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PubMed1983

[SUVA (Swiss Accident Insurance Fund) and silicosis. Silicosis in Switzerland. Development of technological dust control].

In Switzerland the technical measures against quartz dust started in 1948 when wet drilling was compulsoryly introduced, initially in underground mining. The miners using the first wet drilling machines had serious problems with water, and only with the introduction of carriage drilling machines in 1963 did the method fully break through. Dust caused by blasting operations and by loading of the resultant material was limited by ventilation and sprinkling of water. In 1966 the first full-face cutting machines were used, and it was necessary to install a dust chamber behind the drill from which dust could be taken to a dust arrester. The problem of dust limitation when using boom cutters at sectional areas of more than 20 sq. meters without a pilot tunnel has not been resolved. Since 1970, dust in quarries and stone-cutter workshops has been successfully combated by the use of exhaust pumps in combination with filters. The use of quartz sand to clean metal pieces (sandblast) was forbidden in 1960. Today, materials of the same value, but quartz-free, are available. In foundries, dust production can be limited by continuous automation and installation of exhaust pumps in moulding units. For more than 30 years now the technical equipment has been available for successful prevention of quartz dust emissions. However, at some plants it is still difficult to persuade the personnel to use the protective equipment.

Dust↗
PubMed1998

Risk of pulmonary tuberculosis relative to silicosis and exposure to silica dust in South African gold miners.

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.

Adult↗
PubMed2001

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/m(3)-years (or 0.36 mg/m(3)-years of respirable crystalline silica), increasing to 68.7% when CTD exposure was 150 mg/m(3)-years (or 5.4 mg/m(3)-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/m(3), 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/m(3) 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.

Adult↗
PubMed1993

Association of silicosis, lung dysfunction, and emphysema in gold miners.

BACKGROUND: In an earlier study of gold miners men with silicosis were found to have abnormal lung function, including airflow obstruction and reduced diffusing capacity. In a follow up study a sample of these men was examined by computed tomography to determine whether emphysema accounted for these abnormalities, which are associated with silicosis in this working population. METHODS: A sample of 70 men from a cohort of older gold miners with and without silicosis who had worked underground for a mean period of 29 years was examined by computed tomography to determine whether each man had emphysema. In addition, each man had lung function tests and routine chest radiography (125 kV). RESULTS: A total of 48 men had emphysema on examination by computed tomography. On the basis of the results in a chest radiograph 55 of the men had silicosis. Emphysema was related to silicosis, being present in five of the 15 men without silicosis and in 43 of the 55 with silicosis. Diffuse emphysema was apparent in two men without silicosis (14%) and in 25 men with silicosis (45%). The proportion of men with diffuse emphysema increased from 14% in those with International Labour Organisation category 0 nodule profusion to 46% in those with category 1, 48% in those with category 2, and 67% in those with category 3. Emphysema was also related to smoking: eight of the 18 who had never smoked and 40 of the 52 smokers had emphysema. All of those who had never smoked and had emphysema had silicosis with category 2/2 or greater nodule profusion. Lung function tests showed changes associated with silicosis that could be explained by the associated emphysema. CONCLUSIONS: In this population emphysema occurred in association with silicosis and accounted for the abnormalities in lung function associated with silicosis.

Gold↗
PubMed2003

Longitudinal study of the FEV1, cumulative exposure to dusts and silicosis in gold miners.

OBJECTIVES: The aim of this longitudinal study was to assess the rate of decline in FEV1 (deltaFEV1) in gold miners with silicosis and to relate these findings with the radiographic picture, age, smoking habits and cumulative exposure to dusts. METHODS: The study included 73 gold miners with silicosis and 73 miners exposed to dusts but without silicosis. The clinical, radiological and functional assessment was made at least twice in each miner at the beginning and at the end of an adequate interval of the investigation which was extended for a mean period of 38.9 months for the group with silicosis and 33.6 months for the group without silicosis. RESULTS: In the group of miners with silicosis deltaFEV1 was much higher (187 ml/year) as compared with the mean value found in the miners without silicosis (43.2 ml/year). No significant differences were found for deltaFEV1 according to the age criterion (in both groups) and to their smoking habits (in the group with silicosis). In silicosis, a very good correlation exists between the index of cumulative exposure to dusts and the magnitude of the decline rate of FEV1. In the miners, group without silicosis, deltaFEV1 had not any significant correlation with cumulative exposure to dusts. CONCLUSIONS: Our observations revealed that the cumulative exposure to dusts affected the decline rate of FEV1 only to the extent to which it determined silicosis and intervened less in the functional decline in miners without silicosis. Smoking habits increased AFEV1 only in miners without silicosis.

Adult↗
PubMed1998

Silica, compensated silicosis, and lung cancer in Western Australian goldminers.

OBJECTIVES: Silica has recently been reclassified as carcinogenic to humans based largely on the observed increase in rates of lung cancer in subjects with silicosis. Other recent reviews have arrived at different conclusions as to whether silicosis or silica itself is carcinogenic. This study aims to examine exposure-response relations between exposure to silica and subsequent silicosis and lung cancer in a cohort of goldminers. METHODS: 2,297 goldminers from Kalgoorlie in Western Australia were examined in 1961, 1974, and 1975. Data were collected on respiratory symptoms, smoking habits, and employment history. Subjects were followed up to the end of 1993. Survival analyses for lung cancer mortality and incidence of compensated silicosis were performed with age and year matched conditional logistic regression analyses. RESULTS: 89% of the cohort were traced to the end of 1993. 84% of the men had smoked at some time and 66% were current smokers. 1386 deaths occurred during the follow up period, 138 from lung cancer, and 631 subjects were compensated for silicosis. A strong effect of smoking on mortality from lung cancer, and a smaller effect on the incidence of compensated silicosis was found. There was a strong effect of duration and intensity of exposure on the incidence of silicosis. The risk of mortality from lung cancer increased after compensation for silicosis. Of all direct measures of exposure to silica, only log cumulative exposure was significantly related to incidence of lung cancer, but this effect disappeared once the onset of silicosis was taken into account. CONCLUSIONS: The incidence of silicosis was clearly related to exposure to silica and the onset of silicosis conferred a significant increase in risk for subsequent lung cancer, but there was no evidence that exposure to silica caused lung cancer in the absence of silicosis.

Adolescent↗
PubMed1999

Crystalline silica exposure, radiological silicosis, and lung cancer mortality in diatomaceous earth industry workers.

BACKGROUND: The role of silicosis as either a necessary or incidental condition in silica associated lung cancer remains unresolved. To address this issue a cohort analysis of dose-response relations for crystalline silica and lung cancer mortality was conducted among diatomaceous earth workers classified according to the presence or absence of radiological silicosis. METHODS: Radiological silicosis was determined by median 1980 International Labour Organisation system readings of a panel of three "B" readers for 1809 of 2342 white male workers in a diatomaceous earth facility in California. Standardised mortality ratios (SMR) for lung cancer, based on United States rates for 1942-94, were calculated separately for workers with and without radiological silicosis according to cumulative exposures to respirable crystalline silica (milligrams per cubic meter x years; mg/m3-years) lagged 15 years. RESULTS: Eighty one cases of silicosis were identified, including 77 with small opacities of > or = 1/0 and four with large opacities. A slightly larger excess of lung cancer was found among the subjects with silicosis (SMR 1.57, 95% confidence interval (CI) 0.43 to 4.03) than in workers without silicosis (SMR 1.19, 95% CI 0.87 to 1.57). An association between silica exposure and lung cancer risk was detected among those without silicosis; a statistically significant (p = 0.02) increasing trend of lung cancer risk was seen with cumulative exposure, with SMR reaching 2.40 (95% CI 1.24 to 4.20) at the highest exposure level (> or = 5.0 mg/m3-years). A similar statistically significant (p = 0.02) dose-response gradient was observed among non-silicotic subjects when follow up was truncated at 15 years after the final negative radiograph (SMR 2.96, 95% CI 1.19 to 6.08 at > or = 5.0 mg/m3-years), indicating that the association among non-silicotic subjects was unlikely to be accounted for by undetected radiological silicosis. CONCLUSIONS: The dose-response relation observed between cumulative exposure to respirable crystalline silica and lung cancer mortality among workers without radiological silicosis suggests that silicosis is not a necessary co-condition for silica related lung carcinogenesis. However, the relatively small number of silicosis cases in the cohort and the absence of radiographic data after employment limit interpretations.

Adult↗