RESUMO
Formaldehyde (FA) is a xenobiotic air pollutant and its universal distribution causes a widespread exposure to humans. This review aimed to bring updated information concerning FA toxicity in humans and animals based on in vitro and in vivo studies from 2013 to 2019. Researches were carried out in Pubmed, Scopus, and Science Direct databases to determine the effects of FA exposure on inflammation, oxidative stress and genotoxicity in experimental studies with animals (rats and mice) and humans. Besides, in vitro studies assessing FA cytotoxicity focusing on cell viability and apoptosis in different cell line cultures were reviewed. Studies with humans gave evidence regarding significant deleterious effects on health associated to chronic FA occupational exposure. Evaluations carried out in experimental studies showed toxic effects on different organs as lung, upper respiratory tract, bone marrow and brain as well as in cells. In summary, this study demonstrates that knowing the mechanisms underlying FA toxicity is essential to understand the deleterious effects that this xenobiotic causes on biological systems.
Assuntos
Hipersensibilidade Respiratória , Xenobióticos , Animais , Formaldeído/efeitos adversos , Formaldeído/toxicidade , Camundongos , Estresse Oxidativo , Ratos , Hipersensibilidade Respiratória/metabolismo , Xenobióticos/toxicidadeRESUMO
There is a well-recognized association between environmental air pollution exposure and several human diseases. However, the relationship between diseases related to occupational air pollution exposure on roads and high levels of traffic-related air pollutants (TRAPs) is less substantiated. Biomarkers are essential tools in environmental and occupational toxicology, and studies on new biomarkers are increasingly relevant due to the need to determine early biomarkers to be assessed in exposure conditions. This review aimed to investigate the main advances in the biomonitoring of subjects occupationally exposed to air pollution, as well as to summarize the biomarkers of exposure, effect, and susceptibility. Furthermore, we discuss how biomarkers could be used to complement the current application of methods used to assess occupational exposures to xenobiotics present in air pollution. The databases used in the preparation of this review were PubMed, Scopus, and Science Direct. Considering the significant deleterious effects on health associated with chronic occupational exposure to xenobiotics, this topic deserves attention. As it is difficult to avoid occupational exposure to TRAPs, biomonitoring should be applied as a strategy to reduce the toxic effects of workplace exposure.
Assuntos
Poluição do Ar/efeitos adversos , Monitoramento Biológico , Exposição Ocupacional/efeitos adversos , Poluição Relacionada com o Tráfego/efeitos adversos , Emissões de Veículos/toxicidade , Biomarcadores/metabolismo , Ecotoxicologia , Humanos , Saúde OcupacionalRESUMO
Formaldehyde (FA) exposure has been proven to increase the risk of asthma and cancer. This study aimed to evaluate for 28 days the FA inhalation effects on oxidative stress, inflammation process, genotoxicity, and global DNA methylation in mice as well as to investigate the potential protective effects of melatonin. For that, analyses were performed on lung, liver and kidney tissues, blood, and bone marrow. Bronchoalveolar lavage was used to measure inflammatory parameters. Lipid peroxidation (TBARS), protein carbonyl (PCO), non-protein thiols (NPSH), catalase activity (CAT), comet assay, micronuclei (MN), and global methylation were determined. The exposure to 5-ppm FA resulted in oxidative damage to the lung, presenting a significant increase in TBARS and NO levels and a decrease in NPSH levels, besides an increase in inflammatory cells recruited for bronchoalveolar lavage. Likewise, in the liver tissue, the exposure to 5-ppm FA increased TBARS and PCO levels and decreased NPSH levels. In addition, FA significantly induced DNA damage, evidenced by the increase of % tail moment and MN frequency. The pretreatment of mice exposed to FA applying melatonin improved inflammatory and oxidative damage in lung and liver tissues and attenuated MN formation in bone marrow cells. The pulmonary histological study reinforced the results observed in biochemical parameters, demonstrating the potential beneficial role of melatonin. Therefore, our results demonstrated that FA exposure with repeated doses might induce oxidative damage, inflammatory, and genotoxic effects, and melatonin minimized the toxic effects caused by FA inhalation in mice.