scombrid

Those air filters work eh? I'll give them a look. Are they quiet? Thanks. I never noticed the smoke much until I moved out.

Of course mom smokes more now than when I was younger. I always wonder why she doesn't mind aggravating my asthma. "Oh no! your asthma is bothering you? <puff puff puff> that's awful <puff puff puff> my smoke isn't bothering you is it? <puff puff puff>". Man that nicotene is powerful. She even risked a security deposit on a rented beach house because it was cold outside and she wanted to light up in spite of the NO SMOKING signs of every wall.

scigirl

God did it!

I just finished reading a critique of that article at WebMD. Here's some interesting information about that british study, and studies in general about second hand smoke.

Click Here.

Call me crazy, but any study sponsored by the tobacco companies is a big warning flag in my book.

scigirl

scigirl

No they didn't. See the above critique of the article - it was flawed on several levels.

Yet another flaw in the study.

scigirl

Nuno Figueira

That's why I put "proved", and not proved.

ps418

You have yet to demonstrate that anything I've written amounts to misinformation, but if you're curious, I was a smoker until 1 year ago. I quit because of heart problems, and I was deathly afraid of dying while my daughter is still young. My grandmother died a horrible death from lung cancer (filterless camels for 50 years), and I think that anyone who values their health should quit smoking immediately. I have no interest whatsoever in assisting the tobacco industry in any way, though I do have an interest in the legitimate debate as to whether ETS is signficantly associated with heart disease and lung cancer.

What makes you think magic is required, other than your own apparent ignorance that carcinogenesis is dose-dependent? There are plenty of substances that are carcinogenic at high levels, but are not associated with cancer at much lower levels of exposure. By the same logic, eating 10-20 donuts a day is associated with obesity and heart disease, therefore there must be excess mortality associated with eating 1 donut a week, absent some magical mechanism.

You mean, if a substance is associated with elevated risk of cancer at high doses, but not at low doses, this requires a miracle? Regardless of how flawed the study in the OP might be, or all studies of ETS, this is just flat wrong.


Ok, you're crazy What matters to me is not how a study is funded --since any study could be dismissed out of hand on those grounds-- but who actually did the research, how big their sample was, how they measured outcomes, how many confounding variables they accounted for, how sophisticated the data analyses are, and so on. I'm more than willing to look at shortcomings in those areas, and change my mind accordingly. Thanks for posting that WebMD critique. I'll have a closer look at that monday. I will be especially interested in comparing the "50 very reputable studies" that find a significant link between ETS and lung cancer/heart disease with those that do not find such a link. For instance, I wonder if this includes the 30 studies that were included in the EPA metanalysis, which found a nonsignficant relative risk of 1.19? It will also be interesting to see how many of these studies meet the high standards being applied to the study in the OP. Furthermore, there is evidence of publication bias in these types of studies in favor of positive results (more on this monday), which further weakens the case for even these nonsignificant ratios.

I wonder if this is, as it sounds, simply a restatement of the conclusion of the EPA meta-nalysis, which concluded that the relative risk is 1.19, or the WHO study, which found a relative risk of 1.16, both of which are in fact nonsignficant results? If so, there is plenty of room to disagree about whether this is signficant.

EDIT TO ADD: I was correct about the extremely low rate ratios, at least with respect to ETS and CHD (I havent seen the CPS II data on lung cancer yet). The authors of the CPS II report on heart disease report a rate ratio of 1.22 (95% CI= 1.07 to 1.40) among never-smoking men married to currently smoking wives, and a rate ratio for women of only 1.10 (95% CI=0.96 to 1.27). The authors of that study also caution that "our data do not show consistent dose-response trends and are possibly subject to confounding by unmeasured risk factors."

Steenland K, Thun M, Lally C, Heath C. Environmental tobacco smoke and coronary heart disease in the American cancer society CPS-II cohort. Circulation 1996;94: 622-8.


Rather than look at the concensus itself, let's look at the evidence that the concensus is based upon. Certainly a signficant part of this concensus is based on the EPA and WHO reports, which produced nonsignficant increases in risk (yet called them signficant anyway), and were based on far smaller sample sizes. I'll change my mind in a heartbeat if the science is against me, but I'm not yet convinced that this is the case.

Patrick

Nuno Figueira

You have a point about concentration levels of carcinogenic sustances, but tell me, how are you going to find out who has the genetic factors that will "protect" them from the occurrence of those cancers and who doesn't and which levels will be acceptable to each?

The data is widely available but you chose to hold on to a missconducted study that didn't even measure the total amount and duration of exposure to second hand smoke and expect people to give you any credit in your views?

The link between ETS exposure and cancer risk is real, as is bewteen sudden infant death syndrome and asthma. What more would it take for you to change your mind?

Have a look at the other side, once again.

Environmental tobacco smoke and risk of malignant lymphoma in pet cats.

Bertone ER, Snyder LA, Moore AS.

Department of Biostatistics and Epidemiology, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003-9304, USA. ebertone@schoolph.umass.edu

Feline malignant lymphoma occurs commonly in domestic cats and may serve as a model for non-Hodgkin's lymphoma in humans. Several studies have suggested that smoking may increase the risk of non-Hodgkin's lymphoma. To evaluate whether exposure to household environmental tobacco smoke (ETS) may increase the risk of feline malignant lymphoma, the authors conducted a case-control study of this relation in 80 cats with malignant lymphoma and 114 controls with renal disease diagnosed at a large Massachusetts veterinary teaching hospital between 1993 and 2000. Owners of all subjects were sent a questionnaire inquiring about the level of smoking in the household 2 years prior to diagnosis. After adjustment for age and other factors, the relative risk of malignant lymphoma for cats with any household ETS exposure was 2.4 (95 percent confidence interval: 1.2, 4.5). Risk increased with both duration and quantity of exposure, with evidence of a linear trend. Cats with 5 or more years of ETS exposure had a relative risk of 3.2 (95 percent confidence interval: 1.5, 6.9; p for trend = 0.003) compared with those in nonsmoking households. These findings suggest that passive smoking may increase the risk of malignant lymphoma in cats and that further study of this relation in humans is warranted.


Involuntary smoking and lung cancer.

Boffetta P.

Unit of Environmental Cancer Epidemiology, International Agency for Research on Cancer, Lyon, France. boffetta@iarc.fr

Involuntary smoking contains human carcinogens. Exposure prevalence among adults is on the order of 40%. A meta-analysis of epidemiologic studies on lung cancer and exposure to involuntary smoking from the spouse included 51 studies. The overall relative risk (RR), based on 7369 cases of lung cancer, was 1.25 [95% confidence interval (95% CI) 1.15-1.37]. No evidence existed of an RR difference between the two genders, and study design had no influence on the results. The summary RR was lower for adenocarcinoma than for other histological types. In the largest studies cumulative exposure suggested a dose-response relationship with a unit risk of similar magnitude. The summary RR was 1.17 (95% CI 1.04-1.32) for workplace exposure. Several sources of bias may lead to both overestimation and underestimation of true association, and the most plausible interpretation favors a causal association. Even if excess risk from exposure to involuntary smoking is small, its large prevalence makes it an important environmental carcinogen.

[To smoke or not to smoke, in restaurants, hotels, and bars]

[Article in Spanish]

Lopez-Antunano FJ, Tovar-Guzman VJ.

Centro de Investigacion en Salud Poblacional, Instituto Nacional de Salud Publica, Cuernavaca, Mexico, Mexico. alantu@correo.insp.mx

A MEDLINE search was conducted to identify relevant references, to review the information on adverse effects of tobacco smoking and environmental tobacco smoke (ETS). Occupational exposure to ETS causes significant damages to food industry workers. High levels of mutagenic substances have been demonstrated in restaurant air as well as in the urine samples from those workers. Exposition to 3-aminophenyl, a hemoglobin-associated carcinogen. The best way to protect these workers is the reduction of tobacco smoking in restaurants, hotels, bars and taverns. In restaurant workers, ETS attributable risk for lung cancer is evident.

[Health impact of exposure to environmental tobacco smoke in Italy]

[Article in Italian]

Forastiere F, Lo Presti E, Agabiti N, Rapiti E, Perucci CA.

Dipartimento di epidemiologia ASL RME, via Santa Costanza 53, 00198 Roma. epiamb1@asplazio.it

Household and workplace exposure to environmental tobacco smoke (ETS) is associated with various deleterious health effects. We evaluated the health impact of ETS in Italy. We considered only those health conditions for which systematic quantitative reviews were available. We used relative risks from the reviews while data on the proportion of the Italian population exposed to ETS were derived from national statistics or from ad hoc studies. A total of 2.033 newborns per year are of low birth weight (< 2500 grams) in Italy (7.9%) because of maternal exposure to ETS during pregnancy. There are 87 sudden infant deaths (16.9%) due to post natal maternal active smoking. 21.3% of acute respiratory infections during the first two years of life are due to parental smoking (about 77.000 children); 27.000 cases of asthma (9.1%), 48.000 cases of chronic respiratory symptoms, 64.000 cases of middle ear effusions among children and adolescents are due to parental smoking exposure. The annual estimates of mortality from lung cancer and ischemic heart disease due to ETS exposure from the spouse are 221 and 1896, respectively. Workplace exposure is associated with 324 lung cancer deaths and 235 deaths from ischemic heart disease. Although these estimate are based on several assumptions and they have large uncertainties, the results underline the need and the urgency of public health measures to reduce ETS exposure in the household and in the workplaces in Italy.

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.


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.




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.

Environmental tobacco smoke and adult asthma.

Eisner MD.

Division of Occupational and Environmental Medicine, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, San Francisco, 350 Parnassus Avenue, Suite 609, San Francisco, CA 94117, USA. eisner@itsa.ucsf.edu

The long-term health consequences of ETS exposure have been established over the past two decades. Consistent epidemiologic evidence links ETS exposure with serious chronic health effects, including lung cancer and cardiovascular disease [1, 48, 49]. In this article, the evidence suggests a causal relationship between ETS exposure and new-onset asthma and asthma exacerbation among adults. Despite the growing knowledge of ETS-related health effects, smoking is still permitted in many public locations and workplaces [50, 51]. Because asthma is a visible condition among the general public, the evidence that links ETS exposure with adverse asthma health outcomes should provide policymakers with additional impetus for regulating public smoking and creating smoke-free public environments.

Risk factors for lung cancer among Canadian women who have never smoked.

Hu J, Mao Y, Dryer D, White K; Canadian Cancer Registries Epidemiology Research Group.

Centre for Chronic Disease Prevention and Control, Population and Public Health Brance, Health Canada, Ottawa, Ont.

Risk factors for lung cancer among women who had never smoked were assessed in a case-control study of 161 newly diagnosed histologically confirmed cases and 483 population controls between 1994 and 1997 in eight Canadian provinces. Measurement included socio-economic status, smoking habits, alcohol use, diet, residential and occupational histories and exposure to environmental tobacco smoke (ETS). Dose-response associations were observed for consumption of tea, adjusted odds ratios (ORs) 0.6 (95% confidence interval (CI) = 0.3-0.9) for 1-7 cups per week and 0.4 (95% CI = 0.2-0.7) for > or = 8 cups per week (P = 0.0008), and smoked meat, adjusted ORs 1.3 (95% CI = 0.8-2.3) for 0.5 slice per week and 2.1 (95% CI = 1.1-4.0) for >0.5 slice per week (P = 0.02). Regular use of shortening in cooking was also related to lung cancer. Increased ORs with borderline significance were found for total consumption of meat, eggs or French fries and fried potatoes. Passive exposure to ETS at home (or at work) may be associated with lung cancer risk among never-smoker women; the adjusted ORs were 0.7 (95% CI = 0.2-2.3), 1.2 (95% CI = 0.4-3.2), 1.5 (95% CI = 0.5-4.0) for 1-16, 17-30, and 31 or more years of combined residential and/or occupational ETS exposure, respectively, with a similar pattern for smoker-years of ETS exposure.

ps418

To make this easier, pick out the one study you think provides the most convincing evidence that ETS caused lung cancer or heart disease, and is not subject to the uncertainties and confounders plaguing the one you just got done criticising as more or less worthless. Surely you will want to apply the same high standards to those studies as you do to the one in the BMJ I cited.

Patrick

ps418

That the data is widely available should have tipped you off to the fact that we are in disagreement about what that evidence indicates.

Let's do. And this time, let's remove everything but the bottom line: the relative risks. Also, let me just concede that there may be a tiny, tiny increase in risk for CHD and lung cancer (the paper I cited said this as well) in those groups of nonsmokers exposed to the most ETS (nonsmoking spouses of smokers, for instance).

You've shown an ability to cut and paste from PubMed, but less ability to understand it. What's amazing here is that you actually seem to think these numbers support the position that ETS exposure is a major risk factor. I can only conclude that you and I have very different definitions of major risk. The first thing to note is that the risk ratios are consistently between about 0.7 and 1.6, usually closer to 1. 1 indicates no increase in risk, less than 1 indicates a protective effects of ETS (yes, some studies find this), and RRs or ORs>1 indicates increased risk due to ETS. Also note the extremely large CI's associated with those miniscule risks (e.g. CI of 0.4-4!), and that one of the studies supported a protective effect of 1-16 years of combined residential and/or occupational ETS exposure.

Let's look at relative risk of 1.2, reported as the RR for CHD, assuming that figure is correct. That means that if the rate of lung cancer in nonsmokers married to nonsmokers is 100 per 1,000,000 or 1 per 10,000, the rate in nonsmokers married to smokers would be 120 per 1,000,000, or 1.2 per 10,000. To call this a 'significant' risk is, in my view, quite misleading, and only serves to reinforce the opinion of some critics that the science is being abused to reach a preordained conclusion about ETS causing disease. And though the significance of these ratios varies depending on the sample size (a RR of less than 2 can be signficant, if the sample size is large enough), frequently ratios greater than 2 are dimissed as insignificant. The following examples were on a site discussing ETS:

And at any rate, even given my concession that the RR may be greater than 0, an overwhelmingly apparent conclusion of all the studies is that if ETS exposure increases relative risk at all, the increase in both relative and absolute risk is indeed very, very small (assuming its greater than 0, which is hardly certain). Its also inappropriate to apply these risk ratios to individuals who are exposed to ETS much less frequently than the study populations in which they were determined. Certainly the evidence does not suggest that if you are exposed to (probably low levels of) ETS once a week at a restaurant that you are at an appreciably increaseed risk of cancer or heart disease.

Patrick

ps418

With adequate ventilation and partitioning, patrons need not be affected at all by either smoke or flatulence. As a nonsmoker with a nonsmoking wife, I find that with a few irritating exceptions, restaurants do a good job of keeping our space smoke-free. Rather than banning smoking in private establishments across the board, I would like to see at least the option in at least some establishments (e.g. bars) of ventilation and partitioning requirements.

Patrick

Nuno Figueira

Listen, I never claimed that ETS resulted in a cancer risk similar to cigarrete smoking, but that the risk is there.

There's no way to measure if the quantities willl be enough to increase the risk of a particular person to get cancer and thus it should be banned from ALL public places. I have nothing against places destined to smokers, but I think I do have the right to walk in public places and not to get my health assaulted by smokers.


So one of the studies doesn't show a significant increase, have you seen the one on cats?


"Cats with 5 or more years of ETS exposure had a relative risk of 3.2 (95 percent confidence interval: 1.5, 6.9; p for trend = 0.003) compared with those in nonsmoking households."

Is 3.2 good enough for you? Or are you going to give that crap that a study on cats can't be extrapolated to humans?

And this is what scientists are concluding:

"Several sources of bias may lead to both overestimation and underestimation of true association, and the most plausible interpretation favors a causal association. Even if excess risk from exposure to involuntary smoking is small, its large prevalence makes it an important environmental carcinogen.
"

"The annual estimates of mortality from lung cancer and ischemic heart disease due to ETS exposure from the spouse are 221 and 1896, respectively. Workplace exposure is associated with 324 lung cancer deaths and 235 deaths from ischemic heart disease. Although these estimate are based on several assumptions and they have large uncertainties, the results underline the need and the urgency of public health measures to reduce ETS exposure in the household and in the workplaces in Italy.
"

"High levels of mutagenic substances have been demonstrated in restaurant air as well as in the urine samples from those workers. Exposition to 3-aminophenyl, a hemoglobin-associated carcinogen. The best way to protect these workers is the reduction of tobacco smoking in restaurants, hotels, bars and taverns. In restaurant workers, ETS attributable risk for lung cancer is evident.
"

"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.
"

If your point is that the risk might have been overestimated, fine. Even stilll, so what? One death is one too much. I don't give a rats ass about smokers because I too have been one and I've quit, but smokers have no rights to interfere with other people freedom.

Go live in denial, what do I care.