Abstract
Crystalline silica, when inhaled occupationally in sufficient concentration of fine particles (respirable size) and duration, was widely identified as a hazard early in this century; some would say much earlier. In spite of the long-term general recognition of lung fibrosis (silicosis) resulting from such exposures in a wide variety of industries, increasingly accurate measurement of airborne crystalline silica, and the establishment of potential for human adverse biological effects by cytotoxicity and animal studies, epidemiologic results from studies of occupationally exposed workers have yielded only limited and variable information on dose–response relationships for silicosis. Adequate risk characterization has, therefore, been slow in evolving, and epidemics of silicosis continue to occur. Workplace standards have been set on the basis of these limited available data, which were reviewed at this conference. In spite of the indicated deficiencies of quantitative estimates of silicosis risk, it is a reasonable conclusion that sufficient information is at hand to effectively prevent silicosis in the workplace. In the last decade, increasing interest has focused on the possibility that crystalline silica is a human lung carcinogen. At present, a definitive conclusion on this question must be regarded as premature. Many studies of silicotics have demonstrated excess lung cancer risk, and while several cohort studies have shown overall excess, only one has convincingly shown the risk to be dose-dependent. Also, few of those with an excess lung cancer risk have been able to account for confounding exposures, or other serious methodologic flaws have been present. That silicotics are at increased risk of lung cancer is clear; that workers exposed to silica at doses which have not produced silicosis are at such risk is not. Public policy is directed at preventing disease produced by occupational exposure to crystalline silica. For silicosis, this means more effective compliance (and enforcement) with the measures already known to mitigate the risk: dust control and respiratory protection. Better dose–response information would facilitate the elimination of residual risk. As the science evolves in regard to the potential lung cancer risk, prevention may require only the same exposure control measures as for silicosis, if the excess cancer risk is found to be related to silicosis, and not silica exposure alone. If, however, excess lung cancer risk is found to be the result of exposure, and not lung fibrosis, dose–response relationships must be sought from appropriate epidemiologic studies. Weill, H.: Risk Analysis and Public Policy in Relation to silica Exposure, Appl. Occup. Environ. Hyg. 10(12):1154–1156; 1995.