Abstract
Photochemical smog is a complex mixture of primary and secondary air pollutants including secondary organic aerosols (SOA), ozone and reactive aldehydes which has been linked to increased risk of adverse cardiovascular and pulmonary responses. The components and related health effects of smog are thought to be determined both by the precursor chemicals and reaction conditions. Here we examined the difference between isoprene- (IS-) and toluene- (TS) generated smog in causing cardiopulmonary effects in rats. Wistar-Kyoto rats were exposed to either filtered air (FA) or smog for 4 hours. IS-smog contained 660ppb NO(2), 335ppb O(3), and 178μg/m(3) SOA while TS-smog had 380ppb NO(2), 250ppb O(3), and 1,250μg/m(3) SOA. Whole-body plethysmography was performed at baseline and after each exposure and left ventricular function was measured using a Millar probe and arrhythmic sensitivity to aconitine. Tidal volume decreased only after IS-smog while inspiratory time and nasal injury increased following both smog atmospheres. Only TL-smog caused an increase in PenH, which is an indicator of airway irritation. On the other hand, only IS-smog caused left ventricular pressure to decrease, while only TL-smog increased sensitivity to cardiac arrhythmia. These data indicate that the source of smog atmosphere plays a large role in the types of responses it elicits and that its relative SOA and gaseous composition determine the extent of cardiovascular versus respiratory effects.