Environmental Research

Fetal development is highly sensitive to environmental influences, including maternal smoking during pregnancy (MSDP) and air pollution. The placenta may play a central role in mediating these effects through epigenetic mechanisms, including small non-coding RNAs (sncRNAs). While most studies have focused on microRNAs (miRNAs), other sncRNA classes remain poorly characterized. Here, we characterized the placental sncRNA landscape and investigated its associations with prenatal exposure to MSDP and air pollution. The sncRNA expression profile of 390 chorionic villi samples from the Barcelona Life Study Cohort (BiSC) was measured using small RNA sequencing and the seqBuster/seqCluster pipeline. MSDP was assessed via questionnaire, and prenatal exposure to black carbon (BC), particulate matter [≤]2.5 m (PM2.5), and nitrogen dioxide (NO2) was estimated using hybrid dispersion-land-use regression (LUR) spatiotemporal models. Associations were evaluated using linear regressions adjusted for relevant covariates. We identified 979 placental sncRNA clusters, assigned primarily to miRNAs (33.2%), piRNAs (26.4%), snoRNAs (12.2%), tRFs (7.8%), and others (20.4%). MSDP was associated with the downregulation of miR-421 and the upregulation of multiple snoRNAs from the imprinted DLK1-DIO3 locus (SNORD113-4, SNORD114-2, SNORD114-3, and SNORD114-17), as well as the piR-26394. No sncRNAs remained significantly associated with air pollution after multiple-testing correction, although several miRNAs showed suggestive associations. Overall, this study provides a comprehensive characterization of placental sncRNAs and identifies previously unreported smoking-associated sncRNAs within the imprinted DLK1-DIO3 locus, expanding our understanding of placental epigenetic responses to prenatal environmental exposures.

Ambient particulate matter (PM) is a well-established environmental risk factor for non-communicable diseases, yet its influence on mitochondrial function remains poorly defined. Mitochondrial DNA copy number (mtDNA-CN) serves as a biomarker of mitochondrial biogenesis, making it a candidate exposure biomarker. We conducted the study per PRISMA guidelines (PROSPERO-CRD420261320957) and examined the association between ambient PM exposure and mtDNA-CN. Risk of bias was assessed using Joanna Briggs Institute tools, and relative and absolute changes in mtDNA-CN were pooled using random-effects models, with subgroup analyses by pollutant type and descriptive synthesis of mechanistic evidence. Of 1,224 records identified, 24 studies met inclusion criteria for quantitative analysis, with 12 reporting percentage change and 12 reporting absolute values, covering 13,092 participants. PM exposure was significantly associated with decreased percentage mtDNA-CN (ES: -4.90; 95% CI: -7.97 to -1.82; p = 0.002), while absolute mtDNA-CN levels increased significantly (ES = 0.55; 95% CI: 0.05 to 1.04; p = 0.030). Mechanistic pathways contributing included mtDNA hypermethylation, impaired mitochondrial biogenesis and dynamics. Our findings show ambient PM exposure alters mtDNA-CN, though directionality differs by metric, pointing to the need for larger prospective studies to validate mtDNA-CN as a reliable biomarker of airborne PM and nanoparticulate exposure.

Background: Observational studies have linked air pollution to otitis media, but confounding and reverse causation preclude causal inference. We used two-sample Mendelian randomization (MR) to assess genetic causal effects of six air pollutants on non-suppurative otitis media, represented by otitis media with effusion (OME). Methods: Exposure GWAS for PM2.5, PM2.5 absorbance, PM2.5-10, PM10, NO2 and NOx were obtained from UK Biobank (MRC-IEU), and the outcome was FinnGen R13 H8_NONSUPPNAS (12,397 cases, 464,237 controls). Inverse-variance weighting was primary, with MR-Egger, weighted median and mode, MR-PRESSO, leave-one-out and Steiger analyses, reverse MR and exploratory multivariable MR (MVMR). Asthma, allergic rhinitis and chronic rhinosinusitis served as positive controls, and three suppurative otitis media phenotypes served as negative controls. Results: After false-discovery-rate correction, none of the six pollutants was significantly associated with OME; the sole nominal signal was PM10 (OR=1.555, 95% CI 0.947-2.553, P=0.081), which reversed with the 88-SNP pooled set (OR=0.64, 0.24-1.69, P=0.365). At 80% power, minimum detectable ORs ranged widely from 1.69 to 32.09; only PM2.5-10 and PM10 had values near 2, so moderate effects (OR 1.2-1.5) cannot be excluded. Confirmatory positive controls using phenotype-specific instruments were strongly positive, whereas negative-control outcomes showed no associations (all FDR>0.85). Every nominal reverse-MR signal had a significant MR-Egger intercept (the PM2.5 absorbance signal also showed significant heterogeneity and MR-PRESSO tests), indicating horizontal pleiotropy rather than reverse causation. MVMR was exploratory only, as conditional F statistics were below 10. Conclusions: We found no evidence for large-effect genetic causal associations between the six air pollutants and OME. These null findings argue against large, lifetime-average causal effects, and the associations reported in observational studies may instead reflect residual confounding, shared comorbidity or differences in exposure windows.

Background: Non-optimal air temperature increases the risk of preterm birth, but how temperature-related risks may translate into future population burden remains uncertain. We aimed to estimate the association between temperature and preterm birth in Sweden and assess how preterm birth burden may change under plausible future temperature conditions. Methods: We conducted a nationwide population-based cohort study of singleton births in Sweden from 1973 to 2018. Weekly mean temperature was assigned at the parish level according to maternal residence. Cox proportional hazards models with a distributed lag nonlinear model were used to estimate nonlinear and delayed associations between temperature and preterm birth. The estimated exposure response relationship and baseline hazards were then incorporated into an individual-based microsimulation of gestational progression under projected temperatures for 2025 to 2055. Future projections were examined across multiple climate models under SSP1-2.6 and SSP3-7.0 scenarios. Outcomes included the annual number and cumulative incidence of preterm births and the temperature-attributable fraction. Results: Among 4,338,825 singleton births, 211,397 (4.9%) were preterm. Temperature preterm birth associations were modest overall. The clearest increase in hazard was observed following exposure to very low temperatures, particularly -10C at short lags. Higher temperatures showed no clear increase in risk. From 2025 to 2055, the annual cumulative incidence of preterm birth and the temperature-attributable fraction was expected to remain broadly stable, with limited differences between emissions scenarios. In contrast, the absolute number of preterm births was expected to over the projection period, primarily reflecting increases in the projected number of pregnancies rather than substantial changes in temperature-associated risk. Conclusions: Very low temperatures were associated with a modest short-term increase in preterm birth risk in Sweden, hot temperatures showed little evidence of increased risk. Applying these associations to future climate conditions suggested limited changes in preterm birth incidence or the proportion attributable to temperature through 2055. However, the absolute burden of preterm birth may increase as the population at risk grows. This highlights the importance of considering demographic change alongside climate projections when assessing future maternal and neonatal health burden.

Total serum perfluorooctane sulfonate (PFOS) concentration and its isomer composition describe different aspects of internal exposure, but their respective associations with depressive symptoms remain uncertain. We examined adults aged 18-25 years in NHANES August 2021-August 2023 using survey-weighted models of the Patient Health Questionnaire-9 (PHQ-9). Total measured PFOS was the sum of linear PFOS and pooled monomethyl-branched PFOS; composition was their log-ratio. The analytic cohort included 169 participants, with 147 complete cases for core adjustment. Median total PFOS was 1.70 ng/mL, the median linear fraction was 72.2%, and the weighted prevalence of PHQ-9 [≥]10 was 22.6%. In the joint adjusted model, a doubling of total PFOS at fixed composition corresponded to -0.49 PHQ-9 points (95% CI, -1.65 to 0.68); a doubling of the linear-to-branched ratio at fixed total corresponded to 0.21 points (-1.94 to 2.36). Algebraic rescaling across the reported interquartile ranges yielded differences of -0.58 points (-1.95 to 0.81) for total PFOS and 0.13 points (-1.16 to 1.41) for composition. The inverse continuous-score association weakened with adjustment, whereas the screening odds ratio primarily lost precision. Excluding three observations with an isomer below detection shifted both joint coefficients. The data therefore do not establish an independent composition association or equivalent isomer effects. Experimental evidence supports candidate oxidative, inflammatory, and synaptic pathways, but differential protein binding and elimination prevent a serum composition ratio from being interpreted directly as brain dose or toxicity. Larger longitudinal analyses with isomer-resolved exposure and toxicokinetic measurements are needed to test these pathways.

Endocrine-disrupting chemicals can target ovaries and interfere with key milestones of reproduction. Previously, we found that mixtures of the chemical exposome measured in follicular fluid (FF) were cumulatively associated with lower oocyte yield. Because ovaries age faster than many other organs, our current aim was to evaluate associations of FF chemical mixtures with epigenetic age acceleration and epigenetic pathways in FF cells. FF was collected during oocyte retrieval from 76 patients undergoing assisted reproduction in Atlanta. The exposome was measured using untargeted high-resolution mass spectrometry with gas (GC) and liquid (LC) chromatography. Weighted quantile sum (WQS-RS) indices were constructed for three mixtures of chemicals in association with oocyte yield, separated by instrument configuration (GC, LC-HILIC, LC-C18). DNA methylation was measured from the cellular component of FF using Illumina MethylationEPIC BeadChip, with age acceleration based on the GrimAge clock. Regression and pathway enrichment analyses elucidated relationships between chemical exposures or mixture indices and epigenetic markers, adjusted for age and technical covariates. All three chemical mixture indices were associated with epigenetic age acceleration in FF (p<0.05). For example, a standard-deviation increase in the GC-detected mixture was associated with 0.23 standard-deviations higher accelerated aging (95% CI: 0.0058-0.45; p=0.048). Twenty-seven frequently detected chemicals, including benzo[a]pyrene, plasticizers, flame retardants, forever chemicals, and pesticides, were associated with epigenetic pathways related to ovarian follicle growth and hormone signaling (p<0.05; six under false discovery rate<5%). In summary, environmental chemicals may accumulate in ovaries, contribute to accelerated epigenetic aging of ovarian somatic cells, and potentially affect follicle development.

Objective: Environmental pollutants are increasingly recognized as potential risk factors for metabolic dysfunction-associated steatotic liver disease (MASLD), yet the effects of mixed exposures and underlying mechanisms remain unclear. We evaluated associations between environmental chemical mixtures and MASLD and the mediating role of inflammation-related biomarkers. Methods: We analyzed 60 environmental chemicals across six categories among 39,061 U.S. adults from the National Health and Nutrition Examination Survey (NHANES) 1999-2020. Principal Component Pursuit with Principal Component Analysis (PCP-PCA) identified latent exposure patterns. MASLD was identified using multisociety Delphi consensus criteria and the Hepatic Steatosis Index (HSI [&ge;] 36). Logistic regression, restricted cubic spline models, and mediation analysis were applied. Results: PCP-PCA generated 5-17 dimensions per chemical category, with first-dimension variance contributions ranging from 30.70% to 98.88%. Six dimensions from four categories were retained, with phthalate esters (PAEs) and organophosphate flame retardants (OPFRs) showing the most consistent associations with MASLD. PAEs Dim.1, explaining 90.71% of variance, showed a significant non-linear dose-response association (P-nonlinear = 0.0001). Significant associations were identified for mono-isobutyl phthalate (MiBP; OR 1.12, 95% CI 1.07-1.19), mono(carboxyoctyl) phthalate (MCOP; OR 1.08, 95% CI 1.02-1.14), mono(carboxynonyl) phthalate (MCNP; OR 1.12, 95% CI 1.03-1.21), and bis(1,3-dichloro-2-propyl) phosphate (BDCP; OR 1.15, 95% CI 1.08-1.23). C-reactive protein (CRP) and red cell distribution width (RDW) were the primary mediators, accounting for 32.42% and 19.62% of the MiBP-MASLD association, respectively (both p < 0.0001). Conclusion: Environmental co-exposure, particularly to PAEs and OPFRs, was associated with higher MASLD risk, with systemic inflammation potentially contributing to these associations.

Background: Lead is a cumulative environmental toxicant for which no safe level of exposure has been identified, and pregnant women and their fetuses are particularly vulnerable because lead readily crosses the placenta and can be mobilised from maternal bone stores. Bangladesh conducted its first nationally representative blood lead testing among pregnant women through the 2025 Multiple Indicator Cluster Survey (MICS), but a detailed, multi-domain analysis of the determinants of elevated blood lead level (BLL) among this population has not yet been reported. Methods: We conducted a secondary cross-sectional analysis of 1,928 pregnant women aged 15-49 years with complete data from the women's dataset of Bangladesh MICS 2025. Elevated BLL was defined as [&ge;]5 g/dL. Survey-weighted logistic regression was used to estimate unadjusted and adjusted odds ratios (aOR) for co-exposure to arsenic, cadmium and mercury and sociodemographic and socioeconomic covariates. Slope Index of Inequality (SII) as well as Relative Index of Inequality (RII) were used to quantify wealth-related inequality. Population attributable fractions (PAF) were estimated for three counterfactual scenarios, and adaptive least absolute shrinkage and selection operator (LASSO) regression was used as a sensitivity analysis. Results: Elevated BLL was present among 6.2% of participants. In the adjusted model, a 2-fold rise in blood cadmium was associated with higher odds of elevated BLL (aOR: 1.54; 95% CI: 1.21-1.96), whereas a 2-fold rise in blood mercury (aOR: 0.63; 95% CI: 0.48-0.83), rural residence (aOR: 0.55; 95% CI: 0.32-0.94), secondary education (aOR: 0.49; 95% CI: 0.28-0.85) and post-secondary education (aOR: 0.22; 95% CI: 0.11-0.46) were associated with lower odds. Belonging to progressively wealthier quintiles was associated with markedly higher odds, BLL rising to an aOR of 10.32 (95% CI: 4.41-24.15) for the richest versus poorest quintile. The RII was 8.59 (95% CI: 4.24-17.40) and the SII was 0.159 (95% CI: 0.101-0.218), indicating a substantial pro-rich gradient in elevated BLL. Counterfactual scenarios suggested that shifting the population to secondary-level education could reduce the prevalence of elevated BLL by 52.9% (95% CI: 20.6-72.0) and shifting to rural residence by 24.3% (95% CI: 1.4-41.9). Adaptive LASSO variable selection produced estimates consistent in direction and magnitude with the fully adjusted model. Conclusion: In this national sample, approximately one out of every 16 pregnant women had blood lead levels that met or exceeded the action threshold set by the World Health Organization, with this issue being particularly prevalent among wealthier, urban, and less-educated women, and was compounded by co-exposure to cadmium. In Bangladesh, the typical pattern observed for maternal and child health indicators does not align with the inverse relationship found between household wealth and lead exposure. This suggests that the sources of exposure are not merely indicators of material poverty. Antenatal blood lead screening, source investigation, and equity-informed lead-reduction strategies that specifically reach wealthier and urban households are warranted.

Abstract Background Air pollution contributes substantially to morbidity and mortality in low-income countries, where reliance on solid fuels leads to high levels of household exposure. Colonisation of the upper respiratory tract by Streptococcus pneumoniae is a prerequisite for pneumococcal disease, and inhaled air pollutants may influence colonisation through impaired mucociliary clearance. Therefore, we investigated the association between S. pneumoniae colonisation and personal exposure to particulate matter (PM2.5) and carbon monoxide (CO) as well as temperature and relative humidity in older children in The Gambia. Methods We conducted a prospective study of 134 children aged 5-14 years across eight visits in rural Gambia. Personal 24-hour PM2.5, CO, temperature and relative humidity exposures were measured using personal monitors. Concurrently, combined nasopharyngeal/oropharyngeal swabs were collected at each visit, and S. pneumoniae colonisation was determined by microbiological culture. Mixed-effects logistic regression models were used to examine associations between environmental exposures and colonisation. Exposures were additionally decomposed into between-child and within-child components. Models were adjusted for age, season, and household income tertile. Results A total of 554 child visits with paired exposure and microbiological data were analysed. Overall, 24-hour geometric mean PM2.5 and CO were 12.6 {micro}g/m3 (95% CI 12.2-13.1) and 0.16 ppm (95% CI 0.14-0.19) respectively and overall S. pneumoniae colonisation prevalence was 39.7%. In conventional models, PM2.5, CO, temperature, and relative humidity were not significantly associated with S. pneumoniae colonisation after adjustment for confounders. In the within-between decomposition analysis, higher between-child temperature exposure was consistently associated with lower odds of colonisation (mutually adjusted model: OR 0.74, 95% CI 0.56-0.98; p = 0.034). Relative humidity showed an inverse within-child association in crude analysis (OR 0.70, 95% CI 0.52-0.93; p = 0.013), which attenuated after adjustment for season and other confounders. No associations were observed for PM2.5 or CO exposures. Conclusion At the exposure levels observed in this cohort of older children, PM2.5 and CO exposures were not independently associated with S. pneumoniae colonisation. The pattern observed for temperature suggests that longer-term temperature conditions may be more relevant to pneumococcal colonisation than short-term exposure variation in this setting.

Plastic products have greatly improved convenience in daily life. However, diverse pollutants released from these materials pose substantial risks to human health. Lactiplantibacillus plantarum PD01 has previously been demonstrated to reduce microplastic (MP) bioaccumulation and toxicity in murine model. In this study, we conducted a randomized, double-blind, placebo-controlled trial to further evaluate the efficacy of L. plantarum PD01 in reducing MPs and MP-associated chemicals in humans. A total of 106 participants were recruited in November 2025. Eligible participants were randomly assigned to either the placebo or intervention group, and orally received placebo or 1.0x1010 colony-forming units (CFU) L. plantarum PD01 after meals three times a day, respectively. Fecal, urinary, and blood samples were collected to determine the MPs contents, plasticizer levels, gut microbiota composition, blood metabolic profiles and biochemical indicators. Among these measurements, the analysis of urinary phthalate metabolites was completed first and revealed a significant reduction after the probiotic intervention. Compared with the placebo group, 6-week L. plantarum PD01 supplementation resulted in significant relative reductions in urinary levels of MCMHP by 60.2% (P = 0.0343), MMP by 51.2% (P < 0.001), MEHP by 49.6% (P = 0.0058), MiBP by 45.7% (P = 0.0085), MnBP by 35.8% (P = 0.0478), and {Sigma}DEHP by 46.2% (P = 0.0461). The interim results presented here provide the first clinical evidence that the probiotic strain PD01 can significantly reduce residual MP-associated chemicals in human body. To the best of our knowledge, this is the first randomized controlled trial (RCT) to evaluate probiotic intervention targeting MPs and MP-associated chemicals in humans.

Background Short-term weather conditions can trigger paediatric hospital admissions, but evidence remains limited on the health relevance of intraday temperature variability, humidity, and precipitation, and generally on which subgroups are most susceptible. Methods We conducted a nationwide case time-series study of Swedish children and adolescents aged 6-18 years using linked register data. Associations between daily mean temperature, intraday temperature variability, relative humidity, and precipitation and inpatient hospitalisations were estimated with Poisson regression (individual fixed effects) combined with distributed lag non-linear models over lags 0-21 days. Outcomes included all-cause hospitalisation and cause-specific admissions. Effect modification was examined by sex, age group, socioeconomic indicators, region, and calendar periods. Findings Among 4,638,247 children and adolescents in the cohort, 1,070,702 (23.1%) experienced at least one inpatient hospitalisation, contributing 1,736,169 hospitalisation events. All-cause hospitalisation increased with higher mean temperature, with risk highest at hot extremes. Intraday temperature variability showed a U-shaped association, with higher rates at both lowest and highest exposure levels. Relative humidity showed no association with hospitalisation risk. Higher precipitation was associated with increased hospitalisation risk, but estimates at high rainfall levels were imprecise. Stratified analyses indicated modest differences by sex and socioeconomic indicators, but clearer heterogeneity by age and region, with the highest risks among younger children and in East Sweden; associations varied across calendar periods and were imprecise for most cause-specific outcomes. Sensitivity analyses mostly showed that the main curve shapes were robust. Interpretation Short-term exposure to hot temperatures, both low and high intraday temperature variability, and higher levels of precipitation were associated with an increased risk of all-cause hospitalisation among children in Sweden, with clearer variation by age group and region than by sex or socioeconomic position. These findings support targeting paediatric climate-health preparedness and early-warning systems toward younger children and higher-risk regions such as eastern Sweden and extending such systems beyond mean temperature to include intraday temperature variability, a distinct, currently overlooked driver of risk that heat-focused systems are not designed to capture. Fundings This research was funded by Formas the Swedish Research Council for Sustainable Development (grant no. 2023-01774 and 2022-01845) and the Swedish Research Council (2025-02804 and 2022-06599).

Background: Chronic arsenic exposure in drinking water causes skin lesions and cancers and raises infant, cardiovascular and all-cause mortality in Bangladesh. National surveys tested source water in 2012-13, 2019 and 2025 with different kits, so the trend is uncertain. Objectives: We estimated how arsenic in source water changed after laboratory adjustment of 2012-13 readings, and how many people remained exposed. We also assessed whether districts high in earlier surveys held most people exposed in 2025. Methods: We analysed 11,624 households in three Multiple Indicator Cluster Surveys. We counted arsenic strictly above 10 and 50 parts per billion (ppb). Results: Estimates reproduced published 2019 and 2025 tables. After laboratory adjustment of 2012-13, the share above 10 ppb fell from 24.0% to 14.4% (adjusted ratio 0.61, sampling 95% CI 0.55 to 0.67; 0.69 with interview month). Above 50 ppb it fell from 10.9% to 8.6% (0.80, 0.69 to 0.93; 0.93 with month). Most of the fall at 10 ppb occurred within source types. Without false positives, it would vanish only if later kits detected 61% of sources above 10 ppb. About 26 million people used such water in 2025 (kit scenarios 23 to 32 million). The 25 districts high in 2012-13 and 2019 held 39% of the population but 72% of those exposed (bootstrap 95% interval 60 to 76). Clustering was evident, but no district was a significant hotspot. Conclusions: Arsenic above 10 ppb was lower in 2025 than in 2012-13, but the size of the fall depends on unverified later kits. Change at 50 ppb and since 2019 was unclear after month adjustment. One household in seven exceeded the WHO guideline in 2025. Districts found high earlier held most exposed people, supporting prioritised well testing there alongside broader surveillance. Future surveys need one kit with a laboratory cross-check.

Background: Exercise training is a cornerstone intervention for cardiovascular disease, yet large cohort studies have reported attenuation of physical activity benefits at elevated air pollution concentrations, creating uncertainty around exercise prescription in polluted settings where cardiovascular disease burden is greatest. Objectives: To determine whether ambient PM2.5 concentration modifies the cardiovascular benefits of structured exercise training, using a global sample of trials spanning a >100-fold pollution gradient. Methods: We conducted a systematic review and multilevel meta-analysis of exercise training interventions reporting pre-post changes in systolic blood pressure (SBP), diastolic blood pressure (DBP), peak oxygen uptake (VO2Max), or resting heart rate (HR) in adults. Annual ambient PM2.5 concentrations (3.5-283 g/m3) were assigned to each study location from CAMS ERA5 reanalysis data. Three-level random-effects models with cluster-robust variance estimation accounted for arms nested within studies. PM2.5 meta-regression was conducted unadjusted and adjusted for world region, exercise mode, trial duration, and health condition, with subgroup analyses by exercise mode and hypertension status. Results: Across 465 studies (27,629 participants), exercise training produced clinically meaningful benefits for all outcomes (SBP - mmHg, DBP - mmHg, VO2Max +3.2 ml/kg/min, HR - bpm; all p < 0.001), with benefits consistently larger in higher-pollution settings. Hypertensive participants showed the greatest improvements, particularly from aerobic exercise (SBP standardised mean difference 0.396 in the Low vs 1.020 in the High PM2.5 stratum). Although aerobic and resistance training participants experience similar chronic ambient PM2.5 exposure, only aerobic exercise showed a stratum gradient (interaction p = 0.074). Discussion: Exercise training delivers clinically meaningful cardiovascular benefits at every pollution level tested. The larger benefits observed in higher-pollution settings reflect the greater cardiovascular risk burden of those populations, and hypertensive patients stand to gain the most, particularly from aerobic exercise.

Background: In coastal Bangladesh, saline drinking water has been linked to raised blood pressure. The 2025 Multiple Indicator Cluster Survey (MICS) measured electrical conductivity (EC), a salinity indicator, in source water, but its report gave no population counts or district estimates. Objectives: To estimate how many people live in households whose tested source has high EC, and to describe patterns by place, household characteristics, source type and arsenic. Methods. EC was measured in source water of 6,040 households in 64 districts, February to June. In 14.5% of households the tested source was not the main drinking-water source. Primary outcomes were EC above 1,500 and 3,000 microsiemen/cm, survey risk classes that are not health-based standards. Estimates were survey weighted; comparisons were observational. Results: EC exceeded 1,500 microsiemen/cm in 5.3% of households (95% CI 4.7 to 5.9), about 9.0 million people, including 1.8 million above 3,000 microsiemen/cm. Coastal-zone districts held 26% of households but 70% of those above 1,500 microsiemen/cm. Shares varied little by wealth or in households with young children or pregnant women. Nationally, deep tube wells more often had high EC because most are coastal. In the coastal zone, deep and shallow wells had similar shares (16.1% and 17.9%). After district adjustment, EC was about 18% lower in deep wells (geometric mean ratio 0.82, 0.73 to 0.92). Within upazilas (restricted sample) it was 0.93 (0.80 to 1.07). Arsenic above 10 ppb was more common where EC was high, but this link weakened after district adjustment. Conclusions: Millions of people live in households whose tested source has high EC, mostly in coastal and south-central districts. Deep wells had modestly lower EC after geographic adjustment, but the difference shrank within upazilas and depended on the handling of implausibly low readings. The findings support measuring EC alongside arsenic, with documented meter calibration.

Socioeconomic inequality in exposure to air pollution possess a significant public health challenge, yet little is known about how the disparities vary across the various economic status areas in Nairobi. Globally, studies have shown that exposure to air pollution is unequal across communities hence disparities in harm to human health. This study examined the association between socioeconomic characteristics and perceived air quality among residents of low- and high-socioeconomic status areas in Nairobi, Kenya. Two regions within Nairobi County were selected for this study: Mukuru kwa Njenga (representing the Low Socioeconomic Status) and Langata (representing the High Socioeconomic Status) with a sample size of 384 in HSES areas and 368 in LSES areas. A cross-sectional study was conducted among 752 respondents residing in selected LSES and HSES areas of Nairobi. Data was collected using a structured questionnaire assessing sociodemographic characteristics, income, education, employment, perceived air quality, and self-reported health outcomes associated with air pollution exposure. Descriptive statistics were used to summarize participant characteristics and perceived air quality. Chi-square tests were used to examine associations between residential area and categorical health outcomes, while ordinal logistic regression was used to assess the association between socioeconomic characteristics and perceived air-quality ratings. Perceived air quality differed significantly between residential socioeconomic groups. Respondents in LSES areas were more likely to rate air quality as poor or very poor, with 45.4% rating it as very poor, compared with only 1.6% of respondents in HSES areas. In contrast, 12.2% of HSES respondents rated air quality as good compared with 0.3% in LSES areas. The association between area of residence and perceived air-quality rating was statistically significant, {chi}2(3) = 282.672, p < 0.001. In the ordinal logistic regression model, HSES residence was associated with significantly lower odds of reporting poorer perceived air quality compared with LSES residence (OR = 0.135, 95% CI: 0.095-0.190, p < 0.001). Income was also significantly associated with perceived air quality, while respondents with no formal education had higher odds of reporting poorer perceived air quality compared with those with secondary education (OR = 3.254, 95% CI: 1.388-7.638, p = 0.007). Significant differences were also observed for several self-reported health outcomes. Respiratory problems were more prevalent among respondents in LSES areas than HSES areas (72.7% versus 50.4%; {chi}2(1) = 29.081, p < 0.001; Cramer's V = 0.224). However, allergies, eye irritation, and headaches were reported more frequently in HSES areas than in LSES areas, with significant associations observed for allergies ({chi}2(1) = 106.479, p < 0.001; Cramer's V = 0.429), eye irritation ({chi}2(1) = 136.577, p < 0.001; Cramer's V = 0.486), and headaches ({chi}2(1) = 149.180, p < 0.001; Cramer's V = 0.508). No statistically significant association was observed for cardiovascular problems, likely reflecting the very low number of reported cases. Substantial socioeconomic disparities in perceived air quality and self-reported respiratory health outcomes were observed. Residents of low-socioeconomic status areas consistently perceived poorer air quality and reported a higher burden of respiratory problems, highlighting the need for targeted interventions to reduce environmental health inequalities.

This study assesses the spatial dynamics of heavy metals and associated trace elements in the water and sediment of the Slana River approximately one and half year after an environmental accident and river contamination caused by mining effluent. Using PCA and standardized environmental indices (CF, PLI), we modelled the distribution of contaminants across the macro-gradient of the river and within the micro-gradient surrounding the source of pollution. We found that although the situation in the water column has improved and stabilized, the sediment remains the primary reservoir of trace elements, including toxic arsenic, with the highest concentrations recorded near the source and in its immediate vicinity. Although the concentration of primary mining indicators decreases relatively rapidly along the stream, this is systematically offset by the accumulation of other elements, including sulphur and aluminium. As a result of these geochemical processes, the total pollution load index (PLI) remains statistically unchanged along the entire stream, but indicates a chronic, spatially uniform (PLI = 1.06-1.16) toxicological burden on the ecosystem.

Essential for nutrient growth, due to intensive farming practices nitrate has become a common water contaminant in agricultural states. US nitrate regulations are designed to protect the health of newborns and infants, but have never been revised to consider potential harms of prenatal exposure. Recent evidence, however, suggests that exposure below the 10 mg/L regulatory limit may be associated with adverse birth outcomes. This current study examines whether first-trimester exposure below the regulatory limit is associated with adverse birth outcomes in Iowa (an intensive agricultural state). Finished drinking-water nitrate measurements from Iowa public water systems were linked to birth records. Nitrate measures were aggregated to a balanced county-quarter panel (1983 to 1988). Each pregnancy was assigned an average nitrate exposure over a 98-day first-trimester window. All births with a first trimester county-quarter nitrate measure >= 10 mg/L were excluded. Linear probability models with county-by-year and year-by-conception-quarter fixed effects, with standard errors clustered by county, estimated both uncorrected and Sidak corrected inference. The final analytic sample included 113,328 singleton births. Relative to lowest exposure category (0.1 mg/L or below), exposure to 5 mg/L or more nitrate was associated with a 1.04 percentage-point increase in the probability of preterm birth (CI = 0.24 to 1.83), a 13.5% relative increase, and associated with a 0.53 percentage-point increase in very preterm birth (CI = 0.08 to 0.97), a 46.2% relative increase. The statistical significance of both estimates persisted after correction for multiple tests. Exposure to > 0.1 mg/L and < 5 mg/L was not associated with any outcome. These preterm and very preterm birth associations were consistent across several sensitivity checks. Because nitrate concentrations between 5 to <10 mg/L comply with current rules, these findings warrant reassessing approaches to protect the health of pregnant women and their children.

Background: Childhood anaemia remains a major public health challenge in low- and middle-income countries. Although nutritional deficiencies are well-established contributors, the population-level role of environmental heavy metal exposure remains poorly understood in South Asia. Objectives: To estimate the prevalence, socioeconomic inequalities, and factors associated with childhood anaemia among children aged 12-59 months in Bangladesh, with particular emphasis on environmental heavy metal exposure. Methods: We analysed nationally representative cross-sectional data from the Bangladesh Multiple Indicator Cluster Survey (MICS) 2025, including 10,343 children aged 12-59 months. Blood concentrations of lead, arsenic, cadmium, and mercury were transformed using base-2 logarithms (log2). The primary outcome was binary child anaemia status. Survey-weighted Bayesian hierarchical logistic regression using R-INLA, with primary sampling unit (PSU)-level random intercepts, was the primary analytical approach. Socioeconomic inequalities were evaluated using the Slope Index of Inequality (SII) and Relative Index of Inequality (RII). Population attributable fractions (PAFs) were estimated separately using counterfactual analyses. Results: Overall, 4779 (44.3%) children had anaemia. In multiple Bayesian models, each 2-fold increase in blood arsenic (posterior aOR 1.12, 95% CrI 1.06-1.18; P(aOR>1): >0.99) and blood cadmium (aOR 1.09, 95% CrI 1.04-1.13; P(aOR>1): >0.99) was independently associated with higher odds of childhood anaemia. Conversely, higher blood mercury was inversely associated (aOR 0.82, 95% CrI 0.78-0.86; P(aOR<1): >0.99). Older child age (aOR 0.69 per 13.2 months increase, 95% CrI 0.65-0.72), higher Height-for-Age Z-score (aOR 0.88, 95% CrI 0.84-0.91), maternal higher education (aOR 0.69, 95% CrI 0.56-0.86), and richest wealth status (aOR 0.80, 95% CrI 0.66-0.97) were associated with lower anaemia odds. Anaemia was more common among children from the poorest households (SII: -12.39%, 95% CI -17.62, -7.17), while anaemia prevalence was lower among wealthier households (RII: 0.76, 95% CI 0.67-0.85). Interpretation: Childhood anaemia in Bangladesh is associated with environmental toxicant exposures, nutritional deficits, and structural socioeconomic disadvantage. The findings highlight the potential importance of integrating nutritional, environmental, and socioeconomic considerations within strategies to address the high burden of child anaemia in Bangladesh.

Toxicants in the environment can significantly impact physiology. Environmental chemical exposures during early developmental stages disturb normal embryonic development and programming, and dramatically impact long-term health as individuals age. Female and male animals show distinct phenotypes when responding to a given chemical exposure. Here, through the TaRGET II (Toxicant Exposures and Responses by Genomic and Epigenomic Regulators of Transcription) consortium, we systematically explored sex-specific transcriptomic and epigenomic alterations in response to various toxicants, including arsenic (As), lead (Pb), tributyltin (TBT), bisphenol A (BPA), di(2-ethylhexyl) phthalate (DEHP), dioxin (TCDD), and fine particulate matter (PM2.5), across three time points in mice exposed two weeks prior to conception through gestation and lactation. After being exposed to toxicants during the embryonic and early postnatal developmental stages, 1,025 omics datasets were generated from the liver and analyzed across three mouse life stages. We discovered a significant sex-biased molecular response to distinct exposures in the liver at both the transcriptomic and epigenetic levels, showing dynamic changes across mouse development and aging. The perturbed pathways and transcription factors in response to different chemical exposures in both sexes were further evaluated to measure the sex-specific impact of each toxic exposure in the liver. Overall, this study presents the most detailed investigation of sex-specific molecular signatures under the influence of developmental exposures to toxic substances.

Introduction: Pesticide exposure has been associated with poorer mental health, yet little is known about whether seasonal fluctuations in agricultural pesticide use are associated with cyclical changes in mood among people living in agricultural communities. We evaluated associations between 10 peak and off-peak pesticide spray seasons and ecological momentary assessment (EMA)-derived mood in a floricultural region in Ecuador. Methods: 496 participants completed repeated EMA surveys across 10 assessment administrations over 2.5 years (2022-2024), including one single-assessment administration and nine 10-day bursts (Nobservations=14,332). Mood outcomes included negative affect (sadness, anxiety, stress, anger, tiredness, difficulty concentrating; overall mean=2.79, Standard Deviation [SD]=1.32), positive affect (happiness, motivation; overall mean=4.21, SD=1.60), and behavioral dysregulation (aggression and impulsivity, overall mean=1.86, SD=1.29). Generalized linear mixed models estimated pooled, between-person and within-person associations between peak pesticide spray seasons and mood, adjusting for demographic and longitudinal factors Effect modification by sex, floricultural occupation, and cohabitation with a floricultural worker was assessed. Results: Peak spray seasons were associated with higher negative affect ({beta}=0.11 [0.06, 0.16]) and behavioral dysregulation ({beta}=0.10 [0.05, 0.15]) but not positive affect ({beta}=0.01 [-0.05, 0.07]). Associations were driven by within-person changes. Sex modified associations with negative affect, which were stronger in males than females. Floricultural occupation modified associations, with poorer mood, greater behavioral dysregulation and lower positive affect among floricultural workers than non-workers. Discussion: Peak pesticide spray seasons were associated with worsening of negative affect and behavioral dysregulation. EMA may provide a sensitive approach for detecting short-term neurobehavioral changes associated with seasonal pesticide exposure.