title: Paternal smoking, genetic polymorphisms in CYP1A1 and childhood leukemia risk.
abstract: 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 from three teaching hospitals in Seoul, Korea. Five single nucleotide polymorphisms in CYP1A1 (-17961T>C, -9893G>A, I462V, 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). An 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.
authors.affiliation: Department of Preventive Medicine, Cancer Research Institute, Seoul National University College of Medicine, 28 Yongon-Dong Chongno-Gu, Seoul, Republic of Korea.
authors.forename: Kyoung-Mu
authors.initials: KM
authors.lastname: Lee
authors.forename: Mary H
authors.initials: MH
authors.lastname: Ward
authors.forename: Sohee
authors.initials: S
authors.lastname: Han
authors.forename: Hyo Seop
authors.initials: HS
authors.lastname: Ahn
authors.forename: Hyoung Jin
authors.initials: HJ
authors.lastname: Kang
authors.forename: Hyung Soo
authors.initials: HS
authors.lastname: Choi
authors.forename: Hee Young
authors.initials: HY
authors.lastname: Shin
authors.forename: Hong-Hoe
authors.initials: HH
authors.lastname: Koo
authors.forename: Jong-Jin
authors.initials: JJ
authors.lastname: Seo
authors.forename: Ji-Eun
authors.initials: JE
authors.lastname: Choi
authors.forename: Yoon-Ok
authors.initials: YO
authors.lastname: Ahn
authors.forename: Daehee
authors.initials: D
authors.lastname: Kang
mesh_terms: D000293:Adolescent; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics*; D004781:Environmental Exposure; D005220:Fathers; D005260:Female; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D007223:Infant; D007938:Leukemia / Q000209:etiology*; D008297:Male; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*
chemical_list: D019363:Cytochrome P-450 CYP1A1