There exists a significant body of research on the potential effects on respiratory health from exposure to environmental (passive) tobacco smoke (ETS) (reviewed in: National Academy of Sciences 2000). Many components of ETS are known lung irritants. There have been direct associations shown between exposure to tobacco smoke and the development of lung cancer, obstructive airway disease, chronic bronchitis, ear infections, and asthma. It is small wonder that ETS is associated with so many disparate disorders, considering that tobacco smoke components include the carcinogens benzene, toluene, and 1,3-butadiene (Mitacek et al. 2002), toxicants such as nickel (Tobacco Research Implementation Group 1998) and polycyclic aromatic hydrocarbons (PAHs) (Besaratinia et al. 2002), and common household chemicals including ammonia, formaldehyde, and acetone (Tobacco Research Implementation Group 1998). Moreover, the effects of tobacco smoke are not limited to the active smoker but to anyone exposed to passive or environmental tobacco smoke, including infants and children. Because ETS represents a large and diverse mixture of chemicals of many different types, it is difficult to ascribe ETS effects on the immune system to any one component. For this reason, most descriptions of relationships between developmental ETS exposure and asthma development require high levels of exposure. Individual molecular effects will remain elusive until complex "mixture" studies are conducted in a developmental setting. One study has shown direct effects of ETS and nicotine on lung function in the developing fetus. In this case, an interaction of tobacco-specific toxicants with the neuronal alpha (7) nicotinic acetylcholine receptor and its associated mitogenic signal transduction pathway was explored, particularly with regard to a potential role in lung carcinogenesis and pediatric lung disorders (Schuller et al. 2000). From that study's findings, the authors suggest that chronic nicotine and ETS exposure in pregnant women who smoke may upregulate the alpha (7) nicotinic receptor as well as components of its associated mitogenic signal transduction pathway. Upregulation of these receptors and downstream biochemical cascades are hypothesized to increase the susceptibilities of the infants for the development of pediatric lung disorders (Schuller et al. 2000). Whether those disorders include the development of asthma remains to be seen. Nonetheless, the adverse effects of maternal smoking on the health of the developing fetus and neonate are well recognized.
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