Tankersley C G, Kleeberger S R
Department of Environmental Health Sciences, Johns Hopkins School of Public Health, Baltimore, MD 21205.
Toxicol Lett. 1994 Jun;72(1-3):279-89. doi: 10.1016/0378-4274(94)90039-6.
We have examined whether the effects of acute (2 ppm/3 h) and subacute (0.3 ppm/72 h) ozone (O3) exposures on airways are mutually predictive. Inbred C57BL/6J (susceptible) and C3H/HeJ (resistant) mice are differentially responsive to inflammation induced by the 2 exposures. Breeding experiments and cosegregation analysis indicated that 2 separate genes control inflammatory responses: Inf (acute), Inf-2 (subacute). The genetic model was also used to examine the effects of both exposures on the magnitude and pattern of breathing. Results imply that mechanisms that control susceptibility to the 2 exposures are not the same, and that one response is not necessarily predictive of the other.