Short-term effects of particulate matter: an inflammatory mechanism?

"Would you tell me please, which way I ought to go from here," asked Alice. "That depends a good deal on where you want to go to," said the cat. (Lewis Carroll, Alice's Adventures in Wonderland) A large number of epidemiological studies show positive correlations between increasing levels of particulate matter (PM) in urban air and short-term morbidity and mortality for diverse acute cardiopulmonary diseases. Brought about by PM increments, inflammation is thought to exacerbate preexisting inflammatory diseases. Experimental evidence suggests a hierarchical oxidative stress model, in which a weakened antioxidant defense, as observed in disease or induced by inhaled particles, increases the PM ability to cause lung inflammation, accounting for exacerbations that occur in asthmatics and in patients with chronic obstructive lung disease. The role of PM-induced inflammation leading to acute cardiovascular events such as arrhythmia, heart failure, and myocardial infarction is more speculative. There is neither clear-cut evidence in humans that inhaled PM could get as far as blood circulation nor that proinflammatory mediators are significantly released from inflamed lung tissues, nor that blood coagulability is critically altered. As a whole, data in humans indicate that short-term inflammatory responses to PM are not always detected; they are usually mild and loosely correlated with functional changes. Among these studies, the diversity of PM characteristics, dose metrics, and endpoints hampers a clear discerning of inflammatory mechanism(s). Thus, the question arises as to whether inflammation represents the mechanism of acute cardiopulmonary PM toxicities in susceptible individuals, or rather an event that may coexist with other relevant mechanism(s). This review article discusses the evidence in humans linking short-term PM increments to inflammation and to exacerbations of cardiopulmonary diseases. Although there is a large amount of data available, there still remains a gulf between the number of epidemiological and panel studies and that of controlled exposures. Research on controlled exposure needs expanding, so that the results of time-series and panel studies will be better understood and short-term standards for human exposure may be more confidently allocated.