Animal studies have provided the toxicologist with useful and scientifically sound information indicating that exposure to oxidant gases can alter the functioning of the host's normal pulmonary defense system, resulting in an increased risk to infectious disease. Since the basic mechanisms of action of the human and the animal pulmonary defenses are similar, it is reasonable to relate these animal's biological responses to human exposures. This paper examines the possibility of quantitatively extrapolating such animal dose-response data to humans.