Effects of concentrated ambient particles in rats and hamsters: an exploratory study.
Considerable controversy surrounds the biological plausibility of adverse effects from exposure to ambient particulate matter (PM)*, chiefly because these adverse effects have been observed at particle mass concentrations below those that have been shown to produce effects in healthy animals and human volunteers in the laboratory. To address this research gap, we examined the potential for concentrated ambient PM to produce pulmonary and cardiovascular changes in compromise rodent models. Normal healthy and monocrotaline-treated rats received single or multiple exposures to concentrated ambient PM, and their responses were tested using functional, cellular, biochemical, and histological endpoints. Analyses determined that no changes in pulmonary function or structure occurred after exposure to concentrated ambient PM. Cardiac arrhythmias did not increase after PM exposure in normal or monocrotaline-treated rats. Increased atrial conduction time, accompanied by a decrease in the duration of the T wave portion of the electrocardiogram (ECG) waveform, was observed in PM-exposed monocrotaline-treated rats in one experiment. In addition, on several but not all exposure days, small yet statistically significant increases in heart rate and peripheral blood cell differential counts were observed in normal and monocrotaline-treated rats within 6 hours after exposure to concentrated ambient PM. The observed changes in cardiovascular parameters in rats returned to control values by 24 hours after exposure. In a hamster cardiomyopathy model, no adverse cardiac or pulmonary changes were detected after exposure to concentrated ambient PM. Thus, these studies found that cardiopulmonary effects could be produced in rats, but not in hamsters with cardiomyopathy, exposed to concentrated ambient PM. None of the changes occurred on every exposure day and none appeared to be life threatening. Thus, the cardiac changes may reflect changes in homeostasis that could affect individuals who are critically ill, and these findings do not resolve the biological plausibility of adverse health effects associated with ambient PM in epidemiologic studies.
Gordon
T
T
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, USA.
Nadziejko
C
C
Chen
L C
LC
Schlesinger
R
R
D000367:Age Factors; D000393:Air Pollutants / Q000009:adverse effects* / Q000633:toxicity*; D000397:Air Pollution / Q000009:adverse effects*; D000818:Animals; D001772:Blood Cell Count; D009202:Cardiomyopathies / Q000097:blood / Q000150:complications* / Q000235:genetics / Q000503:physiopathology; D006224:Cricetinae; D004195:Disease Models, Animal; D006339:Heart Rate; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood / Q000139:chemically induced / Q000150:complications* / Q000503:physiopathology; D017380:Hypertrophy, Right Ventricular / Q000139:chemically induced / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008452:Maximum Allowable Concentration; D008647:Mesocricetus; D016686:Monocrotaline; D009026:Mortality; D010316:Particle Size; D051381:Rats; D011916:Rats, Inbred F344; D013997:Time Factors
D000393:Air Pollutants; D016686:Monocrotaline