Silicosis mortality, prevention, and control--United States, 1968-2002

Silicosis is a preventable occupational lung disease caused by inhaling dust containing crystalline silica; no effective treatment for silicosis is available. Deaths from inhalation of silica-containing dust can occur after a few months' exposure (1). Crystalline silica exposure and silicosis have been associated with work in mining, quarrying, tunneling, sandblasting, masonry, foundry work, glass manufacture, ceramic and pottery production, cement and concrete production, and work with certain materials in dental laboratories. To describe patterns of silicosis mortality in the United States, CDC analyzed data from the National Institute for Occupational Safety and Health (NIOSH) National Occupational Respiratory Mortality System (NORMS) for 1968-2002. This report summarizes the results of that analysis, which indicated a decline in silicosis mortality during 1968-2002 and suggested that progress has been made in reducing the incidence of silicosis in the United States. However, silicosis deaths and new cases still occur, even in young workers. Because no effective treatment for silicosis is available, effective control of exposure to crystalline silica in the workplace is crucial.     

Non-fibrous dust load and smoking in dental technicians: a study using bronchoalveolar lavage.

A study was conducted with transmission electron microscopy to find whether bronchoalveolar lavage could be used to identify subjects with occupational exposure to mineral particles. Non-fibrous mineral particles in bronchoalveolar lavage (BAL) fluid from 46 dental technicians and 41 white collar controls with lung diseases but free from occupational exposure to dusts were analysed. The total particle concentration in BAL fluid was significantly higher in dental technicians than in controls (12.18 x 10(5) particles/ml of BAL fluid, v 2.03 x 10(5) particles/ml, p < 0.001). Dental technicians had significantly more crystalline silica, aluminium, and alloys containing nickel and chromium. There was a non-significant twofold increase of total particle concentration in the lungs of dental technicians who were smokers compared with non-smokers. The results strongly support the use of BAL fluid analysis to assess dust accumulation in workers in heavily exposed occupations such as dental technicians. This is a valid method to evaluate occupational exposure to non-fibrous mineral particles, and may be useful to determine the occupational aetiology of some respiratory diseases.     

Early detection of scleroderma in quartz dust exposed workers and workers with silicosis by determining serum beta-galactosidase activity

Progressive systemic sclerosis (PSS) is a rare disease belonging to the collagen diseases. PSS is frequently observed in workers with an intensive exposure to crystalline silica and with silicosis in the GDR. The recognition as an occupational disease is regulated by law. The elevated beta-galactosidase activity in the serum of patients with silicosis and beginning PSS can be used for detecting of early stages of PSS. References are given to medical care of patients with silicosis and exposure to quartz.     

Highway repair: a new silicosis threat

OBJECTIVES: We describe an emerging public health concern regarding silicosis in the fast-growing highway repair industry. METHODS: We examined highway construction trends, silicosis surveillance case data, and environmental exposure data to evaluate the risk of silicosis among highway repair workers. We reviewed silicosis case data from the construction industry in 3 states that have silicosis registries, and we conducted environmental monitoring for silica at highway repair work sites. RESULTS: Our findings indicate that a large population of highway workers is at risk of developing silicosis from exposure to crystalline silica. CONCLUSIONS: Exposure control methods, medical screenings, protective health standards, and safety-related contract language are necessary for preventing future occupational disease problems among highway repair workers.     

Exposure to crystalline silica, silicosis, and lung disease other than cancer in diatomaceous earth industry workers: a quantitative risk assessment

Objectives: To estimate excess lifetime risk of (a) mortality from lung disease other than cancer (LDOC), and, (b) onset of radiographic silicosis, arising from occupational exposure to respirable crystalline silica dust.

Methods: Data from a cohort of California diatomaceous earth mining and processing workers exposed to crystalline silica dust (mainly as cristobalite) were reanalyzed with Poisson regression methods with internal and external adjustments for potential confounding by calendar time, age, smoking, Hispanic ethnicity, and time since first observation. Model fit was evaluated by comparing deviances and fitting cubic spline models. Lifetime risks of death from LDOC and radiographic silicosis were estimated up to age 85 with an actuarial approach accounting for competing causes of death.

Results: For deaths due to LDOC, a linear relative rate model gave the best fit in Poisson regression analyses. At the mean cumulative exposure of LDOC cases to silica, after adjustment for smoking, the estimated rate ratio was 4.2 (p<0.0001); at the maximum cumulative exposure of cases, the rate ratio was 18.4. The excess lifetime risk for white men exposed to respirable cristobalite dust for 45 years at the current permissible exposure limit (PEL; about 0.05 mg/m³) of the Occupational Safety and Health Administration was 54/1000 (95% confidence interval (95% CI) 17 to 150). For 70 incident cases of radiographic silicosis largely manifest before the end of employment, the best fit was also the linear relative rate model, predicting a rate ratio of 25.6 for silicosis at the mean cumulative exposure of the cases (p<0.0001). The excess lifetime risk for silicosis at the current PEL was 75/1000.

Conclusion: Current occupational health standards for crystalline silica permit risks of lung disease other than cancer far in excess of what is usually considered acceptable by the Occupational Safety and Health Administration (a lifetime risk of less than one in a thousand deaths).

     

Silicosi severa da terre di diatomee nella produzione di alginato ad uso odontoiatrico: uno studio necroscopico

«Severe silicosis due to diatomaceous earth in dental alginate: a necropsy study»Background:Severe silicosis from occupational exposure to calcined diatomaceous earth has been observed in the past, due to the high-temperature transformation of amorphous silica in crystalline phases, mainly cristobalite. In dental alginate production and use a silica exposure may be underestimated. Objectives: To describe the clinical picture, the scenario and pattern of occupational exposure to silica and the corresponding necroscopic findings of a case of silicosis in a worker engaged in the production of alginates for dental use.Methods:A commercial sample of calcinated diatomaceous earth and necroscopic lung samples were analysed by scanning electron microscopy (SEM-EDS) and X-ray diffraction (XRD) for the quali-quantitative determination of crystalline silica. Material safety data sheets (MSDSs) of diatomaceous earth produced in 2002 and 2018 were examined to assess the information content on silicosis risk. Clinical findings and post-mortem examinations of the worker are evaluated.Results:A cristobalite concentration of 36% (wt/wt) was determined in the diatomaceous earth sample and a large amount of diatom fragments were observed in lung samples. The DRX spectra indicated the presence of cristobalite either in the bulk sample or in the lung tissues. The MSDS dated 2002 reported the presence of SLC up to 63% with cristobalite concentrations <60%, and the resulting risk of silicosis, while the MSDS dated 2018 and referred to a commercial product currently on the market indicated a concentration of cristobalite <1% and no risk of silicosis. The worker was suffering from a severe silicosis, histologically confirmed by necropsy.Conclusion:The present case-study revealed that the risk of silicosis from calcined diatomaceous earths used to produce dental alginates has been ignored. The lack of engineering controls and personal protection measures led to a high cristobalite lung burden, consistent with the development of a severe silicosis that were a contributing factor of death. A MSDS of a commercial product currently on the market does not report this serious hazard.Key words: Silicosis, diatomaceous earth, dental alginate     

Silicosis screening in surface coal miners--Pennsylvania, 1996-1997

Silicosis is an occupational respiratory disease caused by inhaling respirable crystalline silica dust. Silicosis is irreversible, often progressive (even after exposure has ceased), and potentially fatal. Exposure to silica dust occurs in many occupations, including mining (1). During 1996-1997, surface coal miners at eight sites in Pennsylvania were screened to estimate the prevalence of silicosis, to identify risk factors for silicosis, and to refer miners with a possible diagnosis of silicosis or other conditions for medical evaluation and treatment. This report summarizes the results of the screening, which indicated that an increased prevalence of and risk for silicosis is associated with miners' age and years of drilling experience, and provides recommendations for preventing silicosis among miners.     

Silicosis compensation in Western Australian gold miners since the introduction of an occupational exposure standard for crystalline silica

Occupational exposure limits for crystalline silica are under review worldwide because of the large numbers of exposed people and, especially, because of the recent International Agency for Research on Cancer classification of silica as a human carcinogen. OBJECTIVES: The aims of this study were to (i) re-examine the incidence of silicosis in Western Australian gold miners and, using estimates of the total population at risk, (ii) estimate the upper confidence limit for the risk of silicosis in Western Australian gold miners since 1974, when the current exposure standard for crystalline silica was implemented. METHODS: Work histories of cases compensated for pneumoconiosis after 1974 were examined. Numbers of workers in the total workforce likely to be exposed to crystalline silica in Western Australia were estimated as the population at risk. RESULTS: There were no cases of compensated silicosis in Western Australian miners whose first dust exposure began during or after 1974. The upper 95% confidence interval for this zero rate was estimated to be 4.8 per 100,000 person-yr. CONCLUSIONS: There have been no compensated cases of silicosis in Western Australia among miners first exposed to crystalline silica after introduction of the current exposure standard. A rate of compensated silicosis higher than five cases per 100,000 person-yr is unlikely.     

Evaluation of exposure to methyl methacrylate among dental laboratory technicians.

Following the diagnosis of two cases of occupational asthma among dental technicians, an industrial hygiene survey was conducted in two dental laboratories to determine time-weighted average and peak concentrations of methyl methacrylate vapor and time-weighted average concentration of acrylic dust. The time-weighted average concentrations of methyl methacrylate vapor were 0.7 ppm and 1.6 ppm and average peak concentrations were 9.3 ppm and 9.7 ppm for the first and second laboratory, respectively. The use of a local exhaust ventilation system was significant in reducing the peak concentration of methyl methacrylate vapor in the breathing zone of dental technicians. However, the local exhaust ventilation was not efficient in reducing the concentration of airborne acrylic dusts. Occupational exposure of dental technicians to dental materials, in particular to methyl methacrylate, requires further investigation. Local exhaust ventilation systems can reduce the concentration of methyl methacrylate in the dental laboratories to a significant extent if installed and used properly.     

Exposure-response analysis and risk assessment for silica and silicosis mortality in a pooled analysis of six cohorts

Aims: To study the relation between exposure to crystalline silica and silicosis mortality. Although mortality is an important endpoint for regulators, there have been no exposure-response studies for silicosis mortality, because of the relative rareness of silicosis as an underlying cause of death, and the limited availability of quantitative exposure estimates. Methods: Data from six occupational cohorts were pooled with good retrospective exposure data in which 170 deaths from silicosis were reported. Standard life table analyses, nested case-control analyses, and risk assessment were performed. Results: The rate of silicosis mortality in the combined data was 28/100 000 py, increasing in nearly monotonic fashion from 4.7/100 000 for exposure of 0–0.99 mg/m³-years to 233/100 000 for exposure of >28.1 mg/m³-years. The estimated risk of death up to age 65 from silicosis after 45 years of exposure at 0.1 mg/m³ silica (the current standard in many countries) was 13 per 1000, while the estimated risk at an exposure of 0.05 mg/m³ was 6 per 1000. Both of these risks are above the risk of 1 per 1000 typically deemed acceptable by the US OSHA. Conclusion: The findings from this pooled analysis add further support to the need to control silica exposure and to lower the occupational standards. Our estimates of lifetime silicosis mortality risk are probably underestimates as, in addition to exposure misclassification, our study might have suffered from outcome misclassification in that silicosis deaths might have been coded to other related causes, such as tuberculosis or chronic obstructive pulmonary disease.     

Change of exposure response over time and long-term risk of silicosis among a cohort of Chinese pottery workers

An analysis was conducted on a cohort of Chinese pottery workers to estimate the exposure-response relationship between respirable crystalline silica dust exposure and the incidence of radiographically diagnosed silicosis, and to estimate the long-term risk of developing silicosis until the age of 65. The cohort comprised 3,250 employees with a median follow-up duration of around 37 years. Incident cases of silicosis were identified via silicosis registries (Chinese X-ray stage I, similar to International Labor Organisation classification scheme profusion category 1/1). Individual exposure to respirable crystalline silica dust was estimated based on over 100,000 historical dust measurements. The association between dust exposure, incidence and long-time risk of silicosis was quantified by Poisson regression analysis adjusted for age and smoking. The risk of silicosis depended not only on the cumulative respirable crystalline silica dust exposures, but also on the time-dependent respirable crystalline silica dust exposure pattern (long-term average concentration, highest annual concentration ever experienced and time since first exposure). A long-term "excess" risk of silicosis of approximately 1.5/1,000 was estimated among workers with all annual respirable crystalline silica dust concentration estimates less than 0.1 mg/m(3), using the German measurement strategy. This study indicates the importance of proper consideration of exposure information in risk quantification in epidemiological studies.     

Is silicosis required for silica-associated lung cancer?

BACKGROUND: Abundant epidemiologic and experimental evidence supports the 1997 International Agency for Research on Cancer classification of crystalline silica as a human lung carcinogen. Nonetheless, there remains uncertainty about whether excessive lung cancer occurs exclusively among workers with silicosis. METHODS: A review was performed of published occupational epidemiologic literature directly pertinent to the interrelations among silica exposure, silicosis, and lung cancer. RESULTS: The association between silica and lung cancer is generally, but not uniformly, stronger among silicotics than nonsilicotics. However, the existing literature is ambiguous due to incomplete or biased ascertainment of silicosis, inadequate exposure assessment, and the inherently strong correlation between silica exposure and silicosis which hinders efforts to disentangle unique contributions to lung cancer risk. CONCLUSIONS: Until more conclusive epidemiologic findings become available, population-based or individually-based risk assessments should treat silicosis and lung cancer as distinct entities whose cause/effect relations are not necessarily linked.     

Silicosis-related years of potential life lost before age 65 years--United States, 1968-2005

Occupational exposure to respirable crystalline silica occurs in construction, mining, manufacturing, and other industries and can result in silicosis and other lung diseases. Classic (chronic) silicosis results from exposure to relatively low concentrations of respirable crystalline silica for >/=years. Exposure to higher concentrations of silica for 5-10 years can cause accelerated silicosis, and symptoms of acute silicosis can sometimes develop within weeks of initial exposure to extreme concentrations of silica. Deaths in young adults from acute or accelerated silicosis generally reflect more recent and intense exposures. Silicosis is incurable, but preventable through effective control and elimination of exposure to respirable crystalline silica. To characterize recent trends in premature mortality attributed to silicosis in the United States, CDC analyzed annual mortality data from 1968-2005, the most recent years for which complete data were available. Years of potential life lost before age 65 years (YPLL) and mean YPLL were calculated using standard methodology. During 1968-2005, total annual YPLL attributed to silicosis (17,130) declined 90.2%, from 1,441 (mean per decedent: 7.7 YPLL) to 141 (mean per decedent: 11.8), with an annual average of 8.6 YPLL per decedent for the period. However, the proportion of YPLL attributable to young silicosis decedents increased; an estimated 3,600-7,300 new silicosis cases occur annually. Hazard surveillance, workplace-specific interventions, and further silicosis prevention and elimination efforts, especially among young adults, are needed.     

Cohort mortality study of North American industrial sand workers. II. Case-referent analysis of lung cancer and silicosis deaths

BACKGROUND: A cohort mortality study of 2670 men in nine North American industrial sand plants resulted in 83 deaths from lung cancer 20 or more years after hire (standardized mortality ratio 139) and 37 deaths from silicosis (including seven from silico-tuberculosis). The lung cancer excess was unrelated to duration of employment and not found in all plants.Objectives: The primary aim was to determine whether lung cancer risk among these employees was related to quantitative estimates of crystalline silica exposure, after allowance for cigarette smoking. A secondary aim was to do the same for silicosis mortality, partly as a means of validating the estimated levels of exposure. METHODS: A nested case-referent study was undertaken with cases matched with up to two controls on plant, age and date of first employment from men who survived the case. Exposures were estimated by linking work histories to a job-exposure matrix, undertaken separately. Cigarette smoking information was obtained from medical records and other sources, blind as to case-control status. Matched statistical analyses were conducted using conditional logistic regression. FINDINGS: Odds ratios for silicosis mortality were significantly related to cumulative silica exposures and tended to a relationship with category of average crystalline silica concentration, but inconsistently with length of employment. After accounting for a strong effect of cigarette smoking, odds ratios for lung cancer were related to cumulative crystalline silica exposure and to average silica concentration, but not to length of employment. CONCLUSION: These findings support a causal relationship between lung cancer and quartz exposure after allowance for cigarette smoking, in the absence of cristobalite or other known occupational carcinogens.     

Silica carcinogenicity: description of a clinical case

BACKGROUND: Until the early 1980's there was a general consensus that no relationship existed between occupational silica exposure and lung cancer, in spite of a number of reports to the contrary. Confirmation arrived later from animal experiments and in 1997 the IARC modified its carcinogenic agents classification to include silica in group 1, human carcinogens. This fact brought about a change in insurance practice regarding occupational diseases due to silica, with greater attention dedicated to pneumoconiosis-related lung cancers. OBJECTIVE: To describe a clinical case of lung cancer due to occupational exposure to silica in a worker of a ceramics industry already receiving compensation for silicosis. METHODS: Diagnosis and recognition of the occupational origin of the disease were achieved via assessment of exposure to silica in the past and review of the medical examinations over the years. RESULTS: The pathogenesis and the causative relationship between pneumoconiosis and cancer is debated and lung cancer was recognized as an occupational disease. CONCLUSIONS: It is concluded that a causative relationship can exist more due to the presence of silicosis than due to occupational exposure to silica.     

Risk of silicosis in cohorts of Chinese tin and tungsten miners, and pottery workers (I): an epidemiological study

BACKGROUND: Epidemiological evaluations of the risk of silicosis in relation to exposure to crystalline silica have raised the question of whether different types of silica dust exposures vary with respect to their ability to cause silicosis. The aim of this study is to compare the risk of silicosis among cohorts of silica dust-exposed Chinese tin miners, tungsten miners, and pottery workers and to assess whether gravimetric measurements of respirable silica dust sufficiently determine the risk of silicosis or whether other factors of exposure may play a significant role. METHODS: Cohorts were selected from 20 Chinese mines and potteries. Inclusion criteria were starting employment after January 1, 1950 and being employed for at least 1 year during 1960-1974 in one of the selected workplaces. Radiological follow-up for silicosis onset was from January 1, 1950 through December 31, 1994. Silicosis was assessed according to the Chinese radiological criteria for diagnosis of pneumoconiosis (as suspect, Stage I, II, or III). Exposure-response relationships were estimated for silicosis of Stage I or higher. Silica dust exposure was estimated in terms of cumulative total dust exposure, calculated from a workplace, job title, and calendar year exposure matrix, and individual occupational histories. Cumulative total dust exposure was converted in two steps into cumulative respirable dust exposure and cumulative respirable silica dust exposure using conversion factors estimated from side-by-side measurements conducted in 1988-89. RESULTS: The male cohorts included 4,028 tin miners, 14,427 tungsten miners, and 4,547 pottery workers who had similar onset of employment and duration of follow-up. For a given exposure level, the risk of silicosis was higher for the tin and tungsten than the pottery workers. CONCLUSION: The observed differences in the risk of silicosis among the three cohorts suggest that silica dust characteristics, in addition to cumulative respirable silica dust exposure, may affect the risk of silicosis.     

Mineralogy of lung tissue in dental laboratory technicians' pneumoconiosis.

This article reports on a case of pneumoconiosis in a dental laboratory technician with a history of respiratory exposure to dental materials. Special attention is paid to the mineralogical analysis of the lung biopsy. The abundance of chromium, cobalt, and silica particles suggests that the dental technician's pneumoconiosis is the result of the combined effects of hard metal dusts and silica particles generated during finishing dental frameworks. Adequate technical protection such as a local ventilation system should be considered in dental laboratories to prevent respiratory exposure of dental technicians to airborne contaminants.     

Silica exposure index in gold mining

OBJECTIVE: To develop a cumulative silica exposure index, including time period, duration and intensity of exposure, and to test this index as for occurrence and severity of silicosis. METHODS: A cross-sectional study was carried out comprising 140 former gold miners from two localities in Southeastern Brazil between November 1997 and December 1999. Complete data on occupational and medical histories, chest x-rays and spirometry were analyzed. Borderline cases on the x-rays were also submitted to high-resolution chest computed tomography. The exposure index was the sum of scores obtained by logarithmic transformation of respirable silica concentration related to job tasks, mines and work time. Parametric tests were used for comparing averages between the groups of interest. RESULTS: The silica exposure index was able to discriminate the main outcome (silicosis) as well as other outcomes (tuberculosis and lung emphysema) in the whole group at p-values of 0.008, 0.016 and <0.001 respectively. In regard to the four main categories of silicosis, the Tukey test showed differences in the averages of the exposure index in the categories 0 and 3 and 1 and 3. However, in the borderline cases subgroup, the exposure index was not satisfactory for cases submitted to x-rays and tomography and it could not differentiate other outcomes. CONCLUSIONS: The silica exposure index represents an advance in exposure evaluation of former miners. However, other information, such as clinical and lung functional data are needed for better understanding disease progress in silica exposed cases, especially among borderline cases.     

Chronic obstructive pulmonary disease and occupational exposure to silica

Prolonged exposure to high levels of silica has long been known to cause silicosis This paper evaluates the evidence for an increased risk of chronic obstructive pulmonary disease (COPD) in occupations and industries in which exposure to crystalline silica is the primary exposure, with a focus on the magnitude of risks and levels of exposure causing disabling health effects. The literature suggests consistently elevated risks of developing COPD associated with silica exposure in several occupations, including the construction industry; tunneling; cement industry; brick manufacturing; pottery and ceramic work; silica sand, granite and diatomaceous earth industries; gold mining; and iron and steel founding, with risk estimates being high in some, even after taking into account the effect of confounders like smoking. Average dust levels vary from about 0.5 mg.m3 to over 10 mg.m3 and average silica levels from 0.04 to over 5 mg.m3, often well above occupational standards. Factors influencing the variation from industry to industry in risks associated with exposure to silica-containing dusts include (a) the presence of other minerals in the dust, particularly when associated with clay minerals; (b) the size of the particles and percentage of quartz; (c) the physicochemical characteristics, such as whether the dust is freshly fractured. Longitudinal studies suggest that loss of lung function occurs with exposure to silica dust at concentrations of between 0.1 and 0.2 mg.m3, and that the effect of cumulative silica dust exposure on airflow obstruction is independent of silicosis. Nevertheless, a disabling loss of lung function in the absence of silicosis would not occur until between 30 and 40 years exposure.     

Commentary on ‘Evaluation of take home (para-occupational) exposure to asbestos and disease: a review of the literature’, Donovan et al.

Abstract

A case-control study (8,740 cases; 83,338 controls) was done to evaluate the association between potential occupational exposure to silica and risk of tuberculosis (TB) mortality, using the National Occupational Mortality Surveillance database for 1983–1992. Potential silica exposure was based on the decedent's usual industry and occupation. Assignment of potential exposure to silica was based on the entire range of industries and occupations. Odds ratios (ORs) for mortality from respiratory TB associated with potential high and intermediate exposures to silica were 1.30 (95% CI 1.14–1.48) and 1.07 (95% CI 0.77–1.47), respectively, adjusting for silicosis, other pneumoconioses, age, gender, race, socioeconomic status, and potential exposure to active TB. The elevated OR was seen in all subgroups: male, female, white, and black. The average age at death/among respiratory TB cases with potential silica exposure was significantly younger by four years than that among cases without potential silica exposure. The findings suggest that potential occupational exposure to silica alone, in the absence of silicosis, is associated with respiratory TB mortality, with a dose-response relationship.