{"title":"Dietary Patterns Modulate Ozone-Induced Reproductive Injury in C57BL/6J Mice","authors":"Yuzhi Guo, Shen Chen, Jiahao Zhang, Miao Li, Xinhang Jiang, Yahan Yang, Lizhu Ye, Zhaohuan Gui, Guanghui Dong, Daochuan Li, Wen Chen","doi":"10.1021/envhealth.5c00865","DOIUrl":"https://doi.org/10.1021/envhealth.5c00865","url":null,"abstract":"<p>Dietary patterns orchestrate systemic metabolism andreproductivehealth, yet whether specific dietary patterns modulate susceptibilityto ozone-induced male reproductive toxicity and its intergenerationalconsequences remains unclear. Here, male C57BL/6J mice were fed adlibitum (AL), a 30% calorie-restricted diet (CR), or a 45% high-fatdiet (HFD), followed by ozone exposure (1 ppm, 4 h/day, 5 days/weekfor 3 months) to recapitulate real-world condition. We found thatozone exposure exacerbated reproductive injury under both CR and HFD,each diet perturbing metabolism through distinct pathways. Under CR,ozone further suppressed glycolysis, the TCA cycle, and amino acidmetabolism, resulting in severe testicular energy depletion and impairedspermatogenic differentiation. In contrast, HFD amplified ozone-inducedmetabolic overload, inflammatory activation, and mitochondrial stress,accompanied by dysregulated lipid metabolism. Integrated metabolomicanalyses identified disruption of the glucose-lactate-TCA axis asa central mechanism underlying testicular energy failure. Furthermore,exposed males (F0) were subsequently mated with unexposed femalesto generate offspring (F1 and F2) for assessment of next-generationhealth risks. The results showed that paternal dietary regimen andozone exposure exclusively perturbed metabolic homeostasis in F1 offspring,indicating a reversible metabolic reprogramming rather than stabletransgenerational inheritance. Collectively, these findings establishsystemic metabolic status as a critical determinant of ozone-inducedreproductive toxicity and reveal that paternal nutritional and environmentalchallenges jointly prime metabolic susceptibility in the next generation(F1).</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2219–2231"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environment & HealthPub Date : 2026-10-16Epub Date: 2026-06-02DOI: 10.1021/envhealth.5c00676
Zijun Li, Xingyao Tang, Xueyan Han, Sinan Wu, Zhaoyang Pan, Linhong Pang, Hailu Zhu, Yicong Wang, Qi Wang, Xinran Shan, Ting Yang, Jing Wei, Tianjia Guan, Ke Huang, Chen Wang, The China Pulmonary Health (CPH) Study Group
{"title":"Associations between Size-Specific Particulate Matter and Lung Function: Results from the China Pulmonary Health Study","authors":"Zijun Li, Xingyao Tang, Xueyan Han, Sinan Wu, Zhaoyang Pan, Linhong Pang, Hailu Zhu, Yicong Wang, Qi Wang, Xinran Shan, Ting Yang, Jing Wei, Tianjia Guan, Ke Huang, Chen Wang, The China Pulmonary Health (CPH) Study Group","doi":"10.1021/envhealth.5c00676","DOIUrl":"https://doi.org/10.1021/envhealth.5c00676","url":null,"abstract":"<p>Emergingevidence suggests that the respiratory health effectsof particulate matter (PM) may vary by aerodynamic diameter. However,comprehensive investigations comparing the effects of size-specificPM on lung function indicators remain limited. We analyzed lung functiondata from the China Pulmonary Health (CPH) Study to assess the associationsbetween long-term exposure to PM<sub>1</sub>, PM<sub>1–2.5</sub>, PM<sub>2.5</sub>, PM<sub>2.5–10</sub>, and PM<sub>10</sub> and indicators of large and small airway function using multivariablelinear models. This study included 50,991 adults aged 20 years andabove. For large airway function, each interquartile range (IQR) increasein PM<sub>1</sub>, PM<sub>1–2.5</sub>, PM<sub>2.5</sub>, andPM<sub>10</sub> was significantly associated with a decrease in FEV<sub>1</sub>, FVC, and FEV<sub>1</sub>/FVC. The associations between FEV<sub>1</sub> and FVC strengthened as the particle size decreased. PM<sub>1</sub> showed the strongest association, with the lowest FEV<sub>1</sub> (−36.84 mL, 95% confidence interval (CI): −45.91,−27.76 mL) and FVC (−34.63 mL, 95% CI: −45.48,−23.79 mL) values. For small airway function, all size-specificparticles were significantly associated with decreases in FEF<sub>75</sub> and FEF<sub>25–75</sub>. Specifically, each IQR increasein PM<sub>2.5–10</sub> exposure was associated with the largestreduction in the airway function indicators. Furthermore, stratifiedanalyses showed stronger adverse associations in vulnerable subpopulations,including females, older adults, former smokers, biomass nonusers,and participants with chronic obstructive pulmonary disease (COPD).Size-specific PM exposure has differential health effects on bothlarge and small airway lung function indicators. Therefore, it isessential to account for particle size in health risk assessmentsand the regulation of PM.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2232–2241"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environment & HealthPub Date : 2026-10-16Epub Date: 2026-09-24DOI: 10.1021/envhealth.6c00429
Lu Jiang, Qian Liu, Yawei Wang, Guibin Jiang
{"title":"Environmental Science at a Transformational Crossroads: Two Decades of the “National Conference on Environmental Chemistry” and the Future of New Pollutants Research","authors":"Lu Jiang, Qian Liu, Yawei Wang, Guibin Jiang","doi":"10.1021/envhealth.6c00429","DOIUrl":"https://doi.org/10.1021/envhealth.6c00429","url":null,"abstract":"<p>Environmental science is undergoing a critical transitionfrompollutant-specific and end-of-pipe control to systemic sustainabilityscience. The development trajectory of the Chinese “NationalConference on Environmental Chemistry (NCEC)” provides an empiricallens through which to examine this broader disciplinary transformation.This study analyzes how evolving governance demands, increasing environmentalcomplexity, and advances in analytical and computational technologieshave collectively reshaped research priorities, disciplinary boundaries,and modes of scientific collaboration. The emergence of new pollutantgovernance as a central frontier reflects the limitations of conventionalsingle-medium and single-pollutant regulatory frameworks. Persistent,low-dose, and mixture-prone contaminants highlight the need for integrativeapproaches that link molecular mechanisms with cross-media processesand system-level outcomes. While it also accelerating methodologicaladvances in non-target screening, computational prediction, systemstoxicology, and cross-media risk assessment. The NCEC experience furtherillustrates how scientific platforms can connect frontier research,interdisciplinary integration, resource mobilization, and science–policydialogue. Drawing on the NCEC, we provide an empirically groundedperspective on how environmental science should move beyond reactiveremediation toward anticipatory risk assessment, upstream prevention,sustainable chemical design, and system-level governance, offeringa broader framework for aligning research innovation with ecologicalresilience in global environmental governance.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2163–2171"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Long-Term Exposure to Ambient Air Pollution and Cervical Cancer Outcomes in Chinese Women: A Prospective Study on Recurrence and Mortality Risks","authors":"Yuanxin Lin, Junjun Qiu, Liwen Jiang, Shuqi Li, Yixuan Jiang, Lu Zhou, Kexin Yu, Bin Lv, Haidong Kan, Jing Cai, Keqin Hua","doi":"10.1021/envhealth.6c00011","DOIUrl":"https://doi.org/10.1021/envhealth.6c00011","url":null,"abstract":"<p>The impact of air pollution on the prognosis of cervicalcancer(CC) remains unclear. This study examined the associations of majorair pollutants on recurrence and mortality among CC patients. We enrolled3,758 women diagnosed with primary CC at the Obstetrics and GynecologyHospital of Fudan University between 2019 and 2022, following themannually until June 2024. Air pollution exposure was estimated usinghigh-resolution spatiotemporal models based on residential addresses.Weighted Cox proportional hazards models based on the Fine–Grayapproach were used to estimate the risk of recurrence, while stratifiedCox proportional hazards models were used to estimate the risk ofdeath, adjusting for demographic, clinical, and meteorological factors.Among the patients (median follow-up ∼ 3 years), 217 recurrences(5.8%) and 113 deaths (3.0%) occurred. Each interquartile range increasein fine particulate matter (PM<sub>2.5</sub>), inhalable particulatematter (PM<sub>10</sub>), nitrogen dioxide (NO<sub>2</sub>), and sulfurdioxide (SO<sub>2</sub>) was associated with elevated recurrence risk,with subdistribution hazard ratios (SHRs) of 1.93 (95% ConfidenceInterval (CI): 1.40–2.66), 1.65 (1.13–2.42), 1.60 (1.14–2.24),and 1.26 (1.07–1.48), respectively. Higher exposure to PM<sub>2.5</sub>, PM<sub>10</sub>, and NO<sub>2</sub> was also linked toincreased mortality risk, with hazard ratios (HRs) of 2.55 (95% CI:1.78–3.67), 2.21 (1.38–3.54), and 1.37 (1.03–1.84),respectively. No significant association was observed for ozone (O<sub>3</sub>). Exposure–response and sensitivity analyses supportedthese findings. This cohort study provides the first evidence thatlong-term exposure to air pollution after surgery is associated withincreased risks of recurrence and mortality in primary CC patients,highlighting it as a modifiable environmental determinant of CC prognosis.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2278–2288"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environment & HealthPub Date : 2026-10-16Epub Date: 2026-06-25DOI: 10.1021/envhealth.5c00818
Lu Zhou, Zhang Shi, Ye Yao, Xihao Du, Xinlei Zhu, Yixiang Zhu, Shuai Xu, Jiang Lin, Renjie Chen, He Wang, Haidong Kan
{"title":"A Comprehensive Assessment of Physiological and Neural Changes Underlying Cognitive Performance after Heat Stress: A Randomized Clinical Trial","authors":"Lu Zhou, Zhang Shi, Ye Yao, Xihao Du, Xinlei Zhu, Yixiang Zhu, Shuai Xu, Jiang Lin, Renjie Chen, He Wang, Haidong Kan","doi":"10.1021/envhealth.5c00818","DOIUrl":"https://doi.org/10.1021/envhealth.5c00818","url":null,"abstract":"<p>Heat stress threatens neurological health as a risk factorforcognitive decline. However, deeper understanding of the psychological,cognitive, and neural changes induced by heat stress, with strongercausal inference and biological evidence, is needed. A randomized,crossover, controlled trial was conducted among 30 healthy adults(15 males, 15 females; mean age 21.5 ± 1.5 years) during October–November2022. Participants were randomly divided into two groups and alternatelyunderwent 2-h exposures to high temperature (32 °C) and moderatetemperature (22 °C) at a laboratory in Shanghai, China. Psychologicaldistress was evaluated using a simplified DASS-21 scale. Cognitivefunction was assessed through neurobehavioral tests (Schulte gridand Stroop tests), with neural activity examined using functionalmagnetic resonance imaging (fMRI) to assess blood oxygen level-dependentsignals. Blood samples were collected for plasma exosome transcriptomicsand targeted biomarker analyses. Acute heat exposure significantlyincreased psychological distress by 27.3%, decreased processing speedby 13.6%, and impaired response inhibition by 3.4%. Heat stress reducedneural activity and synchronization in the precentral gyrus, inferiorfrontal gyrus, and rostral hippocampus. Functional connectivity wasalso attenuated in these regions. These alterations might be drivenby type I interferon-dominated inflammation, excitotoxicity, and oxidativestress. Conversely, neural regulatory responses were observed, includingactivation of the lateral occipital cortex and elevated levels ofneurotrophic factors. This trial demonstrates the relationship betweenacute heat exposure and diminished cognitive function. These findingsunderscore the need for public health strategies to maintain indoortemperatures within a comfortable range and promote active coolingto protect cognitive health.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2312–2322"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149173521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environment & HealthPub Date : 2026-10-16Epub Date: 2026-07-15DOI: 10.1021/envhealth.5c00839
Can Wang, Bhaskar Sharma, Ruonan Peng, Xin Yong, Louis S. Santiago, Ke Du
{"title":"Shape-Dependent Interactions of Gold Nanoparticles with Microalgae: Distinct Cellular and Molecular Responses","authors":"Can Wang, Bhaskar Sharma, Ruonan Peng, Xin Yong, Louis S. Santiago, Ke Du","doi":"10.1021/envhealth.5c00839","DOIUrl":"https://doi.org/10.1021/envhealth.5c00839","url":null,"abstract":"<p>The ecotoxicological effects of engineered nanoparticlesin aquaticenvironments are influenced not only by composition and size but alsoby particle morphology, yet shape-dependent interactions with primaryproducers remain poorly understood. In this study, we evaluated thecellular and molecular responses of freshwater algae (<em>Chlamydomonas reinhardtii</em>) following exposure to100 nm silica-coated gold nanospheres (AuNPs) and nanostars (AuNSs)across multiple concentrations. Exposure to 10 mg/L AuNSs for 72 hresults in significantly stronger inhibition of algal growth and photosyntheticactivity compared to the same concentration of AuNPs. Morphometricprofiling reveals that AuNSs induce pronounced structural injury,including cell enlargement, debris production, and disruption of subcellularorganization, more than AuNPs. Confocal imaging suggested that thisheightened toxicity may stem from two distinct internalization patterns:AuNPs primarily adhered to chloroplast surfaces, whereas AuNSs causedmore extensive membrane disruption and were observed deeper withinintracellular compartments. RNA sequencing identified 9 upregulatedand 38 downregulated differentially expressed genes (DEGs) in the10 mg/L AuNP-treated cells, impairing photosynthesis and energy storagevia the photosystem II subunit S1 (PSBS1)/early light-inducible protein(ELI3) pathway. In contrast, the AuNS group exhibits 246 upregulatedand 145 downregulated DEGs, affecting membrane integrity and nitrogenmetabolism through the nitrate reductase (NIT1)/aminomethyl transferase(AMT1)/protein kinase domain-containing protein (A0A2K3CRU5) pathway.These results demonstrate that the nanoparticle morphology can drivedivergent toxicity mechanisms in algal cells. Our findings highlightthe necessity of incorporating NP morphology into environmental riskassessments and suggest that safer nanomaterial design should considershape-dependent interactions with aquatic microorganisms.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2416–2430"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environment & HealthPub Date : 2026-10-16Epub Date: 2026-06-03DOI: 10.1021/envhealth.6c00080
Natong Liu, Zhongshuo Ma, Xiao Sun, Liyan Zhao, Jie Zhang, Nan Zhang, Xue Liang
{"title":"IL-17 Signaling Pathway: A Potential Signaling Pathway Mediating Neuroinflammation Induced by PM2.5","authors":"Natong Liu, Zhongshuo Ma, Xiao Sun, Liyan Zhao, Jie Zhang, Nan Zhang, Xue Liang","doi":"10.1021/envhealth.6c00080","DOIUrl":"https://doi.org/10.1021/envhealth.6c00080","url":null,"abstract":"<p>Particulate Matter 2.5 (PM<sub>2.5</sub>) in the atmospherecaninvade the central nervous system (CNS) and induce neurotoxicity,yet the mechanism is not well understood. In this study, the viabilityof microglia was significantly reduced by PM<sub>2.5</sub>, and thealteration of several inflammatory factors indicated an inflammatoryresponse in BV2 cells caused by PM<sub>2.5</sub>. Differentially expressedgenes (DEGs) were then screened by a microarray assay. These DEGswere mainly enriched in terms associated with inflammatory reactionsthrough Gene Ontology (GO) annotation. Additionally, the Kyoto Encyclopediaof Genes and Genomes (KEGG) analysis indicated that these DEGs wereprimarily enriched in IL-17 along with its downstream NF-κBand MAPK signaling pathways. Furthermore, the adverse impacts of PM<sub>2.5</sub> exposure were effectively alleviated by the IL-17 signalingpathway inhibitor aIL17A, including improvements in the behavioralbarrier, suppression of IL-17 activation and its downstream NF-κBand MAPK signaling pathways, reduced excessive secretion of inflammationcytokines, and decreased microglial activation. Combining all theseresults, PM<sub>2.5</sub> was found to activate IL-17 along with itsdownstream NF-κB and MAPK signaling pathways, triggering microglialactivation and neuroinflammation, ultimately leading to neurobehavioralimpairments. Overall, the IL-17 signaling pathway may be a potentialtherapeutic target for PM<sub>2.5</sub>-induced neurotoxicity, whichwill contribute to related research in the future.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2242–2252"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environment & HealthPub Date : 2026-10-16Epub Date: 2026-06-03DOI: 10.1021/envhealth.6c00026
Siyi Wang, Xianghui Wang, Kailun Wang, Shi Tang, Xia Sheng, Shunqing Xu, Yahang Lin, Mingxi Zhang, Fengzhen Cui
{"title":"Single-Cell Transcriptomic Profiling of Human Blood Vessel Organoids Exposed to 6-Chloronicotinic Acid","authors":"Siyi Wang, Xianghui Wang, Kailun Wang, Shi Tang, Xia Sheng, Shunqing Xu, Yahang Lin, Mingxi Zhang, Fengzhen Cui","doi":"10.1021/envhealth.6c00026","DOIUrl":"https://doi.org/10.1021/envhealth.6c00026","url":null,"abstract":"<p>6-Chloronicotinic acid (6-ClNA) is a major metaboliteof chloropyridinylneonicotinoids in humans; however, its toxic effect on blood vesseldevelopment remains to be understood. In this study, we utilized ahumanized blood vessel organoid (hBVO) model and single-cell transcriptomicstechnology to investigate the impact of 6-ClNA exposure on hBVO development.Morphologically, 6-ClNA did not significantly alter the growth ofhBVO throughout 20 days of culture. Interestingly, single-cell transcriptomicanalyses revealed that 6-ClNA-treated hBVOs exhibited significantimbalance in cell subpopulation homeostasis, including impaired endothelialcell function and abnormal proliferation of vascular smooth musclecells. This was echoed by the morphological changes in the aorticarch and abdominal aorta of mice after acute exposure to 6-ClNA. Enrichmentanalysis showed that 6-ClNA exposure affected critical biologicalprocesses in a cell-type-specific manner, such as vascular developmentalsignaling, cellular energy metabolism, protein homeostasis, and hemodynamicresponses. In addition, trajectory analysis suggested that 6-ClNAaltered the differentiation trajectory of vascular progenitors. Together,our study profiles the toxicity of 6-ClNA on blood vessel developmentin a humanized 3D model at single-cell resolution, which providesimportant and detailed evidence for understanding the potential riskof early life exposure to chloropyridinyl neonicotinoids.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2253–2268"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Environment & HealthPub Date : 2026-10-16Epub Date: 2026-06-27DOI: 10.1021/envhealth.5c00779
Yihui Ge, Yi Zhang, Jiawen Liao, Yan Lin, Zhenchun Yang, Kiros Berhane, Zhipeng Bai, Bin Han, Jia Xu, Frank Gilliland, Zhanghua Chen, Weili Yan, Guoying Huang, Junfeng Jim Zhang
{"title":"Preconception Folic Acid Supplementation Associated with Attenuated Effects of Air Pollution on Birthweight Outcomes","authors":"Yihui Ge, Yi Zhang, Jiawen Liao, Yan Lin, Zhenchun Yang, Kiros Berhane, Zhipeng Bai, Bin Han, Jia Xu, Frank Gilliland, Zhanghua Chen, Weili Yan, Guoying Huang, Junfeng Jim Zhang","doi":"10.1021/envhealth.5c00779","DOIUrl":"https://doi.org/10.1021/envhealth.5c00779","url":null,"abstract":"<p>Gestational exposure to ambient air pollution has beenlinked toadverse birth outcomes. Folic acid (FA) supplementation supports fetaldevelopment, but the optimal timing for protective effects remainsuncertain. This study aims to determine whether maternal FA supplementationprior to conception modifies the association between gestational airpollution exposure and birthweight-related outcomes in a populationwhere most women also took FA during pregnancy. We analyzed data from10,579 mother–child pairs from a preconception cohort in Shanghai,China. Ambient concentrations of PM<sub>2.5</sub>, PM<sub>10</sub>, NO<sub>2</sub>, and ozone were estimated at a residential levelusing spatiotemporal models for the preconception period and eachtrimester. We assessed whether preconception FA supplementation modifiedthe association between air pollution exposure and birth outcomes,including birthweight, birthweight <em>Z</em>-score, small-for-gestationalage (SGA), and low birthweight (LBW). Linear and logistic regressionmodels with interaction terms, as well as stratified analyses by FAsupplementation status, were applied. Children’s sex-specificassociations were also explored. Significant interactions betweenpreconception FA supplementation and air pollution exposures wereobserved for birthweight and SGA. A 10 μg/m<sup>3</sup> increasein PM<sub>2.5</sub> exposure during pregnancy was associated witha −62.8 g (95% CI: −97.0, −28.6) change in birthweightand a 1.78 (95% CI: 1.16, 2.73) odds ratio for SGA among women withoutpreconception FA supplementation. No such significant associationswere found among women receiving preconception FA supplementation,with an estimated change of −1.7 g in birthweight (95% CI:−65.7 to 62.4) and an odds ratio of 0.70 for SGA (95% CI: 0.32–1.44).The protective effect appeared more pronounced for male infants thanfemales. Maternal preconception FA supplementation can attenuate theadverse effects of gestational air pollution exposure on birthweightand SGA risk in women who also received FA supplementation duringpregnancy. These findings support the importance of incorporatingpreconception FA supplementation as a protective measure against gestationalexposure to air pollution.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2323–2332"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}