Chronic inhalation exposure to ozone and nitric acid elevates stress-inducible heat shock protein 70 in the rat lung.

The ability of urban oxidant and acid air pollutants to induce heat shock proteins (HSPs) in the mammalian lung is not known. Such proteins are known to be correlated with environmental stress and pathophysiological conditions. In this study, stress-inducible HSP 70 was assessed by slot-blotting in rat lungs (N=10 per group) following inhalation exposures for 4 h per day, 3 days per week for 40 weeks to the following pollutants: (a) purified air;(b) 0.15 ppm ozone (O3);(c)50 micrograms/m3 nitric acid (HNO3); or(d) a combination of both 0.15 ppm O3 and 50 micrograms/m3 HNO3. At 24 h following the last exposure, samples from the right apical lobe of the lung were obtained for either slot-blotting or gel electrophoretic separation, subsequent protein immunoblotting, and chemiluminescence detection of HSP 70 levels. Experiments demonstrate that stress-inducible HSP 70 was present constitutively in the control lungs and was separable from the constitutive form of HSP 70. Slot-blotting analysis demonstrate that the O3 and HNO3 exposures alone produced significant elevations of HSP70. Specifically, either O3 or HNO3 alone significantly elevated lung stress-inducible HSP 70 levels by 277% and 221% respectively, above control levels. The group exposed to combined O3 and HNO3 showed a 177% elevation in lung stress-inducible HSP 70 that was significantly greater that the group inhaling purified air, but this effect was less than the effects of either pollutant component alone. Moreover, all exposure groups were significantly different from one another. These results indicate that stress-inducible HSP 70 in the rat lung is highly elevated after chronic inhalation exposures to both O3 and HNO3 when administered either alone or in combination within the range of urban ambient concentrations.