期刊
CHEST
卷 138, 期 5, 页码 1116-1124出版社
ELSEVIER
DOI: 10.1378/chest.10-0187
关键词
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资金
- National Center for Research Resources [5K12RR017672]
- Alpha-1 Foundation
- Jesselon Einstein-Shaare Zedeck Fellowship Program
- National Institute of Occupational Safety and Health through the New York City Fire Department and Montefiore Medical Center
- National Institutes of Health [M01 00096, K23HL084191, K24A1080298, R01HL057879]
- Centers for Disease Control and Prevention [U1Q/CCU2211581]
- National Institute of Occupational Safety and Health [U10-OH008243, U10-OH008242]
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. alpha(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 mu mol/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). CHEST 2010; 138(5):1116-1124
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