Airway responsiveness to acetaldehyde in patients with asthma: relationship to methacholine responsiveness and peak expiratory flow variation

Abstract

These results indicate that airway hyperresponsiveness to acetaldehyde is a sensitive and specific indicator for separating asthmatic and normal subjects. Airway responsiveness to methacholine or acetaldehyde and PEF variation are not reflecting the same pathophysiological process in the airways.

Airway Hyperresponsiveness in Patients With Coronary Spastic Angina Relationship Between Coronary Spasticity and Airway Responsiveness

“…[37][38][39] The differences between these 2 agents regarding their receptor distribution and ability to induce endothelium-derived vasodilation or constriction of arterial smooth muscles may be involved in the different results obtained in the present study and those of Saitoh et al 24 Because ACh and MCh challenges have been reported to yield similar high levels of sensitivity and specificity for revealing airway hyperresponsiveness, we consider that the differences between these 2 agents did not affect our results. 40 Influences of age, 41 sex, smoking habits, 42 allergic factors, [43][44][45] left ventricular ejection fraction 46 and microvascular angina 47 on airway hyperresponsiveness have been reported. However, no significant differences were observed among the present CSA, CP and control groups with respect to age, sex or coronary risk factors, including smoking and allergic factors.…”

Airway Responsiveness to Inhaled Acetaldehyde in Subjects with Allergic Rhinitis: Relationship to Methacholine Responsiveness

“…Finally, a cutoff point of 80 mg/ml separating normal from increased bronchial responsiveness to acetaldehyde may appear arbitrary. We have previously found that 92% of the subjects with asthma had a fall in FEV 1 >20% after inhalation of acetaldehyde in concentrations up to 40 mg/ml, while no healthy subject showed significant bronchoconstriction [6]. Furthermore, the challenge procedure with inhaled acetaldehyde was repeatable to within a single doubling dilution in subjects with asthma [24].…”

“…Myou et al [4]reported that the airways of 9 asthmatic patients were more responsive to inhaled acetaldehyde than those of 9 healthy subjects. In another study [6], 56 of 61 asthmatic patients had a fall in FEV 1 of more than 20% while no healthy subject showed significant bronchoconstriction after inhaled acetaldehyde. In the present study, increased responsiveness to inhaled acetaldehyde was detected in 13 of the 16 asthmatic patients and, therefore, our results confirm that inhaled acetaldehyde causes bronchoconstriction in most, but not all, patients with asthma.…”

“…Some authors suggested a cutoff limit of 8 mg/ml for the provocative concentration causing a 20% fall in forced expiratory volume in 1 s (PC 20 ) methacholine [3]or PC 20 histamine [2], since all their nonasthmatic subjects had a PC 20 value above this value, while all their asthmatic subjects with recent symptoms had a lower PC 20 value. Besides methacholine and histamine, asthmatic subjects also have exaggerated airway responses to inhaled acetaldehyde [4, 5, 6]. The mechanism(s) underlying the bronchoconstriction caused by inhalation of acetaldehyde is not certain, but is probably due to the release of mediators from preactivated inflammatory cells [4, 7].…”

“…From published data in asthmatics, it appears that the degree of airway responsiveness to acetaldehyde is not closely linked to the degree of airway responsiveness to methacholine [6]. In addition, upon methacholine challenge airway constriction is induced in both chronic obstructive pulmonary disease and asthma [8].…”