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Departments of Industria Hygiene and Toxicology [A. H., K. P., K. L.], Epidemiology and Biostatistics [L. T.], and Uusimaa Regional Institute [A. K.], Finnish Institute of Occupational Health, FIN-00250 Helsinki, Finland, and Department of Internal Medicine, Helsinki University Central Hospital, FIN-00290 Helsinki, Finland [K. M.]
Besides asbestos exposure, the factors that determine susceptibility to malignant mesothelioma are unknown. We evaluated the risk of GSTM1 null genotype and slow acetylation-associated NAT2 genotype for malignant mesothelioma in relation to asbestos exposure. Both the GSTM1 null genotype and the NAT2 slow acetylator genotype placed individuals at about 2-fold increased risk of developing malignant mesothelioma [odds ratio (OR) = 1.8, 95% confidence interval (CI) = 1.0–3.5 and OR = 2.1, 95% CI = 1.1–4.1, for the GSTM1 and NAT2 genes, respectively]. When the patients were divided into low/moderate and high exposure groups according to their asbestos exposure histories, the effect of the at-risk genotypes was mostly attributable to the high exposure groups (OR = 2.3, 95% CI = 1.0–5.6 and OR = 3.7, 95% CI = 1.3–10.2, for the GSTM1 and NAT2 genes, respectively). The individuals with combined GSTM1 and NAT2 defects had about a 4-fold risk of developing malignant mesothelioma compared to those with the GSTM1 gene and NAT2 fast acetylator genotype (OR = 3.6; 95% CI = 1.3–9.6). Moreover, the risk among subjects highly exposed to asbestos with the double at-risk genotype was more than 7-fold greater compared to those with the more beneficial genotypes of both GSTM1 and NAT2 genes (OR = 7.4; 95% CI = 1.6–34.0).
1 To whom requests for reprints should be addressed, at Finnish Institute of Occupational Health, Topeliuksenkatu 41 a A, FIN-00250 Helsinki, Finland.
Received 3/20/95. Accepted 6/ 2/95.
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