DNA-DAMAGE IN NASAL RESPIRATORY EPITHELIUM FROM CHILDREN EXPOSED TO URBAN POLLUTION

The nasal cavity is the most common portal of entry to the human body and a well-known target site for a wide range of air pollutants and ch emically induced toxicity and carcinogenicity. DNA single-strand break s (SSB) can be used as a biomarker of oxidant exposure and as an indic ator of the carcinogenicity and mutagenicity of a substance. We examin ed the utility of using the alkaline single cell gel electrophoresis a ssay (SCGE) for measuring DNA damage in children's nasal epithelium ex posed to air pollutants. We studied 148 children, ages 6-12, including 19 control children from a low polluted Pacific port and 129 children from Southwest Metropolitan Mexico City, an urban polluted area with high ozone concentrations year-round. Three sets of two nasal biopsies were taken in a 3-month period. All exposed children had upper respir atory symptoms and DNA damage in their nasal cells. Eleven- and twelve -year-olds had the most DNA damage, and more than 30% of children aged 9-12 exhibited patchy areas of squamous metaplasia over high-flow nas al regions. These areas had the greatest numbers of damaged DNA cells (P less than or equal to 0.001) and a large number of DNA tails > 80 m u m (P < 0.001) when compared to the contralateral macroscopically nor mal site in the same child. The youngest children with significantly l ess outdoor exposure displayed patchy areas of goblet cell hyperplasia and had the least DNA damage. These findings suggest that SCGE can be used to monitor PNA damage in children's nasal epithelium and, furthe r, the identification of DNA damage in nasal proliferative epithelium could be regarded as a sentinel lesion, most likely due to severe and sustained cell injury. (C) 1997 Wiley-Liss, Inc.