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Background: Depression substantially contributes to pregnancy-related morbidity, and pregnancy is increasingly recognized as a vulnerable window for exposure effects on maternal mental health. Exposures to organophosphate esters (OPEs) are ubiquitous and may have neurotoxic effects; however, their impacts on prenatal depression remain unknown. We evaluated associations of third trimester OPE metabolites on maternal depressive symptoms during pregnancy., Methods: This study included 422 participants in the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort, a prospective pregnancy cohort of primarily low-income and Hispanic participants residing in Los Angeles, California. We measured concentrations of nine OPEs in third trimester spot urine samples (mean gestational age = 31.5 ± 2.0 weeks). Using the Center for Epidemiologic Studies-Depression (CES-D) scale, we classified participants as having probable depression during pregnancy (N = 137) or not (N = 285) if one or more CES-D scores administered at each trimester met the suggested cutoff score for clinically significant depressive symptoms (≥16). We estimated associations of prenatal OPE metabolite concentrations in tertiles and risk of prenatal depression using modified Log-Poisson regression. We examined associations of the OPE mixture on depression during pregnancy using Bayesian kernel machine regression (BKMR)., Results: Participants with the highest tertiles of DPHP and BDCIPP exposure had a 67% (95% CI: 22%, 128%) and 47% (95% CI: 4%, 108%) increased risk of maternal depressive symptoms during pregnancy, respectively. No associations between other OPE metabolites and maternal depression symptoms were observed. In mixture analyses, we observed a positive and linear association between higher exposure to the OPE metabolite mixture and odds of prenatal maternal depression, primarily driven by DPHP., Conclusions: Our findings provide new evidence of associations between frequently detected OPE metabolites on maternal depression symptoms during pregnancy. Results could inform future intervention efforts aimed at reducing perinatal maternal depression., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Personal exposure to fine particulate matter (PM 2.5 ) is impacted by different sources each with different chemical composition. Determining these sources is important for reducing personal exposure and its health risks especially during pregnancy., Objective: Identify main sources and their contributions to the personal PM 2.5 exposure in 213 women in the 3rd trimester of pregnancy in Los Angeles, CA., Methods: We measured 48-hr integrated personal PM 2.5 exposure and analyzed filters for PM 2.5 mass, elemental composition, and optical carbon fractions. We used the EPA Positive Matrix Factorization (PMF) model to resolve and quantify the major sources of personal PM 2.5 exposure. We then investigated bivariate relationships between sources, time-activity patterns, and environmental exposures in activity spaces and residential neighborhoods to further understand sources., Results: Mean personal PM 2.5 mass concentration was 22.3 (SD = 16.6) μg/m 3 . Twenty-five species and PM 2.5 mass were used in PMF with a final R 2 of 0.48. We identified six sources (with major species in profiles and % contribution to PM 2.5 mass) as follows: secondhand smoking (SHS) (brown carbon, environmental tobacco smoke; 65.3%), fuel oil (nickel, vanadium; 11.7%), crustal (aluminum, calcium, silicon; 11.5%), fresh sea salt (sodium, chlorine; 4.7%), aged sea salt (sodium, magnesium, sulfur; 4.3%), and traffic (black carbon, zinc; 2.6%). SHS was significantly greater in apartments compared to houses. Crustal source was correlated with more occupants in the household. Aged sea salt increased with temperature and outdoor ozone, while fresh sea salt was highest on days with westerly winds from the Pacific Ocean. Traffic was positively correlated with ambient NO 2 and traffic-related NO x at residence. Overall, 76.8% of personal PM 2.5 mass came from indoor or personal compared to outdoor sources., Impact: We conducted source apportionment of personal PM 2.5 samples in pregnancy in Los Angeles, CA. Among identified sources, secondhand smoking contributed the most to the personal exposure. In addition, traffic, crustal, fuel oil, fresh and aged sea salt sources were also identified as main sources. Traffic sources contained markers of combustion and non-exhaust wear emissions. Crustal source was correlated with more occupants in the household. Aged sea salt source increased with temperature and outdoor ozone and fresh sea salt source was highest on days with westerly winds from the Pacific Ocean., (© 2024. The Author(s).)

Background: Air pollution has been associated with gestational hypertension (GH) and preeclampsia, but susceptible windows of exposure and potential vulnerability by comorbidities, such as prenatal depression, remain unclear., Methods: We ascertained GH and preeclampsia cases in a prospective pregnancy cohort in Los Angeles, CA. Daily levels of ambient particulate matters (with a diameter of ≤10 μm [PM 10 ] or ≤2.5 μm [PM 2.5 ]), nitrogen dioxide, and ozone were averaged for each week from 12 weeks preconception to 20 gestational weeks. We used distributed lag models to identify susceptible exposure windows, adjusting for potential confounders. Analyses were additionally stratified by probable prenatal depression to explore population vulnerability., Results: Among 619 participants, 60 developed preeclampsia and 42 developed GH. We identified a susceptible window for exposure to PM 2.5 from 1 week preconception to 11 weeks postconception: higher exposure (5 µg/m 3 ) within this window was associated with an average of 8% (95% CI, 1%-15%) higher risk of GH. Among participants with probable prenatal depression (n=179; 32%), overlapping sensitive windows were observed for all pollutants from 8 weeks before to 10 weeks postconception with increased risk of GH (PM 2.5 , 16% [95% CI, 3%-31%]; PM 10 , 39% [95% CI, 13%-72%]; nitrogen dioxide, 65% [95% CI, 17%-134%]; and ozone, 45% [95% CI, 9%-93%]), while the associations were close to null among those without prenatal depression. Air pollutants were not associated with preeclampsia in any analyses., Conclusions: We identified periconception through early pregnancy as a susceptible window of air pollution exposure with an increased risk of GH. Prenatal depression increases vulnerability to air pollution exposure and GH., Competing Interests: Disclosures None.

Importance: Recent studies in Canadian and Mexican populations suggest an association of higher prenatal fluoride exposure with poorer neurobehavioral development, but whether this association holds for US-based populations is unknown., Objective: To examine associations of third trimester maternal urinary fluoride (MUF) with child neurobehavior at age 3 years in the US., Design, Setting, and Participants: This prospective cohort study utilized urine samples archived from 2017 to 2020 and neurobehavioral data assessed from 2020 to 2023 from the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) pregnancy cohort, which consisted of predominately Hispanic women residing in Los Angeles, California. Cohort eligibility criteria at recruitment included being 18 years of age or older, less than 30 weeks' gestation, and a fluent English or Spanish speaker. Exclusion criteria included having a disability preventing participation or provision of informed consent, being HIV positive or incarcerated, and having a multiple gestation pregnancy. There were 263 mother-child pairs who completed the 3-year study visit. In this analysis, women who reported prenatal smoking were excluded. Data analysis was conducted from October 2022 to March 2024., Exposure: Specific gravity-adjusted MUF (MUFSG), a biomarker of prenatal fluoride exposure., Main Outcomes and Measures: Neurobehavior was quantified using the Preschool Child Behavior Checklist (CBCL), which included composite scores for Total Problems, Internalizing Problems, and Externalizing Problems. CBCL composite T scores range from 28 to 100. T scores from 60 to 63 are in the borderline clinical range, whereas scores above 63 are in the clinical range. Linear and logistic regression models adjusted for covariates were conducted., Results: A total of 229 mother-child pairs (mean [SD] maternal age, 29.45 [5.67] years; 116 female children [50.7%] and 113 male children [49.3%]) who had MUFSG measured were included in the study. Median (IQR) MUFSG was 0.76 (0.51-1.19) mg/L, and 32 participants (14.0%) had a Total Problems T score in the borderline clinical or clinical range. A 1-IQR (0.68 mg/L) increase in MUFSG was associated with nearly double the odds of the Total Problems T score being in the borderline clinical or clinical range (odds ratio, 1.83; 95% CI, 1.17-2.86; P = .008), as well as with a 2.29-point increase in T score for the Internalizing Problems composite (B = 2.29; 95% CI, 0.47-4.11; P = .01) and a 2.14-point increase in T score for the Total Problems composite (B = 2.14; 95% CI, 0.29-3.98; P = .02)., Conclusions and Relevance: In this prospective cohort study of mother-child pairs in Los Angeles, California, prenatal fluoride exposure was associated with increased neurobehavioral problems. These findings suggest that there may be a need to establish recommendations for limiting fluoride exposure during the prenatal period.

Background: Fluoride is ubiquitous in the United States (US); however, data on biomarkers and patterns of fluoride exposure among US pregnant women are scarce. We examined specific gravity adjusted maternal urinary fluoride (MUFsg) in relation to sociodemographic variables and metal co-exposures among pregnant women in Los Angeles, California., Methods: Participants were from the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort. There were 293 and 490 women with MUFsg measured during first and third trimesters, respectively. An intra-class correlation coefficient examined consistency of MUFsg between trimesters. Kruskal-Wallis and Mann-Whitney U tests examined associations of MUFsg with sociodemographic variables. Covariate adjusted linear regression examined associations of MUFsg with blood metals and specific gravity adjusted urine metals among a subsample of participants within and between trimesters. A False Discovery Rate (FDR) correction accounted for multiple comparisons., Results: Median (IQR) MUFsg was 0.65 (0.5) mg/L and 0.8 (0.59) mg/L, during trimesters one and three respectively. During both trimesters, MUFsg was higher among older participants, those with higher income, and White, non-Hispanic participants than Hispanic participants. MUFsg was also higher for White, non-Hispanic participants than for Black, non-Hispanic participants in trimester three, and for those with graduate training in trimester one. MUFsg was negatively associated with blood mercury in trimester one and positively associated with blood lead in trimester three. MUFsg was positively associated with various urinary metals, including antimony, barium, cadmium, cobalt, copper, lead, nickel, tin, and zinc in trimesters one and/or three., Conclusions: MUFsg levels observed were comparable to those found in pregnant women in Mexico and Canada that have been associated with poorer neurodevelopmental outcomes. Lower urinary fluoride levels among Hispanic and non-Hispanic Black participants in MADRES compared to non-Hispanic White participants may reflect lower tap water consumption or lower fluoride exposure from other sources. Additional research is needed to examine whether MUFsg levels observed among pregnant women in the US are associated with neurodevelopmental outcomes., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Breastfeeding may protect women’s long-term cardiovascular health; however, breastfeeding-related postpartum lipid changes remain unclear. We aim to examine associations of breastfeeding duration with maternal lipids at 12 months postpartum. In a subsample (n = 79) of the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort, breastfeeding status and duration at 3, 6, and 12 months postpartum were self-reported. Serum levels of lipids, including total cholesterol, triglycerides (TG), high-, low-, and very low-density lipoprotein cholesterol (HDL-C, LDL-C, VLDL-C), were measured from blood samples collected at 12 months postpartum. We used linear regression models to compare lipids by breastfeeding duration, adjusting for potential confounders. Women who were breastfeeding at 12 months had higher HDL-C (mean: 41.74 mg/dL, 95% CI: 37.27−46.74 vs. 35.11 mg/dL, 95% CI: 31.42−39.24), lower TG (80.45 mg/dL, 95% CI: 66.20−97.77 vs. 119.11 mg/dL, 95% CI: 98.36−144.25), and lower VLDL-C (16.31 mg/dL, 95% CI: 13.23, 20.12 vs. 23.09 mg/dL, 95% CI: 18.61−28.65) compared to women who breastfed for <6 months. No lipids were significantly different between women who breastfed for 6−11 months and for <6 months. Each month’s increase in breastfeeding duration was significantly, inversely associated with TG and VLDL-C and positively with HDL-C. Adjusting for fasting status, demographics, pre-pregnancy body mass index, breastfeeding frequency, and pregnancy complications did not appreciably change effect estimates. Breastfeeding at 12 months postpartum and a longer duration of breastfeeding in the first year postpartum were both associated with increased HDL-C and decreased TG and VLDL-C at 12 months postpartum.

Background: Fetal growth is predictive of health later in life. Both toxic and essential metals influence fetal growth, but most studies have focused on these elements individually and used birth weight as an indicator of fetal growth. The objective of the current study was to investigate the impact of a mixture of metals on fetal size in mid-pregnancy in a predominately lower income Hispanic pregnancy cohort in Los Angeles., Methods: For our primary analysis, we focused on six elements that have previously been associated individually with fetal size, including arsenic (As), barium (Ba), cadmium (Cd), mercury (Hg), molybdenum (Mo), and tin (Sn), measured in maternal urine samples collected in early pregnancy (median: 12.4 weeks gestation). In an exploratory analysis, we additionally included cobalt (Co), nickel (Ni), antimony (Sb), and thallium (Tl). Using covariate-adjusted Bayesian Kernel Machine Regression (BKMR) as our main mixture modeling approach, we examined the impact of these metals on fetal biometry measures obtained between 18 and 22 weeks gestation, with a focus on estimated fetal weight (EFW)., Results: BKMR identified Mo and Ba as the mixture components that contributed most to associations with EFW. Linear associations were observed for both metals. An increase in Mo from the 25th to 75th percentile was associated with a 0.114 (95% credible interval (CI): 0.019, 0.247) SD higher EFW, equivalent to a 7.4 g difference. Similar associations were observed between Mo and the other fetal measures evaluated. In contrast, an increase in Ba from the 25th to 75th percentile was associated with a -0.076 (95% CI: 0.217, 0.066) SD lower EFW, equivalent to a 4.9 g difference. Similar inverse associations were observed for Ba in relation to abdominal circumference and biparietal diameter. BKMR also identified a possible interaction between Ba and Mo in relation to head circumference, suggesting that the positive associations between Mo and this outcome may be attenuated at high levels of Ba, which was consistent with findings from linear regression (P interaction  = 0.03). In an exploratory analysis accounting for a larger mixture of metals, Mo and Ba consistently contributed most to associations with EFW. An inverse association was also identified between Sb and EFW., Conclusions: Our results suggest that Mo may promote fetal growth, while Ba and Sb may reduce fetal growth, in this population., (Copyright © 2020. Published by Elsevier Inc.)

Background: Hypothalamic-pituitary-adrenal (HPA)-axis dysfunction has been associated with a variety of mental health and cardio-metabolic disorders. While causal models of HPA-axis dysregulation have been largely focused on either pre-existing health conditions or psychosocial stress factors, recent evidence suggests a possible role for central nervous system activation via air pollutants, such as nitrogen dioxide (NO 2 ), ozone (O 3 ) and particulate matter (PM). Therefore, in an observational study of Latino youth, we investigated if monthly ambient NO 2 , O 3 , and PM with aerodynamic diameter ≤ 2.5 (PM 2.5 ) exposure were associated with morning serum cortisol levels., Methods: In this cross-sectional study, morning serum cortisol level was assessed after a supervised overnight fast in 203 overweight and obese Latino children and adolescents (female/male: 88/115; mean age: 11.1 ± 1.7 years; pre-pubertal/pubertal/post-pubertal: 85/101/17; BMI z-score: 2.1 ± 0.4). Cumulative concentrations of NO 2, O 3 and PM 2.5 were spatially interpolated at the residential addresses based on measurements from community monitors up to 12 months prior to testing. Single and multi-pollutant linear effects models were used to test the cumulative monthly lag effects of NO 2 , O 3, and PM 2.5 on morning serum cortisol levels after adjusting for age, sex, seasonality, social position, pubertal status, and body fat percent by DEXA., Results: Single and multi-pollutant models showed that higher O 3 exposure (derived from maximum 8-h exposure windows) in the prior 1-7 months was associated with higher serum morning cortisol (p < 0.05) and longer term PM 2.5 exposure (4-10 months) was associated with lower serum morning cortisol levels (p < 0.05). Stratification by pubertal status showed associations in pre-pubertal children compared to pubertal and post-pubertal children. Single, but not multi-pollutant, models showed that higher NO 2 over the 4-10 month exposure period associated with lower morning serum cortisol (p < 0.05)., Conclusions: Chronic ambient NO 2, O 3 and PM 2.5 differentially associate with HPA-axis dysfunction, a mechanism that may serve as an explanatory pathway in the relationship between ambient air pollution and metabolic health of youth living in polluted urban environments. Further research that uncovers how ambient air pollutants may differentially contribute to HPA-axis dysfunction are warranted.

Predicting PM 2.5 concentrations at a fine spatial and temporal resolution (i.e., neighborhood, hourly) is challenging. Recent growth in low cost sensor networks is providing increased spatial coverage of air quality data that can be used to supplement data provided by monitors of regulatory agencies. We developed an hourly, 500 × 500 m gridded PM 2.5 model that integrates PurpleAir low-cost air sensor network data for Los Angeles County. We developed a quality control scheme for PurpleAir data. We included spatially and temporally varying predictors in a random forest model with random oversampling of high concentrations to predict PM 2.5 . The model achieved high prediction accuracy (10-fold cross-validation (CV) R 2  = 0.93, root mean squared error (RMSE) = 3.23 μg/m 3 ; spatial CV R 2  = 0.88, spatial RMSE = 4.33 μg/m 3 ; temporal CV R 2  = 0.90, temporal RMSE = 3.85 μg/m 3 ). Our model was able to predict spatial and diurnal patterns in PM 2.5 on typical weekdays and weekends, as well as non-typical days, such as holidays and wildfire days. The model allows for far more precise estimates of PM 2.5 than existing methods based on few sensors. Taking advantage of low-cost PM 2.5 sensors, our hourly random forest model predictions can be combined with time-activity diaries in future studies, enabling geographically and temporally fine exposure estimation for specific population groups in studies of acute air pollution health effects and studies of environmental justice issues., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Arsenic (As) is a contaminant of top public health concern, due to its range of detrimental health effects. Arsenic exposure has not been well-characterized among the US Hispanic populations and has been particularly understudied in this population during pregnancy., Methods: As part of the MADRES ongoing pregnancy cohort of predominantly lower-income, Hispanic women in Los Angeles, CA, we examined levels of maternal first trimester urinary As, including total As and As metabolites (inorganic (iAs), monomethylated (MMA) and dimethylated As (DMA)), in relation to participant demographics, lifestyle characteristics, and rice/seafood consumption, to identify factors that may influence As exposure and its metabolites during pregnancy (N = 241)., Results: Total As concentrations ranged from low to high (0.8-506.2 μg/L, mean: 9.0 μg/L, SD: 32.9) in our study population. Foreign-born Hispanic women had 8.6% higher %DMA (95% CI: 3.3%, 13.9%) and -7.7% lower %iAs (95% CI: -12.6%, -2.9%) than non-Hispanic women. A similar trend was observed for US-born Hispanic women. In addition, maternal age was associated with 0.4% higher %iAs (95% CI: 0.1%, 0.6%) and 0.4% lower %DMA (95% CI: -0.7%, -0.1%) per year, which may indicate poor As methylation capacity., Conclusion: Individual factors may predict As exposure and metabolism in pregnancy, and in turn, greater risk of adverse health effects.

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.

Background: Disproportionately high rates of maternal overweight and obesity among the Hispanic population before, during, and after pregnancy pose serious health concerns for both mothers (e.g., preeclampsia, gestational diabetes, weight retention) and children (e.g., elevated lifelong obesity risk). A growing body of evidence implicates environmental exposures (e.g., air pollution, metals) and social stressors (e.g., poverty, violence) in contributing to obesity-related biobehavioral processes, such as physical activity, dietary intake, perceived stress, and cortisol regulation. However, current understanding of the role of environmental exposures and social stressors on obesity-related biobehavioral processes is limited by infrequent, inter-individual measurement, and lack of personal exposure monitoring., Methods: The "Maternal and Developmental Risks from Environmental and Social Stressors" (MADRES) real-time and personal sampling study examines the within-subject day-level effects of environmental and social stressors on maternal pre- and post-partum obesity-related biobehavioral responses. Among a cohort of 65 low-income, Hispanic women in urban Los Angeles, this study uses innovative personal, real-time data capture strategies (e.g., ecological momentary assessment [EMA], personal exposure monitoring, geolocation monitoring, accelerometry) to repeatedly assess obesity-related processes during the 1st and 3rd trimester, and at 4-6 months postpartum. Day-level effects of environmental exposures and social stressors on women's physical activity, diet, perceived stress and salivary cortisol measured across repeated days will be tested using multilevel modeling., Discussion: Hispanic women of childbearing age bear a disproportionately high burden of obesity, and this population is also unduly exposed to numerous obesogenic settings. By using innovative real-time data capture strategies, the current study will uncover the daily impacts of environmental and social stressor exposures on women's obesity-related biobehavioral responses, which over time can lead to excessive gestational weight gain, postpartum weight retention and can pose serious consequences for both mother and child. Findings from the real-time and personal sampling study will identify key mechanistic targets for policy, clinical, and programmatic interventions, with the potential for broad-reaching public health impacts.

Objectives: Growing evidence indicates that ambient (AAP: NO 2 , PM 2.5 and O 3 ) and traffic-related air pollutants (TRAP) contribute to metabolic disease risk in adults; however, few studies have examined these relationships in children., Methods: Metabolic profiling was performed in 429 overweight and obese African-American and Latino youth living in urban Los Angeles, California. This cross-sectional study estimated individual residential air pollution exposure and used linear regression to examine relationships between air pollution and metabolic outcomes., Results: AAP and TRAP exposure were associated with adverse effects on glucose metabolism independent of body fat percent. PM 2.5 was associated with 25.0% higher fasting insulin (p < 0.001), 8.3% lower insulin sensitivity (p < 0.001), 14.7% higher acute insulin response to glucose (p = 0.001) and 1.7% higher fasting glucose (p < 0.001). Similar associations were observed for increased NO 2 exposure. TRAP from non-freeway roads was associated with 12.1% higher insulin (p < 0.001), 6.9% lower insulin sensitivity (p = 0.02), 10.8% higher acute insulin response to glucose (p = 0.003) and 0.7% higher fasting glucose (p = 0.047)., Conclusions: Elevated air pollution exposure was associated with a metabolic profile that is characteristic of increased risk for type 2 diabetes. These results indicate that increased prior year exposure to air pollution may adversely affect type 2 diabetes-related pathophysiology in overweight and obese minority children., (© 2016 World Obesity Federation.)

Evidence suggests that ambient air pollution (AAP) exposure may contribute to the development of obesity and type 2 diabetes. The objective of this study was to determine whether exposure to elevated concentrations of nitrogen dioxide (NO 2 ) and particulate matter with aerodynamic diameter <2.5 (PM 2.5 ) had adverse effects on longitudinal measures of insulin sensitivity (S I ), β-cell function, and obesity in children at high risk for developing diabetes. Overweight and obese Latino children (8-15 years; n = 314) were enrolled between 2001 and 2012 from Los Angeles, CA, and followed for an average of 3.4 years (SD 3.1 years). Linear mixed-effects models were fitted to assess relationships between AAP exposure and outcomes after adjusting for covariates including body fat percent. Higher NO 2 and PM 2.5 were associated with a faster decline in S I and a lower S I at age 18 years, independent of adiposity. NO 2 exposure negatively affected β-cell function, evidenced by a faster decline in disposition index (DI) and a lower DI at age 18 years. Higher NO 2 and PM 2.5 exposures over follow-up were also associated with a higher BMI at age 18 years. AAP exposure may contribute to development of type 2 diabetes through direct effects on S I and β-cell function., (© 2017 by the American Diabetes Association.)