Nonsmokers are frequently exposed to tobacco smoke in indoor environments. The potential health risks of such involuntary, or passive, smoking is a topic of intense interest. Current evidence suggests that passive smoking acutely lowers the angina threshold and that chronic passive smoking may lead to small airways dysfunction or lung cancer. There is a paucity of data on whether asthmatics may be at special respiratory risk from passive smoking.
Asthma is characterized by hyperreactivity of the airways, such that a wide variety of different stimuli may cause bronchospasm and reduced airflow (https://onlineasthmainhalers.com/diagnosis-of-bronchial-asthma-by-clinical-evaluation-methods-and-materials.html). Even if lung function tests are normal, bronchial hyperreactivity can be detected by bronchoprovocation challenge testing with inhaled agents such as histamine or methacholine. In addition, bronchoprovocation testing may be useful for detecting changes in airway reactivity that occur in response to therapeutic interventions or environmental exposures. For example, such studies have demonstrated temporary increases in bronchial responsiveness following viral infections, and antigen inhalation, as well as exposure to ozone and nitrogen dioxide. Changes in nonspecific bronchial responsiveness may be clinically important since many studies have shown a correlation of airway reactivity with the clinical severity of asthma as determined by symptom scores, medication requirements, or dose of specific allergen required to produce airflow obstruction.
Two previous studies which examined the acute effects of passive smoking on lung function in asthmatics report conflicting results. Furthermore, there is no published information concerning the effect of passive smoking on nonspecific airway responsiveness in asthmatics. Therefore, we investigated the effect of acute passive smoking on both lung function and airway reactivity in a group of young stable asthmatic patients.
Subjects and Methods
Nine asthmatic individuals ranging in age from 19 to 30 years were studied. Five subjects were males, and four were females. Subjects were selected from 11 consecutive respondents to an advertisement announcing the study. The diagnosis of asthma was made previously by the individuals physician. Respondents were included oiily if they were currently clinically stable and off oral asthma medications. Four individuals intermittently using inhaled bronchodilators at the time of the study were included. No subject with an upper respiratory infection within the preceding eight weeks was studied. Although the subjects were asymptomatic at the time of this study, five had required hospitalization for asthma in the past. However, no subject had been hospitalized for asthma within the preceding year. All individuals were nonsmokers. Individuals were not selected based upon a history of how they reacted in the presence of tobacco smoke. However, six of the subjects indicated that exposure to cigarette smoke “bothered” their asthma.
Subjects were instructed to avoid coffee, cola drinks, chocolate, and exercise for at least six hours before bronchoprovocation testing. No subject was taking vitamin C supplements. Subjects using an inhaled bronchodilator were instructed to withhold use for six to eight hours preceding the test, in accordance with published guidelines. Before participation in the study, subjects signed a consent form approved by the Yale Human Investigation Committee.
The experimental protocol was carried out in each subject on two separate days (Table 1). This design was utilized in order to avoid the need to do two methacholine challenges on the same day. On the first day, baseline spirometry was measured with a pneumotachy-graph-integrated flow-volume device connected to a Gould 3054 high performance X-Y recorder. The forced vital capacity (FVC), the forced expiratory volume in one second (FEV,), and the maximal expiratory flow rate at 50 percent of the vital capacity (Vmax50) were determined. Following this, a methacholine inhalation challenged test was performed. The challenge test was conducted by delivering sequential doses of methacholine in phenol-buffered saline solution (0.05, 0.5, 1.0, 2.0, 5.0, 10.0, 25.0 mg/ml) via mouthpiece with a DeVilbiss No. 45 nebulizer. A noseclip was used. Each dose was delivered during two minutes of normal tidal breathing. The FEV, was determined at 0.5 and four minutes after each dose. If at either time there was a 20 percent or greater fall in FEV1 from the baseline prechallenge value, the test was terminated. If the FEV1 did not decrease by this amount, then the next dose was delivered. The cumulative dose of methacholine which corresponded to a 20 percent decrease in FEV1 was determined by linear interpolation of the last two points on the dose-response curve. This “provocative dose” of methacholine which causes a 20 percent decrease in FEV, is the PDaoFEV1. A low PD1FEX1 indicates a high degree of nonspecific bronchial responsiveness (see our article on site “Observations Concerning Expiratory Flow and Bronchodilator Response in Asthma“).
On the second experiment day (24 to 48 hours following the first day), subjects returned for spirometry and then a baseline pre-smoke exposure venous blood sample was drawn for carboxyhemoglobin (COHb) analysis. The blood COHb level analysis was performed with a double-wavelength spectrophotometer. The subject then entered a 4.25 m environmental chamber for exposure to machinegenerated cigarette smoke for one hour. Both sidestream and mainstream smoke filled the chamber. The same brand of a leading nonfilter cigarette was used in all experiments. The chamber was maintained at a temperature of about 25°C and the relative humidity was approximately 50 percent. Air turnover in the chamber was adjusted as necessary to maintain a carbon monoxide level in the ambient air of between 40 and 50 ppm. The carbon monoxide level was sampled continuously from an area near the subject. While in the chamber, the subjects were given the option to wear goggles to reduce eye irritation. These goggles did not cover the nose or mouth.
Immediately following one hour of passive smoking, the subject exited from the chamber and a venous blood sample was drawn for COHb analysis. Spirometric testing was performed, followed by a methacholine bronchoprovocation challenge. The chest of each subject was auscultated immediately before and after the passive smoke exposure.
A methacholine challenge test was also administered to 14 individuals (age 18 to 37 years; mean 28 years) who had normal pulmonary function test results and no history of asthma. The purpose was to compare the methacholine responsiveness of this “normal” group with that of the study population, which had been selected based upon a prior history of asthma. The normal individuals did not participate in the passive smoking experiment.
Statistical analyses of spirometric values, carboxyhemoglobin levels, and the PDajFEVj (transformed to log units as is customary) were performed with the paired Students f-test. The nonparametric signed rank test was used to also evaluate changes in PD^FEVj assessed without prior transformation to log units.
Table 1—Protocol
| Day 1 | Day 2 |
| I. Baseline studies | I. Before passive smoking |
| a. Spirometry (FEV^ FVC, Vmax50) | a. Venous COHb analysis |
| b. Spirometry | |
| b. Methacholine inhalation challenge | II. One hour smoke exposure |
| III. After passive smoking | |
| a. Venous COHb analysis | |
| b. Spirometry | |
| c. Methacholine inhalation challenge |