Although cadmium (Cd) is a toxic heavy metal that reportedly causes liver injury, few studies have investigated biomarkers of Cd-induced liver injury. The purpose of this study is to investigate the role of bile acid (BA) in Cd-induced liver injury and determine reliable and sensitive biochemical parameters for the diagnosis of Cd-induced liver injury. In this study, 48 Sprague-Dawley rats were randomly divided into six groups and administered either normal saline or 2.5, 5, 10, 20, and 40 mg/kg/d cadmium chloride for 12 weeks. A total of 403 subjects living in either a control area (n = 135) or Cd polluted area (n = 268) of Dongdagou-Xinglong (DDGXL) cohort were included, a population with long-term low Cd exposure. The BA profiles in rats' liver, serum, caecal contents, faeces, and subjects' serum were detected using high-performance liquid chromatography-tandem mass spectrometry (HPLC–MS/MS). Changes in rats' and subjects' liver injury indices, rats' liver pathological degeneration, and rats' liver and subjects’ blood Cd levels were also measured. Cadmium exposure caused cholestasis and an increase in toxic BAs, leading to liver injury in rats. Among them, glycoursodeoxycholic acid (GUDCA), glycolithocholic acid (GLCA), taurolithocholic acid (TLCA), and taurodeoxycholate acid (TDCA) are expected to be potential biomarkers for the early detect of Cd-induced liver injury. Serum BAs can be used to assess Cd-induced liver injury as a simple, feasible, and suitable method in rats. Serum GUDCA, GLCA, TDCA, and TLCA were verified to be of value to evaluate Cd-induced liver injury and Cd exposure in humans. These findings provided evidence for screening and validation of additional biomarkers for Cd-induced liver injury based on targeted BA metabolomics.

Lead is a metal that exists naturally in the Earth's crust and is a ubiquitous environmental contaminant. The alleviation of lead toxicity is important to keep human health under lead exposure. Biosynthesized selenium nanoparticle (SeNPs) and selenium-enriched Lactobacillus rhamnosus SHA113 (Se-LRS) were developed in this study, and their potentials in alleviating lead-induced injury to the liver and intestinal tract were evaluated in mice by oral administration for 4 weeks. As results, oral intake of lead acetate (150 mg/kg body weight per day) caused more than 50 times and 100 times lead accumulation in blood and the liver, respectively. Liver function was seriously damaged by the lead exposure, which is indicated as the significantly increased lipid accumulation in the liver, enhanced markers of liver function injury in serum, and occurrence of oxidative stress in liver tissues. Serious injury in intestinal tract was also found under lead exposure, as shown by the decrease of intestinal microbiota diversity and occurrence of oxidative stress. Except the lead content in blood and the liver were lowered by 52% and 58%, respectively, oral administration of Se-LRS protected all the other lead-induced injury markers to the normal level. By the comparison with the effects of normal L. rhamnosus SHA113 and the SeNPs isolated from Se-LRS, high protective effects of Se-LRS can be explained as the extremely high efficiency to promote lead excretion via feces by forming insoluble mixture. These findings illustrate the developed selenium-enriched L. rhamnosus can efficiently protect the liver and intestinal tract from injury by lead.

Incomplete combustion of solid fuels (animal dung and bituminous coal) is a common phenomenon during residential cooking and heating in the Qinghai-Tibetan Plateau (QTP), resulting in large amounts of pollutants emitted into the atmosphere. This study investigated the pollutant emissions from six burning scenarios (heating and cooking with each of the three different fuels: yak dung, sheep dung, and bitumite) in the QTP's pastoral dwellings. Target pollutants such as carbon monoxide (CO), gas-phase polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs), fine particles (PM₂.₅, particulate matter with an aerodynamic diameter < 2.5 μm), carbonaceous aerosols, water-soluble ions, and particle-phase PAHs were investigated. Emission factors (EFs) (mean ± standard deviation) of PM₂.₅ from the six scenarios were in the range of 1.21 ± 0.47–7.03 ± 1.95 g kg⁻¹, of which over 60% mass fractions were carbonaceous aerosols. The ratio of organic carbon to elemental carbon ranged from 9.6 ± 2.7–33.4 ± 11.5 and 81.7 ± 30.4–91.9 ± 29.0 for dung and bitumite burning, respectively. These values were much larger than those reported in the literature, likely because of the region's high altitudes—where the oxygen level is approximately 65% of that at the sea level—thus providing a deficient air supply to stoves. However, the toxicity and carcinogenicity of PAHs emitted from solid fuel combustion in the QTP are significant, despite a slightly lower benzo(a)pyrene-equivalent carcinogenic potency (Bapₑq) in this study than in the literature. The gas-to-particle partitioning coefficient of PAHs and VOC emission profiles in the QTP differed significantly from those reported for other regions in the literature. More attention should be paid to the emissions of PAH derivatives (oxygenated PAHs and nitro-PAHs), considering their enhanced light-absorbing ability and high BaPₑq from solid fuel combustion in the QTP.

Mammalian polychlorinated biphenyl (PCB) metabolism has not been systematically explored with nontarget high-resolution mass spectrometry (Nt-HRMS). Here we investigated the importance of the gut microbiome in PCB biotransformation by Nt-HRMS analysis of feces from conventional (CV) and germ-free (GF) adult female mice exposed to a single oral dose of an environmental PCB mixture (6 mg/kg or 30 mg/kg in corn oil). Feces were collected for 24 h after PCB administration, PCB metabolites were extracted from pooled samples, and the extracts were analyzed by Nt-HRMS. Twelve classes of PCB metabolites were detected in the feces from CV mice, including PCB sulfates, hydroxylated PCB sulfates (OH-PCB sulfates), PCB sulfonates, and hydroxylated methyl sulfone PCBs (OH-MeSO₂-PCBs) reported previously. We also observed eight additional PCB metabolite classes that were tentatively identified as hydroxylated PCBs (OH-PCBs), dihydroxylated PCBs (DiOH-PCBs), monomethoxylated dihydroxylated PCBs (MeO-OH-PCBs), methoxylated PCB sulfates (MeO-PCB sulfates), mono-to tetra-hydroxylated PCB quinones ((OH)ₓ-quinones, x = 1–4), and hydroxylated polychlorinated benzofurans (OH-PCDF). Most metabolite classes were also detected in the feces from GF mice, except for MeO-OH-PCBs, OH-MeSO₂-PCBs, and OH-PCDFs. Semi-quantitative analyses demonstrate that relative PCB metabolite levels increased with increasing dose and were higher in CV than GF mice, except for PCB sulfates and MeO-PCB sulfates, which were higher in GF mice. These findings demonstrate that the gut microbiome plays a direct or indirect role in the absorption, distribution, metabolism, or excretion of PCB metabolites, which in turn may affect toxic outcomes following PCB exposure.

Microplastics (<5 mm) are ubiquitous in the global environment and are increasingly recognized as a biological hazard, particularly in the oceans. Zooplankton, at the base of the marine food web, have been known to consume microplastics. However, we know little about the impacts of microplastics across life history stages and on carbon settling. Here, we investigated the effects of ingestion of neutrally buoyant polystyrene beads (6.68 μm) by the copepod Acartia tonsa on (1) growth and survival across life history stages, (2) fecundity and egg quality, (3) and fecal characteristics. We found that microplastic exposure reduced body length and survival for nauplii and resulted in smaller eggs when copepods were exposed during oogenesis. Combining these life history impacts, our models estimate a 15% decrease in population growth leading to a projected 30-fold decrease in abundance over 1 year or 20 generations with microplastic exposure. In addition, microplastic-contaminated fecal pellets were 2.29-fold smaller and sinking rates were calculated to be 1.76-fold slower, resulting in an estimated 4.03-fold reduction in fecal volume settling to the benthos per day. Taken together, declines in population sizes and fecal sinking rates suggest that microplastic consumption by zooplankton could have cascading ecosystem impacts via reduced trophic energy transfer and slower carbon settling.

Microbiome community structure is intimately involved in key biological functions in the gastrointestinal (GI) system including nutrient absorption and lipid metabolism. Recent evidence suggests that disruption of the GI microbiome is a contributing factor to metabolic disorders and obesity. Poor diet and chemical exposure have been independently shown to cause disruption of the GI microbiome community structure and function. We hypothesized that the addition a chemical exposure to overfeeding exacerbates adverse effects on the GI microbiome community structure and function. To test this hypothesis, adult zebrafish were fed a normal feeding regime (Control), an overfeeding regime (OF), or an overfeeding regime contaminated with diethylhexyl phthalate (OF + DEHP), a suspected obesogen-inducing chemical. After 60 days, fecal matter was collected for sequencing, identification, and quantification of the GI microbiome using the 16s rRNA hypervariable region. Analysis of beta diversity indicated distinct microbial profiles between treatments with the largest divergence between Control and OF + DEHP groups. Based upon functional predictions, OF + DEHP treatment altered carbohydrate metabolism, while both OF and OF + DEHP affected biosynthesis of fatty acids and lipid metabolism. Co-occurrence network analysis revealed decreases in cluster size and a fracturing of the microbial community network into unconnected components and a loss of keystone species in the OF + DEHP treatment when compared to Control and OF treatments. Data suggest that the addition of DEHP in the diet may exacerbate microbial dysbiosis, a consequence that may explain in part its role as an obesogenic chemical.

The human pathogenic bacteria (HPB) in animal feces may disseminate to agricultural soils with their land application as organic fertilizer. However, the knowledge about the impacts of different sources and rates of animal manures on the temporal changes of soil HPB remains limited, which hamper our ability to estimate the potential risks of their land application. Here, we constructed an HPB database including 565 bacterial strains. By blasting the 16 S rRNA gene sequences against the database we explored the occurrence and fate of HPB in soil microcosms treated with two rates of swine, poultry or cattle manures. A total of 30 HPB were detected in all of manure and soil samples. Poultry manure at the high level obviously improved the abundance of soil HPB. The application of swine manure could introduce concomitant HPB into the soils. Of which, Pseudomonas syringae pv. syringae B728a and Escherichia coli APEC O78 may deserve more attention because of their survival for a few days in manured soils and being possible hosts of diverse antibiotic resistance genes (ARGs) as revealed by co-occurrence pattern. Bayesian source tracking analysis showed that the HPB derived from swine manure had a higher contribution to soil pathogenic communities than those from poultry or cattle manures in early days of incubation. Mantel test together with variation partitioning analysis suggested that bacterial community and soil physicochemical properties were the dominant factors determining the profile of HPB and contributed 64.7% of the total variations. Overall, our results provided experimental evidence that application of animal manures could facilitate the potential dissemination of HPB in soil environment, which should arouse sufficient attention in agriculture practice and management to avoid the threat to human health.

This study assessed the sources, magnitudes, and chemical compositions of household air pollution (HAP) and personal exposure in traditional Tibetan households. We measured 24-h personal exposures to PM₂.₅ and kitchen area black carbon (BC) concentrations, using MicroPEMs and microAeths, respectively. Particulate polycyclic aromatic hydrocarbon (PAH) and inorganic element concentrations were quantified via post analyses of a subset of MicroPEM sample filters. Household surveys regarding participant demographics, cookstove usage, household fuel, cooking behaviors, and lifestyles were collected. The results reaffirm that burning firewood and yak dung, mainly for cooking, leads to high PM₂.₅ and BC exposures. The geometric mean concentration (95% confidence interval, CI) was 74.3 (53.6, 103) μg/m³ for PM₂.₅ and the arithmetic mean ± standard deviation (SD) concentration was 4.90 ± 5.01 μg/m³ for BC and 292 ± 364 ng/m³ for 15 identified PAHs, respectively. The arithmetic mean ± SD of mass concentrations of 24 detected elements ranged from 0.76 ± 0.91 ng/m³ (Co) to 1.31 ± 1.35 μg/m³ (Si). Our statistical analyses further illustrated that the high concentrations of PM₂.₅, BC, and most PAHs and metals, are significantly associated with nomadic village, poorer stove/chimney conditions and yak dung burning. The results from this study show that substantial HAP exposure is prevalent in Tibetan households and requires immediate actions to mitigate potential negative environmental health impacts. The observational data also revealed the possibility of other important sources (e.g. traffic and garbage burning) that have contributed to personal exposures. These findings improve our understanding of HAP exposure and potential health risks in Tibetan communities and will help inform strategies for reducing HAP in Tibetan households and beyond.

Antimicrobial resistance genes (ARGs) are considered emerging environmental pollutants, posing potential risks for human and animal health: the misuse of antimicrobials in food-producing animals could favour the maintenance and spread of resistances (RMS) in bacteria. The occurrence of ARGs in Italian swine farming – which has specific characteristics – was investigated in order to explore RMS dynamics. Two farrow-to-finish pig farms were longitudinally monitored: faecal samples from animals and environmental samples were collected. DNA was extracted and tetA, ermB, qnrS and mcr1 ARGs were analysed by qPCR for their ability to confer resistance to highly or critically important antimicrobials (CIAs). Moreover, 16SrDNA gene was analysed to assess bacterial abundance. ermB and tetA genes were found in animal samples and manure samples. On the contrary, mcr1 was exclusively found in weaners, while qnrS occurred in all animal categories but sows and finishers. Among the analysed genes, ermB and tetA showed the highest absolute and relative abundances. Our results indicate that ermB and tetA ARGs are widely disseminated in the explored farms, suggesting efficient maintenance among bacteria and persistence in the environment. Interestingly, the presence of qnrS and mcr1, limited to just a few animal categories, highlights inefficient dissemination of these genes in the farm environment, in particular for mcr1, a stable plasmid gene conferring resistance to the last-resort antimicrobial, colistin. Paying close attention only to the finishing phase would have hampered the discovery of resistances to CIAs at farm level, which we instead identified thanks to an intensive longitudinal monitoring programme.

Hyperbranched polymers are nanomaterials belonging to the class of dendritic architectures with increasing applications in many diverse fields. We studied the toxicity of two hyperbranched polymers to the freshwater crustacean Daphnia magna. A hyperbranched hydroxyl-terminated polyester and a commercial hyperbranched polyamidoamine, Helux-3316 were tested for the acute immobilization of daphnids, the overproduction of reactive oxygen species and the activity of the antioxidant enzymes catalase and glutathione S-transferase. The effect for D. magna immobilization was higher for the hyperbranched polyamidoamine Helux-3316, which was attributed to the presence of primary amino groups on its surface. Following exposure to both hyperbranched polymers, a clear overproduction of reactive oxygen species took place accompanied by concentration-dependent enzymatic antioxidant response. Our results showed that the overproduction of reactive oxygen species activated antioxidant defence mechanisms and was responsible for the immobilization of daphnids exposed to both hyperbranched polymers. We showed evidence of the uptake of fluorescently labelled Helux-3316 that accumulated into the gastrointestinal tract of D. magna, and its removal via excretion within fecal pellets. This is the first work reporting the internalization of hyperbranched polymers in aquatic organisms.