We have documented physical symptoms that developed after September 11, 2001 among local residents and local workers as well as in cleanup workers exposed to dust, gas, and fumes from the WTC destruction. These symptoms were present despite the passage of more than 5 years since exposure. Upper and lower respiratory symptoms including DOE, cough, and wheeze were particularly common. Despite the different ways in which WTC dust and fume exposure may have occurred, the symptoms described in each of the exposure categories we defined were strikingly similar to those that have been published for the occupationally exposed rescue and recovery workers.3–5
The symptoms also were similar to those identified in the small number of rescue and recovery workers in our program. Exposure to the dust cloud appeared to increase the risk for DOE in those with non-occupational exposures. Although mean spirometry values were normal for the population as a whole, almost one third had values below the LLN with different patterns of abnormalities. More than half of a sampled population with normal spirometry was hyperresponsive to methacholine, a rate that is higher than that that described in most studies of asymptomatic individuals.24
New-onset and persistent DOE was associated with patterns that included a reduced FVC.
We have grouped our patients by their status and potential for WTC dust, gas, and fume exposures on September 11, 2001 as a local worker, resident, cleanup worker, rescue, and recovery workers. Good exposure measurements for these groups are lacking due to the absence of systematic measurements of the airborne gases and particles, particularly during the first few days after the collapse. Exposure assessments are also limited by the few measurements of the resuspended particles, the variation in components of the substances released over the initial days and months, and differences in patterns of contact.10
Lioy et al10
have proposed a model of five types of environmental and occupational exposures. This model includes exposure to the initial pulverized building materials and jet fuel fires and the most intense period of the WTC plume emissions. This period would correspond to the “dust cloud” period and as expected, this exposure was most common in the local workers and was associated with dyspnea. Additional exposure periods include outdoor exposures from September 11, 2001 to the end of September due to the resuspension of particulate mass and the massive fires at Ground Zero. Evacuated residents and local workers returning to their homes and work, as well as cleanup workers, all had potential for exposure at this time. Over the ensuing months, the fires continued and ambient particulate matter levels were noted to be elevated on particular days. Many in our exposure categories had potential for exposure during this time as well. The last category described by Lioy et al includes indoor exposures. This is the least well characterized exposure type because of non-uniformity in contamination of buildings, differences in the amounts of dust, variations in the procedures employed to clean the dust, and variations in the contact with settled WTC dust and smoke.12
The local workers, residents, and cleanup workers all had potential for this type of exposure.
The chemical components of the toxins in the dust, gas, and fumes generated by the destruction of the WTC towers support the biologic plausibility of adverse health and particularly respiratory effects. Measurements of settled dust documented that these particles were highly alkaline (pH 11),12
and this property alone has been shown to be associated with respiratory effects. Occupational exposure to inhaled alkaline material induces chronic cough, phlegm, and dyspnea as well as upper respiratory tract symptoms.25
Exposure to alkaline dusts in a residential population has been described to produce similar symptoms.26
In vitro and animal studies of settled WTC dust also suggest toxicity.27,28
Although lower respiratory symptoms of DOE, cough, chest tightness, and wheeze were common, these symptoms can be due to a variety of mechanisms. Airway diseases, including reactive airways dysfunction and irritant-induced asthma have been proposed in the responder and firefighter populations.1,15
We and others have suggested involvement of peripheral or small airways in some patients using physiologic techniques and high resolution computerized tomography,29,30
and bronchiolitis obliterans has been described in a case report.31
Parenchymal diseases such as a sarcoid-like illnesses have also been described in firefighters. Only a small number of our patients had abnormalities consistent with obvious airway or parenchymal disease on their CXR.
Identification of lung function abnormalities may be difficult in cross-sectional studies of populations such as ours. Many of the WTC-exposed firefighters had apparently normal lung function, and only longitudinal measurements revealed a much greater than expected loss of lung function.32
Lung function can also be normal in patients with asthma in the absence of an acute exacerbation or until significant airway remodeling has occurred, and distal airway or peripheral lung disease may not be detectable with spirometry.29,30,33
Lung function can also be normal in early interstitial lung diseases. Although the mean spirometry values were normal in our population, one third had measurements below their expected values. We suspect that the symptoms in our population are due to heterogeneous mechanisms. The presence of positive methacholine challenge studies in a sampled population with normal spirometry suggests airway hyperreactivity consistent with irritant-induced asthma, in some, but not all of our patients. Some of the symptoms in the patients with normal spirometry may also be due to distal airway or peripheral lung disease, which would not be detectable with spirometry.29,30,33
The patterns of spirometry in patients with abnormal lung function also suggest heterogeneity in the disease. Those with an “obstructed” pattern had some response to bronchodilator, suggesting the presence of reversible airway disease consistent with asthma. Those with the “obstructed and low FVC” pattern had the lowest spirometry values and had improvement in both FEV1
and FVC in response to bronchodilator, raising the possibility of airway disease associated with air trapping. In contrast, those with a “low FVC” pattern had minimal improvement with bronchodilator, suggesting that this abnormality might be due to a different mechanism. Further studies are warranted for the elucidation of mechanisms of these abnormalities.
There are several potential limitations to the interpretation of our data. This was a self-referred population whose enrollment depended on the presence of any symptom and the potential for exposure to WTC dust. The prevalence and incidence of persistent symptoms that developed after September 11, 2001 remain unknown in the larger population. A recent report suggests the possibility that approximately 120,000 local residents or building occupants may have had new onset or worsening respiratory symptoms and 4100 may have newly diagnosed asthma, consistent with a 3% increase in asthma rates.34
Our data were obtained from patients who reported exposures to WTC dust, gas, or fumes and symptoms thought to be caused by these exposures and thus do not lend themselves to formal tests of association between exposure and disease or symptoms. Because of the unexpected nature of the disaster, the causal relationship between the diverse exposures WTC dust gas and fumes and the described symptoms is difficult to determine and the absence of a specific biomarker of exposure to WTC dust, the complex mixtures of the dust gas and fumes, and the diverse potential for exposures makes biologic assessment of toxicologic effects difficult.10
We have used a combination of the presence of exposure, the temporal pattern of the symptoms, and the consistency of findings to suggest a causal relationship as suggested for occupational health risk assessments.35
The association of a greater risk for DOE with exposure to the dust cloud suggests a relationship to a high intensity exposure, lending further credence to causality. We do not have preexisting medical data as many of the individuals in our program sought little or only sporadic medical care before September 11, 2001 and measurements of lung function are not performed routinely. Our measures are self-reported, and thus there is a risk of recall bias. This bias may be more likely in those with potential for secondary gain, however, few in our population were eligible for monetary reimbursement and worker’s compensation was only available to those with occupational WTC exposure. The resemblance of the symptoms in our population to those reported for the WTC rescue and recovery workers is consistent with a similar process of disease.
In sum, we have described new onset and persistent respiratory symptoms in populations with diverse potential for exposure to WTC dust, gas, and fumes including local workers and residents. The known chemical composition of the dust and fumes and the time sequence of occurrence of symptoms after the collapse of the WTC towers, makes an association between the symptoms and WTC toxicant exposure likely. The similarity of symptoms and lung function abnormalities in residents and local workers with those of cleanup and rescue and recovery workers supports this relationship. Abnormalities in spirometry suggest heterogeneity of disease. The presence of symptoms over 5 years after the event suggests a continued need for provision of services and medical surveillance, which will help clarify mechanisms of disease. The difficulties faced in determining disease causality and assessment underscore the need for rapid monitoring of health effects in all populations in the setting of potential environmental disasters.