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Background: Ambient air pollution during pregnancy has been linked with postpartum depression up to 12 months, but few studies have investigated its impact on persistent depression beyond 12 months postpartum. This study aimed to evaluate prenatal ambient air pollution exposure and the risk of persistent depression over 3 years after childbirth and to identify windows of susceptibility., Methods: This study included 361 predominantly low-income Hispanic/Latina participants with full-term pregnancies in the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort. We estimated daily residential PM 2.5 , PM 10 , NO 2 , and O 3 concentrations throughout 37 gestational weeks using inverse-distance squared spatial interpolation from monitoring data and calculated weekly averaged levels. Depression was assessed by the 20-item Center for Epidemiologic Studies-Depression (CES-D) scale at 12, 24, and 36 months postpartum, with persistent postpartum depression defined as a CES-D score ≥16 at any of these timepoints. We performed robust Poisson log-linear distributed lag models (DLM) via generalized estimating equations (GEE) to estimate the adjusted risk ratio (RR)., Results: Depression was observed in 17.8 %, 17.5 %, and 13.4 % of participants at 12, 24, and 36 months, respectively. We found one IQR increase (3.9 ppb) in prenatal exposure to NO 2 during the identified sensitive window of gestational weeks 13-29 was associated with a cumulative risk ratio of 3.86 (95 % CI: 3.24, 4.59) for persistent depression 1-3 years postpartum. We also found one IQR increase (7.4 μg/m 3 ) in prenatal exposure to PM 10 during gestation weeks 12-28 was associated a cumulative risk ratio of 3.88 (95 % CI: 3.04, 4.96) for persistent depression. No clear sensitive windows were identified for PM 2.5 or O 3 ., Conclusions: Mid-pregnancy PM 10 and NO 2 exposures were associated with nearly 4-fold increased risks of persistent depression after pregnancy, which has critical implications for prevention of perinatal mental health outcomes., Competing Interests: Declaration of competing interest We declare no actual or potential competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Exposure to ambient air pollution is associated with morbidity and mortality, making it an important public health concern. Emissions from motorized traffic are a common source of air pollution but evaluating the contribution of traffic-related air pollution (TRAP) emissions to health risks is challenging because it is difficult to disentangle the contribution of individual air pollution sources to exposure contrasts in an epidemiological study., Objective: This paper describes a new framework to identify whether air pollution differences reflect contrasts in TRAP exposures. Because no commonly measured pollutant is entirely specific to on-road motor vehicles, this exposure framework combined information on pollutants, spatial scale (i.e., geographic extent), and exposure assessment methods and their spatial scale to determine whether the estimated effect of air pollution in a given study was related to differences in TRAP., Methods: The exposure framework extended beyond the near-road environment to include differences in exposure to TRAP at neighborhood resolution ( ≤ 5 km) across urban, regional, and national scales. It also embedded a stricter set of criteria to identify studies that provided the strongest evidence that exposure contrasts were related to differences in traffic emissions., Results: Application of the framework to the transparent selection of epidemiological studies for a systematic review produced insights on assessing and improving comparability of TRAP exposure measures, particularly for indirect measures such as distances from roads. It also highlighted study design challenges related to the duration of measurements and the structure of epidemiological models., Impact Statement: This manuscript describes a new exposure framework to identify studies of traffic-related air pollution, a case study of its application in an HEI systematic review, and its implications for exposure science and air pollution epidemiology experts. It identifies challenges and provides recommendations for the field going forward. It is important to bring this information to the attention of researchers in air pollution exposure science and epidemiology because applying the broader lessons learned will improve the conduct and reporting of studies going forward., Competing Interests: Competing interests The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.)

Autism spectrum disorder (ASD) is a developmental disorder with symptoms that range from social and communication impairments to restricted interests and repetitive behavior and is the 4th most disabling condition for children aged 5-14. Risk factors of ASD are not fully understood. Environmental risk factors are believed to play a significant role in the ASD epidemic. Research focusing on air pollution exposure as an early-life risk factor of autism is growing, with numerous studies finding associations of traffic and industrial emissions with an increased risk of ASD. One of the possible mechanisms linking autism and air pollution exposure is metabolic dysfunction. However, there were no consensus about the key metabolic pathways and corresponding metabolite signatures in mothers and children that are altered by air pollution exposure and cause the ASD. Therefore, we performed a review of published papers examining the metabolomic signatures and metabolic pathways that are associated with either air pollution exposure or ASD risk in human studies. In conclusion, we found that dysregulated lipid, fatty acid, amino acid, neurotransmitter, and microbiome metabolisms are associated with both short-term and long-term air pollution exposure and the risk of ASD. These dysregulated metabolisms may provide insights into ASD etiology related to air pollution exposure, particularly during the perinatal period in which neurodevelopment is highly susceptible to damage from oxidative stress and inflammation., 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. Published by Elsevier Ltd.)

Background: Exposure to ambient air pollutants has emerged as a risk for metabolic-dysfunction associated steatotic liver disease (MASLD)., Objectives: We sought to examine associations between short-term (prior month) and long-term (prior year) ambient air pollution exposure with hepatic fat fraction (HFF) and liver stiffness in Latino youth with obesity. A secondary aim was to investigate effect modification by patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype and liver disease severity., Methods: Data was analyzed from 113 Latino youth (age 11-19) with obesity in Southern California. Individual exposure to particulate matter with aerodynamic diameter ≤ 2.5μm (PM 2.5 ), ≤ 10μm (PM 10 ), nitrogen dioxide (NO 2 ), 8-hour maximum ozone (8hrMax-O 3 ), 24-hr O 3 , and redox-weighted oxidative capacity (O x wt ) were estimated using residential address histories and United States Environmental Protection Agency air quality observations. HFF and liver stiffness were measured using magnetic resonance imaging. Linear models were used to determine associations between short-term and long-term exposure to air pollutants with HFF and liver stiffness. Modification by PNPLA3 and liver disease severity was then examined., Results: Short-term exposure to 8hrMax-O 3 was positively associated with HFF. Relationships between air pollution exposure and HFF were not impacted by PNPLA3 genotype or liver disease severity. Long-term exposure to 8hrMax-O 3 and O x wt were positively associated with liver stiffness. Associations between air pollution exposure and liver stiffness depended on PNPLA3 genotype, such that individuals with GG genotypes exhibited stronger, more positive relationships between short-term exposure to PM 10 , 8hrMax-O 3 , 24-hr O 3, and O x wt and liver stiffness than individuals with CC/CG genotypes. In addition, relationships between short-term exposure to NO 2 and liver stiffness were stronger in those with severe liver disease., Discussion: Air pollution exposure may be a risk factor for liver disease among Latino youth with obesity, particularly in those with other preexisting risks for liver damage., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Rohit Kohli reports a relationship with Mirum Biopharma that includes: consulting or advisory. Rohit Kohli reports a relationship with Ipsen that includes: consulting or advisory. Michael Goran reports a relationship with YUMI foods that includes: consulting or advisory. Michael Goran reports a relationship with Bobbie Labs that includes: consulting or advisory. Michael Goran receives royalties from Penguin Random House for Sugarproof If there are other authors, they 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 The Authors. Published by Elsevier Inc. All rights reserved.)

In this study, associations between prenatal exposure to fine particulate matter (PM2.5) from 9 sources and development of autism spectrum disorder (ASD) were assessed in a population-based retrospective pregnancy cohort in southern California. The cohort included 318,750 mother-child singleton pairs. ASD cases ( N = 4559) were identified by ICD codes. Source-specific PM2.5 concentrations were estimated from a chemical transport model with a 4 × 4 km 2 resolution and assigned to maternal pregnancy residential addresses. Cox proportional hazard models were used to estimate the hazard ratios (HR) of ASD development for each individual source. We also adjusted for total PM2.5 mass and in a separate model for all other sources simultaneously. Increased ASD risk was observed with on-road gasoline (HR [CI]: 1.18 [1.13, 1.24]), off-road gasoline (1.15 [1.12, 1.19]), off-road diesel (1.08 [1.05, 1.10]), food cooking (1.05 [1.02, 1.08]), aircraft (1.04 [1.01, 1.06]), and natural gas combustion (1.09 [1.06, 1.11]), each scaled to standard deviation increases in concentration. On-road gasoline and off-road gasoline were robust for other pollutant groups. PM2.5 emitted from different sources may have different impacts on ASD. The results also identify PM source mixtures for toxicological investigations that may provide evidence for future public health policies.

Background: Little is known about how childhood exposure to traffic-related air pollution (TRAP) and stress interact to affect adults' cardiometabolic health. We examined this interaction and assessed the impact of over 10 years of childhood TRAP exposure on cardiometabolic health., Methods: From 2018 to 2023, 313 young adults from the Southern California Children's Health Study were enrolled in a follow-up assessment. Using CALINE4 line source dispersion model, average childhood TRAP exposures (from pregnancy to age 13) were estimated for nitrogen oxides (NO x ) from all roads. Traffic density was calculated within a 300-m residential buffer. Cardiometabolic health was assessed in adulthood (mean age 24 ± 1.7) based on blood lipids (total cholesterol, high- and low-density lipoprotein [HDL, LDL], triglycerides), glucose metabolism (fasting glucose, fasting insulin, HbA1c), body composition (BMI, android/gynoid ratio [AG ratio], percent body fat), and blood pressure. A PDAY (Pathobiologic Determinants of Atherosclerosis in Youth) score was generated to evaluate overall cardiometabolic health. Participants' perceived stress was assessed in childhood and adulthood (ages 13 and 24 years, respectively)., Results: Results of mixed effects linear models, adjusted for demographics and smoking status, suggested that each standard deviation increase in childhood exposure to traffic-related total NO x was associated with 0.62 increase in PDAY score (95% Confidence Interval [CI]:0.10,1.14), 0.09% increase in HbA1c (95%CI: 0.04, 0.15), 1.19% increase in percent body fat (95%CI: 0.18, 2.20), and 0.96 kg/m 2 increase in BMI (0.11, 1.80) in adulthood. Among participants with higher childhood stress levels, we observed significant associations of traffic-related total NO x with total cholesterol, HDL, LDL, HbA1c, insulin, and BMI. None of these associations were significant among people with lower stress levels. We observed similar statistically significant associations of traffic density., Conclusion: Long-term childhood exposure to TRAP in childhood may have lasting adverse impacts on cardiometabolic health, especially for children with higher stress levels., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Shohreh Farzan reports financial support was provided by National Institutes of Health. Breton, Bastain, Habre reports financial support was provided by National Institutes of Health. Shohreh Farzan reports a relationship with University of Southern California that includes: employment. Guo, Habre, Xu, Chen, Howland, Gauderman, Bastain, Breton reports a relationship with University of Southern California that includes: employment. Lurmann, Pavlovic reports a relationship with Sonoma Technology Inc that includes: employment. If there are other authors, they 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.)

Rationale: Few studies have examined the effects of long-term childhood air pollution exposure on adult respiratory health, including whether childhood respiratory effects underlie this relation. Objectives: To evaluate associations between childhood air pollution exposure and self-reported adult bronchitic symptoms while considering child respiratory health in the Southern California Children's Health Study. Methods: Exposures to nitrogen dioxide (NO 2 ), ozone, and particulate matter <2.5 μm and <10 μm in diameter (PM 10 ) assessed using inverse-distance-squared spatial interpolation based on childhood (birth to age 17 yr) residential histories. Bronchitic symptoms (bronchitis, cough, or phlegm in the past 12 mo) were ascertained via a questionnaire in adulthood. Associations between mean air pollution exposure across childhood and self-reported adult bronchitic symptoms were estimated using logistic regression. We further adjusted for childhood bronchitic symptoms and asthma to understand whether associations operated beyond childhood respiratory health impacts. Effect modification was assessed for family history of asthma, childhood asthma, and adult allergies. Measurements and Main Results: A total of 1,308 participants were included (mostly non-Hispanic White [56%] or Hispanic [32%]). At adult assessment (mean age, 32.0 yr; standard deviation [SD], 4.7), 25% reported bronchitic symptoms. Adult bronchitic symptoms were associated with NO 2 and PM 10 childhood exposures. Odds ratios per 1-SD increase were 1.69 (95% confidence interval, 1.14-2.49) for NO 2 (SD, 11.1 ppb) and 1.51 (95% confidence interval, 1.00-2.27) for PM 10 (SD, 14.2 μg/m 3 ). Adjusting for childhood bronchitic symptoms or asthma produced similar results. NO 2 and PM 10 associations were modified by childhood asthma, with greater associations among asthmatic individuals. Conclusions: Childhood NO 2 and PM 10 exposures were associated with adult bronchitic symptoms. Associations were not explained by childhood respiratory health impacts; however, participants with childhood asthma had stronger associations.

Pregnant people are vulnerable to air pollution exposure, including risk of preterm birth, low birth weight, and stillbirth. Understanding the infiltration of outdoor wildfire smoke into a residential space is critical for the accurate assessment of wildfire smoke exposure and associated health effects in pregnant people. Relying on ambient measurements of wildfire smoke alone can result in exposure misclassification. In this study, we examine the role of physical housing characteristics in the relationship between smoke exposure and preterm birth. In particular, we examine the effect of home size, year of construction, cooling type, and renovation status, as effect modifiers in the relationship between smoke exposure during pregnancy and preterm birth from 2007 to 2015 in California. To do this, we combined data on home characteristics from the California Tax Assessor, birth outcomes from the California birth records database, and the number of smoke days for each pregnancy from theNOAA (National Oceanic and Atmospheric Administration) Hazard Mapping System (HMS). We estimated the association between smoke day exposures and odds of preterm birth using logistic regression models and stratified by air basin and housing characteristics. Our findings reveal that cooling type and renovation status are key factors modifying the smoke exposure-preterm birth relationship. Notably, we found elevated associations for people living in unrenovated homes, those using evaporative cooling systems, and those using central air conditioning units. While we observed elevated odds of preterm birth associated with increasing smoke day exposure for residents of large and new homes, this effect does not significantly differ across home size and age quartiles. This study highlights the need to further examine the relative roles of housing characteristics as well as factors not measured here including behavioral factors, time spent outdoors, window use, and occupational exposures in driving adverse birth outcomes related to wildfire smoke exposure., 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. Published by Elsevier Ltd.)

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).)

While fine particulate matter (PM 2.5 ) has been associated with autism spectrum disorder (ASD), few studies focused on ultrafine particles (PM 0.1 ). Given that fine and ultrafine particles can be highly correlated due to shared emission sources, challenges remain to distinguish their health effects. In a retrospective cohort of 318,371 mother-child pairs (4549 ASD cases before age 5) in Southern California, pregnancy average PM 2.5 and PM 0.1 were estimated using a California-based chemical transport model and assigned to residential addresses. The correlation between PM 2.5 and PM 0.1 was 0.87. We applied a two-step variance decomposition approach: first, decomposing PM 2.5 and PM 0.1 into the shared and unique variances using ordinary least squares linear regression (OLS) and Deming regression considering errors in both exposures; then assessing associations between decomposed PM 2.5 and PM 0.1 and ASD using Cox proportional hazard models adjusted for covariates. Prenatal PM 2.5 and PM 0.1 each was associated with increased ASD risk. OLS decomposition showed that associations were driven mainly by their shared variance, not by their unique variance. Results from Deming regression considering assumptions of measurement errors were consistent with those from OLS. This decomposition approach has potential to disentangle health effects of correlated exposures, such as PM 2.5 and PM 0.1 from common emissions sources., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Anny Xiang reports financial support was provided by National Institutes of Environmental Health Sciences. Rob McConnell reports financial support was provided by National Institute of Environmental Health Sciences. Joel Schwartz reports financial support was provided by US Environmental Protection Agency. Joel Schwartz has testified on behalf of the U.S. Department of Justice in a case involving a Clean Air Act violation If there are other authors, they 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 B.V. All rights reserved.)

Prenatal and early life air pollution exposure has been linked with several adverse health outcomes. However, the mechanisms underlying these relationships are not yet fully understood. Therefore, this study utilizes fecal metabolomics to determine if pre- and postnatal exposure to ambient air pollutants (i.e., PM 10 , PM 2.5 , and NO 2 ) is associated with the fecal metabolome in the first 2 years of life in a Latino cohort from Southern California. The aims of this analysis were to estimate associations between (1) prenatal air pollution exposure with fecal metabolic features at 1-month of age, (2) prior month postnatal air pollution exposure with fecal metabolites from 1-month to 2 years of age, and (3) how postnatal air pollution exposure impacts the change over time of fecal metabolites in the first 2 years of life. Prenatal exposure to air pollutants was associated with several Level-1 metabolites, including those involved in vitamin B6 and tyrosine metabolism. Prior month air pollution exposure in the postnatal period was associated with Level-1 metabolites involved in histidine metabolism. Lastly, we found that pre- and postnatal ambient air pollution exposure was associated with changes in metabolic features involved in metabolic pathways including amino acid metabolism, histidine metabolism, and fatty acid metabolism.

Background: The November 2018 Camp fire was the most destructive wildfire in California history, but its effects on reproductive health are not known., Methods: We linked California birth records from 2017-2019 to daily smoke levels using U.S. EPA Air Quality System (AQS) PM2.5 data and NOAA Hazard Mapping System smoke plume polygons during the Camp fire. In the main analysis, pregnancies were considered exposed if they had median AQS PM2.5 levels above 50 μg/m3 for at least 7 days during November 8-22, 2018. We calculated rates of preterm birth and the infant sex ratio based on week of conception and used the generalized synthetic control method to estimate the average treatment effect on the treated and to propose a novel approach to identify potential critical weeks of exposure during pregnancy., Results: We found associations between Camp fire-related smoke exposure and rates of preterm birth, with a risk difference (RD) = 0.005, 95% CI 0.001, 0.010. Exposure during week 10 of pregnancy was consistently associated with increased preterm birth (RD = 0.030, 95% CI 0.004, 0.056). We did not observe differences in the infant sex ratio., Conclusions: Camp fire smoke exposure was associated with increased rates of preterm birth, with sensitive windows in the first trimester., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Prenatal air pollution exposure has been associated with individual inflammatory, cardiovascular, and metabolic biomarkers in mothers and neonates. However, studies of air pollution and a comprehensive panel of biomarkers across maternal and cord blood samples remain limited. Few studies used data-driven methods to identify biomarker groupings that converge biomarkers from multiple biological pathways. This study aims to investigate the impacts of prenatal air pollution on groups of biomarkers in maternal and cord blood samples., Methods: In the Maternal And Developmental Risks from Environmental and Social Stressors (MADRES) cohort, 87 biomarkers were quantified from 45 trimester 1 maternal blood and 55 cord blood samples. Pregnancy and trimester 1-averaged concentrations of particulate matter ≤2.5 μm and ≤10 μm in diameter (PM 2.5 and PM 10 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) were estimated, using inverse distance squared weighted spatial interpolation from regulatory air monitoring stations. Traffic-related NO x was assessed using California Line Source Dispersion Model: freeway/highway roads, non-freeway major roads, non-freeway minor roads, and their sum as total NOx. Elastic Net (EN) regression within the rexposome R package was used to group biomarkers and assess their associations with air pollution., Results: In maternal samples, trimester 1-averaged PM 10 was associated with elevated inflammation biomarkers and lowered cardiovascular biomarkers. NO 2 exhibited positive associations with cardiovascular and inflammation markers. O 3 was inversely associated with inflammation, metabolic, and cardiovascular biomarkers. In cord blood, pregnancy-averaged PM 2.5 was associated with higher cardiovascular biomarkers and lower metabolic biomarkers. PM 10 was associated with lower inflammation and higher cardiovascular biomarkers. Total and major road NOx was associated with lower cardiovascular biomarkers., Conclusion: Prenatal air pollution exposure was associated with changes in biomarkers related to inflammation, cardiovascular, metabolic, cancer, and neurological function in both mothers and neonates. This study shed light on mechanisms by which air pollution can influence biological function during pregnancy., 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: 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.

Background: Ambient air pollution has been linked to postpartum depression. However, few studies have investigated the effects of traffic-related NO x on postpartum depression and whether any pregnancy-related factors might increase susceptibility., Objectives: To evaluate the association between traffic-related NO x and postpartum depressive and anxiety symptoms, and effect modification by pregnancy-related hypertension., Methods: This study included 453 predominantly low-income Hispanic/Latina women in the MADRES cohort. Daily traffic-related NO x concentrations by road class were estimated using the California LINE-source dispersion model (CALINE4) at participants' residential locations and averaged across pregnancy. Postpartum depressive and anxiety symptoms were evaluated by a validated questionnaire (Postpartum Distress Measure, PDM) at 1, 3, 6 and 12 months postpartum. Multivariate linear regressions were performed to estimate the associations at each timepoint. Interaction terms were added to the linear models to assess effect modification by hypertensive disorders of pregnancy (HDPs). Repeated measurement analyses were conducted by using mixed effect models., Results: We found prenatal traffic-related NO x was associated with increased PDM scores. Specifically, mothers exposed to an IQR (0.22 ppb) increase in NO x from major roads had 3.78% (95% CI: 0.53-7.14%) and 5.27% (95% CI: 0.33-10.45%) significantly higher 3-month and 12-month PDM scores, respectively. Similarly, in repeated measurement analyses, higher NO x from major roads was associated with 3.06% (95% CI: 0.43-5.76%) significantly higher PDM scores across the first year postpartum. Effect modification by HDPs was observed: higher freeway/highway and total NO x among mothers with HDPs were associated with significantly higher PDM scores at 12 months postpartum compared to those without HDPs., Impact: This study shows that prenatal traffic-related air pollution was associated with postpartum depressive and anxiety symptoms. The study also found novel evidence of greater susceptibility among women with HDPs, which advances the understanding of the relationships between air pollution, maternal cardiometabolic health during pregnancy and postpartum mental health. Our study has potential implications for clinical intervention to mitigate the effects of traffic-related pollution on postpartum mental health disorders. The findings can also offer valuable insights into urban planning strategies concerning the implementation of emission control measures and the creation of green spaces., (© 2024. The Author(s).)

Background: Extreme heat and air pollution is associated with increased mortality. Recent evidence suggests the combined effects of both is greater than the effects of each individual exposure. Low neighborhood socioeconomic status ("socioeconomic burden") has also been associated with increased exposure and vulnerability to both heat and air pollution. We investigated if neighborhood socioeconomic burden or the combination of socioeconomic and environmental exposures ("socioenvironmental burden") modified the effect of combined exposure to extreme heat and particulate air pollution on mortality in California., Methods: We used a time-stratified case-crossover design to assess the impact of daily exposure to extreme particulate matter <2.5 μm (PM 2.5 ) and heat on cardiovascular, respiratory, and all-cause mortality in California 2014-2019. Daily average PM 2.5 and maximum temperatures based on decedent's residential census tract were dichotomized as extreme or not. Census tract-level socioenvironmental and socioeconomic burden was assessed with the CalEnviroScreen (CES) score and a social deprivation index (SDI), and individual educational attainment was derived from death certificates. Conditional logistic regression was used to estimate associations of heat and PM 2.5 with mortality with a product term used to evaluate effect measure modification., Results: During the study period 1,514,292 all-cause deaths could be assigned residential exposures. Extreme heat and air pollution alone and combined were associated with increased mortality, matching prior reports. Decedents in census tracts with higher socioenvironmental and socioeconomic burden experienced more days with extreme PM 2.5 exposure. However, we found no consistent effect measure modification by CES or SDI on combined or separate extreme heat and PM 2.5 exposure on odds of total, cardiovascular or respiratory mortality. No effect measure modification was observed for individual education attainment., Conclusion: We did not find evidence that neighborhood socioenvironmental- or socioeconomic burden significantly influenced the individual or combined impact of extreme exposures to heat and PM 2.5 on mortality in California., Impact: We investigated the effect measure modification by socioeconomic and socioenvironmental of the co-occurrence of heat and PM 2.5 , which adds support to the limited previous literature on effect measure modification by socioeconomic and socioenvironmental burden of heat alone and PM 2.5 alone. We found no consistent effect measure modification by neighborhood socioenvironmental and socioeconomic burden or individual level SES of the mortality association with extreme heat and PM 2.5 co-exposure. However, we did find increased number of days with extreme PM 2.5 exposure in neighborhoods with high socioenvironmental and socioeconomic burden. We evaluated multiple area-level and an individual-level SES and socioenvironmental burden metrics, each estimating socioenvironmental factors differently, making our conclusion more robust., (© 2024. The Author(s).)

Background: Wildfires in the Western United States are a growing and significant source of air pollution that is eroding decades of progress in air pollution reduction. The effects on preterm birth during critical periods of pregnancy are unknown., Methods: We assessed associations between prenatal exposure to wildland fire smoke and risk of preterm birth (gestational age < 37 weeks). We assigned smoke exposure to geocoded residence at birth for all live singleton births in California conceived 2007-2018, using weekly average concentrations of particulate matter ≤ 2.5 µm (PM 2.5 ) attributable to wildland fires from United States Environmental Protection Agency's Community Multiscale Air Quality Model. Logistic regression yielded odds ratio (OR) for preterm birth in relation to increases in average exposure across the whole pregnancy, each trimester, and each week of pregnancy. Models adjusted for season, age, education, race/ethnicity, medical insurance, and smoking of the birthing parent., Results: For the 5,155,026 births, higher wildland fire PM 2.5 exposure averaged across pregnancy, or any trimester, was associated with higher odds of preterm birth. The OR for an increase of 1 µg/m 3 of average wildland fire PM 2.5 during pregnancy was 1.013 (95 % CI:1.008,1.017). Wildland fire PM 2.5 during most weeks of pregnancy was associated with higher odds. Strongest estimates were observed in weeks in the second and third trimesters. A 10 µg/m 3 increase in average wildland fire PM 2·5 in gestational week 23 was associated with OR = 1.034; 95 % CI: 1.019, 1.049 for preterm birth., Conclusions: Preterm birth is sensitive to wildland fire PM 2.5 ; therefore, we must reduce exposure during pregnancy., 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 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Human milk oligosaccharides (HMOs) impact neonate immunity and health outcomes. However, the environmental factors influencing HMO composition remain understudied. This study examined the associations between ambient air pollutant (AAP) exposure and HMOs at 1-month postpartum. Human milk samples were collected at 1-month postpartum (n = 185). AAP (PM 2.5 , PM 10 , NO 2 ) exposure included the 9-month pregnancy period through 1-month postpartum. Associations between AAP with (1) HMO diversity, (2) the sum of sialylated and fucosylated HMOs, (3) 6 a priori HMOs linked with infant health, and (4) all HMOs were examined using multivariable linear regression and principal component analysis (PCA). Exposure to AAP was associated with lower HMO diversity. PM 2.5 and PM 10 exposure was positively associated with the HMO 3-fucosyllactose (3FL); PM 2.5 exposure was positively associated with the sum of total HMOs, sum of fucosylated HMOs, and the HMO 2'-fucosyllactose (2'FL). PCA indicated the PM 2.5 , PM 10 , and NO 2 exposures were associated with HMO profiles. Individual models indicated that AAP exposure was associated with five additional HMOs (LNFP I, LNFP II, DFLNT, LNH). This is the first study to demonstrate associations between AAP and breast milk HMOs. Future longitudinal studies will help determine the long-term impact of AAP on human milk composition., (© 2024. The Author(s).)

This study reports results from research conducted at the Observatory of Mount Pico (OMP), 2225 m above mean sea level on Pico Island in the Azores archipelago in June and July 2017. We investigated the chemical composition, mixing state, and cloud condensation nuclei (CCN) activities of long-range transported free tropospheric (FT) particles. FLEXible PARTicle Lagrangian particle dispersion model (FLEXPART) simulations reveal that most air masses that arrived at the OMP during the sampling period originated in North America and were highly aged (average plume age > 10 days). We probed size-resolved chemical composition, mixing state, and hygroscopicity parameter (κ) of individual particles using computer-controlled scanning electron microscopy with an energy-dispersive X-ray spectrometer (CCSEM-EDX). Based on the estimated individual particle mass from elemental composition, we calculated the mixing state index, χ. During our study, FT particle populations were internally mixed (χ of samples are between 53 % and 87 %), owing to the long atmospheric aging time. We used data from a miniature Cloud Condensation Nucleus Counter (miniCCNC) to derive the hygroscopicity parameter, κ CCNC . Combining κ CCNC and FLEXPART, we found that air masses recirculated above the North Atlantic Ocean with lower mean altitude had higher κ CCNC due to the higher contribution of sea salt particles. We used CCSEM-EDX and phase state measurements to predict single-particle κ (κ CCSEM-EDX ) values, which overlap with the lower range of κ CCNC measured below 0.15 % SS. Therefore, CCSEM-EDX measurements can be useful in predicting the lower bound of κ, which can be used in climate models to predict CCN activities, especially in remote locations where online CCN measurements are unavailable., 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 © 2023 Elsevier B.V. All rights reserved.)

Background: There is a long tradition in environmental health of using frameworks for evidence synthesis, such as those of the U.S. Environmental Protection Agency for its Integrated Science Assessments and the International Agency for Research on Cancer Monographs. The framework, Grading of Recommendations Assessment, Development, and Evaluation (GRADE), was developed for evidence synthesis in clinical medicine. The U.S. Office of Health Assessment and Translation (OHAT) elaborated an approach for evidence synthesis in environmental health building on GRADE., Methods: We applied a modified OHAT approach and a broader "narrative" assessment to assess the level of confidence in a large systematic review on traffic-related air pollution and health outcomes., Discussion: We discuss several challenges with the OHAT approach and its implementation and suggest improvements for synthesizing evidence from observational studies in environmental health. We consider the determination of confidence using a formal rating scheme of up- and downgrading of certain factors, the treatment of every factor as equally important, and the lower initial confidence rating of observational studies to be fundamental issues in the OHAT approach. We argue that some observational studies can offer high-confidence evidence in environmental health. We note that heterogeneity in magnitude of effect estimates should generally not weaken the confidence in the evidence, and consistency of associations across study designs, populations, and exposure assessment methods may strengthen confidence in the evidence. We mention that publication bias should be explored beyond statistical methods and is likely limited when large and collaborative studies comprise most of the evidence and when accrued over several decades. We propose to identify possible key biases, their most likely direction, and their potential impacts on the results. We think that the OHAT approach and other GRADE-type frameworks require substantial modification to align better with features of environmental health questions and the studies that address them. We emphasize that a broader, "narrative" evidence assessment based on the systematic review may complement a formal GRADE-type evaluation. https://doi.org/10.1289/EHP11532.

Microplastic particles are of increasing environmental concern due to the widespread uncontrolled degradation of various commercial products made of plastic and their associated waste disposal. Recently, common technology used to repair sewer pipes was reported as one of the emission sources of airborne microplastics in urban areas. This research presents results of the multi-modal comprehensive chemical characterization of the microplastic particles related to waste discharged in the pipe repair process and compares particle composition with the components of uncured resin and cured plastic composite used in the process. Analysis of these materials employs complementary use of surface-enhanced Raman spectroscopy, scanning transmission X-ray spectro-microscopy, single particle mass spectrometry, and direct analysis in real-time high-resolution mass spectrometry. It is shown that the composition of the relatively large (100 μm) microplastic particles resembles components of plastic material used in the process. In contrast, the composition of the smaller (micrometer and sub-micrometer) particles is significantly different, suggesting their formation from unintended polymerization of water-soluble components occurring in drying droplets of the air-discharged waste. In addition, resin material type influences the composition of released microplastic particles. Results are further discussed to guide the detection and advanced characterization of airborne microplastics in future field and laboratory studies pertaining to sewer pipe repair technology.

Background and Aim: Ambient air pollution (AAP) exposure has been associated with altered blood lipids and liver fat in young adults. MicroRNAs regulate gene expression and may mediate these relationships. This work investigated associations between AAP exposure, serum microRNA networks, lipid profiles, and non-alcoholic fatty liver disease (NAFLD) risk in young adults., Methods: Participants were 170 young adults (17-22 years) from the Meta-AIR cohort of the Children's Health Study (CHS). Residential AAP exposure (PM 2.5 , PM 10 , NO 2 , 8-hour maximum O 3 , redox-weighted oxidative capacity [O x wt ]) was spatially interpolated from monitoring stations via inverse-distance-squared weighting. Fasting serum lipids were assayed. Liver fat was imaged by MRI and NAFLD was defined by ≥ 5.5% hepatic fat fraction. Serum microRNAs were measured via NanoString and microRNA networks were constructed by weighted gene correlation network analysis. The first principal component of each network represented its expression profile. Multivariable mixed effects regression models adjusted for sociodemographic, behavioral, and clinical covariates; baseline CHS town code was a random effect. Effects estimates are scaled to one standard deviation of exposure. Mediation analysis explored microRNA profiles as potential mediators of exposure-outcome associations. DIANA-mirPATH identified overrepresented gene pathways targeted by miRNA networks., Results: Prior-month O x wt was associated with NAFLD (OR=3.45; p = 0.003) and inversely associated with microRNA Network A (β = -0.016; p = 0.026). Prior-year NO 2 was associated with non-HDL-cholesterol (β = 7.13; p = 0.01) and inversely associated with miRNA Network A (β = -0.019; p = 0.022). Network A expression was inversely associated with NAFLD (OR=0.35; p = 0.010) and non-HDL-C (β = -6.94 mg/dL; p = 0.035). Network A members miR-199a/b-3p and miR-130a, which both target fatty acid synthase, mediated 21% of the association between prior-month O x wt exposure with NAFLD (p = 0.048) and 23.3% of the association between prior-year NO 2 exposure and non-HDL-cholesterol (p = 0.026), respectively., Conclusions: Exposure to AAP may contribute to adverse lipid profiles and NAFLD risk among young adults via altered expression of microRNA profiles., 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 © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

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 (NO 2 ), particulate matter < 10 µm (PM 10 ), particulate matter < 2.5 µm (PM 2.5 ), and ozone (O 3 ) 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 NO 2 , PM 2.5 , PM 10 , and O 3 were 16.4 (2.9) ppb, 12.0 (1.1) μg/m 3 , 28.5 (4.7) μg/m 3 , 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 PM 2.5 and 1.64% [95%CI 1.27%, 2.13%] for NO 2 ), the growth rate from age 6 months to age 2 years was significantly decreased (0.90% [95%CI 0.82%, 1.00%] for NO 2 ), and the attained weight at age 2 years was significantly lower (- 7.50% [95% CI - 13.57%, - 1.02%] for PM 10 and - 7.00% [95% CI - 11.86%, - 1.88%] for NO 2 )., 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., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Exposure to ambient and near-roadway air pollution during pregnancy has been linked with several adverse health outcomes for pregnant women and their babies. Emerging research indicates that microRNA (miRNA) expression can be altered by exposure to air pollutants in a variety of tissues. Additionally, miRNAs from breast tissue and circulating miRNAs have previously been proposed as a biomarker for breast cancer diagnosis and prognosis. Therefore, this study sought to evaluate the associations between pregnancy exposures to ambient (PM 10 , PM 2.5 , NO 2 , O 3 ) and near-roadway air pollution (total NO x , freeway NO x , non-freeway NO x ) with breast milk extracellular vesicle miRNA (EV-miRNA), measured at 1-month postpartum, in a cohort of 108 Latina women living in Southern California. We found that PM 10 exposure during pregnancy was positively associated with hsa-miR-200c-3p, hsa-miR-200b-3p, and hsa-let-7c-5p, and was negatively associated with hsa-miR-378d. We also found that pregnancy PM 2.5 exposure was positively associated with hsa-miR-200c-3p and hsa-miR-200b-3p. First and second trimester exposure to PM 10 and PM 2.5 was associated with several EV-miRNAs with putative messenger RNA targets related to cancer. This study provides preliminary evidence that air pollution exposure during pregnancy is associated with human milk EV-miRNA expression., (© 2023 The Author(s). Published by IOP Publishing Ltd.)

Background: Autism Spectrum Disorder (ASD) risk is highly heritable, with potential additional non-genetic factors, such as prenatal exposure to ambient particulate matter with aerodynamic diameter < 2.5 µm (PM 2.5 ) and maternal immune activation (MIA) conditions. Because these exposures may share common biological effect pathways, we hypothesized that synergistic associations of prenatal air pollution and MIA-related conditions would increase ASD risk in children., Objectives: This study examined interactions between MIA-related conditions and prenatal PM 2.5 or major PM 2.5 components on ASD risk., Methods: In a population-based pregnancy cohort of children born between 2001 and 2014 in Southern California, 318,751 mother-child pairs were followed through electronic medical records (EMR); 4,559 children were diagnosed with ASD before age 5. Four broad categories of MIA-related conditions were classified, including infection, hypertension, maternal asthma, and autoimmune conditions. Average exposures to PM 2.5 and four PM 2.5 components, black carbon (BC), organic matter (OM), nitrate (NO 3 - ), and sulfate (SO 4 2- ), were estimated at maternal residential addresses during pregnancy. We estimated the ASD risk associated with MIA-related conditions, air pollution, and their interactions, using Cox regression models to adjust for covariates., Results: ASD risk was associated with MIA-related conditions [infection (hazard ratio 1.11; 95% confidence interval 1.05-1.18), hypertension (1.30; 1.19-1.42), maternal asthma (1.22; 1.08-1.38), autoimmune disease (1.19; 1.09-1.30)], with higher pregnancy PM 2.5 [1.07; 1.03-1.12 per interquartile (3.73 μg/m 3 ) increase] and with all four PM 2.5 components. However, there were no interactions of each category of MIA-related conditions with PM 2.5 or its components on either multiplicative or additive scales., Conclusions: MIA-related conditions and pregnancy PM 2.5 were independently associations with ASD risk. There were no statistically significant interactions of MIA conditions and prenatal PM 2.5 exposure with ASD risk., 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 © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Air pollution has been associated with gestational diabetes mellitus (GDM). We aim to investigate susceptible windows of air pollution exposure and factors determining population vulnerability., Methods: We ascertained GDM status in the prospective Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) pregnancy cohort from Los Angeles, California, USA. We calculated the relative risk of GDM by exposure to ambient particulate matter (PM 10 ; PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) in each week from 12 weeks before to 24 weeks after conception, adjusting for potential confounders, with distributed lag models to identify susceptible exposure windows. We examined effect modification by prenatal depression, median-split pre-pregnancy BMI (ppBMI) and age., Findings: Sixty (9.7%) participants were diagnosed with GDM among 617 participants (mean age: 28.2 years, SD: 5.9; 78.6% Hispanic, 11.8% non-Hispanic Black). GDM risk increased with exposure to PM 2.5 , PM 10 , and NO 2 in a periconceptional window ranging from 5 weeks before to 5 weeks after conception: interquartile-range increases in PM 2.5 , PM 10 , and NO 2 during this window were associated with increased GDM risk by 5.7% (95% CI: 4.6-6.8), 8.9% (8.1-9.6), and 15.0% (13.9-16.2), respectively. These sensitive windows generally widened, with greater effects, among those with prenatal depression, with age ≥28 years, or with ppBMI ≥27.5 kg/m 2 , than their counterparts., Interpretation: Preconception and early-pregnancy are susceptible windows of air pollutants exposure that increased GDM risk. Prenatal depression, higher age, or higher ppBMI may increase one's vulnerability to air pollution-associated GDM risk., Funding: National Institutes of Health, Environmental Protection Agency., Competing Interests: The authors declare they have no actual or potential competing financial interests., (© 2023 The Author(s).)

Background: There is increasing evidence for adverse health effects associated with aircraft-emitted particulate matter (PM) exposures, which are largely in the ultrafine (PM 0.1 ) size fraction, but no previous study has examined neurodevelopmental outcomes., Objective: To assess associations between maternal exposure to aircraft ultrafine particles (UFP) during pregnancy and offspring autism spectrum disorder (ASD) diagnosis., Methods: This large, representative cohort study included 370,723 singletons born in a single healthcare system. Demographic data, maternal health information, and child's ASD diagnosis by age 5 were extracted from electronic medical records. Aircraft exposure estimates for PM 0.1 were generated by the University of California Davis/California Institute of Technology Source Oriented Chemical Transport model. Cox proportional hazard models were used to assess associations between maternal exposure to aircraft PM 0·1 in pregnancy and ASD diagnosis, controlling for covariates., Results: Over the course of follow-up, 4,554 children (1.4 %) were diagnosed with ASD. Increased risk of ASD was associated with maternal exposure to aircraft PM 0.1 [hazard ratio, HR: 1.02, (95 % confidence interval (CI): 1.01-1.03) per IQR = 0.02 µg/m 3 increase during pregnancy. Associations were robust to adjustment for total PM 0.1 and fine particulate matter (PM 2.5 ), near-roadway air pollution, and other covariates. Noise adjustment modestly attenuated estimates of UFP effects, which remained statistically significant., Discussion: The results strengthen the emerging evidence that maternal particulate matter exposure during pregnancy is associated with offspring ASD diagnosis and identify aircraft-derived PM 0.1 as novel targets for further study and potential regulation., 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 © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Mounting evidence suggests that air pollution influences lipid metabolism and dyslipidemia. However, the metabolic mechanisms linking air pollutant exposure and altered lipid metabolism is not established. In year 2014-2018, we conducted a cross-sectional study on 136 young adults in southern California, and assessed lipid profiles (triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, very-low-density lipoprotein (VLDL)-cholesterol), and untargeted serum metabolomics using liquid chromatography-high-resolution mass spectrometry, and one-month and one-year averaged exposures to NO 2 , O 3 , PM 2.5 and PM 10 air pollutants at residential addresses. A metabolome-wide association analysis was conducted to identify metabolomic features associated with each air pollutant. Mummichog pathway enrichment analysis was used to assess altered metabolic pathways. Principal component analysis (PCA) was further conducted to summarize 35 metabolites with confirmed chemical identity. Lastly, linear regression models were used to analyze the associations of metabolomic PC scores with each air pollutant exposure and lipid profile outcome. In total, 9309 metabolomic features were extracted, with 3275 features significantly associated with exposure to one-month or one-year averaged NO 2 , O 3 , PM 2.5 and PM 10 (p < 0.05). Metabolic pathways associated with air pollutants included fatty acid, steroid hormone biosynthesis, tryptophan, and tyrosine metabolism. PCA of 35 metabolites identified three main PCs which together explained 44.4% of the variance, representing free fatty acids and oxidative byproducts, amino acids and organic acids. Linear regression indicated that the free fatty acids and oxidative byproducts-related PC score was associated with air pollutant exposure and outcomes of total cholesterol and LDL-cholesterol (p < 0.05). This study suggests that exposure to NO 2 , O 3 , PM 2.5 and PM 10 contributes to increased level of circulating free fatty acids, likely through increased adipose lipolysis, stress hormone and response to oxidative stress pathways. These alterations were associated with dysregulation of lipid profiles and potentially could contribute to dyslipidemia and other cardiometabolic disorders., 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 © 2023 Elsevier Ltd. All rights reserved.)

Background: The health effects of traffic-related air pollution (TRAP) continue to be of important public health interest across the globe. Following its 2010 review, the Health Effects Institute appointed a new expert Panel to systematically evaluate the epidemiological evidence regarding the associations between long-term exposure to TRAP and selected health outcomes. This paper describes the main findings of the systematic review on non-accidental mortality., Methods: The Panel used a systematic approach to conduct the review. An extensive search was conducted of literature published between 1980 and 2019. A new exposure framework was developed to determine whether a study was sufficiently specific to TRAP, which included studies beyond the near-roadway environment. We performed random-effects meta-analysis when at least three estimates were available of an association between a specific exposure and outcome. We evaluated confidence in the evidence using a modified Office of Health Assessment and Translation (OHAT) approach, supplemented with a broader narrative synthesis., Results: Thirty-six cohort studies were included. Virtually all studies adjusted for a large number of individual and area-level covariates-including smoking, body mass index, and individual and area-level socioeconomic status-and were judged at a low or moderate risk for bias. Most studies were conducted in North America and Europe, and a few were based in Asia and Australia. The meta-analytic summary estimates for nitrogen dioxide, elemental carbon and fine particulate matter-pollutants with more than 10 studies-were 1.04 (95% CI 1.01, 1.06), 1.02 (1.00, 1.04) and 1.03 (1.01, 1.05) per 10, 1 and 5 µg/m 3 , respectively. Effect estimates are interpreted as the relative risk of mortality when the exposure differs with the selected increment. The confidence in the evidence for these pollutants was judged as high, because of upgrades for monotonic exposure-response and consistency across populations. The consistent findings across geographical regions, exposure assessment methods and confounder adjustment resulted in a high confidence rating using a narrative approach as well., Conclusions: The overall confidence in the evidence for a positive association between long-term exposure to TRAP and non-accidental mortality was high., 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 © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Objectives: We report results of a systematic review on the health effects of long-term traffic-related air pollution (TRAP) and diabetes in the adult population. Methods: An expert Panel appointed by the Health Effects Institute conducted this systematic review. We searched the PubMed and LUDOK databases for epidemiological studies from 1980 to July 2019. TRAP was defined based on a comprehensive protocol. Random-effects meta-analyses were performed. Confidence assessments were based on a modified Office for Health Assessment and Translation (OHAT) approach, complemented with a broader narrative synthesis. We extended our interpretation to include evidence published up to May 2022. Results: We considered 21 studies on diabetes. All meta-analytic estimates indicated higher diabetes risks with higher exposure. Exposure to NO 2 was associated with higher diabetes prevalence (RR 1.09; 95% CI: 1.02; 1.17 per 10 μg/m 3 ), but less pronounced for diabetes incidence (RR 1.04; 95% CI: 0.96; 1.13 per 10 μg/m 3 ). The overall confidence in the evidence was rated moderate, strengthened by the addition of 5 recently published studies. Conclusion: There was moderate evidence for an association of long-term TRAP exposure with diabetes., Competing Interests: Author FL was employed by the company Sonoma Technology, Inc. The remaining authors declare that they do not have any conflicts of interest., (Copyright © 2023 Kutlar Joss, Boogaard, Samoli, Patton, Atkinson, Brook, Chang, Haddad, Hoek, Kappeler, Sagiv, Smargiassi, Szpiro, Vienneau, Weuve, Lurmann, Forastiere and Hoffmann.)

Background: Higher ambient temperature and air pollution may contribute to increased risk of behaviors harmful to oneself or to others; however, quantitative evidence is limited. We examined the relationship of deaths due to suicide and homicide with temperature and air pollution in California-a state prone to high levels of both exposures., Method: California death certificates from 2014 to 2019 were used to identify deaths due to suicide and homicide. Residential data for decedents were used to assign exposure to daily temperature (maximum[T max ], minimum[T min ]) and daily average air pollution concentrations (particulate matter <10 μm[PM 10 ] and < 2.5 μm[PM 2.5 ], nitrogen dioxide[NO 2 ], ozone[O 3 ]). T min served as a surrogate for nighttime temperature. A time-stratified case-crossover study design using conditional logistic regression was used to assess the effects of daily exposure to temperature and air pollutants on suicide and homicide mortality, adjusting for relative humidity. Effect modification by sex and age was assessed., Results: We observed 24,387 deaths due to suicide and 10,767 deaths due to homicide. We found a monotonic temperature association for both outcomes. A 5 °C increase in T max at lag-2 and T min at lag-0 was associated with 3.1 % (95 % confidence interval [CI]: 1.1 %-5.2 %) and 3.8 % (95%CI: 0.9 %-6.8 %) increased odds of death due to suicide, respectively. The increased odds of homicide mortality per 5 °C increase in T max at lag-0 and T min at lag-1 were 4.9 % (95%CI: 1.6 %-8.1 %) and 6.2 % (95%CI: 1.6 %-11.0 %), respectively. No air pollutant associations were statistically significant. Temperature associations were robust after adjustment for PM 2.5 . Some temperature effects were larger among women for suicide and men for homicide mortality, and among those over age 65 years for both outcomes., Conclusion: Risk of suicide and homicide mortality increases with increasing daily ambient temperatures. Findings have public health relevance given anticipated increases in temperatures due to global climate change., 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 © 2023 Elsevier B.V. All rights reserved.)

Lay Abstract: Autism spectrum disorder is heterogeneous and often accompanied by co-occurring conditions. Previous studies have shown that maternal health conditions during pregnancy including obesity, diabetes, preeclampsia, and asthma were associated with increased likelihood of autism. However, little has been done examining the likelihood associated with autism with co-occurring conditions. This study assessed these maternal health conditions in relationship to autism and gastrointestinal disturbances, a common co-occurring condition in children diagnosed with autism. Data included 308,536 mother-child pairs from one integrated health care system with comprehensive electronic medical records. Among the study cohort, 5,131 (1.7%) children had a diagnosis of autism by age 5. Gastrointestinal disturbances were present in 35.4% of children diagnosed with autism and 25.1% of children without autism diagnoses. Our results showed that each of the four maternal health conditions during pregnancy was associated with increased likelihood of gastrointestinal disturbances, autism without gastrointestinal disturbances, and autism with gastrointestinal disturbances. For all four maternal health conditions, the association was greatest for likelihood of autism with gastrointestinal disturbances. Given that children diagnosed with autism are more likely to have gastrointestinal disturbances and over 80% of gastrointestinal disturbances in this cohort were diagnosed prior to autism diagnosis, this study suggests that there may be common biological pathways between autism and gastrointestinal disturbances impacted by these maternal exposures. Future studies are warranted to assess associations between different exposures and autism with other co-occurring conditions to increase our understanding of autism heterogeneity.

Background: Higher prenatal ambient air pollution exposure has been associated with impaired neurodevelopment in preschoolers and school-aged children. The purpose of this study was to explore the relationships between prenatal ambient air pollution exposure and neurodevelopment during infancy., Methods: This study examined 161 Latino mother-infant pairs from the Southern California Mother's Milk Study. Exposure assessments included prenatal nitrogen dioxide (NO 2 ) and particulate matter smaller than 2.5 and 10 microns in diameter (PM 2.5 and PM 10 , respectively). The pregnancy period was also examined as three windows, early, mid, and late, which describe the first, middle, and last three months of pregnancy. Infant neurodevelopmental outcomes at 2 years of age were measured using the Bayley-III Scales of Infant and Toddler Development. Multivariable linear models and distributed lag linear models (DLM) were used to examine relationships between prenatal exposures and neurodevelopmental scores, adjusting for socioeconomic status, breastfeeding frequency, time of delivery, pre-pregnancy body mass index, and infant birthweight and sex., Results: Higher prenatal exposure to PM 10 and PM 2.5 was negatively associated with composite cognitive score (β = -2.01 [-3.89, -0.13] and β = -1.97 [-3.83, -0.10], respectively). In addition, higher average prenatal exposure to PM 10 was negatively associated with composite motor (β = -2.35 [-3.95, -0.74]), scaled motor (β = -0.77 [-1.30, -0.24]), gross motor (β = -0.37 [-0.70, -0.04]), fine motor (β = -0.40 [-0.71, -0.09]), composite language (β = -1.87 [-3.52, -0.22]), scaled language (β = -0.61 [-1.18, -0.05]) and expressive communication scaled scores (β = -0.36 [-0.66, -0.05]). DLMs showed that higher prenatal air pollution exposure during mid and late pregnancy was inversely associated with motor, cognitive, and communication language scores., Conclusions: Higher exposure to air pollutants during pregnancy, particularly in the mid and late prenatal periods, was inversely associated with scaled and composite motor, cognitive, and language scores at 2 years. These results indicate that prenatal ambient air pollution may negatively impact neurodevelopment in early life., (© 2023. The Author(s).)