Science Inventory

TOXICOLOGICAL EFFECTS OF PARTICULATE MATTER DERIVED FROM THE DESTRUCTION OF THE WORLD TRADE CENTER

Citation:

Gavett, S H., N. H. HaykalCoates, Chen, Lung Chi, Cohen, Mitchell D, AND D L. Costa. TOXICOLOGICAL EFFECTS OF PARTICULATE MATTER DERIVED FROM THE DESTRUCTION OF THE WORLD TRADE CENTER. Presented at American Association for Aerosol Research, Charlotte, NC, October 7-11, 2002.

Description:

May 15, 2002
Abstract submitted by Stephen H. Gavett for American Association for Aerosol Research (AAAR) annual meeting October 7-11, 2002 in Charlotte, NC.

TOXICOLOGICAL EFFECTS OF PARTICULATE MATTER DERIVED FROM THE DESTRUCTION OF THE WORLD TRADE CENTER
Stephen H Gavett, Najwa Haykal-Coates, Lung Chi Chen*, Mitchell D Cohen*, and Daniel L Costa. Pulmonary Toxicology Branch (MD-82), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 and *New York University Medical Center, 57 Old Forge Road, Tuxedo, NY 10987

We examined whether fine particulate matter (PM2.5) derived from the destruction of the World Trade Center (WTC) has detrimental effects on the lungs of mice using biological endpoints that have clinical correlates in humans. The purpose of the studies was to assess respiratory function and lung inflammation in accordance with public complaints regarding perceived irritancy and respiratory impairments. Settled dust samples were collected around Ground Zero on September 12 and 13. The samples were aerosolized and size-fractionated, and the PM2.5 fraction was collected on filters. Filters from 7 of the collection sites were extracted and extensively analyzed by several analytical techniques. A portion was pooled and administered to mice by aspiration directly into the airways at three different doses. Mice were assessed for airway and ventilatory function (general index of irritancy), deep lung diffusing capacity, and lung inflammation and injury. The effects of the pooled WTC dust sample were compared with effects in three control groups which were administered saline vehicle alone, Mt. St. Helens dust PM2.5 which is relatively inert, or residual oil fly ash (ROFA)PM2.5 which is relatively toxic. In a separate study, the health effects of the dust samples from the 7 individual collection sites around the WTC were examined in order to better understand the intrinsic hazards associated with dust samples from different locations around Ground Zero and with varying compositions. These individual site samples were delivered by aspiration and the effects were compared to those from a Standard Reference Material PM2.5 derived from Washington DC ambient air PM (NIST 1649a). In a third study, mice inhaled WTC PM2.5, derived from a bulk dust sample collected in the vicinity of the disaster, or filtered air in nose-only exposure tubes. Mice were exposed for 5 hours to 10.6 mg/m3 PM2.5 which may be comparable to levels in the first day or two post-disaster. The results of these studies indicate that samples of WTC PM2.5 induce mild to moderate degrees of inflammation when administered at a relatively high dose (100 micrograms) directly into the airways of mice. This dose of WTC PM also caused airway hyperresponsiveness (greater sensitivity to an airway-constricting drug) to a greater degree than ROFA and comparable to NIST 1649a. Doses of 10 and 32 micrograms administered directly into the airways, or inhalation at 10.6 mg/m3, did not induce significant inflammation or hyperresponsiveness. The data will contribute to WTC PM2.5 hazard identification, potential mechanisms of action, and the short-term human health risk assessment of WTC PM being conducted by the Environmental Protection Agency.

This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.

Record Details:

Record Type: DOCUMENT (PRESENTATION/ABSTRACT)
Product Published Date: 10/07/2002
Record Last Revised: 06/06/2005
Record ID: 62264

Organization:

U.S. ENVIRONMENTAL PROTECTION AGENCY

OFFICE OF RESEARCH AND DEVELOPMENT

NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LABORATORY

EXPERIMENTAL TOXICOLOGY DIVISION

PULMONARY TOXICOLOGY BRANCH