Frequent drought events and particulate matter pollution from vehicular exhaust seriously affect urban plant growth and provisioning of ecological services. Yet, how plants respond physiologically and morphologically to these two combined stressors remains unknown. Here, we assessed particle retention dynamics and plant morphology and physiology of Euonymus japonicus Thunb. var. aurea-marginatus Hort. under continuous drought with severe exhaust exposure. Our results showed that continuous drought insignificantly lowered particle retention in each of three size fractions by 1.02 μg·cm⁻² on average in the first 28 days, but significantly lowered total particle retention by 35.75 μg·cm⁻² on the 35th day. We observed evident changes in morphology, leaf mass per area (LMA), pigments, gas exchange in all stressed plants. Compared with single stress, combined drought and pollution caused earlier yellowing and shedding of old leaves, significantly lowered LMA by 1.21 mg·cm⁻², caused a greater decline in pigments and net photosynthetic rate (Pₙ). Large particles may mainly explain pigment reduction, lower weekly LMA increases, and stomatal restriction, while coarse particles may be the main drivers of the decline in Pₙ. Continuous drought mediated the influence of all three particle sizes on some parameters, such as weakening the impact of total particles on LMA, strengthening the impact of fine particles on photosynthesis. Our findings suggest that drought accelerates the physiological responses of plants to exhaust pollution. Under controlled severe exhaust pollution conditions, the optimal time to maintain high particle retention during continuous drought without decline in physiological conditions for E. japonicus var. aurea-marginatus was 14 days. Some additional interventions after 14 days (it could be postponed appropriately under field conditions) may help ensure healthy growth of plants and retention of particulate matter.

Perfluoroalkyl substances (PFAS) are known to be endocrine-disrupting compounds, but are nevertheless widely used in consumer and industrial products and have been detected globally in human and wildlife. Data from animal and epidemiological studies suggest that PFAS may affect human fertility. This led us to consider whether maternal or paternal plasma PFAS had effects on in vitro fertilization (IVF) outcomes. The study population consisted of 96 couples who underwent IVF treatment in 2017 due to tubal factor infertility. The concentrations of 10 PFAS in blood samples from both male and female partners were measured. Poisson regression with log link was performed to evaluate the association between the tertiles of PFAS concentrations and numbers of retrieved oocytes, mature oocytes, two-pronuclei (2 PN) zygotes, and good-quality embryos, while multiple linear regression models were used to investigate the correlation between plasma PFAS and semen parameters. Multivariable logistic regression was used to evaluate the association between the tertiles of PFAS concentrations and clinical outcomes. It was found that maternal plasma concentrations of perfluorooctanoic acid (PFOA) were negatively associated with the numbers of retrieved oocytes (pₜᵣₑₙd = 0.023), mature oocytes (pₜᵣₑₙd = 0.015), 2 PN zygotes (pₜᵣₑₙd = 0.014), and good-quality embryos (pₜᵣₑₙd = 0.012). Higher paternal plasma PFOA concentrations were found to be significantly associated with reduced numbers of 2 PN zygotes (pₜᵣₑₙd = 0.047). None of the maternal or paternal PFAS were significantly associated with the probability of implantation, clinical pregnancy, or live birth. To our knowledge, the present study is the first to assess the association between parental exposure to PFAS and IVF outcomes. Our results suggest the potential reproductive effects of PFAS on both men and women, and that exposure to PFAS may negatively affect IVF outcomes. Future studies, particularly with large sample size cohorts, are needed to confirm these findings.

Particulate pollution is closely related to public health. PM₁ (particles with an aerodynamic size not larger than 1 μm) is much more harmful than particles with larger sizes because it goes deeper into the body and hence arouses social concern. However, the sparse and unevenly distributed ground-based observations limit the understanding of spatio-temporal distributions of PM₁ in China. In this study, hourly PM₁ concentrations in central and eastern China were retrieved based on a random forest model using hourly aerosol optical depth (AOD) from Himawari-8, meteorological and geographic information as inputs. Here the spatiotemporal autocorrelation of PM₁ was also considered in the model. Experimental results indicate that although the performance of the proposed model shows diurnal, seasonal and spatial variations, it is relatively better than others, with a determination coefficient (R²) of 0.83 calculated based on the 10-fold cross validation method. Geographical map implies that PM₁ pollution level in Beijing-Tianjin-Hebei is much higher than in other regions, with the mean value of ∼55 μg/m³. Based on the exposure analysis, we found about 75% of the population lives in an environment with PM₁ higher than 35 μg/m³ in the whole study area. The retrieval dataset in this study is of great significance for further exploring the impact of PM₁ on public health.

The search for optimal catalysts to improve the working efficiency of ozonation has always been an important issue in the research field of advanced oxidation processes. In this study, a novel catalyst, ferrosilicon, was selected as the catalyst in heterogeneous catalytic ozonation to degrade ibuprofen (IBP) in water and treat real pharmaceutical wastewater. During the procedure, 45#ferrosilicon exhibited the best catalytic activity. Under the optimized experimental conditions, the IBP removal reached 75%, which was a great improvement compared to the 37% removal by ozone alone. The 45#-ferrosilicon-catalysed ozonation also achieved 68% TOC removal for real pharmaceutical wastewater, which was 31% higher than that by ozone alone. The degradation pathway of IBP was proposed using GC/MS. The EPR test proved that the main active species in the system were free active radicals •OH, and the measured accumulative •OH amount was 102 μmol. The characterization results show that the nascent metallic oxides, hydroxides, and hydroxyoxides on the ferrosilicon surface facilitated the decomposition of ozone molecules and generation of free active radicals. The removal of target organic contaminants in the water was mainly attributed to the oxidization of these highly active species.

Evidence has shown associations between air pollution and traffic-related exposure with accelerated aging, but no study to date has linked the exposure with age at natural menopause, an important indicator of reproductive aging. In this study, we sought to examine the associations of residential exposure to ambient particulate matter (PM) and distance to major roadways with age at natural menopause in the Nurses’ Health Study II (NHS II), a large, prospective female cohort in US. A total of 105,996 premenopausal participants in NHS II were included at age 40 and followed through 2015. Time-varying residential exposures to PM₁₀, PM₂.₅₋₁₀, and PM₂.₅ and distance to roads was estimated. We calculated hazard ratios (HR) and 95% confidence intervals (CIs) for natural menopause using Cox proportional hazard models adjusting for potential confounders and predictors of age at menopause. We also examined effect modification by region, smoking, body mass, physical activity, menstrual cycle length, and population density. There were 64,340 reports of natural menopause throughout 1,059,229 person-years of follow-up. In fully adjusted models, a 10 μg/m³ increase in the cumulative average exposure to PM₁₀ (HR: 1.02, 95% CI: 1.00, 1.04), PM₂.₅₋₁₀ (HR: 1.03, 95% CI: 1.00, 1.05), and PM₂.₅ (HR: 1.03, 95% CI: 1.00, 1.06) and living within 50 m to a major road at age 40 (HR: 1.03, 95%CI: 1.00, 1.06) were associated with slightly earlier menopause. No statistically significant effect modification was found, although the associations of PM were slightly stronger for women who lived in the West and for never smokers. To conclude, we found exposure to ambient PM and traffic in midlife was associated with slightly earlier onset of natural menopause. Our results support previous evidence that exposure to air pollution and traffic may accelerate reproductive aging.

N⁶-methyladenosine (m6A) modification, the most prevalent form of RNA methylation, modulates gene expression post-transcriptionally. Di-(2-ethylhexyl) phthalate (DEHP) is a common environmental endocrine disrupting chemical that induces testicular injury due to the inhibition of the demethylase fat mass and obesity-associated protein (FTO) and increases the m6A modification. How FTO-mediated m6A modification in testicular Leydig cell injury induced by DEHP remains unclear. Here, the TM3 Leydig cell line was treated with mono-(2-ethylhexyl) phthalate (MEHP), the main metabolite of DEHP in the body, as well as FB23-2, an inhibitor of FTO. Decreased levels of testosterone in the culture supernatant, significantly increased apoptosis, and a remarkable upregulation of global m6A modification were found in both TM3 cells treated with MEHP and FB23-2. Transcriptome sequencing showed that both treatments significantly induced apoptosis-associated gene expression. Methylated RNA immunoprecipitation sequencing showed that the Leydig cell injury induced by upregulated m6A modification could be associated with multiple physiological disorders, including histone acetylation, reactive oxygen species biosynthesis, MAPK signaling pathway, hormone secretion regulation, autophagy regulation, and male gonadal development. Overall, the inhibition of FTO-mediated up-regulation of m6A could be involved in MEHP-induced Leydig cell apoptosis.

This study reports on concentrations of short- and medium-chain chlorinated paraffins (SCCPs and MCCPs, respectively) in a wide range of food samples (n = 211) purchased in Belgium during 2020. Samples were analysed by gas chromatography-mass spectrometry (GC-MS) and quantified using chlorine content calibration. ∑SCCPs were present above LOQ in 25% of samples with an overall range of <LOQ to 58 ng/g wet weight (ww), while ∑MCCPs were identified in 66% of samples ranging from <LOQ to 250 ng/g ww. ∑MCCP concentrations were greater than those of ∑SCCPs in all 48 samples in which both groups were detected with an average ∑MCCP/∑SCCP ratio of 5.8 (ranging from 1.3 to 81). In general, the greatest CP concentrations were observed in foods classified as animal and vegetable fats and oils and sugar and confectionary for both SCCPs and MCCPs. Significant correlations between lipid content in food samples and CP levels illustrated the role of lipids in accumulating CPs within foodstuffs, while industrial processing, food packaging and environmental conditions are each likely to contribute to overall CP loads. Selected samples (n = 20) were further analysed by liquid chromatography-high resolution MS (LC-HRMS) to investigate homologue profiles and the occurrence of long-chain CPs (LCCPs). LCCPs were detected in 35% of the 20 subset samples while the HRMS results for SCCPs and MCCPs matched closely with those obtained by GC-MS. This study reveals the widespread occurrence of SCCPs and MCCPs in Belgian food and indicates that LCCPs may represent a substantial contribution to overall CP levels in foodstuffs.

Environmental lead exposure has been linked with reduced kidney function. However, evidence about its role in diabetic kidney damage, especially when considering the nutritional status of vitamin D, is sparse. In this observational study, we investigated the association between low-level lead exposure and urinary albumin-to-creatinine ratio (UACR) and assessed potential impact of vitamin D among 4033 diabetic patients in Shanghai, China. Whole blood lead was measured by graphite furnace atomic absorption spectrometry. Serum 25-hydroxyvitamin D [25(OH)D] was tested using a chemiluminescence immunoassay. The associations of blood lead with UACR and albuminuria, defined as UACR ≥30 mg/g, according to 25(OH)D levels were analyzed using linear and Poisson regression models. A doubling of blood lead level was associated with a 10.7% higher UACR (95% CI, 6.19%–15.5%) in diabetic patients with 25(OH)D < 50 nmol/L, whereas the association was attenuated toward null (2.03%; 95% CI, −5.18% to 9.78%) in those with 25(OH)D ≥ 50 nmol/L. Similarly, the risk ratios of prevalent albuminuria per doubling of blood lead level between the two groups were 1.09 (95% CI, 1.03–1.15) and 0.99 (95% CI, 0.86–1.14), respectively. Joint analysis demonstrated that a combination of high blood lead and low 25(OH)D corresponded to significantly higher UACR. Among diabetic patients with 25(OH)D < 50 nmol/L, the increment of UACR relative to blood lead was more remarkable in those with reduced estimated glomerular filtration rate (<60 mL/min/1.73 m²). These results suggested that higher blood lead levels were associated with increased urinary albumin excretion in diabetic patients with vitamin D deficiency. Further prospective studies are needed to validate our findings and to determine whether vitamin D supplementation yields a benefit.

Nanotechnology provides a wide range of benefits in the food industry in improving food tastes, textures, sensations, quality, shelf life, and food safety. Recently, potential adverse effects such as toxicity and safety concerns have been associated with the increasing use of engineered nanoparticles in food industry. Additionally, very limited information is known concerning the behavior, properties and effects of food nano-materials in the gastrointestinal tract. There is explores the current advances and provides insights of the potential risks of nanoparticles in the food industry. Specifically, characteristics of food nanoparticles and their absorption in the gastrointestinal tract, the effects of food nanoparticles against the gastrointestinal microflora, and the potential toxicity mechanisms in different organs and body systems are discussed. This review would provide references for further investigation of nano-materials toxicity effect in foods and their molecular mechanisms. It will help to develop safer foods and expand nano-materials applications in safe manner.

In the past decade, particulate matter with aerodynamic diameter less than 2.5 μm (PM₂.₅) has reached unprecedented levels in China and posed a significant threat to public health. Exploring the long-term trajectory of the PM₂.₅ attributable health burden and corresponding disparities across populations in China yields insights for policymakers regarding the effectiveness of efforts to reduce air pollution exposure. Therefore, we examine how the magnitude and equity of the PM₂.₅-related public health burden has changed nationally, and between provinces, as economic growth and pollution levels varied during 2005–2017. We derive long-term PM₂.₅ exposures in China from satellite-based observations and chemical transport models, and estimate attributable premature mortality using the Global Exposure Mortality Model (GEMM). We characterize national and interprovincial inequality in health outcomes using environmental Lorenz curves and Gini coefficients over the study period. PM₂.₅ exposure is linked to 1.8 (95% CI: 1.6, 2.0) million premature deaths over China in 2017, increasing by 31% from 2005. Approximately 70% of PM₂.₅ attributable deaths were caused by stroke and IHD (ischemic heart disease), though COPD (chronic obstructive pulmonary disease) and LRI (lower respiratory infection) disproportionately affected poorer provinces. While most economic gains and PM₂.₅-related deaths were concentrated in a few provinces, both gains and deaths became more equitably distributed across provinces over time. As a nation, however, trends toward equality were more recent and less clear cut across causes of death. The rise in premature mortality is due primarily to population growth and baseline risks of stroke and IHD. This rising health burden could be alleviated through policies to prevent pollution, exposure, and disease. More targeted programs may be warranted for poorer provinces with a disproportionate share of PM₂.₅-related premature deaths due to COPD and LRI.