Epidemiological studies suggest an association between
ambient particulate matter and cardiopulmonary diseases in humans. The mechanisms underlying these health effects are poorly understood. To better understand the potential relationship between
particulate-matter-induced
inflammation and
vascular disease, a 2-phase retrospective study was conducted. Phase one included the review of heart, lung, and kidney tissues from high-dose and control male B6C3F1 mice exposed by inhalation to 9 particulate compounds for a 2-year period. The results showed that high-dose males developed significantly increased incidences of coronary and renal
arteritis over controls in 2 of the 9 studies (
indium phosphide and
cobalt sulfate heptahydrate), while marginal increases in
arteritis incidence was detected in 2 additional studies (
vanadium pentoxide and
gallium arsenide). In contrast,
arteritis of the muscular arteries of the lung was not observed. Morphological features of
arteritis in these studies included an influx of mixed inflammatory cells including neutrophils, lymphocytes, and macrophages. Partial and complete effacement of the normal vascular wall architecture, often with extension of the inflammatory process into the periarterial connective tissue, was observed. Phase 2 evaluated the heart, lung, kidney, and mesentery of male and female B6C3F1 mice from the 90-day studies of the 4 compounds demonstrating
arteritis after a 2-year period. The results showed
arteritis did not develop in the 90-day studies, suggesting that long-term chronic exposure to lower-dose metallic
particulate matter may be necessary to induce or exacerbate
arteritis.