Tobacco smoke exposure and the risk of childhood acute lymphoblastic and myeloid leukemias by cytogenetic subtype

Catherine Metayer, Luoping Zhang, Joseph L. Wiemels, Karen Bartley, Joshua Schiffman, Xiaomei Ma, Melinda C. Aldrich, Jeffrey S. Chang, Steve Selvin, Cecilia H. Fu, Jonathan M Ducore, Martyn T. Smith, Patricia A. Buffler

Research output: Contribution to journalArticle

42 Citations (Scopus)

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 highhyperdiploidy (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 ofAMLwith 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. Impact: Parents should limit exposures to tobacco smoke before and after the child's birth.

Original languageEnglish (US)
Pages (from-to)1600-1611
Number of pages12
JournalCancer Epidemiology Biomarkers and Prevention
Volume22
Issue number9
DOIs
StatePublished - Sep 2013

Fingerprint

Precursor Cell Lymphoblastic Leukemia-Lymphoma
Acute Myeloid Leukemia
Smoke
Cytogenetics
Tobacco
Myeloid Leukemia
Smoking
Tobacco Smoke Pollution
Parturition
Aneuploidy
Confidence Intervals
Chromosomes
Chromosome Deletion
Polyploidy
B-Lymphoid Precursor Cells
Fluorescence In Situ Hybridization
Karyotype
Germ Cells
Carcinogens
B-Lymphocytes

ASJC Scopus subject areas

  • Epidemiology
  • Oncology

Cite this

Tobacco smoke exposure and the risk of childhood acute lymphoblastic and myeloid leukemias by cytogenetic subtype. / Metayer, Catherine; Zhang, Luoping; Wiemels, Joseph L.; Bartley, Karen; Schiffman, Joshua; Ma, Xiaomei; Aldrich, Melinda C.; Chang, Jeffrey S.; Selvin, Steve; Fu, Cecilia H.; Ducore, Jonathan M; Smith, Martyn T.; Buffler, Patricia A.

In: Cancer Epidemiology Biomarkers and Prevention, Vol. 22, No. 9, 09.2013, p. 1600-1611.

Research output: Contribution to journalArticle

Metayer, C, Zhang, L, Wiemels, JL, Bartley, K, Schiffman, J, Ma, X, Aldrich, MC, Chang, JS, Selvin, S, Fu, CH, Ducore, JM, Smith, MT & Buffler, PA 2013, 'Tobacco smoke exposure and the risk of childhood acute lymphoblastic and myeloid leukemias by cytogenetic subtype', Cancer Epidemiology Biomarkers and Prevention, vol. 22, no. 9, pp. 1600-1611. https://doi.org/10.1158/1055-9965.EPI-13-0350
Metayer, Catherine ; Zhang, Luoping ; Wiemels, Joseph L. ; Bartley, Karen ; Schiffman, Joshua ; Ma, Xiaomei ; Aldrich, Melinda C. ; Chang, Jeffrey S. ; Selvin, Steve ; Fu, Cecilia H. ; Ducore, Jonathan M ; Smith, Martyn T. ; Buffler, Patricia A. / Tobacco smoke exposure and the risk of childhood acute lymphoblastic and myeloid leukemias by cytogenetic subtype. In: Cancer Epidemiology Biomarkers and Prevention. 2013 ; Vol. 22, No. 9. pp. 1600-1611.
@article{9c7b317b679b4a6fa4346b37b8a4abf8,
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 highhyperdiploidy (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 ofAMLwith 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. Impact: Parents should limit exposures to tobacco smoke before and after the child's birth.",
author = "Catherine Metayer and Luoping Zhang and Wiemels, {Joseph L.} and Karen Bartley and Joshua Schiffman and Xiaomei Ma and Aldrich, {Melinda C.} and Chang, {Jeffrey S.} and Steve Selvin and Fu, {Cecilia H.} and Ducore, {Jonathan M} and Smith, {Martyn T.} and Buffler, {Patricia A.}",
year = "2013",
month = "9",
doi = "10.1158/1055-9965.EPI-13-0350",
language = "English (US)",
volume = "22",
pages = "1600--1611",
journal = "Cancer Epidemiology Biomarkers and Prevention",
issn = "1055-9965",
publisher = "American Association for Cancer Research Inc.",
number = "9",

}

TY - JOUR

T1 - Tobacco smoke exposure and the risk of childhood acute lymphoblastic and myeloid leukemias by cytogenetic subtype

AU - Metayer, Catherine

AU - Zhang, Luoping

AU - Wiemels, Joseph L.

AU - Bartley, Karen

AU - Schiffman, Joshua

AU - Ma, Xiaomei

AU - Aldrich, Melinda C.

AU - Chang, Jeffrey S.

AU - Selvin, Steve

AU - Fu, Cecilia H.

AU - Ducore, Jonathan M

AU - Smith, Martyn T.

AU - Buffler, Patricia A.

PY - 2013/9

Y1 - 2013/9

N2 - 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 highhyperdiploidy (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 ofAMLwith 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. Impact: Parents should limit exposures to tobacco smoke before and after the child's birth.

AB - 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 highhyperdiploidy (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 ofAMLwith 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. Impact: Parents should limit exposures to tobacco smoke before and after the child's birth.

UR - http://www.scopus.com/inward/record.url?scp=84884145100&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84884145100&partnerID=8YFLogxK

U2 - 10.1158/1055-9965.EPI-13-0350

DO - 10.1158/1055-9965.EPI-13-0350

M3 - Article

VL - 22

SP - 1600

EP - 1611

JO - Cancer Epidemiology Biomarkers and Prevention

JF - Cancer Epidemiology Biomarkers and Prevention

SN - 1055-9965

IS - 9

ER -