The use of DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane) in some countries, although regulated, is contributing to an increased worldwide risk of exposure to this organochlorine pesticide or its derivative p,p’-DDE [1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene]. Many studies have associated p,p’-DDE exposure to type 2 diabetes, obesity and alterations of the reproductive system, but their molecular mechanisms of toxicity remain poorly understood. We have addressed this issue by using commercial microarrays based on probes for the entire Mus musculus genome to determine the hepatic transcriptional signatures of p,p’-DDE in the phylogenetically close mouse species Mus spretus. High-stringency hybridization conditions and analysis assured reliable results, which were also verified, in part, by qRT-PCR, immunoblotting and/or enzymatic activity. Our data linked 198 deregulated genes to mitochondrial dysfunction and perturbations of central signaling pathways (kinases, lipids, and retinoic acid) leading to enhanced lipogenesis and aerobic glycolysis, inflammation, cell proliferation and testosterone catabolism and excretion. Alterations of transcript levels of genes encoding enzymes involved in testosterone catabolism and excretion would explain the relationships established between p,p´-DDE exposure and reproductive disorders, obesity and diabetes. Further studies will help to fully understand the molecular basis of p,p´-DDE molecular toxicity in liver and reproductive organs, to identify effective exposure biomarkers and perhaps to design efficient p,p’-DDE exposure counteractive strategies.

Osteoporosis or enhanced bone loss is one of the most commonly occurring bone conditions in the world, responsible for higher incidence of fractures leading to increased morbidity and mortality in adults. Bone loss is affected by various environmental factors including diet, age, drugs, toxins etc. Microcystins are toxins produced by cyanobacteria with microcystin-LR being the most abundantly found around the world effecting both human and animal health. The present study demonstrates that MC-LR treatment induces bone loss and impairs both trabecular and cortical bone microarchitecture along with decreasing the mineral density and heterogeneity of bones in mice. This effect of MC-LR was found due to its immunomodulatory effects on the host immune system, wherein MC-LR skews both T cell (CD4+ and CD8+ T cells) and B cell populations in various lymphoid tissues. MC-LR further was found to significantly enhance the levels of osteoclastogenic cytokines (IL-6, IL-17 and TNF-α) along with simultaneously decreasing the levels of anti-osteoclastogenic cytokines (IL-10 and IFN-γ). Taken together, our study for the first time establishes a direct link between MC-LR intake and enhanced bone loss thereby giving a strong impetus to the naïve field of “osteo-toxicology”, to delineate the effects of various toxins (including cyanotoxins) on bone health.

Interactions between organic toxicants and nano-particles in the aquatic environment may modify toxicant bioavailability and consequently the toxicant's fate and toxicity. To evaluate the potential impact of nano-titanium dioxide (TiO₂) on the bio-concentration and reproductive endocrine disruption of tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) in fish, a comparative bioaccumulation study was conducted on zebrafish (Danio rerio, AB strain) treated with 0, 5.74, 23.6, or 90.7 μg L⁻¹ TDCIPP alone or co-exposed to TDCIPP and 0.09 mg L⁻¹ nano-TiO₂ for 21 days. Nano-TiO₂ can absorb TDCIPP and nano-TiO₂ is taken up into zebrafish. Chemical measurements showed that TDCIPP was bio-concentrated in zebrafish, and the highest level was detected in the liver, followed by the brain and gonads. Compared with TDCIPP treatment, increased tissue burdens of both TDCIPP were observed in the liver, brain, and gonads suggesting that nano-TiO₂ adsorbed TDCIPP and acted as a carrier facilitating the uptake and translocation of TDCIPP in tissues. Higher bio-concentration in the presence of nano-TiO₂ resulted in a significant decrease in the hepatic-somatic index, gonad-somatic index and brain-somatic index in F0 females but not F0 males. Moreover, a further gender-dependent reduction in testosterone (T), estradiol (E2), follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and induction of plasma vitellogenin (VTG) concentrations in adults were observed following co-exposure. Co-exposure also inhibited egg production and caused significant developmental toxicity in F1 larvae. The results obtained using this multi-marker approach suggested that nano-TiO₂ is a carrier of TDCIPP and accelerated its bio-concentration in adult zebrafish, resulting in adverse reproduction outcomes.

While numerous studies worldwide have evaluated the short-term associations of fine and coarse particulate matter (PM) air pollution with mortality and morbidity, these studies may be susceptible to short-term harvesting effect. We aimed to investigate the short-term association between mortality and PM with aerodynamic diameter less than 2.5 μm (PM2.5) and those between 2.5 and 10 μm (PMc) within a month prior to death, and assess the mortality displacement by PM2.5 and PMc among elderly population in Hong Kong.We obtained air pollution data from January 2011 to December 2015 from Environmental Protection Department, and daily cause-specific mortality data from Census and Statistical Department of Hong Kong. We performed generalized additive distributed lag model to examine the acute, delayed and long-lasting effects of PM2.5 and PMc within one month on mortality.We observed a statistically significant association of PM2.5 and PMc exposure over lags 0–6 days with all natural mortality and cardio-respiratory mortality. The overall cumulative effect of PM2.5 over 0–30 lag days was 3.44% (95% CI: 0.30–6.67%) increase in all natural mortality and 6.90% (95% CI: 0.58–13.61%) increase of circulatory mortality, which suggested the absence of mortality displacement by PM2.5. On the other hand, no significant cumulative association with mortality was found for PMc over 0–30 lag exposure window, and thus mortality displacement by PMc cannot be ruled out. Findings remained robust in various sensitivity analyses.We found adverse effect of both PM2.5 and PMc exposure within one week prior to death. While there was no evidence of mortality displacement in the association of PM2.5 exposure over one month prior with all natural and circulatory mortality, mortality displacement by PMc cannot be ruled out. PM2.5 may contribute more to the longer term effect of particulate matter than PMc.

Communities resident in urban areas located near active volcanoes can experience volcanic ash exposures during, and following, an eruption, in addition to sustained exposures to high concentrations of anthropogenic air pollutants (e.g., vehicle exhaust emissions). Inhalation of anthropogenic pollution is known to cause the onset of, or exacerbate, respiratory and cardiovascular diseases. It is further postulated similar exposure to volcanic ash can also affect such disease states. Understanding of the impact of combined exposure of volcanic ash and anthropogenic pollution to human health, however, remains limited.The aim of this study was to assess the biological impact of combined exposure to respirable volcanic ash (from Soufrière Hills volcano (SHV), Montserrat and Chaitén volcano (ChV), Chile; representing different magmatic compositions and eruption styles) and freshly-generated complete exhaust from a gasoline vehicle. A multicellular human lung model (an epithelial cell-layer composed of A549 alveolar type II-like cells complemented with human blood monocyte-derived macrophages and dendritic cells cultured at the air-liquid interface) was exposed to diluted exhaust (1:10) continuously for 6 h, followed by immediate exposure to the ash as a dry powder (0.54 ± 0.19 μg/cm2 and 0.39 ± 0.09 μg/cm2 for SHV and ChV ash, respectively). After an 18 h incubation, cells were exposed again for 6 h to diluted exhaust, and a final 18 h incubation (at 37 °C and 5% CO2). Cell cultures were then assessed for cytotoxic, oxidative stress and (pro-)inflammatory responses.Results indicate that, at all tested (sub-lethal) concentrations, co-exposures with both ash samples induced no significant expression of genes associated with oxidative stress (HMOX1, NQO1) or production of (pro-)inflammatory markers (IL-1β, IL-8, TNF-α) at the gene and protein levels. In summary, considering the employed experimental conditions, combined exposure of volcanic ash and gasoline vehicle exhaust has a limited short-term biological impact to an advanced lung cell in vitro model.

Although hexachlorobutadiene (HCBD) has been listed as a persistent organic pollutant (POP) under Annexes A and C of the Stockholm Convention, information about its unintentional production and emission is still very limited. We estimated the historical unintentional production and emission of HCBD during 1992–2016 in China based on aggregated activity data and emission functions. The unintentional production of HCBD increased from 60.8 (95% confidence interval, 38.2–88.5) MT/yr to 2871.5 (2234.2–3530.0) MT/yr during 1992–2016, representing an average annual growth rate of 17.4%. The main unintentional source of HCBD changed from carbon tetrachloride to trichloroethylene production during this period. We estimated that China's cumulative emissions of HCBD were 8211.3 (6131.5–10,579.5) MT during the same period. HCBD consumption and the chlorinated hydrocarbon production sector were the major contributors to total HCBD emissions. Owing to the long-range transport capability of HCBD (8784 km), such high emissions in China may cause adverse effects in other regions.

Groundwater is an essential public and drinking water supply and its protection is a goal for global policies. Here, we investigated the presence and prevalence of antibiotic residues, antibiotic resistance genes (ARGs), mobile genetic elements (MGEs), and microbial contamination in groundwater environments at various distances from urban areas. Antibiotic concentrations ranged from below detection limit to 917 ng/L, being trimethoprim, macrolide, and sulfonamide the most abundant antibiotic classes. A total of eleven ARGs (aminoglycoside, β-lactam, chloramphenicol, Macrolide-Lincosamide-Streptogramin B - MLSB, sulfonamide, and tetracycline), one antiseptic resistance gene, and two MGEs were detected by qPCR with relative abundances ranging from 6.61 × 10−7 to 2.30 × 10−1 copies/16S rRNA gene copies. ARGs and MGEs were widespread in the investigated groundwater environments, with increased abundances not only in urban, but also in remote areas. Distinct bacterial community profiles were observed, with a higher prevalence of Betaproteobacteria and Bacteroidetes in the less-impacted areas, and that of Firmicutes in the contaminated groundwater. The combined characteristics of increased species diversity, distinct phylogenetic composition, and the possible presence of fecal and/or pathogenic bacteria could indicate different types of contamination. Significant correlations between ARGs, MGEs and specific taxa within the groundwater bacterial community were identified, revealing the potential hosts of resistance types. Although no universal marker gene could be determined, a co-selection of int1, qacEΔ1 and sulI genes, a proxy group for anthropogenic pollution, with the tetC, tetO, tetW resistance genes was identified. As the tet group was observed to follow the pattern of environmental contamination for the groundwater samples investigated in this study, our results strongly support the proposal of this group of genes as an environmental tracer of human impact. Overall, the present study investigated several emerging contaminants in groundwater habitats that may be included in monitoring programs to enable further regulatory and protection measures.

This study evaluated associations between the bioreactivity of PM2.5in vitro and emission sources in the vicinity of a petrochemical complex in Taiwan. The average PM2.5 was 30.2 μg/m3 from 9 February to 23 March 2016, and the PM2.5 was clustered in long-range transport (with major local source) (12.8 μg/m3), and major (17.3 μg/m3) and minor industrial emissions (4.7 μg/m3) using a k-means clustering model. A reduction in cell viability and increases in the cytotoxicity-related lactate dehydrogenase (LDH), oxidative stress-related 8-isoprostane, and inflammation-related interleukin (IL)-6 occurred due to PM2.5 in a dose-dependent manner. The PM2.5 from major industrial emissions was significantly correlated with increased 8-isoprostane and IL-6, but this was not observed for long-range transport or minor industrial emissions. The bulk metal concentration was 9.52 ng/m3 in PM2.5. We further observed that As, Ba, Cd, and Se were correlated with LDH in the long-range transport group. Pb in PM2.5 from the major industrial emissions was correlated with LDH, whereas Pb and Se were correlated with 8-isoprostane. Sr was correlated with cell viability in the minor industrial emissions group. We demonstrated a new approach to investigate particle bioreactivity, which suggested that petrochemical-emitted PM2.5 should be a concern for surrounding residents' health.

Whilst attention is increasingly being focused on embodied pollutant emissions along supply chains in China, relatively little attention has been paid to dynamic changes in this process. This study utilized environmental extended input-output analysis (EEIOA) and structural path analysis (SPA) to investigate the dynamic variation of the SO2 emissions embodied in 28 economic sectors in Chinese supply chains during 2002–2012. The main conclusions are summarized as follows: (1) The dominant SO2 emission sectors differed under production and consumption perspectives. Electricity and heat production dominated SO2 emissions from the point of view of production, while construction contributed most from the consumption perspective. (2) The embodied SO2 emissions tended to change from the path (staring from consumption side to production side): “Services→Services→Power” in 2002 to the path: “Construction and Manufacturing→Metal and Nonmetal→Power” in 2012. (3) Metal-driven emissions raised dramatically from 15% in 2002 to 22% in 2012, due to increasing demand for metal products in construction and manufacturing activities. (4) Power generation was found to result in the greatest volume of production-based emissions, a burden it tended to transfer to upstream sectors in 2012. Controlling construction activities and cutting down end-of-pipe discharges in the process of power generation represent the most radical interventions in reducing Chinese SO2 emissions. This study shed light on changes in SO2 emissions in the supply chain, providing a range of policy implications from both production and consumption perspectives.

The spatial distribution of old and new halogenated flame retardants (HFRs), including polybrominated diphenyl ethers (PBDEs), hexabromocyclododecanes (HBCDs), and Dechlorane Plus (DPs) and related compounds (Dechloranes), were investigated in the South Shetland Islands of Antarctica, employing mosses (Andreaea depressinervis and Sanionia uncinata) and lichens (Himantormia lugubris and Usnea antarctica) as bioindicators. The levels of PBDEs, HBCDs, and Dechloranes ranged from 3.2 to 71.5, 0.63–960, and 2.04–2400 pg/g dw (dry weight) in the mosses, and from 1.5 to 188, 0.1–21.1, and 1.0–83.8 pg/g dw in the lichens, respectively. HFRs were detected in all of the collected samples, even in those from the remote regions. The dominance of high brominated-BDE, anti-DP fraction, and HBCD diastereomeric ratio in the samples from remote regions suggested the long-range atmospheric transport (LRAT) of the HFRs. The relatively high HBCDs and Dechloranes contamination and their similar chemical profile with commercial products in the vicinity of Antarctic research stations indicated that human activities might act as local sources, while PBDEs appeared to be more influenced by LRAT and bioaccumulation rather than local emission. Lastly, the relatively high HFR levels and dominance of more brominated BDEs at the Narębski Point and in the wet lowlands suggested that penguin colonies and melting glacier water could be secondary HFR sources in Antarctica. The HFR levels differed by sample species, suggesting that further research on the factors associated with the HFR accumulation in the different species is necessary. This study firstly reports the alternative HFR levels in a wide area of the Antarctica, which could improve our understanding of the source, transport, and fate of the HFRs.