Brianna F. Moore

Bovine Milk Protein-Induced Intestinal Malabsorption of Lactose and Fat in Infants

Summary A nonbovine, dextrose-containing formula was fed to 4 babies with lactose malabsorption in remission. Substitution of lactose for dextrose in the formula did not produce steatorrhea, flattening of the oral lactose tolerance curves, or acid, watery stools, but the prior feeding of selected bovine milk proteins, skim milk, or whole cows milk did. Thus, it would seem that in certain human subjects, at least, it is the proteins, and not the carbohydrate, in cows milk that can precipitate intestinal malabsorption.

The Fort Collins Commuter Study: impact of route type and transport mode on personal exposure to multiple air pollutants

Traffic-related air pollution is associated with increased mortality and morbidity, yet few studies have examined strategies to reduce individual exposure while commuting. The present study aimed to quantify how choice of mode and route type affects personal exposure to air pollutants during commuting. We analyzed within-person difference in exposures to multiple air pollutants (black carbon (BC), carbon monoxide (CO), ultrafine particle number concentration (PNC), and fine particulate matter (PM2.5)) during commutes between the home and workplace for 45 participants. Participants completed 8 days of commuting by car and bicycle on direct and alternative (reduced traffic) routes. Mean within-person exposures to BC, PM2.5, and PNC were higher when commuting by cycling than when driving, but mean CO exposure was lower when cycling. Exposures to CO and BC were reduced when commuting along alternative routes. When cumulative exposure was considered, the benefits from cycling were attenuated, in the case of CO, or exacerbated, in the case of particulate exposures, owing to the increased duration of the commute. Although choice of route can reduce mean exposure, the effect of route length and duration often offsets these reductions when cumulative exposure is considered. Furthermore, increased ventilation rate when cycling may result in a more harmful dose than inhalation at a lower ventilation rate.

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

Proinflammatory Diets during Pregnancy and Neonatal Adiposity in the Healthy Start Study

Objective To evaluate the association between dietary inflammatory index (DII) scores during pregnancy and neonatal adiposity. Study design The analysis included 1078 mother–neonate pairs in Healthy Start, a prospective prebirth cohort. Diet was assessed using repeated 24‐hour dietary recalls. DII scores were obtained by summing nutrient intakes, which were standardized to global means and multiplied by inflammatory effect scores. Air displacement plethysmography measured fat mass and fat‐free mass within 72 hours of birth. Linear and logistic models evaluated the associations of DII scores with birth weight, fat mass, fat‐free mass, and percent fat mass, and with categorical outcomes of small‐ and large‐for‐gestational age. We tested for interactions with prepregnancy BMI and gestational weight gain. Results The interaction between prepregnancy BMI and DII was statistically significant for birth weight, neonatal fat mass, and neonatal percent fat mass. Among neonates born to obese women, each 1‐unit increase in DII was associated with increased birth weight (53 g; 95% CI, 20, 87), fat mass (20 g; 95% CI, 7–33), and percent fat mass (0.5%; 95% CI, 0.2–0.8). No interaction was detected for small‐ and large‐for‐gestational age. Each 1‐unit increase in DII score was associated a 40% increase in odds of a large‐for‐gestational age neonate (1.4; 95% CI, 1.0–2.0; P = .04), but not a small‐for‐gestational age neonate (1.0; 95% CI, 0.8–1.2; P = .80). There was no evidence of an interaction with gestational weight gain. Conclusions Our findings support the hypothesis that an increased inflammatory milieu during pregnancy may be a risk factor for neonatal adiposity. Trial registration Clinicaltrials.gov: NCT02273297.

Exposure to secondhand smoke, exclusive breastfeeding and infant adiposity at age 5 months in the Healthy Start study.

Infant adiposity may be influenced by several environmental risk factors, but few studies have explored these interactions.

Ozone-Related Respiratory Morbidity in a Low-Pollution Region

Objective: We evaluated the effects of ozone on respiratory-related hospital admissions in three counties in Washington State from 1990 to 2006. We further examined vulnerability to ozone by key demographic factors. Method: Using linked hospital admission and ambient monitoring data, we estimated the age-, sex-, and health insurance-stratified associations between ozone (0 to 3 days’ lag) and respiratory-related hospital admissions in King, Spokane, and Clark County, Washington. Results: The adjusted relative risk (RR) for a 10 ppb increase in ozone at 3 days’ lag was 1.04 (95% confidence interval [CI]: 1.02, 1.07) for Clark County, 1.03 (95% CI: 1.01, 1.05) for Spokane County, and 1.02 (95% CI: 1.01, 1.03) for King County. There was consistent evidence of effect modification by age. Conclusion: Ozone at levels below federal standards contributes to respiratory morbidity among high-risk groups in Washington.

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

BackgroundPrevious 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.ObjectivesTo 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.MethodsWe 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.ResultsCompared 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.ConclusionsOffspring 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.

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.