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.     

Occupational exposure to crystalline silica dust in the United States, 1988-2003

The purposes of this study were a) to summarize measurements of airborne (respirable) crystalline silica dust exposure levels among U.S. workers, b) to provide an update of the 1990 Stewart and Rice report on airborne silica exposure levels in high-risk industries and occupations with data for the time period 1988-2003, c) to estimate the number of workers potentially exposed to silica in industries that the Occupational Safety and Health Administration (OSHA) inspected for high exposure levels, and d) to conduct time trend analyses on airborne silica dust exposure levels for time-weighted average (TWA) measurements. Compliance inspection data that were taken from the OSHA Integrated Management Information System (IMIS) for 1988-2003 (n = 7,209) were used to measure the airborne crystalline silica dust exposure levels among U.S. workers. A second-order autoregressive model was applied to assess the change in the mean silica exposure measurements over time. The overall geometric mean of silica exposure levels for 8-hr personal TWA samples collected during programmed inspections was 0.077 mg/m3, well above the applicable American Conference of Governmental Industrial Hygienists threshold limit value of 0.05 mg/m3. Surgical appliances supplies industry [Standard Industrial Classification (SIC) 3842] had the lowest geometric mean silica exposure level of 0.017 mg/m3, compared with the highest level, 0.166 mg/m3, for the metal valves and pipe fitting industry (SIC 3494), for an 8-hr TWA measurement. Although a downward trend in the airborne silica exposure levels was observed during 1988-2003, the results showed that 3.6% of the sampled workers were exposed above the OSHA-calculated permissible exposure limit.     

Risk of silicosis in a Colorado mining community

We investigated exposure-response relations for silicosis among 134 men over age 40 who had been identified in a previous community-based random sample study in a mining town. Thirty-two percent of the 100 dust-exposed subjects had radiologic profusions of small opacities of 1/0 or greater at a mean time since first silica exposure of 36.1 years. Of miners with cumulative silica exposures of 2 mg/m³-years or less, 20% had silicosis; of miners accumulating > 2 mg/m³-years, 63% had silicosis. Average silica exposure was also strongly associated with silicosis prevalence rates, with 13% silicoties among those with average exposure of 0.025–0.05 mg/m³, 34% among those with exposures of > 0.05–0.1 mg/m³, and 75% among those with average exposures > 0.1 mg/m³. Logistic regression models demonstrated that time since last silica exposure and either cumulative silica exposure or a combination of average silica exposure and duration of exposure predicted silicosis risk. Exposure-response relations were substantially higher using measured silica exposures than using estimated silica exposures based on measured dust exposures assuming a constant silica proportion of dust, consistent with less exposure misclassification. The risk of silicosis found in this study is higher than has been found in workforce studies having no follow-up of those leaving the mining industry and in studies without job title-specific silica measurements, but comparable to several recent studies of dust exposure-response relationships which suggest that a permissible exposure limit of 0.1 mg/m³ for silica does not protect against radiologic silicosis. © 1996 Wiley-Liss, Inc.     

Occupational Exposure to Crystalline Silica at Alberta Work Sites

Although crystalline silica has been recognized as a health hazard for many years, it is still encountered in many work environments. Numerous studies have revealed an association between exposure to respirable crystalline silica and the development of silicosis and other lung diseases including lung cancer. Alberta Jobs, Skills, Training and Labour conducted a project to evaluate exposure to crystalline silica at a total of 40 work sites across 13 industries. Total airborne respirable dust and respirable crystalline silica concentrations were quite variable, but there was a potential to exceed the Alberta Occupational Exposure Limit (OEL) of 0.025 mg/m³ for respirable crystalline silica at many of the work sites evaluated. The industries with the highest potentials for overexposure occurred in sand and mineral processing (GM 0.090 mg/m³), followed by new commercial building construction (GM 0.055 mg/m³), aggregate mining and crushing (GM 0.048 mg/m³), abrasive blasting (GM 0.027 mg/m³), and demolition (GM 0.027 mg/m³). For worker occupations, geometric mean exposure ranged from 0.105 mg/m³ (brick layer/mason/concrete cutting) to 0.008 mg/m³ (dispatcher/shipping, administration). Potential for GM exposure exceeding the OEL was identified in a number of occupations where it was not expected, such as electricians, carpenters and painters. These exposures were generally related to the specific task the worker was doing, or arose from incidental exposure from other activities at the work site. The results indicate that where there is a potential for activities producing airborne respirable crystalline silica, it is critical that the employer include all worker occupations at the work site in their hazard assessment. There appears to be a relationship between airborne total respirable dust concentration and total respirable dust concentrations, but further study is require to fully characterize this relationship. If this relationship holds true, it may provide a useful hazard assessment tool for employers by which the potential for exposure to airborne respirable silica at the work site can be more easily estimated.     

Relation between exposure to respirable silica dust and silicosis in a tungsten mine in China.

To estimate the quantitative relation between exposure to respirable silica dust and risk of an attack of silicosis, 1151 workers exposed to silica dust and employed from 1958 to 1987 in a tungsten mine in China were investigated. The results showed that the ratio of respirable silica dust concentration to total silica dust concentration was 0.529. Then, the total silica dust concentration in historical surveillance and monitoring data was converted to respirable silica dust concentration. The free silica content in respirable dust determined by x ray diffraction averaged 24.7%. Multiple logistic regression was used for the dichotomous dependent variables (presence or absence of silicosis). The independent variables in the multiple logistic regression with presence of silicosis as the dependent variable were age when first exposed, tuberculosis (presence or absence), and cumulative exposure to respirable silica dust. The partial regression coefficient of individual cumulative exposure was estimated as 0.079. It implied a positive association between exposure to respirable silica dust and risk of an attack of silicosis. The exposure limit for respirable silica dust was estimated as 0.24 mg/m3 under given conditions.     

Relation between exposure to respirable silica dust and silicosis in a tungsten mine in China.

To estimate the quantitative relation between exposure to respirable silica dust and risk of an attack of silicosis, 1151 workers exposed to silica dust and employed from 1958 to 1987 in a tungsten mine in China were investigated. The results showed that the ratio of respirable silica dust concentration to total silica dust concentration was 0.529. Then, the total silica dust concentration in historical surveillance and monitoring data was converted to respirable silica dust concentration. The free silica content in respirable dust determined by x ray diffraction averaged 24.7%. Multiple logistic regression was used for the dichotomous dependent variables (presence or absence of silicosis). The independent variables in the multiple logistic regression with presence of silicosis as the dependent variable were age when first exposed, tuberculosis (presence or absence), and cumulative exposure to respirable silica dust. The partial regression coefficient of individual cumulative exposure was estimated as 0.079. It implied a positive association between exposure to respirable silica dust and risk of an attack of silicosis. The exposure limit for respirable silica dust was estimated as 0.24 mg/m3 under given conditions.     

Occupational causes of chronic obstructive pulmonary disease

The relation between Chronic Obstructive Pulmonary Disease (COPD, including chronic bronchitis and emphysema (CBE), and exposure to coal dust is well established. This paper reviews the evidence relating to other occupational causes of COPD, including industries associated with exposure to fumes, chemical substances, and dusts. A review of key literature has been carried out with a focus on the magnitude of risks and levels of exposure causing disabling health effects. The literature suggests that elevated risks of developing COPD are clearly associated with several occupations, with risk estimates being high in some, even after taking into account the effect of confounders, such as smoking. Of particular concern are agricultural workers who can be exposed to a variety of gases and organic dusts, among whom CBE is clearly elevated, particularly for pig farmers and exposure to endotoxins, with an increased annual decline in lung function. Similarly, cotton textile workers are exposed to a mixture of substances affecting development of atopy, byssinosis, and CBE, and across-shift and long-term decline in lung function. Atopy also has an important role in the development of COPD in flour mill workers and bakers, with those sensitized to bakery allergens having a greater lung function decline than non-sensitized individuals. Welding processes involve a range of potential chemical, physical and radiation hazards. The average reduction in FEV1 associated with welding fumes is similar to that associated with smoking. Challenges in assessing the evidence include variation in diagnostic methods; concurrent exposure to cigarette smoke (direct or second-hand) and multiple work-place irritants; healthy worker selection/survivor effects; poor exposure definition. Raising awareness of occupational causes of COPD among employers, employees, and health service professionals is important.     

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.     

Engineering controls for selected silica and dust exposures in the construction industry--a review

This literature review summarizes engineering control technology research for dust and silica exposures associated with selected tasks in the construction industry. Exposure to crystalline silica can cause silicosis and lung fibrosis, and evidence now links it with lung cancer. Of over 30 references identified and reviewed, 16 were particularly significant in providing data and analyses capable of documenting the efficacy of various engineering controls. These reports include information on generation rates and worker exposures to silica and dust during four different tasks: cutting brick and concrete block, grinding mortar from between bricks, drilling, and grinding concrete surfaces. The major controls are wet methods and local exhaust ventilation. The studies suggest that while the methods provide substantial exposure reductions, they may not reduce levels below the current ACGIH threshold limit value (TLV) of 0.05 mg/m(3) for respirable quartz. Although further research on controls for these operations is indicated, it is clear that effective methods exist for significant exposure reduction.     

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.     

Pulmonary alveolar proteinosis induced by silica dust?

Abstract Pulmonary alveolar proteinosis (PAP) is a rare disease, with several aetiologies. This study reports the first Finnish case of PAP with possible induction by silica dust. A 58-year-old male patient had a documented history of heavy exposure to silica dust over a long period, although he himself considered the exposure to be low. The patient's cumulative exposure to silica dust was approximately 10 mg m(-3) years according to the workplace measurements. The patient developed classical symptoms and signs of PAP that closely mimicked those of acute silicosis, but he did not have any signs of classic silicosis. We conclude that significant chronic exposure to silica favours the diagnosis of PAP rather than acute silicosis in this case. PAP should be taken into account when patients exposed to silica dust complain of respiratory symptoms. A patient's assessment of his/her exposure to silica may not always be reliable.     

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.     

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.       

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.


     

锡矿工人接尘与矽肺危险度评价

目的探讨粉尘暴露与矽肺危险度之间的接触效应关系。方法选择广西４个锡矿１９６０～１９６５年间工作１年以上的３０１０名接尘工人进行队列研究。用生存分析法统计累积粉尘接触量和矽肺出现的关系。结果追访到１９９４年底,检出矽肺１０１５例（３３．７％）。矽肺平均潜伏期２１．３年。总粉尘浓度７．５ｍｇ／ｍ３（ＴＷＡ）。拟合生存分析模型表明：矽肺发病危险度与累积接尘量的关系适合Ｗｅｉｂｕｌ分布。累积总粉尘接触量低于１０ｍｇ·ｍ－３·ａ－１时,矽肺危险小于１％;累积总粉尘接触量超过２０ｍｇ·ｍ－３·ａ－１时,矽肺累积危险度升高加快;累积总粉尘接触量达１５０ｍｇ·ｍ－３·ａ－１时,矽肺危险超过６８％。接尘时间与接尘量和矽肺危险度呈正相关。结论矽肺危险度与累积接尘量之间存在接触效应关系。     

Silicosis among gold miners: exposure--response analyses and risk assessment.

OBJECTIVES. This study sought to estimate the risk of silicosis by cumulative exposure-years in a cohort of miners exposed to silica, as well as the lifetime risk of silicosis under the current Occupational Safety and Health Administration (OSHA) standard (0.09 mg/m3). METHODS. In a cohort study of 3330 gold miners who worked at least 1 year underground from 1940 to 1965 (average 9 years) and were exposed to a median silica level of 0.05 mg/m3 (0.15 mg/m3 for those hired before 1930), 170 cases of silicosis were determined from either death certificates or two cross-sectional radiographic surveys. RESULTS. The risk of silicosis was less than 1% with a cumulative exposure under 0.5 mg/m3-years, increasing to 68% to 84% for the highest cumulative exposure category of more than 4 mg/m3-years. Cumulative exposure was the best predictor of disease, followed by duration of exposure and average exposure. After adjustment for competing risks of death, a 45-year exposure under the current OSHA standard would lead to a lifetime risk of silicosis of 35% to 47%. CONCLUSIONS. Almost 2 million US workers are currently exposed to silica. Our results add to a small but increasing body of literature that suggests that the current OSHA silica exposure level is unacceptably high.     

Mortality from non-malignant respiratory diseases among people with silicosis in Hong Kong: exposure-response analyses for exposure to silica dust

Objectives

To examine the exposure–response relationships between various indices of exposure to silica dust and the mortality from non‐malignant respiratory diseases (NMRDs) or chronic obstructive pulmonary diseases (COPDs) among a cohort of workers with silicosis in Hong Kong.

Methods

The concentrations of respirable silica dust were assigned to each industry and job task according to historical industrial hygiene measurements documented previously in Hong Kong. Exposure indices included cumulative dust exposure (CDE) and mean dust concentration (MDC). Penalised smoothing spline models were used as a preliminary step to detect outliers and guide further analyses. Multiple Cox''s proportional hazard models were used to estimate the dust effects on the risk of mortality from NMRDs or COPDs after truncating the highest exposures.

Results

371 of the 853 (43.49%) deaths occurring among 2789 workers with silicosis during 1981–99 were from NMRDs, and 101 (27.22%) NMRDs were COPDs. Multiple Cox''s proportional hazard models showed that CDE (p = 0.009) and MDC (p<0.001) were significantly associated only with NMRD mortality. Subgroup analysis showed that deaths from NMRDs (p<0.01) and COPDs (p<0.05) were significantly associated with both CDE and MDC among underground caisson workers and among those ever employed in other occupations with high exposure to silica dust. No exposure–response relationship was observed for surface construction workers with low exposures. A clear upward trend for both NMRDs and COPDs mortality was found with increasing severity of radiological silicosis.

Conclusion

This study documented an exposure–response relationship between exposure to silica dust and the risk of death from NMRDs or COPDs among workers with silicosis, except for surface construction workers with low exposures. The risk of mortality from NMRDs increased significantly with the progression of International Labor Organization categories, independent of dust effects.Excessive mortality from non‐malignant respiratory diseases (NMRDs) including chronic obstructive pulmonary disease (COPD) has been reported among cohorts exposed to silica dust or among cohorts with disease silicosis.^{1,2,3,4,5,6,7} However, inconsistent or even conflicting evidence existed on the exposure–response relationship between exposure to silica dust and death from NMRDs or COPD.^{1,3,4,5,6,7,8,9} Besides the potential differences in methods or toxicity of quartz polymorphs and exposure levels, discrepancies between studies might reflect the differences in biological effectiveness of various exposure indices.^3,10 The potential limitations of cumulative dust exposure (CDE) had been emphasised by Smith,¹¹ who said that CDE might be a poor dose index in examining the association with lung diseases by using a pharmacokinetic model. Hughes et al¹² found a substantially steeper relationship with silicosis among diatomaceous earth workers exposed at the highest concentrations of crystalline silica. More recently, Buchanan et al¹³ provided supportive evidence on this issue and suggested that quantifying the risks of silicosis should take into account the variations in quartz exposure intensity, particularly for concentrations >1 or 2 mg/m³, even if exposures were for relatively short periods. Studies comparing the possible effect of cumulative exposure to silica dust and mean dust concentration (MDC) on the risk of NMRD or COPD remain sparse and in demand. We report here the exposure–response analyses between various indices of exposure to silica dust and mortality from NMRDs or COPD among a cohort of 2789 workers with silicosis in Hong Kong, taking into consideration the effect of cigarette smoking.     

Dust exposure during small-scale mining in Tanzania: a pilot study

Small-scale mining in developing countries is generally labour-intensive and carried out with low levels of mechanization. In the Mererani area in the northern part of Tanzania, there are about 15000 underground miners who are constantly subjected to a poor working environment. Gemstones are found at depths down to 500 m. The objectives of this pilot study were to monitor the exposure to dust during work processes, which are typical of small-scale mining in developing countries, and to make a rough estimation of whether there is a risk of chronic pulmonary diseases for the workers. Personal sampling of respirable dust (n = 15) and 'total' dust (n = 5) was carried out during three consecutive days in one mine, which had a total of 50 workers in two shifts. Sampling started immediately before the miners entered the shaft, and lasted until they reappeared at the mine entrance after 5-8 h. The median crystalline silica content and the combustible content of the respirable dust samples were 14.2 and 5.5%, respectively. When drilling, blasting and shovelling were carried out, the exposure measurements showed high median levels of respirable dust (15.5 mg/m(3)), respirable crystalline silica (2.4 mg/m(3)), respirable combustible dust (1.5 mg/m(3)) and 'total' dust (28.4 mg/m(3)). When only shovelling and loading of sacks took place, the median exposures to respirable dust and respirable crystalline silica were 4.3 and 1.1 mg/m(3). This study shows that the exposure to respirable crystalline silica was high during underground small-scale mining. In the absence of personal protective equipment, the miners in the Mererani area are presumably at a high risk of developing chronic silicosis.     

Respiratory effects of exposure to low levels of concrete dust containing crystalline silica

BACKGROUND: Dusts containing crystalline silica are generated in mining, construction, glass, granite and concrete production industries. The association between exposure to low levels of concrete dust containing crystalline silica and reduction in lung function, was evaluated in a cross-sectional study. METHODS: The study was carried out among 144 concrete workers, from two factories, with exposure assessment of respirable dust and silica by personal samplers. Results of respiratory questionnaires and standardized measurements of lung function were compared with the results in a control population. Multiple linear regression analysis was used in selecting factors that predict (age and standing height standardized residual) lung function. RESULTS: The average concentration of respirable dust in both factories was 0.8 mg/m(3) and 0.06 mg/m(3) for respirable silica. The average silica content of the dust was 9%. The average cumulative dust exposure was 7.0 mg/m(3) year and cumulative silica exposure was 0.6 mg/m(3) year. Significant associations between exposure to concrete dust and a small lung function (FEV(1)/FVC ratio, MMEF) loss were found, independent of smoking habits and of a history of allergy. CONCLUSIONS: Our results indicate that, concrete workers with chronic obstructive pulmonary symptoms and/or work-related lower respiratory symptoms are at risk of having a reduction in lung function (FEV&(1)/FVC ratio) outside the 5th percentile of the external reference population, and therefore, of mild chronic obstructive pulmonary disease, at respirable concrete dust levels below 1 mg/m(3) with a respirable crystalline silica content of 10% (TWA, 8 hr).     

Exposure to respirable crystalline silica in eastern North Carolina farm workers

Occupational exposure to crystalline silica has been linked to silicosis, some forms of cancer, and certain autoimmune diseases. Little information exists on exposure levels of respirable silica in the agricultural industry. This study assessed respirable silica exposure of farm workers in eastern North Carolina. Sandy soils in this region have been shown to contain high levels of respirable silica. Personal breathing zone samples (n = 37) were collected from 27 workers at seven farms during various agricultural activities. The highest respirable silica concentrations were measured during sweet potato transplanting (3.91 +/- 2.07 mg/m3). Respirable silica exposure was observed to be associated with agricultural activity, soil moisture, relative humidity, and wind speed. Most of the variation in exposure (79%) was explained by agricultural activity and soil moisture. The observed percentage of silica levels (mean 34.7%) were almost twice as high as was reported in studies of California agriculture. This may be due to the loamy sand and sandy loam soil types in the regions in this study. In agriculture, respirable silica exposure is highly variable, but the potential for exposures above the threshold limit value of 0.05 mg/m3 exists during particular agricultural activities.