Comparison of impulse oscillometry and spirometry for detection of airway hyperresponsiveness to methacholine, mannitol, and eucapnic voluntary hyperventilation in children.

BACKGROUND: Forced expiratory maneuvers are usually difficult in young children. Impulse oscillometry (IOS) requires no active cooperation, is noninvasive, rapid, and easy to perform. This study aimed to compare IOS indexes and forced expiratory volume in 1 second (FEV1) in children for the assessment of bronchial hyperreactivity to methacholine, mannitol, and eucapnic voluntary hyperventilation (EVH). MATERIALS: Children aged 3-14 years (mean 10.0 ± 3.1) with symptoms suggestive of asthma were recruited. IOS measurements were taken before spirometry. Methacholine, mannitol, and EVH tests were performed without a specific order. RESULTS: We included 190 children, whose mean age was 10.0 ± 3.1 years. Changes in FEV1 correlated significantly with variation in IOS indexes (P < .05). The indexes with the greatest discriminative capacity were Z5, R5, and X5. Optimal cut-offs were: for methacholine tests, ≧22% in R5, ≧82% for reactance area (AX), and ≦41% for X5; for the mannitol test, ≧18% in R5, ≧40% in AX, and ≦21% for X5. In the EVH test, ≧23% for R5, ≧40% for AX, and a fall of 29% for X5. When using the optimal cut-off points obtained from IOS, the mean number of steps and doses required for methacholine and mannitol tests to induce significant bronchoconstriction were significantly lower compared with spirometry ( P < .05). CONCLUSIONS: The effectiveness of R5, X5, and AX indexes were comparable to FEV1 in assessing bronchial obstruction during bronchial challenge testing. Therefore, IOS may be useful in assessing bronchial obstruction in children who cannot reliably perform spirometric maneuvers during bronchial challenge testing.

Nasal response in patients with diisocyanate asthma.

BACKGROUND: To date, no studies have assessed nasal and bronchial response to diisocyanates during specific inhalation challenges (SIC). OBJECTIVES: This study was performed to assess nasal response during SIC with diisocyanates (nasal and oral breathing) in patients with suspected occupational asthma due to these agents. METHODS: Fourteen patients with suspected clinical history of diisocyanate-induced asthma were challenged with diisocynates in a 7m3 chamber. Nasal response testing during challenges was assessed by acoustic rhinometry, peak nasal inspiratory flow (PNIF), and visual analog scale (VAS), alongside bronchial responses. RESULTS: Eleven patients had a significant asthmatic response to diisocyanates. None reported clear work-related nasal symptoms. In patients with positive bronchial response to diisocyanates, nasal mean minimal cross-sectional area (MCA) decreased by 26.9%, nasal volume at 5 cm decreased by 33.5%, and PNIF decreased by 28.3%, all from baseline. A positive nasal response was elicited in 45%, 54%, and 45% of patients, respectively. A significant increase in VAS was observed in 4 patients. Three patients with negative bronchial response had a negative nasal response. CONCLUSION: SIC revealed an objective nasal response in around 50% of patients with occupational asthma due to diisocyanates, in spite of the fact that none of them reported work-related nasal symptoms. The clinical significance of this finding is a poor association between nasal symptoms at work and an objective nasal response during positive SIC with diisocyanates.

Occupational asthma caused by triglycidyl isocyanurate.

BACKGROUND: Several cases of allergic contact dermatitis, two cases of occupational asthma from over one decade ago and one case of hypersensitivity pneumonitis have been documented in painters who use polyester powder paint containing triglycidyl isocyanurate (TGIC). METHODS: We report a 28-year-old female who, 4 months after beginning work in a powder-coating factory, developed asthma-like symptoms. In her workplace, aluminium frames were treated with an electrostatic powder paint containing 2.5-10% TGIC. RESULTS: Serial peak-flow measurements performed during both working and non-working periods demonstrated peak-flow variability of up to 46% on work days. Bronchial methacholine test results also varied between times at work and away from work. PC(20) methacholine was 0.32 mg/ml and fraction of exhaled nitric oxide (FENO) was 18 ppb. A controlled exposure challenge was performed with a placebo yielding no changes in FEV(1) over a 24-hour period. On visit 2, the patient was placed in the chamber and exposed to TGIC (4% in lactose) at a mean concentration of 3.61 mg/m(3) for a total of 15 min. A 20% fall in FEV(1) from baseline was elicited at 10 min, together with cough and wheezing. No late response was demonstrated. Twenty-four hours after the challenge, neither methacholine PC(20) nor FENO levels varied from baseline values. No IgE was detected by ELISA testing and no IgE-binding bands were found by immunoblot analysis of patient and control serum. CONCLUSIONS: The aforementioned results demonstrate that TGIC inhalation induced immunologic occupational asthma, although no IgE mechanism was evidenced.