TY - JOUR
T1 - Human nasal mucosal changes after exposure to urban pollution
AU - Calderon-Garciduenas, L.
AU - Rodriguez-Alcaraz, A.
AU - Garcia, R.
AU - Sanchez, G.
AU - Barragan, G.
AU - Camacho, R.
AU - Ramirez, L.
PY - 1994
Y1 - 1994
N2 - Millions of people worldwide are living in areas where ozone (O3) concentrations exceed health standards (an hourly average of 235 μg/m3/0.12 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 O3 as the main pollutant, we studied a population of healthy, young males newly arrived to southwest metropolitan Mexico City (SWMMC). The study included 49 non-smoking residents in an unpolluted port, Veracruz City; 14 subjects stayed in the port and served as controls while 35 subjects traveled to SWMMC and had serial nasal lavages at different times after arriving in SWMMC. Subjects had exposures to ambient O3 an average of 10.2 hr/day, with a total cumulative O3 exposure of 10.644 ppm.hr. Nasal inflammatory responses, polymorphonuclear leukocyte PMN-CD11b surface expression, rhinoscopic changes, and respiratory symptoms were evaluated. Exposed subjects had massive nasal epithelial shedding and significant responses in PMN nasal influx (p < 0.00001) and in PMN-CD11b expression (p < 0.05). Cumulative O3 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 epithelial changes persisted 2 weeks after the exposed subjects returned to their nonpolluted environment. Exposure to an urban polluted atmosphere induces significant and persistent nasal epithelial alterations in healthy subjects. Because O3 is the main pollutant for SWMMC and concentrations of other pollutants (e.g., sulfur dioxide, nitrogen dioxide, total suspended particulates, formaldehyde) were well below the standard levels or undetectable, we suggest that O3 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.
AB - Millions of people worldwide are living in areas where ozone (O3) concentrations exceed health standards (an hourly average of 235 μg/m3/0.12 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 O3 as the main pollutant, we studied a population of healthy, young males newly arrived to southwest metropolitan Mexico City (SWMMC). The study included 49 non-smoking residents in an unpolluted port, Veracruz City; 14 subjects stayed in the port and served as controls while 35 subjects traveled to SWMMC and had serial nasal lavages at different times after arriving in SWMMC. Subjects had exposures to ambient O3 an average of 10.2 hr/day, with a total cumulative O3 exposure of 10.644 ppm.hr. Nasal inflammatory responses, polymorphonuclear leukocyte PMN-CD11b surface expression, rhinoscopic changes, and respiratory symptoms were evaluated. Exposed subjects had massive nasal epithelial shedding and significant responses in PMN nasal influx (p < 0.00001) and in PMN-CD11b expression (p < 0.05). Cumulative O3 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 epithelial changes persisted 2 weeks after the exposed subjects returned to their nonpolluted environment. Exposure to an urban polluted atmosphere induces significant and persistent nasal epithelial alterations in healthy subjects. Because O3 is the main pollutant for SWMMC and concentrations of other pollutants (e.g., sulfur dioxide, nitrogen dioxide, total suspended particulates, formaldehyde) were well below the standard levels or undetectable, we suggest that O3 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.
KW - Adhesion molecules
KW - Air pollution
KW - Human nasal mucosa
KW - Nasal lavage
KW - Ozone
UR - http://www.scopus.com/inward/record.url?scp=0028607058&partnerID=8YFLogxK
U2 - 10.1289/ehp.941021074
DO - 10.1289/ehp.941021074
M3 - Article
C2 - 7713020
AN - SCOPUS:0028607058
SN - 0091-6765
VL - 102
SP - 1074
EP - 1080
JO - Environmental Health Perspectives
JF - Environmental Health Perspectives
IS - 12
ER -