DNA STRAND BREAKS IN HUMAN NASAL RESPIRATORY EPITHELIUM ARE INDUCED UPON EXPOSURE TO URBAN POLLUTION

All organisms have the ability to respond and adapt to a myriad of env ironmental insults, The human respiratory epithelium, when exposed to oxidant gases in photochemical smog, is at risk of DNA damage and requ ires efficient cellular adaptative responses to resist the environment ally induced cell damage. Ozone and its reaction products induce in vi tro and in vivo DNA single strand breaks (SSBs) in respiratory epithel ial cells and alveolar macrophages. To determine if exposure to a poll uted atmosphere with ozone as the main criteria pollutant induces SSBs in nasal epithelium, we studied 139 volunteers, including a control p opulation of 19 children and 13 adult males who lived in a low-pollute d Pacific port, 69 males and 16 children who were permanent residents of Southwest Metropolitan Mexico City (SWMMC), and 22 young males newl y arrived to SWMMC and followed for 12 weeks. Respiratory symptoms, na sal cytology and histopathology, cell viabilities, and single-cell gel electrophoresis were investigated. Atmospheric pollutant data were ob tained from a fixed-site monitoring station. SWMMC volunteers spent >7 hr/day outdoors and all had upper respiratory symptoms. A significant difference in the numbers of DNA-damaged nasal cells was observed bet ween control and chronically exposed subjects, both in children (p<0.0 0001) and in adults (p<0.01). SSBs in newly arrived subjects quickly i ncreased upon arrival to the city, from 39.8 +/- 8.34% in the first we ek to 67.29 +/- 2.35 by week 2. Thereafter, the number of cells with S SBs remained stable in spite of the continuous increase in cumulative ozone, suggesting a threshold for cumulative DNA nasal damage. Exposur e to a polluted urban atmosphere induces SSBs in human nasal respirato ry epithelium, and nasal SSBs could serve as a biomarker of ozone expo sure. Further, because DNA strand breaks are a threat to cell viabilit y and genome integrity and appear to be a critical lesion responsible for p53 induction, nasal SSBs should be evaluated in ozone-exposed ind ividuals.