Ultrastructural nasal pathology in children chronically and sequentially exposed to air pollutants

Southwest Metropolitan Mexico City (SWMMC) children are repeatedly exposed to a complex mixture of air pollutants, including ozone, particulate matter , and aldehydes. Nasal biopsies taken from these children exhibit a wide ra nge of histopathologic alterations: marked changes in ciliated and goblet c ell populations, basal cell hyperplasia, squamous metaplasia, and mild dysp lasias. We studied the ultrastructural features of 15 nasal biopsies obtain ed from clinically healthy children 4 to 15 yr of age, growing up in SWMMC. The results were compared with nasal biopsies from 11 children growing up in Veracruz and exposed to low pollutant levels. Ultrathin sections of nasa l biopsies revealed an unremarkable mucociliary epithelium in control child ren, whereas SWMMC children showed an epithelium comprised of variable numb ers of basal, ciliated, goblet, and squamous metaplastic as well as interme diate cells. Nascent ciliated cells, as evidenced by the presence of migrat ory kinetosomes, were common, as were ciliary abnormalities, including abse nt central microtubules, supernumerary central and peripheral tubules, cili ary microtubular discontinuities, and compound cilia. Dyskinesia associated with these abnormal cilia was suggested by the altered orientation of the central microtubules in closely adjacent cilia. A transudate was evident be tween epithelial cells, suggesting potential deficiencies in epithelial jun ction integrity. Particulate matter was present in heterolysosomal bodies i n epithelial cells and it was also deposited in intercellular spaces. The s evere structural alteration of the nasal epithelium together with the promi nent acquired ciliary defects are likely the result of chronic airway injur y in which ozone, particulate matter, and aldehydes are thought to play a c rucial role. The nasal epithelium in SWMMC children is fundamentally disord ered, and their mucociliary defense mechanisms are no longer intact. A comp romised nasal epithelium has less ability to protect the lower respiratory tract and may potentially leave the distal acinar airways more vulnerable t o reactive gases. Impairment of mucociliary clearance has the potential to increase the contact time between deposited mutagenic particulate matter an d the epithelial surface, thus increasing the risk for nasal carcinogenesis . Chronic exposures to air pollutants affect the whole respiratory tract; t he nasal epithelium is an accessible and valuable sentinel to monitor expos ures to toxic or carcinogenic substances.