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SUMMARY: Quantifying the impact of exposure to environmental chemical mixtures is important for identifying risk factors for diseases and developing more targeted public health interventions. The National Institute of Environmental Health Sciences (NIEHS) held a workshop in July 2015 to address the need to develop novel statistical approaches for multi-pollutant epidemiology studies. The primary objective of the workshop was to identify and compare different statistical approaches and methods for analyzing complex chemical mixtures data in both simulated and real-world data sets. At the workshop, participants compared approaches and results and speculated as to why they may have differed. Several themes emerged: a) no one statistical approach appeared to outperform the others, b) many methods included some form of variable reduction or summation of the data before statistical analysis, c) the statistical approach should be selected based upon a specific hypothesis or scientific question, and d) related mixtures data should be shared among researchers to more comprehensively and accurately address methodological questions and statistical approaches. Future efforts should continue to design and optimize statistical approaches to address questions about chemical mixtures in epidemiological studies. [ABSTRACT FROM AUTHOR]

Background: Reported associations between gestational tobacco exposure and autism spectrum disorders (ASDs) have been inconsistent. Objective: We estimated the association between maternal smoking during pregnancy and ASDs among children 8 years of age. Methods: This population-based case-cohort study included 633,989 children, identified using publicly available birth certificate data, born in 1992, 1994, 1996, and 1998 from parts of 11 U.S. states subsequently under ASD surveillance. Of these children, 3,315 were identified as having an ASD by the active, records-based surveillance of the Autism and Developmental Disabilities Monitoring Network. We estimated prevalence ratios (PRs) of maternal smoking from birth certificate report and ASDs using logistic regression, adjusting for maternal education, race/ethnicity, marital status, and maternal age; separately examining higher- and lower-functioning case sub­groups; and correcting for assumed under-ascertainment of autism by level of maternal education. Results: About 13% of the source population and 11% of children with an ASD had a report of maternal smoking in pregnancy: adjusted PR (95% confidence interval) of 0.90 (0.80, 1.01). The association for the case subgroup autistic disorder (1,310 cases) was similar: 0.88 (0.72, 1.08), whereas that for ASD not otherwise specified (ASD-NOS) (375 cases) was positive, albeit including the null: 1.26 (0.91, 1.75). Unadjusted associations corrected for assumed under-ascertainment were 1.06 (0.98, 1.14) for all ASDs, 1.12 (0.97, 1.30) for autistic disorder, and 1.63 (1.30, 2.04) for ASD-NOS. Conclusions: After accounting for the potential of under-ascertainment bias, we found a null association between maternal smoking in pregnancy and ASDs, generally. The possibility of an association with a higher-functioning ASD subgroup was suggested, and warrants further study. [ABSTRACT FROM AUTHOR]

Prenatal tobacco smoke exposure has been implicated as a risk factor for cognitive deficits in children. The purpose of this study is to examine the association between prenatal tobacco smoke exposure and diagnosis of intellectual disabilities (ID) among 8-year-old children living in Arkansas, Georgia, North Carolina and Utah. In 2002 and 2004, 965 ID case children were identified through a surveillance network and compared with the population of children born in the surveillance region during the same period (n = 104 607). Prenatal tobacco smoke exposure was determined from birth certificates. We estimated the effect of prenatal tobacco smoke exposure (none, <10, 10-19 and > or =20 cigarettes per day) on ID using logistic regression. Generally, the risk of ID was mildly elevated among children whose mothers smoked > or =20 cigarettes per day during pregnancy [RR 1.34; 95% (confidence interval) CI 0.96, 1.87] after adjustment for maternal education, maternal race, maternal age, marital status, child sex, birth year and study site. However, the effect of exposure to > or =20 cigarettes per day significantly differed for males [RR 1.77, 95% CI 1.20, 2.62] compared with females [RR 0.81, 95% CI 0.44, 1.50]. Supplemental analyses reveal substantial confounding of this relationship by socio-economic indicators. A differential effect of tobacco smoke exposure on the risk of ID is suggested for males and females and deserves further investigation; however, the interpretation is tempered by the potential for residual confounding. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The purpose of this study was to examine the association of exposures to tobacco smoke and environmental lead with attention deficit hyperactivity disorder (ADHD). METHODS: Data were obtained from the National Health and Nutrition Examination Survey 1999-2002. Prenatal and postnatal tobacco exposure was based on parent report; lead exposure was measured using blood lead concentration. ADHD was defined as having current stimulant medication use and parent report of ADHD diagnosed by a doctor or health professional. RESULTS: Of 4,704 children 4-15 years of age, 4.2% were reported to have ADHD and stimulant medication use, equivalent to 1.8 million children in the United States. In multivariable analysis, prenatal tobacco exposure [odds ratio (OR) = 2.5; 95% confidence interval (CI), 1.2-5.2] and higher blood lead concentration (first vs. fifth quintile, OR = 4.1; 95% CI, 1.2-14.0) were significantly associated with ADHD. Postnatal tobacco smoke exposure was not associated with ADHD (OR = 0.6; 95% CI, 0.3-1.3; p = 0.22). If causally linked, these data suggest that prenatal tobacco exposure accounts for 270,000 excess cases of ADHD, and lead exposure accounts for 290,000 excess cases of ADHD in U.S. children. CONCLUSIONS: We conclude that exposure to prenatal tobacco and environmental lead are risk factors for ADHD in U.S. children. [ABSTRACT FROM AUTHOR]

Objectives: To estimate the impact of gestational and childhood bisphenol A (BPA) exposures on behavior and executive function at 3 years of age and to determine whether child gender modified those associations., Methods: We used a prospective birth cohort of 244 mothers and their 3-year-old children from the greater Cincinnati, Ohio, area. We characterized gestational and childhood BPA exposures by using the mean BPA concentrations in maternal (16 and 26 weeks of gestation and birth) and child (1, 2, and 3 years of age) urine samples, respectively. Behavior and executive function were measured by using the Behavior Assessment System for Children 2 (BASC-2) and the Behavior Rating Inventory of Executive Function-Preschool (BRIEF-P)., Results: BPA was detected in >97% of the gestational (median: 2.0 μg/L) and childhood (median: 4.1 μg/L) urine samples. With adjustment for confounders, each 10-fold increase in gestational BPA concentrations was associated with more anxious and depressed behavior on the BASC-2 and poorer emotional control and inhibition on the BRIEF-P. The magnitude of the gestational BPA associations differed according to child gender; BASC-2 and BRIEF-P scores increased 9 to 12 points among girls, but changes were null or negative among boys. Associations between childhood BPA exposure and neurobehavior were largely null and not modified by child gender., Conclusions: In this study, gestational BPA exposure affected behavioral and emotional regulation domains at 3 years of age, especially among girls. Clinicians may advise concerned patients to reduce their exposure to certain consumer products, but the benefits of such reductions are unclear.