Happy Wonderer

Several friends of my family have died of smoking-related illnesses. (Many of the WWII generation picked up the habit in the service, where cigarettes were handed out free.) Ask anyone over 50 who has smoked for most of their life if they would recommend that young people start.

Our friend Lloyd was a brilliant, charming man who smoked two packs a day. For the 25 years that I knew him he had a terrible cough that made him sound like he was on his last legs. During his life I think he encountered almost every possible respriatory illness in some form or another. He preservered through them and did brilliant research and was a beloved teacher up until lung cancer got him.

Fred Kerlinger was another family friend (you may know of him if you are into statistics and psychometrics.) He too had a persistant cough, and died of smoking related illnesses. An incredible waste in both cases, the time and energy he spent fighting for breath could have been spent writing another book...

It is not just the length of life that matters, it is the quality of life. Breathing is something we take for granted when we are (relatively) young. Watching these people fight respiratory diseases convinced me even as a kid that I would never want to do that. Besides, they smelled bad -- I could tell if any of them had been doing research with my Dad long after they had left the house -- and they didn't smoke inside. (It is sadly amusing that some smokers think they can 'sneak' a smoke in a public place and that nobody will know who did it.)

Non-scientific ancedote: I belong to a club where almost all of the members are older than my wife and I. It is very easy to spot the life-long smokers, they look at least 10 years older than the nonsmokers (I do the database so I know roughly how old people really are...) Not smoking doesn't guarentee you a healthy life, but smoking garentees you an unhealthy one.

Has anybody met an older lifelong smoker who didn't have respiratory problems? (Serious question, I don't know if some people are more affected than others.)

George

By the way, one takeaway from the club is that you shouldn't throw away your old age. There is a couple in their early 80's who are on their way to the ski slopes right now. Another couple in their 70's can easily outwalk my wife and I (in our 40's and in decent shape.)

I do not desire long life as much as being healthy during all the life that I have...

Jesse

Oxymoron:
But smoking is intrusive. Even if I don't get sarcomae as a result of sniffing your cigarette in the streer, I don't like it, it isn't good for me, it makes my clothes and hair smell, it affects my skin, I don't want it. I have just as much a right to not get it as you have to smoke it.

But unless there is evidence of an actual health risk from second-hand smoke (and there may well be, I don't know), "it smells bad" is a pretty poor argument for passing laws against smoking in public places--after all, there is no law against refusing to bathe and wearing the same clothes for weeks on end, just as there is no law against public flatulance. Do you think there should be?

Mad Kally

I still have no anecdotal evidence or have ever heard of any regarding 2nd hand smoke (ETS) for lung CA or COPD. (although I'm sure it could aggravate COPD symptoms) It may be out there as Dr. Rick said. Because I haven't come across a case of it does not mean it doesn't exist. I wouldn't think it would be very swift for people to smoke around a person with asthma either.

Kally

Oxymoron

No, not as such. It's - yet again - about changing the culture over a peiod of time that is longer than the span of an individual's life. Banning smoking in cinemas and restaurants is a good start. I have no issue with smoking-only places where it it understood that is what they are. But less of the "it's optional everywhere" attitude - I want to be able to vote with my feet. Oh, and a clamp down on the ejection of stubs in the street and from cars (which freaks me when I've just filled up with petrol) under littering laws.

redstar2000

Dr. Rick, I thank you for your post...at least you offer something other than self-righteousness and neo-puritanical banalities.

As I understand the first study, they took 14,697 sick people (people already diagnosed with coronary heart disease) of which 1,055 of them died from that disease over six years.

I am not clear on what the numbers 1.75, 1.67, etc. actually mean; does that mean someone was 1.75 times more likely to die than someone who did not fit that particular parimeter?

In any event, I note that "current smoking" was the worst of the three "predictors" of mortality.

Even more interesting, these were people who were already sick with a very serious condition. What does this have to do with people who smoke and are in normal health?

Do you understand what I want to see? Give me 100,000 people at age 15...divide them into smokers and non-smokers (move them from one group to the other as appropriate)...follow them through their lives and record when and how they die (do autopsies, not just mechanically write down "died from smoking" on a certificate)...then publish real numbers with real odds.

And if that is too difficult, then extrapolate from smaller samples. Somewhere there are some real numbers, aren't there?

I hope you will not hold it against me but I cannot accept anything from the CDC on this issue; as a federal agency with an "anti-tobacco" agenda, I don't consider them trustworthy on this matter. If you can cite more studies like the one above, I promise to read them.

In the meantime, I ask your thoughts on the social utility of yet another "front" on the "war against drugs". Do you think that making it more and more difficult for people to acquire and use tobacco products will be "worth" what the ever more draconian measures will "cost"?

Nuno Figueira

Hi, I couldn't avoid participating in this thread, in fact I registred just so I could have a saying. This is one of those topics that extremely passionate about and usually triggers very strong emotions in me.

First let me tell you I'm an ex smoker. I too was once a selfish bastard that polluted the air everyone else breath and was uterly convinced that I was in full rights of doing so.

These days, besides admiting how wrong I was, I hate smokers and the way they actively and unpunishedly attack my health, diminush my life quality and restricted the amount of social activities I can engage in without having my asthma seriously aggravated to the point of not being able to sleep for a few days after any contact with second hand smoke. Worst of all, at times I have to endure hypocritical attitude of trying to deny the extent of the damage smokers impose on others.

It goes way beyond the lung cancer thing, the health impact of 30 minutes of second hand smoke exposure are measurable.

Studies? They are all around. A quick search on pubmed returned 107 pages of references, I took the time to copy and paste a few.

Treatment compliance, passive smoking, and asthma control: a three year cohort study.

Soussan D, Liard R, Zureik M, Touron D, Rogeaux Y, Neukirch F.

INSERM U408 Epidemiologie, Faculte de Medecine Xavier Bichat, B.P. 416, 75870 Paris Cedex 18, France. dsoussan@bichat.inserm.fr

AIMS: To study the role of treatment compliance and parents' smoking on asthma control in children with recently diagnosed mild or moderate persistent asthma who were prescribed inhaled anti-inflammatory treatment. METHODS: Prospective cohort study of 167 children aged 6-12 years (64% boys). Patients were examined at inclusion and followed up for three years with a visit every four months. Peak expiratory flow (PEF) was measured twice a day during the week before each visit. Two control criteria were monitored: (1) symptom control = having diurnal or nocturnal exacerbations less than once a week and no symptoms between exacerbations, at all visits; and (2) PEF control = daily PEF variability <20% on each of the seven days before each visit. RESULTS: Symptom control was achieved by 25.1% of children and PEF control by 53.3%. Symptom control was positively related to having understood the way in which the medication worked and taking the prescribed doses (odds ratios (OR) = 3.38 and 4.82 respectively). It was inversely related to smoking within the home (OR = 0.34). PEF control was positively related to taking the prescribed doses (OR = 3.58). It was less frequently achieved if the mother smoked within the home (OR = 0.34). CONCLUSIONS: Results suggest that, to maximise the benefits of available asthma medication and to improve health outcomes, further efforts should be made to convince the parents of asthmatic children not to smoke in the house, and to improve compliance by increasing the patients' understanding of the disease and its treatment.

Passive smoking and vascular disease.

Ahijevych K, Wewers ME.

College of Nursing and College of Medicine and Public Health, The Ohio State University, Columbus, Ohio, USA.

Passive smoking, or environmental tobacco smoke, is a causative factor in cardiovascular disease. A 30-minute passive smoking exposure was found to affect coronary flow velocity reserve in nonsmokers, indicating endothelial dysfunction in coronary circulation. This article summarizes empirical work on passive smoking and heart disease. Clinically relevant findings include a dose-response relationship between passive smoking exposure and heart disease and partial reversibility of physical effects after eliminating passive smoking exposure. Appropriate assessment of passive smoking exposure in a variety of settings is warranted, as well as recommendations to avoid such exposure. Policy-based public health initiatives to eliminate passive smoking in the workplace and other public areas are needed.

Anti-smoking declaration.

Fujiwara H.

The Anti-Smoking Promotion Committee,The Japanese Circulation Society.

The number of deaths from cardio- and cerebro-vascular diseases (CVDs) rivals that from cancer in Japan. In the year 2000, heart disease, including coronary artery disease, claimed the lives of 147,000 Japanese persons, while cerebrovascular disease took the lives of 133,000 people, and cancer deaths were 295,000. Vascular diseases are clearly a major cause of deaths in adults. Further, a significant number of patients suffer from a variety of CVD-related illnesses. The prevention of these diseases and the improvement of quality of life through the reduction of morbidity and mortality is the ultimate goal for all researchers and physicians in cardiovascular disease. Reducing the number and severity of risk factors for heart disease and stroke should be the immediate goal of the Japanese Circulation Society (JCS).The JCS has been strongly involved in efforts to reduce the risk factors of hypertension, obesity, hyperlipidemia, and diabetes mellitus. Smoking is a well-recognized risk factor, and, for example, is associated with an increased risk of 1.7 to 3.0 times for coronary artery disease, 1.7 to 8.0 times for stroke, and 1.4 to 10.0 times for sudden death. For patients with CVDs, the longer the history of smoking, the more it aggravates the severity of the disease itself, and has greater affects on the activities of daily living by reducing oxygen availability in the patient. Passive smoking recently has been accepted as a major risk of coronary artery disease, stroke, and cancers. The prevalence of smoking in teenagers and women is now increasing in Japan, giving the prospect of serious consequences for the incidence, morbidity, and mortality of CVDs in the future. In particular, the combination of smoking and the oral contraceptive pill multiplies the risk of CVDs. Therefore, a national campaign to quit smoking and to eliminate passive smoking is needed. In terms of primary prevention, the excellent cost-benefit ratio of a non-smoking policy will help control the present spiraling increase in medical expenditures.Non-smoking measures are extremely important for the prevention and treatment of CVDs. A survey in 2002, however, revealed a high prevalence of smoking by Japanese physicians in the circulatory field (14% of men and 13% of women physicians). This prevalence is worse than in the United States 20 years ago. As for medical institutions recognized by the JCS, the same survey shows that only 5% completely ban smoking, and only 5% run a smoking cessation clinic in their cardiovascular departments. These figures clearly show that the importance of smoking issues is not recognized, and that cardiovascular physicians in Japan have been slow to act against tobacco use.The Japanese Circulation Society, as the leading professional association for cardiovascular specialists in Japan, hereby declares that we will vigorously fight against smoking by working to ban smoking, encouraging smoking cessation, and preventing passive smoking exposure. This effort will begin within our own membership. The JCS will promote the importance of these counter measures to the public. The JCS has defined 10 specific targets for this effort to decrease smoking and its negative effects and will focus on 3 audiences: the JCS and its membership, hospitals and medical schools, and the general public.








Why is smoking a risk factor for sudden infant death syndrome?

Gordon AE, El Ahmer OR, Chan R, Al Madani OM, Braun JM, Weir DM, Busuttil A, Blackwell CC.

Medical Microbiology and Forensic Medicine, University of Edinburgh, Edinburgh, UK. a.e.gordon@dundee.ac.uk

Smoking is a major risk factor for both Sudden Infant Death Syndrome (SIDS) and respiratory tract infections. Such infections, both viral and bacterial, also increase the SIDS risk. This study investigated the effect of cigarette smoke at two stages of infection: 1) mucosal surface colonization; 2) induction and control of inflammatory responses. For colonization, RSV or influenza A infected cells bound several bacterial species in significantly higher numbers due to increased expression of host cell antigens. Buccal epithelial cells from smokers bound significantly more bacteria. For Staphylococcus aureus, this was associated with increased tar levels. Some SIDS deaths have been proposed to result from high levels of pro-inflammatory mediators elicited by infection and/or cigarette smoke during a developmental period when infants are less able to control inflammatory responses. Inflammatory reponses were compared between blood samples from smokers (n = 42) and non-smokers (n = 60) stimulated with TSST-1 or LPS. Non-smokers had significantly higher IL-6 (P = 0.011), IFN (P = 0.003) and IL-10 (P = 0.000) baseline levels. Non-smokers had higher IFN (P = 0.008) and IL-1 (P = 0.001, 0.007) responses to LPS and higher IL-10 responses to TSST-1 (P < 0.05) and LPS (P < 0.000). This study highlights that smoking increases the SIDS risk by greater susceptibility to viral and bacterial infections and enhanced bacterial binding after passive coating of mucosal surfaces with smoke components. In animal models, IL-10 reduced the lethal effect of staphylococcal toxins. In this study, smokers had lower IL-10 responses toTSST-1 and LPS. Dose response effects of cigarette smoke exposure needs to be established in relation to inflammatory response control and infantile infections.

Household smoking behavior and ETS exposure among children with asthma in low-income, minority households.

Berman BA, Wong GC, Bastani R, Hoang T, Jones C, Goldstein DR, Bernert JT, Hammond KS, Tashkin D, Lewis MA.

Division of Cancer Prevention and Control Research, Jonsson Comprehensive Cancer Center, University of California at Los Angeles, A2-125 CHS, Box 956900, 90095-6900, Los Angeles, CA, USA

Environmental tobacco smoke (ETS) exposure was measured among 242 children with asthma who live in homes where at least one person smokes. Subjects were identified through clinics, schools, community agencies, and hospitals serving low-income, medically underserved communities in Los Angeles. Parents were surveyed about smoking behaviors in the household, children's ETS exposure, and attitudes towards smoking and smoking behavior change. Validation measures included urine cotinine for the child with asthma and passive air nicotine monitors placed in the subjects' homes. Overall reported levels of household smoking and ETS exposure were low, with a significant amount of household smoking taking place outside rather than inside the home. Over 47% of the respondents reported absolute restrictions against smoking in the home, and these restrictions were associated with lower reported levels of smoking, ETS exposure, and air nicotine and urine cotinine concentrations.

increase gamma-tocopherol in vivo after adjustment for dietary antioxidant intakes.

Dietrich M, Block G, Norkus EP, Hudes M, Traber MG, Cross CE, Packer L.

School of Public Health, University of California, Berkeley 94720-7360, USA. mdietric@uclink.berkeley.edu

BACKGROUND: Free radicals in cigarette smoke may cause oxidative damage to macromolecules, contributing to cardiovascular diseases and cancer. Decreased plasma antioxidant concentrations may indicate cigarette smoke-related oxidative stress. OBJECTIVE: We compared the effects on plasma antioxidant concentrations in cotinine-confirmed active and passive smokers with those in nonsmokers, independent of differences in dietary intakes and other covariates. DESIGN: Plasma samples from 83 smokers, 40 passive smokers, and 36 nonsmokers were analyzed for total ascorbic acid, alpha- and gamma-tocopherols, 5 carotenoids, retinol, and cotinine. Groups were compared by using analysis of variance with adjustment for sex, age, race, body mass index, alcohol intake, triacylglycerol concentration, fruit and vegetable intakes, and dietary antioxidants. RESULTS: After adjustment for dietary antioxidant intakes and other covariates, smokers and passive smokers had significantly lower plasma beta-carotene concentrations than did nonsmokers (0.15, 0.17, and 0.24 micro mol/L, respectively) and significantly higher gamma-tocopherol concentrations (7.8, 7.8, and 6.5 micro mol/L, respectively). Smokers had significantly lower plasma ascorbic acid and beta-cryptoxanthin concentrations than did nonsmokers and passive smokers (ascorbic acid: 43.6, 54.5, and 54.6 micro mol/L, respectively; beta-cryptoxanthin: 0.12, 0.16, and 0.16 micro mol/L, respectively) and significantly lower concentrations of lutein and zeaxanthin than did nonsmokers (0.33 compared with 0.41 micro mol/L). The P values for all the differences described above were < 0.05. No significant differences in plasma concentrations of alpha-tocopherol, alpha-carotene, total carotenoids, lycopene, or retinol were observed. CONCLUSIONS: These results indicate that cigarette smokers and nonsmokers exposed to cigarette smoke have a significantly lower plasma antioxidant status than do unexposed nonsmokers, independent of differences in dietary antioxidant intakes. Further research is required to explain why plasma gamma-tocopherol concentrations were significantly higher in smokers and passive smokers than in nonsmokers.

Passive smoking and its impact on employers and employees in Hong Kong.

McGhee SM, Hedley AJ, Ho LM.

Department of Community Medicine, University of Hong Kong, 5th Floor, University of Hong Kong Medical Centre, 21 Sassoon Road, Hong Kong. smmcghee@hkucc.hku.hk

AIMS: To estimate the prevalence of passive smoking at work in the whole workforce in Hong Kong (population 6.8 million), the characteristics of the passive smokers, any extra use of health care among passive smokers, and who pays for that health care. METHODS: A random sample of 14,325 households was contacted by telephone; 6,186 responding adults who worked full time were asked about their employment, their most recent use of health care and the cost of that care, their medical benefits, and their exposure to secondhand smoke in the workplace. After weighting the sample for sex, age, household size, and income, 4,739 subjects were included in the analysis. RESULTS: Of 1,961 full time workers who did not smoke, 47.5% were exposed to secondhand smoke in the workplace compared with only 26% exposed at home. Exposure at work was associated with being younger, male, married, less educated, and having a lower income. Those exposed at work were 37% more likely to report having visited a doctor for a respiratory illness in the previous 14 days. Employers were paying 28% of the cost of these visits, the government paid 8%, and the individuals paid 63%. If extrapolated to the 3 million workers in the Hong Kong population, employers would pay just over US$9 million per year, while the affected workers would pay around US$20 million. CONCLUSION: As well as the costs of active smoking, the cost of extra health care utilisation associated with passive smoking is an additional cost being paid by those employers who have not established smoke free workplaces and by their employees.

Bronchitis symptoms in young teenagers who actively or passively smoke cigarettes.

Manning P, Goodman P, Kinsella T, Lawlor M, Kirby B, Clancy L.

Department of Respiratory Medicine, CResT Directorate, St. James Hospital & Trinity College, Dublin, Ireland. manningp@tcd.ie

This study was undertaken to examine the prevalence of bronchitis (cough with phlegm) symptoms in teenagers who either smoked cigarettes on a regular basis (active smokers) or were non-smokers but who are exposed to passive smoking (passive smokers) in the home. The study was undertaken in 1995 and repeated in 1998. The 1995 study was a cross sectional questionnaire survey of smoking habits in secondary school children aged 13-14 years and was undertaken as part of the ISAAC questionnaire survey. Thirty representative and randomly selected schools from throughout the Republic of Ireland took part in the study. In the 1995 study, 3066 students completed a questionnaire on their current smoking habits and symptoms of cough and phlegm. We found that 634 (20.7%) of these young teenagers actively smoked cigarettes with significantly more females smoking than males with 23.3% of girls compared to 17.6% boys (p = 0.0001). We found that 46.3% of non-smoking children were exposed to smoking in the home (passive smokers) with parental smoking accounting for most of the passive smoking. Bronchitis symptoms were more commonly reported in active smokers compared to non-smokers with an odds ratio of 3.02 (95% CI 2.34-3.88) (p < 0.0001) or in passive smokers compared to those not exposed to smoking with odds ratio of 1.82 (95% CI 1.32-2.52) (p < 0.0001). The 1998 study showed similar results for smoking habits, passive smoking and prevalence of bronchitis symptoms as with the 1995 study. These results document that increased bronchitis symptoms occur in teenagers exposed to active or passive smoking.

Association between passive cigarette smoking and the risk of developing acute coronary syndromes: the CARDIO2000 study.

Pitsavos C, Panagiotakos DB, Chrysohoou C, Tzioumis K, Papaioannou I, Stefanadis C, Toutouzas P.

Department of Cardiology, School of Medicine, University of Athens, Greece.

Although the effect of smoking on human health has been established as a major risk factor, the effect of passive smoking is controversial. The purpose of this study was to investigate the association between passive smoking and the risk of acute coronary syndromes (ACS) among nonsmokers. Eight hundred and forty-eight patients with the first event of ACS and 1078 cardiovascular disease-free matched controls completed a detailed questionnaire regarding their exposure to environmental smoke. Two hundred and ninety-seven (35%) of the patients and 259 (24%) of the controls were defined as nonsmokers and passive smokers, respectively. After controlling for several potential confounders, the results showed that nonsmokers exposed to cigarette smoke increased the risk of ACS by 51% (odds ratio = 1.51, 95% confidence interval 1.21-2.99) compared with nonsmokers not exposed to smoke. It was estimated that 34 coronary events per 134 subjects would occur as a result of passive smoking during their lifetime. Consequently, this study supports the hypothesis that passive smoking increases the risk of developing acute coronary syndromes. Given the high prevalence of cigarette smoking in many developing societies, the public health consequences of passive smoking with regard to coronary heart disease may be important.

Environmental tobacco smoke and the risk of cardiovascular disease.

Jousilahti P, Patja K, Salomaa V.

University of Helsinki, Department of Public Health, Finland. pekka.jousilahti@ktl.fi

Disease risk due to smoking is not limited to smokers only. Passive smoking, exposure to environmental tobacco smoke, is associated with adverse health effects, and it increases the risk of several diseases. This paper summarizes the cardiovascular effects of tobacco smoke and the current data on the effects of environmental tobacco smoke on the development of cardiovascular disease. According to the results of epidemiologic and experimental studies, environmental tobacco smoke has marked harmful effects on the cardiovascular system. It is estimated that it increases the risk of an acute event of coronary heart disease by 25-35%. Even though the number of studies conducted in the work environment is small, there is no reason to assume that the cardiovascular effects of environmental tobacco smoke differ markedly between the home and the workplace. Firm and timely actions are needed to protect people from exposure to environmental tobacco smoke, both in occupational and other environments.

Health effects of tobacco use and exposure.

Bartal M.

Department of Respiratory Diseases, CHU Ibnou Rochd, University Hospital, Casablanca, Morocco. bartal@iam.net.ma

Tobacco is still widely consumed in a variety of different ways, mainly as smokeless tobacco and cigarette smoking. Four traits characterize tobacco use whatever the way of using it: 1) addiction linked to nicotine is behind all the tobacco hazards; 2) individual variation in tobacco susceptibility; 3) dose-response relationship; 4) time-lag effect. Smokeless tobacco, chewed or snuffed can lead mainly to inflammation of the oral cavity and oral cancers. Cigarette smoking accounts for 65-85% of global tobacco consumption. Active smoking can cause: 1) respiratory disorders culminating in chronic obstructive pulmonary disease (COPD) and emphysema; 2) cardiovascular hazards by way of increased vascular spasm and atherosclerosis leading to acute and chronic myocardial events, cerebral and peripheral vascular diseases; 3) cancers: twelve types are caused or related to cigarette smoking. Lung cancer is still the leading cause of cancer death in most high-income countries where data are available. An excess mortality is associated with smoking, with a 2-fold greater risk in smokers than in nonsmokers throughout middle age. The exposed pregnant woman subjects herself and her pregnancy to risks, and her fetus to growth retardation and perinatal morbidity and mortality. Passive smoking implicates 20-80% of the whole population. It can be nearly as harmful as active smoking depending upon risk factors, and can lead to short as well as to long-term effects. Children are the most vulnerable population particularly during the first years of life. Passive smoking increases risks for higher and lower respiratory tract illness but a smoke-free environment improves all these disorders. Ischemic heart diseases and lung cancer are the main risks for non smoking adults exposed to cigarette smoke. Tobacco use and exposure is the single most important source of preventable morbidity, disability and premature mortality. But giving up smoking helps at any time, the sooner the better. Health professionals should be the key advocates in tobacco prevention.

Negative effects of passive smoking on the (unborn) child]

[Article in Dutch]

Hofhuis W, Merkus PJ, de Jongste JC.

Erasmus Medisch Centrum, Sophia Kinderziekenhuis, afd. Longziekten, Postbus 2060, 3000 CB Rotterdam.

The negative effects of passive smoking on the health of the foetus or child continue to receive little attention, despite the large volume of research in this area. Passive smoking during pregnancy is associated with low birth weight, a reduction in head circumference at birth, and a far higher incidence of sudden infant death syndrome. Exposure to cigarette smoke also leads to a decreased lung function, an increased risk of severe infections, including respiratory syncytial virus bronchiolitis, meningococcal disease and middle ear infections. There is no association between passive smoking and the development of allergic asthma, but passive smoking does cause an increase in the prevalence of respiratory symptoms in children with or without asthma. Finally, there is a relation between passive smoking and behavioural disorders including attention deficit/hyperactivity disorder (ADHD). Passive smoking before birth seems even more harmful than after birth. A causal relationship is suggested in most studies, or has been proven by animal experiments. A decreased birth weight in general increases the risk of developing chronic diseases as an adult, such as hypertension, cardiovascular disease and type 2 diabetes mellitus. This extensive knowledge about the adverse health effects of smoke exposure in (unborn) children deserves greater attention in the counselling of pregnant women, and in anti-smoking campaigns.

Smoking and asthma]

[Article in Danish]

Ulrik CS, Lange P.

Lungemedicinsk klinik 223, H:S Hvidovre Hospital, DK-2650 Hvidovre. csulrik@dadlnet.dk

Cigarette smoking is a well-known health hazard, probably not least for patients suffering from asthma. This review gives a short overview of the effects of passive and active smoking on the inception and outcome with of longitudinal changes in the lung function and mortality of patients with asthma. Substantial evidence suggests that smoking affects asthma adversely. Exposure to environmental tobacco smoke, especially maternal smoking in children, may be a significant risk factor for asthma. Such exposure in patients with established asthma is not only associated with more severe symptoms, but also with a poorer quality of life, reduced lung function, and increased utilisation of health care including hospital admissions. Active smoking does not appear to be a significant risk factor for asthma, but is associated with a worse outcome with regard to both longitudinal changes in lung function and asthma-related mortality. Based on current knowledge, it is therefore of utmost importance to encourage patients with asthma not to smoke, and accordingly these patients should be given full support in their right to a smoke-free environment.

[Lung injury caused by passive smoking and its effects on cytokines in rats]

[Article in Chinese]

Pang B, Wang C, Weng X, et Al.

Red Cross Chaoyang Hospital, Beijing 100020, China.

OBJECTIVE: A rat model with chronic bronchitis was replicated by passive inhalation of cigarette smoking fume to study its long-term effects on lung injury and nitric oxide (NO), interluekin-6 (IL-6), interleukin-8 (IL-8). METHODS: Levels of nitrogen dioxide (NO(2)) and nitrogen trioxide (NO(3)) were measured with spectrophotometry in rats indicating their level of nitric oxide (NO). Levels of IL-6 and IL-8 were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Levels of NO in serum, bronchial alveolar lavage fluid (BALF) and lung tissue in the smoking group were significantly lower than those in the normal controls (P < 0.01). But, levels of IL-6 and IL-8 were higher in the smoking group than those in the controls. CONCLUSION: Long-term passive smoking could cause injury of lung tissue to certain extent, reduction in secretion of NO in endothelial cells and damage to pulmonary vessels.

The public health harm of tobacco and its prevention in Hong Kong.

Lam TH.

Department of Community Medicine, The University of Hong Kong, Patrick Manson Building South Wing, 7 Sassoon Road, Pokfulam, Hong Kong.

This paper briefly reviews the health hazards associated with smoking, including passive smoking, with specific reference to local (Hong Kong) evidence. A Medline search of Hong Kong papers from January 1966 to January 1998 was made, and these and other relevant papers were reviewed. In Hong Kong, at least 10 people die daily from smoking- related diseases. Local studies show that smoking is associated with lung cancer, oesophageal cancer, liver cancer, ischaemic heart disease, peripheral vascular disease, ischaemic stroke, peptic ulcer, osteoporosis, impaired lung function, respiratory symptoms, and other adverse health effects. Smoking in pregnant women can result in smaller babies being born. Pooled results from four case-control studies show a 60% excess risk of lung cancer due to exposure to environmental tobacco smoke. Several studies confirm the link between exposure to environmental tobacco smoke and respiratory illness, hospitalisation, and asthma in children. The risks of smoking (one of every two smokers will be killed by tobacco) are not well known and are underestimated by both doctors and the public. Stronger health messages and more local evidence are needed to support tobacco control in Hong Kong.

Smoking, passive smoking and lung cancer cell types among women in Poland.

Rachtan J.

Epidemiology Unit, Centre of Oncology, M. Sklodowska-Curie Memorial Institute, Garncarska 11, 31-115 Cracow, Poland. z5rachta@cyf-cr.edu.pl

A case-control study involving 242 women with histologically confirmed lung cancer and 352 healthy controls, was conducted in Cracow, Poland between 1991 and 1997. Subjects were interviewed about their exposure to smoking, passive smoking and other suspected risk factors, according to a structured questionnaire. Multivariate analysis has shown that cigarette smoking was the most strongly active risk factor in female lung cancer. The strongest influence of this factor was observed with reference to small cell carcinoma and squamous cell carcinoma. It has also been observed that passive smoking exposure during childhood before the age of 18, significantly increased risk of squamous cell carcinoma, small cell carcinoma and all cell types combined. A similar effect was observed for adenocarcinoma, but there was no statistical significance.

Effect of passive smoking on respiratory symptoms, bronchial responsiveness, lung function, and total serum IgE in the European Community Respiratory Health Survey: a cross-sectional study.

Janson C, Chinn S, Jarvis D, Zock JP, Toren K, Burney P; European Community Respiratory Health Survey.

Department of Medical Sciences, Respiratory Medicine and Allergology, Uppsala University, Akademiska sjukhuset, Uppsala, Sweden. christer.janson@medsci.uu.se

BACKGROUND: Passive smoking is widespread, and environmental tobacco smoke contains many potent respiratory irritants. This analysis aimed to estimate the effect of passive smoking on respiratory symptoms, bronchial responsiveness, lung function, and total serum IgE in the European Community Respiratory Health Survey. METHODS: This analysis included data from 7882 adults (age 20-48 years) who had never smoked, from 36 centres in 16 countries. Information on passive smoking, respiratory symptoms, asthma, and allergic rhinitis was gathered through a structured interview. Spirometry and methacholine challenge were carried out, and total and specific IgE were measured. The effect of passive smoking was estimated by means of logistic and multiple linear regression for each country and combined across countries by random-effects meta-analysis. FINDINGS: In 12 of the 36 centres, more than half the participants were regularly involuntarily exposed to tobacco smoke. The prevalence of passive smoking in the workplace varied from 2.5% in Uppsala, Sweden, to 53.8% in Galdakao, Spain. Passive smoking was significantly associated with nocturnal chest tightness (odds ratio 1.28 [95% CI 1.02 to 1.60]), nocturnal breathlessness (1.30 [1.01 to 1.67]), breathlessness after activity (1.25 [1.07 to 1.47]), and increased bronchial responsiveness (effect -0.18 [-0.30 to -.05]). Passive smoking in the workplace was significantly associated with all types of respiratory symptoms and current asthma (odds ratio 1.90 [95% CI 0.90 to 2.88]). No significant association was found between passive smoking and total serum IgE. INTERPRETATION: Passive smoking is common but the prevalence varies widely between different countries. Passive smoking increased the likelihood of experiencing respiratory symptoms and was associated with increased bronchial responsiveness. Decreasing involuntary exposure to tobacco smoke in the community, especially in workplaces, is likely to improve respiratory health.

Turning science into junk: the tobacco industry and passive smoking.

Samet JM, Burke TA.

Department of Epidemiology, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, Md 21205, USA. jsamet@jhsph.edu

In this issue, Glantz and Ong offer a powerful analysis of the tobacco industry's attempt to discredit the scientific evidence on passive smoking, particularly the industry's use of the label "junk science." Environmental epidemiologic studies in other arenas have also been targets for the "junk science" label. Lessons for researchers involved in high-stakes issues in the public policy arena include a need for awareness of competing interests, for transparency concerning funding, and for adherence to rigorous quality assurance and peer review practices. The goal of "sound science" seems an admirable one; it should not, however, be used to dismiss available but uncertain evidence in order to delay action.

Environmental tobacco smoke and lung function in employees who never smoked: the Scottish MONICA study.

Chen R, Tunstall-Pedoe H, Tavendale R.

Cardiovascular Epidemiology Unit, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, UK. rchen@cve.dundee.ac.uk

OBJECTIVES: To investigate the relation between lung function in employees and exposure to environmental tobacco smoke (ETS) at work and elsewhere. METHODS: Never smokers in employment (301) were identified from the fourth Scottish MONICA survey. They completed a self administered health record, which included details of exposure to ETS, and attended a survey clinic for physical and lung function measurements, and for venepuncture for estimation of serum cotinine. Differences in lung function in groups exposed to ETS were tested by analysis of variance (ANOVA), the exposure-response relation by a linear regression model, and a case-control analysis undertaken with a logistic regression model. RESULTS: Both men and women showed effects on forced expiratory volume in the first second (FEV(1)) and forced vital capacity (FVC) from exposure to ETS-higher exposure going with poorer lung function. This was found at work, and in total exposure estimated from ETS at work, at home, and at other places. Linear regression showed an exposure-response relation, significant for ETS at work, total exposure, and exposure time/day, but not at home or elsewhere. Compared with those not exposed to ETS at work, those who were exposed a lot had a 254 ml (95% confidence interval (95% CI) 84 to 420) reduction in FEV(1), and a 273 ml (60 to 480) reduction in FVC after adjusting for confounders. Although lung function was not significantly associated with serum cotinine in all the data, a significant inverse relation between cotinine concentration and FVC occurred in men who had had blood collected in the morning. Case-control analysis also showed a significant exposure-response relation between ETS, mainly at work, and lung function. A higher exposure measured both by self report and serum cotinine went with lower lung function. CONCLUSION: The exposure-response relation shows a reduction in pulmonary function of workers associated with passive smoking, mainly at work. These findings endorse current policies of strictly limiting smoking in shared areas, particularly working environments.

Health consequences of passive smoking]

[Article in German]

Haustein KO.

Institut fur Nikotinforschung und Raucherentwohnung, Erfurt. haustein@inr-online.de

Environmental tobacco smoking (ETS) represents a main risk factor for the generation of diseases of the respiratory tract and of the cardiovascular system in spite of statements to the contrary. ETS enhances the risk of lung cancer by a factor of 2-3. Newborn and small children (< 2 years of life) are at high risk if they live within this period of time in a household exposed to maternal more than fraternal smoking. Endothelial cells of the blood vessels are damaged as early as during the first month of life of passive smoking children, and these defects can be detected during the first decade of life. ETS over a period of more than ten years changes the intima/media ratio by enhancing the thickness of the vessel wall. Additionally, poor health behaviour is seen in households of smokers because the behaviour of the parents is transferred to that of their children, and this behaviour is the starting point of further health risks and damages. The presented data should cause a call for primary smoking prevention preferably among children and young persons on the one hand, and the organisation of programs against ETS at the workplace and in public buildings, as well as in the private house on the other hand. Non-smokers must be informed about the risks and dangers of ETS more than it is the case up to now.

Acute effects of passive smoking on the coronary circulation in healthy young adults.

Otsuka R, Watanabe H, Hirata K, Tokai K, Muro T, Yoshiyama M, Takeuchi K, Yoshikawa J.

Department of Internal Medicine and Cardiology, Osaka City University Medical School, 1-4-3 Asahimachi Abeno-ku, Osaka City, Japan 545-8585.

CONTEXT: Recent studies have shown that passive smoking is a risk factor for ischemic heart disease and may be associated with vascular endothelial dysfunction. The acute effects of passive smoking on coronary circulation in nonsmokers are not known. OBJECTIVE: To determine the acute effects of passive smoking on coronary circulation using coronary flow velocity reserve (CFVR), assessed by noninvasive transthoracic Doppler echocardiography. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional study conducted from September 2000 to November 2000 among 30 Japanese men (mean age, 27 years; 15 healthy nonsmokers and 15 asymptomatic active smokers) without history of hypertension, diabetes mellitus, or hyperlipidemia. MAIN OUTCOME MEASURES: Coronary flow velocity reserve, calculated as the ratio of hyperemic to basal coronary flow velocity induced by intravenous infusion of adenosine triphosphate and measured in each participant before and after a 30-minute exposure to environmental tobacco smoke. RESULTS: Heart rate and blood pressure responses to adenosine triphosphate infusion were not affected by passive smoking exposure in either group. Passive smoking exposure had no effect on basal coronary flow velocity in either group. Mean (SD) CFVR in nonsmokers was significantly higher than that in active smokers before passive smoking exposure (4.4 [0.91] vs 3.6 [0.88], respectively; P =.02), while CFVR after passive smoking exposure did not differ between groups (P =.83). Passive smoking exposure significantly reduced mean (SD) CFVR in nonsmokers (4.4 [0.91] vs 3.4 [0.73], respectively; P<.001). CONCLUSIONS: Passive smoking substantially reduced CFVR in healthy nonsmokers. This finding provides direct evidence that passive smoking may cause endothelial dysfunction of the coronary circulation in nonsmokers.

The miseries of passive smoking.

Nelson E.

Institute of Hygiene and Occupational Medicine, University Medical Center, Essen, Germany.

Passive smoking is defined as an involuntary exposure to a combined but diluted cigarette sidestream smoke (SS, gas and particle phases that are evolved from the smoldering end of a cigarette while the smoker is not puffing) and the exhaled smoke from smokers. SS contains numerous cytotoxic substances such as polycyclic aromatic hydrocarbons (PAHs), aromatic amines, nitrosamines, heavy metals, poisonous gases, pesticide residues, and radioactive elements in quantities much higher than those found from the cigarette mainstream smoke (MS) which is puffed by smokers. Passive smoking is found to be the cause of death from cancers and cardiac disease. Furthermore, it damagingly involves reproductive organs, the nervous system, genetic materials, and is particularly hazardous to mother and child during pregnancy and to those with a history of asthma, chronic infections, induced or earned immune deficiency, or predisposed susceptibility.

Active and passive tobacco exposure.

Gidding SS.

Nemours Cardiac Center, 1600 Rockland Road, 19899, Wilmington, DE, USA

Both passive and active exposure to tobacco smoke have adverse cardiovascular consequences for children and adolescents. Smoking as a habit begins in mid-adolescence and is perpetuated by the highly addictive nature of nicotine. Smoking has been associated with decreased life expectancy from all causes and early atherogenesis. The physiologic effects of active, and possibly passive smoke exposure include endothelial injury, increased oxidizability of LDL cholesterol, lower HDL cholesterol, impaired exercise performance, and altered oxygen delivery. Physician roles have been limited to research into the harmful nature of tobacco in the past, but new roles in advocacy against tobacco companies and the treatment of nicotine addiction are evolving.

Mad Kally

With all those illnesses from 2nd hand smoke, it's a wonder that there's anyone left alive on the planet. There is no question that smoking causes all these things. I am not a smoker, I am a hospice nurse. I watch people die for a living, I haven't seen one from 2nd hand smoke yet. I've seen hundreds with primary lung CA and other illnesses who were smokers. Some turn off their O2 and keep smoking until the day they die. They might as well, quitting at that point isn't going to save them.

I was an Oncology Certified Nurse and chemo certified before hospice. I didn't run into any then either. Where are they? I'm really curious.

Dr Rick

Yes, this study was designed to look at predictors of mortality in patients with known coronary artery disease (CAD), and it found that current smokers with CAD had an odds ratio of 1.29 to 1.66 of dying during the study period over nonsmokers. The odds ratios are reported as a range in which the numbers can be "confidently" considered accurate instead of due to random chance, as any statistic, no matter how large of a pool it is drawn upon, can be due to random variations.

Age was the strongest predictor (odds ratios 1.75 and 2.25), so those with CAD should avoid both aging and cigarette smoking to decrease their risk of death during a given time period. However, it is much harder for people to do the former than the latter, so doctors often counsel smokers to stop smoking but rarely counsel anyone to stop aging.

The finding that current smoking is a risk factor coincides with many other studies that have shown a marked decline in morbidity and mortality rates when smokers quit smoking. The risk of cardiac deaths for a former smoker drops almost to that of a "never-smoker" within 3 years of smoking cessation; the risk of lung cancer drops to similar levels over about 10 years.

By itself, perhaps nothing, but this is just one of thousands of studies performed over the past 40 years on various populations including those without underlying illnesses. It is clear from this large body of evidence that, regardless of your current health status, cigarette smoking increases the chances that you will get sick or die over a given time period.

The numbers have been published extensively in the primary literature. Here's one published just last month:

Epidemiology, January 1, 2003; 14(1): 24-9.

Smoking, blood pressure and serum cholesterol-effects on 20-year mortality.

S Houterman, WM Verschuren, and D Kromhout

"BACKGROUND To study the impact of smoking and blood pressure conditional on serum total cholesterol levels, we investigated the 20-year mortality risk associated with high systolic blood pressure (>/=140 mmHg) and smoking, at low (<5.2 mmol/Liter), medium (5.2-6.49mmol/Liter), and high (>/=6.5 mmol/Liter) serum total cholesterol levels.METHODS The study population comprised a cohort of 50,000 men and women age 30-54 years, examined between 1974 and 1980, in five Dutch towns. The duration of follow-up averaged 20 years. Age-adjusted relative risks (RRs) for mortality from coronary heart disease (CHD), cardiovascular diseases (CVD) and all causes were estimated, for six risk profiles (based on levels of total cholesterol, systolic blood pressure and smoking), using Cox proportional hazards analysis.RESULTS Given a low cholesterol level, smoking had a larger impact than elevated blood pressure on CHD, CVD and all-cause mortality. The combination of elevated blood pressure and smoking among persons with low cholesterol was associated with RRs of 3.0 for CHD, 6.0 for CVD and 4.1 for all-cause mortality in men, and 2.3, 3.6 and 2.6, respectively, in women. Among persons with high cholesterol, the combination of high blood pressure and smoking was associated with RRs of 9.7 for CHD, 13.9 for CVD and 5.7 for all-cause mortality in men, and 15.9, 9.3 and 4.3, respectively, in women. For each risk profile, the absolute number of CHD, CVD and total deaths was larger in men than in women.CONCLUSIONS The results demonstrate the potential power of a multifactorial approach to risk factor reduction in the prevention of cardiovascular diseases and all-cause mortality."

You can find thousands more on medline, or you can save yourself the bother and just look at Nuno Figueira's post above.


The one above is from the Netherlands; similar studies from around the world can be found in the medical literature.

I think that the worth of something should be balanced against its costs, so I don't think that we should restrict smoking no matter what the costs. But that's a seperate though related argument from the health effects of smoking and second-hand smoke.

Nobody is suggesting that exposure to second-hand smoke will certainly kill everyone, just as no one would reasonably suggest that not wearing a seatbelt will result in certain death. The fact is, the vast majority of people that are exposed to second-hand smoke or that don't wear their seatbelts don't die from either of these, but nonetheless, the risks of an adverse efect upon one's health or life is increased by living with a curent smoker and/or by not wearing a seatbelt while travelling by car.

Studies, like the one I cited above, show that even people with serious illnesses can benefit by not smoking. In other studies, patients with head, neck, and lung cancers that quit smoking have been found to have longer survivals than those that don't

Come-on, now, Kally; did you really take a thorough history about second-hand smoke exposure from every single patient you saw?


Rick

Mad Kally

Indeed it is...Ricky, I really did ask them if they were or ever were smokers. THEY ALL WERE! I swear on the babble. lol

LeftCoast

My Wife's Father died at the age of 50 of a smoking caused heart attack about 15 years ago (this was before I met her so I really don't think of him as my FIL). He was a multiple pack-a-day smoker for all of his adult life. From what they were told, it was probably better that he died that way (unpleasant to be sure, but relatively quick), as the autopsy showed that he was at most 2 or 3 years away from developing lung cancer.