Environmental exposure to mineral coal and by-products: Influence on human health and genomic instability.

Environmental exposure to pollution generated by mining and burning coal is inevitable for people living nearby. Therefore, the aim of this study was to evaluate the influence of coal dust on health conditions and genomic instability of individuals who live near coal mines and thermoelectric power plants, and to relate the results to inorganic elements and inflammatory responses. Thus, we evaluated 284 individuals from four cities in the south of Brazil around a region with coal mines and a thermoelectric power plant (one city was considered a negative control). The results of the Comet assay and Micronucleus (MN) test did not show a genotoxic or mutagenic effect related to environmental exposure to coal, but the inflammatory cytokine tumor necrosis factor-α (TNF-α) was increased in all cities around the power plant when compared to the control conditions. Higher levels of MN were associated with body mass index and cardiovascular risk, and higher levels of Damage Index (DI), TNF-α and interleukin1ß (IL-1ß) with number of cigarettes/day. Principal component analysis (PCA) was used to integrate DNA damage and inflammatory results with inorganic elements. This study also demonstrated the relationship between zinc and MN, copper, and interleukin10 (IL-10), and among silicon and sulfur with DI and nucleoplasmic bridge. A relationship was also observed between the reduction of inorganic elements and both aging and quality of health. The use of different methodologies and the relationship between the results obtained in these studies, including different lifestyles, can increase the understanding of the interaction between this mineral and the health status of residents of regions affected by coal pollution.

Amido Black 10B a widely used azo dye causes DNA damage in pro- and eukaryotic indicator cells.

Acid Black 10B (AB10B) is widely used for the production of textiles, leather and prints. It is a representative of azo dyes and it is well documented that some of these compounds are mutagenic per se, and that cleavage products (in particular aromatic amines) may cause damage of the genetic material and cancer. Since no toxicological data on AB10B have been published, we evaluated its mutagenic activity in Salmonella/microsome assays and studied its acute toxic and genotoxic properties in a human derived liver cell line (HepG2) which retained the activities of drug metabolizing enzymes. The compound did not cause cytotoxicity (MTT assay), but clear genotoxic effects were detected in pro- and eukaryotic indicator cells. Dose dependent induction of his+ revertants was seen in strain TA98 which detects frameshift mutations without metabolic activation; a more pronounced effect was seen in its derivative YG1024 which overexpresses N-acetyltransferase. Induction of single/double strand breaks by Comet assay was detected with concentrations > 0.125 mg/mL in liver derived cells; as well as increased rates for micronucleus (reflecting structural and numeric chromosomal aberrations) and nuclear buds which are a consequence of gene amplifications were seen with a higher dose (2.0 mg/mL) (p < 0.05; Tukey's test). The mutational pattern which was observed in the bacterial tests indicates that the cleavage product p-nitroaniline may cause the genotoxic effects of the dye. Our findings indicate that exposure of humans and the release of the compound into the environment may lead to adverse effects due to its DNA damaging activity.

Genotoxicity induced by water and sediment samples from a river under the influence of brewery effluent.

Brewery effluents contain complex mixtures that are discharged into rivers. Therefore, it is necessary to evaluate the genotoxic potential of these effluents. The study evaluated the genotoxicity of surface water and sediment samples from the Jacuí River in the state of Rio Grande do Sul, Brazil, which received effluents discharged from a brewery. The Salmonella/microsome test, Comet Assay and Micronucleus test on V79 cells, as well as the element profile (PIXE) and PAHs levels were used for this purpose. The surface water and sediment samples were collected in summer at three sites: 1 km upstream from the brewery discharge site (Site A); in front of the effluent discharge site, after chemical and biological treatment (Site B); about 1 km downstream from the discharge site (Site C). Only a sediment sample from Site A induced a mutagenic effect using the Salmonella/microsoma test (TA97a). All three sites presented genotoxicity (A, B and C), both for water and sediments using comet assay, and mutagenicity in the samples from Site B (surface water) and Site A and Site C (sediments) using the micronuclei tests. The results of PIXE and PAHs showed higher levels of elements for samples obtained from sites upstream and downstream from the effluent discharge. Environmental samples consist of complex mixtures of chemicals, and it is difficult to associate DNA damage with a specific element. This study showed that brewery effluent contains metals and PAHs that can induce in vitro genotoxicity under the conditions of this study.