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Manufactured and Airborne Nanoparticle Cardiopulmonary Interactions: A Review of Mechanisms and the Possible Contribution of Mast Cells
Citation:
Shannahan, J., U. Kodavanti, AND J. Brown. Manufactured and Airborne Nanoparticle Cardiopulmonary Interactions: A Review of Mechanisms and the Possible Contribution of Mast Cells. INHALATION TOXICOLOGY. Informa Healthcare, London, Uk, 24(5):320-39, (2012).
Impact/Purpose:
This review was prepared to summarize the mechanisms of particulate matter induced cardiovascular effects. There are a number of mechanisms being investigated in EPA labs and other institutes. This effort was to bring studies done at EPA and nationwide to understand the commonality and distinct features of cardiopulmonary interactions. Based on the research done at East Carolina University, this review also provides insights into the role of mast cells in eliciting cardiovascular response following ultrafine particle exposure
Description:
Human inhalation exposures to manufactured nanoparticles (NP) and airborne ultrafine particles (UFP) continues to increase in both occupational and environmental settings. UFP exposures have been associated with increased cardiovascular mortality and morbidity, while ongoing research supports adverse systemic and cardiovascular health effects after NP exposures. Adverse cardiovascular health effects include alterations in heart rate variability, hypertension, thrombosis, arrhythmias, increased myocardial infarction, and atherosclerosis. Exactly how UFP and NP cause these negative cardiovascular effects is poorly understood, however a variety of mediators and mechanisms have been proposed. UFP and NP, as well as their soluble components, are known to systemically translocate from the lung. Translocated particles could mediate cardiovascular toxicity through direct interactions with the vasculature, blood, and heart. Recent study suggests that sensory nerve stimulation within the lung may also contribute to UFP- and NP-induced acute cardiovascular alterations. Activation of sensory nerves,such as C-fibers, within the lung may result in altered cardiac rhythm and function. Lastly, release of pulmonary-derived mediators into systemic circulation has been proposed to facilitate cardiovascular effects. In general, these proposed pulmonary derived mediators include pro-inflammatory cytokines, oxidatively-modified macromolecules, vasoactive proteins, and prothrombotic factors. These pulmonary derived mediators have been postulated to contribute to the subsequent prothrombotic,atherogenic, and inflammatory effects after exposure. This review will evaluate the potential contribution of individual mediators and mechanisms in facilitating cardiopulmonary toxicity following inhalation of UFP and NP. Lastly we will appraise the literature and propose a hypothesis regarding the possible role of mast cells in contributing to these systemic effects.