The epidemiological evidence for PM-associated health effects continues to
mount. The effects, including morbidity and mortality, are most evident in
the elderly and those with preexisting impairments in cardiopulmonary healt
h. Recent preliminary field and controlled clinical studies support these a
ssociations by suggesting that PM can alter cardiac risk factors in a manne
r consistent with a higher risk of second heart attack. Empirical studies i
n healthy animals have provided evidence that PM and its emission surrogate
s cause lung injury, and perhaps more importantly these PM can exaggerate i
nflammatory, biochemical, hematologic, and physiologic impairments in anima
l models of cardiopulmonary disease. These findings have brought attention
to the often underappreciated, integral structural and physiological interp
lay of the heart and lungs within the cardiopulmonary system, especially in
conventional inhalation toxicology studies, if animal models are to enhanc
e our understanding of PM health effects in humans, it is critical that we
expand our knowledge of this interplay in both humans and animal models whe
n the lung is challenged with PM or its copollutants. How PM modulates auto
nomic and other homeostatic functions of the cardiopulmonary system, partic
ularly in those with preexisting impairments or heart-lung disease, will en
hance our understanding of public health risks and the likely multiplicity
of factors that determine the responsiveness of any individual.