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Excerpt
Joint Departments of Epidemiology and Biostatistics, and Occupational Health, Faculty of Medicine, McGill University; Research Center, Hôpital Sainte-Justine; and Department of Pediatrics, Université de Montréal, Montréal, Québec, Canada
Epidemiology 2002;13:277–281
Although alcohol metabolism produces reactive oxygen species that conceivably might promote carcinogenesis, little is known of the association, if any, between parental alcohol use before and during pregnancy and the risk of childhood leukemia. The potential role of genetic polymorphisms, such as those associated with genes of the glutathione-S-transferase (GST) gene family, also remains an open question. The authors report a population-based, case-control study of 491 incident cases of acute lymphoblastic leukemia (ALL) in children aged 9 years or younger, matched for age and gender with healthy control subjects. Parents were interviewed separately by telephone about their alcohol consumption. In 186 cases, interaction odds ratios between prenatal exposure and child DNA variants in the GSTM1 and CYP2E1 genes, the latter a cytochrome P450 gene, were estimated.
ALL was inversely related to maternal alcohol consumption before or during pregnancy; the adjusted odds ratio for any alcohol consumption during pregnancy was 0.7. Comparable results were obtained when wine and beer drinking (but not spirits) were considered separately. The odds ratio for drinking wine or beer at any time was 0.6, and that for consumption during pregnancy was 0.7. This inverse relationship was most evident with small amounts of alcohol intake. The effect was strongest in subjects who drank only during pregnancy. The interaction odds ratio for the GSTM1 null genotype during late pregnancy was 2.4, and that for CYP2E1 variant G-1295C (allele *5) during the time of nursing was 4.9. The risk associated with any type of alcohol exposure increased with the dose.
These findings, suggesting that maternal alcohol consumption during pregnancy and nursing might protect against ALL, could reflect the potential chemopreventive effects of flavonoids present in wine and beer. More data are needed, but it seems possible that these effects of alcohol are at least in part genetically determined. Variant polymorphisms of genes that metabolize carcinogens might alter the risk associated with prenatal alcohol exposure.
