Environment & Health最新文献

The increasing prevalence of microplastics in the environment has raised concerns about their potential environmental and health implications. Biofilms readily colonize microplastics upon their entry into the environment, altering their surface characteristics. While most studies have explored how biofilms influence the adsorption and transportation of other contaminants by microplastics, the reciprocal interplay between microplastics and biofilms and the resulting ecological risks remain understudied. This review comprehensively reviews the impact of microplastic properties on biofilm formation and composition, including the microbial community structure. We then explore the dynamic interactions between microplastics and biofilms, examining how biofilms alter the physicochemical properties, migration, and deposition of microplastics. Furthermore, we emphasize the potential of biofilm-colonized microplastics to influence the environmental fate of other pollutants. Lastly, we discuss how biofilm-microplastic interactions may modify the bioavailability, biotoxicity, and potential health implications of microplastics.

The increasing prevalence of microplastics in the environment has raised concerns about their potential environmental and health implications. Biofilms readily colonize microplastics upon their entry into the environment, altering their surface characteristics. While most studies have explored how biofilms influence the adsorption and transportation of other contaminants by microplastics, the reciprocal interplay between microplastics and biofilms and the resulting ecological risks remain understudied. This review comprehensively reviews the impact of microplastic properties on biofilm formation and composition, including the microbial community structure. We then explore the dynamic interactions between microplastics and biofilms, examining how biofilms alter the physicochemical properties, migration, and deposition of microplastics. Furthermore, we emphasize the potential of biofilm-colonized microplastics to influence the environmental fate of other pollutants. Lastly, we discuss how biofilm–microplastic interactions may modify the bioavailability, biotoxicity, and potential health implications of microplastics.

Manganese (Mn) exposure leads to pathological accumulation of Tau-associated neurodegenerative disease and has become a major public health concern. However, the precise mechanism underlying this effect remains unclear. Here, the mechanism by which Mn induces dysfunction of autophagy-lysosomal pathway-mediated tauopathy by activating the cGAS-STING pathway was explored both in vitro and in vivo. Mn exposure induced tauopathy in microglia and in mice while activating the cGAS-STING pathway, inducing type I interferon production, and impairing the degradation function of the autophagy-lysosomal pathway. Importantly, inactivation of the cGAS-STING pathway rescued the degradation activity of the autophagy-lysosomal pathway, while tauopathy was markedly attenuated, as shown in both cGAS-knockout and STING-knockout BV2 microglia and in mice. Moreover, the autophagy inhibitor 3-methyladenine (3-MA) restored the impaired degradation activity of the autophagy-lysosomal pathway by inactivating the cGAS-STING pathway, thereby clearing Tau aggregation. Taken together, these results indicate that Mn exposure induces tauopathy by impairing the function of the autophagy-lysosomal pathway through the activation of the cGAS-STING pathway. Thus, this study identifies a novel mechanism by which Mn exposure induces Tau aggregation, which in turn triggers potential neurotoxicity, providing a foundation for future drug target research.

Manganese (Mn) exposure leads to pathological accumulation of Tau-associated neurodegenerative disease and has become a major public health concern. However, the precise mechanism underlying this effect remains unclear. Here, the mechanism by which Mn induces dysfunction of autophagy–lysosomal pathway-mediated tauopathy by activating the cGAS–STING pathway was explored both in vitro and in vivo. Mn exposure induced tauopathy in microglia and in mice while activating the cGAS–STING pathway, inducing type I interferon production, and impairing the degradation function of the autophagy–lysosomal pathway. Importantly, inactivation of the cGAS–STING pathway rescued the degradation activity of the autophagy–lysosomal pathway, while tauopathy was markedly attenuated, as shown in both cGAS-knockout and STING-knockout BV2 microglia and in mice. Moreover, the autophagy inhibitor 3-methyladenine (3-MA) restored the impaired degradation activity of the autophagy–lysosomal pathway by inactivating the cGAS–STING pathway, thereby clearing Tau aggregation. Taken together, these results indicate that Mn exposure induces tauopathy by impairing the function of the autophagy–lysosomal pathway through the activation of the cGAS–STING pathway. Thus, this study identifies a novel mechanism by which Mn exposure induces Tau aggregation, which in turn triggers potential neurotoxicity, providing a foundation for future drug target research.

Previous studies have shown that methyl tert-butyl ether (MTBE) could interfere with lipid metabolism. However, there is still a lack of epidemiological reports on the association between MTBE exposure and the risk of nonalcoholic fatty liver disease (NAFLD). In this study, a cross-sectional study was performed with data from the 2017–2020 cycles of the National Health and Nutrition Examination Survey (NHANES). The target population consisted of adults with reliable vibration controlled Transient elastography (VCTE) and blood MTBE concentration results. The hepatic steatosis and fibrosis were assessed by the values of the controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), respectively. Generalized linear mixed model analysis was performed to evaluate the association between MTBE exposure and both steatosis and early liver fibrosis after adjustment for potential confounders. A total of 1303 subjects were enrolled and divided into NAFLD groups (CAP ≥ 248) and non-NAFLD groups (CAP < 248) based on the values of CAP in this study. Generalized linear mixed analysis suggested that blood MTBE concentration was positively associated with NAFLD risk in whole populations (OR: 2.153, 95% confidence interval [CI], 1.176–3.940) and female populations (OR: 11.019, 95% CI: 2.069–58.676). Blood MTBE concentration still showed an obvious positive correlation with the NAFLD risk after excluding factors such as diet and exercise in whole populations. Similarly, a positive correlation between blood MTBE concentration and liver fibrosis was also observed, although the results did not show significant statistical differences. In conclusion, our results indicate that MTBE exposure might be a potential important environmental pathogenic factor for NAFLD.

Previous studies have shown that methyl tert-butyl ether (MTBE) could interfere with lipid metabolism. However, there is still a lack of epidemiological reports on the association between MTBE exposure and the risk of nonalcoholic fatty liver disease (NAFLD). In this study, a cross-sectional study was performed with data from the 2017-2020 cycles of the National Health and Nutrition Examination Survey (NHANES). The target population consisted of adults with reliable vibration controlled Transient elastography (VCTE) and blood MTBE concentration results. The hepatic steatosis and fibrosis were assessed by the values of the controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), respectively. Generalized linear mixed model analysis was performed to evaluate the association between MTBE exposure and both steatosis and early liver fibrosis after adjustment for potential confounders. A total of 1303 subjects were enrolled and divided into NAFLD groups (CAP ≥ 248) and non-NAFLD groups (CAP < 248) based on the values of CAP in this study. Generalized linear mixed analysis suggested that blood MTBE concentration was positively associated with NAFLD risk in whole populations (OR: 2.153, 95% confidence interval [CI], 1.176-3.940) and female populations (OR: 11.019, 95% CI: 2.069-58.676). Blood MTBE concentration still showed an obvious positive correlation with the NAFLD risk after excluding factors such as diet and exercise in whole populations. Similarly, a positive correlation between blood MTBE concentration and liver fibrosis was also observed, although the results did not show significant statistical differences. In conclusion, our results indicate that MTBE exposure might be a potential important environmental pathogenic factor for NAFLD.

Respiratory infections and tuberculosis ranked as the second leading global causes of mortality in 2021. Following the methodology from the Global Burden of Disease Study (GBD) 2021, we aimed to estimate the attributable burden and risk factors of respiratory infections and tuberculosis among China's population under 20 from 1990 to 2021. In 2021, there were 652 million new cases and 12 699 deaths of respiratory infections and tuberculosis among people under 20 years old in China. We estimated 9054 (71.2%) deaths and 818 498 (54.6%) disability-adjusted life years (DALYs) from respiratory infections attributed to all evaluated risk factors. Mortality rates were the highest in Xizang, Xinjiang, and Qinghai in 2021, while they constantly decreased since 1990. Ambient particulate matter pollution was the second leading cause of death among males and first among females, accounting for nearly 1/5 of deaths from respiratory infections and tuberculosis in 2021. In 23 of 33 provinces, ambient particulate matter pollution was the first leading cause of death and DALY, while in Xizang and Gansu, it was not the major contributor to the burden. From 1990 to 2021, the burden from household air pollution declined remarkably in all 33 provinces except for Xizang and Gansu, while the population attributable fraction (PAF) of ambient particulate matter pollution continuously increased. The overall burden of respiratory infections and tuberculosis showed a declining trend, while it remained a fatal threat to infants in relatively less developed regions. The raised hazard of ambient particulate matter pollution underscored the necessity of the shift into the formulation of prevention and intervention strategies.

Respiratory infections and tuberculosis ranked as the second leading global causes of mortality in 2021. Following the methodology from the Global Burden of Disease Study (GBD) 2021, we aimed to estimate the attributable burden and risk factors of respiratory infections and tuberculosis among China’s population under 20 from 1990 to 2021. In 2021, there were 652 million new cases and 12 699 deaths of respiratory infections and tuberculosis among people under 20 years old in China. We estimated 9054 (71.2%) deaths and 818 498 (54.6%) disability-adjusted life years (DALYs) from respiratory infections attributed to all evaluated risk factors. Mortality rates were the highest in Xizang, Xinjiang, and Qinghai in 2021, while they constantly decreased since 1990. Ambient particulate matter pollution was the second leading cause of death among males and first among females, accounting for nearly 1/5 of deaths from respiratory infections and tuberculosis in 2021. In 23 of 33 provinces, ambient particulate matter pollution was the first leading cause of death and DALY, while in Xizang and Gansu, it was not the major contributor to the burden. From 1990 to 2021, the burden from household air pollution declined remarkably in all 33 provinces except for Xizang and Gansu, while the population attributable fraction (PAF) of ambient particulate matter pollution continuously increased. The overall burden of respiratory infections and tuberculosis showed a declining trend, while it remained a fatal threat to infants in relatively less developed regions. The raised hazard of ambient particulate matter pollution underscored the necessity of the shift into the formulation of prevention and intervention strategies.