Association between organophosphate esters exposure and all-cause and cause-specific mortality: a national population-based cohort study.

Exposure to organophosphate esters (OPEs) is associated with several chronic diseases, but the relationship with mortality risk is unclear. Therefore, we used the National Health and Nutrition Examination Survey 2011-2018 data to evaluate these relationships. 6,869 participants aged 18 years or older were included. Survival status information was obtained through the National Death Index through 31 December 2019. Multivariable COX regression model was adopted to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the relationships of urinary OPEs metabolites with mortality risk. During an average of 5.0 years of follow-up, 406 deaths were documented. After adjusting for confounders, bis(2-chloroethyl) phosphate was associated with an increased risk of all-cause mortality [HR (95%CI) = 1.12(1.05-1.20)] and cardiovascular mortality [HR (95%CI) = 1.15(1.04-1.26)]. Our study found that exposure to OPEs was significantly associated with increased risks of all-cause and cardiovascular mortality. Consequently, controlling OPEs exposure is needed to alleviate the health-related burden.

Recognition and detection technology for microplastic, its source and health effects.

Microplastic (MP) is ubiquitous in the environment which appeared as an immense intimidation to human and animal health. The plastic fragments significantly polluted the ocean, fresh water, food chain, and other food items. Inadequate maintenance, less knowledge of adverse influence along with inappropriate usage in addition throwing away of plastics items revolves present planet in to plastics planet. The present study aims to focus on the recognition and advance detection technologies for MPs and the adverse effects of micro- and nanoplastics on human health. MPs have rigorous adverse effect on human health that leads to condensed growth rates, lessened reproductive capability, ulcer, scrape, and oxidative nervous anxiety, in addition, also disturb circulatory and respiratory mechanism. The detection of MP particles has also placed emphasis on identification technologies such as scanning electron microscopy, Raman spectroscopy, optical detection, Fourier transform infrared spectroscopy, thermo-analytical techniques, flow cytometry, holography, and hyperspectral imaging. It suggests that further research should be explored to understand the source, distribution, and health impacts and evaluate numerous detection methodologies for the MPs along with purification techniques.

Upregulated LncRNA-Meg3 modulates the proliferation and survival of MEPM cells via interacting with Smad signaling in TCDD-induced cleft palate.

Exposure to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in utero can result in high rates of cleft palate (CP) formation, yet the underlying mechanisms remain to be characterized. In vivo, the lncRNA Meg3 was upregulated following TCDD treatment in CP-associated murine embryonic palatal tissue, with concomitant changes in proliferative and apoptotic activity in these murine embryonic palatal mesenchymal (MEPM) cells. Meg3 can modulate the TGF-ß/Smad to control the proliferation, survival, and differentiation of cells. Accordingly, TCCD and TGF-ß1 were herein used to treat MEPM cells in vitro, revealing that while TCDD exposure altered the proliferative activity and apoptotic death of these cells, exogenous TGF-ß1 exposure antagonized these effects via TGF-ß/Smad signaling. TCDD promoted Meg3 upregulation, whereas TGF-ß1 suppressed TCDD-driven upregulation of this lncRNA. Meg3 was additionally determined to directly interact with Smad2, with significant Meg3 enrichment in Smad2-immunoprecipitates following TCDD treatment. When Meg3 was silenced, the impact of TCDD on Smad signaling, proliferative activity, and apoptosis were ablated, while the effects of exogenous TGF-ß1 were unchanged. This supports a model wherein Meg3 is upregulated in TCDD-exposed palatal tissue whereupon it can interact with Smad2 to suppress Smad-dependent signaling, thus controlling MEPM cell proliferation and apoptosis, contributing to TCDD-induced CP, which provides a theoretical support for the precautions of cleft palate induced by TCDD.

Green space, air pollution and gestational diabetes mellitus: A retrospective cohort study in central China.

Emerging evidence suggests residential surrounding green space is beneficial for human health. The association between green space and GDM showed inconsistent results, and potential effect modification of green space with air pollution is still unclear. This study aims to evaluate the association between green space and GDM, and further explore potential interaction and medication effects. Participants were recruited from a retrospective cohort study between 2015 and 2020 in Henan, China. Residential green space based on normalized difference vegetation index (NDVI) and air pollution exposure were estimated using spatial-statistical models. Multivariate logistic regression was applied to evaluate the association between per 0.1 unit increase in NDVI with 4 buffer sizes (250 m, 500 m, 1000 m, 2000 m) and GDM. We examined potential interaction of green space and air pollutants on GDM. Mediating effects of air pollution associated with green space exposure on GDM were also investigated by causal mediation analyses. A total of 46,665 eligible pregnant women were identified. There were 4092 (8.8 %) women diagnosed with GDM according to the IADPSG criteria. We found that per 0.1-unit increment in NDVI250 m, NDVI500 m, NDVI1000 m and NDVI2000 m in second trimester were associated with the decreased risk of GDM, with adjusted OR of 0.921(95 %CI: 0.890-0.953), 0.922 (95 %CI: 0.891-0.953), 0.921 (95 %CI: 0.892-0.952) and 0.921 (95 %CI: 0.892-0.951), respectively. We identified significant interactions between second trimester PM2.5 and O3 exposure and NDVI for GDM (Pinteraction < 0.001). The causal mediation analysis showed that PM2.5 mediated approximately 2.5-5.5 % of the association between green space and GDM, while the estimated mediating effect of O3 was approximately 30.1-38.5 %. In conclusion, our study indicates that residential green space was associated with a reduced risk of GDM, particularly second trimester. Green space may benefit to GDM partly mediated by a reduction in PM2.5 and O3.