Kilts & Pipe Smoking

[GlassMan]

I noticed in the thread on the Grand Opening of Rocky's new storefront for USAK, that two members who went had to extinquish their tobacco pipes at the bar later that night.

That started me thinking, I wonder how many other people on this board also enjoy a good tobacco pipe every know and then? Personally I love my pipes both as collectibles and as sources of physical enjoyment.

If you are into pipes, what types do you have and what is your favorite type of blend?

Personally I have an affection for Italian pipes so my collection includes Castello, La N'Atra, Viprati, & Ser Jacopo. From England I have Dunhill & Ferndown. I've also got some Peterson's, a few Meerschaums, and an assortment of other makers from the US & Europe. As for tobacco, I'm partial to English & Scottish blends, although every now and again I smoke a Balkan.

[Graham]

I noticed in the thread on the Grand Opening of Rocky's new storefront for USAK, that two members who went had to extinquish their tobacco pipes at the bar later that night.

Not quite on topic, sorry, but the big news here is that a lot more people will be leaving their tobacco habits at the door of the pubs here downunder.
From Jan 1 all pubs and clubs will be smoke free.

Naturally, the pubs are complaining that revenue will be lost, I believe more people if anything, especially families will return to the pubs.

Time will tell.

Sorry, I know nothing about those kind of pipes, but the Highland pipes..I know a lot about them :mrgreen:

[macwilkin]

I have a Peterson Briar pipe that I smoke on very selected occasions (stag Burns Suppers, etc.) There is a Norwegian tobacco I love called "Highland Whisky"! ;)

Cheers,

Todd

[MACKAY]

I don't personally smoke a pipe, but do enjoy the smell of a burning pipe a heck of a lot more than a cigar or a cigarette.

Brian Mackay

[Jerry]

I don't know much about pipes, but my grandfather from Northern Ireland used to be a pipe smoker. I have a few of his old pipes including one or two which I am sure he brought over when the family immigrated to the USA in the late 1920s.

[James]

Keep up the good work-there are too many inhibitions these days: there is room for all, without this or that group infringing upon the activities of others.

Too the smell of smoke is much pleasanter that the stench of non-smoking bars, public transport and the like.

Of course the big joke is when the medical profession will once again decide that smoking is good for people.

James

[GlassMan]

Sadly, there have been an almost endless number of research papers that have shown that the causal linkage between smoking and cancer is only in the minds of the anti-smoking activists. However, many of these papers failed to receive much press or were actively covered up by the sponsoring organization because the data did not agree with the preconceived opinions of the sponsors (most notably the World Health Organization).

Here is a partial list of excerpts & papers:

Relative risk of lung cancer for asbestos workers was "highest for those who had never smoked, lowest for current smokers, and intermediate for ex-smokers. The trend was statistically significant. There was no significant association between smoking and deaths from mesothelioma,".
0565. University of London, School of Hygiene and Tropical Medicine. "Cancer of the Lung Among Asbestos Factory Workers."

"Lung volume parameters were found to decrease with age, but there was no significant modification related to tobacco consumption."
0241. Institut D'Etudes Et Recherches Pneumophtisiologiques (Institute of Studies on Tuber-culosis). France. Keisbauer, J.P. "Longitudinal Study of the Methods of Early Detection of Respiratory Diseases in a Population of Cab Drivers."

"No statistically significant relationship was found in either community between smoking and coronary heart disease, hypertension or somatic complaints"
University of Texas School of Allied Health Sciences. Philips, B.U., Jr.; Bruhn, J.G. "Smoking Habits and Reported Illness in Two Communities With Different Systems of Social Support." FUNDING: Univ. of Texas; National Institute of Mental Health. 1981-83.

"Preliminary data indicate greater frequency of anterior infarctions among nonsmokers." "Among patients with unstable angina, smoking was associated with less persistent rest pain and a lower proportion of smokers had chronic angina of effort prior to hospital admission. Preliminary analysis suggests a marginally lower in-hospital mortality rate among smokers after controlling for age and other prognostic factors."
St. Vincent's Hospital, Dept. of Preventive Cardiology and Cardiac Dept. (Dublin, Ireland). Cohort of 898 males and 415 female heart patients. 12/80-1/86.

"Recent secular trends in sex and age specific mortality from ischemic heart disease, both in the United Kingdom and in the United States, appear to be independent of changes in cigarette consumption."
University of Leeds, Dept. of Medical Physics (England). Burch, P.R.J. "Tests of Causal, Constitutional and Mixed Hypotheses of Associations between Smoking and Disease in Man," 1972 and continuing. Funding: Univ. Leeds.

"In asymptomatic male aviators (aged 20 to 60), age and ratio of total cholesterol to high density lipoprotein cholesterol are most highly correlated with degree of coronary artery disease found on angiography. After removing the effect of age and this ratio, no statistically significant additional variance is explained by other risk factors [including smoking]."
Department of Defense, Department of the Air Force, School of Aerospace Medicine (Brooks Air Force Base, Texas). Tolan, G.D.; Honck, P.; Hickman, R. et al. "Multivariate Approaches to the Detection of Asymptomatic Coronary Artery Disease." Funded by USAF. 1971 - continuing.

"Secular trends in mortality from oesophageal cancer in the United Kingdom are independent of secular changes in cigarette consumption, but well correlated with secular changes in alcohol consumption...alcohol acts as an indirect causal agent. The proximal causal agent is likely to be a precipitator, such as a microorganism. Genetic predisposition is also implicated"
University of Leeds. Dept. of Medical Physics (England). Burch, P.R.J. "Tests of Causal, constitutional, and Mixed Hypotheses of Associations Between Smoking and Disease in Man." Funding: Univ. of Leeds. 1972 - continuing.

"Preliminary results implicate relative weight in both men and women as a principal risk factor in renal cell carcinoma. Comparison with population controls failed to implicate cigarette smoking of beverage use as risk factors."
University of Oklahoma, Health Sciences Canter. Asal, N.R.; Geyer, J. "Risk Factors in Kidney Cancer." Oct. 1981 - Feb., 1985. FUNDING:< National Cancer Institute.

"No association was found for exposure to side-stream {second-hand} smoke, coffee drinking, or artificial sweetener use. The association of several occupations with bladder cancer risk has been found in males..."
American Health Foundation. Wynder, E.L.; Goodman, M.T.; Kabat, G.C., et al. "Studies in Tobacco-Related Cancers." FUNDING: National Cancer Institute.

"Overall, smoking was not found to be associated with any of the cancers studied." Centres for Disease Control.
Epidemiologic Studies Branch. Division of Reproductive Health. Rubin, G.; Tyler, C.W.; Franks, A.L.; Stroup, M. "Smoking and Endometrial, Ovarian, and Breast Cancer."

1. Smoking improves human information precessing.
2. Higher nicotine cigarettes produce greater improvements [in information processing] than low-nicotine cigarettes.
3. Nicotine tablets produce similar effects.
4. Nicotine can reverse the detrimental effects of scopolamine on performance
5. Smoking effects are accompanied by increases in EEG arousal and decreases in the latency of the late positive component of the evoked potential."
University of Reading, Department of Psychology (England). Warburton., D.M.; Wesnes, K. "The Effects of Cigarette Smoking on Human Information Processing and the role of Nicotine in These Effects "

"Smokers in general are thinner than nonsmokers, even when they ingest more calories."
Kentucky State University. Lee. C.J.: Panemangalore. M. "Obesity Among Selected Elderly Females In Central Kentucky." FUNDING: USDA 0942. University of Louisville. Belknap Campus School of Medicine. Satmford, B.A.; Matter, S.; Fell, R.D., et al. "Cigarette Smoking, Exercise and High Density Lipoprotein Cholesterol" FUNDING: American Heart Association.

"...all smokers had less plaque, gingival inflammation and tooth mobility than nonsmokers and similar periodontal pocket depth."
Veterans Administration, Outpatient Clinic (Boston). Chauncey. H.H,; Kapur, K.K.; Feldmar, R S. "The Longitudinal and Cross-Sectional Study of Oral Health: in Healthy Veterans (Dental Longitudinal Study)

"Smokers have lower incidence of postoperative deep vein thrombosis than nonsmokers."
Guy's Hospital Medical School (England). Jones, R.M. "Influence of Smoking on Peri-Operative Morbidity." Hypertension (High blood pressure) is less common among smokers.

"Hypertension and postpartum hemorrhage were lower in smokers."
University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. "An Assessment of Smoking in Pregnancy."

"Several epidemiological studies have indicated that there may be an inverse relationship between smoking and Parkinson's disease." There is an "apparent protective effect of cigarette smoke."
Carr, L.A.; Rowell, P.P. "Attenuation of 1methyl-4-phenyl-1,2,3,6-tetrahydrophyridine- induced neurotoxicity by tobacco smoke." Published in Neuro-pharmacology 29(3):311-4, Mar 1990.

"There is a low prevalence of smoking in ulcerative colitis. The disease often starts or relapses after stopping smoking."
Prytz, H.; Benoni, C.; Tagesson, C. "Does smoking tighten the gut?" In Scandinavian Journal of Gastroenterology 24(9):1084-8, Nov. 1989.

[GlassMan]

And here are some quotes from a review of articles that cover smokers & non-smokers:

In February, 1991, a paper was published in the Journal, Cancer, entitled "Comparative Epidemiology of Cancer Between the United States and Japan". The authors, Ernst L. Wynder, M.D., et al, started out with the assumption that smoking causes lung cancer. In fact, Dr. Wynder has been crusading against smoking since the 1950's and the authors' report was paid for by the anti-smoking National Cancer Institute. As we will see, the authors took some liberties with the figures presented in their report, so as to try to make the data fit their preconception that smoking causes lung cancer, but eventually had to admit that the data did not support that assumption.

On January 13, 1995, the Wall Street Journal reported another study, this one involving animals and funded, in part, by the U.S. National Institutes of Health. According to the report, the study was inspired when a researcher in Buffalo, John Pauly, was studying some tissue from a smoker and lung cancer victim and found a tiny particle of cellulose acetate, the material used to make cigarette filters. He apparently decided that pieces of cigarette filters, imbedded in the lungs, are the cause of lung cancer and decided to do an experiment with mice. He implanted pieces of filters, coated with cigarette tar, in the lungs of six mice and found that they remained intact in the lungs for six months. This finding was haled as a great break-through, demonstrating that pieces of cigarette filters may lodge in the lungs and cause cancer. What this ignores, however, is a simple fact: no cancers were found in the mice! What the study really proves, therefore, is merely that implanting pieces of cigarette filters, drenched with tar, in the lungs of mice does the mice no apparent harm!

To this day, it remains unconfirmed and it remains true, to this day, that despite hundreds of experiments18, nobody has been able to induce a single cancer in lab animals by exposing them to ordinary tobacco products or smoke.

To this day, it remains unconfirmed and it remains true, to this day, that despite hundreds of experiments18, nobody has been able to induce a single cancer in lab animals by exposing them to ordinary tobacco products or smoke.

What these studies show is that low class people tend to smoke more than higher class people, and that low class people tend to die sooner than high class people: considerably sooner. There may be many reasons for the higher death rates in people with lower SES. They tend to work in hazardous occupations, exposed to hazardous fumes and chemicals. They eat a different diet, tend to become obese, tend to receive less medical care and lower quality care. Moreover, they tend to suffer more from mental depression 23 . So the Committee's concern that the study results might be biased by SES turns out to have been well founded. Subsequent studies confirm that, smoking aside, it is risky to belong to the lower socio-economic strata.

Recently, I posed a question to Ed Uthman, M.D., a pathologist practicing in Dallas, TX. The question was whether a surgeon, at autopsy, could determine from an examination of the deceased's lungs, whether the deceased was or was not a smoker. Here is Dr. Uthman's response: I don't think one can tell if the deceased were a tobacco smoker or not by the appearance of the lungs. The absence of any black pigment suggests that the person was either a nonsmoker or a very light smoker. Heavy black pigmentation suggests that the person was either a heavy smoker, or lived in a city with heavy particulate air pollution, or was a coal miner, or some combination of the three. The black pigment in question is elemental carbon, which most investigators believe to be inert in its effects on the lungs (although in the extremely heavy doses that coal miners used to get, it may have had a partial role in coal-workers' lung disease).

Apparently, the "advanced inhalation device" referred to by the SG is the "Maddox-ornl smoking machine". It is referred to in an article by A.P. Wehner, et al., which appeared in 1981 in Toxicology and Applied Pharmacology at pages 1-17. There, the authors describe an experiment in which 80 female rat were forced to consume 8 cigarettes per day, seven days per week, for 2 years. One of the rats developed a carcinoma of the lung.

Before getting too excited about these experiments, however, we need to consider this: the largest known rats weigh no more than an average of one pound. Forcing a one pound rat to smoke 8 cigarettes per day is the equivalent of forcing a 160 pound human to smoke 1280 cigarettes per day (64 packs). Such experiments are not realistic and in no way replicate exposure to ordinary tobacco smoke. Given the enormous concentrations of smoke used by the experimenters, it is wonder that any of the animals even survived the ordeal; yet, they did, and only a small percentage developed tumors.

In recent years, new smoking machines have been devised that subject rats to second hand smoke. In an article in the May 28, 1994 issue of The Los Angeles Times, writer Sheryl Stolberg describes experiments that have been going on for three years, exposing rats to continuous concentrations of smoke as high as 4,000 micrograms per cubic meter, concentrations many times the concentrations encountered in the real world, even in times of brief exposure, e.g., bars. Bottom line: no significant harm to the animals has been shown,

In 1998, however, an event took place which enables me to resolve the unanswered questions. In that year, the State of Minnesota brought a lawsuit against tobacco companies to recover damages to the State, allegedly caused by smoking. The case was settled before any judgment could be rendered, but not before a few trial sessions were held.

At these sessions, testimony was taken from experts for both the plaintiff (the State) and the Defendants (the tobacco companies). Experts for both sides agreed that, despite many, many animal inhalation experiments over a period of many years, all of the experiments had failed, i.e., nobody has ever been able to demonstrate, through animal experiments, that inhaling tobacco smoke - no matter in what quantities or concentrations - causes lung cancer.

In the same WSJ article, there is an interesting quote from Neil E. Caporaso, a researcher at the government-owned National Cancer Institute in Bethesda, MD. According to Mr. Caporaso, one out of eight smokers will be stricken with lung cancer (which is another way of saying that seven out of eight will not). Considering the fact that one out of every five Americans dies from some form of cancer, and that lung cancer is the most common form of cancer in persons between the ages of 45 and 74, and the second commonest form in persons over that age, Mr. Caporaso's estimate of the risk seems very modest and wholly at variance with the position taken by most government scientists, who shriek hysterically that smoking "causes" lung cancer.

That's on of my favorite statistics since if anything it shows a negative correlation between smoking & lung cancer.

"Since 1950, the incidence of all cancers in people between the ages of 50 and 60 years has increased by 44%, with even higher increases in some of the more deadly forms of cancer. Breast and colon cancer went up 60%, prostate up 100% and testicular cancer for men between the ages of 28 and 35 went up 300%. Lung cancer has gone up 262%, an increase that is obviously not related to cigarette smoking, because over the same period the number of people smoking cigarettes dropped from 50% to 25%..."

Recent studies, reported by the National Institute on Drug Addiction (NIDA), seem to bear out my hunch. These studies suggest that tobacco contains a monoamine oxidase inhibitor (MAOI). MAOI's are anti-depressants, which work by increasing serotonin levels in the brain. They are used in medicine to treat Parkinson's disease, which may explain why a number of studies have shown that smokers have a far lower rate of Parkinson's than non-smokers. In any event, the MAOI in tobacco smoke may play as great a role in smoking as nicotine.

[GlassMan]

In the mid 1970's, some researchers decided to do a study on the effects of smoking cessation as well as other "healthy behaviors". They sought to avoid the flaws that had plagued other epidemiological studies and, to that end, they sought to study groups that were not self selected, but rather were selected, at least in part, on a random basis. The study group was called the "Multiple Risk Factor Intervention Trial (MRFIT) Research Group".
12,866 high risk men, aged 35 to 57 years, were randomly assigned to one of two groups. One group was treated to a special intervention program, consisting of drug-care treatment for hypertension, counseling to stop cigarette smoking, and dietary advice for lowering blood cholesterol (I will call this the "special intervention" or"SI group"). The other group, which I will call the "control group", was left to smoke, eat, and have high blood pressure, without intervention.
The MRFIT Research Group rendered its first report in 1982, reflecting an average follow-up time of 7 years. To the disappointment of the researchers, there was no statistically significant difference between the mortality in the SI group, from that in the control group - despite the fact that, as a result of the nagging, the participants in the SI group significantly "improved" their health habits, i.e., stopped smoking, and lowered their blood pressure and cholesterol levels. {Multiple risk factor intervention trial, JAMA, 248, 1465-77 (1982). }
In 1990, the MRFIT group produced another report, reflecting 10.5 years of research, using the same two groups. This time, the results appeared to show a statistically significant reduction in coronary heart disease (CHD) in the intervention group, but this was attributed not to smoking cessation, but rather to reduction in hypertension 41 . It turned out that there were more deaths from ischemic heart disease in the SI group than in the control group (96 vs. 86 deaths). Moreover, there were more deaths from cancer of the respiratory and intrathoracic organs in the SI group than in the control group (66 vs. 55) {Mortality rates after 10-15 years for participants in the Multiple Risk Factors Intervention Trial, JAMA, 263, 1795-1801 (1990).}

And here are some comments on methodologies used in many of the studies that link smoking to health problems:

"As a general rule of thumb, we are looking for a relative risk of 3 or more before accepting a paper for publication." - Marcia Angell, editor of the New England Journal of Medicine"

"My basic rule is if the relative risk isn't at least 3 or 4, forget it." - Robert Temple, director of drug evaluation at the Food and Drug Administration.

In 1993 the EPA issued a report which claimed that Environmental Tobacco Smoke (ETS) caused 3,000 deaths per year. The first step in a meta analysis is identifying all of the relevant studies. The EPA located 33 studies that compared ETS exposure to lung cancer rates. The EPA selected 31 of the 33 studies. Later they rejected one of their chosen studies, bringing the total to 30. On page 3-46 of the report the EPA estimates, based on nicotine measurements in non-smokers blood, "this would translate to the equivalent of about one-fifth of a cigarette per day." {from second hand smoke} Studies that measured actual exposure by having non-smokers wear monitors indicate even this low estimate is exaggerated. Actual exposure (for people who live and/or work in smoky environments) is about six cigarettes per year. (See also the study by Oak Ridge National Laboratories.)
In 1995 The Congressional Research Service (CRS) released a review of the EPA report. The CRS pointed out that "from a group of 30 studies. . six found a statistically significant (but small) effect, 24 found no statistically significant effect and six of the 24 found a passive smoking effect opposite to the expected relationship." The EPA based their numbers on a meta analysis of just 11 studies. The analysis showed no increase in risk at the 95% confidence level. Even after excluding most of the studies, the EPA couldn't come up with 3,000 deaths, but they had already announced the results. So they doubled their margin of error. Let me repeat that, because it may seem hard to believe: After failing to achieve their pre-announced results by ignoring half of the data, they doubled their margin of error!
After juggling the numbers, The EPA came up with an RR (Relative Risk) of ETS causing lung cancer 1.19. A RR of less than 2.0 is usually written off as and insignificant result, most likely to be due to error or bias. An RR of 3.0 or higher is considered desirable. Although the EPA declared ETS was a Class A carcinogen with an RR of 1.19, in analysis of other agents they found relative risks of 2.6 and 3.0 insufficient to justify a Group A classification.

In 1998 Judge William Osteen vacated the study - declaring it null and void after extensively commentating on the shoddy way it was conducted. His decision was 92 pages long. Osteen used the term "cherry-picking" to describe he way the EPA selected their data. "First, there is evidence in the record supporting the accusation that EPA "cherry picked" its data. Without criteria for pooling studies into a meta- analysis, the court cannot determine whether the exclusion of studies likely to disprove EPA's a priori hypothesis was coincidence or intentional. Second, EPA's excluding nearly half of the available studies directly conflicts with EPA's purported purpose for analyzing the epidemiological studies and conflicts with EPA's Risk Assessment Guidelines." Osteen found other deep flaws in the the EPA's methodology. In his judgment he stated: "The record and EPA's explanations to the court make it clear that using standard methodology, EPA could not produce statistically significant results with its selected studies. Analysis conducted with a .05 significance level and 95% confidence level included relative risks of 1. Accordingly, these results did not confirm EPA's controversial a priori hypothesis. In order to confirm its hypothesis, EPA maintained its standard significance level but lowered the confidence interval to 90%. This allowed EPA to confirm its hypothesis by finding a relative risk of 1.19, albeit a very weak association. EPA's conduct raises several concerns besides whether a relative risk of 1.19 is credible evidence supporting a Group A classification. First, with such a weak showing, if even a fraction of Plaintiffs' allegations regarding study selection or methodology is true, EPA cannot show a statistically significant association between ETS and lung cancer." The following is another direct quote from Judge Osteen's decision: "In this case, EPA publicly committed to a conclusion before research had begun; excluded industry by violating the Act's procedural requirements; adjusted established procedure and scientific norms to validate the Agency's public conclusion, and aggressively utilized the Act's authority to disseminate findings to establish a de facto regulatory scheme intended to restrict Plaintiffs, products and to influence public opinion. In conducting the ETS Risk Assessment, disregarded information and made findings on selective information; did not disseminate significant epidemiologic information; deviated from its Risk Assessment Guidelines; failed to disclose important findings and reasoning; and left significant questions without answers. EPA's conduct left substantial holes in the administrative record. While so doing, produced limited evidence, then claimed the weight of the Agency's research evidence demonstrated ETS causes cancer. Gathering all relevant information, researching, and disseminating findings were subordinate to EPA's demonstrating ETS a Group A carcinogen."

[QUOTE]The World Health Organization conducted a study of Environmental Tobacco Smoke (ETS) and lung cancer in Europe. ETS is commonly referred to as Second Hand Smoke (SHS). The two terms are interchangeable.
This was a case control study using a large sample size. The purpose of the study was to provide a more precise estimate of risk, to discover any differences between different sources of ETS, and the effect of ETS exposure on different types of lung cancer. The study was conducted from twelve centers in seven European countries over a period of seven years. The participants consisted of 650 patients with lung cancer and 1542 control subjects. Patients with smoking related diseases were excluded from the control group. None of the subjects in either group had smoked more than 400 cigarettes in their lifetime. The study found no statistically significant risk existed for non-smokers who either lived or worked with smokers. The only statistically significant number was a decrease in the risk of lung cancer among the children of smokers. The study found a Relative Risk (RR) for spousal exposure of 1.16, with a Confidence Interval (CI) of .93 - 1.44. The 1.16 number is not statistically significant.

[GlassMan]

On March 8, 1998, the British newspaper The Telegraph reported "The world's leading health organization has withheld from publication a study which shows that not only might there be no link between passive smoking and lung cancer but that it could have even a protective effect." [/QUOTE]
Here's a link to the article: http://www.junkscience.com/news/euwsjets.htm

Here's another great article: http://www.sepp.org/controv/healthhoax.html

And here's a great quote from a conference seminar being given by an Anti-Smoking group about how to convince people not to smoke:

Key Points: Research shows that a compelling story will beat true facts, even when the listener knows ahead of time that the story is fiction and the facts are true. Our movement has many true stories to tell. We’ll take a look at what the research says, what goes into telling a persuasive, compelling story and then real life examples of how these stories can be used to help accomplish advocacy or other goals.

And there has even been research in Scandinavia between twins (one a pipe smoker and one a non-smoker) which showed that pipe smokers LIVE LONGER than the non-smoker after eliminating all other risk factors.

Yet, no matter what actual research science finds, be prepared to hear everyone screaming the "truth" that tobacco kills.