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Objective To estimate the mortality and years of life lost among youth aged 18-44 in Chongqing from 2011 to
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<p><b>OBJECTIVE</b>To analyze the changes in endogenous small molecule metabolites after benzo[a]pyrene (B[a]P) exposure in rat cerebral cortex and explore the mechanism of B[a]P neurotoxicity.</p><p><b>METHODS</b>Five-day-old SD rats were subjected to gavage administration of 2 mg/kg B[a]P for 7 consecutive weeks. After the exposure, the rats were assessed for spatial learning ability using Morris water maze test, ultrastructural changes of the cortical neurons under electron microscope, and metabolite profiles of the cortex using GC/MS. The differential metabolites between the exposed and control rats were identified with partial least squares discriminant analysis (PLS-DA) and the metabolic pathways related with the differential metabolites were analyzed using Cytoscape software.</p><p><b>RESULTS</b>Compared with the control group, the rats exposed to B[a]P showed significantly increased escape latency (P<0.05) and decreased time spent in the target area (P<0.05). The exposed rats exhibited widened synaptic cleft, thickened endplate membrane and swollen cytoplasm compared with the control rats. Eighteen differential metabolites (VIP>1, P<0.05) in the cortex were identified between the two groups, and 9 pathways associated with B[a]P neurotoxicity were identified involving amino acid metabolism, tricarboxylic acid cycle and Vitamin B3 (niacin and nicotinamide) metabolism.</p><p><b>CONCLUSION</b>B[a]P can cause disturbance in normal metabolisms and its neurotoxicity is possibly related with disorders in amino acid metabolism, tricarboxylic acid cycle and vitamin metabolism.</p>
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<p><b>OBJECTIVE</b>To investigate the effect of air pollution on respiratory health in school-aged children in the main urban area of Chongqing, China.</p><p><b>METHODS</b>The main urban area of Chongqing was divided into polluted area and clean area according to the air pollution data shown on the Environmental Protection Agency Website of Chongqing between 2010 and 2015. A cluster sampling method was used to select 695 third- or fourth-grade children from 2 primary schools in the clean or polluted area as study subjects, with 313 children from the clean area and 382 children from the polluted area. Pulmonary function was examined for all children and a standard American epidemiological questionnaire (ATS-DLD-78-C) was used to investigate the prevalence of respiratory diseases and symptoms.</p><p><b>RESULTS</b>Compared with the clean area, the polluted area had significantly higher concentrations of inhalable particles (PM), fine particulate matter (PM), and nitric oxide (NO) (P<0.05). The multivariate logistic regression analysis was performed after adjustment for confounding factors, and the results showed that compared with those in the clean area, the children in the polluted area had significantly higher risks of cough (OR=1.644), cough during cold (OR=1.596), expectoration during cold (OR=2.196), persistent expectoration (OR=1.802), and wheezing (OR=2.415). The boys and girls in the clean area had significantly higher forced vital capacity and forced expiratory volume in one second than those in the polluted area (P<0.05).</p><p><b>CONCLUSIONS</b>Air pollution in the main urban area of Chongqing is associated with the increased prevalence of respiratory symptoms in school-aged children and has certain effect on children's pulmonary function.</p>
Assuntos
Criança , Feminino , Humanos , Masculino , Poluição do Ar , Volume Expiratório Forçado , Modelos Logísticos , Doenças Respiratórias , Capacidade VitalRESUMO
<p><b>OBJECTIVE</b>To explore the effect of exposure to vehicle exhaust in pregnant mice on the reproductive function and DNA methylation in male offspring mice.</p><p><b>METHODS</b>Twenty pregnant mice were randomized into control group and vehicle exhaust exposure group (n=10) and exposed to routine laboratory condition and to vehicle exhaust for 10 consecutive days (8 h per day) in a tunnel with a heavy traffic, where the concentrations of TSP, PM10, PM2.5, SO2 and NOX and the decibel of noise were measured. The offspring mice were raised till reaching maturity, and the epididymides of the male mice were collected to test the weight coefficients, DNA methylation level, and mRNA levels of Aldh7a1 and Rpe.</p><p><b>RESULTS</b>The body weight and the weight coefficients of the epididymides and testes differed significantly between the exposure group and the control group (P>0.05). The concentrations of TSP, PM2.5, PM10 and NOx and the decibel of noise were significantly higher in the traffic environment and the control environment (P<0.05). Reduced representation bisulphite sequencing (RRBS) and Gene ontology (GO) showed that 58 genes had significantly different methylation levels between the two groups, mostly relating to the process of spermatogenesis (P<0.05). Compared with the control group, Aldh7a1 and Rpe mRNA expressions in the testes were down-regulated significantly in the exposure group (P<0.05).</p><p><b>CONCLUSION</b>Exposure of pregnant mice to vehicle exhaust causes damages of the reproductive function in the male offspring mice.</p>
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<p><b>OBJECTIVE</b>To observe the effect of chronic arsenic exposure on cerebral cortex and serum metabolics of mice and explore the mechanism of arsenic neurotoxicity.</p><p><b>METHODS</b>Twelve 3-week-old male C57BL/6J mice were randomly assigned into exposure group and control group and exposed to sodium arsenite (50 mg/L) via drinking water and deionized water for 12 weeks, respectively. After the exposure, arsenic level in the cerebrum was determined by hydride generation-atomic fluorescence spectrometry. The metabolites in the cerebral cortex and serum were determined using gas chromatography-mass spectrometry (GC/MS) analysis. Principal component analysis (PCA) was used to analyze the difference of the metabolites between the exposure and the control groups. Online tools for analyzing metabolic pathways were used to identify the related metabolites pathways.</p><p><b>RESULTS</b>Arsenic content in the brain of exposure group was significantly higher than that in the control group (P<0.05). The mice exposed to arsenic had a higher level of citric acid, phenylalanine, tyrosine, histidine and lysine in the cerebral cortex (P<0.05). Serum levels of serine, glycine, proline, aspartate and glutamate were significantly higher while α-ketoglutaric acid level was significantly lower in the exposure group than in the control group (P<0.05). PCA analysis showed a significant difference in cerebral cortex and serum metabolites between the two groups.</p><p><b>CONCLUSION</b>Chronic arsenic exposure may affect the function of the central nervous system by interfering with amino acid metabolism and tricarboxylic acid cycle, which may be one of the mechanisms of arsenic neurotoxicity.</p>