Microplastics (MPs) are one novel environmental pollutant sized < 5 mm that is ubiquitously present in numerous environmental media and particularly susceptible to interact with various toxic chemicals. Importantly, MPs can enter the food chain, and are bio-enriched and bio-accumulated with trophic levels, eventually endangering ecosystems and human health. However, there need to be more understanding regarding the bio-interaction of MPs with the host, particularly for biological barriers. This review aimed to summarize the latest findings regarding the main exposure routes of MPs that generated health burdens on humans. Furthermore, their interactions with biological barriers that generate adverse health effects and the underlying mechanisms were also reviewed. Additionally, we provided a comprehensive overview of recent advances regarding the removing and controlling of MPs. Finally, we discussed the future directions for MPs hazard prevention to provide helpful information for regulating decision-making and guiding safer plastics applications.

As the concerned emerging pollutants, several lines of evidence have indicated that nanoplastics (NPs) lead to reproductive toxicity. However, the biological mechanism underlying NPs disturbed spermatogenesis remains largely unknown. Therefore, we aimed to reveal the potential mechanism of impaired spermatogenesis caused by long-term NPs exposure from the perspective of integrated metabolome and microbiome analysis. After 12 weeks of gavage of polystyrene nanoplastics (PS-NPs) and animo-modified polystyrene nanoplastics (Amino-NPs), a well-designed two-exposure stages experimental condition. We found that NPs exposure induced apparent abnormal spermatogenesis, which appeared more severe in the Amino-NPs group. Mechanistically, 14 floras associated with glucose and lipid metabolism were significantly altered, as evidenced by 16 S rRNA sequencing. Testicular metabolome revealed that the Top 50 changed metabolites were also enriched in lipid metabolism. Subsequently, the combined gut microbiome and metabolome analysis uncovered the strong correlations between Klebsiella, Blautia, Parabacteroides, and lipid metabolites (e.g., PC, LysoPC and GPCho). We speculate that the dysbiosis of gut microbiota-related disturbed lipid metabolism may be responsible for long-term NPs-induced damaged spermatogenesis, which provides new insights into NPs-induced dysregulated spermatogenesis.

The COVID-19 pandemic has dramatically changed the patterns of lifestyle and posed psychological stress on pregnant women. However, the association of sleep duration and screen time with anxiety among pregnant women under the backdrop of the COVID-19 pandemic scenario has been poorly addressed. We conducted one large-scale, multicenter cross-sectional study which recruited 1794 pregnant women across middle and west China. Self-reported demographic characteristics, lifestyle, and mental health status were collected from 6th February to 8th May 2020. We investigated the association of sleep duration and screen time with the risk of anxiety by multivariable logistic regression analysis and linear regression analysis after adjusting potential confounders. The dose-response relationship of sleep duration and screen time with anxiety was visualized using a cubic spline plot. Our data revealed that almost 35% of pregnant women suffered from anxiety during the COVID-19 pandemic. Sleep duration was dose-dependently associated with a lower risk of anxiety among pregnant women (OR = 0.41, 95% CI: 0.27–0.63), while screen time exhibited a conversed effect (OR = 2.01, 95% CI:1.00–4.39). Notably, sleep duration (≥8 h/day) synergistically combined with screen time (3–7 h/day) to diminish the risk of anxiety (OR = 0.70, 95% CI: 0.50–0.99). Taken together, sleep duration and screen time were independently and jointly associated with anxiety (P < 0.05). Therefore, promoting a more active lifestyle and maintaining higher sleep quality could improve the mental health of pregnant women, especially under public health emergency.

Cumulative evidence has demonstrated that exposure to polycyclic aromatic hydrocarbons (PAHs) or phthalates (PAEs) contributes to a variety of adverse health effects. However, the association of PAHs and PAEs co-exposure with blood cell-based inflammatory indicators during early pregnancy is still unclear. We aimed to investigate the single and mixed associations of exposure to PAHs and PAEs with blood cell-based inflammatory indicators among early pregnant women. A total of 318 early pregnant women were included in this study. General linear regressions were used to estimate the relationships of individual OH-PAHs and mPAEs with blood cell-based inflammatory indicators. The key pollutants were selected by an adapted least absolute shrinkage and selection operator (LASSO) penalized regression model and wasemployed to build the Bayesian kernel machine regression (BKMR) and quantile g-computation (Q-g) models, which can assess the joint association of OH-PAHs and mPAEs with blood cell-based inflammatory indicators. General linear regression indicated that each 1% increase in MOP was associated with a 4.92% (95% CI: 2.12%, 7.68%), 3.25% (95% CI: 0.50%, 6.18%), 5.87% (95% CI: 2.22%, 9.64%), and 6.50% (95% CI: 3.46%, 9.64%) increase in WBC, lymphocytes, neutrophils, and monocytes, respectively. BKMR and Q-g analysis showed that the mixture of OH-PAHs and mPAEs was linked with increased levels of white blood cells (WBC), neutrophils, monocytes, and lymphocytes, and MOP was identified as the dominant contributor. OH-PAHs and mPAEs co-exposure in early pregnancy was associated with elevated blood cell-based inflammatory indicators reactions. More attention should be paid to the inflammation induced by environmental pollution for perinatal women, especially early pregnant women.