Chapter Summary

The purpose of this chapter was to address the influence of maternal/fetal immu-notoxicant exposure on the development of asthma. Deciphering exactly how developmental exposures can lead to postnatal asthma onset or affect the sensitivity to triggers of asthmatic attacks remains an elusive goal due to insufficient evidence and a lack of mechanism studies. This chapter provided a molecular overview of asthma sensitization and triggering, asthmatic inflammation, and the inter- and intracellular mediators that may be affected by toxicants and allergens during asthma pathogenesis. Following this molecular review were discussions of the influences of maternal-fetal interactions during physiologic fetal sensitization and the development of normal immune responses. The processes involved included the generation of atopy-related fetal IgE, the bias towards a TH2 phenotype in the neonatal immune system, and the genetic components of asthma sensitization. The chapter concluded with discussions of how asthma as an exacerbated postnatal immune response may be acquired or influenced by developmental exposures to: 1.) aeroallergens such as dust mites, cockroaches, molds, pet dander, and pollens; 2.) toxicants such as pesticides, polycyclic halogenated hydrocarbons including PCBs and dioxins, and heavy metals, with particular emphasis on lead; and 3.) environmental tobacco smoke, with its sundry components including polycyclic aromatic hydrocarbons. It is our hope that this review will inspire further research into the effects of environmental toxicants on the development of asthma, particularly because of the paucity of studies currently able to provide insight into the mechanisms of interaction between molecular moieties of the environment and the various components of the immune system at discrete stages of development in utero and in the antenatal period.

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