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School of Medicine, University of Southern California, Los Angeles, California 90089 [J. D. B., R. S., D. H. G., P. M., J. M. P., G. D. H.]; Department of Pediatrics, University of Minnesota, Duluth, Minnesota 55812 [L. L. R., M. E. N., W. G. W.]; Joint Section of Hematology/Oncology, University of Chicago, Chicago, Illinois 60637 [M. L.]; and Department of Hematology-Oncology, University of Colorado, Colorado Springs, Colorado 80933 [L. O.]
The Childrens Cancer Study Group conducted a case-control study of occupational exposures of parents of 204 children (under 18 yr of age) with acute nonlymphoblastic leukemia. The most consistent finding was an association of acute nonlymphoblastic leukemia risk with pesticide exposure. Controls matched by date of birth and race were obtained through random digit dialing. Odds ratio (OR) for paternal pesticide exposure in jobs held for longer than 1000 days was 2.7 (95% confidence interval, 1.0 to 7.0; trend, P = 0.06), and seven case mothers and no control mothers had prolonged exposure (trend, P = 0.008). Risk estimates for parental pesticide exposure were substantally incrased for children under age 6 at diagnosis (OR for prolonged exposure to either parent = 11.4; trend, P = 0.003) and for those with myelomonocytic and monocytic subtypes (OR, 13.6; trend, P = 0.007). Moreover, there were significantly elevated risks for direct exposure of the child to pesticides in the household (OR for exposure most days = 3.5; trend, P = 0.04) and for maternal exposure to household pesticides at the time of pregnancy (eight case mothers versus no controls for exposure most days; trend, P = 0.05). Paternal exposures to solvents (OR, 2.1; P = 0.003) and petroleum products (OR, 2.4; P = 0.002) were reported more commonly for cases than controls. Other occupational exposures reported significantly more often by case parents were paternal exposure to plastics or lead and maternal exposure to paints and pigments, metal dusts, and sawdust. These data provide further evidence for a role of occupational risk factors in the etiology of childhood cancer.
1 Support for this study was provided by a grant from the NIH (CA35314), the University of Minnesota's Children's Cancer Research Fund, and an American Cancer Society Institutional Award (IN-13-V62). Contributing Childrens Cancer Study Group investigators, institutions, and grant numbers are given in the "Appendix." Grant support from the Division of Cancer Treatment, National Cancer Institute, NIH, Department of Health and Human Services.
2 To whom (Childrens Cancer Study Group) requests for reprints should be addressed, at 199 North Lake Avenue, Third Floor, Pasadena, CA 91101.
3 Supported in part by a Research Caneer Development Award from the NIH.
4 Recipient of a fellowship award from the Leukemia Society of America.
5 Recipient of a Special Fellow Award from the Leukemia Society of America.
Received 9/28/88. Revised 2/17/89. Accepted 4/13/89.
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