Abstract Background: Ambient fine and ultrafine particles are linked to the progression of atherosclerotic cardiovascular diseases, wherein gut microbiome may play a critical role. However, the underlying mechanisms and relevant metabolic pathways are not yet fully understood. Objectives: To identify the features and metabolic pathways of gut microbiome, and to explore their potential roles in the pro-inflammatory and pro-atherosclerotic effects of particles in size ranges of 5–560 nm (measured as number concentration, PNC5–560). Methods: We conducted a longitudinal panel study of 152 young adults in Beijing, China, with four monthly clinical examinations between September 2019 and January 2020. Gut microbiome, fecal metabolome, and circulating pro-inflammatory and pro-atherosclerotic biomarkers were measured. Linear mixed-effects models were used to examine the associations linking short-term PNC5–560 exposure to health indicators. We further evaluated whether gut microbiota could mediate changes in these biomarkers and identified the underlying metabolic pathways. Results: Major sources of PNC5–560 in the study area were identified as diesel vehicle emissions (37.9%), gasoline vehicle emissions (39.4%), nucleation (9.2%), and secondary aerosols (11.9%). Per interquartile range increment in PNC5–560 over the preceding 7 days was associated with significant elevations in circulating pro-inflammatory and pro-atherosclerotic biomarkers, with effect estimates ranging from 2.1% (95% CI: 0.4%, 3.8%) to 198.6% (95% CI: 29.3%, 365.8%). PNC5–560 exposure was also associated with decreased gut microbial α-diversity (e.g., Shannon, Simpson, and Chao1) and altered taxonomic composition. Several microbial species (e.g., Solibaculum mannosilyticum, Bacteroides stercoris, and Bifidobacterium longum) were identified as potential mediators of the effects of PNC5–560 on pro-inflammatory and pro-atherosclerotic responses, with mediation proportions up to 9.8% (95% CI: 0.8, 38.3) and 4.8% (95% CI: 0.09, 22.5), respectively. Functional analyses further revealed that these mediating effects involved perturbations in nucleotide and amino acid metabolism pathways. Conclusions: This study provides evidence suggesting that gut microbiome may regulate nucleotide and amino acid metabolism, thereby partially mediating the detrimental cardiovascular effects of size-fractioned ambient particles.
Abstract Floods are increasingly frequent under climate change and may influence zoonotic disease transmission through environmental and ecological pathways. However, the spatiotemporal heterogeneity and potential causal relationship between floods and disease risk remain insufficiently characterized. We combined nationwide surveillance data on hemorrhagic fever with renal syndrome (HFRS) with multisource flood records in China from 2005 to 2022 to evaluate the association between flood exposure and HFRS risk. A Bayesian spatiotemporal hierarchical model was used to estimate lagged associations, identify high-risk clusters, and assess effect modification by environmental and socioeconomic factors. To strengthen causal inference, we further applied a stacked difference-in-differences design with propensity score matching. Flood exposure was associated with a biphasic lagged response in HFRS risk, characterized by a short-term decrease during the flood month and the subsequent month, followed by a delayed increase peaking at 4–6 months (maximum at 5 months: RR = 1.05, 95% CrI 1.02–1.08). Spatially, elevated risks were concentrated in flood-prone areas, particularly in northeast China. The delayed increase in risk was more pronounced in midtemperate regions, Apodemus-type endemic areas, and agricultural zones. Effect modification analyses indicated higher flood-associated risks in areas with lower socioeconomic status, including lower GDP, limited healthcare resources, and lower agricultural mechanization. The quasi-experimental analysis supported a causal association between flood exposure and increased HFRS risk, with the largest effect observed at approximately 3 months post-flood. These findings are consistent with environmentally mediated changes in host ecology and human exposure that may influence disease transmission following flood events. Our results provide evidence that flood exposure can increase zoonotic disease risk with a delayed and spatially heterogeneous pattern. Accounting for these lagged and context-specific effects may improve risk assessment and inform targeted public health interventions following extreme hydrological events.
Abstract Large-scale residential energy transitions from solid fuel to clean energy are promising strategies to mitigate climate change and improve population health, but rigorous evaluation of their impacts is rare. China’s Clean Heating Policy (CHP) aimed to transition tens of millions of households from coal to electric and gas-based space heating. Following evidence of policy-driven improvements in indoor air pollution and indoor temperature, we evaluated the CHP’s impact on blood pressure (BP). In winter 2018–2019, we enrolled 1,003 adults aged >40 years from 50 Beijing villages not yet treated by the CHP; 20 villages were treated during follow-up (winters 2019–2020 and 2021–2022). Brachial and central BP and covariates were measured during household visits by trained staff. Policy impacts were estimated using an extended two-way fixed-effects difference-in-differences approach with village-clustered standard errors and adjustment for key BP predictors to improve precision. We found evidence of reductions (in mmHg) in brachial systolic BP (−1.4, 95% confidence interval [CI]: −3.3, 0.5), central systolic BP (−1.5, 95% CI: −3.3, 0.4), brachial diastolic BP (−1.6, 95% CI: −2.9, −0.3), and central diastolic BP (−1.6, 95% CI: −2.9, −0.3) among villages treated by the CHP compared with those untreated. Treatment effects varied by the year villages were treated by the CHP (p for homogeneity = 0.00 to 0.14) with greater BP reductions among participants in earlier-treated villages. Household energy policies like the CHP may serve as effective population-level interventions to reduce BP in China and complement high-risk cardiovascular prevention strategies.
Abstract Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) is associated with small-for-gestational age (SGA), an adverse pregnancy outcome indicative of intrauterine growth restriction (IUGR). Evidence from previous environmental epidemiologic work suggests that lipids contribute to this association through oxidative stress and inflammation. Therefore, we conducted an exploratory study by analyzing the maternal lipidome with the meet-in-the-middle approach to identify potential intermediates. In the Atlanta African American Maternal–Child Cohort, pregnant participants provided serum samples between 6 and 17 weeks gestation, which underwent targeted PFAS analysis (N: total = 513, SGA = 61) and untargeted lipidomics analysis (N: total = 330, SGA = 36). A lipidome-wide association study (LWAS) was conducted for PFNA, PFOA, PFOS, and PFHxS with multivariable regression and their mixture with quantile g-computation. A separate LWAS was performed for SGA with multivariable regression. Lipid pathway analysis was performed in LIPEA (Lipid Pathway Enrichment Analysis). Lipidomic signatures that overlapped between any PFAS LWAS and the SGA LWAS were considered intermediates. A simultaneous, 1-quartile increase in serum concentrations of PFNA, PFOA, PFOS, and PFHxS at early pregnancy was associated with a 43% increase in delivery of an SGA newborn (Odds Ratio = 1.43; 95% Confidence Interval = 1.02, 2.00). The overall mixture effect was driven by PFNA (weight = 0.42). There were 321 features associated with the PFAS mixture and 25 features associated with SGA in the maternal lipidome (all p < 0.05, but none remained significant after false discovery rate correction). After confirmation and annotation, three intermediate metabolites were identified, including phosphatidylinositol 18:1–20:4, phosphatidylcholine 32:0, and monoacylglycerol 18:0. The pathways for glycerophospholipid metabolism, retrograde endocannabinoid signaling, insulin resistance, and long-term depression were also enriched in the LWAS for PFNA, PFOA, PFOS, PFHxS, the PFAS mixture, and SGA. Global analysis of the maternal lipidome during early pregnancy revealed diverse bioactive lipid involvement in the PFAS-SGA association. Additional research is warranted to understand if antioxidants and anti-inflammatory nutrients would attenuate exposure effects on adverse maternal–child health outcomes.
Abstract To elucidate the sex-specific associations of per- and polyfluoroalkyl substances (PFASs) on type 2 diabetes (T2D) risk and to explore whether genetic susceptibility and baseline lipid profiles may help explain these associations. A nested case-control study including 985 matched case-control pairs from the Dongfeng-Tongji Cohort was conducted. Serum PFAS concentrations, T2D-related pathway polygenic risk scores (PRSs), blood lipid profiles, and plasma lipidomes were integrated. Conditional logistic regression, weighted quantile sum (WQS) regression, mediation analysis, and gene-environment interaction analysis were used to explore the associations and mechanisms. Sex-specific associations were observed between PFAS exposure and incident T2D, with PFOA and PFNA being associated with higher T2D risk in females. Liver-lipid pathway PRS strengthened these sex-specific associations. PFAS exposure was associated with triglyceride-related lipid profiles in females. Exploratory analyses suggested that the lipid score statistically accounted for part of the selected PFAS-T2D associations. CYP19A1-rs2414098 modified the association in females, with 50% mediation by the lipid score in the CC genotype (higher estrone). Baseline lipid profiles may partly account for the observed sex-specific associations between PFAS exposure and incident T2D. The observed effect modification by CYP19A1 rs2414098 suggests that hormonal pathways may contribute to the sex-specific associations, although this hypothesis requires confirmation in studies with direct hormone measurements and experimental validation.
BACKGROUND: The vertebrate nervous system is vulnerable to chemical toxicity, and the widespread release of chemicals into the environment outstrips the capacity to assess their safety. The zebrafish (Danio rerio) is a powerful vertebrate model that can bridge the gap between in vitro- and mammalian-based in vivo studies. However, the behavior-rich repertoire of larval zebrafish, a 3R-compliant model amenable to higher throughput chemical screens, has yet to be fully deployed to identify and characterize chemical compounds that cause neurotoxicity. OBJECTIVE: We sought to establish a multibehavioral phenotyping approach in larval zebrafish to identify and mechanistically elucidate neuroactive chemicals, with particular focus on chemical compounds that affect nonassociative habituation learning. METHODS: We devised a battery of automated behavioral assays in larval zebrafish. The battery captures stereotypical visual and acoustic behaviors including habituation, a form of nonassociative learning. To elucidate mechanisms underlying exposure-induced behavioral alterations in zebrafish, in silico target predictions, pharmacological interventions, patch-clamp recordings in cultured mouse cortical neurons, and human multineurotransmitter (hMNR) assay in 3D BrainSpheres were used. RESULTS: Known pharmacological modulators of habituation in zebrafish evoked distinct behavioral patterns. By screening chemicals positive for ex vivo N-methyl-d-aspartate receptor (NMDAR) modulation, we identified chlorophene, a biocide that caused sedation, paradoxical excitation, and reduced habituation in zebrafish. Using in silico target predictions and pharmacological interventions, we discovered that chlorophene acts via gamma-aminobutyric acid A receptors (GABAARs), a previously unknown target site. Orthogonal validation in cultured mouse cortical neurons and human stem cell-derived BrainSpheres confirmed chlorophene's interaction with GABAARs. Chlorophene's behavioral profile resembled that of flupirtine, a Kv7 potassium channel (M-current) activator, suggesting that habituation deficits stem from M-current rather than GABAAR modulation. CONCLUSIONS: These studies combined a series of behavior assays in a phenotypically rich, rapid, and inexpensive nonmammalian vertebrate test system to screen chemicals for neurotoxicity. Together with in silico target predictions and mouse- and human-based models, our findings establish multibehavioral phenotyping in zebrafish as a powerful toolkit for neurotoxicity testing and mechanism identification, with relevance for humans.
BACKGROUND:Fat-soluble toxicants, such as chlorpyrifos (CPF) can accumulate in adipose tissue and the liver. During weight loss, these compounds may be released into the circulation, but the metabolic consequences of this mobilization remain poorly understood. OBJECTIVES:This study aimed to investigate the mobilization of CPF during weight loss and its effects on liver health and adipose tissue metabolism in mice. METHODS:C57BL/6J mice were fed a high-fat diet (HFD) or a low-fat diet (LFD) and exposed to 2 mg/kg BW/day CPF by oral gavage. Weight loss was induced by β3-adrenergic stimulation (CL316243) or treadmill exercise for 4 or 10 weeks. CPF was quantified in serum and tissues using HPLC. Tissue histology, expression of genes related to CPF metabolism, liver injury markers, and metabolic protein levels were assessed. RESULTS:CPF-exposed LFD mice showed more severe liver fibrosis and adipose inflammation than did their HFD counterparts. While obese mice had lower adipose CPF concentrations, they showed higher hepatic accumulation. CPF-exposed weight loss mice had higher levels of CPF in adipose tissue, liver, and brain and higher expression of CPF metabolism-related genes, including Paraoxinase-1 and cytochrome P450 genes, and greater glucose intolerance compared to their counterparts without CPF administration. Molecular analyses revealed suppressed AMPK signaling and P62 accumulation, indicating mitophagy disruption in CPF-exposed mice after weight loss. These effects occurred even at human-relevant low doses (0.45 mg/kg of BW/day) and persisted across sexes. DISCUSSION:Weight loss mobilizes CPF and its metabolites from fat stores, leading to tissue accumulation and damage. Even low-dose exposure contributes to hepatic and metabolic disruption in mice, highlighting the potential risk of toxicant mobilization during fat reduction.
BACKGROUND: Growing evidence links air pollution to cognitive dysfunction in older adults. The gut microbiome and circulating metabolites present an important yet unexplored pathway given their crucial role in the gut-brain axis. OBJECTIVES: We aimed to explore the potential roles of gut bacteria, fungi, microbial functional potentials, and circulating metabolites in the association of residential PM2.5 and O3 exposure with cognitive dysfunction. METHODS: We analyzed gut microbiome data from 1,027 older adults using metagenome and internal transcribed spacer sequencing to profile bacterial and fungal taxa, functional pathways, and enzyme abundances. Targeted metabolomics quantified 195 circulating metabolites, such as amino acids and organic acids. Annual average ambient PM2.5 and O3 exposures were estimated by using satellite-based models. Cognitive outcomes, including mild cognitive impairment and cognitive decline, were assessed using the Mini-Mental State Examination and Hasegawa Dementia Scale. Statistical analyses included Microbiome Multivariable Association with Linear Models (with a false discovery rate threshold of 0.25) for microbial associations and multivariate regression for metabolites and cognitive outcomes. RESULTS: Higher PM2.5 and O3 exposures were associated with disturbances in microbial composition, altered taxonomic profiles (e.g., decreased abundances of Blautia obeum and Gordonibacter pamelaeae), and disrupted functional pathways, particularly those regulating 2-oxoglutarate. These findings were partially replicated in an independent population. Higher air pollution levels were associated with increased circulating levels of 2-oxoglutarate and l-glutamine (key metabolites in neurodegenerative progression), which were further linked to higher odds of concurrent mild cognitive impairment (OR: 1.39-1.56) and an increased 2-year risk of cognitive decline (OR: 1.26-1.37). These associations were partially mediated by air pollution-related changes in microbial anaerobic energy metabolism pathways, especially involving 2-oxoglutarate metabolism and the enzyme aspartate transaminase. CONCLUSIONS: Our findings highlight the role of the gut microbiome and microbial metabolites in mediating the detrimental impact of air pollution on cognitive health in older adults, providing new insights into the underlying etiology for future hypothesis generation.
BACKGROUND: Diarrheal diseases remain a leading cause of mortality and morbidity among under-five children in South Asia. In rural Bangladesh, deep tubewells that tap into low-arsenic deep aquifers have been installed to provide microbially safe and arsenic-free drinking water at the source. However, unlike more widely used shallow tubewells, deep tubewells are sparsely distributed, and households often travel farther for drinking-water consumption from such wells. Hence, benefits from deep tubewells may be abated by higher levels of microbial contamination during water handling and storage that could increase the risk of diarrheal diseases. OBJECTIVES: We examined the association between deep tubewell use and diarrheal disease risk in under-five children and investigated the role of social and environmental factors on modifying the association. METHODS: We implemented community diarrheal disease surveillance across households with under-five children using deep and shallow tubewells in Matlab, Bangladesh from March 2018 to October 2019. We used Generalized Estimating Equations (GEE) to estimate the association between deep tubewell versus shallow tubewell use and diarrheal disease prevalence. RESULTS: Children in households using deep tubewells had diarrheal disease prevalence 0.83 times that of children in households using shallow tubewells (95% confidence interval (CI): 0.71-0.96). Protective effects of deep tubewell use on diarrhea risk were observed among children in households that drank from wells within their household compound (risk ratio (RR) = 0.70, 95% CI: 0.54 - 0.91), were in flood-prone areas (RR = 0.83, 95% CI: 0.75 - 0.92), and used unimproved latrines (RR = 0.62, 95% CI: 0.43-0.89). Deep tubewell use was more protective against diarrhea than shallow tubewell use during the dry season (RR = 0.71, 95% CI: 0.52-0.97). CONCLUSIONS: Despite concerns, using deep tubewells may not translate to higher diarrhea risk among under-five children and may reduce diarrhea further, especially in social and environmental contexts associated with higher groundwater microbial contamination.
BACKGROUND:Exposomics is a conceptual framework positioned at the intersection of environmental health sciences and precision medicine. It seeks to comprehensively understand how environmental exposures and the body's response to these exposures impact human health across the life course. Introduced in 2005, the exposome concept represents a paradigm shift from single-pollutant studies to an integrated approach considering a broad range of exposures. OBJECTIVES:This commentary explores the ongoing efforts to operationalize the exposome, with a focus on NIH initiatives aimed at building capacity in exposomics research and integrating lifecourse exposure data into health research. METHODS:This commentary draws on a structured review of current NIH funding opportunities, initiatives, and strategic documents related to exposomics. Key NIH-supported projects and collaborations were identified through analysis of publicly available agency reports, grant announcements, and program descriptions. Additional insights were gathered from relevant literature and international research activities to contextualize the NIH's role in promoting exposomics and integrating life-course exposure data into health research. DISCUSSION:Operationalizing the exposome is essential for advancing the field of environmental health and precision medicine. NIH-supported initiatives, alongside international collaborations, aim to standardize methodologies, develop tools, and promote interdisciplinary research. Addressing the complexities of exposomics requires integrating diverse datasets and fostering global coordination, paving the way for innovative strategies to improve human health outcomes. https://doi.org/10.1289/EHP15561.
BACKGROUND:Antimicrobial use in food-animal production selects for antimicrobial-resistant Escherichia coli (E. coli) that can be transmitted to humans via contaminated meat products. California Senate Bill 27 (SB27), which took effect on January 1, 2018, restricts the use of medically important antimicrobials in California food-animal production. Over time, SB27 could reduce the prevalence of antimicrobial-resistant E. coli on meat produced in California. OBJECTIVES:We aimed to assess whether the implementation of SB27 was associated with significant decreases in resistance to medically important antimicrobials among E. coli strains contaminating raw chicken produced in California. METHODS:We purchased raw chicken products in Southern California, including those produced in and outside of California, from 2017 to 2021 and cultured them for E. coli. Susceptibility to 19 antimicrobials was determined using the disk diffusion method. Changes in antimicrobial susceptibility over the course of the study were evaluated using the Mann-Kendall test. RESULTS:We observed significant decreases in resistance to multiple classes of antimicrobials in E. coli isolated from retail chicken meat from 2017 to 2021. Resistance to penicillins had a relative decrease of 14-18% annually in E. coli from chicken raised in California but not from chicken raised outside California, potentially indicating that SB27 was effective. Resistance to multiple other classes of antimicrobials saw an absolute decrease of up to 8% in chicken produced both inside and outside California. DISCUSSION:Our findings suggest that the downward trends in antimicrobial resistance among E. coli populations from California-produced chicken products reflect national trends. It is possible that the California SB27 legislation helped motivate industry-wide decreases in antimicrobial use among broiler chicken producers. Alternatively, the changes observed in California may have been driven by industry-wide trends independent of SB27. The lack of publicly available data regarding actual antimicrobial use in California and non-California broiler chicken production limits our ability to make stronger conclusions about our observations. https://doi.org/10.1289/EHP16115.
BACKGROUND:Environmental epidemiology studies increasingly integrate "big" geospatial and health data sets to examine associations between environmental factors and health outcomes. Using such data sets ─ and linking between them ─ presents a number of complexities with regard to study design and analytic approaches. These complexities are often magnified with the integration of additional contextual data representing other neighborhood characteristics including socioeconomic factors. Guidance regarding the design of environmental health studies that leverage "big" geospatial and health outcome data is limited and fragmented. OBJECTIVE:Drawing on methodological literature and case studies, this commentary outlines common challenges related to geospatial and health data linkages, posing a series of guiding questions and considerations for investigators conducting environmental health studies, particularly analyses with an etiological focus. DISCUSSION:Recommendations include: 1) using a target trial approach to guide causal analysis, 2) aligning measures with hypothesized causal mechanisms, 3) exploring opportunities to "groundtruth" and validate data, and 4) prioritizing interdisciplinary science. The goal of the commentary is to consolidate insights from multiple disciplines ─ including exposure science, epidemiology, and sociology ─ to provide a foundation for etiologic research focused on advancing environmental health for all populations.
BACKGROUND: Organophosphate ester flame retardants and plasticizers (OPEs) have myriad uses in industry and consumer products. Increasing human exposure to OPEs has raised concerns about their potential effects on child neurodevelopment during the pregnancy. Objective: We investigated whether OPE urinary concentrations during pregnancy were associated with child's autism-related outcomes. METHODS: We included 4159 mother-child pairs from 15 cohorts in the NIH Environmental influences on Child Health Outcomes (ECHO) Consortium, with children born from 2006-2020 (median age [interquartile range]: 6 [4,10] years). Nine OPE biomarkers were measured in urine samples collected mid- to late pregnancy. Dilution-adjusted biomarkers were modeled continuously, categorically (high [>median], moderate [≤median], nondetect), or as detect/nondetect depending on their detection frequency. We assessed child autism-related traits via a) parent report on the Social Responsiveness Scale (SRS) and b) clinical autism diagnosis. We examined associations of OPEs with child outcomes, including modification by child sex, using generalized estimating equations to account for clustering by ECHO cohort. RESULTS: Compared with nondetectable concentrations, high exposure to bis-(butoxyethyl) phosphate (BBOEP) was associated with higher autistic trait scores (adj-β 0.97, 95% confidence interval [CI]: 0.42, 1.52) and greater odds of autism diagnosis (adjusted odds ratio [adj-OR]: 1.27, 95% CI: 1.07, 1.50). Bis-(1-chloro-2-propyl) phosphate (BCPP) showed associations with autistic trait scores (BCPP adj-β for high exposure vs nondetect: 0.34, 95% CI: -0.46, 1.13; BCPP adj-β for moderate exposure vs nondetect: 0.72, 95% CI: 0.24, 1.20). High exposure to bis-(2-chloroethyl) phosphate (BCETP) was associated with lower odds of autism diagnosis (adj-OR: 0.76, 95% CI: 0.60, 0.95). Other OPEs showed no associations in adjusted models. Associations between BBOEP and higher autistic trait scores were stronger in males than females. DISCUSSION: Prenatal exposure to OPEs, specifically BCPP and BBOEP, may be associated with a higher risk of autism diagnosis and related traits in childhood.
BACKGROUND:The relationship between prenatal exposure to low-level air pollution and child autism spectrum disorder (ASD) is unclear. OBJECTIVE:To examine associations of prenatal air pollution exposure with autism. METHODS:We analyzed data from 8,035 mother-child pairs from 44 United States cohorts in the Environmental influences on Child Health Outcomes (ECHO) Cohort. Fine particulate matter (PM2.5), nitrogen dioxide (NO2), and 8-h-max ozone (O3) levels were estimated at residential addresses during pregnancy. Parents rated children's autism-related traits using the Social Responsiveness Scale (SRS) (mean age 9.4 years, SD = 3.6) and reported physician-diagnosed ASD. We examined associations of the three air pollutants with SRS scores (10th, 50th, and 90th quantiles) using quantile regression and with ASD diagnosis using logistic regression. Models were run within census divisions, and coefficients were pooled in a meta-analysis. RESULTS:Average (SD) pregnancy exposures were 9.3 μg/m3 (2.7) for PM2.5, 21.8 ppb (8.8) for NO2, and 40.3 ppb (5.5) for O3, with variations across census divisions. The median SRS T-score was 46 (IQR = 41 to 52), and 444 children (5.5%) had an ASD diagnosis. Higher PM2.5 was associated with higher SRS scores at the 10th quantile (β = 0.74, 95% CI: 0.09, 1.40) but not at the median or highest quantile. The association between PM2.5 and ASD diagnosis was highly heterogeneous, with associations present in the South Central, Mountain, and Pacific census divisions. Heterogeneity was also high in the association between NO2 and SRS at the median and only in the mid-Atlantic, West North Central, and South Atlantic census divisions. Higher O3 was associated with higher SRS scores at the median (β per IQR increment = 0.83, 95% CI: 0.05, 1.61) and highest quantile (β = 2.19, 95% CI: 0.06, 4.32) in the meta-analysis. Higher O3 also was associated with ASD. DISCUSSION:Associations with ASD outcomes were present even at low levels of air pollutants.
INTRODUCTION: Disparities in exposure to and harm associated with pesticides are established. However, high resolution spatial data on exposure to pesticides are lacking. PURPOSE: To describe the development of a pesticide metric for Washington State and to evaluate the associations between pesticide exposure and sociodemographic characteristics of census tracts. METHODS: We used the US cropland data set to quantify the location and size of agricultural land. These data were overlaid with state- and county-level estimated annual agricultural pesticide use to estimate pesticide exposure at the census tract level. Sociodemographic characteristics of census tracts were from the US Centers for Disease Control and Prevention's Social Vulnerability Index (SVI). Generalized additive models evaluated the associations between pesticide exposure and each of the SVI variables. RESULTS: The median exposure to pesticides was 1.5 lbs/sq mi. Significant associations were observed between exposure to pesticides and a higher percentage of population below poverty, populations unemployed, populations 65 and older, non-Hispanic white populations, those with limited English language proficiency, mobile homes, and group quarters. CONCLUSIONS: The results inform public health and policy efforts to identify areas and populations that are most vulnerable to pesticide exposure and improve the health and well-being of farmworkers and populations residing near agricultural areas.
BACKGROUND: While numerous studies have examined associations between prenatal air pollution exposure and fetal growth measures, investigations assessing longitudinal growth trajectories across multiple time points during mid-to-late pregnancy remain limited. OBJECTIVES: The aim of this study is to explore the effects of prenatal exposure to air pollution on fetal growth trajectories. METHODS: From a prospective birth cohort in Wuhan, China, recruited from 2013 to 2016, we included a total of 4283 eligible pregnant women. At 16, 24, 31, and 38 weeks of gestation, we collected ultrasound measurements, including biparietal diameter (BPD), abdominal circumference (AC), femur length (FL), and estimated fetal weight (EFW). Exposure to air pollution during pregnancy was estimated for the participants' residential addresses using a spatial interpolation method. Associations between air pollutants and fetal growth parameters across four exposure windows were examined by using multiple informant models. Group-based trajectory modeling (GBTM) combined with a multinomial logistic regression model was used to explore the effect of air pollution exposure on fetal growth trajectories. RESULTS: Four trajectory groups for AC, FL, and EFW, and three trajectory groups for BPD were selected based on GBTM. Compared with the reference trajectory group, exposure to higher PM2.5 during weeks 1-16 was significantly associated with lower odds of being in the "fast growth group" for AC (OR = 0.68, 95% CI: 0.55, 0.84) and EFW (OR = 0.71, 95% CI: 0.56, 0.91). Exposures to PM2.5, PM10, NO2, SO2, and CO during 1-16 weeks were negatively associated with AC, FL, and EFW at 16 weeks as well as BPD, FL, and EFW at 24 weeks. Similar negative associations were observed between air pollution exposure during 25-38 weeks and AC and EFW at 38 weeks. DISCUSSION: Our study provided evidence of negative associations between air pollution exposure during 1-16 weeks of gestation and the fast growth trajectory group. In addition, we observed distinct lagged associations between air pollution and fetal growth, with early pregnancy exposure negatively related to early and midgestational growth, and mid-to-late pregnancy exposure negatively related to growth in the late window. These results underscore the importance of identifying critical windows of susceptibility during pregnancy and support early intervention strategies to mitigate adverse fetal developmental outcomes.
BACKGROUND:Long-term exposure to arsenic (As) can cause many health effects and As metabolism is key in the detoxification and elimination of As. We hypothesize that hepatic steatosis might affect As metabolism efficiency. We evaluated the association of As exposure and As metabolism biomarkers with hepatic steatosis. METHODS:In this cross-sectional analysis, we analyzed data from 3,577 participants in the Multi-Ethnic Study of Atherosclerosis (MESA), an ethnically diverse US adult population, with urinary metals and liver CT scan data available. We measured total As and As species in urine, and summarized As methylation biomarkers as inorganic (iAs%), monomethylarsonic acid (MMA%), and dimethylarsinic acid (DMA%). The ratio of liver-to-spleen (L/S) Hounsfield units (HU) < 1.0 and liver attenuation < 40 HU were used to assess the presence and severity of liver fat content. We used logistic regression to estimate the odds ratio (OR) (95%CI) of steatosis per higher interquartile range (IQR) of log-transformed total urinary As levels (ΣAs, μg/L), and per 5% higher in log-transformed As species (iAs%, MMA%, DMA%). RESULTS:The adjusted ORs (95%CI) for L/S < 1.0 were 1.09 (0.91, 1.30) per higher IQR of ΣAs, and 0.80 (0.68, 0.95), 0.69 (0.61, 0.77), and 1.24 (1.15, 1.34) per 5% higher iAs%, MMA%, and DMA%, respectively. The corresponding ORs (95% CI) for HU < 40 were 0.99 (0.75, 1.30) per higher IQR of increase ΣAs, and 0.70 (0.50, 0.91), 0.65 (0.55, 0.78), and 1.31 (1.16, 1.48) per 5% higher iAs%, MMA%, and DMA%, respectively. The associations were consistent by self-reported race/ethnicity and sex. CONCLUSIONS:Arsenic methylation capacity, but not exposure, was associated with the prevalence of hepatic steatosis. Studies are needed to examine the longitudinal association between the progression of hepatic steatosis with As metabolism biomarkers and As-related disease. https://doi.org/10.1289/EHP16728.
