Pub Date : 2025-12-01DOI: 10.1016/j.heha.2025.100159
Na Li , Ting Fan Leung , Linwei Tian , Huachang Hong , Wen-Jing Deng
Organophosphate esters (OPEs), widely employed as flame-retardants and plasticizers, have been linked to adverse health outcomes in children. This study evaluated the predictors of OPE exposure in children aged 1 to 12 years in Guangxi, China. Eleven OPEs were detected in a cohort of 84 children and their parents’ urine, with geometric mean (GM) levels ranging from 0.11 ng/gcrea (tri-n-propyl phosphate, TPP) to 25.93 ng/gcrea (tris(2,3-dichloropropyl) phosphate, TDCPP) in children, and from 0.04 ng/gcrea (triphenyl phosphate, TPHP) to 18.71 ng/gcrea (TDCPP) in parents. These findings are consistent with values reported in several large-scale national urinary biomonitoring studies on OPEs. Significant positive correlations among most target OPEs and no significant gender and age differences in children’s urine were found. The eXtreme Gradient Boosting (XGBoost) coupled with Shapley Additive explanations (SHAP), was employed to analyse the importance of 93 variables from the questionnaire and interpret the levels of OPEs in children’s urine. Models for six OPEs were constructed, revealing that daily use of fans affected the levels of five OPEs. Additionally, egg consumption and the number of family members were associated with higher levels of TPP/TCEP, and CDP/TEHP, respectively. There is a need to conduct more precise quantitative assessments of OPE exposure routes.
{"title":"Exposure to organophosphate esters (OPEs) of children (1-12y) in Guangxi, China: Predictors evaluation by machine learning","authors":"Na Li , Ting Fan Leung , Linwei Tian , Huachang Hong , Wen-Jing Deng","doi":"10.1016/j.heha.2025.100159","DOIUrl":"10.1016/j.heha.2025.100159","url":null,"abstract":"<div><div>Organophosphate esters (OPEs), widely employed as flame-retardants and plasticizers, have been linked to adverse health outcomes in children. This study evaluated the predictors of OPE exposure in children aged 1 to 12 years in Guangxi, China. Eleven OPEs were detected in a cohort of 84 children and their parents’ urine, with geometric mean (GM) levels ranging from 0.11 ng/g<sub>crea</sub> (tri-n-propyl phosphate, TPP) to 25.93 ng/g<sub>crea</sub> (tris(2,3-dichloropropyl) phosphate, TDCPP) in children, and from 0.04 ng/g<sub>crea</sub> (triphenyl phosphate, TPHP) to 18.71 ng/g<sub>crea</sub> (TDCPP) in parents. These findings are consistent with values reported in several large-scale national urinary biomonitoring studies on OPEs. Significant positive correlations among most target OPEs and no significant gender and age differences in children’s urine were found. The eXtreme Gradient Boosting (XGBoost) coupled with Shapley Additive explanations (SHAP), was employed to analyse the importance of 93 variables from the questionnaire and interpret the levels of OPEs in children’s urine. Models for six OPEs were constructed, revealing that daily use of fans affected the levels of five OPEs. Additionally, egg consumption and the number of family members were associated with higher levels of TPP/TCEP, and CDP/TEHP, respectively. There is a need to conduct more precise quantitative assessments of OPE exposure routes.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100159"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145623864","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 : 2025-12-01DOI: 10.1016/j.heha.2025.100144
Youxing Li , Yaqin Pang , Wenxue Li , Dongshun Chen , Caiping Zhang , Yufang Cen , Junhong Wei , Rongqing Xiao , Wenlian Rao , Yinxia Lin , Ahmad Razali Ishak , Mohd Shukri Bin Mohd Aris , Guangzi Qi
Mild cognitive impairment (MCI) is an early stage of Alzheimer's disease and is the result of interactions between environmental and genetic factors. However, their impact on aluminum workers is not yet clear. This study aimed to explore the interaction between occupational exposure and NLRP3 gene polymorphisms on the odds of MCI among aluminum production workers. We assessed the cognitive function of 478 workers in a factory in Guangxi, China, and identified two main occupational exposure factors: principal component 1 (PC1: noise, high temperature, carbon monoxide, sulfur dioxide, nitrogen oxides) and principal component 2 (PC2: aluminum oxide dust, magnetic field, fluoride, manganese dioxide). Genotyping of polymorphisms in the NLRP3 gene (rs10754558, rs10925027, rs3806265, rs4612666) was performed. The results of the analysis showed that high PC2 exposure significantly increased the odds of MCI [OR (95 % CI): 1.99 (1.36, 2.91)], and the rs10754558 G/C genotype was independently associated with MCI [OR (95 % CI): 1.56 (1.05, 2.33)]. PC2 interacted with rs3806265 C/T [OR (95 % CI):2.13 (1.16, 3.92)] and rs4612666 C/T [OR (95 % CI): 2.84 (1.19,6.81)], further increasing the odds of MCI. These findings suggest that alumina dust, magnetic fields, fluoride, and manganese dioxide are the main occupational hazards factors for MCI. rs10754558 G/C is an independent susceptibility genotype for MCI, while rs3806265 C/T and rs4612666 C/T are environmental susceptibility genotypes for MCI. This study emphasizes that reducing occupational exposure and screening for susceptibility genes can provide a basis for targeted interventions to reduce the odds of MCI in this population.
{"title":"Effects of occupational exposure factors interacting with NLRP3 gene polymorphisms on mild cognitive impairment: A cross-sectional study of workers in an aluminum electrolysis production environment","authors":"Youxing Li , Yaqin Pang , Wenxue Li , Dongshun Chen , Caiping Zhang , Yufang Cen , Junhong Wei , Rongqing Xiao , Wenlian Rao , Yinxia Lin , Ahmad Razali Ishak , Mohd Shukri Bin Mohd Aris , Guangzi Qi","doi":"10.1016/j.heha.2025.100144","DOIUrl":"10.1016/j.heha.2025.100144","url":null,"abstract":"<div><div>Mild cognitive impairment (MCI) is an early stage of Alzheimer's disease and is the result of interactions between environmental and genetic factors. However, their impact on aluminum workers is not yet clear. This study aimed to explore the interaction between occupational exposure and NLRP3 gene polymorphisms on the odds of MCI among aluminum production workers. We assessed the cognitive function of 478 workers in a factory in Guangxi, China, and identified two main occupational exposure factors: principal component 1 (PC1: noise, high temperature, carbon monoxide, sulfur dioxide, nitrogen oxides) and principal component 2 (PC2: aluminum oxide dust, magnetic field, fluoride, manganese dioxide). Genotyping of polymorphisms in the NLRP3 gene (rs10754558, rs10925027, rs3806265, rs4612666) was performed. The results of the analysis showed that high PC2 exposure significantly increased the odds of MCI [OR (95 % CI): 1.99 (1.36, 2.91)], and the rs10754558 G/C genotype was independently associated with MCI [OR (95 % CI): 1.56 (1.05, 2.33)]. PC2 interacted with rs3806265 C/T [OR (95 % CI):2.13 (1.16, 3.92)] and rs4612666 C/T [OR (95 % CI): 2.84 (1.19,6.81)], further increasing the odds of MCI. These findings suggest that alumina dust, magnetic fields, fluoride, and manganese dioxide are the main occupational hazards factors for MCI. rs10754558 G/C is an independent susceptibility genotype for MCI, while rs3806265 C/T and rs4612666 C/T are environmental susceptibility genotypes for MCI. This study emphasizes that reducing occupational exposure and screening for susceptibility genes can provide a basis for targeted interventions to reduce the odds of MCI in this population.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100144"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693001","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}
Microplastics (MPs) have become a widespread and novel threat to agriculture by degrading soils, damaging plant productivity and ultimately threatening food security. Research on MP contamination paths through plastic mulching, biosolids, compost, and wastewater irrigation has led to a greater understanding the problem, but the physiological and ecological impacts on plants have not been quantified and explained. MPs affect the biophysical properties of the soils, including the water and nutrients, which impacts their flow to the MP-affected plants. Biophysical changes caused by the MPs to the soils include changes to bulk density, porosity, and hydraulic conductivity. In the rhizosphere, they cause disruption to the microbial networks, suppression of enzymes, and the destabilization of symbiotic relationships, which impacts the plants’ ability to biogoechemically cycle and mitigate stress. MP-affected plants result in reduced germination, depressed photosynthetic productivity, oxidative stress leading to altered carbon distribution, secondary metabolites, and loss of other metabolites.
While there are many studies on the microbial and physicochemical approaches to remediation, the plant pathway and approaches to remediation are still largely unexplored and present a novel opportunity to address the problem. Symbiotic microbial consortia associated with root systems will help with enzymatic transformation of aggregating, immobilizing, and in some cases, biochemically transforming MPs. The detoxification capacity of PGPR and rhizosphere biochar are often situational and short-lived. Most importantly, the short-term laboratory studies using pristine MPs and over concentrated MPs will not accurately influence or predict the ecological impact and applicability to the field.
This review underscores the need for an integrated, nature-based strategies to combat MP pollution and protect agroecosystem integrity by bridging microbiology, soil science, and sustainable agriculture. Furthermore, a comprehensive understanding of the root system physiology, chemical exudation patterns, and microbial associations has been explored to determine the fate of the MP in deriving implementable plant-driven approaches. Such a framework is necessary to develop resilient self-remediating agroecosystems that can degrade plastic waste while maintaining productive agriculture.
{"title":"Plant-driven strategies for mitigating microplastic pollution in agricultural ecosystems","authors":"Anindita Banerjee , Pranav Kumar , Arkaprobha Ghosh , Soumita Reja , Surjit Singh","doi":"10.1016/j.heha.2025.100160","DOIUrl":"10.1016/j.heha.2025.100160","url":null,"abstract":"<div><div>Microplastics (MPs) have become a widespread and novel threat to agriculture by degrading soils, damaging plant productivity and ultimately threatening food security. Research on MP contamination paths through plastic mulching, biosolids, compost, and wastewater irrigation has led to a greater understanding the problem, but the physiological and ecological impacts on plants have not been quantified and explained. MPs affect the biophysical properties of the soils, including the water and nutrients, which impacts their flow to the MP-affected plants. Biophysical changes caused by the MPs to the soils include changes to bulk density, porosity, and hydraulic conductivity. In the rhizosphere, they cause disruption to the microbial networks, suppression of enzymes, and the destabilization of symbiotic relationships, which impacts the plants’ ability to biogoechemically cycle and mitigate stress. MP-affected plants result in reduced germination, depressed photosynthetic productivity, oxidative stress leading to altered carbon distribution, secondary metabolites, and loss of other metabolites.</div><div>While there are many studies on the microbial and physicochemical approaches to remediation, the plant pathway and approaches to remediation are still largely unexplored and present a novel opportunity to address the problem. Symbiotic microbial consortia associated with root systems will help with enzymatic transformation of aggregating, immobilizing, and in some cases, biochemically transforming MPs. The detoxification capacity of PGPR and rhizosphere biochar are often situational and short-lived. Most importantly, the short-term laboratory studies using pristine MPs and over concentrated MPs will not accurately influence or predict the ecological impact and applicability to the field.</div><div>This review underscores the need for an integrated, nature-based strategies to combat MP pollution and protect agroecosystem integrity by bridging microbiology, soil science, and sustainable agriculture. Furthermore, a comprehensive understanding of the root system physiology, chemical exudation patterns, and microbial associations has been explored to determine the fate of the MP in deriving implementable plant-driven approaches. Such a framework is necessary to develop resilient self-remediating agroecosystems that can degrade plastic waste while maintaining productive agriculture.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100160"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145623809","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 : 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":"2025-11-28","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 : 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":"2025-11-27","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 : 2025-11-09DOI: 10.1016/j.heha.2025.100157
Zhongzhi Xu , Xin Xu , Shao Lin , Bing Xia , Shanyu Zhou , Shu Wang , Yawei Guo , Lulu Lin , Huiyuan Zhong , Lerong Liu , Yongshun Huang , Wangjian Zhang
This study aimed to examine the independent and joint effects of occupational dust exposure (ODE) and pulmonary function abnormalities (PFA) on the incidence of hypertension, and to assess whether pre-existing PFA modifies the ODE–hypertension relationship. A prospective cohort design was used, drawing data from the Guangdong Key Occupational Diseases Surveillance Project (2021–2023), which included 144,627 workers from 21 cities in Guangdong, China. ODE and PFA were assessed using standardized protocols, and hypertension was defined as elevated blood pressure or use of antihypertensive medication. Cox proportional hazards models, restricted cubic splines, and interaction analyses were performed to evaluate associations, and Mendelian randomization (MR) using UK Biobank data was conducted to assess causality. At baseline, 33,766 participants (23.3 %) had PFA, and during follow-up, 14,996 (10.4 %) developed hypertension. Both ODE (HR = 1.12, 95 % CI: 1.08–1.16) and PFA (HR = 1.19, 95 % CI: 1.14–1.23) were independently associated with increased hypertension risk (P < 0.001), with a higher combined effect (HR = 1.39, 95 % CI: 1.31–1.47). A positive trend was observed between dust exposure duration and hypertension risk (HR = 1.11 for ≥6 years vs. <2 years; P for trend = 0.017). Respirable dust (≤10 μm) and inorganic dust were significantly associated with increased hypertension risk (HR = 1.16 and 1.13). MR analysis supported a causal relationship between ODE, PFA, and hypertension. These findings indicate that pre-existing PFA amplifies the hypertensive effects of ODE, highlighting the importance of respiratory health interventions to reduce hypertension risk among dust-exposed workers.
{"title":"Pre-existing pulmonary function abnormality exacerbates the impact of occupational dust exposure on incident hypertension: Evidence from a large occupational cohort","authors":"Zhongzhi Xu , Xin Xu , Shao Lin , Bing Xia , Shanyu Zhou , Shu Wang , Yawei Guo , Lulu Lin , Huiyuan Zhong , Lerong Liu , Yongshun Huang , Wangjian Zhang","doi":"10.1016/j.heha.2025.100157","DOIUrl":"10.1016/j.heha.2025.100157","url":null,"abstract":"<div><div>This study aimed to examine the independent and joint effects of occupational dust exposure (ODE) and pulmonary function abnormalities (PFA) on the incidence of hypertension, and to assess whether pre-existing PFA modifies the ODE–hypertension relationship. A prospective cohort design was used, drawing data from the Guangdong Key Occupational Diseases Surveillance Project (2021–2023), which included 144,627 workers from 21 cities in Guangdong, China. ODE and PFA were assessed using standardized protocols, and hypertension was defined as elevated blood pressure or use of antihypertensive medication. Cox proportional hazards models, restricted cubic splines, and interaction analyses were performed to evaluate associations, and Mendelian randomization (MR) using UK Biobank data was conducted to assess causality. At baseline, 33,766 participants (23.3 %) had PFA, and during follow-up, 14,996 (10.4 %) developed hypertension. Both ODE (HR = 1.12, 95 % CI: 1.08–1.16) and PFA (HR = 1.19, 95 % CI: 1.14–1.23) were independently associated with increased hypertension risk (<em>P</em> < 0.001), with a higher combined effect (HR = 1.39, 95 % CI: 1.31–1.47). A positive trend was observed between dust exposure duration and hypertension risk (HR = 1.11 for ≥6 years vs. <2 years; <em>P</em> for trend = 0.017). Respirable dust (≤10 μm) and inorganic dust were significantly associated with increased hypertension risk (HR = 1.16 and 1.13). MR analysis supported a causal relationship between ODE, PFA, and hypertension. These findings indicate that pre-existing PFA amplifies the hypertensive effects of ODE, highlighting the importance of respiratory health interventions to reduce hypertension risk among dust-exposed workers.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100157"},"PeriodicalIF":2.7,"publicationDate":"2025-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528404","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}
Access to clean toilets in schools is essential for a conducive learning environment and safeguarding pupils' health. Urban schools often face sanitation challenges stemming from overcrowding, inadequate facilities, and differences in management practices across school categories such as public or private, primary or secondary, day or boarding, and service level classifications. Identifying key factors influencing toilet cleanliness is vital for improving urban school sanitation. This study investigated the drivers of toilet cleanliness through a cross-sectional study conducted in Kampala City, in Uganda. Kampala City has 852 schools of which 274 were selected for this study. Data collection comprised 274 structured observations guided by a checklist, 548 questionnaires administered to Head Teachers and Sanitation Teachers, and 40 key informant interviews. Logistic regression and decision tree modeling were used for data analysis. Across all school types, significant associations were observed between toilet cleanliness and facility privacy, sex segregation, presence of health clubs, handwashing facilities with soap and water, rainwater harvesting systems, sanitation budget, and toilet paper availability. The decision tree model identified rainwater harvesting, handwashing facilities, and health clubs as the strongest predictors of toilet cleanliness, in that order. Findings indicate that policymakers and school administrators should prioritize investment in water access, hygiene infrastructure, and health clubs to improve and sustain toilet cleanliness in urban schools.
{"title":"What drives toilet cleanliness in urban schools? Roles of infrastructure, resources, and hygiene promotion in Kampala","authors":"Jude Zziwa Byansi , Swaib Semiyaga , Alex Yasoni Katukiza , Najib Lukooya Bateganya , Frank Kansiime , Robinah Nakawunde Kulabako","doi":"10.1016/j.heha.2025.100158","DOIUrl":"10.1016/j.heha.2025.100158","url":null,"abstract":"<div><div>Access to clean toilets in schools is essential for a conducive learning environment and safeguarding pupils' health. Urban schools often face sanitation challenges stemming from overcrowding, inadequate facilities, and differences in management practices across school categories such as public or private, primary or secondary, day or boarding, and service level classifications. Identifying key factors influencing toilet cleanliness is vital for improving urban school sanitation. This study investigated the drivers of toilet cleanliness through a cross-sectional study conducted in Kampala City, in Uganda. Kampala City has 852 schools of which 274 were selected for this study. Data collection comprised 274 structured observations guided by a checklist, 548 questionnaires administered to Head Teachers and Sanitation Teachers, and 40 key informant interviews. Logistic regression and decision tree modeling were used for data analysis. Across all school types, significant associations were observed between toilet cleanliness and facility privacy, sex segregation, presence of health clubs, handwashing facilities with soap and water, rainwater harvesting systems, sanitation budget, and toilet paper availability. The decision tree model identified rainwater harvesting, handwashing facilities, and health clubs as the strongest predictors of toilet cleanliness, in that order. Findings indicate that policymakers and school administrators should prioritize investment in water access, hygiene infrastructure, and health clubs to improve and sustain toilet cleanliness in urban schools.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100158"},"PeriodicalIF":2.7,"publicationDate":"2025-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528406","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 : 2025-10-01DOI: 10.1016/j.heha.2025.100156
Xin Wang , Ziqin Cao , Kelly M. Bakulski , Henry L. Paulson
Background
Cerebrovascular diseases are a leading cause of death in the U.S., and emerging evidence suggests that environmental toxicants such as cadmium may contribute to cerebrovascular risk. This study investigates the association between cadmium exposure and cerebrovascular mortality in a nationally representative sample of U.S. adults.
Methods
We analyzed data from adults aged ≥40 years in the National Health and Nutrition Examination Survey (NHANES) 1999–2016 cycles, with mortality follow-up through 2019. Blood cadmium was measured in 23,455 participants, and urinary cadmium was measured in 8929 participants. Cerebrovascular deaths were identified through linkage with the National Death Index. Survey-weighted Cox proportional hazards models evaluated associations between cadmium concentrations and cerebrovascular mortality.
Results
Over a mean follow-up of 10.2 years, 247 cerebrovascular deaths were observed. Each interquartile range increase in blood cadmium (0.40 µg/L) was associated with a 23 % higher risk of cerebrovascular mortality (HR = 1.23, 95 % CI: 1.04–1.46). Urinary cadmium was also associated with higher cerebrovascular mortality, although marginally significant (HR = 1.36 per doubling, 95 % CI: 0.99–1.87). Associations appeared stronger among former and current smokers, though interaction terms were not statistically significant.
Conclusions
Cadmium exposure is associated with increased cerebrovascular mortality in the U.S. population. These findings support cadmium as a modifiable environmental risk factor and underscore the need for public health interventions to reduce exposure through tobacco control, dietary regulations, and environmental policy.
{"title":"Exposure to cadmium and cerebrovascular mortality in the United States","authors":"Xin Wang , Ziqin Cao , Kelly M. Bakulski , Henry L. Paulson","doi":"10.1016/j.heha.2025.100156","DOIUrl":"10.1016/j.heha.2025.100156","url":null,"abstract":"<div><h3>Background</h3><div>Cerebrovascular diseases are a leading cause of death in the U.S., and emerging evidence suggests that environmental toxicants such as cadmium may contribute to cerebrovascular risk. This study investigates the association between cadmium exposure and cerebrovascular mortality in a nationally representative sample of U.S. adults.</div></div><div><h3>Methods</h3><div>We analyzed data from adults aged ≥40 years in the National Health and Nutrition Examination Survey (NHANES) 1999–2016 cycles, with mortality follow-up through 2019. Blood cadmium was measured in 23,455 participants, and urinary cadmium was measured in 8929 participants. Cerebrovascular deaths were identified through linkage with the National Death Index. Survey-weighted Cox proportional hazards models evaluated associations between cadmium concentrations and cerebrovascular mortality.</div></div><div><h3>Results</h3><div>Over a mean follow-up of 10.2 years, 247 cerebrovascular deaths were observed. Each interquartile range increase in blood cadmium (0.40 µg/L) was associated with a 23 % higher risk of cerebrovascular mortality (HR = 1.23, 95 % CI: 1.04–1.46). Urinary cadmium was also associated with higher cerebrovascular mortality, although marginally significant (HR = 1.36 per doubling, 95 % CI: 0.99–1.87). Associations appeared stronger among former and current smokers, though interaction terms were not statistically significant.</div></div><div><h3>Conclusions</h3><div>Cadmium exposure is associated with increased cerebrovascular mortality in the U.S. population. These findings support cadmium as a modifiable environmental risk factor and underscore the need for public health interventions to reduce exposure through tobacco control, dietary regulations, and environmental policy.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100156"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145268132","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 : 2025-10-01DOI: 10.1016/j.heha.2025.100154
Daniel Tomčík , Miloš Gejdoš
This study assessed the airborne particulate matter (PM) in urban heating plants, potentially affecting respiratory health in workers and nearby residents. The objectives of this study were to characterize occupational exposure during chip-loading activities and to evaluate ambient PM concentrations in the surrounding environment. Occupational exposure was assessed in accordance with the relevant standards using the Temtop M2000C, while continuous ambient monitoring was conducted with the AirNote device. The results indicate a significant increase in PM concentrations during woodchip loading activities. Mean PM2.5 concentrations were 24.03 µg/m3 during loading and 8.07 µg/m3 during non-loading, while PM10 levels were 38.75 µg/m3 and 12.80 µg/m3, respectively. Continuous monitoring revealed that daily mean PM2.5 concentrations were above the WHO 24-h guideline value of 15 µg/m3 on 3 days. The maximum daily mean PM2.5 concentration was 43.7 µg/m3, while the median daily mean was 22.5 µg/m3. For PM10, the maximum daily mean reached 70.9 µg/m3 and the median daily mean was 35.6 µg/m3, with exceedance of the WHO 24-hour guideline of 45 µg/m3 observed on one day. Distance from the woodchip pile also had a significant effect on PM concentrations (p < 0.001), with short-term mean levels at 50 m exceeding the WHO 24-h guideline value by 2.9 times for PM2.5 and 1.6 times for PM10. These guideline values are provided for context only, as they represent 24-hour mean concentrations and not instantaneous limits. Beyond 100 m, no further significant reduction in PM levels was observed. Biomass storage operations can cause temporary PM exceedances, particularly during handling and near storage areas. These findings underscore the importance of implementing mitigation strategies to reduce airborne particulate emissions.
{"title":"Assessment of particulate matter exposure associated with biomass storage in urban heating plant","authors":"Daniel Tomčík , Miloš Gejdoš","doi":"10.1016/j.heha.2025.100154","DOIUrl":"10.1016/j.heha.2025.100154","url":null,"abstract":"<div><div>This study assessed the airborne particulate matter (PM) in urban heating plants, potentially affecting respiratory health in workers and nearby residents. The objectives of this study were to characterize occupational exposure during chip-loading activities and to evaluate ambient PM concentrations in the surrounding environment. Occupational exposure was assessed in accordance with the relevant standards using the Temtop M2000C, while continuous ambient monitoring was conducted with the AirNote device. The results indicate a significant increase in PM concentrations during woodchip loading activities. Mean PM2.5 concentrations were 24.03 µg/m<sup>3</sup> during loading and 8.07 µg/m<sup>3</sup> during non-loading, while PM10 levels were 38.75 µg/m<sup>3</sup> and 12.80 µg/m<sup>3</sup>, respectively. Continuous monitoring revealed that daily mean PM2.5 concentrations were above the WHO 24-h guideline value of 15 µg/m<sup>3</sup> on 3 days. The maximum daily mean PM2.5 concentration was 43.7 µg/m<sup>3</sup>, while the median daily mean was 22.5 µg/m<sup>3</sup>. For PM10, the maximum daily mean reached 70.9 µg/m<sup>3</sup> and the median daily mean was 35.6 µg/m<sup>3</sup>, with exceedance of the WHO 24-hour guideline of 45 µg/m<sup>3</sup> observed on one day. Distance from the woodchip pile also had a significant effect on PM concentrations (<em>p</em> < 0.001), with short-term mean levels at 50 m exceeding the WHO 24-h guideline value by 2.9 times for PM2.5 and 1.6 times for PM10. These guideline values are provided for context only, as they represent 24-hour mean concentrations and not instantaneous limits. Beyond 100 m, no further significant reduction in PM levels was observed. Biomass storage operations can cause temporary PM exceedances, particularly during handling and near storage areas. These findings underscore the importance of implementing mitigation strategies to reduce airborne particulate emissions.</div></div>","PeriodicalId":73269,"journal":{"name":"Hygiene and environmental health advances","volume":"16 ","pages":"Article 100154"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145268131","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号