HUMAN NASAL MUCOSAL CHANGES AFTER EXPOSURE TO URBAN POLLUTION

Millions of people worldwide are living in areas where ozone (O-3) con centrations exceed health standards (an hourly average of 235 mu g/m(3 )/0.12 ppm, not to be exceeded more than once per year). Ozone induces acute nasal inflammatory responses and significant epithelial lesions in experimental animals and humans. To determine the nasal effects of a 15-day exposure to an urban polluted atmosphere with O-3 as the mai n pollutant, we studied a population of healthy, young males newly arr ived to southwest metropolitan Mexico City (SWMMC). The study included 49 nonsmoking residents in an unpolluted port, Veracruz City; 14 subj ects stayed in the port and served as controls, while 35 subjects trav eled to SWMMC and had serial nasal lavages at different times after ar riving in SWMMC. Subjects had exposures to ambient O-3 an average of 1 0.2 hr/day, with a total cumulative O-3 exposure of 10.644 ppm.hr. Nas al inflammatory responses, polymorphonuclear leukocyte PMN-CD11b surfa ce expression, rhinoscopic changes, and respiratory symptoms were eval uated. Exposed subjects had massive nasal epithelial shedding and sign ificant responses in PMN nasal influx (p<0.00001) and in PMN-CD11b exp ression (p<0.005). Cumulative O-3 exposure correlated with respiratory symptoms, PMNs (r(s) = 0.2374, p<0.01), and CD11b (r(s) = 0.3094, p<0 .01); 94% of exposed subjects experienced respiratory symptoms, and 97 % left the city with an abnormal nasal mucosa by rhinoscopy. Nasal epi thelial changes persisted 2 weeks after the exposed subjects returned to their nonpolluted environment. Exposure to an urban polluted atmosp here induces significant and persistent nasal epithelial alterations i n healthy subjects. Because O-3 is the main pollutant for SWMMC and co ncentrations of other pollutants (e.g., sulfur dioxide, nitrogen dioxi de, total suspended particulates, formaldehyde) were well below the st andard levels or undetectable, we suggest that O-3 is likely to play a role in the etiopathogenesis of the nasal alterations along with the effects of other atmospheric pollutants which were not measured.