Cancer Epidemiology, Biomarkers & Prevention
Tobacco smoke exposure and the risk of childhood acute lymphoblastic and myeloid leukemias by cytogenetic subtype
Metayer C et al.
Abstract
Background: Tobacco smoke contains carcinogens known to damage somatic
and germ cells. We investigated the effect tobacco smoke on the risk of
childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML),
especially subtypes of pre-natal origin like 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% 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 before were 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. Impact: Parents should limit exposures to tobacco smoke
before and after the child's birth.