Oolon Colluphid

This got me thinking. Just guessing here, but I’m inclined to think that second-hand smoke is likely to be rather ‘better’ than the primary stuff.

The reason would be that the majority of the smoke in the air doesn’t come direct from the cigarette: it is exhaled. So before it gets to another person, it has been through the fag’s filter, and then been down into a pair of nice warm moist lungs, where much of the nasties (as well as the nicotine) are dissolved into the mucus linings.

So what a smoker blows out would have had much of the worst stuff removed. This could make cigarette smoke little worse than the smoke from, say, a bonfire... which would fit in with Penn, Teller and co’s claims.

So I suppose this means that pipe and cigar smoke, which is neither filtered nor inhaled, and comes in larger quantities, is worse for surrounding people than it is for the smoker (since the smoker at least gets the relaxing -- ie a good thing -- effects of the nicotine and flavour).

Can anyone corroborate any of these musings?

Cheers, DT

Oolon Colluphid

Thinking of bonfire smoke reminds me: from what I’ve read, we should be more concerned about the dollops of free radicals in the blackened bits of barbequed food....

Cheers, DT

doghouse

But…think of the kitty cats!

Last year a study found the relative risk for developing malignant lymphoma in cats is more than doubled if they live with a smoker. The risk was even higher with long-term exposure.

Regarding the question as to if I smoke, I don’t. Both grandfathers died of lung cancer at an early age, and one grandmother died of emphysema; all 3 were smokers. My other grandmother who never smoked is alive at 91 years. I don’t need a statistician to tell me my DNA doesn’t like tobacco.

Bertone ER, Snyder LA, Moore AS. Environmental tobacco smoke and risk of malignant lymphoma in pet cats. Am J Epidemiol. 2002 Aug 1;156:268-73.

scombrid

Do you have the source for this. My dad's favorite cat is currently dieing of malignant lymphoma. It's a nasty way to go, he's just hanging on. He weighed 28lbs last time he was weighed healthy. Now he's a 16lb anemic skeleton with his eyes sunk into his head. I wonder if there were some causal link between smoking and the cat dieing if it'd give my mother pause regarding the smoking. She didn't care that smoke irritated my asthma and she obviously doesn't give a rat's ass about her health either as her mother died of emphysema after hanging on for 11years with half a lung. I doubt she'd care about the cat either. She loves her nicotene.


Even if I demonstrated that she killed the cat (she's ultra emotional so the sick cat is tearing her up anyway) she'd still find a way to rationalize cigarette use. She won't go more than an hour without a cigarette. If we go to a restaurant and have the option of getting seated immediately in the non-smoking section or waiting an hour for the smoking section we wait. IPU forbid that she'd eat a meal without smoking and then she can smoke her brains out in the car (which she'll do anyway). I feel bad for my dad bankrolling that habit (mom spends almost as much per week on cigarettes as I do on food) and then having to face the medical bills and suffering that will result from the cigarettes.

Walross

Darwin's Terrier wrote:

But what about the smoke that comes off the end of the cigarette? I suspect there is at least as much of that as there is the exhaled smoke, and I suspect that it is at least as harmful as the smoke that is being inhaled (since it's not filtered). Does anyone know if there have been any studies to learn what percentage of second-hand smoke comes from exhalation and what just comes off the tip of the cig?

Walross

Mad Kally

"...The National Cancer Institute (NCI)."
from LadyShea's link:

Journal of the National Cancer Institute, Vol. 90, No. 19, October 7, 1998:


"An association between exposure to environmental tobacco smoke (ETS) and lung cancer risk has been suggested. To evaluate this possible association better, researchers need more precise estimates of risk, the relative contribution of different sources of ETS, and the effect of ETS exposure on different histologic types of lung cancer. To address these issues, we have conducted a case-control study of lung cancer and exposure to ETS in 12 centers from seven European countries.


RESULTS: ETS exposure during childhood was not associated with an increased risk of lung cancer. No clear dose-response relationship could be demonstrated for cumulative spousal ETS exposure. No increase in risk was detected in subjects whose exposure to spousal or workplace ETS ended more than 15 years earlier. Ever exposure to ETS from other sources was not associated with lung cancer risk. Risks from combined exposure to spousal and workplace ETS were higher for squamous cell carcinoma and small-cell carcinoma than for adenocarcinoma, but the differences were not statistically significant.


CONCLUSIONS: Our results indicate no association between childhood exposure to ETS and lung cancer risk. We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS. There was no detectable risk after cessation of exposure."

Dr Rick

Passive tobacco smoke exposure has been found in some studies to be associated with an increased risk of childhood asthma, exacerbations of chronic obstructive pulmonary disease (COPD), coronary artery disease (CAD), lung cancer, sudden infant death syndrome (SIDS) and erectile dysfunction. Some of the compounds from cigarette smoke have been found in the breast tissue and milk of women exposed to second-hand smoke, but evidence that these findings are directly associated with diseases of the breast or pose a risk to nursing infants is lacking.

Lung cancer is uncommon among nonsmokers; a statistically increased risk of an uncommon disease can still leave the disease uncommon, and that might explain why our outstanding IIDB hospice nursing staff may not have had any antedotal experience with passive smoking and lung cancer even though a statistical relationship has been found.

Rick

Mad Kally

How did I know you'd show up?

xoxoxox
Kally

doghouse

That would be the journal citation I put at the bottom of my post.

I'm sorry to hear about your dad's cat. Realize that lymphoma is one of the most common types of cancer in cats. Many cases are caused by infection with the Feline Leukemia Virus (FeLV). In an individual patient, I'm not sure there is a way to know for sure if the cancer was caused by tobacco smoke or not.

simian

I looked through them. They strike me as only slightly better than creationist links or HIV doesn't cause AIDS links.

I also looked at the "Life Sciences" database (the closest I have to a source to look at medical journals). Dates of the database: 1999 to 2002/12 (which does not necessarily mean no earlier journals show up in it). I used lung cancer and environmental tobacco smoke at the words to search. I am sure there are limits for the links of articles, so I am limiting myself to posting the first 5 that came up. Here are the first 5 I found:

TI: Lifetime environmental exposure to tobacco smoke and primary lung cancer of non-smoking Taiwanese women
AU: Lee,-C.-H.*; Ko,-Y.-C.; Goggins,-W.; Huang,-J.-J.; Huang,-M.-S.; Kao,-E.-L.; Wang,-H.-Z.
AF: School of Public Health, Kaohsiung Medical University, No. 100 Shih-Chuan 1st Road, Kaohsiung, Taiwan, ROC 807; E-mail: ycko@mail.nsysu.edu.tw
SO: International-Journal-of-Epidemiology [Int.-J.-Epidemiol.] 2000 vol. 29, no. 2, pp. 224-231
*LHM: International Journal of Epidemiology Full-Text Available Online
IS: ISSN 0300-5771
PY: 2000
LA: English
LS: English
PT: J (Journal-Article)
AB: 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.
DE: Cigarette-smoke; Passive-smoking; Carcinogenesis-; Taiwan-; lung-cancer; Females-
ID: man-; females-
CL: -Social-poisons-and-drug-abuse-24180
JA: Toxicology-Abstracts
AN: 4762591
TI: Exposure Misclassification Bias in Studies of Environmental Tobacco Smoke and Lung Cancer
AU: Wu,-A.H.
AF: University of Southern California, Dept. of Preventive Medicine, 1441 Eastlake Ave., MS#44, Los Angeles, CA 90089, USA; E-mail: annawu@hsc.usc.edu
SO: Environmental-Health-Perspectives [Environ.-Health-Perspect.] 1999 vol. 107, Suppl. 6, pp. 873-877
*LHM: Environmental Health Perspectives Full-Text Available Online
IS: ISSN 0091-6765
PY: 1999
LA: English
LS: English
PT: J (Journal-Article)
AB: It is now recognized that exposure to environmental tobacco smoke (ETS) in the workplace and other settings outside the home may be equally as important as residential ETS exposure. This review examines the sources of misclassification in the assessment of workplace ETS exposure in questionnaire-based epidemiologic studies. Cogent to this discussion is the role of misclassification of ever smokers as never smokers, which is important in studies of both workplace and residential ETS exposure and lung cancer and is discussed first. The collective evidence from studies that have used direct or indirect approaches to estimate smoker misclassification shows that although some misclassification of ever smokers as never smokers exists in studies of ETS and lung cancer, the potential bias from the misclassification of smokers is unlikely to explain the observed increased risk of lung cancer associated with ETS exposure.
DE: Cigarette-smoke; Passive-smoking; Polluted-environments; Reviews-; lung-cancer
ID: man-; epidemiology-
CL: -Social-poisons-and-drug-abuse-24180
JA: Toxicology-Abstracts
AN: 4670672
TI: p53 Mutations and Exposure to Environmental Tobacco Smoke in a Multicenter Study on Lung Cancer
AU: Husgafvel-Pursiainen,-K.; Boffetta,-P.; Kannio,-A.; Nyberg,-F.; Pershagen,-G.; Mukeria,-A.; Constantinescu,-V.; Fortes,-C.; Benhamou,-S.
AF: Laboratory of Molecular and Cellular Toxicology, Finnish Institute of Occupational Health, Topeliuksenkatu 41 aA, FIN-00250 Helsinki, Finland; E-mail: Kirsti.Husgafvel-Pursiainen@occuphealth.fi
SO: Cancer-Research [Cancer-Res.] 2000 vol. 60, no. 11, pp. 2906-2911
*LHM: Cancer Research Full-Text Available Online
IS: ISSN 0008-5472
PY: 2000
LA: English
LS: English
PT: J (Journal-Article)
AB: Biomarker data may provide a way to strengthen the link between environmental tobacco smoke (ETS) exposure and lung cancer shown in epidemiological studies. We conducted a multicenter case-control study to investigate the association between ETS exposure and lung cancer in never-smokers using p53 mutations as a biomarker of tobacco-related carcinogenesis. Paraffin-embedded tissue or fresh tissue samples from 91 never-smokers and 66 smokers with histologically confirmed lung cancer and interview data about smoking habits and ETS exposure were analyzed for mutations in the p53 gene. Statistical analysis was performed using multivariate logistic regression. Among the lifelong nonsmokers, the overall mutation prevalence was 10% (nine cases). Among 48 never-smokers ever exposed to spousal ETS, 13% (six cases) showed mutations. Smokers exhibited 17 (26%) mutations. A 3-fold [odds ratio, 2.9; 95% confidence interval (CI), 1.2-7.2] increased risk of p53 mutation was observed for smokers as compared with all never-smokers combined (i.e., irrespective of ETS exposure). The increase was 4.4-fold (95% CI, 1.2-16.2) when compared with never-smokers without ETS exposure. Among never-smokers, the risk of mutation was doubled (odds ratio, 2.0; 95% CI, 0.5-8.7) for exposure to spousal ETS only, based on 6 exposed cases with mutation and 42 exposed cases without mutation. The risk was 1.5 (95% CI, 0.2-8.8) for those ever exposed to spousal or workplace ETS as compared with those never exposed to spousal or workplace ETS. For smokers, the most common mutation type was G:C to T:A transversion (31%), whereas G:C to A:T transitions were predominant among never smokers (57%). In conclusion, our study indicates a significant 3-4-fold increased risk of p53 mutation in smoking lung cancer cases, and it suggests that mechanisms of lung carcinogenesis in ETS-exposed never-smokers include mutations in the p53 gene, similar to that seen in smokers. However, the mutation patterns observed also suggest a difference between smokers and never-smokers. Clearly, additional investigations of the role of p53 mutation as a biomarker for tobacco-related carcinogenesis, including that related to ETS, are indicated.
DE: p53-protein; Cigarette-smoke; Lung-; Carcinogenesis-; Mutation-; Passive-smoking
ID: man-
CL: Tumor-suppressor-genes-and-anti-oncogenes:-p53-gene,-anti-suppressor-genes-K-rev-rap-rab-RSU-1-26405
JA: Oncogenes-&-Growth-Factors-Abstracts
AN: 4738569
TI: A case-control study of lung cancer and environmental tobacco smoke among nonsmoking women living in Shanghai, China
AU: Zhong,-L.; Goldberg,-M.S.*; Gao,-Y.-T.; Jin,-F.
AF: Joint Departments of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Canada; E-mail: mark@polair.epi.mcgill.ca
SO: Cancer-Causes-and-Control 1999 vol. 10, no. 6, pp. 607-616
*LHM: Cancer Causes & Control Full-Text Available Online
IS: ISSN 0957-5243
PY: 1999
LA: English
LS: English
PT: J (Journal-Article)
AB: The incidence of lung cancer in women living in China is among the highest in the world but it does not appear that tobacco smoking is a major risk factor for lung cancer. As tobacco smoking is highly prevalent in Chinese men, exposure to environmental tobacco smoke (ETS) may play an important role in the development of lung cancer in Chinese women who never smoked. We conducted the present investigation because previous studies did not account for dietary habits or indoor air pollution from Chinese-style cooking and they did not assess the effect of occupational exposure to ETS. A population-based, case-control study was conducted to evaluate the relationship between lung cancer and exposure to ETS among nonsmoking women living in Shanghai, China. Five-hundred and four women diagnosed with incident, primary lung cancer between February 1992 and January 1994 were identified through the population-based Shanghai Cancer Registry. A control group of 601 nonsmoking women was selected randomly from the Shanghai Residential Registry, and was approximately frequency-matched to the age distribution of the lung cancer cases. Information on lifetime domestic and occupational exposure to ETS was obtained through face-to-face interviews. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated by unconditional logistic regression. The OR for ever exposed to ETS from spouses was 1.1 (95% CI: 0.8-1.5), and the OR for ever exposed to ETS at work was 1.7 (95% CI: 1.3-2.3). Furthermore, the OR increased with increasing number of hours of daily exposure to ETS in the workplace and with increasing number of smoking co-workers. No associations were found for exposure to ETS during childhood. The main findings of the present study are that long-term occupational exposure to ETS, both alone or in combination with exposures at home, conferred an increased risk of lung cancer among women who never smoked. The inconsistency of the results regarding exposure to ETS at home and at work may have been due to lower exposures at home.
DE: Cancer-; Passive-smoking; Cigarette-smoke; Risk-assessment; Occupational-exposure; Lung-; China,-Shangai; Tobacco-; Females-; Air-pollution; Pollution-effects; Lung-cancer; China,-Shanghai
ID: man-; females-
CL: -Social-poisons-and-drug-abuse-24180
JA: Toxicology-Abstracts
AN: 4682421
TI: Lung Cancer and Environmental Tobacco Smoke: Occupational Risk to Nonsmokers
AU: Brown,-K.G.
AF: Kenneth G. Brown, Inc., 4917 Erwin Rd., Durham, NC 27707, USA; E-mail: kbinc@mindspring.com
SO: Environmental-Health-Perspectives [Environ.-Health-Perspect.] 1999 vol. 107, no. Supp. 6, pp. 885-890
*LHM: Environmental Health Perspectives Full-Text Available Online
IS: ISSN 0091-6765
PY: 1999
LA: English
LS: English
PT: J (Journal-Article)
AB: The principal epidemiologic evidence that environmental tobacco smoke (ETS) increases the risk of lung cancer in (lifelong) nonsmokers is from studies of nonsmoking women married to smokers. This article estimates exposure-response curves for 14 studies (1,249+ cases, 7 countries) with data on lung cancer categorized by the number of cigarettes/day smoked by the husband. The pooled results from the five U.S. studies alone are extrapolated to ETS levels in the workplace using measures of serum cotinine and nicotine samples from personal monitors as markers of exposure to ETS. It is predicted that the increase in lung cancer risk for nonsmoking women from average ETS exposure at work (among those exposed at work) is on the order of 25% (95% confidence interval (CI) = 8, 41) relative to background risk (i.e., with no ETS exposure from any source). This compares to an estimate of 39% (95% CI = 5, 65) for nonsmoking women whose husbands smoke at the adult male smoker's average of 25 cigarettes/day. At the 95th percentiles of exposure, the estimate from spousal smoking is 85% (95% CI = 32, 156), compared to 91% (95% CI = 34, 167) from workplace ETS exposure. Subject to the validity of the assumptions required in this approach, the outcome supports the conclusion that there is a significant excess risk from occupational exposure to ETS. The excess risk from ETS at work is typically lower than that from spousal smoking, but may be higher at the 95th percentiles of exposure.
DE: Occupational-exposure; Passive-smoking; Cigarette-smoke; Risk-assessment; lung-cancer
ID: man-
CL: -Social-poisons-and-drug-abuse-24180
JA: Toxicology-Abstracts
AN: 4670674
TI: Estimating Lung Cancer Risk with Exposure to Environmental Tobacco Smoke
AU: Lubin,-J.H.
AF: Division of Cancel Epidemiology and Genetics, NCI, 6120 Executive Blvd., EPS/8042, Bethesda, MD 20892-7244, USA; E-mail: lubinj@exchange.nih.gov
SO: Environmental-Health-Perspectives [Environ.-Health-Perspect.] 1999 vol. 107, no. Supp. 6, pp. 879-883
*LHM: Environmental Health Perspectives Full-Text Available Online
IS: ISSN 0091-6765
PY: 1999
LA: English
LS: English
PT: J (Journal-Article)
AB: Estimates of lung cancer in nonsmokers due to exposure to environmental tobacco smoke (ETS) in the workplace or in the home may be developed in several ways. Estimates may be based on a) models developed using the full range of data in smokers; b) models developed using data restricted to smokers with a low smoking rate, for example, less than or equal to 10 cigarettes per day; c) models developed using data from studies of residential exposure to ETS of nonsmokers, with exposures based on smoking rates of spouses; and d) models using data from studies of occupational exposure to ETS of nonsmokers. Methods a and b require an estimate of cigarette equivalent exposure for ETS as well as assumptions on the cigarette equivalent dose to target cells from ETS and on the comparability of lung cancer risk per unit dose from smokers and nonsmokers. Summary relative risks (RRs) and 95% confidence intervals (CI) from ETS studies of nonsmokers with exposures based on smoking patterns of spouses are 1.24 (1.1, 1.4) for females and 1.34 (1.0, 1.8) for males, whereas the RR estimate for occupational ETS exposure and its 95% CI is 1.39 (1.2, 1.7). Using RR estimates for ETS exposure, cigarette equivalents for ETS range from 0.1 to 1.0, based on a range of descriptive and biologically motivated models in active smokers; a cigarette equivalent is 0.2 based on a comparison of log-linear trends in RR with number of cigarettes smoked per day in active smokers and in spouses of nonsmokers.
DE: Cigarette-smoke; Passive-smoking; Risk-assessment; Polluted-environments; lung-cancer; Pollution-effects; Occupational-exposure
ID: man-
CL: -Social-poisons-and-drug-abuse-24180
JA: Toxicology-Abstracts
AN: 4670673


Simian