portance in considering harm reduction strategies is the contribution of ETS to asthma and respiratory infections in children. Abatement strategies for susceptible children exposed to environmental tobacco smoke may differ from those used to reduce harm in tobacco smokers.

An extensive knowledge base exists describing the contribution of tobacco smoke exposure to nonneoplastic respiratory disease, and key points are described briefly here. The major goal of this chapter is to summarize studies designed to test whether reducing exposure to tobacco toxicants improves health outcomes for respiratory diseases. As will be described below, there are considerable gaps in information about reducing harm and uncertainties about the quality of the existing knowledge base in this regard. Consequently, a research agenda is proposed to guide future studies aimed at reducing the harm from smoking in COPD.

There are currently no specific biomarkers of respiratory disease due to smoking tobacco products (see Chapter 11). The rare genetic deficiency of α₁-antitrypsin is a risk factor for disease, not a biomarker (see below). No unique molecular or genetic defect specific for tobacco-related respi-