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.     

Exposure to silica and silicosis among tin miners in China: exposure-response analyses and risk assessment

OBJECTIVES—To investigate the risk of silicosis among tin miners and to investigate the relation between silicosis and cumulative exposure to dust (Chinese total dust and respirable crystalline silica dust).
METHODS—A cohort study of 3010 miners exposed to silica dust and employed for at least 1 year during 1960-5 in any of four Chinese tin mines was conducted. Historical total dust data from China were used to create a job exposure matrix for facility, job title, and calendar year. The total dust exposure data from China were converted to estimates of exposure to respirable crystalline silica for comparison with findings from other epidemiological studies of silicosis. Each worker''s work history was abstracted from the complete employment records in mine files. Diagnoses of silicosis were based on 1986 Chinese pneumoconiosis Roentgen diagnostic criteria, which classified silicosis as stages I-III—similar to an International Labour Organisation (ILO) classification of 1/1 or greater.
RESULTS—There were 1015 (33.7%) miners identified with silicosis, who had a mean age of 48.3 years, with a mean of 21.3 years after first exposure (equivalent to 11.0 net years in a dusty job). Among those who had silicosis, 684 miners (67.4%) developed silicosis after exposure ended (a mean of 3.7 years after). The risk of silicosis was strongly related to cumulative exposure to silica dust and was well fitted by the Weibull distribution, with the risk of silicosis less than 0.1% when the Chinese measure of cumulative exposure to total dust (CTD) was under 10 mg/m³-years (or 0.36 mg/m³-years of respirable crystalline silica), increasing to 68.7% when CTD exposure was 150 mg/m³-years (or 5.4 mg/m³-years of respirable crystalline silica). Latency period was not correlated to the risk of silicosis or cumulative dose of exposure. This study predicts about a 36% cumulative risk of silicosis for a 45 year lifetime exposure to these tin mine dusts at the CTD exposure standard of 2 mg/m³, and a 55% risk at 45 years exposure to the current United States Occupational Safety and Health Administration and Mine Safety and Health Administration standards of 0.1 mg/m³ 100% respirable crystalline silica dust.
CONCLUSIONS—A clear exposure-response relation was detected for silicosis in Chinese tin miners. The study results were similar to most, but not all, findings from other large scale exposure-response studies.


     

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).

     

Silicosis in the 1980's

At the request of the Mine Safety and Health Administration (MSHA), the National Institute for Occupational Safety and Health (NIOSH) recently investigated the health of workers at two silica flour mills. Both mills have a long history of failure to maintain workplace concentrations of dust containing free silica below the MSHA exposure standard. Thirty-seven percent of sixty-one workers and ex-workers with one or more years of silica dust exposure had chest radiographic evidence of silicosis. Because of the high prevalence of silicosis in workers at these two silica flour producers, MSHA silica dust measurements were reviewed for twenty-five other active U.S. silica flour producers. Eighty-nine percent of the work force in these 27 silica flour producers are employed at workplaces where more than twenty-five percent of the dust samples reviewed were above the exposure standard. Fifty-three percent of all samples were above the MSHA standard. No significant decline in silica dust levels occurred during the period (1974-1979) covered by the data supplied by MSHA. Based on the NIOSH study and MSHA data, it is apparent that the risk of silicosis is very high among workers in this industry. Prevention of this disease will require a concerted effort of government enforcement agencies, workers and management.     

Estimating historical respirable crystalline silica exposures for Chinese pottery workers and iron/copper, tin, and tungsten miners.

Collaborative studies of Chinese workers, using over four decades of dust monitoring data, are being conducted by the National Institute for Occupational Safety and Health (NIOSH) and Tongji Medical University in China. The goal of these projects is to establish exposure-response relationships for the development of diseases such as silicosis or lung cancer in cohorts of pottery and mine workers. It is necessary to convert Chinese dust measurements to respirable silica measurements in order to make results from the Chinese data comparable to other results in the literature.This article describes the development of conversion factors and estimates of historical respirable crystalline silica exposure for Chinese workers. Ambient total dust concentrations (n>17000) and crystalline silica concentrations (n=347) in bulk dust were first gathered from historical industrial hygiene records. Analysis of the silica content in historical bulk samples revealed no trend from 1950 up to the present. During 1988-1989, side-by-side airborne dust samples (n=143 pairs) were collected using nylon cyclones and traditional Chinese samplers in 20 metal mines and nine pottery factories in China. These data were used to establish conversion factors between respirable crystalline silica concentrations and Chinese total dust concentrations. Based on the analysis of the available evidence, conversion factors derived from the 1988-1989 sampling campaign are assumed to apply to other time periods in this paper. The conversion factors were estimated to be 0.0143 for iron/copper, 0.0355 for pottery factories, 0.0429 for tin mines, and 0.0861 for tungsten mines. Conversion factors for individual facilities within each industry were also calculated. Analysis of variance revealed that mean conversion factors are significantly different among facilities within the iron/copper industry and within the pottery industry. The relative merits of using facility-specific conversion factors, industry-wide conversion factors, or a weighted average of the two are discussed. The exposure matrix of the historical Chinese total dust concentrations was multiplied by these conversion factors to obtain an exposure matrix of historical respirable crystalline silica concentrations.     

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.     

Metal and non-metal miners' exposure to crystalline silica, 1998-2002

BACKGROUND: Crystalline silica is well known to cause silicosis and other diseases. Exposure is common in the mining industry and consequently, the US Mine Safety and Health Administration (MSHA) evaluates miners exposure to silica to determine compliance with its exposure limit. METHODS: MSHA exposure measurements were obtained for the 5-year period from 1998 to 2002 and average exposure was calculated classified by occupation and by mine. Evaluation criteria were whether average values exceeded MSHA's permissible exposure limit or the limit recommended by the National Institute for Occupational Safety and Health (NIOSH), whether there was a risk of exposure to freshly fractured silica, and whether there was a risk of a high rate of exposure to silica. RESULTS: Miners in certain jobs are exposed to silica above permissible and recommended exposure limits. Some miners may also be exposed at a high rate or to freshly fractured silica. CONCLUSIONS: Known dust control methods should be implemented and regular medical surveillance should be provided.     

Silica exposure, silicosis, and lung cancer: a necropsy study

Recent studies of the association between lung cancer and silicosis and silica dust have been inconclusive; some showing positive association and some showing none. The present study matched 231 cases of lung cancer with 318 controls by year of birth. Subjects were selected from the necropsy records of the National Centre for Occupational Health. Data on intensity and duration of exposure to silica dust were obtained from personnel records. Presence or absence of lung cancer and the presence and severity of silicosis of the parenchyma, pleura, and hilar glands were documented from necropsy reports. Smoking data were abstracted from records of routine examinations. No case-control differences were noted for any of the exposure indicators including cumulative dust exposure, total dusty shifts, weighted average intensity of exposure, total underground shifts, and shifts in high dust. Similarly, no association was found between lung cancer and the presence or severity of silicosis and any site. Stratified analyses showed neither significant nor suggestive trends when case-control comparisons for silicosis were examined by level of dust exposure or smoking. Reasons for disparity between these results and those of some other studies may include concomitant exposures to radon daughters, asbestos, diesel emissions, and cigarette smoking; idiosyncracies of the compensation process; and the possibility of a threshold in the relation(s).     

Silicosis mortality with respiratory tuberculosis in the United States, 1968-2006

The presence of tuberculosis (TB) in patients with silicosis increases mortality risk. To characterize silicosis-respiratory TB comortality in the United States, the authors used 1968-2006 National Center for Health Statistics multiple cause-of-death data for decedents aged ≥25 years. The authors calculated proportionate mortality ratios (PMRs) using available information on decedents' industries and occupations reported from 26 states from 1985 through 1999. Among 16,648 silicosis deaths, 2,278 (13.7%) had respiratory TB listed on the death certificate. Of silicosis-respiratory TB deaths, 1,666 decedents (73.1%) were aged ≥65 years, 2,255 (99.0%) were male, and 1,893 (83.1%) were white. Silicosis-respiratory TB deaths declined 99.5% during the study period (P < 0.001 for time-related trend), from 239.8 per year during 1968-1972 to 1.2 per year during 2002-2006, with no reported deaths in 2006. Silicosis-respiratory TB deaths reported from Pennsylvania (n = 525; 1.29 per million population), Ohio (n = 258; 0.81 per million), and West Virginia (n = 146; 2.35 per million) accounted for 40.8% of all such deaths in the United States. The highest PMR for silicosis-respiratory TB death was associated with the "miscellaneous nonmetallic mineral and stone products" industry (PMR = 73.7, 95% confidence interval: 33.8, 139.8). In the United States, 2006 marked the first year since 1968 with no silicosis-respiratory TB deaths. The substantial decline in silicosis-respiratory TB comortality probably reflects prevention and control measures for both diseases.     

Silica exposure, silicosis, and lung cancer: a necropsy study.

Recent studies of the association between lung cancer and silicosis and silica dust have been inconclusive; some showing positive association and some showing none. The present study matched 231 cases of lung cancer with 318 controls by year of birth. Subjects were selected from the necropsy records of the National Centre for Occupational Health. Data on intensity and duration of exposure to silica dust were obtained from personnel records. Presence or absence of lung cancer and the presence and severity of silicosis of the parenchyma, pleura, and hilar glands were documented from necropsy reports. Smoking data were abstracted from records of routine examinations. No case-control differences were noted for any of the exposure indicators including cumulative dust exposure, total dusty shifts, weighted average intensity of exposure, total underground shifts, and shifts in high dust. Similarly, no association was found between lung cancer and the presence or severity of silicosis and any site. Stratified analyses showed neither significant nor suggestive trends when case-control comparisons for silicosis were examined by level of dust exposure or smoking. Reasons for disparity between these results and those of some other studies may include concomitant exposures to radon daughters, asbestos, diesel emissions, and cigarette smoking; idiosyncracies of the compensation process; and the possibility of a threshold in the relation(s).     

Silica exposure, silicosis, and lung cancer: a mortality study of South African gold miners.

The effects of exposure to gold mining dust with a high concentration of free silica and tobacco smoking on mortality from lung cancer was assessed in a sample of 2209 white South African gold miners who started mining exposure during 1936-43, and were selected for a study of respiratory disorders in 1968-71 when they were aged 45-54. The mortality follow up was from 1968-71 to 30 December 1986. The relative risk for the effect of dust cumulated to the start of the follow up period was estimated as 1.023 (95% confidence interval (CI) 1.005-1.042) for a unit of 1000 particle-years. The combined effect of dust and tobacco smoking was better fitted by the multiplicative model than the additive model, suggesting that the two exposures act synergistically. No association between lung cancer and silicosis of the parenchyma or pleura was found, but a positive association existed between silicosis of the hilar glands and lung cancer.     

Silica exposure, silicosis, and lung cancer: a mortality study of South African gold miners.

The effects of exposure to gold mining dust with a high concentration of free silica and tobacco smoking on mortality from lung cancer was assessed in a sample of 2209 white South African gold miners who started mining exposure during 1936-43, and were selected for a study of respiratory disorders in 1968-71 when they were aged 45-54. The mortality follow up was from 1968-71 to 30 December 1986. The relative risk for the effect of dust cumulated to the start of the follow up period was estimated as 1.023 (95% confidence interval (CI) 1.005-1.042) for a unit of 1000 particle-years. The combined effect of dust and tobacco smoking was better fitted by the multiplicative model than the additive model, suggesting that the two exposures act synergistically. No association between lung cancer and silicosis of the parenchyma or pleura was found, but a positive association existed between silicosis of the hilar glands and lung cancer.     

Silicosis in dental laboratory technicians--five states, 1994-2000

Silicosis is a debilitating, sometimes fatal, yet preventable occupational lung disease caused by inhaling respirable crystalline silica dust. Although crystalline silica exposure and silicosis have been associated historically with work in mining, quarrying, sandblasting, masonry, founding, and ceramics, certain materials and processes used in dental laboratories also place technicians at risk for silicosis. During 1994--2000, occupational disease surveillance programs in five states identified nine confirmed cases of silicosis among persons who worked in dental laboratories; four persons resided in Michigan, two in New Jersey, and one each in Massachusetts, New York, and Ohio. This report describes three of the cases and underscores the need for employers of dental laboratory technicians to ensure appropriate control of worker exposure to crystalline silica.     

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.     

Risk of pulmonary tuberculosis relative to silicosis and exposure to silica dust in South African gold miners [published erratum appears in Occup Environ Med 1999 Mar;56(3):215-6]

OBJECTIVES: To investigate the following questions. (1) Is silica dust on its own, without the presence of silicosis, associated with an increased risk of pulmonary tuberculosis (PTB) in workers exposed to silica dust? (2) In the absence of silicosis is the excess risk dose related? (3) What is the predominant chronological sequence between the development of PTB and the development of silicosis after the end of exposure to dust? METHODS: A cohort of 2255 white South African gold miners has been followed up from 1968 to 1971, when they were 45-55 years of age, to 31 December 1995 for the incidence of PTB. During the follow up 1592 (71%) men died. Of these, 1296 (81%) had a necropsy done at the National Centre for Occupational Health (NCOH) to determine the presence of silicosis and PTB. The incidence of PTB in the cohort was studied relative to cumulative exposure to dust and the onset of silicosis. For the miners with necropsy, the incidence for PTB was studied relative to the severity of silicosis found at necropsy. RESULTS: There were 115 subjects who developed PTB. The total person- years of follow up was 39,319. For the whole cohort, the factors associated with increased risk of PTB were cumulative exposure to dust (mg/m3.y) (the adjusted rate ratio (RR) 1.07; (95% confidence interval (95% CI) 1.04 to 1.10)), silicosis diagnosed radiologically (3.96 (2.59 to 6.06)), and tobacco pack-years (1.02 (1.01 to 1.03)). The RR (95% CI) for PTB increased with increasing quartiles of cumulative exposure to dust 1.0, 1.51 (0.78 to 2.91), 2.35 (1.28 to 4.32), and 3.22 (1.75 to 5.90). In miners who did not have radiologically diagnosed silicosis (n = 1934, PTB = 74), the adjusted RR (95% CI) for PTB and cumulative exposure to dust was 1.10 (1.06 to 1.13), and increased with quartiles of cumulative exposure to dust as 1.00, 1.46 (0.70 to 3.03), 2.67 (1.37 to 5.23), and 4.01 (2.04 to 7.88). For the subjects who had a necropsy (n = 1296, PTB = 70), the adjusted RR (95% CI) for PTB increased with the severity of silicosis found at necropsy; 1.0 for no silicosis, 1.88 (0.97 to 3.64) for negligible, 2.69 (1.35 to 5.37) for slight, and 2.30 (1.16 to 4.58) for moderate or marked silicosis. For subjects who had a necropsy and no silicosis (n = 577, PTB = 18), the adjusted RR (95% CI) increased slightly with quartiles of cumulative dust 1.0, 1.11 (0.31 to 4.00), 1.42 (0.43 to 4.72), and 1.38 (0.33 to 5.62). CONCLUSION: Exposure to silica dust is a risk factor for the development of PTB in the absence of silicosis, even after exposure to silica dust ends. The risk of PTB increases with the presence of silicosis, and in miners without radiological silicosis, with quartiles of exposure to dust. The severity of silicosis diagnosed at necropsy was associated with increasing risk of PTB and even < 5 nodules--that is, undetectable radiologically--was associated with an increased risk of PTB. The diagnosis of PTB was on average 7.6 years after the end of exposure to dust, at around 60 years of age. The onset of radiological silicosis preceded the diagnosis of PTB in 90.2% of the cases with PTB who had silicosis. The results have implications for medical surveillance of workers exposed to silica dust after the end of exposure.       

Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence

Occupational exposure is an important risk factor for chronic obstructive pulmonary disease (COPD), and silica dust is one of the most important occupational respiratory toxins. Epidemiological and pathological studies suggest that silica dust exposure can lead to COPD, even in the absence of radiological signs of silicosis, and that the association between cumulative silica dust exposure and airflow obstruction is independent of silicosis. Recent clinicopathological and experimental studies have contributed further towards explaining the potential mechanism through which silica can cause pathological changes that may lead to the development of COPD. In this paper we review the epidemiological and pathological evidence relevant to the development of COPD in silica dust exposed workers within the context of recent findings. The evidence surveyed suggests that chronic levels of silica dust that do not cause disabling silicosis may cause the development of chronic bronchitis, emphysema, and/or small airways disease that can lead to airflow obstruction, even in the absence of radiological silicosis.     

Respirable concrete dust--silicosis hazard in the construction industry

Concrete is an extremely important part of the infrastructure of modern life and must be replaced as it ages. Many of the methods of removing, repairing, or altering existing concrete structures have the potential for producing vast quantities of respirable dust. Since crystalline silica in the form of quartz is a major component of concrete, airborne respirable quartz dust may be produced during construction work involving the disturbance of concrete, thereby producing a silicosis hazard for exposed workers. Silicosis is a debilitating and sometimes fatal lung disease resulting from breathing microscopic particles of crystalline silica. Between 1992 and 1998, the National Institute for Occupational Safety and Health (NIOSH) made visits to construction projects where concrete was being mechanically disturbed in order to obtain data concerning respirable crystalline silica dust exposures. The construction activities studied included: abrasive blasting, concrete pavement sawing and drilling, and asphalt/concrete milling. Air samples of respirable dust were obtained using 10-mm nylon cyclone pre-separators, 37-mm polyvinyl chloride (PVC) filters, and constant-flow pumps calibrated at 1.7 L/min. In addition, high-volume respirable dust samples were obtained on 37-mm PVC filters using 1/2" metal cyclones (Sensidyne model 18) and constant-flow pumps calibrated at 9.0 L/min. Air sample analysis included total weight gain by gravimetric analysis according to NIOSH Analytical Method 600 and respirable crystalline silica (quartz and cristobalite) using x-ray diffraction, as per NIOSH Analytical Method 7500. For abrasive blasting of concrete structures, the respirable crystalline silica (quartz) concentration ranged up to 14.0 mg/m3 for a 96-minute sample resulting in an eight-hour time-weighted average (TWA) of 2.8 mg/m3. For drilling concrete highway pavement the respirable quartz concentrations ranged up to 4.4 mg/m3 for a 358-minute sample, resulting in an eight-hour TWA of 3.3 mg/m3. For concrete wall grinding during new building construction the respirable quartz measurements ranged up to 0.66 mg/m3 for a 191-minute sample, resulting in an eight-hour TWA of 0.26 mg/m3. The air sampling results for concrete sawing ranged up to 14.0 mg/m3 for a 350-minute sample resulting in an eight-hour TWA of 10.0 mg/m3. During the milling of asphalt from concrete highway pavement, the sampling indicated a respirable quartz concentration ranging up to 0.34 mg/m3 for a 504-minute sample, resulting in an eight-hour TWA of 0.36 mg/m3. The results of this work indicate the potential for respirable quartz concentrations involving disturbance of concrete to range up to 280 times the NIOSH Recommended Exposure Limit (REL) of 0.05 mg/m3 assuming exposure for an eight- to ten-hour workday. Considering the aging of the concrete infrastructure in the United States, these results pose a challenge to all who have an interest in preventing silica exposures and the associated disease silicosis.     

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.     

Silicosis among semiprecious gem cutters in Joaquim Felício, Minas Gerais State, Brazil

A cross-sectional study was performed to determine the prevalence of silicosis among semiprecious gem cutters (n=70) and describe their clinical, epidemiological, and occupational profiles in Joaquim Felício, Minas Gerais State, Brazil, from April to December 2002. Occupational history was used with a respiratory questionnaire, chest x-ray, and spirometry. Silicosis prevalence was 7.1%. All affected individuals were men, with a mean age of 21.5 and mean exposure to silica of 7.1 years. All belonged to the informal economy and had been working at small and rudimentary workshops, using improvised lathes, with intense exposure to silica dust. According to the ILO Radiological Classification, four of the five cases of silicosis were classified as grade 1 and one as grade 3. Silicosis among gem cutters constitutes a serious public health problem that requires efforts to minimize risk through work by multidisciplinary teams from government agencies and nongovernmental organizations, with active participation by the workers themselves.     

Field evaluation of an engineering control for respirable crystalline silica exposures during mortar removal

During mortar removal with a right angle grinder, a building renovation process known as "tuck pointing," worker exposures to respirable crystalline silica can be as high as 5 mg/m(3), 100 times the recommended exposure limit developed by the National Institute for Occupational Safety and Health. To reduce the risk of silicosis among these workers, a vacuum cleaner can be used to exhaust 80 ft(3)/min (2.26 m(3)/min) from a hood mounted on the grinder. Field trials examined the ability of vacuum cleaners to maintain adequate exhaust ventilation rates and measure exposure outcomes when using this engineering control. These field trials involved task-based exposure measurement of respirable dust and crystalline silica exposures during mortar removal. These measurements were compared with published exposure data. Vacuum cleaner airflows were obtained by measuring and digitally logging vacuum cleaner static pressure at the inlet to the vacuum cleaner motor. Static pressures were converted to airflows based on experimentally determined fan curves. In two cases, video exposure monitoring was conducted to study the relationship between worker activities and dust exposure. Worker activities were video taped concurrent with aerosol photometer measurement of dust exposure and vacuum cleaner static pressure as a measure of airflow. During these field trials, respirable crystalline silica exposures for 22 samples had a geometric mean of 0.06 mg/m(3) and a range of less than 0.01 to 0.86 mg/m(3). For three other studies, respirable crystalline silica exposures during mortar removal have a geometric means of 1.1 to 0.35. Although this field study documented noticeably less exposure to crystalline silica, video exposure monitoring found that the local exhaust ventilation provided incomplete dust control due to low exhaust flow rates, certain work practices, and missing mortar. Vacuum cleaner airflow decrease had a range of 3 to 0.4 ft(3)/min (0.08 to 0.01 m(3)/sec(2)) over a range of vacuum cleaners, hose diameters, and hose lengths. To control worker exposure to respirable crystalline silica, local exhaust ventilation needs to be incorporated into a comprehensive silica control program that includes respiratory protection, worker training, and local exhaust ventilation.