Pub Date : 2026-03-01Epub Date: 2025-12-20DOI: 10.1016/j.heha.2025.100163
Ziyi Zhang , Nan Li , Zeping Yang , Ming Jin , Xiaojing Liu , Yanyan Zhang , Nan Lin , Zhiwen Li , Lili Zhuang , Hongchu Bao , Ran Zhao , Bin Wang
Per- and polyfluoroalkyl substances (PFASs) can interfere with the endocrine and central nervous systems, and may further disrupt sleep quality. To address this concern, we investigated the association between the whole-blood levels of several PFASs and insomnia. A total of 394 female adults were recruited and 30 PFASs were measured. Multivariate logistic regression models were employed to test the individual associations between the level of each component and insomnia. Quantile-based g-computation and Bayesian kernel machine regression models were used to estimate whether co-exposure to PFASs increased the risk of insomnia. The individual exposure analyses revealed that the levels of perfluorodecanoic acid [odds ratio (OR) = 1.22, 95 % confidence interval (CI): 1.03, 1.45)], perfluoroundecanoic acid [OR = 1.59 (95 % CI: 1.02, 2.47)], perfluorononanoic acid [OR = 2.20 (95 % CI: 1.15, 4.21)], and 6:2 chlorinated polyfluorinated ether sulfonate [OR for quartile 2 (Q2) = 2.07 (95 % CI: 1.10, 3.88), OR for Q4 = 2.27 (95 % CI: 1.17, 4.42)] were positively associated with the risk of insomnia. Our findings nonetheless suggest that reducing exposure to such substances would probably lower the risk of insomnia in adults.
{"title":"Potential effect of co-exposure to Per- and polyfluoroalkyl substances on the risk of insomnia","authors":"Ziyi Zhang , Nan Li , Zeping Yang , Ming Jin , Xiaojing Liu , Yanyan Zhang , Nan Lin , Zhiwen Li , Lili Zhuang , Hongchu Bao , Ran Zhao , Bin Wang","doi":"10.1016/j.heha.2025.100163","DOIUrl":"10.1016/j.heha.2025.100163","url":null,"abstract":"<div><div>Per- and polyfluoroalkyl substances (PFASs) can interfere with the endocrine and central nervous systems, and may further disrupt sleep quality. To address this concern, we investigated the association between the whole-blood levels of several PFASs and insomnia. A total of 394 female adults were recruited and 30 PFASs were measured. Multivariate logistic regression models were employed to test the individual associations between the level of each component and insomnia. Quantile-based g-computation and Bayesian kernel machine regression models were used to estimate whether co-exposure to PFASs increased the risk of insomnia. The individual exposure analyses revealed that the levels of perfluorodecanoic acid [odds ratio (OR) = 1.22, 95 % confidence interval (CI): 1.03, 1.45)], perfluoroundecanoic acid [OR = 1.59 (95 % CI: 1.02, 2.47)], perfluorononanoic acid [OR = 2.20 (95 % CI: 1.15, 4.21)], and 6:2 chlorinated polyfluorinated ether sulfonate [OR for quartile 2 (Q2) = 2.07 (95 % CI: 1.10, 3.88), OR for Q4 = 2.27 (95 % CI: 1.17, 4.42)] were positively associated with the risk of insomnia. Our findings nonetheless suggest that reducing exposure to such substances would probably lower the risk of insomnia in adults.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100163"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927215","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}
Pub Date : 2026-03-01Epub Date: 2026-01-05DOI: 10.1016/j.heha.2026.100168
Randy T. Tangang , Yineng Chen , Junrong Ma , Samantha Friedman , Imran Hossain Mithu , Zhongguo Huang , Najm Alsadat Madani , Bennett Gayle DeeDee , Xiaobo X Romeiko , Shao Lin
Background
With increasing environmental disparities and understudied older adult populations, our study aims to evaluate whether older adults and subgroups are more likely to live in communities with higher environmental hazards.
Methods
Using 2014–2019 data from the American Community Survey, we identified census county subdivisions with elevated proportions (≥ 75%) of four subgroups: adults aged ≥ 65 years, older adults living alone, older adults below the poverty line, and Black older adults, while comparing them with other groups. We integrated data for extreme weather and several air pollutants (UFP, PM₂.₅, O₃, SO₂, NH₃, NO2, and CO), as well as the Disaster Risk Index derived from FEMA, using the 75th percentile as the cutoff point for these exposures. We then applied a multivariate mixed-effects logistic regression to examine exposure disparities.
Results
Older adults living alone resided in areas with greater vulnerability to disaster (P < 0.001). Additionally, poor older adults were more likely to live in areas with multiple environmental hazards, including higher levels of UFP (OR: 1.89, 95% CI: 1.11–3.21) and SO2 (OR: 1.68, 95% CI: 1.04–2.70), 5–8 extreme events (OR=3.1, 95% CI: 1.90–5.12), as well as significant overall disaster risk index. Furthermore, areas with a higher % of Black older adults faced more environmental hazards, such as a higher likelihood of living in communities with high levels of extreme heat (OR: 4.08; 95% CI: 1.69–9.86), high PM₂.₅ (OR: 2.69; 95% CI: 1.43–5.05), and UFP (OR: 2.1; 95% CI: 1.26–3.49), as well as multiple extreme events (OR=2.18, 95%CI: 1.36–3.64 for 1–4 events; OR=14.83, 95%CI: 8.54–26.77 for 5–8 events).
Conclusion
We conclude that poor or Black older adults, face significantly greater exposure to multiple environmental hazards, extreme weather events, and disaster vulnerabilities – compared to other subgroups.
{"title":"Environmental health disparities among elderly population in New York State","authors":"Randy T. Tangang , Yineng Chen , Junrong Ma , Samantha Friedman , Imran Hossain Mithu , Zhongguo Huang , Najm Alsadat Madani , Bennett Gayle DeeDee , Xiaobo X Romeiko , Shao Lin","doi":"10.1016/j.heha.2026.100168","DOIUrl":"10.1016/j.heha.2026.100168","url":null,"abstract":"<div><h3>Background</h3><div>With increasing environmental disparities and understudied older adult populations, our study aims to evaluate whether older adults and subgroups are more likely to live in communities with higher environmental hazards.</div></div><div><h3>Methods</h3><div>Using 2014–2019 data from the American Community Survey, we identified census county subdivisions with elevated proportions (≥ 75%) of four subgroups: adults aged ≥ 65 years, older adults living alone, older adults below the poverty line, and Black older adults, while comparing them with other groups. We integrated data for extreme weather and several air pollutants (UFP, PM₂.₅, O₃, SO₂, NH₃, NO<sub>2,</sub> and CO), as well as the Disaster Risk Index derived from FEMA, using the 75th percentile as the cutoff point for these exposures. We then applied a multivariate mixed-effects logistic regression to examine exposure disparities.</div></div><div><h3>Results</h3><div>Older adults living alone resided in areas with greater vulnerability to disaster (<em>P</em> < 0.001). Additionally, poor older adults were more likely to live in areas with multiple environmental hazards, including higher levels of UFP (OR: 1.89, 95% CI: 1.11–3.21) and SO<sub>2</sub> (OR: 1.68, 95% CI: 1.04–2.70), 5–8 extreme events (OR=3.1, 95% CI: 1.90–5.12), as well as significant overall disaster risk index. Furthermore, areas with a higher % of Black older adults faced more environmental hazards, such as a higher likelihood of living in communities with high levels of extreme heat (OR: 4.08; 95% CI: 1.69–9.86), high PM₂.₅ (OR: 2.69; 95% CI: 1.43–5.05), and UFP (OR: 2.1; 95% CI: 1.26–3.49), as well as multiple extreme events (OR=2.18, 95%CI: 1.36–3.64 for 1–4 events; OR=14.83, 95%CI: 8.54–26.77 for 5–8 events).</div></div><div><h3>Conclusion</h3><div>We conclude that poor or Black older adults, face significantly greater exposure to multiple environmental hazards, extreme weather events, and disaster vulnerabilities – compared to other subgroups.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100168"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978100","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}
Pub Date : 2026-03-01Epub Date: 2025-12-19DOI: 10.1016/j.heha.2025.100165
Senyuan Huang , Lei Fang , Shengbing Yu , Chaoyang Long , Yingxin Yu
Anthropogenic activities have exacerbated the environmental contamination of polycyclic aromatic hydrocarbons (PAHs) with adverse health effects on human health. In response, various human biomonitoring utilizing urine, hair, nails, breast milk or blood have been established to assess PAH exposure levels as alternatives to external exposure assessment, with monohydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) used as biomarkers. However, comprehensive summaries of internal exposure levels of OH-PAHs remain scarce, except for the urinary OH-PAHs in children. In this review, available studies on OH-PAHs in human biomatrices were synthesized to estimate the internal levels of PAH exposure along with health risks in populations worldwide. While the composition profiles of urinary OH-PAHs among countries were similar with OHNap as the predominant metabolite, variations among different human biomatrices were observed. Influencing factors such as gender, age, living environment, smoking, season, and occupation could affect OH-PAH levels. The carcinogenic risk posed by PAH exposure warranted greater attention than non-carcinogenic risk. Currently, significant gaps persist in human biomonitoring in South America and Africa particularly. Future research should conduct human biomonitoring of OH-PAHs frequently and refine health risk assessment to inform evidence-based regulatory decisions.
{"title":"Human internal exposure to polycyclic aromatic hydrocarbon: A global review of monohydroxylated metabolites and associated health risks","authors":"Senyuan Huang , Lei Fang , Shengbing Yu , Chaoyang Long , Yingxin Yu","doi":"10.1016/j.heha.2025.100165","DOIUrl":"10.1016/j.heha.2025.100165","url":null,"abstract":"<div><div>Anthropogenic activities have exacerbated the environmental contamination of polycyclic aromatic hydrocarbons (PAHs) with adverse health effects on human health. In response, various human biomonitoring utilizing urine, hair, nails, breast milk or blood have been established to assess PAH exposure levels as alternatives to external exposure assessment, with monohydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) used as biomarkers. However, comprehensive summaries of internal exposure levels of OH-PAHs remain scarce, except for the urinary OH-PAHs in children. In this review, available studies on OH-PAHs in human biomatrices were synthesized to estimate the internal levels of PAH exposure along with health risks in populations worldwide. While the composition profiles of urinary OH-PAHs among countries were similar with OH<img>Nap as the predominant metabolite, variations among different human biomatrices were observed. Influencing factors such as gender, age, living environment, smoking, season, and occupation could affect OH-PAH levels. The carcinogenic risk posed by PAH exposure warranted greater attention than non-carcinogenic risk. Currently, significant gaps persist in human biomonitoring in South America and Africa particularly. Future research should conduct human biomonitoring of OH-PAHs frequently and refine health risk assessment to inform evidence-based regulatory decisions.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100165"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927217","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}
Pub Date : 2026-03-01Epub Date: 2026-02-28DOI: 10.1016/j.heha.2026.100172
Chi-An Hsiao , Wen-Chin Lee , Wan-Ting Huang , Fu-Jen Cheng , Chia-Te Kung , Chien-Te Lee , Chin-Chou Wang , Kai-Fan Tsai , Liang-Jen Wang , Shau-Hsuan Li , Yu-Che Ou
Phthalate exposure can cause health hazards, including nephrotoxicity. However, the daily intake and adverse renal effects of phthalate exposure in patients with chronic kidney disease (CKD) remain unclear. Participants with non-dialysis-dependent CKD (i.e., not requiring long-term hemodialysis or peritoneal dialysis) stages 3–5 were enrolled in this one-year longitudinal investigation. We calculated the estimated daily intakes (EDIs) of five main phthalate compounds from their urinary biomonitoring data to evaluate the impact of phthalate exposure on urinary renal biomarkers reflecting oxidative damage and renal tubular injury. The overall urinary phthalate detection rate was 100% among 112 male and 57 female participants. Our analyses demonstrated that EDIs of di-(2-ethylhexyl) phthalate, diethyl phthalate (DEP), and dibutyl phthalate (DBP) independently correlated with the increases in kidney injury molecule-1 (β (95% confidence interval (CI)), 0.352 (0.193–0.512), 0.240 (0.135–0.345), and 0.312 (0.193–0.431) log ng/g creatinine per log ng/kg body weight/day of corresponding EDIs; p <0.001). Furthermore, the EDIs of DEP, dimethyl phthalate, and DBP were independently associated with the elevations in 8-hydroxy-2’-deoxyguanosine (β (95% CI), 0.278 (0.206–0.350), 0.509 (0.361–0.658), and 0.319 (0.215–0.423) log μg/g creatinine per log ng/kg body weight/day, respectively; p <0.001). The mediating role of oxidative damage in phthalate-associated renal tubular injury was also identified. Our study highlights the nephrotoxicity of phthalate exposure in patients with CKD and suggests that renal tubular injury and oxidative damage play crucial roles in phthalate-associated nephrotoxicity, which is underestimated using traditional renal surrogates.
{"title":"Associations between phthalate exposure and kidney injury in chronic kidney disease","authors":"Chi-An Hsiao , Wen-Chin Lee , Wan-Ting Huang , Fu-Jen Cheng , Chia-Te Kung , Chien-Te Lee , Chin-Chou Wang , Kai-Fan Tsai , Liang-Jen Wang , Shau-Hsuan Li , Yu-Che Ou","doi":"10.1016/j.heha.2026.100172","DOIUrl":"10.1016/j.heha.2026.100172","url":null,"abstract":"<div><div>Phthalate exposure can cause health hazards, including nephrotoxicity. However, the daily intake and adverse renal effects of phthalate exposure in patients with chronic kidney disease (CKD) remain unclear. Participants with non-dialysis-dependent CKD (i.e., not requiring long-term hemodialysis or peritoneal dialysis) stages 3–5 were enrolled in this one-year longitudinal investigation. We calculated the estimated daily intakes (EDIs) of five main phthalate compounds from their urinary biomonitoring data to evaluate the impact of phthalate exposure on urinary renal biomarkers reflecting oxidative damage and renal tubular injury. The overall urinary phthalate detection rate was 100% among 112 male and 57 female participants. Our analyses demonstrated that EDIs of di-(2-ethylhexyl) phthalate, diethyl phthalate (DEP), and dibutyl phthalate (DBP) independently correlated with the increases in kidney injury molecule-1 (β (95% confidence interval (CI)), 0.352 (0.193–0.512), 0.240 (0.135–0.345), and 0.312 (0.193–0.431) log ng/g creatinine per log ng/kg body weight/day of corresponding EDIs; <em>p</em> <0.001). Furthermore, the EDIs of DEP, dimethyl phthalate, and DBP were independently associated with the elevations in 8-hydroxy-2’-deoxyguanosine (β (95% CI), 0.278 (0.206–0.350), 0.509 (0.361–0.658), and 0.319 (0.215–0.423) log μg/g creatinine per log ng/kg body weight/day, respectively; <em>p</em> <0.001). The mediating role of oxidative damage in phthalate-associated renal tubular injury was also identified. Our study highlights the nephrotoxicity of phthalate exposure in patients with CKD and suggests that renal tubular injury and oxidative damage play crucial roles in phthalate-associated nephrotoxicity, which is underestimated using traditional renal surrogates.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100172"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147420127","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}
Pub Date : 2026-03-01Epub Date: 2025-11-27DOI: 10.1016/j.heha.2025.100161
Sarawut Sangkham , Nattapon Pansakun , Patipat Vongruang , Mohammad Nayeem Hasan , Saksin Simsin
Fine particulate matter (PM2.5) is a significant contributor to air pollution and is associated with many diseases of global public health concern. In this study, the burden of lung cancer and cardiopulmonary disease attributed to PM2.5 exposure in Thailand's upper northern region is estimated. Additionally, generalised additive models (GAMs) were used to examine the relationship between PM2.5 and ozone (O3) levels and the incidence of cardiovascular diseases (CVDs) and chronic obstructive pulmonary disease (COPD). The results indicated all eight provinces showed a positive relative risk (RR) for lung cancer and cardiopulmonary disease. The estimated long-term exposure to PM2.5 during 2015–2023 showed that the regional average relative risk (RR) was 1.558 (95 % CI: 1.530–1.586) for lung cancer and 1.344 (95 % CI: 1.328–1.361) for cardiopulmonary disease. This study examined the short-term effects of PM2.5 and ozone (O3) exposure on morbidity from COPD and CVD. PM2.5 exposure was significantly associated with increased COPD risk only in Lampang province, where the incidence rate ratio [IRR] was 1.009 (95 % CI: 1.002–1.017), p < 0.05. Ozone exposure showed significant associations with COPD risk in Chiang Mai, Chiang Rai, and Nan provinces, with the IRRs of 1.021 (95 % CI: 1.009–1.033), 1.020 (95 % CI: 1.007–1.032), and 1.026 (95 % CI: 1.012–1.040), respectively (p < 0.05). Ozone exposure was associated with an increased IRR for CVD risk in Chiang Mai, Chiang Rai, and Nan provinces; however, the association was not statistically significant. In contrast, no significant association in IRR was observed for short-term PM2.5 exposure in relation to CVD. Joint exposure to PM2.5 and O3 was significantly associated with increased risk of COPD in Chiang Mai, Chiang Rai, and Nan provinces (p < 0.05). Interaction analyses revealed synergistic effects on COPD in Nan and CVD in Chiang Rai and Nan. Male sex, older age (≥ 60 years), and seasonal variation of particulate matter and ozone concentration were identified as significant effect modifiers. These findings elucidate the differential impacts of air pollutants on respiratory and cardiovascular health in upper northern Thailand. Furthermore, they emphasise the heightened vulnerability of older adults and males, underscoring the urgent need for targeted, region-specific public health interventions.
{"title":"Estimated burden of disease and health effects attributable to fine particulate matter and ozone exposure in relation to COPD and cardiovascular disease in Upper Northern Thailand","authors":"Sarawut Sangkham , Nattapon Pansakun , Patipat Vongruang , Mohammad Nayeem Hasan , Saksin Simsin","doi":"10.1016/j.heha.2025.100161","DOIUrl":"10.1016/j.heha.2025.100161","url":null,"abstract":"<div><div>Fine particulate matter (PM<sub>2.5</sub>) is a significant contributor to air pollution and is associated with many diseases of global public health concern. In this study, the burden of lung cancer and cardiopulmonary disease attributed to PM<sub>2.5</sub> exposure in Thailand's upper northern region is estimated. Additionally, generalised additive models (GAMs) were used to examine the relationship between PM<sub>2.5</sub> and ozone (O<sub>3</sub>) levels and the incidence of cardiovascular diseases (CVDs) and chronic obstructive pulmonary disease (COPD). The results indicated all eight provinces showed a positive relative risk (RR) for lung cancer and cardiopulmonary disease. The estimated long-term exposure to PM<sub>2.5</sub> during 2015–2023 showed that the regional average relative risk (RR) was 1.558 (95 % CI: 1.530–1.586) for lung cancer and 1.344 (95 % CI: 1.328–1.361) for cardiopulmonary disease. This study examined the short-term effects of PM<sub>2.5</sub> and ozone (O<sub>3</sub>) exposure on morbidity from COPD and CVD. PM<sub>2.5</sub> exposure was significantly associated with increased COPD risk only in Lampang province, where the incidence rate ratio [IRR] was 1.009 (95 % CI: 1.002–1.017), <em>p</em> < 0.05. Ozone exposure showed significant associations with COPD risk in Chiang Mai, Chiang Rai, and Nan provinces, with the IRRs of 1.021 (95 % CI: 1.009–1.033), 1.020 (95 % CI: 1.007–1.032), and 1.026 (95 % CI: 1.012–1.040), respectively (<em>p</em> < 0.05). Ozone exposure was associated with an increased IRR for CVD risk in Chiang Mai, Chiang Rai, and Nan provinces; however, the association was not statistically significant. In contrast, no significant association in IRR was observed for short-term PM<sub>2.5</sub> exposure in relation to CVD. Joint exposure to PM<sub>2.5</sub> and O<sub>3</sub> was significantly associated with increased risk of COPD in Chiang Mai, Chiang Rai, and Nan provinces (<em>p</em> < 0.05). Interaction analyses revealed synergistic effects on COPD in Nan and CVD in Chiang Rai and Nan. Male sex, older age (≥ 60 years), and seasonal variation of particulate matter and ozone concentration were identified as significant effect modifiers. These findings elucidate the differential impacts of air pollutants on respiratory and cardiovascular health in upper northern Thailand. Furthermore, they emphasise the heightened vulnerability of older adults and males, underscoring the urgent need for targeted, region-specific public health interventions.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100161"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145718984","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}
Pub Date : 2026-03-01Epub Date: 2025-12-19DOI: 10.1016/j.heha.2025.100164
Akriti Ashesh, Ningombam Linthoingambi Devi
Contamination of dieldrin in soil and vegetables are reported even after its regulatory ban in many countries. However, monitoring of such persistent organic pollutants is not consistent in India. Still regional-level studies and report on dieldrin contamination are limited. Gaya Ji, being the 2nd largest economic district of the 3rd most populous state, Bihar, in India, is chosen for monitoring regional dieldrin contamination levels in soil and vegetable grown in the area. The present study monitored contamination of dieldrin in soil-vegetable samples to assess the health and ecological risk related to its exposure. 53 soil and vegetable samples were collected from Gaya district. Dieldrin was extracted with soxhlet extraction unit and estimated by Gas Chromatography Mass Spectrometry Detector (GCMSD). 2,4,5,6-tetrachloro-m-xylene (TCmX) was used as a surrogate standard, which yielded 71.94% - 89.91% recovery. Dieldrin concentration in soil and vegetable ranged from 0.04–1.33μg/g and 0.0019–0.97μg/g, respectively. 95.75% of the contaminated soil samples showed higher concentration than limit set by the Dutch Serious Risk Concentration (SRC) in 1976. 93.75% of vegetable samples showed contamination above the MRLs set by EU/WHO in 1994. Human risk assessment indicated that children (5–11 years) and adults (≥20 years) were the most vulnerable to cancer risk due to dieldrin exposure via dermal route. Adults and toddlers (7 months- 4 years) were the most vulnerable to the non-cancerous risk due to dieldrin exposure via ingestion route. Ecological risk assessment carried for earthworms, rats, and birds based on their modeled toxicity values given by Agriculture & Environment Research Unit (AERU) at the University of Hertfordshire, UK in 2016. The assessment indicated moderate risk for 47.82% soil and 12.5% vegetable samples. The findings of the present research reveal serious contamination and risks related to dieldrin exposure. Thus, demands regular monitoring and remediation studies to reduce its persistence in the environment.
{"title":"Ecological risk assessment of dieldrin presence in soil and vegetables: a case study in Indo-Gangetic region, Gaya, India","authors":"Akriti Ashesh, Ningombam Linthoingambi Devi","doi":"10.1016/j.heha.2025.100164","DOIUrl":"10.1016/j.heha.2025.100164","url":null,"abstract":"<div><div>Contamination of dieldrin in soil and vegetables are reported even after its regulatory ban in many countries. However, monitoring of such persistent organic pollutants is not consistent in India. Still regional-level studies and report on dieldrin contamination are limited. Gaya Ji, being the 2nd largest economic district of the 3rd most populous state, Bihar, in India, is chosen for monitoring regional dieldrin contamination levels in soil and vegetable grown in the area. The present study monitored contamination of dieldrin in soil-vegetable samples to assess the health and ecological risk related to its exposure. 53 soil and vegetable samples were collected from Gaya district. Dieldrin was extracted with soxhlet extraction unit and estimated by Gas Chromatography Mass Spectrometry Detector (GCMSD). 2,4,5,6-tetrachloro-m-xylene (TCmX) was used as a surrogate standard, which yielded 71.94% - 89.91% recovery. Dieldrin concentration in soil and vegetable ranged from 0.04–1.33μg/g and 0.0019–0.97μg/g, respectively. 95.75% of the contaminated soil samples showed higher concentration than limit set by the Dutch Serious Risk Concentration (SRC) in 1976. 93.75% of vegetable samples showed contamination above the MRLs set by EU/WHO in 1994. Human risk assessment indicated that children (5–11 years) and adults (≥20 years) were the most vulnerable to cancer risk due to dieldrin exposure via dermal route. Adults and toddlers (7 months- 4 years) were the most vulnerable to the non-cancerous risk due to dieldrin exposure via ingestion route. Ecological risk assessment carried for earthworms, rats, and birds based on their modeled toxicity values given by Agriculture & Environment Research Unit (AERU) at the University of Hertfordshire, UK in 2016. The assessment indicated moderate risk for 47.82% soil and 12.5% vegetable samples. The findings of the present research reveal serious contamination and risks related to dieldrin exposure. Thus, demands regular monitoring and remediation studies to reduce its persistence in the environment.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100164"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927216","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}
Pub Date : 2026-03-01Epub Date: 2026-02-13DOI: 10.1016/j.heha.2026.100171
Bo Peng , Yixuan Lu , Wei Zheng , Ruihua Yang , Xin Yan , Di Wu , Xingyan Liu , Ya Zhang , Yuan Zhang , Yujie Zhang , Ziyu Wang , Xincong Shi , Yuanyuan Wang , Guanghui Li , Xu Ma
Background
Air pollution is a significant environmental risk factor linked to neurodevelopmental disorders and cognitive impairments. Most research focuses on particulate matter, while studies on gaseous pollutants like ozone and preconceptional exposures are limited.
Methods
Data from 9869 mother-child dyads in the Beijing Birth Cohort Study (BBCS) were used. Ozone and six particulate pollutants were obtained from the Tracking Air Pollution in China (TAP) database, a nationwide spatiotemporal air pollution modeling platform of China mainland. Neurodevelopmental outcomes at 2 months were assessed using the Ages and Stages Questionnaires, Third Edition (ASQ-3). Multivariable linear regression models estimated the effects of ozone exposure on ASQ scores, stratified by sex.
Results
Preconceptional ozone exposure (per 10 μg/m³ increase) was negatively associated with gross motor (β= -0.16, P = 0.003), communication (β= -0.20, P = 0.03), personal-social (β= -0.18, P = 0.02), and problem-solving (β= -0.20, P = 0.02) scores in all infants. Third-trimester ozone exposure was associated with lower fine motor scores (β= -0.14, P = 0.04) and personal-social scores (β= -0.14, P = 0.02). These associations remained robust after adjustment for co-exposure to fine particulate matter and its components. Sex-stratified analyses revealed boys were more sensitive to late pregnancy ozone exposure, while girls were more sensitive to preconceptional exposure.
Conclusion
Preconceptional and gestational ozone exposure was associated with lower cognitive and motor function scores in infants, highlighting the potential importance of early-life exposure windows for neurodevelopment and informing future mechanistic research and public health prevention strategies.
背景：空气污染是与神经发育障碍和认知障碍相关的重要环境风险因素。大多数研究都集中在颗粒物上，而对臭氧等气态污染物和先入为主的接触的研究则很有限。方法采用北京出生队列研究（BBCS）中9869对母子对的数据。臭氧和6种颗粒污染物的数据来源于中国大陆空气污染时空模拟平台——中国空气污染追踪数据库（TAP）。使用年龄和阶段问卷第三版（ASQ-3）评估2个月时的神经发育结果。多变量线性回归模型估计臭氧暴露对ASQ评分的影响，按性别分层。结果孕期臭氧暴露（每增加10 μg/m³）与大肌肉运动（β= -0.16, P = 0.003）、沟通（β= -0.20, P = 0.03）、个人-社交（β= -0.18, P = 0.02）、问题解决（β= -0.20, P = 0.02）得分呈负相关。孕晚期臭氧暴露与精细运动评分（β= -0.14, P = 0.04）和个人-社会评分（β= -0.14, P = 0.02）降低相关。在调整了共同暴露于细颗粒物及其成分后，这些关联仍然很强。性别分层分析显示，男孩对怀孕后期接触臭氧更敏感，而女孩对孕前接触臭氧更敏感。结论：孕前和妊娠期臭氧暴露与婴儿较低的认知和运动功能评分有关，突出了生命早期暴露窗口对神经发育的潜在重要性，并为未来的机制研究和公共卫生预防策略提供了信息。
{"title":"Associations between preconceptional and gestational ozone exposure and early infant neurodevelopment: A birth cohort study","authors":"Bo Peng , Yixuan Lu , Wei Zheng , Ruihua Yang , Xin Yan , Di Wu , Xingyan Liu , Ya Zhang , Yuan Zhang , Yujie Zhang , Ziyu Wang , Xincong Shi , Yuanyuan Wang , Guanghui Li , Xu Ma","doi":"10.1016/j.heha.2026.100171","DOIUrl":"10.1016/j.heha.2026.100171","url":null,"abstract":"<div><h3>Background</h3><div>Air pollution is a significant environmental risk factor linked to neurodevelopmental disorders and cognitive impairments. Most research focuses on particulate matter, while studies on gaseous pollutants like ozone and preconceptional exposures are limited.</div></div><div><h3>Methods</h3><div>Data from 9869 mother-child dyads in the Beijing Birth Cohort Study (BBCS) were used. Ozone and six particulate pollutants were obtained from the Tracking Air Pollution in China (TAP) database, a nationwide spatiotemporal air pollution modeling platform of China mainland. Neurodevelopmental outcomes at 2 months were assessed using the Ages and Stages Questionnaires, Third Edition (ASQ-3). Multivariable linear regression models estimated the effects of ozone exposure on ASQ scores, stratified by sex.</div></div><div><h3>Results</h3><div>Preconceptional ozone exposure (per 10 μg/m³ increase) was negatively associated with gross motor (β= -0.16, <em>P</em> = 0.003), communication (β= -0.20, <em>P</em> = 0.03), personal-social (β= -0.18, <em>P</em> = 0.02), and problem-solving (β= -0.20, <em>P</em> = 0.02) scores in all infants. Third-trimester ozone exposure was associated with lower fine motor scores (β= -0.14, <em>P</em> = 0.04) and personal-social scores (β= -0.14, <em>P</em> = 0.02). These associations remained robust after adjustment for co-exposure to fine particulate matter and its components. Sex-stratified analyses revealed boys were more sensitive to late pregnancy ozone exposure, while girls were more sensitive to preconceptional exposure.</div></div><div><h3>Conclusion</h3><div>Preconceptional and gestational ozone exposure was associated with lower cognitive and motor function scores in infants, highlighting the potential importance of early-life exposure windows for neurodevelopment and informing future mechanistic research and public health prevention strategies.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100171"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147420128","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}
Pub Date : 2026-03-01Epub Date: 2026-01-09DOI: 10.1016/j.heha.2026.100170
Changda Yu , Zeeshan Mohammed , Hong-Zhi Zhang , Dao-Sen Wang , Yun-Ting Zhang , Guang-Hui Dong , Mei-Po Kwan , Li-Zi Lin
Diabetes is a prevalent chronic disease. Its interaction with environmental factors, especially greenspace, has garnered substantial scholarly attention. However, prevailing research has yielded disparate outcomes. The objective of our research was to elucidate the association between individual eye-level greenspace exposure and diabetes risk, employing data acquired from the 33 Communities Chinese Health Study, comprising 15,477 participants in Liaoning Province, China. Greenspace exposure was measured using the Greenness Visibility Index (GVI) from street view images, while the markers of blood glucose were ascertained via a systematic oral glucose tolerance test. Our findings indicate that eye-level greenspace exposure retains a substantial inverse association with the risk of diabetes, fasting and 2-hour glucose levels. Nevertheless, no significant associations were identified between eye-level greenspace exposure and either fasting or 2-hour insulin levels when gender was not considered. However, upon taking gender into consideration, a positive association was manifested between greenspace exposure and fasting insulin levels in male subjects, while a reverse association was exhibited in females. Regarding markers of Homeostasis Model Assessment, eye-level greenspace exposure had a significant negative relationship with the HOMA-IR index, which implies a conceivable connection with diminished levels of insulin resistance. Concurrently, a positive association was discerned between eye-level greenspace exposure and the HOMA-β index, hinting at a possible relationship with augmented beta-cell functionality. Nonetheless, these associations varied across different greenspace components and gender groups. This study provides novel evidence in revealing a negative association between individual eye-level greenspace exposure in residential environments and the prevalence of diabetes. It also sheds light on the intricate relationships between eye-level greenspace exposure and diverse markers of blood glucose homeostasis.
{"title":"Eye-level greenspace exposure and residents’ diabetes/glucose homeostasis status in Northeast China: A gender perspective","authors":"Changda Yu , Zeeshan Mohammed , Hong-Zhi Zhang , Dao-Sen Wang , Yun-Ting Zhang , Guang-Hui Dong , Mei-Po Kwan , Li-Zi Lin","doi":"10.1016/j.heha.2026.100170","DOIUrl":"10.1016/j.heha.2026.100170","url":null,"abstract":"<div><div>Diabetes is a prevalent chronic disease. Its interaction with environmental factors, especially greenspace, has garnered substantial scholarly attention. However, prevailing research has yielded disparate outcomes. The objective of our research was to elucidate the association between individual eye-level greenspace exposure and diabetes risk, employing data acquired from the 33 Communities Chinese Health Study, comprising 15,477 participants in Liaoning Province, China. Greenspace exposure was measured using the Greenness Visibility Index (GVI) from street view images, while the markers of blood glucose were ascertained via a systematic oral glucose tolerance test. Our findings indicate that eye-level greenspace exposure retains a substantial inverse association with the risk of diabetes, fasting and 2-hour glucose levels. Nevertheless, no significant associations were identified between eye-level greenspace exposure and either fasting or 2-hour insulin levels when gender was not considered. However, upon taking gender into consideration, a positive association was manifested between greenspace exposure and fasting insulin levels in male subjects, while a reverse association was exhibited in females. Regarding markers of Homeostasis Model Assessment, eye-level greenspace exposure had a significant negative relationship with the HOMA-IR index, which implies a conceivable connection with diminished levels of insulin resistance. Concurrently, a positive association was discerned between eye-level greenspace exposure and the HOMA-β index, hinting at a possible relationship with augmented beta-cell functionality. Nonetheless, these associations varied across different greenspace components and gender groups. This study provides novel evidence in revealing a negative association between individual eye-level greenspace exposure in residential environments and the prevalence of diabetes. It also sheds light on the intricate relationships between eye-level greenspace exposure and diverse markers of blood glucose homeostasis.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100170"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037756","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}
Pub Date : 2026-03-01Epub Date: 2025-11-28DOI: 10.1016/j.heha.2025.100162
Gaowei Duan , Hong Hong , Yuanhang Liu , He Xiao , Yuan Ding , Muhammad Amjad , Peixuan Wu , Li Zhong , Xu Wang , Xin Meng , Haiyan Zhang
Perfluorooctanoic acid (PFOA), a widely distributed environmental pollutant, exerts toxic effects on multiple human organs and tissues. However, its impact on skeletal muscle function and the underlying molecular mechanisms remain poorly understood. In this study, we first observed that PFOA exposure caused muscle dysfunction in juvenile mice, characterized by reduced grip strength and impaired motor coordination; to explore the underlying mechanism, we further conducted in vitro experiments using C2C12 myoblasts. Long-term treatment with 100 μacid (PFOA), a widely distributed environmental pollutant, exerts toxic effects on multiple human organs and tissues. However, its impact on myotubes. Transcriptome sequencing revealed a significant decrease in the expression of key myogenic regulatory factors (e.g., myosin heavy chain MYHC and myogenin) in PFOA-treated cells, findings that were confirmed by RT-qPCR and Western blot analyses. Mechanistically, PFOA treatment activated the Hippo signaling pathway, as evidenced by increased phosphorylation of the YAP protein. Treatment with taurine, an indirect activator of YAP, significantly restored the expression of myogenic genes and effectively promoted myotube formation. In summary, this study demonstrates that PFOA impairs muscle function by activating the Hippo signaling pathway and suppressing the transcription of key myogenic factors, providing new insights into PFOA-induced myotoxicity.
{"title":"Perfluorooctanoic acid impairs myogenic differentiation and muscle function via activation of the hippo-YAP pathway in mice and C2C12 myoblasts","authors":"Gaowei Duan , Hong Hong , Yuanhang Liu , He Xiao , Yuan Ding , Muhammad Amjad , Peixuan Wu , Li Zhong , Xu Wang , Xin Meng , Haiyan Zhang","doi":"10.1016/j.heha.2025.100162","DOIUrl":"10.1016/j.heha.2025.100162","url":null,"abstract":"<div><div>Perfluorooctanoic acid (PFOA), a widely distributed environmental pollutant, exerts toxic effects on multiple human organs and tissues. However, its impact on skeletal muscle function and the underlying molecular mechanisms remain poorly understood. In this study, we first observed that PFOA exposure caused muscle dysfunction in juvenile mice, characterized by reduced grip strength and impaired motor coordination; to explore the underlying mechanism, we further conducted in vitro experiments using C2C12 myoblasts. Long-term treatment with 100 μacid (PFOA), a widely distributed environmental pollutant, exerts toxic effects on multiple human organs and tissues. However, its impact on myotubes. Transcriptome sequencing revealed a significant decrease in the expression of key myogenic regulatory factors (e.g., myosin heavy chain MYHC and myogenin) in PFOA-treated cells, findings that were confirmed by RT-qPCR and Western blot analyses. Mechanistically, PFOA treatment activated the Hippo signaling pathway, as evidenced by increased phosphorylation of the YAP protein. Treatment with taurine, an indirect activator of YAP, significantly restored the expression of myogenic genes and effectively promoted myotube formation. In summary, this study demonstrates that PFOA impairs muscle function by activating the Hippo signaling pathway and suppressing the transcription of key myogenic factors, providing new insights into PFOA-induced myotoxicity.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100162"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145791656","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}
Pub Date : 2026-03-01Epub Date: 2025-12-19DOI: 10.1016/j.heha.2025.100166
Yongke He , Yixian Ren , Hangqian Zhang , Runping Liang , Kangyong Wu , Zhenming Zheng , Zhou Li , Wanmin Liang , Liping Zhou , Jiu Chen , Guanhao Guo , Shihua Wu , Xueji Yang , Weijie Ling , Jiaming Guo , Yanmei Ruan , Wenchong Tan , Bin Wang , Zhi Wang
Noise, a significant environmental stressor, has been demonstrated to induce dysregulated glucose and lipid metabolism. However, the precise molecular mechanisms driving liver dysfunction in noise-induced dysregulated glucose and lipid metabolism remain incompletely elucidated. Recent studies have underscored the pivotal role of the NLRP3 (Nod-like receptor protein 3) inflammasome in the context of liver pathology. To this end, a noise-exposure rat model was established (100 dB, 4 h/day for 30 days) to investigate whether the NLRP3 inflammasome mediates noise-caused hepatic injury and dysfunction. Exposure to noise resulted in significant alterations to liver architecture and dysfunction in rats. Furthermore, we found that noise triggered assembly and activation of the NLRP3 inflammasome, effects that were suppressed by the NLRP3 inhibitor MCC950. Such inhibition thereby attenuated liver damage and improved hepatic function. In conclusion, our findings indicate that noise-induced NLRP3 inflammasome activation promotes hepatic inflammation, contributing to liver injury and dysregulation of glucose and lipid metabolism. These results provide new mechanistic insights into the pathogenesis of noise-induced liver damage and dysfunction.
{"title":"NLRP3 inflammasome inhibition attenuates liver injury and dysfunction induced by noise exposure in rats","authors":"Yongke He , Yixian Ren , Hangqian Zhang , Runping Liang , Kangyong Wu , Zhenming Zheng , Zhou Li , Wanmin Liang , Liping Zhou , Jiu Chen , Guanhao Guo , Shihua Wu , Xueji Yang , Weijie Ling , Jiaming Guo , Yanmei Ruan , Wenchong Tan , Bin Wang , Zhi Wang","doi":"10.1016/j.heha.2025.100166","DOIUrl":"10.1016/j.heha.2025.100166","url":null,"abstract":"<div><div>Noise, a significant environmental stressor, has been demonstrated to induce dysregulated glucose and lipid metabolism. However, the precise molecular mechanisms driving liver dysfunction in noise-induced dysregulated glucose and lipid metabolism remain incompletely elucidated. Recent studies have underscored the pivotal role of the NLRP3 (Nod-like receptor protein 3) inflammasome in the context of liver pathology. To this end, a noise-exposure rat model was established (100 dB, 4 h/day for 30 days) to investigate whether the NLRP3 inflammasome mediates noise-caused hepatic injury and dysfunction. Exposure to noise resulted in significant alterations to liver architecture and dysfunction in rats. Furthermore, we found that noise triggered assembly and activation of the NLRP3 inflammasome, effects that were suppressed by the NLRP3 inhibitor MCC950. Such inhibition thereby attenuated liver damage and improved hepatic function. In conclusion, our findings indicate that noise-induced NLRP3 inflammasome activation promotes hepatic inflammation, contributing to liver injury and dysregulation of glucose and lipid metabolism. These results provide new mechanistic insights into the pathogenesis of noise-induced liver damage and dysfunction.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"17 ","pages":"Article 100166"},"PeriodicalIF":2.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927214","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}
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