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Coal is a mixture of several chemicals, many of which have mutagenic and carcinogenic effects and are a key contributor to the global burden of mortality and disease. Previous studies suggest that coal is related to telomeric shortening in individuals occupationally exposed, however little is known about the effects of mining and burning coal on the telomeres of individuals living nearby. Therefore, the primary objective of this investigation was to assess the impact of proximity to coal power plants and coal mines on the genomic instability of individuals, while also exploring potential associations with individual characteristics, oxidative stress, inflammatory responses, and the presence of inorganic elements. This study involved 80 men participants from three cities around a thermoelectric power plant and one city unexposed to coal and byproducts. DNA was extracted from peripheral blood samples obtained from each participant, and the length of telomeres (TL) was assessed using quantitative real-time polymerase chain reaction (qPCR) methodology. No significant difference was observed between exposed individuals (6,227 ± 2,884 bp) when compared to the unexposed group (5,638 ± 2,452 bp). Nevertheless, TL decrease was associated with age and risk for cardiovascular disease. Longer telomere length was found to be linked with increased concentrations of Si and P in blood samples. No correlations were observed between TL with comet assay, micronucleus test, oxidative stress, and inflammatory results. Additional research is required to ascertain the potential correlation between these changes and the onset of diseases and premature mortality.

Coal is a mixture of several chemicals, many of which have mutagenic and carcinogenic effects and a key contributor to the global burden of mortality and disease. Previous studies suggest that coal is related to telomeric shortening in individuals occupationally exposed, however little is known about the effects of mining and burning coal on the telomeres of individuals living nearby. Therefore, the aim of this study was to evaluate the influence of this exposure on genomic instability of individuals who live near coal activities, besides correlating results with individual characteristics, inflammatory responses, oxidative stress and inorganic elements. The study involved 80 men participants from three cities around a thermoelectric power plant and one city unexposed to coal and byproducts. DNA was isolated from peripheral blood samples from all individuals and telomeres (TL) were measured by quantitative real time polymerase chain reaction (qPCR). No significant difference was observed between exposed individuals (6.227 ± 2.884 pb) when compared to the unexposed group (5.638 ± 2.452 bp). Nevertheless, TL decrease was associated with age and risk for cardiovascular disease. Higher concentrations of Si and P in blood samples were associated with longer telomeres length. No correlations were observed between TL with comet assay, micronucleus test, oxidative stress, and inflammatory results. Further studies are needed to determine whether these alterations are associated with diseases and premature deaths.

Exposure of tobacco workers handling dried tobacco leaves has been linked to an increased risk of toxicity and respiratory illness due to the presence of nicotine and other chemicals. This study aimed to evaluate the DNA damage caused by the exposure of tobacco growers during the dry leaf classification process and the relation to cellular mechanisms. A total of 86 individuals participated in the study, divided into a group exposed to dry tobacco (n = 44) and a control group (n = 42). Genotoxicity was evaluated using the alkaline comet assay and lymphocyte micronucleus (MN) assay (CBMN-Cyt), and measurement of telomere length. The levels of oxidative and nitrosative stress were evaluated through the formation of thiobarbituric acid reactive species, and nitric oxide levels, respectively. The inorganic elements were measured in the samples using particle-induced X-ray emission method. The combination of variables was demonstrated through principal component analysis and the interactions were expanded through systems biology. Comet assay, MN, death cells, thiobarbituric acid reactive species, and nitrosative stress showed a significant increase for all exposed groups in relation to the control. Telomere length showed a significant decrease for exposed women and total exposed group in relation to men and control groups, respectively. Bromine (Br) and rubidium (Rb) in the exposed group presented higher levels than control groups. Correlations between nitrate and apoptosis; Br and MN and necrosis; and Rb and telomeres; besides age and DNA damage and death cells were observed. The systems biology analysis demonstrated that tobacco elements can increase the nuclear translocation of NFKB dimers inducing HDAC2 expression, which, associated with BRCA1 protein, can potentially repress transcription of genes that promote DNA repair. Dry tobacco workers exposed to dry leaves and their different agents showed DNA damage by different mechanisms, including redox imbalance.