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Objective. To test the hypotheses that there is an excess percentage of slow acetylators among patients with idiopathic systemic lupus erythematosus (SLE) and that these patients had excessive exposure to environmental amines and hydrazines before the onset of illness. Methods. Case–control study with structured interview and acetylation phenotyping. Results. No excess proportion of slow acetylators or environmental amine exposure was found. Conclusion. Slow acetylation phenotype and exposure to environmental amines are not principal causes of idiopathic SLE.