Posted on 11/21/2006 5:04:27 AM PST by SJackson
There are few personal confessions more likely to alienate many Americans than to admit to smoking. Singles ads are filled with people who will never even go on a first date with someone who smokes. I strongly suspect that more women would date a millionaire who earned his money disreputably than a millionaire who smoked.
Drinkers are far more highly regarded than smokers, as are playboys, gamblers, lawyers, politicians and almost anyone else except child molesters.
So I have no doubt that some readers who until now have held me in esteem will lose respect for me when they learn that not only do I smoke cigars and a pipe, but I love doing so, have no interest in stopping and have been happy to pass this pleasure on to my older son. In fact, we regularly have some of our best talks while we enjoy our cigars.
For the record, I never smoke cigarettes, which I happen to dislike the smell of, and which I acknowledge to be dangerous. But what I write here largely applies to cigarette smokers as well. In fact, I find anti-smoking zealots far more dangerous to society than cigarette smokers, and would much sooner date a cigarette smoker than one of the zealots.
Having said that, however, it does need to be pointed out that there is little in common between cigar (or pipe) smoking and cigarette smoking. Most important, we don't inhale. This is not meant in the way former President Bill Clinton meant it when he said he "never inhaled." The purpose and joy of cigar and pipe smoking are to enjoy the taste of tobacco in one's mouth. The purpose and joy of cigarette smoking are only vaguely related to the taste of tobacco.
And that leads to two other great differences between cigarette smoking and cigar (and pipe) smoking: First, there is no issue of addiction regarding cigars or pipes. I have been smoking both since I was 15 years old, and could stop tomorrow if I wanted to. Indeed, as a Jew who observes the Sabbath prohibition on kindling fire, I do not smoke for a day every week, and it is effortless. Likewise, I am frequently on the road lecturing, and often miss days at a time with absolutely no discernible effect. Second, because one does not inhale when smoking a cigar or pipe, the likelihood of lung cancer is minimal.
Yes, I am warned by doctors that I am more liable to contract mouth or lip cancer, but while physicians may see such diseases, in 40 years of smoking I have never met or heard of one person with either cancer.
Indeed, I am quite convinced that my one-a-day cigar or pipe may well have had a positive impact on my health given how much relaxation it induces. Stress kills far more people than cigars or pipes do.
It is a sign of the times that the latest James Bond film has prohibited 007 from smoking a cigar. One of the most benign practices a person can engage in was banned, but our macho hero can be shown drinking alcohol and bedding women (and without any mention of condoms!), not to mention killing people and engaging in behaviors infinitely more dangerous than cigar smoking.
We live in the Age of Stupidity. This new age has been induced by widespread college education and widespread secularism -- Psalms is entirely accurate: "Wisdom begins with fear of the Lord" -- which explains, for example, why only well-educated secularists came to believe that there were no innate nonphysical differences between men and women.
Nearly 100 years ago, before widespread college education and before widespread secularism, when America tried to prohibit a vice, it chose alcohol, not tobacco. It knew that there were immoral consequences to alcohol consumption -- most child abuse, most spousal abuse, about half of violent crimes and most rapes are accompanied by alcohol. Nobody has ever raped because smoking a cigarette or a cigar numbed his conscience. And no one fears smoking drivers; we rightly fear drinking drivers.
Both in my hometown and on the road, I find great joy in visiting cigar stores and schmoozing with the owners and with the guys smoking there. In fact, cigar stores may be the last place men can get together without women.
Of course if you think I am really killing people due to the secondhand smoke they inhale from my cigar or pipe, I presume all discussion ends. I am then simply a killer who needs to be stopped. I find absurd the notion that more than 50,000 Americans are killed every year just by being in the presence of smokers. But if you believe it, all you need to do is open a window and enjoy yourself.
The late legendary comedian George Burns was a listener to my radio talk show. When he was around 90 years old, he invited me to his Beverly Hills home. In the course of our two hours together, he smoked two cigars and had a couple of martinis. I asked him what his doctor said about those habits. George looked at me and responded, "My doctor died."
My father is 88 years old and has been smoking a few cigars a day (in my 87-year-old mother's presence, I might add). They are both in near-perfect health. He not only taught me the joys of cigars. He also taught me the importance of thinking for myself and how to lead an honorable life that includes as much joy as possible.
Almost every one of them is in every breath you exhale, smoker or not.
Serving poisnous chemicals like hydrogen cyanide, hdyrazine, formaldehyde, vinly-chrloride is not serving fat ??
geez....! since when did a happy meal have hhydrogen cyanide, dyrazine, formaldehyde, vinly-chrloride in it, how stupid some of these pro-cirgarete agruments can get.
Lets see - find all these chemicals (very small sample of the total) in a happy meal for me (see middle of article):
Cigarette smoke contains over 4,700 chemical compounds including 60 known carcinogens. No threshold level of exposure to cigarette smoke has been defined but there is conclusive evidence to indicate that long-term (years) smoking greatly increases the likelihood of developing numerous fatal conditions.
Cigarette smoking is responsible for more than 85% of lung cancers and is also associated with cancers of the mouth, pharynx, larynx, oesophagus, stomach, pancreas, uterine cervix, kidney, ureter, bladder and colon. Cigarette smoking has also been linked to Leukaemia. Apart from the carcinogenic aspects of cigarette smoking, links to increased risks of cardiovascular diseases (including stroke), sudden death, cardiac arrest, peripheral vascular disease and aortic aneurysm have also been established. Many components of Cigarette smoke have also been characterised as Ciliotoxic materials that irritate the lining of the respiratory system resulting in increased bronchial mucus secretion and chronic decreases in pulmonary and mucociliary function.
A 1992 report by the Environmental Protection Agency (EPA) examined the effects of Passive Smoking (also known as Environmental Tobacco Smoke (ETS) or Second-hand smoke) and concluded that it posed a similar risk to direct cigarette smoking. The report actually resulted in cigarette smoke being classified as a "group A" carcinogen by the EPA, a category reserved for the more potent known human carcinogens.
Cigarette smoke itself may be broken down into two categories of smoke - Mainstream smoke (MS) and Sidestream smoke (SS). MS is that smoke which is inhaled by the smoker from the cigarette during a puff. SS is that smoke which is emitted by the burning cigarette between puffs. The chemical compositions of both types of smoke are qualitatively similar since they are both derived from burning tobacoo, however, there are some significant quantitative differences between MS and SS. The temperature at which MS is formed is much higher than the temperature at which SS is formed, since the smoker is actively inhaling from the cigarette during the generation of MS. A result of this is that SS contains larger quantities of many organic chemical compounds than MS. One study has tentatively suggested that SS may be more carcinogenic than MS at the same concentrations.
Regulations governing Cigarette smoking have been increasingly strict since July 1957, when Dr. Leroy E. Burney (US Surgeon General) issued the first Public Health services statement on cigarette smoking - smoking was identified as a cause of lung cancer. This observation was based more on epidemiological data than specific scientific evidence that identified carcinogenic materials in cigarette smoke, however research in the last 30 years has confirmed the epidemiological observations made previously. ETS has become the latest aspect of cigarette smoking to come under regulation with the realisation that ETS does contribute to increased risk of lung cancer amongst exposed non-smokers. Most US states have legislation controlling or restricting smoking in public areas including restaurants. Many states have or are implementing complete bans on smoking in or within the vicinity of public areas, while many businesses have adopted non-smoking policies. In Ireland, legislation has not reached the same level, but it is inevitable and currently, the Public Health Act restricts smoking in public areas and on public transport services.
Cigarette Smoke Chemical constituents
As mentioned previously, cigarette smoke contains over 4,700 chemical compounds of which about 60 are carcinogenic. The following tables, sourced from US Surgeon General Reports on the Health Consequences of smoking summarise the toxic components of cigarettes.
Primary Toxic and Carcinogenic components of Cigarette Smoke including vapour-phase and particulate phase components
Agent Toxic Ciliotoxic Carcinogenic Co-carcinogenic
/ Promoter
Carbon Monoxide x
Nitrogen Oxides (NOx) x
Hydrogen Cyanide x x
Formaldehyde x x
Acrolein x
Acetaldehyde x
Ammonia x
Hydrazine x
Vinyl Chloride x
Urethane x
2-Nitropropane x
Quinoline x
Benzo[a]pyrene x x
Dibenz[a,h]anthracene x x
Benzo[b]fluoranthene x x
Benzo[j]fluoranthene x x
Dibenzo[a,h]pyrene x x
Dibenzo[a,i]pyrene x x
Dibenz[a,j]acridine x x
Indeno[1,2,3-cd]pyrene x x
Benzo[c]phenanthrene x x
Benz[a]anthracene x x
Benzo[e]pyrene x x
Chrysene x x
Methylchrysene x x
Mehtylfluoranthene x x
Dibenz[a,c]anthracene x x
Dibenz[a,h]acridine x x
Dibenzo[c,g]carbazole x x
Mehtylnaphtalenes x
1-Methylindoles x
Dichlorostilbene x
Catechol x
3-Methycatechol x
4-Methycatechol x
4-Ethycatechol x
4-n-Propylcatechol x
Nitrosodimethylamine x
Nitrosoethymethylamine x
Nitrosodiethylamine x
Nitrosodi-n-propylamine x
Nitrosodi-n-butylamine x
Nitrosopyrrolidine x
Nitrosopiperidine x
Nitrosomorpholine x
N'-Nitrosonornicotine x
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone x
N'-Nitrosoanabasine x
N'-Nitrosoanatabine x
Aromatic Amines x
Aromatic Nitrohydrocarbons x
Polonium-210 x
Nickel x
Arsenic x
Cadmium x
While it is not possible to examine all the compounds and their respective toxicological effects, this report will focus on the primary carcinogens found in cigarette smoke. The primary cancer causing agents found in cigarette smoke may be broadly categorised as follows,
Carcinogenic
Polycyclic Aromatic Hydrocarbons (PAH)
N-nitrosaminous compounds
Aromatic Amines
Trace metals
Promoters
Catechols
Pyrenes
Co-carcinogens / Potentiators (not present in Cigarette smoke)
Asbestos
Alcohol
Polycyclic Aromatic Hydrocarbons (PAH)
Aromatic compounds that have rings which share at least one side are described as Fused-ring systems or Polycyclic Aromatic Hydrocarbons. There are many PAHs in cigarette smoke including Benzo[a]pyrene, Dibenz[a,h]anthracene and Benz[a]anthracene (see table).
These are reactive compounds that tend to form epoxides when metabolised becoming extremely genotoxic. They act as tumour initiators. Benzo[a]pyrene is a particularly good example of a cigarette smoke PAH which has been studied extensively. About 40 of it's oxygenated metabolites have been isolated and characterised with at least one of them being a potent mutagen. The resulting epoxide metabolite, benzo[a]pyrene-7,8-diol-9,10-epoxide forms an adduct with DNA in mouse embryo cells, indicating that the diol-epoxide is the metabolic intermediate responsible for reacting with DNA.
N-nitrosamines
N-nitrosamines are formed by the nitrosation of amines. Cigarette smoke contains two major types of N-nitrosamines, Volatile N-nitrosamines (VNA) and Tobacoo Specific N-nitrosamines (TSNA). Practically all Volatile N-nitrosamines are retained by the respiratory system upon cigarette smoke inhalation. Typical cigarette smoke VNAs include N-nitrosdiethylamine (NDEA) and N-nitrosodimethylamine (NDMA), both of which are classified as potent environmental carcinogens.
As of the International Agency for Research on Cancer's (IARC) 1986 report, these substances had not been classified as Human carcinogens due to lack of scientific research, however, on the basis of large amounts of research on laboratory animals indicating carcinogenicity it is generally felt that they should be regarded as carcinogenic to humans. In a 1968 study for instance, in which 36 Syrian Golden Hamsters were given a single dose of only 6 mg of NDEA, 29 suffered Tumours of the respiratory trace.
Studies of N-nitrosamines indicate that it is a metabolically activated carcinogen which disrupts DNA. The metabolic activation is brought about by the demethylating enzyme Cytochrome P-450 which requires NADPH and O2. The presence of alcohol seems to enhance N-nitrosamine metabolism to it's carcinogenic metabolite. This would appear to indicate that alcohol potentiates the effects of N-nitrosamines as carcinogens and would explain the observed increased incidence of cancer of the oral cavity and oesophagus in smokers who also drink large amounts of alcohol.
Aromatic Amines
Epidemiological studies of dye workers have documented that certain aromatic amines such as 2-naphthylamine and 4-aminobiphenyl are human bladder carcinogens. 2-naphthylamine is converted to an N-hydroxy derivative metabolic intermediate, which is capable of forming adducts with guanine in nucleic acids.
Trace Metals
While it is generally felt that the quantities of Cadmium, Nickel, Arsenic and Polonium-210 found in cigarette smoke do not significantly contribute to an increased risk of lung cancer or other smoking-related cancers, their role as potentiators or co-factors has not been researched to-date in any great detail.
These metals tend to accumulate in the body and could possibly act as promoters in conjunction with carcinogens in cigarette smoke. Cadmium for instance (several forms of which are suspected carcinogens) is only present at concentrations of 50-100 ng in cigarette smoke but it has been suggested that a heavy smoker will retain up to 1.5 g of it per day leading to a lifetime accumulation of 0.5 mg.
The importance of Arsenic as a toxic component of cigarette smoke has diminished following the removal of Arsenic containing compounds from the list if recommended pesticides in the US for the control of hornworms on tobacco. This has resulted in a large decrease in the amount of Arsenic in tobacco and consequently cigarette smoke. A review by the International Agency for Cancer (IARC) suggested that arsenic compounds could potentially act as human skin carcinogens.
Nickel, classified as a suspected human carcinogen (IARC, 1986) is present in concentrations up to 80 ng in cigarette smoke (MS). Nickel has been shown to induce sarcomas by subcutaneous injection in laboratory animals. Nickel Subsulphide (Ni3S2) has been shown to have even greater potency, inducing a high rate of renal carcinomas in rats after exposure to only a single 5 mg dose (Intravenally injected).
Polonium-210, a radioactive material that emits -particles, accumulates at a higher rate in the parenchyma and bronchial mucosa of smokers. Studies on Syrian Golden Hamsters using multiple intratracheal instillations of Polonium-210 have revealed a dose-response relationship with bronchocarcinomas and adenocarcinomas in the respiratory system.
Environmental Tobacco Smoke (ETS)
The 1986 report by the US Surgeon General on Involuntary Smoking came to the following conclusions,
Environmental Tobacco Smoke is a cause of disease including lung cancer in healthy non-smokers.
Children exposed to ETS (due to the fact that one or both of their parents were smokers) have an increased frequency of respiratory infections, increased respiratory problems and a slightly reduced rate of increase in lung function as they develop.
The separation of smokers and non-smokers in the same airspace may result in reductions, but does not eliminate exposure of non-smokers to ETS.
As mentioned in the opening paragraph, cigarette smoke can be categorised as either Mainstream smoke (MS) or Sidestream smoke (SS). ETS is derived mainly from SS which is qualitatively similar to MS. However, due to the lower temperature of formation of SS, it actually contains higher concentrations of toxic and carcinogenic agents than MS. Laboratory tests on animals have indicated that SS is more carcinogenic than MS. It must, however, also be borne in mind that while SS may be more toxic/carcinogenic, ETS is essentially a diluted form of SS so one cannot directly correlate the toxicity of SS to ETS.
ETS, like cigarette smoke, is undoubtedly a causative agent for a number of human diseases including various cancers and diseases of the respiratory tract aswell as middle ear infections in exposed children. Non-carcinogenic lung disease may be broken down into two major areas, disease of the lung airways (inflammation of the airways, increased bronchial mucus secretions,etc.) and disease of the lung parenchyma (alveolar tissue damage resulting in emphysema). Non-smokers exposed to ETS generally do not suffer from lung parenchyma disease unless they have a genetic predisposition to weakened lung tissue, however, disease of the lung airways can be induced by much smaller doses of cigarette smoke. With regard to Lung cancer, there is a tentative dose-response relationship which indicates that higher ETS exposure levels increases the risk of lung cancer but lower doses could also result in cancer.
Studies have been conducted on the effects of ETS on both children and adults. With regard to ETS, the main risk group is children and infants, particularly up to the age of 2 years.
Effects of ETS exposure on children
ETS exposure due to parental smoking, especially the mother's, contributes to 150,000 to 300,000 cases annually of lower respiratory tract infection (pneumonia, bronchitis, and other infections) in infants and children under 18 months of age. ETS exposure is also associated with increased respiratory irritation (cough, phlegm production, and wheezing) and middle ear infections, as well as upper respiratory tract symptoms (sore throats and colds) in infants and children. Two other infant-specific conditions known to be linked to ETS exposure have been researched in recent times, these being middle ear infections (MEI) and sudden infant death syndrome (SIDS).
A report in May, 1995 entitled Passive Smoke Exposure and Otitis Media sought to clarify the link between ETS exposure in infants and occurrence of otitis media (middle ear infections). It concluded that a significant increase in MEI risk was caused by exposure to ETS with the threshold being a maternal smoking level of 20 or more cigarettes a day. The mechanisms by which MEI are brought about by ETS include increased general risk of infection in individuals exposed to ETS and increased mucus secretion and ciliostasis effects bringing about an accumulation of mucus and bacteria in the middle ear region.
Sudden Infant Death Syndrome is a significant cause of death in infants aged from 1 month to a year and studies have established a conclusive link between it's occurrence and maternal smoking. Increased maternal smoking which results in increased ETS exposure to infants leads to a higher risk of SIDS independently of other confounding risk factors including low birth weight and low gestational age (both of which, incidentally are associated with maternal active smoking during pregnancy).
Effects of ETS exposure on adults
Estimates that ETS exposure causes 3,000 lung cancer deaths annually have been made. This is the primary area of risk associated with ETS exposure to adult non-smokers. The 1992 report by the EPA Respiratory Health Effects of Passive smoking: Lung Cancer and other Disorders classified ETS as a Group A carcinogen - a category reserved only for the most dangerous cancer-causing agents in humans. The risks of other cancers due to ETS exposure have not currently been evaluated in great detail at this stage but it seems likely that most cancers linked to cigarette smoking will be linked to ETS following suitable study. Other effects of ETS exposure in adults include chronic coughing, phlegm and wheezing; decreased pulmonary function (a 1980 report on 2100 adults found that the magnitude of the effects of ETS on pulmonary function was comparable to active smoking of 1 to 10 cigarettes per day) and bronchoconstriction.
Asthmatics appear to have a heightened sensitivity to ETS exposure, with studies showing 25% decreased lung function in asthmatics exposed in the laboratory to levels of ETS that had no effect on smokers.
Conclusions
Cigarette smoke appears to be one the main, preventable causes of disease in the modern world and it seems likely that conventional cigarette smoking will become increasingly restricted as public awareness of the effects of ETS increases and other dangers of smoking become more apparent. Cigarette smoking as a habit is also threatened by the US Food and Drug Administration (FDA) which is currently contemplating reclassification of cigarettes as a drug delivery device, this would inevitably result in much tighter controls on cigarette sales. Environmental Tobacco Smoke exposure presents a definite health risk, particularly to young infants and high-risk groups (including groups with genetic predispositions to ETS exposure risk and workers dealing with materials such as asbestos which appears to potentiate the effects of carcinogens in cigarette smoke) and it is the responsibility of smokers to ensure that they do not provide unnecessary health hazards to non-smokers. It has so far been impossible to define a threshold level below which ETS or direct cigarette smoker exposure can be deemed safe and free from risks since it the whole concept of whether a carcinogen can possibly have a safe threshold level is currently under debate.
References:
The Medical Effects of Tobacco Consumption, Scientific American. May 1995
Harrisons' Principles of Internal Medicine, 10th Ed. Petersdorf, Adams, Braunwald Isselbacher, Martin and Wilson. Chap 244:1302-1305
The Health Consequences of Smoking - Cancer, a report of the Surgeon General. US Department of Health and Human Services, 1982.
The Health Consequences of Involuntary Smoking, a report of the Surgeon General. US Department of Health and Human Services, 1986.
Organic Chemistry, 2nd Ed.. Ege, S. Published by D.C. Heath and Co.
Biochemistry, Voet, D., Voet, J. G.. Published by Wiley
National Cancer Institute World-Wide-Web site
I never eat at Mickey-Ds, I can't stand the place.
I think quite a few of you smoking freepers forget that you smokers are a minority and the majority of Americans can pass laws to keep you away from the rst of us.
Of course you could go wine to to ACLU that majority is surpressing the rights of the minority.
You made the analogy between an increased probability of poor health and criminal prosecution, not me. I was just carrying it out to logical extension. Why draw the line at "increases probability of cancer"? There are other causes of death (cardio-vascular disease).
Your litany of chemicals does not mention anything other than a confirmation of epidemiological evidence. What quantities of smoke are required to cause cancer in non-smokers? Excesses of any chemical can cause death from one direction or another (even water).
Are there any chemicals coming out of your car that might cause cancer in sufficient quantities?
What quantities of these chemicals would you find acceptable in the air around you (in ppm)? Any?
This is entirely misleading
It is true that breathing secondhand smoke for a short time can have immediate adverse effects on the cardiovascular system and one could reasonably state that these effects represent something other than normal functioning of the heart, blood, and vascular systems. However, there is not evidence that these effects, which have been shown to be transient, increase the risk of a heart attack.
The statement is misleading, then, because it suggests that the adverse acute effects of a brief exposure to secondhand smoke have been shown to increase the risk of a heart attack. This is simply not the case.
Moreover, even if the statement were accurate, it misrepresents the conclusions of the actual Surgeon General's report, which is devoid of any conclusion that short-term exposure to secondhand smoke increases heart attack risk.
If you read through or search the entire 727-page report, you will not find any conclusion that a brief exposure to secondhand smoke increases heart attack risk. And for good reason: there is no such evidence. The report itself is very carefully reviewed science and it is cautious in drawing causal conclusions. Not so the summary of the conclusions of the report provided by the Surgeon General.
It is as if the Surgeon General didn't even read his own report. It is as if he simply decided in advance the claims he wanted to make, and made them, regardless of whether there was evidence in the report to support them, or whether the report had drawn those conclusions.
It is important to add that even the speculation about the potential effects of a brief secondhand smoke exposure on heart attack risk apply only to people with severe existing coronary artery disease, who are essentially so fragile that virtually any insult (even eating a hamburger) could cause a heart attack. Without qualifying the claim to make it clear that it is referring only to people with severe coronary artery disease, the claim is very misleading.
He also said, "Short exposures to secondhand smoke can cause blood platelets to become stickier, damage the lining of blood vessels, decrease coronary flow velocity reserves, and reduce heart rate variability, potentially increasing the risk of a heart attack."
Another misleading statement.
It is true that short exposure to secondhand smoke can increase platelet aggregation, cause endothelial dysfunction (damage to the lining of blood vessels), decrease coronary velocity reserves, and reduce heart rate variability. However, there is not evidence that these effects, which have been shown to be transient, increase the risk of a heart attack.
The statement is misleading, then, because it suggests that the adverse acute effects of a brief exposure to secondhand smoke have been shown to increase the risk of a heart attack. This is simply not the case.
Moreover, even if the statement were accurate, it misrepresents the conclusions of the actual Surgeon General's report, which is devoid of any conclusion that short-term exposure to secondhand smoke increases heart attack risk.
If you read through or search the entire 727-page report, you will not find any conclusion that a brief exposure to secondhand smoke increases heart attack risk. And for good reason: there is no such evidence. The report itself is very carefully reviewed science and it is cautious in drawing causal conclusions. Not so the summary of the conclusions of the report provided by the Surgeon General.
Once again, it is as if the Surgeon General didn't even read his own report. It is as if he simply decided in advance the claims he wanted to make, and made them, regardless of whether there was evidence in the report to support them, or whether the report had drawn those conclusions.
It is important to add, again, that even the speculation about the potential effects of a brief secondhand smoke exposure on heart attack risk apply only to people with severe existing coronary artery disease, who are essentially so fragile that virtually any insult (even eating a hamburger) could cause a heart attack. Without qualifying the claim to make it clear that it is referring only to people with severe coronary artery disease, the claim is very misleading.
What this means is that there really wasn't much of a need for a 727-page report. If the Surgeon General was just going to communicate alarmist claims to the public that weren't in the report itself, why waste the effort preparing the 727 pages?
Well it occurs to me that there is a potential reason: to make it appear that the conclusions being communicated were carefully reviewed and scrutinized and that they are therefore not subject to questioning.
There is no way that the public, or even most anti-smoking advocates or groups, are going to read through the entire 727-page report to figure out what claims made by the Surgeon General are well-documented and supported by the evidence and conclusions drawn in the report and which are not. By attaching what basically amounts to a propaganda statement along with the report, it makes it appear to all that these conclusions are documented, when in fact they are not.
And in every breath you exhale you find
Acetone, Isoprene, Acetonitrile, pTolualdehyde, Toluene, P,SDimethylhexane, Ethyl Alcohol, Acetaldehyde, Dichloronitromethane, 2,2,4-Trimethyl-l-pentanol, n-Propyl acetate, 2,2-Dimethyl-l-pentanol, Cyclohexane, Hexane, Thiolacetic acid, I-Heptanol, Cyclohexyl alcohol, Benzene, 2-Ethyl-l-hexanone, 2,3,5 Trimethylhexane, Ethyl Imercaptopropionate, Cycloheptatriene, p-Xylene, n-Butyl alcohol, 3,4 Dimethylhexane, Limonene, Isooctyl alcohol, Methyl-n-propyl sulfide, Ethyl-4-methyl-1-pentanol, Neopentyl acetate, Trans4nonenal, n-Heptane, Ethylbenzene, 5-Methyl4heptanone, Dimethylsulfide, P-Methyl-l-pentanol, pl)ichlorobenzene, Trans-3-hexen-l-ol, Capryl alcohol, Mesitylene, n-Hexylmercaptan, 3,4-Dimethylheptane, 2,3,3,4-Tetramethylpentane, 1Chlorohexane, Dichloroacetylene, 2,P-Dimethyl-l-octanol, 2,2,3,3 - Tetramethylhexane, o-Xylene, 2,3,3 - Trimethylhexane, Isopropylalcohol, 2,2-Dimethyl-l-hexanol, 5-Ethyl-l-butanol, Z,P-Dimethylheptane, Furan, Naphthalene, Thiocyclopentane, Cyclopentylalcohol, n-l\lonane, Ethyl phenyl acetate, n-Amyl alcohol, Z,CDimethylheptane, 5-Nitropropane, 2,6 - Di-tert-butyl-4-methyl-phenol, Methyl-tert-butyl-ketone, Di-Tert-butyldisulfide, 2,2-Dimethyl-Shexanone, 1,2-Diethylbenzene, 2,5-Dimethylheptane, 2-Methyl-3-heptanone, Isobutyl alcohol, m-Xylene, 2,2,5,5Tetramethylhexane, n-Decanal, SMethyl-2-butanol, Propiophenone, Ethylacetate, n-Decane, Isopropylbenzene, IEthylpentane, Di-n-Butylamine, N-Dodecane, o-Dichlorobenzene, Allylacetate, S,SDiethylpentane, n-Butyl acetoacetate, Benzylamine, Indene, Methylnaphthalene, 'L-Methyl-Spentanone, Coumarin, Phenylacetic acid, Ethyl valerate, 5-Methyl-3-heptanone, n-Octane, Cumic alcohol, Methanol, 2,4-Dimethyl-Shexanone, Octylacetate, Cycloheptadiene, 2-Methyl-1-octene, Ethyl Lmethylvalerate, o-Nitrotoluene
They are all commonly found in human exhalations, in other words, normal human breath. Natural stuff. Just goes to show that a "little bit of knowledge is indeed a dangerous thing."
Oh, and by the way, OSHA was asked to declare that there was NO safe exposure to ETS.
OSHA came back and said that for every component found in ETS there was alreasy a PEL (Permissible Exposure Limit) and that it would take, on the order of, a 10X10 foot room, hermetically sealed, with thousands of cigarettes lit at the same time in order for even ONE of those components to reach the PEL.
If you want to debate facts - let's do it.
Property rights are essential to the existence and operation of a free market, and, for a business, these rights include the right to determine which amenities and services to provide on your premises.
If a business decides not to reimburse employees for commuting costs, the business is well within its rights to do so. If a business decides to provide a lounge for its employees, it may do so. If a business decides to validate parking for a customer, it may do so.
The freedom to smoke on the premises is like any of these other amenities-it is within the purview of the owner to provide it. The freedom to permit smoking is part of the property rights a business enjoys that permit it to serve its customers effectively in the marketplace.
The only difference between the freedom to smoke and the other amenities mentioned is that smoking is deemed socially undesirable and may pose a health risk (the carcinogenic properties of second-hand smoke have yet to be conclusively established).
The social undesirability of smoking does not give the government, municiple/county/state/etc, carte blanche to run roughshod over property rights.
A free society-that includes property owners-can decide for itself what is undesirable behavior and employ its own arsenal to combat it, without the aid of state coercion.
Property owners and restaurateurs, while many times victims, are not the immediate victims, however, of smoking bans - smokers are. Anti-smoking activists support these bans ostensibly to limit second hand smoke, but the real reason is often to limit smoking itself and make it socially unacceptable.
Bans like these are predicated on the notion that smokers are incapable of deciding for themselves. Bans like these also assume that non-smokers cannot decide for themselves whether or not to expose themselves to second-hand smoke.
This paternalistic premise runs counter to the American founding principles of freedom and self-government.
If non-smokers do not want to expose themselves to smoke, they can choose to dine at establishments that prohibit smoking on their own.
Public health busybodies should not dragoon the government into social engineering for their desires.
Alternatively, cigars have fewer if any chemicals. Here are the ingredients on a pint of Haagen Dazs Cigar Explosion:
Cream, skim milk, sugar, natural tobacco butter, egg yolks.
Fat chance.
What about breathing in the air the nonsmokers exhale? Should everybody around you stop breathing? It might have germs, you know?
This chart looks at substances found in Environmental Tobacco Smoke (ETS) for which measurements have actually been obtained – very few, of course, because it is difficult to even find these chemicals in diffuse and diluted ETS.
It calculates the volume of a 100m3 sealed and unventilated enclosure (about 20 by 20 feet with a 9- foot ceiling).
Taking Environmental Protection
Agency (EPA) figures for ETS yields per cigarette, it determines the number of cigarettes required to reach the lowest, most stringent published threshold for these substances.
For Benzo[a]pyrene, 222,000 cigarettes would be needed to reach the
lowest published "danger" threshold.
For Acetone, 118,000.
For Hydrazine, slightly more than 14,000.
Toluene would require 50,000 packs of smoldering cigarettes. At 20
cigarettes per pack, that's one million cigarettes.
Of course, the moment one introduces real world factors to the room –
a door, an open window or two, or a healthy level of mechanical air
exchange – achieving these levels becomes even more implausible.
Frankly, it is difficult to imagine a situation where these threshold
limits could be realized.
CALCULATED NUMBER OF CIGARETTES REQUIRED TO REACH A THRESHOLD LIMIT FROM ETS IN A SEALED, UNVENTILATED 100m3 ENCLOSURE AT STP (1)
| ETS Component | CAS Number | Molecular Weight | ETS Output (mg/cigarette)(2) | Threshold Limit (ppm) | Threshold Limit (mg/m3) | Cigarettes Required |
| 2-Toluidine | (3 isomers) (3) | 107.15 | 0.003 | 2 | 8.7 | 290,000 |
| Acetaldehyde | 75-07-0 | 44.05 | 1.26 | 111 | 180 (4) | 14,285 |
| Acetic acid | 64-19-7 | 60.05 | 1.5 | 10 | 25 | 1,666 |
| Acetone | 67-64-1 | 58.05 | 1 | 500 | 1187 | 118,700 |
| Benzene | 71-43-2 | 78.11 | 0.24 | 1 | 3.1 (5) | 1,290 |
| Benzo[a]Pyrene | 50-32-8 | 252.30 | 0.00009 | 0.02 | 0.2 (6) | 222,000 |
| Cadmium | 7440-43-9 | 112.40 | 0.0007 | 0.002 | 0.01 | 1,430 |
| Catechol | 120-80-9 | 110.11 | 0.14 | 5 | 22 | 15,700 |
| Dimethylamine | 124-40-3 | 45.08 | 0.036 | 10 (7) | 9.2 | 25,555 |
| Formic acid | 64-18-6 | 46.02 | 0.525 | 5 (8) | 9.4 | 1,790 |
| Hydrazine | 302-01-2 | 32.05 | 0.00009 | 0.01 | 0.013 | 14,444 |
| Hydroquinone | 123-31-9 | 110.11 | 0.16 | 0.4 | 2 | 1,250 |
| Methylamine | 74-89-5 | 31.09 | 0.1 | 5 | 13 | 13,000 |
| Methylchloride | 74-87-3 | 50.49 | 0.88 | 50 | 103.0 | 11,170 |
| Nickel | 7440-02-0 | 58.71 | 0.0025 | 0.4 | 1 | 40,000 |
| Phenol | 108-95-2 | 94.11 | 0.25 | 5 | 19 | 7,600 |
| Polonium 210 (9) | 210 | 0.4pCi | na | 3pCi/liter (10) | 750,000 | |
| Pyridine | 110-86-1 | 70.01 | 0.39 | 5 | 16 | 4,100 |
| Toluene | 108-88-3 | 92.13 | 0.000035 | 50 | 375 | 1,000,000 |
(TLV in ppm)(gram mol wt of substance) (TLV in mg/m3)(24.45)
TLV in mg/m3 = ______________________________ TLV in ppm = ___________________
24.45 gram mol wt of substance
1. Limits expressed in ppm have been translated to mg/m3 for the sake of clarity and volume calculation. New values have been incorporated, and the lowest threshold (irrespective of source) has been used. Unless otherwise noted, lowest threshold limit values were found in “1999 TLVs and BEIs,” American Conference of Governmental Industrial Hygienists.
2. Data from NTP RoC ETS, December 2-3, 1998, Table 1-1, pp 1-3, per EPA.
3. Three isomers o-Toluidine [95-53-4], m-Toluidine [108-44-1], p-Toluidine [106-49-0]. Mol wt for each is 107.15, TWA/TLV is 2 ppm for each.
4. OSHA, PEL-TWA has been raised to 200ppm, vacating a previous lower level of 180 mg/m3. I used the lower limit.
5. This calculation based on the lowest possible calculated OSHA/NIOSH threshold of 1 ppm.
6. Based on coal tar pitch volatiles [65996-93-2], as benzene solubles
7. OSHA PEL
8. NIOSH PEL-TWA, and HSDB
9. “Levels of polonium-210 in tobacco smoke are not believed to be great enough to significantly impact lung cancer” Hecht S, Tobacco smoke carcinogens and lung cancer. JNCI 1999;91:1194-1210.
10. EPA (1990c).
Have you figured out a way to live forever? Just wanted that secret.... I mean the world needs to know this.
Nothing like a thousand word post to justify that you don't like the smell of burning tobacco.
Exactly...
Here is a tiny list for you "..... we live in a world of carcinogens. They are everywhere. They are in the food we eat, the air we breathe, the water we drink, the soil we walk on. They are produced by plants, trees, bacteria, fungi, and our own bodies. Human blood contains many carcinogens; if it were an industrial product, it would be classed as a toxic substance. Our saliva contains nitrates, which are carcinogens. All human sex hormones are carcinogens.
Here are some of the food carcinogens listed in my book: sucrose, the common sugar from sugar cane and sugar beets, is a reported carcinogen. So if fructose, which is found in all fruits. Orange, lemon, lime and grapefruit oils are carcinogens or carcinogen promoters. Corn oil, cottonseed oil and sunflower oil are carcinogens. Raisins and walnuts contain malonaldehyde, which is a carcinogen. Salt is a carcinogen. Black pepper, cinnamon, ginger and nutmeg contain saffrole, which is a carcinogen. All fruits and vegetables and animal feed contain terpenes, which are carcinogens. The Paris-based International Agency for Research on Cancer reports that “virtually every food stuff or food product is potentially susceptible to contamination by [carcinogenic] aflatoxin...Samples of nearly every dietary staple have been found to contain [it].” These staples include coconuts, sunflower seeds, hazelnuts, Brazil nuts, walnuts, pecans, peanuts, corn, wheat, oats, barley, rye, sorghum, rice, black pepper, cocoa, wine, peas and sweet potatoes. Bread contains ethyl carbamate, a carcinogen. Yogurt and beer have it, too. Beets, celery and lettuce contain carcinogenic nitrosamines. Raw beef, pork, turkey and chicken contain carcinogens, and cooking makes things worse. Broiling, roasting, baking, braising, boiling, frying and smoking foods produce a variety of carcinogens. Mother's milk contains lactose. Lactose is a carcinogen. A cup of coffee contains over a hundred carcinogens, far more than secondhand smoke--Makers & Takers Edmund Contoski.
I would't not want you left entirely out of the denial game or finding other you can spend your time being disgusted with.
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.