Differential cardiopulmonary effects of size-fractionated ambient particulate matter in mice.
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.
Tong
Haiyan
H
Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA. tong.haiyan@epa.gov
Cheng
Wan-Yun
WY
Samet
James M
JM
Gilmour
M Ian
MI
Devlin
Robert B
RB
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D005260:Female; D019570:Inhalation Exposure; D051379:Mice; D009203:Myocardial Infarction / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D011014:Pneumonia / Q000139:chemically induced*; D020127:Recovery of Function; D018570:Risk Assessment; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects; D017725:Ventricular Pressure / Q000187:drug effects
D052638:Particulate Matter