Paternal smoking, genetic polymorphisms in CYP1A1 and childhood leukemia risk

We conducted a case-control study to evaluate the association between paternal smoking and childhood leukemia and to evaluate potential modification by polymorphisms in CYP1A1. Histologically confirmed childhood leukemia cases (n = 164) and non-cancer controls (n = 164) were recruited front three teaching, hospitals in Seoul. Korea. Five single nucleotide polymorphisms in CYP1A1 (-17961T>C. -9893G>A. 1462V. 1188C>T (*2A), and 11599C>G) were genotyped and haplotypes were estimated by the expectation-maximization method. We also conducted a meta-analysis of 12 studies that have reported the association between paternal smoking and childhood leukemia risk. Paternal smoking at home was associated with all leukemias (OR = 1.8. 95% CI = 1.1-2.8) and acute lymphoblastic leukemia (ALL) (2.0, 1.2-3.4). Ail increasing trend in risk was observed for pack-years smoked after birth (P-trend = 0.06 and 0.02, respectively) and the number of smokers in the home during, the child's life (P-trend =0.05 and 0.03. respectively). Among those without the CGACC haplotype, ALL risk was significantly increased by the father's smoking at home (2.8. 1.5-5.3) and the presence of at least one smoker in the home (2.3, 1.2-4.4). and the test for interaction was significant (P-interaction = 0.03 and 0.02, respectively). The meta-analysis showed that overall paternal smoking (1.13. 1.04-1.24) and smoking before the pregnancy of the child (1.12, 1.04-1.21) were significantly associated with childhood leukemia risk. Our results suggest that paternal smoking is a risk factor for childhood leukemia and the effect may be modified by CYP1A1 genotype. (C) 2008 Elsevier Ltd. All rights reserved.