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American Journal of Respiratory and Critical Care Medicine Vol 174. pp. 235-236, (2006)
© 2006 American Thoracic Society
doi: 10.1164/rccm.200605-636ED


Editorials

The World Trade Center Collapse

A Continuing Tragedy for Lung Health?

John R. Balmes, M.D.

University of California at San Francisco Lung Biology Center and Division of Occupational and Environmental Medicine, San Francisco, California

While the tragedy of the World Trade Center (WTC) collapse still sears the consciousness of those who value human life, some important lessons in occupational and environmental respiratory disease have been learned as a result of this disaster. Perhaps the most striking of these lessons is the value of medical surveillance for workers in jobs with high risk for inhalational exposure to toxicants. Because the New York City Fire Department (NYFD) had preexposure pulmonary function test results on virtually all of the firefighters involved in the emergency response to the attack on the WTC, as well as the infrastructure in place to continue to follow them longitudinally, Prezant and colleagues (1) and Banauch and colleagues (2, 3) have been able to describe the sequelae of exposure to WTC "dust" in a remarkable series of papers. The first paper reported that the relatively high-level exposure to WTC "dust" experienced by NYFD emergency responders in the initial weeks after September 11 was associated in a cross-sectional analysis with persistent bronchitis and substantial decrements in ventilatory function (1). A subsequent paper documented that a number of the NYFD responders whose symptoms failed to resolve with time away from WTC dust exposure had airway hyperresponsiveness, consistent with irritant-induced asthma (also known as "reactive airways dysfunction syndrome") (2). In an article published in this issue of the Journal (pp. 312–319), these investigators now present strong evidence from a longitudinal analysis that exposure to WTC dust caused a decrease in ventilatory function in the first year of post–September 11 surveillance equal to that of 12 years of age-related decline (3).

The ongoing follow-up of the NYFD cohort has thus provided strong evidence for several concepts that previously were more speculative. A single, massive exposure to an irritant is not the only route to irritant-induced asthma since multiple, submassive exposures to WTC dust appear to have caused the syndrome in WTC responders (2). Such exposures now also appear to have caused accelerated decline of lung function, which suggests that this cohort is also at risk of developing chronic obstructive pulmonary disease (COPD) (3). Continued longitudinal follow-up of the cohort will be necessary to determine whether the early evidence of accelerated decline in FEV1 will indeed lead to COPD since other irritant-exposed cohorts have demonstrated excessive decline in the first postexposure year with subsequent recovery (4, 5).

Despite the power of the data generated from the medical surveillance of the NYFD responders, some limitations must be acknowledged. The responders present at the time of the collapse of the towers and while fires were still burning were exposed to smoke as well as WTC dust (6), making it difficult to disentangle the independent effect of the dust. The exposure assessment approach used to date by Prezant and colleagues allows only a crude classification of relative exposure to WTC dust that is not particularly informative about the exposure–response relationship. Improved knowledge of this relationship would allow improved assessment of risk in other occupationally and environmentally exposed groups (7, 8). Analyses of the dust suggest that the primary irritant effect was derived from its alkalinity (9), but further toxicologic investigation to better understand mechanism of injury is warranted (10).

If most of the respiratory tract injury that has been carefully documented in the NYFD cohort was due to exposure to the WTC dust in the days and weeks following the collapse of the towers, then an additional element to the tragedy of September 11 is that this occupational morbidity could have been prevented with early and well-trained use of simple respiratory protective equipment (e.g., N95 masks) (11). Let us be better prepared for future disasters in many ways, including institution of plans to protect emergency responders from unnecessary occupational exposures to irritant dusts.

FOOTNOTES

Conflict of Interest Statement: J.R.B. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

  1. Prezant DJ, Weiden M, Banauch GI, McGuinness G, Rom WN, Aldrich TK, Kelly KJ. Cough and bronchial responsiveness in firefighters at the World Trade Center site. N Engl J Med 2002;347:806–815.[Abstract/Free Full Text]
  2. Banauch GI, Alleyne D, Sanchez R, Olender K, Cohen HW, Weiden M, Kelly KJ, Prezant DJ. Persistent hyperreactivity and reactive airway dysfunction in firefighters at the World Trade Center. Am J Respir Crit Care Med 2003;168:54–62.[Abstract/Free Full Text]
  3. Banauch GI, Hall C, Weiden M, Cohen HW, Aldrich TK, Christodoulou V, Arcentales N, Kelly KJ, Prezant DJ. Pulmonary function after exposure to the World Trade Center in the New York City Fire Department. Am J Respir Crit Care Med 2006;174:312–319.[Abstract/Free Full Text]
  4. Jones RN, Hughes JM, Glindmeyer H, Weill H. Lung function after acute chlorine exposure. Am Rev Respir Dis 1986;134:1190–1195.[Medline]
  5. Abhyankar A, Bhambure N, Kamath NN. Pajankar SP, Nabar ST, Shrenivas A, Shah AC, Deshmukh SN. Six month follow-up of fourteen victims with short-term exposure to chlorine gas. J Soc Occup Med 1989;39:131–132.[Medline]
  6. Lioy PJ, Weisel CP, Millette JR, Eisenreich S, Vallero D, Offenberg J, Buckley B, Turpin B, Zhong M, Cohen MD, et al. Characterization of the dust/smoke aerosol that settled east of the World Trade Center (WTC) in lower Manhattan after the collapse of the WTC 11 September 2001. Environ Health Perspect 2002;110:703–714.[Medline]
  7. Skloot G, Goldman M, Fischler D, Goldman C, Schechter C, Levin S, Teirstein A. Respiratory symptoms and physiologic assessment of ironworkers at the World Trade Center disaster site. Chest 2004;125:1248–1255.[Abstract/Free Full Text]
  8. Reibman J, Lin S, Hwang SA, Gulati M, Bowers JA, Rogers L, Berger KI, Hoerning A, Gomez M, Fitzgerald EF. The World Trade Center residents' respiratory health study: new-onset respiratory symptoms and pulmonary function. Environ Health Perspect 2005;113:406–411.[Medline]
  9. Landrigan PJ, Lioy PJ, Thurston G. Berkowitz G, Chen LC, Chillrud SN, Gavett SH, Georgopoulos PG, Geyh AS, Levin S, Perera F, Rappaport SM, Small C; NIEHS World Trade Center Working Group. Health and environmental consequences of the world trade center disaster. Environ Health Perspect 2004;112:731–739.[Medline]
  10. Gavett SH, Haykal-Coates N, Highfill JW, Ledbetter AD, Chen LC, Cohen MD, Harkema JR, Wagner JG, Costa DL. World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice. Environ Health Perspect 2003;111:981–991.[Medline]
  11. Feldman DM, Baron SL, Bernard BP, Lushniak BD, Banauch G, Arcentales N, Kelly KJ, Prezant DJ. Symptoms, respirator use, and pulmonary function changes among New York City firefighters responding to the World Trade Center disaster. Chest 2004;125:1256–1264.[Abstract/Free Full Text]



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