ps418

Thank no-God that this same type of logic is not be applied to all environmental pollutants! There'd be no industry, no driving, no food additives, no safe levels of manufacturing waste. And what's more, the study I cite below shows that with proper ventilation, the concentration of ETS in no-smoking sections is not significantly greater than in buildings where smoking is banned altogether, which is obviously a satisfactory level for anyone.

I basically agree with you. Both smokers and nonsmokers can be accomodated without across the board bans with proper partioning and ventilation.

Not a single one the sources you quoted reported what I would call a 'significant' increase in risk. Furthermore, contrary to what you appear to think, many studies that have looked at the association between ETS and risk for CHD and lung cancer have reported a lack of significant association. You're making it sound like the one I cited in the OP is the only one, which is simply incorrect.

You mean, that crap called common sense? The study was a case-control with only 80 subjects (who were cats). Why pay particular attention to this one, when the one I cited was a prospective study and included tens of thousands of human subjects, other than a desire to reach a particular conclusion?

Yes, some scientists are concluding this, while others are concluding that the most plausible interperetation does not favor a causal association.

Or simply improve ventilation and partitioning, which will reduce the concentrations to extremely low levels not significantly different from that in places where smoking is banned altogether. See for instance:

Jenkins et al, 2001. Environmental Tobacco Smoke in the Nonsmoking Section of a Restaurant: A Case Study. Regulatory Toxicology and and Pharmacology 34, 213-220.

In this study it is shown that with good ventilation, ETS in nonsmoking sections is no worse than in establishments bannign smoking altogether. In addition, there are plenty of studies on workplace ETS exposure's relationship with heart disease and cancer that find a null or insignificant result, so as with the risk of cancer in nonsmoking spouses of smokers, the evidence for increased risk is weak at best. See for instance:

Wu] AH, Henderson BE, Pike MC, Yu MC. Smoking and other risk factors for lung cancer in women. Journal National Cancer Institute 1985;74(4):747-751. Nonsmoker data given for adeno-carcinoma only. "For nonsmoking ADC cases, we did not observe any elevated risk associated with passive smoke exposure ... at work (RR=1.3; 95% CI=0.5, 3.3)." 29 ADC cases.

Kabat GC, Wynder EL. Lung cancer in nonsmokers. Cancer 1984;53:1214-1221. (Men) "Eighteen of 25 cases reported havin]g been exposed to cigarette smoke at work compared to 11 of 25 controls. The difference is just statistically significant (p=0.05)." (Women) "No differences on exposure to passive smoking at home or at work were found in women,...26 of 53 cases were exposed at work compared to 31 of 53 controls." [Calculated RRs=1.6 & 0.6; 1.1 all. Male controls may have underreported exposure, since it is supposedly less than females despite more male smoking.]

Garfinkel L, Auerbach O, Joubert L. Involuntary smoking and lung cancer: A case-control study. Journal National Cancer Institute 1985;75(3):463-469. "OR for exposure at work during the last 5 years was 0.88; for the last 25 years, it was 0.93." CIs 0.66-1.18 and 0.73-1.18. 134 cases.

Janerich DT, Thompson WD, Varela LR, Greenwald P, Chorost S, Tucci C, Zaman MB, Melamed MR, Kiely M, McKneally MF. Lung cancer and exposure to tobacco smoke in the household. New England Journal Medicine 1990;323:632-636. "Estimating the odds ratio as a continuous variable for an equivalent differential of 150 person-years of exposure gave an odds ratio of 0.91 (95 percent confidence interval, 0.80 to 1.04), indicating no evidence of an adverse effect of environmental tobacco smoke in the workplace...." 191 cases.

Stockwell HG, Goldman AL, Lyman GH, Noss CI, Armstrong AW, Pinkham PA, Candelora EC, Brusa MR. Environmental tobacco smoke and lung cancer risk in nonsmoking women. Journal National Cancer Institute 1992;84(18):1417-1422. "We found no statistically significant increase in risk associated with environmental tobacco smoke at work or during social activities (data not shown)." 210 cases.

http://www.forces.org/evidence/carol/carol37.htm

Denial of what? The evidence that ETS exposure is not signficantly associated with risk of CHD and lung cancer? I have no interest in living in denial of any true fact, including the carcinogenicity of ETS exposure, provided it is a true fact. If you wish to end the conversation, thats fine, but it would seem that you are the one who wishes to live in denial, not me.

Patrick

ps418

A few more points:

Since the researchers were only interested in the nonsmoking spouses of smokers, this is perfectly appropriate, and still leaves the researchers with a huge sample size. It would have been impossible to include the entire CPS group in the analyses.

That's right. Tobacco companies have every right to do this. By the same logic, pharmaceutical companies or researchers receiving money from pharmaceutical companies have every right to conduct research on their products, so long as they declare their interests and make their data available for peer review. The great thing about science is we don't have to ad hominem or guilt-by-association each other to death. Theoretically at least, we can set our standards of evidence and then let the data decide.

That's just a silly and totally unjustified ad hominem. I dont see any way in which Enstrom and Kabat are attempting to 'confuse' anyone. One could turn it around and say that anti-ETS are confusing the public by repeatedly calling insignificant results significant.

If this study is flawed, then at least it has the virtue of being much less flawed than the majority of the "50 very reputable studies" that report positive associations. This is what Gio Gori, former director of the Smoking and Health Program of the US National Cancer Institute, for which he received the US Public Health Service Superior Service Award, had to say about the study:

To boot, this paper controls for more confounding variables than do other studies. Richard Smith, editor of the BMJ, after explaining that the paper was deemed acceptable by the journals top two epidemiologist reviewers, writes:

George Davey Smith, a well-known and respected epidemiologist who reviewed Enstrom and Kabat, also said he thought the analyses were fine and the data unbiased. What is interesting to note here is not simply what some people are considering "flaws," but the steadfast and complete refusal of some critics to admit any value at all [e.g. No one is saying "Hmm, that's very interesting, but I'm still concerned about variable x. . ." ]. I can guarantee you that if the results supported a significant positive association, we'd be hearing from the very same people how detailed, thorough, and convincing the study is. How do I know this? Simple. Look at the enthusiastic endorsements of these same critics of much less-rigorous studies which appear to show an association.

It would be quite interesting to compare point by point the 50 studies that are being referred to "very reputable" to that of Enstrom and Kabat. As I pointed out, meta-analyses of these studies routinely fails to give a clearly signficant positive result, and to boot there is clear evidence of publication bias favoring positive associations, which would serve to skew meta-analyses towards a spurious positive association. LaVois and Layard (1995) write:

Publication bias in the environmental tobacco smoke/coronary heart disease epidemiologic literature. Regul Toxicol Pharmacol 1995 Feb;21(1):184-91.

From WeMD again:

As I already pointed out, I regard this as an uncritical interpretation of the CPS II data. A RR of 1.2 is of extremely doubtful significance to begin with, even more so when you consider that the RR for CHD for women exposed to ETS was only 1.1(!), that there was no significant dose-dependent risk increase, and that the authors admit that even this extremely weak association could be subject to confounding variables. And this is some of the 'best' evidence!

And now that I've seen the CPS II data for ETS-associated lung cancer, I can say the same thing about those conclusions. As reported by Cardenas et al (1997), the RR for nonsmoking men whose wives smoked was 1.1 (CI = 0.6-1.8), and RR among women was 1.2 (CI = 0.8-1.8).Included in their abstract for all the world to see is their cautionary note that "Most CIs included the null. Although generally not statistically significant, these results agree with the EPA summary estimate that spousal smoking increases lung cancer risk by about 20 percent in never-smoking women. Even large prospective studies have limited statistical power to measure precisely the risk from ETS."

In fairness, one subgroup did yield a higher RR: women married to men who smoked more than 40 cigarettes a day had a RR of 1.9, but with a very broad 95% CI of 1-3.6. By comparison, the CPS II data shows that the relative risk of lung cancer in smoking versus nonsmoking men is about 20, and in women about 8 -- undeniable epidemiological evidence that smoking significantly increases the risk of lung cancer.

At any rate, that the CPS II data was singled out as a proper study 'refuting' Enstrom and Kabat is telling, since Enstrom and Kabat actually control for more confounding variables and for pre-existing disease, and report a RR that is just 0.1-0.2 less. I can't think of any other area of public health science where people are making such emphatic and sweeping claims based on RR's hovering around 1.1-1.2.

Cardenas et al, Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study II. Cancer Causes Control 1997 Jan;8(1):57-64.

Patrick

Nuno Figueira

There you go. I'm also against placing exaustion pipes pumping into people faces, and I also keep my car below 2500 RPM and use unleaded fuel to minimize pollution, I'm also against the use of hydrogenated and trans fats in foods, against the stand the FDA is taking on the issue of fish contamination with heavy metals, etc....

I am a part of the solution, you, in this particular issue at least, are a part of the problem because you're fighting for the right of a few to hurt everyone else's health. I've said before, even if it was completely impossible for ETS to cause lung (or other) cancers you are still killing or simply degrading others life quality with your nasty habit. Smokers, as far as I'm concerned, have no rights so powerfull that allow them to disrespect others.




So answer these questions for me.

1- How much time do the average couples you know spend together?

2- How many of them have children and smoke in the house?

If you honestly answer these questions then you'll have discredited completely your dear research.








Denial of the fact that people die from ETS (1), that thousands of children get asthma, die from infant sudden death sindrome or develop some kind of respiratory disease thanks to your selfish disregard for others health.

And you know what really makes me sick? I once was one of you.



1-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

NialScorva

Except Patrick's entire point is that there's very little correlation showing that it's damaging to people's health at all. Are you reading?

And then you're legislating morality, not safety. Are people coming into your house and smoking? Where does your right to "quality of life" come from, and when does it end with respect to others being able to enjoy their "quality of life"? Do we ban peanuts from all public places since a few people have reactions far worse than any asthma patient's reaction to smoke? If not, then why and what is your line?

Saying it's "distgusting" and "nasty" is a rather pathetic criteria for banning things, altogether. You bait and switch from the science to the philosophical/moral issue. I'm a fence sitter on the issue, though I'm starting to lean towards treating ETS with the same respect as cell phone radiation and environmental EM as a health threat.

With you're last post, you seem to have given up on ETS as a scientific and public safety issue altogether? Why not just come out and say it?

Tenspace

If second-hand smoke got you really high, created a vicious addiction, and made you spend all your money and ruin your life, then yes, it would be an appropriate analogy. And you'd need to consider the government subsidies and popular culture/advertising that created this smoking problem to begin with. A much different case than putting heroin in the water supply.

Tenspace

Nuno Figueira

Wow!! Now this is truly amazing. Patrick is not saying that at all. The question is, are you reading? Have you seen any of the studies I posted?

My right to breath is a basic right, and to put it bluntly, since your habit is agravating my quality of life because a single hour of ETS will result in at least a couple of sleepness nights with asthma attacks I think I have the right to have my health respected and even to fight back to the point of physically assaulting you to protect my health.

You are completely delirious my friend. I posted around 15 studies showing adverse health effects resulting from ETS. Patrick showed one missconducted research and you showed nothing.

IF you are saying that no adverse health effects result from ETS then show me some scientifc evidence. I'm all hears (or eyes).

Tenspace

Quoting scientific research without providing references... kinda kills the credibility of what you're trying to say.

What a dangerous position to take. You don't give a rat's ass about smokers and they have no right to interfere with other's freedoms.... Okay, take your opinion and replace "Smoker" with "Obese Person" (or "Fatty" if you really are that insensitive).... Or, "SUV Drivers". There are a hell of alot of vices that we humans tolerate of each other. And many are more dangerous to outsiders than second-hand smoke. My concern is the venom you spew at smokers in your post: What other vices drive you to the edge like this?

Tenspace

Nuno Figueira

What? Don't dare to put words in my mouth. How the hell are you to do that?

Fat people don't hurt my health and expect me to stay silent about it.

And for the record. I didn't provide references because I posted the abstracts were I took that from in this same thread.

Nuno Figueira

And NialScorva,


You accused me of dropping science, well, here it is. Please do read it. How can you say that there are no adverse health effects resulting from ETS?

Passive smoking and lung cancer: a cumulative meta-analysis.

Taylor R, Cumming R, Woodward A, Black M.

Department of Public Health and Community Medicine, Faculty of Medicine, The University of Sydney, New South Wales. richardt@health.usyd.edu.au

OBJECTIVE: To review the epidemiological evidence for the association between passive smoking and lung cancer. METHOD: Primary studies and meta-analyses examining the relationship between passive smoking and lung cancer were identified through a computerised literature search of Medline and Embase, secondary references, and experts in the field of passive smoking. Primary studies meeting the inclusion criteria were meta-analysed. RESULTS: From 1981 to the end of 1999 there have been 76 primary epidemiological studies of passive smoking and lung cancer, and 20 meta-analyses. There were 43 primary studies that met the inclusion criteria for this meta-analysis; more studies than previous assessments. The pooled relative risk (RR) for never-smoking women exposed to environmental tobacco smoke (ETS) from spouses, compared with unexposed never-smoking women was 1.29 (95% CI 1.17-1.43). Sequential cumulative meta-analysed results for each year from 1981 were calculated: since 1992 the RR has been greater than 1.25. For Western industrialised countries the RR for never-smoking women exposed to ETS compared with unexposed never-smoking women, was 1.21 (95% CI 1.10-1.33). Previously published international spousal meta-analyses have all produced statistically significant RRs greater than 1.17. CONCLUSIONS: The abundance of evidence in this paper, and the consistency of findings across domestic and workplace primary studies, dosimetric extrapolations and meta-analyses, clearly indicates that non-smokers exposed to ETS are at increased risk of lung cancer. IMPLICATIONS: The recommended public health policy is for a total ban on smoking in enclosed public places and work sites.

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.

Indoor and outdoor smoking: impact on children's health.

Johansson A, Halling A, Hermansson G.

Division of Paediatrics, Department of Molecular and Clinical Medicine, Linkoping University, Linkoping, Sweden. anjoh@imv.liu.se

BACKGROUND: Many children are exposed to ETS (environmental tobacco smoke), which has both immediate and long-term adverse health effects. The aim was to determine the prevalence and nature of smoking among parents with infants and the association of indoor or outdoor smoking with the health of their children. METHODS: Mail-questionnaire study, which was performed in a county in the south-east of Sweden, as a retrospective cross-sectional survey including 1990 children, 12-24 months old. RESULTS: 20% of the children had at least one smoking parent; 7% had parents who smoked indoors and 13% parents who smoked only outdoors. Indoor smoking was most prevalent among single and blue-collar working parents. In the case of smoking cessation during pregnancy, smoking was usually resumed after delivery or at the end of the breast-feeding period. Coughing more than two weeks after a URI (upper respiratory infection), wheezing without a URI as well as pooled respiratory symptoms differed significantly between children of non-smokers and indoor smokers. CONCLUSION: Further research of the common belief that outdoor smoking is sufficient to protect infants from health effects due to ETS exposure is warranted.


Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Eisner MD.

Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, California, USA. eisner@itsa.ucsf.edu

The impact of environmental tobacco smoke (ETS) exposure on adult pulmonary function has not been clearly determined. Because adults with asthma have chronic airway inflammation, they may be a particularly susceptible group. Using data from the Third National Health and Nutrition Examination Survey (NHANES III), I examined the cross-sectional relationship between serum cotinine, a biomarker of ETS exposure, and pulmonary function among 10,581 adult nonsmokers and 440 nonsmoking adults with asthma whose cotinine and spirometry data were available. I generated residuals, which are observed minus predicted values (based on Crapo equations), for forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio to adjust for age, sex, and height. In addition, I used multivariate linear regression to control for sociodemographic characteristics and previous smoking history. Most adults with and without asthma had detectable serum cotinine levels, indicating recent ETS exposure (85.7% and 83.4%, respectively). Among nonsmoking male participants, I found no evidence that ETS exposure was related to decreased pulmonary function. In the nonsmoking female stratum, the highest cotinine tertile was associated with a lower FEV1 [-100 mL; 95% confidence interval (CI), -143 to -56 mL], FVC (-119 mL; 95% CI, -168 to -69 mL), and FEV1/FVC ratio (-1.77%; 95% CI, -2.18% to -1.36%). Among women with asthma, the highest cotinine tertile was also associated with decreased FEV1 (-261 mL; 95% CI, -492 to -30 mL), FVC (-291 mL; 95% CI, -601 to 20 mL), and FEV1/FVC ratio (-1.6%; 95% CI, -3.3% to 0.19%). In conclusion, ETS exposure is associated with decreased pulmonary function in adult females, especially those with asthma. This analysis should provide further impetus for public policies that promote smoke-free environments.

Environmental tobacco smoke exposure and nocturnal symptoms among inner-city children with asthma.

Morkjaroenpong V, Rand CS, Butz AM, Huss K, Eggleston P, Malveaux FJ, Bartlett SJ.

Department of Medicine, Johns Hopkins School of Medicine, the Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21224, USA.

BACKGROUND: Environmental tobacco smoke (ETS) is a frequent exposure and is linked to asthma among inner-city children. OBJECTIVE: We sought to examine the relationship among ETS exposure, select asthma symptoms, and consequences among inner-city children with asthma. METHODS: Data from interviews with primary caregivers of inner-city elementary school children with asthma were evaluated (n = 590). Caregiver reports of child asthma symptoms, exercise limitations, asthma management, health care use, and ETS exposure were examined. RESULTS: Smoking in the home was reported by 29.4% of primary caregivers. ETS exposure (yes/no) was not related to frequency of child nocturnal symptoms or other select asthma morbidity markers. However, among children exposed to ETS, the frequency and severity of child nocturnal symptoms were highest among children exposed to moderate-to-heavy levels of ETS. After controlling for child age, anti-inflammatory medication use, asthma primary care, and caregiver's education, exposure to higher levels of ETS was associated with nearly a 3-fold increase in nocturnal symptoms in children (odds ratio, 2.83; 95% CI, 1.22-6.55). CONCLUSION: Among elementary school inner-city children with asthma, exposure to higher levels of ETS was associated with increased frequency of nocturnal symptoms. Reducing the exposure of children with asthma to ETS should be a clear priority in developing effective asthma management plans for inner-city families.

The effects of environmental tobacco smoke on children: Information and implications for PNPs.

Brown ML.

School of Nursing, University of Texas Health Science Center, 1100 Holcombe Boulevard, Houston, TX 77030, USA.

Although much information is available about the harmful effects of smoking and exposure to environmental tobacco smoke (ETS), many children are in contact with ETS in their home every day. Health effects related to ETS vary from minor nasal irritation to an increased susceptibility to sudden infant death syndrome. ETS can also cause future health problems as exposed children become adults. Assessment of ETS exposure is an essential component of a patient's health history, and parents should be educated about the harmful effects of ETS and how to protect young children from it. Strategies for prevention of ETS exposure must be pursued to ensure improved health outcomes for all children.


Exposure to environmental tobacco smoke: association with personal characteristics and self reported health conditions.

Iribarren C, Friedman GD, Klatsky AL, Eisner MD.

Kaiser Permanente Division of Research, Oakland, California 94611, USA. cgi@dor.kaiser.org

STUDY OBJECTIVE: To examine the association between exposure to environmental tobacco smoke (ETS) and demographic, lifestyle, occupational characteristics and self reported health conditions. DESIGN: Cross sectional study, using data from multiphasic health checkups between 1979 and 1985. SETTING: Large health plan in Northern California, USA. PARTICIPANTS: 16 524 men aged 15-89 years and 26 197 women aged 15-105 years who never smoked. RESULTS: Sixty eight per cent of men and 64 per cent of women reported any current ETS exposure (at home, in small spaces other than home or in large indoor areas). The exposure time from all three sources of ETS exposure correlated negatively with age. Men and women reporting high level ETS exposure were more likely to be black and never married or separated/divorced, to have no college or partial college education, to consume three alcoholic drink/day or more and to report exposure to several occupational hazards. Consistent independent relations across sexes were found between any current exposure to ETS and a positive history of hay fever/asthma (odds ratio (OR)=1.22 in men, 1.14 in women), hearing loss (OR=1.30 in men, 1.27 in women), severe headache (OR=1.22 in men, 1.17 in women), and cold/flu symptoms (OR=1.52 in men, 1.57 in women). Any current ETS exposure was also associated with chronic cough (OR=1.22) in men and with heart disease (OR=1.10) in women. Self reported stroke was inversely associated with any current ETS exposure in men (OR=0.27). No associations were noted for cancer or tumour and for migraine. CONCLUSION: ETS exposure correlated with several personal characteristics potentially associated with adverse health outcomes. Although the study design precluded causal inference, ETS exposure was associated with several self reported acute and chronic medical conditions.

Tenspace

So, you don't see a difference between a casual smoker five seats over in a restaurant, and a guy blowing smoke in your face from the next barstool? I empathize with your health problems, but you seem a bit too eager to resort to physical violence.

Tenspace