title: Tobacco smoke exposure and the risk of childhood acute lymphoblastic and myeloid leukemias by cytogenetic subtype.
abstract: BACKGROUND
  Tobacco smoke contains carcinogens known to damage somatic and germ cells. We investigated the effect of tobacco smoke on the risk of childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML), especially subtypes of prenatal origin such as ALL with translocation t(12;21) or high-hyperdiploidy (51-67 chromosomes).
  
  
  METHODS
  We collected information on exposures to tobacco smoking before conception, during pregnancy, and after birth in 767 ALL cases, 135 AML cases, and 1,139 controls (1996-2008). Among cases, chromosome translocations, deletions, or aneuploidy were identified by conventional karyotype and fluorescence in situ hybridization.
  
  
  RESULTS
  Multivariable regression analyses for ALL and AML overall showed no definite evidence of associations with self-reported (yes/no) parental prenatal active smoking and child's passive smoking. However, children with history of paternal prenatal smoking combined with postnatal passive smoking had a 1.5-fold increased risk of ALL [95% confidence interval (CI), 1.01-2.23], compared to those without smoking history (ORs for pre- or postnatal smoking only were close to one). This joint effect was seen for B-cell precursor ALL with t(12;21) (OR = 2.08; 95% CI, 1.04-4.16), but not high hyperdiploid B-cell ALL. Similarly, child's passive smoking was associated with an elevated risk of AML with chromosome structural changes (OR = 2.76; 95% CI, 1.01-7.58), but not aneuploidy.
  
  
  CONCLUSIONS
  Our data suggest that exposure to tobacco smoking was associated with increased risks of childhood ALL and AML; and risks varied by timing of exposure (before and/or after birth) and cytogenetic subtype, based on imprecise estimates.
  
  
  CONCLUSIONS
  Parents should limit exposures to tobacco smoke before and after the child's birth.
authors.affiliation: School of Public Health, University of California, 1995 University Avenue, Suite 460, Berkeley, CA94704-7392, USA. cmetayer@berkeley.edu
authors.forename: Catherine
authors.initials: C
authors.lastname: Metayer
authors.forename: Luoping
authors.initials: L
authors.lastname: Zhang
authors.forename: Joseph L
authors.initials: JL
authors.lastname: Wiemels
authors.forename: Karen
authors.initials: K
authors.lastname: Bartley
authors.forename: Joshua
authors.initials: J
authors.lastname: Schiffman
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Ma
authors.forename: Melinda C
authors.initials: MC
authors.lastname: Aldrich
authors.forename: Jeffrey S
authors.initials: JS
authors.lastname: Chang
authors.forename: Steve
authors.initials: S
authors.lastname: Selvin
authors.forename: Cecilia H
authors.initials: CH
authors.lastname: Fu
authors.forename: Jonathan
authors.initials: J
authors.lastname: Ducore
authors.forename: Martyn T
authors.initials: MT
authors.lastname: Smith
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Buffler
mesh_terms: D000293:Adolescent; D002140:California / Q000453:epidemiology; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003582:Cytogenetics; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007951:Leukemia, Myeloid / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics; D008297:Male; D015999:Multivariate Analysis; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology; D012307:Risk Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects / Q000706:statistics & numerical data*
chemical_list: D014028:Tobacco Smoke Pollution