Hypertension and Vascular Toxicity of PM
A growing body of data implicates particulate matter air pollution (PM) as an important factor in the pathogenesis of cardiovascular disease. PM influences susceptibility to adverse cardiovascular events and may be particularly harmful in individuals with pre-existing cardiovascular disease (CVD) risk factors such as diabetics, hypertensives and smokers. The synergistic interaction of PM with other conventional risk factors is internally consistent with our current understanding of how risk factors mediate complex diseases such as hypertension, whereby the pathways involved in mediating the adverse effects often converge on final common mechanisms. A number of studies have now demonstrated rapid effects of inhaled particulates on cardiovascular variables such as vascular tone and function, arguing for mechanisms transducing PM signals within minutes to hours. There is also good evidence to suggest sub-acute and chronic effects of PM with persuasive lines of evidence to support a role for reactive oxygen species (ROS) dependent mechanisms. The extent of these effects depend on the source, composition and duration of exposure to PM and the underlying susceptibility of the individual or the animal. Our understanding of the locus of generation of these mediators (lung versus extra-pulmonary), the source(s), time course of release and the relative contribution to various vascular effects continues to evolve. In this section we will discuss recent studies that have enhanced our understanding of PM-mediated vascular effects with a focus on hypertension, and we will discuss the relative biological significance of these findings.