Inflammation and the coagulation cascade are considered to be the potential mechanisms of ambient particulate matter (PM) exposure-induced adverse cardiovascular events. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), and fibrinogen are arguably the four most commonly assayed markers to reflect the relationships of PM with inflammation and blood coagulation. This review summarized and quantitatively analyzed the existing studies reporting short- and long-term associations of PM₂.₅(PM with an aerodynamic diameter ≤2.5 μm)/PM₁₀ (PM with an aerodynamic diameter≤10 μm) with important inflammation and blood coagulation markers (TNF-α, IL-6, IL-8, fibrinogen). We reviewed relevant studies published up to July 2020, using three English databases (PubMed, Web of Science, Embase) and two Chinese databases (Wang-Fang, China National Knowledge Infrastructure). The OHAT tool, with some modification, was applied to evaluate risk of bias. Meta-analyses were conducted with random-effects models for calculating the pooled estimate of markers. To assess the potential effect modifiers and the source of heterogeneity, we conducted subgroup analyses and meta-regression analyses where appropriate. The assessment and correction of publication bias were based on Begg’s and Egger’s test and “trim-and-fill” analysis. We identified 44 eligible studies. For short-term PM exposure, the percent change of a 10 μg/m³ PM₂.₅ increase on TNF-α and fibrinogen was 3.51% (95% confidence interval (CI): 1.21%, 5.81%) and 0.54% (95% confidence interval (CI): 0.21%, 0.86%) respectively. We also found a significant short-term association between PM₁₀ and fibrinogen (percent change = 0.17%, 95% CI: 0.04%, 0.29%). Overall analysis showed that long-term associations of fibrinogen with PM₂.₅ and PM₁₀ were not significant. Subgroup analysis showed that long-term associations of fibrinogen with PM₂.₅ and PM₁₀ were significant only found in studies conducted in Asia. Our findings support significant short-term associations of PM with TNF-α and fibrinogen. Future epidemiological studies should address the role long-term PM exposure plays in inflammation and blood coagulation markers level change.

Natural environments are receiving an increasing number of contaminants. Therefore, the evaluation and identification of early responses to pollution in these complex habitats is an urgent and challenging task. Doñana National Park (DNP, SW Spain) has been widely used as a model area for environmental studies because, despite its strictly protected core, it is surrounded by numerous threat sources from agricultural, mining and industrial activities. Since many pollutants often induce oxidative stress, redox proteomics was used to detect redox-based variations within the proteome of Mus spretus mice captured in DNP and the surrounding areas. Functional analysis showed that most differentially oxidized proteins are involved in the maintenance of homeostasis, by eliciting mechanisms to respond to toxic substances and oxidative stress, such as antioxidant and biotransformation processes, immune and inflammatory responses, and blood coagulation. Furthermore, changes in the overall protein abundance were also analysed by label-free quantitative proteomics. The upregulation of phase I and II biotransformation enzymes in mice from Lucio del Palacio may be an alert for organic pollution in the area located at the heart of DNP. Metabolic processes involved in protein turnover (proteolysis, amino acid catabolism, new protein biosynthesis and folding) were activated in response to oxidative damage to these biomolecules. Consequently, aerobic respiratory metabolism increased to address the greater ATP demands. Alterations of cholesterol metabolism that could cause hepatic steatosis were also detected. The proteomic detection of globally altered metabolic and physiological processes offers a complete view of the main biological changes caused by environmental pollution in complex habitats.

PBDEs and heavy metals are two major contaminants at e-waste disposal sites, but their combined effects remain largely unexplored. In the present study, the transcriptomic profiles of zebrafish larvae were examined after acute exposure of embryos to 200 μg/L BDE-209, 20 μg/L lead (Pb) or their mixture (Mix). Stimulation of steroidogenic pathway and vitellogenesis in the BDE-209 and Mix treatments indicated the estrogenic activities of BDE-209, while Pb antagonized those estrogenic effects in the Mix treatment. Increased heart rates were observed in zebrafish exposed to the Pb and Mix treatments. The cardiac dysfunction probably resulted from the promotion of angiogenesis, increased adrenergic drive and induction of the formation of blood clot. Furthermore, the Pb and Mix treatments activated neuroendocrine regulation of the pituitary in a positive feedback loop, via the thyrotropin-releasing hormone receptor, thus increasing thyroid hormone production self-adaptively. Overall, the interaction between BDE-209 and Pb led to synergistic and antagonistic effects on gene transcriptions, with concerted contribution from their individual toxicological properties.

This study aimed to assess the effects of Basagran® on zebrafish (Danio rerio) embryos. The embryos were exposed to Basagran® at concentrations ranging from 120.0 to 480.6 mg/L, and the effects on embryo development (up to 96 h) and bacterial communities of 96 h-larvae were assessed. The embryo development response was time-dependent and concentration-dependent (106.35 < EC50 < 421.58 mg/L). The sensitivity of embryo-related endpoints decreased as follows: blood clotting in the head and/or around the yolk sac > delay or anomaly in yolk sac absorption > change in swimming equilibrium > development of pericardial and/or yolk sac oedema > scoliosis. A PCR-DGGE analysis was used to evaluate changes in the structure, richness, evenness and diversity of bacterial communities after herbicide exposure. A herbicide-induced structural adjustment of bacterial community was observed.In this study, it was successfully demonstrated that Basagran® affected zebrafish embryos and associated bacterial communities, showing time-dependent and concentration-dependent embryos' developmental response and structural changes in bacterial community. Thus, this work provides for the first time a complementary approach, which is useful to derive robust toxicity thresholds considering the embryo-microbiota system as a whole. The aquatic hazard assessment will be strengthened by combining current ecotoxicological tests with molecular microbiology tools.

Exposure to elevated levels of ambient air pollutants can lead to adverse cardiovascular effects. Perturbation of the coagulation balance is one of the potential mechanisms. However, evidence regarding the impact of improvement in air pollution on blood coagulability in COPD patients has never been reported. Coagulation processes are known to be of relevance for cardiovascular pathology; therefore, this study aimed to investigate the association of short-term air pollution exposure with blood marker (D-dimer) of coagulation. A 3-year (through the Asian game) cohort study based on the GIRD COPD Biobank Project was conducted in 36 COPD patients to estimate whether changes in measurements of D-dimer were associated with changes in pollutant concentration, comparing for 51 intervention days (November 1–December 21) in 2010 with the same calendar date of baseline years (2009 and 2011). Daily mean concentrations of air pollutants and meteorological variables were measured during the time. Daily PM₁₀ decreased from 65.86 μg/m³ during the baseline period to 62.63 μg/m³ during the Asian Games period; daily NO₂ decreased from 51.33 to 42.63 μg/m³. SO₂ and other weather variables did not differ substantially. We did not observe statistically significant improvements in D-dimer levels by 9.86 % from a pre-Asian game mean of 917 ng/ml to a during-Asian game mean of 1007 ng/ml, platelet number by 11.66 %, PH by −0.15 %, PCO₂ by −6.54 %, and PO₂ by −1.16 %. In the post-Asian game period, when pollutant concentrations increased, most outcomes approximated pre-Asian game levels, and similar effects were also demonstrated in D-dimer, platelet number, and arterial blood gas. For D-dimer and platelet number, we observed statistically significant increases associated with increases in NO₂ at lag 1–3 and SO₂ at lag 2–4. For PH, PCO₂, and PO₂, any significant effect was not demonstrated. This study gives no support to the hypothesis that reduction in air pollution levels during the 2010 Asian game is associated with activation of blood coagulation with COPD patients. However, one step forward has been made on the gap between improved air pollution and blood coagulability. Meanwhile, our study also provides evidence for the presence of a hypercoagulative state in systemic circulation in COPD patients. Additional studies employing other susceptible populations and endpoints are pending.

Distribution of perfluorooctane sulfonate (PFOS) was investigated in tissues (plasma, blood clot, mucus, skin, liver, muscle, and gonad) of tiger puffer fish Takifugu rubripes. A single dose of PFOS was intraperitoneally injected at 0.1 mg/kg body weight with samples taken over a 14-day period. The highest concentration of PFOS was found in the plasma, 861 ng/mL at 14 days, followed by the mucus, liver, blood clot, gonads, muscles, and skin of fish. A gradual upward trend in PFOS concentration was observed in the mucus and liver whereas there was no change in the plasma, blood clot, gonad, muscle, and skin after the initial increase in PFOS concentrations following injection. No significant trend for estimated total PFOS content in whole body was observed during the experimental period. Relatively high concentrations of PFOS (690 ng/g ww after 14 days) were detected in body surface mucus that continuously oozes from the skin. These results may suggest that mucus is one of the elimination pathways of PFOS in tiger puffer fish.