Artificial Stone Silicosis: Technical Report

Dr. Rosenfeld’s Analysis of Occupational Exposure to Respirable Crystalline Silica from Cutting, Grinding, Polishing, Transporting, and Installing Artificial Stone Countertops

Date: July 20, 2026

Prepared By:

Paul Rosenfeld Ph.D.

RoseyFields LLC

1317 12th Street,

Santa Monica, California 90405

1. Artificial Stone Silicosis, Nanoparticles, Exposure Studies and Epidemiology 3

1.1 Engineered Stone Created a New Occupational Disease 3

1.2 Chronology of Artificial Stone–Associated Silicosis (AS Silicosis) 5

1.3 Engineered Stone Is Fundamentally Different Than Natural Stone 6

1.4. Engineered Stone Produces Far More Nanoparticles Than Granite 8

1.5. Why Smaller Particles Are More Hazardous & Biologically Active 12

1.6 Engineered Stone Epidemiological Evidence 15

1.7 Traditional Silica Controls Failed to Protect Engineered Stone Workers 17

1.8 Regulatory Experience Demonstrates That Traditional Controls Were Insufficient 19

1.9 Studies Showing Low-Dose Silica Exposure Causes Silicosis 26

1.10 Demonstrative Application of the Park et al. (2002) Exposure-Response Model 32

1.11 Exposure Activities 34

1.12 Qualifications of Paul E. Rosenfeld, Ph.D. 38

2 State of Knowledge of Engineered Stone 40

2.1 Definition of Silica 40

2.2 Environmental Background Concentrations of Silica 41

2.3 Engineered Stone Silica is Distinct From Environmental Silica 44

2.4 Knowledge of Hazards of Silica in ES Countertop Cutting 51

2.5 Regulatory Agency Guidance and Regulations on Silica 56

2.6 Respirators as a Protective Measure Against Silicosis 66

3 Silica Toxicology, Disease Mechanisms, and Medical Effects 72

4 Engineered Stone as a Distinctly High-Risk Product 75

4.1 Silica Content of Natural and Engineered Stone Countertops 75

4.2 Engineered Stone Is Not Natural Stone 77

4.3 Additional Dangers from Engineered Stone 83

4.3.1 Respiratory Protection Against Ultrafine Particles 90

4.3.2. Silicosis Outbreaks from Engineered Stone 94

4.4 Australia’s Engineered Stone Ban 99

4.5 Cal/OSHA’s Engineered Stone Ban 103

5 Industrial Hygiene and Exposure Science 108

5.1 Task-Based Exposure Studies 109

5.2 8-hr TWA Studies 127

6 Epidemiology and Dose-Response Evidence 139

6.1 Silicosis 140

6.1.1 Radiological Measurements of Silicosis 140

6.1.2 Low Dose Exposure Studies 142

6.1.3 Odds Ratio Studies 147

6.1.4 Relative Risk Studies 148

6.1.5 Hazard and Rate Ratio Studies 149

6.1.6 Other Epidemiological Studies 150

6.1.7 Epidemiological Studies (NMRD and Pneumonociosis) 152

6.1.8 Risk Level Studies 153

6.1.9 Linear Dose-Response Relationship Studies 158

6.1.10 Summary Table of Epidemiological Studies 161

6.2 OSHA’s Silicosis Epidemiological Study Comparison 164

6.3 Lung Cancer 165

6.4 COPD 167

6.5 Quantitative Risk Assessments for Silica-Related Diseases 170

7.6 Toxicology of Respirable Crystalline Silica 176

7 Feasible Safer Alternatives and Controls 180

7.1 Substitutions for Engineered Stone 181

7.2 Silica Dust Mitigation Measures and Engineering Controls 184

7.2.1 Wetting 185

7.3 Local Exhaust Ventilation and Dust Collection Systems 187

7.4 Personal Protective Equipment 188

7.4.1 Scientific Peer-reviewed Literature on Lack of Fit-testing 191

7.4.2 Scientific Peer-reviewed Literature on Nano Particle Penetration of Respirators 193

8 Standard of Care and Negligence Analysis 193

8.1 Employer Compliance 193

8.1.1 Engineered Stone Manufacturers 194

8.1.2 Makita Angle Grinder Engineering Controls 206

9 Exposure Matrices 208

9.1 Methodology 208

9.5 Demonstrative Nanoparticle Calculation 213

10 Findings And Opinions 215

1. Artificial Stone Silicosis, Nanoparticles, Exposure Studies and Epidemiology

This report demonstrates that engineered stone presents a fundamentally different occupational hazard than natural stone. Engineered stone typically contains more than 90% crystalline silica, generates substantially higher airborne silica concentrations during fabrication, produces far greater numbers of ultrafine and nanoparticle-sized dust particles, and possesses surface characteristics that increase its biological activity. These differences have resulted in a worldwide epidemic of rapidly progressive silicosis among engineered stone workers.

In 2026, the American Thoracic Society (ATS) formally recognized Artificial Stone–Associated Silicosis (AS Silicosis) as a distinct occupational disease characterized by shorter latency, more rapid progression, greater severity, and higher mortality than traditional silicosis. The ATS further concluded that conventional engineering controls—including wet methods, local exhaust ventilation, and respiratory protection—have not consistently protected workers and identified elimination or substitution of engineered stone as the most effective preventive measure.

My dose reconstruction demonstrates that Mr. Gonzalez Sanchez’s cumulative silica exposure greatly exceeded doses associated with increased disease risk in published epidemiological studies. Even under conservative assumptions assuming continuous wet cutting, grinding, and polishing, his estimated cumulative exposure remained well above levels associated with significantly increased risks of silicosis.

The opinions presented in this report are based upon peer-reviewed scientific literature, regulatory findings, industrial hygiene measurements, epidemiological evidence, and quantitative dose reconstruction discussed throughout this report.

1.1 Engineered Stone Created a New Occupational Disease

For decades, respirable crystalline silica was considered a well-characterized occupational hazard. OSHA responded to decades of epidemiological evidence by lowering the permissible exposure limit (PEL) in 2016 to 50 µg/m³ and requiring engineering controls, exposure monitoring, medical surveillance, respiratory protection, and wet-cutting methods to reduce worker exposure. OSHA nevertheless concluded that measurable lifetime risks of silicosis and lung cancer would remain even at the revised exposure limit.

Shortly after engineered stone became widely used, physicians around the world began identifying an unexpected pattern of disease among countertop fabrication workers. Unlike traditional silicosis, affected workers frequently developed severe disease after relatively short exposure durations, often at young ages, with rapid progression to progressive massive fibrosis and, in many cases, lung transplantation or death.

After reviewing the worldwide scientific evidence, the American Thoracic Society concluded that this represents a distinct occupational disease now known as Artificial Stone–Associated Silicosis (AS Silicosis).

One of the most striking epidemiologic differences between traditional occupational silicosis and engineered stone-associated silicosis is the substantially younger age at which disease is diagnosed. Historically, chronic silicosis has primarily been a disease of older workers, typically developing after 20 years or more of exposure. In contrast, engineered stone-associated silicosis is characterized by a markedly shorter latency period, with disease typically diagnosed after only 7 to 19 years of exposure. A recent comprehensive review by Fazio et al. (2025) concluded that engineered stone silicosis represents a distinct occupational disease entity because of its accelerated clinical course, younger age at presentation, and substantially poorer prognosis compared with traditional silicosis. The review further recognized that this form of accelerated silicosis can develop within 2 to 10 years after initial exposure to high levels of silica.

Individual epidemiologic studies support these findings. In California, the largest U.S. case series reported a median age at diagnosis of 45 years among 52 engineered stone workers. Australia’s national surveillance program similarly reported a median age of approximately 42 years among affected workers, while Spanish investigators reported a median age of only 33 years in workers with engineered stone silicosis. These studies collectively demonstrate that workers fabricating engineered stone frequently develop clinically significant silicosis decades earlier than workers exposed to silica in traditional industries, reflecting the exceptionally high respirable crystalline silica exposures generated during cutting, grinding, and polishing of engineered stone materials.

1.2 Chronology of Artificial Stone–Associated Silicosis (AS Silicosis)

Engineered stone countertops, introduced commercially in the late 1980s, unintentionally triggered a worldwide resurgence of silicosis. Unlike natural stone, engineered stone is manufactured from crushed quartz bound with resins and typically contains more than 90% crystalline silica. Cutting, grinding, and polishing these materials generates extremely high concentrations of respirable crystalline silica, resulting in a new form of accelerated silicosis that develops more rapidly and progresses more aggressively than the disease historically observed in miners and foundry workers.

The first major outbreak was identified in Israel, where young countertop fabricators developed end-stage silicosis requiring lung transplantation. Similar outbreaks were soon reported in Spain, where investigators documented rapidly progressive disease that often continued to worsen even after exposure ended, frequently progressing to progressive massive fibrosis (PMF). Australia subsequently reported widespread disease among engineered stone workers, with government screening programs identifying radiographic silicosis in approximately 20–30% of workers.

The epidemic soon spread to the United States. The first documented U.S. case was reported in Texas in 2014, followed by CDC investigations identifying additional cases across multiple states. California became the epicenter of the U.S. outbreak, with surveillance documenting more than 500 engineered stone silicosis cases by early 2026 and reported cases increasing at approximately 88% per year. Additional cases have now been reported in Texas, Washington, Colorado, and other states, while nationwide industrial hygiene studies continue to document excessive respirable crystalline silica exposures and deficiencies in respiratory protection, fit testing, and medical surveillance among countertop fabrication shops.

1.3 Engineered Stone Is Fundamentally Different Than Natural Stone

Although engineered stone resembles natural stone, it is fundamentally a different material with substantially different occupational hazards. Natural stones such as granite and marble are geologic materials formed over millions of years through natural mineralization. In contrast, engineered stone is a manufactured composite consisting primarily of finely crushed quartz bound together with polymer resins and pigments using a process known as vacuum vibrocompression. As a result, engineered stone typically contains more than 90% crystalline silica by weight, compared with less than 10% for marble and approximately 20% to 50% for most granites. This difference alone substantially increases the amount of respirable crystalline silica generated during fabrication.

Thompson and Qi compared the respirable dust generated during grinding of granite and engineered stone. Rather than measuring the composition of the countertop itself, they analyzed the airborne respirable dust that workers actually inhale. The study demonstrated that respirable dust generated from engineered stone contained approximately 57% to 75% crystalline silica, compared with approximately 25% crystalline silica for granite. Thus, for the same amount of airborne dust, fabrication of engineered stone exposes workers to approximately two to three times more crystalline silica than fabrication of granite.

However, engineered stone differs from granite in far more than silica content alone. Because engineered stone is manufactured from finely crushed quartz, cutting and grinding generate substantially greater numbers of respirable and ultrafine particles. Many of these particles are within the nanoparticle size range (<100 nanometers), allowing them to penetrate deeply into the lungs where they deposit within the alveoli.

Research has consistently detected VOC emissions from ES fabrication, which has included known toxins and carcinogens such as styrene and benzene. Studies have suggested that these VOCs are generated during active machining during the breakdown of inhalared resins. Atmospheric sampling during the fabrication of engineered stones, has detected concentrations of phthalic anhydride, styrene, benzene, ethylbenzene, toluene, and acetone. The presence of VOCs raises the potential for synergistic reactions in the lung between carcinogenic VOCs and RCS.

1.4. Engineered Stone Produces Far More Nanoparticles Than Granite

Carrieri et al. (2020) compared airborne particle-number distributions generated during fabrication of engineered stone and granite under identical laboratory conditions. Engineered stone produced a dominant nanoparticle peak centered at approximately 50–70 nanometers, whereas granite generated comparatively few particles within this size range. Because this figure measures particle number rather than particle mass, it demonstrates that fabrication of engineered stone generates a much finer aerosol containing substantially more inhalable particles than fabrication of granite.

Smaller particles are not simply easier to inhale, but they are also more biologically active. As particle diameter decreases, total surface area increases dramatically. Freshly fractured engineered stone particles also expose highly reactive surface chemical groups known as nearly free silanols. Pavan and colleagues demonstrated that these reactive surface groups readily damage cell membranes and initiate inflammatory reactions leading to fibrosis. Consequently, freshly fabricated engineered stone exposes workers not only to more respirable crystalline silica, but also to silica particles with substantially greater biological reactivity.

If I take the approximate mid-point of the engineered stone values and assume a mean value of 0.05 microns and the approximate midpoint of the granite of 0.15 microns, engineered stone would have approximately 27 times more particles than granite.

Ophir et al. (2019) compared respirable dust generated during fabrication of engineered stone and natural stone. As shown in Figure 1-5, engineered stone dust (red dashed line) contained a substantially greater proportion of smaller respirable particles, peaking at approximately 2–3 µm, whereas natural stone dust (blue line) peaked at approximately 4–5 µm. These findings independently demonstrate that fabrication of engineered stone generates a finer respirable aerosol with substantially more particles and greater biologically active surface area than natural stone.

To better understand why engineered stone has produced a worldwide epidemic of accelerated silicosis, Ramkissoon et al. (2022) compared the physical and chemical characteristics of respirable dust generated during fabrication of 12 commercially available engineered stone products with dust generated from natural granite and marble. The investigators analyzed the freshly generated respirable dust using multiple analytical techniques, including scanning electron microscopy (SEM), to examine the size, shape, and surface characteristics of the particles.

The SEM images below provide a direct visual comparison of the respirable dust generated from engineered stone (top) and natural stone (bottom). The engineered stone images reveal a dense collection of numerous tiny fractured particles attached to and surrounding larger particles, whereas the natural stone images are dominated by comparatively larger, smoother particles with far fewer ultrafine fragments. Even without understanding the microscopy, the difference is readily apparent that engineered stone produces a much finer cloud of respirable dust than natural stone.

Although these images are qualitative, they visually reinforce the quantitative findings reported by Ramkissoon et al. and other investigators that fabrication of engineered stone generates substantially more ultrafine particles and nanoparticles than fabrication of natural stone. These smaller particles remain airborne longer, penetrate deeper into the lungs, and provide substantially greater biologically active surface area than larger particles of the same mass, increasing their potential to injure lung tissue.

1.5. Why Smaller Particles Are More Hazardous & Biologically Active

The hazard posed by engineered stone depends not only on the amount of respirable crystalline silica generated, but also on the size of the particles. As particle diameter decreases, the number of particles and their total surface area increase dramatically, even when the total dust mass remains unchanged. Consequently, a cloud of nanoparticles presents a substantially more reactive surface to lung tissue than the same mass of larger particles.

Smaller particles also remain airborne longer, are more readily inhaled, and penetrate deeper into the lungs where they deposit within the alveoli. These characteristics increase the likelihood of prolonged contact with lung tissue and contribute to inflammation and pulmonary fibrosis.

The hazard posed by engineered stone is not limited to the amount of respirable crystalline silica it generates. Cutting, grinding, and polishing continuously fracture quartz crystals, creating millions of freshly broken microscopic surfaces. These freshly fractured surfaces are chemically different from older, weathered quartz because they expose highly reactive chemical groups known as nearly free silanols.

Think of freshly fractured quartz like freshly broken glass. Immediately after the surface is broken, it is chemically “active” and readily reacts with its surroundings. Over time, those fresh surfaces gradually weather and become less reactive. Workers fabricating engineered stone continuously generate and inhale these freshly fractured silica particles while they are at their most biologically active.

In their 2023 study, Pavan et al. demonstrated that crystalline silica particles containing nearly free silanols readily attach to and damage cell membranes, whereas particles lacking these reactive surface groups produce little or no membrane injury. Cell membrane damage is one of the earliest events that initiates inflammation, recruits immune cells, and ultimately leads to pulmonary fibrosis (silicosis). These findings provide a biologically plausible explanation for why freshly fractured engineered stone dust is substantially more hazardous than older, weathered silica dust. Figure 1-10 below is a demonstrative image of a silanol, highlighting characteristics that make them far more damaging to cells.

In that same study, Pavan et al. investigated why some crystalline silica particles are more harmful than others by comparing their ability to damage cells with the chemistry of their particle surfaces. In Panel A, the y-axis (% hemolysis) represents the percentage of red blood cells whose outer membranes were damaged or ruptured after exposure to silica particles, with higher values indicating greater cell injury. The x-axis (surface area dose, cm²/mL) represents the total surface area of silica particles exposed to the cells. Panel B examines the chemistry of the particle surfaces using infrared spectroscopy. The y-axis (Normalized Kubelka-Munk Units) is a relative measure of the strength of the infrared signal from chemical groups on the particle surface, with higher peaks indicating a greater abundance of those surface chemical groups. The x-axis (wavenumber, cm⁻¹) is simply a chemical “fingerprint” that identifies different chemical bonds present on the surface of the silica particles. Panel B’ enlarges the shaded region of Panel B containing highly reactive surface chemical groups known as nearly free silanols.

When the three panels are considered together, they demonstrate that the silica particles causing the greatest cell membrane damage are the same particles that contain these highly reactive surface groups. This finding is particularly important for engineered stone because every cut, grind, and polish creates millions of freshly fractured quartz particles with newly exposed reactive surfaces. Like freshly broken glass, these fresh surfaces are more chemically active than older, weathered silica particles. Because engineered stone workers continuously create and inhale freshly fractured quartz throughout the workday, they are repeatedly exposed to silica at its most reactive state, helping explain the unusually short latency and rapid progression of silicosis observed in engineered stone workers.

Engineered stone also contains approximately 5% to 15% polymer resins and additives that are absent from natural stone. During cutting and polishing, heat and friction can degrade these resins, releasing volatile organic compounds including styrene, benzene, toluene, ethylbenzene, phthalic anhydride, and other hazardous chemicals into the worker’s breathing zone. Thus, engineered stone workers are exposed not only to respirable crystalline silica, but also to a complex mixture of nanoparticles, reactive silica surfaces, volatile organic compounds, and trace metals.

1.6 Engineered Stone Epidemiological Evidence

Engineered stone (ES) is unique to occupational medicine and has only recently become the subject of epidemiological studies. ES first became commercially available in 1986, however it wasn’t until 2010, that scientific literature began reporting an association between ES and silicosis. Since the publication of that initial report, an increasing number of cases have been reported in Spain, Israel, Australia, and the United States. These studies have been markedly consistent, with engineering stone workers consistently developing silicosis after far shorter exposure durations, and experiencing far more rapid disease progression than workers exposed to traditional stone dusts.

The first major ES silicosis study, Kramer et al. (2012), evaluated patients diagnosed with silicosis between 1997 and 2010. The study found 25 young countertop fabricators with end-stage silicosis associated with their work with engineered stone products. Similar outbreaks were soon reported in Spain, with investigators documenting a high incidence of silicosis among young ES workers who had an average exposure time of 14 years. Studies further demonstrated that disease progression often continued after the exposure ceased, with many worker’s diagnoses progressing to progressive massive fibrosis (PMF). Reports from the United States, Australia, China, and other countries further confirmed these findings, with studies consistently finding a pattern of accelerated disease, severe radiographic abnormalities, and disproportionate impacts on young workers. These studies are summarized in Table 1-1 below.

Table 1-1: Epidemiological Studies Showing Evidence of Engineered Stone Toxicity

The most compelling ES silicosis evidence comes from large-scale screening and surveillance programs, most notably from Australia and the United States. Australia screening initiatives identified radiographic evidence of silicosis in approximately 21 to 24% of engineering stone workers. In 2023, a California-based study identified approximately 52 sefer cases of ES silicosis, many of whom were Latino immigrant workers. Three years later, in 2026 that value rose to 531 indicating a tenfold increase in approximately three years. The consistency of these findings across continents, industries, and studies, provides overwhelming evidence that ES exposure produces a uniquely aggressive form of silicosis that substantially differs from other silica dust exposures.

1.7 Traditional Silica Controls Failed to Protect Engineered Stone Workers

For decades, occupational health professionals believed that respirable crystalline silica could be adequately controlled through engineering controls, including wet cutting, local exhaust ventilation, respiratory protection, exposure monitoring, and medical surveillance. Consistent with this understanding, OSHA lowered the permissible exposure limit (PEL) to 50 µg/m³ in 2016 after concluding that the previous standard failed to adequately protect workers.

Figure 1-12 is OSHA’s Final Quantitative Risk Assessment for Lifetime Silica Exposure, published in the Final Rule for Occupational Exposure to Respirable Crystalline Silica in March of 2016. The agency conducted an extensive toxicological, epidemiological and experimental review of available literature on the adverse health effects of occupational exposure to RCS, pooling data from historical cohort studies of highly exposed workers across major sectors like mining, pottery, and diatomaceous earth facilities. Using this information, OSHA developed quantitative estimates of excess risk of mortality and morbidity in comparison to historical and revised PELS, projecting the lifetime health risks of workers exposed to various levels of airborne silica over a standard 45-year working career. Importantly, OSHA acknowledged that measurable risks of silicosis, lung cancer, and other diseases would remain even at the revised PEL, recognizing that the standard would reduce—but not eliminate—worker risk.

As demonstrated in Figure 1-12, even at the updated PEL of 50 µg/m³, across a 45-year working lifetime, OSHA found that the risk of silicosis remained unacceptably high. For silicosis and non-malignant lung disease mortality, studies found that 7 to 44 out of 1,000 workers exposed at the PEL will die from those diseases. For silicosis morbidity, the literature has found that exposure to silica at the PEL is associated with 20 to 170 out of 1,000 workers developing the disease. These levels remain above the OSHA acceptable risk level of 1 per 1,000.

1.8 Regulatory Experience Demonstrates That Traditional Controls Were Insufficient

Australia and California provide two important real-world examples showing that traditional silica controls were not sufficient to stop engineered stone silicosis. Both jurisdictions first attempted to control exposure through stricter workplace rules, including prohibitions on dry cutting, respiratory protection, dust controls, air monitoring, medical surveillance, inspections, and worker training. Despite these measures, disease continued to occur, leading regulators to conclude that engineered stone presented a hazard that could not be reliably controlled through conventional industrial hygiene measures alone.

Australia was the first jurisdiction to reach this conclusion. After engineered stone silicosis cases emerged in 2015, Queensland and Victoria adopted increasingly strict controls beginning in 2018 and 2019, including bans on dry processing and requirements for PPE, exposure monitoring, health surveillance, and dust-control practices. However, inspections revealed continued noncompliance, and dry processing continued to occur. After reviewing the scientific and medical evidence, Australia ultimately concluded that enforcement, licensing, and partial restrictions were insufficient to protect workers. In 2024, Australia banned the manufacture, supply, processing, and installation of engineered stone containing more than 1% crystalline silica.

Figure 1-13 summarizes Australia’s regulatory progression. The figure demonstrates that Australia did not begin with a ban. While regulators first attempted conventional controls, those measures failed to reliably prevent disease and exposure. Australia’s final decision to eliminate engineered stone from the market reflects the conclusion that removal of the hazard was necessary to protect workers.

California’s history with engineered stone follows a similar pattern. California first identified engineered stone silicosis cases in 2019, including fatal cases among workers in their 30s. Cal/OSHA responded with a Special Emphasis Program focused on respirable crystalline silica and respiratory protection compliance. The program found overexposures in approximately two-thirds of inspected workplaces, with repeated failures involving exposure assessment, hazard communication, respiratory protection, and medical surveillance.

In 2023, California physicians and public health officials reported 52 engineered stone silicosis cases, primarily among Spanish-speaking Latino immigrant countertop workers. Many diagnoses were delayed, many workers had already developed progressive massive fibrosis, and nearly one in five of the initially reported workers had died. Cal/OSHA then adopted an Emergency Temporary Standard, later made permanent, requiring stronger respiratory protection, prohibiting dry cutting, and imposing stricter dust-control requirements. In spite of more stringent standards, California surveillance showed that engineered stone silicosis cases continued to increase rapidly, at approximately 88% per year.After careful consideration, in May 2026, Cal/OSHA reached a unanimous decision to initiate the process to prohibit the fabrication and installation of artificial stone products containing more than 1% crystalline silica.

Figure 1-14 shows the year-by-year increase in reported California cases. It demonstrates that the epidemic continued to grow even after regulators recognized the hazard and began imposing stricter requirements.

Figure 1-15 shows the cumulative burden of disease in California. This illustrates the scale and acceleration of the epidemic: engineered stone silicosis was not an isolated cluster, but a rapidly expanding occupational disease outbreak.

These regulatory experiences demonstrate why engineered stone cannot be treated like ordinary natural stone. Australia and California both attempted to address the hazard through conventional silica controls, but the continued rise in disease showed that those controls were not reliably protective. This conclusion is consistent with the NIOSH hierarchy of controls, which recognizes elimination and substitution as the most effective methods of hazard prevention.

Figure 1-16 explains the basic industrial hygiene principle underlying these regulatory decisions: when a severe hazard cannot be reliably controlled by ventilation, work practices, respirators, and enforcement, the most protective solution is to eliminate or substitute the hazard. Applied to engineered stone, this means that the most effective way to prevent disease is to remove or replace high-silica engineered stone rather than relying solely on worker-level controls.

Even when engineering controls and respiratory protection are implemented, practical and scientific limitations reduce their effectiveness. Respirators require medical clearance, fit testing, proper maintenance, and consistent worker compliance, all of which are difficult to achieve in many countertop fabrication shops. Wet-cutting methods and powered air-purifying respirators (PAPRs) may also interfere with visibility, communication, and mobility, creating incentives for workers to modify or remove protective equipment during fabrication.

Table 1-2.1 summarizes published studies demonstrating that fabrication of engineered stone consistently generates extremely small respirable particles, including nanoparticles as small as 20–40 nanometers. These findings are visually reinforced by the SEM images below, which illustrate that engineered stone produces a much finer cloud of respirable dust than natural stone.

Table ES-2.1 Summary of Nanoparticle Literature

Table 1-2.2 summarizes laboratory studies demonstrating that the most penetrating particle size for N95 respirators is approximately 30–50 nanometers—essentially the same particle-size range generated during engineered stone fabrication.

Table 1-2.2 Summary of Respirator Particle Penetration Literature

Even when controls are present, practical limitations can also reduce their effectiveness. Respirators require medical clearance, fit-testing, and strict worker compliance which may not be maintained within many of these fabrication shops. Wet-cutting and powered air-purifying respirators may also interfere with visibility and communication within shops, which may create safety hazards or reasons for workers to remove protections. The Table ES-3 below summarizes scientific literature on the inadequacies of non fit-tested respirators for ES.

Table 1-3 Summary of Scientific Literature of Nanoparticle Penetration of Non Fit-tested N95 Filtering Facepiece Respirators (FFRs)

Collectively, these studies demonstrate a critical relationship: engineered stone generates nanoparticles that fall within the particle-size range that is most difficult for N95 respirators to capture. Consequently, although respirators and engineering controls can substantially reduce worker exposure, they cannot completely eliminate exposure to the smallest and most biologically reactive engineered stone particles.

In addition, respirable dust settles throughout fabrication shops and is repeatedly resuspended during routine activities such as sweeping, material handling, and worker movement, extending exposures well beyond active cutting and grinding. Similar limitations occur during countertop installation, where wet methods and local exhaust ventilation are often impractical inside finished homes and commercial buildings. For these reasons, regulators in Australia and California ultimately concluded that while engineering controls and respiratory protection reduce risk, they cannot reliably eliminate the hazards associated with engineered stone. Consistent with the NIOSH Hierarchy of Controls, elimination or substitution of the hazard provides the highest level of worker protection.

1.9 Studies Showing Low-Dose Silica Exposure Causes Silicosis

Kreiss and Zhen (1996) conducted one of the landmark epidemiological studies of respirable crystalline silica exposure by evaluating former and current hard-rock miners who had been followed for more than three decades. Unlike many earlier occupational studies that evaluated only active workers, the investigators included retired workers and reconstructed each worker’s lifetime silica exposure using historical industrial hygiene measurements, allowing them to evaluate the long-term health effects of cumulative silica exposure. Figure 1-17 below groups workers according to their average airborne respirable crystalline silica exposure and shows the percentage of workers in each group who developed radiographic silicosis. Figure 1-17 demonstrates a clear exposure-response relationship: workers exposed to average silica concentrations as low as 0.025–0.05 mg/m³, well below historical occupational exposure limits, still developed silicosis, and disease prevalence increased steadily with increasing exposure. This study demonstrates that reducing silica exposure lowers risk but does not eliminate it and provides strong evidence that there is no practical safe average exposure level below which silicosis cannot occur.

Kreiss and Zhen (1996) also evaluated workers based on their lifetime cumulative respirable crystalline silica exposure, the exposure metric most commonly used by occupational epidemiologists. Figure 1-18 below groups workers according to their cumulative silica dose and shows the percentage of workers who developed radiographic silicosis within each exposure category. Approximately 12% of workers whose cumulative exposure was less than 1 mg/m³-year developed silicosis, with disease prevalence increasing progressively as cumulative exposure increased. Figure 1-18 demonstrates that silicosis is fundamentally a cumulative-dose disease and that measurable lung injury occurs even at relatively low cumulative silica exposures. This concept provides the scientific basis for comparing Mr. Gonzalez Sanchez’s reconstructed cumulative exposure with the published epidemiological literature.

Steenland and Brown (1995) evaluated 3,330 underground gold miners who were followed for an average of 37 years to determine whether cumulative silica exposure predicted silicosis. Using detailed work histories and historical industrial hygiene measurements, the investigators reconstructed each worker’s lifetime cumulative silica exposure and compared it with radiographic evidence of silicosis. Figure 1-19 below summarizes their findings by cumulative exposure category. Importantly, silicosis was observed even among workers in the lowest lifetime exposure group (0–0.2 mg/m³-years), and both the number of cases and disease rate increased steadily with increasing cumulative exposure. The authors concluded that “in no cumulative exposure category is there no silicosis.” This study independently confirms that cumulative silica exposure is the principal determinant of silicosis risk and that no practical cumulative exposure threshold was identified.

Chen et al. (2001) conducted one of the largest quantitative epidemiological investigations of silicosis ever published, following 3,010 Chinese tin miners, including 1,015 confirmed cases of radiographic silicosis, over several decades. The investigators reconstructed each worker’s cumulative respirable crystalline silica exposure using detailed employment histories and historical industrial hygiene measurements, allowing them to directly compare cumulative exposure with silicosis risk. Figure 1-20 below demonstrates a continuous increase in disease prevalence as cumulative silica exposure increased. The study is particularly important because of its large sample size, long follow-up period, and detailed quantitative exposure assessment. Its findings closely mirror those reported in mining populations throughout North America and Europe, demonstrating that cumulative silica exposure consistently predicts silicosis regardless of worker population or geographic location.

Howlett et al. (2024) conducted one of the most comprehensive reviews of the silica epidemiology literature to date. Rather than studying a single workforce, the investigators systematically reviewed more than 1,200 scientific publications and identified eight high-quality epidemiological studies representing ten independent worker cohorts from mining, foundries, pottery manufacturing, and other silica-exposed industries. The left side of Figure 1-21 below compares the actual exposure-response relationships reported by each individual study, while the right side presents smoothed exposure-response curves to facilitate comparison among worker populations. Although the studies involved different industries, countries, and exposure conditions, every investigation demonstrated the same fundamental finding: the risk of silicosis increased progressively with cumulative respirable crystalline silica exposure, and no practical cumulative exposure threshold was identified. The remarkable agreement among independent investigators provides compelling evidence that cumulative silica exposure is the primary determinant of silicosis risk.

1.10 Demonstrative Application of the Park et al. (2002) Exposure-Response Model

Park et al. (2002) conducted one of the most comprehensive quantitative risk assessments of occupational respirable crystalline silica exposure and silicosis published in the peer-reviewed scientific literature. The study is a foundational risk assessment that has consistently been cited by reputable institutions including OSHA in their 2016 evaluation of occupational exposures to Silica. Furthermore, based on Web of Science, Park et al. (2002) has been cited 9 times by NIOSH and the CDC, six times by 3 times by IARC, 3 times by the World Health Organization (WHO), and once by the National Institutes of Health, among the 73 citations.

Park et al. (2002) reconstructed cumulative respirable crystalline silica exposures for more than 2,300 diatomaceous earth workers using historical industrial hygiene measurements and detailed employment histories. They evaluated multiple competing exposure-response models to determine which best described the observed epidemiologic data. After comparing several statistical models, the investigators concluded that a linear relative-rate model provided the most appropriate description of the relationship between cumulative respirable crystalline silica exposure and radiographic silicosis when the analysis was restricted to cumulative exposures below 10 mg/m³-years, where the exposure-response relationship was most reliable. They therefore used this linear model as the basis for estimating excess lifetime silicosis risk. This methodology was subjected to peer review and published in Occupational and Environmental Medicine.

Table 1 4: Demonstrative Exhibit Showing Silicosis Morbidity After 45 Years and 1 Year At Various Exposure Concentrations.

The demonstrative table above does not constitute a new epidemiologic study, independent risk assessment, or novel statistical analysis. Rather, it is a transparent mathematical application of the published exposure-response model selected by Park et al. (2002) using the same cumulative exposure principles employed throughout the occupational silica epidemiology literature. Cumulative respirable crystalline silica exposure is calculated using the well-established exposure assessment equation:

Cumulative Exposure = Average Respirable Crystalline Silica Concentration × (Duration of Exposure/2000 Hour)

This cumulative exposure metric has been used for decades by occupational epidemiologists, industrial hygienists, NIOSH, OSHA, and numerous peer-reviewed investigations evaluating silica-related disease. The calculations presented in the table rely on these universally accepted principles of exposure assessment and simply illustrate how the published Park et al. (2002) model applies to occupational exposure scenarios of varying airborne silica concentrations.

The second column illustrates the estimated excess lifetime risk of radiographic silicosis associated with a single occupational year of exposure at each average respirable crystalline silica concentration by proportionally applying the published linear exposure-response relationship selected by Park et al. (2002). For example, an average occupational exposure of 1 µg/m³ corresponds to an estimated excess lifetime risk of approximately 36 excess radiographic silicosis cases per one million exposed workers following one occupational year of exposure. The third column presents the corresponding 45-year lifetime risk estimates reported by Park et al. for continuous occupational exposure at the same average concentration. As average airborne silica concentration increases, the estimated excess lifetime risk increases in a nearly proportional manner, consistent with the linear exposure-response model selected by the authors.

The purpose of this demonstrative is illustrative rather than predictive. It is not offered to establish that any particular worker will develop silicosis after one year of exposure, nor does it create a new epidemiologic opinion. Instead, it provides the Court with a simplified application of the published Park et al. (2002) model so that cumulative occupational exposures can be understood using familiar exposure assessment principles. The demonstrative merely translates the peer-reviewed exposure-response relationship into occupational scenarios that are easier for the trier of fact to understand.

The methodology underlying this demonstrative is based entirely upon generally accepted principles of occupational exposure assessment, including the use of cumulative exposure as the relevant dose metric and the application of a peer-reviewed linear exposure-response model selected by the original investigators. The calculations are transparent, reproducible, independently verifiable, and rely solely upon published scientific methods rather than any new statistical modeling or subjective assumptions. Accordingly, this demonstrative is intended solely as an aid to explain the scientific concepts described in Park et al. (2002) and does not alter, expand, or replace the conclusions reported by the original authors. It is a mathematical illustration derived from a published, peer-reviewed exposure-response model using accepted industrial hygiene and epidemiologic principles.

1.11 Exposure Activities

For demonstrative purposes, the mean silica exposure concentrations from wet activities are plotted and compared to background silica concentrations in Figures 1-22 and 1-23 below. Even when wet processes are used, airborne silica concentrations during processing of engineered stone often exceed Permissible Exposure Limits.

I performed a demonstrative particle-count calculation using 1 µg/m3 of respirable crystalline silica. It is a demonstrative calculation and is not intended to estimate the exact number of particles inhaled since engineered stone dust consists of a broad distribution of particle sizes rather than particles of a single diameter. Instead, it illustrates a fundamental principle of aerosol science: even a very small inhaled mass of respirable crystalline silica represents an extraordinarily large number of biologically active particles.

Assuming spherical crystalline silica particles with a density of 2.65 g/cm³, Figure ES-24 below demonstrates the approximate number of nanoparticles in 1 µg/m3 of respirable crystalline silica. This nanoparticle mass corresponds to approximately 1.1 × 10¹⁰ individual particles at a particle diameter of 40 nanometers, 5.8 × 10⁹ particles at 50 nanometers, 3.3 × 10⁹ particles at 60 nanometers, and 7.2 × 10⁸ particles at 100 nanometers.

This demonstrative calculation is consistent with multiple independent lines of scientific evidence discussed throughout this report. Carrieri et al. (2020) demonstrated that fabrication of engineered stone produces a dominant particle-number distribution centered at approximately 50–70 nanometers, whereas granite generated comparatively few particles within this size range. Ophir et al. (2019) and Ramkissoon et al. (2022) independently showed that engineered stone produces a substantially finer respirable aerosol than natural stone, resulting in greater numbers of ultrafine particles capable of remaining airborne longer and penetrating more deeply into the distal lung. Together, these studies demonstrate that workers fabricating engineered stone are exposed to substantially greater numbers of respirable and nanoparticle-sized silica particles than workers fabricating granite.

The importance of these particles extends beyond particle number alone. As particle diameter decreases, the number of particles and the total available surface area per unit mass increase dramatically, providing substantially more surface for interaction with lung tissue. In addition, in their 2023 paper, Pavan et al. demonstrated that freshly fractured quartz generated during cutting and grinding exposes nearly free silanols, highly reactive surface chemical groups that readily damage cell membranes and initiate inflammatory and fibrotic responses. These freshly fractured surfaces are considerably more biologically reactive than weathered silica particles and provide a biologically plausible explanation for the unusually rapid onset, accelerated progression, and increased severity of artificial stone-associated silicosis reported worldwide.

1.12 Qualifications of Paul E. Rosenfeld, Ph.D.

My name is Paul Rosenfeld, Ph.D and I prepared this report. I am the founder and principal at the environmental consulting firm of RoseyFields, located at 1317 12th Street, Suite 7, in Santa Monica, California 90401. I have practiced as an environmental risk and exposure assessor for over 25 years and have specific knowledge and experience that qualifies

I received a B.A. in Environmental Studies from the University of California, Santa Barbara in 1991, an M.S. in Environmental Science from the University of California, Berkeley in 1995, and a Ph.D. in Soil Chemistry from the University of Washington in 1999. In addition to my education, I have extensive experience in evaluating the fate and transport of environmental contaminants, risk and exposure assessment of contaminants released from pollution sources, historical dose reconstruction, and monitoring and modeling of pollution sources that may cause impacts on human health. I am presently a principal environmental scientist and risk assessor at Roseyfields LLC, which I founded in 2025.

I obtained much of my experience in evaluating contaminated sites while working for the United States Navy, where I served as a Remedial Project Manager for the Navy Base Realignment and Closure (“BRAC”) Team, South West Division on Treasure Island, California. While working for BRAC, I managed many sites with environmental contamination concerns and oversaw remediation activities. While working for BRAC I managed the remediation of asbestos contaminated pipes and soils underneath structures with friable asbestos on Treasure Island. I managed the testing of the soils and the cleanup activities. This experience encompassed a considerable amount of work including on-site investigations, air monitoring, and remedial actions. I have previously taught courses on the subject of environmental health at the University of California, Los Angeles (“UCLA”), presented at professional environmental conferences on various subjects involving environmental contamination and remediation, and have published scientific studies of contaminant fate and transport of odorous chemicals. I have also co-authored several books concerning environmental contamination and best practices in the chemical industry. These publications include The Risks of Hazardous Waste (2011), Handbook of Pollution Prevention and Cleaner Production: Best Practices in the Agrochemical Industry (2011), Handbook of Pollution Prevention and Cleaner Production: Best Practices in the Wood and Paper Industries (2010), and Handbook of Pollution Prevention and Cleaner Production, Best Practices in The Petroleum Industry (2009).

I have 25 years of experience conducting quantitative exposure assessments and chemical dose reconstruction. I have published several papers involving dose reconstruction including “Cancer Risk and Diesel Exhaust Exposure Among Railroad Workers” and “Camp Lejeune Marine Cancer Risk Assessment for Exposure to Contaminated Drinking Water From 1955 to 1987.” Because of my strong air sampling and analytical skills, I take on very challenging exposure assessment projects, for instance my firm was hired by the Missouri Department of Natural Resources to evaluate hundreds of chemicals emitted from a radioactive landfill that was experiencing an exothermic reaction similar to a fire.

I have been trained to be a Hazwopper by Industrial Hygienists and I utilize many industrial hygiene principles in my practice. I co-authored a book entitled The Risks of Hazardous Waste (2011) which addresses several issues relating to asbestos and other hazardous substances. I have been fit tested for a respirator, know how to don and doff hazardous waste personal protective equipment, have tested toxic air to ensure the safety of remediation staff, set up zones of exclusion, and have tested for hundreds of different chemicals using a variety of industrial hygiene testing methods.

I have participated in measuring asbestos levels in building materials and air. While working for Navy BRAC, I oversaw the remediation of friable fibers coating hot water heating pipes underneath old military structures. I have modeled asbestos emissions from serpentine soils in road dust in California, and calculated the exposure to nearby residents and school children. While getting my doctorate in Soil Chemistry at the University of Washington, I took courses on mineralogy, soil formation, and electron microscopy which directly relate to information presented in this report.

I use my education, expertise, and knowledge to conduct investigations and prepare exposure and risk assessments. I have performed numerous investigations, monitoring projects, and assessments for governmental and private entities concerning risks to human health and the environment due to contamination from asbestos, diesel particulate matter, formaldehyde, odorous chemicals, pesticides, polychlorinated biphenyls, petroleum hydrocarbons, polycyclic aromatic hydrocarbons, dioxins/furans, volatile organic compounds, perchlorate, heavy metals, perfluorochemicals, mold, bacteria, and other contaminants. I have conducted numerous risk assessments over a period of more than twenty years specifically relating to air contaminants and have testified at deposition and/or at trial as an expert witness on numerous cases involving environmental contamination, exposure, and human health risk.

I have an expertise in epidemiology and regularly incorporate the results of epidemiological studies into my practice. I co-authored an epidemiological paper entitled “Hospital, Health and Community Burden After Oil Refinery Fires, Richmond, California, 2007 to 2017.” which evaluated the increased hospitals after a large fire in Richmond California. In addition, I have utilized epidemiological analysis in many of his peer reviewed publications. I have been lead author and co-author of the following peer reviewed publications that incorporate epidemiological studies in the analysis including “Camp Lejeune Marine Cancer Risk Assessment for Exposure to Contaminated Drinking Water from 1955 to 1987”, “Cancer Risk and Diesel Exhaust Exposure Among Railroad Workers” and “Perfluoroalkyl substances exposure in firefighters: Sources and implications” Moreover, I taught medical doctors and nurses epidemiological practices focusing on cancer clusters while serving as an Adjunct Professor and Lecturer at UCLA’s School of Public Health.

I have prepared hundreds of reports on exposure to compounds and chemicals including: asbestos, AFFF, benzene, silica, diesel particulate matter, silica, carbon monoxide, chlorinated solvents such as TCE, pesticides, cigarette smoke, PCBs, dioxins, PAHs, and mold. I use a variety of methods to calculate the dose to impacted individuals including EPA, NIOSH, and OSHA methodology.

2 State of Knowledge of Engineered Stone

2.1 Definition of Silica

Silica, or silicon dioxide (SiO₂), is a colorless, white chemical compound composed of natural elements from the earth’s crust. It occurs in crystalline and amorphous forms in natural rock and synthetic materials. The three most common forms of crystalline silica are quartz, tridymite, and cristobalite, which occur naturally in rocks and soil. Cristobalite is the most biologically active form of crystalline silica, followed by tridymite and then quartz. Sub-classifications of crystalline silica based on temperature phase include a-quartz, b-quartz, a-tridymite, B-tridymite, a-cristobalite, B-cristobalite. A-quartz is the thermodynamically stable form of crystalline silica in ambient conditions and is the most abundant form of crystalline silica. As a result, “quartz” is often used in place of the term “crystalline silica.”

2.2 Environmental Background Concentrations of Silica

Low concentrations of silica are commonplace in the natural environment because silica is a significant component of the Earth’s crust. Environmental concentrations of respirable crystalline silica (RCS) are predominantly influenced by natural processes such as soil erosion, wind transport of dust, and volcanic activity, with nearly 100% of the mass of free silica in the ambient air coming from geologic sources. In addition, anthropogenic activities, like mining, construction, and agricultural operations contribute to environmental background silica. Despite the ubiquity of potential RCS-generating processes, environmental background silica concentrations remain low.

According to Davis et al.’s 1984 study, in urban regions, the annual average of PM2.5 and PM10 silica concentrations ranged from 0 to 1.9 µg/ and 0.9 to 8 µg/ respectively. These results were corroborated by the USEPA in 1996, which found an average ambient PM10 silica concentration of 1.9 µg/m³ in urban regions, generally ranging from 0.3 to 5 µg/. Even in dust-prone regions of the United States, the USEPA noted that background silica concentrations were unlikely to exceed 8 μg/m³ on average. Ambient average concentrations of silica in 22 cities in the United States are demonstrated in the following table:

Table 2.1: Average Coarse and Fine Quartz Concentrations in Cities in the United States

Even near RCS-generating industrial facilities, ambient environmental concentrations of silica remain low. Studies in Wisconsin near frac sand mining facilities reported localized background RCS levels ranging from 0.2 µg/m³ to 1.73 µg/m³. In their 2020 report, the Texas Department on Environmental Quality found that RCS concentrations around APOs (Aggregate Production Operations), which are industrial facilities where crushed stone and sand are extracted and processed for construction or pavement, ranged from 0 to 2.8 5 µg/, with many samples below the limit of detection.

Critically, environmental background silica concentrations also predominantly consist of coarser particles. As demonstrated in Table 2.1, the average concentrations of fine quartz were much lower than coarse quartz and close to or below the limit of detection for many of the sampled cities. The USEPA, in their 1996 report, concluded that there was “less silica in the PM2.5 fraction” in the background environmental silica when compared to occupational silica samples. Because these ambient environmental silica particles are coarser than the ones encountered in occupational settings, they are unable to penetrate deep into the lung tissue. Therefore, the ATSDR / USEPA does not believe that ambient exposures to silica will cause individuals to develop silicosis, noting that they have not observed adverse effects from “incidental exposure to low levels of c-silica in the environment (e.g. at beaches) or from exposure particles that exceed the respirable size range.”

In contrast, when manipulating engineered stone in indoor environments, respirable crystalline exposures can be thousands of times higher, making ambient environmental silica a negligible contributor to silicosis. Additionally, because occupational silica has a greater fraction of particles being in the respirable to nano-particle range, particularly when fabricating engineered stone, comparisons between concentrations of RCS in the ambient environment and concentrations of RCS in occupational settings are not always appropriate.

2.3 Engineered Stone Silica is Distinct From Environmental Silica

While ambient levels of crystalline silica exist in the natural environment, engineered stone silica poses a fundamentally distinct hazard to workers due to unique characteristics that pose specific biological hazards.

Ambient levels of crystalline silica, as previously mentioned in Section 2.2, are found at low concentrations, generally ranging between 0 to 1.9 µg/ and 0.9 to 8 µg/ for PM2.5 and PM10 respectively. Fabrication of engineered stone countertop products, on the other hand, creates drastically higher levels of dust exposure during the cutting, grinding, and polishing of ES. These concentrations are explained in detail in Section 6. Table 3.2. and Table 3.3 below compare background levels of silica with data from ES exposure studies.

Beyond large disparities in exposure concentrations, the lethality of ES is not strictly limited to the sheer amount of silica dust released during ES activities. As described in Section 3.2, most concentrations of environmental silica are primarily coarser dusts that are far too massive to be deeply inhaled into the respiratory tract. Even when environmental silica is released into air, concentrations remain minimal, as the ATSDR reports that no adverse effects have been associated with incidental oral exposures to environmental silica.

These particles are compositionally different from ambient airborne silica particles, which creates unique hazards when inhaled. During ES activities, quartz becomes fractured, creating nearly free silanols (NFS), a chemical group that provides unique toxic effects to the body. More specifically, studies have found that fractured synthetic quartz is associated with damage to cellular membranes, triggering inflammatory processes within the body. This is described in further detail in Sections 4 and 5. The images below demonstrate the compositional disparities between engineered stone dust and environmental silica dust.

Figure 2.1 provides Scanning Electron Microscope (SEM) images of repairable dusts from machined engineered stones. Scientific literature has noted that engineered stone dust particles observe more irregular shapes, sharp edges, and fractures along the surface than dust particles from natural stone.

Figure 2.2 provides a comparison of four sizes of crystalline silica particles purchased directly from a nanomaterials facility. The crystalline silica particles were subsequently sorted into distinct size ranges, including coarse, respirable, submicron, and ultrafine as summarized in the table below.

Figure 2.2 compares the particle sizes accordingly by taking four images of the different particle sizes at the same magnification. This allows for direct comparison between coarse silica particles, respirable silica particles, and ultrafine or nanoparticles. As previously discussed in Section 3.2, environmental silica is typically coarse, with a fraction of dusts in the respirable range. This is demonstrated in images C (Respirable) and D (Coarse) in Figure 2.2. Silica dust derived from ES manufacturing activities can be found in the ultrafine, submicron, and respirable sizes, represented in images A (Ultrafine), B (Submicron) and C (Respirable) in Figure 2.2. Since these particles are all derived from synthetic manufacturing, it allows for a demonstrative comparison between crystalline silica particle sizes in the environment and crystalline silica particle sizes derived from ES work but is not directly reflective of the exact nature of environmental crystalline particles.

Additional studies have found that fabricating engineered stone products produces disproportionately more nanoparticles. In 2020, Carrieri et al. investigated respirable crystalline dust production when cutting and grinding engineered and natural stones. As demonstrated in Figure 3.3, the main peak in particle number concentration occurred in the nanoparticle range (0.01 to 0.1 µm) for materials A and B, which were high-silica engineered stones. In contrast, the peak in particle diameter for granite occurred between 0.1 to 1 µm, outside of the nanoparticle range. Ophir et al., in their 2019 study, found similar results when evaluating nanoparticle production from engineered stone and the distribution of respirable crystalline silica particle sizes in engineered stone-exposed subjects’ lungs. Sputum samples from the exposed group had a significantly greater proportion of nanoparticles, with 12% of particles in the nanoparticle range compared to 1% in the non-exposed controls. When the study examined the particle distribution of engineered stone dust, 15% of the sample was found to be nanoparticle-sized and the particle size distribution peaked earlier than natural stone dust, indicating that engineered stone produced smaller particles.

In 2025, DeVaughn et al. conducted a field investigation monitoring Chicago-area fabricators’ exposure to dust when performing wet cutting with small hand tools. Shop A fabricated 90% engineered stone while shop B fabricated 65%. Overall, the study found that between 90.3 to 98.7% of the dust emitted were under 2.5 µm, and 62.4 to 91.6% of all particles were “very fine ultrafine particles” with a size under 1 µm. As demonstrated in Figure 2.4, across both shops and both visits, the peak in particle size was in the smallest category <0.3 µm, with up to almost 40% of the particles in that range, indicative of potentially large nanoparticle production.

In 2016, Pavan et al. examined artificial stone dust supplied by stone manufacturers, consisting of material that was dry cut using a grinder or wet cut using a circular saw. The study found that 90% of the particles were <4 µm, with dry cutting producing slightly finer particles than wet cutting. Figure 3.5 provides a comparison between particle sizes and shapes between engineered stone processed using wet (A, B, E, F) and dry (C, D, G, H) cutting methods.

Ultimately, environmental silica dust is profoundly different to silica dust generated through engineered stone activities. Beyond simply the volume of dust generated from ES activities, the particles themselves are drastically smaller in size and possess a far higher inhalation hazard.

2.4 Knowledge of Hazards of Silica in ES Countertop Cutting

When a worker performs tasks that cut, break, grind, abrade, or drill stone countertops, respirable silica dust arises. Respirable crystalline silica (“RCS”) refers to the portion of airborne crystalline silica dust capable of entering gas-exchange regions of the lungs if inhaled. These particles have diameters smaller than 10 micrometers.

Silicosis is an irreversible respiratory disease caused by inhaling RCS dust, and is often progressive and potentially fatal. Silicosis causes permanent lung damage, as silica dust particles become trapped in lung tissue and reduces the lungs ability to consume oxygen, often resulting in shortness of breath, cough, and fatigue. Exposure to airborne crystalline silica increases the risk of lung cancer, chronic obstructive pulmonary disease, and kidney disease. In some cases, silicosis has been associated with tuberculosis.

Between 1987 and 1989, the first engineered stone manufacturing plants for the fabrication of stone countertops were being built in Israel and Spain. These manufacturing plants followed Bretonstone’s initial development of engineered stone in the 1960’s and successful efforts in inventing a vibrocompression fabrication method that had allowed for the creation of engineered stone countertops in 1975.

In 1997, Simcox et. al performed work site studies at several granite countertop businesses in the state of Washington to assess silicosis exposure, stating that:

“The health consequences have been known for years for workers in mining and manufacturing. It has been known for over 80 years that fabrication of granite produces silicosis.”

The 1999 report on these surveys stated several countertop businesses still used dry cutting processes and that every work site had at least one personal exposure greater than Washington’s personal exposure limit (PEL) of 0.1 mg/m³. Work sites that used dry processes routinely had exposures over 1 mg/m³, the 1999 OSHA PEL. Many of the measurements for wet processes were above 0.5 mg/m³, the NIOSH recommended exposure limit (REL). The study concluded that granite countertop fabricators were at risk of silicosis, and recommended wet processes and ventilation techniques that would reduce silica exposures to as low a level as possible.

In 2002, NIOSH published a hazard review about the health effects of occupation exposure to RCS, describing the various types of silicosis a worker may develop:

“A worker may develop one of three types of silicosis, depending on the airborne concentration of respirable crystalline silica: (1) chronic silicosis, which usually occurs after 10 or more years of exposure at relatively low concentrations; (2) accelerated silicosis, which develops 5 to 10 years after the first exposure; or (3) acute silicosis, which develops after exposure to high concentrations of respirable crystalline silica and results in symptoms within a period ranging from a few weeks to 5 years after the initial exposure [NIOSH 1996b; Parker and Wagner 1998; Ziskind et al. 1976; Peters 1986].”

The report identified masonry, stonework, tile setting and plastering as one of the top nonmining industries with the largest number of workers exposed to respirable crystalline silica during 1986.

In 2008, OSHA identified the Cut Stone and Stone Product Manufacturing Industry as an industry with potential overexposure to crystalline silica exposure in the National Emphasis Program on Crystalline Silica.

In 2011, Mao et al. published a report regarding lung transplantation for end-stage silicosis. The study examined outcomes in five consecutive cases of end-stage silicosis in individuals aged 25 to 56. All patients were miners with 2 to 5 years of exposure to silica-containing dust. Of these, four received single lung transplants, and one underwent a bilateral lung transplant. Two patients passed away—one two days after the transplant and another from sepsis seven months post-transplant. The remaining three survivors are alive at 5, 3, and 2 years post-transplant. The authors described silicosis as follows:

“This disease slowly and relentlessly leads to end stage lung disease several decades after inhalation of silica containing fine particles. Unfortunately, there is no treatment for end-stage silicosis once the patient’s condition deteriorates. Lung transplant may be lifesaving treatment.”

In 2012, Kramer et al. systematically assessed a silicosis outbreak among patients, referring to silicosis as “preventable through appropriate workplace practices.” Researchers reported an outbreak of end-stage silicosis caused by dry cutting engineered countertop applications, stating:

“We found that all 25 patients shared an exposure history of working with the same commercial brand of decorative, synthetic stone material, performing a similar work task of dry cutting the stone for end use in construction, predominantly for kitchens and other countertop applications. Review of the manufacturer’s material safety data sheet for product information documented that this material, CaesarStone, contains >85% crystalline silica.”

The study suggests adequate measures should be undertaken to prevent future occurrences of a “needless tragedy”:

“In summary, we report an outbreak of end-stage silicosis leading to LTX, a disease epidemic caused by dust generated through dry cutting engineered decorative stone with very high silica content. Strict enforcement of occupational safety and health regulations could have prevented this needless tragedy. Appropriate public health interventions to prevent future occurrences should be undertaken.”

In 2015, OSHA and NIOSH released a Hazard Alert for silica exposure during countertop manufacturing, finishing, and installation. In their report, OSHA and NIOSH noted the following work operations in the natural and engineered stone fabrication industry released respirable crystalline silica:

“Workers operating powered hand tools, such as saws, grinders, and high-speed polishers, have some of the highest silica dust exposures in the countertop manufacturing, finishing and installation industries. These exposures come from dry cutting, grinding, edging, and contouring stone, and may occur in shop environments as well as on job sites where finishing work is completed. In the manufactured stone industry, workers may also be exposed to silica dust when opening bags of ground quartz, moving or mixing bulk raw materials, cleaning and scraping mixers, or cleaning dust collector bag houses.”

The report additionally highlighted that despite there being OSHA regulations to reduce respirable crystalline silica exposure, such as wet-cutting or dust suppression systems, there is scarce adherence to these rules and recommendations:

“In many shops, current practices still involve dry cutting, grinding, polishing, and other work that releases silica dust into the air. Phillips et al. (2012) found that approximately 74% of 47 countertop shops in three metropolitan areas of Oklahoma reported using predominantly dry methods in at least one step of their work, and only four shops (9%) reported using dust collection or suppression systems at all.”

In 2016, the CDC published a report regarding silica dust from stone countertop fabrication and installation. The report discusses silicosis outbreaks in Israel, Spain, and the United States, regarding occupational exposure to silica in engineered stone countertops, and assessed respirable crystalline silica exposure during countertop fabrication tasks.

In 2022, Surasi et al. examined respirable crystalline silica concentrations in engineered stone fabrication workplaces following Cal/OSHA’s special emphasis program (SEP), initiated to reduce worker exposure to respirable crystalline silica (RCS). The study analyzed silica exposures for 152 employees across 47 workplaces. Approximately 38 workers (25%) had exposures above the PEL, with concentrations as high as 670.7 μg/m³. Another 17 workers (11%) ,had exposures between the permissible exposure limit (PEL) and action level (AL). 24 (51%) of workplaces had at least one exposure above the PEL, and another 7 (15%) had an exposure between the PEL and AL. In total, 34 (72%) of workplaces were cited for at least one respiratory crystalline silica standard violation, and 27 (57%) of workplaces were cited for at least one respiratory protection standard violation.

In 2023, OSHA launched their own inspection initiative focused on the engineered stone fabrication and installation industries. This initiative followed silicosis outbreaks in the stone product manufacturing industry, with OSHA identifying these manufacturers as having “workplaces where workers are typically exposed to high levels of silica.” They identified “Cutting, grinding, chipping, sanding, drilling, and polishing engineered or manufactured stone products” and ”Operating powered hand tools, such as saws, grinders, and high-speed polishers” as especially high risk activities.

In July 2023, the California Department of Public Health released a Health Advisory reporting that more than 1,000 cases of silicosis in workers who fabricate countertops had been reported worldwide since 2010. In response to this silicosis outbreak, in December 2023, Cal/OSHA unanimously adopted an emergency temporary standard (ETS) for respirable crystalline silica.

The ETS, however, proved largely ineffective, as the public health consequences continued to demonstrate that silicosis cases among ES workers was continually on the rise. In December of 2025, the Western Occupational and Environmental Medical Association (WOEMA) filed Petition 609 to the California Occupational Safety and Health Standards Board requested revisions to the crystalline silica standard to prohibit all fabrication and installation tasks on engineered stone containing more than 1% crystalline silica. After careful consideration, in May 2026, Cal/OSHA reached a unanimous decision to initiate the process to prohibit the fabrication and installation of artificial stone products containing more than 1% crystalline silica.

As this epidemic continued, physicians began identifying an unexpected pattern of disease among countertop fabrication workers. Unlike traditional silicosis, affected workers frequently developed severe disease after relatively short exposure durations, often at young ages, with rapid progression to progressive massive fibrosis and, in many cases, lung transplantation or death. After reviewing the worldwide scientific evidence, the American Thoracic Society concluded that this represents a distinct occupational disease now known as Artificial Stone–Associated Silicosis (AS Silicosis).

2.5 Regulatory Agency Guidance and Regulations on Silica

In 1971, OSHA adopted permissible exposure limits (“PEL”) for respirable crystalline silica for general, construction, and maritime industries. The PEL was expressed as “a formula of volume of crystalline silica per cubic meter of air, divided by the percentage of silicon dioxide (SiO2); or as millions of particles per cubic foot of air, divided by the percentage of SiO2.” The PEL for respirable crystalline silica was calculated for each sample and expressed in terms of total respirable dust using the following formula:

PEL for respirable crystalline silica =

These old-standards, when expressed in μg/m³, measured as an 8-hour TWA, are approximated with the following values: 100 μg/m³ for quartz in general industry, 250 μg/m³ for quartz in construction and maritime industries, 50 μg/m³ for cristobalite, and 50 μg/m³ for tridymite.

In 1972, NIOSH and the USBM issued joint approval for single-use respirators to protect against inhalation of silica dust particles. Therefore, countertop employees could have protected their workers from the harms of silica exposure with inexpensive disposable respirators as early as 1972.

In 1974, NIOSH published a recommended exposure limit (“REL”) for respirable crystalline silica of 50.0 μg/m³ as a TWA for up to 10 hours per day during a 40-hour workweek. In their recommendation, NIOSH highlighted the 10 million particles per cubic foot (mppcf) standard in the granite industry, equivalent to an 100 μg/m³ standard, “has not been entirely adequate for protection of workers.” Moreover, in their review of data across multiple industries where workers are exposed to respirable crystalline silica, the results did “not reveal any significant difference in the degree of toxicity of free silica in the form of quartz to which workers are exposed as compared with that in the granite industry.” For this reason, they concluded that their REL is applicable to all work environments where workers may be exposed to respirable crystalline silica.

NIOSH recognized the adverse health effects of exposure to silica as a potential cause of silicosis in its 1977 guide to occupational diseases.

IARC classified silica as a probable human carcinogen in 1987, stating:

“A number of studies have shown that persons diagnosed as having silicosis after occupational exposure to dust containing crystalline silica have an increased risk for dying from lung cancer. This increase has been seen among miners, quarry workers, foundry workers, ceramic workers, granite workers and stone cutters.”

In 1988, NIOSH, in an OSHA hearing on the proposed rules for air contaminants, argued that crystalline silica should be considered a potential occupational carcinogen as defined by OSHA carcinogen policies. The NIOSH recommended exposure limit of 50.0 μg/m³ for respirable crystalline silica is 16 times higher than the 2005 OEHHA chronic inhalation reference exposure level of 3 μg/m³ for respirable crystalline silica.

In 1989, OSHA updated their PELs from the now-obsolete particle counting formula into μg/m³ of air. This did not result in any decreases in PELs. In 1992, OSHA updated the PEL for quartz to 100 μg/m³ for all industries, including construction and maritimes ones, which had a higher PEL of 250 μg/m³. However, in 1992, the 11th Circuit Court of Appeals vacated the 1989 OSHA changes to their PEL formulas and 1992 OSHA proposed updates to the quartz PELs, returning the PEL standards to the 1971 values when OSHA was founded.

In 1997, IARC published Volume 68 of IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. The organization found that there was sufficient evidence in both experimental animal models and human occupational studies for the carcinogenicity of inhaled silica. IARC updated its classification of silica in 1997 to state: 

“Crystalline silica inhaled in the form of quartz or cristobalite from occupational sources is carcinogenic to humans (Group 1).”

In 1997, the American Thoracic Society specifically identified stone cutting as a “high risk occupation” for developing silicosis. The report states:

“When modern technology is not accompanied by modern controls (such as rock drilling without appropriate dust suppression), it may lead to increased airborne concentrations of silica dust. Exposure to silica of a respirable size occurs in mining, quarrying, drilling, and tunneling operations. Silica exposure is also a hazard to sandblasters, stonecutters, and pottery, foundry, ground silica, and refractory brick workers.”

In 2001, OSHA, in their semiannual agenda of regulations, highlighted the current regulatory deficiencies in mitigating respirable crystalline silica exposure. The report notes that “more than 30 percent of OSHA-collected silica samples 1982 through 1991” exceeded OSHA’s PEL, endangering two million workers exposed to silica, including more than 100,000 workers in high risk jobs, a category that includes “abrasive blasting, foundry work, stonecutting, rock drilling, quarry work, and tunneling.”

Even when adhering to the 1971 OSHA PELs, the report emphasized that multiple studies indicated that those PELs were not stringent enough to be health protective:

“In the interval since the limit was promulgated, there have been a number of studies of workers that have estimated that close to 50 percent of workers exposed to silica in the current limit for a 45-year working lifetime would develop silicosis, a disabling, progressive and sometimes fatal disease involving the scarring of the lung, coughing, and shortness of breath. There are currently about 300 deaths reported per year from silicosis. However, the actual number of cases and true risk is unknown due to inadequate case identification, which means that the number of deaths is probably underreported. Also, since the promulgation of OSHA’s permissible exposure limit, studies have demonstrated a statistically significant, dose-related increase in lung cancer in several occupational groups.”

The report concluded that because recent studies have found that “the current OSHA standard is insufficient to protect against silicosis,” OSHA would conduct a risk assessment to determine whether the 1971 OSHA PELs should be lowered to adequately protect worker health.

The California Office of Environmental Health Hazard Assessment (OEHHA) adopted a chronic Inhalation Reference Exposure Level (“REL”) for crystalline silica at 3 μg/m³ in 2005. This REL was selected to protect the health of the general population from chronic exposure to crystalline silica, based on ACGIH and ISO definitions of respirable particles. The OEHHA Chronic Toxicity Summary states:

“In the absence of comprehensive data on the silicosis-inducing activity of different particle sizes, it is not possible to adjust the REL for different particle size distributions, which might be found in the general environment, or for different measurement methods. The REL is therefore specified as applicable to concentrations of particles having a size range (and reactivity) similar to those measured in the occupational studies [respirable as defined occupationally (ISO, 1995; NIOSH, 2003; ACGIH, 2004)].”

In their 2005 report, the California OEHHA additionally highlighted that the then-OSHA PEL of 100 μg/m³ failed to adequately protect worker health, noting that silicosis mortality was still occurring among workers exposed to levels of silica deemed acceptable. OEHHA states:

“Silicosis is still being diagnosed at death in workers who were supposed to be exposed to occupational levels of 50-100 μg/m³. Thus, there have been recommendations that the occupational exposure limit for respirable, crystalline silica (specifically alpha-quartz) be lowered from the current level of 100 μg/m³ to 50μg/m³ (NIOSH, 1974; Rosenman et al., 1996; ACGIH, 1999; Finkelstein, 2000). In 2000, the ACGIH lowered its TLV for quartz from 100 to 50 μg/m³. In 1986, WHO recommended that the occupational level be set at 40 μg/m³ (WHO, 1986). Greaves (2000) recommended that the TLV be lowered to 10 μg/m³.”

In 2010, OSHA described health risks associated with exposure to silica and silica dust, stating: 

“Health hazards associated with exposure to crystalline silica-containing dusts arise from the inhalation of the respirable dust fraction, which is comprised of particles sufficiently small to reach the deep lung.”

In 2013, OSHA published its proposed rule on occupational exposure to crystalline silica. In the risk assessment supporting the proposal, OSHA estimated that long-term exposure to respirable crystalline silica at a concentration of 0.025 mg/m³ over a 45-year working lifetime would result in an estimated silicosis risk of approximately 4 cases per 1,000 exposed workers:

In 2014, OSHA released 29 CFR Parts 1910, 1915, 1917, 1918, and 1926, detailing and reviewing OSHA’s approach to managing chemical exposures in the workplace. In the release, OSHA consistently describes how PELs are inadequate or fail to protect workers. OSHA specifically stated that PELs “may be outdated or inconsistent with the best available current science. The CFR further acknowledges that “it may be evident from scientific literature or readily available evidence that risk at the existing PEL is clearly significant and that it can be more substantially reduced by a more stringent regulation.” The CFR further states that, “at times, it is evidence without extensive analysis the the most stringent PEL feasible can only reduce, not eliminate significant risk.”

In 2015, OSHA and National Institute for Occupational Safety and Health (NIOSH) published a Hazard Alert: Worker Exposure to Silica during Countertop Manufacturing, Finishing and Installation. This hazard alert highlighted the risks of silica exposure for workers involved in the manufacturing, finishing, and installation of natural and manufactured stone countertops and how these hazards can be mitigated.

In 2016, OSHA published a final rule regulating occupational exposure to respirable crystalline silica, written as two standards: one for construction and one for general industry and maritime. This rule lowered the PEL for respirable crystalline silica to 50.0 μg/m³ calculated as an 8-hour time-weighted average (“TWA”). The rule included an action level of 25 µg/m³ as an 8-hour time-weighted average, requiring exposure monitoring and control measures at that level. Employers were also required to use engineering controls, provide respiratory protection when necessary, implement exposure control plans, and conduct medical surveillance for at-risk workers.

OSHA highlighted the health risks associated with respirable crystalline silica exposure, particularly under the previous permissible exposure limits, stating:

“Occupational Exposure to Respirable Crystalline Silica standards on March 25, 2016 (81 FR 16286), after determining that employees exposed to respirable crystalline silica at the previous permissible exposure limits face a significant risk of material impairment to their health. The evidence in the record for this rulemaking indicates that workers exposed to respirable crystalline silica are at increased risk of developing silicosis and other nonmalignant respiratory diseases, lung cancer, and kidney disease. These requirements are necessary to provide protection from these hazards. The silica final rule becomes effective on June 23, 2016.”

OSHA’s 2016 Final Rule states that “The Agency considers the level of risk remaining at the new PEL to be significant. However, based on the evidence evaluated during the rulemaking process, OSHA has determined a PEL of 50 μg/m³ is appropriate because it is the lowest level feasible for all affected industries.”

In 2018, OSHA began enforcement of the updated respirable crystalline silica standard for the general industry and maritime sectors. This included requiring employers to limit access to high-exposure areas, using dust controls, and providing respirators when controls are insufficient. Housekeeping methods should avoid generating airborne dust, and a written exposure control plan must be in place. Furthermore, workers exposed above the action level for 30+ days annually should receive medical exams, including chest X-rays and lung function tests, every three years. Additionally, workers should be trained on silica-related risks and exposure controls, and exposure data and medical records must be maintained.

In 2019, the Agency for Toxic Substances and Disease Registration (ATSDR) and the Environmental Protection Agency (EPA) released their updated toxicological profile for silica. The report noted that no minimal risk level (MRL) for respirable crystalline silica, that is the minimum exposure before the development of adverse health risks, could be determined for the following reason:

“However, a no-observed-adverse-effect level (NOAEL) for silicosis has not been defined, with silicosis and death due to silicosis observed for the lowest estimated cumulative exposure ranges reported. For the lowest estimated cumulative exposure range reported in the available literature (0–0.2 mg/-year), silicosis was observed in 5 of 3,330 gold miners (Steenland and Brown 1995a). At the estimated cumulative exposure range of 0.1–1.23 mg/-year, death due to silicosis was observed in 2,857 of 74,040 mining and pottery workers in China (Chen et al. 2012). In other occupational studies, cumulative exposure levels associated with silicosis and silicosis-related death are higher.”

In 2022, OSHA inspected respirable crystalline silica (RCS) exposure in workplaces handling natural and engineered stone slabs. The data revealed that:

“Approximately one quarter of the breathing zone samples for RCS exceeded the OSHA Permissible Exposure Limit (PEL). The highest measured 8-hour time weighted average RCS exposure value recorded was approximately 20 times the PEL value. Nearly two thirds of the employers with RCS overexposures had not completed medical surveillance on exposed employees.”

In July 2023, the California Department of Public Health released a Health Advisory reporting that more than 1,000 cases of silicosis in workers who fabricate countertops had been reported worldwide since 2010. In response to this silicosis outbreak, in December 2023, Cal/OSHA unanimously adopted an emergency temporary standard (ETS) for respirable crystalline silica. The new regulations apply to stone fabrication shops that process artificial stone with >0.1% silica and natural stone with >10% silica. These revisions were specifically designed to “protect workers engaged in high-exposure trigger tasks (cutting, grinding, polishing, cleanup, etc.) involving artificial stone and natural stone containing more than 10% crystalline silica.”

The ETS mandates that the new protections apply to all fabrication shops, regardless of the respirable crystalline silica levels measured by the employer. It also grants Cal/OSHA the ability to issue an Order Prohibiting Use (OPU) when dry cutting or other dust generating activities are observed, without having to conduct air monitoring beforehand. The regulations propose a number of compliance methods, including wet-cutting methods that ensure running water covers the entire surface, installation of local exhaust ventilation systems, and use of dust capture systems such as shrouds or vacuums. In addition, the regulations state that employers must offer medical exams to certain workers, avoid housekeeping practices that expose workers to excess silica dust, such as dry sweeping, communicate the hazards of silica exposure in compliance with regulations, and keep records or air monitoring data, objective data, and medical surveillance. The regulations also require the use of a full-face, tight-fitting powered air-purifying respirator. Should workplaces demonstrate severe violations that endanger an employee’s health, the ETS allows Cal/OSHA to immediately suspend operations.

Following the implementation of the ETS, Cal/OSHA found the following:

“As part of this effort, 26% of the shops inspected received Orders Prohibiting Use (OPUs), which temporarily shutdown equipment or processes that pose immediate safety risks until the issues are fixed. Additionally, citations were issued in approximately 95% of the closed inspections, with 53 out of 56 resulting in violations. This highlights the significant enforcement actions taken to improve workplace safety around silica exposure.”

From the 1st of July 2024, Safe Work Australia prohibited work related to the manufacturing, supplying, processing, or installation of engineered stone benchtops, panels, and slabs. This included implementing a nationwide prohibition of engineered stone containing more than 1% crystalline silica. Australia was the first government in the world to ban engineered stone entirely. The decision arose after a consistent failure of other regulatory standards, including robust controls and measures, and extensive scientific evidence that indicated the most effective and cost-efficient solution was a complete ban of the product.

In December 2024, Cal/OSHA unanimously made permanent the ETS, “protecting workers from respirable crystalline silica (RCS), especially those who work with artificial, man-made stone.” These regulations were set to begin in 2025.

In 2024, OSHA published a Hazard Analysis: Lessons and Findings from OSHA’s Emphasis Program on Silica in Engineered Stone, stating:

“The connection between workplace exposure to fine airborne silica dust and the uncurable and progressive lung disease silicosis has been known for hundreds of years.”

After consistent failures of the ETS to reduce the silicosis epidemic, in December of 2025, the Western Occupational and Environmental Medical Association (WOEMA) filed Petition 609 to Cal/OSHA requesting revisions to the crystalline silica standard to prohibit the fabrication and installation tasks on engineered stone containing more than 1% crystalline silica. After extensive review of the petition and available evidence, CAl/OSHA concluded that the fabrication and installation of engineered stone products with greater than 1% silica is “inherently dangerous, highly toxic, and harmful to workers.” They further added that “worker exposure should be prohibited.”

In 2026, the Cal/OSHA board moved forward with Petition 609, beginning to evaluate state-wide prohibition, concluding that the prohibition on all fabrication and installation tasks on engineered stone that contains more than silica may be the quickest and most cost-effective way to reduce silicosis in California.

2.6 Respirators as a Protective Measure Against Silicosis

In 1934, The United States Bureau of Mines (“USBM”) issued the first dust/fume/mist respirator approval standards: 30 CFR Part 14, Schedule 21. USBM issued this standard as a response to one of the worst industrial disasters in American history: the Hawks Nest Tunnel disaster, in which up to one thousand workers died after developing silicosis while working in an underground tunnel in West Virginia during the early 1930’s. Schedule 21 included tests to ensure that specified respirators were capable of protecting workers from exposure to silica dust.

In 1963, E.C. Hyatt published a study titled “Current Problems and New Developments in Respiratory Protection” underscoring the critical role of fit testing in ensuring the reliability of respiratory protective devices. Researchers developed a gas chamber test using iso-amyl acetate to evaluate the reliability of face seals in respirators. Hyatt’s work revealed that improper peripheral face fit is a leading cause of leakage in respirators, compromising their protective efficacy. Testing over 1,200 individuals demonstrated significant variation in the effectiveness of face fits, even with commercially available respirators. This highlights the importance of iterative testing to identify models that achieve better sealing across diverse facial structures. Hyatt’s research underscores that routine fit testing is not merely a precaution but a necessity to ensure respirators provide consistent and dependable protection across various conditions and users.

In 1964, Hounam et al. published a study titled “The Evaluation of Protection Provided by Respirators,” highlighting the critical importance of fit testing in ensuring the efficacy of respiratory protective equipment. The study developed and applied two methods to assess respirator performance using sodium chloride aerosol and halogenated hydrocarbon vapor tests. Results demonstrated that leakage around the face seal was a primary factor compromising protection. Hounam emphasized that many respirators initially fitted by users provided inadequate protection due to improper adjustments, with tests showing significant penetration above 0.1%. However, when proper fit testing and adjustments were conducted, these failures were reduced to negligible levels. The study emphasizes the importance of fit testing, alongside the subject being clean-shaven:

“To ensure optimum protection, proper care must be taken in the use of respirators and in their maintenance. In use, attention must be paid to careful fitting, particularly when spectacles are worn and the wearer must be clean-shaven.”

This research laid a foundation for modern fit testing protocols, emphasizing that even well-designed respirators could fail without proper fit and maintenance, reinforcing the need for systematic evaluation and training in their use.

According to the CDC, as respiratory protection became mandatory around the 1990s, the importance of a tight and proper respirator fit increased. OSHA revised the certification regulations for fit testing in 1995, leading to further research in 1996 regarding exposure in the workplace, causing researchers to use simulated workplace protection factors and exposure simulations.

In January of 1998, OSHA issued a revised Respiratory Protection Standard and Final Rule in the Federal Register, codified as 29 CFR 1910.134. The Standard details key methods in regulating respiratory health in any workplace where employers require respirators, including a requirement of “fit testing procedures for tight fitting respirators.” Specifically, OSHA mandates that respirator fit testing be performed prior to any employee being required to use any “negative or positive pressure respiratory” with a tight fitting facepiece. The Final Rule states the following on fit testing:

“This paragraph requires that, before an employee may be required to use any respirator with a negative or positive pressure tight-fitting facepiece, the employee must be fit tested with the same make, model, style,and size of respirator that will be used. This paragraph specifies the kinds of fit tests allowed, the procedures for conducting them, and how the results of the fit tests must be used.

(1) The employer shall ensure that employees using a tight-fitting facepiece respirator pass an appropriate qualitative fit test (QLFT) or quantitative fit test (QNFT) as stated in this paragraph.

(2) The employer shall ensure that an employee using a tight-fitting facepiece respirator is fit tested prior to initial use of the respirator, whenever a different respirator facepiece (size, style, model or make) is used, and at least annually thereafter.

(3) The employer shall conduct an additional fit test whenever the employee reports, or the employer,PLHCP, supervisor, or program administrator makes visual observations of, changes in the employee’s physical condition that could affect respirator fit. Such conditions include, but are not limited to, facial scarring, dental changes, cosmetic surgery, or an obvious change in body weight.

(4) If after passing a QLFT or QNFT, the employee subsequently notifies the employer, program administrator,supervisor, or PLHCP that the fit of the respirator is unacceptable, the employee shall be given a reasonable opportunity to select a different respirator facepiece and to be retested.”

The Standard states:

“Throughout this preamble, OSHA has demonstrated that adequate fit testing, proper respirator selection, worker training, and thorough inspection and maintenance are essential elements of a respirator program. Without these requirements, OSHA believes that there is a greater chance that a respirator user will inhale potentially dangerous air contaminants, either by improper selection of equipment, excessive respirator leakage, improper use of the respirator, or any combination of these.”

OSHA’s Respiratory Protection Standard, codified as 29 CFR 1910.134, mandates that employers provide appropriate respiratory protection to employees exposed to hazardous airborne contaminants, including silica dust. A critical component of this standard is the requirement for fit testing to ensure that the selected respirator forms an adequate seal on the user’s face, thereby providing the intended level of protection. OSHA provides a detailed explanation of differentiation between qualitative and quantitative fit tests. It states that a respiratory user should verify that the respiratory has been properly positioned on the face to ensure a proper seal. Specifically, it states a user seal check does not substitute for a respirator fit test.

OSHA defines approved methods of fit testing, categorized into qualitative and quantitative testing:

“Qualitative fit testing (QLFT) involves the introduction of a gas, vapor, or aerosol test agent into an area around the head of the respirator user. If the respirator user can detect the presence of the test agent through subjective means, such as odor, taste, irritation, the respirator fit is inadequate. In a quantitative respirator fit test (QNFT), the adequacy of respirator fit is assessed by measuring the amount of leakage into the respirator, either by generating a testaerosol as a test atmosphere, using ambient aerosol as the test agent, using controlled negative pressure to measure the volumetric leak rate.”

A 1998 report by Rink in response to OSHA’s 1998 regulations states that studies indicate a complete respirator program, including fit testing, will reduce exposures to toxic substances by 96% compared to a control group without the same program.

A systematic review of dust control measures by Anlimah et al. (2023) emphasized that while interventions like water suppression and ventilation are essential, the effectiveness of respiratory protective equipment heavily depends on proper fit and usage. The study emphasizes the critical role of fit testing in protecting workers from respirable crystalline silica. Without proper fit testing, the study suggests, respirators may not provide adequate protection, leading to increased risk of silica-related diseases.

When a worker has a beard, the efficacy of his mask and respirator is compromised. In as early as 1998, Stobbe et al. published a review of the existing literature regarding facial hair and respirator fit. They reviewed twelve studies from the years 1964 to 1987 that measured the positive and negative pressure of respirator use. The results, they found, were generally consistent, “with all but one showing that the presence of facial hair produced leakage that was 50 to 1000 times greater than that found with clean-shaven persons.” The study elaborates, stating:

“The author’s opinion is that when a competent industrial hygiene evaluation has demonstrated that no health hazard exists or is likely to exist, the situation requires the exercise or professional judgment. Under these conditions respirator use with facial hair may pose a number of administrative problems and risks, the significance of which must be balanced carefully against the restrictions on personal freedom associated with a ban on facial hair.”

The study advises that if facial hair is allowed in a workplace, all other aspects of a complete respirator program should be met, including training because a “beared respirator user cannot safely enter an area where respirator use is required.”

OSHA’s 1998 Respiratory Protection Standard also identifies facial hair as a potential disruptor of respirator effectiveness, stating that:

“1)Facepiece seal protection.

(i) The employer shall not permit respirators with tight-fitting facepieces to be worn by employees who have:

(A) Facial hair that comes between the sealing surface of the facepiece and the face or that interferes with valve function; or (B) Any condition that interferes with the face-to-face piece seal or valve function.”

In 2004, NIOSH published a report called the Respirator Selection Logic. This document highlights the importance of fit testing, especially when an employee has a beard:

“The following requirements and restrictions must be considered to ensure that the respirator selected will provide adequate protection under the conditions of intended use” […]

“2. Qualitative or quantitative fit tests must be provided as appropriate to ensure that the tight-fitting facepiece respirator fits the individual. NIOSH endorses the OSHA standard 29 CFR1910.134 for fit testing except for irritant smoke (see the Appendix, page 27). Employees must pass a fit test with the exact model and size that they will wear in the workplace.”[…]

“4. Respirators with tight-fitting facepieces (including pressure-demand respirators) should not be used when facial hair interferes with the face seal.”

As demonstrated, OSHA and NIOSH have published guidance specifically addressing silica exposure in the countertop fabrication industry. These publications underscore the necessity of implementing comprehensive respiratory protection programs, including fit testing, to protect workers. OSHA’s guidance on worker exposure to silica during countertop manufacturing, finishing, and installation highlights that when respirators are required, employers must have a respiratory protection program that includes proper respirator selection, fit testing, medical evaluations, and training.

3 Silica Toxicology, Disease Mechanisms, and Medical Effects

Freshly fractured silica surfaces can be highly reactive and promote oxidative stress, macrophage injury, persistent inflammation, and fibrotic remodeling. Fine and ultrafine particles penetrate deeply into the lung where clearance may be limited.

Silicon radicals are generated when silica is ground, breaking silicon-oxygen bonds on the surface. These silicon radicals have the ability to react with water to produce hydroxyl free radicals. In addition, this process also produces other reactive compounds, such as silanols and carboxyls. In 1988, Vallyathan et al. examined the radical generating potential of freshly cut quartz. The study found that fresh silica generated significantly more silicon radicals and was able to produce hydroxyl radicals in an aqueous solution. In addition, the study found lipid peroxidation of cellular membranes as another pathway for the generation of hydroxyl radicals. In their 2016 study, Pavan et al. found that artificial stone generated significantly greater hydroxyl free radicals when compared to quartz in cellular models regardless of whether the stone was cut wet or dry. In contrast, wet cutting was effective in reducing carboxyl radicals. Generation of these surface radicals is higher among freshly cut or ground quartz when compared to aged surfaces, meaning that quartz workers, who are consistently exposed to fresh particles, may have higher than expected exposures. These results were corroborated by Turci et al. in their 2016 study. When quartz, both synthetic and mineral, were mechanically ground, surface radicals were generated. In particular, ground synthetic quartz was even more effective at generating carbon-centered free radicals, with the reactivity sustained for up to an hour in testing. Because cutting and mechanical grinding produce highly irregular and disordered structures, increasing surface area and promoting reactivity, these effects are enhanced.

Generation of these hydroxyl radicals can be augmented through contamination of quartz with trace metals, such as iron. In their 1997 study, Castranova et al. found that iron contaminated quartz produced 57% more reactive species, such as hydroxyl and hydroperoxide, in water when compared to a low iron sample through Fenton-like reactions. Dissolution of silica in acids, such as ascorbic acid, can also increase the toxicity of silica by increasing the number of radical sites on the crystal’s surface.

Another mechanism for silica toxicity could be nearly free silanols (NFS), moieties or chemical groups formed when quartz is freshly fractured. This process produces silicon-based radicals, which are hydrolyzed to form silanols. According to Pavan et al., their 2020 study demonstrated that NFS promote favorable conditions for membranolytic activity and other toxic cellular effects. Because NFS are weakly bonded together, they have increased ability to interact with biological molecules. Specifically, computational models suggest that NFS bonds with phospholipids in the cellular membrane, stiffening them and causing them to rupture. Additionally, Vallyathan et al., in their 1988 study, found that silanols also may have the potential to form hydrogen bonds with the cellular membrane, initiating lipid peroxidation on the surface.

Respirable crystalline silica is directly cytotoxic to cells. Fractured synthetic quartz is associated with reduced cell count and increased cell membrane permeability, indicating damage to the membrane. In 1988, Vallyathan et al. found that freshly crushed quartz induced a greater alveolar macrophage burst and cytotoxicity. The study found that even silicon dust that had been aged for years still had cytotoxic effects, including decreasing the cellular membrane integrity, promoting lipid peroxidation, and stimulating alveolar macrophages. Turci et al., in their 2016 study, found increased lysosomal stress in macrophages and lysis in red blood cells and liposomes in cells. Silica moieties, like NFS, rupture or damage the cellular membranes of immune cells, such as macrophages. In samples contaminated with iron, which increased production of hydroxyl radicals, there was increased damage to the air-blood barrier in the alveoli and lipid peroxidation in lung tissue along with oxygen radical generation by phagocytes.

Damage to immune cells triggers an inflammatory response, such as the recruitment of inflammatory neutrophil cells and release of inflammatory cytokines. In their 2009 study, Scarfi et al. found that silica treated with acid had a significant increase in inflammatory cytokine synthesis and secretion from macrophages following membrane lipid peroxidation.

Exposure to respiratory crystalline silica from both natural and artificial stones has been associated with promoting epithelial-to-mesenchymal transition (EMT) in cells. EMT is a process where epithelial cells lose their polarity and cell-cell contact and reorganize their shape, allowing them to become mobile and invasive. During this process, these epithelial cells may further produce inflammatory cytokines and growth factors or fully complete this transition, which promotes the generation of fibroblasts and myofibroblasts that cause silicosis and other fibrotic diseases. Pavan et al., in their 2016 study, found that EMT induction may have resulted from exposure to these hydroxyl and carboxyl radicals.

This persistent inflammation, resulting from a combination of cell damage, release of inflammatory compounds, and neutrophil recruitment, has been associated with genotoxic effects and increased risk of cancer.

4 Engineered Stone as a Distinctly High-Risk Product

The fabrication of engineered stone has several unique hazards in comparison to natural stone, including the higher silica content in comparison to natural stone; increased generation of ultrafine particles, and resin composition of the stone. Published outbreaks show younger workers with shorter latency periods than historically expected.

4.1 Silica Content of Natural and Engineered Stone Countertops

Various materials contain crystalline silica, including brick, block, mortar, and concrete. Stone countertop products specifically can contain over 90% crystalline silica. According to a study conducted in 2020, artificial stone is becoming a more common choice in homes than natural stone because of desirable properties including stain-free and scratch-proof surfaces, acid and fire resistance, and non-toxicity.

Silica content is typically lower in natural stone products as opposed to engineered stone. In contrast to natural stone products, engineered stone contains more than three times the silica content (90% vs 3%-30%). Worksafe Australia, an Australian Government statutory agency established in 2009 and represents the interests of workers and members representing the interests of employers, estimated that the silica content in engineered stone can be as high as 97%. Limestone and certain types of marble are calcium-based stones, and contain little or no silica. The table below describes the silica and quartz content of natural and engineered stones.

Table 4.1: Silica Content of Stone Countertop Materials

Multiple peer-reviewed publications have assessed the mass and composition of respirable crystalline silica (“RCS”) when abrading engineered stone in comparison to natural stone such as granite or marble.

A 2020 study by Carrieri et al. analyzes the characterization of silica exposure during manufacturing artificial stone countertops. The study found that manipulation processes such as cutting and grinding artificial countertop materials posed a substantial health risk due to silica inhalation. Carrieri assessed four stone types: A and B with high silica content (>85%), artificial stone C with lower silica levels (<11%), and granite. Bulk samples found the following percentages for total crystalline silica weight: artificial stone A (90.8%), artificial stone B (91.2%), artificial stone C (9.6%), and granite (30.7%). Of all the respirable particles, by weight, 51.4% and 53.6% were for quartz for materials A and B. For material C and granite, these values were 4.4% and 7.9% silica. While granite generated larger amounts of respirable dust than artificial stones A and B, the mean crystalline quartz content in granite was 33.5 mg/m³, as opposed to mean respirable crystalline quartz value of 50.8 mg/ for stone A and 47.7 mg/m³ for stone B.

Hall et al. 2021 assessed the crystalline mineral and non-crystalline composition of granite, sandstone, resin-artificial stone and sintered-artificial stone through bulk material testing. The study used dust tunnel testing to assess airborne dust concentrations during cutting and polishing of each stone material. While the levels of respirable dust during cutting were comparable for both natural and engineered stone, Hall et al. found that resin-artificial stone and sandstone had higher percentages of crystalline silica within dust (69% and 55% respirable silica respectively), as opposed to granite and sintered-artificial stone (5% and 3.5% respirable silica respectively).

An estimated 100,000 stone fabricators in the US are at potential risk for silicosis associated with exposure to respirable crystalline silica.

Fazio et al. (2025) conducted a multidisciplinary review of the epidemiology, occupational risks, and clinical challenges associated with engineered stone (ES) processing. The review noted that ES materials typically contain greater than 90% crystalline silica by weight, which significantly exceeds the content of natural stones such as granite (40-50%) and marble (<10%). During the fabrication process, personal breathing zone samples and area monitoring data consistently showed that respirable crystalline silica (RCS) levels frequently exceeded safe occupational exposure limits (OELs). The review found that even when engineering controls such as wet saws, integrated water delivery systems, and exhaust ventilation were used, exposure levels often remained above established limits (1).

Thompson and Qi also assessed the characterization of the emissions and crystalline silica content of respirable dust in granite and ES by finding the normalized generation rate for four stones. Stone A is composed of up to 90% crystalline silica, Stone B is composed of less than 50% crystalline silica, Stone C is composed of under 0.2% crystalline silica, and granite was composed of 72% silica. A handheld pneumatic angle grinder was used to cut the stone. The study found that bulk dust from Stone A contained 60% silica, Stone B 25%, Stone C 0%, and granite 30%. For the mean normalized generation rates of RCS, the stones, from highest to lowest, were in the following order: Stone A (15.6 mg/cm³), Granite (10.8 mg/cm³), Stone B (6.31 mg/cm³), and Stone C (not detected).

4.2 Engineered Stone Is Not Natural Stone

Engineered stone (ES), while often marketed as quartz, is fundamentally different despite visual similarities. The materials are fundamentally different, as engineered stones are synthetic, manufactured composites that present drastically different and more severe hazards than natural stones derived from geological formulations.

Natural stones (NS), such as granite and marble, are naturally occurring stones that have been quarried from mines and cut into the desired shape. These formed over millions of years ago through natural processes, such as heat, pressure, and mineral accumulation. Engineered stone, on the other hand, is an artificial product manufactured in a factory through the crushing of different mined materials into a fine powder. These powders are blended together using pigment and resins through the process known as vacuum vibrocompression which uses heat and pressure to form a dense, non-porous slab.

The primary distinction between natural stones and engineered stones is the disparity in crystalline silica content. Engineered stone typically has a crystalline silica content between 90 or more silica by weight, while natural stones like granite have at most 40-50% silica by weight. Other natural stones, such as marble and limestone, are primarily calcite and contain little to no crystalline silica. While there are some natural stones, such as quartzite, that contain over 90 percent crystalline silica, the most common natural stones have baseline crystalline silica levels drastically lower than engineered stone. This disparity in silica content between engineered and natural stone can result in a two to 90-fold increase in exposure to nanosized crystalline silica.

Since engineered stone is derived from crushed silica powder, it requires synthetic binding agents to hold its shape. Manufacturers add polymer resins, such as polyethylene terephthalate, polyester-styrene, acrylic and epoxy, which typically make up between 5% and 15% of the slab’s total weight. These resins add to the toxic and carcinogenic compounds into the dust generated from fabrication. Natural stones, on the other hand, do not have synthetic resins, pigments, or adhesives added.

The compositional differences lead to distinctly different hazards generated during the fabrication of both materials. When natural stone slabs are cut using a bridge saw or hand grinder, the dust primarily consists of natural mineral compounds and a lower concentration of RCS. However when the same equipment is used on engineered stone, this generates dust clouds with a drastically higher composition of RCS. This is demonstrated in the Figures below.

Beyond the disparity in quantity of silica generated, the size of particles generated from engineered stone drastically differs from natural stone. Since engineered stone was derived through the binding of finely crushed crystalline silica, the cutting of the product generated a disproportionate amount of ultrafine particles. Studies demonstrate that the dry-cutting of engineered stone products can produce ultra fine particles that engineering controls cannot adequately capture. These nano particles have diameters of less than 100 nanometers and are able to penetrate the human body more deeply due to their smaller size.

The morphology and reactivity of dust particles generated from engineered stone are clearly distinct from particles generated from natural stone. NS dust observes natural layers with less conchoidal fractures on the surface. ES dust, on the other hand, observes more irregular shapes, with sharp edges and fractures. These disparities are pictured below.

The irregular fractures in artificial stone create a surface with molecules known as “nearly free silanols” (NFS). NFS molecules are present far more abundant in crystalline silica materials. NFS are highly reactive and have the optimal structure and shape to attach to cell membranes in the lung and cause damage.

Research has found that the specific surface area of ES dust is greater than the surface area of NS dust particles. This increased surface area is accompanied by a heightened electrical surface charge, which when combined with the presence of NFS, makes engineered stone dust exceptionally biologically reactive. Scientific evidence has demonstrated that exposure to artificial stone dust increases oxidative stress and compromises the epithelial barrier in lung cells. This increased surface area is demonstrated in Figure 4.5 below.

As previously mentioned the hazards of ES dust are increased by the presence of synthetic resins, which are entirely absent from NS dust. Studies have shown that respirable dust generated by the dry-cutting of Es comprises between 8.6 and 20% resin. Research has found that resin within artificial stone may prevent RCS particles from naturally being eliminated in the air through interactions with other reactive airborne species. Essentially, resin protection can allow for more transportation of NFS into the deep lung. Once inside of the deep lung, acidic fluids in the lung can remove this resin protection, exposing the NFS.

Research has consistently detected VOC emissions from ES fabrication, which has included known toxins and carcinogens such as styrene and benzene. Studies have suggested that these VOCs are generated during active machining during the breakdown of inhalared resins. Atmospheric sampling during the fabrication of engineered stones, has detected concentrations of phthalic anhydride, styrene, benzene, ethylbenzene, toluene, and acetone. The presence of VOCs raises the potential for synergistic reactions in the lung between carcinogenic VOCs and RCS.

Engineered stone additionally incorporates trace or transition metals which are often used as pigments or catalysts in the manufacturing process. These aerosolized metals may create a “cocktail effect” with resins and may contribute to increased cancer risks. The potential synergistic toxicity between VOCs, RCS, and trace metals, may create a unique hazard specific to ES.

4.3 Additional Dangers from Engineered Stone

The studies described in this Section characterize the dust produced during the cutting, grinding, and fabrication of engineered stone. Multiple studies found that dust from engineered stone contains particles on the nanometer scale, with diameters less than 0.1 μm (also known as ultrafine particles). Because of their size, nanoparticles have high deposition efficiency in the lungs and are the most toxic component of airborne particulate matter. In addition, nanoparticles have been observed to be more reactive than their micron-sized counterparts due to their large surface area to molecule ratio, which increases exponentially with smaller particles. This is conducive to the formation of free radicals, which create oxidative stress and prompt inflammatory responses, such as silicosis. The additional dangers associated with small particle size reinforce the need to move away from engineered stone products because of the hazards they produce in occupational settings.

In 2019, Ophir et al. evaluated the presence and effects of ultrafine particles (“UFP”) generated from engineered stone dust in exposed workers to better understand their role in respiratory disease. The study focused on a group of 68 individuals in the countertop production industry who had worked primarily with engineered stone over the previous 20 years. The authors analyzed the particle distribution in induced sputum samples in the study group and found that the particle distribution was practically identical to that of dust samples from an engineered stone factory in the region. In the induced sputum samples, collected from patients’ lungs, approximately 12% of particles were nano-ranged compared to approximately 15% from the artificial stone dust. In contrast, only 1.56% of the particles in the induced sputum samples in the control group were nano-ranged. Additionally, the smallest fraction of particles for the induced sputum from patients (32.08 to 108.9 nm) was “almost identical” to the dust samples (28.1 to 110.1 nm). The smallest fraction of particles for the control group’s induced sputum samples was significantly larger. This is demonstrated in Figure 5.6 below.

In addition, the authors found that there was a positive correlation between the accumulation of nanoparticles and inflammatory cytokines in the induced sputum samples, providing evidence that the nanoparticles elicit an immune response. The authors noted that ultrafine particles are more toxic than larger particles due to their increased surface area, reactivity, and ability to penetrate deeply into the lungs and translocate to other organ systems.

In 2020, Carrieri et al. characterized silica exposure during cutting and grinding of three engineered stone samples and one natural granite sample. The study found that two of the three engineered stone samples contained over 90% crystalline silica, significantly higher than the 31% found in the granite sample. When analyzing the respirable mass concentrations of the materials, the authors found that the two engineered stone samples with high silica content had the main particle diameter distribution peak in the nanometer range: 0.01 and 0.1 μm. In comparison, the granite sample had a particle size distribution peak at 0.15 to 0.4 μm. Representative images of the airborne grinding particles for the two engineered stone and granite samples are demonstrated in Figure 5.7 below. It must be noted that the authors discussed that grinding particles with irregular shapes were found in high counts of silica in Materials A and B (demonstrated in Figure 5.7.1) and in low counts for granite (demonstrated in Figure 5.7.2.). The authors further noted that nanoparticles have been documented to translocate from the respiratory system to other organs, such as the liver and kidneys, and can contribute to multiorgan accelerated silicosis. In addition, the authors stated that exposure was far above the OSHA mineral dust exposure PEL for all materials tested and that their results also “suggest that the standard control measures used during manufacturing and installation processes (such as wet cutting) and use of personal protective equipment (such as respirators) are to be reevaluated.”

In 2022, Ramkissoon et al. characterized respirable dust generated during the machining of engineered and natural stones to better understand the hazards associated with engineered stone exposure. The study found that respirable engineered stone dust contained concentrations of crystalline silica that generally exceed 80%, compared to much lower levels in natural stones such as granite and marble. In addition, the authors found that dry cutting engineered stone produced extremely fine particles, with over 90% having diameters between 190 and 825 nm. While the study noted that the three natural stones used as controls had similar particle size distributions, there was a “clear difference” in surface area. The engineered stone particles had greater surface areas and more irregular and fractured morphologies than natural stone dust, as demonstrated in Figure 5.8 below. This can increase surface reactivity and has been reported to play an important role in cytotoxicity.

Figure 5.8.1: Representative SEM Images of Respirable Dusts from Machined Engineered Stones

In 2024, Ramkissoon published another article discussing the generation of VOCs in processing engineered stone, including both ES with high levels of silica content and newer low-silica content ES products. The resin present in these products contributes to the release of VOCs including styrene, toluene, benzene, polychlorinated biphenyls (PCBs), and polyaromatic hydrocarbons (PAHs).

Rishi et al. (2024) assessed the release of crystalline silica during the fabrication of engineered stone, specifically focusing on the characterization of nanocrystalline silica (NCS) in the sub-100 nm size fraction. The researchers found that 70% of the total aerosol mass in the sub-100 nm aerosol fraction was crystalline silica. While this sub-100 nm fraction accounted for only about 1% of the total aerosol mass, the researchers determined it contributed a disproportionate 4-24% of the total aerosol surface area deposited in the lung. The authors stated that because current engineering controls primarily use mass as an exposure metric, they may significantly underestimate the health risks posed by the high surface area of nanocrystalline silica.

DeVaughn et al. (2025) conducted a field investigation of respirable crystalline silica exposure among eight engineered stone fabricators in two Chicago-area workshops, combining personal breathing zone sampling, real-time particle monitoring, and material characterization of dust. They found consistently elevated RCS exposures, with time-weighted average concentrations ranging from 11 to 203 µg/m³ (median 90 µg/m³), and 78% of samples exceeding the OSHA 50 µg/m³ exposure limit. Engineered stone dust exhibited very high silica content (56-95%) compared to natural stone (~30%), and particle size analysis showed that over 90% of emitted particles were <2.5 µm. For workers using hand tools, between 62.4 and 91.6% of particles had a diameter of less than 1 micron. These small particles can penetrate deep into the lungs and cause an inflammatory response. The authors emphasized the need for improved engineering controls, regulatory measures, and enforcement to protect workers in the engineered stone fabrication sector from exposure scenarios with high silica content, elevated airborne concentrations, and predominance of fine particles.

In their 2023 study, Pavan et al. demonstrated that crystalline silica particles containing nearly free silanols readily attach to and damage cell membranes, whereas particles lacking these reactive surface groups produce little or no membrane injury. Cell membrane damage is one of the earliest events that initiates inflammation, recruits immune cells, and ultimately leads to pulmonary fibrosis (silicosis). These findings provide a biologically plausible explanation for why freshly fractured engineered stone dust is substantially more hazardous than older, weathered silica dust.

In that same study, Pavan et al. investigated why some crystalline silica particles are more harmful than others by comparing their ability to damage cells with the chemistry of their particle surfaces. In Panel A of Figure 5.9 below, the y-axis (% hemolysis) represents the percentage of red blood cells whose outer membranes were damaged or ruptured after exposure to silica particles, with higher values indicating greater cell injury. The x-axis (surface area dose, cm²/mL) represents the total surface area of silica particles exposed to the cells. Panel B examines the chemistry of the particle surfaces using infrared spectroscopy. The y-axis (Normalized Kubelka-Munk Units) is a relative measure of the strength of the infrared signal from chemical groups on the particle surface, with higher peaks indicating a greater abundance of those surface chemical groups. The x-axis (wavenumber, cm⁻¹) is simply a chemical “fingerprint” that identifies different chemical bonds present on the surface of the silica particles. Panel B’ enlarges the shaded region of Panel B containing highly reactive surface chemical groups known as nearly free silanols.

When the three panels are considered together, they demonstrate that the silica particles causing the greatest cell membrane damage are the same particles that contain these highly reactive surface groups. This finding is particularly important for engineered stone because every cut, grind, and polish creates millions of freshly fractured quartz particles with newly exposed reactive surfaces. Like freshly broken glass, these fresh surfaces are more chemically active than older, weathered silica particles. Because engineered stone workers continuously create and inhale freshly fractured quartz throughout the workday, they are repeatedly exposed to silica at its most reactive state, helping explain the unusually short latency and rapid progression of silicosis observed in engineered stone workers.

4.3.1 Respiratory Protection Against Ultrafine Particles

NIOSH emphasizes that because respirators are subject to stringent certification requirements, the most important aspect of a NIOSH-certified respirator is its fit and the amount of leakage. In addition, NIOSH emphasizes that respirators are tested against a “worst case” scenario, which includes a charge-neutralized test aerosol with particles at or near the most penetrating particle size and high air flow measured with a precise and sensitive detection method.

However, Rengasamy and Eimer (2012) concluded that current NIOSH certification test methods may not represent the most challenging conditions for nanoparticle exposure, and recommended that more stringent testing incorporate aerosols with a higher fraction of nanoparticles and use number-based detection methods to better capture true filtration performance. The study evaluated the filtration performance of 17 NIOSH-certified filtering facepiece respirators using both traditional photometric (mass-based) and particle number-based methods, with a focus on nanoparticle penetration. They found that the photometric method consistently underestimated filter penetration compared to number-based measurements, particularly for nanoparticles (<100 nm) because photometric detection is relatively insensitive to particles with low mass. Across most respirator models, particularly those with electrostatic filter media, penetration was significantly higher when measured using particle counting. The most penetrating particle size had a diameter of approximately 50 nm, indicating that most of the penetration not measured with photometric detection is due to nanoparticles.

In addition, several authors have found that nanoparticle penetration exceeds permissible levels. Balazy et al. (2006) evaluated the performance of two models of N95 respirators against NaCl nanoparticles at inhalation flow rates of 30 and 85 liters per minute. The study used particles with diameters ranging from 10 to 600 nm and found that peak penetration values occurred for particles between 30 and 70 nm when using pre-charged fiber filters. For mechanical filters, peak penetration occurred for particles with diameters of approximately 300 nm. Overall, the study found that nanoparticle penetration may be in excess of 5% at high inhalation flow rates. The fraction of N95 respirators for which nanoparticle penetration was over 5% was as high as 9/10 at a flow rate of 85 liters per minute.

Rengasamy et al. (2009) compared the nanoparticle filtration performance of various NIOSH and European Norms (“ENs”) approved filtering facepiece respirators (“FFR”). The study evaluated the penetration abilities of polydisperse NaCl aerosols with a mass median diameter of 238 nm, as well as the penetration abilities of monodisperse NaCl aerosols with a diameters ranging from 20 to 400 nm and silver particles with diameters between four and 30 nm. The study tested two FFR models of each type – N95, P100, FFP2 and FFP3 – at a flow rate of 85 L/min. Penetrations from the polydisperse NaCl aerosol test were less than one percent for the N95 and FFP2 models and less than 0.03% for the P100 and FFP3 models. The tests using monodisperse particles found that the most penetrating particle size (“MPPS”) was in the 30-60 nm range for all FFR models tested. The penetration percentages at the MPPS ranged from 0.009% to approximately 4% for all the FFR models tested. When the FFRs were treated with liquid isopropanol to remove the electrostatic charge, the MPPS shifted to 200 to 300 nm and penetration increased for all particle types, showing the importance of electret filters. Overall, the study concluded that the NIOSH-approved N95 and P100 and EN-certified FFP2 and FFP3 respirators used in the study provided expected levels of laboratory filtration performance against nanoparticles.

Zhou and Cheng (2016) evaluated the efficacy of N95 filtering facepiece respirators (“FFR”) of filtering engineered nanoparticles. The study used two commercial N95 FFR filters that were previously fit-tested to the manikin used in the study. Penetration of various engineered nanoparticles, including carbon nanotubes, titanium dioxide, and carbon-based fullerene, was evaluated at inhalation flow rates of 30, 85, and 130 L/min and compared to NaCl aerosol penetration, which is often used in NIOSH evaluations. The authors found that for new respirator filters, penetration of the NaCl aerosol was less than 5% and the most penetrating particle size (“MPPS”) was 40 nm. In contrast, penetration of the engineered nanoparticles exceeded 5% and was often greater than 5% near the MPPS, which was between 90 and 150 nm. For respirators treated with isopropanol to remove the electrostatic force, penetration increased substantially for both the NaCl aerosol and the nanoparticles. The MPPS increased as well, with the average particle size being 150 nm. The authors concluded that a possible reason for the higher penetrations of engineered nanoparticles could be due to electrostatic collection processes.

Ntlailane and Wichmann (2019) conducted a meta-analysis on studies evaluating the penetration of nanoparticles through N95 respirators. The authors reviewed 14 laboratory studies and ultimately included 13 in the meta-analysis for a total of 29 data points. The included studies evaluated penetrations of particles with diameters ranging from 1 nm to 10 μm. Ntlailane and Wichmann (2019) found that the most penetrating particle size (“MPPS”) consistently occurred in the nanoscale range (approximately 39-100 nm), confirming a shift from the traditionally assumed 100-400 nm range due to electret filter media. Across studies, mean penetration ranged from 1-6%, with an overall pooled estimate of 2.79%, below the NIOSH 5% performance threshold, but several individual studies exceeded this limit. Subgroup and sensitivity analyses showed higher penetration for monodispersed aerosols and non-manikin test setups. The authors concluded that while N95 respirators are generally effective for nanoparticle filtration under controlled conditions, their performance is influenced by factors such as aerosol characteristics, respirator design, and testing methodology, and current certification approaches may not fully capture variability relevant to real-world nanoparticle exposures.

Because respirators may not be properly fit-tested or lack an adequate seal, several other studies examined the potential for nanoparticle inward leakage under these conditions.

In 2011, Rengasamy and Eimer examined the nanoparticle penetration through N95 FFRs. Using a manikin simulating human breathing volumes of 20, 30, and 40 L/min, N95 FFRs were tested after artificial leaks were introduced to simulate seal leakage when respirators were not fit-tested. With an artificial leak of 2.41 mm, the study found that for particles sized 50 nm, the penetration rate ranged from 6.97 to 7.62%. For particles sized 100 nm, with the same-sized artificial leak, the study found a penetration rate of 6.88 to 7.68%. Additionally, when artificial leaks were introduced, especially for smaller leaks, the particle penetration capabilities for the most penetrating size, 50 nm, was two-fold higher than smaller or larger particles, though all saw increases. In 2012, Rengasamy and Eimer performed an additional study similarly examining nanoparticle penetration in N95, investigating the potential for direct penetration through the filter or inward leakage from poor fit-testing, using artificial leaks to simulate this. Four models of N95 were tested on a mannikin simulating human breathing volumes of 8, 20, 30, and 40 L/min, and an artificial leak sized 3 mm was introduced. The study found that particles sized 45 nm, which is in the nanoparticle range, were the most penetrating particles. With an artificial leak, the study found that 13.6 to 30.4% breakthrough for 45 nm particles.

In 2014, Rengasamy et al. continued their research by evaluating submicron-size aerosol penetration and inward leakage through N95 FFRs. Two N95 models were tested on a manikin, with 8 and 40 L/min breathing models, simulating human inhalation rates. Various numbers of artificial leaks sized 3 mm were introduced to simulate masks without fit-testing. The study found that 45 nm particles were the most penetrating. For a mask with two 3 mm artificial leaks, the study found that the leakage rate for 45 nm particles ranged from 8.56 to 11.75% using N95 masks. When this increased to four 3 mm leaks, the study found that the inward leakage for 45 nm increased to 27.86 to 30.66%, and with six 3 mm leaks, the study found an inward leakage for 45 nm to be between 31.45 to 38.75%.

4.3.2. Silicosis Outbreaks from Engineered Stone

In 2010, Martinez et al.’s study was the first documented report of a silicosis outbreak from engineered stone. Three construction workers in Spain were exposed to high concentrations of silica from working with artificial stone and developed silicosis at an atypically young age. In 2010, a study by Garcia Vadillo et al. in Spain also found an outbreak of silicosis among quartz conglomerates or engineered stone workers. These workers were between the ages of 26 and 37, with an average of 29, and had relatively short periods of exposure, with a range of 5 to 12 years and average of 9 years.

In 2011, Pascual et al. identified another outbreak of silicosis among Spanish engineered stone workers who had worked with engineered stone since 1995. Of the eleven workers, six (54.5%) were diagnosed with silicosis. In 2012, Kramer et al. conducted a retrospective cohort study to investigate a silicosis outbreak in Israel among artificial stone workers. Between 1997 and 2010, Israel documented 25 silicosis cases, 10 of which were serious enough to warrant a lung transplant. All patients presented with moderate to severe restrictive lung disease and were responsible for dry cutting high-silica engineered stone products. The study found a highly significant incidence ratio for the development of silicosis among these artificial stone workers. In 2012, Bartoli et al. noted seven cases of silicosis, one of which was severe, among 29 engineered stone workers in Tuscany, Italy.

In 2014, Perez-Alonzo et al. documented 46 cases of silicosis among male workers in the artificial stone industry diagnosed between 2012 and 2014. Diagnosed workers had a median age of 33 years and a median of 11 years manufacturing engineered stone countertops. In 2015, Yates et al. identified the first case of silicosis in Australia from engineered stone in a 52-year old man. He had worked as a stone cutter for over 20 years and was responsible for cutting and polishing engineered stone countertops. That same year Friedman et al. published their study documenting the first case of silicosis from artificial stone processing in Texas. A 37-year old worker who had worked at the company for 10 years as a polisher, laminator, and fabricator was diagnosed with progressive massive fibrosis, the most advanced stage of silicosis. In 2018, Hoy et al. documented seven cases of silicosis from artificial stone fabrication in Australia. Workers had a median age of 44 years, with a range of 26 to 61, and between 4 and 10 years of exposure, with a median of 7 years. 85.7% of cases demonstrated progression to progressive massive fibrosis.

In 2019, Rose et al. identified several cases of silicosis among artificial stone workers in the United States. In California, six cases of silicosis at an engineered stone countertop fabrication company were identified. There were two deaths resulting from silicosis at this facility: a 38-year old man who worked at the company for 9 years and a 36-year old man who worked at the company for 13 years. Another 36-year old man was diagnosed with silicosis after working with the company for 11 years. The remaining three workers, aged 35 to 59, were positive for silicosis. In Colorado, seven cases of silicosis were reported between June 2017 to December 2018. These workers were employed at stone fabrication companies that worked mainly with engineered stone. Five reported direct exposure to engineered stone through cutting, grinding, and polishing while two were exposed through “workplace housekeeping.” Multiple patients had developed severe complications, with two having developed silicotuberculosis and five demonstrating evidence of progressive silicosis. Between March and April 2019 in Texas, a cluster of silicosis cases were identified at an engineered stone countertop fabrication facility. The four confirmed cases were aged 40 to 59 years old and were responsible for cutting, gluing, and finishing artificial stone countertops. Half of the cases reported moderate to severe reductions in pulmonary function. In 2018, a silicosis case was identified in Washington. The 36-year old worker had only worked in the stone countertop fabrication industry for 6 years, with tasks including cutting, polishing, and laminating natural and engineered stone. He was diagnosed with progressive massive fibrosis, the most advanced form of silicosis.

In 2019, Ronsmans et al. identified two cases of silicosis in a two-man company that produced and installed kitchen countertops. One man was 41 years old and only worked for 9.5 years in engineered stone fabrication while the other man was 46 years old and worked for 9 years in artificial stone manufacturing. In 2019, Ophir et al. examined 68 non-smoking patients with up to 20 years of artificial stone dust exposure. The study found that 29 of them had silicosis.

Leso et al. (2019) conducted a systematic review to understand the association between AS derived silica exposure and silicosis development. The study reviewed over 109 peer-reviewed studies that focused on AS dust and silicosis. The authors found that while many of the studies were observational, they recognized an unusually high incidence of silicosis over short periods of investigation associated with occupational exposure to RC in AS activities. The authors suggested that this may indicate a cause-effect relationship between RC exposure from AS and silicosis.

Wu et al. (2020) conducted an investigation comparing 18 patients with artificial stone associated silicosis with 63 patients with natural stone-associated silicosis. The study focused on 81 patients with newly diagnosed silicosis that were recruited from the Department of Occupational Medicine and Toxicology in Beijing Chao-Yang Hospital. The study required all patients to complete a standardized questionnaire regarding their occupational histories, where they were subsequently sorted into two groups: artificial stone-associated silicosis and natural stone silicosis. The authors found that compared with natural-stone associated silicosis, AS silicosis was associated by a shorter latency period, rapid radiological progression, and an accelerated decline in lung function and high mortality. These findings support the notion that AS silicosis is distinct from NS-associated silicosis with shorter onset periods.

In 2020, Leon-Jimenez et al. expanded upon Perez-Alonzo et al.’s 2014 study examining silicosis prevalence among artificial stone workers in the Bay of Cadiz region in Spain. In total, the study found 104 cases of silicosis, with 7 having progressive massive fibrosis, the most severe form of silicosis. The average age of silicosis diagnosis was 36.2 years, with an average exposure of 12 years. After an average of four years of follow-up, the number of progressive massive fibrosis cases had greatly increased to 40 (37.7% of silicosis cases). In 2020, Hoy et al. identified 86 cases of silicosis among artificial stone countertop fabricators in Victoria, Australia. 25.6% of the workers diagnosed with silicosis had worked in the industry for under 10 years, indicating the development of accelerated silicosis.

In 2022, Hua et al. performed a meta-analysis of 169 engineered stone workers with silicosis across Israel, Spain, Australia, and the United States to examine their demographics and characteristics. The mean age of diagnosis was 51.7 years old, with an average work duration of 19.9 years. 32.5% workers had progressive massive fibrosis, 18.5% of which had 10 or few years of work in the engineered stone industry, a relatively short period of time. In 2022, Ronsmans identified an outbreak of silicosis among workers in the skirting board manufacturing industry. Skirting boards are similar to engineered stone countertops, composed of a silica-polymer mixture. Four workers were diagnosed with silicosis, with ages as young as 38 years and years of exposure as little as 7. In 2022, Edwards documented the prevalence of silicosis among 1509 engineered stone workers in Queensland and Victoria, Australia. 362 of workers (24%) sampled had silicosis.

In 2023, Hoy et al. screened 544 stone and benchtop workers in Australia to determine the prevalence of silicosis in this industry. 95% of subjects worked with artificial stone and 86.2% dry processed the stone or were exposed to dry processing activities. Of the 544 workers, 117 (21.5%) were diagnosed with silicosis, with a median age of diagnosis of 42.1 years. The median duration from the first exposure to silicosis diagnosis was 12 years. In 2023, Fazio et al. examined the prevalence of silicosis among immigrant engineered stone fabrication workers in California, identifying 52 cases. The median age of diagnosis was 45 years, and 38% presented with progressive massive fibrosis. In 2024, Feary et al. identified the first eight cases of silicosis from artificial stone fabrication in the United Kingdom. The median age at diagnosis was 34 years old with a median dust exposure of 12.5 years, though half the subjects had exposures between 4 to 8 years. In 2024, Reynolds et al. identified a case of silicosis in a 31 year old who was responsible for operating a CNC machine at a stone fabrication facility that “mostly” processed artificial stone. He had only worked there for five years. In 2025, Flattery et al. published the results of silicosis surveillance in California from 2019 until 2024. Overall, the study documented 296 cases of silicosis, with 243 (82%) being associated with engineered stone exposures. Workers with engineered stone silicosis were much younger than those non-engineered stone silica (46 years old compared to 65 years old). Among those diagnosed with engineered stone silicosis, the median age of death was 46 years old, with a median interval from diagnosis to death being approximately 2 years.

In 2026, the American Thoracic Society published a report on Artificial Stone-associated silicosis, calling for the elimination of high-silica artificial stone. The report specifically identified artificial stone-associated silicosis (AS silicosis) as an emerging epidemic of preventable occupational disease. Figure 4.10 below demonstrates the rising number of AS-Silicosis cases throughout various locations from 2005 until 2025. The report additionally highlighted the rapid emergence of AS silicosis and more importantly the ineffectiveness of regulatory controls on mitigating this growth. The report ultimately calls for more stringent regulations, suggesting that where appropriate, material substitution and elimination should be implemented.

4.4 Australia’s Engineered Stone Ban

In response to extensive scientific evidence gathered by respiratory and occupational health experts, the Australian government became the first in the world to ban engineered stone entirely. After finding out that regulatory action alone was ineffective, in July of 2024, the government implemented a nationwide prohibition of engineered stone containing more than 1% crystalline silica.

The decision was backed by extensive scientific evidence funded by the Australian government. This included wide-scale health screening programs for the stone benchtop industry. The screenings found high prevalence rates among active fabricators. An initial screening conducted in Queensland found 98 cases of silicosis among the first 400 workers screened, while another initiative discovered 99 confirmed cases of silicosis among 400 screened workers. One of the cohorts, as discussed in Edwards (2019), had workers as young as 23, finding that while many were asymptomatic many also had progressive massive fibrosis (PMF).

Australia did not initially ban engineered stone after these discoveries, initially attempting to manage the hazard through regulatory enforcement. In Australia, the silicosis outbreak began in 2015 as a result of heavy artificial stone use in countertop fabrication. Starting in 2018, Queensland began prohibiting the dry cutting of artificial stone, further requiring the use of PPE, air and health monitoring, dust control practices, and training for all workers and employers. In spite of these robust controls and measures, they failed to address these issues. Following aggressive workplace inspections, where Queensland inspectors investigated all 138 known workplaces that cut artificial stone, they issued 552 violations to the 138 shops, averaging approximately four violations per shop. This demonstrates that in spite of these regulations, there was rampant, systemic non-compliance across the entire state.

In 2019, the Australian government created a National Dust Disease Taskforce (NDDT), to formally investigate and review scientific and medical evidence regarding ES silicosis. In 2021, the NDDT warned stakeholders that if “significant improvements in work safety” were not achieved within three years, the product should be banned. Further research provided evidence that preventative measures did not protect workers effectively.

In September of 2019, the state of Victoria prohibited dry processing of artificial stone entirely. Subsequent research demonstrated that even after regulatory changes, 24% of jobs in the stone benchtop industry had exposure to dry processing. While this value was down from 87% prior to the regulatory changes, it provided evidence that in spite of the ban, dry processing continued illegally.

After NDDT’s recommendations, Safe Work Australia (SWA), the federal Occupational Health and Safety body in Australia, began to investigate the best ways of managing the risks of RCS at work. In August of 2023, SWA released its Decision Regulation Impact Statement (RIS) which discussed their evaluation of three primary options: a ban on the use of all engineered stone, a ban on the use of engineered stone with a crystalline silica content of 40% or more, and a ban on the use of ES with CS greater than 40% or more and a licensing scheme for ES with less than 40% CS.

SWA ultimately concluded that traditional enforcement and licensing was far too costly and insufficient in protecting workers from the toxicity of engineered stone dust. A critical factor in determining this decision was the availability of alternative products that manufacturers could switch to less hazardous alternatives such as natural stone.

This analysis further evaluated the economic feasibility of a complete ban of ES. Their formal breakeven analysis demonstrated that the prevention of 51 cases of silicosis of the appraisal period could offset the estimated $251.1 million economic cost of prohibition. They further concluded that the ban was the most economically viable option to address the silicosis crisis as it did not lead to a loss of jobs and viable alternatives, such as natural stone, were readily available and price-competitive.

Based on the weight of this evidence, in March of 2024, the federal, state, and territory governments of Australia agreed to release a full ban that prohibited the manufacture, supply, processing,and installation of ES containing more than 1% CS. Australia has demonstrated that the banning of artificial stone has had no negative economic effects, with fabricators and manufacturers making and selling countertops at the same rate as they had prior to the ban. The Australian government has further concluded that the ban is working as intended, with crystalline silica containing artificial stone virtually disappearing from the Australian market.

Figure 4.11 summarizes Australia’s regulatory progression. The figure demonstrates that Australia did not begin with a ban. While regulators first attempted conventional controls, those measures failed to reliably prevent disease and exposure. Australia’s final decision to eliminate engineered stone from the market reflects the conclusion that removal of the hazard was necessary to protect workers.

While California faces a similar silicosis epidemic among their own fabrication workers, the extent to which their ban could replicate Australia’s success could face some legal challenges. Most notably, Australia controlled the entire supply chain for artificial stone, including imports, manufacture, and sale. Australia, therefore, was able to institute nationwide import bans, supply bans, and tight custom controls to remove the ES from the market entirely.

California Division of Occupational Safety and Health (Cal/OSHA), on the other hand, can only regulate the sites of employment including where fabrication and installation occurs. They lack the authority to ban the importation of ES or prohibit the retail sale of the material. Cal/OSHA further highlights that if ES remains commercially available to consumers in California, non-compliant shops may go “underground” to avoid regulations. Regulators further raise concerns that worker risks may therefore concentrate in least regulated spaces, or that fabricators may move out of California in order to evade this enforcement.

4.5 Cal/OSHA’s Engineered Stone Ban

In the United States, California has been the primary focus of the engineered stone silicosis epidemic since the first reported ES silicosis outbreak in 2019, which led to two fatalities of workers in their 30s. In response, California initiated a Special Emphasis Program (SEP) focused on reducing worker exposures to RCS through enforcing compliance with respiratory protection standards and silica standards. The SEP discovered overexposures occurred in two-thirds of workplaces, most commonly for failures to perform exposure assessments, communicate RCS hazards, and to perform medical surveillance.

In 2023, public health officials and physicians published the largest US case series of ES silicosis, which included 52 cases. The cases primarily consisted of Spanish-speaking Latino immigrant men employed in countertop fabrication shops. Diagnosis was delayed in 58% of these cases, with many of those cases having already developed progressive massive fibrosis (PMF), the most severe form of silicosis. Nearly one in five of those initial cases resulted in death, which highlighted the urgent need to address the emerging issue of silicosis among ES workers.

Figure 4.12 shows the year-by-year increase in reported California cases. It demonstrates that the epidemic continued to grow even after regulators recognized the hazard and began imposing stricter requirements.

Figure 5.13 shows the cumulative burden of disease in California. This illustrates the scale and acceleration of the epidemic: engineered stone silicosis was not an isolated cluster, but a rapidly expanding occupational disease outbreak.

As California’s silicosis epidemic among engineered stone intensified, California regulators began to realize that even the most stringent regulations were failing to adequately protect workers. In 2023, California adopted an Emergency Temporary Standard (ETS), which was later made permanent in 2025, which attempted to eliminate silicosis among artificial workers. The initial ETS required the use of wet methods, HEPA vacuums, and powered air-purifying respirators (PAPRs).

However, employer compliance of the standard was drastically low, as CAL/OSHA cited 94% of inspected shops for violations, with 20% requiring emergency shutdown orders. Cal/OSHA further acknowledged that even in fully compliant shops, workers may still be exposed to harmful silica levels from nanoparticles that engineering controls “cannot adequately capture.”

The ETS was proving largely ineffective, and the public health consequences in California were severe. Surveillance data indicated that silicosis cases among ES workers were still on the rise, effectively doubling every 13 months. Regulators further identified that among the hundreds of affected workers, the most affected are a deeply vulnerable population, estimating that approximately 98 to 99% of the work force Latino men, the majority of whom are foreign-born. They further recognized that immigration enforcement concerns reduce the likelihood that workers report unsafe conditions, which may create an environment where exploitation and health harms go unchecked.

In December of 2025, the Western Occupational and Environmental Medical Association (WOEMA) filed Petition 609 to the California Occupational Safety and Health Standards Board requested revisions to the crystalline silica standard to prohibit all fabrication and installation tasks on engineered stone containing more than 1% crystalline silica. The petition was driven by the growing body of knowledge that existing regulations, enforcement efforts, and respiratory protection programs had repeatedly failed to halt the accelerating silicosis among countertop fabrication workers.

Cal/OSHA, upon reviewing the petition, concluded that the fabrication and installation of engineered stone products with greater than 1% silica is “inherently dangerous, highly toxic, and harmful to workers.” They further added that “worker exposure should be prohibited.” This conclusion arose after years of escalating regulatory invention. Cal/OSHA has further recognized the economic realities of widespread compliance is unlikely, noting that a fully compliant fabrication shop may require investments of at least $250,000, which may still be inadequate for protecting workers from CS. Meanwhile, based on the current Cal/OSHA penalties, non-compliant operations can set up for approximately $30,000 and face modest penalties with the average Cal/OSHA penalty being approximately $14,000. This large disparity in costs between compliance and non-compliance is unlikely to sufficiently incentivize compliance.

Based on these findings, California regulators determined that ES presents inherently hazardous occupational exposures that cannot be adequately controlled under real-world conditions, even with the best practices. In 2026, the Cal/OSHA board moved forward with Petition 609, beginning to evaluate state-wide prohibition, concluding that the prohibition on all fabrication and installation tasks on engineered stone that contains more than silica may be the quickest and most cost-effective way to reduce silicosis in California.

This is supported by NIOSH’s Hierarchy of Controls, which ranks hazard control strategies from most to least effective. This includes elimination, substitution, engineering controls, administrative controls, and personal protective equipment (PPE). This is demonstrated in the figure below.

The hierarchy essentially assumes that in the absence of elimination or substitution of the product, engineering controls such as engineering controls, administrative controls, and PPE can reduce airborne concentrations to reduce worker risk to acceptable levels. While this approach is successfully applied to many industrial exposures, engineering stone has demonstrated that these controls are largely inadequate. The extreme silica content of engineered stone, combined with its generation of highly reactive nanoparticles and VOCs, creates hazards that are unusually difficult to control with conventional protective measures.

California’s experiences with silicosis among engineered stone illustrates these challenges. California has made rigorous attempts to eliminate silicosis through the requirement of wet methods, HEPA vacuums,and powered air-purifying respirators (PAPRs). In spite of these efforts, Employer compliance of the standard was drastically low, as CAL/OSHA cited 94% of inspected shops for violations, with 20% requiring emergency shutdown orders. Cal/OSHA further acknowledged that even in fully compliant shops, workers may still be exposed to harmful silica levels from nanoparticles that engineering controls “cannot adequately capture.”

Even when controls are present, practical limitations can also reduce their effectiveness. Respirators require medical clearance, fit-testing, and strict worker compliance which may not be maintained within many of these fabrication shops. Wet-cutting and powered air-purifying respirators may also interfere with visibility and communication within shops, which may create safety hazards or reasons for workers to remove protections.

Furthermore, unique characteristics of ES dust create significant challenges to traditional control strategies. Engineering controls that are effective at removing relatively larger particles do not function well with nanoparticles due to their size. Research also demonstrates that the most penetrating particle size for common N95 respirators falls within the same nanometer range generated during ES fabrication. Additionally, large quantities of settled dust accumulate throughout the fabrication shop and can be resuspended during routine activities, which may extend worker exposures beyond direct operation of saws and grinders.

Similar challenges occur during countertop installation, as wet methods and enclosed ventilation are not often viable options within finished homes and businesses. Regulators, therefore, have recognized that while respiratory protection and engineering controls can reduce risk, they cannot fully eliminate exposures. Therefore, the most effective long-term solution to addressing hazards associated with ES, likely involves the elimination of the product and the substitution of the product with safer alternatives.

5 Industrial Hygiene and Exposure Science

Silica exposure assessments have been conducted as personal samples in countertop facility settings and in task-based experimental environments. They assess silica exposure for workers in different occupations, while doing different tasks, using different tools, and using different dust mitigation techniques.

The majority of existing respirable crystalline silica exposure literature measures silica exposure in broad categories of small and large tool operation and dry and wet operation. Operation of small hand tools, such as angle grinders and pneumatic polishers, is often considered within a single category. However, Philips and other scientific studies demonstrate that the respirable crystalline silica levels are highly variable depending on the specific task and tools used. Furthermore, worker time spent polishing, cutting, and grinding depends on the employer, job position, and work responsibilities. Grouping these exposures may result in an underestimate or overestimate of an individual workers exposure.

Phillips et al. 2013 Task Exposure Ranking

Furthermore, the methodology used to calculate an 8-hour time-weighted average often results in an underestimate of exposure. When the sampling time is shorter than the 8-hour or 10-hour period, exposure is often considered to be zero for the unsampled time period. This results in an underestimate of worker exposure.

The EPA’s Guidelines for the Statistical Analysis of Occupational Exposure Data states about TWA: “This approach is only valid when you can assume that there was no exposure during the remainder of the workday. This is a key assumption that should not be made without good information indicating that this is indeed the case.”

TWA-based studies are presented in Section 6.2 because many of them demonstrate that respirable crystalline silica (RCS) levels occurring during countertop work exceed historical and current regulatory limits for RCS.

5.1 Task-Based Exposure Studies

Whether or not wet methods were used, airborne silica levels during grinding, polishing, and cutting tasks are often above the OSHA PEL, posing danger to workers. Exposure studies demonstrate that airborne silica levels are consistently higher during processing of engineered stone in comparison to processing of both or processing of granite. This Section presents several peer-reviewed scientific publications that were referenced to establish the concentration of respirable crystalline silica present during various activities or tasks conducted during stone countertop fabrication.

In a 2016 CDC survey report, Qi conducted personal task based air sampling and an industrial hygiene evaluation of Stone Systems in Houston, Texas, to measure five workers’ exposures to respirable dust and respirable crystalline silica. The workers used handheld tools in the stone countertop fabrication process, and assessed tasks primarily involved polishing, grinding, and surface lamination. The engineering control utilized was supplying water to the tools throughout the fabrication process to suppress dust at its source. In accordance with NIOSH methods 0600 and 7500, air sampling for respirable crystalline silica showed that short-term exposures ranged from 27.1 to 142.6 µg/m³ for polishing and from 57.8 to 450.8 µg/m³ for grinding. The average short-term respirable crystalline silica exposures were 62.2 µg/m³ for polishing and 159.4 µg/m³ for grinding. Excluding the two outlier sampling periods, which found respirable crystalline exposures of 650 and 1535.8 µg/m³ when the laminator was cleaning stone with compressed air and performing initial grinding, the laminating short-term respirable crystalline silica exposure ranged from 48.0 to 119.0 µg/m³, with an average of 90.8 µg/m³. Overall, workers using grinders were exposed to substantially higher levels of respirable crystalline silica compared to workers using polishers. According to the authors, wet grinding and wet polishing of both granite and engineered quartz stone can result in overexposure to respirable crystalline silica, and exposure levels during wet grinding were particularly significant.

In 2014, Zwack et al. evaluated employees’ exposure to airborne crystalline silica in a manufacturing plant that made natural and engineered stone countertops. The report, prepared in response to a worker in the plant being diagnosed with silicosis, found overexposures to respirable crystalline silica despite the company using wet methods to control dust. These exposures, above OSHA’s permissible exposure limits (“PELs”), were highest for employees that used pneumatic wet grinders with diamond cup wheels. The authors conducted personal air sampling, evaluation of ventilation systems, observation of work practices, review of health and safety records, including spirometry results, and medical interviews. Air samples were analyzed for respirable particulates using NIOSH Method 0600 with a detection limit of 50 micrograms per sample. Air and bulk samples were analyzed for three types of respirable crystalline silica (quartz, cristobalite, and tridymite) using X-ray diffraction in accordance with NIOSH Method 7500. The detection limits were 5 μg per sample for quartz and cristobalite, and 10 μg per sample for tridymite. The quantitation limits were 17 μg per sample for quartz and cristobalite, and 33 μg per sample for tridymite. The polishers operated resin-bonded discs at approximately 4,500 RPM, while the grinders used diamond cup wheels running at around 7,000 RPM.

From task-based air sampling, respirable crystalline silica exposures varied from non-detects to 140 µg/m³ for polishers and from 50 to 140 µg/m³ for the grinders. Notably, exposure to engineered quartz was higher than granite or a combination of stone types, with polishers being exposed to 31 to 140 µg/m³ of respirable crystalline silica. For full-shift samples, the study found that pneumatic diamond cup wheel grinders had respirable silica levels between 93 and 140, all of which exceed the current OSHA PEL of 50 µg/m³.

In a CDC survey report, Qi and Lo conducted personal, short-term and task based air sampling of Stone Systems in Mendota Heights, Minnesota in 2016. During the site visit, researchers measured six workers’ exposures to respirable dust and respirable crystalline silica in the stone countertop fabrication process. The workers used handheld tools to polish and grind, employing the engineering control measure of utilizing water to stop dust at the source. Air sampling for respirable crystalline silica showed that short-term exposure levels ranged from 21.4 to 122.9 µg/m³ for polishing and from 114.8 to 583.2 µg/m³ for grinding. The geometric mean short-term exposures were 65.7 µg/m³ for polishing and 223.3 µg/m³ for grinding. The geometric mean silica content in respirable dust samples was 38.1% for polishing and 62.2% for grinding. Respirable dust samples from grinding contained significantly more crystalline silica than those of polishing, using p < 0.0001.

In a 2024 study in Spain, Martínez-González et al. examined the concentration of dust generated during dry cutting and polishing assessed across three different materials: granite, marble, and silica agglomerates, like silestone. The granite used was approximately 42% quartz, the silestone 80.8% quartz and 16.5% cristobalite, and the marble less than 2% quartz. This comparative observational analytical study took place in a marble shop, where a worker carried out multiple operations of these stone materials. The worker used pneumatic grinders and sanders for wet work and electric grinders and disc sanders for dry work. Among the materials tested, silica agglomerates produced the highest concentrations of respirable crystalline silica particles, particularly during dry fabrication. For dry cutting, the average respirable crystalline silica exposure was 16.79 mg/m³ and 26.13 mg/m³ for granite and silestone respectively. For dry polishing, the average respirable crystalline silica concentration was 5.44 mg/m³ and 10.73 mg/m³ for granite and silestone respectively. Even wet operations produced high levels of respirable silica. When doing wet cutting, respirable crystalline silica exposures were 1.48 µg/m³ for granite and 2.35 for silestone. Moreover, silestone had much greater silica content when compared to granite. When dry cutting, the respirable dust for granite was composed of 23.70% silica while for silestone, that number was 73.07%. For dry polishing, the respirable dust was 25.48% silica for granite and 61.31% silica for silestone while for wet cutting, the respirable dust was 22.77% silica for granite and 59.49% silica for silestone. For marble, the study found that respirable crystalline silica concentrations below the limit of detection for dry cutting and wet cutting. For dry polishing of marble, the study found that the dust was 2.49% silica, with an average respirable silica concentration of 0.34 mg/m³. According to the authors, the increased generation of fine particles in both dry and wet operation of silica agglomerates indicates that water injection alone is an insufficient dust control measure.

In 2017, Johnson et al. published a study evaluating methods for controlling respirable crystalline silica dust exposure during stone countertop fabrication tasks. The experiment times ranged from 2-minute to 20-minute averages. Specifically, they focused on measuring dust from cup grinding techniques, silicon carbon (SiC) wheels, and blade cutting. The researchers tested the efficiency of two dust suppression approaches: wet methods (using water spray or sheet-flow-wetting) and on-tool local exhaust ventilation (LEV) during activities like grinding, polishing, cutting, and drilling of engineered stone.

For diamond cups, the study found the following respirable crystalline silica concentrations across a 20 minute sampling period: grinding with water-spray wetting and LEV: 2.988 µg/m³; grinding with water-spray wetting and no LEV: 0.434 µg/m³; grinding with sheet-flow wetting and LEV: 1.128 µg/m³; grinding with sheet-flow wetting and no LEV: 2.115. For silicon carbide, using a 20-minute sampling period, the study found the following respirable crystalline silica concentrations: wheel grinding with sheet-flow wetting and LEV (0.248 µg/m³), wheeling grinding with sheet flow wetting and no LEV (2.249 µg/m³), dry wheel grinding with LEV (0.767 µg/m³), and dry wheel grinding with no LEV (4.819 µg/m³). For blade cutting using a diamond blade, the study found the following respirable silica levels produced by the activity across two minutes: sheet flow wetting and LEV (1.212 µg/m³), sheet flow wetting and no LEV (2.075 µg/m³), dry and LEV (3.203 µg/m³), and dry blade cutting and no LEV (4.332 µg/m³). The study found that respirable silica made up about 53% of the total respirable dust generated.

In 2020, Carrieri et al. investigated silica exposure during the manufacturing of artificial stone countertops, focusing on the risks posed by inhalation of respirable crystalline silica particles generated during seven minutes of continuous cutting and grinding. The study simulated these practices in an experimental, enclosed chamber, and analyzed silica content in various materials: artificial stone A (85-95% silica), artificial stone B (>85% silica), artificial stone C (<11%), and granite (unspecified). Bulk samples found the following percentages for total crystalline silica weight: artificial stone A (90.8%), artificial stone B (91.2%), artificial stone C (9.6%), and granite (30.7%). Of all the respirable particles, by weight, 51.4% and 53.6% were for quartz for materials A and B. For material C and granite, these values were 4.4% and 7.9% silica. When cutting and grinding material A, the study found an average respirable silica concentration of 50.8 µg/m³ and when performing the aforementioned actions on material B, the study found an average of 47.7 µg/m³. For material C, the average respirable silica concentration produced by cutting and grinding was 3.7 µg/m³ and for granite, they were 33.5 µg/m³ on average.

In 2015, Cooper et al. evaluated the effectiveness of three control measures in reducing respirable silica exposure during artificial stone countertop cutting with a handheld circular saw. The authors compared the standard wetted-blade condition to a wetted blade with an additional water curtain spray and a wetted blade with local exhaust ventilation (LEV). Stone countertop cutting activities occurred in an enclosed outdoor tent measuring 3.1 m x 3.1 m with a ceiling height of 2.7 m. Results showed that respirable quartz concentrations (µg/m³) ranged from 1.87 to 4.85 for the wet blade alone, 0.92 to 3.41 for the wet blade with a water curtain, and <0.12 to 0.20 for the wet blade with LEV, while dry cutting resulted in significantly higher exposures (44,370 µg/m³ quartz). The average silica concentration of the respirable dust was 58.5%.

In 2015, OSHA and NIOSH published a Hazard Alert for occupational exposure to silica. In this report, OSHA noted that in their inspection of a marble shop, they found that two finishers dry grinding green marble without any engineering controls were exposed to 39 to 45 µg/m³ of respirable crystalline silica.

Some additional studies, such as Bartoli et al. 2012, contain exposure concentrations but were excluded from our analysis because they were not written in English.

Whether or not wet methods were used, airborne silica levels during grinding, polishing, and cutting tasks are often above the OSHA PEL, posing danger to workers. Exposure studies demonstrate that airborne silica levels are consistently higher during processing of engineered stone in comparison to processing of both or processing of granite.

Table 5.1.1 below presents the mean, UCL, and maximum silica exposure concentrations during countertop fabrication tasks for short-term task-based exposures. This table includes field based studies that involved Natural Stone. It must be noted that for natural stone, all task-based studies and all field studies had the same values.

Table 5.1.1: Summary of Task-Based Exposure for Natural Stone Countertop Cutting (All-Task Based Studies)

For demonstrative purposes, the mean, UCL, and maximum silica exposure concentrations presented in Table 5.1.1 are plotted and compared to background silica concentrations in Figure 5.1.1 below.

Table 5.1.2 below presents the mean, UCL, and maximum silica exposure concentrations during countertop fabrication tasks for short-term task-based exposures. This table only includes field studies and is inclusive of engineered and natural stone exposures.

Table 5.1.2: Summary of Task-Based Exposure for Engineered and Natural Stone Countertop Cutting (Field Studies)

For demonstrative purposes, the mean, UCL, and maximum silica exposure concentrations presented in Table 5.1.2 are plotted and compared to background silica concentrations in Figure 5.1.3 and Figure 5.1.4 below.

Figure 5.1.4: Summary of Silica Exposure Values from all Wet Processing Activities (Field Studies)

Table 5.1.3 below presents the mean, UCL, and maximum silica exposure concentrations during engineered stone countertop fabrication tasks for short-term task-based exposures. This table only includes field studies that involved engineered stone.

Table 5.1.3: Summary of Task-Based Exposure for Engineered Stone Countertop Cutting (Field Studies)

For demonstrative purposes, the mean, UCL, and maximum silica exposure concentrations presented in Table 5.1.3 are plotted and compared to background silica concentrations in Figure 5.1.5 and Figure 5.1.6 below.

Table 5.2.1 below presents the mean, UCL, and maximum silica exposure concentrations during countertop fabrication tasks for short-term task-based exposures. This table includes all task-based studies that involved natural and engineered stone.

Table 6.2.1: Summary of Task-Based Exposure for Countertop Cutting (All Task-Based Studies)

For demonstrative purposes, the mean, UCL, and maximum silica exposure concentrations presented in Table 5.2.1 are plotted and compared to background silica concentrations in Figure 5.2.1 and Figure 5.2.2 below.

Table 5.2.2 below presents the mean, UCL, and maximum silica exposure concentrations during countertop fabrication tasks for short-term task-based exposures. This table includes all task-based studies that involve only engineered stone.

Table 5.2.2: Summary of Task-Based Exposure for Engineered Stone Countertop Cutting (All Task-Based Studies)

For demonstrative purposes, the mean, UCL, and maximum silica exposure concentrations presented in Table 5.2.2 are plotted and compared to background silica concentrations in Figure 5.2.3 and Figure 5.2.4 below.

Table 5.2.3 below presents the UCL during countertop fabrication tasks for granite and engineered stone. This table only includes field studies.

Table 5.2.3: UCL of Task-Based Exposures for Granite and Engineered Stone (Field Studies)

For demonstrative purposes, the granite and engineered stone UCL exposure concentrations presented in Table 5.2.3 are plotted and compared to each other in Figure 5.2.5 below.

Table 5.2.4 below presents the UCL during countertop fabrication tasks for granite and engineered stone. This table includes all task-based studies.

Table 5.2.4: UCL of Task-Based Exposures for Granite and Engineered Stone (All Task-Based Studies)

For demonstrative purposes, the granite and engineered stone UCL exposure concentrations presented in Table 5.2.4 are plotted and compared to each other in Figure 5.2.6 below.

5.2 8-hr TWA Studies

For demonstrative reasons, this Section presents several peer-reviewed scientific publications that calculated the time-weighted average concentration of respirable crystalline silica present during various activities conducted during stone countertop fabrication.

In 1999, Simcox et al. published a study regarding silica exposure during granite countertop fabrication in Applied Occupational and Environmental Hygiene. The study focused on six small businesses fabricating granite countertops and similar products, each employing 3 to 10 workers. Crystalline silica exposure was linked to specific tasks like cutting, grinding, and finishing granite, tasks that produce airborne silica dust. Light-colored granite had higher silica content (25–45%) compared to darker granite (0–15%). Researchers collected 43 air samples to measure respirable crystalline silica concentrations, providing time-weighted average (“TWA”) exposure levels across work shifts. For the purpose of this case study, they divided the six work sites into two types of processes: those who used handheld grinders and saws without water were called dry processes, and those who used wet methods such as water-fed angle grinders and milling tools were identified as wet processes.

In total, they collected 19 samples of workers that used dry processes and 18 that used wet processes. Workers using dry processes experienced exposure levels significantly above the then-permissible limits (100 µg/m³), with exposures up to 700 µg/m³. Approximately 63% of samples from dry processes exceeded this limit, and every company’s average silica concentrations were greater than the PEL, recording average respirable crystalline levels of 430, 490, 220, and 160 µg/m³. Wet processes, including water-fed tools and milling machines, reduced silica concentrations to below the then-PEL of 100 µg/m³. However, the majority of wet processes would violate the updated OSHA 50 µg/m³ that was adopted in 2016. These include the following activities: Retrofitted angle grinders with water-fed angle grinders (60 µg/m³), water-fed milling machine with water-fed angle grinders (60 µg/m³), water-fed milling machine (60 µg/m³), and water-fed wet grinders, wet curtains, and automatic edge profilers (60 µg/m³). 70% of personal samples represented at least six hours of an eight hour shift, and unsampled time was assumed to have zero exposure.

A paper by Fairfax and Oberbeck (2010) discusses a case study that examined employees involved in cutting, grinding, and polishing granite and marble slabs using specialized tools such as bridge saws, pneumatic power tools, and a computer-controlled borer. The employees who were monitored over multiple inspections were either fabricators or bridge saw operators. The fabricators performed buffing, grinding, and polishing jobs using pneumatic power tools. Some employees sampled were wearing respiratory protection such as N95 filtering facepiece respirators, while others were not. Personal samples were collected from workers and adjusted to be an 8-hour TWA, and the respirable crystalline silica PEL for each sample was calculated using the following formula:

PEL for respirable crystalline silica = .

In their first inspection, when engineering controls, such as water spray systems for bridge saws and a water mist coupled with a cascade system and a push-pull ventilation system for hand tools, had not been implemented, there were two violations of OSHA’s PEL, both from the fabricators. One fabricator was exposed to 3070 µg/m³ of respirable dust that was 14% quartz, above the calculated PEL of 625 µg/m³. The other was exposed to 1340 µg/m³ of respirable dust that was 11% quartz, above the calculated PEL of 769 µg/m³. The bridge saw operators were exposed to 330 µg/m³ of dust that was 15% quartz and 550 µg/m³ of dust that was 13% quartz, both below the calculated PELs of 588 µg/m³ and 667 µg/m³. After the engineering controls had been implemented, two subsequent inspections found respirable dust exposures of 400 µg/m³ with 8.2% quartz and 470 µg/m³ with 10.8% quartz for fabricators, which were below the PELs of 980 µg/m³ and 780 µg/m³.

In the third set of inspections, despite the implementation of water-based controls, there were numerous violations of the PEL. One fabricator was exposed to silica concentrations over four times the PEL, their sampling recording respirable dust levels of 1810 µg/m³ with 20.4% quartz, above the calculated PEL of 450 µg/m³. Two other fabricators were also exposed to respirable silica concentrations above the PEL: 490 µg/m³ with 18.8% quartz, above the PEL of 480 µg/m³, and 490 µg/m³ with 18.6% quartz, above the PEL of 485 µg/m³. Only the bridge saw operator had exposures below the PEL, being exposed to 90 µg/m³ with 15.9% quartz, below the PEL of 560 µg/m³. Even after implementing their abatement process, which included prohibiting the use of compressed air for cleaning and adding improved ventilation, the company still recorded violations. One of their fabricators was exposed to 7400 µg/m³ of silica with 0.7% quartz, above the calculated PEL of 3700 µg/m³. This study demonstrates that wet fabrication methods alone may not reduce silica exposure to below Permissible Exposure Limits, even when the silica content of the stone is lower. It does not assess ultrafine particle count or other hazardous components of engineered stone.

In 2013, Phillips et al. investigated respirable silica exposure in stone countertop fabrication shops. Sampling was conducted in four shops using various fabrication techniques, including hand tools, automated machines, and wet and dry methods. For partial shift samples, the study found the following geometric average respirable crystalline silica concentrations: all wet (60 µg/m³), mostly wet (65 µg/m³), wet and dry (1200 µg/m³), mostly dry (1200 µg/m³), and all dry (1200 µg/m³). Particularly for the dry samples, silica concentrations for the most-exposed workers were several times greater than the then-PEL of 100 µg/m³. Critically, even among shops that predominantly or completely use wet methods, the presence of another worker performing dry work nearby had elevated silica concentrations to 308 µg/m³ and 770 µg/m³, much greater than the geometric mean of 60 µg/m³. When looking at TWA exposures, the study found violations of the then-OSHA PEL of 100 µg/m³ among workshops that used wet and dry methods, mostly dry methods, and all dry methods, with geometric average silica concentrations of 1200 µg/m³, 1000 µg/m³, and 870 µg/m³ respectively. Additionally, the geometric mean of the TWA exposure for mostly wet methods was 83 µg/m³, exceeding the now-OSHA PEL and 1974 NIOSH REL of 50 µg/m³. This study demonstrates that wet fabrication methods alone may not reduce silica exposure to below Permissible Exposure Limits, even when the silica content of the stone is lower. It does not assess ultrafine particle count or other hazardous components of engineered stone.

In 2020, Guarnieri et al. examined the prevalence of silicosis among engineered stone countertop fabrication workers in northeastern Italy. 45 workers from 11 stone companies, eight family or artisan companies and three large factories, were sampled. In the smaller shops, these workers were responsible for dry-cutting and polishing kitchen countertops. In two of the factories, wet finishing was used. The 8-hour TWA for these activities ranged from 260 to 744 µg/m³.

In 2021, Salamon et al. analyzed occupational exposure to crystalline silica in artificial stone processing at four different facilities in Northern Italy. The facilities utilized wet or dry manual finishing, along with preventative measures such as wet mechanical processing and local exhaust ventilation. Personal silica exposure was measured using GS3 cyclones placed in the breathing zone throughout the work shift, and silica concentrations were quantified through X-ray diffraction analysis. For wet mechanical processing, the average respirable silica concentration was 16 µg/m³. For dry manual finishing, the average respirable silica concentration was 39 µg/m³, with concentrations up to 98 µg/m³, and for wet finishing, the average respirable silica concentration was 20, with levels up to 54 µg/m³. The highest exposure was observed during dry finishing operations.

A 2024 study by Seneviratne et al. investigated respirable silica exposure among migrant workers working at engineered stone fabrication workshops. 6 workshops responsible for making bathroom countertops were chosen, with 24 workers being sampled. In total, approximately 79% of the sampled workers had personal exposures greater than the Australian Workplace Exposure Standard (WES) of 100 µg/m³ for respirable crystalline silica. Workers responsible for dry finishing tasks had the highest exposures, with those using hand-held power tools having levels more than 7 to 14 times the WES. Approximately 85% of dry finishing workers experienced silica exposures greater than the WES. “Most” wet finishing workers were exposed to concentrations above the WES, with one worker, who operated a high-pressure water-fed pneumatic grinder being exposed to respirable silica almost 20 times the WES. “Some” wet cutting bridge saw operators were also exposed to silica levels above the WES, with a maximum concentration for workers responsible for wet cutting being slightly greater than 200 µg/m³. Across the workers that performed tasks using water-fed tools, 71% experienced respirable crystalline silica concentrations above the WES.

A 2024 study by Weller et al. evaluated respirable crystalline silica exposure among workers that work at engineered stone fabricating workshops. 30 stone fabrication workshops in the Sydney metropolitan areas were selected for personal sampling, all of them using wet methods of fabrication, which included the use of large stonecutting tools, such as bridge saws, and pneumatic hand tools for cutting, grinding, and polishing. The sampling duration was at least 75% of the worker’s full shift, and, in total, 123 personal samples were collected. Among the semiautomated tools, miter saw and bridge saw workers had the highest respirable silica exposures at 47 and 39 mg/m³ respectively. For semiautomated edge polishers and routers, the study found silica exposures of 19 and 22 mg/m³ respectively. Hand grinding/cutting and polishing produced a respirable silica concentration of 62 mg/m³, hand polishing only 36 mg/m³, and hand laminating 32 mg/m³. Hand cutting /grinding activities combined with hand polishing were conducted while working inside of a walk-in booth. Pneumatic hand grinding/cutting and hand laminating activities were sampled within workshops. The authors described hand laminating as including gluing of the ES in order to finish and finalize the product. The authors discussed how hand lamination does not generate airborne dust or mist, and the similarity in exposure concentrations could be due to close proximity to hand polishing activities. Other activities, which include hand grinding and polishing for short periods of time, transportation of material, and wet clean-up of debris, had a respirable silica exposure of 33 mg/m³.

McGowan et al. (2025) examined respirable silica concentrations in stone fabrication workshops across the United States. 1,100 stone fabrication companies were surveyed, and data from 257 countertop workshops was analyzed. Almost all the stores fabricated both natural and engineered stone, with the approximate percentage of natural to fabricated among stores that do both being 37% natural and 52% engineered. Respirable silica concentrations were broken down by activity: large tools, small tools, installation, handling, and support. Activities under the large tools include using CNCs to cut, shape, and drill, bridge saws to cut stone, and machines for polishing. Activities under the small tools include cutting with hand saws, hand grinding, shaping and drilling, hand polishing, edge laminating, and preparing the miter. All samples have been converted to 8-hour time weight average (“TWA”) exposures for respirable crystalline silica. For large tools, the study found the following average respirable silica exposures: dry: 35 µg/m³; dry with local exhaust ventilation (LEV): 12 µg/m³; wet: 19 µg/m³; wet with wall exhaust: 5.7 µg/m³. For small tools, the study found the following average respirable silica concentrations: dry: 1,258 µg/m³; dry with local exhaust ventilation (LEV): 286.5 µg/m³; wet: 21.3 µg/m³; wet with wall exhaust: 5.9 µg/m³; wet and dry 55 µg/m³. When installing stone countertops, handling stone material, and performing support activities, the study found average respirable silica concentrations of 47.8 µg/m³, 10.7 µg/m³, and 8.4 µg/m³ respectively.

Dry methods are more dangerous than wet methods. Whether or not wet methods were used, airborne silica levels during grinding, polishing, and cutting of engineered stone are often above the OSHA PEL, posing danger to workers.

Demonstrative images of dust production during various stone fabrications tasks are presented in the figures below.

6 Epidemiology and Dose-Response Evidence

Relative risk (or risk ratio), odds ratio, and hazard ratio are three statistical measures used in epidemiology to compare the likelihood of an outcome between two groups.

To understand the difference between risk ratios and odds ratios, it is important to understand the difference between risk and odds.

Risk is calculated by comparing the number of members in a group with disease to the total number of members in a group. Risk of disease within an exposed group (or an unexposed group) is calculated using the following formula:

Risk = Number of Members in Exposed Group with Disease / Total Number of Members in Exposed Group

Relative risk (or risk ratio) compares the probability of an event occurring in an exposed group to the probability of an event occurring in an unexposed group. It is often used in cohort studies. It is calculated using the following formula:

Relative Risk = Risk of Disease in Exposed Group / Risk of Disease in Nonexposed Group

Odds, on the other hand, are calculated by comparing the number of members in an exposed group (or unexposed group) with disease to the number of members in an exposed group (or unexposed group) without disease. This is described by the following formula:

Odds = Number of Members in Exposed Group with Disease / Number of Members in Exposed Group without Disease

An odds ratio is the odds of disease in an exposed group compared to the odds of disease in an unexposed group. Odds ratios provide a measure of the strength of association of two variables and are often used in case-control studies. An odds ratio is calculated using the following formula:

Odds Ratio = Odds of Disease in Exposed Group / Odds of Disease in Unexposed Group

For both relative risk and odds ratios, a result of 1.0 indicates that there is no difference in risk of disease in exposed and unexposed populations. A relative risk or odds ratio of greater than 1.0 indicates that there is a greater risk of disease in the exposed population, while a relative risk or odds ratio of less than 1.0 indicates that there is a greater risk of disease in the unexposed population.

A hazard ratio compares the rate at which events, such as disease diagnosis, occur over time between groups. Hazard ratios are calculated by comparing the hazard rate of the exposed group to the hazard rate of the unexposed group.

6.1 Silicosis

This Section details epidemiological studies demonstrating the minimum threshold of cumulative silica dust exposure that has been shown to increase the risk of silicosis. The epidemiological studies in this Section demonstrate the increased risk of silicosis from varying levels of cumulative silica dust exposure. These studies show more than a statistically significant doubling of the risk for silicosis. However, it must be noted that these studies use the lowest exposure group as the comparison group. This means that these risks are likely underestimations of true risk since they do not compare to an unexposed group. These studies are therefore included to be holistic but may not fully represent the risk associated with silica exposure.

6.1.1 Radiological Measurements of Silicosis

To determine if a given individual has silicosis, the International Labor Organization (ILO) has created a classification system for systematically describing and recording radiographic abnormalities in postero-anterior chest radiographs that are consistent with forms of pneumoconiosis. Parenchymal abnormalities are classified into small and large opacities, with small opacities further categorized by shape, size, affected area of the lung, and profusion (concentration of small opacities in affected zones of the lung.) Profusion is subcategorized into one of four categories (0, 1, 2, and 3) each of which is further divided into 12 ordered subcategories. Radiographs are recorded using two numbers separated by an oblique stroke. The first number denotes the assigned profusion category, and the second number indicates any alternative category that was seriously considered during classification. For example, a radiograph that shows profusion similar to subcategory 2/2, and neither 1 nor 3 was seriously considered as an alternative, the final classification would be 2/2.

Many epidemiological studies (Vacek at al. 2018, Kreiss and Zhen 1996, Hughes et. al 1998) that assess risk of silicosis measure presence of profusions within these subcategories, typically in ones that are consistent with a subcategorization greater than 1/0 and/or presence of large opacities. Some studies limit their assessment to rounded opacities (Vacek at al. 2018 & Hnizdo 1993). Kreiss and Zhen chose to assess both, citing previous studies that had found that both irregular and rounded opacities were related to cumulative silica exposure.

A 1993 report by Hnizdo et al. assessed correlation between radiological and pathological diagnosis of silicosis. For workers who were exposed to high average levels of silicosis, the study advised that radiograph readers should consider radiographs with category 0/1 profusions or larger to increase the accuracy of radiological positive silicosis diagnoses in comparison to diagnosis of silicosis after autopsy. For workers exposed to lower average concentrations of respirable dust, the study recommends using category 1/0 or 1/1 for a positive radiological diagnosis of silicosis.

6.1.2 Low Dose Exposure Studies

Many epidemiological studies have demonstrated that exposure to low concentrations of silica is still linked to silicosis. The following studies below provide evidence that even at low exposure concentrations, workers have an increased risk of silicosis.

Kreiss and Zhen (1996) evaluated exposure-response relationships between silica exposure and silicosis among a mining town. The study utilized a population-based cohort including subjects with silicosis, dust exposure without silicosis, and community residents with no occupational history of silica exposure. This included 100 former miners, and 34 controls. The subjects were independently classified for silicosis using chest radiographs. The authors assessed exposure-response relationships for silicosis using three exposure indices. Figure 7.1 below groups the workers according to their average airborne respirable crystalline silica exposures and demonstrates what percentage of workers in each group had developed radiographic silicosis. The figure demonstrates a clear exposure-response relationship. The study demonstrated that workers exposed to average silica concentrations as low as 0.025–0.05 mg/m³, well below historical occupational exposure limits, still developed silicosis, and disease prevalence increased steadily with increasing exposure. This provides evidence that while reducing silica exposures may lower risk, it does not eliminate it.

The authors also evaluate workers based on their lifetime cumulative exposure to silica exposure. Figure 7.2 below groups workers based on their cumulative lifetime silica dose, showing the percentage of workers within each group that had developed radiographic silicosis. The figure demonstrates that silicosis is fundamentally a cumulative-dose disease, for which measurable lung injury occurs even in the lowest exposure groups.

Steenland and Brown (1995) investigated a cohort of 3,330 gold miners with an average employment duration of 9 years. The study relied upon an average follow-up of 37 years, reconstructing exposures using job-exposure matrices and estimated dust exposures for each job. The study evaluated silicosis rates across the cohort, based on level of cumulative exposure, further calculating cumulative risk of silicosis. This is summarized below in Figure 7.3. The data provides evidence that men can get silicosis after only brief exposures to low levels of silica.

Chen et al. (2001) conducted a cohort study of 3,010 miners exposed to silica dust while employed within four Chinese tin mines. The authors utilized historical total dust data from China in order to develop a job exposure-matrix to estimate individual exposures. Medical data was obtained from personnel and medical examination records for each employee, with silicosis diagnoses determined based on chest radiographs, with each diagnosis defined by at least two radiologists. The authors utilized cumulative silica exposures to calculate cumulative exposure risk of silicosis in relation to respirable crystalline silica, comparing these results with the results from Steenland & Brown (1995), Kreiss & Zhen (1996), and Hnizdo &Sluis-Cremer (1993 ). This is summarized below in Figure 7.4. This demonstrates a dose-response relationship between cumulative silica exposure and disease prevalence, further illustrating that even low exposures to silica can result in increases in silicosis prevalence.

Howlett et al. (2024) conducted a systematic review of existing literature on the relationship between cumulative respirable crystalline silica (RCS) exposure and silicosis. The authors reviewed eight studies, including 10 cohorts, extracting concentrations and categorical cumulative RCS exposures. The authors re-calculated cumulative risk of silicosis across those studies, developing a dose-response meta-analysis that demonstrated the estimated cumulative risk attributable to reductions in silica exposures. The authors additionally compared the cumulative risk across the eight studies analyzed. This comparison is summarized in Figure 7.5 below. While the studies involve investigations into different industries, each study consistently demonstrates that the risk of silicosis progressively increases with crystalline silica exposure while further demonstrating increases in risk at low exposures.

6.1.3 Odds Ratio Studies

A 1996 study by Kreiss and Zhen evaluated the exposure-response relationship between cumulative silica exposure and silicosis among residents of a hardrock mining town in Leadville, Colorado. The study included a community-based random sample of 134 men over age 40, with 100 miners and 34 controls who had never been exposed to dust. Researchers found that a cumulative silica exposure of 1 mg/ was associated with an odds ratio (OR) of 4.9 (95% CI 2.3 – 10.5) for a ILO category profusion greater than or equal to 1/0 and an OR of 4.3 (95% CI 1.9 – 9.6) for an ILO category profusion greater than or equal to 1/1.

A 2011 study by Vacek et al. examined relationships between silica exposure and mortality from silicosis among workers in the Vermont granite industry. The cohort included 7052 granite industry workers, among whom 55 deaths from silicosis were identified. They found that cumulative silica exposure between 3.65 and 6.71 mg/ years was associated with silicosis risk at an OR of 8.62 (95% CI 1.86 – 39.95) with the uppermost interval of cumulative exposure greater than 10.261 mg/ associated with an OR of 10.55 (95% CI 2.3-48.4). All these silicosis deaths occurred in people born before 1925, which was consistent with earlier studies that indicated that silicosis mortality happened in workers with documented exposure prior to the introduction of dust controls in 1938 -1940.

A 2018 study by Vacek et al. evaluated the exposure-response relationship between respirable quartz exposure and radiographic silicosis among 1,902 production workers with 67 cases of radiographic silicosis identified. The study cohort consisted of men employed between 1938-203 by two industrial sand companies at 40 different plants in 22 US states. To be included in the study, workers had to be employed for more than 10 years and have at least 1 posterior-anterior analog chest radiographs obtained 10 or more years after hire. The study assessed risk of small opacity profusions that were categorized as ≥1/0. Through a conditional logistic regression, they found that the risk of silicosis increased with cumulative exposure. Vacek et al. found that risk of silicosis increased with cumulative silica exposure, with an OR of 12.57 (95% CI 2.08-55.47) for a cumulative exposure between 3.01-5.5 mg/years and an OR of 25.50 (95% CI 5.52-117.82) for a cumulative exposure greater than 5.50 mg/years.

6.1.4 Relative Risk Studies

A 1998 study by Hughes et al. evaluated the exposure-response relationship between crystalline silica exposure and silicosis. They evaluated a cohort of 1,809 workers in the diatomaceous earth industry where the primary structure of silica is the cristobalite form. Researchers evaluated radiograph images for presence of small opacities with a profusion category greater than 1/0 and/or presence of large opacities. Researchers found that cumulative silica exposure and average concentration of exposure impacted risk of radiological protrusions. For workers exposed to silica concentrations ≤0.5 mg/m³, the relative risk of radiographic opacities at cumulative exposures of 3-6 mg/m³-years was 3.88 (95% CI: 1.22–12.4). For workers exposed to concentrations >0.5 mg/m³, the relative risk at the same cumulative exposure range was 11.88 (95% CI: 1.55–89.2)..

6.1.5 Hazard and Rate Ratio Studies

A 2002 study by Mannetje et al. studied the relation between exposure to crystalline silica and silicosis mortality among six cohorts that ranged from various industries such as diatomaceous earth, granite, industrial sand, and gold. Data from these cohorts were pooled in which 170 deaths from silicosis were reported. The study found significant rate ratios (RR) for the relationship between occupational exposure to silica and silicosis mortality. For the lowest cumulative exposure category (0.99-1.97 g/m³-years), the study found a significant RR of 3.39 (95% CI: 1.42-8.08), increasing to 6.22 (95% CI: 2.56-15.12) for the next exposure category (1.97-2.87 g/m³-years). For the highest exposure category (>28.10 g/m³-years), the RR was found to be 63.63 (95% CI: 19.87 to 203.8).

In 2004, OSHA’s contractor, Toxichemica Inc. commissioned Steenland and Bartell to update the silicosis mortality analyses presented in the 2002 study by Mannetje et al. The report used the same six cohorts used by Mannetje et al. in their 2002 paper. Sources of random measurement error, which were errors from assigning a mean exposure to each job and conversion errors for measurements, were combined in a Monte Carlo analysis. Additionally, a nested case-control model was used to control for the effects of age by performing an exact match over categorical. After these adjustments, in the lowest exposure category (0.99-1.97 g/m³-years), the study found an RR of 2.18 (95% CI: 0.64-7.38), which increases to 3.35 (95% CI: 1.00-11.27) at an exposure of 1.97-2.87 g/m³-years and 4.27 (95% CI: 1.26-14.55) for an exposure of 2.87-4.33 g/m³-years. For the highest exposure category of >28.10 mg/m³-years, the RR is 12.83 (95% CI: 3.34 to 49.82). Even under the more stringent 2004 modeling, workers in the highest exposure group remained over twelve times more likely to die from silicosis than non-exposed workers.

A 2020 study by Wang et al. compared the risk of silicosis in metal mines to pottery factories. They studied 39,808 workers from January 1, 1960 to December 31, 2003 in China. A cumulative respirable silica dust exposure (CDE) was conducted by creating a job-exposure matrix to personal work history. Resulting hazard ratios of silicosis for each 1 mg/m³ year increase in CDE were 1.08 for tungsten mines, 1.41 for iron and copper mines, 1.14 for tin mines, and 1.03 for pottery factories. At an exposure limit of 0.05 mg/m³ of respirable silica dust for 45 years, cumulative risk for metal mines was 2.3% and 0.6% for pottery factories.

6.1.6 Other Epidemiological Studies

A 1996 study by Rosenman et al. examined the silicosis prevalence among current and retired workers at an iron foundry that produced engine blocks. The study had 1,072 male subjects, with approximately half having worked at the foundry for at least 20 years. With 20 years of work at 100 μg/m³, the study found an odds ratio of 1.45, and with 40 years of work at 100 μg/m³, the odds ratio was 2.10. Additionally, even at the lowest cumulative exposure category of 0.2 mg/m³-years, the study found a statistically significant odds ratio (OR) of 1.04 (95% CI: 1.02-1.15), increasing to 2.10 (95% CI: 1.56-2.82) at 4 mg/m³-years and 3.04 (95% CI: 1.96-4.72) at 6 mg/m³-years.

A 2001 study by Hughes et al. performed a cohort mortality study of 2,670 men including 30 men whose deaths were ascribed to silicosis and 7 men whose deaths were ascribed to silico-tuberculosis. The study also included 50 controls. Hughes et al. integrated job histories with job-exposure matrices to calculate cumulative exposure up to the date of the death of each case. The study also addressed potential latency periods by also using lagged exposure indices, where years employed, cumulative exposure, and average concentration were calculated up to 15 years before the death of the case. The study found that a cumulative exposure greater than 5 mg/m³ years was associated with risk of silicosis (OR of 2.62) for non-lagged exposure indices. No confidence intervals were provided for the odds ratios.

A 2011 study by Mundt et al. examined the exposure-response relationship between silicosis morbidity and cumulative silica exposure in the porcelain industry. In this cohort study, the paper evaluated the work histories and medical records of 17,644 employees that had participated in silicosis screening programs from 1985 until 1988 and worked at least six months. For cumulative exposures, the study found a hazard ratio (HR) of 0.3 (95% CI: <0.1-2.6) for the lowest cumulative exposure category of 0.5-1.0 mg/m³-years, and an HR of 3.1 (95% CI: 1.1-9.3) for the highest exposure category of >3.0. The study found significant HRs for cumulative exposure levels greater than 3: 5.3 (95% CI: 1.6-17.3), 7.3 (95% CI: 2.6-20.8), and 6.8 (95% CI: 3.0-15.3) for >4-5, >5-6, and >6 mg/m³-years respectively.

OSHA noted multiple limitations with this study that could have resulted in underestimation of risk. The cohort was young, with a mean age of 35 years, and had excluded workers over 75 years old, and chronic silicosis has a long latency period of 20 to 30 years, meaning that symptoms of silicosis may not have been evident within the timeline of the study. As noted in the report, the average age of silicosis diagnosis was 56 years old, and only 9.2% of the cohort had died. Furthermore, while males accounted for only 47% of the cohort, they represented 85% of silicosis cases, therefore combining male and female data in a silicosis analysis may have depressed the effects seen. As OSHA noted, “risks of silicosis were lower among females, possibly because they did not have job assignments with exposures as high as males.” In addition, OSHA highlighted how “​​regrouping of the reference group into a cumulative exposure category of <3.0 mg/m³-year and restratification of exposure categories resulted in a baseline with greater exposures and therefore diminished ability to see effects; it is unclear if enough workers were exposed to levels above 3.0 mg/m³-year to detect a trend.” There was also evidence of exposure misclassification.

6.1.7 Epidemiological Studies (NMRD and Pneumonociosis)

A 1997 study by Checkoway et al. evaluated the dose-response relationship between silica exposure and nonmalignant respiratory disease (NMRD) mortality among diatomaceous earth workers. The study examined 2,037 non-Hispanic and 533 Hispanic white men who worked at least 12 months at the factory between 1942 and 1987. Silica exposure was quantified using air monitoring data provided by the factory. The study reported increasing mortality rate ratios (RR) for NMRD with increasing cumulative silica exposure. For example, the RR was 1.52 (95% CI: 0.55-4.20) for the lowest cumulative exposure category of 0.5-<1.1 mg/m³-years and 4.79 (95% CI: 2.01-11.9) for the highest exposure category (>=5.0 mg/m³-years). When applying a 15-year exposure lag, the study found the association remained with the RR found to be 2.04 (95% CI: 0.77-5.45), 1.96 (95% CI: 0.71-5.43), 3.17 (95% CI: 1.25-8.05), and 5.35 (95% CI: 2.23-12.8) across increasing cumulative exposure categories.

A 2002 study by Park et al. examined the relationship between exposure to respirable crystalline silica and lung disease, including silicosis, in the diatomaceous earth industry. 2,342 workers at a diatomaceous factory, composed of employees who worked at least a year between 1942 and 1994, were chosen. Crystalline silica exposure was estimated using the measured total dust concentrations, workers’ employment history, and a linear relative rate Poisson regression model. For a cumulative exposure at 1.0 mg/m³-years, the study found a rate ratio (RR) of 1.55 for the development of a lung disease other than cancer, which includes silicosis. For the mean exposure (5.79 mg/m³-years), the RR was 4.17 and for the maximum exposure (31.8 mg/m³-years), the RR was 18.4. When examining the onset of radiographic opacities that are ≥1/0, the study found an RR of 7.10 at an exposure level of 1.0 mg/m³-years. With increased cumulative exposure, there was greater risk, with the study finding an RR of 27.27 at the mean cumulative exposure (5.79 mg/m³-years) and an RR of 84.64 at the maximum recorded exposure (31.8 mg/m³-years).

A 2012 study by Chen et al. performed a cohort study of workers at metal mines and pottery factories in China to determine the relationship between exposure to silica dust and mortality to respiratory diseases. In total, the study examined 74,040 workers across 29 mines and factories who had worked for at least a year between 1960 and 1974, with a follow up at the end of 2003. Low exposure to silica dust was defined as 0.01-1.23 mg/m³-years, medium was 1.24-4.46 mg/m³-years, and high was >4.46 mg/m³-years. For nonmalignant respiratory diseases (NMRD), which includes silicosis, the study found a hazard ratio (HR) of 1.89 (95% CI: 1.60-2.24) for low exposure, 4.28 (95% CI: 3.74-4.91) for medium exposure, and 6.68 (95% CI: 5.85-7.61). For pneumoconiosis, a sub-category of NMRD that includes silicosis, the study found a hazard ratio of 4.36 (95% CI: 3.49-5.44) for medium exposure and 7.75 (95% CI: 6.21-9.67) for high exposure. This study indicates that even low levels of silica that are considered “safe” increase the risk of disease and death.

6.1.8 Risk Level Studies

A 1993 study by Hnizdo and Sluis-Cremer examined silicosis risk among white South African gold miners. Approximately 14% of the cohort, or 212 miners, had developed silicosis. For a cumulative exposure of 3.3 mg/m³-year, the modeled risk was 0.156, which increased to 0.227 when the cumulative exposure of silica was 4.5 mg/m³-year. For the actual percent of workers with silicosis, at a cumulative exposure of 3.3 mg/m³-year, the study found that 36.7% of workers had a diagnosis. For 4.5 mg/m³-year, this value was 45.5%.

A 1994 study by Ng and Chan studied the prevalence of silicosis amongst granite quarry workers in Hong Kong. The study examined 338 male workers employed between 1967 and 1985, and silicosis was determined by 1/1 ILO classification according to the majority of readers examining the chest radiographs. For employees exposed to 3.1 mg/m³-year of cumulative exposure, the study found 13% of workers had silicosis, a value that rises to 25% for 7.1 mg/m³-year and 22% for 22 mg/m³-year.

A 1995 study by Steenland and Brown evaluated the silicosis risk of a cohort of 330 gold miners in South Dakota that had worked underground for at least 1 year between 1940 and 1965. For cumulative silica exposure of 0 to 0.2 mg/m³-years and 0.2 to 0.5 mg/m³-years, the cumulative risk of developing silicosis was 0.2% and 0.5% respectively. As silica exposure increased, the cumulative risk of developing silicosis increased. At 0.5 to 1.0 mg/m³-years, the cumulative risk was 1.7% to 2.2%, and at the highest exposure category of >4.0 mg/m³-years, the cumulative risk of silicosis is 67.8% to 84%. After adjusting for competing risks of death, the study found that a 45-year exposure to 90-100 μg/m³ of silica, the then-OSHA PEL for silica, would result in a lifetime risk of silicosis of 35% to 47% for gold miners.

A 1996 study by Rosenman et al. investigated the prevalence of silicosis among 1,077 male workers, both current and retired, at an iron foundry that produced engine blocks. Approximately half of the workers had worked at the foundry for at least 20 years. For those exposed to the OSHA standard of 90-100 μg/m³, 0.3-2.7% had developed silicosis, a proportion that rises to 4.9-9.9% among workers exposed to over 100 μg/m³ of silica. For cumulative exposure <240 mg-days/m³ of silica, equating approximately 0.658 mg/m³-years, the percentage of workers that developed silicosis was 0.6%. For 240-720 mg-days/m³ (0.66-1.97 mg/m³-years), the percentage was 0.3%, for 720-2,160 mg-days/m³ (1.97-5.91 mg/m³-years), the percentage was 2.7%, and for >2,160 mg-days/m³ (>5.91 mg/m³-years), the percentage was 9.9%.

A 1996 study by Kreiss and Zhen examined the exposure-response relationship between occupational respirable crystalline silica exposure and the development of silicosis in a mining town. 134 male Leadville residents were chosen; their occupational history was recorded and they had a chest radiograph to scan for symptoms of silicosis. Among those exposed to >0-1 mg/m³-years of silica, a median of 12.5% had silicosis. This value greatly increased with higher cumulative silica exposure. For >1-2 mg/m³-years of silica exposure, the prevalence of silicosis was a median of 26.3%; for >2-3 mg/m³-years of silica exposure, the prevalence of silicosis was a median of 55.6%; for >3 mg/m³-years of silica exposure, the prevalence of silicosis was a median of 83.3%. Using logistic regression, the study estimated that for an average exposure of 0.05 mg/m³, the silicosis risk was 50% for miners who worked for 45 years and 9% for miners that had worked 25 years. After another 20 years, the 25 year miners had a 36% risk of silicosis, a percentage that increased to 67% with an additional 15 years of follow-up. For 45-year miners followed after 15 years, the silicosis risk was 78%.

A 1998 study by Hughes et al. performed a cohort mortality study of 2,323 men whose employment at a diatomaceous plant was from 1942 until 1987. For a cumulative crystalline exposure of 2.0 mg/m³-years, the risk of developing silicosis was 1.1% among the cohort exposed to an average of <0.50 mg/m³ and 3.7% among the cohort exposed to an average of >0.50 mg/m³. For a cumulative exposure of 4.0 mg/m³-years, the risk of developing silicosis was 3.3% for the lower average exposure and 12.4% for the higher average exposure.

A 2001 study by Chen et al. investigated the relationship between exposure to respirable crystalline dust and the development of silicosis among tin miners. The cohort was composed of 3,010 miners that had worked at least for one of four Chinese tin mines between 1960 and 1965. Chest radiographs were taken to determine silicosis status. For 2 mg/m³-years of exposure to respirable silica, the study found a 14% risk of developing silicosis, a value that rose to 47% for 4 mg/m³-years of exposure. For 4.5 mg/m³-years of exposure, which translates to 45 years of silica exposure at the then-OSHA PEL of 0.1 mg/m³, the study found the risk of developing silicosis to be 55%.

A 2002 study by Park et al. evaluated the association between respirable crystalline silica exposure and the development of silicosis. The cohort was comprised of 2,341 workers at a diatomaceous earth plant who had worked at least a year between 1942 and 1994. Excess risk estimates were calculated assuming workers were exposed to constant silica concentrations between 20 and 65. At the then-OSHA PEL of 0.1 mg/m³ for silica and <10 mg/m³-years of cumulative exposure, the excess risk of developing silicosis was 100/1,000. For all workers, regardless of cumulative exposure, the excess risk was 140/1,000. Using the updated OSHA PEL of 0.05 mg/m³ for silica, the excess risk of developing silicosis was 68/1,000 for workers with <10 mg/m³-years of cumulative exposure and 75/1,000 for all workers. For the lowest exposure category of 0.001 mg/m³ of constant silica exposure and <10 mg/m³-years of cumulative exposure, the excess risk of developing silicosis was modeled to be 1.6/1,000. For all workers, the excess risk of developing silicosis was 6.2/1,000. All of these are above OSHA’s acceptable risk level of 1 per 1,000.

A 2002 study by Mannetje et al. examined six cohorts across multiple industries, including diatomaceous earth, granite, industrial sand, and gold, to determine the relationship between crystalline silica exposure and silicosis mortality. Pooled data from these cohorts revealed that 170 deaths from silicosis were reported. The results showed the estimated risk of death up to age 65 from silicosis after 45 years of exposure at 0.1 mg/ silica was 13 per 1000, while the estimated risk at an exposure at 0.05 mg/ was 6 per 1000. Both of these are above the risk level of 1 per 1000 deemed acceptable by the US OSHA.

A 2004 study by Churchyard et al. investigated the exposure-response relationship between silicosis and the inhalation of respirable crystalline silica dust from gold mining. This cross-sectional study examined 520 black gold miners from South Africa, performing interviews to understand their job history and taking chest radiographs to determine whether they have silicosis. For a cumulative quartz exposure of 0 to 0.80 mg/m³-years, the percent of workers who developed silicosis was 10.7%. This value increased to 32% under the highest cumulative quartz exposure category: 1.48 to 3.08 mg/m³-years.

A 2022 study by Ranaan et al. examined the risk of developing silicosis and other diseases when occupationally exposed to silica. This cross-sectional study examined 261 Israeli workers, with 42.15% of them having been employed in the artificial marble industry and 29.5% in manufacturing and construction. The average total duration of exposure was 15.6 years, with an average yearly silica exposure level of 0.23 mg/m³ or a cumulative silica exposure of 3.59 mg/m³. In total, 25 or 9.58% of workers surveyed were diagnosed with silicosis, with an average respirable crystalline silica exposure of 0.42 mg/m³ and cumulative respirable crystalline silica exposure of 7.60 mg/m³. When compared with other scientific literature with similar endpoints, the study found that for a cumulative respirable crystalline silica exposure of 3.59 mg/m³, with an average exposure of 0.23 mg/m³ across an average of 15.6 years, the cumulative silicosis rate was 2.67% cases per mg/m³/year. Thus, after 10 years of exposure of 0.1 mg/m³ or a cumulative respirable crystalline silica exposure of 1 mg/m³, 2.67% of workers will develop silicosis, an incidence that doubles after 20 years. This translated to a relative risk of 20.54 (95% CI: 9.85 – 42.86).

A 2025 study by Wang et al. investigated the prevalence of silicosis among workers exposed to long-term low doses of respirable crystalline silica. This cohort study of 30,697 workers in China had their cumulative respirable silica exposure estimated using a job-exposure matrix based on title and facility. For workers with a lifetime silica dust exposure of less than or equal to 0.05 mg/m³, the study found that the average duration of silica dust exposure was 20.6 years with a silicosis prevalence of 3.1%. For workers with a lifetime silica dust exposure of less than or equal to 0.10 mg/m³, the study found that the average duration of silica dust exposure was 18.8 years, with a silicosis presence of 5.4%. For workers with a lifetime silica dust exposure of less than or equal to 0.35 mg/m³, the study found the average duration of silica dust exposure was 19.9 mg/m³, with a silicosis rate of 13.7%. Among the workers with silica dust exposure less than or equal to 0.05 mg/m³, when compared to Q1 cumulative exposures, the study found that the hazard ratio (HR) for Q2 was 1.32 (95% CI: 0.82 – 2.10), Q3 was 1.87 (95% CI: 1.22 – 2.88), and Q4 was 2.00 (95% CI: 1.30 – 3.09). Among workers with a silica dust exposure of less than or equal to 0.10 mg/m³, when compared to Q1 cumulative exposures, the study found the following HRs: Q2 HR was 2.52 (95% CI: 1.88 – 3.38), Q3 HR was 4.08 (95% CI: 3.09 – 5.39), and Q4 HR was 4.02 (95% CI: 3.04 – 5.32). Among workers with a silica dust exposure of less than or equal to 0.35 mg/m³, in comparison to Q1 cumulative exposures, the study found an HR of 2.8 (95% CI: 2.38 – 3.28) for Q2, 5.76 (95% CI: 4.93 – 6.73) for Q3, and 7.14 (6.07 – 8.40) for 8.40 for Q4. The study concluded that to keep the lifetime silicosis risk within 0.1%, a maximum of 11, 3, and 1 years for a cumulative exposure of 0.05 mg/m³, 0.10 mg/m³, and 0.35 mg/m³ respectively should be adhered to.

A 2026 study by DeBono et al. examined the relationship between cumulative respirable crystalline silica exposure and the development of respiratory diseases, including lung cancer and silicosis. This cohort study consisted of 93,526 miners that received medical exams from 1928 until 1988 in Ontario, Canada. Disease follow-ups were taken from 1964 until 2023. For clinically-detected silicosis, consisting of cases from 1999 to 2022, the study found elevated IRRs: relatively low cumulative exposures had an IRR of 3.56 (95% CI: 1.53 – 8.27), medium exposures had an IRR of 10.8 (95% CI: 4.84 – 24.3), high exposures had an IRR of 42.4 (95% CI: 18.6 – 95.9) and very high exposures an IRR of 55.5 (95% CI: 23.7 – 129.9).

6.1.9 Linear Dose-Response Relationship Studies

Numerous epidemiological studies have demonstrated that the risk of silicosis observes a dose-response relationship with exposure to respirable silica. This Section summarizes studies that demonstrate that this relationship may be linear.

Park et al. (2002) performed a quantitative risk assessments of silicosis morbidity on a retrospective cohort study of 2,342 white male workers who were employed for at least one year at some point between 1942 and 1994 at a California diatomaceous earth plant, and primarily exposed to cristobalite, a crystalline silica polymorph formed during the calcination of diatomaceous earth. The cohort was assembled using company employment records, and workers were followed through a comprehensive medical surveillance program that included periodic chest radiographs and occupational health evaluations.

To estimate individual worker exposures, the researchers reconstructed historical exposure levels using an extensive database of industrial hygiene measurements collected throughout the facility going back over 80 years. These measurements were linked to detailed job histories, allowing the researchers to estimate silica exposure for each worker during each period of employment. Cumulative exposure was calculated by multiplying estimated respirable silica concentrations by the duration of employment for each job category and summing the products across the worker’s employment history.

The lifetime health risks evaluated by Park et al. (2002) were twofold; mortality from lung disease other than cancer (LDOC) and the incident of onset radiographic silicosis, which was determined by reviewing decades of surveillance chest x-rays using standardized International Labour Organisation (ILO) criteria. Workers who developed radiographic findings consistent with silicosis during follow-up were classified as incident cases. Approximately 70 incident cases of silicosis were identified within the cohort and used for the development of the exposure-response model. They use this to evaluate if both of these health risks arise from respirable crystalline silica that was primarily in the form of cristobalite.

The researchers evaluated Poisson regression models to characterize the relationship between cumulative silica exposure and silicosis risk, including linear relative-rate models, additive excess-rate models, power functions, log-linear models, and spline-based models. Model performance was compared using standard epidemiologic goodness-of-fit criteria. The authors concluded that the linear relative-rate model provided the most appropriate fit to the observed data and used that model to estimate lifetime silicosis risk. While authors have disagreed with Park et al. (2002)’s use of a linear relative rate model, OSHA has explicitly disagreed with criticisms, supporting Park et al. (2002)’s model.

Rice et al. (2001) evaluated the same California diatomaceous earth worker cohort as Park et al.(2002) , comprising approximately 2,342 workers employed in mining and processing operations with substantial exposure to cristobalite. Using detailed historical industrial hygiene measurements, employment records, quantitative exposure reconstruction, Poisson regression modeling, Cox proportional hazards analyses, and actuarial life-table methods, the researchers examined the relationship between cumulative respirable crystalline silica exposure and lung cancer mortality. With these tools, the authors evaluated multiple exposure-response models, and concluded that the linear relative-rate model provided the best overall fit to the observed data. The study demonstrated a statistically significant increase in lung cancer mortality with increasing cumulative silica exposure and further illustrated that cumulative exposure can be used to generate quantitative lifetime risk estimates through age 85.

Regulatory agencies have additionally supported the assumption of a low-dose relationship between outcomes and exposure metrics in epidemiological investigations for carcinogenic and non carcinogenic materials.

In OSHA’s 2016 Final Rule of Occupational Exposure to Crystalline Silica, Dr. Ginsberg, one of contracted peer-reviewers for OSHA, stated:

“it is logical for OSHA to strongly consider inter-subject variability…as the reason for linearly-appearing regression slopes in silica-related non-cancer and cancer studies. This explanation does not imply an artifact [that is, a false appearance of linear exposure-response] but that the linear (or log linear) regression coefficient extending down to low dose reflects the inherent variability in susceptibility such that the effect of concern…may occur in some individuals at doses well below what might be a threshold in others”

As OSHA notes, the persistent appearance of linear or log-linear trends at low doses is driven by inter-subject variability. Population-level data effectively aggregates a spectrum of individual thresholds, meaning that for highly susceptible workers, adverse health effects can still trigger at exposures well below what might otherwise appear to be a ‘safe’ population threshold.” This supports the use of low-dose extrapolation utilizing silicosis epidemiological studies.

Park (2025) conducted a NIOSH review of quantitative risk assessments and PELs to identify exposure response relationships for known occupational carcinogens and calculate occupational exposure limits. The author conducted a comprehensive literature review, identifying relevant cohort or nested case-control studies containing quantitative and cancer mortality data. The authors subsequently utilized this data to derive exposure-response relationships using four methods. These exposure-responses were subsequently utilized in life table analyses to incorporate competing causes of death to calculate the working lifetime exposure concentration corresponding to one-per-thousand excess lifetime risk. The authors concluded that there was a massive systematic gap between current occupational regulatory standards and public health protection targets. The author further cited the National Academy of Sciences’ guidance that supports the assumption of a low-dose linear relationship between outcomes and exposure metrics in epidemiological investigations for carcinogenic and non-carcinogenic materials.

6.1.10 Summary Table of Epidemiological Studies

These epidemiological studies demonstrate the minimum threshold of cumulative silica dust exposure that has been shown to increase the risk of silicosis. A summary of the epidemiological studies in the table below shows the increased risk of silicosis from varying levels of cumulative silica dust exposure. These multiple studies show more than a statistically significant doubling of the risk for silicosis. However, it must be noted that these studies use the lowest exposure group as the comparison group. This means that these risks are likely underestimations of true risk since they do not compare to an unexposed group. These studies are therefore included to be holistic but may not fully represent the risk associated with silica exposures.

Table 6.1: Summary of Relative Risk Studies on Silica Exposure And Silicosis

Table 6.2: Summary of Odds Ratio Studies on Silica Exposure And Silicosis

Table 6.3: Summary of Rate Ratio Study on Silica Exposure And Silicosis

Table 6.4: Summary of Hazard Ratio Study on Silica Exposure And Silicosis

6.2 OSHA’s Silicosis Epidemiological Study Comparison

OSHA’s Final Rule for Occupational Exposure to Respirable Crystalline Silica, published in March of 2016 included a Risk Assessment for Lifetime Silica Exposure. This risk assessment included an extensive toxicological, epidemiological, and experimental review of existing literature on the adverse health effects of occupational exposures to RCS, including polling data from historical cohort studies of highly exposed workers across major sectors like mining, pottery, and diatomaceous earth facilities. Using this information, OSHA developed quantitative estimates of excess risk of mortality and morbidity in comparison to historical and revised PELS, projecting the lifetime health risks of workers exposed to various levels of airborne silica over a standard 45-year working career. Importantly, OSHA acknowledged that measurable risks of silicosis, lung cancer, and other diseases would remain even at the revised PEL, recognizing that the standard would reduce—but not eliminate—worker risk.

Figure 6.6 below summarizes OSHA’s final quantitative mortality risk estimates based on their review of available scientific literature. The column delineated in red illustrates the risk associated with exposures at the revised OSHA PEL of 50 µg/m³. The sections highlighted in yellow illustrate silicosis risk associated with exposures to RCS. As demonstrated in Figure 6.6, even at the updated PEL of 50 µg/m³, across a 45-year lifetime, OSHA still finds silicosis risk remains unacceptably high. For silicosis and non-malignant lung disease mortality, studies found that 7 to 44 out of 1,000 workers exposed at the PEL will die from those diseases. For silicosis morbidity, the literature has found that exposure to silica at the PEL is associated with 20 to 170 out of 1,000 workers developing the disease. These levels remain above the OSHA acceptable risk level of 1 per 1,000.

6.3 Lung Cancer

Brüske-Hohlfed et al. (2000) pooled 2 case-control studies conducted in Germany between 1988 and 1996, with 3,498 male cases of lung cancer and 3541 male population controls, to investigate the association of lung cancer with various occupational exposures, including crystalline silica. For silica, the study found an odds ratio of 1.41 (95% CI: 1.22 – 1.62), indicative of an elevated risk of lung cancer.

McDonald et al. (2005) built on a previous cohort study of approximately 2670 employees of the North American sand industry between 1940 and 1979, with the goals to determine whether estimates of lung cancer and silicosis risk were confirmed by mortality in the six years since the first study. Updated data showed similar results for lung cancer odds ratios (OR), specifically in the highest category of silica exposure concentration (OR = 2.36, 95% CI: 1.00 – 5.59), and highest cumulative silica exposure category (OR = 2.64, with the original study OR = 2.58). In addition, the study found a significant exposure-response association, with increasing cumulative exposure to silica associated with increased OR of developing lung cancer (p = 0.011). The study concluded that their findings supported a casual relationship between lung cancer and quartz exposure after allowance for cigarette smoking.

Lai et al. (2018) conducted a retro-prospective study of 7665 workers from one Chinese iron mine, investigating both smoking and long-term exposure to crystalline silica on lung cancer and other diseases in the cohort. The study found that in the highest silica exposure group compared to unexposed, the hazard ratio (HR) for lung cancer was 1.671 (95% CI: 1.216 – 2.298). There was a significant exposure-response association, with increasing silica exposure associated with increasing HR of developing lung cancer (p-value = 0.001). Additionally, workers who were ever-smokers and were also exposed to silica had a lung cancer hazard ratio of 6.586 (95% CI: 3.616 – 11.992). The study concluded that the findings indicated that silica exposure, especially when combined with smoking, was a contributing factor to the deaths within the cohort.

McLaughlin et al. (1992) conducted a nested case-control study of 316 male lung cancer cases and 1352 controls among silica exposed workers in China, assessing whether silica induces lung cancer. 29 mines and factories from 5 Chinese factories were included in this study. The study showed that in tin mines, workers who were exposed to high categorical levels of cumulative respirable silica had an odds ratio (OR) of 3.1 (with a 95% CI excluding 1.00) for lung cancer. Additionally, in iron-copper and tin mines with present cases of silicosis, the ORs for lung cancer were 3.1 and 2.0 (both with 95% CIs excluding 1.00), respectively.

6.4 COPD

Calvert et al. (2003) utilized data from the U.S. National Occupational Mortality Surveillance (NOMS) system, identifying 94,922 death certificates with a mention of Chronic Obstructive Pulmonary Disease (COPD) to investigate its association with occupational crystalline silica exposure. When comparing those with any detectable silica exposure (medium, high, and super high categories combined) to the low/no exposure reference group, a significantly increased mortality odds ratio (MOR 1.12, 95% CI 1.10–1.14) was found. Further analysis revealed a significant trend of increasing risk with increasing exposure category, with the “super high” exposure group showing an MOR of 1.47 (95% CI 1.30-1.66) compared to the lowest group and “high” exposure vs low having an elevated MOR of 1.29 (95% CI 1.25–1.33) with a p trend of p<0.001. An even stronger association was noted for individuals whose death certificates listed silicosis, exhibiting an MOR of 4.38 (95% CI 3.39–5.67) for COPD compared to non-silicotics. The study thus corroborated the association between crystalline silica exposure and COPD mortality.

Grahn et al. (2021) conducted a study involving 43,641 subjects in Stockholm, Sweden, assessed the smoking-adjusted risk of developing COPD (identified by medication or physician diagnosis) associated with occupational particle exposure, specifically respirable crystalline silica (RCS). The unexposed group served as the reference for calculating hazard ratios (HR). Among men, exposure to RCS was associated with an increased risk, with ever-exposed men having an HR of 1.46 (95% CI 1.13–1.90) when adjusted for smoking. A significant positive exposure-response trend was found for RCS and COPD incidence (p=0.016). Notably, men characterized as highly exposed, ≥ 0.048 mg/(with a mean concentration of 0.052 mg/ of RCS) had a significant HR of 1.63 (95% CI 1.17–2.27). The authors concluded that occupational exposure to RCS increased the risk of developing COPD, and the finding that risks were elevated at levels below the European occupational exposure limit of 0.1mg/.

Lenander-Ramirez et al. (2022) conducted a cohort study of 1,752 Swedish iron foundry workers to evaluate the morbidity and mortality from respiratory diseases, specifically focusing on COPD and respirable silica exposure. Using data from the National Non-primary Outpatient Register, the study determined a statistically significant increased morbidity risk for COPD across all three cumulative respirable silica exposure groups (tertiles) compared to the general Swedish population. The highest cumulative exposure group, > 0.39mg/ year (corresponding to an average silica exposure level of about <0.05mg/), yielded a standardized incidence ratio (SIR) of 1.64 (95% CI 1.17–2.24). The intertertile, 0.15-0.38mg/ year, showed an SIR of 2.07 (95% CI 1.43–2.91).The lowest cumulative exposure group (≤14 mg/ year) also showed a significant SIR of 2.35 (95% CI 1.56–3.40). The authors concluded that the statistically increased morbidity for COPD was determined at silica exposure levels well below the current Swedish occupational exposure limit of 0.1 mg/.

Reid and Sluis-Cremer (1996) investigated the mortality of a cohort of 4,925 white South African gold miners using a cohort study and nested case-control analysis. The overall standardized mortality ratio (SMR) for COPD (ICD-9 416 + 490-505) in the cohort was significantly elevated at 189% (95% CI: 162.1-219.0, p<0.0001) compared to the reference population. After adjusting for smoking, cumulative dust exposure (expressed in y-mg/) was also found to increase the risk; the relative risk for cumulative dust exposure, after entering smoking into the model, was 1.20 (95% CI 1.0–1.4). The authors concluded that dust exposure likely contributes toward the development of COPD, especially in conjunction with smoking.

Steenland and Brown (1995) investigated an update on 3,328 gold miners exposed to silica and nonasbestiform amphibole minerals. While COPD mortality was not analyzed as a distinct underlying cause, the broader category of Nonmalignant Respiratory Disease, which largely reflected silicosis and other dust-related lung disease, was significantly elevated (SMR 1.86, 95% CI 1.58-2.16). . Crucially, the category of Pneumoconioses and other respiratory diseases showed a strong, statistically significant positive exposure-response trend with increasing estimated cumulative dust exposure, with the SMR rising from 1.79 in the lowest exposure category (<8,000 dust-days, equivalent to 1mppcf of dust) to 8.87 in the highest category (48,000+ dust-days). The authors concluded that substantial silica exposure led to large excess mortality from diseases known to be silica-related, and the strong positive dose-response trends validated the link between cumulative dust exposure and severe nonmalignant lung disease.

Ulvestad et al. (2000) compared 212 male tunnel workers (exposed group) with 205 outdoor heavy construction workers (reference group) in Norway to assess the occurrence of respiratory symptoms and airflow limitation related to years of occupational exposure. The exposure assessments showed that tunnel workers had significantly higher geometric mean exposures to respirable dust (1.2, 95% CI: 1.09-1.31mg/), alpha-quartz (0.034, 95% CI: 0.028-0.041 mg/) and oil mist compared to the reference group. The prevalence of Chronic Obstructive Pulmonary Disease (COPD) was significantly higher in tunnel workers (14%) than in the reference subjects (8%) (p=0.03). The odds ratio (OR) for COPD among tunnel workers versus construction workers was 2.50 (95% CI 1.31 to 4.96), adjusted for smoking, years employed, and atopy. Furthermore, the adjusted decrease in forced expiratory volume in one second () was 17 mL for each year of tunnel work, compared to 0.5 mL per year in the reference group. The authors concluded that combined exposure to dust, alpha-quartz, diesel exhaust, and nitrogen dioxide in tunnel work enhances the risk for accelerated decline in , respiratory symptoms, and COPD.

6.5 Quantitative Risk Assessments for Silica-Related Diseases

In order to evaluate the significance of health risks resulting from occupational exposures to RCS, regulatory agencies like OSHA rely on quantitative risk assessments. These assessments involve the using epidemiological data, experimental data, and statistical models to provide a quantitative assessment of exposed workers’ risks, assuming exposure over a working lifetime. By calculating risk estimates at different exposure concentrations, regulators can objectively determine whether a hazard poses a material impairment and quantify the benefits of reducing permissible exposure limits (PELs).

The standard methodology for conducting occupational risk assessment involves evaluating exposures over a 45-year working lifetime, assuming 8-hour work days, 250 days per year. To develop estimates, OSHA relied upon studies that quantify the exposure-response relationship between silica dust exposure and silicosis, across epidemiological studies. These studies were integrated into a life table analysis that accounted for the competing causes of death due to background causes and cumulated risk up until the age of 85.

OSHA’s quantitative risk assessment demonstrates the disease burden at previously allowed exposure limits. Specifically, the analysis found that employees exposed to RCS at the preceding PELs were at increased risk of lung cancer mortality, silicosis mortality, and morbidity. The findings also suggested that exposures to RCS increased the risk of death from other nonmalignant respiratory diseases, such as COPD. The table below summarizes the estimated excess lifetime risk per 1,000 workers at the previous PEL of 100 µg/m³ and the revised PEL of 50 µg/m³.

Table 7.5: OSHA Estimated Excess Lifetime Risk per 1,000,000 Workers (45-Year Working Life)

For lung cancer mortality, OSHA relied upon risk assessments from several epidemiological studies that investigated the exposure-response relationship between RCS and lung cancer. These studies focused on ten different cohorts from several industries, including granite workers, industrial sand workers, earth workers, and coal miners. Based on these studies, OSHA estimated lung cancer mortality associated with 45 years of exposure to be between 11 to 54 deaths per 1,000 workers at the previous PEL of 100 µg/m³. At the revised PEL of 50 µg/m³, OSHA estimated this would decrease to between 5 and 23 deaths per 1,000 workers.

For silicosis mortality, the authors relied upon two published, peer-reviewed studies including a pooled analysis of six epidemiological studies (Mannetje et al. 2002). This pooled analysis included 18,634 subjects, with 150 silicosis deaths, demonstrating an increased mortality rate with exposure to silica. In order to better control for age and exposure measurement uncertainty, OSHA relied upon the model used in Mannetje et al. (2002) using the rate ratios estimated from sensitivity analyses. Using this adjusted mode, OSHA estimated the lifetime silicosis mortality risk using the previous PEL of 100 µg/m³ was approximately 11 deaths per 1,000 workers. This decreased to 7 deaths per 1,000 workers using the revised PEL of 50 µg/m³.

While significant, regulatory epidemiologists further recognized that risk estimates based solely on silicosis mortality can underestimate the true respiratory disease burden. OSHA recognizes that chest radiographs provide the most reliable estimates of silicosis morbidity, further acknowledging that the low sensitivity of chest radiography in detecting silicosis may lead to underestimates of true risk. Furthermore, silicosis has frequently been misclassified as a cause of death, often being misidentified as emphysema or chronic bronchitis. Silica exposure has also been associated with COPD, among other diseases, which may mean that the underlying cause of death may be attributed to another disease rather than silicosis.

In order to address the potential for underreporting, OSHA conducted an assessment of Non-Malignant Respiratory Disease (NMRD), relying heavily on Park et al. (2002). This analysis included pneumoconiosis, silicosis, chronic bronchitis, and emphysema. OSHA’s estimate of excess lifetime NMRD mortality using the previous PEL of 100 ug/m3 calculated 85 deaths per 1,000 workers µg/m³. This value decreased to 44 deaths per 1,000 workers at the revised PEL of 50 µg/m³.

OSHA additionally assessed the risk of end-stage renal diesel mortality associated with silica exposure. This analysis relied on Steenland et al. (2002), which included an analysis of 18,382 workers across three cohorts. The researchers found a positive exposure-response relationship for multiple cause mortality and underlying cause mortality. OSHA utilized this data to find a lifetime excess cancer risk of 39 deaths per 1,000 workers at the previous general industry PEL of 100 µg/m³. This cancer risk decreased to 32 deaths per 1,000 workers at the revised PEL of 50 µg/m³.

OSHA additionally conducted a risk assessment evaluating silicosis morbidity, or the probability of a worker acquiring silicosis while still alive. The risk assessment relied upon five studies that evaluated silicosis morbidity after workers left their jobs. These studies specifically focused on cohorts of gold miners, coal miners, tin miners, and pottery workers. The morbidity risk estimates generated from these studies was severe, with a high probability for workers to develop silicosis. The estimated cumulative risk model for developing radiological silicosis after a 45-year exposure at 100 µg/m³was approximately between 60 and 773 cases per 1,000 workers. This value was reduced to 20 to 170 cases per 1,000 workers when exposed to the revised PEL of 50 µg/m³.

These risk assessments ultimately demonstrate that respirable crystalline silica is exceptionally dangerous at concentrations historically deemed acceptable. In establishing workplace safety standards, OSHA relies upon the Supreme Court’s precedent on Benzene, which establishes that a lifetime excess risk of 1 death per 1,000 workers indicates a clearly significant risk of a material on health, warranting heavy regulatory action. Since the estimated risks of lung cancer, NMRD, and silicosis at both the previous and revised PELs exceed this 1 in 1,000 benchmark, the data confirms that silica-exposed workers face an extreme, life-threatening occupational hazard.

Park et al. (2002) performed one of the most detailed quantitative risk assessments of silicosis morbidity available in the occupational epidemiology literature. This was a retrospective cohort study of 2,342 white male workers who were employed for at least one year at some point between 1942 and 1994 at a California diatomaceous earth plant, and primarily exposed to cristobalite, a crystalline silica polymorph formed during the calcination of diatomaceous earth. The cohort was assembled using company employment records, and workers were followed through a comprehensive medical surveillance program that included periodic chest radiographs and occupational health evaluations.

To estimate individual worker exposures, the researchers reconstructed historical exposure levels using an extensive database of industrial hygiene measurements collected throughout the facility going back over 80 years. These measurements were linked to detailed job histories, allowing the researchers to estimate silica exposure for each worker during each period of employment. Cumulative exposure was calculated by multiplying estimated respirable silica concentrations by the duration of employment for each job category and summing the products across the worker’s employment history.

The lifetime health risks evaluated by Park et al. (2002) were twofold; mortality from lung disease other than cancer (LDOC) and the incident of onset radiographic silicosis, which was determined by reviewing decades of surveillance chest x-rays using standardized International Labour Organisation (ILO) criteria. Workers who developed radiographic findings consistent with silicosis during follow-up were classified as incident cases. Approximately 70 incident cases of silicosis were identified within the cohort and used for the development of the exposure-response model. They use this to evaluate if both of these health risks arise from respirable crystalline silica that was primarily in the form of cristobalite.

The researchers evaluated Poisson regression models to characterize the relationship between cumulative silica exposure and silicosis risk, including linear relative-rate models, additive excess-rate models, power functions, log-linear models, and spline-based models. Model performance was compared using standard epidemiologic goodness-of-fit criteria. The authors concluded that the linear relative-rate model provided the most appropriate fit to the observed data and used that model to estimate lifetime silicosis risk. Finally, the authors performed actuarial life-table analyses to estimate excess lifetime risk associated with various occupational exposure concentrations. These life-table calculations incorporated age-specific background mortality rates and projected risk through age 85 for workers exposed for 45 years, or from ages 20 to 65. The resulting estimates represent excess lifetime risks rather than simple proportions observed within the study cohort.

Since Park et al. (2002)’s analysis was based on observed worker exposures, observed radiographic disease outcomes, quantitative exposure reconstruction, and formal actuarial modeling, it is widely regarded as one of the strongest quantitative studies of silicosis morbidity available in the literature and has been cited extensively by OSHA, OEHHA, NOISH, and other regulatory agencies.

Table 7.6 below includes a Demonstrative Silicosis Morbidity Risk based on Park et al. (2002). The 45 year exposure excess cases comes directly from Park’s paper. For demonstrative purposes I divided 45 year exposure by 45 to come up with the risk values of a one year exposure. This is useful because it shows that individuals exposed for only 1 year, for demonstrative purposes have a risk treater of 1 in 1000 which is OSHA regulatory threshold for requiring PPE.

Table 6.6: Demonstrative Exhibit Showing Silicosis Morbidity After 45 Years and 1 Year At Various Exposure Concentrations.

7.6 Toxicology of Respirable Crystalline Silica

The toxicological profile for respirable crystalline silica, defines a complex, cascading sequence of events that transforms the mineral into a severe occupational hazard. Adverse effects of inhaled crystalling silica are strictly associated with the respirable size, or particles less than 10 micrometers. The inhalation of crystalline silica has adverse effects on the respiratory, renal, and immune systems, with scientific evidence demonstrating the respiratory system is most susceptible. Health effects are primarily associated with prolonged occupational exposures to crystalline silica. However, intermediate duration exposures to high levels have also been associated with health outcomes. RCS exposure has been extensively linked to Silicosis and Lung Cancer.

Various industrial activities can further generate different types of crystalline silica particles, with variations in particle size, surface reactivity and fibrogenic potential. Crystalline silica compounds in the nanoparticle range, with diameters less than 100 nanometers, observe different toxicokinetic and toxicodynamics and can provide substantially different hazards to larger, respirable particles. Nanoparticles are able to penetrate the human body more deeply than larger respirable particles due to their size. In the context of engineered stone fabrication, nearly free silanols (NFS) develop on the surface of these particles during fabrication activities that fracture the stone. The noticeably high surface area of these nanoparticles provide a large surface area for these active NFS groups. NFS is highly reactive and has the optimal structure and shape to attach to cell membranes in the lung and cause damage.

Research has shown that NFS enriched silica particles cause severe and acute lung injury and cellular death by binding to the alveolar macrophage membranes and rupturing the cells. This triggers NALP3-dependent proinflammatory responses that lead to the release of inflammatory cytokines and chemokines, ROS and reactive nitrogen species, and arachidonic acid metabolites. The release of these chemicals damages nearby cells, recruiting macrophages, or white blood cells. This creates a recurring cycle of macrophage phagocytosis, death, and release of intracellular contents. This results in a chronic inflammatory process known as alveolitis.

Oxidative stress originates from two sources: from particle-derived reactive oxygen species (ROS) and cell derived ROS. Cell-derived ROS originates from the previously described alveolitis onset by NFS. Particle-derived ROS originates from dust generated during fabrication activities, which creates silica-derived free radicals that cause direct damage to the epithelial cells. These biological processes and their impacts on fibrosis, silicosis, and lung cancer summarized in the Figure 7.7 below.

Fibrosis is a direct, maladaptive response to inflammation and oxidative tissue damage. Excessive cycling between inflammatory and reparative phases within the lung leads to excess extracellular matrix deposition, which may ultimately culminate in fibrosis.

Silicosis is a form of fibrosis specifically caused by inhalation of silica, and most frequently occurs as a form of nodular pulmonary fibrosis. Silica exposure leads to silicosis as a result of a cycle of cell damage, oxidant generation, inflammation, scarring, and fibrosis. A silica particle can damage the lung directly through their unique surface properties, or through stimulation of alveolar macrophages. Silica particles are not digested or degrade once entering the body, and continue to rupture cells within the lung, leading to continuous chronic inflammation (alveolitis) and excessive tissue repair. Consistent cycling between inflammatory and reparative phases leads to excess extracellular matrix deposition, which subsequently leads to fibrosis of the lung, or silicosis.

Silicosis can be categorized into different forms depending on the frequency, intensity, and duration of exposures. Silicosis primarily occurs as acute silicosis, simple silicosis, progressive massive fibrosis (PMF) or accelerated silicosis. Silicosis is a progressive disease that continually progresses beyond initial diagnosis. Pulmonary function studies have identified that while functional impairment may be mild in the beginning, as it advances it may lead to significant loss of lung volumes, gas exchange function,and increased airflow obstruction.

Silica exposures have further been linked towards lung cancer incidence. The primary pathway for lung cancer is derived from the chronic inflammatory pipeline in which inhalation of silica ruptures cells within the lungs and results in chronic inflammation and excessive tissue repair. While the inflammatory process typically leads to fibrosis and silicosis, the inflammatory process can also release proteolytic enzymes and oxidants that can cause damage to cells and DNA. This damage can result in genotoxic events that can trigger a carcinogenic process.

While the toxicity of respirable silica is not solely confined to the respiratory system, the nature of silica nanoparticles can allow translocation from the lungs into the bloodstream and potentially migrate to other organs. This systematic distribution of highly reactive particles, combined with chronic inflammatory cycles, heavily implicates crystalline silica in the development of severe, autoimmune disorders.

7 Feasible Safer Alternatives and Controls

The previous sections document the health hazards of silica inhalation through countertop fabrication and presents literature demonstrating the magnitude of RCS exposure during cutting, grinding, and polishing of natural and engineered stone.

NIOSH has determined a hierarchy of controls, assessing which categories and methods are most effective at controlling occupational exposure to hazards.

NIOSH lists each control in order of preferred actions and effectiveness. Starting with the most effective, this list includes:

• Elimination
• Substitution
• Engineering Controls
• Administrative Controls
• PPE

This section discusses these controls in relation to controls present in the countertop fabrication industry. It also discusses the failure of stone fabrication employers, stone manufacturers, and tool manufacturers to properly implement controls, and the feasibility of controls such as Personal Protective Equipment.

7.1 Substitutions for Engineered Stone

Multiple peer-reviewed studies and industrial hygiene assessments have demonstrated that wet processes alone are not enough to reduce RCS levels below the safe exposure level. The NIOSH Hierarchy of Controls state that elimination or substitution are the most effective way of protecting workers from occupational hazards. This Section discusses countertop material alternatives to engineered stone and granite.

In July 2024, Australia banned the supply and manufacture of engineered stone benchtops, panels, and slabs. Specifically, the ban applies to engineered stone products composed of greater than 1% crystalline silica, manufactured by mixing natural stone with water, resins, and other polymers. Although SafeWork Australia had considered a ban on high-silica engineered stone products, defined by manufacturers as containing above 40% silica, and implementation of a licensing scheme, the organization ultimately recommended a complete ban. The department cited the overrepresentation of engineered stone workers amongst workers diagnosed with silicosis, particularly amongst younger workers, the disproportionately high respiratory crystalline silica content and potential for additive hazards from the resins binding the stone, and systemic failure of the industry to follow safety laws. These concerns also follow research that has demonstrated that even when complying with wetting techniques when cutting or grinding engineered stone, exposures may exceed permissible limits. In addition, the SafeWork Australia reiterated their opposition to allowing engineered stone products with 40% silica, stating that permitting work with lower silica content engineered stones may create the incorrect perception that these products are safer even though there is no toxicological evidence of safe levels for these materials. In their announcement, they highlighted alternatives to engineered stone in countertops that have been exempted from the ban, such as porcelain, ceramic, sintered stone, concrete, natural stones, and stones composed of other non-crystalline silicas.

These materials have been shown in research to produce lower respirable crystalline silica levels than engineered stone. In 2022, Hall et al. evaluated the respirable crystalline silica composition of common stoneworking materials, such as granite, sandstone, marble, resin-bound engineered stone with varying silica content, sintered stone, and ceramic. For the resin-bound engineered stones, the study found crystalline silica percentage compositions that ranged up to 90%. In addition, the study found that sandstone, a natural stone considered high in silica, was composed of 62% silica. In contrast, marble, sintered stone, ceramic, and some resin-bound artificial stones all had much lower values. Artificial stones R8 and R9, which were composed of 88% and 99% noncrystalline material, reported crystalline silica concentrations below the detection limit and 0.7%, respectively. Marble, similarly, reported no crystalline silica detected. The crystalline silica composition for sintered stone ranged from 6.9% to 17% and the study found that ceramic was composed of 0.9% crystalline silica.

In 2023, Thompson and Qi tested respirable crystalline silica release from multiple types of stones used in the manufacturing of countertops when fabricated. Stone C was composed of recycled glass, which is an amorphous silica, in a cement matrix and had a respirable crystalline silica content of under 0.2%. After using an angle grinder to cut the stone, the study found that the bulk sample of Stone C had no crystalline silica and produced non-detectable emissions of respirable crystalline silica.

In 2024, Martinez-Gonzalez et al. examined the concentration and composition of dust assessed across multiple work activities generated from three different materials: granite (42% quartz), marble (2% quartz), and silica agglomerates, like silestone (80.8% quartz and 16.5% cristobalite). Dry cutting of granite and silestone produced an average respirable crystalline silica exposures of 16.79 mg/m³ and 26.13 mg/m³ respectively, while marble produced no detectable emissions of respirable crystalline silica. For wet cutting, respirable crystalline silica exposures were 1.48 mg/m³ for granite and 2.35 mg/m³ for silestone but below the detection limit for marble. Only for dry polishing did the study find detectable levels of respirable crystalline silica for marble, but concentrations were much lower than for granite or silestone. Marble had respirable silica concentrations of 0.34 mg/m³, translating to 2.49% silica, whereas granite and silestone had average respirable crystalline silica concentrations of 5.44 mg/m³ and 10.73 mg/m³, respectively.

In 2025, Ramkissoon et al. investigated respirable crystalline silica emissions from various low and no-silica stones. The study examined five engineered stone materials, one of which (MH1) was high crystalline silica, one of which (MH2) was low crystalline silica, and three of which (MH3, MH4, MH5) contained no crystalline silica. MH3 was composed of 89% fused silica, 1% titanium dioxide, and 10% resin while MH5 was composed of 78-80% aluminum hydroxide and 18 to 20% resin. Composition details were not available for MH4. The study also examined the following low-silica non-engineered stones: porcelain (MH6), ceramic (MH7), and sintered stone (MH8, MH9). Porcelain contained 5 to 11% crystalline silica along with zircon, additives, silicoaluminates, and amorphous silica. Ceramic contained 15 to 20% crystalline silica and was composed of 60 to 70% amorphous silica and 5 to 10% silicoaluminates. MH8, a sintered stone, contained 9 to 13% silica, with 52% kaolin, 5% talc, 40% feldspar, and 3% cornish stone, while MH9, another sintered stone, contained 0 to 11% crystalline silica, with the remaining materials composing the stone being silicoaluminates, amorphous silica, zirconium silicate, and pigments.

Each stone slab was cut using an angle grinder in a controlled test chamber. For MH1, the high-silica engineered stone, the dust produced was 73.5% silica. For MH2, the low-silica engineered stone, the respirable crystalline silica percentage was 23%. The respirable crystalline silica percentages for MH3, MH4, and MH5 – the silica-free engineered stones – were below the detection limit. Dust from the sintered stones, MH8 and MH9, was composed of 7.32% and 21.9% respirable crystalline silica, ceramic dust was found to contain 15% respirable crystalline silica, and porcelain contained 4.71% respirable crystalline silica.

These alternatives to engineered stone existed long before engineered stone was invented and remain commercially viable. Ceramic tiles and marble, which contain 0.9-32% and 2-11% crystalline silica respectively, have been historically used in countertop production.

In a 2001 article from Fine Homebuilding, Gibson described multiple alternatives to engineered stone for kitchen countertops that were commercially available at the time. These include concrete, glazed and porcelain ceramic tiles, solid surfacing, stainless steel, high-pressure laminate (phenolic resins), and plastic laminates. For concrete countertops using CHENG materials, a manufacturer highlighted in the article, the MSDS sheet stated the concrete was composed of 0.1 to 0.7% crystalline silica. Other alternatives, such as stainless steel, solid surfacing, high-pressure laminates, and plastic laminates, are not known to contain crystalline silica. In 2010, sintered stone was first manufactured for stone countertops by Neolith, and in 2013, the sintered, porcelain slab Dekton countertop was released by Cosentino. Sintered stone countertops have been shown to contain 6.9 to 21.9% crystalline silica while porcelain have recorded a silica content of 4.71% to 11%.

To demonstrate that alternatives, such as natural stone and low to no-silica products, were competitive with engineered stone products, SafeWork Australia provided cost comparisons between materials. For Si90 engineered stone from Caesarstone, which contains approximately 41-90% silica, the price per square meter was $416 to $1,190, excluding installation. Low-silica or silica-free materials including porcelain, marble, stainless steel, and polished concrete ranged in cost from $700 to $2,500 per square meter, including installation costs. Cost estimates for additional non-stone alternatives, such as bamboo, hardwood timber, and laminate ranged from $120 to $1,200 per square meter.

7.2 Silica Dust Mitigation Measures and Engineering Controls

OSHA had a broad list of regulations for silica exposure protections including engineering controls and personal protective requirements. However, Cal/OSHA and Safe Work Australia have further recognized that engineering control methods are ineffective for reducing ES dust exposures. Cal/OSHA explicitly highlighted the fact that wet methods are “not proven to be effective for airborne nanoparticle mitigation,” further stating that wet methods “can reduce but not eliminate harmful exposures.” Cal/OSHA further discusses how the effectiveness of exhaust ventilation is dependent on proper implementation and use of airflow rates, placement, size and speed, and other factors, stating that if not properly implemented, local exhaust ventilation can be ineffective and counterproductive.

When citing reasons behind the ban, Cal/OSHA explicitly discussed how the “combined approach of engineering controls, PPE, and enforcement have not led to a reduction in exposures but have instead revealed industry-wide non-compliance.”

Australia’s stringent enforcement including the prohibition of large scale enforcement and the prohibition of dry cutting was ultimately deemed ineffective in mitigating the silicosis crisis associated with Engineered Stone activities. Australia later banned the use of Engineered Stone products containing more than 1% silica after finding that traditional enforcement and licensing was insufficient in protecting workers.

7.2.1 Wetting

Various regulatory guidance documents have recommended wet processes such as water sprays and wet-edge milling. Peer-reviewed scientific publications have assessed the effectiveness of these various processes in facility evaluations and in controlled settings. While wetting processes significantly reduce exposure in comparison to dry processes many studies have recorded exposures above the established PELS when processing engineered stone. Multiple studies call into question the feasibility and cost of wetting procedures.

As early as 1999, Simcox et. al published a study regarding silica exposure during granite countertop fabrication in the journal of Applied Occupational and Environmental Hygiene. The study focused on six small businesses fabricating granite countertops and similar products in Washington state, each employing 3 to 10 workers. Crystalline silica exposure was linked to specific tasks like cutting, grinding, and finishing granite, tasks that produce airborne silica dust. Light-colored granite had higher silica content (25–45%) compared to darker granite (0–15%). Researchers collected 43 air samples to measure respirable crystalline silica concentrations, providing time-weighted average (TWA) exposure levels across work shifts. For the purpose of this case study, they divided the six work sites into two types of processes: those who used handheld grinders and saws without water were called dry processes and those who used wet methods such as water-fed angle grinders and milling tools were identified as wet processes. They collected 19 samples of workers that used dry processes and 18 that used wet processes. Workers using dry processes experienced exposure levels significantly above permissible limits (0.1 mg/m³). About 63% of samples from dry processes exceeded this limit. Wet processes, including water-fed tools and milling machines, reduced silica concentrations to below permissible levels in all cases. It should be noted that wet processes reduced exposure to RCS below 0.10 mg/m^3 (Washington’s PEL at the time), but not below the NIOSH REL or OSHA’s current PEL. Dry sweeping and lack of proper respiratory protection were common in shops with higher exposure. The study advises medical monitoring, proper use of personal protective equipment, and ventilation systems, along with emphasizing training workers on silica hazards and adopting housekeeping practices.

A 2008 case study conducted by the Occupational Safety and Health Administration (OSHA) examined employees involved in cutting, grinding, and polishing granite and marble slabs using specialized tools such as bridge saws, pneumatic power tools, and a computer-controlled borer. The employees who were monitored over multiple inspections were either fabricators or bridge-saw operators. Some employees sampled were wearing respiratory protection such as N95 filtering facepiece respirators, while others were not. As a result of previous OSHA citations, the facility implemented various dust control measures, including water spray systems for the bridge saws, and a water mist coupled with a cascade system and a push-pull ventilation system for hand tools. The study emphasizes the importance of engineering controls and strict adherence to respiratory protection protocols in silica-exposure industries.

In 2013, Phillips et al. investigated respirable silica exposure in stone countertop fabrication shops. Sampling was conducted in four shops using various fabrication techniques, including hand tools, automated machines, and wet and dry methods. The study found that workers using dry methods consistently exceeded the threshold limit value (TLV) for respirable quartz of 0.025 mg/m³, with some exposures approaching or exceeding OSHA’s PEL of 0.1 mg/m³. Wet methods reduced exposure significantly but did not eliminate the risk, particularly when nearby dry work was performed. The study showed the highest silica exposures occurred during dry sweeping, dry sawing/cutting, and dry grinding. The study emphasized the need for improved engineering controls, ventilation, and stricter adherence to wet methods.

Phillips at al. 2013 Task Exposure Ranking

In 2017, Johnson et. al explored the efficacy of on-tool water sprays, center-feed wetting, and sheet-flow wetting on various grinding, polishing, cutting, and drilling tasks involving quartz stone. The study concluded that sheet-flow-wetting was effective in reducing dust exposures , especially in combination with on-tool local exhaust ventilation.

In a 2021 facility evaluation, NIOSH scientists conducted three site visits to measure the effectiveness of water spray, center-feed wetting, and a mixture of water spray and sheet-wetting on reducing RCS exposure during grinding. NIOSH scientists similarly concluded that sheet-flow-wetting was most effective, while water spray and center-feed wetting would still overexpose workers to RCS without additional control measures. Zwack et al. performed a similar facility evaluation in 2015 at a facility that only used cutting and polishing tools with water spray, finding that water suppression alone was not sufficient to reduce RCS exposure below PELs.

7.3 Local Exhaust Ventilation and Dust Collection Systems

In their 1996 Preventing Silicosis and Death in Construction Workers report, NIOSH noted that “dust collection equipment [was] available for many types of dust-generating equipment.” NIOSH recommended purchasing tools with dust control systems and advised to “always” use and maintain them. These recommendations were reaffirmed by OSHA and NIOSH reports in 2008 and 2009, respectively. In their Special Emphasis Program (SEP) for silica, OSHA noted that one strategy to reduce silica exposures was the “use of tools with dust collection systems,” which NIOSH found to reduce dust from concrete by approximately 90%.

In 2015, Cooper et al. evaluated the effectiveness of three control measures in reducing respirable silica exposure during artificial stone countertop cutting with a handheld circular saw. The authors compared the standard wetted-blade condition to a wetted blade with an additional water curtain spray and a wetted blade with local exhaust ventilation (LEV). Stone countertop cutting activities occurred in an enclosed outdoor tent measuring 3.1 m x 3.1 m with a ceiling height of 2.7 m. Results showed that respirable quartz concentrations (µg/m³) ranged from 1.87 to 4.85 for the wet blade alone, 0.92 to 3.41 for the wet blade with a water curtain, and <0.12 to 0.20 for the wet blade with LEV, while dry cutting resulted in significantly higher exposures (44,370 µg/m³ quartz). The average silica concentration of the respirable dust was 58.5%.

7.4 Personal Protective Equipment

As previously discussed in Section 8.1, according to NIOSH’s hierarchy of controls, respiratory protection is the least effective protection against hazardous dust. This is consistent with the American Industrial Hygiene Association, which recognizes process ventilation and enclosure as primary means of silica dust control ahead of respiratory protective devices. OSHA understands that a combination of engineering controls, work practices, protective equipment, and other measures are required in order to prevent overexposure to silica during countertop manufacturing, finishing and installation.

OSHA recommends that workers use “at least” a NIOSH-approved N95 respirator. These standard NIOSH respirators have an Assigned Protection Factor (APF) of 10, which can only be achieved if a respirator is quantitatively fit tested on an individual worker. An APF of 10, refers to the minimum anticipated protection provided by a respirator, meaning that respirators, when fit-tested, theoretically reduce the inhaled dust to 10 percent of its ambient level. Therefore, if the silica level is more than 10 times the OSHA Permissible Exposure Limit (PEL), a half-mask respirator with an APF of 10 is inadequate. Data from OSHA and NIOSH air monitoring and other published studies provide evidence that countertop industry worker exposure to airborne crystalline silica exceeds the OSHA PEL by a magnitude of over 10 when there’s a lack of engineered controls.

Scientific evidence has additionally shown that electrostatic respirators, such as NIOSH-approved N95 masks, often fail to adequately protect from the nano particles, the deadliest particle size for RCS. The intense mechanical pulverization of artificial stone produces large quantities of particles in the nanometer scale, with diameters less than 100 nanometers. As previously discussed in Section 5, nanoparticles have high deposition efficiency in lungs and are the most toxic component of airborne particulate matter. Systematic reviews of NIOSH-approved respirators, including N95 respirators, have found that their most penetrating particle size (MPPS) generally falls between 40 and 100 nanometers. These biologically destructive particles, therefore, are likely to slip through the filtering mouthpiece respirators. These studies are summarized in Section 8.4.1.

However, even when the filter media is effective, studies have further found that nanoparticles can easily bypass the filter through other pathways. Grinshpun et al. (2009) evaluated the different pathways that nanoparticles penetrate through N95 masks. The study found that the number of particles penetrating through faceseal leakage far exceeded penetrations through the filter medium. The authors further noted that normal movements, such as the wearer moving their head or bending over, increases the faceseal leakage. This is further acknowledged in OSHA’s 2016 report on Occupational Exposures to RCS, which describes how “movement of the jaw in speaking can cause leakage.” This suggests that masks may be highly ineffective during active physical labor conducted by workers.

Facial hair provides another common failure for respirator protection. In order for a tight-fitting respirator to properly function, it must create an absolute seal against the face. Industrial hygiene literature has consistently demonstrated that the presence of facial hair produces respirator leakage that is 50 or 1,000 times greater than in the among clean-shaven individuals. While OSHA regulations prohibit the use of tight-fitting respirators by employees with facial hair, studies have consistently observed stone countertop workers and shop managers actively fabricating stone with facial hair that compromises respirator seals.

OSHA has also acknowledged that wearing a respirator can cause additional burdens on the wearer and can “create safety problems of their own.” OSHA discusses how use of a respirator in some instances can make it difficult for the wearer to see and communicate with other workers. OSHA specifically highlights how movement of the jaw during communication can cause leakage and can reduce the efficiency of the respirator. Furthermore, OSHA also discusses how wearing a respirator can cause skin irritation and difficulty breathing. From a safety standpoint, OSHA discusses how respirators can affect vision or communication, which can create safety hazards in difficult or dangerous jobs.OSHA acknowledges that these stressors can cause employees to refrain from wearing a respirator.

CDC investigations of stone fabrication shops have continually documented widespread misuse of respirators due to these burdens. Investigators observed workers wearing N95 masks incorrectly, wearing both straps around the base of the neck, only wearing one strap, or cutting off one of the straps.

While OSHA describes Powered Air-Purifying Respirators (PAPRs) as offering far more protection than half-face air purifying respirators, these respirators have their own safety hazards. PAPRs are respirators that force air through a filter into a loose fitting hood or helmet. These masks provide a higher APF than N95s, and can overcome the issue of workers with facial hair. However, while working during wet cutting and polishing of engineered stone, workers have reported having their visibility obscured by water splashing onto their visor and excessive weight on their headtops. This can create safety hazards, especially with workers conducting high-speed cutting operations that require high precision and accuracy.

Due to the strain that respirators place on the cardiovascular and respiratory systems, OSHA mandates that a physician or licensed healthcare professional clears an employee before they can be fit-tested to wear a respirator. This often means that workers with pre-existing conditions, such as asthma, may be medically disqualified from wearing a respirator. Therefore if a workplace solely relies upon respirators for dust control, these workers may effectively be forced out.

Deven Johnson, a former cement mason, specifically described employees hiding injuries from supervisors to avoid being blacklisted from their jobs. She further clarified that she knew for a fact that “it happens.” Similarly, Dr. L. Christine Oliver, an associate clinical professor of medicine at Harvard Medical School, testified that her patients do not want their medical information reported to their employers out of “fear of losing their jobs.” Industry representatives have also confirmed this discrimination based on medical results. Construction Industry Safety Coalition (CISC) noted that employers may refuse to hire an employee with silicosis since they did not want to be held liable if the disease progressed or since they may have to offer workers’ compensation.

When approved industrial respirators are unavailable, workers sometimes substitute them with common cloth or surgical masks that offer little protection. Rengasamy et al. (2008) tested non NIOSH approved respirators, which demonstrated widespread failure to prevent nanoparticle infiltration, finding particle penetration levels ranging from 1 to 87%. Additionally, since these substitute masks do not offer a tight facial seal and contain inferior filter media, the use of non-NIOSH-approved respirators is inadequate for RCS protection.

Ultimately, the regulatory and scientific evidence does not deem respirators adequate for hazard control. Engineering controls like ventilation and water suppression offer stronger protections, while masks may offer additional protections, they should not be the primary protector against RCS.

7.4.1 Scientific Peer-reviewed Literature on Lack of Fit-testing

As previously discussed in Section 5.3.1, scientific literature has historically shown that use of a respirator without fit-testing can expose workers to far higher concentrations of contaminants than respirator clearance theoretically allows. Oftentimes ES manufacturing workers are not fit-tested for the respirators they use. This can create a false sense of security amongst workers as they are not as adequately protected.

OSHA assigns all respirators an Assigned Protection Factor (APF), which indicates that the workplace respiratory protection a certain class of respirators is expected to provide employees. These APFs are intended to be used to advise employers regarding which respirators are effective for specific work environments. Assigned protection factors are a ratio between the concentration outside of the respirator, and the concentration within the respirator. APFs can be used to calculate the maximum use concentration (MUC), or the maximum atmospheric concentration of a hazardous substance an employee can be expected to be protected from while wearing a respirator.

The MUC can be calculated by multiplying the permissible exposure limit (PEL) by the assigned protection factor of the respirator in use. The lowest APF allowed by OSHA is 10, which is assigned to half mask/dust masks and elastomeric half-masks. An APF of 10, indicates that the wearer is only exposed to 1/10th of the airborne concentration. For half mask respirators, OSHA requires they are fit-tested to ensure an adequate seal and appropriate protection for workers.

NIOSH conducted investigations of simulated workplace protection factors (SWPFs) for non-fit tested respirators. Simulated Workplace Protection Factors (SWPFs), are the ratio between the contaminant concentration outside of a respirator to the concentration inside of a respirator while a worker is performing tasks. Coffey et al. (2004) conducted an evaluation of N95 respirators with and without fit-testing, finding drastic disparities in SWPF. Across 18 N95 respirators without fit-testing, the study found an average SWPF of 3, drastically lower than the APF of 10 assigned to N95 respirators. Duling et al. (2007) conducted a similar investigation of N95 filtering facepiece respirators (FFR), finding average SWPFs of 3.3 across 15 N95 FFRs. These studies are summarized in Table 8.1 below.

Table 7.1 Summary of Scientific Literature of SWPFs of Non Fit-tested N95 Respirators

7.4.2 Scientific Peer-reviewed Literature on Nano Particle Penetration of Respirators

Scientific, peer-reviewed literature and documentation from regulatory agencies provide evidence that masks and personal protective equipment are often inadequate for protection from nano-particles, which may be developed during the fabrication of artificial stone countertops. This has been described in detail in Section 5.3.1. Literature also demonstrates that respirators that have not been properly fit-tested or lack an adequate seal can further expose workers to higher concentrations of nanoparticles. Table 7.2 below summarizes NIOSH studies investigating the impact of facial seal leakage on the penetration of 45 nm particles through N95 respirators. These studies demonstrate a high potential for nanoparticle penetration.

Table 7.2 Summary of Scientific Literature of Nanoparticle Penetration of Non Fit-tested Respirators

8 Standard of Care and Negligence Analysis

By the relevant time periods, silica hazards were well known, occupational limits existed, and feasible controls were available. Failure to implement effective controls, monitor worker exposure, communicate risks, and provide safer alternatives fell below reasonable industrial hygiene and occupational safety standards.

Where workers inhaled substantial respirable crystalline silica during countertop fabrication, those exposures materially increased the risk of silicosis and related disease. By the relevant time periods, silica hazards were well known, occupational limits existed, and feasible controls were available.

Failure to implement effective controls, monitor worker exposure, communicate risks, and provide safer alternatives fell below reasonable industrial hygiene and occupational safety standards.

8.1 Employer Compliance

Evidence shows that stone fabrication workshops have consistently failed to adhere to regulatory standards regarding personal protective equipment, inadequately protecting workings from crystalline silica.

In 2025, McGowan et al. evaluated respiratory silica concentrations in stone fabrication workshops across the United States. Out of the 1,100 stone fabrication companies surveyed, 257 countertop workshops provided data for analysis. A majority of the workshops fabricated both natural and engineered stone. Among those handling both, the average product mix was 37% natural and 52% engineered. Approximately 37% of the surveyed workshops did not require respirators, with 46.3% having respirable crystalline silica levels above OSHA’s PEL. Among the shops that required respirators, 58% did not perform fit testing, and 46% did not have a written respiratory protection program. The study concluded that:

“Thus, despite recent increased attention regarding the hazards of RCS exposure in this industry and OSHA silica regulations, real‐world practices regarding sampling for RCS, medical surveillance, and respiratory protection were highly variable and frequently not in compliance with the OSHA silica standard.”

In 2025, Soo et al. conducted a study that assessed personal air sampling results and job description notes from 17 industrial hygiene air sampling visits conducted at 11 stone fabrication facilities in Georgia. The study used similar exposure groups to assess workers performing stone fabrication. Respiratory protection was often improperly implemented at these facilities, with contractors documenting instances of improperly-fitting respiratory protection, respiratory protection worn with facial hair, improper storage of respirator protection, and removal of respirator protection during work tasks.

8.1.1 Engineered Stone Manufacturers

The following Section provides an overview of the various Safety Data Sheet(SDS) warnings provided by manufacturers of engineered stone manufacturers. Manufacturers of engineered stone have historically failed to provide clear, consistent warnings on the safe use of their products and the associated dangers within their MSDS documents.

Across all of these SDSs, Engineered Stone manufacturers have failed to acknowledge the unique hazards posed by fabrication of Engineered Stone, notably failing to discuss the potential for nanoparticle exposure. As previously described in Section 3.3, fabrication of ES releases respirable crystalline silica nanoparticles that penetrate deeply into the lungs and create a uniquely toxic hazard for workers. Not only do these SDSs fail to acknowledge the potential for nanoparticle exposure, they do not list adequate protections for nanoparticles.

As described in Section 5.3 and Section 8.4, scientific literature has demonstrated that nanoparticles are the most penetrating particle sizes for filtering facepiece respirators. As discussed below, these SDSs recommend the use of filtering facepiece respirators and do not recommend the use of more protective equipment such as Self-Contained Breathing Apparatuses (SCBA). This represents a systemic failure on behalf of engineered stone manufacturers to adequately warn and protect workers. As previously mentioned, these safety sheets further fail to warn workers about the potential for nanoparticle exposure and fail to recognize the increased toxicity of engineered stone products in comparison to natural stone products. This provides misleading information to workers, who may be deceived into thinking that their exposures from natural stone dust are comparable to those from natural stone.

Furthermore, between manufacturers, their warnings are inconsistent and contradictory, providing workers with confusing narratives on the safety of Engineered Stone products and the proper respiratory protection needed.

Consentino’s 1999 SDS for Silestone, which describes the product as being approximately 70 to 90% crystalline silica by weight. This MSDS includes the following personal protective equipment warning:

“Use [a] respirator or particulate mask when cutting or abrading materials. Use only respirators that meet NIOSH AND OSHA STANDARDS UNDER 29CFR 1910.134 and only N-95 filtering capability or greater should be used to protect against cristalline silica and other dust.”

The SDS additionally provides suggested engineering controls, specifically the use of “ASTME-1132-86 Standard Practice for Health Requirements Relating to Occupational Exposure to Dust.” The MSDS report describes potential health concerns arising from prolonged inhalation of airborne silica, including the potential for silicosis. The MSDS also discusses how the International Agency for Research (IARC) and the National Toxicological Program (NTP) have recognized the carcinogenic nature of silica.

A later, 2010 SDS provided by Cosentino for Silestone uses descriptive language that may confuse workers when trying to understand the best practices to follow when handling these materials. The SDS states:

“Exposure to dust may be monitored and controlled with suitable control measures such as:

• Machinery and tools involving the use of water
• Natural and/or mechanical ventilation systems that ensure the renewal of air in the workplace.
• Cleaning and maintenance. Use of vacuum and/or water cleaning systems, avoid sweeping and the use of compressed air, which creates dust. Preventative maintenance programmes of the installations to ensure the correct conditions of order, cleaning and operation of work equipment
• Respiratory protection for P3 type particulates according to EN 143:2001 and its revisions EN 143/AC 2002, EN 143/AC 2005, including working with water as a dust-reducing agent during the preparation of Silestone
• Hand Protection: We recommend the use of gloves to avoid the risk of cutting when handling pieces.
• Eye protection: We recommend the use of eye protection in accordance with regulation EN166:2001
• Skin Protection: Skin protection is not necessary but we recommend that work clothes are worn to avoid the contact of dust with skin. Wash hands and face with soap and water to remove dust before breaks and at the end of the shift
• Work Clothes: do not clean up using compressed air, use vacuum cleaning methods.”

This guidance can easily be misinterpreted based on language used. The SDS lists control measures after stating that exposures “may be” monitored using those methods. This may provide a level of ambiguity for those interpreting the listed control measures. While the SDS explicitly uses the language “we recommend the use of” when describing the use of gloves and eye protection, the document inconsistently does not use that language when describing respiratory protection. The SDS additionally states that it “recommends methods that involve the use of water in the manufacturing of this product” but does not use similar language when describing the need for respiratory protection. The 2010 SDS additionally did not include the same inhalation warning that crystalline silica has been recognized as a probable carcinogen by IARC and NTP, as had been discussed in the 2004 SDS.

This is further muddled by the fact that under hazard identification, the SDS includes the use of personal protective equipment P3. Additionally, under handling and storage recommendations, the SDS includes individual precautions and environmental precautions. The individual precautions advise that workers wear safety shoes and gloves while the environmental precautions include the use of water-cooled tools to prevent the creation of dust. The inconsistent discussion of respirator use in this SDS may make it difficult for workers to interpret which safety precautions to take, especially since it explicitly discusses the using wetting controls to reduce dust exposure.

The revised, 2013 SDS for Silestone from Cosentino, was consistent with the 2010 SDS that did not discuss the carcinogenic nature of crystalline silica. This MSDS utilized the same language when describing how exposure to dust “may be monitored and controlled” by their listed measures. While the 2013 SDS includes recommendations for the use of respiratory protection in its hazards identification sections and its exposure controls/personal protection sections, it does not include discussion of respiratory protection in its handling and storage sections.

Cosentino’s 2015 SDS for Silestone has consistent issues with previous sheets. While it does include the recommendation to use a respirator in its hazards identification and exposure controls/personal protection sections, the handling and storage section only includes discussion of helmets, safety shoes, safety glasses, and gloves under personal protective equipment. The safety data sheet additionally does not include any warnings under accidental release measures, which according to OSHA is supposed to include recommendations on appropriate responses to releases, including what personal protective equipment to use and cleanup procedures to follow.

The 2023 edition of the SDS for Silestone includes respiratory protection recommendations under its precautionary statements. Under its “Measures to take in case of accidental spillage,” it details that personal precautions and protective equipment are “not applicable,” further citing that the “finished material poses no spillage risks.” This same language is used regarding environmental precautions and cleaning containment methods under that same section. While the final subsection, “Reference to other Section” includes referrals to Section 8 and Section 13 that discuss personal protective equipment, this can be rather confusing for the worker interpreting the need for personal protective equipment and cleaning containment methods while working with this material.

Handling and Storage guidance within the 2023 SDS advise the use of dust exposure controls such as water supply systems and vacuum cleaning. This section, consistent with previous safety data sheets, does not include discussion of respirator usage despite inclusion of a personal protective equipment section and heavy discussion of the potential for respirable crystalline silica exposure during mechanical processing and installation. This further contributes to potential confusion among workers, as the next section,focused on exposure control and individual protection, explicitly calls for the use of Respiratory protection under its personal protective equipment section. This is further muddled by the fact that the other personal protective equipment listed in this section: gloves, eye protection, and work clothing, was previously listed in the handling and storage section of the SDS, that did not include respiratory protection.

The inconsistencies in description of hazards in Silestone SDS reports for engineered stone leave room for interpretation, placing undue responsibility on the manufacturing workers to assess what protections or controls are necessary in specific scenarios. While early SDS reports, like the 1999 Silestone SDS, advise that crystalline silica is recognized by IARC and NTP as a possible carcinogen, this warning was removed from later editions of Cosentino safety data sheets. This creates an environment in which the potential dangers of airborne particles, including crystalline, could be underestimated or ignored, resulting in possible overexposure.

This confusion is exacerbated in more recent Cosentino SDS documents that often juxtapose hazard recommendations that clearly call for respirator use with handling and storage recommendations that either don’t discuss respiratory protection or do not explicitly state that respirators are recommended despite discussing the use of wetting methods for dust control. Additionally, these SDS documents do not include any warnings under the Accidental Release Measures section, which according to OSHA, are supposed to provide “recommendations on the appropriate response to spills, leaks, or releases.”

A 2024 SDS for Cambria Quartz Surfaces, under Hazards Identification, describes the product as “not hazardous” while also highlighting concerns regarding the potential for release of “significant amounts of respirable (airborne) crystalline silica dust.” Furthermore, while the Hazards Identification Section highlights concerns for exposures to “dangerous concentrations of respirable dust,” the section does not advise the use of respiratory protection. The Section additionally includes hazard statements that discusses potential cancer associated with inhalation, and damage to organs from prolonged or repeated inhalation exposure. However, while providing these warnings, when listing protective gear in the same section, the SDS advises that users “wear protective gloves, protective clothing and eye protection,” notably not including respirator use. These hazards are re-emphasized in Section 4, which discusses first-aid measures. The section in particular lists silicosis as a potential risk from short-term, heavy exposure or long term exposure. It additionally discusses how long term exposure to respirable crystalline silica “results in a significant risk of developing” lung cancer. In the toxicological information section for the product, the product is “not classified” for acute toxicity for inhalation exposure, but the same section discusses how respirable crystalline silica is a known human carcinogen as has been recognized by IARC, NTP, and OSHA.

In the Section 6, which covers accidental release measures, the SDS discusses the use of personal protective equipment, including warnings advising that personnel do not breathe in dust. This warning starkly contrasts with safety data sheets from other manufacturers, like Consentino’s Silestone SDSs, which advise that personal protective equipment is “not applicable”, or that quartz products have no risk of accidental releases. This inconsistency between manufacturers can make it difficult for workers to determine whether or not personal protective equipment is needed when working with engineered stone products. Additionally, the Cambria 2024 SDS, in its Exposure Controls/Personal Protection Section, describes respiratory protection to be used “if exposure limits are exceeded or irritation is experienced,” or when there’s insufficient ventilation. This relies on the subjective judgement of the user to determine if respiratory protection is required. The 2024 SDS additionally discusses engineering controls, recommending the use of “dust extraction equipment, wet processing techniques, or local ventilation.” This provides vague guidance regarding which controls are optimal to use to mitigate dust exposure, leaving it up to the interpretation of the employer or employee to select control methods.

These trends are consistent with earlier SDS documentation, which presents similar issues regarding its warnings. A 2013 Cambria SDS for quartz describes the product as “non-hazardous” in its Hazards Identification Section while also including warnings of “serious damage to health” from inhalation, advising the use of respiratory equipment “in case of insufficient ventilation.” This demonstrates inconsistencies with later SDSs that do not discuss respiratory protection in the Hazards Identification Section. The Accidental Release Measures Section describes the material as not containing “any hazardous substances that would be of environmental concern upon accidental release.” This directly contradicts later SDS reports that recommend the use of respiratory protection and advise personnel to avoid inhalation of dust. The Exposure Control/Personal Protection Section of the SDS advises the use of respiratory protection, describing the use of NIOSH approved respiratory protection as “necessary to avoid inhalation of excessive air contaminants.” Later SDSs, as previously discussed, advise that respiratory protection is used when irritation is observed. This highlights contradictory guidelines provided by Cambria, as variations between guidance could develop confusing narratives regarding the appropriate use of PPE.

These SDSs reflect a systemic failure of communication on behalf of Cambria, as they provided confusing guidelines regarding the use of PPE, endangering manufacturing workers. These guidelines varied from year to year, which may have contributed to confusion among workers regarding the appropriate personal protective equipment and the hazards associated with their work.

Caesarstone (2010) in its 2010 Safety Data Sheet, described their product as “not classified as hazardous” in their Hazards Identification section. The Section later discusses potential health effects from operations working with the material, specifically discussing inhalation of crystalline silica dust as a possible cause of silicosis. The section later describes crystalline silica as recognized carcinogens by IARC, NTP, OSHA, and ACGIH. These descriptions can be misleading for manufacturing workers, who may not fully understand the extent to which the material they’re working with can be dangerous.

Under Accidental Release Measures, the SDS advises the use of “suitable respiratory protection and protective equipment when necessary.” This warning requires the user to determine the usage of a respirator based on their own subjective judgement and not according to standards or thresholds in place. This is similarly consistent with the Handling and Storage section, which states “good industrial hygiene practices should be followed when handling this material.” These guidelines are vague and leave room for interpretation by the user, not according to specific standards.

The Engineering Controls/Personal Protection section describes respiratory protection as “necessary to avoid inhalation of excessive air contaminants,” deferring to NIOSH guidelines regarding the type of respirator to use based on the magnitude of exposure. NIOSH Guidelines regarding respirable crystalline silica, provide respirator recommendations based on airborne concentrations of silica. The SDS further recommends the use of a positive pressure supplied respirator “if there is a potential for an uncontrolled release, exposure levels are not known or under any circumstances where air purifying respirators may not provide adequate protection. Ultimately, this SDS provides different narratives regarding the use of respiratory protection, describing their use“when necessary” in some scenarios, and calling for positive, pressure supplied respirators in other scenarios. These inconsistent recommendations may leave selection of respiratory protection up to the interpretation of the user. These same issues are present in the later 2012 SDS for the same product.

The 2016 Caesarstone SDS specifies the use of P3 respirators in its Hazards Identification Section. The Exposure Controls Section, which describes that the appropriate respirator “depends on the type and magnitude of exposure.” The Section additionally requires the use of “properly fitted respiratory protection approved by the National Institute for Occupational Safety and Health.” NIOSH’s guide for crystalline silica respiratory protection does not include P3 respirators at all, as P3 respirators are outside of the NIOSH classification system and belong to European respiratory protection classifications. This may cause confusion with users, who may not be familiar with international respiratory protection guidelines and may not know the equivalence of a P3 respirator with a NIOSH approved respirator. By not specifying the NIOSH equivalent for P3 respirators, represents a failure to clearly communicate the proper respiratory protection needed. These issues were partially addressed in the 2024 edition of the SDS, which describes an N95 or higher mask as an equivalent respirator to a P3.

A 2011 SDS for HanStone, when it was owned by Hanwha, stated, “this product is not classified as dangerous” under its Hazard Identification Section. The same section discusses how operations with the material, such as sawing, routing, drilling and sanding can generate dust that may cause silicosis if overexposed. This is further elaborated upon in the Toxicological Information Section, which discusses symptoms of silicosis and epidemiological studies that provide “limited evidence” that lung cancer is associated with exposure to crystalline silica. Under Exposure Controls and Personal Protection, the SDS recommends the use of “Eye/Face/Hand Protection” and wearing a “safety protector” during operations that include “sawing, sanding, drilling or routing.” The SDS does not include any specific mention of respiratory protection. The SDSs failure to specifically discuss respiratory protection or to provide specificity regarding the proper respiratory protection needed represents a failure to communicate the proper hazards and associated protections needed while working with engineered stone products.

Some of these issues persisted when Hyundai took over Hanstone operations. A 2019 SDS for HanStone quartz similarly described the product as “non-hazardous” and as posing “no health hazard” in its solid form in its Hazard Identification Section. The section further discusses potential exposure to crystalline silica dust during fabrication or demolition activities, specifying its carcinogenicity. Part of the precautionary statements in the Hazards Identification Section includes the use of P3 respiratory protection for particulates, further recommending the use of “personal protective equipment as required.” Under Accidental Release Measures, the SDS recommends the use of “appropriate respirator protection and safety glasses where a risk of exposure to dust is present.” This warning requires the user to determine the usage of a respirator based on their own subjective judgement and not according to standards or guidelines that advise the use of respirators in specific scenarios. Under Handling and Storage, the SDS warns against the potential for breathing in dust, recommending the use of wet production methods and ventilation. The section, however, fails to include any recommendation for respiratory use.

Under Exposure Controls/Personal Protection, the SDS recommends the use of NIOSH approved filtering face piece respirators, or higher level respiratory protection “where there is potential to exceed the exposure limits.” This contradicts prior recommendations that include the use of P3 respiratory protection, which are not included in NIOSH respiratory guidance for respirable crystalline silica exposure. By not specifying the NIOSH equivalent for P3 respirators, represents a failure to clearly communicate the proper respiratory protection needed.

The 2020 SDS for HanStone addressed some of these issues, with the Handling and Storage section including guidelines to wear protective equipment when working, including the use of a P3 mask. The Accidental Release Measures further included the use of “appropriate personal protective [equipment] during clean up,” however did not specify the type of personal protective equipment. The Exposure Controls and Personal Protection section included more details regarding respiratory protection, advising the use of respiratory protection for P3 type particulates. This updated SDS resolved some of the issues from the 2019 SDS, notably consistently recommending the use of a consistent respirator throughout its different sections. However, this did not address the issues with inconsistencies with regulatory agencies relied upon. The Exposure Controls and Personal Protection Section relies upon European Union standards for selection of respiratory protection, however relies upon OSHA standards for occupational exposure limits. The OSHA standards provided in the SDS were further not accurate to the most recent TWA, which includes a level of 0.05 mg/m3, rather than the 0.1 presented in the SDS. If relying on both European and US regulatory agencies, this document should provide a holistic overview of regulations in the EU and the US, including NIOSH equivalents of P3 respirators. US Workers may be confused by the recommendations within this SDS report, as P3 respirators are not included in NIOSH respiratory guidance for respirable crystalline silica exposure.

Additionally, consistent with the previous 2019 SDS, it similarly classified the product as not dangerous, while citing the potential for exposure to silica dust which may cause silicosis. These descriptions may be misleading for manufacturing workers, who may not fully understand the extent to which the material they’re working with is dangerous. These issues highlight a failure to communicate the proper hazards and associated protections needed while working with engineered stone products.

The Hazard Identification Section of the 2023 SDS for HanStone classified the product as “non-hazardous,” while also classifying it as a Category 1A carcinogen when the product is cut, drilled, grinded, and polished. The Section further recommends the use of respiratory protection “in [the] case of inadequate ventilation.” Under Accidental Release Measures, the SDS recommends that individuals wear “appropriate protective clothing and equipment where risk of exposure to dust is present.” Under Handling and Storage, the SDS recommends the use of an approved respirator (referring to Section 8, Exposure Controls/Personal Protection) when cutting, drilling, grinding and polishing, or any process that generates dust. The Exposure Controls/Personal Protection section requires the use of NIOSH approved respiratory equipment “if it is not possible to reduce the limits to below the permissible limits.” The section further advises the use of respirators based on the requirements of the user’s jurisdiction. Using a respirator “if it is not possible to reduce the limits to below the permissible limits” contradicts previous sections that suggest the use of respirators in scenarios “where risk of dust exposure is present” or during a “process that generates dust.” This may create confusion among users as to when respiratory protection is needed.

The 2024 Hanstone SDS provides precautionary statements that includes recommendations to “wear protective gloves/protective clothing/eye protection/face protection/hearing protection.” While this same section specifically discusses inhalation exposure to airborne quartz as being a cause of silicosis, the Section does not explicitly advise the use of respiratory protection. The Handling and Storage Section explicitly recommends the use of protective equipment when working, specifying the use of a P3 mask. The Exposure Controls/Personal Protection Section advises the use of “NIOSH or European EN 149 full or half face piece respiratory protective equipment when necessary.” The Section further advises the use of respiratory protection for P3 type particulates and working with water as a dust-reducing agent. The Section further advises the use of supplied-air respirators or self-contained breathing apparatuses when there’s a lack of oxygen. The term “when necessary” may provide ambiguity when users are selecting respiratory protection, especially since earlier guidance within the same SDS recommends use of respiratory protection while working. Consistent with previous SDS reports from Hanstone, they cite outdated OSHA TWA’s for silica.

Hanstone SDSs have historically provided contradictory and confusing guidelines regarding the use of PPE and have misreported OSHA PELs. This reflects a systematic failure of communication on behalf of HanStone manufacturers to inform users of the hazards of their product.

Documentation from peer-reviewed literature and from regulatory agencies has additionally found issues with SDSs from engineering stone manufacturers. These are briefly summarized below.

In 2024, the Australian Government banned the use of Engineered Stone in Australia, citing concerns regarding occupational exposures to silica. Safe Work Australia released a report on behalf of the Australian government highlighting the reasons behind this ban. The report in particular provides critiques of Safety Data Sheets, specifically the tendency for manufacturers to describe engineered stone products as, “not classified as hazardous“ while also disclosing that dust created through the processing of the material may contain respirable silica dust. This is consistent with MSDS reports provided by Cambria and other manufacturers, as previously discussed.

Safety data sheets from stone manufacturers additionally provided silica content estimates that were inconsistent with the actual silica content found in laboratory testing. Kumarasamy et al. (2022) conducted a comparative analysis, comparing the information provided in artificial stone product safety data sheets, with physiochemical data. The study determined the contents of 25 individual artificial stone products from six different providers, comparing them with their corresponding safety data sheet information. The studies found inconsistencies between SDSs from different suppliers, discussing how suppliers often would categorize silica constituents differently, if at all. The authors specifically focused on categorization of quartz and cristobalite in SDS files, finding that while some manufacturers would separate Quartz and cristobalite percentages, others would not report cristobalite concentration at all, even when it had been determined to be present. The authors found that in most of the safety data sheets analyzed, the concentrations of components fell within the ranges of the SDSs, however they further noted that the ranges were “unusually wide” for many constituents. The authors further noted that in spite of the wide ranges of values presented in many SDSs, testing of samples of artificial stone found concentrations outside of the SDS-specified compositional range. This highlights further negligence on behalf of manufacturers who have failed to adequately inform users of the contents within their products.

Ultimately, the lack of alignment between different sections of the same SDS documents, SDS documents from different years, and among documents from different manufacturers, suggest a broader negligence in ensuring worker safety. By failing to provide clear, enforceable, and uniform standards for respiratory protection, engineered stone manufacturers have contributed to the ongoing exposure of manufacturing workers to respirable crystalline silica.

8.1.2 Makita Angle Grinder Engineering Controls

In their 1996 Preventing Silicosis and Death in Construction Workers report, NIOSH noted that “dust collection equipment [was] available for many types of dust-generating equipment.” NIOSH recommended purchasing tools with dust control systems and advised to “always” use and maintain them. These recommendations were reaffirmed by OSHA and NIOSH reports in 2008 and 2009, respectively. In their Special Emphasis Program (SEP) for silica, OSHA noted that one strategy to reduce silica exposures was the “use of tools with dust collection systems,” which NIOSH found to reduce dust from concrete by approximately 90%.

Makita has acknowledged the hazards of dust exposure produced by their equipment in their own manuals and press releases. In their angle grinder manual, they stated that “power sanding, sawing, grinding, drilling, and other construction activities” releases “crystalline silica from bricks and cement and other masonry products,” which were described as harmful to human health. In their general catalogue, they described the use of a “commercially available water delivery system or dust shroud” as a “requirement.” Makita was also aware of the demand for more dust protection equipment, with a Makita Product Manager stating that “contractors are demanding more dust extraction solutions to reduce the amount of concrete dust created during tool usage.”

Despite their knowledge of the dust generated by the use of Makita tools and health hazards of silica dust inhalation, Makita routinely sold dust-producing tools, such as grinders, without dust mitigation attachments included with the product. In a Makita angle grinder manual, dust collecting wheel guards were described as “optional accessories” for “cutting stone materials.”

It is not unprecedented for Makita to have provided complementary equipment for Makita tools to meet regulatory requirements. According to their angle grinder overview, Makita states that wheel guards are provided as part of standard equipment. This is to meet OSHA regulations that mandate the use of safety guards for all grinding equipment. Makita’s angle grinder manual instructs to “always” use the “dust collecting wheel guard if required by domestic regulation” for the cut-off wheel. In addition, the manual states that optional accessories “may be included in the tool package as standard accessories” depending on a country’s standards. Given that Makita understood the importance of the dust collecting wheel in reducing dust exposure and thus complying with regulations, Makita should have provided this safety equipment to all customers instead of relegating it as an optional accessory.

Additionally, Makita failed to adequately inform users about the health hazards of cutting stone without the dust collecting wheel attachment. Although Makita was aware of the risks, the angle grinder manual does not emphasize that the angle grinder should always be used with the dust collecting wheel guard when cutting stone. Instead, they noted that dust collecting wheel guards should only always be used “if required by domestic regulation,” which underplays the health risks from respiratory crystalline silica exposure.

9 Exposure Matrices

9.1 Methodology

An exposure year is a standardized unit used to quantify occupational exposure to airborne respiratory crystalline silica over a defined period, based on a standard work year of 2,000 hours (approximately 40 hours per week for 50 weeks). This metric is widely used in occupational health to assess cumulative exposure and associated risks. In scientific literature, exposure year units are often expressed as mg/cubic meter-year (“mg/-Year” or “(mg/)-y”), The cumulative silica dose over the exposure time frame is calculated by summing the products of probability, frequency, intensity and duration of exposure, and involves the following steps:

First, the respirable crystalline silica concentration in a meter of air is found in scientific literature for each relevant activity for the individual at issue (e.g. dry cutting and grinding with hand tools, wet polishing and grinding with hand tools, operating bridge-saws or other machinery) in micrograms per meters cubed (“ug/”).

Second, the total time for each relevant exposure activity is calculated and converted to occupational years. Then, the exposure time in occupational years is multiplied by the fiber concentration for each activity to calculate the fiber years.

Exposure-years/m³ for each activity = (Total hours exposed/2,000) × (Respirable Crystalline Silica concentration for each exposure activity)

Third, the cumulative exposure-years is calculated by summing the exposure years for each activity.

Total Exposure-years/m³ = Σ (Exposure years for each exposure activity)

This methodology provides a standardized approach to quantifying respirable silica exposure, ensuring consistency and accuracy in dose assessments. This methodology and the use of respirable exposure years is consistent with silica epidemiological and exposure literature.

Since exposure studies varied methodologically, these studies were sorted into “Field-based studies” and “All task-based studies.” Field-based studies only include studies that were conducted at stone manufacturing facilities, while “all-task based studies” consider all studies that utilized task-based sampling. Three publications on wet polishing, one on dry polishing, one on dry cutting, one on wet cutting, and three on wet grinding were field based studies. One publication on wet cutting, two on dry cutting, one on wet grinding, and one on dry grinding were additionally included in the all-tasked based studies exposure. These studies, which are summarized in Section 5, were used to calculate respirable crystalline silica concentrations (ug/).

For each study, an average, upper confidence level (“UCL”), and maximum were calculated. To evaluate various summary statistics for exposure concentrations for silica, the United States Environmental Protection Agency’s ProUCL software (Version 5.1.00) was used. ProUCL is a statistical tool developed by the USEPA to calculate the one-sided 95 percent upper confidence limit (“95% UCL”) on the arithmetic mean concentration for environmental datasets. ProUCL additionally provided the average and maximum concentrations for these scientific studies.

The US EPA Risk Assessment Guidance of 1989 explains that the reasonable maximum exposure should be utilized for risk assessment. When discussing the exposure concentration, the guidance documents states:

“Because of the uncertainty associated with any estimate of exposure concentration, the upper confidence limit (i.e., the 95 percent upper confidence limit) on the arithmetic average will be used for this variable. There are standard statistical methods which can be used to calculate the upper confidence limit on the arithmetic mean.”

Scientific, peer-reviewed literature has additionally extensively used 95% UCLs when conducting risk assessments and estimating exposures.

If an UCL or maximum were unable to be calculated, the average was used. To calculate the average UCL of silica exposure from each task, the average of each study’s mean and UCL was taken, respectively. To calculate the maximum silica exposure from each task, the maximum silica exposure value across all the studies was used.

These studies are summarized in the tables below. Table 9.1 summarizes exposure concentrations for all silica stone activities, including solely granite, engineered stone and natural stone, and solely engineered studies, for both field and task based studies. Figures 9.1 and 9.2 summarize the exposure concentrations from task-based studies for engineered stone and granite work. Because most peer-reviewed literature that assess both engineered stone and granite fabrication do not specify the percentage of engineered stone or granite used in tasks. The data points underlying these calculations and graphs are presented in supplemental files.

Table 9.1: Summary of Exposure Values for All Silica Stone Activities

9.5 Demonstrative Nanoparticle Calculation

Assuming spherical crystalline silica particles with a density of 2.65 g/cm³, the nanoparticle mass of 1 ug of silica, corresponds to approximately 7.9 × 10¹⁰ individual particles at a particle diameter of 40 nanometers, 4.0 × 10¹⁰ particles at 50 nanometers, 2.3 × 10¹⁰ particles at 60 nanometers, and 5.0 × 10⁹ particles at 100 nanometers.

This demonstrative calculation is consistent with multiple independent lines of scientific evidence discussed throughout this report. Carrieri et al. (2020) demonstrated that fabrication of engineered stone produces a dominant particle-number distribution centered at approximately 50–70 nanometers, whereas granite generated comparatively few particles within this size range. Ophir et al. (2019) and Ramkissoon et al. (2022) independently showed that engineered stone produces a substantially finer respirable aerosol than natural stone, resulting in greater numbers of ultrafine particles capable of remaining airborne longer and penetrating more deeply into the distal lung. Together, these studies demonstrate that workers fabricating engineered stone are exposed to substantially greater numbers of respirable and nanoparticle-sized silica particles than workers fabricating granite.

The importance of these particles extends beyond particle number alone. As particle diameter decreases, the number of particles and the total available surface area per unit mass increase dramatically, providing substantially more surface for interaction with lung tissue. In addition, in their 2023 paper, Pavan et al. demonstrated that freshly fractured quartz generated during cutting and grinding exposes nearly free silanols, highly reactive surface chemical groups that readily damage cell membranes and initiate inflammatory and fibrotic responses. These freshly fractured surfaces are considerably more biologically reactive than weathered silica particles and provide a biologically plausible explanation for the unusually rapid onset, accelerated progression, and increased severity of artificial stone-associated silicosis reported worldwide.

Accordingly, the demonstrative particle calculations should not be viewed in isolation. Rather, they corroborate the consistent findings from industrial hygiene studies, aerosol characterization, toxicological investigations, epidemiological studies, and regulatory evaluations demonstrating that engineered stone fabrication exposes workers to extraordinarily large numbers of highly reactive respirable crystalline silica particles.

10 Findings And Opinions

• The figure below demonstrates a global epidemic of a distinct occupational disease now recognized by the American Thoracic Society as Artificial Stone–Associated Silicosis (AS Silicosis), with major outbreaks reported in Israel, Spain, Australia, the United States, and numerous other countries. Unlike traditional silicosis, AS silicosis develops after relatively short exposure durations, progresses rapidly to progressive massive fibrosis, frequently continues to worsen after exposure ceases, and has resulted in lung transplantation and premature death among many affected workers.

Figure 10.1: Cumulative Number of Artificial Stone–Associated Silicosis Cases Around The World

• Natural stones such as granite and marble are geologic materials formed over millions of years through natural mineralization. In contrast, engineered stone is a manufactured composite consisting primarily of finely crushed quartz bound together with polymer resins and pigments using a process known as vacuum vibrocompression. As a result, engineered stone typically contains more than 90% crystalline silica by weight, compared with less than 10% for marble and approximately 20% to 50% for most granites. This difference alone substantially increases the amount of respirable crystalline silica generated during fabrication.

• Engineered stone generates nanoparticles during fabrication. Nano particles have been found to be more likely to deposit deep within the lungs and are more reactive due to their large surface area. These nanoparticles are more biologically reactive and provide a plausible explanation for the rapid onset and accelerated progression for artificial stone-associated silicosis reported worldwide.
• Engineered stone nanoparticles contain a highly reactive chemical group known as nearly free silanols on their surfaces. Pavan et al. (2023) demonstrated that crystalline silica particles with high concentrations of nearly free silanols cause the greatest cell membrane damage due to their uniquely high reactive surface. Engineered stone nanoparticles have drastically higher surface areas than larger particles, presenting a substantially greater, more reactive surface that damages lung tissue. This is demonstrated in Figure 10.3 below.

• While manufacturers recommend the use of wet methods to mitigate exposures, peer-reviewed literature has demonstrated that even wet activities often generated silica concentrations above permissible exposure limits, showing that partial controls alone were inadequate. Figure 10.4 below summarizes respirable silica concentrations reported across task-based studies of engineered stone fabrication using only wet methods.

• Figure 10.5 below summarizes respirable crystalline silica concentrations reported across task-based studies of engineered stone fabrication and demonstrates that dry fabrication processes produce dramatically higher exposures than wet methods. In particular, dry cutting and dry polishing generated the highest silica concentrations—often hundreds of times greater than wet cutting, grinding, and polishing—highlighting the importance of engineering controls and wet-cutting techniques to reduce worker exposures.

• OSHA PELs are NOT health protective. The Assistant Secretary of Labor for OSHA stated, “many of our chemical exposure standards are dangerously out of date and do not adequately protect workers.” OSHA has further acknowledged that “a broad consensus exists among public health experts and practitioners, chemical manufacturers, and labor and employer groups that OSHA’s PELs are woefully outdated and insufficiently protective of worker health.” OSHA”s 29 CFR explicitly stated that “the most stringent PEL feasible can only reduce, not eliminate, significant risk.”
• In 1971, OSHA established a Permissible Exposure Limit (“PEL”) of Quartz of 100 μg/m³ TWA for respirable quartz. NIOSH stated in 1974 that PELS in the granite industry were inadequate to protect human health, setting a Recommended Exposure Limit (“REL”) of 50 μg/m³ TWA. While the PEL was updated in 2016 to 50 μg/m³ TWA, OSHA has acknowledged that significant risk still exists at 50 μg/m³.
• Evidence from regulatory agencies, Cal/OSHA and Safe Work Australia, has demonstrated that traditional controls including use of PPE, air and health monitoring, dust control practices and training of workers and employers are inadequate for protecting workers from silicosis associated with ES fabrication work.
• Cal/OSHA has recognized that while respiratory protection and engineering controls can reduce risk, they cannot fully eliminate exposures. They have further recognized that the most effective solution to addressing hazards associated with ES, involves the elimination of the product entirely and the substitution with safer alternatives. Research has demonstrated that engineering controls do not function well with nanoparticles due to their size. Published evidence further demonstrates that the most penetrating particle size for common N95 respirators falls within the nanometer range generated during ES fabrication.
• Assuming spherical crystalline silica particles with a density of 2.65 g/cm³, Figure 11.6 below demonstrates the approximate number of nanoparticles in 1 µg/m3 of respirable crystalline silica. This nanoparticle mass corresponds to approximately 5.8 × 10⁹ individual particles at 50 nanometers.

• ES dust has unique characteristics that make it uniquely and substantially more hazardous than traditional NS dust. There is epidemiological evidence demonstrating that even short term exposures to ES dust demonstrates an increased risk of silicosis.
• There is epidemiological evidence that demonstrates that silicosis risk observes a linear, dose-response relationship with silica exposure. These studies evaluated mortality among a large cohort, demonstrating that linear relative-rate models provide the most appropriate fit for cumulative silica exposure and silicosis risk.
• Natural Stone and 1% silica ES Products are safer alternatives to widely-used ES Products, yet many of the Defendants failed to provide safer alternatives to ES Products despite the availability of far less hazardous, economically viable alternatives.
• In 2017, NIOSH published Bulletin 68, which stated there is no known safe level of exposure to most carcinogens. Bulletin 68 states: “for most carcinogens, there is no known safe level of exposure… Risk management based on a premise of no safe level does provide employers with a uniform approach to handling occupational carcinogens, including those with possible thresholds, that is easier to apply across different work processes and is more health protective for workers”.
• II reserve the right to supplement or amend my report as new information becomes available.
• I hold these and other opinions expressed herein to a reasonable degree of scientific certainty.

Paul E. Rosenfeld, Ph.D.