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OBJECTIVE: To explore the effect of occupational aluminum exposure on the blood of male workers. METHODS: A total of 249 male workers were selected as the research subjects by cluster sampling method in the electrolytic workshop of an aluminum plant. Blood samples were collected for determination of the blood aluminum concentration and blood routine. The subjects were divided into low-, medium-, and high-aluminuml groups based on the tertile of blood aluminum level(P_(33) is 13.9 μg/L, P_(67) is 37.7 μg/L). RESULTS: The red blood cell(RBC) count and hemoglobin level in patients of the high-aluminum group were lower than that of the low-aluminum group(P<0.05). There was no significant difference of the RBC count and hemoglobin level of patients in middle-aluminum group compared with that of the low-and high-aluminum groups(P>0.05). There was no statistical significant difference in white blood cell count and platelet count among the three groups(P>0.05). The results of the generalized linear regression model showed that the higher the blood aluminum level, the lower the RBC count and hemoglobin level of workers(P<0.05) after eliminating confounding factors such as age, length of service, education level, smoking, and drinking. CONCLUSION: Occupational aluminum exposure can cause a decrease of RBC count and hemoglobin level with a dose-effect relationship in workers.
RESUMO
OBJECTIVE: To explore the relationship between occupational aluminum exposure and fasting blood glucose level in workers. METHODS: A cluster sampling method was used to select 178 occupational aluminum-exposed workers as the exposure group, and 178 workers without occupational aluminum exposure as the control group in a large aluminum factory in Shanxi Province. Glucose oxidase method was used to measure the fasting blood glucose level, and inductively coupled plasma mass spectrometry was used to measure the plasma aluminum level in these workers. A generalized linear model was used to analyze the correlation between plasma aluminum exposure level and fasting blood glucose in these workers. RESULTS: The blood aluminum level of workers in the exposure group was higher than that of the control group [median: 39.58 vs 16.67 μg/L, P<0.01]. The fasting blood glucose level of workers in the exposure group was higher than that of the control group [(5.33±0.79) vs(5.15±0.41) mmol/L, P<0.01]. The results of the generalized linear model analysis showed that the blood aluminum level of workers was positively correlated with their fasting blood glucose level after adjusting for age, body mass index, smoking, drinking, exercise, family history of diabetes, and incidence of diabetes(P<0.05). There was a dose-response relationship between the blood aluminum level and fasting blood glucose level of workers in the groups of junior high school and below and high school(all P_(trend)<0.01). There was no correlation found between blood aluminum level and fasting blood glucose level in the group of college and above(P_(trend)>0.05). There was a dose-response relationship between the blood aluminum level and the fasting blood glucose level in the workers in the non-exercise group(P_(trend)<0.01). There was no correlation found between the blood aluminum level and the fasting blood glucose level in the exercise group(P_(trend)>0.05). CONCLUSION: The blood aluminum level of workers exposed to occupational aluminum is positively correlated with their fasting blood glucose level. Higher education level or exercise can moderately reduce the effect of blood aluminum level on fasting blood glucose.
RESUMO
OBJECTIVE: To explore the mechanism of ubiquitin-proteasome pathway(UPP) in the degradation of hyperphosphorylated tau protein in aluminum-induced mouse neuroblastoma N2 a cells. METHODS: N2 a cells in logarithmic growth period were randomly divided into control group and MG132 group. Cells in control group were exposed to concentrations of 0 or 1 mmol/L aluminum chloride for 24 hours. Cells in MG132 group were pretreated with MG132 at a concentration of 5 μmol/L for 6 hours, then exposed to concentrations of 0 or 1 mmol/L aluminum chloride for 24 hours. After exposure, the cells were collected. Western blotting was used to detect the relative expression of tau-5, P-tau181, P-tau231, P-tau262, P-tau396, heat shock protein 70(Hsp70) and carboxyl terminus of the Hsp70-interacting protein(CHIP). The ubiquitin relative expression was detected by enzyme-linked immunosorbent assay. RESULTS: The results of factorial analysis showed that the relative expression of tau-5, P-tau231, P-tau262, P-tau396, CHIP, Hsp70 and ubiquitin in N2 a cells were statistically significant in the main effect and interaction effect of aluminum chloride and MG132 treatment(P<0.05). Both in the control group and MG132 group, the relative expression of tau-5, P-tau231, P-tau262, P-tau396, CHIP, Hsp70 and ubiquitin in N2 a cells exposed to 1 mmol/L aluminum chloride increased(P<0.05) when compared with the N2 a cells without exposed to aluminum chloride. No matter aluminum chloride exposed or not, the relative expression of tau-5, P-tau231, P-tau262, P-tau396, CHIP, Hsp70 and ubiquitin in N2 a cells of MG132 group was higher than that of control group(P<0.05). CONCLUSION: UPP is involved in the regulation of hyperphosphorylated tau protein by proteasome degradation in aluminum-induced N2 a cells. UPP mainly regulates P-tau231, P-tau262, and P-tau396 sites. CHIP and Hsp70 played an important role in the UPP pathway.