Chlorinated polycyclic aromatic hydrocarbons (ClPAHs) receive increasing attention as hazardous pollutants in terms of the high environmental persistence and toxicities. Ambient concentrations of 24 ClPAHs and 24 PAHs were investigated at 14 sites in the Tokyo Bay area of Japan. Twelve of 18 ClPAH species were detected in air samples, in spite of small sampling volumes. Mean concentrations of total PAHs in gas and particle phases were 5400 and 1400 pg/m³, and mean concentrations of total ClPAHs in gas and particle phases were 40 and 14 pg/m³, respectively. The spatial distributions of both total ClPAH and PAH concentrations indicated heavy pollution at sites in industrial activity areas. Principal component analysis suggested that the dominant sources of gaseous and particulate ClPAHs differed substantially from each other. In particular, gaseous ClPAHs could be produced by specific sources different from those of particulate ClPAHs. However, the dominant sources of particulate ClPAHs could be the same as those of particulate PAHs, including industrial activities such as steel and gas-production plants and natural gas-fired power plants. The influences of spatial relationships among sampling sites were represented using a network analysis. The constructed network showed that ambient ClPAHs and PAHs were dominated by local rather than regional pollution, because there were weaker relationships among nearby sites. Finally, exposure risks for ClPAHs were dominated by 7-chlorobenz[a]anthracene, followed by 9-chlorophenanthrene and 6-chlorobenzo[a]pyrene, and total risk was ∼1/200 that of PAHs.

The primary objective of the present study was to review the impact of Cd exposure on gut microbiota and intestinal physiology, as well as to estimate whether gut may be considered as the target for Cd toxicity. The review is based on literature search in available databases. The existing data demonstrate that the impact of Cd on gut physiology is two-sided. First, Cd exposure induces a significant alteration of bacterial populations and their relative abundance in gut (increased Bacteroidetes-to-Firmicutes ratio), accompanied by increased lipopolysaccharide (LPS) production, reflecting changed metabolic activity of the intestinal microbiome. Second, in intestinal wall Cd exposure induces inflammatory response and cell damage including disruption of tight junctions, ultimately leading to increased gut permeability. Together with increased LPS production, impaired barrier function causes endotoxinemia and systemic inflammation. Hypothetically, Cd-induced increase gut permeability may also result in increased bacterial translocation. On the one hand, bacteriolysis may be associated with aggravation of endotoxemia. At the same time, together with Cd-induced impairment of macrophage inflammatory response, increased bacterial translocation may result in increased susceptibility to infections. Such a supposition is generally in agreement with the finding of higher susceptibility of Cd-exposed mice to infections. The changed microbiome metabolic activity and LPS-induced systemic inflammation may have a significant impact on target organs. The efficiency of probiotics in at least partial prevention of the local (intestinal) and systemic toxic effects of cadmium confirms the role of altered gut physiology in Cd toxicity. Therefore, probiotic treatment may be considered as the one of the strategies for prevention of Cd toxicity in parallel with chelation, antioxidant, and anti-inflammatory therapy.

Although weekly consumption of fish is recommended, the presence of contaminants in seafood has raised many concerns regarding the benefits of fish intake. In the present study microplastics (MPs) and metals’ concentration in muscles of both benthic and pelagic fish species from northeast of Persian Gulf were investigated and the risk/benefit of their consumption was assessed. The results demonstrated that MPs and Hg in all species and Se in benthic species increase with size, while relationship between other metals, and fish size is not consistent. Consumption of a meal ration of 300 and < 100 g/week for adults and children, respectively, is recommended since it would provide the required essential elements with no human health risk. On the other hand, the estimated intake of MPs from fish muscles revealed that the mean intake of MPs for P. indicus, E. coioides, A. djedaba, and S. jello consumption is 555, 240, 233, and 169 items/300 g-week, respectively. Moreover, the relationship between MPs and metals in fish muscles were positive for A. djedaba, and negative for E. coioides. Considering the chemical toxicity of MPs and metals, and their good linear relationships in some species, consumption of high doses of the studied fish may pose a health threat to the consumers.

Gasoline vehicles are a major source of anthropogenic secondary organic aerosols (SOAs). However, current models based on known precursors fail to explain the substantial SOAs from vehicle emissions due to the inadequate understanding of the formation mechanism. To provide more information on this issue, the formation of SOAs from ozonolysis of four light-duty gasoline vehicle exhaust systems was investigated with a vacuum ultraviolet photoionization mass spectrometer (VUV-PIMS). Remarkable SOAs formation was observed and the SOAs were primarily aliphatic alkenes. PI mass spectra of the SOAs from all vehicles exhibited similar spectral patterns (a regular mass group with m/z at 98, 112, 126 …). Interestingly, most carbonyl products of aliphatic alkenes observed as major gaseous products have specific molecular weights, and the main formation pathway of SOAs can be explained well using aldol condensation reactions of these carbonyls. This is a direct observation of the aldol condensation as a dominated pathway for SOAs formation, and the first report on the composition and formation mechanism of the SOAs from the ozonolysis of gasoline vehicle exhaust is given. The study reveals that low molecular weight alkenes may play a more significant role in vehicle-induced SOAs formation than previously believed. More importantly, the PI mass spectra of SOAs from vehicles show similarities to the field aerosol sample mass spectra, suggesting the possible significance of the aldol condensation reactions in ambient aerosol formation. Since carbonyls are a major degradation product of biogenic and anthropogenic VOCs through atmospheric oxidation processes, the mechanism proposed in this study can be applied more generally to explain aerosol formation from the oxidation of atmospheric hydrocarbons.

Acrylamide (AA), an environmental pollutant, has been linked to neurotoxicity, genotoxicity and carcinogenicity. AA is widely used to synthesize polymers for industrial applications, is widely found in Western-style carbohydrate-rich foods and cigarette smoke, and can also be detected in human umbilical cord blood and breast milk. This is the first study that demonstrated the cardiac developmental toxicity of AA in zebrafish embryos. Post-fertilization exposure to AA caused a clearly deficient cardiovascular system with a shrunken heart and abortive morphogenesis and function. Disordered expression of the cardiac genes, myl7, vmhc, myh6, bmp4, tbx2b and notch1b, as well as reduced number of myocardial cells and endocardial cells, indicated the collapsed development of ventricle and atrium and failed differentiation of atrioventricular canal (AVC). Although cell apoptosis was not affected, the capacity of cardiomyocyte proliferation was significantly reduced by AA exposure after fertilization. Further investigation showed that treatment with AA specifically reduced the expressions of nkx2.5, myl7 and vmhc in the anterior lateral plate mesoderm (ALPM) during the early cardiogenesis. In addition, AA exposure disturbed the restricted expressions of bmp4, tbx2b and notch1b during atrioventricular (AV) valve development and cardiac chambers maturation. Our results showed that AA-induced cardiotoxicity was related to decreased cardiac progenitor genes expression, reduced myocardium growth, abnormal cardiac chambers morphogenesis and disordered AVC differentiation. Our study demonstrates that AA exposure during a time point analogous to the first trimester in humans has a detrimental effect on early heart development in zebrafish. A high ingestion rate of AA-containing products may be an underlying risk factor for cardiogenesis in fetuses.

Ambient concentrations of fine particulate matter (PM₂.₅) concentration is often used as an exposure surrogate to estimate PM₂.₅ health effects in epidemiological studies. Ignoring the potential variations in the amount of outdoor PM₂.₅ infiltrating into indoor environments will cause exposure misclassification, especially when people spend most of their time indoors. As it is not feasible to measure the PM₂.₅ infiltration factor (Fᵢₙf) for each individual residence, we aimed to build models for residential PM₂.₅Fᵢₙf prediction and to evaluate seasonal Fᵢₙf variations among residences. We repeated collected paired indoor and outdoor PM₂.₅ filter samples for 7 continuous days in each of the three seasons (hot, cold and transitional seasons) from 48 typical homes of Shanghai, China. PM₂.₅-bound sulfur on the filters was measured by X-ray fluorescence for PM₂.₅Fᵢₙf calculation. We then used stepwise-multiple linear regression to construct season-specific models with climatic variables and questionnaire-based predictors. All models were evaluated by the coefficient of determination (R²) and root mean square error (RMSE) from a leave-one-out-cross-validation (LOOCV). The 7-day mean (±SD) of PM₂.₅Fᵢₙf across all observations was 0.83 (±0.18). Fᵢₙf was found higher and more varied in transitional season (12–25 °C) than hot (>25 °C) and cold (<12 °C) seasons. Air conditioning use and meteorological factors were the most important predictors during hot and cold seasons; Floor of residence and building age were the best transitional season predictors. The models predicted 60.0%–68.4% of the variance in 7-day averages of Fᵢₙf, The LOOCV analysis showed an R² of 0.52 and an RMSE of 0.11. Our finding of large variation in residential PM₂.₅Fᵢₙf between seasons and across residences within season indicated the important source of outdoor-generated PM₂.₅ exposure heterogeneity in epidemiologic studies. Our models based on readily available data may potentially improve the accuracy of estimates of the health effects of PM₂.₅ exposure.

Environmental pollution is a topic of great interest because it directly affects the quality of ecosystems and of all living organisms at different trophic and systematic levels. Together with the global climate change, the long-term surviving of many species of plants and animals is threaten, distributional patterns at global and regional levels are altered and it results in local assemblages of species that are quite different from those that currently constitute coevolved communities. .For this study, the species Myotis myotis was used as bioindicator and it was sampled from two caves in the south-east of Sicily, Pipistrelli chosen as control area and Palombara chosen as polluted area, to measure the concentrations of trace elements in fur and liver tissues. Results showed higher content of essential elements in fur in bats sampled from Pipistrelli. Conversely, higher concentrations of toxic metals in liver such as As, Cd, Pb and Hg were measured in bat samples in Palombara cave, where specimens have a hunting area extended within the boundaries of the petrochemical plant. Nevertheless, we cannot consider Palombara population as polluted by metal contamination since their tissue concentrations are overall lower than toxic thresholds values suggested for small mammals. Likewise, we cannot exclude other kind of pollutants as potential stressors of the examined population, contributing with the decreasing of bat colonies in Sicily.

The contribution of diesel exhaust to atmospheric pollution is a major concern for public health, especially in terms of occurrence of lung cancers. The present study aimed at addressing the toxic effects of a repeated exposure to these emissions in an animal study performed under strictly controlled conditions. Rats were repeatedly exposed to the exhaust of diesel engine. Parameters such as the presence of a particle filter or the use of gasoil containing rapeseed methyl ester were investigated. Various biological parameters were monitored in the lungs to assess the toxic and genotoxic effects of the exposure. First, a transcriptomic analysis showed that some pathways related to DNA repair and cell cycle were affected to a limited extent by diesel but even less by biodiesel. In agreement with occurrence of a limited genotoxic stress in the lungs of diesel-exposed animals, small induction of γ-H2AX and acrolein adducts was observed but not of bulky adducts and 8-oxodGuo. Unexpected results were obtained in the study of the effect of the particle filter. Indeed, exhausts collected downstream of the particle filter led to a slightly higher induction of a series of genes than those collected upstream. This result was in agreement with the formation of acrolein adducts and γH2AX. On the contrary, induction of oxidative stress remained very limited since only SOD was found to be induced and only when rats were exposed to biodiesel exhaust collected upstream of the particle filter. Parameters related to telomeres were identical in all groups. In summary, our results point to a limited accumulation of damage in lungs following repeated exposure to diesel exhausts when modern engines and relevant fuels are used. Yet, a few significant effects are still observed, mostly after the particle filter, suggesting a remaining toxicity associated with the gaseous or nano-particular phases.

The estimation of PM₂.₅-related mortality is becoming increasingly important. The accuracy of results is largely dependent on the selection of methods for PM₂.₅ exposure assessment and Concentration-Response (C-R) function. In this study, PM₂.₅ observed data from the China National Environmental Monitoring Center, satellite-derived estimation, widely collected geographic and socioeconomic information variables were applied to develop a national satellite-based Land Use Regression model and evaluate PM₂.₅ exposure concentrations within 2013–2015 with the resolution of 1 km × 1 km. Population weighted concentration declined from 72.52 μg/m³ in 2013 to 57.18 μg/m³ in 2015. C-R function is another important section of health effect assessment, but most previous studies used the Integrated Exposure Regression (IER) function which may currently underestimate the excess relative risk of exceeding the exposure range in China. A new Shape Constrained Health Impact Function (SCHIF) method, which was developed from a national cohort of 189,793 Chinese men, was adopted to estimate the PM₂.₅-related premature deaths in China. Results showed that 2.19 million (2013), 1.94 million (2014), 1.65 million (2015) premature deaths were attributed to PM₂.₅ long-term exposure, different from previous understanding around 1.1–1.7 million. The top three provinces of the highest premature deaths were Henan, Shandong, Sichuan, while the least ones were Tibet, Hainan, Qinghai. The proportions of premature deaths caused by specific diseases were 53.2% for stroke, 20.5% for ischemic heart disease, 16.8% for chronic obstructive pulmonary disease and 9.5% for lung cancer. IER function was also used to calculate PM₂.₅-related premature deaths with the same exposed level used in SCHIF method, and the comparison of results indicated that IER had made a much lower estimation with less annual amounts around 0.15–0.5 million premature deaths within 2013–2015.