CD-sens seems to be very useful for the determination of a patient's allergen sensitivity and should be evaluated for the measurement and monitoring of anti-IgE treatment efficacy. CD-max, the conventional approach to basophil allergen challenge, which mirrors cell reactivity, gives incorrect information.
We investigated whether exposure to a low level (490 micrograms/m3) of nitrogen dioxide (NO2) affects bronchial responsiveness to allergen and enhances allergen-induced increase in airway responsiveness to histamine. Eighteen subjects with asthma and allergy to pollen were exposed at rest to either purified air or NO2 for 30 min followed 4 h later by an allergen inhalation challenge. Responsiveness to histamine was measured the day after. Lung function during NO2 exposure and allergen challenge was measured by plethysmography and after exposure by a portable spirometer hourly. The order of exposure to NO2 and air was randomized and separated by at least 2 wk. The asthmatic reaction during the late phase was enhanced by NO2, and peak expiratory flow after allergen challenge was on average 6.6% lower (p = 0.02) after NO2 than after air exposure. The number of subjects having a late asthmatic reaction (fall in FEV1 > 15%) was seven after air and 10 after NO2 (NS). Peripheral blood samples were analyzed for differential cell counts before and after NO2/allergen and serum levels of eosinophil cationic protein (ECP). NO2 effect on lung function was neither associated with an increase in eosinophil numbers nor with ECP levels. NO2 did not affect lung function before allergen challenge, early asthmatic reaction, and allergen-induced increase in responsiveness to histamine. These results indicate that short exposure to an ambient level of NO2 followed several hours later by allergen inhalation enhances allergen-induced late asthmatic reaction.
The prevalence and variability of ventilation-perfusion (VA/Q) inequality was examined in 26 stable, symptomatic, asthmatic subjects (mean FEV1/FVC, 79% predicted; mean FEF75, 43% predicted) studied once a week for 9 consecutive weeks. We used a recent modification of the multiple inert gas elimination technique allowing frequent serial studies without the need for sampling arterial blood. The VA/Q inequality was expressed as log SD (the second moment) of the distributions of blood flow (Q) and ventilation (V) on a log scale. Log SDQ averaged 0.74, and in every patient log SDQ exceeded the 95% upper limit of normal (0.60) in 2 wk or more. In only 5 patients was mean log SDQ less than 0.6. The ventilation distribution was less abnormal, with mean log SDV exceeding the 95% normal upper limit in only 4 patients. Bimodal blood-flow distributions containing low VA/Q units were observed at some point in 24 of 26 subjects, but occurrence was variable, and in only one third of all measurements was bimodality found. Analysis of variance showed that 70 to 75% of the total variance of log SD was due to intersubject differences, about 20% was due to random changes over time, and the remaining 7 to 9% was not explained by either and was due mostly to experimental error. Arterial PO2 measured 3 times in each subject was inversely related to log SDQ (r = 0.76), but only 60% of the variance in PaO2 was explained by VA/Q mismatch, the rest being due presumably to variation in mixed venous PO2 and similar extrapulmonary factors.(ABSTRACT TRUNCATED AT 250 WORDS)
Nitrogen dioxide (NO 2 ) is a major air pollutant produced by combustion, the main sources being traffic exhaust outdoors and gas appliances indoors. Evidence from several epidemiological studies suggests that ambient levels of nitrogen dioxide may increase the risk for exacerbations of asthma [1,2]. Controlled human exposure studies on the other hand have not shown that lung function is affected by ambient levels of NO 2 [3,4]. However, an increase in airway responsiveness to nonspecific stimuli like histamine and methacholine has been reported in asthmatics at NO 2 concentrations <1,000 µg·m -3 [5][6][7]. It is possible that NO 2 may exert its effects by an interaction with other air pollutants, such as particles, SO 2 and O 3 . In a study by JÖRRES et al. [8], the lung function response was increased after NO 2 followed by SO 2 in asthmatics, and in healthy females when NO 2 was followed by O 3 exposure 3 h later [9], but not in asthmatics exposed to NO 2 and O 3 simultaneously [10]. Furthermore, in a recent study, bronchial response to birch and timothy pollen was enhanced by prior exposure to 500 µg·m -3 NO 2 for 30 min [11]. Similar results were shown for house dust mite after exposure to 800 µg·m -3 (0.4 ppm) NO 2 for 1 h [12]. These latter reports show that ambient levels of NO 2 can also enhance the airway responsiveness to allergens in humans. However, the allergen doses given in the experiments mentioned above considerably exceed those encountered in normal life. This makes it difficult to draw any firm conclusions on the clinical implications of the findings. As an increase in nonspecific bronchial responsiveness and the presence of late asthmatic reactions have also been reported after low doses of pollen allergen [13,14], the use of a nonsymptomatic allergen dose would imitate seasonal exposure better.In order to mimic real-life exposure, the aim of the present study was to investigate the effect of daily repeated exposure to a nonsymptomatic allergen dose preceded by a short exposure to 500 µg·m -3 NO 2 . We wanted to determine whether the NO 2 effect on asthmatic response was reproducible with this significantly lower allergen dose and whether the magnitude of the response to NO 2 changed during repeated exposure. Methods SubjectsSubjects were recruited through the hospital outpatient clinic and by local advertising. All subjects gave informed Repeated exposure to an ambient level of NO 2 enhances asthmatic response to a nonsymptomatic allergen dose. V. Strand, M. Svartengren, S. Rak, C. Barck, G. Bylin. ©ERS Journals Ltd 1998. ABSTRACT: We investigated the effects of NO 2 and allergen on lung function in a repeated exposure model. For 4 subsequent days, 16 subjects with mild asthma and allergy to birch or grass pollen were exposed at rest to either purified air or 500 µg·m -3 NO 2 for 30 min in an exposure chamber. Four hours later, an individually determined nonsymptomatic allergen dose was inhaled. Lung function (forced expiratory volume in one second (FEV1)) was measured by a portable spirome...
Ten subjects with asthma inhaled 3.6 micron particles labeled with 111In in air and in a helium-oxygen mixture (He-O2) at 0.5 and at 1.2 L/s. Lung retention was measured after zero and after 24 h, and the percentage 24-h retention (Ret24) was taken to represent the fraction deposited in the alveolar part of the lung. For both inhalation rates, Ret24 was significantly higher when particles were inhaled with He-O2 than with air. The increase in Ret24 seemed to be larger in subjects with asthma than in healthy persons earlier studied. Ret24 was correlated with changes in both large and small airways, especially when the particles were inhaled with He-O2. Our data suggest that inhalation of drugs in He-O2 might be of therapeutic value when treating patients with severely obstructed airways.
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