Abstract
This study was designed to determine the sequence of events leading to cardiopulmonary effects following acute inhalation of diesel engine exhaust in rats. Rats were exposed for 2 h to diesel engine exhaust (1.9 mg/m3), and biological parameters related to antioxidant defense, inflammation, and procoagulation were examined after 4, 18, 24, 48, and 72 h. This in vivo inhalation study showed a pulmonary anti-oxidant response (an increased activity of the anti-oxidant enzymes glutathione peroxidase and superoxide dismutase and an increase in heme oxygenase-1 protein, heme oxygenase activity, and uric acid) which precedes the inflammatory response (an increase in IL-6 and TNF-α). In addition, increased plasma thrombogenicity and immediate anti-oxidant defense gene expression in aorta tissue shortly after the exposure might suggest direct translocation of diesel engine exhaust components to the vasculature but mediation by other pathways cannot be ruled out. This study therefore shows that different stages in oxidative stress are not only affected by dose increments but are also time dependent.
Highlights
Epidemiological studies have shown associations between daily changes in air pollution such as particulate matter (PM) and cardiopulmonary morbidity and mortality [1, 2]
To evaluate the sequence of events following diesel engine exhaust (DEE)-induced oxidative stress, key components of the anti-oxidant defense system as well as markers for inflammation were analyzed in bronchoalveolar lavage fluid (BALF) (Table 3)
Albumin in fluid obtained from the BALF, as an indicator of permeability of the alveolar barrier, was not altered upon exposure to DEE and not different among all investigated time points
Summary
Epidemiological studies have shown associations between daily changes in air pollution such as particulate matter (PM) and cardiopulmonary morbidity and mortality [1, 2]. Journal of Toxicology tissues, such as those of the cardiovascular system, may be injured either directly via translocation of particles or soluble components into the circulation or indirectly via pulmonary inflammatory effects. The reactive organic soluble substances of particles, which can consist of several redox-active quinones, may play a role due to their electrophilic properties [11]. These can be generated during metabolism of several polycyclic aromatic hydrocarbons (PAHs) by cytochrome P-450 (CYP1A1) [12]. The present study was designed to determine the sequence of events leading to cardiopulmonary effects following an acute inhalation of diesel engine exhaust (DEE) in rats
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