World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice

被引:101
作者
Gavett, SH
Haykal-Coates, N
Highfill, JW
Ledbetter, AD
Chen, LC
Cohen, MD
Harkema, JR
Wagner, JG
Costa, DL
机构
[1] US EPA, Pulm Toxicol Branch, Off Res & Dev, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA
[2] NYU, Sch Med, Nelson Inst Environm Med, Tuxedo Pk, NY USA
[3] Michigan State Univ, E Lansing, MI 48824 USA
关键词
airway hyperresponsiveness; inflammation; neutrophil; nose-only inhalation; oropharyngeal aspiration; risk assessment;
D O I
10.1289/ehp.5931
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Pollutants originating from the destruction of the World Trade Center (WTC) in New York City on 11 September 2001 have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter [particulate matter with a mass median aerodynamic diameter < 2.5 mum (PM2.5)] has detrimental respiratory effects in mice 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 12 and 13 September 2001. Aspirated samples of WTC PM2.5 induced mild to moderate degrees of pulmonary inflammation 1 day after exposure but only at a relatively high dose (100 mug). This response was not as great as that caused by 100 muG PM2.5 derived from residual oil fly ash (ROFA) or Washington, DC, ambient air PM [National Institute of Standards and Technology, Standard Reference Material (SRM) 1649a]. However, this same dose of WTC PM2.5 caused airway hyperresponsiveness to methacholine aerosol comparable to that from SRM 1649a and to a greater degree than that from ROFA. Mice exposed to lower doses by aspiration or inhalation exposure did not develop significant inflammation or hyperresponsiveness. These results show that exposure to high levels of WTC PM2.5 can promote mechanisms of airflow obstruction in mice. Airborne concentrations of WTC PM2.5 that would cause comparable doses in people are high (similar to 425 mug/m(3) 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.
引用
收藏
页码:981 / 991
页数:11
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