title: Accelerated spirometric decline in New York City firefighters with α₁-antitrypsin deficiency.
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. 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 FEV(1) 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).
authors.affiliation: Division of Pulmonary, Department of Medicine, Montefiore Medical Center, Bronx, NY, USA. banauchg@ummhc.org
authors.forename: Gisela I
authors.initials: GI
authors.lastname: Banauch
authors.forename: Mark
authors.initials: M
authors.lastname: Brantly
authors.forename: Gabriel
authors.initials: G
authors.lastname: Izbicki
authors.forename: Charles
authors.initials: C
authors.lastname: Hall
authors.forename: Alan
authors.initials: A
authors.lastname: Shanske
authors.forename: Robert
authors.initials: R
authors.lastname: Chavko
authors.forename: Ganesha
authors.initials: G
authors.lastname: Santhyadka
authors.forename: Vasilios
authors.initials: V
authors.lastname: Christodoulou
authors.forename: Michael D
authors.initials: MD
authors.lastname: Weiden
authors.forename: David J
authors.initials: DJ
authors.lastname: Prezant
mesh_terms: D000328:Adult; D018450:Disease Progression; D005260:Female; D005390:Fires; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume / Q000502:physiology*; D006801:Humans; D008297:Male; D009519:New York City; D009784:Occupational Diseases / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D016273:Occupational Exposure / Q000009:adverse effects*; D011446:Prospective Studies; D018635:Rescue Work; D047851:September 11 Terrorist Attacks; D015208:Smoke Inhalation Injury / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D013147:Spirometry / Q000379:methods; D000078329:Workforce; D019896:alpha 1-Antitrypsin Deficiency / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*