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.

A previous study observed high blood lead levels (BLL) in preschool children attending 50 day care centers (DCC) in São Paulo, Brazil.To identify whether lead levels found in both homes and DCC environments are associated with high blood lead levels.Children attending 4 DCCs, quoted here as NR, VA, PS and PF, were divided into two groups according to BLL: high exposure (HE: ≥13.9 μg/dL; 97.5 percentile of the 2013 year sample) and low exposure (LE: <5 μg/dL). For in situ lead measurements (lead paint mode: mg/cm² and ROHS mode: μg/g) in the children's households and in the DCC environments, a field portable X-ray-fluorescence analyzer was used. Multiple logistic regressions were performed to control for confounding factors. Odds ratios were adjusted for age, sex, day care center's measured lead, and tobacco.In an NR DCC building, 33.8% of the measurements had lead levels >600 μg/g, whereas such levels were observed in 77.1% of NR playground measurements. In VA DCC, 22% and 23% of the measurements in the building and in the playgrounds had levels higher than 600 μg/g, respectively. The percentage of high lead levels in the children's houses of the LE group was 5.9% (95% CI: 4.3–7.6%) and 13.2 (95% CI: 8.3–18.0%) in the HE group. Moreover, a significant association was found between high BLLs and lead levels found both in households and DCCs (p < 0.001). Most of the high lead measurements were found in tiles and playground equipment.Lead exposure estimated from the DCCs, where children spend about 10 h/day, can be as relevant as their household exposure. Therefore, public authorities should render efforts to provide a rigorous surveillance for lead-free painting supplies and for all objects offered to children.

To examine the mechanism of hexavalent chromium [Cr(VI)]-induced carcinogenesis, a cross-sectional study in workers with or without exposure to Cr(VI) as well as in vitro administration of Cr(VI) in 16HBE cells was conducted. We explored the associations between Cr(VI) exposure, methylation modification of DNA repair genes and their expression levels, and genetic damage. Results showed that hypermethylation of CpG sites were observed in both occupationally exposed workers and 16HBE cells administrated Cr(VI). DNA damage markers including 8-hydroxydeoxyguanosine (8-OHdG) and micronucleus frequency in Cr(VI)-exposed workers were significantly higher than the control group. Among workers, blood Cr concentration was positively correlaed with the methylation level of CpG sites in DNA repair genes including CpG6,7, CpG8, CpG9,10,11 of MGMT, CpG11 of HOGG1; CpG15,16,17, CpG19 of RAD51, and genetic damage markers including 8-OHdG and micronucleus frequency. Significant negative association between methylation levels of CpG sites in DNA repair genes and corresponding mRNA was also observed in 16HBE cells. This indicated that Cr(VI) exposure can down-regulate DNA repair gene expression by hypermethylation, which leads to enhanced genetic damage. The methylation level of these CpG sites of DNA repair genes can be potential epigenetic markers for Cr(VI)-induced DNA damage.

Adult coho salmon (Oncorhynchus kisutch) prematurely die when they return from the ocean to spawn in urban watersheds throughout northwestern North America. The available evidence suggests the annual mortality events are caused by toxic stormwater runoff. The underlying pathophysiology of the urban spawner mortality syndrome is not known, and it is unclear whether closely related species of Pacific salmon are similarly at risk. The present study co-exposed adult coho and chum (O. keta) salmon to runoff from a high traffic volume urban arterial roadway. The spawners were monitored for the familiar symptoms of the mortality syndrome, including surface swimming, loss of orientation, and loss of equilibrium. Moreover, the hematology of both species was profiled by measuring arterial pH, blood gases, lactate, plasma electrolytes, hematocrit, and glucose. Adult coho developed behavioral symptoms within a few hours of exposure to stormwater. Various measured hematological parameters were significantly altered compared to coho controls, indicating a blood acidosis and ionoregulatory disturbance. By contrast, runoff-exposed chum spawners showed essentially no indications of the mortality syndrome, and measured blood hematological parameters were similar to unexposed chum controls. We conclude that contaminant(s) in urban runoff are the likely cause of the disruption of ion balance and pH in coho but not chum salmon. Among the thousands of chemicals in stormwater, future forensic analyses should focus on the gill or cardiovascular system of coho salmon. Because of their distinctive sensitivity to urban runoff, adult coho remain an important vertebrate indicator species for degraded water quality in freshwater habitats under pressure from human population growth and urbanization.

In Brazil, there are scarce data on lead (Pb) and cadmium (Cd) contamination, especially for more vulnerable populations such as preschool children. In this paper, we answer two questions: (1) What are the exposure levels of lead and cadmium in preschool children, in Sao Paulo, Brazil? and (2) What are the risk factors associated with this exposure? This cross-sectional study included 50 day care centers (DCCs), totaling 2463 children aged 1–4 years. Venous blood samples were analyzed by ICP-MS. Questionnaires were administered to the parents. Multiple logistic regression models were used to identify associations between blood lead levels (BLLs) and blood cadmium levels (BCLs) and potential risk factors. The geometric mean for BLLs was 2.16 μg/dL (95% CI: 2.10–2.22 μg/dL), and the 97.5th percentile was 13.9 μg/dL (95% CI: 10.0–17.3 μg/dL). For cadmium exposure, the geometric mean for BCLs was 0.48 μg/L (95% CI: 0.47–0.50 μg/L), and the 95th percentile was 2.57 μg/L (95% CI: 2.26–2.75 μg/L). The DCCs’ geographic region was associated with high BLLs and BCLs, indicating hot spots for lead and cadmium exposures. In addition, it was found that the higher the vehicles flow, the higher were the BLLs in children. Red lead in household gates was also an important risk factor for lead exposure. Comparing these results with the findings of the Fourth National Report on Human Exposure to Environmental Chemicals by CDC-2013, it was found that in Brazilian preschool children the BLLs are almost three times higher (97.5th percentile) and the BCLs are almost twelve times higher (95th percentile) than those in U.S. children. This information is essential to formulate public health policies.

Studies of circulating levels in difference sex and age classes, and maternal transfer of bisphenol A, 4-tert-octylphenol and 4- nonylphenol in the Baltic grey seal were performed from 2014-2017. Blood was collected from long-term captive adult males, pregnant females and pups. Milk was collected from nursing females. The aim of this study was not only to determine the concentrations of phenol derivatives, i.e. bisphenol A (BPA), 4-tert-octylphenol (OP) and 4-nonylphenol (NP), but also to try to evaluate the transfer of these compounds to the next generation in the final stage of foetal life and in the first few weeks of life in juvenile marine mammals. The measurements were carried out using high performance liquid chromatography. The obtained data show that all phenol derivatives are present in the blood of males, females and pups (range <0.07–101 ng·cm⁻³) and in female milk (range <0.1–406.3 ng·cm⁻³). The main source of phenol derivatives in organisms is food exposure. Gender, age, or number of births were not observed to have a significant effect on changes in phenol derivative levels in seal blood within the breeding group. In the prenatal stage of life, a small amount of BPA and alkylphenols was passed on to the offspring through the placenta. In the blood of the offspring the concentration of these compounds exceeded the concentration in the mother's blood 1.5-fold. During nursing, females detoxified their systems. Level of phenol derivatives in the pups blood increased linearly with its increasing concentrations in the mother's milk. On the other hand, the seafood diet which started after the physiological fasting stage of the pup, stabilised the levels of phenol derivatives below 10 ng ∙ cm⁻³.

Polycyclic aromatic hydrocarbons (PAH) are well-known to be carcinogenic and the mechanisms that it contributes to oxidative DNA damage and aryl hydrocarbon receptor (AhR)-dependent induction are also well understood. However, little is known about the associations between PAH exposure, AhR expression, and oxidative DNA damage. We investigated their associations of AhR expression and oxidative DNA damage related to PAH exposure among 310 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; 9-hydroxyphenanthren, 9-PHE; and 1-hydroxypyrene, 1-OHP) and a marker of oxidative damage (8-hydroxy- 2′- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. AhR expression in venous blood was measured by reverse transcription -polymerase chain reaction. The results showed that increasing levels of urinary 1-OHP was positively associated with high 8-OHdG (OR (95% CI) was 4.01 (1.41–11.45) for 4th quartile, compared with 1st quartile, P for trend = 0.013). The similar associations were also found between urinary 1-OHP and high-AhR expressions (4th vs. 1st quartile = 3.50, 95% CI: 1.24–9.87, P for trend = 0.029). A significant association between AhR expression and high 8-OHdG was also found (4th vs. 1st quartile = 2.44, 95% CI: 1.05–5.70, P for trend = 0.027). In addition, mediation analysis showed the AhR expression could explain 35.9% of the association of oxidative DNA damage related to PAH exposure. Our findings implicated that the association between PAH exposure and oxidative DNA damage may be mediated by AhR expression among Chinese occupational workers.

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.

Decabromodiphenyl Ethane (DBDPE), a kind of new brominated flame retardants (NBFRs) used to replace DecaBDE, has been frequently detected in the environment and human samples. In this study, we explored its toxic effects on male mouse offspring after perinatal exposure to DBDPE. During the perinatal period, pregnant ICR mice were exposed to DBDPE (100 μg/kg body weight) via oral gavage. After weaning, male offspring were fed on a low-fat diet and a high-fat diet, respectively. We measured and recorded body weight, liver weight, and epididymis fat mass, blood biochemical markers, metabolites changes in liver, and gene expression involved in lipid and glucose homeostasis. The results showed that perinatal exposure to DBDPE increased the risk of obesity in mouse offspring and affected triglyceride synthesis, bile secretion, purine synthesis, mitochondrial function and glucose metabolism, furthermore, the use of HFD feeding may further exacerbate these effects. All of these results show that early-life exposure to low doses of DBDPE can promote the development of metabolic dysfunction, which in turn induces obesity.

Mercury (Hg) is a pervasive environmental contaminant that can impair avian health, consequently there is a need to gauge exposures. Bird blood provides a measure of recent dietary exposure to Hg, but blood collection and storage can be complex and costly. Dried blood spots (DBS) may help overcome challenges of whole blood analyses, therefore, this study aimed to develop and validate a novel method to assess Hg exposure in birds using DBS. First, accuracy and precision of blood Hg concentrations for entire DBS and DBS punches were determined for white leghorn chicken (Gallus gallus domesticus) dosed with methylmercury (MeHg) via egg injection. Next, we investigated Hg stability in chicken DBS subjected to time, temperature, and humidity treatments. Lastly, we applied the method to DBS created using standard field methods from zebra finch (Taeniopygia guttatato) in the laboratory and American golden-plover (Pluvalis dominica) sampled in the field. All samples were analyzed for total Hg (THg) using direct Hg analysis. Accuracy was determined by comparing DBS concentrations with those of corresponding whole blood and reported as percent recovery. Accuracy for entire chicken DBS was 101.8 ± 5.4%, while DBS punches revealed lower recovery (87.7 ± 4.0 to 92.4 ± 4.1%). There was little effect of time, temperature, and humidity storage treatments on Hg concentrations of DBS, with mean DBS THg concentrations within ±8% of whole blood (n = 10 treatments). For zebra finch, DBS punches were more accurate (93.7 ± 9.7%) compared to entire DBS (126.8 ± 19.4%). While for American golden-plover, entire DBS resulted in the most accurate THg concentrations (111.5 ± 7.6%) compared to DBS punches (edge: 115.4 ± 18.9%, interior: 131.4 ± 16.1%). Overall, results indicate that DBS analysis using direct Hg analysis can accurately evaluate Hg exposure in birds.