Executive Summary

Background
Engineered stone workers face some of the highest risks for developing silicosis, a severe and irreversible lung disease caused by exposure to respirable crystalline silica dust. Unlike traditional industries, engineered stone contains over 90% crystalline silica, and fabrication tasks release extremely hazardous levels of dust. Workers are developing silicosis at younger ages, after shorter exposure durations, and with more aggressive disease progression than seen in other industries.

Problem
Despite legal requirements, many workers are not being screened or medically monitored. A recent study by Surasi et al. (2022) found that over one-third of employers failed to provide required medical surveillance. Self-employed workers, those in small shops, and employees in financially strained workplaces are especially vulnerable. Cal/OSHA lacks the staffing and resources to ensure compliance. As a result, the current system is failing to detect disease early, leaving workers at risk of severe disability and premature death.

Our Recommendation
We propose a comprehensive, independent medical surveillance program for all workers exposed to engineered stone dust for at least 30 days, including both current and former workers. The program is specifically designed for individuals without established parenchymal silicosis, though those with only lymph node calcifications are eligible.

Key Testing Components

• Medical History and Physical Exam: Annual history and physical exam focusing on heart, lungs, skin, joints, ENT (ear, nose, mouth, and throat), and extremities with medical and exposure history including exposure questionnaire. Performed by an occupational medicine or pulmonary physician.

• Symptom and quality of life screening: Annual standardized questionnaires (KBILD, MMRC, PROMIS-29).

• Chest CT scans: Annually during employment; annually for 15 years after leaving the industry; then every 3 years thereafter, with the option to stop at age 75 following joint decision with physician.

• Pulmonary function testing: Full annual testing (spirometry, lung volumes, DLCO, 6-minute walk) on the same schedule as CT scans.

• Cardiopulmonary exercise test (CPET): At baseline, then every 3–5 years, or sooner if clinically indicated.

• Infectious disease screening: Annual tuberculosis (Quantiferon Gold + sputum cultures) and nontuberculous mycobacterial screening.

• Systemic disease markers: Routine labs including basic metabolic panel, liver panel, complete blood count with differential, IgE, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and angiotensin-converting enzyme (ACE). These tests provide critical information about systemic inflammation, immune dysregulation, and organ function.

• Autoimmune testing: Comprehensive laboratory panel at baseline, then every 5 years, with earlier repeat if symptoms arise.

• Emerging tools: Biomarkers, breath biopsy, and forced oscillometry may be used at physician discretion.

Oversight
The protocol will be developed by experienced occupational medicine physicians and pulmonologists who specialize in silicosis and pneumoconiosis. It will be reviewed and updated every two years to reflect new clinical evidence and diagnostic tools.

Why This Matters
Silicosis is preventable but irreversible once established. Early detection allows for removal from exposure, closer monitoring, and better long-term outcomes. Independent, expert-led surveillance is necessary to close the gaps left by employer-based systems and ensure that all exposed workers—past and present—receive the medical care they need.

Table 1. Recommended Testing and Frequency for Artificial Stone Workers

Screening recommendations for exposed artificial stone workers without evidence of parenchymal silicosis

Introduction

Disease surveillance for silicosis involves the systematic and ongoing monitoring of workers at risk of developing lung disease due to exposure to respirable crystalline silica. This process typically includes periodic health evaluations such as symptom screening, imaging, and pulmonary function testing, with the goal of detecting disease at an early, potentially asymptomatic stage to enable timely intervention and prevent progression. Surveillance is especially critical for workers involved in engineered stone countertop fabrication, a sector associated with exceptionally high-intensity silica exposure. Engineered stone contains over 90% crystalline silica, which far exceeds that of natural stone, and fabrication tasks such as cutting, grinding, and polishing generate hazardous levels of respirable dust. As a result, engineered stone workers are developing silicosis at younger ages, after shorter exposure durations, and with more aggressive progression than historically observed in other industries. Given this severe clinical course and the potential for preventable morbidity, comprehensive and frequent disease surveillance is essential to protect the health of this high-risk workforce.

Despite the importance of medical surveillance, current strategies often fall short, especially in the engineered stone industry. A key limitation is the overreliance on air monitoring, which, while valuable, is expensive and often infeasible in many workplace settings. Recognizing the high baseline risk in this sector, jurisdictions such as California and Australia have revised their surveillance protocols to include universal screening of engineered stone workers, rather than relying solely on exposure measurements. Furthermore, effective surveillance must extend beyond imaging alone. A comprehensive approach should incorporate standardized symptom questionnaires, complete pulmonary function testing with diffusion capacity, and emerging biomarkers that may signal early, subclinical silica-related inflammation. While healthcare systems and regulatory frameworks differ across regions, occupational medicine providers and public health officials should adopt and tailor these strategies to their local contexts, ensuring that the core goals of early detection, accurate exposure assessment, and prompt clinical intervention are maintained.

Early identification of silicosis is particularly critical for workers with ongoing exposure to respirable crystalline silica, as continued exposure significantly accelerates disease progression. Historical data show that between one-third and nearly 90 percent of individuals with silicosis experience worsening disease over time. Engineered stone workers are especially vulnerable due to the intensity of exposure, even after relatively short periods of work. Evidence from Swedish registries and studies in South African and Brazilian miners consistently demonstrates that ongoing silica exposure after diagnosis leads to more rapid progression, including to severe forms like progressive massive fibrosis (PMF). Although disease can continue to progress even after exposure ceases, the rate of deterioration tends to slow. However, among engineered stone workers, progression may occur with alarming speed. For example, one Spanish study found that over half of workers with simple silicosis progressed within four years, and more than one-third developed PMF. Because PMF has a poor prognosis and often culminates in cardiopulmonary failure requiring lung transplantation, detecting disease early, ideally before or at the time of diagnosis, offers a vital opportunity to reduce exposure and potentially alter the trajectory of this otherwise devastating condition.

Medical Necessity of Non-employer-based Screening Programs

Medical surveillance and diagnostic testing for workers exposed to respirable crystalline silica, particularly in the engineered stone industry, is medically necessary due to the high risk of early, aggressive, and irreversible lung disease. Many affected workers are not covered by employer-sponsored surveillance programs because they are self-employed, work in very small shops, or are employed in workplaces with limited financial resources and no capacity to provide such monitoring. As a result, there is a critical gap in access to appropriate medical evaluation and ongoing surveillance.

Furthermore, while Cal/OSHA has adopted emergency standards, the agency does not have adequate staffing or resources to ensure that mandated testing is consistently implemented across workplaces. This lack of enforcement and oversight has left a large segment of high-risk workers without the protections necessary to detect disease early and prevent progression.

The current system is therefore failing to protect this workforce. Independent medical testing and surveillance programs are required to fill this gap and ensure that at-risk individuals receive timely and comprehensive evaluation. As documented by Surasi et al., significant shortcomings in existing surveillance infrastructure underscore the urgent need for accessible, standardized, and medically directed testing for silica-exposed workers.

Eligibility

Workers would be eligible for participation in this screening program if they have a history of occupational exposure to artificial stone dust for a cumulative lifetime duration of at least 30 days. The program is designed for individuals who do not have established evidence of parenchymal silicosis. Eligible participants therefore include those without any radiographic abnormalities suggestive of silicosis, as well as those whose only radiographic findings are isolated lymph node calcifications, which may reflect exposure but do not constitute parenchymal disease. Importantly, eligibility extends to both current and former workers, recognizing that individuals who are no longer employed in the industry remain at risk for disease development and progression.

Protocol Development and Oversight

This protocol would be developed by a multidisciplinary team of occupational medicine physicians and pulmonologists with extensive experience caring for patients with silicosis and other pneumoconioses. Their expertise ensures that the recommended evaluations reflect both best clinical practices and the unique needs of silica-exposed workers. To maintain relevance and scientific rigor, the protocol will undergo systematic review every two years. During each review cycle, the team will evaluate the most current clinical recommendations, incorporate advances in diagnostic testing, and assess the feasibility of integrating novel tools that may not yet exist at the time of this documentation.

Medical History and Physical Exam

Given the complexity of diagnosing and managing silicosis, particularly in workers exposed to high concentrations of respirable crystalline silica from engineered stone, it is essential that affected individuals be evaluated by specialists in occupational and pulmonary medicine with specific expertise in silica-related lung disease. These clinicians are uniquely trained to interpret the interplay between work history, radiographic findings, pulmonary function data, laboratory results, and symptom progression. Accurate diagnosis is especially challenging in early or atypical cases, where imaging and pulmonary function testing may be equivocal. Misclassification can lead to under-recognition of at-risk individuals or, conversely, to unnecessary anxiety and over-treatment. Evaluation by experienced specialists ensures accurate interpretation, timely removal from exposure when needed, and the initiation of interventions that may slow disease progression. Ideally, these assessments should occur within dedicated Silicosis Centers of Excellence, where multidisciplinary teams can deliver standardized, high-quality care, facilitate early detection through advanced diagnostics, and contribute to broader surveillance and research efforts.

Occupational questionnaires are a critical component of the medical assessment for engineered stone workers. These tools systematically capture information about work history, job tasks, exposure duration and intensity, use of personal protective equipment, and the presence or absence of dust-control measures. In the context of engineered stone fabrication—an industry associated with exceptionally high levels of respirable crystalline silica—questionnaires provide essential context that imaging and pulmonary function testing alone cannot offer. They help identify high-risk workers who may require more frequent medical surveillance or earlier diagnostic evaluation, even in the absence of symptoms. Furthermore, standardized occupational questionnaires strengthen epidemiologic research, guide exposure mitigation strategies, and inform regulatory responses by highlighting patterns of unsafe practices.

The medical assessment itself will include a detailed exposure history obtained through these standardized questionnaires and a full physical examination, with emphasis on the heart, lungs, skin, joints, ears, nose, throat, and extremities. Physicians will also integrate results from symptom and quality-of-life questionnaires, imaging studies, pulmonary function testing, infectious disease screening, autoimmune and systemic laboratory markers, and other relevant diagnostics. Together, these elements provide a holistic understanding of both respiratory and systemic health, ensuring early detection, guiding individualized treatment, and supporting evidence-based policy and workplace protections.

Symptoms-based Questionnaires

Respiratory symptom questionnaires provide essential clinical information that complements imaging and physiologic testing. Many early manifestations of silicosis, such as cough, sputum production, or exertional breathlessness, may not be captured by CT scans or pulmonary function tests. Standardized questionnaires allow clinicians to systematically track changes in symptoms over time and ensure that subtle but clinically important declines are not overlooked. 

Quality of life assessments extend beyond respiratory symptoms to capture the broader impact of silica-related disease on daily functioning. Workers with silicosis or early lung impairment frequently experience fatigue, anxiety, sleep disturbance, musculoskeletal pain, and reduced participation in work or social activities. By using validated instruments such as the King’s Brief Interstitial Lung Disease (KBILD) questionnaire, the Modified Medical Research Council (MMRC) dyspnea scale, and thePROMIS-29, clinicians can quantify how disease affects physical, emotional, and social well-being. This information not only guides individualized treatment decisions but also highlights the real-world burden of disease for policymakers, insurers, and employers.

Imaging testing

Traditional chest X-rays are inadequate for detecting early-stage silicosis, especially when compared to the significantly greater sensitivity and diagnostic clarity offered by high-resolution computed tomography (HRCT). HRCT is now widely recognized as the superior imaging tool for surveillance, given its ability to detect subtle abnormalities that are not visible on standard radiographs. Despite some emerging interest in low-dose CT as a potential alternative, no studies have directly compared it to chest X-rays for this purpose, and current evidence is insufficient to conclude that it offers a reliable replacement.

In cases of simple silicosis, HRCT allows for much more precise identification of characteristic features, such as centrilobular and subpleural nodules with a perilymphatic distribution, and provides improved visualization of hilar lymphadenopathy. It can also differentiate silicotic nodules from other causes of nodularity. In complicated silicosis, HRCT is particularly useful for clearly defining mass borders, internal architecture, and associated paracicatricial emphysema. Additional pathologic findings—including lymph node calcification, pleural plaques, or superimposed infections such as tuberculosis—are also better visualized on HRCT.

Data from Australian and Italian studies underscore this superiority: 35–43% of engineered stone workers with CT-confirmed silicosis had normal chest X-rays, and only 42% of Italian workers diagnosed with silicosis via CT had abnormal chest radiographs. These findings have led regulatory bodies in Australia and California to transition from chest X-rays to mandatory chest CT scans for surveillance, underscoring the critical need to adopt more sensitive imaging to enable earlier diagnosis and intervention.

We recommend that all eligible people undergo chest CT imaging as part of medical surveillance. For individuals who remain actively employed in the industry, CT scans should be performed annually during work tenure and for 15 years after cessation of work, and then every 3 years thereafter (aligned with CT chest intervals, with the option to stop testing at age 75 following a joint decision between the patient and the examining physician) throughout the duration of their work tenure, reflecting their continued risk of exposure and disease progression. For those who have left the industry, annual CT scans are advised for the first 15 years following cessation of exposure, given the ongoing risk of delayed disease development. After this period, the interval may be extended to every three years with the option to stop testing at age 75 following a joint decision between the patient and the examining physician. Shorter-interval follow-up scans (e.g., every 3–6 months) may be warranted at the discretion of the treating physician if concerning radiographic findings such as isolated lymph node calcifications or pulmonary nodules are identified.

This approach aligns with practices adopted in Australia and reflects the high-intensity silica exposure associated with engineered stone fabrication, as well as the increased risk of disease progression in this population. After evaluation by a specialist in occupational and pulmonary medicine, the surveillance interval may be extended to every two years in cases where there is compelling evidence of clinical and radiographic stability. Such decisions should be individualized and based on specialist judgment.

Pulmonary function testing

Pulmonary function testing (PFT) refers to a group of non-invasive tests that assess how well the lungs are working, including measurements of lung volume, airflow, and gas exchange capacity. These tests, such as spirometry and diffusing capacity for carbon monoxide (DLCO), are essential tools in the early detection of respiratory impairment. For workers exposed to respirable crystalline silica, particularly in the engineered stone industry, regular PFTs can help identify early signs of lung damage before symptoms appear or radiographic abnormalities develop.

In Australia, it is recommended that workers in high-risk industries such as engineered stone fabrication undergo baseline pulmonary function tests (PFTs) at the start of employment, followed by annual testing to monitor for any decline in lung function over time. This approach is more rigorous than current U.S. OSHA requirements, which do not mandate routine pulmonary function surveillance for silica-exposed workers. The increased frequency of testing in Australia reflects the recognized rapid progression of silicosis in engineered stone workers and the need for more intensive monitoring. Both Safe Work Australia and the [Australian] National Dust Disease Taskforce emphasize that repeated PFTs allow for the identification of meaningful changes by establishing trends and distinguishing true physiological decline from normal variability. When significant changes are detected or clinical concerns arise, more frequent testing and referral to a respiratory specialist are warranted. As with imaging surveillance, this proactive approach to lung function monitoring is a critical strategy for early detection, prevention of disease progression, and protection of workers’ respiratory health in this high-risk population.

Pulmonary function testing in engineered stone workers can reveal a variety of abnormalities, with restrictive patterns being the most frequently observed. However, many individuals with CT evidence of silicosis may still have normal pulmonary function tests, particularly at the time of diagnosis. In an Italian case series, only 33% of workers with CT-confirmed silicosis had abnormal spirometry, whereas 50% had a reduced diffusing capacity for carbon monoxide (DLCO), highlighting the greater sensitivity of diffusion measurements. Similarly, in an Australian study, more than half of the individuals with progressive massive fibrosis showed normal spirometry results. These findings underscore the limited sensitivity of spirometry alone for early disease detection. Including DLCO in routine testing provides a more comprehensive assessment and improves the likelihood of detecting physiologic impairment. While pulmonary function testing is less sensitive than chest CT for diagnosing silicosis, it remains an important tool for monitoring disease progression and assessing functional disability—particularly when full testing, including DLCO, is performed.

We recommend full pulmonary function testing which includes spirometry, lung volumes, diffusion capacity, and 6-minute walk test to be completed annually during work tenure and for 15 years after cessation of work, and then every 3 years thereafter (aligned with CT chest intervals, with the option to stop testing at age 75 following a joint decision between the patient and the examining physician) during work tenure and for 15 years after cessation of work, and then every 3 years thereafter (aligned with CT chest intervals, with the option to stop testing at age 75 following a joint decision between the patient and the examining physician).

Cardiopulmonary Exercise Testing (CPET) offers a valuable diagnostic advantage in dust‑exposed workers by assessing the combined performance of the respiratory, cardiovascular, and muscular systems during exertion. Unlike resting spirometry or DLCO alone, CPET can detect ventilatory inefficiency and reduced aerobic capacity even in individuals who appear normal at rest. For instance, in coal miners with small airway dysfunction, CPET revealed that at modest exercise workloads they used a significantly higher fraction of their maximal voluntary ventilation, had elevated ventilatory equivalents (VE/VO₂ and VE/VCO₂), and exhibited a 27% lower peak oxygen consumption—despite normal resting spirometry and DLCO . Similarly, in a cohort of former U.S. coal miners, resting DLCO strongly predicted abnormalities in CPET gas exchange measures such as elevated A‑a gradient and reduced VO₂ max, while FEV₁ was less predictive. These studies highlight CPET’s ability to unmask early functional limitation, even when resting pulmonary tests and imaging are relatively preserved. Incorporating CPET into surveillance of silica‑exposed workers—such as those in engineered stone fabrication—can therefore provide critical insights into subclinical impairment, guide targeted evaluations, and enhance early detection of disease progression and disability risk. Cardiopulmonary exercise testing (CPET) has been used to evaluate veterans exposed to burn pit smoke, providing a detailed assessment of exercise intolerance and revealing abnormalities in gas exchange, ventilatory efficiency, and cardiovascular response that may not be apparent on resting pulmonary function tests. 

Cardiopulmonary exercise testing is currently being used as part of expansive clinical protocols in the diagnosis of early lung disease in exposed workers, including the Department of Labor’s Black Lung Program and the Veterans’ Administration’s Post-Deployment Cardiopulmonary Evaluation Network. Cardiopulmonary exercise testing (CPET) should be performed at baseline and then repeated every 3–5 years, with shorter intervals if recommended by the examining physician based on clinical findings.

Infectious diseases

A well-established link exists between silicosis and tuberculosis, with a recent meta-analysis reporting a pooled relative risk of 4.01 for developing TB in individuals with silicosis. For example, among 2,758 former South African miners, the prevalence of silicotuberculosis was 25.7%. In California, among engineered stone countertop workers, 2 out of 45 individuals (4%) were diagnosed with active tuberculosis. However, due to overlapping clinical and radiographic features, particularly the micronodular pattern in the upper lung zones, 10 of the 45 workers (22%) were initially misdiagnosed with active pulmonary TB rather than silicosis. Many of these individuals underwent prolonged multidrug TB treatment before silicosis was correctly identified. Thus, while tuberculosis is an important comorbidity in engineered stone-associated silicosis, it is also a potential source of diagnostic confusion due to similar imaging patterns.

Nontuberculous mycobacterial (NTM) infection is linked to underlying lung diseases like cystic fibrosis, COPD, and silicosis. Once thought to be harmless colonizers, NTMs were defined as true pathogens in 2007, with diagnosis requiring symptoms, positive cultures (two sputum or one BAL), and characteristic imaging. In engineered stone (ES) silicosis, studies from Israel, California, and Brazil show a 9% NTM disease prevalence, often with cavitary lesions. Common species include M. kansasii, M. abscessus, M. intracellulare, M. fortuitum, and M. xenopi. NTM is more frequent in progressive massive fibrosis and may worsen outcomes. Species distribution varies by region; in the U.S., NTM surpasses TB prevalence, which may explain its prominence in ES silicosis despite many patients being Latin American immigrants. Further research is needed to clarify biological and epidemiologic risk factors.

For this reason, all those exposed to silica dust, especially those with engineered stone dust exposure must be screened for tuberculosis and other mycobacterial lung diseases. The recommended screening test would be a Quantiferon Gold blood test along with 3 expectorated sputum cultures to be completed annually during work tenure and for 15 years after cessation of work, and then every 3 years thereafter (aligned with CT chest intervals, with the option to stop testing at age 75 following a joint decision between the patient and the examining physician) during work tenure and for 15 years after cessation of work, and then every 3 years thereafter (aligned with CT chest intervals, with the option to stop testing at age 75 following a joint decision between the patient and the examining physician).

Markers of Systemic Disease

In addition to imaging and pulmonary function testing, baseline and periodic laboratory evaluation provides essential information about systemic health in silica-exposed workers. A basic metabolic panel and liver panel help assess kidney and liver function, which may be impaired either by silica-associated autoimmune disease or by medications used to treat related conditions. A complete blood count with white blood cell differential can identify anemia, cytopenias, or elevated inflammatory markers that may indicate systemic involvement of silica-related disease, infections such as tuberculosis or nontuberculous mycobacteria, or autoimmune processes. Measurement of IgE levels is important for evaluating allergic or atopic disease and may provide clues to immune dysregulation associated with silica exposure, including vasculitis. In addition, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) serve as nonspecific but sensitive markers of systemic inflammation, useful in tracking autoimmune activity or identifying occult infection. Though often elevated in sarcoidosis, angiotensin-converting enzyme (ACE) levels can also be abnormal in silicosis and may serve as a marker of granulomatous inflammation.

Autoimmune biomarkers

The connection between silicosis and autoimmune diseases has been recognized since the early-to-mid 20th century. Notably, scleroderma was reported in stone masons, systemic sclerosis (SSc) in South African gold miners (known as Erasmus Syndrome), and rheumatoid arthritis (RA) in coal miners (Caplan’s Syndrome). In addition to these, silica exposure has been associated with conditions such as systemic lupus erythematosus (SLE), dermatomyositis, polymyositis, and ANCA-associated vasculitis, among other autoimmune diseases.

Recent studies of engineered stone (ES) countertop workers have shown continued links between silicosis and autoimmune conditions, with approximately 20% affected—about seven times higher than in the general population. The most commonly reported conditions are RA, SSc, and SLE, but cases of ANCA vasculitis and others have also been observed. Furthermore, the presence of autoimmune and inflammatory markers increases with disease severity. Among ES workers, the prevalence of positive antinuclear antibodies (ANA) and elevated angiotensin-converting enzyme (ACE) levels rose from 24.2% and 10.3% in exposed individuals without silicosis to 34.0% and 34.8% in those with simple silicosis, and to 47.1% and 55.6% in those with complex silicosis, respectively. The likelihood of detecting autoantibodies in silicosis is also linked to older age, smoking history, and higher levels of respirable crystalline silica (RCS) exposure. In a large group of over 1,000 exposed workers, confirmed autoimmune disease was identified in about 1%.

To evaluate, for autoimmune diseases, these biomarkers are recommended: 

Systemic disease testing

• Complete blood count with white blood cell differential

• Complete metabolic panel (evaluate kidney and liver function)

• IgE (immunoglobulin in asthma and some rheumatologic diseases such as vasculitis)

Rheumatoid Arthritis (RA)

• RF (Rheumatoid Factor)
• Anti-CCP (Cyclic Citrullinated Peptide)

Systemic Lupus Erythematosus (SLE)

• ANA
• Anti-dsDNA (Double-Stranded DNA)
• Anti-Smith (Sm)
• Anti-Ro/SSA and Anti-La/SSB (also seen in Sjögren's, may overlap with lupus)
• Low complement levels (C3, C4)

Systemic Sclerosis (Scleroderma)

• ANA
• Anti-centromere antibodies (limited cutaneous SSc)
• Anti-Scl-70 / Anti-topoisomerase I (diffuse cutaneous SSc)
• Anti-RNA polymerase III

ANCA-Associated Vasculitis

• p-ANCA (MPO – Myeloperoxidase)
• c-ANCA (PR3 – Proteinase 3)

Dermatomyositis / Polymyositis

• ANA
• Anti-Mi-2 (more specific to dermatomyositis)
• Anti-Jo-1 (associated with antisynthetase syndrome)
• Anti-SRP (Signal Recognition Particle)
• Anti-MDA5, Anti-TIF1-γ, Anti-NXP2 (subtypes, associated with different clinical features)
• CK (Creatine Kinase): Elevated in myositis (dermatomyositis, polymyositis)

Sarcoidosis

• Angiotensin-Converting Enzyme (ACE): May be elevated in sarcoidosis but can also rise in chronic inflammation like silicosis

Additional biomarkers

Several biomarkers have been investigated for their potential to distinguish early silicosis from simple occupational exposure to crystalline silica. Among these, CC16 (Clara cell protein 16) has shown the most consistent ability to differentiate silicosis, even at early stages, from silica exposure, with significantly lower serum levels in affected individuals. KL-6 (Krebs von den Lungen 6) also appears elevated in silicosis patients relative to exposed controls and correlates with fibrotic disease severity, although further silica-specific validation is needed. In contrast, pro- and anti-inflammatory cytokines such as TNF-α, IL-1, IL-6, and IL-10, along with neopterin, tend to be elevated in both exposed individuals and those with silicosis, limiting their standalone diagnostic specificity. The MUC5B gene, while associated with fibrotic susceptibility, does not clearly distinguish exposure from disease. However, it is important to emphasize that this body of research is still in its early stages. While some markers currently lack specificity, they may ultimately contribute valuable predictive power as part of a multi-biomarker model for early disease detection. Future work should avoid prematurely excluding any candidates and instead focus on validating their combined utility across diverse cohorts and exposure profiles.

Other early surveillance techniques

Breath Biopsy

There is emerging research exploring the use of breath biopsy, a noninvasive method analyzing volatile organic compounds (VOCs) in exhaled breath, as a potential tool for early detection and exposure surveillance in silicosis. Recent studies have profiled VOCs in the breath of workers exposed to crystalline silica dust and individuals with confirmed silicosis. In a case–control study of silica-exposed workers and silicosis patients, investigators identified significantly elevated levels of VOCs such as acetaldehyde, hexanal, nonanal, decane, pentadecane, 2-propanol, and 3-hydroxy-2-butanone compared with healthy controls. These findings suggest oxidative stress and inflammatory responses as underlying mechanisms. A larger study combining VOC analysis with machine learning models achieved nearly 90% accuracy in distinguishing silicosis cases from healthy individuals by identifying nine breath biomarkers, including 2,3-butanedione, ethyl acetate, chlorobenzene, and phthalic anhydride. A corporate research effort (Owlstone Medical) also used a VOC atlas to cross-reference compounds produced in silicosis patients, reinforcing that specific exhaled VOC patterns could serve as candidate biomarkers of disease and silica exposure.

Despite promising findings, there are currently no validated or clinically approved breath-biopsy–based tests for silicosis surveillance. Further research is needed to replicate these VOC signatures in broader populations, establish standardized sampling protocols, and determine clinical utility. Nonetheless, breath biopsy offers a compelling future avenue for noninvasive early detection of silica-related lung injury, particularly in high-risk groups such as engineered stone workers. 

Forced Oscillation Technique

The forced oscillation technique (FOT) is an emerging pulmonary function tool that offers distinct advantages in the early detection of silicosis, particularly in engineered stone workers at high risk for rapid disease progression. Unlike spirometry, which often remains normal until moderate or advanced disease, FOT can detect subtle changes in airway resistance and reactance during tidal breathing, making it highly suitable for screening and surveillance. In a study of never-smoking silicosis patients, FOT parameters—including total respiratory resistance and indicators of ventilation heterogeneity—were found to worsen progressively even in the early stages of disease, providing sensitivity to physiologic abnormalities not captured by traditional tests. Further evidence showed that FOT metrics such as resistance at 4 Hz (Rrs₄) and zero-intercept resistance (R₀) were significantly elevated even in patients with mild spirometric obstruction, while reactance and dynamic compliance declined with increasing disease severity. Importantly, these metrics demonstrated high diagnostic accuracy, with area under the curve (AUC) values exceeding 0.80 for mild disease and 0.90 for moderate to severe disease. Additionally, these functional changes have been shown to correlate with radiographic findings of parenchymal damage. Given its ability to detect early small airway and parenchymal abnormalities during normal breathing, FOT may be particularly valuable for identifying subclinical or early silicosis in high-risk workers, facilitating earlier intervention and removal from exposure before irreversible lung damage occurs.

References

1. Australian Government Department of Health and Aged Care. National Guidance for Doctors Assessing Workers Exposed to Respirable Crystalline Silica Dust. Canberra: Department of Health; 2022. https://www.health.gov.au/sites/default/files/documents/2022/07/national-guidance-for-doctors-assessing-workers-exposed-to-respirable-crystalline-silica-dust-practice-guide.pdf. Accessed May 1, 2025.

2. Bartûňková J, Pelclová D, Fenclová Z, et al. Exposure to silica and risk of ANCA-associated vasculitis. Am J Ind Med. 2006;49(7):569-576.

3. Bramwell B. Diffuse Sclerodermia. Edinb Med J. 1914;12(5):387-401.

4. Cal/OSHA, California S of. Standards Board Adopts Emergency Temporary Standard to Protect Workers from Silicosis | California Department of Industrial Relations. https://www.dir.ca.gov/DIRNews/2023/2023-93.html. Accessed May 30, 2025.

5. Carneiro APS, Barreto SM, Siqueira AL, Cavariani F, Forastiere F. Continued exposure to silica after diagnosis of silicosis in Brazilian gold miners. Am J Ind Med. 2006;49(10):811-818.

6. Căluțu IM, Smărăndescu RA, Rașcu A. Biomonitoring exposure and early diagnosis in silicosis: a comprehensive review of the current literature. Biomedicines. 2022;11(1):100.

7. Cohen RA, Go LHT, Friedman LS, Zell Baran LM, Rose CS, Almberg KS. Resting diffusing capacity and severity of radiographic disease predict gas exchange abnormalities with exercise in former US coal miners. Am J Ind Med. 2024;67(8):732-740.

8. Corbett EL, Churchyard GJ, Clayton T, et al. Risk factors for pulmonary mycobacterial disease in South African gold miners. Am J Respir Crit Care Med. 1999;159(1):94-99.

9. Ehrlich R, Akugizibwe P, Siegfried N, Rees D. The association between silica exposure, silicosis and tuberculosis: a systematic review and meta-analysis. BMC Public Health. 2021;21(1):953.

10. Erasmus LD. Scleroderma in gold-miners on the Witwatersrand with particular reference to pulmonary manifestations. South African J Lab Clin Med. 1957;3(3):209-231.

11. Fazio JC, Gandhi SA, Flattery J, et al. Silicosis among immigrant engineered stone (quartz) countertop fabrication workers in California. JAMA Intern Med. 2023;183(9):991-998.

12. Flattery J, Woolsey C, Fazio JC, et al. Silicosis associated with engineered stone exposures and tuberculosis: overlaps in clinical presentation and delayed diagnosis. In: B22. New Frontiers in Environmental and Occupational Lung Disease Research. Am Thorac Soc Int Conf Abstracts. 2024:A3105-A3105.

13. Go LHT, Almberg KS, Friedman LL, Zell Baran LM, Rose CS, Cohen RA. Small airway dysfunction and abnormal exercise responses in coal miners exposed to respirable dust. Ann Am Thorac Soc. 2016;13(7):1076-1080.

14. Griffith DE, Aksamit T, Brown-Elliott BA, et al. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175(4):367-416.

15. Guarnieri G, Mauro S, Lucernoni P, et al. Silicosis in finishing workers in quartz conglomerates processing. La Medicina del Lavoro. 2020;111(2):99.

16. Hessel PA, Sluis-Cremer GK, Hnizdo E, Faure MH, Thomas RG, Wiles FJ. Progression of silicosis in relation to silica dust exposure. Ann Occup Hyg. 1988;32(inhaled particles VI):689-696.

17. Hoa JT, Zell-Baran L, Go LHT, et al. Demographic, exposure and clinical characteristics in a multinational registry of engineered stone workers with silicosis. Occup Environ Med. 2022;79(9):586-593.

18. Hoy RF, Dimitriadis C, Abramson M, et al. Prevalence and risk factors for silicosis among a large cohort of stone benchtop industry workers. Occup Environ Med. Published online June 16, 2023.

19. Hoy RF, Glass DC, Dimitriadis C, Hansen J, Hore-Lacy F, Sim MR. Identification of early-stage silicosis through health screening of stone benchtop industry workers in Victoria, Australia. Occup Environ Med. 2021;78(4):296-302.

20. Hoy RF, Jones C, Newbigin K, et al. Chest x-ray has low sensitivity to detect silicosis in artificial stone benchtop industry workers. Respirology. 2024;29(9):785-794.

21. Izhakian S, Gorelik O, Kramer M. Nontuberculous mycobacteria infections in patients with silicosis. Eur Respir J. 2020;56(suppl 64).

22. Jalali M, Zare Sakhvidi MJ, Bahrami A, Berijani N, Mahjub H. Oxidative stress biomarkers in exhaled breath of workers exposed to crystalline silica dust by SPME-GC-MS. J Res Health Sci. 2016;16(3):153-161.

23. Kramer MR, Blanc PD, Fireman E, et al. Artificial stone silicosis: disease resurgence among artificial stone workers. Chest. 2012;142(2):419-424.

24. León-Jiménez A, Hidalgo-Molina A, Conde-Sánchez MÁ, et al. Artificial stone silicosis: rapid progression following exposure cessation. Chest. 2020;158(3):1060-1068.

25. Levin K, McLean C, Hoy R. Artificial stone-associated silicosis: clinical-pathological-radiological correlates of disease. Respirol Case Rep. 2019;7(7):e00470.

26. Lopes AJ, Mafort TT, da Costa CH, et al. Comparison of respiratory impedance measured by the forced oscillation technique and spirometry with a fixed cutoff for diagnosing obstructive respiratory diseases. Biomed Eng Online. 2013;12:122.

27. Maboso BM, Moyo DM, Muteba KM, et al. Occupational lung disease among Basotho ex-miners in a large outreach medical assessment programme. Occup Health South Afr. 2020;26(4):145-152.

28. Makol A, Reilly MJ, Rosenman KD. Prevalence of connective tissue disease in silicosis (1985-2006)—a report from the state of Michigan surveillance system for silicosis. Am J Ind Med. 2011;54(4):255-262.

29. Marrocco A, Ortiz LA. Role of metabolic reprogramming in pro-inflammatory cytokine secretion from LPS or silica-activated macrophages. Front Immunol. 2022;13.

30. Medeiros D, Lopes AJ, Faria AC, et al. Correlations between quantitative computed tomography and respiratory mechanics in patients with silicosis. J Bras Pneumol. 2015;41(4):323–330.

31. Mesquita Júnior JÁ, Lopes AJ, Jansen JM, Melo PL. Changes in respiratory mechanics in silicosis patients as assessed by forced oscillation technique. Clinics (Sao Paulo). 2006;61(6):497–502.

32. Mizutani RF, Santos UP, Sales RKB, et al. Risk of mycobacterial infections in a cohort of silicosis patients with autoimmune rheumatic diseases. J Bras Pneumol. 50(5):e20240265.

33. Mohebbi I, Zubeyri T. Radiological progression and mortality among silica flour packers: a longitudinal study. Inhal Toxicol. 2007;19(12):1011-1017.

34. Ng TP, Chan SL, Lam KP. Radiological progression and lung function in silicosis: a ten year follow up study. Br Med J (Clin Res Ed). 1987;295(6591):164-168.

35. Owlstone Medical. Identifying Confident Breath Biomarkers for a Potential Silicosis Test with Breath Biopsy VOC Atlas®. https://www.owlstonemedical.com/about/blog/2025/apr/28/identifying-breath-biomarkers-for-silicosis-test-with-breath-biopsy-voc-atlas/. Accessed May 14, 2025.

36. Rangel DA de S, Garcia MVF, Mizutani RF, Sales RKB, Santos U de P, Terra-Filho M. Case series on nontuberculous mycobacterial (NTM) lung disease and silicosis in Brazil. Eur Respir J. 2017;50(suppl 61).

37. Remy-Jardin M, Degreef JM, Beuscart R, Voisin C, Remy J. Coal worker’s pneumoconiosis: CT assessment in exposed workers and correlation with radiographic findings. Radiology. 1990;177(2):363-371.

38. Remy-Jardin M, Remy J, Farre I, Marquette CH. Computed tomographic evaluation of silicosis and coal workers’ pneumoconiosis. Radiol Clin North Am. 1992;30(6):1155-1176.

39. Safe Work Australia. Crystalline Silica and Health Monitoring: Guide for Persons Conducting a Business or Undertaking. Canberra: Safe Work Australia; 2021. https://www.safeworkaustralia.gov.au/sites/default/files/2021-09/health-monitoring-guidance-crystalline-silica.pdf. Accessed May 26, 2025.

40. SafeWork. Respirable crystalline silica. SafeWork SA. August 31, 2022. https://safework.sa.gov.au/workplaces/chemicals-substances-and-explosives/silica. Accessed May 15, 2025.

41. Schreiber J, Koschel D, Kekow J, Waldburg N, Goette A, Merget R. Rheumatoid pneumoconiosis (Caplan’s syndrome). Eur J Intern Med. 2010;21(3):168-172.

42. Shtraichman O, Blanc PD, Ollech JE, et al. Outbreak of autoimmune disease in silicosis linked to artificial stone. Occup Med. 2015;65(6):444-450.

43. Song X, Shen H, Zhou L, et al. Survival analysis of 15,402 pneumoconiosis cases in Jiangsu Province of China from 1961 to 2019. Ann Palliat Med. 2022;11(7):2291301-2292301.

44. Surasi K, Ballen B, Weinberg JL, et al. Elevated exposures to respirable crystalline silica among engineered stone fabrication workers in California, January 2019–February 2020. American Journal of Industrial Medicine. 2022;65(9):701-707. doi:10.1002/ajim.23416

45. Tomic D, Hoy RF, Sin J, et al. Autoimmune diseases, autoantibody status and silicosis in a cohort of 1238 workers from the artificial stone benchtop industry. Occup Environ Med. Published online August 12, 2024.

46. Westerholm P. Silicosis. Observations on a case register. Scand J Work Environ Health. 1980;6(2):1-86.

47. Yi Z, Dong S, Wang X, Xu M, Li Y, Xie L, et al. Exploratory study on noninvasive biomarker of silicosis in exhaled breath by solid-phase microextraction–gas chromatography–mass spectrometry analysis. Int Arch Occup Environ Health. 2023;96(6):857-868.

Authors: Sheiphali A. Gandhi MD, MPH; Robert J. Harrison MD, MPH

Updated December 17, 2025