© 2002 American Thoracic Society
A New York City FirefighterOverwhelmed by World Trade Center DustDepartment of Environmental Medicine University of Rochester School of Medicine and Dentistry Rochester, New York Terrible disasters sometimes jolt medical thinking forward. When a 1929 hospital fire caused 97 deaths from smoke inhalation, investigators learned that combustion products of synthetic materials (in this case, nitrocellulose X-ray film) produced nitrogenous gases in swiftly fatal concentrations—pointing the way to the addition of military gas masks to firefighters' safety equipment (1). Clinical observations of surviving families of the victims of another terrible fire formed our modern understanding of the natural history and management of acute grief reactions (2). Protracted dust storms of wind-blown soil in the Dust Bowl states of the 1930s caused the acute illness and death of previously healthy adults and children from dust pneumonia, an entity still incompletely characterized. More recently, the clustering of 34 deaths and 182 cases of pneumonia in a convention hotel spurred the identification of Legionella pneumophila (3), while the release of a pesticide intermediary reagent, methyl isocyanate, demonstrated to the world the fearsome hazards of juxtaposing industrial facilities with densely populated areas (4). History is full of such painful discoveries in the wake of terrible events. In this issue of AJRCCM (pp. 797–800), Rom and colleagues (5) describe a patient, one of thousands of firefighters, rescue workers, ironworkers, and others intensely exposed to dust and smoke shortly after the collapse of the World Trade Center towers in New York. This firefighter was intensely exposed over 13 long days of rescue and recovery work. When he developed fever, pulmonary infiltrates, and hypoxemia, his physicians treated him with standard antimicrobials and corticosteroids, but also investigated his illness by bronchoalveolar lavage, cell surface marker typing, and analysis of retained dust. Their finding of an eosinophilic alveolitis in the absence of infection, and a gratifying response to corticosteroids, met criteria for acute eosinophilic pneumonia, a condition recognized only in the last 15 years and of uncertain etiopathogenesis. The authors point out that five other World Trade Center firefighters were treated under similar circumstances, but without the bronchoalveolar lavage that could distinguish them as having eosinophilic pneumonitis. It is common for firefighters with smoke inhalation to be hospitalized with acute pulmonary infiltrates, to be treated with antibiotics and corticosteroids, and to make a good recovery—raising the question of how many firefighters over the centuries may have suffered from a similar condition. Yet it is difficult to guess whether this firefighter's illness may have resulted solely from a prolonged and intense exposure, or whether some other inherited or acquired susceptibility made him more vulnerable than others similarly exposed. Cases of acute eosinophilic pneumonia were described in 1989 by two groups that distinguished it from chronic eosinophilic pneumonia as described by Liebow and Carrington (6). But why should acute and sometimes severe alveolar infiltrates occur in previously healthy, nonallergic adults? Allen and colleagues did not believe it likely that recent environmental exposures triggered the acute pneumonias, citing the fact that return to work in the previous environment did not lead to relapse (7). Badesch and colleagues wondered whether their patient suffered from a hypersensitivity reaction to some component of inhaled, rural Colorado soil, which would imply an amplified anamnestic response to rechallenge with environmental antigens (8). Since then, many additional case reports and small case series have been published, some hypothesizing links of this entity to prescription drug reactions, smoking or resumption of smoking, inhaled heroin, acetylene, smoke from fireworks, or scouring powder. Rom and colleagues, in their detailed analysis of the foreign material recovered from the bronchi and alveoli of this firefighter, focus on the presence of asbestos as a component of the dust created by the collapse of the World Trade Center tower. For firefighters and demolition workers, asbestos exposure remains a hazard in the ruins of asbestos-laden structures. Good work practices dictate that water should be sprayed over the rubble during building demolition to keep levels of asbestos and other dusts down—a practice that was not feasible in this instance. Analyses of dust from the World Trade Center site found predominantly coarse particles of cement and gypsum with an extremely alkaline pH, thus making the dust potentially very irritating to the respiratory system. Those working on "the pile" at ground zero were heavily exposed both to dust and the pyrolysis products of the collapsed buildings, and residents of neighborhoods adjacent to the site have raised many questions about community exposure in the days that followed. An impressive number of follow-up studies, both for rescue workers and neighborhood residents, are now in progress, and will make it possible to assess any long-term effects of these exposures. One aspect of this firefighter's occupational history is quite typical of new-onset occupational lung disease—an unusually intense work schedule, with much overtime just before the onset of his illness. Starting on September 11, efforts were made to provide respiratory protective devices ("mask" respirators) to all rescue, recovery, and building trade crews. These respirators are the engineering descendants of the gas masks used in the trenches of World War I to protect against chlorine, mustard, and nerve warfare gases, and later adapted for firefighting and industrial use. Observers in New York have noted that, even after sufficient protective devices became available, many experienced rescuers did not use them consistently, foregoing their own safety in the effort to work more effectively. Long experience and considerable research have demonstrated that most users find the discomfort of such masks difficult to tolerate for more than brief periods of use (9, 10). The individual respirator, like the seat belt, is effective only when actively used. Passive engineering control of the air quality for a large work area is a much superior method for preventing inhalation exposures in most work places. Yet in the case of uncontrolled emergencies such as this one, there will always be a need for an effective means to protect the individual's lungs. Perhaps this disaster can spur engineers and materials scientists to find new ways to protect the lungs of those who risk their lives to save others. REFERENCES
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