Objective　To explore the characteristics of toxic heavy metal pollution in atmospheric PM2.5 (Particulate matter 2.5) during winter in Nanning City and to evaluate the health risks for the population. Methods　Atmospheric PM2.5 samples were continuously collected in the urban areas of Nanning from January to February 2019. The concentrations of seven toxic heavy metals, including cadmium (Cd), arsenic (As), chromium (Cr), lead (Pb), nickel (Ni), mercury (Hg), and manganese (Mn) in atmospheric PM2.5 were analyzed by X-ray fluorescence spectrometry. The pollution characteristics of toxic heavy metals were studied by geo-accumulation index and enrichment factor methods, and their health risks to children and adults were assessed using the health risk assessment model of the United States Environmental Protection Agency. Results　The mass concentration of atmospheric PM2.5 in Nanning in winter 2019 was (44±29) μg/m3, which was generally at a low level. Different degrees of pollution were found for Hg, Cd, As, Cr, and Pb in PM2.5, with Hg and Cd being more seriously polluted. Hg and Cd were highly enriched in PM2.5, followed by Pb with moderate enrichment. These three elements mainly originated from man-made pollution. As, Cr and Ni were mildly enriched and affected by both natural and anthropogenic sources. The non-carcinogenic risks were in the order of As>Pb>Hg>Cr>Cd>Mn>Ni. The total non-carcinogenic risks for the three populations were all less than 1, which is within acceptable limits. The carcinogenic risks were ranked as Cr>As>Cd>Ni, with Cr, As, and Cd posing carcinogenic risks to children and adults ranging from 1×10-6 to 1×10-4. Moreover, the total carcinogenic risks of heavy metals (Cr, As, Cd, and Ni) were higher than 1×10-4 for children, indicating a potential carcinogenic risk. Conclusions　The mass concentration of PM2.5 and heavy metal elements in Nanning City during the winter of 2019 was relatively low, but the pollution of heavy metals still exists. The non-carcinogenic risk of heavy metals is within an acceptable range, but the carcinogenic risk poses a potential danger to children.

Increased intestinal barrier permeability, leaky gut, has been reported in patients with autism. However, its contribution to the development of autism has not been determined. We selected dextran sulfate sodium (DSS) to disrupt and metformin to repair the intestinal barrier in BTBR T⁺tf/J autistic mice to test this hypothesis. DSS treatment resulted in a decreased affinity for social proximity; however, autistic behaviors in mice were improved after the administration of metformin. We found an increased affinity for social proximity/social memory and decreased repetitive and anxiety-related behaviors. The concentration of lipopolysaccharides in blood decreased after the administration of metformin. The expression levels of the key molecules in the toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-nuclear factor kappa B (NF-κB) pathway and their downstream inflammatory cytokines in the cerebral cortex were both repressed. Thus, "leaky gut" could be a trigger for the development of autism via activation of the lipopolysaccharide-mediated TLR4-MyD88-NF-κB pathway.
Mice ; Animals ; NF-kappa B ; Myeloid Differentiation Factor 88/metabolism* ; Lipopolysaccharides/pharmacology* ; Toll-Like Receptor 4/metabolism* ; Autistic Disorder/metabolism* ; Signal Transduction/physiology*