Inhalational Diesel Exhaust Exposure in Submariners: Observational Study

Written By: Sam Savage

Published Date: August 9, 2008 Last Edited: August 9, 2008

By Duplessis, Christopher A Gumpert, Barton

ABSTRACT Objective: An observational study was performed with a convenience sample of 38 submariners exposed to diesel exhaust for 9 hours, to assess the development of reactive airways dysfunction syndrome (RADS) after prophylactic corticosteroid treatment. Methods: Twenty-four subjects were available for baseline physical examinations, pulmonary function tests, and chest radiographs, and 16 more subjects were available for interviews; 30 subjects were available for 6-month follow-up surveys. Subjects were treated on the basis of presenting symptoms; 19 subjects were treated with a 10- day course of orally administered prednisone, accompanied by 30 days of inhaled fluticasone/ salmeterol therapy. Results: There were no cases of RADS diagnosed at 6-month follow-up evaluations. Conclusion: There were no cases of RADS diagnosed at 6-month follow- up evaluations in submariners with uncontrolled, isolated, heavy diesel exhaust exposure, despite many initial symptoms that portended the diagnosis. To our knowledge, this is the largest reported case study of corticosteroid treatment initiated with an expressed intention to prevent the development of RADS after an isolated diesel exhaust exposure. Although we cannot prove that early intervention with corticosteroids prevented RADS, we think that the implementation of prompt prophylactic treatment expedited symptom resolution and might have prevented RADS development, on the basis of previous historical control data. RADS resulting from diesel exhaust may be an important public health issue, and our hope is to promote increased recognition of the diagnosis, which often is not suspected upon initial presentation but is delayed by up to several years. Increasing awareness may prompt pursuit of more- aggressive interventions with acute and protracted corticosteroid treatment and execution of the necessary controlled trials to establish treatment efficacy in mitigating the severity and/or circumventing the development of RADS. INTRODUCTION

Diesel exhaust exposure is pervasive, given the increased use of diesel power in industrial applications. Concerns have arisen regarding the potential acute and chronic health decrements, notably carcinogenic, neurobehavioral, and cardiorespiratory, resulting from exposure.1-3 Diesel fuels are long-chain hydrocarbons encompassing both aliphatic and aromatic constituents. Exhaust products include oxides of nitrogen and sulfur, volatile organic compounds, alkanes, alkenes, aldehydes (formaldehyde, acetaldehyde, and acrolein), benzene, aliphatic hydrocarbons (polycyclic aromatic hydrocarbons), carbon monoxide (CO), carbon dioxide, dioxins, and carbonaceous particulates.2,3 The particulate matter includes elemental carbon and adsorbed organic compounds, with small amounts of sulfate, nitrates, metals, and trace elements. The fine and ultra-fine particles possess diameters of

Population-based studies suggest that diesel exhaust, as a toxicologie pulmonary irritant, may provoke bronchial hyperresponsiveness, exacerbate preexisting allergies and asthma, and engender new-onset asthma.3-7 There is a paucity of data documenting the duration and severity of exposure (isolated or chronic) that may cause respiratory injury.1-10 Toxic inhalational injuries are often self-limited but may cause severe respiratory injury, bronchiolitis obliterans, pulmonary edema, asphyxia, acute respiratory distress syndrome, and death. Occasionally, irritant- induced pulmonary injury may engender reactive airways dysfunction syndrome (RADS).

RADS manifests as protracted airway disease, encompassing nonimmunologic bronchial hyper-responsiveness and airflow obstruction.10 The development of respiratory symptoms occurs shortly after isolated exposure to elevated concentrations of irritant gases, aerosols, vapors, fumes, smokes, or particles. A prolonged period of airway hyper-responsiveness then ensues, with reversible airway obstruction persisting for at least 3 months, often for years, and sometimes permanently.1,10-13 The acute exposure typically occurs in the setting of workplace accidents or situations involving poor ventilation.10 Allergic sensitization is not a prerequisite in the pathogenesis of RADS, differentiating RADS from occupational asthma (which requires a requisite sensitization period, with symptoms predictably surfacing at work). RADS does not appear to require atopic genetic predisposition for its diagnosis, in contradistinction to occupational asthma.13,14 Risk factors for the development of RADS may include premorbid pulmonary conditions and smoking.15 Finally, many cases may evolve through a conditioning phenomenon, whereby previous subthreshold exposures sensitize or potentiate development.

RADS has been noted after exposure to a myriad of inhalational irritants, including combustion products,3,8 with diesel exhaust being implicated as the seventh most common cause.1,15 Diesel- powered trucks have dominated the industry, and diesel paniculate matter now represents an appreciable proportion of the total burden of environmental airborne particulate pollutants. Diesel exhaust exposure may represent a significant public health hazard, as evidenced by recent articles documenting acute decrements in respiratory function among asthmatic individuals and increased susceptibility to coronary vascular events.4,6 Diesel exhaust injuries have been reported for various Navy diesel engines.16

Empirically administered inhaled and/or oral corticosteroid treatment is commonplace (although perhaps controversial) for initial presentations of presumed chemical pneumonias and/or bronchitis produced by various inhalational irritants. However, there is a dearth of documentation establishing treatment efficacy in ameliorating pulmonary injury. To our knowledge, no documented evidence has established the efficacy of expeditious and/or protracted administration of corticosteroids to circumvent pulmonary remodeling and RADS development.15,17-19 Early parenteral corticosteroid administration after inhalational exposures attenuated the otherwise-anticipated severity of bronchial hyper- responsiveness in animal and human models.15,17,20 One case report documented improvement in pulmonary function and mitigation of bronchial hyper-responsiveness with inhaled steroid treatment after an irritant exposure. The authors documented deterioration in pulmonary performance after cessation of steroid treatment, with improvement upon its reintroduction. That article provides some indirect evidence of the potential efficacy of inhaled steroids in mitigating the severity and/or circumventing the development of RADS.17

Ultimately, we hope to emphasize the importance of considering the diagnosis of RADS, which is often not suspected, upon initial presentation of presumed chemical pneumonitis or bronchitis. Our results, coupled with future dedicated controlled trials, may establish the efficacy of administration of acute and protracted courses of corticosteroids to circumvent the development and to minimize the severity of RADS.

INDEX CASE

A submariner presented to our medical facility ~24 hours after diesel exhaust exposure sustained during drills performed aboard a pier-side submarine (opened to the atmosphere). He complained of a persistent productive cough, wheezing, shortness of breath, chest tightness, and pain with deep inspiration; all symptoms developed several hours after commencement of drills. His physical examination was significant for diffuse end-expiratory wheezing. Laboratory results, including complete blood count, arterial blood gas analysis, and complete metabolic panel, were normal, as were electrocardiographic findings. Chest radiographic findings were normal. Pulmonary function test (PFT) results were significant for a forced expiratory volume in 1 second (FEV^sub 1^) of 2.65 L/min (58% of predicted), a forced vital capacity of 3.27 L/min (62% of predicted), and a decreased diffusion capacity for CO (50% of expected). The laboratory was unable to process a request for a carboxyhemoglobin level because of a machine malfunction. The patient was diagnosed as having chemically induced pneumonitis and was treated with a 10-day course of 40 mg of orally administered prednisone.

Subsequent interrogation regarding the patient’s occupational exposure revealed that the submarine filled with diesel exhaust while pier-side drills were being performed for ~9 hours. The events leading to this exposure involved inadvertent positioning of the air intake manifold in close proximity to the diesel exhaust; this stemmed from a failure of the hydraulic actuator to reposition the manifold.

Realizing that the entire ship’s complement was exposed and vulnerable to experiencing acute pneumonitis, bronchitis, and RADS,1 our pulmonary department communicated to the ship the importance of facilitating medical evaluations of all submariners involved. The submariners almost by consensus described this exposure as the highest concentration of diesel exhaust experienced, admitting that it is not uncommon to experience some low-level exposure during typical pier-side drilling while operating the diesel engine. We elected to prophylactically treat subjects with orally administered and/or inhaled steroids, on the basis of presenting symptoms. Appreciating this unique cohort and exposure history, we performed an observational study cataloging symptoms consistent with fume- induced pneumonitis, assessing for the development of RADS attributable to diesel exhaust after administration of prophylactic steroid treatment. METHODS

Human testing was approved by ethical review boards for the protection of human subjects at Naval Medical Center Portsmouth. Each subject provided written informed consent before participating. The setting was a U.S. fleet ballistic missile submarine performing pier-side maneuvering drills on diesel power. Forty submariners (all male; average age, 29 years; age range, 22-43 years) from the submarine who participated in the pier-side exercise were enrolled. Twentyfour subjects who expressed significant symptoms and desired examinations were available for baseline physical examinations, PFTs, and chest radiographs; 16 additional exposed submariners were interviewed (one of whom exhibited significant pulmonary symptoms warranting treatment but did not feel compelled to be examined), and 30 subjects were available for 6-month follow-up surveys. The 24 subjects examined presented within 4 days after the exposure. Medical histories were acquired in direct interviews, with verification through review of subjects’ medical records. The rest of the submariners who were attached to the submarine and who had participated in the exercise either denied symptoms or were not exposed. Given the delay in the initial interviews, invasive bronchoscopic inspection of the airways and inflammatory biomarker analyses were not undertaken (Table I).

All except four enrolled participants admitted to experiencing the maximum 9-hour exposure. Six subjects donned respiratory protection, via the emergency air breathers (EABs) installed throughout the ship, for variable time periods.

PFTs were conducted in accordance with guidelines for acceptability and reproducibility from the American Thoracic Society.9 A FEV^sub 1^/forced vital capacity ratio of

Subjects were treated on the basis of the severity of presenting symptoms; 19 subjects were treated with a 10-day course of orally administered prednisone with concomitant inhaled steroid therapy (250 [mu]g fluticasone/50 [mu]g salmeterol) for 15 to 30 days, and six subjects received 2 weeks of treatment with inhaled corticosteroid (fluticasone) alone. Severity was based on identification of significant decrements in PFT findings, persistent symptoms at presentation, or significant examination findings, all warranting oral steroid therapy.

RESULTS

Significant medical histories included one subject with a history of pneumonia, one with mitral valve prolapse, and one with reflux disease, two subjects treated for hypertension, and four subjects intermittently treated for allergic rhinitis (with one subject admitting to symptoms before the exposure). Twelve subjects reported current tobacco use. Notably, 10 of the 12 smokers were represented among the initial 24 subjects who presented with appreciable symptoms and were available for baseline PFTs. Physical examinations identified two subjects manifesting acute wheezing.

The symptoms reported within the initial 24 hours after exposure are presented in Table II. Four subjects exhibited obstructive findings in PFTs. With the use of 80% of the reference value as the standard, seven subjects exhibited decrements in diffusion capacity for CO. There were no identifiable abnormalities on chest radiographs (Table III).

Of the four subjects who exhibited reduced FEV^sub 1^, one was a smoker. Five of seven subjects who exhibited decrements in diffusion capacity for CO were smokers. None of the subjects who used EABs manifested decrements on PFTs. In 6-month follow-up evaluations, the 30 interviews retrieved revealed that all symptoms had abated except for two subjects who exhibited continued, intermittent, mild dyspnea, one subject who admitted lightheadedness, and one subject who was experiencing continued nasal congestion. We have no reports of symptoms attributable to the incident among those who did not participate in the study. The two subjects with persistent mild dyspnea exhibited normal methacholine challenge test results. To date, no subjects have developed RADS.

DISCUSSION

Because of the prolonged periods within the confined, closed, recirculated atmosphere of a submarine, attention must be directed vigilantly toward atmospheric purity. The toxic diesel exhaust exposure might have exposed the submariners to CO poisoning.21 Submarines are equipped with H2CO burners to scavenge CO produced while the submarine is underway. Submarines use centralized atmospheric monitoring systems that monitor CO levels, emitting alarms if threshold limit values (TLVs) are exceeded. Unfortunately, the system was inoperable, given pier-side operations, and CO levels were unavailable. Neither trace gas analysis nor Draeger tube monitoring of select contaminants was available. Fortunately, no submariner experienced loss of consciousness or neurologic deficits. Prompt treatment with 100% normobaric oxygen or hyperbaric oxygen may avert potential morbidity, cognitive deficits, and neuropsychologic sequelae resulting from significant CO exposure.21 No subjects presented with significant rhinitis warranting nasal steroid treatment, indicating the existence of a reactive upper airways dysfunction syndrome.

Clinical manifestations of acute irritant exposures that may lead to RADS include the onset of a burning sensation in the eyes, nose, throat, and lungs, dyspnea, pleuritic chest pain, coughing, wheezing, hemoptysis, rhinitis, dizziness, headache, and nausea.1,10,22,23 Symptoms occur acutely, within 24 hours (often within minutes), without an accompanying latency period after the exposure (as differentiated from occupational asthma), and persist for at least several months when leading to RADS.14

The pathogenesis of RADS involves an isolated respiratory insult that produces respiratory epithelial injury and mucosal damage (loss of epithelial integrity, desquamation, and denudation).15 Most patients recover from a toxic insult with normalized pulmonary function. In patients predisposed to RADS, there is an exaggerated epithelial injury, with derangement of the healing process. Recovery is accompanied by a chronic, nonspecific, airway inflammatory response, architectural changes, airway remodeling, and activation of neuronal reflexes, in a self-sustaining perpetual inflammatory cascade.10,14,24 The bronchial mucosal reepithelialization and reinnervation after the pulmonary inflammatory injury may alter the threshold of the subepithelial irritant receptors, rendering them hyper-reactive to reexposure to the inciting insult, as well as other subsequent irritants (e.g., cold, exercise, dusts, and various fumes and vapors).1,10,15 The increased airway hyper-reactivity is not specific to RADS but has been identified after various pathologic pulmonary injuries, including adult respiratory distress syndrome and pulmonary infections, resulting from the pulmonary inflammatory process. Patients with RADS may exhibit less airway reversibility than patients with asthma (occupational asthma), which supports the distinct airway remodeling and pathophysiologic injury inflicted in this disease.24

RADS diagnosis is formally defined according to the American College of Chest Physician consensus statement as (1) documented absence of preceding respiratory complaints; (2) onset of symptoms after an isolated exposure; (3) identification of the exposure as a gas, smoke, fume, or vapor present in high concentrations, with inherent irritant qualities; (4) symptom onset within 24 hours and persistence for at least 3 months; (5) symptoms simulating asthma (cough, wheezing, and dyspnea); (6) PFTs demonstrating airflow obstruction or nonspecific bronchial hyper-responsiveness (positive methacholine challenge test results); and (7) exclusion of alternative 0 diagnoses.10,15 RADS treatment is primarily supportive, with the use of bronchodilators and possibly inhaled anticholinergic agents and inhaled and/or orally administered corticosteroids.15

Presently, there is no permissible exposure limit promulgated by the Occupational Safety and Health Administration for diesel exhaust as a unique hazard. However, there are permissible exposure limits imposed upon many of its constituents (both gaseous and paniculate fractions) that are known to contribute to the respirable occupational and environmental pollutant burden. There are no imposed limitations on diesel exhaust paniculate matter, which may constitute 6% to 10% of total paniculate matter; however, it is limited indirectly via the limitations on total environmental paniculate matter established by the National Ambient Air Quality Standard designated by the Environmental Protection Agency.3,25

As stated above, there is a paucity of literature investigating the potential efficacy of prompt and/or protracted prophylactic corticosteroid treatment in circumventing RADS development resulting from inhalational irritants. Although we cannot prove that early intervention with corticosteroids prevented RADS, we think that the prompt prophylactic treatment might have expedited symptom resolution and prevented RADS, on the basis of previous historical control data. This assertion stems from documentation of a duration of diesel exhaust exposure similar to that experienced by our cohort (with the acknowledgment this is merely a surrogate for the concentration and total amount of exposure), which ultimately yielded the diagnosis of RADS.1 Unfortunately, this investigation, like most such publications, can only infer the total composite exposure on the basis of surrogate measures such as the total duration of exposure, given the absence of concentration measurements during the acute, isolated, unanticipated exposure. This assertion is offered with the acknowledgment that specific subjects who develop RADS after an isolated exposure might have experienced numerous previous subclinical exposures, which might have conditioned them (although this is only speculative). Although it was not statistically significant, the qualitative observation that more smokers were represented in the cohort that sought early treatment and manifested significant decrements in PFT results is noteworthy; it suggests smoking as a risk factor for the acute development of respiratory symptoms resulting from nonspecific environmental insults, which is likely attributable to reduced pulmonary reserve and the presence of baseline, nonspecific, bronchial hyper-reactivity.10 This assertion is consistent with documentation that premorbid pulmonary pathologic conditions and smoking may be risk factors for the development of RADS.15

We hope to emphasize the importance of education and training to prevent future incidences and to optimize treatment. We specifically wish to eliminate delays in treatment or transfer to higher-echelon medical care, where potentially efficacious therapies can be administered. We advocate training of medical support personnel to remain vigilant in recognizing scenarios that place shipmates at risk for inhalational incidents and to execute strategies to prevent such situations. Practical measures suggested include real-time monitoring of the submarine atmosphere for carbon dioxide, CO, and nitrogen oxides by using Draeger tubes or portable gas analyzers, continued development of particulate monitors, and implementation of such monitors when the submarine is operating on the diesel engine, particularly when the centralized atmospheric monitoring system is nonfunctional. Suggested policy implementations include (1) administrative controls yielding regulations in work practices to minimize deleterious exposures, including the establishment of 8- hour TLVs for nitrogen oxides and other diesel exhaust constituents, with alarms when TLVs are exceeded that mandate punctual donning of respiratory protection (EABs); (2) engineering controls, including measures to eliminate the risk of diesel exhaust entry into the submarine compartment and institution of filtering units to decrease levels of particulate and volatile organic materials1,13; and (3) education in personal protective controls (training to recognize the acrid odor or visual haze suggesting excessive atmospheric diesel exhaust and necessitating personal isolation or donning of an EAB).

Finally, we advocate acute administration of inhaled and/or orally administered corticosteroids, potentially coupled with inhaled bronchodilator therapy and anticholinergic treatment, with 100% normobaric oxygen therapy (to treat concomitant CO exposure) during transfer to higher-echelon medical care, until definitive, evidence-based studies become available. We hope to promote vigilance in identifying opportunities to perform controlled studies investigating the utility of inhaled and/or orally administered corticosteroids in mitigating pulmonary symptoms and decreasing the severity and incidence of RADS after significant respiratory exposures. With the acknowledgment that most cases of acute, chemically induced pneumonitis/bronchitis would be treated with corticosteroids, investigations may be predicated predominantly on pursuing the utility of protracted courses in expediting symptom resolution and preventing RADS development. Future investigations may identify the exposures, clinical manifestations, biomarkers, genetic polymorphisms, PFT results, and comorbidities that predict subsequent development of RADS and may identify potential chemoprotectants to mitigate its severity, to expedite its resolution, and to circumvent its development.26,27

CONCLUSIONS

There were no cases of RADS diagnosed at 6-month follow-up evaluations among submariners with uncontrolled, isolated, heavy diesel exhaust exposure, despite the manifestation of many initial symptoms that portended the diagnosis. To our knowledge, this is the largest reported case study of corticosteroid treatment initiated with the expressed intention to prevent the development of RADS after an isolated diesel exhaust exposure. Although we cannot prove that early intervention with corticosteroids prevented RADS, we think that the implementation of prompt prophylactic treatment expedited symptom resolution and might have prevented the development of RADS, on the basis of previous historical control data. RADS resulting from diesel exhaust may be an important public health issue, and our hope is to promote increased recognition of the diagnosis, which often is not suspected upon initial presentation but is delayed by up to several years. Increasing awareness may prompt pursuit of more-aggressive interventions with acute and protracted corticosteroid treatment and execution of the necessary controlled trials to establish treatment efficacy in mitigating the severity and/or circumventing the development of RADS.

Naval Medical Center Portsmouth, 620 John Paul Jones Circle, Portsmouth, VA 23708-2197.

This manuscript was received for review in August 2007. The revised manuscript was accepted for publication in March 2008.

REFERENCES

1. Wade JF III, Newman LS: Diesel asthma reactive airways disease following overexposure to locomotive exhaust. ACOEM 1993; 35: 149- 54.

2. Nordholm AF, Ritchie GD, Malcolm WJ, et al: Repeated exposure of rats to JP-4 vapor induces changes in neurobehavioral capacity and 5-HT/5-HIAA levels. J Toxicol Environ Health 1999; 56: 471-99.

3. U.S. Environmental Protection Agency: Health Assessment Document for Diesel Engine Exhaust. Washington, DC, Environmental Protection Agency, 2002. Available from National Technical Information Service, Springfield, VA and http://www.cpa.gov/ncea.

4. McCreanor J, Cullinan P, Nieuwenhuijsen MJ, et al: Respiratory effects of exposure to diesel traffic in persons with asthma. N Engl J Med 2007; 357: 2348-58.

5. Wichmann HE: Diesel exhaust particles. Inhal Toxicol 2007; 19(Suppl 1): 241-4.

6. Mills NL, Tornqvist H, Gonzales MC, et al: Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease. N Engl J Med 2007; 357: 1075-82.

7. Riedl M, Diaz-Sanchez D: Biology of diesel exhaust effects on respiratory function. J Allergy Clin Immunol 2005; 115: 221-8.

8. Sallie B, McDonald C: Inhalation accidents reported to the Sword Surveillance Project 1990-1993. Ann Occup Hyg 1996; 40: 211- 21.

9. American Thoracic Society: Single-breath carbon monoxide diffusing capacity (transfer factor): recommendations for a standard technique: 1995 update. Am J Respir Crit Care Med 1995; 152: 2185- 98.

10. Brooks SM, Weiss MA, Bernstein IL: Reactive airways dysfunction syndrome (RADS): persistent asthma syndrome after high level irritant exposures. Chest 1985; 88: 376-83.

11. Bherer L, Cushman R, Courteau JP, et al: Survey of construction workers repeatedly exposed to chlorine over a three to six month period in a pulpmill, part II: follow up of affected workers by questionnaire, spirometry, and assessments of bronchial responsiveness 18 to 24 months after exposure ended. Occup Environ Med 1994; 51: 225.

12. Emad A, Rezaian GR: The diversity of the effects of sulfur mustard gas inhalation on respiratory system after a single, heavy exposure: analysis of 197 cases. Chest 1997; 112: 734-8.

13. Henneberger PK, Derk SJ, Davis L, et al: Work-related reactive airways dysfunction syndrome cases from surveillance in selected U.S. states. J Occup Environ Med 2003; 45: 360-8.

14. Tilles SA, Jerath-Tatum A: Differential diagnosis of occupational asthma. Immunol Allergy Clin North Am 2003; 23: 167- 76.

15. Alberts WM, do Pico GA: Reactive airways dysfunction syndrome. Chest 1996; 109: 1618-26.

16. Slavin DE: A Longitudinal Study of Lung Function and Symptoms of 34 Royal Navy Submariners Exposed to Diesel Exhaust Fumes. Faculty of Occupational Medicine of the Royal College of Physicians, Doctoral Dissertation, London, U.K., 1998.

17. Lemiere C: Reactive airways dysfunction syndrome due to chlorine: sequential bronchial biopsies and functional assessment. Eur Respir J 1997; 10: 241-4.

18. Lemiere C, MaIo JL, Boulet LP, Beutet M: Reactive airways dysfunction syndrome induced by exposure to a mixture containing isocyanate: functional and histopathologic behavior. Allergy 1996; 51: 262-5.

19. do Pico GA: Toxic gas inhalation. Curr Opin PuIm Med 1995; 1:102-8.

20. Demnati R, Fraser R, Martin JG: Effects of dexamethasone on functional and pathological changes in rat bronchi caused by high acute exposure to chlorine. Toxicol Sci 1998; 45: 242.

21. Weaver LK, Hopkins RO, Chan KJ, et al: Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002; 347: 1057-67.

22. Cullinan P, Acquula S, Dhara VR: Respiratory morbidity 10 years after the Union Carbide gas leak at Bhopal: a cross sectional survey. BMJ 1997; 314: 338.

23. Meggs WJ: RADS and RUDS: the toxic induction of asthma and rhinitis. J Toxicol Clin Toxicol 1994; 32: 487-501.

24. Gautrin D, Boulet LP, Boulet M, et al: Is reactive airways dysfunction syndrome (RADS) a variant of occupational asthma? J Allergy Clin Immunol 1994; 93: 12.

25. Environmental Protection Agency, Integrated Risk Information System: Diesel engine exhaust. Available at http://www.epa.gov/iris/ subst/ 0642.htm; accessed March 2007.

26. Bobb AJ, Jederberg WW: JV-Acetylcysteine as a Provisional, Commercial Off-the-Shelf (COTS) Chemoprotectant against Sulfur Mustard. Publication NHRC/TD TOXDET-03-01. San Diego, CA, Naval Health Research Center Detachment, 2003.

27. Banauch GI, Dhala A, Alleyne D, et al: Bronchial hyperreacctivity and other inhalation lung injuries in rescue/ recovery workers after the World Trade Center collapse. Crit Care Med 2005; 33(Suppl): S102-6. LCDR Christopher A. Duplessis, USN; CAPT Barton Gumpert, USN

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