Do urban environmental pollutants exacerbate childhood lung diseases?

Childhood lung diseases in the United States are on the rise. This is especially true for chronic respiratory diseases such as allergic asthma, where the incidence among children in polluted inner cities has reached epidemic proportions. We believe that the recent marked increase in the incidence of childhood asthma results from the convergence of six separate factors (three of which are characteristics of lung biology and three ofwhich are environmental factors) that individually would not be sufficient to compromise the respiratory health ofchildren. The first of the biologic factors is the extended period of postna-tal life required for complete development of the human lung. For long-lived mammalian species such as humans, this period involves the first 6-8 years of childhood (1). The developmental events occurring during this postnatal period are the same events that begin before birth and include cytodifferentiation of epithelial and intersti-tial cell populations, morphogenesis and reorganization of the gas exchange area, and the development of the respiratory mucosal immune system. Further, the complex trophic interrelationships between various cellular and acellular components of the conducting airway wall are established during this extended postnatal period (2. As with prenatal development, many postnatal developmental processes exhibit critical windows in which minor alterations in function or exposure to mild irritants or toxicants can markedly modify developmental processes. The timing and interaction between these developmental events appear to play a role as susceptible targets for environmental perturbation. The second aspect of human lung biology which appears to play a role is the wide genetic variability that modulates predisposition to enhanced perturbation by allergic and other environmental contaminants. As the complexities of the human genome have been defined, a large variety of genetic polymorphisms are being identified. These polymorphisms are dosely associated with susceptibility to a wide variety of environmental contaminants, including aller-gens (3,4). Both of these characteristics of human biology (postnatal development and genetic variability) provide the platform on which perturbations by environmental contaminants could alter respiratory health. These differences in genetic composition of even dosely related individuals could predispose some of them to disease processes produced by environmental contaminants. When these two biologic factors are subjected to our dedining environmental quality, coexposure to a combination of environmental contaminants may have a decidedly negative impact. One of the environmental factors relevant to childhood lung disease is the recent increase in complexity and distribution, if not the levels, of airborne pollutants, including environmental …