The dangerous link between coal dust exposure and DNA damage: unraveling the role of some of the chemical agents and oxidative stress.

Exposure to coal mining dust poses a substantial health hazard to individuals due to the complex mixture of components released during the extraction process. This study aimed to assess the oxidative potential of residual coal mining dust on human lymphocyte DNA and telomeres and to perform a chemical characterization of coal dust and urine samples. The study included 150 individuals exposed to coal dust for over ten years, along with 120 control individuals. The results revealed significantly higher levels of DNA damage in the exposed group, as indicated by the standard comet assay, and oxidative damage, as determined by the FPG-modified comet assay. Moreover, the exposed individuals exhibited significantly shorter telomeres compared to the control group, and a significant correlation was found between telomere length and oxidative DNA damage. Using the PIXE method on urine samples, significantly higher concentrations of sodium (Na), phosphorus (P), sulfur (S), chlorine (Cl), potassium (K), iron (Fe), zinc (Zn), and bromine (Br) were observed in the exposed group compared to the control group. Furthermore, men showed shorter telomeres, greater DNA damage, and higher concentrations of nickel (Ni), calcium (Ca), and chromium (Cr) compared to exposed women. Additionally, the study characterized the particles released into the environment through GC-MS analysis, identifying several compounds, including polycyclic aromatic hydrocarbons (PAHs) such as fluoranthene, naphthalene, anthracene, 7H-benzo[c]fluorene, phenanthrene, pyrene, benz[a]anthracene, chrysene, and some alkyl derivatives. These findings underscore the significant health risks associated with exposure to coal mining dust, emphasizing the importance of further research and the implementation of regulatory measures to safeguard the health of individuals in affected populations.

Auto repair workers exposed to PM2.5 particulate matter in Barranquilla, Colombia: Telomere length and hematological parameters.

Exposure to 2.5 µm particulate matter (PM2.5) in automotive repair shops is associated with risks to health. We evaluated the effects of occupational exposure to PM2.5 among auto repair-shop workers. Blood and urine samples were collected from 110 volunteers from Barranquilla, Colombia: 55 active workers and 55 controls. PM2.5 concentrations were assessed at each of the sampling sites and chemical content was analyzed by SEM-EDS electron microscopy. The biological samples obtained were peripheral blood (hematological profiling, DNA extraction) and urine (malondialdehyde concentration). Telomere length was assessed by qPCR and polymorphisms in the glutathione transferase genes GSTT1 and GSTM1 by PCR-RFLP, with confirmation by allelic exclusion. White blood cell (WBC), lymphocyte (LYM%) and platelet (PLT) counts and the malondialdehyde concentration were higher (4.10 ± 0.93) in the exposed group compared to the control group (1.56 ± 0.96). TL was shorter (5071 ± 891) in the exposed individuals compared to the control group (6271 ± 805). White blood cell (WBC) and platelet counts were positively associated with exposure. Age and TBARS were correlated with TL in exposed individuals. The GSTT1 gene alleles were not in Hardy-Weinberg (H-W) equilibrium. The GSTM1 gene alleles were in H-W equilibrium and allelic exclusion analysis confirmed the presence of heterozygous GSTM1 genotypes. SEM-EDS analysis showed the presence of potentially toxic elements, including Mg, Al, Fe, Mn, Rh, Zn, and Cu. Auto repair shop workers showed effects that may be associated with exposure to mixtures of pollutants present in PM2.5. The GSTM1 and GSTT1 genes had independent modulatory effects.

Analysis of the cytotoxic and genotoxic effects in a population chronically exposed to coal mining residues.

During coal mining activities, many compounds are released into the environment that can negatively impact human health. Particulate matter, polycyclic aromatic hydrocarbons (PAHs), metals, and oxides are part of the complex mixture that can affect nearby populations. Therefore, we designed this study to evaluate the potential cytotoxic and genotoxic effects in individuals chronically exposed to coal residues from peripheral blood lymphocytes and buccal cells. We recruited 150 individuals who lived more than 20 years in La Loma-Colombia and 120 control individuals from the city of Barranquilla without a history of exposure to coal mining. In the cytokinesis-block micronucleus cytome (CBMN-Cyt) assay, significant differences in the frequency of micronucleus (MN), nucleoplasmic bridge (NPB), nuclear bud (NBUD), and apoptotic cells (APOP) were observed between the two groups. In the buccal micronucleus cytome (BM-Cyt) assay, a significant formation of NBUD, karyorrhexis (KRX), karyolysis (KRL), condensed chromatin (CC), and binucleated (BN) cells was observed in the exposed group. Considering the characteristics of the study group, a significant correlation for CBMN-Cyt was found between NBUD and vitamin consumption, between MN or APOP and meat consumption, and between MN and age. Moreover, a significant correlation for BM-Cyt was found between KRL and vitamin consumption or age, and BN versus alcohol consumption. Using Raman spectroscopy, a significant increase in the concentration of DNA/RNA bases, creatinine, polysaccharides, and fatty acids was detected in the urine of individuals exposed to coal mining compared to the control group. These results contribute to the discussion on the effects of coal mining on nearby populations and the development of diseases due to chronic exposure to these residues.

Exposure to coal mining can lead to imbalanced levels of inorganic elements and DNA damage in individuals living near open-pit mining sites.

Coal mining activities are considered harmful to living organisms. These activities release compounds to the environment, such as polycyclic aromatic hydrocarbons (PAHs), metals, and oxides, which can cause oxidative damage to DNA. In this study, we compared the DNA damage and the chemical composition of peripherical blood of 150 individuals exposed to coal mining residues and 120 non-exposed individuals. Analysis of coal particles revealed the presence of elements such as copper (Cu), aluminum (Al), chrome (Cr), silicon (Si) and iron (Fe). The exposed individuals in our study had significant concentrations of Al, sulfur (S), Cr, Fe, and Cu in their blood, as well as hypokalemia. Results from the enzyme-modified comet assay (FPG enzyme) suggest that exposure to coal mining residues caused oxidative DNA damage, particularly purine damage. Furthermore, particles with a diameter of <2.5 µm indicate that direct inhalation could promote these physiological alterations. Finally, a systems biology analysis was performed to investigate the effects of these elements on DNA damage and oxidative stress pathways. Interestingly, Cu, Cr, Fe, and K are key nodes that intensely modulate these pathways. Our results suggest that understanding the imbalance of inorganic elements caused by exposure to coal mining residues is crucial to understanding their effect on human health.

Association of buccal micronucleus cytome assay (BMNCyt) biomarkers with inorganic element concentration and genetic polymorphisms in welders.

Welding fumes are classified as carcinogenic to humans. The aim of the present study was to measure buccal micronucleus cytome assay biomarkers and to evaluate their association with inorganic elements and genetic polymorphisms (XRCC1, OGG1, XRCC3, GSTM1, and GSTT1) in welders (n = 98) and control individuals (n = 100). Higher levels of DNA damage and cell death were observed in the exposed group. Also, a significant correlation between the frequency of micronuclei and Na, Si, Cl, Ti, Cr, Zn and Mg concentrations. The formation of micronuclei, binucleated cells, cell death was associated with polymorphisms in repair pathways. The OGG1Ser326Cys and XRCC3 241Thr/Met genotypes were associated with cell death. Individuals with GSTM1 null genotype had a higher frequency of micronuclei. These results demonstrate that the deleterious effects of exposure to welding fumes are exacerbated by lifestyle habits, and genetic polymorphisms can influence DNA damage and cell death.

Genotoxicity biomarkers in car repair workers from Barranquilla, a Colombian Caribbean City.

Exposure to chemicals and particles generated in automotive repair shops is a common and underestimated problem. The objective of this study was to assess the genotoxic status of auto repair workers with (1) a questionnaire to gather sociodemographic information and self-reported exposure to hazardous chemicals and (2) measurement of various biochemical parameters. Blood and oral mucosa samples were collected from 174 male volunteers from Barranquilla, Colombia, aged 18-55 years: 87 were active car repairmen and 87 were individuals with no known exposure to hazardous chemicals. Peripheral blood lymphocytes were collected for the comet and cytokinesis-blocking micronucleus (CBMN) assays, while oral mucosal epithelium extracted to quantify micronucleated cells (MNC). DNA was extracted to assess polymorphisms in the DNA repair (XRCC1) and metabolism-related genes (GSTT1 and GSTM1) using PCR-RFLP. DNA damage and frequency of micronuclei (MN) in lymphocytes and oral mucosa were significantly higher in exposed compared to control group. In both groups genotypes and allelic variants for XRCC1 and GSTT1 met the Hardy-Weinberg equilibrium (HWE). In contrast, GSTM1 deviated from HWE. In the exposed group genotypic variants were not correlated with DNA damage or MN presence in cells. DNA damage and occurrence of MN in mucosa and lymphocytes correlated with age and time of service (occupational exposure ≥ 3 years). In summary, workers in car repair shops exhibited genotoxic effects depending upon exposure duration in the workplace which occurred independent of DNA repair XRCC1 gene and metabolism genes GSTT1 and GSTM1. Date demonstrate that health authorities improve air quality in auto repair facilities to avoid occupational DNA damage.

Cytokinesis-block micronucleus cytome (CBMN-CYT) assay and its relationship with genetic polymorphisms in welders.

Fumes generated in the welding process are composed of micrometric and nanometric particles that form when metal fumes condense. The International Agency for Research on Cancer established that many compounds derived from the welding process are carcinogenic to humans. Still, there are few studies related to the role of genetic polymorphisms. This work aimed to analyze the influence of OGG1 Ser326Cys, XRCC1 Arg280His, XRCC1 Arg194Thr, XRCC1 Arg399Gln, XRCC3 Thr241Met, GSTM1, and GSTT1 gene polymorphisms on DNA damage of 98 subjects occupationally exposed to welding fumes and 100 non exposed individuals. The results showed that individuals exposed to welding fumes with XRCC3 Thr241Thr, XRCC3 Thr241Met, and GSTM1 null genotypes demonstrated a significantly higher micronucleus frequency in lymphocytes. In contrast, individuals with XRCC1 Arg399Gln and XRCC1 Gln399Gln genotypes had significant levels of NPBs. OGG1 326 Ser/Cys, OGG1 326 Cys/Cys, XRCC1 194Arg/Thr, XRCC1 194Thr/Thr, and GSTT1 null genotypes exhibited significantly higher apoptotic values. Also, XRCC1 194Arg/Trp, XRCC1 194Thr/Thr, and GSTM1 null genotype carriers had higher necrotic levels compared to XRCC1 194Arg/Arg and GSTM1 nonnull carriers. Compositional analysis revealed the presence of iron, manganese, silicon as well as particles smaller than 2 µm that adhere to each other and form agglomerates. These results may be associated with a mixture of components, such as nitrogen dioxide, carbon monoxide, and metallic fumes, leading to significant DNA damage and cell death processes. These findings demonstrated the importance of the association between individual susceptibility and DNA damage levels due to occupational exposure to welding fumes; and constitute one of the first studies carried out in exposed workers from Colombia.

Cytokinesis-block micronucleus cytome (CBMN-CYT) assay biomarkers and telomere length analysis in relation to inorganic elements in individuals exposed to welding fumes.

During the welding activities many compounds are released, several of these cause oxidative stress and inflammation and some are considered carcinogenic, in fact the International Agency for Research on Cancer established that welding fumes are carcinogenic to humans. The aim of the present study was to analyze the cytotoxic and genotoxic potential of exposure to welding fumes and to determine concentrations of metals in blood and urine of occupationally exposed workers. We included 98 welders and 100 non-exposed individuals. Our results show significant increase in the frequency of micronuclei (MN), nucleoplasmic bridges (NPB), nuclear buds (NBUD) and necrotic cells (NECR) in cytokinesis-block micronucleus cytome (CBMN-Cyt) assay, as well as in the telomere length (TL) of the exposed individuals with respect to the non-exposed group. In the analysis of the concentrations of inorganic elements using PIXE method, were found higher concentrations of Cr, Fe and Cu in the urine, and Cr, Fe, Mg, Al, S, and Mn in the blood in the exposed group compared to the non-exposed group. A significant correlation was observed between MN and age and between NPB and years of exposure. Additionally, we found a significant correlation for TL in relation to MN, NPB, age and years of exposure in the exposed group. Interestingly, a significant correlation between MN and the increase in the concentration of Mg, S, Fe and Cu in blood samples of the exposed group, and between MN and Cr, Fe, Ni and Cu in urine. Thus, our findings may be associated with oxidative and inflammatory damage processes generated by the components contained in welding fumes, suggesting a high occupational risk in welding workers.

DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure.

Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many of the compounds in this mixture can cause oxidative damage to DNA and are considered carcinogenic for humans. Further, chronic DEE exposure increases risks of cardiovascular and pulmonary diseases. Despite these pervasive health risks, there is limited and inconsistent information regarding genetic factors conferring susceptibility or resistance to DEE genotoxicity. The present study evaluated the effects of polymorphisms in two base excision repair (BER) genes (OGG1 Ser326Cys and XRCC1 Arg280His), one homologous recombination (HRR) gene (XRCC3 Thr241Met) and two xenobiotic metabolism genes (GSTM1 and GSTT1) on the genotoxicity profiles among 123 mechanics exposed to workplace DEE. Polymorphisms were determined by PCR-RFLP. In comet assay, individuals with the GSTT1 null genotype demonstrated significantly greater % tail DNA in lymphocytes than those with non-null genotype. In contrast, these null individuals exhibited significantly lower frequencies of binucleated (BN) cells and nuclear buds (NBUDs) in buccal cells than non-null individuals. Heterozygous hOGG1 326 individuals (hOGG1 326 Ser/Cys) exhibited higher buccal cell NBUD frequency than hOGG1 326 Ser/Ser individuals. Individuals carrying the XRCC3 241 Met/Met polymorphism also showed significantly higher buccal cell NBUD frequencies than those carrying the XRCC3 241 Thr/Thr polymorphism. We found a high flow of particulate matter with a diameter of < 2.5 µm (PM2.5) in the workplace. The most abundant metals in DEPs were iron, copper, silicon and manganese as detected by transmission electron microscopy-energy-dispersive X-ray spectroscopy (TEM-EDX). Scanning electron microscopy (SEM-EDS) revealed particles with diameters smaller than PM2.5, including nanoparticles forming aggregates and agglomerates. Our results demonstrate the genotoxic effects of DEE and the critical influence of genetic susceptibility conferred by DNA repair and metabolic gene polymorphisms that shed light into the understanding of underlying mechanisms.

Efecto genotóxico de las mezclas complejas de hidrocarburos en trabajadores de estaciones de servicio de gasolina / Genotoxiceffect of complex hydrocarbon mixtures in workers gasoline service stations

Objetivo: Evaluar el efecto genotóxico de las mezclas complejas de hidrocarburos en los trabajadores de estaciones de servicio de gasolina en Barranquilla (Atlántico, Colombia) a través de la prueba Cometa(CA) alcalina. Materiales y métodos: Se realizó un estudio transversal, prospectivo inferencial de casos y controles. El grupo control estuvo conformado por 15 personas no expuestas laboralmente a hidrocarburos y el expuesto por 38 personas que trabajaron al menos 1 año como despachador de combustible. Se realizó un ensayo cometa alcalino en sangre venosa. Se determinó el efecto genotóxico utilizando el porcentaje de ADN n la cola y por Unidades Arbitrarias de daño. La comparación entre grupos se realizó por la prueba t-student o W-Wilcoxon. Los datos fueron modelados con una regresión simple ajustada. Los análisis de datos fueron realizados con el paquete estadístico R. Resultados: Las edades de los grupos control y experimental fueron de 33±9 y 38±10 años, respectivamente; no hubo diferencia estadísticamente significativa para esta variable (t = -1.82; p-valor > 0,05; a = 95%). Hubo asociación entre Edad y Tiempo de Exposición (x² = 24.9; p-valor < 0,05; a = 95%). El %ADN en la cola para el grupo control fue de 20,67±25,79, mientras que para el grupo expuesto fue 53,35±40,28. El modelo de degradación de ADN es «y=√l(512,687+733,899√1(t))¼. Conclusiones: Las mezclas complejas de heterocíclicos son potencialmente genotóxicas. El daño progresivo se encuentra al 80 % después de 6 años de exposición, siendo igual a los 9 años de exposición que a los 15.

Objective: To evaluate the genotoxic effects of complex mixtures of hydrocarbons in gasoline stations's workers in Barranquilla (Atlántico, Colombia) using the alkaline Comet Assay (CA). Materials and methods: Study was transversal, prospective inferential of case and control. The controls were 15 persons without occupationally exposed to hydrocarbons and the exposed were 38 persons that were working at least one year as fuel dispenser. The alkaline Comet Assay was performed on venous blood. Genotoxic effects was determined throug DNA percentage in tail and damage Arbitrary Units. The comparison between groups was performed by t-student or W-Wilcoxon test. The data were modeled with a simple regression adjusted. The data analyses were performed with the statistical package R. Results: Age of control and experimental groups were 33±9 and 38±10 years respectively, there was no statistically significant difference for this variable (t = -1.82; p-value > 0.05; a = 95 %). There was an association between Age and Exposure Time (x² = 24.9; p-value < 0.05, a = 95%). The %DNA tail for the control group was 20.67 ± 25.79, while for the exposed group was 53.35± 40.28. The DNA degradation model is «y=√ (512.687+733,899√ (t))¼. Conclusions: The complex mixtures of heterocyclic are potentially genotoxic. As the progressive damage is 80 % after 6 years of exposure, being equal damage to the 9 to 15 years of exposure.