Pub Date : 2026-03-01Epub Date: 2026-03-07DOI: 10.1016/j.envint.2026.110186
Houman Kahroba , Kenneth Vanbrabant , Julian Krauskopf , Jacco Briedé , Marcel Ameloot , Michelle Plusquin , Maarten Roeffaers , Theo M. de Kok , Tim Nawrot
Prenatal exposure to ambient air pollution, particularly black carbon (BC), has been linked to adverse pregnancy outcomes and life-long neurodevelopmental disorders. Yet the mechanism by which inhaled nanoparticles cross the placenta and reach fetal tissues is unclear. Here we show that black carbon (BC) is detectable in association with small extracellular vesicles (sEVs) in fetal circulation and in tissue-enriched sEV subsets. Using label-free two-photon microscopy, we visualised BC associated with individual sEVs isolated from cord-blood plasma of 20 mother-infant pairs. BC-sEV association occurred in 27 % of total cord-blood sEVs, 54 % of placental alkaline-phosphatase-positive (PLAP+) placental vesicles and 68 % of fetal-brain-derived (Contactin-2+) vesicles. Among BC-positive fetal-brain sEVs, >90 % of the vesicle fluorescence co-localised with BC, demonstrating extensive pollutant loading. These findings provide evidence that BC can be detected in association with sEV-enriched preparations in fetal circulation, consistent with a possible role for sEV-associated carriage following transplacental particle transfer, though the dominant transport mechanism remains unestablished.
{"title":"Black carbon is detectable in association with small extracellular vesicles in fetal circulation","authors":"Houman Kahroba , Kenneth Vanbrabant , Julian Krauskopf , Jacco Briedé , Marcel Ameloot , Michelle Plusquin , Maarten Roeffaers , Theo M. de Kok , Tim Nawrot","doi":"10.1016/j.envint.2026.110186","DOIUrl":"10.1016/j.envint.2026.110186","url":null,"abstract":"<div><div>Prenatal exposure to ambient air pollution, particularly black carbon (BC), has been linked to adverse pregnancy outcomes and life-long neurodevelopmental disorders. Yet the mechanism by which inhaled nanoparticles cross the placenta and reach fetal tissues is unclear. Here we show that black carbon (BC) is detectable in association with small extracellular vesicles (sEVs) in fetal circulation and in tissue-enriched sEV subsets. Using label-free two-photon microscopy, we visualised BC associated with individual sEVs isolated from cord-blood plasma of 20 mother-infant pairs. BC-sEV association occurred in 27 % of total cord-blood sEVs, 54 % of placental alkaline-phosphatase-positive (PLAP<sup>+</sup>) placental vesicles and 68 % of fetal-brain-derived (Contactin-2<sup>+</sup>) vesicles. Among BC-positive fetal-brain sEVs, >90 % of the vesicle fluorescence co-localised with BC, demonstrating extensive pollutant loading. These findings provide evidence that BC can be detected in association with sEV-enriched preparations in fetal circulation, consistent with a possible role for sEV-associated carriage following transplacental particle transfer, though the dominant transport mechanism remains unestablished.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"209 ","pages":"Article 110186"},"PeriodicalIF":9.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147407208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-03-06DOI: 10.1016/j.envint.2026.110183
Katie L. Land , Hong Xu , James W. Akin , Patrick R. Hannon
Ovulatory defects are the leading cause of female infertility. Widespread exposure to endocrine-disrupting chemicals, such as phthalates, may contribute to the high prevalence of failed ovulation among infertile women. Using primary ovarian granulosa cells obtained from women, we tested the hypothesis that exposure to an environmentally relevant mixture of phthalate metabolites (MPTmix) impairs essential mediators of the ovulatory process, including progesterone (P4), progesterone receptor (PGR), and prostaglandins (PGs). The composition of the MPTmix was derived from urinary phthalate levels in women. Ovarian granulosa cells, obtained from in vitro fertilization patients, were acclimated in culture to regain responsiveness to hCG (human chorionic gonadotropin, clinical luteinizing hormone analogue). Following acclimation, cells were treated for 0.5-36hr with media containing DMSO (dimethyl sulfoxide, vehicle control), ± hCG (to initiate the ovulatory cascade), and ± MPTmix (1–500 µg/ml). Compared to hCG controls, treatment with hCG + MPTmix reduced active ovulatory PG levels by up to 77%, likely via decreased synthesis (lower PTGS2 and PTGES levels/activity), enhanced catabolism of PGE2 to PGF2α (elevated AKR1C1 and AKR1C3 levels), and increased metabolism (elevated HPGD levels/activity). MPTmix exposure further impaired PG function by altering the levels of PG transporters (ABCC4 and SLCO2A1) and receptors (PTGER1-4 and PTGFR). These MPTmix-induced disruptions were accompanied by upstream defects in LH/hCG receptor signaling (cAMP/PKA, ERK1/2), P4 steroidogenesis, and PGR expression. Together, these findings demonstrate that exposure to phthalates impairs P4/PGR-driven PG production/function in human ovarian cells and advances our mechanistic understanding of how phthalate exposure may contribute to ovulatory dysfunction in women.
{"title":"An environmentally relevant phthalate mixture impairs ovulatory prostaglandin and progesterone receptor pathways in human granulosa cells in vitro","authors":"Katie L. Land , Hong Xu , James W. Akin , Patrick R. Hannon","doi":"10.1016/j.envint.2026.110183","DOIUrl":"10.1016/j.envint.2026.110183","url":null,"abstract":"<div><div>Ovulatory defects are the leading cause of female infertility. Widespread exposure to endocrine-disrupting chemicals, such as phthalates, may contribute to the high prevalence of failed ovulation among infertile women. Using primary ovarian granulosa cells obtained from women, we tested the hypothesis that exposure to an environmentally relevant mixture of phthalate metabolites (MPTmix) impairs essential mediators of the ovulatory process, including progesterone (P4), progesterone receptor (PGR), and prostaglandins (PGs). The composition of the MPTmix was derived from urinary phthalate levels in women. Ovarian granulosa cells, obtained from <em>in vitro</em> fertilization patients, were acclimated in culture to regain responsiveness to hCG (human chorionic gonadotropin, clinical luteinizing hormone analogue). Following acclimation, cells were treated for 0.5-36hr with media containing DMSO (dimethyl sulfoxide, vehicle control), ± hCG (to initiate the ovulatory cascade), and ± MPTmix (1–500 µg/ml). Compared to hCG controls, treatment with hCG + MPTmix reduced active ovulatory PG levels by up to 77%, likely via decreased synthesis (lower PTGS2 and <em>PTGES</em> levels/activity), enhanced catabolism of PGE<sub>2</sub> to PGF<sub>2α</sub> (elevated <em>AKR1C1</em> and <em>AKR1C3</em> levels), and increased metabolism (elevated HPGD levels/activity). MPTmix exposure further impaired PG function by altering the levels of PG transporters (<em>ABCC4</em> and <em>SLCO2A1</em>) and receptors (<em>PTGER1</em>-<em>4</em> and <em>PTGFR</em>). These MPTmix-induced disruptions were accompanied by upstream defects in LH/hCG receptor signaling (cAMP/PKA, ERK1/2), P4 steroidogenesis, and <em>PGR</em> expression. Together, these findings demonstrate that exposure to phthalates impairs P4/PGR-driven PG production/function in human ovarian cells and advances our mechanistic understanding of how phthalate exposure may contribute to ovulatory dysfunction in women.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"209 ","pages":"Article 110183"},"PeriodicalIF":9.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147407832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-24DOI: 10.1016/j.envint.2026.110158
Jing Zhao , Yu Wu , Wenhao Zhang , Zeyu Wang , Donghai Xie , Zhenxuan Liu , Ziqi Zhang
Aerosols exert a significant influence on Earth’s climate system via radiative forcing, cloud formation, and air quality. Despite regional variability in their optical properties, coastal boundary aerosols remain poorly characterized, which limits the accuracy of climate assessments. In this study, we develop a hybrid classification framework that combines k-means clustering and a multilayer perceptron neural network to classify coastal aerosols. Using observations from 58 global sites in the Aerosol Robotic Network, we identify four representative coastal aerosol regimes: urban and industrial pollution aerosol, mineral dust aerosol, biomass-burning smoke aerosol, and marine aerosol dominated by sea salt. Our findings reveal strong seasonal dominance in coastal aerosol composition, with mineral dust accounting for up to 75% of the total aerosol burden in summer. Multiwavelength optical properties indicate that the wavelength gradient of aerosol optical depth may decrease from 0.3 to 0.12, highlighting regime-dependent spectral variability. Coarse-mode aerosol optical depth also increases substantially in winter, reaching levels approximately three times those observed in other seasons. Distinguishing coastal aerosol regimes across regions and seasons can improve climate-model evaluation and support evidence-based policies to protect vulnerable coastal ecosystems worldwide.
{"title":"Seasonal aerosol variations at the Land-Ocean boundary: Insights from a global AERONET network analysis","authors":"Jing Zhao , Yu Wu , Wenhao Zhang , Zeyu Wang , Donghai Xie , Zhenxuan Liu , Ziqi Zhang","doi":"10.1016/j.envint.2026.110158","DOIUrl":"10.1016/j.envint.2026.110158","url":null,"abstract":"<div><div>Aerosols exert a significant influence on Earth’s climate system via radiative forcing, cloud formation, and air quality. Despite regional variability in their optical properties, coastal boundary aerosols remain poorly characterized, which limits the accuracy of climate assessments. In this study, we develop a hybrid classification framework that combines k-means clustering and a multilayer perceptron neural network to classify coastal aerosols. Using observations from 58 global sites in the Aerosol Robotic Network, we identify four representative coastal aerosol regimes: urban and industrial pollution aerosol, mineral dust aerosol, biomass-burning smoke aerosol, and marine aerosol dominated by sea salt. Our findings reveal strong seasonal dominance in coastal aerosol composition, with mineral dust accounting for up to 75% of the total aerosol burden in summer. Multiwavelength optical properties indicate that the wavelength gradient of aerosol optical depth may decrease from 0.3 to 0.12, highlighting regime-dependent spectral variability. Coarse-mode aerosol optical depth also increases substantially in winter, reaching levels approximately three times those observed in other seasons. Distinguishing coastal aerosol regimes across regions and seasons can improve climate-model evaluation and support evidence-based policies to protect vulnerable coastal ecosystems worldwide.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"209 ","pages":"Article 110158"},"PeriodicalIF":9.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147279733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Microplastics (MPs) are pervasive environmental contaminants that pose potential health risks through multiple exposure routes. Although their toxic effects have attracted increasing concern, their multigenerational impacts remain poorly understood. This study investigated the reproductive effects of maternal exposure to polystyrene microplastics (PS-MPs) during gestation and lactation, on male offspring across two generations (F1 and F2) of Sprague-Dawley rats. Results demonstrated that maternal PS-MPs exposure induced significant reproductive toxicity in both F1 and F2 male offspring, manifesting as impaired testicular development with reduced sperm count, and accompanied by increased oxidative stress and DNA damage, as indicated by elevated levels of ROS, 8-OHdG, and γ-H2AX. In the F1 generation, we observed suppressed testosterone synthesis and endoplasmic reticulum (ER) stress, characterized by decreased levels of testosterone and steroidogenic acute regulatory protein (StAR), along with increased GRP78. Interestingly, the F2 generation exhibited a distinct adaptive response, characterized by the upregulation of StAR and Serine arginine-rich splicing factor 1 (SRSF1), suggesting that modulation of steroidogenesis and RNA splicing may partially counteract the reproductive impairment induced by ancestral exposure. In conclusion, gestational and lactational exposure to PS-MPs induces multigenerational reproductive toxicity in male offspring. However, compensatory mechanisms appear to attenuate these effects in the F2 generation. These findings provide crucial experimental evidence for the comprehensive assessment of multigenerational reproductive risks from microplastic exposure.
{"title":"Perinatal exposure to polystyrene microplastics induces multigenerational impairment of male reproduction via disrupted steroidogenesis and proteostasis","authors":"Mengling Jiang , Shuxin Wang , Huilin Zeng, Bowen Tan, Yuqi Qin, Qi Zhou, Xiaojing Lv, Jian Wan, Mingqing Chen","doi":"10.1016/j.envint.2026.110165","DOIUrl":"10.1016/j.envint.2026.110165","url":null,"abstract":"<div><div>Microplastics (MPs) are pervasive environmental contaminants that pose potential health risks through multiple exposure routes. Although their toxic effects have attracted increasing concern, their multigenerational impacts remain poorly understood. This study investigated the reproductive effects of maternal exposure to polystyrene microplastics (PS-MPs) during gestation and lactation, on male offspring across two generations (F1 and F2) of Sprague-Dawley rats. Results demonstrated that maternal PS-MPs exposure induced significant reproductive toxicity in both F1 and F2 male offspring, manifesting as impaired testicular development with reduced sperm count, and accompanied by increased oxidative stress and DNA damage, as indicated by elevated levels of ROS, 8-OHdG, and γ-H2AX. In the F1 generation, we observed suppressed testosterone synthesis and endoplasmic reticulum (ER) stress, characterized by decreased levels of testosterone and steroidogenic acute regulatory protein (StAR), along with increased GRP78. Interestingly, the F2 generation exhibited a distinct adaptive response, characterized by the upregulation of StAR and Serine arginine-rich splicing factor 1 (SRSF1), suggesting that modulation of steroidogenesis and RNA splicing may partially counteract the reproductive impairment induced by ancestral exposure. In conclusion, gestational and lactational exposure to PS-MPs induces multigenerational reproductive toxicity in male offspring. However, compensatory mechanisms appear to attenuate these effects in the F2 generation. These findings provide crucial experimental evidence for the comprehensive assessment of multigenerational reproductive risks from microplastic exposure.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"209 ","pages":"Article 110165"},"PeriodicalIF":9.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147278405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-24DOI: 10.1016/j.envint.2026.110169
Anna H. Wu , Jun Wu , Chiuchen Tseng , Burcu F. Darst , Song-Yi Park , Daniel O. Stram , Timothy Larson , Scott Fruin , Veronica W. Setiawan , Xian Yu , Lynne R. Wilkens , Howard Hu , Christopher Haiman , Beate Ritz , Eileen M. Crimmins , Unhee Lim , Iona Cheng , Loïc Le Marchand
Background and Objectives
Meta-analysis results, based largely among Whites, suggested that fine particulate matter (PM2.5) exposure increases the risk of clinical dementia. This study investigated the association of air pollution and incidence of Alzheimer’s disease and related dementias (ADRD) by race and ethnicity.
Methods
We investigated incidence of AD (n = 4,010) and other dementia (n = 4,971) among 44,954 California Multiethnic Cohort (MEC) participants (28% African American, 14% Japanese American, 44% Latino, 14% White adults) who were enrolled in the fee-for-service component of Medicare (2001–2016). We used Cox proportional hazards regression to examine associations between exposure to PM, airport-related ultrafine particles (aUFP) and gaseous pollutants and incidence of AD, other dementia, and ADRD in a minimally- and fully-adjusted model, considering 12 established ADRD risk factors. We conducted stratified analyses to examine associations by sex, and race/ethnicity.
Results
ADRD incidence was associated with PM2.5 (per 2 µg/m3), airport-related UFP (aUFP, per 4400 particles/cm3) and nitrogen dioxide (NO2, per 10 µg/m3) with hazard ratios (HRs, 95%CI), respectively, of 1.04 (1.02–1.06), 1.03 (1.01–1.05) and 1.09 (1.06–1.12). The AD-associations with PM2.5 and NO2, were stronger than the corresponding associations with other dementia (Pheterogeneity ≤ 0.003). Similar patterns of results were observed by sex and across race and ethnicity. Statistically significant findings for ADRD with PM2.5, aUFP and NO2 were observed among African American (respective HRs 1.03, 1.04, 1.09), and Latino and White participants for NO2 (HR 1.10, 1.08). Results in all and African American participants remained statistically significant in fully-adjusted models. Although the effect of PM2.5 was diluted in a co-pollutant with NO2, both PM2.5 and aUFP were significantly associated with ADRD incidence in a co-pollutant model, and NO2 and aUFP (but not PM2.5) remained associated in a multipollutant model. We did not observe consistent modifying effects for any of the 12 established ADRD risk factors.
Conclusions
In this multiethnic population, incidence of ADRD increased with exposures to PM2.5, aUFP, and NO2 in all subjects and this pattern was most prominent among African American adults. These results emphasize that ADRD prevention should include not only individual-level factors but also population-wide policies and regulation to curb air pollution.
{"title":"Racial and ethnic differences in the impact of air pollution on the risk of Alzheimer’s disease and related dementias in the Multiethnic Cohort Study","authors":"Anna H. Wu , Jun Wu , Chiuchen Tseng , Burcu F. Darst , Song-Yi Park , Daniel O. Stram , Timothy Larson , Scott Fruin , Veronica W. Setiawan , Xian Yu , Lynne R. Wilkens , Howard Hu , Christopher Haiman , Beate Ritz , Eileen M. Crimmins , Unhee Lim , Iona Cheng , Loïc Le Marchand","doi":"10.1016/j.envint.2026.110169","DOIUrl":"10.1016/j.envint.2026.110169","url":null,"abstract":"<div><h3>Background and Objectives</h3><div>Meta-analysis results, based largely among Whites, suggested that fine particulate matter (PM<sub>2.5</sub>) exposure increases the risk of clinical dementia. This study investigated the association of air pollution and incidence of Alzheimer’s disease and related dementias (ADRD) by race and ethnicity.</div></div><div><h3>Methods</h3><div>We investigated incidence of AD (n = 4,010) and other dementia (n = 4,971) among 44,954 California Multiethnic Cohort (MEC) participants (28% African American, 14% Japanese American, 44% Latino, 14% White adults) who were enrolled in the fee-for-service component of Medicare (2001–2016). We used Cox proportional hazards regression to examine associations between exposure to PM, airport-related ultrafine particles (aUFP) and gaseous pollutants and incidence of AD, other dementia, and ADRD in a minimally- and fully-adjusted model, considering 12 established ADRD risk factors. We conducted stratified analyses to examine associations by sex, and race/ethnicity.</div></div><div><h3>Results</h3><div>ADRD incidence was associated with PM<sub>2.5</sub> (per 2 µg/m<sup>3</sup>), airport-related UFP (aUFP, per 4400 particles/cm<sup>3</sup>) and nitrogen dioxide (NO<sub>2,</sub> per 10 µg/m<sup>3</sup>) with hazard ratios (HRs, 95%CI), respectively, of 1.04 (1.02–1.06), 1.03 (1.01–1.05) and 1.09 (1.06–1.12). The AD-associations with PM<sub>2.5</sub> and NO<sub>2,</sub> were stronger than the corresponding associations with other dementia (P<sub>heterogeneity</sub> ≤ 0.003). Similar patterns of results were observed by sex and across race and ethnicity. Statistically significant findings for ADRD with PM<sub>2.5,</sub> aUFP and NO<sub>2</sub> were observed among African American (respective HRs 1.03, 1.04, 1.09), and Latino and White participants for NO<sub>2</sub> (HR 1.10, 1.08). Results in all and African American participants remained statistically significant in fully-adjusted models. Although the effect of PM<sub>2.5</sub> was diluted in a co-pollutant with NO<sub>2</sub>, both PM<sub>2.5</sub> and aUFP were significantly associated with ADRD incidence in a co-pollutant model, and NO<sub>2</sub> and aUFP (but not PM<sub>2.5</sub>) remained associated in a multipollutant model. We did not observe consistent modifying effects for any of the 12 established ADRD risk factors.</div></div><div><h3>Conclusions</h3><div>In this multiethnic population, incidence of ADRD increased with exposures to PM<sub>2.5</sub>, aUFP, and NO<sub>2</sub> in all subjects and this pattern was most prominent among African American adults. These results emphasize that ADRD prevention should include not only individual-level factors but also population-wide policies and regulation to curb air pollution.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"209 ","pages":"Article 110169"},"PeriodicalIF":9.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147279736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-24DOI: 10.1016/j.envint.2026.110166
Feiyan Cao , Xinxin Feng , Yong Han , Yingjun Chen , Hongxing Jiang , Tian Chen , Yu Shang , Yu Peng , Zeyu Liu , Junjie Cai , Dan Li
Haze episodes pose substantial health risks to human-beings, yet the connections between the sources and chemical composition of fine particulate matter (PM2.5) and health effects remain inadequately understood. This study employed the high time-resolution (1-h) offline sampling and investigated the chemical characteristics and oxidative potential (OP) of the methanol-soluble organic matter (MSOM) in PM2.5 during three haze events in the North China Plain in 2020. The average volume-normalized and mass-normalized OP (OPv and OPm) during the three episodes (EP1-EP3) were 4.1 ± 1.6, 3.4 ± 1.2, 5.5 ± 1.9 pmol/min/m3, and 20.3 ± 4.9, 27.9 ± 6.7, 22.4 ± 5.3 pmol/min/μg, respectively. Positive matrix factorization model analysis revealed that the contributions of primary combustion (vehicle emission, biomass burning and coal combustion) accounted for ∼60% of total OPm, and the first- and secondary-generation aqueous-phase secondary organic aerosol formation processes (aqSOA I and aqSOA Ⅱ) contributed ∼36% of total OPm. The average OPm in nighttime showed higher values than that in daytime, with the nighttime OPm being predominantly influenced by primary emissions, whereas daytime SOA processes making a major contribution to OPm. Non-targeted screening based on Fourier-transform ion cyclotron resonance mass spectrometry (FT-ICR MS) analysis suggested that nitrogen-containing organic compounds were the dominant contributors to OPm (61%), especially those nitro-/oxygenated-condensed aromatics (Nitro-/O-ConA) and high-oxygen highly unsaturated compounds (HO-HUPC). By integrating the source information with molecular fingerprinting, we find that nitro- ConA were key toxic components in primary emissions, whereas secondary sources were enriched with HO-HUPC. Overall, our results improved the molecular-level understanding of the sources and evolution of key toxic components during haze events.
{"title":"Dynamic oxidative potential of organic matter and their source-specific key toxicants during haze episodes in North China","authors":"Feiyan Cao , Xinxin Feng , Yong Han , Yingjun Chen , Hongxing Jiang , Tian Chen , Yu Shang , Yu Peng , Zeyu Liu , Junjie Cai , Dan Li","doi":"10.1016/j.envint.2026.110166","DOIUrl":"10.1016/j.envint.2026.110166","url":null,"abstract":"<div><div>Haze episodes pose substantial health risks to human-beings, yet the connections between the sources and chemical composition of fine particulate matter (PM<sub>2.5</sub>) and health effects remain inadequately understood. This study employed the high time-resolution (1-h) offline sampling and investigated the chemical characteristics and oxidative potential (OP) of the methanol-soluble organic matter (MSOM) in PM<sub>2.5</sub> during three haze events in the North China Plain in 2020. The average volume-normalized and mass-normalized OP (OP<sub>v</sub> and OP<sub>m</sub>) during the three episodes (EP1-EP3) were 4.1 ± 1.6, 3.4 ± 1.2, 5.5 ± 1.9 pmol/min/m<sup>3</sup>, and 20.3 ± 4.9, 27.9 ± 6.7, 22.4 ± 5.3 pmol/min/μg, respectively. Positive matrix factorization model analysis revealed that the contributions of primary combustion (vehicle emission, biomass burning and coal combustion) accounted for ∼60% of total OP<sub>m</sub>, and the first- and secondary-generation aqueous-phase secondary organic aerosol formation processes (aqSOA I and aqSOA Ⅱ) contributed ∼36% of total OP<sub>m</sub>. The average OP<sub>m</sub> in nighttime showed higher values than that in daytime, with the nighttime OP<sub>m</sub> being predominantly influenced by primary emissions, whereas daytime SOA processes making a major contribution to OP<sub>m</sub>. Non-targeted screening based on Fourier-transform ion cyclotron resonance mass spectrometry (FT-ICR MS) analysis suggested that nitrogen-containing organic compounds were the dominant contributors to OPm (61%), especially those nitro-/oxygenated-condensed aromatics (Nitro-/O-ConA) and high-oxygen highly unsaturated compounds (HO-HUPC). By integrating the source information with molecular fingerprinting, we find that nitro- ConA were key toxic components in primary emissions, whereas secondary sources were enriched with HO-HUPC. Overall, our results improved the molecular-level understanding of the sources and evolution of key toxic components during haze events.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"209 ","pages":"Article 110166"},"PeriodicalIF":9.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147319812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-13DOI: 10.1016/j.envint.2026.110068
Amanda J. Goodrich , Deborah H. Bennett , Michael J. Kleeman , Daniel J. Tancredi , Yunin J. Ludeña , Irva Hertz-Picciotto , Rebecca J. Schmidt
Background
Particulate matter (PM) composition varies by source components and size. While studies show prenatal and early life exposure to total PM2.5 mass to be associated with autism spectrum disorder (ASD), little is known about the role of ultrafine (PM0.1) and fine PM specific components, especially PM0.1.
Objectives
We investigated associations between prenatal and early life exposure to size-resolved PM components and ASD in the CHARGE case–control study.
Methods
We analyzed 1,281 children (751 ASD, 530 typically developing) from the CHARGE study (enrolled 2003–2020). Daily PM0.1 and PM2.5 component concentrations were estimated using a chemical transport model with 4- or 24-km km resolution (for 95% and 5% of addresses, respectively) and bias correction. Daily exposures were averaged over preconception, pregnancy, and the first year of life, and log transformed. Using logistic regression, we estimated PM0.1 odds ratios (ORs) for ASD per interquartile range (IQR) increase in each component, adjusting for confounders, PM2.5 remainder, and NO2.
Results
First-year PM0.1 iron, manganese, black carbon, and sodium were consistently associated with increased odds of ASD (OR (95% CI): 1.60 (1.21, 2.12), 1.27 (1.04, 1.55), 1.54 (1.00, 2.38), and 1.92 (1.24, 2.99), respectively). Similar results were observed with first-year PM0.1-2.5 iron and manganese (OR (95% CI): 1.54 (1.13, 2.09) and 1.46 (1.07, 2.01), respectively).
Discussion
Our findings suggest that exposure to specific PM components during early life, especially in the ultrafine fraction, contribute to ASD risk, with less consistent evidence for prenatal exposures, underscoring the importance of particle composition and exposure timing.
{"title":"Fine and ultrafine particulate matter components and autism spectrum disorder (ASD)","authors":"Amanda J. Goodrich , Deborah H. Bennett , Michael J. Kleeman , Daniel J. Tancredi , Yunin J. Ludeña , Irva Hertz-Picciotto , Rebecca J. Schmidt","doi":"10.1016/j.envint.2026.110068","DOIUrl":"10.1016/j.envint.2026.110068","url":null,"abstract":"<div><h3>Background</h3><div>Particulate matter (PM) composition varies by source components and size. While studies show prenatal and early life exposure to total PM<sub>2.5</sub> mass to be associated with autism spectrum disorder (ASD), little is known about the role of ultrafine (PM<sub>0.1</sub>) and fine PM specific components, especially PM<sub>0.1</sub>.</div></div><div><h3>Objectives</h3><div>We investigated associations between prenatal and early life exposure to size-resolved PM components and ASD in the CHARGE case–control study.</div></div><div><h3>Methods</h3><div>We analyzed 1,281 children (751 ASD, 530 typically developing) from the CHARGE study (enrolled 2003–2020). Daily PM<sub>0.1</sub> and PM<sub>2.5</sub> component concentrations were estimated using a chemical transport model with 4- or 24-km km resolution (for 95% and 5% of addresses, respectively) and bias correction. Daily exposures were averaged over preconception, pregnancy, and the first year of life, and log transformed. Using logistic regression, we estimated PM<sub>0.1</sub> odds ratios (ORs) for ASD per interquartile range (IQR) increase in each component, adjusting for confounders, PM<sub>2.5</sub> remainder, and NO<sub>2</sub>.</div></div><div><h3>Results</h3><div>First-year PM<sub>0.1</sub> iron, manganese, black carbon, and sodium were consistently associated with increased odds of ASD (OR (95% CI): 1.60 (1.21, 2.12), 1.27 (1.04, 1.55), 1.54 (1.00, 2.38), and 1.92 (1.24, 2.99), respectively). Similar results were observed with first-year PM<sub>0.1-2.5</sub> iron and manganese (OR (95% CI): 1.54 (1.13, 2.09) and 1.46 (1.07, 2.01), respectively).</div></div><div><h3>Discussion</h3><div>Our findings suggest that exposure to specific PM components during early life, especially in the ultrafine fraction, contribute to ASD risk, with less consistent evidence for prenatal exposures, underscoring the importance of particle composition and exposure timing.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110068"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145962754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-01-21DOI: 10.1016/j.envint.2026.110096
D. Lopez-Rodriguez , G. Guerrero-Limón , N. Chèvre
With over 350,000 chemicals and mixtures currently registered for production and use worldwide, around 83% of authorized chemicals lack adequate toxicity data, leaving the majority of chemicals poorly characterized. International agencies urge scientists to develop screening methods to explore, identify, and predict chemical hazards, supporting the prioritization of chemical risk assessment. Here, Tree Manifold Approximation and Projection (TMAP) were applied, with the aim of reducing the dimensionality of large toxicological dataset, providing the foundations to data imputation methods allowing to get an understanding of chemical modes of action. Specifically, TMAP was implemented using MHFP6 fingerprints and the NORMAN SusDat database, which contains over 100,000 compounds. To ensure that the TMAP layout preserves chemical structural similarity, a quantitative parameter optimization procedure was developed. The defined optimal parameter set allowed us to define the embeddings that preserves the most structural similarity among nearest connected neighbors, with similarity progressively decreasing as the distance between nodes increases. Leveraging this approach, a graph-based spatial imputation function was generated to obtain insights into the potential ecotoxicity mechanisms of data poor chemicals using physicochemical properties and CTD toxicogenomic data. The relevance and meaningfulness of TMAP chemical space was explored for Daphnia magna, Pimephales promelas and Algae. Chemical classes known to be structurally similar were found to be grouped together in the TMAP chemical space, while heterogeneous classes were found to be sparse. Data imputation allowed for the identification of known and potential chemical mechanisms of action. Indeed, acetylcholinesterase and transthyretin were confirmed as major mechanisms of action of organothiophosphate and brominated flame retardant toxicity in Daphnia magna and Pimephales promelas, respectively. Overall, transdisciplinary toxicological databases combined with TMAP, stand out as a computationally efficient and suitable method to explore and analyze large datasets, allowing for the inference of associations between chemical structures and chemical hazard identification and other potential applications of this hypotheses-generating tool.
{"title":"A chemical space model for the exploration of eco-toxicological data","authors":"D. Lopez-Rodriguez , G. Guerrero-Limón , N. Chèvre","doi":"10.1016/j.envint.2026.110096","DOIUrl":"10.1016/j.envint.2026.110096","url":null,"abstract":"<div><div>With over 350,000 chemicals and mixtures currently registered for production and use worldwide, around 83% of authorized chemicals lack adequate toxicity data, leaving the majority of chemicals poorly characterized. International agencies urge scientists to develop screening methods to explore, identify, and predict chemical hazards, supporting the prioritization of chemical risk assessment. Here, Tree Manifold Approximation and Projection (TMAP) were applied, with the aim of reducing the dimensionality of large toxicological dataset, providing the foundations to data imputation methods allowing to get an understanding of chemical modes of action. Specifically, TMAP was implemented using MHFP6 fingerprints and the NORMAN SusDat database, which contains over 100,000 compounds. To ensure that the TMAP layout preserves chemical structural similarity, a quantitative parameter optimization procedure was developed. The defined optimal parameter set allowed us to define the embeddings that preserves the most structural similarity among nearest connected neighbors, with similarity progressively decreasing as the distance between nodes increases. Leveraging this approach, a graph-based spatial imputation function was generated to obtain insights into the potential ecotoxicity mechanisms of data poor chemicals using physicochemical properties and CTD toxicogenomic data. The relevance and meaningfulness of TMAP chemical space was explored for <em>Daphnia magna</em>, <em>Pimephales promelas</em> and <em>Algae</em>. Chemical classes known to be structurally similar were found to be grouped together in the TMAP chemical space, while heterogeneous classes were found to be sparse. Data imputation allowed for the identification of known and potential chemical mechanisms of action. Indeed, acetylcholinesterase and transthyretin were confirmed as major mechanisms of action of organothiophosphate and brominated flame retardant toxicity in <em>Daphnia magna</em> and <em>Pimephales promelas</em>, respectively. Overall, transdisciplinary toxicological databases combined with TMAP, stand out as a computationally efficient and suitable method to explore and analyze large datasets, allowing for the inference of associations between chemical structures and chemical hazard identification and other potential applications of this hypotheses-generating tool.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110096"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146034186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-02-05DOI: 10.1016/j.envint.2026.110124
Bin Yang , Xiangkai Zhao , Mengqing Yan , Yangyang Jia , Zhiguang Gu , Xiaoyu Hao , Sihua Wang , Zhiheng Li , Xiangwei Zhao , Yongli Yang , Pengpeng Wang , Wei Wang
Benzene, toluene and xylenes (BTX) are common workplace volatile organic compounds, but evidence linking BTX exposure to biological aging is limited. We examined associations between urinary BTX metabolites and biological age acceleration, and explored biological plausibility using computational analyses (network toxicology and molecular docking). We enrolled 301 BTX-exposed workers and 741 unexposed controls (Henan, China, 2022–2023), and selected 301 matched controls using 1:1 propensity score matching. Biological age was estimated with the Klemera–Doubal method (KDM) from clinical biomarkers, and biological age acceleration (KDM-BA.Accel) was defined as biological age minus chronological age. Creatinine-adjusted urinary metabolites of benzene (S-phenylmercapturic acid [SPMA] and trans, trans-muconic acid [TTMA]), toluene (S-benzylmercapturic acid [SBMA]) and xylenes (2-methylhippuric acid [2MHA] and 3-/4-methylhippuric acids [3&4MHA]) were analyzed using generalized linear models, and mixture associations were assessed with Bayesian kernel machine regression (BKMR). In fully adjusted models, higher SPMA (β = 0.15, 95% CI: 0.07 to 0.24) and TTMA (β = 0.08, 95% CI: 0.01 to 0.14) were associated with higher KDM-BA.Accel, and xylene metabolites also showed positive associations. BKMR suggested a positive overall association of the BTX mixture with KDM-BA.Accel, with SPMA and TTMA contributing most prominently. Network toxicology prioritized eight hub genes (TP53, TNF, NFKB1, TGFB1, MAPK3, CTNNB1, FOS and JUN), and enrichment analyses were consistent with oxidative stress response, inflammatory signaling, and cell-cycle regulation pathways. Overall, higher urinary BTX metabolites, particularly benzene biomarkers SPMA and TTMA, was associated with higher biological age acceleration. Future work should include prospective cohorts with repeated biomonitoring and experimental studies to validate the associations and test the implicated mechanisms.
{"title":"Exposure to benzene, toluene and xylenes (BTX) and biological aging: epidemiological evidence from Chinese industrial workers and mechanistic insights","authors":"Bin Yang , Xiangkai Zhao , Mengqing Yan , Yangyang Jia , Zhiguang Gu , Xiaoyu Hao , Sihua Wang , Zhiheng Li , Xiangwei Zhao , Yongli Yang , Pengpeng Wang , Wei Wang","doi":"10.1016/j.envint.2026.110124","DOIUrl":"10.1016/j.envint.2026.110124","url":null,"abstract":"<div><div>Benzene, toluene and xylenes (BTX) are common workplace volatile organic compounds, but evidence linking BTX exposure to biological aging is limited. We examined associations between urinary BTX metabolites and biological age acceleration, and explored biological plausibility using computational analyses (network toxicology and molecular docking). We enrolled 301 BTX-exposed workers and 741 unexposed controls (Henan, China, 2022–2023), and selected 301 matched controls using 1:1 propensity score matching. Biological age was estimated with the Klemera–Doubal method (KDM) from clinical biomarkers, and biological age acceleration (KDM-BA.Accel) was defined as biological age minus chronological age. Creatinine-adjusted urinary metabolites of benzene (S-phenylmercapturic acid [SPMA] and trans, <em>trans</em>-muconic acid [TTMA]), toluene (S-benzylmercapturic acid [SBMA]) and xylenes (2-methylhippuric acid [2MHA] and 3-/4-methylhippuric acids [3&4MHA]) were analyzed using generalized linear models, and mixture associations were assessed with Bayesian kernel machine regression (BKMR). In fully adjusted models, higher SPMA (β = 0.15, 95% CI: 0.07 to 0.24) and TTMA (β = 0.08, 95% CI: 0.01 to 0.14) were associated with higher KDM-BA.Accel, and xylene metabolites also showed positive associations. BKMR suggested a positive overall association of the BTX mixture with KDM-BA.Accel, with SPMA and TTMA contributing most prominently. Network toxicology prioritized eight hub genes (<em>TP53</em>, <em>TNF</em>, <em>NFKB1</em>, <em>TGFB1</em>, <em>MAPK3</em>, <em>CTNNB1</em>, <em>FOS</em> and <em>JUN</em>), and enrichment analyses were consistent with oxidative stress response, inflammatory signaling, and cell-cycle regulation pathways. Overall, higher urinary BTX metabolites, particularly benzene biomarkers SPMA and TTMA, was associated with higher biological age acceleration. Future work should include prospective cohorts with repeated biomonitoring and experimental studies to validate the associations and test the implicated mechanisms.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110124"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146184845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2026-02-10DOI: 10.1016/j.envint.2026.110142
Yannan Li, Blesson Mathew Varghese, Olga Anikeeva, Jingwen Liu, Peng Bi
Background
High temperature is a well-documented public health threat affecting people of all age groups. While occupational studies have assessed heat impacts on workers, the broader health effects on the working-age population remain underexplored. This study systematically reviewed and quantified the health effects of high temperatures and heatwaves among working-age adults.
Method
Systematic searches were conducted in PubMed, Scopus, and Embase for peer-reviewed epidemiological studies published up to January 2025. Eligible studies examined the effects of high temperatures and heatwaves on all-cause and cause-specific morbidity and mortality in individuals aged 15–64 years. A random-effects meta-analysis was performed to pool relative risks (RRs) per 1°C increase in temperature and across heatwave intensities. The study protocol was registered with PROSPERO (CRD42024528637).
Findings
Of 4,755 identified studies, 165 met the inclusion criteria, with 138 eligible for meta-analysis. A 1°C increase in heat exposure was associated with a 2.3% increase in morbidity (RR 1.023 [95% CI 1.019–1.027], I2 = 99.7%) and a 1.6% increase in mortality (RR 1.016 [95% CI 1.013–1.018], I2 = 78.9%) among working-age adults. The risk of morbidity and mortality associated with rising temperatures was greater in lower-income countries. Heatwaves also significantly affected health among working-age adults, with a 5.3% increase in morbidity (RR 1.053 [95% CI 1.042–1.064], I2 = 90.7%) and a 3.8% increase in mortality (RR 1.038 [95% CI 1.020–1.057], I2 = 57.7%). The greatest risk of morbidity was observed during middle-intensity heatwaves, while the highest risk of mortality was found during high-intensity heatwaves. The risk of morbidity from heat-related illnesses and genitourinary disorders showed the strongest associations with rising temperatures and heatwaves.
Interpretation
High temperatures and heatwaves significantly increase morbidity and mortality among working-age adults (15–64 years), particularly due to occupational and environmental factors. Greater risks were observed in humid subtropical and Mediterranean climates, with notable increases in heat-related illnesses and genitourinary disorders. These findings highlight the need for broader heat vulnerability assessments and inclusive prevention strategies beyond workplace settings.
高温是一个有据可查的公共卫生威胁，影响所有年龄组的人。虽然职业研究已经评估了高温对工人的影响，但对工作年龄人口的更广泛的健康影响仍未得到充分探讨。本研究系统地回顾和量化了高温和热浪对工作年龄成年人健康的影响。方法系统检索PubMed、Scopus和Embase中截至2025年1月发表的同行评议流行病学研究。符合条件的研究检查了高温和热浪对15-64岁个体的全因和病因特异性发病率和死亡率的影响。进行了随机效应荟萃分析，以汇总温度每升高1°C和热浪强度的相对风险（rr）。研究方案已在PROSPERO注册（CRD42024528637）。在4755项研究中，165项符合纳入标准，138项符合meta分析。在工作年龄的成年人中，热暴露每增加1°C，发病率增加2.3% (RR 1.023 [95% CI 1.019-1.027], I2 = 99.7%)，死亡率增加1.6% （RR 1.016 [95% CI 1.013-1.018], I2 = 78.9%）。在低收入国家，与气温上升相关的发病和死亡风险更大。热浪也显著影响工作年龄成年人的健康，发病率增加5.3% (RR 1.053 [95% CI 1.042-1.064], I2 = 90.7%)，死亡率增加3.8% （RR 1.038 [95% CI 1.020-1.057], I2 = 57.7%）。在中等强度热浪期间观察到的发病率风险最大，而在高强度热浪期间发现的死亡率风险最高。与热有关的疾病和泌尿生殖系统疾病的发病率与气温上升和热浪的关系最为密切。高温和热浪显著增加了工作年龄成年人（15-64岁）的发病率和死亡率，特别是由于职业和环境因素。在潮湿的亚热带和地中海气候中观察到更大的风险，与热有关的疾病和泌尿生殖系统疾病显著增加。这些发现强调了在工作场所之外进行更广泛的热脆弱性评估和包容性预防策略的必要性。
{"title":"The impact of high temperatures and heatwaves on health outcomes among working-age adults (15–64 years): a systematic review and meta-analysis","authors":"Yannan Li, Blesson Mathew Varghese, Olga Anikeeva, Jingwen Liu, Peng Bi","doi":"10.1016/j.envint.2026.110142","DOIUrl":"10.1016/j.envint.2026.110142","url":null,"abstract":"<div><h3>Background</h3><div>High temperature is a well-documented public health threat affecting people of all age groups. While occupational studies have assessed heat impacts on workers, the broader health effects on the working-age population remain underexplored. This study systematically reviewed and quantified the health effects of high temperatures and heatwaves among working-age adults.</div></div><div><h3>Method</h3><div>Systematic searches were conducted in PubMed, Scopus, and Embase for peer-reviewed epidemiological studies published up to January 2025. Eligible studies examined the effects of high temperatures and heatwaves on all-cause and cause-specific morbidity and mortality in individuals aged 15–64 years. A random-effects <em>meta</em>-analysis was performed to pool relative risks (RRs) per 1°C increase in temperature and across heatwave intensities. The study protocol was registered with PROSPERO (CRD42024528637).</div></div><div><h3>Findings</h3><div>Of 4,755 identified studies, 165 met the inclusion criteria, with 138 eligible for <em>meta</em>-analysis. A 1°C increase in heat exposure was associated with a 2.3% increase in morbidity (RR 1.023 [95% CI 1.019–1.027], I<sup>2</sup> = 99.7%) and a 1.6% increase in mortality (RR 1.016 [95% CI 1.013–1.018], I<sup>2</sup> = 78.9%) among working-age adults. The risk of morbidity and mortality associated with rising temperatures was greater in lower-income countries. Heatwaves also significantly affected health among working-age adults, with a 5.3% increase in morbidity (RR 1.053 [95% CI 1.042–1.064], I<sup>2</sup> = 90.7%) and a 3.8% increase in mortality (RR 1.038 [95% CI 1.020–1.057], I<sup>2</sup> = 57.7%). The greatest risk of morbidity was observed during middle-intensity heatwaves, while the highest risk of mortality was found during high-intensity heatwaves. The risk of morbidity from heat-related illnesses and genitourinary disorders showed the strongest associations with rising temperatures and heatwaves.</div></div><div><h3>Interpretation</h3><div>High temperatures and heatwaves significantly increase morbidity and mortality among working-age adults (15–64 years), particularly due to occupational and environmental factors. Greater risks were observed in humid subtropical and Mediterranean climates, with notable increases in heat-related illnesses and genitourinary disorders. These findings highlight the need for broader heat vulnerability assessments and inclusive prevention strategies beyond workplace settings.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110142"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146153212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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