Weber-Tschopp et al. (1977) reported the acute effects of acrolein on human volunteers. Groups of healthy subjects were exposed to acrolein at 0–0.6 ppm under the following three sets of experimental conditions:
Group I. 53 subjects (31 males and 22 females), 40 min at continuously increasing concentration.
Group II. 42 subjects (17 males and 25 females), four 1.5 min exposures at various concentrations.
Group III. 46 subjects (21 males and 25 females), 60 min at constant at 0.3 ppm.
Irritation, discomfort, and eye blinking rate were measured during exposures; all increased with increasing acrolein concentration and duration of exposure. Respiratory frequency was also measured. For deriving 1-h EELs, the data derived from Group III are most appropriate. Those subjects experienced discomfort during the first 20–30 min, but the intensity of discomfort did not increase thereafter. Irritation of the throat was significant at 10 min. Acute (subjective) irritation was reported as “considerable” after 10–20 min at 0.3 ppm. In this same group, respiratory frequency decreased during the course of the experiment, and a 10% decrease in frequency was observed in 60% of exposed subjects within 20 min. A summary of the effects of continuous exposure at 0.3 ppm (Group III) is presented in Table 6.
The most extensive animal study of acrolein toxicity available is that reported by Lyon et al. (1970). The study featured both repeated and continuous exposures to acrolein under conditions relevant to the establishment of 90-d CELs for humans. There are other recently reported animal data which are reviewed here. These studies do not provide data useful for establishing CELs, but they do afford some insight into the mode of action of acrolein and suggest a possible treatment for intoxication.
Murphy et al. (1963) observed a significant decrease in respiratory frequency and a significant increase in total respiratory flow resistance and tidal volume in guinea pigs after exposure to acrolein at 0.4–1.0 ppm for 2 h. The authors postulated that acrolein primarily increases the respiratory resistance and that, as a compensatory mechanism, the tidal volume increases and the respiratory frequency decreases. The change in respiratory resistance was said to be caused by bronchoconstriction, inasmuch as this change was eliminated by treatment with bronchodilating substances, such as atropine and epinephrine.
Davis et al. (1967) observed an increase in respiratory resistance and tidal volume in guinea pigs after exposure at 17 ppm for 60 min. Decreases in respiratory frequency and minute volume and prolongation of the expiration cycle were also noted. The authors presumed that the receptors were stimulated by an irritant to trigger a reflex-like