Prospective study of e-cigarette use and respiratory symptoms in adolescents and young adults.

RATIONALE: Electronic cigarette (e-cigarette) aerosol contains volatile aldehydes, including flavourings and oxidant metals with known pulmonary toxicity. OBJECTIVES: To evaluate the associations of e-cigarette use with symptoms of wheeze, bronchitic symptoms and shortness of breath (SOB) across 4 years of prospective data. METHODS: Participants completed questionnaires on respiratory symptoms and past 30-day e-cigarette, cigarette and cannabis use in 2014 (wave 1; N=2094; mean age 17.3 years, SD=0.6 years). Follow-up information was collected in 2015 (wave 2; n=1609), 2017 (wave 3; n=1502) and 2018 (wave 4; n=1637) using online surveys. Mixed-effects logistic regression models evaluated associations of e-cigarette use with respiratory symptoms. MEASUREMENTS AND MAIN RESULTS: Participants were mostly Hispanic white (51.8%) and evenly representative by sex (49.6% female; 50.4% male). Compared with never e-cigarette users, past 30-day e-cigarette users reported increased odds of wheeze (OR 1.81; 95% CI 1.28, 2.56), bronchitic symptoms (OR 2.06; 95% CI 1.58, 2.69) and SOB (OR 1.78; 95% CI 1.23, 2.57), adjusting for study wave, age, sex, race, lifetime asthma diagnosis and parental education. Effect estimates were attenuated (wheeze (OR 1.41; 95% CI 0.99, 2.01), bronchitic symptoms (OR 1.55; 95% CI 1.18, 2.05), SOB (OR 1.48; 95% CI 1.01, 2.18)), after adjusting additionally for current cigarette use, cannabis use and secondhand exposure to e-cigarettes/cigarettes/cannabis. CONCLUSIONS: E-cigarette use in young adults was associated with respiratory symptoms, independent of combustible cannabis and cigarette exposures.

Air pollution and age-dependent changes in emotional behavior across early adolescence in the U.S.

Recent studies have linked air pollution to increased risk for behavioral problems during development, albeit with inconsistent findings. Additional longitudinal studies are needed that consider how emotional behaviors may be affected when exposure coincides with the transition to adolescence - a vulnerable time for developing mental health difficulties. This study investigates if annual average PM2.5 and NO2 exposure at ages 9-10 years moderates age-related changes in internalizing and externalizing behaviors over a 2-year follow-up period in a large, nationwide U.S. sample of participants from the Adolescent Brain Cognitive Development (ABCD) Study®. Air pollution exposure was estimated based on the residential address of each participant using an ensemble-based modeling approach. Caregivers answered questions from the Child Behavior Checklist (CBCL) at the baseline, 1-year follow-up, and 2-year follow-up visits, for a total of 3 waves of data; from the CBCL we obtained scores on internalizing and externalizing problems plus 5 syndrome scales (anxious/depressed, withdrawn/depressed, rule-breaking behavior, aggressive behavior, and attention problems). Zero-inflated negative binomial models were used to examine both the main effect of age as well as the interaction of age with each pollutant on behavior while adjusting for various socioeconomic and demographic characteristics. Against our hypothesis, there was no evidence that greater air pollution exposure was related to more behavioral problems with age over time.

Prenatal ambient air pollution exposure and child weight trajectories from the 3rd trimester of pregnancy to 2 years of age: a cohort study.

BACKGROUND: Prenatal air pollution exposure may increase risk for childhood obesity. However, few studies have evaluated in utero growth measures and infant weight trajectories. This study will evaluate the associations of prenatal exposure to ambient air pollutants with weight trajectories from the 3rd trimester through age 2 years. METHODS: We studied 490 pregnant women who were recruited from the Maternal and Development Risks from Environmental and Social Stressors (MADRES) cohort, which comprises a low-income, primarily Hispanic population in Los Angeles, California. Nitrogen dioxide (NO2), particulate matter < 10 µm (PM10), particulate matter < 2.5 µm (PM2.5), and ozone (O3) concentrations during pregnancy were estimated from regulatory air monitoring stations. Fetal weight was estimated from maternal ultrasound records. Infant/child weight measurements were extracted from medical records or measured during follow-up visits. Piecewise spline models were used to assess the effect of air pollutants on weight, overall growth, and growth during each period. RESULTS: The mean (SD) prenatal exposure concentrations for NO2, PM2.5, PM10, and O3 were 16.4 (2.9) ppb, 12.0 (1.1) µg/m3, 28.5 (4.7) µg/m3, and 26.2 (2.9) ppb, respectively. Comparing an increase in prenatal average air pollutants from the 10th to the 90th percentile, the growth rate from the 3rd trimester to age 3 months was significantly increased (1.55% [95%CI 1.20%, 1.99%] for PM2.5 and 1.64% [95%CI 1.27%, 2.13%] for NO2), the growth rate from age 6 months to age 2 years was significantly decreased (0.90% [95%CI 0.82%, 1.00%] for NO2), and the attained weight at age 2 years was significantly lower (- 7.50% [95% CI - 13.57%, - 1.02%] for PM10 and - 7.00% [95% CI - 11.86%, - 1.88%] for NO2). CONCLUSIONS: Prenatal ambient air pollution was associated with variable changes in growth rate and attained weight from the 3rd trimester to age 2 years. These results suggest continued public health benefits of reducing ambient air pollution levels, particularly in marginalized populations.

Identifying critical windows of air pollution exposure during preconception and gestational period on birthweight: a prospective cohort study.

BACKGROUND: Few studies have assessed air pollution exposure association with birthweight during both preconception and gestational periods. METHODS: Leveraging a preconception cohort consisting of 14220 pregnant women and newborn children in Shanghai, China during 2016-2018, we aim to assess associations of NO2 and PM2.5 exposure, derived from high-resolution spatial-temporal models, during preconception and gestational periods with outcomes including term birthweight, birthweight Z-score, small-for-gestational age (SGA) and large-for-gestational age (LGA). Linear and logistic regressions were used to estimate 3-month preconception and trimester-averaged air pollution exposure associations; and distributed lag models (DLM) were used to identify critical exposure windows at the weekly resolution from preconception to delivery. Two-pollutant models and children's sex-specific associations were explored. RESULTS: After controlling for covariates, one standard deviation (SD) (11.5 µg/m3, equivalent to 6.1 ppb) increase in NO2 exposure during the second and the third trimester was associated with 13% (95% confidence interval: 2 - 26%) and 14% (95% CI: 1 - 29%) increase in SGA, respectively; and one SD (9.6 µg/m3) increase in PM2.5 exposure during the third trimester was associated with 15% (95% CI: 1 - 31%) increase in SGA. No association have been found for outcomes of birthweight, birthweight Z-score and LGA. DLM found that gestational weeks 22-32 were a critical window, when NO2 exposure had strongest associations with SGA. The associations of air pollution exposure tended to be stronger in female newborns than in male newborns. However, no significant associations of air pollution exposure during preconception period on birthweight outcomes were found. CONCLUSION: Consistent with previous studies, we found that air pollution exposure during mid-to-late pregnancy was associated with adverse birthweight outcomes.

In Utero Exposure to Mercury Is Associated With Increased Susceptibility to Liver Injury and Inflammation in Childhood.

BACKGROUND AND AIMS: Nonalcoholic fatty liver disease (NAFLD) is the most prevalent cause of liver disease in children. Mercury (Hg), a ubiquitous toxic metal, has been proposed as an environmental factor contributing to toxicant-associated fatty liver disease. APPROACH AND RESULTS: We investigated the effect of prenatal exposure to Hg on childhood liver injury by combining epidemiological results from a multicenter mother-child cohort with complementary in vitro experiments on monocyte cells that are known to play a key role in liver immune homeostasis and NAFLD. We used data from 872 mothers and their children (median age, 8.1 years; interquartile range [IQR], 6.5-8.7) from the European Human Early-Life Exposome cohort. We measured Hg concentration in maternal blood during pregnancy (median, 2.0 µg/L; IQR, 1.1-3.6). We also assessed serum levels of alanine aminotransferase (ALT), a common screening tool for pediatric NAFLD, and plasma concentrations of inflammation-related cytokines in children. We found that prenatal Hg exposure was associated with a phenotype in children that was characterized by elevated ALT (≥22.1 U/L for females and ≥25.8 U/L for males) and increased concentrations of circulating IL-1ß, IL-6, IL-8, and TNF-α. Consistently, inflammatory monocytes exposed in vitro to a physiologically relevant dose of Hg demonstrated significant up-regulation of genes encoding these four cytokines and increased concentrations of IL-8 and TNF-α in the supernatants. CONCLUSIONS: These findings suggest that developmental exposure to Hg can contribute to inflammation and increased NAFLD risk in early life.

The Role of Childhood Asthma in Obesity Development: A Nationwide US Multicohort Study.

RATIONALE: Asthma and obesity often co-occur. It has been hypothesized that asthma may contribute to childhood obesity onset. OBJECTIVES: To determine if childhood asthma is associated with incident obesity and examine the role of asthma medication in this association. METHODS: We studied 8,716 children between ages 6 and 18.5 years who were nonobese at study entry participating in 18 US cohorts of the Environmental influences on Child Health Outcomes program (among 7,299 children with complete covariate data mean [SD] study entry age = 7.2 [1.6] years and follow up = 5.3 [3.1] years). MEASUREMENTS AND MAIN RESULTS: We defined asthma based on caregiver report of provider diagnosis. Incident obesity was defined as the first documented body mass index ≥95th percentile for age and sex following asthma status ascertainment. Over the study period, 26% of children had an asthma diagnosis and 11% developed obesity. Cox proportional hazards models with sex-specific baseline hazards were fitted to assess the association of asthma diagnosis with obesity incidence. Children with asthma had a 23% (95% confidence intervals [CI] = 4, 44) higher risk for subsequently developing obesity compared with those without asthma. A novel mediation analysis was also conducted to decompose the total asthma effect on obesity into pathways mediated and not mediated by asthma medication use. Use of asthma medication attenuated the total estimated effect of asthma on obesity by 64% (excess hazard ratios = 0.64; 95% CI = -1.05, -0.23). CONCLUSIONS: This nationwide study supports the hypothesis that childhood asthma is associated with later risk of obesity. Asthma medication may reduce this association and merits further investigation as a potential strategy for obesity prevention among children with asthma.

Modeling the longitudinal transitions of electronic cigarettes and conventional cigarettes with time-dependent covariates among adolescents.

E-cigarettes may help combustible cigarette smokers switch to a less harmful alternative, or may increase the risk of subsequent initiation of cigarettes among non-smokers. Among youth, it is not clear whether both pathways occur equally, or whether one direction is more likely than the other. We used data from a prospective cohort study of youth in Southern California followed twice annually from Fall 2013 (9th grade) to Fall 2015 (11th grade) (N = 1977). A polytomous logistic regression model was used to simultaneously estimate transition rates for initiation of and abstention from e-cigarettes and cigarettes. Use of e-cigarettes was positively associated with initiation of cigarettes (OR = 7.57; 95%CI:[5.32, 10.8]) and negatively associated with cigarette abstention (OR = 0.58; 95%CI:[0.33, 0.99]) in adjusted models; cigarette use was positively associated with e-cigarette initiation (OR = 2.54; 95%CI:[1.45, 4.47]) and negatively associated with e-cigarette abstention (OR = 0.31; 95%CI:[0.17,0.57]). Uni-directional transition from e-cigarettes only to cigarettes only occurred less frequently than expected under independence (OR = 0.33; 95% CI [0.20, 0.55]), whereas simultaneously initiating both products (OR = 9.79; 95%CI:[7.22, 13.3]) and simultaneously abstaining (OR = 2.84; 95%CI:[1.50, 5.37]) were more frequent than expected. E-cigarettes were more strongly associated with subsequent cigarette initiation than the reverse, though both models indicated that use of either product seems to encourage use of the other. Models also indicated that use of either e-cigarettes or cigarettes resulted in reduced abstention of the other product. Findings suggest that prevention efforts for that continue to focus on both e-cigarettes and cigarettes are needed.

Plasma concentrations of lipophilic persistent organic pollutants and glucose homeostasis in youth populations.

BACKGROUND: Exposure to lipophilic persistent organic pollutants (POPs) is ubiquitous. POPs are metabolic disrupting chemicals and are potentially diabetogenic. METHODS: Using a multi-cohort study including overweight adolescents from the Study of Latino Adolescents at Risk (SOLAR, N = 301, 2001-2012) and young adults from the Southern California Children's Health Study (CHS, N = 135, 2014-2018), we examined associations of POPs and risk factors for type 2 diabetes. SOLAR participants underwent annual visits for a median of 2.2 years and CHS participants performed a single visit, during which a 2-h oral glucose tolerance test was performed. Linear mixed models were used to examine associations between plasma concentrations of POPs [4,4'-dichlorodiphenyldichloroethylene (4,4'-DDE), hexachlorobenzene (HCB), PCBs-153, 138, 118, 180 and PBDEs-154, 153, 100, 85, 47] and changes in glucose homeostasis across age and pubertal stage. RESULTS: In SOLAR, exposure to HCB, PCB-118, and PBDE-153 was associated with dysregulated glucose metabolism. For example, each two-fold increase in HCB was associated with approximately 2 mg/dL higher glucose concentrations at 30 min (p = 0.001), 45 min (p = 0.0006), and 60 min (p = 0.03) post glucose challenge. Compared to individuals with low levels of PCB-118, individuals with high levels exhibited a 4.7 mg/dL (p = 0.02) higher glucose concentration at 15 min and a 3.6 mg/dL (p = 0.01) higher glucose concentration at 30 min. The effects observed with exposure to organochlorine compounds were independent of pubertal stages. PBDE-153 was associated with the development of dysregulated glucose metabolism beginning in late puberty. At Tanner stage 4, exposure to PBDE-153 was associated with a 12.7 mg/dL higher 60-min glucose concentration (p = 0.009) and a 16.1 mg*dl-1*hr-1 higher glucose AUC (p = 0.01). These associations persisted at Tanner 5. In CHS, PBDE-153 and total PBDE were associated with similar increases in glucose concentrations. CONCLUSION: Our results suggest that childhood exposure to lipophilic POPs is associated with dysregulated glucose metabolism.

Effects of policy-driven hypothetical air pollutant interventions on childhood asthma incidence in southern California.

Childhood asthma is a major public health concern and has significant adverse impacts on the lives of the children and their families, and on society. There is an emerging link between air pollution, which is ubiquitous in our environment, particularly in urban centers, and incident childhood asthma. Here, using data from 3 successive cohorts recruited from the same 9 communities in southern California over a span of 20 y (1993 to 2014), we estimated asthma incidence using G-computation under hypothetical air pollution exposure scenarios targeting nitrogen dioxide (NO2) and particulate matter <2.5 µm (PM2.5) in separate interventions. We reported comparisons of asthma incidence under each hypothetical air pollution intervention with incidence under the observed natural course of exposure; results that may be more tangible for policymakers compared with risk ratios. Model results indicated that childhood asthma incidence rates would have been statistically significantly higher had the observed reduction in ambient NO2 in southern California not occurred in the 1990s and early 2000s, and asthma incidence rates would have been significantly lower had NO2 been lower than what it was observed to be. For example, compliance with a hypothetical standard of 20 ppb NO2 was estimated to result in 20% lower childhood asthma incidence (95% CI, -27% to -11%) compared with the exposure that actually occurred. The findings for hypothetical PM2.5 interventions, although statistically significant, were smaller in magnitude compared with results for the hypothetical NO2 interventions. Our results suggest a large potential public health benefit of air pollutant reduction in reduced incidence of childhood asthma.

Prenatal Exposure to Perfluoroalkyl Substances Associated With Increased Susceptibility to Liver Injury in Children.

BACKGROUND AND AIMS: Per- and polyfluoroalkyl substances (PFAS) are widespread and persistent pollutants that have been shown to have hepatotoxic effects in animal models. However, human evidence is scarce. We evaluated how prenatal exposure to PFAS associates with established serum biomarkers of liver injury and alterations in serum metabolome in children. APPROACH AND RESULTS: We used data from 1,105 mothers and their children (median age, 8.2 years; interquartile range, 6.6-9.1) from the European Human Early-Life Exposome cohort (consisting of six existing population-based birth cohorts in France, Greece, Lithuania, Norway, Spain, and the United Kingdom). We measured concentrations of perfluorooctane sulfonate, perfluorooctanoate, perfluorononanoate, perfluorohexane sulfonate, and perfluoroundecanoate in maternal blood. We assessed concentrations of alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase in child serum. Using Bayesian kernel machine regression, we found that higher exposure to PFAS during pregnancy was associated with higher liver enzyme levels in children. We also measured child serum metabolomics through a targeted assay and found significant perturbations in amino acid and glycerophospholipid metabolism associated with prenatal PFAS. A latent variable analysis identified a profile of children at high risk of liver injury (odds ratio, 1.56; 95% confidence interval, 1.21-1.92) that was characterized by high prenatal exposure to PFAS and increased serum levels of branched-chain amino acids (valine, leucine, and isoleucine), aromatic amino acids (tryptophan and phenylalanine), and glycerophospholipids (phosphatidylcholine [PC] aa C36:1 and Lyso-PC a C18:1). CONCLUSIONS: Developmental exposure to PFAS can contribute to pediatric liver injury.

The Potential Effects of Policy-driven Air Pollution Interventions on Childhood Lung Development.

Rationale: Although elevated air pollution exposure impairs lung-function development in childhood, it remains a challenge to use this information to estimate the potential public health benefits of air pollution interventions in exposed populations.Objectives: Apply G-computation to estimate hypothetical effects of several realistic scenarios for future air pollution reductions on lung growth.Methods: Mixed-effects linear regression was used to estimate FEV1 and FVC from age 11 to 15 years in 2,120 adolescents across 3 cohorts (1993-2001, 1997-2004, and 2007-2011). Models included regional pollutants (nitrogen dioxide [NO2] or particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5]) and other important covariates. Using G-computation, a causal inference-based method, we then estimated changes in mean lung growth in our population for hypothetical interventions on either NO2 or PM2.5. Confidence intervals (CIs) were computed by bootstrapping (N = 1,000).Measurements and Main Results: Compared with the effects of exposure from observed NO2 concentrations during the study period, had communities remained at 1994 to 1997 NO2 levels, FEV1 and FVC growth were estimated to have been reduced by 2.7% (95% CI, -3.6 to -1.8) and 4.2% (95% CI, -5.2 to -3.4), respectively. If NO2 concentrations had been reduced by 30%, we estimated a 4.4% increase in FEV1 growth (95% CI, 2.8-5.9) and a 7.1% increase in FVC growth (95% CI, 5.7-8.6). Comparable results were observed for PM2.5 interventions.Conclusions: We estimated that substantial increases in lung function would occur as a result of interventions that reduce NO2 or PM2.5 concentrations. These findings provide a quantification of potential health benefits of air quality improvement.

The Dynamic Relationship Between Asthma and Obesity in Schoolchildren.

Asthma and obesity are among the most prevalent chronic health conditions in children. Although there has been compelling evidence of co-occurrence of asthma and obesity, it is uncertain whether asthma contributes to the development of obesity or obesity contributes to the onset of asthma or both. In this study, we used a joint transition modeling approach with cross-lagged structure to understand how asthma and obesity influence each other dynamically over time. Subjects for this study included 5,193 kindergarten and first-grade students enrolled from 13 communities in 2002-2003 in the Southern California Children's Health Study, with up to 10 years of follow-up. We found that nonobese children with diagnosed asthma at a study visit were at 37% higher odds of becoming obese by the next annual visit compared with children without asthma (odds ratio = 1.38; 95% credible interval: 1.12, 1.71). However, the presence of obesity at the current visit was not statistically significantly associated with asthma onset in the next visit (odds ratio = 1.25; 95% credible interval: 0.94, 1.62). In conclusion, childhood asthma appears to drive an increase in the onset of obesity among schoolchildren, while the onset of obesity does not necessarily imply the future onset of asthma, at least in the short term.

Patterns and determinants of exhaled nitric oxide trajectories in schoolchildren over a 7-year period.

Fractional exhaled nitric oxide (F ENO50 ), a marker of allergic airway inflammation, is used in respiratory research and asthma clinical care; however, its trajectory with increasing age during childhood has not been well characterised. We examined F ENO50 longitudinally during a period of important somatic growth to describe trajectories across childhood and adolescence in healthy participants and evaluate clinical factors as potential determinants of trajectories.F ENO50 was collected at six visits over 8 years in a population-based cohort of 1791 schoolchildren without asthma (median age at entry 8.4 years). Smooth sex-specific F ENO50 trajectories were estimated using generalised additive mixed models, with participant-level random effects. We evaluated whether sex-specific trajectories were influenced by race/ethnicity, body mass index (BMI) percentile, allergic rhinitis or puberty.Different F ENO50 patterns were observed by sex in later childhood and several factors were associated with either F ENO50 level or change in F ENO50 as participants aged. F ENO50 -age trajectories were similar by sex until age ∼11.5 years, after which males had greater F ENO50 change than females. This divergence in F ENO50 -age trajectories coincides with puberty. Males with higher starting BMI percentile had attenuated F ENO50 -age slopes. Among males, F ENO50 levels were lower in non-Hispanic white subjects. Among both sexes, participants with rhinitis had higher F ENO50 F ENO50 levels within individuals tracked over time; however, there was considerable variation in F ENO50 patterns across participants.F ENO50 trajectories from longitudinal data provide evidence of sex differences coinciding with puberty, suggesting potential hormone link. Improved understanding of determinants of F ENO50 trajectories is needed to realise the potential for using individualised predicted F ENO50 trajectories.

Arsenic and birth outcomes in a predominately lower income Hispanic pregnancy cohort in Los Angeles.

Prenatal arsenic exposure has been associated with reduced fetal growth and increased risk for preterm birth, but most studies have been conducted in highly exposed populations outside the U.S. or in non-Hispanic populations in the rural U.S. The objectives of the current study were to: 1) examine the impact of early pregnancy exposure to arsenic on birth weight and gestational age at birth in a predominately lower income Hispanic pregnancy cohort in urban Los Angeles and 2) compare multiple biomarkers of arsenic exposure (blood, urine, and hair) assessed in early pregnancy (mean ± SD gestational age at biospecimen collection: 14 ± 4 weeks). Total arsenic (blood, hair) was measured by ICP-MS and speciated arsenic (urine) was measured by HPLC coupled to ICP-MS. Associations between log2-transformed arsenic measures and birth outcomes were evaluated using multivariable linear regression. A doubling in hair arsenic was associated with a 72.2 g (95% CI: -144.3, -0.1, P = 0.05) lower birth weight, after adjusting for potential confounders and gestational age at birth. A similar but non-significant trend was observed for blood arsenic, but not urine arsenic. The inverse association between hair arsenic and birth weight was more pronounced among infants whose mothers gained greater amounts of weight during pregnancy (Pinteraction = 0.02). The association between urinary monomethyl arsenic and GA at birth differed by pre-pregnancy BMI (Pinteraction<0.01). This study provides evidence that even at relatively low levels of exposure, arsenic exposure (measured in hair samples collected in early pregnancy) may adversely affect fetal growth in this understudied population, particularly in combination with greater gestational weight gain. Future studies with larger sample sizes are needed to confirm these findings and to further investigate some of the inconsistencies observed for the different arsenic biomarkers evaluated.

Electronic Cigarette and Cigarette Social Environments and Ever Use of Each Product: A Prospective Study of Young Adults in Southern California.

BACKGROUND: A supportive youth cigarette social environment, for example, friends' approval of use, leads to cigarette use initiation, and cigarette users develop a more supportive social environment. Whether there is a bidirectional relationship of electronic cigarette (e-cigarette) social environment with e-cigarette use has not been studied. METHODS: Prospective data were collected from 1441 Children's Health Study participants in 2014 (median age = 17.3 years) and at follow-up 1.5 years later. Associations were examined of (1) supportive e-cigarette social environment with subsequent e-cigarette use initiation and (2) baseline e-cigarette use with supportive e-cigarette social environment at follow-up (among those with a nonsupportive baseline social environment). RESULTS: Participants with three to four friends using e-cigarettes at baseline (vs. no friends) had an odds ratio (OR) of 4.08 of subsequent initiation (95% confidence interval [CI] = 1.96 to 8.49); those with best friends who would have a very friendly (vs. unfriendly) reaction to e-cigarette use had an OR of 2.54 of initiation (95% CI = 1.57 to 4.10); and those with someone in the home using e-cigarettes had an OR of 1.94 of initiation (95% CI = 1.19 to 3.15). Participants who had ever used e-cigarettes at baseline developed a supportive social environment at follow-up (OR of 2.06 of having any friends who used e-cigarettes [95% CI = 1.29 to 3.30] and OR of 2.33 of having friends who were friendly toward use [95% CI = 1.32 to 4.11]). Similar bidirectional associations were observed between ever cigarette use and a supportive cigarette social environment. CONCLUSIONS: The bidirectional relationship between a supportive e-cigarette social environment and ever use of e-cigarettes was similar to that previously observed between cigarette social environment and cigarette use. IMPLICATIONS: Disrupting the social acceptability of youth e-cigarette use merits consideration as a strategy for preventing initiation of e-cigarette use, just as the social denormalization of cigarette use has proven to be effective in preventing cigarette initiation.

Tobacco Marketing and Subsequent Use of Cigarettes, E-Cigarettes, and Hookah in Adolescents.

INTRODUCTION: Tobacco marketing has expanded from cigarettes to other tobacco products through many promotional channels. Marketing exposure is associated with use of that tobacco product. However, it is unclear if marketing for one product leads to subsequent use of other tobacco products. METHODS: This prospective cohort study assessed self-reported marketing exposure for six tobacco products across five marketing channels in 11th and 12th grade students in 2014. Approximately 16 months later, a follow-up survey was conducted online (N = 1553) to assess initiation of cigarettes, electronic cigarettes (e-cigarettes), and hookah. RESULTS: Adolescent never-smokers with frequent exposure to cigarette marketing on the Internet and in stores are more than two times as likely to begin smoking as young adults (Internet OR = 2.98 [95% CI = 1.56 to 5.66]; stores OR = 2.83 [95% CI = 1.23 to 6.50]). Never users of e-cigarettes were significantly more likely to initiate use, if exposed to Internet, store, and outdoor e-cigarette marketing. Never users of hookah were more likely to use hookah after seeing it marketed in stores. Youth exposed to marketing of e-cigarettes, hookah, cigars, smokeless tobacco, and pipe tobacco in stores were two to three times more likely to begin smoking cigarettes even though the marketed products were not cigarettes. CONCLUSIONS: Adolescent exposure to marketing of tobacco products is associated with initiation of those products as young adults. Exposure to marketing for non-cigarette tobacco products is associated with subsequent cigarette smoking, even when the promoted products are not cigarettes. Future research and interventions should consider the influence of marketing from multiple tobacco products on adolescent tobacco use. IMPLICATIONS: Adolescents grow up in a rich media environment with exposure to tobacco marketing in both their homes (eg, through the Internet and television) and their communities (eg, stores and billboards). This prospective study provides evidence that adolescents exposed to tobacco marketing for multiple tobacco products are more likely to subsequently begin using those products and to begin smoking cigarettes even when the marketing they recall is for different tobacco products. Adolescent exposure to tobacco marketing can increase likelihood of cigarette smoking, e-cigarette, and hookah use with potential lifelong health effects.

Study Design, Protocol and Profile of the Maternal And Developmental Risks from Environmental and Social Stressors (MADRES) Pregnancy Cohort: a Prospective Cohort Study in Predominantly Low-Income Hispanic Women in Urban Los Angeles.

BACKGROUND: The burden of childhood and adult obesity disproportionally affects Hispanic and African-American populations in the US, and these groups as well as populations with lower income and education levels are disproportionately affected by environmental pollution. Pregnancy is a critical developmental period where maternal exposures may have significant impacts on infant and childhood growth as well as the future health of the mother. We initiated the "Maternal And Developmental Risks from Environmental and Social Stressors (MADRES)" cohort study to address critical gaps in understanding the increased risk for childhood obesity and maternal obesity outcomes among minority and low-income women in urban Los Angeles. METHODS: The MADRES cohort is specifically examining whether pre- and postpartum environmental exposures, in addition to exposures to psychosocial and built environment stressors, lead to excessive gestational weight gain and postpartum weight retention in women and to perturbed infant growth trajectories and increased childhood obesity risk through altered psychological, behavioral and/or metabolic responses. The ongoing MADRES study is a prospective pregnancy cohort of 1000 predominantly lower-income, Hispanic women in Los Angeles, CA. Enrollment in the MADRES cohort is initiated prior to 30 weeks gestation from partner community health clinics in Los Angeles. Cohort participants are followed through their pregnancies, at birth, and during the infant's first year of life through a series of in-person visits with interviewer-administered questionnaires, anthropometric measurements and biospecimen collection as well as telephone interviews conducted with the mother. DISCUSSION: In this paper, we outline the study rationale and data collection protocol for the MADRES cohort, and we present a profile of demographic, health and exposure characteristics for 291 participants who have delivered their infants, out of 523 participants enrolled in the study from November 2015 to October 2018 from four community health clinics in Los Angeles. Results from the MADRES cohort could provide a powerful rationale for regulation of targeted chemical environmental components, better transportation and urban design policies, and clinical recommendations for stress-coping strategies and behavior to reduce lifelong obesity risk.

Association of Changes in Air Quality With Incident Asthma in Children in California, 1993-2014.

Importance: Exposure to air pollutants is a well-established cause of asthma exacerbation in children; whether air pollutants play a role in the development of childhood asthma, however, remains uncertain. Objective: To examine whether decreasing regional air pollutants were associated with reduced incidence of childhood asthma. Design, Setting, and Participants: A multilevel longitudinal cohort drawn from 3 waves of the Southern California Children's Health Study over a period of air pollution decline. Each cohort was followed up from 4th to 12th grade (8 years): 1993-2001, 1996-2004, and 2006-2014. Final follow-up for these data was June 2014. Population-based recruitment was from public elementary schools. A total of 4140 children with no history of asthma and residing in 1 of 9 Children's Health Study communities at baseline were included. Exposures: Annual mean community-level ozone, nitrogen dioxide, and particulate matter less than 10 µm (PM10) and less than 2.5 µm (PM2.5) in the baseline year for each of 3 cohorts. Main Outcomes and Measures: Prospectively identified incident asthma, collected via questionnaires during follow-up. Results: Among the 4140 children included in this study (mean [SD] age at baseline, 9.5 [0.6] years; 52.6% female [n = 2 179]; 58.6% white [n = 2273]; and 42.2% Hispanic [n = 1686]), 525 incident asthma cases were identified. For nitrogen dioxide, the incidence rate ratio (IRR) for asthma was 0.80 (95% CI, 0.71-0.90) for a median reduction of 4.3 parts per billion, with an absolute incidence rate decrease of 0.83 cases per 100 person-years. For PM2.5, the IRR was 0.81 (95% CI, 0.67-0.98) for a median reduction of 8.1 µg/m3, with an absolute incidence rate decrease of 1.53 cases per 100 person-years. For ozone, the IRR for asthma was 0.85 (95% CI, 0.71-1.02) for a median reduction of 8.9 parts per billion, with an absolute incidence rate decrease of 0.78 cases per 100 person-years. For PM10, the IRR was 0.93 (95% CI, 0.82-1.07) for a median reduction of 4.0 µg/m3, with an absolute incidence rate decrease of 0.46 cases per 100 person-years. Conclusions and Relevance: Among children in Southern California, decreases in ambient nitrogen dioxide and PM2.5 between 1993 and 2014 were significantly associated with lower asthma incidence. There were no statistically significant associations for ozone or PM10.

Long-Term Ambient Temperature and Externalizing Behaviors in Adolescents.

The climate-violence relationship has been debated for decades, and yet most of the supportive evidence has come from ecological or cross-sectional analyses with very limited long-term exposure data. We conducted an individual-level, longitudinal study to investigate the association between ambient temperature and externalizing behaviors of urban-dwelling adolescents. Participants (n = 1,287) in the Risk Factors for Antisocial Behavior Study, in California, were examined during 2000-2012 (aged 9-18 years) with repeated assessments of their externalizing behaviors (e.g., aggression, delinquency). Ambient temperature data were obtained from the local meteorological information system. In adjusted multilevel models, aggressive behaviors significantly increased with rising average temperatures (per 1°C increment) in the preceding 1, 2, or 3 years (respectively, ß = 0.23, 95% confidence interval (CI): 0.00, 0.46; ß = 0.35, 95% CI: 0.06, 0.63; or ß = 0.41, 95% CI: 0.08, 0.74), equivalent to 1.5-3.0 years of delay in age-related behavioral maturation. These associations were slightly stronger among girls and families of lower socioeconomic status but greatly diminished in neighborhoods with more green space. No significant associations were found with delinquency. Our study provides the first individual-level epidemiologic evidence supporting the adverse association of long-term ambient temperature and aggression. Similar approaches to studying meteorology and violent crime might further inform scientific debates on climate change and collective violence.

Association of improved air quality with lung development in children.

BACKGROUND: Air-pollution levels have been trending downward progressively over the past several decades in southern California, as a result of the implementation of air quality-control policies. We assessed whether long-term reductions in pollution were associated with improvements in respiratory health among children. METHODS: As part of the Children's Health Study, we measured lung function annually in 2120 children from three separate cohorts corresponding to three separate calendar periods: 1994-1998, 1997-2001, and 2007-2011. Mean ages of the children within each cohort were 11 years at the beginning of the period and 15 years at the end. Linear-regression models were used to examine the relationship between declining pollution levels over time and lung-function development from 11 to 15 years of age, measured as the increases in forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) during that period (referred to as 4-year growth in FEV1 and FVC). RESULTS: Over the 13 years spanned by the three cohorts, improvements in 4-year growth of both FEV1 and FVC were associated with declining levels of nitrogen dioxide (P<0.001 for FEV1 and FVC) and of particulate matter with an aerodynamic diameter of less than 2.5 µm (P= 0.008 for FEV1 and P<0.001 for FVC) and less than 10 µm (P<0.001 for FEV1 and FVC). These associations persisted after adjustment for several potential confounders. Significant improvements in lung-function development were observed in both boys and girls and in children with asthma and children without asthma. The proportions of children with clinically low FEV1 (defined as <80% of the predicted value) at 15 years of age declined significantly, from 7.9% to 6.3% to 3.6% across the three periods, as the air quality improved (P = 0.001). CONCLUSIONS: We found that long-term improvements in air quality were associated with statistically and clinically significant positive effects on lung-function growth in children. (Funded by the Health Effects Institute and others.).