The greatest environmental health concern to the entire world's population is air pollution. While 92 percent of the world's population is thought to breathe poisonous air, it is predicted to cause 7 million premature deaths annually [1, 2]. Polluting fuels continue to be an issue in low- and middle-income countries (LMICs), such as Nigeria, affecting 83 % of the African population. Children under the age of five living within the WHO African and Eastern Mediterranean areas are exposed to particulate matter (PM2.5) levels that exceed the World Health Organisation air quality standards. Furthermore, one in every eight fatalities worldwide in 2016 was attributed to the cumulative effects of ambient and residential air pollution, accounting for 7 million deaths, including around 543,000 deaths in children under the age of five and 52,000 deaths in children aged five to fifteen [3]. Data from the World Bank indicates that approximately 72 % of the Nigerian population is exposed to PM2.5 levels above the WHO guideline threshold, and several cities, notably megacities, have air quality rules that exceed the requirements of air pollution [4, 5]. Due to a shortage of energy, irregular power supply, or lengthy power outages, homes and companies have had to rely largely on privately owned generators to meet their power requirements. The classification of air pollution based on emittance and/or production sources has a global impact on morbidity and mortality, with industrial and biological operations emitting primary air pollutants into the atmosphere [2, 6, 7]. Particulate matter in ambient air is a complex combination of fine and ultrafine particles constituting chemical components, such as metals ions and organics, and its concentration has been linked to several clinical manifestations of various diseases, as well as morbidity and mortality caused by respiratory diseases in both humans and animals [8, 9]. The inhalation of coarse, fine and ultrafine particulate matter into the lungs via the nasal olfactory pathway adversely affects the health and can lead to local activation of immune cells thus leading to a systemic increase in circulating cytokines which causes secondary tissue damage as well as cardiovascular events and atherosclerosis [6, 10, 11, 12]. Our previous investigations on the genotoxic and histopathological impacts of gasoline engine emissions demonstrated the detrimental impact of exhaust emissions in mammalian cells with associated organs such as the liver and kidneys, as well as haematological abnormalities identified [13, 14, 15], Furthermore, studies by Ifegwu et al [16] also reported the harmful impact of Polycyclic Aromatic Hydrocarbons (PAHs), a major component of gasoline generator emissions, had a deleterious impact in adult Swiss male rats. Additional investigations utilising mouse models confirmed that the smoke from the tyres contains particulate matter (PM), further demonstrating that the inhalation of PM is related to undesired toxic consequences such as cardiopulmonary toxicity. When burned, fossil fuels used to power petrol and diesel generators emit pollutants such as nitrogen oxides (NOx), carbon monoxide (CO), sulphur oxides (SOx), carbon dioxide (CO₂), particulate matter (PM2.5 and PM₁₀), and so on, and they are a significant source of air pollution around homes and workplaces, with the toxins they emit contaminating the air we breathe and having health consequences [17]. Aromatics such as benzene, xylene, toluene, and ethylbenzene are large sources of particulate matter emissions via two principal ways which include incomplete combustion leading to soot emissions from the tailpipe, and a secondary organic aerosol formation, which in turn contributes to ultrafine particle formation [18]. Reactive oxygen species (ROS) refer to oxygen-containing molecules having reactive properties, including superoxide anion (O₂•−), hydroxyl radical (HO•), and hydrogen peroxide (H₂O₂) [19]. They are essential for the immune system, redox balance maintenance, and the activation of numerous cellular signalling pathways, as well as the regulation of normal physiological functions such as cell cycle progression and proliferation, differentiation, migration, and cell death. However, excess accumulation of ROS within cells can damage macromolecules, membranes, nucleic acids and organelles, which activates cell death processes like apoptosis [20]. The mechanism by which air pollution impacts human health is extremely complicated and not well understood. According to a previous report by Adenubi and Mmom [21] generating sets have a significant impact on the concentration level of pollutants in relation to certain dwelling characteristics, which may put people at risk for contracting various diseases and disorders. Studies by Phosri et al. [22] reported a significant association between PM₁₀, SO₂, CO, NO₂, and O₃ increases the risk of respiratory hospital admissions. Anthropogenic human activities will continue to exacerbate air pollution, especially in emerging countries with inadequate infrastructure, urbanisation, and economic development. Consistent exposure to pollutants such as exhaust fumes from gasoline engines is unavoidable in Nigeria due to the country's enormous population and growing demand for energy to power its economy. The purpose of this study is to evaluate the oxidative stress response of adult male wistar rats to exhaust emissions from gasoline generator engines.

The oxidative stress parameters evaluated in this study revealed the deleterious impact of gasoline generator exhaust in the exposed rats. Observation in this study indicated that rats sub-acutely and chronically exposed to gasoline generator exhaust had derangement in the oxidant-antioxidant ratio. Inhaling petroleum hydrocarbons has been linked to oxidative stress, which may play a role in the development of respiratory dysfunction [15, 29]. The oxidative stress parameters in the lungs of exposed rats showed elevated oxidant (MDA, NO and H₂O₂) levels and a decline in antioxidant levels (SOD, GPx, GST, GSH, and CAT) in the exposed rats across the weeks at the various time points of exposure (4, 8 and 12 weeks) suggests an impaired ability to counteract the harmful effects of ROS, further exacerbating oxidative stress. The finding aligns with Xu et al. [10] and Afsar et al. [30] who reported the adverse effects of particulate matter on the lungs, including elevated oxidative stress, inflammation, impairment of phagocytosis, dysregulated cell immunity, epigenetic modification, and disruption of cellular signalling pathways. Also, spillover can cause systemic inflammation and oxidative stress, which can activate leukocytes, and platelets and increase myeloperoxidase coupled with elevated cytokine expression and depleted antioxidant levels observed in this study [13]. Ifegwu et al [16] also reported an increase in 1-hydroxypyrene blood concentration levels after 42 days of exposure, depending on the distance from the source of exposure, while Obasi et al. [31] reported that exposure to particulate matter daily for 21 days at exposure periods of 15, 30, 60, and 120 minutes caused biochemical parameter derangement in the exposed rats. In this study, the antioxidant activities of GPX, GST, GSH, and CAT, which are known to mop up free radicals in the body, were shown to be reduced in the exposed rats, leading to a significant decline in the total antioxidant status across all exposed groups.

The total antioxidant status is a measure of the combined activity of all antioxidants present in the body, including enzymatic antioxidants like SOD, CAT, and GPx, as well as non-enzymatic antioxidants such as glutathione and vitamins [32]. The TAS reflects the overall antioxidant capacity and plays a crucial role in maintaining the oxidant-antioxidant balance within the body. In this study, the TAS levels were significantly reduced in the rats exposed to gasoline generator exhaust emissions across all exposure time points (2 hr, 4 hr, and 8 hr) and durations (4, 8, and 12 weeks) compared to the unexposed control group. This depletion in TAS was observed in conjunction with elevated levels of oxidants like MDA, NO, and H₂O₂, as well as decreased levels of individual antioxidant enzymes such as SOD, GPx, GST, and GSH.

The comparative analysis across different exposure time points and weeks revealed significant reductions in TAS values in specific exposure conditions. Rats exposed daily for 2 hr showed a significant decrease in TAS at 8 weeks vs. 12 weeks, while those exposed for 4 hr exhibited significantly reduced TAS at 4 weeks vs. 8 weeks and 8 weeks vs. 12 weeks. Rats exposed for 8hr had a significantly elevated TAS at 4 weeks vs. 8 weeks and 4 weeks vs. 12 weeks, suggesting a potential adaptive response or variable antioxidant dynamics at different exposure durations. The depletion of TAS in the exposed rats can be attributed to the increased oxidative stress induced by gasoline generator exhaust emissions.

As the levels of ROS and oxidants rise, the antioxidant defence mechanisms are overwhelmed, leading to a decrease in the overall antioxidant capacity [19, 33, 34]. This imbalance between oxidants and antioxidants can result in oxidative damage to cellular components, such as lipids, proteins, and nucleic acids, potentially contributing to the development of various diseases and adverse health effects [12, 35]. The study indicates that exposure to exhaust emissions from gasoline engines impairs oxidant-antioxidant homeostasis. In rats with underlying chronic obstructive lung disease, exposure to air pollution exacerbates inflammation, as reported by Wang et al. [36]. Reactive oxygen species production is initiated by oxidative stress, intracellular reactive oxygen species, and exogenous environmental factors. Oxidative stress then causes DNA/lipid/protein degradation, which results in apoptosis, autophagy, necrosis, and the production of proinflammatory cytokines [33]. Through lipid peroxidation, protein carbonyl formation, and glutathione oxidation, oxidative stress causes an excessive buildup of reactive oxygen and nitrogen species within the cell, which can harm macromolecules like DNA, RNA, and proteins. It also causes an imbalance in the cell's oxidant-antioxidant system [34]. Various diseases ranging from cardiovascular disease, diabetes mellitus, immunological disorders, asthma, and chronic respiratory disease could be induced as a result of particulate matter selectively bioaccumulation in various organs [37]. However, the heterogenicity of the gasoline exhaust fume makes the mechanism unclear [38]. Studies have indicated that air pollution can adversely impact lung function, with particulate matter traversing the bloodstream to bioaccumulate in other regions of the body thus impairing their function [15, 39]. According to Rossner et al. [40], air pollution adversely impacts the cells at the molecular level by damaging macromolecules, resulting in protein or DNA adducts, nucleic acid strand breaks, and modifications that may be predisposed to mutations, which can further initiate carcinogenesis. Furthermore, environmental and occupational exposure to gasoline combustion exhaust in automobiles increases cancer risk [18]. Studies by Choi et al. [37] also documented the adverse effects of PM and their role in disease development coupled with alteration in the oxidantantioxidant homeostasis and elevated proinflammatory indicators [41] while Afsar et al. [30] indicated that exposure to PM could trigger an inflammatory response, endothelial dysfunction, autonomic nervous system imbalance, oxidative stress, increase white blood cell and fibrinolytic levels, plasma viscosity, and insulin resistance, all of which could negatively affect the kidneys by resulting in vascular damage, intraglomerular hypertension, glomerulosclerosis, and tubulointerstitial damage that results in chronic kidney disease. As seen in this study, exposure to exhaust emissions from gasoline generator engines elevates biomarkers that can contribute to tissue damage and inflammation. The comparative analysis across different exposure time points and weeks revealed significant changes in the oxidative stress parameters, indicating a time/exposure-dependent response to exhaust exposure. Furthermore, this study found that exposure to exhaust emissions from gasoline generator engines coupled with clastogenic components can alter the biochemical and physiological processes thus predisposing to the development of various diseases.

This study demonstrated the detrimental effect of gasoline generator exhaust exposure on mammalian cells. Exhaust emissions from gasoline generators induced intracellular oxidative stress in rats in a time and exposure-dependent manner, with substantial increases in NO, MDA, and H₂O₂, as well as depletion of antioxidant markers GPX, GST, GSH, CAT, and TAS. It proved how hazardous petrol generator exhaust pollutants could be to human redox balance and lung health, especially in urban areas with limited energy and extensive usage of petrol generators. Long-term exposure to these pollutants has the potential to deplete antioxidant reserves, resulting in an imbalance between antioxidants and oxidants and the accumulation of hazardous ROS in lung tissues. Oxidative stress increases the risk of respiratory disorders such as asthma, COPD, and lung cancer by producing cellular damage, inflammation, and impaired lung function. The ability to counteract the effects of ROS is further compromised by the depletion of antioxidant enzymes and decreased total antioxidant status.

Electricity is the favoured energy source because it promotes urbanisation, higher living standards, industrial expansion, and economic growth. It is proposed that cleaner energy policies and efforts in energy generation and utilisation be implemented rather than thermal plants and a strong dependence on fossil fuels since this would help in reducing atmospheric pollution and so improve air quality.