Passive Smoking

Passive Smoking

I ~I I I ----I I ---=- CHEST editOrials Passive Smoking Acute Effects in Asthma King James the Firsts "counterblaste to toSince bacco,"1 it has bee...

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I ~I I I ----I

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CHEST editOrials

Passive Smoking Acute Effects in Asthma King James the Firsts "counterblaste to toSince bacco,"1 it has been generally appreciated that

breathing tobacco smoke is not pleasant. Early medical papers2.3 recorded eye and mucosal irritation, coughing, and wheezing in sizable proportions of normal subjects and asthmatic patients. More recently, there has been interest in documenting the exact physiologic effects of passive smoking fur two good reasons. From a medical point ofview, one would like to know why large numbers of asthmatic patients (and some normal individuals) complain of cough and wheeze when exposed to cigarette smoke. Understanding the mechanisms involved should be helpful to future research into asthma and environmental lung disease. From a political point ofview, the current movement fur smoke-free environments would be strengthened if one were able to show objective laboratory changes on acute exposure to "second-hand" cigarette smoke. Contemporary studies of pulmonary function have delineated three interrelated effects of tobacco smoke that are germane to the ongoing debate about the importance of second-hand smoke: 1. Chronic exposure to second-hand tobacco smoke in the workplace has been documented to result in decrements in the FEF25-75%4 and a similar exposure in the home5 showed reductions in FEV1 as well as FEF25-75%. 2. Actually smoking cigarettes produces certain acute effects, including highly significant increases in airways resistance. 8 . 7 One might accordingly speculate that second-hand smoke should have similar acute effects. 3. Increased bronchial reactivity as compared with nonsmokers has been recorded in a group of smokers with otherwise normal pulmonary function tests. 8 In this issue of Chest (see page 180), a careful study by Wiedemann and co-workers has shown no measurable acute effects ofpassive smoking in young asthmatic patients; both resting ventilatory function and airway reactivity were unchanged. Only two other papers have looked directly at this question. Shephard et al9 fuund no effect, while Dahms et allO documented a deleterious effect of passive smoking in asthmatic

VOWME 89 I NUMBER 2 I FEBRUARY, 1986

subjects. The discussions offered by the authors ofthose three articles give cause fur further reflection about passive smoking and asthma. Could it be that a considerably longer duration of exposure is the key? Pimm et alll exercised normal subjects in a smoky atmosphere, and showed an increase in coughing but no significant pulmonary function changes. Mild exercise of asthmatic patients in the exposure chamber would also be interesting. This should mimic the reallife situation more closely than any chair-bound experiment. Delayed effects, too, require consideration. It may well be that future studies should fullow asthmatic patients up to 48 hours after the passive smoking insult. Finally, let us not forget that medical history abounds in examples of physicians dismissing symptoms because neither our crude physical examination techniques nor our routine laboratory tests could uncover supporting evidence. Other tests may yet prove more sensitive than those currently employed in studying the physiology of passive smoking. Neville M. Lefcoe, M.D. London, Ontario, Canada University of Westem Ontario. Reprint requests: Dr: Lefcoe, VICtoria Hospital, 375 South Street, London, Ontario, Cal'l66a N6A 4G5

REFERENCES 1 James First, King of Great Britain and Ireland. The Essays of a Prentise. in the Divine Art ofPoesie. Edinburgh. 1585. A Counterblaste to Tobacco. London. 1604 2 Pipes DM. Allergy to tobacco smoke. Ann Allergy 1945; 28: 277-82 3 Speer F. Tobacco and the non-smoker: a study of subjective symptoms. Arch Environ Health 1968; 16:443-46 4 White JR. Froeb HF. Small-airways dysfunction in non-smokers chronically exposed to tobacco smoke. N Eng) J Med 1980; 302: 720-23 5 Kaullinan F. Tessier JF. Paul 0. Adult passive smoking in the home environment: a risk factor fOr chronic airflow limitation. Am J Epidemioll983; 117(3):269-80 6 Chiang Sl: Wang BC. Acute effects ofcigarette smoking on pulmonary function. Am Rev Respir Dis 1970; 101:860-68 7 Sobol BJ, van Voorhies L, Emirgil C. Detection ofacute effects of cigarette smoking on airways dynamics. Thorax 1977; 32:312-16 8 Gerrard JW. Cockcroft D\v, Mink]'I; Cotton DJ, Poonawala R. Dosman JA. Increased nonspecific bronchial reactivity in cigarette smokers with normal lung function. Am Rev Respir Dis 1980; 122:577-81 CHEST I 89 I 2 I FEBRUARY, 1988

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9 Shephard RJ, Collins R, Silverman F: "Passive" exposure ofasthmatic subjects to cigarette smoke. Environ Res 1979; 20: 392-402 10 Dahms TE t Bolin JFt Slavin RG. Passive smoking: effects on bronchial asthma. Chest 1981; 80:530-34 11 Pimm PEt Silverman Ft Shephard RJ. Physiologic effects ofacute passive exposure to cigarette smoke. Arch Environ Health 1978; July/Aug. :201-08

An End to "ARDS"

Few medical acronyms have become so popular and yet are so misleading as that of the "adult respira-

tory distress syndrome!'!' or "ARDS." Certainly, no one would argue that this rather common pulmonary disorder could not occur in children, and in its milder forms, it seems likely that there may be relatively little evidence for pulmonary insufficiency. The term was originally adopted to indicate a respiratory disorder characterized by the acute onset of tachypnea, hypoxemia, and decreased compliance. 1 On chest x-ray films, pulmonary infiltrates were visibly suggestive of local edema, and histologic studies of pulmonary tissues obtained from these patients frequently showed hyaline membranes covering the pulmonary epithelium and both interstitial and intra-alveolar hemorrhage and edema. This early study recognized the basic physiology, course, and incidence of this illness and the therapeutic advantages of ventilation with positive end-expiratory pressure. It can be said without exaggeration that the report permanently changed the practice of pulmonary medicine and helped give it a central role in intensive care medicine. Reference to an "adultl'l' fOrm of respiratory distress was used to distinguish it from the neonatal illness, which was also characterized by noncardiogenic pulmonary edema and hyaline membrane formation. The basic problem in the neonate is attributable to the immaturity of the lung at the time of birth and is probably related to a deficiency of surfactant production. Although there may also be a deficiency in surfactant in the adult disease, and although there may eventually be some role for administering surfactant in these patients, the cause of the illness is presumably related to an injury involving the lungs which results in formation of edema. However; there is a somewhat more subtle problem with the term which has led to some confusion in both clinical and investigational circles. Although it had long been recognized that specific agents such as toxic fumes could cause pulmonary injury and edema in the absence of congestive heart failure, it was not recognized just how common an event this could be until the introduction of the Swan-Ganz catheter into clinical practice some 15 years ago. 2 Prior to that time, it had been common practice to attribute the development of edema following injuries or surgical catastrophes to 182

some obscure failure ofthe heart. This became untenable when low pulmonary arterial occlusion pressures were measured in many of these patients. The causes of edema were presumably related to some form of pulmonary injury which was sustained in patients with severe injuries related either to wartime or civilian activities, but the pathogenesis of the injury was and remains obscure. This mysterious illness obviously and embarassingly must have been prevalent for many years but remained unrecognized because left atrial pressures were not readily estimated and arterial oxygen tensions were difficult to obtain. Furthermore, the frequency of the problem undoubtedly increased when emergency services improved and patients could be delivered to the hospital with much greater dispatch. It was natural to assume that this very serious problem was a specific disorder of the lungs with a well-defined set of causes and a natural history of its own. Difficulties quickly arose with this approach. The list of potential factors that can precipitate ARDS grew dramatically with experience. From the diagnostic point of view, it became particularly difficult to say when a patient had a severe bacterial or viral pneumonia or a picture of ARDS, and complaints were expressed that the term referred to a miscellaneous collection of disorders which might have little to do with one anothet: Furthermore, it has gradually become evident that the edema found in the lungs of these patients might simply represent the most obvious and indeed the most serious manifestation of a generalized capillary injury. This sequence ofevents must be familiar to even the most casual medical historian. Following the introduction ofthe clinical thermometer in the latter part ofthe nineteenth century, considerable attention was given to a variety of "fevers!'!' which were assumed to represent specific illnesses. 3 Advances in bacteriology soon made it obvious that fever was simply a manifestation of the disease, which would require specific therapy; at best, treatment of the fever itself could provide only temporary relief. Now that it has become technically practical to rule out congestive heart failure as the cause for pulmonary edema, care must be taken that a similar error is not made. For the sake of clarity, it would seem preferable to make a specific statement regarding the pathogenesis of the edema, rather than referring to it as "ARDS.l'l' For example, if no cardiac cause for the edema can be found, then it is "noncardiogenic pulmonary edema.l'l' H the clinician is convinced that the edema is related to some injury to the endothelial or epithelial membranes (or both) which leads to the leakage of protein and fluid into the interstitium or alveolar spaces, then it would be n appropriate to refer to an "exudative or an "inflammatoryl'l' edema, rather than a "transudative!'!' or "nonEditorials