Essential trace element zinc is associated with decreased lung cancer risk, but underlying mechanisms remain unclear. This study aimed to investigate role of DNA methylation in zinc-lung cancer association. We conducted a case-cohort study within prospective Dongfeng-Tongji cohort, including 359 incident lung cancer cases and a randomly selected sub–cohort of 1399 participants. Epigenome-wide association study (EWAS) was used to examine association of plasma zinc with DNA methylation in peripheral blood. For the zinc-related CpGs, their mediation effects on zinc-lung cancer association were assessed; their diagnostic performance for lung cancer was testified in the case-cohort study and further validated in another 126 pairs of lung cancer case-control study. We identified 28 CpGs associated with plasma zinc at P < 1.0 × 10⁻⁵ and seven of them (cg07077080, cg01077808, cg17749033, cg15554270, cg26125625, cg10669424, and cg15409013 annotated to GSR, CALR3, SLC16A3, PHLPP2, SLC12A8, VGLL4, and ADAMTS16, respectively) were associated with incident risk of lung cancer. Moreover, the above seven CpGs were differently methylated between 126 pairs of lung cancer and adjacent normal lung tissues and had the same directions with EWAS of zinc. They could mediate a separate 7.05%∼22.65% and a joint 29.42% of zinc-lung cancer association. Compared to using traditional factors, addition of methylation risk score exerted improved discriminations for lung cancer both in case-cohort study [area under the curve (AUC) = 0.818 vs. 0.738] and in case-control study (AUC = 0.816 vs. 0.646). Our results provide new insights for the biological role of DNA methylation in the inverse association of zinc with incident lung cancer.

Triphenyl phosphate (TPHP) is a frequently used flame retardant and indoor semi-volatile pollutant exposing humans with endocrinal disrupting effects. However, its respiratory tract toxicity remains unclear. Herein, we mainly focused on exploring the cytotoxicity of TPHP to the cells from five different parts of the human respiratory tract (from top to bottom): human nasal epithelial (HNEpC) cells, human bronchial epithelial (16HBE) cells, normal nasopharyngeal epithelial (NP69) cells, human lung epithelial cells (Beas-2B) cells, and human lung fibrocells (HFL1 cells) cells. The cell viability, micronucleus induction, endoplasmic reticulum stress gene, intracellular Ca²⁺ concentration, mitochondrial membrane potential (MMP) were investigated in short-term as well as extended exposure of TPHP. HFL1 and HNEpC cells were found to be irreversible damage, while other three type cells achieved homeostasis through self-rescue. Moreover, expression of downstream genes of Nrf2 signaling pathway were upregulated for 1.3–7.0 times and glutathione detoxification enzyme activity changed for 2–10 (U/mg protein) in HNEpC cells. Furthermore, the vascular endothelial growth factor (VEGF), a disease-related factor, increased 1.0–3.5-fold in HNEpC cells. RNA-sequencing results suggested that protein linkage recombination, molecular function regulation and metabolic processes signal pathway were all affected by TPHP exposure in HNEpC. This is a first report to compare respiratory cytotoxicity in whole human respiratory tract under OPFR exposure and found HNEpC cells were the most sensitive target of TPHP. Molecular biological mechanisms uncovered that TPHP exposure in HNEpC can induce the activation of MAPK signal pathway and demonstrate potential respiratory growth differentiation and stress disorder in human nasal cells upon TPHP exposure.

Organic ultraviolet absorbents (UVAs) are increasingly reported in environmental matrices and organisms. However, available information on the bioaccumulation of UVAs in freshwater species is insufficient and their trophodynamics in lake food webs remain unknown. We measured the concentrations of twelve UVAs in the wild species from Lake Chaohu. Except for UV-320 not detected, the other UVAs were prevalent in the study species and their total concentrations were in the range of 5.44–131 ng/g dry weight, which were comparable to the concentrations reported in other waters. Compound and species-specific accumulations of UVAs in the organisms were observed. In the lake, the log-transformed concentrations of 4-methyl benzylidene camphor, octyl p-dimethylaminobenzoate, UV-326, and UV-327 related significantly to the trophic levels of species separately. The calculated trophic magnification factors (TMFs) of the four UVAs were 3.79, implying trophic magnification, and 0.18, 0.40 and 0.58, suggesting trophic dilution, respectively. These suggested that the magnification potential and the associated risks of individual UVAs in freshwater lake differed. To our knowledge, this is the first report of these TMFs in lake food webs. However, more investigation is needed to characterize their trophodynamic behaviors in lakes because food web characteristics likely affect trophic transfer of these chemicals.

Although BHPF has been widely used in plastic manufacturing as a substitute for BPA, current evidence suggests that BHPF also causes harmful effects on reproduction. However, effects of BHPF on mammalian early pregnancy are still poorly defined. This study aimed to explore the effects of BHPF on early pregnancy, especially decidualization and embryonic development in mice and human beings. The results showed that 50 and 100 mg/kg BHPF exposure reduced birth weight, and implantation site weight on the day 8 of pregnancy in mice. Because BHPF inhibits both embryo development and artificial decidualization in mice, suggesting that the detrimental effects of BHPF should be from its effects on embryo development and decidualization. Under in vitro decidualization, 10 μM BHPF inhibits decidualization and leads to disordered expression of Lamin B1 and collagen in mice. In addition, 10 μM BHPF also inhibits decidualization, and causes disordered expression of both collagen III and Lamin B1 under human in vitro decidualization. However, collagen III supplementation can rescue BHPF inhibition on decidualization. Further, our study demonstrates that BHPF impairs human decidualization through the HB-EGF/EGFR/STAT3/Collagen III pathway. Taken together these data suggest that exposure to BHPF impairs mouse and human decidualization during early pregnancy.

The UN Sustainable Development Goal, SDG 7.3, is to double the global rate of improvement in energy efficiency by 2030. To meet this and other energy targets, countries encourage the development and adoption of energy-efficient products. An extensively researched phenomenon in this context is the energy rebound effect, especially in transportation. However, the direct relationship between the energy rebound effect and car emission levels has barely been investigated. Understanding this relationship is important, because energy-related emissions are closely linked to mortality, morbidity, and climate change. We assess the emission consequences in the private car market in Israel of a rebound effect associated with a policy promoting energy-efficient cars. We find that the baseline rebound before introduction of the policy was 40%. In the following three periods marked by policy changes, it grew to 54%, 69%, and 88%. Using household data with specific car characteristics and usage, we calculate the added greenhouse gas (GHG) emission consequences of this rebound by the end of the studied period to be about 5% of the country's per-capita target. Notably, estimates for the emission consequences using “average car” values were almost twice as high. The reason for this gap derives from the co-dependance between car usage and car efficiency. We discuss the implications of this gap in meeting emission goals.

Ciprofloxacin (Cipro) is commonly detected in water worldwide, however, the ecotoxicological effects to aquatic biota is still not fully understood. In this study, using multiple biomarkers, it was investigated sublethal effects of short-term exposure to Cipro concentrations (1, 10 and 100 μg.L⁻¹) in the Neotropical catfish Rhamdia quelen compared to non-exposure treatment (Control). After 96 h of exposure, the fishes were anesthetized for blood collection to hematological and genotoxicity biomarkers analysis. After euthanasia, the brain and muscle were sampled for biochemical biomarkers analyses. Gills, liver and posterior kidney for genotoxicity, biochemical and histopathological biomarkers analysis and anterior intestine for histopathological biomarkers analysis. Genotoxicity was observed in all tissues, regardless of the Cipro concentrations. Hematological alterations, such as reduction of the number of erythrocytes and leucocytes, as well as in hematocrit concentration and histopathological damages, such as reduction of microridges in gill epithelium and necrosis in liver and posterior kidney, occurred mainly at 100 μg.L⁻¹. In addition, at 100 μg.L⁻¹, Cipro increased antioxidant system activity (Catalase in liver and posterior kidney). These results demonstrated that under short-term exposure, Cipro causes toxic effects in R. quelen that demands attention and surveillance of environmental aquatic concentrations of this antibiotic.

Selenium engineered nanomaterials (Se ENMs)-enabled agriculture has developed rapidly, however, the roles of surface charge in the bioavailability and enrichment efficiency of Se ENMs are still unknown. Herein, various Se ENMs of homogenous size (40–60 nm) and different surface charges (3.2 ± 0.7, −29.0 ± 0.4, and 45.5 ± 1.3 mV) were prepared to explore the Se content and nutritional quality in Brassica chinensis L. The results demonstrated that soil application of various Se ENMs (0.05 mg kg⁻¹) displayed different bio-availabilities via modulating the secretion of root exudates (e.g., tartaric, malic, and citric acids), microbial community composition (e.g., Flavobacterium, Pseudomonas, Paracoccus, Bacillus and Rhizobium) and root cell wall. Negatively charged Se ENMs (Se (−)) showed the highest Se content in the shoot of B. chinensis (3.7-folds). Se (−) also significantly increased yield (156.9%) and improved nutritional quality (e.g., ascorbic acid, amino acids, flavonoids, fatty acids, and tricarboxylic acid) of B. chinensis. Moreover, after harvest, the Se (−) did not lead to significant change in Se residue in soil, but the amount of Se residue in soil was increased by 5.5% after applying the traditional Se fertilizer (selenite). Therefore, this study provides useful information for producing Se-fortified agricultural products, while minimizing environmental risk.

Transfer parameters are key inputs for modeling radionuclide transfer in the environment and estimating risk to humans and wildlife. However, there are no data for many radionuclide-foodstuff/wildlife species combinations. The use of parameters derived from stable element data when data for radionuclides are lacking is increasingly common. But, do radionuclides and stable elements behave in a sufficiently similar way in the environment? To answer this question, at least for soil to plant transfer, sampling was conducted in four different countries (England, Kazakhstan, Spain and Ukraine) affected by different anthropogenic radionuclide source terms (in chronological order: global fallout, Semipalatinsk Test Site, the 1957 Windscale accident and the 1986 Chernobyl accident) together with a bibliographical review. Soil to grass transfer parameters (ratio between dry matter concentrations in plant and soil), Fᵥ, for ¹³⁷Cs and ⁹⁰Sr were significantly higher than those for stable elements, suggesting that the use of the latter could lead to underestimating radionuclide concentrations in plant samples Transfer parameters for ¹³⁷Cs and stable Cs were linearly correlated, with a slope of 1.54. No such correlation was observed for ⁹⁰Sr and stable Sr, the mean value of the ⁹⁰Sr:Sr ratio was 35 ranging (0.33–126); few data were available for the Sr comparison. The use of radionuclide transfer parameters, whenever possible, is recommended over derivation from stable element concentrations. However, we acknowledge that for many radionuclides there will be few or no radionuclide data from environmental studies. From analyses of the data collated there is evidence of a decreasing trend in the Fᵥ(¹³⁷Cs)/Fᵥ(Cs) ratio with time from the Chernobyl accident.

Eutrophic lakes are hot spots of CH₄ and volatile sulfur compound (VSC) emissions, especially during algal blooms and decay. However, the response of CH₄ and VSC emissions to lake eutrophication and algae growth as well as the underlying mechanisms remain unclear. In this study, the emissions of CH₄ and VSCs from four regions of Lake Taihu with different eutrophic levels were investigated in four months (i.e., March, May, August and December). The CH₄ emissions ranged from 20.4 to 126.9 mg m⁻² d⁻¹ in the investigated sites and increased with eutrophic levels and temperature. H₂S and CS₂ were the dominant volatile sulfur compounds (VSCs) emitted from the lake. The CH₄ oxidation potential of water ranged from 2.1 to 14.9 μg h⁻¹ L⁻¹, which had positive correlations with trophic level index and the environmental variables except for the NH₄⁺-N concentration. Eutrophic levels could increase the abundances of bacteria and methanotrophs in lake water. α-Proteobacteria methanotroph Methylocystis was more abundant than γ-Proteobacteria methanotrophs in March and May, while the latter was more abundant in August and November. The relative abundance of Cyanobacteria, including Microcystis, A. granulata var. angustissima and Cyanobium had significantly positive correlations with temperature, turbidity, SO₄²⁻-S, and total sulfur. Partial least squares path modelling revealed that the algal growth could promote VSC emissions, which had a positive correlation with CH₄ oxidation potential, likely due to the positive correlation between the CH₄ and VSC emissions from lakes. These findings indicate that water eutrophication and algae growth could increase the emissions of CH₄ and VSCs from lakes. Controlling algae growth might be an effective way to mitigate the emissions of CH₄ and VSCs from freshwater lakes.

Polybrominated diphenyl ethers (PBDEs) are aromatic compounds that containing bromine atoms, which possess high efficiency, good thermal stability. However, PBDEs had various known toxic effects and were characterized as persistent environmental pollutants. Exposure to a quinone-type metabolite of PBDEs (PBDEQ) is linked with excess production of intracellular reactive oxygen species (ROS) in our previous studies. Here, we observed that PBDEQ exposure led to ROS and mitochondrial dysfunction, which promoted canonical and non-canonical Nod-like receptor protein 3 (NLRP3) inflammasome activation. Further experiments demonstrated that PBDEQ exposure activated Toll-like receptors (TLRs), subsequently regulating nuclear factor kappa B (NF-κB) signaling. Moreover, lysosomal damage and K⁺ efflux were involved in PBDEQ-driven NLRP3 inflammasome activation. Our in vivo study also illustrated that PBDEQ administration induced liver inflammation in male C57BL/6J mice. Cumulatively, our current finding provided novel insights into PBDEQ-induced pro-inflammatory responses.