Tobacco smoke and risk of childhood acute lymphoblastic leukemia: findings from the SETIL case–control study View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2014-04-04

AUTHORS

Andrea Farioli, Patrizia Legittimo, Stefano Mattioli, Lucia Miligi, Alessandra Benvenuti, Alessandra Ranucci, Alberto Salvan, Roberto Rondelli, Valentino Conter, Corrado Magnani

ABSTRACT

Purpose Tobacco smoke could cause childhood acute lymphoblastic leukemia (ALL) through at least three pathways: (1) prenatal parental smoking; (2) fetal exposure through maternal smoking during pregnancy; and (3) childhood exposure to secondhand smoke (SHS). We tested these hypotheses in a large population-based case–control study (SETIL) primarily designed to evaluate the role of electromagnetic fields in childhood hematopoietic malignancies.MethodsFrom 1998 to 2003, we enrolled 602 incident cases of ALL from 14 Italian Regions, and 918 controls were individually matched by birthdate, sex, and area of residence. Cases (n = 557) and controls (n = 855) with complete information were analyzed; odds ratios (OR) and 95 % confidence intervals (95 % CI) were estimated with logistic regression models conditioned on matching variables and adjusted by birth order, birthweight, duration of breastfeeding, parental age at delivery, education, and occupational exposure to benzene.ResultsNo evidence associating paternal smoking in the conception period or maternal smoking during the pregnancy with ALL was found. An association of ALL with maternal exposure to SHS during pregnancy (adjusted OR for mothers exposed more than 4 h/day = 2.18, 95 % CI 1.39–3.42) was observed, but recall bias cannot be excluded. Exposure of the children to SHS was associated with ALL only in unadjusted analysis (unadjusted OR for highly exposed children = 1.64; 95 % CI 1.10–2.45).ConclusionsThis study does not support the hypothesis that parental active smoking is associated with ALL. We found very weak evidence of increased risk of ALL for children exposed to SHS. Maternal exposure to SHS was associated with ALL, but recall bias is likely to inflate our estimates. More... »

PAGES

683-692

References to SciGraph publications

  • 2009. Parental Smoking and Childhood Leukemia in CANCER EPIDEMIOLOGY
  • 2006-02-09. Infection, immune responses and the aetiology of childhood leukaemia in NATURE REVIEWS CANCER
  • 2002-01-31. Breast-feeding, fetal loss and childhood acute leukaemia in EUROPEAN JOURNAL OF PEDIATRICS
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s10552-014-0371-9

    DOI

    http://dx.doi.org/10.1007/s10552-014-0371-9

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1038765333

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/24699944


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    23 schema:description Purpose Tobacco smoke could cause childhood acute lymphoblastic leukemia (ALL) through at least three pathways: (1) prenatal parental smoking; (2) fetal exposure through maternal smoking during pregnancy; and (3) childhood exposure to secondhand smoke (SHS). We tested these hypotheses in a large population-based case–control study (SETIL) primarily designed to evaluate the role of electromagnetic fields in childhood hematopoietic malignancies.MethodsFrom 1998 to 2003, we enrolled 602 incident cases of ALL from 14 Italian Regions, and 918 controls were individually matched by birthdate, sex, and area of residence. Cases (n = 557) and controls (n = 855) with complete information were analyzed; odds ratios (OR) and 95 % confidence intervals (95 % CI) were estimated with logistic regression models conditioned on matching variables and adjusted by birth order, birthweight, duration of breastfeeding, parental age at delivery, education, and occupational exposure to benzene.ResultsNo evidence associating paternal smoking in the conception period or maternal smoking during the pregnancy with ALL was found. An association of ALL with maternal exposure to SHS during pregnancy (adjusted OR for mothers exposed more than 4 h/day = 2.18, 95 % CI 1.39–3.42) was observed, but recall bias cannot be excluded. Exposure of the children to SHS was associated with ALL only in unadjusted analysis (unadjusted OR for highly exposed children = 1.64; 95 % CI 1.10–2.45).ConclusionsThis study does not support the hypothesis that parental active smoking is associated with ALL. We found very weak evidence of increased risk of ALL for children exposed to SHS. Maternal exposure to SHS was associated with ALL, but recall bias is likely to inflate our estimates.
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