Urban air particulate inhalation alters pulmonary function and induces pulmonary inflammation in a rodent model of chronic bronchitis

Epidemioiogical studies have reported increased morbidity in human populati ons following inhalation of elevated levels of urban particulate matter. Th ese responses are especially prevalent in populations with chronic obstruct ive pulmonary diseases, including chronic bronchitis. Toxicological studies have reported altered pulmonary function and increased pulmonary inflammat ion following particulate inhalation in the laboratory setting. However, mo st of these studies have utilized artificial particles that may not accurat ely mimic outdoor air pollutant conditions. Few studies have utilized actua l urban air particle samples in inhalation studies. in the present study, t he effects of inhaled concentrated urban air particulates on pulmonary func tion and pulmonary inflammation are addressed. Normal rats and rats with ch ronic bronchitis induced by similar to 200 ppm SO2 for 6 wk were subsequent ly subjected to filtered air or concentrated air particles (CAPs). Twelve r ats per group in 4 groups (48 rats total) were exposed for 5 h/day for 3 co nsecutive days. The CAPs aerosol levels were 206, 733, and 607 mu g/m(3) (M MAD = 0.18 mu m, sigma(g) = 2.9) on days 1, 2, and 3, respectively. Followi ng the final day of exposure, pulmonary function parameters, including peak expiratory flow (PEF), tidal volume (TV), respiratory frequency (RF), and minute volume (MV), were measured and compared to preexposure baseline leve ls. Twenty-four hours following the final day of exposure, bronchoalveolar lavage was performed for total cell counts, differential cell counts, and t otal lavage protein levels. Pulmonary responses to CAPs in Chronic bronchit ic animals indicated a significant increaser in tidal volume as well as pea k expiratory flow. In CAPs-exposed animals without underlying bronchitis, s ignificantly increased tidal volume was observed. Significant pulmonary inf lammation was observed in the CAPs-exposed animals, particularly those with chronic bronchitis. Significant increases in neutrophils, lymphocytes, and total lavage protein were observed. These results suggest two distinct mec hanistic responses to inhaled particles: a stress-type pulmonary function r esponse marked by increases in flow and volume, that is, deeper breathing; and acute pulmonary inflammation marked by cellular influx, particularly ne utrophils. From these data it is concluded that inhaled urban air particles and pulmonary breathing parameters and increase pulmonary inflammation.