The Hebei Spirit oil spill (HSOS) occurred on the west coast of South Korea (Taean county) on December 7, 2007, and studies revealed that exposure to the oil spill was associated with various adverse health issues in the inhabiting population. However, no studies evaluated the association between crude-oil exposure and epigenetic changes. This study aimed to investigate the HSOS exposure-associated longitudinal and cross-sectional variations in global DNA methylation (5-mc) and/or hydroxymethylation (5-hmc) and expression profiles of related genes in Taean cohort participants from 2009 (AH-baseline) and 2014 (AH-follow-up) relative to the reference group (AL). We measured global DNA 5-mc and 5-hmc levels and related gene expression levels in whole blood. We identified significant associations between HSOS exposure and AH-baseline-5-mc, AH-baseline-5-hmc, and AH-follow-up-5-hmc. HSOS exposure was associated with lower %5-mc content and higher %5-hmc content in the same individuals from both the cross-sectional and longitudinal studies. In addition, we found a strong correlation between 5-mc and DNMT3B expression, and between 5-hmc and TET1 expression. Our findings suggested that epigenetic changes are important biomarkers for HSOS exposure and that 5-hmc is likely to be more sensitive for environmental epidemiological studies.

Although huge interspecies differences in the response to dioxins have been acknowledged, toxic equivalency factors derived from rodent studies are often used to assess human health risk. To determine interspecies differences, we first developed a toxicokinetic model in humans by measuring dioxin concentrations in environmental and biomonitoring samples from Southern China. Significant positive correlations between dioxin concentrations in blood and age were observed for seven dioxin congeners, indicating an age-dependent elimination rate. Based on toxicokinetic models in humans, the half-lives of 15 dioxin congeners were estimated to be 1.60–28.55 years. In consideration that the highest contribution to total toxic equivalency in blood samples was by 12378-polychlorinated dibenzo-p-dioxin (P₅CDD), this study developed a physiologically based pharmacokinetic (PBPK) model of 12378-P₅CDD levels in the liver, kidney, and fat of C57/6J mice exposed to a single oral dose, and the half-life was estimated to be 26.1 days. Based on estimated half-lives in humans and mice, we determined that the interspecies difference of 12378-P₅CDD was 71, much higher than the default usually used in risk assessment. These results could reduce the uncertainty human risk assessment of 12378-P₅CDD, and our approach could be used to estimate the interspecies differences of other dioxin congeners.

Nightjars are considered human-tolerant species due to the population densities reached in strongly managed landscapes. However, no studies have been done evaluating metal-related effects on physiology, condition or fitness in any nightjar species. The main aim of this study was to evaluate how metal exposure affects physiology and condition in red-necked nightjar (Caprimulgus ruficollis) populations inhabiting three different environments in southeastern Spain: agricultural-urban area (n = 15 individuals), mining area (n = 17) and control area (n = 16).Increased plasma mineral levels (magnesium and calcium) and alkaline phosphatase (ALP) activity were observed in breeding females, and ALP was significantly higher in young birds due to bone growth and development. In the mining-impacted environment, nightjars showed decreased retinol (17.3 and 23.6 μM in the mining area and control area), uric acid (28.8 and 48.6 mg/dl in the mining area and control area) and albumin (16.2 and 19.6 g/l in the mining area and control area), probably impaired by a combination of toxic metal exposure and low prey quantity/quality in that area. Moreover, they showed increased plasma tocopherol levels (53.4 and 38.6 μM in the mining area and control area) which may be a response to cope with metal-induced oxidative stress and lipid peroxidation. Blood concentrations of toxic metals (As, Pb, Cd and Hg) were negatively associated with calcium, phosphorus, magnesium, ALP, total proteins and body condition index. This could lead to metal-related disorders in mineral metabolism and ALP activity that may potentially increase the risk of skeletal pathologies and consequent risk of fractures in the long term, compromising the survival of individuals. Further studies need to be carried out to evaluate potential metal-related effects on the antioxidant status and bone mineralization of nightjars inhabiting mining environments.

Mosaic loss of chromosome Y (mLOY) is the most common structure somatic event that related to increased risks of various diseases and mortality. Environmental pollution and genetic susceptibility were important contributors to mLOY. We aimed to explore the associations of polycyclic aromatic hydrocarbons (PAHs) exposure, as well as their joint effects with age, smoking, and genetic variants on peripheral blood mLOY. A total of 1005 male coke-oven workers were included in this study and their internal PAHs exposure levels of 10 urinary PAH metabolites and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts were measured. mLOY was defined by the median log R ratio(mLRR) of 1480 probes in male-specific region of chromosome-Y from genotyping array. We found that the PAHs exposure levels were linearly associated with mLOY. A 10-fold increase in urinary 1-hydroxynaphthalene (1-OHNa), 1-hydroxyphenanthrene (1-OHPh), 2-OHPh, 1-hydroxypyrene (1-OHP), ΣOH-PAHs, and plasma BPDE-Alb adducts could generate 0.0111, 0.0085, 0.0069, 0.0103, 0.0134, and 0.0152 decrease in mLRR-Y, respectively. Additionally, mLOY accelerated with age, smoking pack-years, and TCL1A rs1122138-C allele, and we observed the most severe mLOY among subjects carrying more than 3 of the above risk factors. Our results revealed the linear dose-effect associations between PAHs exposure and mLOY. Elder male smokers carrying rs1122138CC genotype were the most susceptible subpopulations to mLOY, who should be given protections for PAHs exposure induced chromosome-Y aberration.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that are linked to adverse health outcomes. PCB tissue levels are determinants of PCB toxicity; however, it is unclear how factors, such as an altered metabolism and/or a fatty liver, affect PCB distribution in vivo. We determined the congener-specific disposition of PCBs in mice with a liver-specific deletion of cytochrome P450 reductase (KO), a model of fatty liver with impaired hepatic metabolism, and wild-type (WT) mice. Eight-week-old male WT (MWT, n = 3), male KO (MKO, n = 5), female WT (FWT, n = 4), and female KO mice (FKO, n = 4) were exposed orally to Aroclor 1254. PCBs were quantified in adipose, blood, brain, and liver tissues by gas chromatography-mass spectrometry. The ΣPCB levels followed the rank order adipose > liver ∼ brain > blood in WT and adipose ∼ liver > brain > blood in KO mice. PCB levels were much higher in the liver of KO than WT mice, irrespective of the sex. A comparison across exposure groups revealed minor genotype and sex-dependent differences in the PCB congener profiles (cos Θ > 0.92). Within each exposure group, tissue profiles showed small differences between tissues (cos Θ = 0.85 to 0.98). These differences were due to a decrease in metabolically more labile PCB congeners and an increase in congeners resistant to metabolism. The tissue-to-blood ratio of PCBs decreased for adipose, increased for the brain, and remained constant for the liver with an increase in chlorination. While these ratios did not follow the trends predicted using a composition-based model, the agreement between experimental and calculated partition coefficients was reasonable. Although the distribution of PCBs differs between KO and WT mice, the magnitude of the partitioning of PCBs from the blood into tissues can be approximated using composition-based models.

Data (N = 10336) from National Health and Nutrition Examination Survey for 2003–2016 for US adults aged ≥ 20 years were analyzed to evaluate the concentrations of blood and urine cadmium across the various stages of glomerular function. Estimated glomerular filtration rate (eGFR) > 90 mL/min/1.73 m2 was defined to be glomerular function stage 1 (GF-1), eGFR between 60 and 90 mL/min/1.73 m2 defined as GF-2, eGFR between 45 and 60 mL/min/1.73 m2 as GF-3A, and eGFR between 15 and 45 mL/min/1.73 m2 as GF-3B/4. Regression models stratified by GF-stages were fitted to estimate associations between the observed levels of blood and urine cadmium across stages of GF. Based on the results of stratified modes, there were consistent increases in adjusted geometric means (AGMSM) for both blood and urine cadmium from GF-1 to GF-3A although increases were not uniform from one GF stage to another. For the total population, AGMSM for blood and urine cadmium were GF-1 (0.47, 0.24), GF-2 (0.60, 0.37), GF-3A (0.72, 0.45), and GF-3B/4 (0.73, 0.45) μg/L. respectively. Although females had higher AGMSMs than males for both blood and urine cadmium, the difference in blood cadmium narrowed as kidney function deteriorated. Smokers had the steepest increases in AGMSMs for blood and urine cadmium across the stages of glomerular function and smoker-nonsmoker differences for blood cadmium narrowed as kidney function deteriorated but smoker-nonsmoker differences for urine cadmium widened as kidney function deteriorated. The important physiologic messages are that both blood and urine cadmium cease to increase from GF-3A to GF-3B/4, suggesting a new steady state based on renal failure. And, the narrowed difference in blood cadmium in smokers vs. nonsmokers suggests why this happens. Incremental exposures to cadmium are offset by excretion as renal failure progresses.

Assessing the fate of both legacy and newer persistent organic pollutants (POPs) is an ongoing challenge. Top predators, including seabirds, are effective monitors of POPs because they forage over a range of marine habitats, integrating signals over space and time. However, migration patterns can make unravelling contaminant sources, and potentially assessments of the effectiveness of regulations, challenging if chemicals are acquired at distant sites. In 2014, we fitted geolocators on ancient murrelets (Synthliboramphus antiqueus) at four colonies on the Pacific Coast of Canada to obtain movement data throughout an annual cycle. All birds underwent a post-breeding moult in the Bering Sea. Around one-third then returned to overwinter on the British Columbia (BC) coast while the rest migrated to overwinter in waters along the north Asian coast. Such a stark difference in migration destination provided an opportunity to examine the influence of wintering location on contaminant signals. In summer 2015, we collected blood samples from returned geo-tagged birds and analyzed them for a suite of contaminants, including polybrominated diphenyl ethers (PBDEs), non-PBDE halogenated flame retardants, perfluoroalkyl substances (PFASs), organochlorines, and mercury. Feathers were also collected and analyzed for stable isotopes (δ¹³C, δ¹⁵N, and δ³⁴S). We found no significant differences in blood concentrations of any contaminant between murrelets from the two different overwinter areas, a result that indicates relatively rapid clearance of POPs accumulated during winter. Spatial variation in diet (i.e., δ¹³C) was associated with both BDE-47 and -99 concentrations. However, individual variation in trophic level had little influence on concentrations of any other examined contaminants. Thus, blood from these murrelets is a good indicator of recent, local contaminants, as most signals appear independent of overwintering location.

Both microplastics and persistent organic pollutants (POPs) are ubiquitously present in natural water environment, posing a potential threat to aquatic organisms. While it has been suggested that the immune responses of aquatic organisms could be hampered by exposure to microplastics and POPs, the synergistic immunotoxic impact of these two types of pollutants remain poorly understood. In addition, little is known about the mechanism behind the immunotoxic effect of microplastics. Therefore, in the present study, the immunotoxicity of microplastics and two POPs, benzo[a]pyrene (B[a]P) and 17β-estradiol (E2), were investigated alone or in combination in a bivalve species, Tegillarca granosa. Evident immunotoxicity, as indicated by alterations of haemocyte count, blood cell composition, phagocytic activity, intracellular content of ROS, concentration of Ca²⁺ and lysozyme, and lysozyme activity, was revealed for both microplastics and the two POPs examined. In addition, the expression of six immune-, Ca²⁺ signalling-, and apoptosis-related genes was significantly altered by exposure of clams to the contaminants studied. Furthermore, the toxicity of POPs was generally aggravated by smaller microplastics (500 nm) and mitigated by larger ones (30 μm). This size dependent effect on POP toxicity may result from size dependent interactions between microplastics and POPs. Data obtained in this study also indicate that similar to exposure to B[a]P and E2, exposure to microplastics may hamper the immune responses of clams through a series of interdependent physiological and molecular processes.

Soil contaminants can cause direct harm to lizards due to their regular swallowing of soil particles. As the world’s fastest growing insecticide with long half-life in soil, the endocrine disrupting effect of neonicotinoids on lizards deserves more attention. In this report, we assessed the endocrine disrupting effect of imidacloprid on Eremias argus during 28 days of continuous exposure. Among the imidacloprid and its metabolites, only the metabolite 6-chloropyridic acid had a significant accumulation in the gonads and was positively correlated with its blood concentration. Imidacloprid might cause endocrine disrupting effects on lizards in two ways. First, the desnitro metabolites of imidacloprid could accumulate in the brain, inhibited the secretion of gonadotropin-releasing hormone, and ultimately affected the feedback regulation of hypothalamic-pituitary-gonadal related hormones. Secondly, imidacloprid severely inhibited the gene expression of the corresponding enzymes in the gonadal anti-oxidative stress system, causing histological damage to the gonads and ultimately affecting gonadal function. Specifically, exposure to imidacloprid resulted in abnormal arrangement of spermatogenic epithelial epithelium, hyperplasia of epididymal wall, and oligospermia of male lizard. Meanwhile, gene expressions of cyp17, cyp19, and hsd17β were severely inhibited in the imidacloprid exposure group, consistent with decreased levels of testosterone and estradiol in plasma. Imidacloprid exposure could cause insufficient androgen secretion and less spermatogenesis in male lizards. The risk of imidacloprid exposure to female lizards was not as severe as that of male lizards, but it still inhibited the expression of cyp19 in the ovaries and led to a decrease in the synthesis of estradiol. This study firstly reported the endocrine disruption of imidacloprid to lizards, providing new data for limiting the use of neonicotinoids.