Although sources of airborne lead have been reduced over the last decade, particularly with the use of lead-free gasoline, there are still relatively high levels of lead contamination in soils and the residential housing stock built before the 1970s, which pose a risk for continued direct exposure through ingestion or airborne exposure if resuspended. Neurobehavioral effects, particularly as a result of early childhood exposures, have been documented, and, because of the way lead is stored in the body, late effects can become manifest during periods of high bone turnover (e.g., pregnancy, lactation, or hyperthyroidism). Late consequences not only relate to lead excretion affecting the fetus or newborn but also appear to be associated with hypertension in adults. Control of exposure in early life is an important component of appropriate preventive action.

In clinical studies of inhaled pollutants, the investigator controls the concentration of the pollutants and the temporal profile of exposure; by varying the degree of exertion during exposure, the investigator can further affect the dose delivered to the respiratory tract. Of necessity, the protocols for clinical studies limit exposures to brief periods, typically from lh or less to no more than 5 or 6h. In most protocols, subjects are exposed at only a single concentration, although a recent study imposed “peaks” of NO2 exposure on a lower background (Utell et al. 1990). In selecting concentrations of inhaled pollutants for a clinical study, some relevant considerations include expectations of producing effects on outcome measures based on the results of previous studies, evidence from animal studies, the need to describe “safe” levels of exposure for regulatory purposes, and ethical constraints.