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PURPOSE OF REVIEW: Environmental chemical exposures may disrupt child development, with long-lasting health impacts. To date, U.S. studies of early environmental exposures have been limited in size and diversity, hindering power and generalizability. With harmonized data from over 60,000 participants representing 69 pregnancy cohorts, the National Institutes of Healths Environmental influences on Child Health Outcomes (ECHO) Program is the largest study of U.S. childrens health. Here, we: (1) review ECHO-wide studies of chemical exposures and maternal-child health; and (2) outline opportunities for future research using ECHO data. RECENT FINDINGS: As of early 2024, in addition to over 200 single-cohort (or award) papers on chemical exposures supported by ECHO, ten collaborative multi-cohort papers have been made possible by ECHO data harmonization and new data collection. Multi-cohort papers have examined prenatal exposure to per- and polyfluoroalkyl substances (PFAS), phthalates, phenols and parabens, organophosphate esters (OPEs), metals, melamine and aromatic amines, and emerging contaminants. They have primarily focused on describing patterns of maternal exposure or examining associations with maternal and infant outcomes; fewer studies have examined later child outcomes (e.g., autism) although follow up of enrolled ECHO children continues. The NICHDs Data and Specimen Hub (DASH) database houses extensive ECHO data including over 470,000 chemical assay results and complementary data on priority outcome areas (pre, peri-, and postnatal, airway, obesity, neurodevelopment, and positive health), making it a rich resource for future analyses. ECHOs extensive data repository, including biomarkers of chemical exposures, can be used to advance our understanding of environmental influences on childrens health. Although few published studies have capitalized on these unique harmonized data to date, many analyses are underway with data now widely available.

California faces several serious direct and indirect climate exposures that can adversely affect public health, some of which are already occurring. The public health burden now and in the future will depend on atmospheric greenhouse gas concentrations, underlying population vulnerabilities, and adaptation efforts. Here, we present a structured review of recent literature to examine the leading climate risks to public health in California, including extreme heat, extreme precipitation, wildfires, air pollution, and infectious diseases. Comparisons among different climate-health pathways are difficult due to inconsistencies in study design regarding spatial and temporal scales and health outcomes examined. We find, however, that the current public health burden likely affects thousands of Californians each year, depending on the exposure pathway and health outcome. Further, while more evidence exists for direct and indirect proximal health effects that are the focus of this review, distal pathways (e.g., impacts of drought on nutrition) are more uncertain but could add to this burden. We find that climate adaptation measures can provide significant health benefits, particularly in disadvantaged communities. We conclude with priority recommendations for future analyses and solution-driven policy actions.

In the modern "omics" era, measurement of the human exposome is a critical missing link between genetic drivers and disease outcomes. High-resolution mass spectrometry (HRMS), routinely used in proteomics and metabolomics, has emerged as a leading technology to broadly profile chemical exposure agents and related biomolecules for accurate mass measurement, high sensitivity, rapid data acquisition, and increased resolution of chemical space. Non-targeted approaches are increasingly accessible, supporting a shift from conventional hypothesis-driven, quantitation-centric targeted analyses toward data-driven, hypothesis-generating chemical exposome-wide profiling. However, HRMS-based exposomics encounters unique challenges. New analytical and computational infrastructures are needed to expand the analysis coverage through streamlined, scalable, and harmonized workflows and data pipelines that permit longitudinal chemical exposome tracking, retrospective validation, and multi-omics integration for meaningful health-oriented inferences. In this article, we survey the literature on state-of-the-art HRMS-based technologies, review current analytical workflows and informatic pipelines, and provide an up-to-date reference on exposomic approaches for chemists, toxicologists, epidemiologists, care providers, and stakeholders in health sciences and medicine. We propose efforts to benchmark fit-for-purpose platforms for expanding coverage of chemical space, including gas/liquid chromatography-HRMS (GC-HRMS and LC-HRMS), and discuss opportunities, challenges, and strategies to advance the burgeoning field of the exposome.

BACKGROUND: Interventions are needed to help people reduce exposure to harmful chemicals from everyday products and lifestyle habits. Report-back of individual exposures is a potential pathway to increasing environmental health literacy (EHL) and readiness to reduce exposures. OBJECTIVES: Our objective was to determine if report-back of endocrine-disrupting chemicals (EDCs) can reduce EDC exposure, increase EHL, and increase readiness to change (i.e., to implement EDC exposure-reduction behaviors). METHODS: Participants in the Healthy Nevada Project completed EHL and readiness-to-change surveys before (n = 424) and after (n = 174) a report-back intervention. Participants used mail-in kits to measure urinary biomarkers of EDCs. The report-back of results included urinary levels, information about health effects, sources of exposure, and personalized recommendations to reduce exposure. RESULTS: EHL was generally very high at baseline, especially for questions related to the general pollution. For questions related to chemical exposures, responses varied across several demographics. Statistically reliable improvements in EHL responses were seen after report-back. For readiness to change, 72% were already or planning to change their behaviors. Post-intervention, women increased their readiness (p = 0.053), while men decreased (p = 0.007). When asked what challenges they faced in reducing exposure, 79% cited not knowing what to do. This dropped to 35% after report-back. Participants with higher propylparaben were younger (p = 0.03) and women and participants who rated themselves in better health had higher levels of some phthalates (p = 0.02-0.003 and p = 0.001-0.003, respectively). After report-back, monobutyl phthalate decreased among the 48 participants who had valid urine tests before and after the intervention (p < 0.001). CONCLUSIONS: The report-back intervention was successful as evidenced by increased EHL behaviors, increased readiness to change among women, and a decrease in monobutyl phthalate. An EHL questionnaire more sensitive to chemical exposures would help differentiate high and low literacy. Future research will focus on understanding why men decreased their readiness to change and how the intervention can be improved for all participants.

BACKGROUND: Midlife residential exposure to greenspace may slow cognitive decline by increasing opportunities for physical activity and social connection, restoring attention, or reducing stress or adverse environmental exposures. However, prospective studies on the association between greenness and cognitive decline are sparse. OBJECTIVE: We investigated the prospective association between greenness at midlife and cognitive decline later in life. We explored effect measure modification by apolipoprotein E (APOE)-ɛ4 carrier status, neighborhood socioeconomic status (NSES), and rural/urban regions. METHODS: The Nurses Health Study (N=121,700) started in 1976 with married female nurses, 30-55 years of age, located across 11 US states. We examined 16,962 nurses who were enrolled in a substudy starting in 1995-2001 (mean age=74y) through 2008. We assessed average summer residential greenness in a 270-m buffer using Landsat Normalized Difference Vegetation Index data from 1986-1994. Starting in 1995-2001, participants underwent up to four repeated measures of five cognitive tests. A global composite score was calculated as the average of all z-scores for each task to evaluate overall cognition. We used linear mixed models to evaluate the association of average greenness exposure at midlife with cognitive decline in later life, adjusted for age, education, NSES, and depression. RESULTS: In adjusted models, higher midlife greenness exposure [per interquartile range (IQR): 0.18] was associated with a 0.004-unit (95% CI: 0.001, 0.006) slower annual rate of cognitive decline. For comparison, we found that 1 year of age is related to a -0.006 mean annual difference for global cognition in the full sample; thus, higher midlife greenness appeared equivalent to slowing cognitive decline by ∼8 months. In analysis exploring gene-environment interactions, we found that among APOE-ɛ4 carriers, an IQR increase in greenness was associated with a rate of decline that was slower by 0.01 units of global composite score (95% CI: 0.0004, 0.02). This association was attenuated among APOE-ɛ4 noncarriers. We did not observe associations between greenness and baseline or annual rate of cognitive decline of verbal memory. DISCUSSION: Higher midlife greenness exposure is associated with slower cognitive decline later in life. Future research is necessary to confirm these findings. https://doi.org/10.1289/EHP13588.

Background: Repeated exposure to heat (ie, plasma volume expansion) or altitude (ie, increase in total hemoglobin mass), in conjunction with exercise, induces hematological adaptations that enhance endurance performance in each respective environment. Recently, combining heat and altitude training has become increasingly common for athletes preparing to compete in temperate, sea-level conditions. Purpose: To review the physiological adaptations to training interventions combining thermal and hypoxic stimuli and summarize the implications for temperate, sea-level performance. Current Evidence: To date, research on combining heat and hypoxia has employed 2 main approaches: simultaneously combining the stressors during training or concurrently training in the heat and sleeping at altitude, sometimes with additional training in hypoxia. When environmental stimuli are combined in a training session, improvements in aerobic fitness and time-trial performance in temperate, sea-level conditions are generally similar in magnitude to those observed with heat, or altitude, training alone. Similarly, training in the heat and sleeping at altitude does not appear to provide any additional hematological or nonhematological benefits for temperate; sea-level performance relative to training in hot, hypoxic, or control conditions. Conclusions: Current research regarding combined heat and altitude interventions does not seem to indicate that it enhances temperate, sea-level performance to a greater extent than "traditional" (heat or hypoxia alone) training approaches. A major challenge in implementing combined-stressor approaches lies in the uncertainty surrounding the prescription of dosing regimens (ie, exercise and environmental stress). The potential benefits of conducting heat and altitude exposure sequentially (ie, one after the other) warrants further investigation. [ABSTRACT FROM AUTHOR]

First-ever measurements of particulate matter (PM2.5, PM10, and TSP) along with gaseous pollutants (CO, NO2, and SO2) were performed from June 2019 to April 2020 in Faisalabad, Metropolitan, Pakistan, to assess their seasonal variations; Summer 2019, Autumn 2019, Winter 2019-2020, and Spring 2020. Pollutant measurements were carried out at 30 locations with a 3-km grid distance from the Sitara Chemical Industry in District Faisalabad to Bhianwala, Sargodha Road, Tehsil Lalian, District Chiniot. ArcGIS 10.8 was used to interpolate pollutant concentrations using the inverse distance weightage method. PM2.5, PM10, and TSP concentrations were highest in summer, and lowest in autumn or winter. CO, NO2, and SO2 concentrations were highest in summer or spring and lowest in winter. Seasonal average NO2 and SO2 concentrations exceeded WHO annual air quality guide values. For all 4 seasons, some sites had better air quality than others. Even in these cleaner sites air quality index (AQI) was unhealthy for sensitive groups and the less good sites showed Very critical AQI (> 500). Dust-bound carbon and sulfur contents were higher in spring (64 mg g-1) and summer (1.17 mg g-1) and lower in autumn (55 mg g-1) and winter (1.08 mg g-1). Venous blood analysis of 20 individuals showed cadmium and lead concentrations higher than WHO permissible limits. Those individuals exposed to direct roadside pollution for longer periods because of their occupation tended to show higher Pb and Cd blood concentrations. It is concluded that air quality along the roadside is extremely poor and potentially damaging to the health of exposed workers.

Exposure to ambient air pollution has significant adverse health effects; however, whether air pollution is associated with urological cancer is largely unknown. We conduct a systematic review and meta-analysis with epidemiological studies, showing that a 5 μg/m3 increase in PM2.5 exposure is associated with a 6%, 7%, and 9%, increased risk of overall urological, bladder, and kidney cancer, respectively; and a 10 μg/m3 increase in NO2 is linked to a 3%, 4%, and 4% higher risk of overall urological, bladder, and prostate cancer, respectively. Were these associations to reflect causal relationships, lowering PM2.5 levels to 5.8 μg/m3 could reduce the age-standardized rate of urological cancer by 1.5 ~ 27/100,000 across the 15 countries with the highest PM2.5 level from the top 30 countries with the highest urological cancer burden. Implementing global health policies that can improve air quality could potentially reduce the risk of urologic cancer and alleviate its burden.

BACKGROUND: Cardiovascular disease (CVD) is the leading cause of death worldwide. It has been known for some considerable time that radiation is associated with excess risk of CVD. A recent systematic review of radiation and CVD highlighted substantial inter-study heterogeneity in effect, possibly a result of confounding or modifications of radiation effect by non-radiation factors, in particular by the major lifestyle/environmental/medical risk factors and latent period. METHODS: We assessed effects of confounding by lifestyle/environmental/medical risk factors on radiation-associated CVD and investigated evidence for modifying effects of these variables on CVD radiation dose-response, using data assembled for a recent systematic review. RESULTS: There are 43 epidemiologic studies which are informative on effects of adjustment for confounding or risk modifying factors on radiation-associated CVD. Of these 22 were studies of groups exposed to substantial doses of medical radiation for therapy or diagnosis. The remaining 21 studies were of groups exposed at much lower levels of dose and/or dose rate. Only four studies suggest substantial effects of adjustment for lifestyle/environmental/medical risk factors on radiation risk of CVD; however, there were also substantial uncertainties in the estimates in all of these studies. There are fewer suggestions of effects that modify the radiation dose response; only two studies, both at lower levels of dose, report the most serious level of modifying effect. CONCLUSIONS: There are still large uncertainties about confounding factors or lifestyle/environmental/medical variables that may influence radiation-associated CVD, although indications are that there are not many studies in which there are substantial confounding effects of these risk factors.

BACKGROUND: Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. METHODS: In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). RESULTS: Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032-1.053) vs OR = 1.009 (95% CI, 0.996-1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019-1.047), RERI = 0.039 (95% CI, 0.025-0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. CONCLUSIONS: The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users.

In California, wildfire risk and severity have grown substantially in the last several decades. Research has characterized extensive adverse health impacts from exposure to wildfire-attributable fine particulate matter (PM2.5), but few studies have quantified long-term outcomes, and none have used a wildfire-specific chronic dose-response mortality coefficient. Here, we quantified the mortality burden for PM2.5 exposure from California fires from 2008 to 2018 using Community Multiscale Air Quality modeling system wildland fire PM2.5 estimates. We used a concentration-response function for PM2.5, applying ZIP code-level mortality data and an estimated wildfire-specific dose-response coefficient accounting for the likely toxicity of wildfire smoke. We estimate a total of 52,480 to 55,710 premature deaths are attributable to wildland fire PM2.5 over the 11-year period with respect to two exposure scenarios, equating to an economic impact of $432 to $456 billion. These findings extend evidence on climate-related health impacts, suggesting that wildfires account for a greater mortality and economic burden than indicated by earlier studies.

Prenatal per- and poly-fluoroalkyl substances (PFAS) exposure may influence gestational outcomes through bioactive lipids─metabolic and inflammation pathway indicators. We estimated associations between prenatal PFAS exposure and bioactive lipids, measuring 12 serum PFAS and 50 plasma bioactive lipids in 414 pregnant women (median 17.4 weeks' gestation) from three Environmental influences on Child Health Outcomes Program cohorts. Pairwise association estimates across cohorts were obtained through linear mixed models and meta-analysis, adjusting the former for false discovery rates. Associations between the PFAS mixture and bioactive lipids were estimated using quantile g-computation. Pairwise analyses revealed bioactive lipid levels associated with PFDeA, PFNA, PFOA, and PFUdA (p < 0.05) across three enzymatic pathways (cyclooxygenase, cytochrome p450, lipoxygenase) in at least one combined cohort analysis, and PFOA and PFUdA (q < 0.2) in one linear mixed model. The strongest signature revealed doubling in PFOA corresponding with PGD2 (cyclooxygenase pathway; +24.3%, 95% CI: 7.3-43.9%) in the combined cohort. Mixture analysis revealed nine positive associations across all pathways with the PFAS mixture, the strongest signature indicating a quartile increase in the PFAS mixture associated with PGD2 (+34%, 95% CI: 8-66%), primarily driven by PFOS. Bioactive lipids emerged as prenatal PFAS exposure biomarkers, deepening insights into PFAS' influence on pregnancy outcomes.

We examined associations between prenatal fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) exposures and child respiratory outcomes through age 8-9 years in 1279 ECHO-PATHWAYS Consortium mother-child dyads. We averaged spatiotemporally modeled air pollutant exposures during four fetal lung development phases: pseudoglandular (5-16 weeks), canalicular (16-24 weeks), saccular (24-36 weeks), and alveolar (36+ weeks). We estimated adjusted relative risks (RR) for current asthma at age 8-9 and asthma with recent exacerbation or atopic disease, and odds ratios (OR) for wheezing trajectories using modified Poisson and multinomial logistic regression, respectively. Effect modification by child sex, maternal asthma, and prenatal environmental tobacco smoke was explored. Across all outcomes, 95% confidence intervals (CI) included the null for all estimates of associations between prenatal air pollution exposures and respiratory outcomes. Pseudoglandular PM2.5 exposure modestly increased risk of current asthma (RRadj = 1.15, 95% CI: 0.88-1.51); canalicular PM2.5 exposure modestly increased risk of asthma with recent exacerbation (RRadj = 1.26, 95% CI: 0.86-1.86) and persistent wheezing (ORadj = 1.28, 95% CI: 0.86-1.89). Similar findings were observed for O3, but not NO2, and associations were strengthened among mothers without asthma. While not statistically distinguishable from the null, trends in effect estimates suggest some adverse associations of early pregnancy air pollution exposures with child respiratory conditions, warranting confirmation in larger samples.

BackgroundAlthough ~18 million people live within a mile from active oil and gas development (OGD) sites in the United States, epidemiological research on how OGD affects the health of nearby urban residents is sparse. Thousands of OGD sites are spread across Los Angeles (LA) County, California, home to the largest urban oil production in the country. Air pollution and noise from OGD may contribute to cardiovascular morbidity.ObjectiveWe examined the association between proximity to OGD and blood pressure in a diverse cohort of residents in LA.MethodsWe recruited residents in South LA who lived

BACKGROUND: Epidemiological findings regarding the association of particulate matter ≤2.5 μm (PM2.5) exposure with hypertensive disorders in pregnancy (HDP) are inconsistent; evidence for HDP risk related to PM2.5 components, mixture effects, and windows of susceptibility is limited. We aimed to investigate the relationships between HDP and exposure to PM2.5 during pregnancy. METHODS AND FINDINGS: A large retrospective cohort study was conducted among mothers with singleton pregnancies in Kaiser Permanente Southern California from 2008 to 2017. HDP were defined by International Classification of Diseases-9/10 (ICD-9/10) diagnostic codes and were classified into 2 subcategories based on the severity of HDP: gestational hypertension (GH) and preeclampsia and eclampsia (PE-E). Monthly averages of PM2.5 total mass and its constituents (i.e., sulfate, nitrate, ammonium, organic matter, and black carbon) were estimated using outputs from a fine-resolution geoscience-derived model. Multilevel Cox proportional hazard models were used to fit single-pollutant models; quantile g-computation approach was applied to estimate the joint effect of PM2.5 constituents. The distributed lag model was applied to estimate the association between monthly PM2.5 exposure and HDP risk. This study included 386,361 participants (30.3 ± 6.1 years) with 4.8% (17,977/373,905) GH and 5.0% (19,381/386,361) PE-E cases, respectively. In single-pollutant models, we observed increased relative risks for PE-E associated with exposures to PM2.5 total mass [adjusted hazard ratio (HR) per interquartile range: 1.07, 95% confidence interval (CI) [1.04, 1.10] p < 0.001], black carbon [HR = 1.12 (95% CI [1.08, 1.16] p < 0.001)] and organic matter [HR = 1.06 (95% CI [1.03, 1.09] p < 0.001)], but not for GH. The population attributable fraction for PE-E corresponding to the standards of the US Environmental Protection Agency (9 μg/m3) was 6.37%. In multi-pollutant models, the PM2.5 mixture was associated with an increased relative risk of PE-E ([HR = 1.05 (95% CI [1.03, 1.07] p < 0.001)], simultaneous increase in PM2.5 constituents of interest by a quartile) and PM2.5 black carbon gave the greatest contribution of the overall mixture effects (71%) among all individual constituents. The susceptible window is the late first trimester and second trimester. Furthermore, the risks of PE-E associated with PM2.5 exposure were significantly higher among Hispanic and African American mothers and mothers who live in low- to middle-income neighborhoods (p < 0.05 for Cochrans Q test). Study limitations include potential exposure misclassification solely based on residential outdoor air pollution, misclassification of disease status defined by ICD codes, the date of diagnosis not reflecting the actual time of onset, and lack of information on potential covariates and unmeasured factors for HDP. CONCLUSIONS: Our findings add to the literature on associations between air pollution exposure and HDP. To our knowledge, this is the first study reporting that specific air pollution components, mixture effects, and susceptible windows of PM2.5 may affect GH and PE-E differently.

A multimorbidity-focused approach may reflect common etiologic mechanisms and lead to better targeting of etiologic agents for broadly impactful public health interventions. Our aim was to identify clusters of chronic obesity-related, neurodevelopmental, and respiratory outcomes in children, and to examine associations between cluster membership and widely prevalent chemical exposures to demonstrate our epidemiologic approach. Early to middle childhood outcome data collected 2011-2022 for 1092 children were harmonized across the ECHO-PATHWAYS consortium of 3 prospective pregnancy cohorts in six U.S. cities. 15 outcomes included age 4-9 BMI, cognitive and behavioral assessment scores, speech problems, and learning disabilities, asthma, wheeze, and rhinitis. To form generalizable clusters across study sites, we performed k-means clustering on scaled residuals of each variable regressed on study site. Outcomes and demographic variables were summarized between resulting clusters. Logistic weighted quantile sum regressions with permutation test p-values associated odds of cluster membership with a mixture of 15 prenatal urinary phthalate metabolites in full-sample and sex-stratified models. Three clusters emerged, including a healthier Cluster 1 (n = 734) with low morbidity across outcomes; Cluster 2 (n = 192) with low IQ and higher levels of all outcomes, especially 0.4-1.8-standard deviation higher mean neurobehavioral outcomes; and Cluster 3 (n = 179) with the highest asthma (92 %), wheeze (53 %), and rhinitis (57 %) frequencies. We observed a significant positive, male-specific stratified association (odds ratio = 1.6; p = 0.01) between a phthalate mixture with high weights for MEP and MHPP and odds of membership in Cluster 3 versus Cluster 1. These results identified subpopulations of children with co-occurring elevated levels of BMI, neurodevelopmental, and respiratory outcomes that may reflect shared etiologic pathways. The observed association between phthalates and respiratory outcome cluster membership could inform policy efforts towards children with respiratory disease. Similar cluster-based epidemiology may identify environmental factors that impact multi-outcome prevalence and efficiently direct public policy efforts.

Wildfires have become more frequent and intense due to climate change and outdoor wildfire fine particulate matter (PM2.5) concentrations differ from relatively smoothly varying total PM2.5. Thus, we introduced a conceptual model for computing long-term wildfire PM2.5 and assessed disproportionate exposures among marginalized communities. We used monitoring data and statistical techniques to characterize annual wildfire PM2.5 exposure based on intermittent and extreme daily wildfire PM2.5 concentrations in California census tracts (2006 to 2020). Metrics included: 1) weeks with wildfire PM2.5 < 5 μg/m3; 2) days with non-zero wildfire PM2.5; 3) mean wildfire PM2.5 during peak exposure week; 4) smoke waves (≥2 consecutive days with

Urbanization has altered land surface properties driving changes in micro-climates. Urban form influences peoples activities, environmental exposures, and health. Developing detailed and unified longitudinal measures of urban form is essential to quantify these relationships. Local Climate Zones [LCZ] are a culturally-neutral urban form classification scheme. To date, longitudinal LCZ maps at large scales (i.e., national, continental, or global) are not available. We developed an approach to map LCZs for the continental US from 1986 to 2020 at 100 m spatial resolution. We developed lightweight contextual random forest models using a hybrid model development pipeline that leveraged crowdsourced and expert labeling and cloud-enabled modeling - an approach that could be generalized to other countries and continents. Our model achieved good performance: 0.76 overall accuracy (0.55-0.96 class-wise F1 scores). To our knowledge, this is the first high-resolution, longitudinal LCZ map for the continental US. Our work may be useful for a variety of fields including earth system science, urban planning, and public health.

Extreme heat and wildfire smoke events are increasingly co-occurring in the context of climate change, especially in California. Extreme heat and wildfire smoke may have synergistic effects on population health that vary over space. We leveraged high-resolution satellite and monitoring data to quantify spatially varying compound exposures to extreme heat and wildfire smoke in California (2006-2019) at ZIP Code Tabulation Area (ZCTA) level. We found synergistic effects between extreme heat and wildfire smoke on daily cardiorespiratory hospitalizations at the state level. We also found spatial heterogeneity in such synergistic effects across ZCTAs. Communities with lower education attainment, lower health insurance coverage, lower income, lower proportion of automobile ownership, lower tree canopy coverage, higher population density, and higher proportions of racial/ethnic minorities experienced higher synergistic effects. This study highlights the need to incorporate compound hazards and environmental justice considerations into evidence-based policy development to protect populations from increasingly prevalent compound hazards.

BACKGROUND: Wildfire smoke exposure has become a growing public health concern, as megafires and fires at the wildland urban interface increase in incidence and severity. Smoke contains many pollutants that negatively impact health and is linked to a number of health complications and chronic diseases. Communicating effectively with the public, especially at-risk populations, to reduce their exposure to this environmental pollutant has become a public health priority. Although wildfire smoke risk communication research has also increased in the past decade, best practice guidance is limited, and most health communications do not adhere to health literacy principles: readability, accessibility, and actionability. This scoping review identifies peer-reviewed studies about wildfire smoke risk communications to identify gaps in research and evaluation of communications and programs that seek to educate the public. METHODS: Four hundred fifty-one articles were identified from Web of Science and PubMed databases. After screening, 21 articles were included in the final sample for the abstraction process and qualitative thematic analysis. Ten articles were based in the US, with the other half in Australia, Canada, Italy, and other countries. Fifteen articles examined communication materials and messaging recommendations. Eight papers described communication delivery strategies. Eleven articles discussed behavior change. Six articles touched on risk communications for vulnerable populations; findings were limited and called for increasing awareness and prioritizing risk communications for at-risk populations. RESULTS: This scoping review found limited studies describing behavior change to reduce wildfire smoke exposure, characteristics of effective communication materials and messaging, and communication delivery strategies. Literature on risk communications, dissemination, and behavior change for vulnerable populations was even more limited. CONCLUSIONS: Recommendations include providing risk communications that are easy-to-understand and adapted to specific needs of at-risk groups. Communications should provide a limited number of messages that include specific actions for avoiding smoke exposure. Effective communications should use mixed media formats and a wide variety of dissemination strategies. There is a pressing need for more intervention research and effectiveness evaluation of risk communications about wildfire smoke exposure, and more development and dissemination of risk communications for both the general public and vulnerable populations.

BackgroundPrior studies suggested that air pollution exposure may increase the risk of Parkinson's Disease (PD). We investigated the long-term impacts of traffic-related and multiple sources of particulate air pollution on PD in central California.MethodsOur case-control analysis included 761 PD patients and 910 population controls. We assessed exposure at residential and occupational locations from 1981 to 2016, estimating annual average carbon monoxide (CO) concentrations - a traffic pollution marker - based on the California Line Source Dispersion Model, version 4. Additionally, particulate matter (PM2.5) concentrations were based on a nationwide geospatial chemical transport model. Exposures were assessed as 10-year averages with a 5-year lag time prior to a PD diagnosis for cases and an interview date for controls, subsequently categorized into tertiles. Logistic regression models were used, adjusting for various factors.ResultsTraffic-related CO was associated with an increased odds ratio for PD at residences (OR for T3 vs. T1: 1.58; 95% CI: 1.20, 2.10; p-trend = 0.02) and workplaces (OR for T3 vs. T1: 1.91; 95% CI: 1.22, 3.00; p-trend

BACKGROUND: The penetrance of common genetic risk variants for Parkinsons disease (PD) is low. Pesticide exposure increases PD risk, but how exposure affects penetrance is not well understood. OBJECTIVE: To determine the relationship between occupational pesticide exposure and PD in people with LRRK2 and GBA risk variants. METHODS: Participants of the Parkinsons Progression Markers Initiative (PPMI) with a LRRK2-G2019 S or GBA risk variant provided information about occupational pesticide exposure. We compared exposure in carriers with and without PD. Among carriers with PD, we used Cox proportional hazard models to compare time-to impairment in balance, cognition, and activities of daily living (ADLs) between participants with and without prior occupational pesticide exposure. RESULTS: 378 participants with a risk variant provided exposure information; 176 with LRRK2-G2019 S (54 with and 122 without PD) and 202 with GBA variants (47 with and 155 without PD). Twenty-six participants reported pesticide exposure. People with a GBA variant and occupational pesticide exposure had much higher odds of PD (aOR: 5.4, 95% CI 1.7-18.5, p

Environmental justice research has focused on the distribution of environmental inequalities, such as proximity to landfills, across the U.S. and globally.BackgroundPublic health research and environmental health research, specifically, have focused on toxic exposure-encompassing individuals or communities that are disproportionately exposed to contaminants that are harmful or potentially harmful to them. Yet, little research has applied critical environmental justice theory-characterized by the idea that marginalized communities need to be treated as indispensable rather than disposable-to the study of toxic exposure. To fill this gap, the current paper offers a case study approach applying critical environmental justice theory to the study of disproportionate and unequal exposure to toxic contaminants.MethodsThis case study is of Kettleman City, a rural, unincorporated community in the heart of California's Central Valley (USA). This community experiences the co-location of environmental hazards, including residing at the intersection of two major highways and hosting a class I hazardous-waste landfill, which is one of the few licensed to accept PCBs. PCBs are a contaminant that has been linked with several adverse health outcomes, including cancers and low birthweight. Residents may also experience poor air quality from proximity to the highways.ResultsThis case highlights the uneven distribution of pollution and environmental degradation that may be shouldered by the community, along with their experiences of adverse health and social impacts. This analysis reveals the importance of incorporating a critical environmental justice perspective to unpack experiences of not only disproportionate exposure but also disproportionate procedural and recognitional inequality.ConclusionsThis research highlights the untapped potential of environmental justice to catalyze exposure science in challenging the unequal distribution of contaminants.

BackgroundA growing body of literature investigated childhood exposure to environmental chemicals in association with attention-deficit/hyperactivity disorder (ADHD) symptoms, but limited studies considered urinary mixtures of multiple chemical classes. This study examined associations of concurrent exposure to non-persistent chemicals with ADHD symptoms in children diagnosed with autism spectrum disorder (ASD), developmental delay (DD), and typical development (TD).MethodsA total of 549 children aged 2-5 years from the Childhood Autism Risks from Genetics and Environment (CHARGE) case-control study were administered the Aberrant Behavior Checklist (ABC). This study focused on the ADHD/noncompliance subscale and its two subdomains (hyperactivity/impulsivity, inattention). Sixty-two chemicals from four classes (phenols/parabens, phthalates, organophosphate pesticides, trace elements) were quantified in child urine samples, and 43 chemicals detected in > 70% samples were used to investigate their associations with ADHD symptoms. Negative binomial regression was used for single-chemical analysis, and weighted quantile sum regression with repeated holdout validation was applied for mixture analysis for each chemical class and all chemicals. The mixture analyses were further stratified by diagnostic group.ResultsA phthalate metabolite mixture was associated with higher ADHD/noncompliance scores (median count ratio [CR] = 1.10; 2.5th, 97.5th percentile: 1.00, 1.21), especially hyperactivity/impulsivity (median CR = 1.09; 2.5th, 97.5th percentile: 1.00, 1.25). The possible contributors to these mixture effects were di-2-ethylhexyl phthalate (DEHP) metabolites and mono-2-heptyl phthalate (MHPP). These associations were likely driven by children with ASD as these were observed among children with ASD, but not among TD or those with DD. Additionally, among children with ASD, a mixture of all chemicals was associated with ADHD/noncompliance and hyperactivity/impulsivity, and possible contributors were 3,4-dihydroxy benzoic acid, DEHP metabolites, MHPP, mono-n-butyl phthalate, and cadmium.ConclusionsEarly childhood exposure to a phthalate mixture was associated with ADHD symptoms, particularly among children with ASD. While the diverse diagnostic profiles limited generalizability, our findings suggest a potential link between phthalate exposure and the comorbidity of ASD and ADHD.

Prenatal exposures to chemical and psychosocial stressors can impact the developing brain, but few studies have examined their joint effects. We examined associations between prenatal phthalate exposures and child behavior, hypothesizing that prenatal stressful life events (PSLEs) may exacerbate risks. To do so, we harmonized data from three U.S. pregnancy cohorts comprising the ECHO-PATHWAYS consortium. Phthalate metabolites were measured in single mid-pregnancy urine samples. When children were ages 4-6 years, mothers completed the Child Behavior Checklist (CBCL), from which a Total Problems score was calculated. Mothers additionally provided recall on their exposure to 14 PSLEs during pregnancy. Primary models examined problem behaviors in relation to: (1) phthalate mixtures calculated through weighted quantile sums regression with permutation test-derived p-values; and (2) joint exposure to phthalate mixtures and PSLEs (counts) using interaction terms. We subsequently refitted models stratified by child sex. Secondarily, we fit linear and logistic regression models examining individual phthalate metabolites. In our main, fully adjusted models (n = 1536 mother-child dyads), we observed some evidence of weak main effects of phthalate mixtures on problem behaviors in the full cohort and stratified by child sex. Interaction models revealed unexpected relationships whereby greater gestational exposure to PSLEs predicted reduced associations between some phthalates (e.g., the metabolites of di-2-ethylhexyl phthalate, di-n-octyl phthalate, di-iso-nonyl phthalate) and problem behaviors, particularly in males. Few associations were observed in females. Additional research is needed to replicate results and examine potential mechanisms.

BACKGROUND: Consuming ultra-processed foods may increase exposure to phthalates, a group of endocrine disruptors prevalent in food contact materials. OBJECTIVES: Investigate associations between ultra-processed food intake and urinary phthalates during pregnancy, and evaluate whether ultra-processed foods mediate socioeconomic disparities in phthalate exposures. METHODS: In a socioeconomically diverse sample of 1031 pregnant women from the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) Study in the urban South, the Block Food Frequency Questionnaire was administered and urinary phthalate metabolites were measured in the second trimester. Linear regressions modeled associations between phthalates and overall ultra-processed food consumption, individual ultra-processed foods, and exploratory factor analysis dietary patterns. Causal mediation analyses examined whether ultra-processed food intake mediates relationships between socioeconomic disparities and phthalate exposures. RESULTS: Ultra-processed foods constituted 9.8-59.0 % (mean = 38.6 %) of participants diets. 10 % higher dietary proportion of ultra-processed foods was associated with 13.1 % (95 %CI: 3.4 %-22.9 %) higher molar sum concentrations of di(2-ethylhexyl) phthalate metabolites (ΣDEHP). 10 % higher consumption of minimally-processed foods was associated with lower ΣDEHP (10.8 %: 3.4 %-22.9 %). Ultra- and minimally-processed food consumption were not associated with non-DEHP metabolites. Standard deviation higher consumptions of hamburger/cheeseburger, French fries, soda, and cake were associated with 10.5 % (4.2 %-17.1 %), 9.2 % (2.6 %-16.2 %), 7.4 % (1.4 %-13.6 %), and 6.0 % (0.0 %-12.4 %), respectively, higher ΣDEHP. Exploratory factor analysis corroborated positive associations of processed food with ΣDEHP, and uncovered a healthy dietary pattern associated with lower urinary ΣDEHP, mono(2-ethyl-5-hydroxyhexyl) (MEHHP), mono(2-ethyl-5-carboxypentyl) (MECPP), mono(2-carboxymethylhexyl) (MCMHP), and mono-isononyl (MINP) phthalates. Significant indirect effects indicated that lower income and education levels were associated with 1.9 % (0.2 %-4.2 %) and 1.4 % (0.1 %-3.3 %) higher ΣDEHP, respectively, mediated via increased ultra-processed food consumption. CONCLUSIONS: Consumption of ultra-processed foods may increase exposure to phthalates. Policies to reduce dietary phthalate exposures from food packaging and processing are needed, as socioeconomic barriers can preclude dietary recommendations as a sole means to reduce phthalate exposures.

Introduction Military exposures may present a cumulative load and increased individual susceptibility to negative health outcomes. Currently, there are no comprehensive and validated environmental exposure assessment tools covering the full spectrum of occupational and environmental exposures for Veterans. The Veterans Affairs (VA) War Related Illness and Injury Study Center in Washington, DC, developed the Veteran Military Occupational and Environmental Exposure Assessment Tool (VMOAT) to establish a structured, comprehensive self-report tool that captures military and non-military occupational and environmental exposures. The VMOAT is clinically insightful, modular, and flexible for adding novel exposures, meeting the needs of modern evolving threats and exposures in both clinical and research settings. This manuscript reviews the ongoing development and validation plans for the VMOAT. Materials and Methods The VMOAT is a self-reported structured questionnaire, and VMOAT 1.0 was developed to cover an individual's 3 life phases (pre, during, post-military service); 5 exposure domains (chemical, physical, biological, injuries including ergonomic, and psychological stress exposures, plus military preventive health measures); and 64 specific exposures nested within exposure categories. VMOAT 1.0 addresses exposure dose (frequency, duration, proximity, route), and can be administered online via VA approved Qualtrics survey software. VMOAT 1.0 to 2.0 updates began in December 2022 with changes focused on readability, streamlining the exposure history, refining the exposure metrics, and improving the skip logic embedded within the survey design. Results The initial VMOAT 1.0 development included face and construct validation with expert internal and external academic and military collaborators, undergoing an iterative 5-cycle review as well as sample testing among a small group of Veterans. The VMOAT 1.0 was used in Institutional Review Board (IRB)-approved longitudinal study, which has been examined preliminarily to compare the VMOAT 1.0 with other exposure assessments and to compare responses of Explosive Ordnance Disposal Veterans, a high occupational exposure cohort, to non-Explosive Ordnance Disposal Veterans. Ongoing VMOAT 2.0 updates will include integration of experiences from piloting the VMOAT 1.0 as well as additional face and content validation and survey cognitive testing with Veterans. VMOAT 2.0 data will improve the development of exposure-informed models using composite survey data to create scored- and scale-based exposure metrics for specific exposures and exposure domains. These data will highlight the effectiveness of the VMOAT as a structured comprehensive occupational and environmental exposure assessment instrument. Conclusions VMOAT development supports the 2022 Promise to Address Comprehensive Toxics Act and fits into the existing VA exposure assessment approach as a standardized, comprehensive self-reported exposure assessment tool. It can be utilized as a stand-alone instrument or supplemented by clinician interviews in research or specialty evaluation programs. The collected VMOAT self-report information on military occupational and environmental exposures will allow direct evaluation with objective measures of exposure and health outcomes. These data outcomes have a high potential to guide the DoD and VA environmental exposure risk mitigation and risk communication efforts. [ABSTRACT FROM AUTHOR]

Existing evidence suggested that the risk of tuberculosis (TB) infection was associated to the variations in temperature and PM2.5. A total of 9,111 cases of TB were reported in Ningxia Hui Autonomous Region, China from 2013 to 2015 on a daily basis, and 57.2% of them were male. The TB risk was more prominent for a lower temperature in males (RR of 1.724, 95% CI: 1.241, 2.394), the aged over 64 years (RR of 2.241, 95% CI: 1.554, 3.231), and the high mobility occupation subpopulation (RR of 2.758, 95% CI: 1.745, 4.359). High concentration of PM2.5 showed a short-term effect and was only associated with an increased risk in the early stages of exposure for the female, and aged 36–64 years group. There were 15.06% (1370 cases) of cases of TB may be attributable to the temperature, and 2.94% (268 cases) may be attributable to the increase of PM2.5 exposures. Low temperatures may be associated with significantly increase in the risk of TB, and high PM2.5 concentrations have a short-term association on increasing the risk of TB. Strengthening the monitoring and regular prevention and control of high risk groups will provide scientific guidance to reduce the incidence of TB. [ABSTRACT FROM AUTHOR]

The association of air pollution and greenspace with respiratory pathogen acquisition and respiratory health was investigated in a community-based birth-cohort of 158 Australian children. Weekly nasal swabs and daily symptom-diaries were collected for 2-years, with annual reviews from ages 3-7-years. Annual exposure to fine-particulate-matter (PM2.5), nitrogen-dioxide (NO2), and normalised-difference-vegetation-index (NDVI) was estimated for pregnancy and the first 2-years-of-life. We examined rhinovirus, any respiratory virus, Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae detections in the first 3-months-of-life, age at initial pathogen detection, wheezing in the first 2-years, and asthma at ages 5-7-years. Our findings suggest that higher NDVI was associated with fewer viral and M. catarrhalis detections in the first 3-months, while increased PM2.5 and NO2 were linked to earlier symptomatic rhinovirus and H. influenzae detections, respectively. However, no associations were observed with wheezing or asthma. Early-life exposure to air pollution and greenspace may influence early-life respiratory pathogen acquisition and illness. [ABSTRACT FROM AUTHOR]

This study explores the association between phthalates and total vitamin D levels and the link between phthalates exposure and subclinical inflammation using monocyte percentage to high-density lipoprotein cholesterol ratio (MHR), utilizing three National Health and Nutrition Examination Survey (NHANES) survey cycles 2013-2018. This study is cross-sectional, utilizing one-time urine samples from randomly selected NHANES participants to assess phthalate metabolites. An inverse association between vitamin D and all Di(2-ethylhexyl) phthalate (DEHP) metabolites was found. The molar sum of DEHP metabolites was inversely associated with vitamin D (β −2.329; 95% CI −3.937,−0.720). An inverse association was observed between monocarboxynonyl phthalate and vitamin D (β −0.0278; 95% CI −0.0527,−0.00298). A similar relationship was found between monocarboxyoctyl phthalate and vitamin D (β −0.0160; 95% CI −0.0242,−0.00775). There was no association between phthalate metabolites and MHR. Stratified analysis showed that the association between phthalate metabolites and MHR may vary according to vitamin D status. [ABSTRACT FROM AUTHOR]

This study examined the heavy metal content in dust storm samples from Erbil, Iraq, along with four other locations. Using ICP-MS, Cd, Ni, Cr, Hg, Pb, Zn, Mn, Cu, Co, Fe and As were determined. The health risks due to exposure to these metals through ingestion, inhalation and dermal contact were assessed for both adults and children. Non-carcinogenic risks were evaluated using the hazard quotient (HQ) and hazard index (HI). Children faced a cumulative risk with HQ > 0.2 for As and Cr and HI > 1. The carcinogenic risk was measured using the carcinogenic risk factor (CRF), which fell below 10–6, indicating low cancer risk. However, children had a higher cancer risk (10−4 to 10−6) for As. The pollution indices revealed varying pollution levels from unpolluted to moderately polluted in the studied areas. Overall, this study highlights potential health risks associated with heavy metal exposure during dust storms, particularly for children, and emphasises the importance of addressing these concerns to safeguard public health. [ABSTRACT FROM AUTHOR]

Since the completion of the Human Genome Project (HGP), biomedical sciences have moved away from a gene-centred view and towards a multi-factorial one in which environment, broadly speaking, plays a central role in the determination of human health and disease. Environmental exposures have been shown to be highly prevalent in disease causation. They are considered as complementary to genetic factors in the etiology of diseases, hence the introduction of the concept of the "exposome" as encompassing the totality of human environmental exposures, from conception onwards (Wild in Cancer Epidemiol Biomark Prev 14:1847–1850, 2005), and the launch of the Human Exposome Project (HEP) which aims to complement the HGP. At first sight, and seen as complementary to the genome, the exposome could thus appear as contributing to the rise of novel postgenomic deterministic narratives which place the environment at their core. Is this really the case? If so, what sort of determinism is at work in exposomics research? Is it a case of environmental determinism, and if so, in what sense? Or is it a new sort of deterministic view? In this paper, we first show that causal narratives in exposomics are still very similar to gene-centred deterministic narratives. They correspond to a form of Laplacian determinism and, above all, to what Claude Bernard called the "determinism of a phenomenon". Second, we introduce the notion of "reversed heuristic determinism" to characterize the specific deterministic narratives present in exposomics. Indeed, the accepted sorts of external environmental exposures conceived as being at the origins of diseases are determined, methodologically speaking, by their identifiable internal and biological markers. We conclude by highlighting the most relevant implications of the presence of this heuristic determinism in exposomics research. [ABSTRACT FROM AUTHOR]

Chemical modifications of proteins induced by ambient ozone (O 3) and nitrogen oxides (NO x) are of public health concerns due to their potential to trigger respiratory diseases. The laboratory and environmental exposure systems have been widely used to investigate their relevant mechanism in the atmosphere. Using bovine serum albumin (BSA) as a model protein, we evaluated the two systems and aimed to reduce the uncertainties of both the reactants and products in the corresponding kinetic study. In the laboratory simulation system, the generated gaseous pollutants showed negligible losses. Ten layers of BSA were coated on the flow tube with protein extraction recovery of 87.4%. For environmental exposure experiment, quartz fiber filter was selected as the upper filter with low gaseous O 3 (8.0%) and NO 2 (1.7%) losses, and cellulose acetate filter was appropriate for the lower filter with protein extraction efficiency of 95.2%. The protein degradation process was observed without the exposure to atmospheric oxidants and contributed to the loss of protein monomer mass fractions, while environmental factors (e.g., molecular oxygen and ultraviolet) may cause greater protein monomer losses. Based on the evaluation, the study exemplarily applied the two systems to protein modification and both showed that O 3 promotes the protein oligomerization and nitration, while increased temperature can accelerate the oligomerization and increased relative humidity can inhibit the nitration in the environmental exposure samples. The developed laboratory and environmental systems are suitable for studying protein modifications formed under different atmospheric conditions. A combination of the two will further reveal the actual mechanism of protein modifications. [Display omitted] [ABSTRACT FROM AUTHOR]