C Infante-Rivard1, M Krajinovic, D Labuda, D Sinnett. 1. Joint Department of Epidemiology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada. cirivard@epid.lan.mcgill.ca
Abstract
OBJECTIVE: To evaluate the effect of parental smoking on childhood acute lymphoblastic leukemia and to determine if it is modified by child genetic polymorphisms. METHODS: We carried out a case-control study in Quebec, Canada, including 491 incident cases aged 0-9 years and as many healthy controls matched on age and sex. Each parent was interviewed separately with respect to smoking habits during and after pregnancy. In addition, we carried out a case-only substudy with 158 cases classified according to presence or absence of the alleles *2A, *2B, and *4 in the CYP1A1 gene. RESULTS: There were small risk increases with maternal smoking during the later trimesters. Interaction odds ratios were increased (although often not significantly) for the CYP1A1*4 allele at high levels of maternal smoking in the last trimesters and at low level of paternal postnatal smoking, and decreased for the CYP1A1*2B allele. The latter appeared to confer a protective advantage at low levels for maternal prenatal smoking and at high levels for paternal postnatal smoking. CONCLUSIONS: Reported smoking habits showed no association with leukemia; risks for genetic polymorphisms lacked precision but indicated that the effect of parental smoking could be modified by variant alleles in the CYP1A1 gene.
OBJECTIVE: To evaluate the effect of parental smoking on childhood acute lymphoblastic leukemia and to determine if it is modified by child genetic polymorphisms. METHODS: We carried out a case-control study in Quebec, Canada, including 491 incident cases aged 0-9 years and as many healthy controls matched on age and sex. Each parent was interviewed separately with respect to smoking habits during and after pregnancy. In addition, we carried out a case-only substudy with 158 cases classified according to presence or absence of the alleles *2A, *2B, and *4 in the CYP1A1 gene. RESULTS: There were small risk increases with maternal smoking during the later trimesters. Interaction odds ratios were increased (although often not significantly) for the CYP1A1*4 allele at high levels of maternal smoking in the last trimesters and at low level of paternal postnatal smoking, and decreased for the CYP1A1*2B allele. The latter appeared to confer a protective advantage at low levels for maternal prenatal smoking and at high levels for paternal postnatal smoking. CONCLUSIONS: Reported smoking habits showed no association with leukemia; risks for genetic polymorphisms lacked precision but indicated that the effect of parental smoking could be modified by variant alleles in the CYP1A1 gene.
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Authors: Catherine Metayer; Elizabeth Milne; Jacqueline Clavel; Claire Infante-Rivard; Eleni Petridou; Malcolm Taylor; Joachim Schüz; Logan G Spector; John D Dockerty; Corrado Magnani; Maria S Pombo-de-Oliveira; Daniel Sinnett; Michael Murphy; Eve Roman; Patricia Monge; Sameera Ezzat; Beth A Mueller; Michael E Scheurer; Bruce K Armstrong; Jill Birch; Peter Kaatsch; Sergio Koifman; Tracy Lightfoot; Parveen Bhatti; Melissa L Bondy; Jérémie Rudant; Kate O'Neill; Lucia Miligi; Nick Dessypris; Alice Y Kang; Patricia A Buffler Journal: Cancer Epidemiol Date: 2013-02-09 Impact factor: 2.984