You are here:
WORLD TRADE CENTER FINE PARTICULATE MATTER CAUSES RESPIRATORY TRACT HYPERRESPONSIVENESS IN MICE
Citation:
Gavett, S H., N. H. HaykalCoates, J W. Highfill, A. D. Ledbetter, Chen, Lung Chi, Cohen, Mitchell D, J. R. Harkema, J. G. Wagner, AND D L. Costa. WORLD TRADE CENTER FINE PARTICULATE MATTER CAUSES RESPIRATORY TRACT HYPERRESPONSIVENESS IN MICE. ENVIRONMENTAL HEALTH PERSPECTIVES 111(7):981-991, (2003).
Description:
World Trade Center Fine Particulate Matter Causes Respiratory Tract Hyperresponsiveness in Mice
Stephen H. Gavett1, Najwa Haykal-Coates1, Jerry W. Highfill1, Allen D. Ledbetter1, Lung Chi Chen2, Mitchell D. Cohen2, Jack R. Harkema3, James G. Wagner3, and Daniel L. Costa1.
1National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA; 2Nelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY, USA
3Michigan State University, East Lansing, MI, USA
Abstract
Pollutants originating from the destruction of the World Trade Center (WTC) have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter (PM2.5) has detrimental respiratory effects in mice in order to contribute to the risk assessment of WTC-derived pollutants. Samples of WTC PM2.5 were derived from settled dust collected at several locations around Ground Zero on September 12 and 13. Aspirated samples of WTC PM2.5 induced mild to moderate degrees of pulmonary inflammation one day after exposure, but only at a relatively high dose (100 mg). This response was not as great as that caused by 100 mg PM2.5 derived from residual oil fly ash (ROFA) or Washington DC ambient air PM (NIST 1649a). However, this same dose of WTC PM2.5 caused airway hyperresponsiveness to methacholine aerosol comparable to NIST 1649a and to a greater degree than ROFA. Mice exposed to lower doses by aspiration or inhalation exposure did not develop significant inflammation or hyperresponsiveness. These results show that a high dose of WTC PM2.5 can promote mechanisms of airflow obstruction in mice. Airborne concentrations of WTC PM2.5 which would cause comparable doses in people are high (~ 425 mg/m3 for 8 hr) but conceivable in the aftermath of the collapse of the towers when rescue and salvage efforts were in effect. We conclude that a high-level exposure to WTC PM2.5 could cause pulmonary inflammation and airway hyperresponsiveness in people. The effects of chronic exposures to lower levels of WTC PM2.5, the persistence of any respiratory effects, and the effects of coarser WTC PM are unknown and were not examined in these studies. Degree of exposure and respiratory protection, individual differences in sensitivity to WTC PM2.5, and species differences in responses must be considered in assessing the risks of exposure to WTC PM2.5.