Bridging Differences in Cohort Analyses of the Relationship between Secondhand Smoke Exposure during Pregnancy and Birth Weight: The Transportability Framework in the ECHO Program.

BACKGROUND: Estimates for the effects of environmental exposures on health outcomes, including secondhand smoke (SHS) exposure, often present considerable variability across studies. Knowledge of the reasons behind these differences can aid our understanding of effects in specific populations as well as inform practices of combining data from multiple studies. OBJECTIVES: This study aimed to assess the presence of effect modification by measured sociodemographic characteristics on the effect of SHS exposure during pregnancy on birth weights that may drive differences observed across cohorts. We also aimed to quantify the extent to which differences in the cohort mean effects observed across cohorts in the Environmental influences on Child Health Outcomes (ECHO) consortium are due to differing distributions of these characteristics. METHODS: We assessed the presence of effect modification and transportability of effect estimates across five ECHO cohorts in a total of 6,771 mother-offspring dyads. We assessed the presence of effect modification via gradient boosting of regression trees based on the H-statistic. We estimated individual cohort effects using linear models and targeted maximum likelihood estimation (TMLE). We then estimated transported effects from one cohort to each of the remaining cohorts using a robust nonparametric estimation approach relying on TMLE estimators and compared them to the original effect estimates for these cohorts. RESULTS: Observed effect estimates varied across the five cohorts, ranging from significantly lower birth weight associated with exposure [-167.3g; 95% confidence interval (CI): -270.4, -64.1] to higher birth weight with wide CIs, including the null (42.4g; 95% CI: -15.0, 99.8). Transported effect estimates only minimally explained differences in the point estimates for two out of the four cohort pairs. DISCUSSION: Our findings of weak to moderate evidence of effect modification and transportability indicate that unmeasured individual-level and contextual factors and sources of bias may be responsible for differences in the effect estimates observed across ECHO cohorts. https://doi.org/10.1289/EHP13961.

Prenatal Exposure to Tobacco and Childhood Cognition and Behavior: Effect Modification by Maternal Folate Intake and Breastfeeding Duration.

In this exploratory analysis, we assessed whether nutrition modified the association between prenatal exposure to tobacco and childhood cognition/behavior among 366 Colorado-based mothers and their offspring (born ≥ 37 weeks with birthweights ≥ 2500 g). Interaction by folate ( 5 months, but not for shorter durations. Our findings support the need for smoking cessation campaigns throughout pregnancy and throughout the postpartum period breastfeeding to reduce neurobehavioral risks in the offspring.

Associations between Prenatal and Postnatal Exposure to Cannabis with Cognition and Behavior at Age 5 Years: The Healthy Start Study.

BACKGROUND: Prenatal exposure to cannabis may influence childhood cognition and behavior, but the epidemiologic evidence is mixed. Even less is known about the potential impact of secondhand exposure to cannabis during early childhood. OBJECTIVE: This study sought to assess whether prenatal and/or postnatal exposure to cannabis was associated with childhood cognition and behavior. STUDY DESIGN: This sub-study included a convenience sample of 81 mother-child pairs from a Colorado-based cohort. Seven common cannabinoids (including delta 9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD)) and their metabolites were measured in maternal urine collected mid-gestation and child urine collected at age 5 years. Prenatal and postnatal exposure to cannabis was dichotomized as exposed (detection of any cannabinoid) and not exposed. Generalized linear models examined the associations between prenatal or postnatal exposure to cannabis with the NIH Toolbox and Child Behavior Checklist T-scores at age 5 years. RESULTS: In this study, 7% (n = 6) of the children had prenatal exposure to cannabis and 12% (n = 10) had postnatal exposure to cannabis, with two children experiencing this exposure at both time points. The most common cannabinoid detected in pregnancy was Δ9-THC, whereas the most common cannabinoid detected in childhood was CBD. Postnatal exposure to cannabis was associated with more aggressive behavior (ß: 3.2; 95% CI: 0.5, 5.9), attention deficit/hyperactivity problems (ß: 8.0; 95% CI: 2.2, 13.7), and oppositional/defiant behaviors (ß: 3.2; 95% CI: 0.2, 6.3), as well as less cognitive flexibility (ß: -15.6; 95% CI: -30.0, -1.2) and weaker receptive language (ß: -9.7; 95% CI: -19.2, -0.3). By contrast, prenatal exposure to cannabis was associated with fewer internalizing behaviors (mean difference: -10.2; 95% CI: -20.3, -0.2) and fewer somatic complaints (mean difference: -5.2, 95% CI: -9.8, -0.6). CONCLUSIONS: Our study suggests that postnatal exposure to cannabis is associated with more behavioral and cognitive problems among 5-year-old children, independent of prenatal and postnatal exposure to tobacco. The potential risks of cannabis use (including smoking and vaping) during pregnancy and around young children should be more widely communicated to parents.

Using non-parametric Bayes shrinkage to assess relationships between multiple environmental and social stressors and neonatal size and body composition in the Healthy Start cohort.

BACKGROUND: Both environmental and social factors have been linked to birth weight and adiposity at birth, but few studies consider the effects of exposure mixtures. Our objective was to identify which components of a mixture of neighborhood-level environmental and social exposures were driving associations with birth weight and adiposity at birth in the Healthy Start cohort. METHODS: Exposures were assessed at the census tract level and included air pollution, built environment characteristics, and socioeconomic status. Prenatal exposures were assigned based on address at enrollment. Birth weight was measured at delivery and adiposity was measured using air displacement plethysmography within three days. We used non-parametric Bayes shrinkage (NPB) to identify exposures that were associated with our outcomes of interest. NPB models were compared to single-predictor linear regression. We also included generalized additive models (GAM) to assess nonlinear relationships. All regression models were adjusted for individual-level covariates, including maternal age, pre-pregnancy BMI, and smoking. RESULTS: Results from NPB models showed most exposures were negatively associated with birth weight, though credible intervals were wide and generally contained zero. However, the NPB model identified an interaction between ozone and temperature on birth weight, and the GAM suggested potential non-linear relationships. For associations between ozone or temperature with birth weight, we observed effect modification by maternal race/ethnicity, where effects were stronger for mothers who identified as a race or ethnicity other than non-Hispanic White. No associations with adiposity at birth were observed. CONCLUSIONS: NPB identified prenatal exposures to ozone and temperature as predictors of birth weight, and mothers who identify as a race or ethnicity other than non-Hispanic White might be disproportionately impacted. However, NPB models may have limited applicability when non-linear effects are present. Future work should consider a two-stage approach where NPB is used to reduce dimensionality and alternative approaches examine non-linear effects.

Early-life exposure to tobacco and childhood adiposity: Identifying windows of susceptibility.

BACKGROUND: Early-life exposure to tobacco is associated with obesity, but the most susceptible developmental periods are unknown. OBJECTIVE: To explore windows of susceptibility in a cohort of 568 mother-child pairs. METHODS: We measured seven measures of tobacco exposure (five self-reported and two biomarkers) spanning from pre-conception to age 5 years. Mothers self-reported active smoking (pre-conception, 17 weeks, and delivery) and household smokers (5 and 18 months postnatally). Cotinine was measured in maternal urine (27 weeks) and child urine (5 years). Adiposity (fat mass percentage) was measured at birth and 5 years via air displacement plethysmography. Using a multiple informant approach, we tested whether adiposity (5 years) and changes in adiposity (from birth to 5 years) differed by the seven measures of tobacco exposure. RESULTS: The associations may depend on timing. For example, only pre-conception (ß = 3.1%; 95% CI: 1.0-5.1) and late gestation (ß = 4.0%; 95% CI: 0.4-7.6) exposures influenced adiposity accretion from birth to 5 years (p for interaction = 0.01). Early infancy exposure was also associated with 1.7% higher adiposity at 5 years (95% CI: 0.1-3.2). Mid-pregnancy and early childhood exposures did not influence adiposity. CONCLUSIONS: Pre-conception, late gestation, and early infancy exposures to tobacco may have the greatest impact on childhood adiposity.

Prenatal exposure to tobacco and adverse birth outcomes: effect modification by folate intake during pregnancy.

BACKGROUND: Fetal exposure to tobacco increases the risk for many adverse birth outcomes, but whether diet mitigates these risks has yet to be explored. Here, we examined whether maternal folate intake (from foods and supplements) during pregnancy modified the association between prenatal exposure to tobacco and with preterm delivery, small-for-gestational age (SGA) births, or neonatal adiposity. METHODS: Mother-child pairs (n = 701) from Healthy Start were included in this analysis. Urinary cotinine was measured at ~ 27 weeks gestation. Diet was assessed using repeated 24-h dietary recalls. Neonatal adiposity (fat mass percentage) was measured via air displacement plethysmography. Interaction was assessed by including a product term between cotinine (< / ≥ limit of detection [LOD]) and folate (< / ≥ 25th percentile [1077 µg/day]) in separate logistic or linear regression models, adjusting for maternal age, race, ethnicity, education, pre-pregnancy body mass index, and infant sex. RESULTS: Approximately 26% of women had detectable levels of cotinine. Folate intake was significantly lower among women with cotinine ≥ LOD as compared to those with cotinine < LOD (1293 µg/day vs. 1418 µg/day; p = 0.01). Folate modified the association between fetal exposure to tobacco with neonatal adiposity (p for interaction = 0.07) and SGA (p for interaction = 0.07). Among those with lower folate intake, fetal exposure to tobacco was associated with lower neonatal adiposity (mean difference: -2.09%; 95% CI: -3.44, -0.74) and increased SGA risk (OR: 4.99; 95% CI: 1.55, 16.14). Conversely, among those with higher folate intake, there was no difference in neonatal adiposity (mean difference: -0.17%; 95% CI: -1.13, 0.79) or SGA risk (OR: 1.15; 95% CI: 0.57, 2.31). CONCLUSIONS: Increased folate intake during pregnancy (from foods and/or supplements) may mitigate the risk of fetal growth restriction among those who are unable to quit smoking or cannot avoid secondhand smoke during pregnancy.

Joint effects of ambient air pollution and maternal smoking on neonatal adiposity and childhood BMI trajectories in the Healthy Start study.

Coexposure to air pollution and tobacco smoke may influence early-life growth, but few studies have investigated their joint effects. We examined the interaction between fetal exposure to maternal smoking and ozone (O3) or fine particulate matter (PM2.5) on birth weight, neonatal adiposity, and body mass index (BMI) trajectories through age 3 years. METHODS: Participants were 526 mother-child pairs, born ≥37 weeks. Cotinine was measured at ~27 weeks gestation. Whole pregnancy and trimester-specific O3 and PM2.5 were estimated via. inverse-distance weighted interpolation from stationary monitors. Neonatal adiposity (fat mass percentage) was measured via. air displacement plethysmography. Child weight and length/height were abstracted from medical records. Interaction was assessed by introducing cotinine (<31.5 vs. ≥31.5 ng/mL [indicating active smoking]), O3/PM2.5 (low [tertiles 1-2] vs. high [tertile 3]), and their product term in linear regression models for birth weight and neonatal adiposity and mixed-effects models for BMI trajectories. RESULTS: The rate of BMI growth among offspring jointly exposed to maternal smoking and high PM2.5 (between 8.1 and 12.7 µg/m3) in the third trimester was more rapid than would be expected due to the individual exposures alone (0.8 kg/m2 per square root year; 95% CI = 0.1, 1.5; P for interaction = 0.03). We did not detect interactions between maternal smoking and O3 or PM2.5 at any other time on birth weight, neonatal adiposity, or BMI trajectories. CONCLUSIONS: Although PM2.5 was generally below the EPA annual air quality standards of 12.0 µg/m3, exposure during the third trimester may influence BMI trajectories when combined with maternal smoking.

Examining Associations Between Dietary Inflammatory Index in Pregnancy, Pro-inflammatory Cytokine and Chemokine Levels at Birth, and Offspring Asthma and/or Wheeze by Age 4 Years.

BACKGROUND: Few studies have demonstrated associations between maternal dietary inflammatory index (DII) during pregnancy and offspring asthma and/or wheeze. OBJECTIVE: The study aimed to assess associations between maternal DII during pregnancy and 1) offspring cord sera pro-inflammatory cytokines (interleukin [IL]-1ß, IL-4, IL-6, IL-10, tumor necrosis factor-α) and chemokines (IL-8, monocyte chemoattractant protein-1) at birth and 2) offspring asthma and/or wheeze at age 4 years. DESIGN: The Healthy Start study is a prospective prebirth longitudinal study that recruited pregnant women in Denver, Colorado and tracked their offspring. PARTICIPANTS AND SETTING: This study used data from 1228 mother-child dyads enrolled in the Healthy Start study. Pregnant women were recruited in Denver, Colorado, between 2009 and 2014, and offspring tracked until age 4 years. MAIN OUTCOME MEASURES: Cord sera cytokines and chemokines were analyzed with multiplex panel immunoassays. Offspring diagnosis of asthma and/or wheeze by age 4 years was extracted from electronic medical records. STATISTICAL ANALYSES PERFORMED: Unadjusted and adjusted linear and logistic regression models were used to assess associations. Covariates included factors such as nulliparity, race/ethnicity, gestational smoking, and maternal history of asthma. RESULTS: Unadjusted analysis showed that increasing maternal DII scores were associated with increased odds of child asthma and/or wheeze by 4 years (odds ratio = 1.17; 95% CI: 1.07-1.27), but the association was attenuated and no longer statistically significant in the adjusted model (odds ratio = 1.15; 95% CI: 0.99-1.33). There were no significant associations between DII scores and cord sera cytokine or chemokine levels. CONCLUSIONS: The study showed that the inflammatory profile of the maternal diet was not associated with cytokines and chemokine levels at birth. The results suggested that a more inflammatory maternal diet was associated with increased odds of offspring asthma and/or wheeze by age 4 years, which could be considered of clinical relevance but the finding was not statistically significant at the .05 level.

Prenatal Exposure to Tobacco and Offspring Neurocognitive Development in the Healthy Start Study.

OBJECTIVE: To explore the associations between prenatal exposure to tobacco and neurocognitive development, in the absence of prematurity or low birth weight. STUDY DESIGN: We followed mother-child pairs within Healthy Start through 6 years of age. Children were born at ≥37 weeks of gestation with a birth weight of ≥2500 g. Parents completed the Third Edition Ages and Stages Questionnaire (n = 246) and children completed a subset of the National Institutes of Health Toolbox Cognition Battery (n = 200). The Ages and Stages Questionnaire domains were dichotomized as fail/monitor and pass. Maternal urinary cotinine was measured at approximately 27 weeks of gestation. Separate logistic regression models estimated associations between prenatal exposure to tobacco (cotinine below vs above the limit of detection) and the Ages and Stages Questionnaire domains. Separate linear regression models estimated associations between prenatal exposure to tobacco and fully corrected T-scores for inhibitory control, cognitive flexibility, and receptive language, as assessed by the National Institutes of Health Toolbox. A priori covariates included sex, maternal age, maternal education, daily caloric intake during pregnancy, race/ethnicity, household income, maternal psychiatric disorders, and, in secondary models, postnatal exposure to tobacco. RESULTS: Compared with unexposed offspring, exposed offspring were more likely to receive a fail/monitor score for fine motor skills (OR, 3.9; 95% CI, 1.5-10.3) and decreased inhibitory control (B: -3.0; 95% CI, -6.1 to -0.7). After adjusting for postnatal exposure, only the association with fine motor skills persisted. CONCLUSIONS: Prenatal and postnatal exposures to tobacco may influence neurocognitive development, in the absence of preterm delivery or low birth weight. Increased developmental screening may be warranted for exposed children.

Diet, Secondhand Smoke, and Glycated Hemoglobin (HbA1c) Levels among Singapore Chinese Adults.

The combination of poor diet and exposure to secondhand smoke may increase hemoglobin A1c (HbA1c) levels, but few studies have explored this interaction. We explored an interaction among 574 never-smoking adults from the Singapore Chinese Health Study. At baseline (age 59 ± 8 years), intakes of omega-3 polyunsaturated fatty acids, vitamin C, vitamin E and fiber were estimated using a modified food frequency questionnaire. At follow-up (age 64 ± 9 years), HbA1c and cotinine were measured. A product term between cotinine (above or below the median value) and each nutrient (high or low intake) was included in separate linear regression models with HbA1c as the outcome. HbA1c among those with high cotinine and low omega-3 polyunsaturated fatty acids intakes were higher than would be expected due to the individual effects alone (p-for-interaction = 0.05). Among those with lower intakes of omega-3 polyunsaturated fatty acids, high cotinine levels were associated with 0.54% higher HbA1c levels (95% confidence interval [CI]: 0.02, 1.06). Conversely, among those with higher intakes of omega-3 polyunsaturated fatty acids, HbA1c differ not differ by exposure (-0.09%; 95% CI: -0.45, 0.30). No evidence of interaction was observed for other nutrients. Diets high in omega-3 polyunsaturated fatty acids may ameliorate secondhand smoke-induced increases in HbA1c.

Fetal exposure to maternal active and secondhand smoking with offspring early-life growth in the Healthy Start study.

BACKGROUND: Previous studies have modeled the association between fetal exposure to tobacco smoke and body mass index (BMI) growth trajectories, but not the timing of catch-up growth. Research on fetal exposure to maternal secondhand smoking is limited. OBJECTIVES: To explore the associations between fetal exposure to maternal active and secondhand smoking with body composition at birth and BMI growth trajectories through age 3 years. METHODS: We followed 630 mother-child pairs enrolled in the Healthy Start cohort through age 3 years. Maternal urinary cotinine was measured at ~ 27 weeks gestation. Neonatal body composition was measured using air displacement plethysmography. Child weight and length/height were abstracted from medical records. Linear regression models examined the association between cotinine categories (no exposure, secondhand smoke, active smoking) with weight, fat mass, fat-free mass, and percent fat mass at birth. A mixed-effects regression model estimated the association between cotinine categories and BMI. RESULTS: Compared to unexposed offspring, birth weight was significantly lower among offspring born to active smokers (-343-g; 95% CI: -473, -213), but not among offspring of women exposed to secondhand smoke (-47-g; 95% CI: -130, 36). There was no significant difference in the rate of BMI growth over time between offspring of active and secondhand smokers (p = 0.58). Therefore, our final model included a single growth rate parameter for the combined exposure groups of active and secondhand smokers. The rate of BMI growth for the combined exposed group was significantly more rapid (0.27 kg/m2 per year; 95% CI: 0.05, 0.69; p < 0.01) than the unexposed. CONCLUSIONS: Offspring prenatally exposed to maternal active or secondhand smoking experience rapid and similar BMI growth in the first three years of life. Given the long-term consequences of rapid weight gain in early childhood, it is important to encourage pregnant women to quit smoking and limit their exposure to secondhand smoke.

The Fort Collins commuter study: Variability in personal exposure to air pollutants by microenvironment.

This study investigated the role of microenvironment on personal exposures to black carbon (BC), fine particulate mass (PM2.5 ), carbon monoxide (CO), and particle number concentration (PNC) among adult residents of Fort Collins, Colorado, USA. Forty-four participants carried a backpack containing personal monitoring instruments for eight nonconsecutive 24-hour periods. Exposures were apportioned into five microenvironments: Home, Work, Transit, Eateries, and Other. Personal exposures exhibited wide heterogeneity that was dominated by within-person variability (both day-to-day and between microenvironment variability). Linear mixed-effects models were used to compare mean personal exposures in each microenvironment, while accounting for possible within-person correlation. Mean personal exposures during Transit and at Eateries tended to be higher than exposures at Home, where participants spent the majority of their time. Compared to Home, mean exposures to BC in Transit were, on average, 129% [95% confidence interval: 101% 162%] higher and exposures to PNC were 180% [101% 289%] higher in Eateries.

Interactions Between Diet and Exposure to Secondhand Smoke on Glycated Hemoglobin Levels Among US Children: Results From NHANES 2007-2012.

INTRODUCTION: Antioxidant-rich diets may lessen the adverse metabolic responses triggered by exposure to secondhand smoke (SHS), but no studies have investigated these potential interactions. OBJECTIVE: To examine the interaction between diet and exposure to SHS on glycated hemoglobin (HbA1c) levels among 2551 children, ages 12-19 years, who participated in the 2007-2012 National Health and Nutrition Examination Survey (NHANES). METHODS: Exposure to SHS was assessed by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), cotinine, and self-report. Weighted linear regression models evaluated the cross-sectional association between exposure to SHS and HbA1c levels. Additive interaction was assessed by introducing product terms (with SHS) of individual nutrients (dietary fiber, eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA], vitamin C, and vitamin E) to separate models. RESULTS: Over half of the children had NNAL or cotinine levels above the limit of detection (56% and 71%, respectively). The median HbA1c level was 5.2% (95% confidence interval: 5.17%, 5.23%). The interaction results suggest that the effects of exposure to SHS and certain dietary nutrients (EPA, DHA, vitamin C) on HbA1c levels may not be independent. For example, although there was only a slight difference in adjusted mean HbA1c levels across NNAL categories among children with high EPA intakes, the adjusted mean HbA1c level was 0.09% higher for high NNAL as compared to low NNAL among children with low EPA intakes. CONCLUSIONS: Further research is needed to inform public health strategies for limiting increases in HbA1c levels among children. Messages may need to focus both on reducing exposure to SHS and improving diets to obtain the maximum benefit. IMPLICATIONS: Our results suggest that the effects of exposure to SHS and diet on HbA1c levels may not be independent. For example, although there was little effect of exposure to SHS on HbA1c levels among children with high EPA intakes, high exposure to SHS was associated with an increase in HbA1c levels among children with low EPA intakes. Further research is necessary; however, based on these joint effects, strategies for limiting increases in HbA1c levels that focus both on reducing exposure to SHS and improving diets may achieve the largest public health benefits.

Interactions Between Diet and Exposure to Secondhand Smoke on Metabolic Syndrome Among Children: NHANES 2007-2010.

CONTEXT: Metabolic syndrome is likely influenced by a complex interaction between exposure to secondhand smoke (SHS) and diet, but no studies have evaluated this relationship. OBJECTIVE: This study aimed to investigate the interaction between diet and exposure to SHS on metabolic syndrome among 12-19 year olds. DESIGN AND PARTICIPANTS: We used weighted logistic regression, adjusting for potential confounders, to examine interaction of these risk factors on the prevalence of metabolic syndrome among 12-19 year olds participating in the National Health and Nutrition Examination Survey (2007-2010). Interaction was assessed by introducing product terms between SHS (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol, cotinine, and self-report) and the individual nutrients (dietary fiber, eicosapentaenoic acid, docosahexaenoic acid, vitamin C, and vitamin E) and nutrient patterns in separate models; the relative excess risk due to interaction was used to evaluate interaction on the additive scale. RESULTS: The joint effect between high exposure to SHS and low levels of certain nutrients (vitamin E and omega-3 polyunsaturated fatty acids) on metabolic syndrome risk was greater than would be expected from the effects of the individual exposures alone (for example, relative excess risk due to interaction for SHS and vitamin E = 7.5; 95% confidence interval, 2.5-17.8). CONCLUSIONS: Prevention strategies for metabolic syndrome aimed at reducing SHS exposures and improving diet quality may exceed the expected benefits based on targeting these risk factors separately.

Interactions between Diet and Exposure to Secondhand Smoke on the Prevalence of Childhood Obesity: Results from NHANES, 2007-2010.

BACKGROUND: Exposure to secondhand smoke (SHS) may increase risk for obesity, but few studies have investigated the joint effects of exposure to SHS and diet. OBJECTIVES: We examined the interaction of exposure to SHS and diet on the prevalence of obesity among 6- to 19-year-olds who participated in the 2007-2010 National Health and Nutrition Examination Survey. METHODS: We characterized exposure using a novel biomarker [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL)], an established biomarker (cotinine), and self-report. Multinomial logistic regression models examined the association of SHS exposure on the prevalence of overweight and obesity as separate outcomes (compared with normal/underweight). Interaction by diet was assessed by introducing interaction terms (with SHS) of the individual nutrients [dietary fiber, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), vitamin C, and vitamin E] into separate models. RESULTS: Approximately half of the children had NNAL and cotinine levels above the limit of detection, indicating exposure to SHS. Interaction results suggest that the prevalence of obesity among children with both high exposure to SHS and low levels of certain nutrients (dietary fiber, DHA, or EPA) is greater than would be expected due to the effects of the individual exposures alone. Little or no evidence suggesting more or less than additive or multiplicative interaction was observed for vitamin C or vitamin E. The association between SHS and obesity did not appear to be modified by dietary vitamin C or vitamin E. CONCLUSIONS: Childhood obesity prevention strategies aimed at reducing SHS exposures and improving diets may exceed the expected benefits based on targeting either risk factor alone. CITATION: Moore BF, Clark ML, Bachand A, Reynolds SJ, Nelson TL, Peel JL. 2016. Interactions between diet and exposure to secondhand smoke on the prevalence of childhood obesity: results from NHANES, 2007-2010. Environ Health Perspect 124:1316-1322; http://dx.doi.org/10.1289/ehp.1510138.