IntroductionAlthough the effects of ionizing radiation on radiation workers have been extensively studied in China, no prospective cohort study has been conducted in Chongqing. Furthermore, previous cohorts have not provided a broad-gauge assessment of the temporal relationship between low-dose occupational radiation exposure and the risk of health outcomes.MethodsA prospective cohort study will be carried out focusing on radiation workers in Chongqing. Health examination outcomes and radiation dose monitoring data will be collected and analyzed using the distributed lag non-linear model (DLNM) combined with generalized additive model (GAM) or generalized linear model (GLM) to evaluate the exposure-lag response relationship.DiscussionOur study will enhance our understanding of the exposure-lag response association between occupational radiation exposure and the health of radiation workers based on DLNM.Clinical trial registrationChinese Clinical Trials Registry, ChiCTR2400081804.

Zinc oxide nanoparticles (ZnONPs) are widely utilized across various industries, raising concerns about their potential toxicity, especially in the respiratory system. This study explores the role of autophagy, regulated by microtubule-associated protein 1A/1Blight chain 3B (LC3B), in ZnONPs-induced toxicity using both in vivo (LC3B knockout mice) and in vitro (BEAS-2B cells) models. Our findings demonstrate that LC3B-regulated autophagy mitigates ZnONPs-induced epithelial cell dysfunction and acute lung injury. In the absence of LC3B, oxidative stress, inflammation, and intracellular zinc accumulation are exacerbated, resulting in mitochondrial dysfunction and epithelial cell death. In vitro, LC3B knockdown disrupted zinc ion transporter expression and impaired mitophagic flux in BEAS-2B cells. Treatment with zinc ion chelators alleviated these toxic effects, confirming that free zinc ions play a critical role in driving ZnONPs toxicity. These findings highlight that targeting autophagy and maintaining zinc homeostasis could offer therapeutic strategies to reduce ZnONPs-induced lung damage.

Environmental arsenic has been extensively documented to induce neuroinflammation and various neurological disorders. Iron overload has been demonstrated to induce microglial activation, subsequently resulting in neurological dysfunction, while the precise molecular mechanisms remain to be elucidated. In this study, we demonstrated that iron chelation therapy ameliorated arsenic-induced iron overload and microglial activation, which was mediated by ferritinophagy. Upon arsenic exposure, N6-methyladenosine (m6A) modification levels were significantly elevated, corresponding to a reduction in fat mass and obesity-associated protein (FTO). Notably, both systemic and microglial-specific Fto knock-in transgenic mice demonstrated resistance to arsenic-induced microglial activation and neurological dysfunction. Conversely, systemic knock-down and conditional microglial-specific knock-out of Fto exacerbated arsenic-induced microglial activation. Through m6A-sequencing analysis, ATG9A was identified as the predominant m6A-modified autophagy-related gene in arsenic-induced ferritinophagy. The expression of ATG9A was found to be regulated by FTO in an m6A-dependent manner. Importantly, ATG9A knock-down significantly attenuated ferritin degradation in arsenic-treated microglial cells. Human cortical tissues result revealed a positive correlation between arsenic concentration and levels of iron, ATG9A, and inflammatory factors, while FTO and Ferritin levels were inversely correlated with arsenic content. These findings suggest that FTO represents a promising therapeutic target for the amelioration of arsenic-related neurotoxicity .

People are paying more and more attention to the effects of environmental factors such as heavy metals on depression, and heavy metals may destroy the homeostasis of vitamin D in the body by affecting human metabolism, and the lack of vitamin D will increase the risk of depression. There are few studies on vitamin D deficiency in depression caused by heavy metals, and it is not deep enough. Therefore, this study used logistic regression, restricted cubic spline curve, weighted quantile and Quantile g-computation model to analyze the effects of heavy metal exposure alone and in combination on vitamin D and depression, as well as the potential role of vitamin D deficiency in the process of heavy metal-induced depression. The results showed that cadmium exposure alone or in combination increased the risk of depression (P < 0.05). When Cd increased by 1 unit, the risk of depressive symptoms increased by 1.178 units. Arsenic and its compounds and lead affected vitamin D levels in the body and contributed the second highest or highest weight in the mixture (P < 0.05). It is worth noting that after grouping according to vitamin D deficiency, compared with the normal group, the mixed exposure of heavy metals in the vitamin D deficiency group had more types of metals related to depression and contributed more weight (P < 0.05). This study found that single metal or multi-metal mixed exposure is associated with depression. Vitamin D deficiency may increase the risk of depression. Vitamin D may be a potential factor in the treatment of depression caused by metal, and the specific mechanism of action needs further study.

Objective In order to improve the service quality of the occupational health technical service industry in Chongqing,the status and influencing factors of professional competence among personnel in this industry were surveyed.Methods A questionnaire survey was conducted on 197 participants in the first skills competition of professionals in the occupational health technical service industry.Their competition scores and associations with their characteristics were analyzed.Results The skill competition covered three categories,namely occupational health assessment and testing(64 persons),radiation health assessment and testing(40 persons),and occupational health examination(93 persons),respectively.Among 197 participants,the majority were male(59.9％),held a bachelor's degree(73.1％),had an intermediate professional title(53.3％),and were aged 31-40(49.2％).The pass rates of theoretical examinations in 3 categories were 41.6％,22.5％,and 19.4％,respectively,while the pass rates of practical skills were 81.3％,90.0％,and 5.4％,respectively.Multifactorial logistic regression analysis showed that males,those who participated in occupational health skills training or worked longer,had higher pass rates in this competition(OR=2.447-4.079,P＜0.05),while the elderly had a lower pass rate(OR=0.053,P＜0.05).Conclusions The results of this skill competition indicated that the theoretical knowledge and practical skills of participants were not good enough.The occupational health service industry in Chongqing needs further enhancement or improvement of professional competency,talent allocation,and continuing education for employed staff.

Excessive exposure to metals in daily life has been proposed as an environmental risk factor for neurological disorders. Oxidative stress is an inevitable stage involved in the neurotoxic effects induced by metals, nevertheless, the underlying mechanisms are still unclear. In this study, we used arsenic as a representative environmental heavy metal to induce neuronal oxidative stress and demonstrated that both in vitro and in vivo exposure to arsenic significantly increased the level of N6-methyladenosine (m6A) by down-regulating its demethylase FTO. Importantly, the results obtained from FTO transgenic mice and FTO overexpressed/knockout cells indicated that FTO likely regulated neuronal oxidative stress by modulating activating transcription factor 3 (ATF3) in a m6A-dependent manner. We also identified the specific m6A reader protein, YTHDC1, which interacted with ATF3 and thereby affecting its regulatory effects on oxidative stress. To further explore potential intervention strategies, cerebral metabolomics was conducted and we newly identified myo-inositol as a metabolite that exhibited potential in protecting against arsenic-induced oxidative stress and cognitive dysfunction. Overall, these findings provide new insights into the importance of the FTO-ATF3 signaling axis in neuronal oxidative stress from an m6A perspective, and highlight a beneficial metabolite that can counteract the oxidative stress induced by arsenic.

Phthalates and bisphenol A are recognized as the predominant endocrine-disrupting substances (EDCs) in the environment, but their impact on sleep health remains unclear. Vitamin D has often been reported to play a role in sleep health and may be affected by endocrine-disrupting compounds. The study utilized data from 5476 individuals in the NHANES project to investigate the correlation between combined exposure to environmental EDCs and sleep duration through modeling various exposures. Furthermore, it emphasizes the importance of vitamin D in the present scenario. Preliminary analyses suggested that vitamin D-deficient individuals generally slept shorter than individuals with normal vitamin D (p < 0.05). Exposure to Mono-ethyl phthalate (MEP), triclosan (TRS), and Mono-benzyl phthalate (MZP), either alone or in combination, was associated with reduced sleep duration and a greater risk of vitamin D deficiency. Individuals with low vitamin D levels exposed to TRS experienced shorter sleep duration than those with normal vitamin D levels (p < 0.05). TRS and MZP were identified as crucial factors in patient outcomes when evaluating mixed exposures (p < 0.05). The results provide new data supporting a link between exposure to EDCs and insufficient sleep length. Additionally, they imply that a vitamin D shortage may worsen the sleep problems induced by EDCs.

Background Environmental chemicals, such as Perfluoroalkyl and polyfluoroalkyl substances (PFAS) and volatile organic compounds (VOCs), and the association between the combined exposure of these chemicals and human lung function remains unclear. This study aimed to explore the effects of mixed exposure to PFAS and VOCs on lung function in the general population of the United States and investigate their potential mechanisms. Methods Data from 30442 respondents were selected for analysis during the US National Health and Nutrition Examination Survey (NHANES) database from 2007 to 2012. Linear models, weighted quantile (WQS) regression, quantile g calculation (QGC), and Bayesian kernel machine regression (BKMR) were used to evaluate the contribution of individual components. Moreover, the interactions between substances in the dose-response relationship mixture of multiple environmental chemical exposures and lung function were also evaluated. The Benjamini-Hochberg method was used to correct multiple tests. Findings Univariate analysis showed that nitromethane was negatively correlated with FEV1 (beta =-0.052), FVC (beta =-0.056), and PEF (beta =-0.065), while perfluorohexanesulfonic acid was positively associated with FEV1 (beta = 0.026), FVC (beta = 0.024), FEF25-75% (beta = 0.012), and PEF (beta = 0.029). Multivariate analysis showed that chloroform and perfluorohexane sulfonic acid were positively associated with lung function (P <0.05), and perfluorohexane sulfonic acid contributed the most. Nitromethane and perfluorodecanoic acid were negatively associated with lung function (P < 0.05), and perfluorodecanoic acid contributed the highest weight in the negative direction. When all chemicals were in the 50th percentile, the environmental chemical mixture had no significant consistent effect or dose-response on lung function. There were interactions among various environmental chemicals within the mixture except for 2-N-methyl-PFOSA acetate and bromodichloromethane. Interpretation These results suggest that environmental mixture exposure is associated with abnormal lung function in American adults, and the interaction of various substances in the mixture affects its physiological and chemical effects.

The knowledge of occupational health and occupational medicine is the basis for students of preventive medicine in the future work.The paper expatiates on how to make students build up their thought of preventive medicine during the teaching course,and raise their interest in it and cultivate their comprehensive capability.The purpose of the paper is to enhance the teaching result and quality.

Herein, we explored the overall association between metal mixtures and lung functions in populations of varying ages and the relationship among the associated components. The 2007–2012 National Health and Nutrition Examination Survey data of 4382 American participants was analyzed, and generalized linear, elastic net, quantile g–computation, and Bayesian kernel machine regression models were used to evaluate the relationship between exposure to the metal mixture and lung function at various ages. The results of barium exposure at distinct stages revealed that children and adolescents exhibited greater lung function changes than those in adults and the elderly. Additionally, compared with children and adolescents, cadmium– and arsenic–containing metabolites contributed to nonconductive lung function changes in adults and the elderly exposed to metal mixtures. The results showed that the effects of exposure to metal mixtures on lung function in children and adolescents were predominantly caused by lead and barium. Altogether, children and adolescents were found to be more susceptible to metal–exposure–mediated lung function changes than adults and the elderly.

Objective: We aimed to investigate the relationship between metal exposure and novel immunoinflammatory indicators. Methods: Data on adults participating in the National Health and Nutrition Examination Survey (NHANES) from 2009 to 2018 were analyzed. Various statistical models were employed to assess the association between metal exposure and novel immune-inflammation-related indicators. Additionally, the impact of metal exposure on inflammation in different gender populations was explored. Results: This study included 4482 participants, of whom 51.1% were male. Significant correlations were observed among various metals. Both elastic net (ENET) and linear regression models revealed robust associations between cadmium (Cd), cobalt (Co), arsenic (As), mercury (Hg), and immunoinflammatory indicators. Weighted quantile sum (WQS) and Quantile g-computation (Q-gcomp) models demonstrated strong associations between barium (Ba), Co, and Hg and immunoinflammatory indicators. Bayesian kernel machine regression (BKMR) analysis indicated an overall positive correlation between in vivo urinary metal levels and systemic inflammation response index (SIRI) and aggregate index of systemic inflammation (AISI). Furthermore, Co, As, and Hg emerged as key metals contributing to changes in novel immunoinflammatory indicators. Conclusions: Metals exhibit associations with emerging immunoinflammatory indicators, and concurrent exposure to mixed metals may exacerbate the inflammatory response. Furthermore, this relationship varies across gender populations.

BackgroundThe dietary protein proportion may be crucial in triggering overweight and obesity among children and adolescents.MethodsCross-sectional data from 4,336 children and adolescents who participated in the National Health and Nutrition Survey (NHANES) between 2011 and March 2020 were analyzed. Multivariate logistic regression was used to calculate odds ratio (OR) and 95% confidence interval (CI). Restricted cubic splines assessed the nonlinear relationships between dietary protein intake and the prevalence of overweight and obesity.ResultsAdjusted logistic regression models showed that each 1% increase in dietary protein proportion was associated with a 4% higher risk of overweight and obesity (OR = 1.04, 95% CI: 1.01–1.07). A nonlinear relationship was noted in children aged 6–11 years (P < 0.05), as demonstrated by restricted cubic spline analysis. After dividing dietary protein intake into quartiles, the highest quartile had an adjusted OR of 2.07 (95% CI: 1.35, 3.16, P = 0.001) compared to the lowest, among children aged 6–11 years.ConclusionDietary protein intake is positively linked to overweight and obesity in American children, irrespective of individual characteristics and total energy consumption.

Emerging contaminants (ECs) pollution has attracted global attention, and a large number of ECs spread in the environment, threatening the ecological environment and human health. Gut microbiota is the most complex microbial community, and its high sensitivity to ECs exposure has been widely concerned and reported by researchers. In fact, many studies have demonstrated that the gut microbiota is closely related to host health and is a toxic target of various environmental pollutants including ECs. This review evaluates the interaction of ECs (including persistent organic pollutants, antibiotics, microplastics and environmental endocrine disruptors) with the gut microbiota, and considers the possible harm of ECs to human health, finding that the gut microbiota may be involved in the regulation of various organ damage, endocrine disorders, embryotoxicity, and cancer development and other toxic processes caused by ECs exposure through related mechanisms such as the gut-liver axis, direct effects, and gut-brain axis. In short, we hope that more future studies will pay more attention to the relationship between ECs, gut microbiota and human health.

Arsenite is a well-documented neurotoxicant that widely exists in the environment. However, the detailed mechanisms of arsenite neurotoxicity are not fully clarified. Autophagy has been reported to be involved in many neurological problems induced by arsenite. Since beclin 1 is an essential mediator of autophagy, we herein used both adult wild-type (beclin 1(+/+)) and heterozygous disruption of beclin 1 (beclin 1(+/-)) mice for chronic administration of 50 mg/L arsenite via drinking water for 3 months. Our results demonstrated that exposure of arsenite caused the working memory deficit, anxiety-like behavior and motor coordination disorder in beclin 1(+/ +) mice, accompanied with pathological changes in morphology and electrophysiology in the cortical tissues. This treatment of arsenite significantly reduced the number of neuronal cells and induced microglia activation and synaptic transmission disorders in the wild-type mice as compared with vehicle controls. Intriguingly, by using beclin 1(+/-) mice, we found that heterozygous disruption of beclin 1 profoundly attenuated these neurotoxic effects induced by arsenite, mainly manifested by improvements in the neurobehavioral impairments, abnormal electrophysiologic alterations as well as dysregulation of synaptic transmission. These findings together indicate that regulation of autophagy via beclin 1 would be a potential strategy for treatment against arsenite neurotoxicity.

To assess the association of environmental chemical factors with osteopenia and/or bone fractures. All data were extracted from the National Health and Nutrition Survey (NHANES) 2017–2018 of American adults aged 20–59 years old; invalid data were excluded based on dual-energy X-ray absorptiometry. For the ultimate valid data set, multivariate logistic regression models were applied to evaluate the association of environmental chemical factors with osteopenia and bone fractures. The valid dataset was obtained from 2640 individuals, who completed a questionnaire of demographic characteristics. Urinary manganese and monomethylarsonic acid were positively associated with osteopenia in American adults, but not bone fracture. However, several environmental factors (e.g., arsenous acid, arsenocholine, dimethylarsinic acid, and 2-thioxothiazolidine-4-carboxylic acid) did not affect bone mineral density, but were significantly associated with bone fracture. Multiple environmental chemical factors significantly affect bone mass or fracture risk. However, the risk of environmental chemical factors on fractures is independent of osteopenia in US Adults. The influence of environmental chemical factors on bone quality should be considered and monitored.

在《公共卫生与预防医学概论》双语课程教学中,普遍存在填鸭式教学、学生缺乏学习动力、英文授课效率低下等问题,因此探索行之有效的教学方法,以激发学生学习欲望,提升教学质量,是授课教师面临的一项艰巨的教学难题.本研究以应用统计学专业本科学生为受试对象,探讨案例式教学方法在双语课程教学中的应用效果.具体教学过程分为(1)明确教学目标;(2)精选汇编中英教学案例;(3)设定主要引导性问题,布置学生课前准备相关英文素材;(4)采用全英文积极开展课堂案例体验与讨论;(5)教师总结点评案例,小结重点、难点知识.案例式教学方法可在积极调动学生学习兴趣,培养学生的自学能力、团队协作能力、语言表达能力、独立思考、分析问题和解决问题能力等综合素质能力,对提高双语教学质量有积极的促进作用.

Purpose:The widespread use of zinc oxide nanoparticles (ZnONPs) has raised concerns about its potential toxicity. Melatonin is a neurohormone with tremendous anti-toxic effects. The enterochromaffin cells are an essential source of melatonin in vivo. However, studies on the effects of ZnONPs on endogenous melatonin are minimal. In the present study, we aimed to investigate the effects of ZnONPs exposure on gut-derived melatonin.Methods:In the present study, 64 adult male mice were randomly and equally divided into four groups, and each group was exposed to ZnONPs (0, 6.5, 13, 26 mg/kg/day) for 30 days. Subsequently, the neurobehavioral changes were observed. The effects of ZnONPs on the expression of melatonin-related genes arylalkylamine N-acetyltransferase (Aanat), melatonin receptor1A (Mt1/Mtnr1a), melatonin receptor1B (Mt2/Mtnr1b), and neuropeptide Y (Npy) on melatonin synthesis and secretion in duodenum, jejunum, ileum and colon during day and night were also assessed.Results:The results revealed that oral exposure to ZnONPs induced impairments of locomotor activity and anxiety-like behavior in adult mice during the day. The transcriptional analysis of brain tissues revealed that exposure to ZnONPs caused profound effects on genes and transcriptional signaling pathways associated with melatonin synthesis and metabolic processes during the day and night. We also observed that, in the duodenum, jejunum, ileum and colon sites, ZnONPs resulted in a significant reduction in the expression of the gut-derived melatonin rate-limiting enzyme Aanat, the membrane receptors Mt1 and Mt2 and Npy during the day and night.Conclusion:Taken together, this is the first study shows that oral exposure to ZnONPs interferes with melatonin synthesis and secretion in different intestinal segments of adult mice. These findings will provide novelty insights into the neurotoxic mechanisms of ZnONPs and suggest an alternative strategy for the prevention of ZnONP neurotoxicity.

Emerging evidence indicates that nanoplastics (NPs) can transport organic pollutants such as di-(2-ethylhexyl) phthalate (DEHP) into organisms and induce adverse health effects. Nevertheless, the toxic effects of NPs combined with DEHP on mammalian intestine are still unclear. In this study, the C57BL6J mice were exposed to polystyrene nanoparticles (PSNPs), DEHP or them both for 30 days to determine their effects on different segments of intestine and the gut microbiota. As a result, DEHP alone or co-exposure to DEHP and PSNPs induced histological damages in all intestinal parts, mainly manifested as the decreased villus lengths, increased crypt depths in the duodenum, jejunum and ileum and decreased villus counts accompanied with decreased epithelial area in the colon. Moreover, decreased mucus coverage, down-regulated Muc2 expression levels as well as the broken tight junctions were observed in intestinal epithelium of mice, particularly obvious in the co-treatment groups. In general, as manifested by greater alterations in most of the parameters mentioned above, simultaneously exposed to PSNPs and DEHP seemed to induce enhanced toxic effects on intestine of mouse when compared with DEHP alone. Furthermore, the altered community composition of gut microbiota might at least partially contribute to these abnormalities. Overall, our results highlight the aggravated toxicity on different segments of intestine in mammalians due to co-exposure of PSNPs and DEHP, and these findings will provide valuable insights into the health risk of NPs and plastic additives.

Coexposure of nanoplastics (NPs) with other pollutants adsorbed from the surroundings has received extensive attention. Currently, the combined effects of NPs and plasticizers remain unclear. Di-(2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer that has raised much concern owing to its ubiquitous pollution and endocrine-disrupting potential. This study aimed to investigate the toxic effects on the male reproductive system upon coexposure to NPs and DEHP. The C57BL/6J mice were orally administrated with polystyrene nanoparticles (PSNPs), DEHP or both for 35 days to evaluate their effects on sperm quality, histology of testes and epididymides, testicular transcriptomic characteristics as well as expression of some important genes in the epididymides. The low-dose PSNPs used here did not induce significant changes in sperm quality, while DEHP alone or cotreatment with DEHP and PSNPs caused notable impairment, mainly manifesting as decreased sperm quality and aberrant structure of the testis and epididymis. Moreover, enhanced toxic effects were found in the cotreatment group when compared with the individual DEHP treatment group, as manifested by more obvious alterations in the sperm parameters as well as histological changes in the testis and epididymis. Testicular transcriptomic analysis revealed differential regulation of genes involved in immune response, cytoplasmic pattern recognition receptor signaling pathways, protein ubiquitination, oxidative stress, necrotic cell death, ATP synthesis and the cellular respiratory chain. RT-qPCR verified that the expression patterns of Cenpb, Crisp1 and Mars were changed in testes, and genes relevant to epididymal function including Aqp9 and Octn2 were downregulated in epididymides, particularly in the cotreatment group. Collectively, our results emphasize that DEHP at an environmentally relevant dose can induce male reproductive toxicity, and PSNPs may aggravate the toxic effects.

Gestational exposure to titanium dioxide nanoparticles (TiO2NPs) has been widely reported to have deleterious effects on the brain functions of offspring. However, little attention has been paid to the neurotoxic effects of TiO2NPs on maternal body after parturition. The pregnant mice were orally administrated with TiO2NPs at 150 mg/kg from gestational day 8-21. The potential effects of TiO2NPs on the neurobehaviors were evaluated at postnatal day 60. The gut microbiota, morphological alterations of intestine and brain, and other indicators that involved in gut-brain axis were all assessed to investigate the underlying mechanisms. The results demonstrated that exposure to TiO2NPs during pregnancy caused the persistent neurobehavioral impairments of maternal mice after delivery for 60 days, mainly including behavioural changes, pathological changes in hippocampus, cortex and intestine. Our data also showed that persistent dysfunction and tissue injuries were probably associated with the disruption of gut-brain axis, manifested by the shift in the composition of gut microbial community, alteration of Sstr1, inhibition of enteric neurons and reduction of diamine oxidase contents in maternal mice. These findings provide a novel insight that regulation of gut microecology may be an alternative strategy for the protection against the neurotoxicity of TiO2NPs in pregnant women.