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Occupational exposures and risk of systemic lupus erythematosus
Christine G Parks1, Glinda S Cooper
1Biostatistics and Epidemiology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA. cqp8@cdc.gov
Abstract:
This review summarizes the growing body of epidemiologic and experimental research pertaining to the relationship between SLE and occupational exposures, such as crystalline silica, solvents, and pesticides. Epidemiologic studies, using different designs in different settings, have demonstrated moderate to strong associations between occupational silica exposure and SLE. Recent experimental studies of silica in lupus-prone mice provide support for the idea that, in addition to its known adjuvant effect, silica exposure increases the generation of apoptotic material, an important source of self-antigen. Despite compelling experimental studies of the organic solvent trichloroethylene (TCE) in lupus-prone mice, there is little evidence of an overall association of SLE and occupational exposure to a broad classification of solvents in humans. However, there is a lack of data on SLE in occupational cohorts with exposures to TCE or other specific solvents. One epidemiologic study reported an association of pesticide mixing and SLE, while a recent experimental study reported accelerated disease in pesticide-treated lupus-prone mice. Other occupational exposures worth investigating include asbestos, metals, and UV radiation. Attention should also be given to the role of gene-environment interactions, which may require large, multi-site studies that collect both genetic material and occupational exposure data. The quality of exposure assessment is an important consideration in designing and evaluating these studies. The use of pre-clinical endpoints (e.g. high-titer autoantibodies) in occupational cohorts with well-characterized exposure histories may reveal occupational risk factors for autoimmunity, and may also provide baseline data for studies of determinants of progression to SLE.
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