ELEVATION OF STRESS-INDUCIBLE HEAT-SHOCK PROTEIN-70 IN THE RAT LUNG AFTER EXPOSURE TO OZONE AND PARTICLE-CONTAINING ATMOSPHERES

Heat shock proteins (HSPs) are elicited as part of a ubiquitous cellul ar defense mechanism following exposure to a variety of environmental assaults. Ozone (O-3) is a commonly encountered toxic air pollutant th at is known to produce a variety of effects in the lung. However, the effects of O-3 exposure on lung HSP expression have not been reported. In this study, the expression and elevation of stress-inducible HSP 7 0 was examined in rat lungs (group sizes = 7) following inhalation exp osure to either (a) 0.2 ppm O-3 or (b) a mixture of 0.2 ppm O-3, 350 /- 75 mu g/m(3) road dust particles with mass median aerodynamic diame ter of 5 mu m, 65 +/- 14 mu g/m(3) ammonium sulfate (SO4-2), and 365 /- 35 mu m/m(3) ammonium nitrate (NO3-1). Exposures were episodic at 4 h/day, 4 consecutive days per week for 8 wk; control rats inhaled pur ified air (n = 4). Rats were euthanized at either 4 or 17 days after t he last exposures, and samples of the peripheral lung from the right a pical lobe were obtained for analysis of stress-inducible HSP 70 level s. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE ) and subsequent protein immunoblotting revealed that stress-inducible HSP 70 was present constitutively in the control lungs. There were no differences in HSP 70 levels in the 4-day and 17-day sacrifice groups ; therefore, the groups were pooled for statistical analysis. Statisti cal analysis by analysis of variance demonstrated that inhalation of a tmospheres containing either O-3 or O-3 in combination with particles significantly elevated rat lung stress-inducible HSP 70 levels (p = .0 007) over control animals that inhaled only purified air; a significan t difference could be detected between O-3 inhalation and control air (p = .0003) and O-3 with the other particles versus the control animal s (p = .0092). Furthermore, analysis of the two groups that inhaled ei ther O-3 or O-3 in combination with other particles showed a significa nt difference (p = .0071). The data suggests that lung stress-inducibl e HSP 70 elevation after exposure to airborne pollutants may be import ant and that changes in HSP 70 levels may be an extremely sensitive in dicator of early pulmonary stress and injury.