| The prevalence, morbidity, and mortality of asthma has been increasing at an alarming rate over the past several decades, making it a major public health concern. Epidemiological evidence suggests that particulate matter (PM) may contribute to such increases. In support of this hypothesis is the observation that asthma prevalence, as well as morbidity and mortality, is increasing most rapidly in urban environments where anthropogenic sources of PM are concentrated. Few epidemiological studies have examined the role of PM in induction of asthma. However, animal studies indicate particles from combustion sources (residual oil and coal fly ashes, diesel fuel) can induce asthma-like parameters of airway hyperresponsiveness (AHR) and inflammation, and can alter immune responses. However, such PM surrogates do not address the complex mixture of substances found in ambient PM.; We have examined the effects of ambient particulate matter collected in urban Baltimore on airway reactivity and inflammation in mice. Additionally, efforts were made to begin to determine the mechanisms by which ambient PM elicits such effects.; Results of this research show that ambient PM from Baltimore City induces sustained asthma-like parameters of AHR and inflammation, as well as alterations in local lung cytokine levels and increases in lung permeability. AHR and inflammation occur to a significant degree in a variety of genetically diverse strains of mice, indicating that all individuals may be susceptible to respirable PM to some degree. Furthermore, the effects of multiple low doses of PM appear to be cumulative. Additionally, results indicate that although inflammation and AHR occur concurrently in response to PM challenge, AHR is not dependent on airway inflammation, but is mediated through the innate defense system of complement activation. In conclusion, exposure to ambient PM may be a contributing factor to increases seen in asthma and other respiratory illnesses, particularly in urban environments. |
