Toxicology and Risk Assessment, Swedish National Institute for Working Life, SE-112 79 Stockholm, Sweden
Steenland and Sanderson presented a well-designed cohort study comprising 4,626 industrial sand workers (1). The lung cancer standardized mortality ratio was 1.60, and limited data suggested that smoking might account for 1020 percent of the lung cancer excess as the risk ratio for lung cancer is about 10 (smokers vs. nonsmokers). Nested case-control analyses after exclusion of short-term workers, who had a high overall mortality, yielded a clear relation between cumulative dose and the occurrence of lung cancer. The study also showed a higher standardized mortality ratio regarding ischemic heart disease of 1.22 (95 percent confidence interval: 1.09, 1.36). Smoking might hypothetically be responsible for 24 percent of this increase as the risk ratio for ischemic heart disease (smokers vs. nonsmokers) is about 2 (2
).
A Swedish case-control study comprised 26,847 men with myocardial infarctions, and for each case two controls were selected from the study base through random sampling, stratified by age, county, and socioeconomic group. The second highest risk was found among stone cutters and carvers, with a relative risk of 1.9 (95 percent confidence interval: 1.1, 3.4). This high risk could not be explained by differences in smoking habits based on assumptions of the possible magnitude of the smoking effect (3). That is, on the basis of data from the Swedish Twin Register, the proportion of smokers differed about 5 percent when subjects in occupations with an increased or decreased incidence were compared with all those employed. Theoretically, it can be shown that, if the smoking prevalence among all employed persons is 50 percent, the observed relative risk is 1.5, and smokers have twice the risk of nonsmokers to develop myocardial infarction, stratification would yield a relative risk of 1.32 if the prevalence of smokers was 70 percent in the index occupation (3
).
A cohort of 3,971 White South African gold miners was followed from January 1, 1970. Most of the miners worked that year, and the age of the workers was 3954 years. The miners were followed for 9 years. A case-referent analysis was conducted that comprised the miners who had at least 85 percent of their service in gold mines. A period of 10 years of underground mining was associated with a risk ratio of 1.5 (p = 0.004) regarding ischemic heart disease, after adjustment for smoking, blood pressure, and body mass index (4). The cohort of South African miners was enlarged, comprising 4,925 miners, and followed from January 1, 1970, for 20 years. The mining cohort was compared with the total South African male population. The standardized mortality ratio regarding ischemic heart disease was 1.24 (95 percent confidence interval: 1.15, 1.34). A case-referent analysis revealed a relative risk of 1.0 after adjustment for smoking habits (5
). A longer follow-up period means that a larger proportion of the cohort is retired and consequently not exposed to quartz. Former miners might reduce their risk of ischemic heart disease in the same way as former smokers (2
).
A general hypothesis about exposure to inhaled particles and the occurrence of ischemic heart disease can be expressed in the following way. Long-term inhalation of particles retained in the lungs will create a low-grade inflammation associated with an increase in plasma fibrinogen. The high concentration of fibrinogen will increase the likelihood for blood clotting and thereby the risk for myocardial infarction and ischemic heart disease (6, 7
). This hypothesis will be supported if industrial sand workers have a higher concentration of plasma fibrinogen than do nonexposed workers with control for other possible confounders, such as smoking habits (8
).
The authors have promised to publish an analysis regarding the relation between silica exposure and the occurrence of kidney disease and arthritis. I am eagerly waiting for a further analysis regarding the relation between silica exposure and the occurrence of ischemic heart disease.
NOTES
Editor's note: In accordance with Journal policy, Steenland and Sanderson were asked whether they wished to respond to this letter, but they chose not to do so.
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