© 2003 American Thoracic Society
Reactive Fallout of World Trade Center DustLaboratory of Pneumology Katholicke Universiteit Leuven Leuven, Belgium The collapse of the World Trade Center (WTC) of New York City after the attack on September 11, 2001 constituted a major acute environmental disaster (1, 2). In this issue of AJRCCM (pp. 54–62), Banauch and coworkers (3) describe a prospective study of firefighters and other rescue workers of the Fire Department of New York City (FDNY), who were exposed to dust and smoke in the hours and days after the collapse of the buildings. Their main purpose was to assess how many subjects would develop symptomatic persistent bronchial hyperresponsiveness. Such asthma that is acquired after acute inhalation injury is known as "reactive airways dysfunction syndrome" (RADS) (4), a term that has gained wide acceptance, mainly because of its acronym rather than because of its actual meaning (5). The 151 rescue workers studied by Banauch and coworkers (3) were classified into a highly exposed group (arrival on site within 2 hours of the collapse of the buildings) and a moderately exposed group (arriving later that day or the next day). They underwent spirometry and a methacholine challenge at 1, 3, and 6 months. The main practical outcome of the study was that 20% of highly exposed and 8% of moderately exposed subjects qualified for the diagnosis of RADS at 6 months. Are such high figures credible? In my opinion, yes. The protocol of the study, the performance of the tests, and the analysis of the data, as they are presented, approach the best that could be achieved given the circumstances. Of course, no study is perfect and the findings will need replication and verification in some way or other. In fact, these figures could even be regarded as minimum estimates because participants were selected, by design, toward the healthier portion of the population. Current smokers and subjects with self-reported allergy were excluded, as were those taking asthma medication. We do not know the actual levels of exposure of the FDNY workers during the first few days, when levels were highest and presumably most relevant. Nevertheless, if one assumes, for the sake of simplicity, a 10-fold difference between the high and moderate exposure, then it can be calculated, on the basis of conventional dose–response relationships (expressing response in probit units against the logarithm of dose), that an exposure 10 times lower than the moderate exposure could result in RADS in 2% of the exposed population. The incidence is likely to be higher among people, such as community residents or other workers, having greater susceptibility than firefighters who likely represent a healthier than average population. Given the existence of a background prevalence of a few percent with bronchial hyperresponsiveness in the general population, however, it would be extremely difficult to attribute causality with any certainty. This brings me to the problem of the medicolegal recognition of RADS in individual victims of inhalation injury. In relatively easy cases, such as here in the nonsmoking FDNY firefighters who did not have atopy and who benefited from medical surveillance that included spirometry, it would take a very unwilling expert to deny a diagnosis of RADS on the grounds that there is no proof of the absence of bronchial hyperresponsiveness before the injury. In practice, however, we are often faced with more difficult cases, such as the isolated smoker or the subject with atopy—possibly an immigrant day laborer (6)—claiming that he became asthmatic and can no longer work, engage in sports, or play saxophone because he performed a very dirty job as an industrial cleaner or a demolition worker for a few days or weeks but without any major identifiable inhalation injury. One of the important contributions of the paper by Banauch and coworkers (3) is the demonstration that, contrary to what is often implied (7, 8), RADS does not require a clinically severe inhalation injury necessitating medical care, let alone hospitalization. This notion was already present in the few other cohort studies on RADS (9, 10). Another novel aspect of this article is also that RADS may be an outcome of injury by particulates. Experimental studies should determine which chemical constituents and/or physical characteristics of this complex aerosol are critical in causing acute and chronic injury. Further research should be done to find out why some people develop persistent bronchial hyperresponsiveness after injury, whereas the majority do not. Therapeutic issues also need to be addressed, particularly the value of inhaled glucocorticoids. RADS is not the sole respiratory aftershock of the WTC disaster. The same group of researchers reported that 3% of FDNY workers developed "WTC cough" (11), defined as "persistent cough that ... was accompanied by respiratory symptoms severe enough for FDNY physicians to place the worker on medical leave for at least four consecutive weeks." Interestingly, WTC cough was also accompanied by symptoms of gastroesophageal reflux in almost all subjects. Although there was a relation between WTC cough and RADS, the overlap between both entities is not perfect, in that only half of those with WTC cough also qualified for RADS. The authors also described a rarer condition, namely acute eosinophilic pneumonitis, in one, and possibly five other rescue workers (12, 13). The exposure of the FDNY firefighters was unusual mainly because of the dramatic context and the scale of the disaster and perhaps not so much because of the type of exposure sustained. Thus, workers doing similar dirty jobs, in similarly intense work schedules and without adequate respiratory protection, conceivably are also at risk of developing disabling cough, asthma, acute eosinophilic pneumonia, granulomatous pneumonitis (14) and, why not, "idiopathic" lung fibrosis, without being involved in an epidemiologic survey. On a more global scale it is worth pointing out that many disaster victims will not be so "lucky," such as the thousands (how many?) of victims of the gas leak in Bhopal (5) or firefighters (15) and other direct and collateral victims of fires and building destructions caused by war. Although after 9/11 health research should be encouraged, one cannot but believe that this is yet another manifestation of the lack of equity in respiratory health research (16). REFERENCES
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