Toxic elements (arsenic, cadmium, lead, mercury, selenium, thallium) are a group of contaminants that are known to elicit developmental, reproductive, general health, and immune system effects in reptiles, even at low concentrations. Reptiles, including marine turtles, are susceptible to accumulation of toxic elements due to their long life span, low metabolic rate, and highly efficient conversion of prey into biomass. The objectives of this study were to (1) document concentrations of arsenic, cadmium, lead, mercury, selenium, and thallium in whole blood and keratin from nesting loggerhead sea turtles (Caretta caretta) from Casey Key, Florida and document correlations thereof and (2) correlate whole blood toxic element concentrations to various hematological and plasma biochemistry analytes. Baselines for various hematological and plasma analytes and toxic elements in whole blood and keratin (i.e., scute) in nesting loggerheads are documented. Various correlations between the toxic elements and hematological and plasma biochemistry analytes were identified; however, the most intriguing were negative correlations between arsenic, cadmium, lead, and selenium with and α- and γ-globulins. Although various extrinsic and intrinsic variables such as dietary and feeding changes in nesting loggerheads need to be considered, this finding may suggest a link to altered humoral immunity. This study documents a suite of health variables of nesting loggerheads in correlation to contaminants and identifies the potential of toxic elements to impact the overall health of nesting turtles, thus presenting important implications for the conservation and management of this species.

As the world burden of environmental contamination increases, it is of the utmost importance to develop streamlined approaches to environmental risk assessment in order to prioritize mitigation measures. Whole-cell biosensors or bioreporters and speciation modeling have both become of increasing interest to determine the bioavailability of pollutants, as bioavailability is increasingly in use as an indicator of risk. Herein, we examine whether bioreporter results are able to reflect expectations based on chemical reactivity and speciation modeling, with the hope to extend the research into a wider framework of risk assessment. We study a specific test case concerning the bioavailability of lead (Pb) in aqueous environments containing Pb-complexing ligands. Ligands studied include ethylene diamine tetra-acetic acid (EDTA), meso-2,3 dimercaptosuccinic acid (DMSA), leucine, methionine, cysteine, glutathione, and humic acid (HA), and we also performed experiments using natural water samples from Lake Tai (Taihu), the third largest lake in China. We find that EDTA, DMSA, cysteine, glutathione, and HA amendment significantly reduced Pb bioavailability with increasing ligand concentration according to a log-sigmoid trend. Increasing dissolved organic carbon in Taihu water also had the same effect, whereas leucine and methionine had no notable effect on bioavailability at the concentrations tested. We find that bioreporter results are in accord with the reduction of aqueous Pb2+ that we expect from the relative complexation affinities of the different ligands tested. For EDTA and HA, for which reasonably accurate ionization and complexation constants are known, speciation modeling is in agreement with bioreporter response to within the level of uncertainty recognised as reasonable by the United States Environmental Protection Agency for speciation-based risk assessment applications. These findings represent a first step toward using bioreporter technology to streamline the biological confirmation or validation of speciation modeling for use in environmental risk assessment.

Human studies indicate that phthalate exposure is associated with adverse male reproductive health, and this association may be modified by genetic polymorphisms.We investigated whether apoptosis-related gene polymorphisms modified the associations of phthalate exposure with spermatozoa apoptosis and semen quality.In this Chinese population who sought for semen examination in an infertility clinic, we measured 8 phthalate metabolites in two urine samples to assess the individual's exposure levels. Apoptosis-related gene (Fas, FasL, and caspase3) polymorphisms were performed by real-time PCR. Spermatozoa apoptosis and semen quality parameters were evaluated by Annexin V/PI assay and computer-aided semen analysis, respectively.We found that Fas rs2234767, FasL rs763110, and caspase3 rs12108497 gene polymorphisms significantly modified the associations between urinary phthalate metabolites and spermatozoa apoptosis. For example, urinary monobutyl phthalate (MBP) associated with an increased percentage of Annexin V⁺/PI⁻ spermatozoa of 25.11% (95% CI: 4.08%, 50.53%) were only observed among men with CT/TT genotype of FasL rs763110. In addition, we found that caspase3 rs12108497 gene polymorphisms significantly modified the associations of urinary mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) with decreased sperm concentration and sperm count (both p-values for interactions = 0.02).Our results provided the first evidence that apoptosis-related gene polymorphisms might contribute to the effects of phthalate exposure on male reproductive health.

Temperature variation caused by climate change, seasonal variation and geographic locations affects the physicochemical compositions of chromophoric dissolved organic matter (CDOM), resulting in difference in the fates of CDOM-related environmental pollutants. Exploration into the thermal induced structural transition of CDOM can help to better understand their environmental impacts, but information on this aspect is still lacking. Through integrating fluorescence excitation–emission matrix coupled parallel factor analysis with synchronous fluorescence two-dimensional correlation spectroscopy, this study provides an in–depth insight into the temperature–dependent conformational transitions of CDOM and their impact on its hydrophobic interaction with persistent organic pollutants (with phenanthrene as an example) in water. The fluorescence components in CDOM change linearly to water temperature with different extents and different temperature regions. The thermal induced transition priority in CDOM is protein-like component → fulvic-like component → humic-like component. Furthermore, the impact of thermal–induced conformational transition of CDOM on its hydrophobic interaction with phenanthrene is observed and explored. The fluorescence–based analytic results reveal that the conjugation degree of the aromatic groups in the fulvic– and humic–like substances, and the unfolding of the secondary structure in the protein–like substances with aromatic structure, contribute to the conformation variation. This integrated approach jointly enhances the characterization of temperature–dependent conformational variation of CDOM, and provides a promising way to elucidate the environmental behaviours of CDOM.

We assessed mercury (Hg) pollution in China's coastal waters, including the Bohai Sea, the Yellow Sea, the East China Sea and the South China Sea, based on a nationwide dataset from 301 sampling sites. A methylmercury (MeHg) intake model for humans based on the marine food chain and human fish consumption was established to determine the linkage between water pollutants and the pollutant intake by humans. The predicted MeHg concentration in fish from the Bohai Sea was the highest among the four seas included in the study. The MeHg intake through dietary ingestion was dominant for the fish and was considerably higher than the MeHg intake through water respiration. The predicted MeHg concentrations in human blood in the coastal regions of China ranged from 1.37 to 2.77 μg/L for pregnant woman and from 0.43 to 1.00 μg/L for infants, respectively, based on different diet sources. The carnivorous fish consumption advisory for pregnant women was estimated to be 288–654 g per week to maintain MeHg concentrations in human blood at levels below the threshold level (4.4 μg/L established by the US Environmental Protection Agency). With a 50% increase in Hg concentrations in water in the Bohai Sea, the bioaccumulated MeHg concentration (4.5 μg/L) in the fish consumers will be higher than the threshold level. This study demonstrates the importance in controlling Hg pollution in China's coastal waters. An official recommendation guideline for the fish consumption rate and its sources will be necessary for vulnerable populations in China.

Even though clinical, epidemiological and toxicological studies have progressively provided a better knowledge of the underlying mechanisms by which air pollution-derived particulate matter (PM) exerts its harmful health effects, further in vitro studies on relevant cell systems are still needed. Hence, aiming of getting closer to the human in vivo conditions, primary human bronchial epithelial cells derived from normal subjects (NHBE) or sensitive chronic obstructive pulmonary disease (COPD)-diseased patients (DHBE) were differentiated at the air-liquid interface. Thereafter, they were repeatedly exposed to air pollution-derived PM2.5 to study the occurrence of some relevant genetic and/or epigenetic endpoints. Concentration-, exposure- and season-dependent increases of OH-B[a]P metabolites in NHBE, and to a lesser extent, COPD-DHBE cells were reported; however, there were more tetra-OH-B[a]P and 8-OHdG DNA adducts in COPD-DHBE cells. No increase in primary DNA strand break nor chromosomal aberration was observed in repeatedly exposed cells. Telomere length and telomerase activity were modified in a concentration- and exposure-dependent manner in NHBE and particularly COPD-DHBE cells. There were a global DNA hypomethylation, a P16 gene promoter hypermethylation, and a decreasing DNA methyltransferase activity in NHBE and notably COPD-DHBE cells repeatedly exposed. Changes in site-specific methylation, acetylation, and phosphorylation of histone H3 (i.e., H3K4me3, H3K9ac, H3K27ac, and H3S10ph) and related enzyme activities occurred in a concentration- and exposure-dependent manner in all the repeatedly exposed cells. Collectively, these results highlighted the key role played by genetic and even epigenetic events in NHBE and particularly sensitive COPD-DHBE cells repeatedly exposed to air pollution-derived PM2.5 and their different responsiveness. While these specific epigenetic changes have been already described in COPD and even lung cancer phenotypes, our findings supported that, together with genetic events, these epigenetic events could dramatically contribute to the shift from healthy to diseased phenotypes following repeated exposure to relatively low doses of air pollution-derived PM2.5.

Although organophosphate esters (OPEs) have been detected with growing frequency in water ecosystems, the underlying accumulation mechanisms of these compounds in fish are still unknown. Here, we investigated the tissue-specific accumulation and depuration of seven OPEs in adult zebrafish at three levels (0, 1/150 LC50 (environmentally relevant level), and 1/30 LC50 per OPE congener) in laboratory after 19 days exposure and 3 days depuration. The bioaccumulation of OPEs varied among tissues. Muscle contained the lowest level of OPEs and liver had the highest level of two (TPP and TCEP) of the seven OPEs at steady state. The high levels and slow depuration rates of TDCIPP, TPHP, and TCP observed in roe indicated that the accumulated OPEs were potentially stored in roe and transferred to the next generation. After examination of the major metabolites (organophosphate diesters) in selected tissues, a physiologically based toxicokinetic (PBTK) model used in fish was adopted to explore the key factors affecting the bioaccumulation of OPEs in zebrafish. Biotransformation of OPEs with polychlorinated alkyl moieties (i.e. TDCIPP) and aryl moieties (i.e. TPHP and TCP) has more significant impacts on the accumulation than those of OPEs with alkyl or short chain chlorinated alkyl moieties. Furthermore, the partition process between tissues and blood was also investigated, and was demonstrated to be the dominant process for OPEs accumulation in zebrafish. This study provides critical information on the bioaccumulation, tissue distribution, and metabolization of OPEs in relation with OPE structures in fish, as well as the underlying bioaccumulation mechanisms/pathways of OPEs in aquatic life.

Based on the 12-hour PM2.5 samples collected in an urban site of Beijing, sixteen PM2.5-bound Polycyclic Aromatic Hydrocarbons (PAHs) were measured to investigate the characteristics and potential source regions of particulate PAHs in Beijing. The study period included the summer period in July–August 2014, the APEC source control period during the Asia-Pacific Economic Cooperation (APEC) meeting in the first half of November 2014, and the heating period in the second half of November 2014. Compared to PM2.5, sum of 16 PM2.5-bound PAHs exhibited more significant seasonal variation with the winter concentration largely exceeding the summer concentration. Temperature appeared to be the most crucial meteorological factor during the summer and heating periods, while PM2.5-bound PAHs showed stronger correlation with relative humidity and wind speed during the APEC source control period. Residential heating significantly increased the concentrations of higher-ring-number (≥4) PAHs measured in PM2.5 fraction. Potential source contribution function (PSCF) and concentration weighted trajectory (CWT) analysis as well as the (3 + 4) ring/(5 + 6) ring PAH ratio analysis revealed the seasonal difference in the potential source area of PM2.5-bound PAHs in Beijing. Southern Hebei was the most likely potential source area in the cold season. Using black carbon (BC) and carbon monoxide (CO) as the PAH tracers, regional residential, transportation and industry emissions all contributed to the PAH pollution in Beijing.

Polycyclic aromatic hydrocarbons (PAHs) and nitro-polycyclic aromatic hydrocarbons (NPAHs) are toxic pollutants mainly produced during fossil fuel combustion. Domestic coal stoves, which emit large amounts of PAHs and NPAHs, are widely used in the Chinese countryside. In this study, emission factors (Efs) for 13 PAH species and 21 NPAH species for four raw coal (three bituminous and one anthracite), one honeycomb briquette, and one crop residue pellet (peanut hulls) samples burned in a typical Chinese rural cooking stove were determined experimentally. The PAH and NPAH Efs for the six fuels were 3.15–49 mg/kg and 0.32–100 μg/kg, respectively. Peanut hulls had very high Efs for both PAHs and NPAHs, and honeycomb briquettes had the lowest Efs. 2-Nitropyrene and 2-nitrofluoranthene, which are NPAHs typically found in secondary organic aerosol, were detected in the emissions from some fuels, suggesting that chemical reactions may have occurred in the dilution tunnel between the flue gas leaving the stove and entering the sampler. The 1-nitropyrene to pyrene diagnostic ratios for coal and peanut hulls were 0.0001 ± 0.0001 and 0.0005, respectively. These were in the same order of magnitude as reference ratios for emissions during coal combustion. The 6-nitrobenzo[a]pyrene to benzo[a]pyrene ratios for the fuels were determined, and the ratios for coal and peanut hulls were 0.0010 ± 0.0001 and 0.0014, respectively. The calculated potential toxic risks indicated that peanut hull emissions were very toxic, especially in terms of NPAHs, compared with emissions from the other fuels.

Benzotriazole (BT) and its associated derivatives are used ubiquitously in industrial processes, and can be detected in indoor temperature coolants and in chemicals designed to inhibit corrosion. This chemical has been widely detected in aquatic environments and shows some degree of environmental persistence. Evidence has shown that BT exposure can negatively affect endocrine systems and can result in neurotoxicity in fish. However, no study has examined whether this chemical exhibits hepatotoxicity in fish, and if so, what are the underlying mechanism associated with the damage. To address this knowledge gap, we measured the liver proteome of adult male Chinese rare minnow (Gobiocypris rarus) exposed to either 0.05, 0.5, or 5 mg/L BT for 28 days. Overall, 17 proteins were induced and 9 were reduced in abundance following BT treatment (ratio > 1.5, p < 0.05). Pathway analysis revealed that cellular processes affected by BT included xenobiotic clearance, oxidative stress response, apoptosis, and translation. Moreover, transcripts related to these toxic pathways were also significantly affected by BT. In addition, rare minnows exposed to BT showed signs of hypertrophy of hepatocytes, nuclei pyknosis, and higher levels of cellular vacuolization compared to the controls, thus these early proteomic responses in the liver may be related to pathology (i.e. adverse outcome pathway). Our data demonstrate that BT dysregulates molecular responses in the liver and tissue pathology indicative of damage. This study provides new insight into BT hepatotoxicity in Chinese rare minnow.