Kenneth I Berger1, Joan Reibman2, Beno W Oppenheimer3, Ioannis Vlahos4, Denise Harrison5, Roberta M Goldring6. 1. André Cournand Pulmonary Physiology Laboratory, New York University School of Medicine, New York, NY; World Trade Center Environmental Health Center, Bellevue Hospital, New York University School of Medicine, New York, NY; Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY. Electronic address: kenneth.berger@nyumc.org. 2. World Trade Center Environmental Health Center, Bellevue Hospital, New York University School of Medicine, New York, NY; Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY. 3. André Cournand Pulmonary Physiology Laboratory, New York University School of Medicine, New York, NY; Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY. 4. Department of Radiology, St. George's Healthcare National Health Service Trust, London, England. 5. Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY; New York University World Trade Center Health Program Clinical Center of Excellence, New York, NY. 6. André Cournand Pulmonary Physiology Laboratory, New York University School of Medicine, New York, NY; World Trade Center Environmental Health Center, Bellevue Hospital, New York University School of Medicine, New York, NY; Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, NY.
Abstract
BACKGROUND: The present study (1) characterizes a physiologic phenotype of restrictive dysfunction due to airway injury and (2) compares this phenotype to the phenotype of interstitial lung disease (ILD). METHODS: This is a retrospective study of 54 persistently symptomatic subjects following World Trade Center (WTC) dust exposure. Inclusion criteria were reduced vital capacity (VC), FEV1/VC>77%, and normal chest roentgenogram. Measurements included spirometry, plethysmography, diffusing capacity of lung for carbon monoxide (Dlco), impulse oscillometry (IOS), inspiratory/expiratory CT scan, and lung compliance (n=16). RESULTS: VC was reduced (46% to 83% predicted) because of the reduction of expiratory reserve volume (43%±26% predicted) with preservation of inspiratory capacity (IC) (85%±16% predicted). Total lung capacity (TLC) was reduced, confirming restriction (73%±8% predicted); however, elevated residual volume to TLC ratio (0.35±0.08) suggested air trapping (AT). Dlco was reduced (78%±15% predicted) with elevated Dlco/alveolar volume (5.3±0.8 [mL/mm Hg/min]/L). IOS demonstrated abnormalities in resistance and/or reactance in 50 of 54 subjects. CT scan demonstrated bronchial wall thickening and/or AT in 40 of 54 subjects; parenchymal disease was not evident in any subject. Specific compliance at functional residual capacity (FRC) (0.07±0.02 [L/cm H2O]/L) and recoil pressure (Pel) at TLC (27±7 cm H2O) were normal. In contrast to patients with ILD, lung expansion was not limited, since IC, Pel, and inspiratory muscle pressure were normal. Reduced TLC was attributable to reduced FRC, compatible with airway closure in the tidal range. CONCLUSIONS: This study describes a distinct physiologic phenotype of restriction due to airway dysfunction. This pattern was observed following WTC dust exposure, has been reported in other clinical settings (eg, asthma), and should be incorporated into the definition of restrictive dysfunction.
BACKGROUND: The present study (1) characterizes a physiologic phenotype of restrictive dysfunction due to airway injury and (2) compares this phenotype to the phenotype of interstitial lung disease (ILD). METHODS: This is a retrospective study of 54 persistently symptomatic subjects following World Trade Center (WTC) dust exposure. Inclusion criteria were reduced vital capacity (VC), FEV1/VC>77%, and normal chest roentgenogram. Measurements included spirometry, plethysmography, diffusing capacity of lung for carbon monoxide (Dlco), impulse oscillometry (IOS), inspiratory/expiratory CT scan, and lung compliance (n=16). RESULTS: VC was reduced (46% to 83% predicted) because of the reduction of expiratory reserve volume (43%±26% predicted) with preservation of inspiratory capacity (IC) (85%±16% predicted). Total lung capacity (TLC) was reduced, confirming restriction (73%±8% predicted); however, elevated residual volume to TLC ratio (0.35±0.08) suggested air trapping (AT). Dlco was reduced (78%±15% predicted) with elevated Dlco/alveolar volume (5.3±0.8 [mL/mm Hg/min]/L). IOS demonstrated abnormalities in resistance and/or reactance in 50 of 54 subjects. CT scan demonstrated bronchial wall thickening and/or AT in 40 of 54 subjects; parenchymal disease was not evident in any subject. Specific compliance at functional residual capacity (FRC) (0.07±0.02 [L/cm H2O]/L) and recoil pressure (Pel) at TLC (27±7 cm H2O) were normal. In contrast to patients with ILD, lung expansion was not limited, since IC, Pel, and inspiratory muscle pressure were normal. Reduced TLC was attributable to reduced FRC, compatible with airway closure in the tidal range. CONCLUSIONS: This study describes a distinct physiologic phenotype of restriction due to airway dysfunction. This pattern was observed following WTC dust exposure, has been reported in other clinical settings (eg, asthma), and should be incorporated into the definition of restrictive dysfunction.
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