The prevalence of asthma, measured either as the frequency of hospital
admissions or number of deaths attributed to asthma, has increased ov
er the last 15 to 20 years. Rapid increases in disease prevalence are
more likely to be attributable to environmental than genetic factors.
inferring from past associations between air pollution and asthma. it
is feasible that changes in the ambient environment could contribute t
o this increase in morbidity and mortality. Scientific evaluation of t
he links between air pollution and the exacerbation of asthma is incom
plete, however. Currently, criteria pollutants [SOx, NOx, O-3, CO, Pb,
particulate matter (PM(10))] and other risk factors (exposure to envi
ronmental tobacco smoke. volatile organic compounds, etc.) are constan
tly being evaluated as to their possible contributions to this situati
on. Data from these studies suggest that increases in respiratory dise
ase are associated with exposures to ambient concentrations of particu
late and gaseous pollutants. Similarly. exposure to environmental toba
cco smoke, also a mixture of particulate and gaseous air toxics, has b
een associated with an increase in asthma among children. In addition,
current associations of adverse health effects with existing pollutio
n measurements are often noted at concentrations below those that prod
uce effects in controlled animal and human exposures to each pollutant
alone. These findings imply that adverse responses are augmented when
persons are exposed to irritant mixtures of particles and gases and t
hat current measurements of air pollution are, in part, indirect in th
at the concentrations of criteria pollutants are acting as surrogates
of our exposure to a complex mixture. Other irritant air pollutants. i
ncluding certain urban air toxics, are associated with asthma in occup
ational settings and may interact with criteria pollutants in ambient
air to exacerbate asthma. An evaluation of dose-response information f
or urban air toxics and biological feasibility as possible contributor
s to asthma is therefore needed. However, this evaluation is compounde
d by a lack of information on the concentrations of these compounds in
the ambient air and their effects on asthma morbidity and mortality.
Through an initial review of the current toxicological literature, we
propose a tentative list of 30 compounds that could have the highest i
mpact on asthma and respiratory health. These compounds were selected
based on their ability to induce or exacerbate asthma in occupational
and nonoccupational settings, their allergic potential and ability to
react with biological macromolecules, and lastly, their ability to irr
itate the respiratory passages. We recommend better documentation of e
xposure to these compounds through routine air sampling and evaluation
of total exposure and further evaluation of biological mechanisms thr
ough laboratory and epidemiological studies directed specifically at t
he role these substances play in the induction and exacerbation of ast
hma.