Smoking is Good for You!
AKA, Smokers' Paradoxes

Note that the studies referenced are what is known as "hard science" as opposed to the "soft science" of epidemiological studies. Also, notice that the research here is not in tobacco literature or tobacco-funded literature; in fact, many of the studies cited are actually from antismoking literature funded by Big Tobacco Control and/or Big Pharma. For more information, please see the Must Reads. You can find previously cited Therapeutic Effects of Smoking and Nicotine in the FORCES International archives. An easy-to-read but well-referenced paper is ONE FEELS BETTER TEMPERED: An Investigation Into The Beneficial Effects Of Smoking

The miracle supplement (for skin, heart, brain rejuvenation) Coenzyme Q10 is extracted from tobacco leaf. WebMistress: Coenzyme Q10 is also essential in fighting cancer!!!

In Coenzyme Q10: A Miracle Vitamin , Dr. Richard A. Kunin extols the benefits of Coenzyme Q10. He also says:

The energy of oxidation in cells depends on CoQ in partnership with niacinamide (vitamin B3), riboflavin (vitamin B2), and minerals such as iron and copper to effect the movement of electrons and hydrogen protons in the power plant of cell, the mitochondrion.
Incidentally, tobacco leaf is the champion source, containing 184 mg in a quarter pound.
Note that the doctor follows with the disclaimer, "In fact, the Japanese companies make their CoQ from tobacco, however it is only released by means of bacterial fermentation not by smoking." The fact remains that CoQ 10 is a natural miracle for the human body and its chief source is tobacco! Those MDs just can't get their heads around the fact that tobacco is a valuable gift from nature! Now take a look at what a pharmacy has to say about natural vs. synthetic CoQ10:
The natural CoQ10 in Qmelt is made via fermentation in which a microorganism (in the case of CoQ10, a bacterium or yeast) naturally produces CoQ10. The CoQ10 is then extracted from the organism and concentrated. It is termed natural since it is normally and naturally produced by the yeast or bacterium from which it was taken. This is different from synthetic CoQ10 which is made by taking a compound found in tobacco and then mixing it with other chemicals to form a similar structure of CoQ10. While tobacco is natural, CoQ10 is not taken from tobacco in this synthetic process....the only thing taken from the tobacco is a compound which is used as the starting material for chemically creating CoQ10. That is why it is referred to as a synthetic process. Tobacco or plants in general do not contain significant amounts of CoQ10
The pharmacy "information" is in direct contradiction of what is known by everyone else: (1) tobacco is the chief source of CoQ10 with an abundance of the enzyme and (2) the means by which CoQ10 is extracted is not chemical, although it might involve fermentation. (Note: The fermentation process might involve beets or fermented sugar cane.)

AN IMPORTANT NOTE: The doctor cited above comments on the importance of CoQ in partnership with other nutrients, including niacinamide, AKA nicotinic acid, niacin and vitamin B3. This is a form of nicotine, which could result from the alteration of nicotine as it is very unstable. Please see Facts about Nicotine.

Smoking Reduces Parkinson's
Neurology. 1999 Sep 22;53(5):1158. Smoking and Parkinson's disease: a dose-response relationship Gorell JM, Rybicki BA, Johnson CC, Peterson EL

Department of Neurology, Henry Ford Health System, National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications, Wayne State University, Detroit, MI, USA.

OBJECTIVE: To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers.

METHODS: Smoking and alcohol consumption were analyzed in 144 PD patients and 464 control subjects, who were frequency matched for sex, race, and age (+/-5 years), in a population-based case-control study of men and women > or =50 years old in the Henry Ford Health System.

RESULTS: With never-smokers as the reference category, there was an inverse association between current light smokers (>0 to 30 pack-years) and PD patients (odds ratio [OR], 0.59; 95% CI, 0.23 to 1.53), and a stronger inverse association of PD with current heavy smokers (>30 pack-years; OR, 0.08; 95% CI, 0.01 to 0.62). When former >30-pack-year smokers were stratified by the interval since quitting, there was an inverse association between those who stopped >20 years ago and PD (OR, 0.86; 95% CI, 0.42 to 1.75), and a greater inverse relationship with those who stopped 1 to 20 years ago (OR, 0.37; 95% CI, 0.19 to 0.72). Alcohol consumption had no independent, significant association with PD, but heavy drinking (>10 drink-years) had a greater effect than light-moderate drinking in reducing but not eliminating the inverse association between smoking and PD.

CONCLUSIONS: The inverse dose-response relationship between PD and smoking and its cessation is unlikely to be due to bias or confounding, as discussed, providing indirect evidence that smoking is biologically protective.

Also see Smoking lowers Parkinson's disease risk from Reuters (Mar 20, 2007).

From "Temporal relationship between cigarette smoking and risk of Parkinson disease" (NEUROLOGY 2007;68:764-768):

The lower risk of Parkinson disease among current and former smokers varied with smoking duration, intensity, and recentness. The dependence of this association on the timing of smoking during life is consistent with a biologic effect.

Osteo-arthritis reduced threefold (the most for knee arthritis in women)
IS OSTEOARTHRITIS IN WOMEN AFFECTED BY HORMONAL CHANGES OR SMOKING? from the journal for British Society for Rheumatology (1993).

Internal antioxidant SOD doubled (recent article labels the higher SOD "the elixir of eternal life" based on animal experiments)
From Scientists find elixir of eternal life - in a worm By Roger Highfield, Science Editor, "Detailed work showed that the gene can boost levels of proteins called SODs (superoxide dismutase) which mop up free radicals, harmful chemicals linked with aging. The researchers think that this may be a defense mechanism that helps the creatures tolerate starvation."

Reduced MAO B enzyme (smokers in their 60s have MAO B of nonsmokers in their 20s; also here). Lowering of MAO B is the Holy Grail (deprenyl does it but not as well as tobacco) of life-extension and smart drug circles.
Explained very well by NightLight referencing The American Journal of Psychiatry illustrated by these graphs, and the National Academy of Sciences (September 8, 2003). More can be found on MAO and the importance of MAO-inhibitors in Turkish Journal of Medical Sciences, MAO Inhibitors in Aging: Can They Serve as Protective Agents in Cardiac Tissue Against Oxidative Stress?, Scholar Google and
The real eye-opener comes from theNational Institute on Drug Abuse! That's about as far as you can get from being a shill for Big Tobacco! Yet, this antismoking group's very own study, "Tobacco Smoke May Contain a Psychoactive Ingredient Other Than Nicotine" (NIDA News, Volume 13, Number 3, July, 1998), states plainly:
The amount of the enzyme, called monoamine oxidase (MAO), is reduced by 30 to 40 percent in the brains of smokers, compared to nonsmokers or former smokers, the brain scans show. The reduction in brain MAO levels may result in an increase in levels of dopamine, which scientists associate with the reinforcing effects of drugs of abuse.
A note needs to be on the research paper in the American Journal of Psychiatry, Maintenance of Brain Monoamine Oxidase B Inhibition in Smokers After Overnight Cigarette Abstinence. The Abstract includes these remarks:
OBJECTIVE: The authors' goal was to replicate a previous finding that smokers have lower brain monoamine oxidase B (MAO-B) levels than comparison nonsmoking subjects ...RESULTS: Average MAO-B levels in smokers in the present study were similar to those found in the previous study and averaged 39% (SD=17) lower than those found in a comparison group of nonsmokers. Brain MAO-B levels did not differ between baseline levels and 10 minutes after smoking.
So, the authors of this study were replicating the results that MAO-B levels are lower in smokers!!!

This benefit of inhibiting MAO-B was known as long ago as 1987. From Irreversible inhibition of monoamine oxidase by some components of cigarette smoke, Life Science (1987 Aug 10;41(6):675-82), "Inhibitory activity towards monoamine oxidase has been found in a solution of cigarette smoke. The inhibition was irreversible."

Alas, one must an actual smoker to benefit. From the abstract of "Smoking a single cigarette does not produce a measurable reduction in brain MAO B in non-smokers" (PubMed):

Positron emission tomography (PET) studies with [11C]L-deprenyl-D2 have shown that brain monoamine oxidase (MAO) B is 40% lower in smokers than in non-smokers. ...These results indicate that the reduction in MAO B in smokers probably occurs gradually and requires chronic tobacco smoke exposure.
Telomerase ("fountain of youth") much more active in smokers.

Smoking is associated with increased telomerase activity in short-term cultures of human bronchial epithelial cells, Cancer Letters 2007 Feb 8;246(1-2):24-33. Epub 2006 Mar 6--from the Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.

Glutathione (chief antioxidant in human body) and catalase (another key antioxidant which neutralizes alcohol damage, cyanide,...) doubled in smokers.
Also explained by NightLight.
From The Abstract of Normal alveolar epithelial lining fluid contains high levels of glutathione in the Journal of Applied Physiology (Vol. 63, Issue 1, p. 152-157):
The epithelial cells on the alveolar surface of the human lower respiratory tract are vulnerable to toxic oxidants derived from inhaled pollutants or inflammatory cells. Although these lung cells have intracellular antioxidants, these defenses may be insufficient to protect the epithelial surface against oxidants present at the alveolar surface. This study demonstrates that the epithelial lining fluid (ELF) of the lower respiratory tract contains large amounts of the sulfhydryl-containing antioxidant glutathione (GSH). The total glutathione (the reduced form GSH and the disulfide GSSG) concentration of normal ELF was 140-fold higher than that in plasma of the same individuals, and 96% of the glutathione in ELF was in the reduced form. Compared with nonsmokers, cigarette smokers had 80% higher levels of ELF total glutathione, 98% of which was in the reduced form. Studies of cultured lung epithelial cells and fibroblasts demonstrated that these concentrations of reduced glutathione were sufficient to protect these cells against the burden of H2O2 in the range released by alveolar macrophages removed from the lower respiratory tract of nonsmokers and smokers, respectively, suggesting that the glutathione present in the alveolar ELF of normal individuals likely contributes to the protective screen against oxidants in the extracellular milieu of the lower respiratory tract.
More studies on antioxidants in people who smoke can be found in the Journal of Applied Physiology.
Selective increase of antioxidant enzyme activity in the alveolar macrophages from cigarette smokers and smoke-exposed hamsters. for American Review of Respiratory Disease, (1990 Mar, vol. 141, no 3, p. 678-82).

Nicotine suppresses cell death of neurons (it also promotes vascular growth factor, e.g. growth and branching of capillaries). (Another advantage of nicotine is that Nicotine Slays TB. The link to this mainstream article is prefaced by this comment, "This article was written in 2001 and since then the ban on smoking in public places and taxing tobacco has grown. Extremely-Drug-Resistant Tuberculosis strains will continue to spread and multiply. The resulting global XDR-TB epidemic will be an untreatable and unstoppable calamity.")

Low concentration carbon monoxide (as found in tobacco smoke) protects cells in harsh conditions, such as low oxygen and general cell death.

From CO-RMs: Therapeutic Carbon Monoxide Releasing Molecules (Monday, October 22, 2007; medGadget, Internet journal of Medical Technologies):

Carbon monoxide (CO), a silent and powerful poison gas, might actually lend itself for a variety of promising clinical applications, according to the researchers from Sheffield University in the UK. Professor Brian Mann and colleagues from the University's Department of Chemistry and hemoCORM Ltd, a spinout company, are working on water-soluble molecules that can deliver CO to tissues to "reduce inflammation, widen blood vessels, increase blood flow, prevent unwanted blood clotting and even suppress the activity of cells and macrophages which attack transplanted organs," according to the university's press release.
Nitric oxide stimulates peripheral circulation (this is the mechanism behind Viagra effect).

Raises youth hormones, e.g. DHEA, pregnenolone, testosterone,...

Relation of age and smoking to serum levels of total testosterone and dehydroepiandrosterone sulfate in aged men in Geriatrics & Gerontology International (Volume 6 Issue 1 Page 49-52, March 2006), which found these results, "Serum T did not decrease with age, and was significantly higher in smokers than for non-smokers. Serum DHEA decreased with age more sharply in non-smokers than for smokers."

Smoking reduces IGF-1 (insulin-like growth factor 1)--at least in males for sure. In animal experiments, lowered insulin growth factor IGF-1 change extends lifespan.

From Signals from the reproductive system regulate the lifespan of C. elegans (Nature. 1999 May 27;399(6734):308-9), "Mutants with reduced activity of the insulin/IGF-1-receptor homologue DAF-2 have been shown to live twice as long as normal". From Dietary and Lifestyle Correlates of Plasma Insulin-Like Growth Factor-I (IGF-I) and IGF Binding Protein-3 (IGFBP-3): The Multiethnic Cohort (Cancer Epidemiology Biomarkers & Prevention, Vol. 13, 1444-1451, September 2004), "In addition, we observed associations between current smoking and low IGF-I levels..."--and, on p. 1449, table 3 shows that smoking had strongest reduction effect on IGF-1 in males!

Hmmmmm.... So, IGF-1 is reduced in people who smoke and animals bred to have reduced IGF-1 have a tendency to double their life spans. That goes a long way toward explaining the reason that the people who have lived longest on this earth are all smokers!

Reduced Incidence of Colorectal Cancer--especially in women.

Cigarette Smoking and the Risk of Colorectal Cancer in Women (Journal of the National Cancer Institute, Vol. 80, No. 16, 1329-1333, October 19, 1988) states, "Colorectal cancer incidence rates for smokers, nonsmokers living with smokers (i.e., passive smokers), and non-smokers in smoke-free households were compared in a 12-year prospective study of 25, 369 women who participated in a private census conducted in Washington County, MD, in 1963. Women who smoked had a decreased relative risk of colorectal cancer compared with the risk for nonsmokers (age-adjusted relative risk, 0.76; 95% confidence interval, 0.52-1.10). The risk for passive smokers was similar to that for smokers. The relative risks were significantly reduced for older women; relative risks were 0.42 for smokers and 0.66 for passive smokers over age 65. The data suggest that older women who smoke have a lower risk of colorectal cancer than non-smokers. The effect may be mediated by an antiestrogenic effect of smoking." More evidence can be found in this scanned document

People who smoke fare better than nonsmokers when exposed to occupational hazards.

From Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workersBritish Medical Journal, Occupational and Environmental Medicine (Vol. 56, 468-472, 1999):

Smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers, which was significant for wheezing (2.6% v 17.4% and 28.6% respectively, both p < 0.01), whereas respiratory symptoms in controls tended to be highest in smokers (NS). No effects of potroom work on the prevalence of respiratory symptoms could be detected. In potroom workers, impairment of lung function due to occupational exposure was found only in non-smokers, with lower results for forced vital capacity (FVC) (98.8% predicted), forced expiratory volume in one second (FEV1) (96.1% predicted) and peak expiratory flow (PEF) (80.2% predicted) compared with controls (114.2, 109.9, and 105.9% predicted; each p < 0.001). Conversely, effects of smoking on lung function were only detectable in non-exposed controls (current smokers v non-smokers: FVC 98.8% v 114.2% predicted; p < 0.01; FEV1 95.5 v 109.9% predicted; p < 0.05)." (NOTE: The key result is that for the exposure controlled group (the potroom workers) the smoking reduced the risk of lung damage sixfold compared to never-smokers.)

For asbestos workers, "Effect of Smoking on Immunological Abnormalities in Asbestos Workers" (Institute of Immunology and Experimental Therapy, Poland) by Lange, A.:

Smoking has a protective effect on immunological abnormalities in asbestos workers.

More for asbestos workers is found in "Cancer of the Lung Among Asbestos Factory Workers" (University of London, School of Hygiene and Tropical Medicine), 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,"

And again in The Interaction of Asbestos and Smoking in Lung Cancer by G. BERRY1, and F. D. K. LIDDELL (Oxford Journals, Medicine, Annals of Occupational Hygiene, Volume 48, Number 5, p. 459-462, 2004):

Conclusion: The excess relative risk of lung cancer from asbestos exposure is about three times higher in non-smokers than in smokers. The modified measure has been placed within a more versatile model of interaction. If interaction is present the relative risk from asbestos exposure changes only slightly between light and heavy smokers, but is higher in very light smokers and non-smokers.

Many other studies show protective effects of smoking for asbestos workers. Similar effects are found for other lung cancer risk factors, including radiation and chemical cancerogen exposures. For example:

From "Lung Cancer Dueto Chloromethyl Ethers" (Hahnemann Medical College and Hospital, Philadelphia) by Weiss, W., "Over the 22 years of follow-up, exposed workers have had a very high risk of respiratory cancer, mostly of the lung. The risk has been dose related and has been much higher in nonsmokers and ex-smokers than in current smokers. The epidemic began to subside shortly after exposure to chloromethyl ethers ceased. The mean induction-latency period was 17 years. Most of the lung cancers in the moderate and high dose groups have been small cell carcinoma,"

From "Respiratory Effects of Exposure to Diesel Emissions in Underground Coal Miners" by Ames, R.G. (DHHS, PHS, CDC, NIOSH. Funding: NIOSH), "Presence of chronic respiratory symptoms at baseline was inversely related to cessation of smoking. Respiratory impairment was positively associated with smoking cessation, but failed to reach statistical significance,"

Reduces schizophrenia symptoms.

From "Investigating the Association Between Cigarette Smoking and Schizophrenia in a Cohort Study," Am J Psychiatry (160:2216-2221, December 2003):

Cigarette smoking may be an independent protective factor for developing schizophrenia. These results are consistent with animal models showing both neuroprotective effects of nicotine and differential release of prefrontal dopamine in response to nicotine.
From Cancer in schizophrenia: is the risk higher or lower? in Schizophrenia Research (Volume 73, Issue 2, Pages 333-341) at :
The incidence of cancer in patients diagnosed with schizophrenia was compared with the incidence in the general population. The results showed that the cancer standardized incidence ratios (SIRs) for all sites were significantly lower among men and women with schizophrenia, 0.86 [95% confidence interval (CI) 0.80-0.93] and 0.91 (95% CI 0.85-0.97), respectively. This reduced overall risk was clearest for those born in Europe-America, both men (SIR 0.85, 95% CI 0.74-0.97) and women (SIR 0.86, 95% CI 0.77-0.94).
Appetite Suppressant -- no citations. Common sense. Most stimulants are appetite suppressants, and nicotine does seem to be a stimulant.
Tobacco: the definitive link in healthy aging by Daniel John Richard Date.
Reduces incidence of Alzheimer's, among other degenerative diseases.

From The Straight Dope Classics:

"A statistically significant inverse association between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption" (International Journal of Epidemiology, 1991)

"The risk of Alzheimer's disease decreased with increasing daily number of cigarettes smoked before onset of disease. . . . In six families in which the disease was apparently inherited . . . the mean age of onset was 4.17 years later in smoking patients than in non-smoking patients from the same family" (British Medical Journal, June 22, 1991)

"Although more data are needed . . . [an analysis of 19 studies suggests] nicotine protects against AD" (Neuroepidemiology, 1994)

Nicotine injections significantly improved certain types of mental functioning in Alzheimer's patients (Psychopharmacology, 1992).

One theory: nicotine improves the responsiveness of Alzheimer's patients to acetylcholine, an important brain chemical.

"When chronically taken, nicotine may result in: (1) positive reinforcement [it makes you feel good], (2) negative reinforcement [it may keep you from feeling bad], (3) reduction of body weight [by reducing appetite and increasing metabolic rate], (4) enhancement of performance, and protection against: (5) Parkinson's disease, (6) Tourette's disease [tics], (7) Alzheimer's disease, (8) ulcerative colitis and (9) sleep apnea. The reliability of these effects varies greatly but justifies the search for more therapeutic applications for this interesting compound." ("Beneficial Effects of Nicotine," Jarvik, British Journal of Addiction, 1991)

See more on smoking and reduced incidence of Alzheimer's disease. In this compilation of 19 studies, 15 found a reduce risk in smokers, and none found an increased risk. Also noted is the fact that acute administration of nicotine improves attention and information processing in AD patients, which adds further plausibility to the hypothesis.
Smoking is Good for You: Absence, Presence, and the Ecumenical Appeal of Indian Islamic Healing Centers
In Shop owner says smoking 'doesn't cause disease' a shop owner "tells his customers that smoking calms the nerves and soothes the mind." This is in sync with what Albert Einstein stated upon becoming a lifetime member of the Montreal Pipe Smokers Club at the age of 71, "I believe that pipe smoking contributes to a somewhat calm and objective judgment in all human affairs."
Evidence that smoking is protective against thyroid cancer

Prepublished from the American Journal of Epidemiology (Sep 2007). From the abstract of pubmed's Alcohol Drinking, Tobacco Smoking, and Anthropometric Characteristics as Risk Factors for Thyroid Cancer: A Countrywide Case-Control Study in New Caledonia. (Unité 754, INSERM, Villejuif, France) by Guignard R, Truong T, Rougier Y, Baron-Dubourdieu D, Guénel P., quote (emphasis added):

Exceptionally high incidence rates of thyroid cancer are observed in New Caledonia, particularly in Melanesian women. To investigate further the etiology of thyroid cancer and to clarify the reasons of this elevated incidence, the authors conducted a countrywide population-based case-control study in this multiethnic population. The study included 332 cases with histologically verified papillary or follicular carcinoma (293 women and 39 men) diagnosed in 1993-1999 and 412 population controls (354 women and 58 men) frequency matched by gender and 5-year age group. Thyroid cancer was negatively associated with tobacco smoking and alcohol drinking, but no inverse dose-response relation was observed. Height was positively associated with thyroid cancer, particularly in men. Strong positive associations with weight and body mass index were observed in Melanesian women aged 50 years or more, with an odds ratio of 5.5 (95% confidence interval: 1.5, 20.3) for a body mass index of 35 kg/m(2) or greater compared with normal-weight women, and there was a clear dose-response trend. This study clarifies the role of overweight for thyroid cancer in postmenopausal women. Because of the high prevalence of obesity among Melanesian women of New Caledonia, this finding may explain in part the exceptionally elevated incidence of thyroid cancer in this group.

A Few Words of Caution Concerning Filters
From "Cigarettes with defective filters marketed for 40 years: what Philip Morris never told smokers" (Tobacco Control 2002;11:i51-i61):
Background: More than 90% of the cigarettes sold worldwide have a filter. Nearly all filters consist of a rod of numerous ( > 12 000) plastic-like cellulose acetate fibres. During high speed cigarette manufacturing procedures, fragments of cellulose acetate that form the mouthpiece of a filter rod become separated from the filter at the end face. The cut surface of the filter of nearly all cigarettes has these fragments. In smoking a cigarette in the usual manner, some of these fragments are released during puffing. In addition to the cellulose acetate fragments, carbon particles are released also from some cigarette brands that have a charcoal filter. Cigarettes with filters that release cellulose acetate or carbon particles during normal smoking conditions are defective.
Conclusions: We have shown that: (a) the filter of today's cigarette is defective; (b) Philip Morris, Inc has known of this filter defect for more than 40 years; (c) the existence of this filter defect has been confirmed by others in independent studies; (d) many methods exist to prevent and correct the filter defect, but have not been implemented; and (e) results of investigations substantiating defective filters have been concealed from the smoker and the health community. The tobacco industry has been negligent in not performing toxicological examinations and other studies to assess the human health risks associated with regularly ingesting and inhaling non-degradable, toxin coated cellulose acetate fragments and carbon microparticles and possibly other components that are released from conventional cigarette filters during normal smoking. The rationale for harm assessment is supported by the results of consumer surveys that have shown that the ingestion or inhalation of cigarette filter fibres are a health concern to nearly all smokers.
From "A False Martyr?" from Surreality Times:
The "official" explanation for smokers developing less squamous tumors and more adenocarcinoma tumors, is that modern filters on cigarettes cause smokers to inhale more deeply which deposits irritants into the small airways deep in the lungs where adenocarcinomas develop. But - non-smokers don't inhale second-hand smoke through a filter!

The anti-smoking industry claims, smokers are now developing andenocarcinomas because they are inhaling cigarette smoke through modern filters, specifically. It's the filtering that makes the difference, in smokers, they claim. Non-smokers never inhale SHS through filters, they always inhale unfiltered smoke. That means, if SHS is causing lung cancer in non-smokers, they should be developing Squamous Cell tumours! Unfiltered tobacco smoke = squamous cell tumours, filtered tobacco smoke = andenocarcinoma tumours, according to the American Cancer Society.
Other health risks could be associated with the use of tobacco sheets in cigarette manufacturing. Although "authorities" and "experts" tell us that "there is no safe cigarette"--but then try to legislate for safer cigarettes--the fact is that whole leaf tobacco and organic tobacco are less hazardous. Moreover, whole leaf tobacco burns slower, thus reducing fire hazards.

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