Nasal Biopsies of Children Exposed to Air Pollutants

Abstract

Southwest Metropolitan Mexico City (SWMMC) atmosphere is a complex mixture of air pollutants, including ozone, particulate matter, and aldehydes. Children in SWMMC are exposed chronically and sequentially to numerous toxicants, and they exhibit signi cant nasal damage. The objective of this study was to assess p53 accumulation by immunohistochemistr y in nasal biopsies of SWMMC children. We evaluated 111 biopsies from 107 children (83 exposed SWMMC children and 24 control children residents in a pollutant-compliant Caribbean island). Complete clinical histories and physical examinations, including an ear-nose-throat (ENT) exam were done. There was a signi cant statistical difference in the upper and lower respiratory symptomatolog y and ENT ndings between control and exposed children ( p < 0.001). Control children gave no respiratory symptomatolog y in the 3 months prior to the study; their biopsies exhibited normal ciliated respiratory epithelium and were p53-negative . SWMMC children complained of epistaxis, nasal obstruction, and crusting. Irregular areas of whitish-gray recessed mucosa over the inferior and middle turbinates were seen in 25% of SWMMC children, and their nasal biopsies displayed basal cell hyperplasia, decreased numbers of ciliated and goblet cells, neutrophilic epithelial in ltrates, squamous metaplasia, and mild dysplasia. Four of 21 SWMMC children with grossly abnormal mucosal changes exhibited strong transmural nuclear p53 staining in their nasal biopsies (p 0.005, odds ratio 26). In the context of lifetime exposures to toxic and potentially carcinogenic air pollutants, p53 nasal induction in children could potentially represent. a) a checkpoin t response to toxic exposures, setting up a selective condition for p53 mutation, or b) a p53 mutation has already occurred as a result of such selection. Because the biological signi cance of p53 nuclear accumulation in the nasal biopsies of these children is not clear at this point, we strongly suggest that children with macroscopic nasal mucosal abnormalities should be closely monitored by the ENT physician. Parents should be advised to decrease the children's number of outdoor exposure hours and encourage a balanced diet with an important component of fresh fruits and vegetables.

p53 Mediates Particulate Matter–induced Alveolar Epithelial Cell Mitochondria-regulated Apoptosis

“…In 2002, the U.S. Environmental Protection Agency reported a range of maximal city concentrations of particulate matter smaller than 10 m in diameter (26-534 g/m 3 ) (40). Our findings concur with studies in humans exposed to various types of air pollutants showing increased p53 gene expression in lung cancers, mutations in the p53 gene in nonmalignant epithelial cells from the sputum of individuals without evidence of lung cancer, and p53 protein expression in the nasal epithelium of dysplastic lesions (41)(42)(43)(44). Our data implicating p53 in mediating PM-induced AEC apoptosis are consistent with a recent study showing that silica, which is another particle capable of causing lung cancer, failed to induce apoptosis in lung cells of p53 knockout animals, but did so in p53 wild-type mice (35).…”

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

“…Similarly, increased p53 immunoreactivity was found in nasal inverted papillomas (Schwerer et al, 2001). A study of nasal biopsies of children in Mexico City with nasal pathology revealed strong transmural p53 staining in about 25% of the samples (Calderon-Garciduenas et al, 2001). This was suggested to reflect a response to air pollution toxicity.…”

Odor identification ability and self-reported upper respiratory symptoms in workers at the post-9/11 World Trade Center site

“…inflamed (Moss et al 2001;Calderon-Garciduenas et al 2001, 2003b. Under these conditions, particulates often accumulate within the nasal respiratory epithelium and the nasal respiratory epithelial barrier can break down (Calderon-Garciduenas et al 2002, 2003a, 2008b.…”