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标题：Secondhand Tobacco Smoke: A Source of Lead Exposure in US Children and Adolescents
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作者：Andria Apostolou ; Esther Garcia-Esquinas ; Jeffrey J. Fadrowski 等
期刊名称：American journal of public health
印刷版ISSN：0090-0036
出版年度：2012
卷号：102
期号：4
页码：714-722
DOI：10.2105/AJPH.2011.300161
语种：English
出版社：American Public Health Association
摘要：Objectives. We evaluated the relationship between secondhand tobacco smoke (SHS) exposure and blood lead levels in US children and adolescents. Methods. We analyzed data from 6830 participants aged 3–19 years in the National Health and Nutrition Examination Survey (1999–2004) who were not active smokers and for whom SHS exposure information and blood lead measurements were available. Results. After multivariable adjustment, participants in the highest quartile of serum cotinine (≥ 0.44 μg/L) had 28% (95% confidence interval = 21%, 36%) higher blood lead levels than had those in the lowest quartile (< 0.03 μg/L). Similarly, blood lead levels were 14% and 24% higher in children who lived with 1 or with 2 or more smokers, respectively, than they were in children living with no smokers. Among participants for whom lead dust information was available, the associations between SHS and blood lead levels were similar before and after adjustment for lead dust concentrations. Conclusions. SHS may contribute to increased blood lead levels in US children. Lead dust does not appear to mediate this association, suggesting inhalation as a major pathway of exposure. Eliminating SHS exposure could reduce lead exposure in children. Secondhand tobacco smoke (SHS) remains a major source of indoor air pollution worldwide,^{1 – 3} causing major health effects in children, including sudden infant death syndrome, lower respiratory tract infections, reduced lung growth,¹ and behavioral problems.^{4 – 6} In the United States, around 1 in 5 children aged 3 to 11 years live with at least 1 individual who smokes.^{1 , 7} Globally, the burden of SHS exposure during childhood is even higher.^{3 , 8} Lead, a major neurocognitive and kidney toxicant for children at relatively low levels,⁹ is a tobacco constituent that is measured in mainstream smoke (exhaled by the smoker) and sidestream smoke (from the burning cigarette), including the gas phase.^{10 – 13} During the period 1988 to 1994, US children exposed to SHS showed increased blood lead levels.¹⁴ National and local childhood lead poisoning prevention programs identify and follow children at risk for elevated blood lead levels (≥ 10 μg/dL) by collecting data on age of housing, occupancy status (rental or owner occupied), dwelling type, lead paint hazards (including lead in paint, dust, and soil), drinking water source, and industrial point sources near the home.^{15 – 17} Information on SHS, a potentially preventable source of lead exposure, is generally not considered. Our goal was to evaluate the relationship between SHS exposure (identified by the number of smokers at home and by levels of serum cotinine, a biomarker of recent tobacco smoke exposure that integrates active and passive exposure, including exposure in the home, vehicles, and public places) and blood lead levels in US children aged 3 to 19 years who participated in the National Health and Nutrition Examination Survey (NHANES; 1999–2004). NHANES measured lead dust concentrations in the windows and floors of the homes of children aged 3 to 5 years. Because SHS may increase levels of home lead dust,¹⁸ we evaluated the potential mediation of lead dust concentrations in the association between SHS and blood lead levels in children aged 3 to 5.