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Oscillometry (also known as the forced oscillation technique) measures the mechanical properties of the respiratory system (upper and intrathoracic airways, lung tissue and chest wall) during quiet tidal breathing, by the application of an oscillating pressure signal (input or forcing signal), most commonly at the mouth. With increased clinical and research use, it is critical that all technical details of the hardware design, signal processing and analyses, and testing protocols are transparent and clearly reported to allow standardisation, comparison and replication of clinical and research studies. Because of this need, an update of the 2003 European Respiratory Society (ERS) technical standards document was produced by an ERS task force of experts who are active in clinical oscillometry research.The aim of the task force was to provide technical recommendations regarding oscillometry measurement including hardware, software, testing protocols and quality control.The main changes in this update, compared with the 2003 ERS task force document are 1) new quality control procedures which reflect use of "within-breath" analysis, and methods of handling artefacts; 2) recommendation to disclose signal processing, quality control, artefact handling and breathing protocols ( e.g. number and duration of acquisitions) in reports and publications to allow comparability and replication between devices and laboratories; 3) a summary review of new data to support threshold values for bronchodilator and bronchial challenge tests; and 4) updated list of predicted impedance values in adults and children., Competing Interests: Conflict of interest: G.G. King reports grants from American Thoracic Society and European Respiratory Society, during the conduct of the study; a collaborative research agreement and IP agreement with Restech, grants and personal fees for lectures from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Menarini, MundiPharma and Cyclomedica, grants from NH&MRC, Philanthropic Societies, Sydney University, outside the submitted work. Conflict of interest: J. Bates is a minor shareholder and received personal fees for advisory board work from Oscillavent, LLC, outside the submitted work; and has a patent (patent application US 20160007882 A1; proposes the use of oscillometry in ventilated patients) pending to none, and a patent PCT application WO2015127377 A1 (proposes variable tidal volume ventilation as a means of performing oscillometry in ventilated patients) pending to none. Conflict of interest: K.I. Berger has nothing to disclose. Conflict of interest: P. Calverley has advised Philips Respironics about the clinical application of FOT and spoken on this topic at meetings supported by this company. Conflict of interest: P.L. de Melo has a patent 28727 issued. Conflict of interest: R.L. Dellacà has a patent on the detection of EFL by FOT with royalties paid to Philips Respironics and Restech srl, a patent on monitoring lung volume recruitment by FOT with royalties paid to Vyaire, and a patent on early detection of exacerbations by home monitoring of FOT with royalties paid to Restech, and is co-founder and shareholder of Restech srl, a spin-off company of the Politecnico di Milano University producing medical devices for lung function testing based on FOT. Conflict of interest: R. Farré reports contracts for bench assessment of CPAP devices from Resmed and ANTADIR, outside the submitted work. Conflict of interest: G.L. Hall reports grants from American Thoracic Society and European Respiratory Society, during the conduct of the study. Conflict of interest: I. Ioan has nothing to disclose. Conflict of interest: C.G. Irvin reports other for advisory board work from Methapharm, personal fees and non-financial support for advisory board work from Medical Graphics Corp, grants from NIH and American Lung Association, outside the submitted work. Conflict of interest: D.W. Kaczka reports grants from US Department of Defense (W81XWH-16-1-0434) and National Institutes of Health (R01-HL112986, R01-HL126838 and R41-HL140640), and is co-founder and shareholder from OscillaVent, Inc., during the conduct of the study; grants from ZOLL Medical Corporation, and is shareholder and member of an advisory board for Monitor Mask, Inc., outside the submitted work; and has a patent Systems and methods for multi-frequency oscillator ventilation pending to OscillaVent, Inc. (US20160339191A1), a patent Treatment of respiratory condition using targeted delivery pending (US20150290418A1), a patent System and method for setting positive end expiratory pressure during mechanical ventilation based on dynamic lung function (US20070240717A1, abandoned), a patent Enhanced ventilation waveform device issued (US 6,435,182 B1), and a patent Servo-controlled pneumatic pressure oscillator for respiratory impedance measurements and high-frequency ventilation (US20070006924A1, abandoned). Conflict of interest: D.A. Kaminsky reports personal fees for lectures from MGC Diagnostics, Inc., outside the submitted work. Conflict of interest: H. Kurosawa reports grants and personal fees from Chest M.I. Inc., during the conduct of the study; personal fees from Nippon Boehringer Ingelheim Co. Ltd, outside the submitted work; and has a patent US2012101400 with royalties paid to Tohoku University. Conflict of interest: E. Lombardi reports personal fees from Angelini, Boehringer, GSK, Omron and Vifor, grants and personal fees from Chiesi, Lusofarmaco and Novartis, grants and non-financial support from ResTech, personal fees and non-financial support from Vertex, outside the submitted work. Conflict of interest: G.N. Maksym reports financial support from Thorasys, Thoracic Medical Systems Inc, prior to the submitted work and non-financial support from Thorasys during the submitted work; and has a patent Respiratory Device (design patent) issued to Thorasys, a patent Respiratory Device filter issued to Thorasys, a patent Piezoelectric beam bending actuated Device for measuring respiratory system impedance issued to Thorasys, and a patent Method of assessment of airway variability in airway hyperresponsiveness issued to Thorasys. Conflict of interest: F. Marchal has nothing to disclose. Conflict of interest: B.W. Oppenheimer has nothing to disclose. Conflict of interest: S.J. Simpson has nothing to disclose. Conflict of interest: C. Thamrin has a patent WO 2006130922 A1 issued which is broadly relevant to the work, and has intellectual property arrangements with Thorasys Medical Systems and Restech srl relating to research collaborations, but does not have any financial relationships with either company. Conflict of interest: M. van den Berge reports grants paid to the university from AstraZeneca, TEVA, GSK and Chiesi, outside the submitted work. Conflict of interest: E. Oostveen has nothing to disclose., (Copyright ©ERS 2020.)

The effects of childhood exposure to perfluoroalkyl substances (PFASs) on lung function remain mostly unknown. Previous research indicates that children living or going to school near the World Trade Center (WTC) disaster were exposed to high levels of PFASs, among other toxic chemicals. To explore the effects of PFAS exposure on lung function, we measured serum PFASs in a cohort of children from the WTC Health Registry and a matched control group. Perfluorooctanesulfonate had the highest median concentrations in both groups (WTCHR = 3.72 ng/mL, Comparison = 2.75 ng/mL), while the lowest median concentrations were seen for perfluoroundecanoic acid (WTCHR = 0.12 ng/mL, Comparison = 0.01 ng/mL). Lung function outcomes were measured by spirometry, plethysmography, and oscillometry. Asthma diagnosis and serum eosinophil count were also recorded. We examined the relationships of each PFAS with lung function parameters and eosinophil count using linear regressions. Odds ratios for asthma were obtained for each PFAS using logistic regression. The effect of total PFASs on these outcomes was also assessed. All regression models were adjusted for sex, race/ethnicity, age, body mass index (BMI) and tobacco smoke exposure. We found that serum PFASs were not statistically associated with the measured lung function parameters, asthma diagnosis, or eosinophil count in this cohort (p < 0.05). These findings highlight the need for more longitudinal studies to explore the long-term effects of childhood PFAS exposure on lung function past adolescence and early adulthood., (Copyright © 2019 Elsevier Inc. All rights reserved.)

The role for direct assessment of small airway function in subjects with respiratory symptoms but normal airflow by spirometry is discussed. Small airway disease syndrome is described in numerous disease states using a multidisciplinary approach. Data demonstrate that small airway disease is related to presence of respiratory symptoms, exposure to inhaled toxins, presence of local and systemic inflammation, and presence of histologic abnormalities within the distal lung. Investigation of immunological derangements associated with distal airway dysfunction in the setting of normal spirometry may provide insight into pathophysiological mechanisms that are present at disease onset. For the purposes of this symposium, data were reviewed in selected clinical conditions (obesity, environmental inhalational injury, and cigarette smoking) that have been recently studied in the André Cournand Pulmonary Physiology Laboratory at Bellevue Hospital using the forced oscillation technique.

Rationale: Obesity is characterized by increased systemic and pulmonary blood volumes (pulmonary vascular congestion). Concomitant abnormal alveolar membrane diffusion suggests subclinical interstitial edema. In this setting, functional abnormalities should encompass the entire distal lung including the airways., Objectives: We hypothesize that in obesity: 1) pulmonary vascular congestion will affect the distal lung unit with concordant alveolar membrane and distal airway abnormalities; and 2) the degree of pulmonary congestion and membrane dysfunction will relate to the cardiac response., Methods: 54 non-smoking obese subjects underwent spirometry, impulse oscillometry (IOS), diffusion capacity (DLCO) with partition into membrane diffusion (DM) and capillary blood volume (VC), and cardiac MRI (n = 24). Alveolar-capillary membrane efficiency was assessed by calculation of DM/VC., Measurements and Main Results: Mean age was 45±12 years; mean BMI was 44.8±7 kg/m2. Vital capacity was 88±13% predicted with reduction in functional residual capacity (58±12% predicted). Despite normal DLCO (98±18% predicted), VC was elevated (135±31% predicted) while DM averaged 94±22% predicted. DM/VC varied from 0.4 to 1.4 with high values reflecting recruitment of alveolar membrane and low values indicating alveolar membrane dysfunction. The most abnormal IOS (R5 and X5) occurred in subjects with lowest DM/VC (r2 = 0.31, p<0.001; r2 = 0.34, p<0.001). Cardiac output and index (cardiac output / body surface area) were directly related to DM/VC (r2 = 0.41, p<0.001; r2 = 0.19, p = 0.03). Subjects with lower DM/VC demonstrated a cardiac output that remained in the normal range despite presence of obesity., Conclusions: Global dysfunction of the distal lung (alveolar membrane and distal airway) is associated with pulmonary vascular congestion and failure to achieve the high output state of obesity. Pulmonary vascular congestion and consequent fluid transudation and/or alterations in the structure of the alveolar capillary membrane may be considered often unrecognized causes of airway dysfunction in obesity.

Introduction: Abnormality in distal lung function may occur in obesity due to reduction in resting lung volume; however, airway inflammation, vascular congestion and/or concomitant intrinsic airway disease may also be present. The goal of this study is to 1) describe the phenotype of lung function in obese subjects utilizing spirometry, plethysmography and oscillometry; and 2) evaluate residual abnormality when the effect of mass loading is removed by voluntary elevation of end expiratory lung volume (EELV) to predicted FRC., Methods: 100 non-smoking obese subjects without cardio-pulmonary disease and with normal airflow on spirometry underwent impulse oscillometry (IOS) at baseline and at the elevated EELV., Results: FRC and ERV were reduced (44 ± 22, 62 ± 14% predicted) with normal RV/TLC (29 ± 9%). IOS demonstrated elevated resistance at 20 Hz (R20, 4.65 ± 1.07 cmH2O/L/s); however, specific conductance was normal (0.14 ± 0.04). Resistance at 5-20 Hz (R5-20, 1.86 ± 1.11 cmH2O/L/s) and reactance at 5 Hz (X5, -2.70 ± 1.44 cmH2O/L/s) were abnormal. During elevation of EELV, IOS abnormalities reversed to or towards normal. Residual abnormality in R5-20 was observed in some subjects despite elevation of EELV (1.16 ± 0.8 cmH2O/L/s). R5-20 responded to bronchodilator at baseline but not during elevation of EELV., Conclusions: This study describes the phenotype of lung dysfunction in obesity as reduction in FRC with airway narrowing, distal respiratory dysfunction and bronchodilator responsiveness. When R5-20 normalized during voluntary inflation, mass loading was considered the predominant mechanism. In contrast, when residual abnormality in R5-20 was demonstrable despite return of EELV to predicted FRC, mechanisms for airway dysfunction in addition to mass loading could be invoked.

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.

Rationale: Residents and area workers who inhaled dust and fumes from the World Trade Center disaster reported lower respiratory symptoms in two World Trade Center Health Registry surveys (2003-2004 and 2006-2007), but lung function data were lacking., Objectives: To examine the relationship between persistent respiratory symptoms and pulmonary function in a nested case-control study of exposed adult residents and area workers 7-8 years after September 11, 2001., Methods: Registrants reporting post September 11th onset of a lower respiratory symptom in the first survey and the same symptom in the second survey were solicited as potential cases. Registrants without lower respiratory symptoms in either Registry survey were solicited as potential control subjects. Final case-control status was determined by lower respiratory symptoms at a third interview (the study), when spirometry and impulse oscillometry were also performed., Measurements and Main Results: We identified 180 cases and 473 control subjects. Cases were more likely than control subjects to have abnormal spirometry (19% vs. 11%; P < 0.05), and impulse oscillometry measurements of elevated airway resistance (R5; 68% vs. 27%; P < 0.0001) and frequency dependence of resistance (R₅₋₂₀; 36% vs. 7%; P < 0.0001). When spirometry was normal, cases were more likely than control subjects to have elevated R₅ and R₅₋₂₀ (62% vs. 25% and 27% vs. 6%, respectively; both P < 0.0001). Associations between symptoms and oscillometry held when factors significant in bivariate comparisons (body mass index, spirometry, and exposures) were analyzed using logistic regression., Conclusions: This study links persistent respiratory symptoms and oscillometric abnormalities in World Trade Center-exposed residents and area workers. Elevated R₅ and R₅₋₂₀ in cases despite normal spirometry suggested distal airway dysfunction as a mechanism for symptoms.

There is an increasing awareness of the role of distal airways in the pathophysiology of obstructive lung diseases including asthma and chronic obstructive pulmonary disease. We hypothesize that during induced bronchoconstriction: 1) disparity between distal and proximal airway reactivity may occur; and 2) changes in distal airway function may explain symptom onset in subjects with minimal FEV(1) change. 185 subjects underwent methacholine challenge testing (MCT). In addition to spirometry, oscillometry was performed at baseline and after maximum dose of methacholine; 33/185 also underwent oscillometry after each dose. Oscillometric parameters included resistance at 5 and 20 Hz (R(5), R(20)) and heterogeneity of distal airway mechanics assessed by frequency dependence of resistance 5-20 Hz (R(5-20)) and reactance area (AX). R(5) varied widely during MCT (range -0.8 - 11.3 cmH(2)O/L/s) and correlated poorly with change in FEV(1) (r = 0.17). Changes in R(5) reflected changes in both R(20) and R(5-20) (r = 0.59, p<0.05; r = 0.87, p<0.0001). However, R(20) increased only 0.3 cmH(2)O/L/s, while R(5-20) increased 0.7 cmH(2)O/L/s for every 1cmH(2)O/L/s change in R(5,) indicating predominant effect of distal airway mechanics. 9/33 subjects developed symptoms despite minimal FEV(1) change (<5%), while R(5) increased 42% due to increased distal airway heterogeneity. These data indicate disparate behavior of proximal airway resistance (FEV(1) and R(20)) and distal airway heterogeneity (R(5-20) and AX). Distal airway reactivity may be associated with methacholine-induced symptoms despite absence of change in FEV(1). This study highlights the importance of disparity between proximal and distal airway behavior, which has implications in understanding pathophysiology of obstructive pulmonary diseases and their response to treatment.

Pulmonary function is impaired in untreated mucopolysaccharidosis type VI (MPS VI). Pulmonary function was studied in patients during long-term enzyme replacement therapy (ERT) with recombinant human arylsulfatase B (rhASB; rhN-acetylgalactosamine 4-sulfatase). Pulmonary function tests prior to and for up to 240 weeks of weekly infusions of rhASB at 1 mg/kg were completed in 56 patients during Phase 1/2, Phase 2, Phase 3 and Phase 3 Extension trials of rhASB and the Survey Study. Forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1) and, in a subset of patients, maximum voluntary ventilation (MVV), were analyzed as absolute volume in liters. FEV1 and FVC showed little change from baseline during the first 24 weeks of ERT, but after 96 weeks, these parameters increased over baseline by 11% and 17%, respectively. This positive trend compared with baseline continued beyond 96 weeks of treatment. Improvements from baseline in pulmonary function occurred along with gains in height in the younger group (5.5% change) and in the older patient group (2.4% change) at 96 weeks. Changes in MVV occurred earlier within 24 weeks of treatment to approximately 15% over baseline. Model results based on data from all trials showed significant improvements in the rate of change in pulmonary function during 96 weeks on ERT, whereas little or no improvement was observed for the same time period prior to ERT. Thus, analysis of mean percent change data and longitudinal modeling both indicate that long-term ERT resulted in improvement in pulmonary function in MPS VI patients.

In this work MRI-based spirometry is presented as a method for noninvasively assessing pulmonary mechanical function on a regional basis. A SPAMM tagging sequence was modified to allow continuous dynamic imaging of the lungs during respiration. A motion-tracking algorithm was developed to track material regions from time-resolved grid-tagged images. Experiments were performed to image the lungs during quiet breathing and volumetric strain was calculated from the measured displacement maps. Regional volume calculations, derived from volumetric strain, were integrated over the entire lung and compared to segmented volume calculations with good agreement. Results from this work demonstrate that MRI spirometry has the potential to become a clinically useful tool for measuring regional ventilation and assessing pulmonary diseases that regionally affect the mechanical function of the lung., ((c) 2005 Wiley-Liss, Inc.)