Involuntary smoking produces unpleasant symptoms in many individuals. These subjective complaints may be sufficient cause to regulate smoking in confined public places. However, it remains controversial whether acute passive smoking is associated with important pulmonary physiologic hazards. The present study was designed to investigate whether involuntary smoking presents an acute respiratory risk to asymptomatic asthmatic individuals.
Our data demonstrate that one hour of passive cigarette smoke inhalation by young, clinically stable asthmatics produced no change in maximal expiratory flow rates. Furthermore, passive smoking caused a slight decrease in nonspecific bronchial reactivity assessed via methacholine bronchoprovocation. Our subjects were exposed to a severe simulation of passive smoking, beyond what normally occurs in the majority of social or occupational environments. A carbon monoxide level in the ambient air of 40 to 50 ppm far exceeds the level found in office environments where smoking is permitted and is higher than the peak hourly averages usually found in taverns or nightclubs. Blood carboxyhemoglobin determinations confirmed the degree of passive smoke inhalation by our subjects.
Two previous studies investigated the effect of passive smoking on lung (unction in asthmatics; however, neither evaluated the influence of such involuntary smoking on airway reactivity. Shephard et al studied 14 asthmatic subjects and found that the FEW1 and Vmax50 were unchanged after passive smoking. In their study, the intensity of exposure was less (carbon monoxide level in chamber was about 24 ppm), but the duration was longer (two hours). Their subjects were older than ours. Furthermore, the baseline pulmonary function of their subjects demonstrated airflow obstruction (FEV1 = 68±19 percent of predicted; range 30 percent to 91 percent) and several of the subjects were receiving oral asthma medications. Additionally, four of their subjects gave a specific history of “exacerbation” with exposure to cigarette smoke; nevertheless, this subgroup also experienced no decrement in pulmonary function. In contrast to our results and those of Shephard et al, Dahms et al demonstrated a 20 percent decrease in FEV1 and FVC following passive smoking in ten patients with bronchial asthma. It is difficult to account for the different results based upon experiment design or patient selection, although such factors may have played a role. In Dahms study, the smoke exposure was less intense (one hour of a calculated carbon dioxide concentration of 15 to 20 ppm; the average increase in COHb level during exposure was 0.40). Their patients were young (age 18 to 26 years), and baseline lung function demonstrated only mild impairment; the mean FVC was 79.2 percent of predicted and the mean FEV! was 73.7 percent of predicted. The subjects continued taking medications (except bronchodilators beginning four hours prior to exposure), but the authors did not describe what medications were taken and how many subjects were on medications. However, one-half of their subjects were included because of a history of specific complaints when exposed to cigarette smoke; only the remaining five were recruited at random. In short, our study is in agreement with Shephard et al and acute at variance with Dahms et al regarding the effect of passive smoking on maximal expiratory flow in asthmatics. The present study additionally investigated the effect of passive smoking on bronchial reactivity.
The finding that passive smoking caused a decrease in nonspecific airway responsiveness (increased PDaoFEVj) was unexpected. The clinical significance of the change is uncertain, since the magnitude was small. Only one subject had a change in PDaoFEVj of at least one log dose (tenfold shift), an increment that is considered clinically important. It is not known whether lesser changes in PDjqFEV! are important. Although our data show that passive smoking caused a small decrease in airway reactivity, the possibility that this could be associated with an amelioration of the underlying asthma cannot be determined from our study.
The reduction in nonspecific airway responsiveness that we observed might have been mediated by pharmacologically active substances present in cigarette smoke. Inhalation of cigarette smoke causes increased plasma levels of the sympathetic neurotransmitter norepinephrine as well as the adrenomedullary hormone epinephrine. It is possible that catecholamines released locally from sympathetic nerve ganglia, or into the circulation from the adrenal glands, may modify airway smooth muscle reactions. Catecholamine release in response to tobacco smoke inhalation is probably mediated by nicotine. Increased blood and urinary nicotine levels are found in people with mild to moderate passive smoking exposures. Wallis et al have demonstrated that inhalation of nicotine diminished airway responsiveness to methacholine in baboons who were highly reactive to methacholine, even though nicotine inhalation had no direct bron-chodilator effect on lung function.
All the details about pulmonary function test are depicted on the video:
Quantification of bronchial responsiveness may be affected by the prechallenge airway caliber. This might be due to altered distribution of inhaled aerosol particles, such that a greater portion may deposit on the segmental airways, a site where constriction has a profound effect on the FEV1. Furthermore, the exponential relationship between airway diameter and resistance to airflow may mean that an equivalent amount of airway narrowing may cause a much greater decrement in FEV1 in a patient who started the challenge test with constricted airways. Since the lung function of our subjects was the same prior to each of the two methacholine tests, the influence of baseline airway caliber probably was not important in our results.
The FEV, test requires a forced vital capacity maneuver following inspiration to total lung capacity. Full lung inflation can reduce or abolish bronchocon-striction induced by pharmacologic agents in healthy subjects. Thus, detecting slight airway responses to inhaled agents in healthy nonasthmatic subjects requires the use of lung function tests that do not involve inspiration to total lung capacity. In such cases, partial expiratory flow volume curve initiated from end-tidal inspiration, or plethysmographic measurements of airway resistance (SGaw) can be utilized (https://onlineasthmainhalers.com/outlet-concerning-expiratory-flow-and-bronchodilator-response-in-asthma.html). However, in asthmatics, reduction of bronchomotor tone by lung inflation is minimal or absent, and therefore, the FEV! is a useful and reliable test for assessing bronchial reactivity in such patients. Furthermore, SGaw may be influenced by suggestion, whereas FEV! generally is not. This may be due to vagal pathways causing subtle changes in large airway tone. Eliminating the effect of suggestion is important in this study, where the subject cannot be “blinded” to the presence of cigarette smoke. And finally, the PDaoFEV1 shows less day-to-day variability than PDjysSGaw and may be a better test to use when comparing bronchoprovocation tests performed on different days.
We emphasize that this study did not evaluate several aspects that may be relevant to the “real life” problem of passive smoking by asthmatics. Our investigation evaluated only the immediate effects of a one-hour period of involuntary smoking. We did not test whether delayed effects of an acute exposure may occur. Furthermore, our subjects had virtually normal lung function during the study and the findings might be different for asthmatics exposed to cigarette smoke during an episode of bronchospasm. Not to be overlooked is the possible effect of chronic passive smoking. Chronic cigarette smoking may lead to increased airway reactivity in normal subjects. By analogy, chronic involuntary smoking might lead to clinical deterioration in asthmatics. Also, the development or severity of asthma in children may be influenced by parental smoking. And finally, there may be a subset of asthmatics with a specific allergy to constituents of tobacco smoke; further work will be required to elucidate whether passive cigarette smoking represents a risk to such individuals. Nevertheless, the current study suggests that passive cigarette smoking presents no acute respiratory risk to young asymptomatic asthmatics.
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