The risk of silicosis was investigated in a cohort of 2,235 white South African gold miners who had, on average, 24 years of net service from 1940 to the early 1970s and who were followed up to 1991 for radiological signs of onset of silicosis (ILO category 1/1 or more). There were 313 (14%) miners who developed signs of silicosis at an average age of 55.9 years. The latency period was largely independent of the cumulative dust exposure. In 57% of the silicosis, the radiological signs developed, on average, 7.4 years after mining exposure ceased. The risk of silicosis increased exponentially with the cumulative dust dose, the accelerated increase being after 7 mg/m3-years. At the highest exposure level of 15 mg/m3-years, which represents approximately 37 years of gold mining at an average respirable dust concentration of 0.4 mg/m3, the cumulative risk for silicosis reached 77%. In conclusion, the risk of silicosis was strongly dose dependent; however, the latency period was largely independent of the dose.
An inquiry into the relation between exposure to silica dust, the presence of silicosis, and progressive systemic sclerosis was conducted in white South African gold miners by means of a case-control study. Seventy nine cases of progressive systemic sclerosis were matched by year of birth with an equal number of control miners selected randomly but bearing in mind the administrative channel through which the case had come to be identified. Analysis showed no association between silicosis and PSS but did show that the cumulative life time silica exposure was significantly higher in the cases compared with controls. This difference was due to a difference in the intensity of exposure to silica during mining service rather than a difference in duration of service. The results are discussed in the context of current thought on the aetiology of progressive systemic sclerosis, particularly in relation to autoimmune and genetic factors.
Objectives-This two part study aimed to determine whether there was an excess mortality generally or for some diseases among middle aged white South African gold miners on the Witwatersrand and whether the underground dust exposure of these miners contributed to the development of lung cancer, chronic obstructive pulmonary disease (COPD), or ischaemic heart disease (IHD). Methods-A cohort of 4925 white miners in South Africa, born between 1 January 1916 and 31 December 1930 who were alive and working in the vicinity of Johannesburg on 1 January 1970, then aged between 39 and 54, was followed up for 20 years by which time 2032 had died. Most were gold miners (about 87% had worked 85% or more of their shifts in gold mines). Standardised mortality ratios (SMRs) were calculated as percentages of the number of deaths observed in the cohort for a condition as stated on the death certificate divided by the number expected on the basis of concurrent mortality in the reference population (the total age specific white male population of South Africa). A case-control analysis was performed for three diseases (lung cancer, COPD, and IHD), the results of which are presented for those miners in the cohort who had spent at least 85% of their service on gold mines and had worked at least 15% of their shifts underground. Results-The SMR for all causes of death was 129-6%, raised because of excess mortality due to the following causes: lung cancer (SMR = 139-8%), IHD
The radiological findings for the profusion of rounded opacities were compared to pathological findings for parenchymal silicosis in 557 gold miners who had, on average, 2.7 years between the radiological and pathological examination. Three readers read the radiographs, and ILO category 1/1 or more was defined as a positive diagnosis of silicosis. The sensitivity values were 0.393, 0.371, and 0.236, and the specificity values were 0.987, 0.965, and 0.978, for the three readers, respectively. The sensitivity of the readers improved with increasing degree of autopsy silicosis, but a large proportion of those with a moderate and marked degree of silicosis were not diagnosed radiologically. The diagnostic sensitivity of the radiological test could be improved by using category 0/1 as a cutoff point for workers exposed to a high average concentration of respirable silica dust. The diagnostic specificity of radiology could be improved by using category 1/0 or 1/1 as a cutoff point for a positive diagnosis for workers exposed to a low average concentration of respirable silica dust.
The relationship between rheumatoid arthritis and silicosis was studied by means of a case-control study in South African goldminers. One hundred and fifty seven miners with rheumatoid arthritis classified as "definite" (91) or "probable" (66) were individually matched by year of birth with miners who had no evidence of rheumatoid arthritis. Unmatched analysis of the case-control status for "probable" and "definite" cases yielded an odds ratio of 2-84 (p = 0-0001). Separate analyses yielded an odds ratio of 3 79 (p = 00006) for "definite" cases, a non-significant odds ratio for "probable" cases, and an odds ratio of 500 (p = 00003) for the presence of rheumatoid factor. These results could not be explained on the basis of cumulative dust exposure or intensity of exposure. The rate of progression of silicosis in both the "definite" and the "probable" groups was greater than for the control patients with silicosis, as was the probability of silicosis presenting at the start with larger nodules (type r).The radiological and histological features of silicosis are sometimes modified in a characteristic manner in miners with rheumatoid arthritis1-a phenomenon seen also in coalminers' pneumoconiosis.2 3 The question of whether silicosis occurs more readily in individuals with rheumatoid arthritis exposed to silica has not, however, been addressed.Silicosis occurs in South African gold miners, who may be exposed to dust containing high levels of free silica. The main objective of this study was to determine whether silicosis was present more often in miners with rheumatoid arthritis than in miners without, and to determine whether any differences found in the prevalence of silicosis could be explained by differences in the amount or intensity of exposure to silica dust. Miners with silicosis and rheumatoid arthritis were compared with those without rheumatoid arthritis to establish whether the rate of progression and other features of silicosis were different under conditions of equal exposure to silica dust. Index subjects with silicosis who were seropositive for rheumatoid factor were compared with the control subjects with silicosis to determine whether the presence of rheumatoid factor was relevant to the progression of silicosis.
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