Nuno Figueira

Patrick, and the rest of the health problems related to ETS? Are you going to deny that?

I'm curious as to if you also support things like the US denial to comply to the regulamentiations in Kyoto protocol and are against all the pollution control measures the world is trying to establish.

Again to illustrate my point, a few more studies for you pro smokers to practice your denial skills on, and don't forget you are an active part of this problem:

environmental tobacco smoke and deaths from coronary heart disease in Canada.

de Groh M, Morrison HI.

Centre for Disease Prevention and Control, Health Canada, Ottawa, Ontario. margaret_de_groh@hc-sc.gc.ca

A series of recent meta-analyses have concluded that non-smokers who live with smokers face an elevated risk of coronary heart disease (CHD). In this study, we estimated the number of CHD deaths among non-smokers attributable to environmental tobacco smoke (ETS) exposure in their homes. Population-attributable risk estimates suggest that in 1997 over 800 Canadians died of CHD caused by passive exposure to ETS. This figure is likely an underestimation of the total number of CHD deaths attributable to ETS, since our study did not estimate the number of deaths among non-smokers caused by ETS exposure in the workplace. However, this partial picture can still help to highlight the burden of disease resulting from this pervasive involuntary environmental exposure.

Lifetime environmental exposure to tobacco smoke and primary lung cancer of non-smoking Taiwanese women.

Lee CH, Ko YC, Goggins W, Huang JJ, Huang MS, Kao EL, Wang HZ.

Graduate Institute of Medicine, School of Public Health, Kaohsiung Medical University, Taiwan, ROC.

BACKGROUND: For a female population with a high lung cancer mortality rate, such as Taiwanese women, who smoke relatively rarely, but live in an environment with high male smoking prevalence, the risk and population burden of lung cancer due to environmental tobacco smoke (ETS) are relatively important. METHODS: An age-matched case-control study was designed to investigate the effects of cumulative environmental exposure to tobacco smoke during childhood and adult life on lung cancer risk among non-smoking women in Taiwan. Information on passive smoking from all possible sources and life periods were obtained from interviews with 268 and 445 lifetime non-smoking cases and controls. Conditional logistic regression and synergism 'S' index were applied to the data to assess the independent and joint effects of passive smoking in different life stages while controlling for possible confounding variables. RESULTS: Risks of contracting lung cancer among women near-distantly exposed to the highest level of ETS in childhood (>20 smoker-years) and in adult life (>40 smoker-years) were 1.8-fold (95% CI: 1.2-2.9) and 2.2-fold (95% CI: 1.4-3.7) higher than that among women being never exposed to ETS, and the two variables accounted for about 37% of tumours in this non-smoking female population. Children were found to be more susceptible to ETS than adults and such early exposure was found to modify the effect of subsequent tobacco smoke exposure in adult life based on an additive interaction model. CONCLUSIONS: Environmental tobacco smoke exposure occurring in childhood potentiates the effect of high doses of exposure in adult life in determining the development of lung cancer. Smoking prohibition would be expected to protect about 37% of non-smoking Taiwanese women against lung cancer.

Measurement of environmental tobacco smoke exposure among adults with asthma.

Eisner MD, Katz PP, Yelin EH, Hammond SK, Blanc PD.

Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, California 94117, USA. eisner@itsa.ucsf.edu

Because the morbidity and mortality from adult asthma have been increasing, the identification of modifiable environmental exposures that exacerbate asthma has become a priority. Limited evidence suggests that exposure to environmental tobacco smoke (ETS) may adversely affect adults with asthma. To study the effects of ETS better, we developed a survey instrument to measure ETS exposure in a cohort of adults with asthma living in northern California, where public indoor smoking is limited. To validate this survey instrument, we used a passive badge monitor that measures actual exposure to ambient nicotine, a direct and specific measure of ETS. In this validation study, we recruited 50 subjects from an ongoing longitudinal asthma cohort study who had a positive screening question for ETS exposure or potential exposure. Each subject wore a passive nicotine badge monitor for 7 days. After the personal monitoring period, we readministered the ETS exposure survey instrument. Based on the survey, self-reported total ETS exposure duration ranged from 0 to 70 hr during the previous 7 days. Based on the upper-range boundary, bars or nightclubs (55 hr) and the home (50 hr) were the sites associated with greatest maximal self-reported exposure. As measured by the personal nicotine badge monitors, the overall median 7-day nicotine concentration was 0.03 microg/m(3) (25th-75th interquartile range 0-3.69 microg/m(3)). Measured nicotine concentrations were highest among persons who reported home exposure (median 0.61 microg/m(3)), followed by work exposure (0.03 microg/m(3)), other (outdoor) exposure (0.025 microg/m(3)), and no exposure (0 microg/m(3); p = 0.03). The Spearman rank correlation coefficient between self-reported ETS exposure duration and directly measured personal nicotine concentration during the same 7-day period was 0.47, supporting the survey's validity (p = 0.0006). Compared to persons with no measured exposure, lower-level [odds ratio (OR) 1.9; 95% confidence interval (CI), 0.4-8.8] and higher-level ETS exposures (OR 6.8; 95% CI, 1.4-32.3) were associated with increased risk of respiratory symptoms. A brief, validated survey instrument can be used to assess ETS exposure among adults with asthma, even with low levels of exposure. This instrument could be a valuable tool for studying the effect of ETS exposure on adult asthma health outcomes.


Acute exposure to environmental tobacco smoke and heart rate variability.

Pope CA 3rd, Eatough DJ, Gold DR, Pang Y, Nielsen KR, Nath P, Verrier RL, Kanner RE.

Department of Chemistry & Biochemistry, Brigham Young University, Provo, UT 84602, USA. cap3@email.byu.edu

Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Pathophysiologic pathways leading from ETS exposure to cardiopulmonary disease are still being explored. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. In this study we evaluated acute ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers. We conducted ambulatory electrocardiographic (ECG) monitoring for 8-hr periods while participants alternated 2 hr in nonsmoking and smoking areas. Nicotine and respirable suspended particle concentrations and participants' blood oxygen saturation were also monitored. We calculated time and frequency domain measures of HRV for periods in and out of the smoking area, and we evaluated associations with ETS using comparative statistics and regression modeling. ETS exposure was negatively associated with all measures of HRV. During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ETS exposures were not associated with mean heart rate or blood oxygen saturation. Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.

Nuno Figueira

Non-smoker lung cancer deaths attributable to exposure to spouse's environmental tobacco smoke.

Tredaniel J, Boffetta P, Saracci R, Hirsch A.

Unit of Environmental Cancer Epidemiology, International Agency for Research on Cancer, Lyon, France.

BACKGROUND: The causal relationship between environmental tobacco smoke (ETS) and lung cancer is established; however, the magnitude of the risk is not known. Therefore, it is conceivable that ETS is responsible for a number of lung cancer deaths because of the large number of smokers and the widespread presence of ETS. We estimated the number of lung cancer deaths occurring in 1990 in the European Union (EU), attributable to ETS generated by a spouse. METHODS: In each country and for each sex, we used the proportion of smokers and of married people in 1970 to estimate the number of lung cancer deaths not attributable to tobacco smoking occurring in married people, assuming a relative risk (RR) for active smoking equal to 10. We then assumed a prevalence of smoking among these deaths equal to the population at large, and estimated the number of deaths attributable to ETS based on an RR for ETS of 1.3. Additional analyses were carried out assuming different values of RR for smoking and exposure to spouse's ETS. RESULTS: Based on our best assumptions, we calculated that 1146 (839 females, 307 males) lung cancer deaths were attributable to exposure to spouse's ETS in the EU in 1990. All the hypotheses tested resulted in not less than several hundred deaths. CONCLUSION: Regardless of the limitations of this exercise, our results suggest that exposure to spouse's ETS represents a relatively important public health problem in the EU.

Nuno Figueira

I'm starting to feel like this is totally pointless, but one more:

Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study. II.

Cardenas VM, Thun MJ, Austin H, Lally CA, Clark WS, Greenberg RS, Heath CW Jr.

Epidemiology Division, Rollins School of Public Health, Emory University, Atlanta, GA, USA.

Environmental tobacco smoke (ETS) has been classified as a human lung carcinogen by the United States Environmental Protection Agency (EPA), based both on the chemical similarity of sidestream and mainstream smoke and on slightly higher lung cancer risk in never-smokers whose spouses smoke compared with those married to nonsmokers. We evaluated the relation between ETS and lung cancer prospectively in the US, among 114,286 female and 19,549 male never-smokers, married to smokers, compared with about 77,000 female and 77,000 male never-smokers whose spouses did not smoke. Multivariate analyses, based on 247 lung cancer deaths, controlled for age, race, diet, and occupation. Dose-response analyses were restricted to 92,222 women whose husbands provided complete information on cigarette smoking and date of marriage. Lung cancer death rates, adjusted for other factors, were 20 percent higher among women whose husbands ever smoked during the current marriage than among those married to never-smokers (relative risk [RR] = 1.2, 95 percent confidence interval [CI] = 0.8-1.6). For never-smoking men whose wives smoked, the RR was 1.1 (CI = 0.6-1.8). Risk among women was similar or higher when the husband continued to smoke (RR = 1.2, CI = 0.8-1.8), or smoked 40 or more cigarettes per day (RR = 1.9, CI = 1.0-3.6), but did not increase with years of marriage to a smoker. 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.

ps418

Let's go over a few more of Nuno's refs.

Notice that this article contributes absolutely nothing to the evidence that ETS exposure causes cancer/lung cancer. It simple picks a RR ratio from a review and uses it to estimate a number of deaths.

I agree with all of this -- except the assertion that "can be nearly as harmful as active smoking depending upon risk factors," because its ridiculous and wrong. A possible RR of 1.1 - 1.3 is not at all comparable to a RR or 8 or 20.


Notice again that this article adds absolutely no evidence. It simply claims on the basis of other research that ETS is a major risk factor, which is simply not supportable for CHD or lung cancer. At best it could be argued that it is A risk factor.

The article adds nothing to the debate here about ETS and CHD/lung cancer. I haven't made any claim regarding ETS and asthma.

And I already pointed out the problems with this one -- none of the ORs are even close to being statistically signficant, and the ORs for those exposed to 1-16 years of combined work/home ETS are less than 1, which taken at face value indicates a protective effect, not an increased risk.


As I already pointed, a funnel plot of these studies indicates publication bias. Since publication bias will skew the results of meta-analyses towards a spurious positive association, there are reasons to be less than certain of the reported OR of 1.2. Even a mild publication bias will lead to overestimation of both risk and statistical signficance (See for instance Copas and Shi, 2000. Reanalysis of epidemiological evidence on lung cancer and passive smoking. BMJ 320:417-418; Misakian et al, Publication Bias and Research on Passive Smoking: Comparison of Published and Unpublished Studies. JAMA 280:250-253). This is why I think the two CPS studies have a considerable advantage here. Plus, the inclusion of the Enstrom and Kabat CPS 1 data into will likely result in further reduced RRs/ORs in future meta-analyses.

This article does not provide data on ETS causation of lung cancer or CHD.

As all the data presented in this thread show, this is wrong. At best the data support an excess lung cancer risk of a factor of 0.2 or 20%, and that only in the nonsmoking spouses of smokers.

Smokers as a group display worse health habits and environmental influences do than nonsmokers (diet, non-ETS occupational carcinogens, neighborhood air quality), which is precisely why it is so important to control for all potential confounders in studies which purport to look for causal relationships. At any rate, this article is a review and provides no independent evidence for ETS causation of lung cancer or CHD.


[quote]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

. . . 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. [/quotes]

This article finds no relationship at all between ETS exposure and pulmonary function in males, and a very weak one in females. This article provides no independent evidence for ETS causation of lung cancer or CHD, which is what I'm interested in.

Again, I'm looking at ETS as a cause of CHD/lung cancer, not asthma symptoms. I agreed at the very beginning of this thread that ETS exposure can potentially cause respiratory symptoms.

[quote]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.[quote]

This supports what I said above about those exposed to ETS are more likely to be be exposed to other environmental/lifestyle risk factors, which would have the effect of producing a spurious association, which is why it is so important to correct for confounding variables.

Notice that ETS exposure is associated with hearing loss(OR=1.3!) much more so than with heart disease (OR=1.10), which is pretty interesting given that there is not a shred of evidence that smoking causes hearing loss, that self-reported stroke is "strongly" inversely correlated with ETS exposure (OR=0.27), and that the author specifically states that the study design precludes causal inference.

Patrick

ps418

I cited this study several posts ago. You must not be paying attention. I wrote:


Let's look at what your abstract actually says.

What part of "not statistically significant" don't you understand? What part of "most CIs included the null" don't you understand?

Patrick

ps418

Yet again you prove yourself unable to comprehend what you're posting. This article provides precisely zero evidence for ETS causation of CHD/lung cancer. It assumes an RR of 1.3 on the basis of other research and uses that RR to estimate a number of deaths due to ETS in a particular population.

Patrick

ps418

My answer to this question was made obvious from the get-go. Go back and read what I wrote. I am specifically focusing exclusively on CHD and lung cancer.

I don't know enough about the Kyoto "regulamentiations" to tell you whether I support them or not. I can tell you however that I support efforts to reduce CO2 and pollution emissions, that CO2 emissions are contributing to global warming, and think that CO2 emissions are increasing the risk of abrupt climate change.

Patrick

Nuno Figueira

"Yet again you prove yourself unable to comprehend what you're posting. This article provides precisely zero evidence for ETS causation of CHD/lung cancer. It assumes an RR of 1.3 on the basis of other research and uses that RR to estimate a number of deaths due to ETS in a particular population.
"
Unable to understand my ass. English may not be my first language but I assure you I understood the vast majority of what's in all these studies. The estimations are based on peer reviewed material and thus valid in my book. They're dismissable to you simply because they don't serve to prove your point. At least I provided a logical reason to dismiss your research.

And if you're not negating the adverse health effects of ETS then I'm done here and will walk out feeling victorious. Have a nice day.

Oh, and learn about Kyoto, it's important. Assuming you don't support all kinds of atmospheric pollution, that is.

ps418

Thank you for your time and enthusiasm, Nuno. You've prompted me to look much more closely at the evidence than I otherwise would have, and I've learned a great deal because of that. Have a wonderful day.

Patrick