Acute pulmonary response of asthmatics to 3.0 ppm formaldehyde.

Previous studies have failed to demonstrate bronchoconstriction in unselected asthmatics after brief (less than or equal to 1/2-h), controlled exposures to formaldehyde (HCHO). This study was designed to evaluate the acute pulmonary response to 3 ppm HCHO in nine nonsmoking asthmatic volunteers over a more relevant exposure duration (3 hrs). Pulmonary function, nonspecific airway reactivity and symptoms were assessed before and at intervals during the exposure. No significant changes in pulmonary function (FVC, FEV1, FEF25-27%, SGaw, or FRC) or airway reactivity were observed. There was a significant increase in nose/throat irritation at 30 min. (P less than 0.05) and in eye irritation at 60 min (P less than 0.05) and 180 min (P less than 0.01). These results suggest that individuals with asthma will not experience significant bronchoconstriction when exposed at rest to 3 ppm HCHO; however, most will experience eye and upper respiratory tract irritation.

Acute pulmonary response to formaldehyde exposure in healthy nonsmokers.

The acute pulmonary response to three hours' exposure to 3 ppm formaldehyde (HCHO) during intermittent exercise was evaluated in nine healthy nonsmokers. The protocol consisted of clean air on the first day and HCHO on the second day with a 24-hour follow-up on the third day. Pulmonary function, nonspecific airway reactivity, and symptoms were assessed daily. Thirty minutes of HCHO exposure resulted in a 2% decrease in forced expiratory volume at one second (P less than .05) and a 7% decrease in forced midexpiratory flow rate 25%-75% (P less than .01); however, these effects were no longer present between 60 and 180 minutes. There was also a significant increase in odor (P less than .02), nose or throat irritation (P less than .01), and eye irritation (P less than .01) with exposure. No changes in pulmonary function or airway reactivity were observed 24 hours after exposure. Acute exposure to 3 ppm HCHO produced small, transient decreases in pulmonary function and mild to moderate eye and upper respiratory tract irritation.

Ozone response relationships in healthy nonsmokers.

Significant concentration responses were observed in FVC, FEV1, FEF25-75, SGaw, IC, and TLC in 20 healthy, nonsmoking volunteers exposed randomly to 0.00, 0.10, 0.15, 0.20, and 0.25 ppm O3. In addition, significant response changes for FVC, FEV1, and FEF25-75 were shown with time over the 2-h exposure. Intermittent, heavy exercise (VE, 68 L/min) lasting 14 min was employed every 30 min during exposure. Inspection of the concentration and time response curves suggests that the threshold for the group response is at or below 0.15 ppm O3. Six subjects experienced decreases greater than 5% in FEV1 or greater than 15% in SGaw at 0.15 ppm. This concentration is only slightly higher than the 1-h O3 National Ambient Air Quality Standard. A dose-related response was also seen for cough, nose and throat irritation, and chest discomfort. The work load, length of exposure, and individual sensitivity must be considered for establishing a safe O3 exposure level.

Inhibitability and enhanceability of basophil histamine release in asthmatic and normal subjects.

Circulating human basophils contain histamine, a potent mediator of inflammation. Previous in vitro studies have shown that histamine 'releasability' in asthmatic subjects differs from normal subjects but have not evaluated possible differences in the immunopharmacological control of the release of this mediator which might account for these differences. The purpose of the present study was to examine the immunopharmacologic control of basophil histamine release in 14 asthmatics and 10 normal subjects who were characterized by pulmonary function tests, allergic status (skin tests and serum IgE levels) and nonspecific airways reactivity to methacholine and histamine. Basophils were stimulated with anti-IgE, and the inhibitory effects of the H2 agonist, dimaprit, and dibutyryl cyclic AMP (dbcAMP), as well as the enhancing properties of 5-hydroperoxyeicosatetraenoic acid (5-HPETE) and indomethacin on the modulation of histamine release, were investigated. Although no statistically significant differences were seen in the percent histamine release triggered by anti-IgE in these two groups, enhancement of histamine release by 5-HPETE was more consistent in the asthmatic subjects (10 of 10) than in control subjects (6 of 8). The percent increase in histamine release produced by 5-HPETE in asthmatic subjects averaged 3.9 +/- 1.3% using 0.03 micrograms anti-IgE/ml and 4.8 +/- 3.2% using 0.1 microgram anti-IgE/ml (p less than 0.002, Wilcoxon's signed rank test), and averaged 3.0 +/- 4.3 and 3.1 +/- 5.3%, respectively, in control subjects (p greater than 0.10).(ABSTRACT TRUNCATED AT 250 WORDS)

CO concentration-dependent changes in pulmonary diffusing capacity in humans.

Steady-state CO pulmonary diffusing capacity (DLCO) was measured at different inspired CO concentrations in seven males and one female during light treadmill exercise. As the CO level is increased. DLCO increases, reaches a maximum at an end-tidal CO concentration of approximately 100 ppm, and then decreases. The maximum DLCO is up to twice as large as the DLCO measured at an inspired CO concentration of approximately 1,780 ppm. These results are consistent with the presence of saturation kinetics, one of the basic properties of carrier-mediated transport systems. A similar relationship between DLCO and CO concentration was found in previous studies of mechanically ventilated dogs. Thus there is evidence for carrier-mediated transport of CO in the lungs of both humans and dogs.

A screening test for airways reactivity. An abbreviated methacholine inhalation challenge.

A screening test to measure nonspecific airways reactivity was developed and compared to a standard methacholine inhalation challenge in 13 asthmatic patients and ten normal control subjects. The screening challenge consisted of one deep breath, then four breaths of a 5 mg/ml methacholine solution followed by one and four breaths of 25 mg/ml of methacholine. Subjects with a history of wheezing received the 5 mg/ml of methacholine first while those without a history of asthma began the challenge at the 25 mg/ml methacholine concentration. Spirometric test were employed and the challenge was terminated when FEV1 fell 20 percent from baseline. The standard methacholine challenge used a dosimeter and all subjects took five breaths of saline solution followed by seven increasing concentrations of methacholine. Dose response curves were constructed and the provocation dose of methacholine that caused a 20 percent fall in FEV1 was calculated for each protocol. Results of the screening methacholine challenge correlated with those obtained from the more lengthy standard protocol (r = 0.94), and correctly identified levels of airways reactivity in asthmatic patients and normal subjects. The abbreviated protocol was rapid (6-12 min), safe, and inexpensive. Since the equipment is readily available and easy to transport, it could be used at sites outside the hospital as a screening test for nonspecific airways reactivity.