Inhalation exposure to carbon black induces inflammatory response in rats

A link between exposure to fine particulate matter and cardiovascular events has been established. Inhaled nanoparticles are thought to pass through the lungs to reach other tissues via systemic circulation and to induce cell or tissue injuries. It was recently shown that long-term exposure to intra-tracheal dispersion of nano-sized carbon black (CB) exacerbates atherosclerotic lesions in low-density lipoprotein receptor-deficient mice. Because intra-tracheal dispersion of CB may be associated with aggregate formation and may not be an ideal method for CB exposure, whole-body inhalation exposure was used in the present study, the aim of which was to examine whether exposure of rats to nano-sized CB particles by inhalation leads to translocation of these particles into the circulation, exerting direct adverse effects on extrapulmonary tissues.

Sprague-Dawley rats were exposed to a high dose of CB or filtered air for 6 h/day, 5 days a week for a total of 4 weeks. Although the presence of CB was confirmed in pulmonary macrophages, electron microscopic survey did not detect CB in other tissues including liver, spleen and aorta. CB exposure raised blood pressure levels in an exposure-time dependent manner. Levels of circulating inflammatory marker proteins, including monocyte chemoattractant protein-1, interleukin-6, and C-reactive protein, were higher in the CB-treated group than in the controls.

Evidence of translocation of inhaled CB was not obtained. It is likely that inhaled nano-sized CB particles form aggregations in the lung and do not exert direct adverse effects on extrapulmonary tissues. Air-pollution-mediated cardiovascular events appear to be induced by the low-grade inflammatory response to the accumulation of aggregated nano-sized particles in the lung.