| With the rapid development of economy and the continuous growth of social population,the demand for polymer materials in the fields of transportation,building decoration,electronic devices,textiles,and aviation also increases.Flame retardants are added to polymer materials to improve the safety of products.As commonly used flame retardant materials,short-chain chlorinated paraffins(SCCPs),novel brominated flame retardants(NBFRs),and organophosphate flame retardants(OPFRs)enter the environment in large quantities during production and use,causing pollution to the environment and ecosystem,and endangering human health.Recent years,the prevalence of type 2 diabetes has continued to rise worldwide,with the highest number in China.Animal exposure studies have shown that environmental pollutants are important factors in the development of type 2 diabetes.Currently,there is a lack of epidemiological studies on environmental pollutants and type 2 diabetes caused by the slather of flame retardants.Therefore,a case-control study was designed to investigate the association between SCCPs,NBFRs,and OPFRs exposure and type 2 diabetes risk.The main research results are as follows:1.Serum samples provided by diabetics(n=172)and non-diabetics(n=172)were collected from the First Affiliated Hospital of Shandong Medical University.Initially,the analysis method of three typical flame retardants in human serum was established.The concentrations of SCCPs in serum were determined by gas chromatography time-of-flight mass spectrometry,and the levels of NBFRs and OPFRs in serum were determined by gas chromatography triple quadrupole mass spectrometry.2.The association between SCCPs exposure and type 2 diabetes risk was researched by conditional logistic regression,and results showed that serum concentrations of C10-CPs,C11-CPs,andΣSCCPs were significantly positively correlated with type 2 diabetes risk.Serum SCCP concentrations were divided into quartiles according to the concentration distribution of the control group.Compared to the lowest quartile of C10-CPs,C11-CPs,andΣSCCPs,the highest quartiles had 7.09,31.5,and 10.1times significantly increased risk for type 2 diabetes after adjusting for potential confounders,and exhibiting a nonlinear dose-response correlation(p<0.001).This study also observed a stronger association between serum SCCP concentrations and type 2diabetes risk in males than in females.In a stratified BMI analysis,obese individuals(BMI≥25 kg m-2)exposed to SCCPs had approximately 1.2 to 7.9-folds risk of developing type 2 diabetes as normal-weight individuals(BMI<25 kg m-2),suggesting a synergistic effect of SCCP exposure and obesity on effects of type 2 diabetes.In the control group,no significant association was observed between SCCP exposure and fasting plasma glucose(FPG)after adjusting for confounding factors.SCCP exposure was positively correlated with total cholesterol(TC),low-density lipoprotein-cholesterol(LDL-C),and total lipid levels,which indicated that SCCPs may induce type 2 diabetes by disrupting with lipid metabolic homeostasis in vivo.3.In the study of NBFRs and OPFRs exposure and type 2 diabetes risk,serum concentrations of 2,3-dibromopropyl-2,4,6-tribromophenyl ether(DPTE),2,3-dibromopropyl-2,4,6-tribromophenyl ether(TPrP),triphenyl phosphate(TPP),tris(2-ethylhexyl)phosphate(TEHP),andΣ4OPFRs were significantly associated with an increased risk of type 2 diabetes.In sex stratification,the associations between TPrP and TEHP exposure and type 2 diabetes risk were slightly stronger in males,but stronger for DPTE,TPP,andΣ4OPFRs in females.Among participants in controls,serum NBFR concentrations were significantly negatively associated with FPG,and TPrP concentration was significantly positively associated with FPG.Serum concentrations of NBFRs and OPFRs were significantly positively correlated with TC and HDL levels,while no significant correlation was found between any NBFR and OPFR compounds and triglycerides and LDL-C.Those results indicated that serum concentrations of NBFRs and OPFRs may promote the development of type 2 diabetes by disrupting metabolism of glucose and lipid fractions. |