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Di-(2-ethylhexyl) phthalate (DEHP), an endocrine-disrupting chemical (EDC) commonly used as a plasticizer, is responsible for widespread environmental pollution. Epidemiological and experimental data implicate DEHP and its metabolite mono(2-ethylhexyl) phthalate (MEHP) in the occurrence and development of metabolic syndrome. However, the specific effects and potential mechanisms of action of DEHP on glucose and lipid metabolism in adults are currently unclear. In the current study, adult male mice were continuously exposed to DEHP (0, 5, and 25 mg/kg/day) via oral administration and changes in glucose and lipid metabolism explored. Notably, exposure to DEHP led to a significant increase in plasma glucose and hepatic lipid accumulation but had no effect on insulin secretion. Western blot and real-time quantitative PCR showed that DEHP induced insulin resistance and promoted gluconeogenesis and lipid accumulation via overexpression of forkhead box protein O1 (FoxO1), in keeping with hepatic RNA sequencing data. Variations in gut microbiota aggravated these effects while inhibition of FoxO1 reversed the adverse effects of DEHP. Our findings support a key role of FoxO1 in disorders of glucose and lipid metabolism caused by DEHP.

Volatile methylsiloxanes (VMSs) are widely used in various personal-care products and industrial additives and products. This study focused on VMSs exposure in the general population, workers, and the families of workers living in residential and industrial areas of southwestern China. VMSs concentrations in indoor environmental matrices from six industrial facilities were 3.4 × 102 to 9.0 × 102 μg m−3 in gas-phase samples, 4.7 × 102 to 1.5 × 104 μg g−1 in PM2.5 samples, and 2.3 × 102 to 7.2 × 103 μg g−1 in dust samples, which were two to four orders of magnitude higher than the concentrations measured in residential areas. Exposure to VMSs was investigated by analysis of plasma samples from workers in residential and industrial areas for the presence of cyclic (D4–D6) and linear (L3–L16) VMSs. VMSs concentrations in plasma samples ranged from 84 to 2.3 × 102 ng ml−1 in workers, one to two orders of magnitude higher than those in the general population (2.2 ng ml−1). Daily VMSs indoor exposure via inhalation and ingestion in individuals from residential and industrial areas were estimated and assessed under working-time and leisure-time conditions. This study showed that exposure to VMSs in industrial areas is approximately two to four or one to two orders of magnitude higher than that in residential areas during the working- or leisure-time scenario, respectively. Furthermore, the families of workers (the non-occupational group) experienced higher levels of exposure to VMSs in their homes compared with the general population. The ratios of exposure to linear VMSs via PM2.5 inhalation to that via the gas phase ranged from 7.8% to 43.1% in industrial areas. This study suggests that intake of linear VMSs via PM2.5 inhalation should be considered when estimating human exposure to VMSs in areas with high levels of PM2.5 air pollution.