Context.-Cotinine, a metabolite of nicotine, is a marker of exposure to tobacco smoke. Previous studies suggest that non-Hispanic blacks have higher levels of serum cotinine than non-Hispanic whites who report similar levels of cigarette smoking. Objective.-To investigate differences in levels of serum cotinine in black, white, and Mexican American cigarette smokers in the US adult population. Design.-Third National Health and Nutrition Examination Survey, 1988-1991. Participants.-A nationally representative sample of persons aged 17 years or older who participated in the survey. Outcome Measures.-Serum cotinine levels by reported number of cigarettes smoked per day and by race and ethnicity. Results.-A total of 7182 subjects were involved in the study; 2136 subjects reported smoking at least 1 cigarette in the last 5 days. Black smokers had cotinine concentrations substantially higher at all levels of cigarette smoking than did white or Mexican American smokers (PϽ.001). Serum cotinine levels for blacks were 125 nmol/L (22 ng/mL) (95% confidence interval [CI], 79-176 nmol/L [14-31 ng/mL]) to 539 nmol/L (95 ng/mL) (95% CI, 289-630 nmol/L [51-111 ng/mL]) higher than for whites and 136 nmol/L (24 ng/mL) (95% CI, 85-182 nmol/L [15-32 ng/mL]) to 641 nmol/L (113 ng/mL) (95% CI, 386-897 nmol/L [68-158 ng/mL]) higher than for Mexican Americans. These differences do not appear to be attributable to differences in environmental tobacco smoke exposure or in number of cigarettes smoked. Conclusions.-To our knowledge, this study provides the first evidence from a national study that serum cotinine levels are higher among black smokers than among white or Mexican American smokers. If higher cotinine levels among blacks indicate higher nicotine intake or differential pharmacokinetics and possibly serve as a marker of higher exposure to cigarette carcinogenic components, they may help explain why blacks find it harder to quit and are more likely to experience higher rates of lung cancer than white smokers.

BackgroundThe U.S. Centers for Disease Control and Prevention collected health, housing, and environmental data in a single integrated national survey for the first time in the United States in 1999–2004.ObjectivesWe aimed to determine how floor dust lead (PbD) loadings and other housing factors influence childhood blood lead (PbB) levels and lead poisoning.MethodsWe analyzed data from the 1999–2004 National Health and Nutrition Examination Survey (NHANES), including 2,155 children 12–60 months of age with PbB and PbD measurements. We used linear and logistic regression models to predict log-transformed PbB and the odds that PbB was ≥ 5 and ≥ 10 μg/dL at a range of floor PbD.ResultsThe population-weighted geometric mean (GM) PbB was 2.0 μg/dL (geometric standard error = 1.0). Age of child, race/ethnicity, serum cotinine concentration, poverty-to-income ratio, country of birth, year of building construction, floor PbD by floor surface and condition, windowsill PbD, presence of deteriorated paint, home-apartment type, smoking in the home, and recent renovation were significant predictors in either the linear model [the proportion of variability in the dependent variable accounted for by the model (R2) = 40%] or logistic model for 10 μg/dL (R2 = 5%). At floor PbD = 12 μg/ft2, the models predict that 4.6% of children living in homes constructed before 1978 have PbB ≥ 10 μg/dL, 27% have PbB ≥ 5 μg/dL, and the GM PbB is 3.9 μg/dL.ConclusionsLowering the floor PbD standard below the current standard of 40 μg/ft2 would protect more children from elevated PbB.

The Healthy Communities Study is designed to assess relationships between characteristics of community programs and policies targeting childhood obesity and children’s BMI, diet, and physical activity. The study involved a complex data collection protocol implemented over a 2-year period (2013–2015) across a diverse sample of up to 125 communities, defined as public high school catchment areas. The protocol involved baseline assessment within each community that included in-person or telephone interviews regarding community programs and policies and in-home collection of BMI, nutritional, and physical activity outcomes from a sample of up to 81 children enrolled in kindergarten through eighth grade in public schools. The protocol also involved medical record reviews to establish a longitudinal trajectory of BMI for an estimated 70% of participating children. Staged sampling was used to collect less detailed measures of physical activity and nutrition across the entire sample of children, with a subset assessed using more costly, burdensome, and detailed measures. Data from the Healthy Community Study will be analyzed using both cross-sectional and longitudinal models that account for the complex design and correct for measurement error and bias using a likelihood-based Markov chain Monte Carlo methodology. This methods paper provides insights into the complex design features of the Healthy Communities Study and may serve as an example for future large-scale studies that assess the relationship between community-based programs and policies and health outcomes of community residents.

The impact of the US EPA-required phase-outs starting in 2000-2001 of residential uses of the organophosphate (OP) pesticides chlorpyrifos (CPF) and diazinon (DZN) on preschool children's pesticide exposures was investigated over 2003-2005, in the Raleigh-Durham-Chapel Hill area of North Carolina. Data were collected from 50 homes, each with a child initially of age 3 years (OCh) and a younger child (YCh). Environmental samples (indoor and outdoor air, dust, soil) and child-specific samples (hand surface residue, urine, diet) were collected annually over 24-h periods at each home. Child time-activity diaries and household pesticide use information were also collected. Analytes included CPF and DZN; pentachlorophenol (PCP); 2,4-dichlorophenoxyacetic acid (2,4-D); the CPF metabolite 3,5,6-trichloro-2-pyridinol (TCP); and the DZN metabolite 2-isopropyl-6-methyl-4-pyrimidinol (IMP). Exposures (ng/day) through the inhalation, dietary ingestion, and indirect ingestion were calculated. Aggregate potential doses in ng/kg body weight per day (ng/kg/day) were obtained by summing the potential doses through the three routes of exposure. Geometric mean aggregate potential doses decreased from 2003 to 2005 for both OCh and YCh, with the exception of 2,4-D. Child-specific longitudinal modeling indicated significant declines across time of the potential doses of CPF, DZN, and PCP for both children; declines of IMP for both children, significant only for OCh; a decline of TCP for OCh but an increase of TCP for YCh; and no significant change of 2,4-D for either child. Age-adjusted modeling indicated significant effects of the child's age for all except CPF, and of time for all except PCP and 2,4-D. Within-home variability was small compared with that between homes; variability was smallest for 2,4-D, both within and between homes. The aggregate potential doses of CPF and DZN were well below published reference dose values. These findings show the success of the US EPA restrictions in reducing young children's pesticide exposures.

BackgroundLead-contaminated house dust is a major source of lead exposure for children in the United States. In 1999–2004, the National Health and Nutrition Examination Survey (NHANES) collected dust lead (PbD) loading samples from the homes of children 12–60 months of age.ObjectivesIn this study we aimed to compare national PbD levels with existing health-based standards and to identify housing and demographic factors associated with floor and windowsill PbD.MethodsWe used NHANES PbD data (n = 2,065 from floors and n = 1,618 from windowsills) and covariates to construct linear and logistic regression models.ResultsThe population-weighted geometric mean floor and windowsill PbD were 0.5 μg/ft2 [geometric standard error (GSE) = 1.0] and 7.6 μg/ft2 (GSE = 1.0), respectively. Only 0.16% of the floors and 4.0% of the sills had PbD at or above current federal standards of 40 and 250 μg/ft2, respectively. Income, race/ethnicity, floor surface/condition, windowsill PbD, year of construction, recent renovation, smoking, and survey year were significant predictors of floor PbD [the proportion of variability in the dependent variable accounted for by the model (R2) = 35%]. A similar set of predictors plus the presence of large areas of exterior deteriorated paint in pre-1950 homes and the presence of interior deteriorated paint explained 20% of the variability in sill PbD. A companion article [Dixon et al. Environ Health Perspect 117:468–474 (2009)] describes the relationship between children’s blood lead and PbD.ConclusionMost houses with children have PbD levels that comply with federal standards but may put children at risk. Factors associated with PbD in our population-based models are primarily the same as factors identified in smaller at-risk cohorts. PbD on floors and windowsills should be kept as low as possible to protect children.