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Scientific Activities - Actividades Científicas

Honorary Committee Lecture

Passive smoking - overview
Published in ProCOR

Bernard Lown, MD
Awarded with Nobel Prize

 

Passive smoking - an overview

The medical struggle against tobacco, formally began in 1962 and 1964 when the Royal College of Physicians in London and the Surgeon General in Washington released their landmark reports documenting the relation of smoking to  lung cancer.(1, 2)  The daunting fiscal and political power of the tobacco companies offered little hope that the popular interest will prevail.  Yet a profound historic turn-around is now in the making. In many industrialized countries, in no small measure,  the strong backlash against smoking  relates to the discovery that tobacco is  not merely personally injurious,  but is an environmental pollutant hazardous to  non-smokers.  If smoking is risky for innocent bystanders, then it is no longer a private matter without social accountability. Even those who maintain that society must not legislate adherence to healthy life styles, can not be impervious to circumscribing this habit to prevent harm to others. In fact, John Stuart Mill's principle is apropos, " the only purpose for which power can be rightfully exercised over any member of a civilized community, against his will, is to prevent harm to others."

In the USA appreciation of the harm of environmental tobacco smoke (ETS) has led to prohibition of smoking in public places, such as hotels, movie theaters, restaurants, buses, railways, domestic flights etc. The growing realization that smoke gets in everyone's eyes has undermined the tobacco industry's case. A bellwether is the recent victory of  60,000 flight attendants in their class action  trial on second hand smoke.   In the landmark  settlement five major tobacco companies have agreed to pay several hundred million dollars in damages.(3)

Now the battle has entered the most intimate haunts of the cigarette, the liquor bars, casinos and nightclubs. These sites have hitherto been unthinkable without  a heavy smog of all pervading tobacco smoke.  In the biggest assault yet, the State of California has banned smoking in these places as of January 1, 1998.  The intent is to protect employees like bartenders, waitresses and bellhops from the risk of second-hand smoke.  The New York times characterized the legislation as the "harshest tobacco law" enacted to date.

The problem of passive smoking globally is of enormous dimension and growing. The wide prevalence of smoking in the home, the workplace, and spaces of  public assemblage,  provides no oasis free from toxic tobacco pollutants for the nonsmoker. The magnitude of the problem can be inferred from the experience in the United States prior to enactment of legislation banning smoking in various public places. During the  mid- 1980's,   63.3 percent of American non-smokers reported daily exposure to environmental smoke. (4) Of these,  34.5 per cent were exposed 10 hours or more per week and 15.9 per cent at least 40 hours per week.  About a decade ago approximately  two thirds of  United States children lived in homes where at least one adult smoked.(5) Contemporary data from the European Union, where there have been less aggressive campaigning against tobacco, about 80% of  those over 15 years of age are exposed to environmental tobacco smoke. (6)

What is Passive Smoke? A cigarette emits two components;  the mainstream  which the smoker inhales and the sidestream which enters the environment.   The largest component of environmental pollution,  85 percent, derives from the burning end of the cigarette -- the so called side-stream emission.  Mainstream smoke is a complex aerosol mixture inhaled by the smoker,  filtered by the lung, then exhaled  and accounts for  15 percent of the environmental burden.(7) Cigarette smoking releases into the environment over  4000 chemicals.  The two streams of smoke contribute  qualitatively  similar constituents including oxides of nitrogen, nicotine, carbon monoxide, and various carcinogens.  During inhalation cigarettes burn at higher temperatures resulting in more complete combustion and a greater breakdown of toxic tobacco components.  The undiluted sidestream smoke has a higher pH,  smaller particle size,  higher concentration of  carbon monoxide, as well as the toxic  and carcinogenic compounds which the smoker inhales.

The quantity of these chemicals in the environment depends on  a host of factors such as the  number of smokers, the extent of their cigarette consumption, the rate of smoking,  the type of cigarette (e.g. filter or non filter, low tar, nicotine content, etc.), the proximity of the non-smoker, the duration of exposure, the magnitude of the space,  the home or work ventilation system, the season of the year and many other variables.  Assessing the hazard of environmental tobacco smoke for  non-smokers is, therefore, a formidable problem.

Considerable research has been conducted to identify sensitive markers to measure tobacco smoke exposure in non-smokers. (7) The nicotine metabolite conitine, which is excreted in the urine,  has become widely accepted in epidemiological studies.  It has a long half life of 20 hours, does not fluctuate during smoke exposure and can be readily measured in urine or in saliva. (8, 9 )   A strong correlation has been demonstrated between urinary conitine levels and self reported exposure to tobacco smoke in children and adults,  both at home and work environments. (7)

What then  is the scientific basis indicating that smoking does pollute  the environment? It is supported,  in essence,  by two types of evidence.   First, one finds in the homes of smokers twice the concentration of airborne respirable particulates compared to those in the  homes  of non-smokers.  Second, non-smokers exposed to tobacco smoke have measurable conitine levels in their urine. (7, 10)   In one study of 663 of non-smokers  exposed to environmental smoke, 91%  had an average urinary conitine level of  8ng/L.  (11)   Disquieting is the fact that conitine was also detected in 81% of 162 subjects without known smoke exposure in the preceding  four days. Since one can not identify with assurance  a zero-exposure group, the true health effects of environmental smoke  remain  conjectural.

Based on urinary conitine levels, the National Research Council concluded  that non-smokers exposed to passive smoke absorb nicotine equivalent to 0.1 to 1 cigarette per day.(8)   This is consistent with the fact that the measurable conitine in the urine is  only 0.7 percent of the  1200ng/L found in the urine of smokers.(11)   With such insubstantial exposure there seems little likelihood of adverse health effects resulting from environmental smoke.  However substantial  epidemiological as well as  experimental evidence indicate otherwise.

Epidemiological Data Since passive smoking does not lend itself to randomized study, clinical conclusions are necessarily deduced from epidemiological data. These demonstrate an increase in various pathological states generally in non-smoking spouses compared to people not exposed to a smoking marital partner.  As a large part of the population is exposed to ETS, even small increases in risk of highly prevalent diseases such as cancer and heart disease  could have large adverse health effects.

When the issue of involuntary smoking was first raised in the 1972 report of the  Surgeon General,   only a handful of studies had then been published. (11) With each ensuing report more evidence was pointing to the substantial hazard of ETS.  By 1986, two landmark reports, by the US National Academy of Science (10) and by the Surgeon General (12) reached the conclusion that passive smoking adversely affects the health of adults and children.  A positive association between passive smoking and lung cancer  was found in 11 of the 13 studies then available.(12)   By 1993 the evidence had grown far more persuasive.  In 24 of 30 studies, carried out in eight countries,  passive smoking was implicated in lung cancer.(13) An impressive  body of epidemiological data  then convinced the United States  Environmental Protection Agency (EPA) to classify environmental tobacco smoke as a known human carcinogen. (14) Most persuasive was the large seminal study of  Hirayama in Japan.(15)  He  found a relative risk of lung cancer of 0.63 for nonsmoking wives of non-smoking husbands as contrasted to a near doubling of risk with an RR of 1.12 for non-smoking women married to current or former smokers.(15)

It appears that passive smoking poses a special risk for  adenocarcinomas arising in more distal part of the bronchial tree.(16)  This is unlike the squamous cell carcinoma found predominantly in active smokers. Unlike what the smoker inhales, the sidestream smoke components of ETS are smaller in particulate size, the carcinogens may therefore penetrate to deeper reaches of the lung.

In the United States passive smoking may contribute to as many as 4,700 annual death from  lung cancer. This  equates to a mortality rate of 7.4 non-smokers per 100,000 person years.(17)  The finding is  not dissimilar to the 6.8 such deaths estimated by Hirayama in the large Japanese study.(15)   In the most recently reported meta-analysis involving  37  epidemiological studies on passive smoking and lung cancer, Hackshaw et al (18) concluded that marriage to a smoker increased the risk of lung cancer by a remarkable 26% (95% confidence interval 8% to 49%). The association is bolstered by a consistent dose response relation.

In addition to lung and other cancers throughout the body,  passive smoking is associated with a variety of vexing health problems. It is well established that ETS causes both  acute and chronic respiratory diseases.  Though these are not as threatening to immediate survival as malignancy, nonetheless symptoms of chronic cough, phlegm and wheezing  impair the quality of life.  Children exposed to environmental smoke have more middle ear infections, more respiratory tract infections,  more exacerbations of asthma, as well as decreased lung function.  Passive smoking lowers birth weight. In a prospective study, Martin and Bracken (19) have shown that the adjusted relative risk of delivering a low birth weight baby(less than 2500 gm.) among passive smoking women  was 2.2 times as great as compared to unexposed women.  A larger detrimental effect was reported by Rubin et al (20)  who observed that birth weight in infants of non-smoking mothers was reduced by 120g per pack of cigarettes smoked per day by the father.  There is also a suggestion that sudden infant death syndrome may increase with ETS. Among the elderly, passive smoke has been associated with increase in cataracts, sleep disorders, reduction in bone density and impotence.(21)

All the above cited  complications are relatively picayune compared to the toll passive smoking exacts on the cardiovascular system.  These will be discussed in the next section.

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Bibliography

1.  Royal College of Physicians. Smoking and health. Summary and report of the Royal College of Physicians of London on smoking in relation to cancer of the lung and other diseases. New York: Pittman Publishing, 1962.
2.  Department of Health, Education and Welfare. Smoking and health. Report of the Advisory Committee to the Surgeon General of the Public Health  Service, Atlanta: Public Health Service, Centers for Disease Control, 1964. (PHS Publication No 1103.)
3.  Josefson D. US flight attendants win settlement over passive smoking . BMJ 1997;315:968.
4.  Friedman GD, Pettiti DB, Bawol RD. Prevalence and correlates of passive smoking. Am J Public Health  1983;73:401-5.
5.  Weiss ST. Passive smoking and lung cancer; what is the risk? Am Rev Respir Dis  1986;133:1-3.
6.  Watson R Passive smoking is a major threat BMJ 1998;316:9.
7.  Fielding JE, Phenow KJ.  Health effects of involuntary smoking  New Eng J Med 1988;319:1452-11460 National Research Council. Environmental Tobacco Smoke. Measuring Exposure and Assessing Health Effects. Washington D.C. National Academy Press;1986.
8.  Department of Health, Education and Welfare. The health   consequences of smoking; a report of the Surgeon General. Washington DC Government Printing Office, 1972. (DHEW publications no.(HMS) 72-7516).
9.  Steenland K. Passive smoking and the risk of heart disease. JAMA;1992;267:94.
10. Cummings K. et al Measurement of current exposure to environmental tobacco smoke  Arch Environm Health 1990; 45:75.
11. US Department of Health and Human Services. The health consequences of involuntary smoking. A report of the surgeon general . Rocville, MD:Public Health Service, Office on Smoking and Health, 1986.(DHHS Publication No (CDC)87-
12. Davis RM. Passive smoking: history repeats itself. BMJ 1997;315:961.
13. Environmental Protection Agency. Respiratory health effects of passive smoking:  lung cancer and other disorders. Washington,DC:EPA.1992. (Publication EPA/600/6- 90/006F.
14. Hirayam T. Cancer  mortality in in nonsmoking women with smoking husbands based on  a large- scale cohort study  in Japan. Prev Med 1984;13:680-690.
15. Fontham ETH, Correa P, Wu-Williams A, et al Lung cancer in non-smoking women: a multicenter case-control study. Cancer EpidemiolBiomark Prev
16. Department of Health and Human Services. The health consequences of smoking: cancer,  a report of the Surgeon General. Washington DC Government Printing Office, 1982.  (DHEW publication DHHS(PHS) 82-50179).
17. Hackshaw AK et al. The accumulated evidence on lung cancer and environmental tobacco smoke BMJ 1997;315:980
18. Martin and Bracken   Am J Epidemiology 1986; 124:633-42.
19. Rubin et al  Lancet 1986 ii 415-417. 20. Feldman HA et al.  Impotence and its medical and psychosocial  correlates: results of the Massachusetts aging study  J Urol 1994;151:54-61.

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Nov/16/1999