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Original Research: COPD |

Accelerated Spirometric Decline in New York City Firefighters With α1-Antitrypsin Deficiency

Gisela I. Banauch, MD; Mark Brantly, MD; Gabriel Izbicki, MD; Charles Hall, PhD; Alan Shanske, MD; Robert Chavko, MD; Ganesha Santhyadka, MD; Vasilios Christodoulou; Michael D. Weiden, MD; David J. Prezant, MD, FCCP
Author and Funding Information

From the Pulmonary Division (Drs Banauch, Hall, Chavko, Santhyadka, and Prezant and Lt Christodoulou), Department of Medicine, and the Department of Pediatrics (Dr Shankse) Montefiore Medical Center, and Biostatistics Division, Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY; Pulmonary and Critical Care Division (Dr Brantly), Department of Medicine, University of Florida School of Medicine, Gainesville, FL; Pulmonary Institute (Dr Izbicki), Shaare Zedek Medical Center and the Hebrew University-Hadassah Medical School, Jerusalem, Israel; Division of Pulmonary and Critical Care Medicine (Dr Weiden), New York University School of Medicine, New York, NY; and Bureau of Health Services (Dr Prezant), New York City Fire Department, Brooklyn, NY.

Correspondence to: Gisela I. Banauch, MD, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Room S6-842, University of Massachusetts Memorial Hospital Center, 55 Lake Ave N, Worcester, MA 01655; e-mail: banauchg@ummhc.org


Funding/Support: Dr Banauch received funding from the National Center for Research Resources (5K12RR017672). Dr Brantly received support from the Alpha-1 Foundation. Dr Izbicki was supported by the Jesselon Einstein-Shaare Zedeck Fellowship Program. Dr. Hall received salary support from the National Institute of Occupational Safety and Health through the New York City Fire Department and Montefiore Medical Center. Dr Weiden received funding from the National Institutes of Health [Grants M01 00096, K23HL084191, K24A1080298, and R01HL057879]. Dr Prezant (principal investigator) received funding from the Centers for Disease Control and Prevention [U1Q/CCU221158] and the National Institute of Occupational Safety and Health [U10-OH008243 and U10-OH008242].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(5):1116-1124. doi:10.1378/chest.10-0187
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Background:  On September 11, 2001, the World Trade Center (WTC) collapse caused massive air pollution, producing variable amounts of lung function reduction in the New York City Fire Department (FDNY) rescue workforce. α1-Antitrypsin (AAT) deficiency is a risk factor for obstructive airway disease.

Methods:  This prospective, longitudinal cohort study of the first 4 years post-September 11, 2001, investigated the influence of AAT deficiency on adjusted longitudinal spirometric change (FEV1) in 90 FDNY rescue workers with WTC exposure. Workers with protease inhibitor (Pi) Z heterozygosity were considered moderately AAT deficient. PiS homozygosity or PiS heterozygosity without concomitant PiZ heterozygosity was considered mild deficiency, and PiM homozygosity was considered normal. Alternately, workers had low AAT levels if serum AAT was ≤ 20 μmol/L.

Results:  In addition to normal aging-related decline (37 mL/y), significant FEV1 decline accelerations developed with increasing AAT deficiency severity (110 mL/y for moderate and 32 mL/y for mild) or with low AAT serum levels (49 mL/y). Spirometric rates pre-September 11, 2001, did not show accelerations with AAT deficiency. Among workers with low AAT levels, cough persisted in a significant number of participants at 4 years post-September 11, 2001.

Conclusions:  FDNY rescue workers with AAT deficiency had significant spirometric decline accelerations and persistent airway symptoms during the first 4 years after WTC exposure, representing a novel gene-by-environment interaction. Clinically meaningful decline acceleration occurred even with the mild serum AAT level reductions associated with PiS heterozygosity (without concomitant PiZ heterozygosity).

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