Mechanism of PM-Induced Acute Health Effects

EPA Grant Number: R826244
Title: Mechanism of PM-Induced Acute Health Effects
Institution: New York University Medical Center
EPA Project Officer: Chung, Serena
Project Period: January 23, 1998 through January 22, 2001
Project Amount: $600,799
RFA: Health Effects and Exposures to Particulate Matter and Associated Air Pollutants (1997) RFA Text |  Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air , Human Health


The objective of this study is to determine the biological mechanism for systemic effects associated with acute exposure to ambient particulate matter (PM). We hypothesize that inhaled PM causes immediate effects on the autonomic regulation of the cardiovascular system resulting in a stress response and that the biological changes associated with this response can explain a substantial portion of the mortality associated with acute exposure to PM. Our preliminary studies have demonstrated that concentrated ambient PM induces a stress response in normal rats. We will determine whether environmentally relevant concentrations of PM cause a stress response and whether there is a threshold concentration below which PM does not cause acute cardiovascular changes. Moreover, because of epidemiologic evidence that PM-associated adverse effects may occur in those individuals with pre-existing illness, we also hypothesize that concentrated ambient PM will produce these systemic effects at lower concentrations in an animal model of compromised health. Because of the confounding effects of gaseous co-pollutants on estimates of relative risk of morbidity and mortality attributable to PM exposure, we will test the hypothesis that ozone and sulfur dioxide alter the stress response to inhaled PM. Finally, because there is uncertainty as to the relative contribution of indoor versus outdoor PM to adverse health effects, we will examine the dose-response curves for concentrated indoor and outdoor PM.


Physiologic parameters indicative of a stress response, that can be related to epidemiological findings, will be monitored before, during, and up to 24 hours after a 3 hr exposure of rats to concentrated ambient New York City PM. The primary parameters to be monitored are blood pressure, heart rate, EKG, and sympathetic nerve fiber activity. Levels of stress-response related hormones will also be measured in the blood and urine.

Expected Results:

As determined in preliminary studies, concentrated ambient PM is expected to induce a stress response. Such an observation will provide a biological mechanism for the adverse health effects observed at low PM concentrations. We also expect that the sensitive physiologic and biochemical parameters will identify a lowest observable effective PM concentration for altering cardiovascular function. The data obtained in the proposed study can be extrapolated to infer the potential for the observed effects to contribute to the mortality that is associated with ambient PM inhalation. In summary, the results from this study address a number of the research needs identified in this solicitation, including: biological plausibility, sensitive subpopulations, the role of gaseous co-pollutants, and the contribution of indoor PM.

Publications and Presentations:

Publications have been submitted on this project: View all 9 publications for this project

Journal Articles:

Journal Articles have been submitted on this project: View all 4 journal articles for this project

Supplemental Keywords:

particulates, metals, ambient air, animal, mechanisms., RFA, Health, Scientific Discipline, Air, particulate matter, Toxicology, Health Risk Assessment, Risk Assessments, Biochemistry, Environmental Monitoring, Atmospheric Sciences, co-factors, copollutant exposures, cardiopulmonary responses, inhalability, morbidity, cardiovascular vulnerability, dose response, air pollution, air sampling, biological mechanisms, cardiopulmonary mechanisms, chronic health effects, particulate exposure, Acute health effects, mortality

Progress and Final Reports:

  • 1998
  • 1999 Progress Report
  • Final Report