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Respiratory Effects and Systemic Stress Response Following Acute Acrolein Inhalation in Rats.
Citation:
Snow, S., M. McGee, A. Henriquez, J. Richards, M. Schladweiler, A. Ledbetter, AND U. Kodavanti. Respiratory Effects and Systemic Stress Response Following Acute Acrolein Inhalation in Rats. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 158(2):454-464, (2017).
Impact/Purpose:
Acrolein, a chemically simple but highly reactive gas, is produced and released during organic combustion processes. This study, examined nasal, pulmonary, and systemic effects of acrolein in rats acutely exposed to a range of concentrations to allow a better understanding of the systemic consequences and respiratory effects of acute acrolein inhalation with special emphasis to the relation between respiratory effects and systemic hormonal and metabolic changes. The study therefore informs the risk assessment of acrolein . Acrolein is classified as one the hazardous air pollutants (HAPs) regulated under the Clean Air Act.
Description:
Previous studies have demonstrated that exposure to the pulmonary irritant ozone causes myriad systemic metabolic and pulmonary effects attributed to sympathetic and hypothalamus-pituitary-adrenal (HPA) axis activation, which are exacerbated in metabolically impaired models. We examined respiratory and systemic effects following exposure to a sensory irritant acrolein to elucidate the systemic and pulmonary consequences in healthy and diabetic rat models. Male Wistar and Goto Kakizaki (GK) rats, a nonobese type II diabetic Wistar-derived model, were exposed by inhalation to 0, 2, or 4 ppm acrolein, 4 h/d for 1 or 2 days. Exposure at 4 ppm significantly increased pulmonary and nasal inflammation in both strains with vascular protein leakage occurring only in the nose. Acrolein exposure (4 ppm) also caused metabolic impairment by inducing hyperglycemia and glucose intolerance (GK > Wistar). Serum total cholesterol (GKs only), low-density lipoprotein (LDL) cholesterol (both strains), and free fatty acids (GK > Wistar) levels increased; however, no acrolein-induced changes were noted in branched-chain amino acid or insulin levels. These responses corresponded with a significant increase in corticosterone and modest but insignificant increases in adrenaline in both strains, suggesting activation of the HPA axis. Collectively, these data demonstrate that acrolein exposure has a profound effect on nasal and pulmonary inflammation, as well as glucose and lipid metabolism, with the systemic effects exacerbated in the metabolically impaired GKs. These results are similar to ozone-induced responses with the exception of lung protein leakage and ability to alter branched-chain amino acid and insulin levels, suggesting some differences in neuroendocrine regulation of these two air pollutants.
