Differential Cardiopulmonary Effects of Size-Fractionated Ambient Particulate Matter in Mice

Abstract

A growing body of evidence from epidemiological and toxicological studies provides a strong link between exposure to ambient particulate matter (PM) of varying size and increased cardiovascular and respiratory morbidity and mortality. This study was designed to evaluate the cardiopulmonary effects of ambient coarse, fine, and ultrafine particles collected in Chapel Hill, NC. Mice were exposed to each size fraction by oropharyngeal instillation. Twenty-four hours later, pulmonary inflammation was assessed by bronchoalveolar lavage and cardiac injury was measured using a Langendorff cardiac perfusion preparation. Recovery of post-ischemic left ventricular developed pressure and infarct size were measured as indeces of cardiac ischemia/reperfusion injury. Coronary flow rate was measured before, during, and after ischemia. We demonstrate that coarse PM caused the most significant pulmonary inflammatory responses. In contrast, hearts from ultrafine-exposed mice had significantly lower post-ischemic functional recovery and greater infarct size, while hearts from coarse and fine PM-exposed mice had no significant responses to ischemia/reperfusion. The coronary flow rate was significantly reduced in the ultrafine PM group. This study shows that exposure of mice to coarse PM results in significant pulmonary toxicity while ultrafine PM appears to enhance cardiac ischemia/reperfusion injury.

Associations between short-term exposure to particulate matter and ultrafine particles and myocardial infarction in Augsburg, Germany

“…Further, ultrafine particles may directly interact with the cardiovascular system and affect vascular endothelium and atherosclerotic plaques as well as provoke local inflammation and oxidative stress. A study on mice (Tong et al, 2010) reported that hearts from mice exposed to ultrafine particles showed a significantly lower post-ischemic functional recovery and a greater infarct size, but no effects were seen for mice exposed to coarse particles (PM ranging from 2.5 to 10 m in aerodynamic diameter) or PM 2.5 . Indirect pollutant effects are supposed to evoke rather delayed and chronic cardiovascular responses.…”

Acute systemic and lung inflammation in C57Bl/6J mice after intratracheal aspiration of particulate matter from small-scale biomass combustion appliances based on old and modern technologies

“…Thus, they are usually deposited in the tracheobronchial and alveolar regions of the airways (Lippmann et al, 1980). Due to the small size of PM 1 , these combustion derived particles can even penetrate through the lung tissue and reach the capillary blood vessels and circulating cells (Tong et al, 2010). Exposure to wood combustion-derived particles can lead to upregulation of proinflammatory cytokines, including interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), as well as chemokines including IL-8 and keratinocyte-derived chemoattractant (KC).…”

Combined toxicity of amorphous silica nanoparticles and methylmercury to human lung epithelial cells

“…Mercury in the air is easily taken up through the lungs, and about 74% of inhaled mercury is retained in human body (Syversen and Kaur, 2012). The mercury can be distributed throughout the human body via the blood circulation, which could cause cardiovascular and pulmonary health disease (Tong et al, 2010;Valera et al, 2012). Based on the Global mercury assessment 2013 reported by United Nations Environment Program (UNEP) (Assessment, 2013), the global mercury emissions to air from anthropogenic sources is estimated as 1960 t in 2010, but the emissions are changing in the range of 1010-4070 t. Atmospheric mercury exists primarily as gaseous elemental mercury (GEM-Hg°), reactive gaseous mercury (RGM-Hg 2 þ ) and particulate mercury Hg (p) (Fang et al, 2011).…”