文章基本信息

标题：Biomarker Evidence of Tobacco Smoke Exposure in Children Participating in Lead Screening
本地全文：下载
作者：Anne Joseph ; Logan Spector ; Katherine Wickham 等
期刊名称：American journal of public health
印刷版ISSN：0090-0036
出版年度：2013
卷号：103
期号：12
页码：e54-e59
DOI：10.2105/AJPH.2013.301315
语种：English
出版社：American Public Health Association
摘要：Objectives. We assessed tobacco smoke exposure (TSE), defined according to detection of cotinine, in dried blood spots collected from children for lead screening. Methods. Dried blood spots collected from a national sample of 1541 Black and White children and submitted to a commercial laboratory for lead analysis were analyzed for cotinine. We used an anonymous administrative data set including information on children's characteristics to conduct univariate and multivariate analyses. Results. Cotinine was detected in 61% of dried blood spots; 17% of samples had cotinine levels above 3 nanograms per gram. Median cotinine levels were significantly higher among Black than White children (0.66 ng/g vs 0.30 ng/g) and among Medicaid recipients (0.94 ng/g vs < 0.3 ng/g). In multivariate analyses, significant increases in cotinine levels were associated with Black (vs White) race, older age, Medicaid coverage, higher state smoking rate, and higher average winter temperature. Detectable cotinine levels were significantly associated with higher lead levels. Conclusions. TSE is highly prevalent among children undergoing lead screening, and exposure levels are greater among Black children and children on Medicaid. TSE may contribute to lead exposure. Concurrent lead screening and biological screening for TSE may be a feasible approach to increasing childhood TSE detection. Tobacco smoke exposure (TSE) is responsible for an estimated 60 000 deaths per year among nonsmokers, 1 including more than 5000 deaths in children (3 times the number of deaths from all childhood cancers combined). 2,3 Notably, levels of cotinine—a metabolite of nicotine and a well-established biomarker of TSE levels—are highest in the youngest children and those below the poverty level. 4 Screening for TSE is recommended at all pediatric visits 5 because of its important health consequences. 6,7 Although parent reports suggest that 24% of children are exposed to tobacco smoke, data from the National Health and Nutrition Examination Survey (NHANES) show a much higher rate: in 2008, 54% of children aged 3 to 11 years were exposed to TSE, determined by the presence of cotinine in urine or blood. 8,9 Parents may underreport childhood TSE because of lack of awareness, social desirability bias, or fear of consequences. 9 Requirements for parents to disclose their child’s TSE are an important barrier to delivering interventions to help parents quit smoking and implement smoke-free policies for the home and car. Extant childhood screening programs for lead—another environmental toxin—provide an obvious yet currently untapped opportunity to detect TSE by measuring biomarkers of tobacco exposure in children at well-child visits. The Centers for Disease Control and Prevention and the American Academy of Pediatrics recommend that all US children have blood lead concentrations measured at 1 and 2 years of age. Lead screening is a requirement for all Medicaid-eligible children and is now performed routinely in both high- and low-risk groups. 10–12 Because health care providers already screen children for lead exposure as part of their routine practice, 10 a similar tactic of measuring cotinine in children might institutionalize management of TSE in a comparable fashion. The detrimental health effects of lead exposure 10 and TSE 6 have been well described. Childhood exposure to these toxins is highly prevalent, and the likelihood of exposure is more common in children of lower socioeconomic status. 6,10 No studies of which we are aware have demonstrated the feasibility of large-scale biological screening for TSE in very young children. We assessed rates of TSE (determined according to detection of cotinine) from an analysis of dried blood spots collected for lead screening from very young children (less than 48 months old), an age group generally excluded from population-based TSE biomarker surveys. We hypothesized that TSE would vary significantly according to race and Medicaid coverage. We also postulated that the level of cotinine in dried blood spots would be positively correlated with lead levels owing to shared socioeconomic risk factors for both of these environmental exposures and examined whether TSE might predict lead exposure in small children.