Effects of inhaled acrylic acid derivatives in rats

Chemical reactivity with glutathione, urinary thioether excretion, total (T-SH) and non-protein-SH (NP-SH) groups in tissues and blood glucose were studied in male Wistar rats exposed to acrylic acid derivatives. The 6-h inhalation of acrylonitrile (AN), methyl acrylate (MA), ethyl acrylate (EA), n-butyl acrylate (BA) and 2-ethylhexyl acrylate (2-EHA) in several concentrations increased the urinary thioether excretion; the portion metabolized to thioethers was 35-18% of the acrylonitrile dose, but only 1.5-8% for the acrylates. Total-SH levels in the liver significantly decreased after the inhalation of AN, EA, BA and 2-EHA. In blood there was a decrease only after EA. Most pronounced NP-SH depletion was in the liver, less in blood and moderate in brain and lungs. There was an exponential relationship between the tissue NP-SH and the inhaled concentrations. Calculated concentrations inducing 50% NP-SH depletion indicated that reaction of acrylic acid derivatives with SH groups was decreasing in the order AN much greater than 2-EHA greater than EA = BA for the chemicals and liver greater than blood greater than lungs greater than brain for the tissues. All inhaled acrylates induced hyperglycemia, but acrylic acid was without effect. The chemical reactivity of acrylates with glutathione (GSH) decreased in the order EA greater than BA greater than MA greater than AN greater than 2-EHA. The results suggest that GSH depletion may participate in acute lethal and biochemical toxic effects of acrylic acid esters.