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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 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.)

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.)

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 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: 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.)

Background: Evidence in the literature suggests that air pollution exposures experienced prenatally and early in life can be detrimental to normal lung development, however the specific timing of critical windows during development is not fully understood., Objectives: We evaluated air pollution exposures during the prenatal and early-life period in association with lung function at ages 6-9, in an effort to identify potentially influential windows of exposure for lung development., Methods: Our study population consisted of 222 children aged 6-9 from the Fresno-Clovis metro area in California with spirometry data collected between May 2015 and May 2017. We used distributed-lag non-linear models to flexibly model the exposure-lag-response for monthly average exposure to fine particulate matter (PM 2.5 ) and ozone (O 3 ) during the prenatal months and first three years of life in association with forced vital capacity (FVC), and forced expiratory volume in the first second (FEV 1 ), adjusted for covariates., Results: PM 2.5 exposure during the prenatal period and the first 3-years of life was associated with lower FVC and FEV 1 assessed at ages 6-9. Specifically, an increase from the 5th percentile of the observed monthly average exposure (7.55 μg/m 3 ) to the median observed exposure (12.69 μg/m 3 ) for the duration of the window was associated with 0.42 L lower FVC (95% confidence interval (CI): -0.82, -0.03) and 0.38 L lower FEV 1 (95% CI: -0.75, -0.02). The shape of the lag-response indicated that the second half of pregnancy may be a particularly influential window of exposure. Associations for ozone were not as strong and typically CIs included the null., Conclusions: Our findings indicate that prenatal and early-life exposures to PM 2.5 are associated with decreased lung function later in childhood. Exposures during the latter months of pregnancy may be especially influential., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Andreas Neophytou reports financial support was provided by National Institute of Environmental Health Sciences. John R. Balmes, Liza Lutzker, Stephanie Holm, Elizabeth M. Noth, Sadie Costello, Tim Tyner, Ellen Eisen, Kari C. Nadeau, S Katharine Hammond reports financial support was provided by National Institute of Environmental Health Sciences. John R. Balmes reports a relationship with California Air Resources Board that includes: board membership., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: In-utero exposure to particulate matter with aerodynamic diameter less than 2.5 μm (PM 2.5 ) is associated with low birth weight and health risks later in life. Pregnant women are mobile and locations they spend time in contribute to their personal PM 2.5 exposures. Therefore, it is important to understand how mobility and exposures encountered within activity spaces contribute to personal PM 2.5 exposures during pregnancy., Methods: We collected 48-h integrated personal PM 2.5 samples and continuous geolocation (GPS) data for 213 predominantly Hispanic/Latina pregnant women in their 3 rd trimester in Los Angeles, CA. We also collected questionnaires and modeled outdoor air pollution and meteorology in their residential neighborhood. We calculated three GPS-derived activity space measures of exposure to road networks, greenness (NDVI), parks, traffic volume, walkability, and outdoor PM 2.5 and temperature. We used bivariate analyses to screen variables (GPS-extracted exposures in activity spaces, individual characteristics, and residential neighborhood exposures) based on their relationship with personal, 48-h integrated PM 2.5 concentrations. We then built a generalized linear model to explain the variability in personal PM 2.5 exposure and identify key contributing factors., Results: Indoor PM 2.5 sources, parity, and home ventilation were significantly associated with personal exposure. Activity-space based exposure to roads was associated with significantly higher personal PM 2.5 exposure, while greenness was associated with lower personal PM 2.5 exposure (β = -3.09 μg/m 3 per SD increase in NDVI, p-value = 0.018). The contribution of outdoor PM 2.5 to personal exposure was positive but relatively lower (β = 2.05 μg/m 3 per SD increase, p-value = 0.016) than exposures in activity spaces and the indoor environment. The final model explained 34% of the variability in personal PM 2.5 concentrations., Conclusions: Our findings highlight the importance of activity spaces and the indoor environment on personal PM 2.5 exposures of pregnant women living in Los Angeles, CA. This work also showcases the multiple, complex factors that contribute to total personal PM 2.5 exposure., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Air pollution exposure may make people more vulnerable to COVID-19 infection. However, previous studies in this area mostly focused on infection before May 2020 and long-term exposure., Objective: To assess both long-term and short-term exposure to air pollution and COVID-19 incidence across four case surges from 03/1/2020 to 02/28/2021., Methods: The cohort included 4.6 million members from a large integrated health care system in southern California with comprehensive electronic medical records (EMR). COVID-19 cases were identified from EMR. Incidence of COVID-19 was computed at the census tract-level among members. Prior 1-month and 1-year averaged air pollutant levels (PM 2.5 , NO 2 , and O 3 ) at the census tract-level were estimated based on hourly and daily air quality data. Data analyses were conducted by each wave: 3/1/2020-5/31/2020, 6/1/202-9/30/2020, 10/1/2020-12/31/2020, and 1/1/2021-2/28/2021 and pooled across waves using meta-analysis. Generalized linear mixed effects models with Poisson distribution and spatial autocorrelation were used with adjustment for meteorological factors and census tract-level social and health characteristics. Results were expressed as relative risk (RR) per 1 standard deviation., Results: The cohort included 446,440 COVID-19 cases covering 4609 census tracts. The pooled RRs (95% CI) of COVID-19 incidence associated with 1-year exposures to PM 2.5 , NO 2 , and O 3 were 1.11 (1.04, 1.18) per 2.3 μg/m 3 ,1.09 (1.02, 1.17) per 3.2 ppb, and 1.06 (1.00, 1.12) per 5.5 ppb respectively. The corresponding RRs (95% CI) associated with prior 1-month exposures were 1.11 (1.03, 1.20) per 5.2 μg/m 3 for PM 2.5 , 1.09 (1.01, 1.17) per 6.0 ppb for NO 2 and 0.96 (0.85, 1.08) per 12.0 ppb for O 3 ., Conclusion: Long-term PM 2.5 and NO 2 exposures were associated with increased risk of COVID-19 incidence across all case surges before February 2021. Short-term PM 2.5 and NO 2 exposures were also associated. Our findings suggest that air pollution may play a role in increasing the risk of COVID-19 infection., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Metabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood., Objectives: To assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects., Methods: We studied 299 children (ages 6-8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) - the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO 2 , elemental carbon, and fine particulate matter (PM 2.5 ) - were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome., Results: The study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m 3 increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 μg/m 3 increase in 6-month average PM 2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO 2 was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane., Discussion: Our results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Traffic-related air pollution (TRAP) exposure has been linked to type 2 diabetes and metabolic dysfunction in humans. Animal studies suggest that air pollutants may alter the composition of the gut microbiota, which may negatively impact metabolic health through changes in the composition and/or function of the gut microbiome., Objectives: The primary aim of this study was to determine whether elevated TRAP exposure was correlated with gut bacterial taxa in overweight and obese adolescents from the Meta-AIR (Metabolic and Asthma Incidence Research) study. The secondary aim was to examine whether gut microbial taxa correlated with TRAP were also correlated with risk factors for type 2 diabetes (e.g., fasting glucose levels). We additionally explored whether correlations between TRAP and these metabolic risk factors could be explained by the relative abundance of these taxa., Methods: Participants (17-19 years; n=43) were enrolled between 2014 and 2016 from Southern California. The CALINE4 line dispersion model was used to model prior year residential concentrations of nitrogen oxides (NOx) as a marker of traffic emissions. The relative abundance of fecal microbiota was characterized by 16S rRNA sequencing and spearman partial correlations were examined after adjusting for body fat percent., Results: Freeway TRAP was correlated with decreased Bacteroidaceae (r=-0.48; p=0.001) and increased Coriobacteriaceae (r=0.48; p<0.001). These same taxa were correlated with fasting glucose levels, including Bacteroidaceae (r=-0.34; p=0.04) and Coriobacteriaceae (r=0.41; p<0.01). Further, freeway TRAP was positively correlated fasting glucose (r=0.45; p=0.004) and Bacteroidaceae and Coriobacteriaceae explained 24% and 29% of the correlation between TRAP and fasting glucose levels., Conclusions: Increased TRAP exposure was correlated with gut microbial taxa and fasting glucose levels. Gut microbial taxa that were correlated with TRAP partially explained the correlation between TRAP and fasting glucose levels. These results suggest that exposure to air pollutants may negatively impact metabolic health via alterations in the gut microbiota., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Emerging evidence indicates that the near-roadway air pollution (NRAP) mixture contributes to CHD, yet few studies have evaluated the associated costs., Objective: We integrated an assessment of NRAP-attributable CHD in Southern California with new methods to value the associated mortality and hospitalizations., Methods: Based on population-weighted residential exposure to NRAP (traffic density, proximity to a major roadway and elemental carbon), we estimated the inflation-adjusted value of NRAP-attributable mortality and costs of hospitalizations that occurred in 2008. We also estimated anticipated costs in 2035 based on projected changes in population and in NRAP exposure associated with California's plans to reduce greenhouse gas emissions. For comparison, we estimated the value of CHD mortality attributable to PM less than 2.5μm in diameter (PM 2.5 ) in both 2008 and 2035., Results: The value of CHD mortality attributable to NRAP in 2008 was between $3.8 and $11.5 billion, 23% (major roadway proximity) to 68% (traffic density) of the $16.8 billion attributable to regulated regional PM 2.5 . NRAP-attributable costs were projected to increase to $10.6 to $22 billion in 2035, depending on the NRAP metric. Cost of NRAP-attributable hospitalizations for CHD in 2008 was $48.6 million and was projected to increase to $51.4 million in 2035., Conclusions: We developed an economic framework that can be used to estimate the benefits of regulations to improve air quality. CHD attributable to NRAP has a large economic impact that is expected to increase by 2035, largely due to an aging population. PM 2.5 -attributable costs may underestimate total value of air pollution-attributable CHD., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Objective: Neighborhood greenspace improves mental health of urban-dwelling populations, but its putative neurobehavioral benefits in adolescents remain unclear. We conducted a prospective study on urban-dwelling adolescents to examine the association between greenspace in residential neighborhood and aggressive behaviors., Method: Participants (n = 1,287) of the Risk Factors for Antisocial Behavior Study, a multi-ethnic cohort of twins and triplets born in 1990 to 1995 and living in Southern California, were examined in 2000 to 2012 (aged 9-18 years) with repeated assessments of their aggressive behaviors by the parent-reported Child Behavior Checklist. Normalized Difference Vegetation Index (NDVI) derived from satellite imagery was used as a proxy for residential neighborhood greenspace aggregated over various spatiotemporal scales before each assessment. Multilevel mixed-effects models were used to estimate the effects of greenspace on aggressive behaviors, adjusting for within-family/within-individual correlations and other potential confounders., Results: Both short-term (1- to 6-month) and long-term (1- to 3-year) exposures to greenspace within 1,000 meters surrounding residences were associated with reduced aggressive behaviors. The benefit of increasing vegetation over the range (∼0.12 in NDVI) commonly seen in urban environments was equivalent to approximately 2 to 2.5 years of behavioral maturation. Sociodemographic factors (e.g., age, gender, race/ethnicity, and socioeconomic status) and neighborhood quality did not confound or modify these associations, and the benefits remained after accounting for temperature., Conclusion: Our novel findings support the benefits of neighborhood greenspace in reducing aggressive behaviors of urban-dwelling adolescents. Community-based interventions are needed to determine the efficacy of greenspace as a preemptive strategy to reduce aggressive behaviors in urban environments., (Copyright © 2016 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.)

Background: Few previous studies examined the impact of prenatal air pollution exposures on fetal development based on ultrasound measures during pregnancy., Methods: In a prospective birth cohort of more than 500 women followed during 1993-1996 in Los Angeles, California, we examined how air pollution impacts fetal growth during pregnancy. Exposure to traffic related air pollution was estimated using CALINE4 air dispersion modeling for nitrogen oxides (NOx) and a land use regression (LUR) model for nitrogen monoxide (NO), nitrogen dioxide (NO2) and NOx. Exposures to carbon monoxide (CO), NO2, ozone (O3) and particles <10μm in aerodynamic diameter (PM10) were estimated using government monitoring data. We employed a linear mixed effects model to estimate changes in fetal size at approximately 19, 29 and 37 weeks gestation based on ultrasound., Results: Exposure to traffic-derived air pollution during 29 to 37 weeks was negatively associated with biparietal diameter at 37 weeks gestation. For each interquartile range (IQR) increase in LUR-based estimates of NO, NO2 and NOx, or freeway CALINE4 NOx we estimated a reduction in biparietal diameter of 0.2-0.3mm. For women residing within 5km of a monitoring station, we estimated biparietal diameter reductions of 0.9-1.0mm per IQR increase in CO and NO2. Effect estimates were robust to adjustment for a number of potential confounders. We did not observe consistent patterns for other growth endpoints we examined., Conclusions: Prenatal exposure to traffic-derived pollution was negatively associated with fetal head size measured as biparietal diameter in late pregnancy., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Exposure to ambient air pollution is linked to adverse pregnancy outcomes. Previous reports examining the relationship between ambient air pollution and Hypertensive Disorders of Pregnancy have been inconsistent., Objectives: We evaluated the effects of ambient air pollution on the odds of Hypertensive Disorder of Pregnancy and whether these associations varied by body mass index (BMI)., Methods: We conducted a retrospective, case-control study among 298 predominantly Hispanic women (136 clinically confirmed cases) who attended the Los Angeles County+University of Southern California Women's and Children's Hospital during 1996-2008. Trimester-specific carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), and particulate matter with aerodynamic diameter <10 μm and <2.5 μm (PM10, PM2.5) exposure were estimated based on 24-hour exposure level at residential address. Logistic regression models were fitted to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for two standard deviation increase in exposure levels., Results: Exposures to CO and PM2.5 in the 1st trimester were significantly associated with Hypertensive Disorders of Pregnancy, and these associations were modified by BMI. In non-obese women (BMI <30), 1st trimester exposures to PM2.5 and CO were significantly associated with increased odds of Hypertensive Disorder of Pregnancy (ORs per 2-standard deviation increase in PM2.5 (7 μg/m(3)) and CO (1 ppm) exposures were 9.10 [95% CI: 3.33-24.6] and 4.96 [95% CI: 1.85-13.31], respectively). Additionally, there was a significantly positive association between exposure to O3 in the 2nd trimester and Hypertensive Disorder of Pregnancy (OR per 15 ppb=2.05; 95% CI: 1.22-3.46)., Conclusion: Among non-obese women, 1st trimester exposure to PM2.5 and carbon monoxide are associated with increased odds of Hypertensive Disorder of Pregnancy., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: Two recent case-control studies in Italy reported that long-term exposure to particulate air pollution or living near major traffic roads was associated with an increased risk of deep vein thrombosis (DVT). No prospective evidence exists on the possible association between long-term traffic-related air pollution and incident venous thromboembolism (VTE)., Objectives: To examine the association between long-term traffic exposure and incident VTE in a population-based prospective cohort study., Methods: We studied 13,143 middle-aged men and women in the Atherosclerosis Risk in Communities Study without a history of DVT or pulmonary embolism at baseline examination (1987-1989). The Geographical Information System-mapped traffic density and distance to major roads in the four study communities served as measures of traffic exposure. We examined the association between traffic exposure and incident VTE with proportional hazards regression models., Results: A total of 405 subjects developed VTE in 2005. Traffic density was not significantly associated with VTE. Relative to those in the lowest quartile of traffic density, the adjusted hazard ratios across increasing quartiles were 1.18 (95% confidence interval [CI] 0.88-1.57), 0.99 (95% CI 0.74-1.34) and 1.14 (95% CI 0.86-1.51) (P-value for trend across quartiles = 0.64). For residents living within 150 m of major roads, as compared with subjects living further away, the adjusted hazard ratio was 1.16 (95% CI 0.95-1.42, P = 0.14)., Conclusions: This first prospective study in the general population does not support an association between air pollution exposure or traffic proximity and risk of DVT. More data may be needed to clarify whether traffic or air pollution influences the risk of VTE., (© 2011 International Society on Thrombosis and Haemostasis.)

Background: Whether local exposure to major roadways adversely affects lung-function growth during the period of rapid lung development that takes place between 10 and 18 years of age is unknown. This study investigated the association between residential exposure to traffic and 8-year lung-function growth., Methods: In this prospective study, 3677 children (mean age 10 years [SD 0.44]) participated from 12 southern California communities that represent a wide range in regional air quality. Children were followed up for 8 years, with yearly lung-function measurements recorded. For each child, we identified several indicators of residential exposure to traffic from large roads. Regression analysis was used to establish whether 8-year growth in lung function was associated with local traffic exposure, and whether local traffic effects were independent of regional air quality., Findings: Children who lived within 500 m of a freeway (motorway) had substantial deficits in 8-year growth of forced expiratory volume in 1 s (FEV(1), -81 mL, p=0.01 [95% CI -143 to -18]) and maximum midexpiratory flow rate (MMEF, -127 mL/s, p=0.03 [-243 to -11), compared with children who lived at least 1500 m from a freeway. Joint models showed that both local exposure to freeways and regional air pollution had detrimental, and independent, effects on lung-function growth. Pronounced deficits in attained lung function at age 18 years were recorded for those living within 500 m of a freeway, with mean percent-predicted 97.0% for FEV1 (p=0.013, relative to >1500 m [95% CI 94.6-99.4]) and 93.4% for MMEF (p=0.006 [95% CI 89.1-97.7])., Interpretation: Local exposure to traffic on a freeway has adverse effects on children's lung development, which are independent of regional air quality, and which could result in important deficits in attained lung function in later life.

Human health effects due to chronic exposure to ozone (O3) have not been established due to problems with exposure assignment and the use of measures of lung function which may not reflect the site of O3 toxicity in the lung. We investigated the feasibility of retrospective assessment of O3 exposure-relevant covariates and derived lifetime "effective exposure" to ozone. Mid- and end-expiratory flows (FEF25-75%, FEF75%) were regressed against effective exposure and ecological lifetime exposure. A convenience sample of 130 UC Berkeley freshmen, ages 17-21, participated twice in the same tests (residential history, questionnaire, pulmonary function), 5-7 days apart. Students had to be lifelong residents of Northern (SF) or Southern (LA) California. Monthly ambient O3 concentrations (OZ) were assigned based on the lifetime residential history. An "effective time" (T) spent in OZ environments was derived for each residence and age stratum (0-2, 3-5, 6-11, 12+) with the use of questions about "total time spent outdoors" and time spent in "moderate" and/or "heavy" activity. Effective exposure was calculated over the lifetime (OZ x T) of each subject. Ozone metrics used were 8-hr averages (10 AM-6 PM) and "hours above 60 ppb." FEF25-75% and FEF75% decreased with both effective exposure and ecologic assignment of O3 exposure. For a 20 ppb increase (interquartile range) in 8-hr O3, FEF75% decreased 334 ml/sec (95%Cl:11-657 ml/sec), which corresponds to 14% (1.0-28.3%) of the population mean FEF75%. The corresponding effect on FEF25-75% was -420 ml/sec (95%Cl: +46 to -886, P = 0.08) or 7.2% of the mean. Use of time-activity data to define exposure had no impact on estimates. Negative confounding factors were region (SF vs LA), gender, and ethnicity. Lifetime 8-hr average O3 concentrations ranged from 16 to 74 ppb with little overlap between regions. There was no evidence for different O3 effects across regions. Effects were independent of lifetime mean PM10, NO2, temperature, or humidity. Effects on FEV1 tended to be negative whereas those for FVC, although negative in some models, where inconsistent and small. The strong relationship of lifetime ambient O3 on mid- and end-expiratory flows of college freshmen and the lack of association with FEV1 and FVC are consistent with biologic models of chronic effects of O3 in the small airways. Since the present study was designed as a pilot study, these findings have to be confirmed in a larger sample that is representative of the target population.