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Background: Prenatal exposure to cannabis (or more specifically, delta 9-tetrahydrocannabinol [Δ9-THC]) has been consistently linked to low birthweight. Animal models further show that Δ9-THC is associated with rapid postnatal growth. Whether this association is modified by breastfeeding is unknown., Methods: In this exploratory study, we followed 128 mother-child pairs through 3 years. Urinary Δ9-THC and cannabidiol (CBD) were measured mid-gestation. Generalized linear models estimated the associations between Δ9-THC and neonatal body composition. A mixed-effects model estimated the association between Δ9-THC and body mass index (BMI) z-score trajectories. Interaction was assessed by a three-way product term (Δ9-THC × breastmilk months × age)., Results: Fifteen children (12%) had Δ9-THC exposure; three had concomitant CBD exposure. Prenatal exposure to Δ9-THC alone was associated with lower fat mass (-95 g, 95% confidence interval [CI]: -174, -14) and neonatal adiposity (-2.1%; 95% CI: -4.2, -0.4) followed by rapid postnatal growth (0.42 increase in BMI z-score per square root year; 95% CI: 0.12, 0.72). Breastfeeding modified this association (p = 0.04), such that growth was similar for those breastfed for 5 months whereas a shorter duration of breastfeeding was associated with 1.1 higher BMI z-score at 3 years (95% CI: 0.21, 2.05)., Conclusions: Our study suggests that prenatal exposure to Δ9-THC may alter early-life growth. Breastfeeding may stabilize rapid postnatal growth, but the impact of lactational exposure requires further investigation., (© 2024 The Author(s). Pediatric Obesity published by John Wiley & Sons Ltd on behalf of World Obesity Federation.)

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 [ - 167.3 g ; 95% confidence interval (CI): - 270.4 , - 64.1 ] to higher birth weight with wide CIs, including the null ( 42.4 g ; 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.

Purpose of Review: To consolidate information on the obesogenic and cardiometabolic effects of prenatal exposure to cannabis., Recent Findings: A PubMed search strategy updated from January 1, 2014, through 14 June 2023, produced a total of 47 epidemiologic studies and 12 animal studies. Prenatal exposure to cannabis is consistently associated with small for gestational age and low birth weight. After birth, these offspring gain weight rapidly and have increased adiposity and higher glucose (fat mass percentage) in childhood. More preclinical and prospective studies are needed to deepen our understanding of whether these associations vary by sex, dose, timing, and composition of cannabis (e.g., ratio of delta-Δ9-tetrahydrocannabinol [Δ9-THC] to cannabidiol [CBD]). Addressing these gaps may help to solidify causality and identify intervention strategies. Based on the available data, clinicians and public health officials should continue to caution against cannabis use during pregnancy to limit its potential obesogenic and adverse cardiometabolic effects on the offspring., (© 2023. The Author(s).)

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., (© 2023. The Author(s).)

Background: Overnutrition in utero may increase offspring risk of nonalcoholic fatty liver disease (NAFLD), but the specific contribution of maternal diet quality during pregnancy to this association remains understudied in humans., Objectives: This study aimed to examine the associations of maternal diet quality during pregnancy with offspring hepatic fat in early childhood (median: 5 y old, range: 4-8 y old)., Methods: Data were from 278 mother-child pairs in the longitudinal, Colorado-based Healthy Start Study. Multiple 24-h recalls were collected from mothers during pregnancy on a monthly basis (median: 3 recalls, range: 1-8 recalls starting after enrollment), and used to estimate maternal usual nutrient intakes and dietary pattern scores [Healthy Eating Index-2010 (HEI-2010), Dietary Inflammatory Index (DII), and Relative Mediterranean Diet Score (rMED)]. Offspring hepatic fat was measured in early childhood by MRI. Associations of maternal dietary predictors during pregnancy with offspring log-transformed hepatic fat were assessed using linear regression models adjusted for offspring demographics, maternal/perinatal confounders, and maternal total energy intake., Results: Higher maternal fiber intake and rMED scores during pregnancy were associated with lower offspring hepatic fat in early childhood in fully adjusted models [Back-transformed β (95% CI): 0.82 (0.72, 0.94) per 5 g/1000 kcal fiber; 0.93 (0.88, 0.99) per 1 SD for rMED]. In contrast, higher maternal total sugar and added sugar intakes, and DII scores were associated with higher offspring hepatic fat [Back-transformed β (95% CI): 1.18 (1.05, 1.32) per 5% kcal/d added sugar; 1.08 (0.99, 1.18) per 1 SD for DII]. Analyses of dietary pattern subcomponents also revealed that lower maternal intakes of green vegetables and legumes and higher intake of "empty calories" were associated with higher offspring hepatic fat in early childhood., Conclusions: Poorer maternal diet quality during pregnancy was associated with greater offspring susceptibility to hepatic fat in early childhood. Our findings provide insights into potential perinatal targets for the primordial prevention of pediatric NAFLD., (Copyright © 2023 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

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 (β: 3.2; 95% CI: 0.5, 5.9), attention deficit/hyperactivity problems (β: 8.0; 95% CI: 2.2, 13.7), and oppositional/defiant behaviors (β: 3.2; 95% CI: 0.2, 6.3), as well as less cognitive flexibility (β: -15.6; 95% CI: -30.0, -1.2) and weaker receptive language (β: -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.

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 (β = 3.1%; 95% CI: 1.0-5.1) and late gestation (β = 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., (© 2022 World Obesity Federation.)

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., (© 2022. The Author(s).)

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 (< / ≥ 25 th 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., (© 2022. The Author(s).)

Objective: To assess the impact of fetal exposure to cannabis on adiposity and glucose-insulin traits in early life., Research Design and Methods: We leveraged a subsample of 103 mother-child pairs from Healthy Start, an ethnically diverse Colorado-based cohort. Twelve cannabinoids/metabolites of cannabis (including Δ9-tetrahydrocannabinol and cannabidiol) were measured in maternal urine collected at ~27 weeks' gestation. Fetal exposure to cannabis was dichotomized as exposed (any cannabinoid > limit of detection [LOD]) and not exposed (all cannabinoids < LOD). Fat mass and fat-free mass were measured via air displacement plethysmography at follow-up (mean age: 4.7 years). Glucose and insulin were obtained after an overnight fast. Generalized linear models estimated the associations between fetal exposure to cannabis with adiposity measures (fat mass [kg], fat-free mass [kg], adiposity [fat mass percentage], body mass index [BMI], and BMI z-scores) and metabolic measures (glucose [mg/dL], insulin [uIU/mL], and homeostatic model assessment of insulin resistance [HOMA-IR])., Results: Approximately 15% of the women had detectable levels of any cannabinoid, indicating fetal exposure to cannabis. Exposed offspring had higher fat mass (1.0 kg; 95% CI, 0.3-1.7), fat-free mass (1.2 kg; 95% CI, 0.4-2.0), adiposity (2.6%; 95% CI, 0.1-5.2), and fasting glucose (5.6 mg/dL; 95% CI, 0.8-10.3) compared with nonexposed offspring. No associations were found with fasting insulin (in the fully adjusted model), HOMA-IR, BMI, or BMI z-scores., Conclusions: We provide novel evidence to suggest an association between fetal exposure to cannabis with increased adiposity and fasting glucose in childhood, a finding that should be validated in other cohorts., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society.)

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]-1β, 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., (Copyright © 2021 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved.)

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 (O 3 ) or fine particulate matter (PM 2.5 ) 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 O 3 and PM 2.5 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]), O 3 /PM 2.5 (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 PM 2.5 (between 8.1 and 12.7 μg/m 3 ) in the third trimester was more rapid than would be expected due to the individual exposures alone (0.8 kg/m 2 per square root year; 95% CI = 0.1, 1.5; P for interaction = 0.03). We did not detect interactions between maternal smoking and O 3 or PM 2.5 at any other time on birth weight, neonatal adiposity, or BMI trajectories., Conclusions: Although PM 2.5 was generally below the EPA annual air quality standards of 12.0 μg/m 3 , exposure during the third trimester may influence BMI trajectories when combined with maternal smoking., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Objectives: To explore the longitudinal association of neonatal adiposity (fat mass percentage) with BMI trajectories and childhood overweight and obesity from ages 2 to 6 years., Methods: We studied 979 children from the Healthy Start cohort. Air displacement plethysmography was used to estimate fat mass percentage. Child weight and recumbent length or standing height were abstracted from medical records. Overweight and obesity were defined as BMI levels ≥85th percentile for age and sex. Mixed-effects models were used to examine the association between neonatal fat mass percentage and BMI trajectories from age 2 to 6 years. We tested for effect modification by sex, race and/or ethnicity, and breastfeeding duration. We estimated the proportion of children classified as overweight or obese at specific levels of neonatal fat mass percentage (mean ± SD)., Results: The mean neonatal adiposity level was 9.1% ± 4.0%. Child BMI levels differed by neonatal adiposity. Each SD increase in neonatal adiposity resulted in a 0.12 higher overall BMI level between ages 2 to 6 years (95% confidence interval: 0.03 to 0.20; P < .01), and this association was not modified by offspring sex, race and/or ethnicity, or breastfeeding duration. Increasing neonatal adiposity was associated with an increasing proportion of childhood overweight and obesity by age 5 years ( P = .02)., Conclusions: We provide novel evidence that higher neonatal adiposity is significantly associated with higher overall BMI levels and an increased likelihood of overweight or obesity from ages 2 to 6 years. Because various prenatal exposures may specifically influence offspring fat accretion, neonatal adiposity may be a useful surrogate end point for prenatal interventions aimed at reducing future childhood overweight and obesity., Competing Interests: POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose., (Copyright © 2020 by the American Academy of Pediatrics.)

Objective: The impact of in utero exposure to maternal overweight and obesity on offspring metabolic health is well documented. Neurodevelopmental outcomes among these children are, however, less well studied. To address this gap, the current study investigated brain function among 4- to 6-year-old children exposed to maternal overweight or obesity during gestation compared with that of children born to mothers with healthy BMI in pregnancy., Methods: Resting-state functional magnetic resonance imaging was used to study neuronal activity and connectivity during a passive viewing task (movie) among 101 typically developing children enrolled in the Healthy Start study, a longitudinal prebirth cohort in Colorado., Results: Forty-nine children (48%) were exposed to maternal overweight or obesity in utero (mean age = 5 years, SD = 0.9). Children born to mothers with overweight or obesity demonstrated hyperactivity in the left posterior cingulate cortex and hypoactivity in the dorsal anterior cingulate and the supplementary motor area (P < 0.05 for all). Children born to mothers with overweight or obesity also showed ubiquitously weaker brain connectivity (P < 0.05 for all)., Conclusions: These novel results suggest altered brain function among children exposed to maternal overweight and obesity in utero., (© 2020 The Obesity Society.)

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., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Prenatal exposures to ambient air pollution and traffic have been associated with adverse birth outcomes, and may also lead to an increased risk of obesity. Obesity risk may be reflected in changes in body composition in infancy., Objective: To estimate associations between prenatal ambient air pollution and traffic exposure, and infant weight and adiposity in a Colorado-based prospective cohort study., Methods: Participants were 1125 mother-infant pairs with term births. Birth weight was recorded from medical records and body composition measures (fat mass, fat-free mass, and adiposity [percent fat mass]) were evaluated via air displacement plethysmography at birth (n = 951) and at ~5 months (n = 574). Maternal residential address was used to calculate distance to nearest roadway, traffic density, and ambient concentrations of fine particulate matter (PM 2.5 ) and ozone (O 3 ) via inverse-distance weighted interpolation of stationary monitoring data, averaged by trimester and throughout pregnancy. Adjusted linear regression models estimated associations between exposures and infant weight and body composition., Results: Participants were urban residents and diverse in race/ethnicity and socioeconomic status. Average ambient air pollutant concentrations were generally low; the median, interquartile range (IQR), and range of third trimester concentrations were 7.3 μg/m 3 (IQR: 1.3, range: 3.3-12.7) for PM 2.5 and 46.3 ppb (IQR: 18.4, range: 21.7-63.2) for 8-h maximum O 3. Overall there were few associations between traffic and air pollution exposures and infant outcomes. Third trimester O 3 was associated with greater adiposity at follow-up (2.2% per IQR, 95% CI 0.1, 4.3), and with greater rates of change in fat mass (1.8 g/day, 95% CI 0.5, 3.2) and adiposity (2.1%/100 days, 95% CI 0.4, 3.7) from birth to follow-up., Conclusions: We found limited evidence of an association between prenatal traffic and ambient air pollution exposure and infant body composition. Suggestive associations between prenatal ozone exposure and early postnatal changes in body composition merit further investigation., Competing Interests: Declaration of competing interest The authors state that they have no competing financial interests related to this work., (Copyright © 2020 Elsevier Inc. All rights reserved.)

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.

Aims/hypothesis: We previously showed that intrauterine exposure to gestational diabetes mellitus (GDM) increases selected markers of adiposity in pre-pubertal adolescents. In the present study, we examined these associations in adolescence, and explored whether they are strengthened as the participants transition through puberty., Methods: Data from 597 individuals (505 unexposed, 92 exposed) participating in the longitudinal Exploring Perinatal Outcomes among Children (EPOCH) study in Colorado were collected at two research visits when the participants were, on average, 10.4 and 16.7 years old. Adiposity measures included BMI, waist/height ratio, and visceral and subcutaneous adipose tissue (as determined by MRI). Separate general linear mixed models were used to assess the longitudinal relationships between exposure to maternal GDM and each adiposity outcome. We tested whether the effect changed over time by including an interaction term between exposure and age in our models, and whether the associations were explained by postnatal behaviours., Results: Compared with unexposed participants, those exposed to maternal GDM had higher BMI (β = 1.28; 95% CI 0.35, 2.21; p < 0.007), waist/height ratio (β = 0.03; 95% CI 0.01, 0.04; p = 0.0004), visceral adipose tissue (β = 4.81; 95% CI 1.08, 8.54; p = 0.01) and subcutaneous adipose tissue (β = 35.15; 95% CI 12.43, 57.87; p < 0.003). The magnitude of these differences did not change over time and the associations did not appear to be explained by postnatal behaviours., Conclusions/interpretation: Our data provide further evidence that intrauterine exposure to maternal GDM is associated with increased offspring adiposity, an effect that appears early in life and tracks throughout adolescence. Efforts to prevent childhood obesity following intrauterine exposure to maternal GDM should target the prenatal or early life periods.

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/m 2 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.

This study investigated the role of microenvironment on personal exposures to black carbon (BC), fine particulate mass (PM 2.5 ), 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., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

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., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The extent of the association between temperature and heat-coded deaths, for which heat is the primary cause of death, remains largely unknown. We explored the association between temperature and heat-coded deaths and potential interactions with various demographic and environmental factors. A total of 335 heat-coded deaths that occurred in Oklahoma from 1990 through 2011 were identified using heat-related International Classification of Diseases codes, cause-of-death nomenclature, and narrative descriptions. Conditional logistic regression models examined the association between temperature and heat index on heat-coded deaths. Interaction by demographic factors (age, sex, marital status, living alone, outdoor/heavy labor occupations) and environmental factors (ozone, PM 10 , PM 2.5 ) was also explored. Temperatures ≥99 °F (the median value) were associated with approximately five times higher odds of a heat-coded death as compared to temperatures <99 °F (adjusted OR = 4.9, 95% CI 3.3, 7.2). The effect estimates were attenuated when exposure to heat was characterized by heat index. The interaction results suggest that effect of temperature on heat-coded deaths may depend on sex and occupation. For example, the odds of a heat-coded death among outdoor/heavy labor workers exposed to temperatures ≥99 °F was greater than expected based on the sum of the individual effects (observed OR = 14.0, 95% CI 2.7, 72.0; expected OR = 4.1 [2.8 + 2.3-1.0]). Our results highlight the extent of the association between temperature and heat-coded deaths and emphasize the need for a comprehensive, multisource definition of heat-coded deaths. Furthermore, based on the interaction results, we recommend that states implement or expand heat safety programs to protect vulnerable subpopulations, such as outdoor workers.

Background: The prevalence of diabetes mellitus (DM), chronic kidney disease (CKD), hemodialysis (HD), and renal transplantation (RT) is increasing. This study assessed postoperative complications among diabetic patients with CKD, HD, or post-RT after total hip arthroplasty (THA)., Methods: Four cohorts were created using a nationwide database: DM&THA, DM&CKD&THA, DM&HD&THA, and DM&RT&THA. Cohorts were matched to a control group by age and gender. Thirty-day medical complications and 90-day and 2-year surgical complications were evaluated., Results: All 30-day complications were higher in each cohort. Ninety-day and 2-year surgical complications in the DM&HD&THA cohort were increased compared to the DM&RT&THA cohort. Remarkably, no increased risk of periprosthetic joint infection, periprosthetic fracture, or revision was noted post-THA in the DM&RT&THA cohort., Conclusion: Diabetic patients with worsening kidney function are associated with increased post-THA complications. Postsurgical risks decline following RT. Diabetic patients with kidney failure may want to undergo RT prior to THA to optimize surgical outcomes., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Infant adiposity may be influenced by several environmental risk factors, but few studies have explored these interactions., Objective: To examine the interaction between exposure to secondhand smoke and breastfeeding exclusivity on adiposity at age 5 months., Methods: We studied 813 mother-offspring pairs from the longitudinal Healthy Start study. Fat mass and fat-free mass were measured by air displacement plethysmography. Linear regression analyses were used to estimate the association between household smokers (none, any) with fat mass, fat-free mass, percent fat mass, weight-for-age z-score, weight-for-length z-score and BMI-for-age z-score as separate outcomes. Interaction terms between household smokers and breastfeeding exclusivity (<5 months, ≥5 months) were added to separate models., Results: The combination of exposure to secondhand smoke and a lack of exclusive breastfeeding was associated with increased adiposity at age 5 months. For example, within the not exclusively breastfed strata, exposure to secondhand smoke was associated with increased fat mass (0.1 kg; 95% CI: 0.0-0.2; P = 0.05). Conversely, within the exclusively breastfed strata, there was virtually no difference in fat mass between exposed and non-exposed infants (coefficient: -0.1; 95% CI: -0.3-0.1; P = 0.25)., Conclusions: Our findings may inform new public health strategies with potential relevance for both smoking cessation and obesity prevention., (© 2017 World Obesity Federation.)

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.

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., (© The Author 2016. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Modern unipolar hip hemiarthroplasty, commonly used for displaced femoral neck fracture, is now modular, with both a variable length cobalt-chromium adapter-sleeve and large femoral head. Patients with these modular components may develop symptomatic trunnion corrosion, with elevated serum metal levels. We report the case of an 82-year-old woman, 5.5 years after a modular unipolar hip hemiarthroplasty, who presented with a 4-month history of hip pain and limp. Evaluation showed elevated serum cobalt and chromium levels and an acetabular cyst. At revision, fluid, tissue, and gross inspection were consistent with trunnion corrosion. The hip was revised with a ceramic head and dual mobility acetabular component, with a good result at 1 year. The designs of commercially available, modern unipolar hip hemiarthroplasty prostheses are reviewed.

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.

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.

Weakly binding azide ligands have been used as surface caps in the synthesis of lanthanide oxo and selenido clusters. Addition of NaN3 and Na2O to in situ prepared solutions of Ln(SePh)3 in pyridine results in the formation of (py)18Sm6Na2O2(N3)16 or (py)10Ln6O2(N3)12(SePh)2 (Ln = Ho, Er), with the Sm and Er compounds characterized by low temperature single crystal X-ray diffraction. Attempts to prepare chalcogenido derivatives by ligand-based redox reactions using elemental Se were successful in the preparation of (py)10Er6O2(SeSe)2(N3)10, a diselenido cluster having crystallographic disorder due to some site sharing of both SeSe and N3 ligands. These compounds all detonate when heated.

Ln(SePh)(3) (Ln = Ce, Pr, Nd), prepared by reduction of PhSeSePh with elemental Ln and Hg catalyst, reacts with excess elemental Se to give (py)(11)Ln(7)Se(21)HgSePh, an ellipsoidal polyselenide cluster. The molecular structure contains two square arrays of eight- or nine-coordinate Ln fused at one edge to form a V shape that is also capped on the concave side by a centrally located nine-coordinate (Se(3))pyLn(Se(3)) and on the convex side by a 2-fold disordered SeHgSePh. The central Ln coordinates to selenido, triselenido, and pyridine ligands, while all other Ln coordinate to selenido, diselenido, triselenido, and pyridine ligands. Thermal treatment of the Pr compound at 650 °C gave Pr(2)Se(3) and Pr(3)Se(4). NIR emission studies of the Nd compound show four transitions from the excited-state (4)F(3/2) ion to (4)I(9/2), (4)I(11/2), (4)I(13/2), and (4)I(15/2) states. The (4)F(3/2) ion to (4)I(11/2) transition (1075 nm emission) exhibited 43% quantum efficiency. This is the highest quantum efficiency reported for a 'molecular' Nd compound and leads a group of selenide-based clusters that has shown extraordinary quantum efficiency. In terms of efficiency and concentration, these compounds compare favorably with solid-state materials.

Ln(SePh)(3) (Ln = Ce, Pr, Nd) reacts with elemental Se in the presence of Na ions to give (py)(16)Ln(17)NaSe(18)(SePh)(16), a spherical cluster with a 1 nm diameter. All three rare-earth metals form isostructural products. The molecular structure contains a central Ln ion surrounded by eight five-coordinate Se(2-) that are then surrounded by a group of 16 Ln that define the cluster surface, with additional μ(3) and μ(5) Se(2-), μ(3) and μ(4) SePh(-), and pyridine donors saturating the vacant coordination sites of the surface Ln, and a Na ion coordinating to selenolates, a selenido, and pyridine ligands. NIR emission studies of the Nd compound reveal that this material has a 35% quantum efficiency, with four transitions from the excited state (4)F(3/2) ion to (4)I(9/2), (4)I(11/2), (4)I(13/2), and (4)I(15/2) states clearly evident. The presence of Na(+) is key to the formation of these larger clusters, where reactions using identical concentrations of Nd(SePh)(3) and Se with either Li or K led only to the isolation of (py)(8)Nd(8)Se(6)(SePh)(12).

Reductive cleavage of C(6)F(5)SeSeC(6)F(5) with elemental M (M = Zn, Cd, and Hg) in pyridine results in the formation of (py)(2)Zn(SeC(6)F(5))(2), (py)(2)Cd(SeC(6)F(5))(2), and Hg(SeC(6)F(5))(2). Structural characterization of the Zn and Cd compounds reveals tetrahedral coordination environments, while the Hg compound shows a complicated series of linear structures with two short, nearly linear Hg-Se bonds, up to two longer and perpendicular Hg...Se interactions, and no coordinated pyridine ligands. All three compounds exhibit well-defined intermolecular pi-pi-stacking interactions in the solid state. They are volatile and decompose at elevated temperatures to give MSe and either (SeC(6)F(5))(2) or Se(C(6)F(5))(2).

Mutations in sarcoglycans have been reported to cause autosomal-recessive limb-girdle muscular dystrophies. In skeletal and cardiac muscle, sarcoglycans are assembled into a complex on the sarcolemma from four subunits (alpha, beta, gamma, delta). In this report, we present a detailed structural analysis of sarcoglycans using deletion study, limited proteolysis and co-immunoprecipitation. Our results indicate that the extracellular regions of sarcoglycans consist of distinctive functional domains connected by proteinase K-sensitive sites. The N-terminal half domains are required for sarcoglycan interaction. The C-terminal half domains of beta-, gamma- and delta-sarcoglycan consist of a cysteine-rich motif and a previously unrecognized conserved sequence, both of which are essential for plasma membrane localization. Using a heterologous expression system, we demonstrate that missense sarcoglycan mutations affect sarcoglycan complex assembly and/or localization to the cell surface. Our data suggest that the formation of a stable complex is necessary but not sufficient for plasma membrane targeting. Finally, we provide evidence that the beta/delta-sarcoglycan core can associate with the C-terminus of dystrophin. Our results therefore generate important information on the structure of the sarcoglycan complex and the molecular mechanisms underlying the effects of various sarcoglycan mutations in muscular dystrophies.

Unlabelled: Acute renal failure (ARF) following trauma is rare. Historically, ARF has been associated with a high mortality rate. To investigate this entity we conducted a retrospective review of 72,757 admissions treated at nine regional trauma centers over a 5-year period. Seventy-eight patients (0.098%) developed acute renal failure requiring hemodialysis. Detailed demographic, clinical, and outcome data were collected. Patients with pre-existing medical conditions (group I) had a 70% increase in mortality over those without pre-existing conditions (p less than 0.004). Twenty-four patients (31%) developed ARF less than 6 days after injury (group II). The remainder (group III) developed late renal failure (mean time to first dialysis, 23 days). The predominant cause of death was multiple organ failure (82%). There were no differences in mortality because of multiple organ failure among the three groups of patients. Of the 33 survivors, six (18%) were discharged with renal insufficiency, three (9%) were discharged on dialysis, 23 (70%) were discharged home or to rehabilitation, and 27 (82%) had no significant evidence of renal insufficiency., Conclusion: Posttraumatic renal failure requiring hemodialysis is rare (incidence, 107 per 100,000 trauma center admissions), but the mortality rate remains high (57%). Two thirds of the cases of posttraumatic renal failure develop late and are secondary to multiple organ failure; one third of the cases of posttraumatic renal failure develop early and may result from inadequate resuscitation.

The adaptive behavior of kindergarten children with previous experience in day care centers or in family day care settings was compared and contrasted with that of kindergarten children who had not participated in day care. No significant differences among groups were found on measures of adaptive behavior, communication skills, daily living skills, socialization, or motor skills. The findings suggest that both forms of out-of-home care are suitable options for parents.

The feeding of bovine milk to five highly allergic pediatric patients with bilateral family histories of atopy led to transient malabsorption of glucose and fat as well as systemic autonomic functional changes which may be attributable to pharmacologic actions of histamine and/or acetylcholine. It is hypothesized that during allergic reactions endogenously released smooth muscle stimulating neuromediators could provide rapid propulsion of nutrients through the absorbing portion of the gut, leading to suboptimal absorption, and that bovine milk inducible malabsorption in the atopic patients has an immuno-pharmacologic basis in its pathogenesis.

Regulation of capsular biosynthesis (rcs) genes, encoding the ability to induce the production of a colanic acid polysaccharide capsule, were transferred to Escherichia coli by conjugation with Klebsiella pneumoniae (aerogenes) of capsular serotype K36. Transfer was mediated by a 58.4-MDa conjugative plasmid of incompatibility group IncM, which carried a copy of Tn7 (specifying resistance to trimethoprim and streptomycin) together with determinants for several further resistances. This plasmid did not carry the rcs genes itself, but mediated the conjugative recA-dependent transfer of part of the Klebsiella chromosome to E. coli. Once resident in E. coli, the rcs gene(s) could not be mobilised to other strains of E. coli, and the mobilising plasmid could be cured from capsulate transconjugants without loss of the ability to produce colanic acid. All such cured transconjugants contained an insertion of Tn7 in the chromosome, suggesting that the transposon might be involved in mobilisation of the rcs genes from Klebsiella sp. to E. coli. These findings explain previous observations that the ability to manufacture capsular polysaccharide could be transferred by plasmids between Klebsiella sp. and E. coli.