Effect of passive smoking exposure on risk of type 2 diabetes: a systematic review and meta-analysis of prospective cohort studies.

Objective: The effect of passive smoking exposure on the risk of type 2 diabetes has not been systematically studied. A meta-analysis was conducted to assess the association between passive smoking exposure and the risk of diabetes. Methods: We searched three major databases up to 31 October 2022 to identify relevant prospective cohort studies on the association between passive smoking and the risk of type 2 diabetes. The pooled relative risk (RR) and 95% confidence interval (CI) for the association between passive smoking exposure and the risk of type 2 diabetes were analyzed using a fixed-effect model. Results: Ten prospective cohort studies were included in this meta-analysis, with a total of 251,620 participants involved. The pooled RR showed a significantly positive association between nonsmokers exposed to passive smoking and type 2 diabetes as compared to non-smokers who were not exposed to passive smoking [RR = 1.27; 95% CI (1.19, 1.36); p < 0.001]. Sensitivity analysis indicated that the pooled RR was not substantially affected by any of the individual studies. Conclusion: Exposure to passive smoking increases the risk of type 2 diabetes. This study may have a positive effect on the prevention of type 2 diabetes. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42023372532.

Inhibition of human sulfotransferases (SULTs) by per- and polyfluoroalkyl substances (PFASs) and structure-activity relationship.

Per- and polyfluoroalkyl substances (PFASs) are a family of highly fluorinated aliphatic substances widely used in industrial and commercial applications. This study aims to determine the inhibition of PFASs towards sulfotransferases (SULTs) activity, and trying to explain the toxicity mechanism of PFASs. In vitro recombinant SULTs-catalyzed sulfation of p-nitrophenol (PNP) was utilized as a probe reaction. The incubation system was consisted of PFASs, SULTs, PNP, 3'-phosphoadenosine-5'-phosphosulfate, MgCl2 and Tris-HCl buffer. Ultra-performance liquid chromatography was employed for analysis of the metabolites. All tested PFASs showed inhibition towards SULTs. The longer the carbon chain length of the PFASs terminated with -COOH, the higher is its capability of inhibiting SULT1A3. PFASs with -SO3H had a relatively higher ability to inhibit SULT1A3 activity than those with -COOH, -I and -OH. The inhibition kinetic parameter was 2.16 and 1.42 µM for PFOS-SULT1A1, PFTA-SULT1B1. In vitro in vivo extrapolation showed that the concentration of PFOS and PFTA in human matrices might be higher than the threshold for inducing inhibition of SULTs. Therefore, PFASs could interfere with the metabolic pathways catalyzed by SULTs in vivo. All these results will help to understand the toxicity of PFASs from the perspective of metabolism.