Subchronic inhalation of carbon nanofibers: No apparent cross-talk between local pulmonary and cardiovascular/systemic responses

Pulmonary exposures to air pollution-derived particulate matter (PM) may result in both activation of lung responses and adverse cardiovascular (CV) effects. This suggests a cross-talk relationship between local and systemic responses potentially leading to CV disease in humans. To test this hypothesis in a normal animal model, rats were exposed to aerosols of carbon nanofibers (CNF) for 13 weeks. The highest CNF concentration (25 mg/m³) produced persistent respiratory tract (RT) inflammation/cytotoxicity throughout the exposure and 3-month recovery period, concomitant with translocation of inhaled CNF from airspace to extrapulmonary sites. The finding provided a basis for postulating that local RT effects could translocate to the systemic circulation, thereby producing CV alterations such as inflammation and/or coagulation changes. Therefore, assessments of cardiovascular endpoints such as cardiomyocyte cell proliferation (CP)/histopathology, C-reactive protein (CRP) levels, and 4 different diagnostic coagulation parameters, were investigated. No significant differences were measured between air or CNF-exposed rats when measuring fibrinogen levels, platelet counts, PT and aPTT bleeding times, and CRP levels. In addition, CP and histopathology evaluations were not different in CNF-exposed rats. Cardiac physiology and telemetry responses were not measured in this study. It was concluded that no apparent cross-talk was evident between local respiratory and systemic/cardiovascular compartments.