What is already known about this topic?:Impact of individual and biomechanical risk factors on musculoskeletal disorders (MSDs) has been researched; however, the factors of intervenable work organization (e.g., overtime and rest breaks) require in-depth investigation, particularly in the context of national policy changes in China by 2025. What is added by this report?:Among 88,609 participants, 37.5% (33,247/88,609) had MSDs. We found that working hours [prevalence ratio (PR)=1.18], shift work (lower back, elbows, hips/thighs, and ankles/feet, P<0.05), overtime (PR=1.23), staff shortages (PR=1.23), covering for absent coworkers (PR=1.18), and resuming work after rest (PR=1.09) were all likely associated with a significantly increased prevalence of MSDs and pain scores in several body parts (P<0.05). What are the implications for public health practice?:Our findings contribute to efforts to standardize work organization management to prevent MSDs, providing reference for employers and policymakers to regulate rest breaks, manage overtime, and ensure adequate levels of staffing to comply with occupational health regulations.

The expanding use of ternary lithium-ion batteries has raised growing concerns about their potential ecological and health risks in recent years. This study aimed to investigate the effects and underlying mechanisms of the ternary lithium-ion battery cathode material lithium nickel-cobalt-manganese oxide (NCM523) on planarian locomotor activity, growth, and regeneration, providing insight into the environmental and ecological hazards. Freshwater planarians (Dugesia japonica) were exposed to NCM523-shrimp paste mixtures via feeding. The median lethal concentration (LC50), locomotor activity, growth, regeneration capacity, oxidative stress markers, and expression levels of related genes were evaluated. Exposure to NCM523 induced significant toxicity in planarians, with a 72-h LC50 of 401.5 μg mg⁻¹ (95% CI: 387.7 to 418.1). Elevated malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) activity, together with reduced glutathione peroxidase (GPx) and catalase (CAT) activities, indicated that NCM523 exposure triggered oxidative stress in a concentration-dependent manner. Concurrently, planarians exhibited reduced locomotor activity and marked delays in both growth and regeneration as NCM523 concentrations increased. These physiological impairments were accompanied by upregulation of regeneration-associated genes, including Dj-GATA4/5/6, Dj-PCNA, and Dj-nlg. In conclusion, these findings demonstrate that NCM523 adversely affects planarian locomotor activity, growth, and regeneration, providing crucial in vivo evidence for assessing the potential ecotoxicological risks of ternary lithium-ion battery cathode materials.

BackgroundAcute paraquat (PQ) poisoning is associated with high mortality and rapid multi-organ injury. Early risk stratification is particularly important when plasma or urine PQ concentrations are unavailable. This study aimed to characterize acute PQ poisoning and identify routinely available admission variables associated with in-hospital death.MethodsWe retrospectively enrolled 128 consecutive patients with acute PQ poisoning admitted to Guangzhou Twelfth People’s Hospital between January 2008 and December 2020. Patients were categorized as survivors (n = 46) or non-survivors (n = 82) according to in-hospital outcome. Continuous variables were analyzed using the Mann–Whitney U test and categorical variables using the chi-square test or Fisher’s exact test, as appropriate. Clinically relevant admission variables were screened for collinearity and entered into a backward stepwise binary logistic regression model in SPSS 25.0. ROC curves were generated in R, and AUCs with 95% confidence intervals were calculated.ResultsThe in-hospital mortality rate was 64.06%. Compared with survivors, non-survivors had significantly higher ingested dose, coagulation indices, inflammatory markers, liver injury markers, renal function indices, and myocardial injury markers (all p < 0.05). In multivariable analysis, ingested dose (OR = 1.016, 95% CI: 1.003–1.029, p = 0.015) and AST (OR = 1.027, 95% CI: 1.011–1.042, p = 0.001) were independently associated with in-hospital death. AST showed the best discrimination among single markers (AUC = 0.911, 95% CI: 0.855–0.958).ConclusionIngested dose and AST were independently associated with in-hospital death in acute PQ poisoning, and AST showed the best single-marker discriminative performance.

ObjectivePesticide self-poisoning is a major global public health issue, yet the post-discharge mental health of survivors remains poorly characterized. To investigate the physical and mental health among survivors of diquat self-poisoning after returning to the community, which informs the effective prevention and intervention measures of repeated suicide.MethodsA follow-up study of 25 patients with acute diquat self-poisoning was enrolled from Guangzhou twelfth people’s hospital during 2017 to 2023. The health-related quality of life (HRQoL) was evaluated using the MOS 36-item short-form health survey (SF-36), and anxiety and depression were, respectively, assessed using Generalized Anxiety Disorder-7 (GAD-7) and ‌Patient Health Questionnaire-9 (PHQ-9) scales.ResultsTwenty-five (25) diquat self-poisoning patients were enrolled in a follow-up study, with a median follow-up of 1.58 person-years. Most participants had low scores in mental health of the HRQoL survey, with a median score was 108.15. In SF-36 domains, only Role Physical (RP) scored significantly lower in the high-dose group (p = 0.04). Persistent neurological issues (fatigue, forgetfulness, headache) were the primary physical complaints. HRQoL total scores were significantly shaped by sleep duration, history of major trauma, left-behind child status, and psychological symptoms (p < 0.05). Anxiety and depression symptoms had high prevalent rates of 56 and 68%, respectively. Stratified analysis by toxic dose [low-dose (≤ 50 mL, n = 12) vs. high-dose (> 50 mL, n = 13)] revealed no statistically significant differences in anxiety or depression rates.ConclusionDiquat self-poisoning survivors may experience persistent physical and psychological health difficulties after returning to the community, warranting further attention. The findings highlighted that prevention of repeated self-harm is still necessary among at-risk populations after returning to the community, particularly adolescents and young adults.

This study investigated ‌the protective effect of nuclear factor erythroid 2-related factor 2 (Nrf2) against diquat-induced acute kidney injury (AKI) by regulating mitochondrial ferritin (FtMt). A model of kidney injury was established in male Wistar rats by oral gavage of diquat. The rats were randomly assigned to four experimental groups: control, diquat, diquat + Liproxstatin-1 (Lip-1, a ferroptosis inhibitor), and diquat + Sulforaphane (SFN, an Nrf2 activator). Kidney injury markers, oxidative stress levels, and the expression of ferroptosis-related proteins, Nrf2 and FtMt, were assessed. Results showed that Diquat induced dose- and time-dependent AKI and ferroptosis, with a significant decrease in the expressions of Glutathione Peroxidase 4 (GPX4), cystine/glutamate antiporter solute carrier family 7 member 11 (SLC7A11; also known as xCT), and Nrf2. Concurrently, diquat also upregulated the expression of ferritin heavy chain 1 (FTH1) and FtMt. Inhibition of ferroptosis alleviated AKI while upregulating Nrf2 and downregulating FtMt expression. SFN targeted the activation of Nrf2 expression, which significantly alleviated ferroptosis and downregulated the FtMt expression. Immunofluorescence co-localization analysis further revealed co-localization of Nrf2 and FtMt in kidney tissues. In conclusion, these findings demonstrate that Nrf2 activation attenuates diquat-induced renal ferroptosis by modulating FtMt expression, suggesting that they may serve as a potential therapeutic target for preventing diquat-induced kidney injury.

BackgroundThe increasing cosmetic use of botulinum toxin has been accompanied by poisoning events related to inappropriate administration, including excessive dosing, unapproved or unverifiable products, self-injection, and procedures performed outside regulated medical settings. However, the inpatient clinical profile and predictors of prolonged hospitalization remain insufficiently defined. This study aimed to describe the clinical characteristics of cosmetic botulinum toxin poisoning and identify factors associated with longer hospital stay.MethodsWe conducted a retrospective cohort study of patients hospitalized for cosmetic botulinum toxin poisoning at Guangzhou Twelfth People’s Hospital between August 2024 and January 2025. Demographic data, injection-related characteristics, clinical manifestations, antitoxin treatment, hospitalization duration, and available clinical outcomes were extracted from medical records. Patients were divided into a short-stay group (<7 days) and a prolonged-stay group (≥7 days). Univariate analyses and multivariable Cox regression were performed to identify factors associated with hospitalization duration. A nomogram was developed to estimate length of stay.ResultsA total of 145 patients were included, with a median age of 37 years; 97.93% were female. The most common injection sites were the forehead (26.35%), periocular region (16.77%), and jaw (11.98%). The most frequent manifestations were dizziness (89.66%), dysphagia (85.52%), blurred vision (75.17%), ptosis (68.28%), and slurred speech (24.83%). In multivariable Cox regression, duration of antitoxin therapy, dysphagia, and slurred speech were independently associated with prolonged hospitalization. A nomogram based on these variables showed acceptable calibration performance (MSE = 1.302; MAE = 1.029). No in-hospital deaths occurred.ConclusionCosmetic botulinum toxin poisoning is characterized mainly by cranial nerve-related and bulbar manifestations. Dysphagia, slurred speech, and antitoxin treatment duration were independently associated with prolonged hospitalization. The nomogram may support early risk stratification and inpatient management, although external validation is needed.

While perfluorooctane sulfonate (PFOS) has been epidemiologically associated with ocular disorders, its direct specific role in retinal disease and the underlying molecular mechanisms are still not well understood. We initially examined serum PFAS levels in relation to retinal diseases among 777 participants (666 controls vs. 111 cases) from the Isomer of C8 Health Project in China. Then, C57BL/6 mice were orally gavaged with PFOS at doses of 0.8, 8, and 80 μg/kg/day for 90 days in vivo. The retinal ganglion cell line (RGC-5) was also exposed to PFOS at concentrations of 0, 1, 10, and 100 μM for 24 h in vitro. Epidemiological analysis showed a significant positive association between serum PFOS levels and the risk of retinal disease (OR = 1.46, 95%CI: 1.20, 1.80). In mice, exposure to PFOS caused progressive retinal thinning, retinal ganglion cell (RGC) loss, and retinal inflammation. In RGC-5 cells, PFOS activated Caspase-8, which led to cleavage of both GSDMD and GSDME, thereby inducing pyroptosis. Blocking Caspase-8 significantly reduced pyroptotic cell death involving GSDMD or GSDME. This study identifies PFOS as a new environmental trigger for retinal diseases through Caspase-8-mediated dual cleavage of GSDMD and GSDME. Our findings connect human exposure data with mechanistic toxicology and highlight the Caspase-8-gasdermin axis as a potential therapeutic target for PFOS related retinal disease.

Introduction:Paraquat (PQ) and diquat (DQ) are highly toxic bipyridyl herbicides, but their dominant organ injury patterns and clinical outcomes are not identical. This study aimed to compare the clinical characteristics, organ injury profiles, and prognosis of acute PQ and DQ poisoning. Methods:This retrospective single-center cohort study included consecutive patients with acute oral PQ or DQ poisoning treated at Guangzhou Occupational Disease Prevention and Treatment Hospital between January 2012 and January 2022. Baseline characteristics, clinical manifestations, admission laboratory findings, and in-hospital outcomes were compared between 270 patients with PQ poisoning and 115 patients with DQ poisoning. Results:PQ poisoning was associated with a higher crude in-hospital mortality rate than DQ poisoning (142/270 [52.6%] vs. 29/115 [25.2%], p < 0.001), shorter hospital stay, higher admission creatinine levels, and more frequent mediastinal emphysema. In contrast, DQ patients were younger, reported larger ingestion amounts, presented later to the local hospital, and more often showed nausea/vomiting, disturbance of consciousness, seizures, reduced responsiveness, agitation, dysarthria, anuria, and pleural effusion. The DQ group also had significantly higher CK and CK-MB levels, suggesting more prominent neuromuscular involvement. Kaplan-Meier analysis showed a significant difference in overall survival between the two groups. Conclusion:PQ and DQ poisoning show distinct clinical phenotypes and should not be managed as interchangeable toxic syndromes. Rapid toxin identification and toxin-specific monitoring may help guide early risk stratification and supportive care.

Background Limited research has explored the relationship between occupational noise exposure and liver enzymes, particularly at the individual exposure level. This study examines the association between occupational noise exposure and liver enzyme levels and the mediating role of metabolic dysfunction-associated fatty liver disease (MAFLD). Methods We recruited 3,427 workers from two factories in Guangzhou, China. Cumulative noise exposure (CNE) was estimated based on noise levels and years of exposure. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) levels were obtained from medical examinations. Linear and logistic regression models, along with subgroup and mediation analyses, were employed to assess the associations between CNE and liver enzyme levels. Results Cumulative noise exposure (CNE) demonstrated a dose-response relationship with liver health indicators, with significant associations observed across different statistical models. Specifically, each 10 dB(A)-year increase in CNE was associated with a 2.10 U/L increase in ALT levels and a 26% higher risk of elevated ALT. Concurrently, categorical models revealed that workers in the highest CNE group had significantly increased risks of elevated ALT, AST, and GGT, with the most pronounced effect observed for AST. These associations were significantly strengthened by insufficient physical activity (P- for interaction<0.05). Notably, MAFLD mediated approximately 15-20% of the observed associations between CNE and liver enzymes (such as ALT and GGT). Conclusion Occupational noise exposure is positively associated with liver enzymes, with MAFLD as a partial mediator. Noise control measures and liver function monitoring may help mitigate liver dysfunction.

The deep integration of social media into daily routines has intensified concerns about problematic social media use among students, adversely affecting both educational outcomes and psychological well-being. Drawing on Social Cognitive Theory and Cognitive-behavioral Theory, this study investigates the roles of academic pressure, anxiety, and depression in the development of social media addiction, with particular attention to the mediating effect of self-control and the moderating role of social support. A survey of 900 college students collected data on these key variables. Structural equation modeling revealed that: academic pressure, anxiety, and depression directly increase social media addiction while also reducing self-control, which mediates the associations. Social support weakens the relationship between academic pressure and social media addiction, yet it fails to significantly moderate the link between anxiety and social media addiction. These findings reveal a multi-layered mechanism underlying social media addiction and provide valuable guidance for intervention strategies in higher education contexts.

INTRODUCTION:Diquat-induced toxic encephalopathy remains inadequately understood. METHODS:Data on patients with acute diquat poisoning were retrospectively collected from May 2017 to May 2023. The diagnosis was confirmed qualitatively by ultra-high performance liquid chromatography quadrupole-time of flight mass spectrometry. A follow-up study was designed to explore the long-term health effects of diquat poisoning. RESULTS:A total of 129 patients with acute diquat poisoning were included in this study. Thirty-four patients died (27 of whom developed toxic encephalopathy) following a median dose of diquat (200 g/L) 190 mL (IQR:100-200 mL). Forty-five patients were diagnosed with toxic encephalopathy, mainly involving the brainstem, bilateral cerebellar peduncles, and basal ganglia. The development of toxic encephalopathy was associated with a significantly higher risk of death (odds ratio = 16.5; 95%CI: 6.2-43.8; P <0.001). Twenty-five of the 95 survivors were enrolled in a follow-up study. The main persistent features were peripheral nerve injuries in 20%, suspected peripheral nerve injuries in 40%, and reduced compound muscle action potential in 84%; chronic-phase encephalopathy occurred in 28%. Transcriptomic analysis revealed significant changes in the expression profiles of neuroregulatory factors, including inhibin-βA and sonic hedgehog. DISCUSSION:Toxic encephalopathy represented an important organ injury caused by acute diquat poisoning, which was strongly associated with an increased risk of death. Peripheral nerve injuries were also common at follow-up. Several limitations should be noted, including the lack of diquat concentrations, the small sample size, the short follow-up duration, and the single-center design. CONCLUSIONS:Thirty-four of 129 (26.4%) patients died from diquat poisoning. Toxic encephalopathy was diagnosed in 45 of 129 (34.9%) patients, and its development was associated with a significantly higher risk of death. Follow-up revealed peripheral nerve injuries in 20% of patients, and chronic-phase encephalopathy in 28%.

Introduction1,2-Dichloroethane (1,2-DCE) is a highly toxic industrial organic solvent that can cause acute toxic encephalopathy through occupational exposure, with underreported clinical data in English literature. To explore the clinical characteristics and patients’ response to supportive treatments of toxic encephalopathy caused by 1,2-DCE.MethodsFifty-nine patients with acute 1,2-DCE poisoning admitted to the hospital from January 2009 to December 2022 were selected. Patients were divided into three groups based on clinical manifestations: intracranial hypertension (Group A), limb tremors (Group B), and behavioral changes (Group C).ResultsToxicology testing found that 1,2-DCE was difficult to detect in serum after more than 24 h. Of the 59 patients, 45 (76.27%) achieved complete recovery, 10 (16.95%) achieved partial recovery, and 4 (6.78%) died. Statistical analysis showed a significant difference in recovery rates among the three groups (χ2 = 10.612, P < 0.05). There were no statistically significant differences in symptom and cranial imaging recovery times between the three groups.ConclusionAcute 1,2-DCE poisoning can cause severe toxic encephalopathy. Early and prolonged treatment with dehydrating agents and glucocorticoids is effective in improving prognosis, and patients with intracranial hypertension are at higher risk of death due to brain herniation.

BackgroundOccupational noise exposure has been linked to various adverse health outcomes, including metabolic disorders. However, limited evidence exists regarding its association with metabolic dysfunction-associated fatty liver disease (MAFLD). This study aimed to investigate the association between occupational noise exposure and MAFLD among automotive manufacturing workers, providing scientific evidence for the prevention and management of MAFLD in occupational populations.MethodsA cross-sectional study involving 3,427 male workers from two automobile manufacturing enterprises in Guangzhou, China, was conducted in 2023. Individual occupational noise exposure levels were assessed via cumulative noise exposure (CNE). MAFLD was diagnosed on the basis of ultrasound imaging and metabolic criteria, including obesity, type 2 diabetes, or metabolic dysregulation. Logistic regression models were used to evaluate the associations between CNE and MAFLD, adjusting for demographic, lifestyle, and clinical covariates. The interaction effects of shift work and hearing protection device use were analyzed. Mediation analysis was used to assess the role of body mass index (BMI) in the relationship between CNE and MAFLD.ResultsAccording to the continuous models, each 1 dB-year increase in the CNE was associated with a 1.05-fold increased risk of MAFLD (OR: 1.05, 95% CI: 1.02, 1.08). According to the categorical models, workers in the highest CNE quartile (>89.651 dB-years) had a significantly greater risk of MAFLD (OR: 1.50, 95% CI: 1.05, 2.16) than did those in the lowest quartile. Subgroup analyses revealed that the association was more pronounced among workers who did not use hearing protection devices or worked night shifts (p for interaction<0.01). Body mass index (BMI) partially mediated the association between CNE and MAFLD, accounting for 3.48% of the total effect.ConclusionOccupational noise exposure was associated with higher odds of MAFLD, and BMI partially mediated this association. Night/shift work and hearing protection use affect this relationship. These findings emphasize the need for effective noise control and occupational health interventions to mitigate MAFLD risk among workers exposed to noise.

Objective:This cross-sectional study aimed to investigate the associations between dietary factors and morbidity burden among occupational radiation workers in Guangzhou, China, a population with chronic low-dose radiation exposure. Methods:From January to December 2024, 1,080 medical radiation workers were enrolled. Dietary intake was assessed using a validated food frequency questionnaire, and morbidity burden was defined as the presence of clinically diagnosed chronic conditions. Multivariable logistic regression models were employed to evaluate associations, adjusting for demographic, occupational, and lifestyle confounders. Results:The overall morbidity prevalence was 45.5%, with thyroid diseases being most common (23.5%). Significant dietary differences were observed: higher tea consumption (≥3 times/week: OR 0.41, 95% CI 0.26 ~ 0.64), vegetable intake (≥3 times/week: OR 0.44, 95% CI 0.29 ~ 0.67), and fruit consumption (≥200 g/week: OR 0.71, 95% CI 0.53 ~ 0.95) were associated with lower morbidity odds. In contrast, high red meat intake (≥3 times/week: OR 1.88, 95% CI 1.34 ~ 2.67) and a preference for meat over vegetables were associated with higher morbidity odds. Conclusion:Specific dietary patterns, particularly plant-based foods and tea, are inversely associated with morbidity burden in radiation workers. These findings support integrating tailored nutritional guidelines into occupational health frameworks to improve health outcomes among radiation workers.

Background:Occupational radiation exposure poses unique health challenges, with emerging evidence suggesting links between chronic low-dose exposure, multisystem morbidity, and sleep disturbances. This study examines the relationship between cumulative morbidity burden and the risk of sleep disorders among radiation-exposed workers in southern China. Methods:A cross-sectional investigation was conducted from January to December 2024 at Guangzhou Twelfth People's Hospital. Morbidity burden was assessed through physician-diagnosed conditions classified by ICD-10 codes across seven disease categories. Sleep disorders were identified via a study-specific questionnaire. Multivariable logistic regression models, adjusted for demographic, occupational, and lifestyle confounders, were used to quantify associations between morbidity and sleep disorders. Subgroup analyses evaluated effect modification by sex, service duration, and profession. Results:A consecutive sample of 1,089 radiation workers underwent comprehensive health evaluations. Sleep disorders affected 33.0% of participants. A graded dose-response relationship was observed: workers with one morbidity exhibited 2.28-fold higher risk of sleep disorders (95%CI:1.68-3.10) compared to those without comorbidities. Risk increased to OR = 2.89 (1.97-4.25) for two morbidities and OR = 3.81 (2.42-6.01) for ≥3 morbidities after full adjustment. Subgroup analyses revealed significantly stronger associations in women (OR = 3.97, 1.94-8.42), workers with ≤15 years of service (OR = 4.24, 1.97-9.38), and biomedical engineers (OR = 5.75, 2.38-14.33). Thyroid, respiratory, cardiovascular, and lens opacity prevalence differed substantially between workers with sleep disorders and those without. Conclusion:Accumulating morbidity burden is robustly associated with sleep disorder risk among radiation workers, with occupational factors influencing the strength of this association. Biomedical engineers, women, and early-career personnel represent high-risk subgroups that warrant targeted screening and preventive interventions.

Noise, a significant environmental stressor, has been demonstrated to induce dysregulated glucose and lipid metabolism. However, the precise molecular mechanisms driving liver dysfunction in noise-induced dysregulated glucose and lipid metabolism remain incompletely elucidated. Recent studies have underscored the pivotal role of the NLRP3 (Nod-like receptor protein 3) inflammasome in the context of liver pathology. To this end, a noise-exposure rat model was established (100 dB, 4 h/day for 30 days) to investigate whether the NLRP3 inflammasome mediates noise-caused hepatic injury and dysfunction. Exposure to noise resulted in significant alterations to liver architecture and dysfunction in rats. Furthermore, we found that noise triggered assembly and activation of the NLRP3 inflammasome, effects that were suppressed by the NLRP3 inhibitor MCC950. Such inhibition thereby attenuated liver damage and improved hepatic function. In conclusion, our findings indicate that noise-induced NLRP3 inflammasome activation promotes hepatic inflammation, contributing to liver injury and dysregulation of glucose and lipid metabolism. These results provide new mechanistic insights into the pathogenesis of noise-induced liver damage and dysfunction.

Astigmatism is a common refractive error in early childhood that can affect visual function and potentially cause amblyopia if not treated. Although environmental factors are gaining recognition as influences on eye development, the impact of prenatal exposure to perfluoroalkyl and polyfluoroalkyl substances (PFAS) remains uncertain. In this prospective birth cohort study that included 248 mother-child pairs enrolled from the Maternal and Child Health Hospital in Maoming, Guangdong Province, China, between 2015 and 2018, we aimed to examine the association between maternal serum PFAS concentrations during pregnancy and the risk of astigmatism in preschool-aged children aged 3-6 years. After adjusting for covariates, each interquartile range (IQR) increase in total PFAS concentration was associated with 1.29-fold higher odds of astigmatism (95% CI: 1.02, 1.65; p = 0.033) and more negative cylindrical power. The associations were significantly stronger among children born preterm and those with a smaller head circumference at birth. Our findings suggest that prenatal PFAS exposure may disrupt early ocular development, underscoring the need to incorporate gestational environmental chemical exposure into strategies for preventing childhood refractive errors and their long-term visual consequences.

OBJECTIVE:This study aimed to determine the relationship between occupational noise, shift work and non-alcoholic fatty liver disease (NAFLD) in male workers in the automobile manufacturing industry. DESIGN:Cross-sectional study. SETTING:This study was carried out at the Guangzhou Twelfth People's Hospital using data from April to September 2022. PARTICIPANTS:A total of 4672 eligible participants were included in the study. PRIMARY AND SECONDARY OUTCOME MEASURES:Diagnosis of NAFLD was made using ultrasound. Noise was detected according to the Measurement of Physical Factors in the Workplace-Part 8: Noise. Environmental noise intensity was assessed using an EDGE personal noise dosimeter manufactured by CASELLA (UK). The working status of workers was investigated by questionnaire. RESULTS:The OR of NAFLD was 1.39 (1.03, 1.88) in the cumulative noise exposure (CNE)≥95 group compared with CNE<85 group. Improved risk of NAFLD in workers with shift work compared with those without shift work (OR=1.35, 95% CI: 1.09, 1.68). As stratified analyses showed, the ORs of NAFLD prevalence related to occupational noise and shift work exposure appear to be increased in young workers. When both shift work and noise exposure work are present simultaneously, the synergy index between them was 0.47 (95% CI: 0.25, 0.89). Combined effects analysis revealed that the OR of NAFLD was 2.02 (95% CI: 1.34, 2.99) in CNE≥95 and cumulative length of night shifts work>2920 hours. CONCLUSION:Occupational noise exposure may be an independent risk factor for NAFLD. It may synergistically affect disease when combined with night shift work, particularly among younger workers. These findings underscore the importance for companies to prioritise the management and training of younger workers, along with targeted occupational health education initiatives, as crucial measures for reducing the incidence of NAFLD.

Evidence on the preventable disease and economic burdens associated with increasing green spaces for the Chinese population remains lacking. This health impact assessment study aimed to provide such evidence for China between 2000 and 2020. Using two green space proxies (percentage of green space [GS%] and normalized difference vegetation index [NDVI] within a 300-m buffer around each grid cell) and three burden indices (allcause adult mortality, years of life lost [YLLs], and economic costs), we applied a comparative risk assessment framework to estimate the preventable burdens associated with increasing GS% and NDVI within the 300-m buffer to 25% and 0.35, respectively. Moreover, we monetized the health gains using the "value of statistical life" metric. In 2020, we found that increasing GS% within the 300-m buffer to 25% could prevent 0.05 (95% uncertainty interval: 0.00-0.14) million deaths, equivalent to 1.02 (0.00-2.51) million YLLs and an economic value of $113.73 (0.00-286.53) billion. Similar estimates were observed for NDVI within the 300-m buffer. The estimates of preventable burdens were unevenly distributed within China, with urban, eastern, or high-GDP regions-such as Jiangsu and Guangdong provinces-showing higher estimates than other areas. From 2000 to 2020, the preventable burdens estimated via the GS% proxy showed a significant increase, whereas a notable decreasing trend was observed with the NDVI proxy. These findings provide quantitative evidence supporting the health and economic benefits of green spaces and highlight the necessity for greening initiatives in China, particularly in economically developed areas.

A retrospective study comparing paraquat (PQ) and diquat (DQ) poisoning in 270 PQ and 115 DQ patients revealed significant differences in clinical outcomes and organ injury patterns. While both bipyridine herbicides caused multi-organ damage (lungs, liver, kidneys, pancreas, brain), PQ poisoning was associated with a markedly higher mortality rate (55.6% vs. 25.2%, P = 0.000), shorter median treatment duration (P = 0.005), and greater ingested amounts (P = 0.009). PQ predominantly led to fatal pulmonary fibrosis, whereas DQ exhibited more severe renal injury and neurotoxicity. Laboratory findings showed significant differences in median creatinine (Cr, P = 0.013), amylase (AMY, P < 0.001), creatine kinase (CK, P = 0.009), and CK-MB (P = 0.001) between groups, though white blood cell count, ALT, and AST did not differ. These findings underscore the necessity for differentiated clinical management, with early targeted interventions potentially improving prognosis in these high-mortality poisonings.