BackgroundWork-related musculoskeletal disorders (WMSDs) are common across industries. Workers in the hairdressing industry are frequently exposed to repetitive upper-limb movements and awkward working postures, which may increase their susceptibility to WMSDs. However, evidence on WMSDs among workers in this industry remains limited.ObjectiveThis study aimed to investigate the prevalence of self-reported WMSDs symptoms and associated factors among workers in the hairdressing industry in Hongkou District, Shanghai.MethodsA cross-sectional survey was conducted using quota sampling in all eight subdistricts of Hongkou District, Shanghai. Hair salons in each subdistrict were ranked by the number of hairdressers and shampoo workers, and the 6 salons with the largest staff size in each subdistrict were selected, resulting in 48 survey sites. Hairdressers and shampoo workers who met the inclusion and exclusion criteria were surveyed using the Chinese version of the Musculoskeletal Disorders Questionnaire. Information on their individual characteristics, musculoskeletal symptoms, and work-related factors was collected. Chi-square tests and Firth logistic regression were used to estimate the prevalence of self-reported WMSDs symptoms and identify associated factors.ResultsThe overall prevalence of self-reported WMSDs symptoms among workers in the hairdressing industry was 45.72%. Among hairdressers, the most commonly affected body regions were the neck (31.51%), shoulders (25.57%), lower back (15.98%), and feet (14.61%). Among shampoo workers, the most commonly affected regions were the neck (24.17%), lower back (24.17%), shoulders (20.83%), and upper back (10.83%). Firth logistic regression showed that fatigue in the corresponding body region after several hours of continuous work was positively associated with self-reported WMSDs symptoms in both types of workers (OR=6.544-52.838). Regarding individual characteristics, shorter height (female≤160 cm, male≤165 cm) was positively associated with self-reported neck and foot symptoms among hairdressers, and self-reported shoulder symptoms among shampoo workers (OR=16.324, 15.084, 9.680). Female shampoo workers had higher odds of self-reported neck symptoms than male shampoo workers (OR=4.924). Smoking was positively associated with self-reported upper-back and lower-back symptoms among shampoo workers (OR=10.544, 4.381). Among work-related factors, maintaining a fixed neck posture for long periods among hairdressers and prolonged standing among shampoo workers were positively associated with self-reported neck symptoms (OR=6.123, 3.080). Among shampoo workers, frequent overtime and maintaining a twisted posture were positively associated with self-reported upper-back symptoms (OR=11.710, 35.306). Sufficient rest time was negatively associated with self-reported foot symptoms among hairdressers (OR=0.238).ConclusionThe prevalence of self-reported WMSDs symptoms was relatively high among workers in the hairdressing industry. Work-related fatigue and awkward working postures were strongly associated with WMSDs symptoms. Measures such as optimizing work-rest schedule, improving ergonomic workplace design, implementing fatigue monitoring and management, promoting work-break exercises, and providing training on appropriate working posture may help reduce the burden of WMSDs symptoms in this occupational group.
BackgroundPer- and polyfluoroalkyl substances (PFAS) are synthetic chemicals characterized by environmental persistence and have been ubiquitously detected in pregnant women. Although existing evidence suggests that PFAS may exert endocrine-disrupting effects, evidence remains limited regarding the associations of individual legacy and emerging PFAS congeners, as well as PFAS mixtures, with fetal hormonal homeostasis.ObjectiveBased on the Jiashan Birth Cohort in China, to investigate the associations between maternal plasma concentrations of legacy and emerging PFAS in the second trimester and levels of multiple hormones in fetal cord blood.MethodsA total of 336 women in the second trimester from the Jiashan Birth Cohort were enrolled. Concentrations of 53 legacy and emerging PFAS were measured in maternal plasma, and levels of eight key hormones were determined in fetal cord blood. Multiple linear regression, restricted cubic spline, and Bayesian kernel machine regression models were used to examine the linear, nonlinear, and joint associations of individual PFAS and PFAS mixtures with fetal cord blood hormone levels.ResultsMaternal plasma concentrations of perfluorononanoic acid, perfluorohexane sulfonic acid, perfluorooctanesulfonic acid, and 8:2 chlorinated perfluoroether sulfonic acid were positively associated with cord blood levels of insulin-like growth factor 1 (IGF1), with β values of 0.040, 0.050, 0.040, and 0.030, respectively (all P<0.05). In contrast, perfluoroheptanoic acid was negatively associated with prolactin levels (β=−0.060, P<0.01). Restricted cubic spline models revealed a nonlinear dose–response relationship between perfluorobutane sulfonic acid and growth hormone (likelihood ratio test P=0.045), with a positive association in the intermediate concentration interval (β=0.261, P=0.010) that turned negative at higher concentrations (β=−0.425, P=0.048), as well as a nonlinear trend between 6:2 fluorotelomer sulfonic acid and prolactin (likelihood ratio test P=0.074). Bayesian kernel machine regression analysis indicated a negative trend between PFAS mixture exposure and cord blood prolactin levels.ConclusionMaternal PFAS exposure in the second trimester is associated with higher insulin-like growth factor 1 levels and lower prolactin levels in fetal cord blood. Prolactin appears to be consistently associated with both individual PFAS congeners and PFAS mixtures. These findings suggest that maternal PFAS exposure may affect fetal endocrine homeostasis by disrupting the hypothalamic-pituitary-prolactin regulatory axis.
BackgroundIn the context of climate change, the health burden associated with non-optimal temperature is becoming increasingly substantial. Emergency ambulance calls (EACs) are a sensitive indicator of acute health effects. However, most previous studies have relied on daily mean temperature (MT) or a single thermal stress indicator, and it remains unclear whether different temperature indicators yield materially different estimates of the health burden attributable to non-optimal temperature.ObjectiveTo compare multiple temperature indicators in evaluating the attributable burden of EACs associated with non-optimal temperature in Dezhou City, Shandong Province.MethodsDaily EACs records and corresponding meteorological data in Dezhou from 2014 to 2023 were collected. A time-stratified case-crossover design with conditional logistic regression, combined with distributed lag non-linear models (DLNM), was employed to examine the exposure-response relationships and population attributable burden of EACs associated with the percentiles of daily MT and 12 commonly used thermal stress indicators.ResultsDuring the study period, a total of 952989 EACs were recorded in Dezhou. For all temperature indicators, the cumulative exposure-response curves showed a V-shaped pattern. Among the attributable fraction (AF) estimates, only those derived from the universal thermal climate index for outdoor shaded space (UTCI3) and wet-bulb temperature (WBT) were significantly lower than the estimates based on MT (P < 0.05); no statistically significant differences were observed for the other indicators. The AF based on MT was 5.24% (95%CI: 4.34%, 6.16%), and the attributable burden was mainly driven by cold temperatures (AF=3.57%, 95%CI: 2.65%, 4.48%). Spatially, high heat-attributable EACs rates per 1000 population were primarily concentrated in the central and southern Dezhou, whereas areas with high cold-attributable EACs rates were more dispersed. The overall spatial pattern of EACs attributable to non-optimum temperatures was more consistent with the distribution of cold-related risks. Subgroup analysis showed that, across susceptible population groups, the AF estimates derived from most thermal stress indicators did not differ significantly from those based on MT.ConclusionIn Dezhou, most thermal stress indicators produce attributable burden estimates for EACs associated with non-optimal temperature that are similar to those based on daily MT, and cold temperatures contribute more to the overall attributable burden. The spatial distribution of EACs attributable to non-optimal temperature is dispersed, whereas heat-attributable hotspots are concentrated in central and southern Dezhou.
BackgroundThe crude mortality rate of sudden death has shown a steady upward trend. Pudong New Area, Shanghai, is a highly urbanized and densely populated district that is substantially affected by the urban heat island effect and has experienced frequent extreme temperature events in recent years. However, evidence on the association between ambient temperatures and sudden death among local residents remains limited.ObjectiveTo examine the association between daily mean temperature and sudden death in Pudong New Area, and to provide evidence for reducing temperature-related risks of sudden death.MethodsData on sudden death, meteorological factors (daily average temperature, daily average relative humidity, and daily average air pressure), and air pollutants [inhalable particulate matter (PM10), sulfur dioxide (SO2), and nitrogen dioxide (NO2)] in Pudong New Area from 2016 to 2021 were collected. A distributed lag non-linear model was used to examine the associations of daily mean temperature with total sudden death and sudden death due to cardiovascular and cerebrovascular diseases, including lagged and cumulative effects (lag0, 0-3, 0-7, 0-14, and 0-21 d). Stratified analyses were performed by sex, age, and education level to identify vulnerable populations. The temperature attributable burden of sudden death was assessed by calculating attributable number (AN) and attribute fraction (AF).ResultsA total of 19458 sudden deaths were reported in Pudong New Area from 2016 to 2021, of which 11082 (56.95%) were due to cardiovascular and cerebrovascular diseases. Both low (P5, 4.6 ℃) and high (P95, 30.2 ℃) temperatures were associated with increased risks of sudden death. The cumulative risks associated with low temperature peaked at lag 0-21 d for both total sudden death and sudden death due to cardiovascular and cerebrovascular diseases. In contrast, the cumulative risks associated with high temperature peaked at lag 0-7 d for total sudden death and at lag 0-3 d for sudden death due to cardiovascular and cerebrovascular diseases. Stratified analyses showed that females, individuals aged ≥65 years, and those with primary school education or below were more sensitive to low temperature; whereas females, individuals aged <65 years, and those with secondary school education or above were more sensitive to high temperature. Using 21.5 ℃ as the minimum mortality temperature, the AN of total sudden deaths attributable to non-optimal temperature was 3791 (95%CI: 1853, 5587), with an AF of 20.41% (95%CI: 9.47%, 28.94%); the AN attributable to low temperature was 3358 (95%CI: 1087, 5062), with an AF of 17.26% (95%CI: 5.89%, 26.01%), whereas the AN attributable to high temperature was 225 (95%CI: −274, 655), with an AF of 2.03% (95%CI: −2.53%, 5.78%). For sudden deaths due to cardiovascular and cerebrovascular diseases, the AN attributable to non-optimal temperature was 2721 (95%CI: 1747, 5575), with an AF of 24.55% (95%CI: 9.59%, 28.65%); the AN attributable to low temperature was 2496 (95%CI: 988, 3562), with an AF of 22.53% (95%CI: 8.97%, 32.41%), whereas the AN attributable to high temperature was 614 (95%CI: −15, 1176), with an AF of 3.15% (95%CI: −0.08%, 6.02%).ConclusionsBoth low (P5, 4.6 ℃) and high (P95, 30.2 ℃) temperatures are associated with increased risks of sudden death in Pudong New Area, Shanghai. High temperature shows a relative short-term effect, whereas low temperature shows a stronger cumulative effect. Females, people ≥65 years, and individuals with primary school educational attainment or below are more vulnerable to low temperature, while females, people <65 years, and those with secondary school educational attainment or above are more vulnerable to high temperature. The attributable burden of low temperature is greater than that of high temperature. Targeted health protection measures should be strengthened for vulnerable populations during extreme temperature events.
BackgroundArsenic exposure has been implicated as an important environmental contributor to pulmonary fibrosis, the pathogenesis of which is closely associated with abnormal activation of pulmonary fibroblasts. However, the specific mechanism remain incompletely understood.ObjectiveTo examine sirtuin 3 (SIRT3) expression during arsenite-induced fibrotic responses in lung fibroblasts, and to investigate its effects on aerobic glycolysis and profibrotic progression, as well as its underlying mechanisms.MethodsHuman embryonic lung fibroblasts (HELF) were treated with sodium arsenite (NaAsO2) at different concentrations (0, 2.5, 5, 10, 20, 40, and 80 μmol·L−1) for 48 h. Cell viability was assessed, and lactate and hydroxyproline (HYP) levels were measured as indicator of glycolytic activity and fibrotic response. Western blot and quantitative polymerase chain reaction (q-PCR) were used to determine the protein and mRNA expression levels of SIRT3, hypoxia-inducible factor 1-alpha (HIF-1α), fibrosis-related genes [Collagen type Ⅰ (Collagen-Ⅰ), and α-smooth muscle actin (α-SMA)], and glycolysis-related genes [pyruvate kinase M2 (PKM2), hexokinase 2 (HK2), and lactate dehydrogenase A (LDHA)].ResultsBased on the cell viability results, the NaAsO2 concentrations of 2.5, 5, and 10 μmol·L−1 for 48 h were selected for subsequent experiments. Compared with the control group, HYP levels were significantly increased in the 2.5, 5, and 10 μmol·L−1 NaAsO2 exposure groups (P <0.05). The protein and mRNA expression levels of HIF-1α, glycolysis-related genes (PKM2, HK2, and LDHA) and fibrosis-related genes (Collagen-Ⅰ, and α-SMA) were significantly upregulated, whereas SIRT3 protein and mRNA expression levels were significantly down-regulated, in the NaAsO2 treated groups compared with the control group (P<0.05). SIRT3 overexpression significantly reduced HYP levels and downregulated the protein and mRNA expression levels of HIF-1α, glycolysis-related genes (PKM2, HK2, and LDHA), fibrosis-related genes (Collagen-Ⅰ, and α-SMA) compared with the NaAsO2 + negative control group (P<0.05). Similarly, HIF-1α knockdown significantly decreased HYP levels and downregulated the protein and mRNA expression levels of glycolysis-related genes (PKM2, HK2, and LDHA) and fibrosis-related genes (Collagen-Ⅰ, and α-SMA) compared with the NaAsO2 + negative control group (P<0.05). In contrast, simultaneous overexpression of SIRT3 and HIF-1α abolished the inhibitory effects of SIRT3 overexporession, as HYP levels and the expression of glycolysis- and fibrosis-related markers showed no statistically significant differences compared with the NaAsO2 + negative control group (P>0.05).ConclusionNaAsO2 exposure could induce profibrotic and glycolysis-related responses in HELF cells, accompanied by SIRT3 downregulation and HIF-1α activation. These findings suggest that the SIRT3/HIF-1α regulatory axis may be a potential target for preventing or attenuating arsenic exposure-related pulmonary fibrotic responses.
Antimicrobial resistance (AMR) is a major global public health challenge. In addition to antibiotic selection pressure, insecticides have attracted increasing attention as widely used non-antibiotic chemicals that may contribute to the emergence and dissemination of bacterial resistance in the environment. This review focused on common insecticides, including organophosphorus insecticides, pyrethroids, and neonicotinoids, and summarized current evidence on their effects on the emergence of AMR, and the spread of antibiotic resistance genes (ARGs). Existing studies suggest that exposure to certain insecticides may reduce bacterial susceptibility to antibiotics and is associated with the proliferation of antibiotic-resistant bacteria, enrichment of ARGs, co-enrichment of mobile genetic elements (MGEs), and enhanced horizontal gene transfer. Potential mechanisms include changes in antibiotic target-related pathways, decreased membrane permeability, activation of efflux pumps, and enzymatic modification or degradation of antibiotics. The dissemination of ARGs may also be promoted through reactive oxygen species (ROS) accumulation, activation of the SOS response, altered cell membrane permeability, changes in extracellular polymeric substance (EPS) synthesis, altered energy metabolism, and regulation of transfer-related genes. Overall, insecticides may act as non-antibiotic selective pressures involved in the evolution and dissemination of bacterial resistance. However, current evidence is still largely derived from laboratory exposure experiments and cross-sectional investigations, and differences among compounds, and long-term risks under real environmental conditions require further clarified. This review may help improve understanding of the environmental health implications of insecticide-associated bacterial resistance and inform risk assessment and prevention strategies for AMR in environmental settings.
BackgroundAgainst the background of global warming, frequent heatwaves pose a major threat to public health. ObjectiveTo investigate the effects of heatwaves on outpatient visits for skin diseases in Urumqi, characterize the exposure–response relationship, identify the critical temperature threshold, and provide scientific evidence for targeted prevention and control of heat-related skin diseases.MethodsData on meteorological conditions, air quality, and dermatological outpatient visits from 10 hospitals in Urumqi were collected from January 1, 2016 to December 31, 2024. A time-stratified case-crossover design combined with a distributed lag model was adopted to construct a conditional logistic regression model, with adjustment for potential confounders, including relative humidity, air pollutants, and COVID-19 lockdown measures. With a maximum lag of 14 d, single-lag and cumulative-lag effects of heatwaves were examined, and the exposure–response relationship between temperature and the risk of dermatological outpatient visit was fitted.ResultsA total of 385 heatwave days were identified in Urumqi from January 1, 2016 to December 31, 2024. These days were concentrated between June and September and showed an increasing annual trend. The median daily number of dermatological outpatient visits during heatwave periods (165 cases) was significantly higher than that during control periods (114 cases) (Z=−5.108, P<0.001). After adjusting for confounders, the odds of dermatological outpatient visits during heatwaves were 1.088 times higher than those of the control period (OR=1.088, 95%CI: 1.069, 1.107). Single-lag effects were statistically significant from lag0 to lag11 (P<0.05), peaking at lag0 (OR=1.088, 95%CI: 1.069, 1.107), showing an acute and immediate effect. Cumulative-lag effects were statistically significant from 1 to 14 d (P<0.05), peaking at lag04 (OR=1.117, 95%CI: 1.099, 1.136). The exposure–response relationship indicated that the OR values increased steeply with increasing temperature when the daily mean temperature exceeded 24.2 ℃, peaking at approximately 28.1 ℃ (OR=1.400, 95%CI: 1.189, 1.649).ConclusionsHeatwave exposure is significantly associated with an increased risk of dermatological outpatient visits among residents in Urumqi. The impact of high temperature on skin diseases is predominantly acute, with peak risks observed on the day of exposure and within the subsequent 4 d. A daily mean temperature of 24.2 ℃ can serve as the critical threshold for heightened dermatological consultation risk. Strengthened health education and early warning systems are recommended to mitigate heatwave-related adverse dermatological outcomes.
BackgroundSilicosis is a progressive pulmonary fibrotic disease caused by long-term inhalation of silica (SiO2) dust, and abnormal fibroblast activation is a central pathological mechanism. Galectin 3 (LGALS3) plays a significant role in fibrosis across multiple organs; however, its specific molecular mechanism in SiO2-induced pulmonary fibrosis remains unclear.ObjectiveTo investigate the role of LGALS3 in silica (SiO2) induced pulmonary fibrosis and its potential molecular mechanisms.MethodsDifferentially expressed genes in mouse lung fibroblasts treated with SiO2 for 56 d were analysed using the GSE183682 single-cell RNA sequencing dataset, followed by pathway enrichment analysis. A mouse model of pulmonary fibrosis was established by intratracheal instillation of SiO2 suspension (50 mg·mL−1, 100 μL). Lung index, hydroxyproline content, and histopathological changes (HE staining) were assessed. Western blot and immunofluorescence staining were used to evaluate the expression of LGALS3, MAPK pathway proteins, and fibrosis markers [collagen type I alpha 1 chain (COL1A1) and α-smooth muscle actin (ACTA2)].ResultsSingle-cell RNA sequencing analysis identified 53 differentially expressed genes in fibroblasts, and Lgals3 was significantly upregulated in the SiO2 group. SiO2 exposure successfully induced pulmonary fibrosis in mice, as indicated by weight loss, elevated hydroxyproline content, alveolar structural disruption, and collagen deposition. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that Lgals3-associated genes were enriched in Toll-like receptor/chemokine signaling pathways. After SiO2 exposure, LGALS3 expression was increased in fibrotic lung tissue and co-localized with ACTA2, an activated fibroblast and myofibroblast marker. This was accompanied by activation of the MAPK signaling pathway.ConclusionLGALS3 may be involved in fibroblast activation and collagen deposition, potentially through activation of the MAPK signalling pathway. These findings suggest that LGALS3 may represent a potential regulatory target in SiO2-induced pulmonary fibrosis.
BackgroundChina has the largest elderly population in the world, and age-related cognitive impairment has become an increasingly important public health issue.ObjectiveTo investigate the associations of exposure to selected essential metals (EMs) and non-essential metals (NEMs) with cognitive function among rural older adults and to examine whether EMs modified the association between NEW exposure and cognitive functions.MethodsA total of 1045 adults aged 60 years and above were enrolled using baseline survey data from a cohort study. Inductively coupled plasma mass spectrometry (ICP-MS) was used to determine urinary concentrations of five EMs (selenium, cobalt, vanadium, manganese, and boron) and five NEMs (arsenic, chromium, cadmium, lithium, and tin). The Mini-Mental State Examination (MMSE) scale was used to assess cognitive function. Generalized linear models (GLMs) and restricted cubic spline (RCS) models were used to examine the associations of individual EMs and NEMs with MMSE scores. Quantile g-calculation (QGC) and Bayesian kernel machine regression (BKMR) models were used to evaluate the associations of EM and NEM mixtures with MMSE scores.ResultsThe mean age of the participants was (69.72±6.63) years, and 511 participants (48.90%) were male. The mean MMSE score was 21.06±5.79. After adjustment for covariates, GLM analysis showed that cobalt (β=0.575, 95%CI: 0.233, 0.918), selenium (β=0.440, 95%CI: 0.045, 0.836), and vanadium (β=0.633, 95%CI: 0.251, 1.016) were positively associated with MMSE scores, whereas tin (β=−0.379, 95%CI: −0.728, −0.029) was negatively associated with MMSE scores. After categorizing metal concentrations into quartiles and including them in the GLM, cobalt (βQ4 vs. Q1=1.697, 95%CI: 0.806, 2.589) and vanadium (βQ4 vs. Q1=1.598, 95%CI: 0.719, 2.477) remained positively associated with MMSE scores, whereas tin (βQ4 vs. Q1=−0.890, 95%CI: −1.771, −0.008) and lithium (βQ4 vs. Q1=−0.794, 95%CI: −1.689, −0.007) were negatively associated with MMSE scores. RCS model showed linear positive associations of cobalt and vanadium with MMSE scores, a linear negative association of tin with MMSE scores, and an inverted U-shaped association between lithium and MMSE scores. Both QGC and BKMR models indicated that the EMs mixture was positively associated with MMSE scores, with cobalt contributing the most. The NEM mixture showed a negative but nonsignificant association with MMSE scores, with lithium contributing the most. When EMs and NEMs were jointly modeled, no significant association was observed between the overall metal mixture and MMSE scores. Interaction analysis suggested a positive interaction between EMs and NEMs in relation to MMSE scores. Stratified analysis showed that, compared with participants with high cobalt or EMs exposure, those with low cobalt or EMs exposure had a more pronounced and statistically significant negative association between NEMs exposure and MMSE scores.ConclusionThe EM mixture is significantly and positively associated with MMSE scores, whereas the NEMs mixture shows a negative but nonsignificant association. EMs and NEMs have a positive interaction on MMSE scores; EMs attenuate the association between NEMs and MMSE scores.
BackgroundAs a traditional labor-intensive industry, the manufacturing sector is an important source of occupational exposure to hazards such as dust, toxic chemicals, and noise. ObjectiveTo analyze the current status and spatiotemporal patterns of occupational hazards including dust, toxic chemicals, and noise in manufacturing workplaces in Shanghai from 2020 to 2025, and to provided evidence for optimizing targeted prevention and control strategies.MethodsWorkplace monitoring data for manufacturing enterprises in Shanghai were obtained from the National Occupational Hazard Factor Monitoring System for Workplaces. Descriptive analyses were conducted to evaluate the exceedance rates of occupational hazard factors related to occupational exposure limits. GeoDa software was utilized to perform spatial autocorrelation analysis of hazard-specific exceedance rates to identify spatial clustering patterns.ResultsFrom 2020 to 2025, the number of monitored manufacturing enterprises in Shanghai increased from 374 to 504. The monitored enterprises were mainly small and micro enterprises located in suburban areas. Over the six-year period, the exceedance rate for dust-exposed work posts decreased from 21.05% to 10.03%, whereas the exceedance rate for chemical toxicant-exposed work posts remained below 3%. Noise showed the highest and most persistent exceedance rate remaining over 20% throughout the study period. Spatial autocorrelation analysis indicated that high-high clusters of dust hazards were consistently concentrated in suburban districts, including Qingpu, Jinshan, and Songjiang. The spatial pattern of chemical toxicant hazards changed over time, with high-low clusters later concentrated in Baoshan and Minhang. High-high clusters of noise hazards showed an expanding pattern, spreading from Qingpu and Songjiang to several other districts, including Jiading, Minhang, and Fengxian.ConclusionOccupational hazards in the manufacturing sector of Shanghai are mainly characterized by exceedances related to dust and noise, with noise emerging as the most persistent and spatially expanding monitored hazard. These hazards exhibit clear spatial heterogeneity: dust-related risks are concentrated in traditional industrial areas, chemical toxicant risks change dynamically with the spatial distribution of industries, and noise-related risks expand across multiple districts. Future occupational interventions should prioritize noise control and implement targeted prevention strategies based on spatial clustering characteristics.
BackgroundDiarrhea disease is a common intestinal infectious disease, and its incidence is affected by meteorological conditions. A better understanding of its epidemiological patterns and influencing factors, together with the construction of reliable prediction models, is of great significance for precise public health prevention and control. ObjectiveTo clarify the epidemic characteristics of adult diarrhea disease in Shanghai, analyze the associations of meteorological factors and a web search index with adult diarrhea disease, and develop and compare forecasting models to support precise regional prevention and control.MethodsWeekly surveillance data of adult diarrhea disease cases from the Shanghai Comprehensive Surveillance Information System for Diarrhea Diseases, together with concurrent meteorological observation data and web search index (Baidu index) data from 2014 to 2019, were collected. A distributed lag non-linear model (DLNM) was adopted to analyze the associations of multiple meteorological factors and the web search index with the number of diarrhea disease cases. By integrating meteorological factors and web search index data, three types of forecasting models were developed, including autoregressive integrated moving average (ARIMA), Random Forest, and extreme gradient boosting (Xgboost), and their predictive performances were evaluated.ResultsAdult diarrhea disease in Shanghai exhibited seasonal variation, with an major incidence peak in summer and winter peaks in some years. The number of cases declined annually after 2015. Mean temperature was significantly associated with the risk of diarrhea disease, and both low and high temperature exposures were associated with increased risks. The highest risk was observed at 32.8°C (RR=2.04, 95%CI: 1.62, 2.55), while the strongest effect of low temperature was observed at 0.9 °C (RR=1.53, 95%CI: 1.25, 1.88). When relative humidity exceeded 69%, the risk of diarrhea disease increased with relative humidity, reaching a peak at 81% (RR=1.20, 95%CI: 1.07, 1.35). When weekly cumulative precipitation exceeded 16 mm, the risk also increased with increasing precipitation, reaching a maximum at 105 mm (RR=1.23, 95%CI: 1.07, 1.42). The web search index was positively associated with the risk of diarrhea disease. Model prediction indicated that both the Random Forest model and the Xgboost model adequately captured the overall trend in diarrhea disease cases, with R2 values generally exceeding 0.7. Notably, the Xgboost model demonstrated greater accuracy in capturing peak intensities.ConclusionMeteorological factors are associated with adult diarrhea disease in Shanghai. The web search index may serve as an auxiliary indicator for diarrhea forecasting. Machine learning models, with advantages in integrating multisource data, may provide effective predictive tools for the prevention and control of diarrhea disease.
BackgroundThe air quality index (AQI), which is based on the concentration of a dominant pollutant, and the air quality health index (AQHI), which is constructed using excess risk estimates for individual pollutants, may not fully capture the health risks associated with combined exposure to air pollutants. These approaches also provide limited information on the relative contributions of different pollutants. Given the geographical heterogeneity in the composition and health effects of air pollutant mixtures, it is necessary to develop region- and disease-specific AQHIs for different population groups.ObjectiveTo develop and evaluate a health risk-based AQHI for respiratory disease mortality associated with air pollutant mixtures using the weighted quantile sum (WQS) regression model and to quantify the relative weight contributions of selected pollutants.MethodsDaily data on six air pollutants, the AQI, meteorological factors, and deaths from respiratory diseases in the central urban districts of Tianjin from 2014 to 2019 were collected and integrated into a time-series database. First, generalized additive models (GAMs) were applied to identify indicator pollutants associated with respiratory disease mortality. Second, the WQS regression model was then applied to estimate the relative weight contributions of selected pollutants and to establish the exposure-response relationship between air pollutant mixtures and respiratory disease mortality for AQHI development. Finally, the exposure-response relationships of the AQHI and AQI with respiratory disease mortality were evaluated and compared across population subgroups and seasons.ResultsFine particulate matter (PM2.5), inhalable particulate matter (PM10), sulfur dioxide (SO2), and ozone (O3) were identified as indicator pollutants for combined air pollution exposure. Particulate matter, including PM2.5 and PM10, and O3 contributed the most to the mixture index, followed by SO2. Each interquartile range (IQR) increase in the WQS-based AQHI was significantly associated with respiratory disease mortality in the total population, males, elderly individuals, non-elderly individuals, and during the warm season. The corresponding excess risks (ER) were 3.79% (95%CI: 1.24%, 6.27%), 4.37% (95%CI: 0.96%, 7.67%), 3.16% (95%CI: 0.47%, 5.77%), 9.36% (95%CI: 2.01%, 16.15%), and 7.13% (95%CI: 1.31%, 13.30%), respectively. Compared with the AQI, the AQHI showed stronger associations with respiratory disease mortality across different population subgroups and seasons.ConclusionPM2.5, PM10, and O3 contribute substantially to the association between air pollutant mixtures and respiratory disease mortality in Tianjin. Compared with the AQI, the WQS-based AQHI better characterizes the association between air quality and respiratory disease mortality across population subgroups.
In the context of global warming, protecting outdoor workers from occupational heat exposure has become an important public health concern. This review summarized the principle, applicability, and limitation of three categories of wet bulb globe temperature (WBGT) prediction models: empirical regression models, heat-balance models, and machine-learning models. Drawing on international experience from the United States, Europe, and Japan, this review further examined the technical challenges of applying WBGT-based prediction models to large-scale occupational heat stress early warning systems. In response to gaps in occupational heat stress management in China, WBGT should be considered a core assessment indicator to support a transition from passive response to proactive intervention. A localized implementation pathway is proposed, incorporating mechanism-based model calibration, regional parameter adaptation, and multi-source data fusion. Strengthening collaboration between public health and meteorological departments and developing platform-based flexible intervention strategies for workers in new forms of employment may improve the targeting of occupational heat stress early warning and health protection. Future research should focus on physics-constrained machine learning, refined microenvironmental prediction, and individualized risk assessment to support the development of a digitally enabled occupational heat-health protection framework.
BackgroundAlthough hand-arm vibration syndrome has traditionally been reported more frequently in colder northern regions, recent cases in Guangdong Province, a subtropical region in the south, exhibit a certain degree of clustering in terms of industry distribution and company size, and for a period of time, they account for a high proportion of the total number of cases reported nationwide.Objective To describe the occupational exposure profile of hand-transmitted vibration (HTV) in Guangdong Province in 2025 and to compare exposure levels across industries, enterprise sizes, and occupational categories.Methods Data were sourced from the Guangdong Provincial Occupational Health Quality Control Platform, to which occupational health technical service institutions across Guangdong Province submitted relevant reports in 2025. The dataset included employers with documented HTV hazards, measurement results, and the number of exposed workers. Exposure levels were categorized into four grades according to the 4-h energy-equivalent frequency-weighted vibration acceleration: Grade I (<1 m·s−2), Grade II (1-2.5 m·s−2), Grade III (>2.5-5 m·s−2), and Grade IV (>5 m·s−2).ResultsA total of 12468 employers with identifiable HTV exposure were identified through the platform in 2025, of which 11710 (93.92%) were in the manufacturing sector. By enterprise scale, 274 (2.20%) were large, 934 (7.49%) were medium-sized, 8 749 (70.17%) were small, and 2511 (20.14%) were micro-sized enterprises, with small enterprises accounting for the largest proportion. Among 22298 job posts with identified HTV exposure, grinding, assembly, polishing, burnishing, and welding were the most common tasks. The M (P25, P75) 4-h energy-equivalent frequency-weighted acceleration [a(4)] was 2.1 (1.5, 2.7) m·s−2, with values ranging from 0.1 to 16.2 m·s−2. Exposure levels were distributed as follows: Grade I, 2835 posts (12.71%); Grade II, 12761 posts, (57.23%); Grade III, 6690 posts, (30.00%); and Grade IV, 12 posts (0.05%), with Grade Ⅱ posts accounting for the largest proportion. Within the manufacturing sector, 21013 exposed job posts were identified, accounting for 94.24% of all exposed posts. Twelve job posts exceeded the occupational exposure limit, of which nine were polishing positions. A total of 115955 workers were exposed to HTV, primarily in manufacturing (110879; 95.62%). Among the exposed workers, 21237, 23454, 65047, and 6217 were employed in large, medium, small, and micro-sized enterprises, respectively. Grinding, assembly, polishing, deburring, and welding were the five most common occupational categories among the exposed workers. The distribution of worker by exposure grade was similar to that of exposed posts: Grade I, 11921 workers (10.28%); Grade II, 65463 workers (56.46%); Grade III, 38447 workers (33.16%); and Grade IV, 124 workers (0.11%).Conclusion In Guangdong Province, HTV exposure is mainly concentrated in the manufacturing sector, particularly in metal product manufacturing, and commonly involves tasks such as grinding, assembly, and polishing. Both exposed enterprises and exposed workers are predominantly concentrated in small enterprises. Grade II exposure accounts for the largest proportion of both exposed job posts and exposed workers, and some workers are at a risk of developing hand-arm vibration syndrome. These findings suggest that targeted occupational management and comprehensive control measures should be strengthened to reduce HTV exposure and prevent hand-arm vibration syndrome.
BackgroundCadmium (Cd) is a highly toxic heavy metal. Chronic low-dose cadmium exposure can lead to renal tubular dysfunction. However, the precise mechanisms by which cadmium induces renal tubular injury through disruption of intracellular metabolic networks remain incompletely understood.ObjectiveTo investigate the toxic effects of cadmium exposure on human renal tubular epithelial cells (HK-2) and to elucidate the associated metabolic regulatory network from the perspective of metabolic reprogramming.MethodsAn in vitro HK-2 cell injury model was established using 5 μmol·L−1 cadmium chloride (CdCl2). The expression of the renal injury marker kidney injury molecule-1 (KIM-1) was determined by Western blot (WB). Glycolytic capacity was evaluated by metabolic flux analysis. Mitochondrial reactive oxygen species (ROS) production was assessed with a fluorescent probe. Mitochondrial membrane potential (MMP) was evaluated after JC-1 staining. Intracellular adenosine triphosphate (ATP) levels were measured using an ATP assay kit. In addition, untargeted metabolomics analysis was conducted to characterize alterations in the intracellular metabolic fingerprint profile and to explore the metabolic pathway changes underlying cadmium-induced renal tubular epithelial cell injury.ResultsCadmium exposure induced injury in HK-2 cells, as indicated by mitochondrial membrane depolarization, increased mitochondrial ROS levels, and decreased intracellular ATP levels. Metabolic flux analysis further revealed significant metabolic reprogramming, characterized by compensatory increases in basal glycolytic rate and maximal glycolytic capacity. Untargeted metabolomics showed depletion of the long-chain acylcarnitine pool and deficiency of key metabolic cofactors, suggesting impaired fatty acid oxidation and mitochondrial energy metabolism. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis indicated that the differential metabolites were mainly enriched in oxidative phosphorylation and glycerophospholipid metabolism. Correlation analysis showed that acylcarnitines were negatively correlated with nucleic acid metabolism-related metabolites, whereas ATP was positively correlated with lysophosphatidylcholine, suggesting that cadmium exposure-induced mitochondrial dysfunction may be accompanied by abnormal DNA metabolism and lipid peroxidation.ConclusionCadmium exposure could induce impaired mitochondrial function, and promote glycolytic metabolic reprogramming in renal tubular epithelial cells. These findings provide new insights into the metabolic mechanisms underlying cadmium-induced nephrotoxicity and may help identify potential metabolic targets for intervention.
BackgroundLong-term exposure to ambient fine particulate matter (PM2.5) is a significant risk factor for cardiometabolic disorders. However, the mechanisms of its interaction with the endogenous circadian system remain incompletely understood.ObjectiveTo investigate whether chronic PM2.5 exposure interferes with the rhythmic expression of the cardiac circadian clock, thereby disrupting downstream antioxidant defenses and metabolic homeostasis, and ultimately driving cardiometabolic dysfunction.MethodsSeventy-two male C57BL/6 mice were randomly divided into a PM2.5 exposure group (PM group) and a filtered air control group (FA group). Whole-body exposure was conducted for 8 weeks in a meteorological environmental animal exposure system. Samples were collected at six distinct zeitgeber time (ZT) points post-exposure. The 24 h ambulatory blood pressure and serum lipid profiles were monitored. Rhythm parameters were derived via cosinor analysis to compare differences in Midline statistic of rhythm (Mesor), amplitude, and phase between the two groups. The rhythmic expression of core circadian clock genes and antioxidant genes in the myocardium was detected by quantitative polymerase chain reaction (qPCR). Myocardial reactive oxygen species (ROS) levels and downstream pathway protein expression were analyzed by immunofluorescence and Western blot (WB), respectively. The expression changes of the clock gene retinoic acid receptor-related orphan receptor α (RORα) were assessed at both the mRNA and protein levels. Finally, Spearman correlation analysis was used to explore the relationships among myocardial RORα expression, lipid profiles, and oxidative stress indicators.ResultsCompared to the FA group, mice in the PM group exhibited a blunted circadian rhythm in blood pressure, characterized by sustained elevation throughout the day. Chronic PM2.5 exposure showed a significant interaction with ZT on systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) (F-interaction=9.11, 5.70, and 6.02, respectively; P<0.05), as well as on serum triglycerides (TG), total cholesterol (T-CHO), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) (F-interaction=16.32, 11.12, 15.39, and 28.09, respectively; P<0.05). Cosinor analysis further revealed that the Mesor values of T-CHO, TG, and LDL-C were significantly increased (P<0.05), while that of HDL-C was significantly decreased in the PM group (P<0.05). The oscillation amplitudes of SBP, DBP, and MAP showed a decreasing trend, whereas those of TG and LDL-C were significantly increased (P<0.05). Furthermore, SBP, T-CHO, and HDL-C all exhibited a significant phase delay (P<0.05). Mechanistically, PM2.5 exposure significantly suppressed the expression of the positive circadian regulator RORα in the myocardium, leading to disordered rhythmic expression of core clock genes (Bmal1, Clock, Per1/2, and Cry1/2). This exposure also inhibited the rhythmic expression of antioxidant genes (GPX1, SOD2, and CAT), resulting in increased ROS generation and elevated expression of calcium/calmodulin-dependent protein kinase II (CaMKII) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) proteins. Correlation analysis further revealed that myocardial RORα expression level was negatively correlated with T-CHO, TG, and LDL-C (r=−0.55, −0.63, and −0.51, respectively; P<0.001), and positively correlated with HDL-C (r=0.37, P=0.010), and antioxidant genes GPX1, SOD2, and CAT expression (r=0.34, 0.35, and 0.56, respectively; P < 0.001).ConclusionChronic PM2.5 exposure induces cardiometabolic dysfunction by suppressing myocardial RORα expression. This suppression disrupts the cardiac circadian clock and the diurnal balance of oxidative stress, triggering oxidative damage and elevating expression of CaMKII/NADPH pathway proteins. Collectively, these alterations precipitate the loss of cardiac metabolic rhythms and subsequent functional impairment.
[Background]Organophosphate esters(OPEs)are a class of emerging persistent organic pollutants widely used as flame retardants and plasticizers.Investigating their occurrence and ecological risks in aquatic environments is essential for the water quality monitoring and precise manage-ment of the Haihe River. [Objective]To develop and validate an efficient and accurate liquid chromatography-tandem mass spectrometry(LC-MS/MS)method for the simultaneous determination of 16 OPEs in wa-ter,to systematically investigate their spatiotemporal occurrence and ecological risks in the mainstream of the Haihe River,and to provide robust data to support local water environment governance. [Methods]Surface water samples were collected from the mainstream of the Haihe River across seven sampling campaigns in 2025:at the end of each quarter(March,June,September,and De-cember),and during the normal(May),wet(August),and dry(November)seasons.Target OPE concentrations were determined using the established LC-MS/MS method.The spatiotemporal distribution of OPEs were revealed by cluster analysis and Spearman correlation analysis using SPSS 27.0.Ecological risks were evaluated using the risk quotient(RQ)method. [Results]All 16 target OPEs were detected in the mainstream of the Haihe River.The total OPE concentration ranged from 60.1 to 2.37×103 ng·L-1,with a median of 437 ng·L-1 and a mean of 502 ng·L-1.Halogenated OPEs were the dominant pollutants,accounting for 74.4%of the total OPE load.Total concentrations exhibited significant seasonal variations,peaking in the summer(wet season)and reaching their lowest in winter(dry season).The ecological risk assessment indicated that most individual OPEs posed low risks to aquatic organisms,but the aromatic compound 2-ethylhexyl diphenyl phosphate(EHDPP)exhibited high risks(RQ>1)to crustaceans at specific sampling sites(S13,S15)in the Binhai New Area during the wet season. [Conclusion]The mainstream of the Haihe River is ubiquitously contaminated by OPEs at levels comparable to other major water bodies in China,posing an overall low ecological risk.However,the dominance of halogenated OPEs,elevated pollution levels during the wet season,and localized high risks posed by EHDPP suggest that continuous monitoring and targeted management of OPEs in the Haihe River are imperative to safeguard the health of the aquatic ecosystem.
Toluene, a widely used organic solvent, has emerged as a major occupational health concern due to its central nervous system toxicity. With the advancement of toxicological research, our understanding of its pathogenic mechanisms has evolved from macroscopic neurobehavioural disorders to microscopic molecular networks. This review outlined the physicochemical properties of toluene, the evolution of its occupational exposure limits, and its in vivo metabolic activation pathways. Drawing upon the latest epidemiological and neuroimaging evidence, we systematically reviewed the structural and functional neurological damage induced by its acute and chronic exposure. Building on this foundation, the molecular mechanisms underlying toluene neurotoxicity were discussed from three perspectives: imbalances in synaptic excitation/inhibition networks, oxidative stress and neuroinflammatory cascades, and epigenetic reprogramming (particularly DNA methylation and histone modifications). To address the challenges of real-world complex exposures, this review highlighted risk assessment and targeted intervention strategies driven by multi-omics technologies and novel early-warning biomarkers. Ultimately, this review aims to provide forward-looking evidence to support the scientific revision of toluene occupational exposure limits and to safeguard the brain health of occupationally exposed populations throughout their life cycle.
BackgroundNickel oxide nanoparticles (NiO NPs) are widely used in industrial applications and can enter the body through the respiratory tract, where they may induce oxidative stress, inflammation, and lung tissue injury, posing a substantial occupational and environmental health risk. Sodium houttuyfonate (SH) exhibits anti-inflammatory, antioxidant, and immunomodulatory properties, alongside a favorable safety profile. ObjectiveTo investigate the protective effects of SH against NiO NP-induced oxidative stress and injury, and to explore the possible molecular mechanisms involved. MethodsBoth in vitro and in vivo experiments were conducted to establish NiO NP-induced lung injury models and to evaluate the effects of SH and its different formulations on oxidative stress injury. In the in vitro experiment, a NiO NP-induced injury model was established in rat alveolar type II epithelial cells (ACE-II). Malondialdehyde (MDA) levels, glutathione (GSH) levels, and superoxide dismutase (SOD) activity were measured. The gene and protein expression levels of molecules in the Kelch-like ECH-associated protein 1-nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Keap1-Nrf2/HO-1) signaling pathway were detected by quantitative real-time PCR (qPCR) and Western blotting. In the in vivo experiment, a NiO NP exposure model was established in Wistar rats. SH and its formulations were administered by gavage or aerosol inhalation, and the above oxidative stress and signaling pathway indicators were examined in lung tissue. ResultsAfter NiO NP exposure, GSH levels and SOD activity in ACE-II cells were significantly decreased, while MDA levels were significantly increased (P<0.001, P<0.01, and P<0.001, respectively). SH intervention increased GSH levels and SOD activity and reduced MDA levels (P<0.05). NiO NPs also upregulated the mRNA and protein expression of Keap1 and downregulated the mRNA and protein expression of Nrf2 and HO-1 (P<0.05), while SH treatment reversed these changes to varying degrees. In the in vivo experiment, GSH levels and SOD activity in lung tissue were decreased, whereas MDA levels were increased in the model group (P<0.05). Histopathological examination showed thickening of the alveolar wall, inflammatory cell infiltration, and focal congestion and hemorrhage. All SH formulations increased GSH levels and SOD activity and alleviated pathological lung injury. Among the tested formulations, the nanoemulsion aerosol group showed a more pronounced regulatory effect on molecules related to the Keap1-Nrf2/HO-1 pathway (P<0.05). ConclusionSH significantly alleviates NiO NP-induced pulmonary oxidative stress injury by reducing MDA levels, enhancing GSH levels and SOD activity, and modulating the Keap1-Nrf2/HO-1 signaling pathway. These findings suggest that SH has antioxidant protective potential against NiO NP-induced lung injury. The nanoemulsion aerosol formulation may enhance the bioavailability of SH, providing experimental evidence for developing pharmacological strategy against NiO NP-induced pulmonary injury.
This paper introduced the classification, sources, and human exposure status of synthetic antioxidants as emerging environmental pollutants, highlighting their widespread presence in human biological matrices, including urine, blood, adipose tissue, and follicular fluid. It summarized the physicochemical properties and exposure characteristics of four major classes of synthetic antioxidants—synthetic phenolic antioxidants, amine antioxidants, organophosphite antioxidants, and sulfur-containing antioxidants—and systematically outlined their effects on reproductive function at multiple levels, including testicular development and sperm quality, ovarian reserve, endocrine homeostasis, pregnancy establishment and maintenance, and fetal development. Additionally, this paper analyzed the adverse impacts of synthetic antioxidant exposure on the pregnancy outcomes of assisted reproductive technology. Based on current evidence, this paper contends that synthetic antioxidants exhibit multi-target and multi-mechanism reproductive toxicity, potentially impairing reproductive function through pathways such as the induction of oxidative stress, disruption of calcium homeostasis, and activation of autophagy and apoptosis. However, current epidemiological evidence remains insufficient, particularly with respect to exposure data derived from reproductive-related biological samples, such as follicular fluid and semen. Future research should prioritize the reproductive toxicity of synthetic antioxidants, explore interactions among underlying mechanisms, and promote the identification of relevant biomarkers. These efforts will provide a scientific basis for understanding reproductive toxicity, improved population risk assessment, developing targeted intervention strategies, and optimizing clinical practices in assisted reproductive technology.
