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Could Secondhand Smoke Exposure Harm the Mental Health of Children?

Could Secondhand Smoke Exposure Harm the Mental Health of Children? More than 4 decades have passed since the first population studies showed that exposure to secondhand smoke (SHS) harmed the health of children. Since then, an ever-lengthening list of adverse effects has been causally linked to SHS. The 2006 Report of the Surgeon General provides the most recent systematic review; the adverse consequences causally linked to SHS exposure of children included sudden infant death syndrome and diverse respiratory outcomes.1 The evidence related to SHS exposure and cognitive and behavioral development was reviewed and found to be inadequate for drawing any inferences, echoing the finding of the article by Eskenazi and Castorina.2 In this issue of the Archives of Pediatrics & Adolescent Medicine, Bandiera and colleagues3 present results of analyses of the National Health and Nutrition Examination Survey data for 2001 to 2004 that show the association of SHS exposure with symptoms of mental health disorders in children and adolescents. The article describes straightforward cross-sectional analyses that use the level of serum cotinine, a major nicotine metabolite and a well-established biomarker for SHS exposure, as the exposure indicator and responses to the National Institute of Mental Health Diagnostic Interview Schedule for Children Version IV as the outcomes. Multivariate models find associations of symptoms for several mental health outcomes with SHS exposure—major depressive disorder, generalized anxiety disorder, attention-deficit/hyperactivity disorder, and conduct disorder. The authors also point to variation in the strength of these associations by race/ethnicity and sex, although they did not formally test for interactions. The limitations of the analyses are clear and acknowledged: the cross-sectional nature of the data, misclassification of exposure and outcomes, and the potential for confounding as well as misspecification of underlying causal pathways. Setting aside these limitations, a key question is the plausibility of a causal association of SHS with this spectrum of symptoms. The just-published Surgeon General's Report, How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease,4 provides only indirectly relevant information. The report links maternal smoking during pregnancy to effects on the developing brain and concludes that carbon monoxide may play a role in neurological deficits in the children of smokers. In animal models, fetal exposure to nicotine is damaging to the developing brain.5 The perinatal period also represents a vulnerable window for exposure to nicotine.6 One animal model showed that high levels of SHS exposure affect indicators of brain development.7 The plausibility of associations of SHS exposure with multiple outcomes also needs to be considered; could exposure to SHS increase the risk of mental health outcomes that may not share a common pathogenesis? A further complication comes from the difficulty of separating consequences of postnatal exposure to SHS from those of maternal smoking during pregnancy. To date, there has been little parallel research; thus, the findings of this new study cannot be placed into a larger body of literature to gauge consistency with results of other studies. An analysis of the same data set, but using the outcome of parent report of diagnosed attention-deficit/hyperactivity disorder, found an association with serum cotinine level.8 In 220 children enrolled in an asthma intervention trial, SHS exposure, also assessed with cotinine, was associated with behavioral9 and sleep problems.10 In another study of children with asthma, cotinine level was associated with behavior problems, as assessed by the Behavior Problem Index.11 The total body of evidence is limited. Consequently, the provocative findings of Bandiera et al3 need replication and an expanded foundation of mechanistic understanding. Further research on exposure to SHS might also provide insights into neurodevelopmental effects of inhaled pollutants, a topic of rising interest.12,13 While cross-sectional studies can be most readily conducted, longitudinal data are needed to bolster arguments for potential causality, to separately assess maternal smoking during pregnancy and SHS exposure after pregnancy, and to characterize the relationship between exposure at various ages and risk. Such studies cannot be readily conducted, as they need to be sufficiently large and incorporate accurate exposure assessment and outcome determination. Perhaps some existing cohorts might be used for this purpose, particularly if SHS exposure has been prospectively assessed. In decades to come, the National Children's Study should prove informative. While further research is warranted in follow-up of the findings of Bandiera et al,3 the evidence on SHS exposure and infant and child health has long been sufficient to mandate reduction of SHS exposure. Without consideration of possible links to behavioral disorders and mental health, the global burden of disease attributable to SHS exposure is substantial.14 In many countries, progress is being made in reducing exposure to SHS, particularly with the impetus provided by the World Health Organization's Framework Convention on Tobacco Control (FCTC).15 However, smoking bans are enacted for public places and workplaces, not covering homes, the principal locus of exposure for children. Fortunately, in the United States, most households with a smoker now have a policy in place that is intended to reduce exposure.1 Unfortunately, such policies are not prevalent elsewhere, particularly in low- and middle-income countries.16 Because smoke-free homes cannot be mandated, education of parents is central to protect children from SHS exposure; health care providers should motivate parents to protect their children, beginning with prenatal care and continuing during childhood.17,18 Pediatricians and other health care providers can help eliminate exposure of infants and children to SHS, even while the evidence on mental health continues to evolve. Correspondence: Dr Samet, Department of Preventive Medicine, University of Southern California, 1441 Eastlake Ave, Room 4436, Los Angeles, CA 90089 (jsamet@usc.edu). Financial Disclosure: None reported. References 1. U.S. Department of Health and Human Services, The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta, GA US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health2006; 2. Eskenazi BCastorina R Association of prenatal maternal or postnatal child environmental tobacco smoke exposure and neurodevelopmental and behavioral problems in children. Environ Health Perspect 1999;107 (12) 991- 1000PubMedGoogle Scholar 3. Bandiera FCRichardson AKLee DJHe J-PMerikangas KR Secondhand smoke exposure and mental health among children and adolescents. Arch Pediatr Adolesc Med 2011;165 (4) 332- 338Google Scholar 4. U.S. Department of Health and Human Services, How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Atlanta, GA US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health2010; 5. Slotkin TA Fetal nicotine or cocaine exposure: which one is worse? J Pharmacol Exp Ther 1998;285 (3) 931- 945PubMedGoogle Scholar 6. Slotkin TA Cholinergic systems in brain development and disruption by neurotoxicants: nicotine, environmental tobacco smoke, organophosphates. Toxicol Appl Pharmacol 2004;198 (2) 132- 151PubMedGoogle Scholar 7. Gospe SM JrZhou SSPinkerton KE Effects of environmental tobacco smoke exposure in utero and/or postnatally on brain development. Pediatr Res 1996;39 (3) 494- 498PubMedGoogle Scholar 8. Xu XCook RLIlacqua VAKan HTalbott EO Racial differences in the effects of postnatal environmental tobacco smoke on neurodevelopment. Pediatrics 2010;126 (4) 705- 711PubMedGoogle Scholar 9. Yolton KKhoury JHornung RDietrich KSuccop PLanphear B Environmental tobacco smoke exposure and child behaviors. J Dev Behav Pediatr 2008;29 (6) 450- 457PubMedGoogle Scholar 10. Yolton KXu YKhoury J et al. Associations between secondhand smoke exposure and sleep patterns in children. Pediatrics 2010;125 (2) e261- e268PubMedGoogle Scholar 11. Fagnano MConn KMHalterman JS Environmental tobacco smoke and behaviors of inner-city children with asthma. Ambul Pediatr 2008;8 (5) 288- 293PubMedGoogle Scholar 12. Volk HEHertz-Picciotto IDelwiche LLurmann F McConnell R Residential proximity to freeways and autism in the CHARGE study [published online December 13, 2010]. Environ Health Perspect PubMed10.1289/ehp.1002835Google Scholar 13. Kalkbrenner AEDaniels JLChen JCPoole CEmch MMorrissey J Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8. Epidemiology 2010;21 (5) 631- 641PubMedGoogle Scholar 14. Oberg MJaakkola MSWoodward APeruga APrüss-Ustün A Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries. Lancet 2011;377 (9760) 139- 146PubMedGoogle Scholar 15. Samet JMWipfli HL Globe still in grip of addiction. Nature 2010;463 (7284) 1020- 1021PubMedGoogle Scholar 16. Wipfli HAvila-Tang ENavas-Acien A et al. Famri Homes Study Investigators, Secondhand smoke exposure among women and children: evidence from 31 countries. Am J Public Health 2008;98 (4) 672- 679PubMedGoogle Scholar 17. Hawthorne MAHannan LMThun MJSamet JM Protecting our Children From Second-hand Smoke. >Geneva, Switzerland International Union Against Cancer2008; 18. Committee on Environmental Health, Committee on Substance Abuse, Committee on Adolescence, and Committee on Native American Child Health, From the American Academy of Pediatrics: policy statement—tobacco use: a pediatric disease. Pediatrics 2009;124 (5) 1474- 1487PubMedGoogle Scholar http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Pediatrics & Adolescent Medicine American Medical Association

Could Secondhand Smoke Exposure Harm the Mental Health of Children?

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Publisher
American Medical Association
Copyright
Copyright © 2011 American Medical Association. All Rights Reserved.
ISSN
1072-4710
eISSN
1538-3628
DOI
10.1001/archpediatrics.2011.21
Publisher site
See Article on Publisher Site

Abstract

More than 4 decades have passed since the first population studies showed that exposure to secondhand smoke (SHS) harmed the health of children. Since then, an ever-lengthening list of adverse effects has been causally linked to SHS. The 2006 Report of the Surgeon General provides the most recent systematic review; the adverse consequences causally linked to SHS exposure of children included sudden infant death syndrome and diverse respiratory outcomes.1 The evidence related to SHS exposure and cognitive and behavioral development was reviewed and found to be inadequate for drawing any inferences, echoing the finding of the article by Eskenazi and Castorina.2 In this issue of the Archives of Pediatrics & Adolescent Medicine, Bandiera and colleagues3 present results of analyses of the National Health and Nutrition Examination Survey data for 2001 to 2004 that show the association of SHS exposure with symptoms of mental health disorders in children and adolescents. The article describes straightforward cross-sectional analyses that use the level of serum cotinine, a major nicotine metabolite and a well-established biomarker for SHS exposure, as the exposure indicator and responses to the National Institute of Mental Health Diagnostic Interview Schedule for Children Version IV as the outcomes. Multivariate models find associations of symptoms for several mental health outcomes with SHS exposure—major depressive disorder, generalized anxiety disorder, attention-deficit/hyperactivity disorder, and conduct disorder. The authors also point to variation in the strength of these associations by race/ethnicity and sex, although they did not formally test for interactions. The limitations of the analyses are clear and acknowledged: the cross-sectional nature of the data, misclassification of exposure and outcomes, and the potential for confounding as well as misspecification of underlying causal pathways. Setting aside these limitations, a key question is the plausibility of a causal association of SHS with this spectrum of symptoms. The just-published Surgeon General's Report, How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease,4 provides only indirectly relevant information. The report links maternal smoking during pregnancy to effects on the developing brain and concludes that carbon monoxide may play a role in neurological deficits in the children of smokers. In animal models, fetal exposure to nicotine is damaging to the developing brain.5 The perinatal period also represents a vulnerable window for exposure to nicotine.6 One animal model showed that high levels of SHS exposure affect indicators of brain development.7 The plausibility of associations of SHS exposure with multiple outcomes also needs to be considered; could exposure to SHS increase the risk of mental health outcomes that may not share a common pathogenesis? A further complication comes from the difficulty of separating consequences of postnatal exposure to SHS from those of maternal smoking during pregnancy. To date, there has been little parallel research; thus, the findings of this new study cannot be placed into a larger body of literature to gauge consistency with results of other studies. An analysis of the same data set, but using the outcome of parent report of diagnosed attention-deficit/hyperactivity disorder, found an association with serum cotinine level.8 In 220 children enrolled in an asthma intervention trial, SHS exposure, also assessed with cotinine, was associated with behavioral9 and sleep problems.10 In another study of children with asthma, cotinine level was associated with behavior problems, as assessed by the Behavior Problem Index.11 The total body of evidence is limited. Consequently, the provocative findings of Bandiera et al3 need replication and an expanded foundation of mechanistic understanding. Further research on exposure to SHS might also provide insights into neurodevelopmental effects of inhaled pollutants, a topic of rising interest.12,13 While cross-sectional studies can be most readily conducted, longitudinal data are needed to bolster arguments for potential causality, to separately assess maternal smoking during pregnancy and SHS exposure after pregnancy, and to characterize the relationship between exposure at various ages and risk. Such studies cannot be readily conducted, as they need to be sufficiently large and incorporate accurate exposure assessment and outcome determination. Perhaps some existing cohorts might be used for this purpose, particularly if SHS exposure has been prospectively assessed. In decades to come, the National Children's Study should prove informative. While further research is warranted in follow-up of the findings of Bandiera et al,3 the evidence on SHS exposure and infant and child health has long been sufficient to mandate reduction of SHS exposure. Without consideration of possible links to behavioral disorders and mental health, the global burden of disease attributable to SHS exposure is substantial.14 In many countries, progress is being made in reducing exposure to SHS, particularly with the impetus provided by the World Health Organization's Framework Convention on Tobacco Control (FCTC).15 However, smoking bans are enacted for public places and workplaces, not covering homes, the principal locus of exposure for children. Fortunately, in the United States, most households with a smoker now have a policy in place that is intended to reduce exposure.1 Unfortunately, such policies are not prevalent elsewhere, particularly in low- and middle-income countries.16 Because smoke-free homes cannot be mandated, education of parents is central to protect children from SHS exposure; health care providers should motivate parents to protect their children, beginning with prenatal care and continuing during childhood.17,18 Pediatricians and other health care providers can help eliminate exposure of infants and children to SHS, even while the evidence on mental health continues to evolve. Correspondence: Dr Samet, Department of Preventive Medicine, University of Southern California, 1441 Eastlake Ave, Room 4436, Los Angeles, CA 90089 (jsamet@usc.edu). Financial Disclosure: None reported. References 1. U.S. Department of Health and Human Services, The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta, GA US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health2006; 2. Eskenazi BCastorina R Association of prenatal maternal or postnatal child environmental tobacco smoke exposure and neurodevelopmental and behavioral problems in children. Environ Health Perspect 1999;107 (12) 991- 1000PubMedGoogle Scholar 3. Bandiera FCRichardson AKLee DJHe J-PMerikangas KR Secondhand smoke exposure and mental health among children and adolescents. Arch Pediatr Adolesc Med 2011;165 (4) 332- 338Google Scholar 4. U.S. Department of Health and Human Services, How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Atlanta, GA US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health2010; 5. Slotkin TA Fetal nicotine or cocaine exposure: which one is worse? J Pharmacol Exp Ther 1998;285 (3) 931- 945PubMedGoogle Scholar 6. Slotkin TA Cholinergic systems in brain development and disruption by neurotoxicants: nicotine, environmental tobacco smoke, organophosphates. Toxicol Appl Pharmacol 2004;198 (2) 132- 151PubMedGoogle Scholar 7. Gospe SM JrZhou SSPinkerton KE Effects of environmental tobacco smoke exposure in utero and/or postnatally on brain development. Pediatr Res 1996;39 (3) 494- 498PubMedGoogle Scholar 8. Xu XCook RLIlacqua VAKan HTalbott EO Racial differences in the effects of postnatal environmental tobacco smoke on neurodevelopment. Pediatrics 2010;126 (4) 705- 711PubMedGoogle Scholar 9. Yolton KKhoury JHornung RDietrich KSuccop PLanphear B Environmental tobacco smoke exposure and child behaviors. J Dev Behav Pediatr 2008;29 (6) 450- 457PubMedGoogle Scholar 10. Yolton KXu YKhoury J et al. Associations between secondhand smoke exposure and sleep patterns in children. Pediatrics 2010;125 (2) e261- e268PubMedGoogle Scholar 11. Fagnano MConn KMHalterman JS Environmental tobacco smoke and behaviors of inner-city children with asthma. Ambul Pediatr 2008;8 (5) 288- 293PubMedGoogle Scholar 12. Volk HEHertz-Picciotto IDelwiche LLurmann F McConnell R Residential proximity to freeways and autism in the CHARGE study [published online December 13, 2010]. Environ Health Perspect PubMed10.1289/ehp.1002835Google Scholar 13. Kalkbrenner AEDaniels JLChen JCPoole CEmch MMorrissey J Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8. Epidemiology 2010;21 (5) 631- 641PubMedGoogle Scholar 14. Oberg MJaakkola MSWoodward APeruga APrüss-Ustün A Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries. Lancet 2011;377 (9760) 139- 146PubMedGoogle Scholar 15. Samet JMWipfli HL Globe still in grip of addiction. Nature 2010;463 (7284) 1020- 1021PubMedGoogle Scholar 16. Wipfli HAvila-Tang ENavas-Acien A et al. Famri Homes Study Investigators, Secondhand smoke exposure among women and children: evidence from 31 countries. Am J Public Health 2008;98 (4) 672- 679PubMedGoogle Scholar 17. Hawthorne MAHannan LMThun MJSamet JM Protecting our Children From Second-hand Smoke. >Geneva, Switzerland International Union Against Cancer2008; 18. Committee on Environmental Health, Committee on Substance Abuse, Committee on Adolescence, and Committee on Native American Child Health, From the American Academy of Pediatrics: policy statement—tobacco use: a pediatric disease. Pediatrics 2009;124 (5) 1474- 1487PubMedGoogle Scholar

Journal

Archives of Pediatrics & Adolescent MedicineAmerican Medical Association

Published: Apr 4, 2011

Keywords: passive smoking,child,mental health

References

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