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Human exposure to various N,N′-substituted p-phenylenediamine-derived quinones (PPDQs) has been of increasing concern. Recent studies have examined N-phenyl-N′-(1,3-dimethylbutyl)-p-phenylenediamine-derived quinone (6PPDQ) in human urine to evaluate human exposure. However, other PPDQs in human urine have not been thoroughly investigated. This study analyzed six PPDQs in urine collected from 149 healthy individuals in Taizhou, China. All target PPDQs were detected, with 6PPDQ (mean 2.4 ng/mL, p = 0.013) and 2,5-bis(o-tolylamino)cyclohexa-2,5-diene-1,4-dione (mean 1.1 vs. 0.62 ng/mL; p = 0.027) were significantly higher in females compared to males. For CPPDQ (p < 0.01) and 6PPDQ (p < 0.01), a decrease was observed in urinary concentrations as participants aged. The daily excretion (DE) of PPDQs through urine was estimated for Chinese adults. The highest average DE was recorded for 6PPDQ at 81 ng/kg-bw/day, with a range from

Exposure to perfluoroalkyl acids (PFAAs) has been found to elicit a range of detrimental effects on human health. However, limited research has investigated the impact of PFAAs on immunity and immune disorders such as Sjogren’s syndrome, with existing studies yielding inconsistent results. This study was conducted in Hangzhou, China, with an initial cohort comprising 156 healthy individuals and 162 patients diagnosed with Sjogren’s syndrome. We quantified serum levels of PFAAs and examined associations between PFAAs and both susceptibilities to the development of Sjogren’s syndrome and immune marker concentrations. Nine PFAAs were frequently detected in the serum, with perfluorooctanoate (PFOA) exhibiting the highest concentration, followed by perfluorooctanesulfonate (PFOS). Exposure to PFOA and perfluorotridecanoate (PFTrDA) was inversely associated with the disease. Furthermore, a negative correlation between PFOA and C-reactive protein (CRP) was observed. These findings suggest that exposure to specific PFAAs may impact the immune system and potentially influence the development of Sjogren’s syndrome.

6:2 chlorinated polyfluorinated ether sulfonate (6:2 Cl-PFESA) exhibits pronounced estrogenic effects, potentially influencing the etiology of lung cancer. This study assessed the potential associations between serum concentrations of 6:2 Cl-PFESA and lung cancer risk at the population level. Odds ratios (ORs) for lung cancer across serum 6:2 Cl-PFESA quartiles were assessed using conditional logistic regression. Additionally, we investigated potential effect modification by various confounding factors. Elevated serum levels of 6:2 Cl-PFESA were consistently associated with an increased risk of lung cancer in both the crude model (OR = 1.62, 95% CI: 1.08–2.42, p = 0.018) and the adjusted model (OR = 1.59, 95% CI: 1.06–2.39, p = 0.026). Stratified analyses revealed that elevated serum levels of 6:2 Cl-PFESA were associated with increased risk estimates of lung cancer among males (adjusted OR = 2.04, 95% CI: 1.19–3.51, p = 0.006), smokers (adjusted OR = 2.48, 95% CI: 1.25–4.89, p = 0.003), and drinkers (adjusted OR = 2.20, 95% CI: 0.94–5.16, p = 0.049). The results of this study imply that exposure to 6:2 Cl-PFESA at levels considered environmentally relevant may be linked to an elevated risk of developing lung cancer.

Bisphenol S (BPS), an environmental endocrine disruptor, has been identified in global environmental matrices. Nevertheless, limited studies have investigated the presence of chlorinated analogues of BPS (Clx-BPSs) with potential estrogenic activities in environmental matrices. In this study, the occurrence of BPS and five types of Clx-BPSs was characterized in indoor dust (n = 178) from Hangzhou City. BPS was measurable in 94% of indoor dust samples, with an average level of 0.63 μg/g (1-BPS (2-chloro-4-(4-hydroxyphenyl)sulfonylphenol; detection frequency 70%), Cl2-BPS-2 (2-chloro-4-(3-chloro-4-hydroxyphenyl)sulfonylphenol; 65%), and Cl2-BPS-1 (2,6-dichloro-4-(4-hydroxyphenyl)sulfonylphenol; 61%) were among the frequently detected Clx-BPSs. Cl1-BPS was the most abundant analyte, with an average of 0.048 μg/g (2-BPS-1 (0.035 μg/g, 2-BPS-2 (0.031 μg/g, 1-BPS (p < 0.01), as well as between BPS and Cl2-BPS-1 (p < 0.01). Moreover, an estimation was made for the total daily intake of Clx-BPSs via the ingestion of indoor dust by infants, children, and adults. This study presents the first evidence of the existence of Clx-BPSs in indoor dust, concurrently highlighting the necessity to address their potential human exposure risks.

Bisphenol A (BPA) is a major component of polycarbonate plastics and epoxy resins. While many studies have investigated the effect BPA exposure has upon changes in gut microbial communities, the influence of gut microbiota on an organism’s ability to metabolize BPA remains comparatively unexplored. To remedy this, in this study, Sprague Dawley rats were intermittently (i.e., at a 7-day interval) or continuously dosed with 500 μg BPA/kg bw/day for 28 days, via oral gavage. In the rats which underwent the 7-day interval BPA exposure, neither their metabolism of BPA nor their gut microbiota structure changed greatly with dosing time. In contrast, following continuous BPA exposure, the relative level of Firmicutes and Proteobacteria in the rats’ guts significantly increased, and the alpha diversity of the rats’ gut bacteria was greatly reduced. Meanwhile, the mean proportion of BPA sulfate to total BPA in rat blood was gradually decreased from 30 (on day 1) to 7.4% (by day 28). After 28 days of continuous exposure, the mean proportion of BPA glucuronide to total BPA in the rats’ urine elevated from 70 to 81%, and in the rats’ feces the mean proportion of BPA gradually decreased from 83 to 65%. Under continuous BPA exposure, the abundances of 27, 25, and 24 gut microbial genera were significantly correlated with the proportion of BPA or its metabolites in the rats’ blood, urine, and feces, respectively. Overall, this study principally aimed to demonstrate that continuous BPA exposure disrupted the rats’ gut microbiota communities, which in turn altered the rats’ metabolism of BPA. These findings contribute to the better understanding of the metabolism of BPA in humans.

As a potential threat to human health, ingestion of microplastics (MPs) has become of concern. Limited studies have carefully characterized the occurrence of MPs in polypropylene-made takeout food containers (TOFCs), which have been widely used in China. In this study, TOFC samples (n = 210) were collected from seven Chinese cities (Hangzhou, Guangzhou, Shanghai, Xining, Chengdu, Qingdao, and Dalian) and analyzed for MPs. All the TOFC samples contained MPs, with an abundance of 3–43 items/TOFC. The TOFCs from Chengdu (25 items/TOFC) contained the highest mean abundance of MPs, which is significantly (p < 0.01) higher than that from Shanghai (8.7 items/TOFC). Fiber accounted for 66–87% of the total for the shape of the MPs in the TOFCs from the different Chinese cities. Most of the MPs in the TOFCs from the different cities had a size of 201–500 μm and accounted for a mean 34–42% of the total MPs in the TOFCs. The major color type of the MPs in the TOFCs was transparent, accounting for a mean 39 (Qingdao)–73% (Hangzhou) of the total MPs. Polymer compositions of the MPs in the TOFCs were consistently dominated by polypropylene, which represented a mean 56–73% of the total MPs. The estimated daily intake of MPs for the general Chinese population through using TOFCs was in the range of 0.042–0.14 items/kg bw/day. To our knowledge, this is the most comprehensive study investigating the occurrence of MPs in TOFCs from China, which contributes to a better understanding of the sources of human oral exposure to MPs.