Gavett Stephen H, Haykal-Coates Najwa, Highfill Jerry W, Ledbetter Allen D, Chen Lung Chi, Cohen Mitchell D, Harkema Jack R, Wagner James G, Costa Daniel L
National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
Environ Health Perspect. 2003 Jun;111(7):981-91. doi: 10.1289/ehp.5931.
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 microm (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 microg). This response was not as great as that caused by 100 microg 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 (approximately 425 microg/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.
据报道,2001年9月11日纽约世界贸易中心(WTC)被毁产生的污染物致使救援人员和附近居民出现不良呼吸道反应。我们研究了世贸中心产生的细颗粒物[质量中位空气动力学直径小于2.5微米的颗粒物(PM2.5)]对小鼠是否具有有害的呼吸道影响,以有助于对世贸中心产生的污染物进行风险评估。世贸中心PM2.5样本取自2001年9月12日和13日在归零地周围多个地点收集的沉降灰尘。吸入世贸中心PM2.5样本后1天会引发轻度至中度的肺部炎症,但仅在相对高剂量(100微克)时出现。这种反应不如源自残油飞灰(ROFA)或华盛顿特区环境空气PM [国家标准与技术研究院,标准参考物质(SRM)1649a]的100微克PM2.5所引起的反应强烈。然而,相同剂量的世贸中心PM2.5引起的对乙酰甲胆碱气雾剂的气道高反应性与SRM 1649a相当,且比ROFA引起的程度更大。通过吸入或吸入暴露接触较低剂量的小鼠未出现明显的炎症或高反应性。这些结果表明,暴露于高水平的世贸中心PM2.5可促进小鼠气流阻塞机制。在人群中会导致相当剂量的世贸中心PM2.5的空气传播浓度很高(8小时内约为425微克/立方米),但在塔楼倒塌后救援和打捞工作进行期间是可以想象的。我们得出结论,高水平暴露于世贸中心PM2.5可能会导致人体肺部炎症和气道高反应性。长期暴露于较低水平的世贸中心PM2.5的影响、任何呼吸道影响的持续性以及更粗的世贸中心PM的影响尚不清楚,且在这些研究中未进行检测。在评估暴露于世贸中心PM2.5的风险时,必须考虑暴露程度和呼吸防护、对世贸中心PM2.5敏感性的个体差异以及反应的物种差异。