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

• Published in: Environmental science and pollution research international Vol. 27; no. 16; pp. 20516 - 20526
• Main Authors: León-Mejía, Grethel, Quintana-Sosa, Milton, de Moya Hernandez, Yurina, Rodríguez, Ibeth Luna, Trindade, Cristiano, Romero, Marco Anaya, Luna-Carrascal, Jaime, Ortíz, Ludis Oliveros, Acosta-Hoyos, Antonio, Ruiz-Benitez, Martha, Valencia, Karen Franco, Rohr, Paula, da Silva, Juliana, Henriques, João Antônio Pêgas
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.06.2020; Springer Nature B.V
• Subjects: Agglomerates; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; Base excision repair; Benzene; Bioassays; Carcinogens; Chromosome aberrations; Comet assay; Damage detection; Deoxyribonucleic acid; Diesel; Diesel engines; Diesel fuels; DNA; DNA damage; DNA repair; Earth and Environmental Science; Ecotoxicology; Electron microscopy; Environment; Environmental Chemistry; Environmental Health; Environmental science; Exhaust emissions; Exhaust gases; Exposure; Gene polymorphism; Genes; Genetic factors; Genotoxicity; GSTM1 protein; GSTT1 protein; Halogenated hydrocarbons; Health risks; Heavy metals; Homologous recombination; Homologous recombination repair; Homology; Lung diseases; Lymphocytes; Manganese; Metabolism; Microscopy; Nanoparticles; Nuclear fuels; Occupational exposure; Particulate matter; Polycyclic aromatic hydrocarbons; Polymerase chain reaction; Polymorphism; Repair; Research Article; Resistance factors; Restriction fragment length polymorphism; Scanning electron microscopy; Transmission electron microscopy; Waste Water Technology; Water Management; Water Pollution Control; X-ray spectroscopy; Mechanics; Diesel exhaust particles; DNA oxidative damage; DNA repair; Polymorphism
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-020-08533-6

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 (PM 2.5 ) 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 PM 2.5 , 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.