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Environmental Health Perspectives (EHP) is a monthly journal of peer-reviewed research and news on the impact of the environment on human health. EHP is published by the National Institute of Environmental Health Sciences and its content is free online. Print issues are available by paid subscription.DISCLAIMER
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Comparative Toxicogenomics Database (CTD)

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Environmental Health Perspectives Volume 104, Number 2, February 1996 Open Access
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DNA Strand Breaks in Human Nasal Respiratory Epithelium Are Induced upon Exposure to Urban Pollution

Lilian Calderón-Garcidueñas, Norma Osnaya-Brizuela, Leticia Ramírez-Martínez, and Anna Villarreal-Calderón

Experimental Pathology Section, Instituto Nacional de Pediatría, Mexico City, 14410 Mexico

Abstract
All organisms have the ability to respond and adapt to a myriad of environmental insults. The human respiratory epithelium, when exposed to oxidant gases in photochemical smog, is at risk of DNA damage and requires efficient cellular adaptative responses to resist the environmentally induced cell damage. Ozone and its reaction products induce in vitro and in vivo DNA single strand breaks (SSBs) in respiratory epithelial cells and alveolar macrophages. To determine if exposure to a polluted atmosphere with ozone as the main criteria pollutant induces SSBs in nasal epithelium, we studied 139 volunteers, including a control population of 19 children and 13 adult males who lived in a low-polluted Pacific port, 69 males and 16 children who were permanent residents of Southwest Metropolitan Mexico City (SWMMC) , and 22 young males newly arrived to SWMMC and followed for 12 weeks. Respiratory symptoms, nasal cytology and histopathology, cell viabilities, and single-cell gel electrophoresis were investigated. Atmospheric pollutant data were obtained 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 between control and chronically exposed subjects, both in children (p<0.00001) and in adults (p<0.01) . SSBs in newly arrived subjects quickly increased upon arrival to the city, from 39.8 +/- 8.34% in the first week to 67.29 +/- 2.35 by week 2. Thereafter, the number of cells with SSBs remained stable in spite of the continuous increase in cumulative ozone, suggesting a threshold for cumulative DNA nasal damage. Exposure to a polluted urban atmosphere induces SSBs in human nasal respiratory epithelium, and nasal SSBs could serve as a biomarker of ozone exposure. Further, because DNA strand breaks are a threat to cell viability and genome integrity and appear to be a critical lesion responsible for p53 induction, nasal SSBs should be evaluated in ozone-exposed individuals. Key words: , , , , . Environ Health Perspect 104:160-168 (1996)


Address correspondence to L. Calderón-Garcidueñas, Cerro del Vigilante #96, Romero de Terreros, Coyoacan, 04320 Mexico DF, Mexico.
We are grateful to all the children and adults that took part in the study. We extend special thanks to Reynaldo Ojeda and his staff for kindly giving us access to atmospheric data ; to Hilda Ramos for the diet analysis ; to Raquel García and Felipe Díaz for FCM technical support ; to Humberto Garnica for the artwork ; and to Gerardo Barragán for statistical help. We thank M.C. Madden and J.G. Lee for their encouragement and technical advice while L.C.-G. was at their laboratory at the University of North Carolina-Chapel Hill ; Dorothy E. Lewis, Baylor College of Medicine, for her expert advice with flow cytometer measurements ; and Allen Lefohn for his assessment of the ozone data. We acknowledge the support of the Chemical Industry Institute of Toxicology, Research Triangle Park, NC, and Kevin Morgan for supplying the electrophoresis apparatus.
Received 21 August 1995 ; accepted 17 October 1995.


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