Short-chain chlorinated paraffin (SCCP) exposure and type 2 diabetes risk: A population-based case-control study in East China

中国 2型糖尿病 人口 糖尿病 医学 内分泌学 环境卫生 地理 考古
作者
Gaoxin Zhang,Qinghua Zhang,Xiaoling Guan,Mei Liu,Lingling Meng,Xu Han,Yingming Li,Guibin Jiang
出处
期刊:Science of The Total Environment [Elsevier BV]
卷期号:908: 168192-168192 被引量:7
标识
DOI:10.1016/j.scitotenv.2023.168192
摘要

Exposure to persistent organic pollutants may be associated to type 2 diabetes, but the studies on associations between short-chain chlorinated paraffin (SCCP) exposure and type 2 diabetes risk in humans are still scarce. Here, we conducted a case-control study involving 344 participants in Shandong Province, East China, to explore the effects of SCCPs on type 2 diabetes risk and their correlations with glycemic biomarker and serum lipid parameters. SCCPs were detected in all serum samples with a median concentration of 24 ng mL-1 in cases and 19 ng mL-1 in controls. Exposure to C10-CPs, C11-CPs, and ΣSCCPs were positively associated with the risk of type 2 diabetes after adjusting for confounders. The associations remained consistent in stratified analyses but stronger in male participants and obese individuals. In the control group, there were significant and positive correlations between SCCP exposure and levels of total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), total lipid, and non-high-density lipoprotein-cholesterol. Significant joint effects on SCCP exposure and lipid parameters were observed in females when analyzed by the quantile-based g-computation model, and C10-CPs showed the highest contribution. Mediation analysis showed that LDL-C had significant mediation effects on the associations between C10-CPs, C11-CPs, and ΣSCCPs exposure and risk of type 2 diabetes. Moreover, TC and high-density lipoprotein-cholesterol were mediators in the relationship between C11-CPs and type 2 diabetes. Taken together, our study revealed that human exposure to SCCPs may increase the risk of type 2 diabetes and disrupt lipid metabolism.
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