Accelerated spirometric decline in New York City firefighters with α1-antitrypsin deficiency

Gisela I. Banauch, Mark Brantly, Gabriel Izbicki, Charles B. Hall, Alan Shanske, Robert Chavko, Ganesha Santhyadka, Vasilios Christodoulou, Michael D. Weiden, David J. Prezant

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

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. a 1 -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).

Original languageEnglish (US)
Pages (from-to)1116-1124
Number of pages9
JournalChest
Volume138
Issue number5
DOIs
StatePublished - Nov 1 2010

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Firefighters
Serum
Gene-Environment Interaction
Air Pollution
Protease Inhibitors
Cough
Longitudinal Studies
Cohort Studies
Lung

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Accelerated spirometric decline in New York City firefighters with α1-antitrypsin deficiency. / Banauch, Gisela I.; Brantly, Mark; Izbicki, Gabriel; Hall, Charles B.; Shanske, Alan; Chavko, Robert; Santhyadka, Ganesha; Christodoulou, Vasilios; Weiden, Michael D.; Prezant, David J.

In: Chest, Vol. 138, No. 5, 01.11.2010, p. 1116-1124.

Research output: Contribution to journalArticle

Banauch, GI, Brantly, M, Izbicki, G, Hall, CB, Shanske, A, Chavko, R, Santhyadka, G, Christodoulou, V, Weiden, MD & Prezant, DJ 2010, 'Accelerated spirometric decline in New York City firefighters with α1-antitrypsin deficiency', Chest, vol. 138, no. 5, pp. 1116-1124. https://doi.org/10.1378/chest.10-0187
Banauch, Gisela I. ; Brantly, Mark ; Izbicki, Gabriel ; Hall, Charles B. ; Shanske, Alan ; Chavko, Robert ; Santhyadka, Ganesha ; Christodoulou, Vasilios ; Weiden, Michael D. ; Prezant, David J. / Accelerated spirometric decline in New York City firefighters with α1-antitrypsin deficiency. In: Chest. 2010 ; Vol. 138, No. 5. pp. 1116-1124.
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T1 - Accelerated spirometric decline in New York City firefighters with α1-antitrypsin deficiency

AU - Banauch, Gisela I.

AU - Brantly, Mark

AU - Izbicki, Gabriel

AU - Hall, Charles B.

AU - Shanske, Alan

AU - Chavko, Robert

AU - Santhyadka, Ganesha

AU - Christodoulou, Vasilios

AU - Weiden, Michael D.

AU - Prezant, David J.

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N2 - 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. a 1 -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).

AB - 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. a 1 -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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