NICOTINE and SMOKING
NICOTINE and SMOKING BENEFITSBENEFITS
By Wanda Hamilton By Wanda Hamilton Researchers have long been aware that
Researchers have long been aware that fewer smokers get Alzheimer's and Parkinson's diseasesfewer smokers get Alzheimer's and Parkinson's diseases than non-smokers. Up to April l992, of the
than non-smokers. Up to April l992, of the 17 studies on Alzheimer's and smoking which had been17 studies on Alzheimer's and smoking which had been published in peer-reviewed journals, 13 reported a reduced risk
published in peer-reviewed journals, 13 reported a reduced risk for smokers and only four found nofor smokers and only four found no difference between smokers and non-smokers. Similar findings have been published on the effect of difference between smokers and non-smokers. Similar findings have been published on the effect of smoking and Parkinson's disease.
smoking and Parkinson's disease. In an article in
In an article in The Times of London (9/7/93), Dr. James The Times of London (9/7/93), Dr. James Le Fanu provided an examination of theLe Fanu provided an examination of the research on smoking and its apparent protective effect for certain diseases. Dr. Le Fanu stated research on smoking and its apparent protective effect for certain diseases. Dr. Le Fanu stated unequivocally: "Smokers have a 50 per
unequivocally: "Smokers have a 50 per cent reduced risk of cent reduced risk of developing Alzheimer's--and the moredeveloping Alzheimer's--and the more smoked the greater the protection." He als
smoked the greater the protection." He also noted that emerging research points to a o noted that emerging research points to a similar effectsimilar effect of smoking on Parkinson's disease.
of smoking on Parkinson's disease. So striking was the apparent protective e
So striking was the apparent protective effect of smoking on Alzheimer's and Parkinson's thatffect of smoking on Alzheimer's and Parkinson's that increasingly biomedical researchers are experimenting with nicotine to treat
increasingly biomedical researchers are experimenting with nicotine to treat the symptoms of thesethe symptoms of these dread disease in-patients who have been diagnosed as having them. Results
dread disease in-patients who have been diagnosed as having them. Results from thesefrom these experiments have all showed promise in alleviating the
experiments have all showed promise in alleviating the symptoms of these diseases with thesymptoms of these diseases with the administration of nicotine.
administration of nicotine.
The mechanism by which the nicotine in tobacco works to protect
The mechanism by which the nicotine in tobacco works to protect smokers is that it smokers is that it increases theincreases the number of so-called "nicotinic" receptors in the brain,
number of so-called "nicotinic" receptors in the brain, which in turn influence the production andwhich in turn influence the production and release of the neurotransmitter acetylcholine. Those who come down with Alzheimer's show a release of the neurotransmitter acetylcholine. Those who come down with Alzheimer's show a marked loss of "nicotinic" receptors in their brains and thus have reduced levels of acetylcholine, marked loss of "nicotinic" receptors in their brains and thus have reduced levels of acetylcholine, which is necessary for
which is necessary for memory and other brain functions.memory and other brain functions. Research has shown that tobacco smoke (and the
Research has shown that tobacco smoke (and the nicotine therein) inhibits the activity of nicotine therein) inhibits the activity of monoamine oxidase B (MAOB). Experiments on mice which were genetically engineered to be monoamine oxidase B (MAOB). Experiments on mice which were genetically engineered to be without the gene for MAOB "were resistant to
without the gene for MAOB "were resistant to the neurodegenerative effects of MPTP, a toxin thatthe neurodegenerative effects of MPTP, a toxin that induces a condition reminiscent of Parkinson's disease," (Dr. Je
induces a condition reminiscent of Parkinson's disease," (Dr. Je an C. Shih researcher at thean C. Shih researcher at the University of Southern California, as reported in Reuters, 1
University of Southern California, as reported in Reuters, 1 0/7/97, "Isoenzyme Inhibited by cigarette0/7/97, "Isoenzyme Inhibited by cigarette Smoke May Have Role in Aging and Neurodegeneration"). The findings of Dr. Shih and her
Smoke May Have Role in Aging and Neurodegeneration"). The findings of Dr. Shih and her colleagues point to a protective effect
colleagues point to a protective effect from smoking on the aging of the brain.from smoking on the aging of the brain. Other diseases for which smoking and nicotine appear to be
Other diseases for which smoking and nicotine appear to be protective are ulcerative protective are ulcerative colitis,colitis, Tourette's Syndrome, and possibly rheumatoid arthritis and colorectal cancer.
Tourette's Syndrome, and possibly rheumatoid arthritis and colorectal cancer. Below are excerpts from some
Below are excerpts from some recent articles and studies on recent articles and studies on nicotine, Alzheimer's, Parkinson's,nicotine, Alzheimer's, Parkinson's, cognitive abilities, Tourette's and ulcerative colitis.
cognitive abilities, Tourette's and ulcerative colitis.
"In human studies, reported performance improvements with post-trial administration of nicotine have all "In human studies, reported performance improvements with post-trial administration of nicotine have all involved associated learning (Mangan and Golding l883; Colrain et al, l992; Warburton et al, l992).... involved associated learning (Mangan and Golding l883; Colrain et al, l992; Warburton et al, l992).... Nicotine improves performance by increasing the attentional resources available for such strategic Nicotine improves performance by increasing the attentional resources available for such strategic proces
processing," sing," [Rusted JM, et al,[Rusted JM, et al, "Facilitation of memory by post-trial administration of nicotine:"Facilitation of memory by post-trial administration of nicotine: evidence for attentional e
evidence for attentional explanation,"xplanation," Psychopharmacology, 108(4):452-5, l992].Psychopharmacology, 108(4):452-5, l992].
"1. Nicotine improves attention in a wide variety of tasks in healthy volunteers. 2. Nicotine improves "1. Nicotine improves attention in a wide variety of tasks in healthy volunteers. 2. Nicotine improves immediate and longer-term memory in healthy volunteers. 3. Nicotine improves attention in patients with immediate and longer-term memory in healthy volunteers. 3. Nicotine improves attention in patients with probabl
probable Alze Alzheimerheimer's Dis's Disease," ease," [Warburton D M,[Warburton D M, "Nicotine as a cognitive enhancer,""Nicotine as a cognitive enhancer," Progress in Neuro-Progress in Neuro-Psychopharmacology and Biological Psychiatry, 16(2): 181-91, Mar l992]
"Researchers observed lessening of tic frequency and severity 3 minutes after subjects chewed [nicotine] "Researchers observed lessening of tic frequency and severity 3 minutes after subjects chewed [nicotine] gum, even more so at 10 minutes."
gum, even more so at 10 minutes." [Rickards E H,[Rickards E H, "Nicotine gum in Tourette's disorder,""Nicotine gum in Tourette's disorder," AmericanAmerican Journal of Psychiatry, 149(3):417, Mar l992. Note: the subjects were all children with Tourette's disorder]. Journal of Psychiatry, 149(3):417, Mar l992. Note: the subjects were all children with Tourette's disorder]. "In humans, nicotine-induced improvement of rapid information processing is particularly well
"In humans, nicotine-induced improvement of rapid information processing is particularly well
documented.... Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's documented.... Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's disease can be attenuated by nicotine."
disease can be attenuated by nicotine." [Levin E D,[Levin E D, "Nicotinic systems and "Nicotinic systems and cognitive function,"cognitive function," Psychopharmacology, 108(4):417-31, l992]
Psychopharmacology, 108(4):417-31, l992]
"Improvement in attention, learning, reaction time, and problem solving have been reported.... Different "Improvement in attention, learning, reaction time, and problem solving have been reported.... Different proces
processes, incses, including luding attentiattention, stion, stimulus mulus evaluaevaluation, ation, and resnd response seponse selectiolection, appen, appear to bar to be invole involved in ved in thethe effect of nicotine on human information processing."
effect of nicotine on human information processing." [Le Houezec J, Benowitz N L,[Le Houezec J, Benowitz N L, "Basic and clinical"Basic and clinical psychopharmaco
psychopharmacology of logy of nicotine,"nicotine," Clinics in Chest Medicine, 12(4):681-99, Dec l991].Clinics in Chest Medicine, 12(4):681-99, Dec l991].
"Despite the absence of change in memory functioning, these results demonstrate that DAT [Alzheimer's "Despite the absence of change in memory functioning, these results demonstrate that DAT [Alzheimer's disease] patients have significant perceptual and visual attentional deficits which are improved by nicotine disease] patients have significant perceptual and visual attentional deficits which are improved by nicotine administration."
administration." [Jones G M, Sahakian B J, et al,[Jones G M, Sahakian B J, et al, "Effects of acute "Effects of acute subcutaneous nicotine on attention,subcutaneous nicotine on attention, information processing and short-term memory in
information processing and short-term memory in Alzheimer's disease,"Alzheimer's disease," Psychopharmacology,Psychopharmacology, 108(4):485-94, l992].
108(4):485-94, l992].
"When you look at people who smoke, and people who don't smoke...you find those who smoke cigarettes "When you look at people who smoke, and people who don't smoke...you find those who smoke cigarettes are about half as likely to get Parkinson's disease."
are about half as likely to get Parkinson's disease." [Dr. David Morens of the University of Hawaii School of [Dr. David Morens of the University of Hawaii School of Public Health as quoted in
Public Health as quoted in "Stunned docs discover cigarettes stop Parkinson's,""Stunned docs discover cigarettes stop Parkinson's," by Roger Field, Newby Roger Field, New York Post, 6/15/95. Dr. Morens and colleagues examined 34 studies on smoking and Parkinson's. Their York Post, 6/15/95. Dr. Morens and colleagues examined 34 studies on smoking and Parkinson's. Their study was published in the June, l995 issue of Neurology].
study was published in the June, l995 issue of Neurology]. Accord
According to ing to a study a study conduconducted at cted at Surrey Surrey UniveUniversity arsity and pubnd published ilished in the jn the journal ournal PsychopPsychopharmacharmacology,ology, smokers are more mentally alert at night than non-smokers. Rosemary Brook, spokeswoman for Surrey smokers are more mentally alert at night than non-smokers. Rosemary Brook, spokeswoman for Surrey University's psychopharmacology unit, said,
University's psychopharmacology unit, said, "The results showed that smokers were subsequently able to"The results showed that smokers were subsequently able to perfor
perform varim various tesous tests of rts of reactioeaction, memn, memory recory recall and all and other rother related telated tasks casks consisteonsistently bently better ttter than the han the non- non-smokers,"
smokers," [Reported on the BBC News, 4/8/98, "Cigarettes 'keep you sharp after dark'."[Reported on the BBC News, 4/8/98, "Cigarettes 'keep you sharp after dark'."
In a presentation at the 151st annual meeting of the American Psychiatric Association (June 8, l998 in In a presentation at the 151st annual meeting of the American Psychiatric Association (June 8, l998 in Toronto), Dr. Paul Newhouse of the University of Vermont reported on his research on treating Parkinson's Toronto), Dr. Paul Newhouse of the University of Vermont reported on his research on treating Parkinson's disease with nicotine.
disease with nicotine. "Preliminary analysis shows improvements after acute nicotine administration in"Preliminary analysis shows improvements after acute nicotine administration in several areas of cognitive performance."
several areas of cognitive performance." These areas included reaction time and central processing speed.These areas included reaction time and central processing speed. The researchers also reported that after chronic use of nicotine on Parkinson's patients, motor function and The researchers also reported that after chronic use of nicotine on Parkinson's patients, motor function and the ability to move also improved. [Reported by Reuters, 6/8/98,
the ability to move also improved. [Reported by Reuters, 6/8/98, "Nicotine patch promising for "Nicotine patch promising for Parkinson's"
Parkinson's"].].
"The influence of smoking on the risk of developing ulcerative colitis is well documented. Compared with "The influence of smoking on the risk of developing ulcerative colitis is well documented. Compared with lifetime nonsmokers, the risk is reduced in smokers...."
lifetime nonsmokers, the risk is reduced in smokers...." [Tysk C, Jarnerot G,[Tysk C, Jarnerot G, "Has smoking changed the"Has smoking changed the epidemiology of ulcerative colitis?"
epidemiology of ulcerative colitis?" Scandinavian Journal of Gastroenterology, 27(6):508-12, Jun l992].Scandinavian Journal of Gastroenterology, 27(6):508-12, Jun l992]. "When association between cigarette smoking and UC [ulcerative colitis] are examined, never-smokers are "When association between cigarette smoking and UC [ulcerative colitis] are examined, never-smokers are approximately three times more likely to develop UC than smokers. A consistent finding from study to study approximately three times more likely to develop UC than smokers. A consistent finding from study to study is that quitters have a mildly increased risk of developing UC which suggests that cigarette smoking may is that quitters have a mildly increased risk of developing UC which suggests that cigarette smoking may have a protective effect,"
have a protective effect," [Lashner B A,[Lashner B A, "Inflammatory bowel disease: family patterns and risk factors,""Inflammatory bowel disease: family patterns and risk factors," Comprehensive Therapy, 18(8):2-4, Aug l992].
Comprehensive Therapy, 18(8):2-4, Aug l992].
"It is beyond doubt that smokers are protected against ulcerative colitis, and the more that is smoked the "It is beyond doubt that smokers are protected against ulcerative colitis, and the more that is smoked the greater the protection--so those on 25 cigarettes a day or more have a risk as little as one-tenth that of greater the protection--so those on 25 cigarettes a day or more have a risk as little as one-tenth that of non-smokers,"
smokers," (Dr. Martin Osbourne, surgeon at the Royal Free Hospital in London, as quoted in the Daily(Dr. Martin Osbourne, surgeon at the Royal Free Hospital in London, as quoted in the Daily Telegraph, 9/7/93).
THE ANTI-SMOKERS LIED ABOUT OSTEOPOROSIS AND ABOUT ESTROGEN THE ANTI-SMOKERS LIED ABOUT OSTEOPOROSIS AND ABOUT ESTROGEN
Antismokers grasping at straws: Antismokers grasping at straws:
Lying at any cost, even when all the evidence is against them Lying at any cost, even when all the evidence is against them
The media flooded the country
The media flooded the country with the anti-smoker claim with the anti-smoker claim that smoking increases osteoporosisthat smoking increases osteoporosis (Danielle HW.
(Danielle HW.Osteoporosis of the slender smokerOsteoporosis of the slender smoker. Arch Intern Med 1976;136:298-304).. Arch Intern Med 1976;136:298-304). There
There was was no no publicity publicity when when the the claim claim was was later later refuted refuted (Jensen (Jensen GF.GF.Osteoporosis of the slenderOsteoporosis of the slender smoker revisited by epidemiologic approach.
smoker revisited by epidemiologic approach.Eur J Clin Investig Eur J Clin Investig 1986;16:239-242).1986;16:239-242).
The Danielle study used two "ill-defined" patient populations; the second included all 70 year-old The Danielle study used two "ill-defined" patient populations; the second included all 70 year-old women in nine suburbs of Copenhagen, and
women in nine suburbs of Copenhagen, and had more cases, 180 versus 72. The first had more cases, 180 versus 72. The first asserted that thereasserted that there was no relation between weight and bone mass in non-smokers, while the second, and most other studies, was no relation between weight and bone mass in non-smokers, while the second, and most other studies, have found correlation in both.
have found correlation in both. Most importantly, there was
Most importantly, there was no difference between smokers and non-smokers in the frequency of no difference between smokers and non-smokers in the frequency of definite osteoporotic or other fractures. The smokers actually
definite osteoporotic or other fractures. The smokers actually had fewer. Since all the had fewer. Since all the cases were thecases were the same age, there is no way to use age adjustment to manipulate the data. Referring to smoking, another same age, there is no way to use age adjustment to manipulate the data. Referring to smoking, another researcher has admitted,
researcher has admitted,"this factor is a more manipulable one than some of the other factors which have"this factor is a more manipulable one than some of the other factors which have been shown to be important in the etiology of fracture."
been shown to be important in the etiology of fracture." A number of studies have found t
A number of studies have found that smokers have slightly higher bone hat smokers have slightly higher bone mass and density than non-mass and density than non-smokers, both pre- or
smokers, both pre- or post-menopausal.post-menopausal."No association between bone mass and smoking was observed. A"No association between bone mass and smoking was observed. A subgro
subgroup witup with patth patterns of erns of substasubstantial cntial combinombined tobed tobacco anacco and alcohd alcohol use ol use having having a lowa lower meaer mean bone n bone massmass could not be identified"
could not be identified" (MF Sowers et al. Prev Med (MF Sowers et al. Prev Med 1985;14:585-596).1985;14:585-596)."Smoking history in pack "Smoking history in pack years
years did not did not correlcorrelate wate with bonith bone densie density at ety at either sither skeletakeletal sitel site," ," spine or forearm (MM Luckey et al. Jspine or forearm (MM Luckey et al. J Clin Endocrinol Metab 1989;69:762-770).
Clin Endocrinol Metab 1989;69:762-770).
In the Framingham Study, Felson et al found that
In the Framingham Study, Felson et al found that"Cigarette smoking was not associated with risk of "Cigarette smoking was not associated with risk of fractu
fracture in are in any anany analyses ilyses includincluding modng models wels without aithout alcohollcohol." ." This was in 217 cases, 174 of them female, inThis was in 217 cases, 174 of them female, in an
an ongoing ongoing prospective prospective of of over over 40 40 years' years' duration duration (Felson (Felson DT DT et et al. al. Am Am J J EpidemiolEpidemiol 1988;128(5):1102-1110).
1988;128(5):1102-1110).
And in a study the next year which separately analyzed radiographs of the white, middle class And in a study the next year which separately analyzed radiographs of the white, middle class Framingham subjects, and poorer, more nonwhite
Framingham subjects, and poorer, more nonwhite HANES I subjects, Felson also HANES I subjects, Felson also found a borderlinefound a borderline statistically significant protective association between smoking and osteoarthritis, which was strongest in statistically significant protective association between smoking and osteoarthritis, which was strongest in the
the heaviest heaviest smokers smokers (Arthr (Arthr Rheum Rheum 1989;32:166-172).1989;32:166-172).
However, true to their anti-smoker psychosis, they had to find something bad to say about smoking. However, true to their anti-smoker psychosis, they had to find something bad to say about smoking. Although they admitted that very few of their subjects ever used estrogen, they claimed that smokers did Although they admitted that very few of their subjects ever used estrogen, they claimed that smokers did not benefit from estrogen therapy on the
not benefit from estrogen therapy on the basis of a mere 29 ever-users, 8 of basis of a mere 29 ever-users, 8 of them smokers.them smokers. Never mind that this claim was opposite to that of
Never mind that this claim was opposite to that of a large 1982 study which claimed both big risks of a large 1982 study which claimed both big risks of fractures, and big benefits from estrogen for smokers. With
fractures, and big benefits from estrogen for smokers. With this study, the anti-smokers couldthis study, the anti-smokers could simultaneously fear-monger against smoking and promote pharmacological intervention. simultaneously fear-monger against smoking and promote pharmacological intervention. But in the
Smoking and Lung Cancer Smoking and Lung Cancer Though there seem to be strong
Though there seem to be strong links between smoking and lung links between smoking and lung cancer, anti-tobacco propaganda often infers thatcancer, anti-tobacco propaganda often infers that smoking is THE cause of lung cancer, with the implicit message that if smoking could be eliminated, so could lung smoking is THE cause of lung cancer, with the implicit message that if smoking could be eliminated, so could lung cancer. This is, of course, false.
cancer. This is, of course, false. Smoking is by no means Smoking is by no means the only risk factor for lung cancer, and the only risk factor for lung cancer, and in somein some occupations cigarette smoking appears actually to help protect against getting the disease. Lung cancer is occupations cigarette smoking appears actually to help protect against getting the disease. Lung cancer is
acknowledged to be on the rise both in the U.S. and elsewhere despite the decline in cigarette smoking which began acknowledged to be on the rise both in the U.S. and elsewhere despite the decline in cigarette smoking which began more than 25 years ago.
more than 25 years ago.
Further, lung cancer among nonsmokers seems to be i
Further, lung cancer among nonsmokers seems to be increasing, while the rate of ncreasing, while the rate of lung cancer among smokers islung cancer among smokers is decreasing, thanks to the advent of
decreasing, thanks to the advent of filtered cigarettes, which nearly every study filtered cigarettes, which nearly every study has shown decreases risk anywherehas shown decreases risk anywhere from 20% to 30% (only one
from 20% to 30% (only one such study is listed here).such study is listed here).
"Rising lung cancer mortality rates during 1953-1982 were similar for both sexes in all parts of "Rising lung cancer mortality rates during 1953-1982 were similar for both sexes in all parts of Oregon; the steepest increases were among women living in the coastal counties."
Oregon; the steepest increases were among women living in the coastal counties."
"Occupational risk differences among both sexes far exceeded those noted with other risk factors, suggesting "Occupational risk differences among both sexes far exceeded those noted with other risk factors, suggesting that occupational exposures deserve primary emphasis in future efforts at lung cancer control."
that occupational exposures deserve primary emphasis in future efforts at lung cancer control." "Causes of lung cancer o
"Causes of lung cancer other than smoking which are associated with ther than smoking which are associated with particular occupations will be identifiedparticular occupations will be identified in the hope of eventually reversing the epidemic trend of this disease."
in the hope of eventually reversing the epidemic trend of this disease."
1375. University of Oregon, School of Medicine. Morton, W.E. "epidemiology of Lung Cancer in Oregon." 1375. University of Oregon, School of Medicine. Morton, W.E. "epidemiology of Lung Cancer in Oregon." Methods: Following data have been
Methods: Following data have been collected:collected:
•
• (1) sex-specific, age-standardized, mean annual death rates for 5-year periods since 1953 for all (1) sex-specific, age-standardized, mean annual death rates for 5-year periods since 1953 for all countiescounties [Portland-Vancouver area]
[Portland-Vancouver area] •
• (2) occupations from death certificates since 1963(2) occupations from death certificates since 1963 •
• (3) all cases occurring in the (3) all cases occurring in the Portland metropolitan area during 1963-1977 by search of tumour Portland metropolitan area during 1963-1977 by search of tumour registriesregistries and hospital record
and hospital record roomsrooms •
• (4) age-adjusted incidence rates by sex for geographic regions, socioeconomic strata, (4) age-adjusted incidence rates by sex for geographic regions, socioeconomic strata, and occupationaland occupational categories.
categories.
"Prospective contribution of pack-years to development of lung cancer was reduced by "Prospective contribution of pack-years to development of lung cancer was reduced by cross-sectional adjustment, but remained significant." But more important than pack years
sectional adjustment, but remained significant." But more important than pack years was airflow obstruction.was airflow obstruction. "Data suggest that smokers who will develop lung cancer may be recognized by prior development of
"Data suggest that smokers who will develop lung cancer may be recognized by prior development of ventilatory obstruction."
ventilatory obstruction."
1006. Johns Hopkins University, School of Hygiene and Public Health. Tockman, M.S.; Anthoisen, N.R.; Wright 1006. Johns Hopkins University, School of Hygiene and Public Health. Tockman, M.S.; Anthoisen, N.R.; Wright E.C. "Airways Obstruction and the Risk of Lung Cancer."
E.C. "Airways Obstruction and the Risk of Lung Cancer."
AND AND
"AO was significantly associated with advanced age, male sex, PiZ allete, blood group A antigen, heavy coffee intake (> 3 cups/day) and first degree relationship to a patient with chronic obstructive pulmonary [lung] disease [genetical predisposition]" "Both AO and CB were associated with cigarette smoking and low socioeconomic status."
1005. Johns Hopkins University, School of Hygiene and Public Health. Tockman, M.S.; Khoury, M.J.; Cohen, B.H. "Different Risk Factor Distributions for Airways Obstruction [AO] and Chronic Bronchitis."
"A cross-geographical analysis of lung cancer mortality for white male residents of Harris County for 1979 to 1981 is being made to assess the contribution of air pollution." "Regression techniques will be used to examine the relationship between mortality rates and measures of air pollution while statistically controller for variables that are known to be linked with excess lung cancer mortality, including age, smoking, and socioeconomic status, [emphasis added]"
Results not available at time of printing.
1472. University of Texas Health Science Centre, School of Public Health. Buffler, P.A.; Stallones, R. "Air Pollution and Lung Cancer in Harris County, Texas." Funding: EPA (CR807108-01) 10/79-4/84.
Results to date (Sept, 1976-May, 1981):"A possible flattening in the dose-response [between smoking and lung cancer] was found and a low relative risk in an area of the world with one of the highest recorded incidence of lung cancer. The flattening of the dose-response curve occurred with an above-average
consumption of 20 cigarettes/day" [emphasis added]
0590. West of Scotland Cancer Surveillance Unit (Glasgow) and University of Michigan, School of Public Health. Gillis, C.R.; Hoie, D.J.; Hawthorne, VIM et al. "Retrospective Case Control Study of Smoking Habits and Lung Cancer in the West of Scotland." Funding: National Institutes of Health (N01-CP-05646).
"Excess risks of lung cancer found in miners and foundry workers could not be fully explained by the high prevalence of smoking among these occupations," [emphasis added].
0495. University of Zurich, Institute of Pathology (Switzerland). Schuler, G. "Epidemiology of Lung Cancer in Switzerland."
Smoking has a protective effect on immunological abnormalities in asbestos workers. 0429. Institute of Immunology and Experimental Therapy (Poland). Lange, A. "Effect of Smoking on Immunological Abnormalities in Asbestos Workers.
AND
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," [emphasis added].
0565. University of London, School of Hygiene and Tropical Medicine. "Cancer of the Lung Among Asbestos Factory Workers."
[Many other studies show similar findings for asbestos workers].
"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," [emphasis added].
1388. Hahnemann Medical College and Hospital (Philadelphia). Weiss, W. "Lung Cancer Dueto Chloromethyl Ethers."
Method: "A cohort of 125 workers (91 exposed to chloromethyl ethers) have been followed since 1963, and semi-quantitative estimates of degree of exposure and records of duration of exposure have been maintained. Information on smoking habits was obtained at the beginning of the observation period."
"Marked atypia were found only in workers chemically exposed to BCME (4.8 percent of smokers and 6.2 percent of nonsmokers). The biological mechanism for increased injury in nonsmokers...has not yet been determined [emphasis added]."
[Index number not recorded]. Labour Protection and Hygiene Centre, Laboratory of Cytology (Romania). Herivan, R.: Constantinescu, V.; Melinte, L. "BCME, Soot, Smoking and Lung Cancer.
"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," [emphasis added].
1544. DHHS, PHS, CDC, NIOSH. Ames, R.G. "Respiratory Effects of Exposure to Diesel Emissions in Underground Coal Miners." Funding: NIOSH.
"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."
"Neither smokers nor nonsmokers showed any changes in bronchial responsiveness after smoking cigarettes."
0391. Yokohama City University, School of Medicine (Japan). Okubo, T; Suzuki, S; Sano, F. "Acute Effect of Smoking on Bronchial Responsiveness."
"Chronic bronchitis was found more often in suburban inhabitants than in rural inhabitants, a significant difference."
"It is concluded that chronic bronchitis is twice as common in the city as in rural areas, however, in both areas, air pollution and cigarette smoking lead to higher incidence."
0427. Copernicus Academy of Medicine (Poland). Nikodemowicz, E.; Owsinski, J.M.; Chomicka, Z. et al. "Influence of Urban Factors on the Incidence of Chronic Bronchitis in Rural Populations."
Smoking and Heart Disease
The connection between smoking and heart disease is far more tenuous than that between smoking and lung disease. Though the medical establishment considers smoking to be a risk factor (among many risk factors) for heart disease, the fact remains that anywhere from 30 to 50% of those admitted to hospitals for coronary problems exhibit none of the known risk factors (including smoking), and that the research is by no means either consistent of conclusive in linking smoking the heart disease. It is true that deaths from heart disease, which is still the number one cause of death, are declining but most researchers attribute this to better surgical and medical techniques, not to a decline in smoking rates, since deaths from heart disease are declining world-wide, even in countries with high smoking rate.
"No statistically significant relationship was found in either community between smoking and coronary heart disease, hypertension or somatic complaints" [emphasis added]
1477. 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." [emphasis added].
0298. 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.
"Preliminary data indicate a high prevalence of IHD [Ischemic Heart Disease] in South Wales. A significant association between white cell count and IHD defined cross-sectionally is not explained by smoking habits. Prevalent IHD is not explained by smoking habit" [emphasis added]
0598. Medical Research Council, Epidemiology Unit (Wales). Yarnell, J.W.G; Elwood, P.C.; Sweetnam, P.M. "Caerphilly Prospective Study of Ischemic Heart Disease." Cohort study of 2,400 men (aged 44-60) began in 1979. Two samples of women also studied.
"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."
0564. 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.
While smoking was more common among women who had myocardial infarction, "no such
difference was observed between women with angina pectoris and other women." Also no significant differences were observed between smoking and nonsmoking women with respect to myocardial infarction and death during the 12-year follow-up.
0464. Sahlgrenska Hospital, Medical Dept. (Sweden). Bengtsson, C.: Lapidus, L; Hallstrom, T. "The Population Study of Women in Gothenburg, Sweden."
"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]." [emphasis added]
1465. 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
Pipe smokers have a higher intake of nicotine than cigarette smokers (as measured by serum and urinary cotinine levels). "Since pipe smokers have little excess risk of CHD [chronic heart disease], higher chronic nicotine exposure is unlikely to be the cause of the excess seen in cigarette smokers."
0534. Medical College of St. Bartholomew's Hospital. Dept. of Environmental and Preventative Medicine (England). Wald, M.J.; Bailey, A. "Nicotine and Heart Disease.".
ETS and Heart Disease
"No difference in prevalence of cardiovascular symptoms was found [between those living with smokers and those not]"
0591. West of Scotland Cancer Surveillance Unit, Ruchill Hospital (Scotland). Gillis, C.R.; Hole, D.J.; Hawthorne, V.M. "Health Effects of Exposure to ETS (Environmental Tobacco Smoke] in the West of Scotland." Cohort of 16,171 (45-64 years old) screened in 1972 and 1976.
Smoking and "Throat" Cancer (See also appended bibliography for additional studies on this)
"All countries experienced a sharp increase in lung cancer mortality; [but] laryngeal and oral cavity cancers showed divergent trends (10 countries had steady or decreasing rates). Results suggest that tobacco may not be the major causative factor for laryngeal and oral cavity cancers." [emphasis added]
0244. Institut National de Recherche et de Security (France). Moulin, J.J; Mur, J.M.; Cavelier, C. "Comparative Epidemiology, In Europe, of Tobacco-Related Cancers (Lung, Larynx, Pharynx, Buccal Cavity)." Data is from World Health Organization 1950-1977.
"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"
0564. 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.
..."alcohol consumption was the dominant risk factor [for oesophageal cancer" [em. add.]
Dept. of HHS, National Cancer Institute. Blot, W.J.; Brown, L.M.; Ershow, A. et al. "Epidemiologic Studies of Tobacco Use and Risk Cancer."
Smoking and Renal [Kidney] Cancer
"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." [emphasis added]
1363. University of Oklahoma, Health Sciences Canter. Asal, N.R.; Geyer, J. "Risk Factors in Kidney Cancer." Oct. 1981 - Feb., 1985. FUNDING:< National Cancer Institute.
"A weak positive association with cigarette smoking has been found, but only after controlling for selection biases." "Findings appear to confirm previously observed associations with obesity, northeastern European ancestry, renal calculi [kidney stones], and use of phenacetin-containing analgesics." [emphasis added]
1060. Harvard University, School of Public Health, Dept. of Epidemiology. MacMahon, B; Maclure, K.M. "A Casa Control Study of Renal Adenocarcinoma." Method: Used Cancer registries, pathology logs and medical records at 37 participating hospitals in the Boston area and follow-up interviews by phone. FINDING: Harvard School of Public Health; National Cancer Institute.
"No association was found for exposure to side-stream smoke, coffee drinking, or artificial sweetener use. The association of several occupations with bladder cancer risk has been found in males..."
1216. American Health Foundation. Wynder, E.L.; Goodman, M.T.; Kabat, G.C., et al. "Studies in Tobacco-Related Cancers." FUNDING: National Cancer Institute.
Smoking and Endometrial, Ovarian and Breast Cancer
"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." FUNDING: NICHD.
"The risk of breast cancer does not appear to be influenced by cigarette smoking"
1039. Boston University Medical Centre. Drug Epidemiology Unit. Shapiro. S Rosenberg. L.; Kaufman. D. "Multiple Case-Control Study of the Long Term Effects of Drug, Use in the Treatment of Chronic Disease." FUNDING: FDA (U01 FD01222-03) and NICHD [National Institute nf Child Health & Human Development].
Emphasis added.
Smoking and Cervical Cancer
"Sexual Behaviour and socioeconomic indicators predict cervical cancer incidence, as has been demonstrated in numerous other studies.: [emphasis added]"
University of Utah. School of Medicine. Lyon J.L. "Epidemiologic Investigation of Cervical Cancer in an Area of Low Incidence " FUNDING: NCI (Dept. of Health &HS)
Smoking and Pregnancy
Some studies have found a correlation between maternal smoking during pregnancy and lower birth weight in babies. However, there are many factors which correlate with low birth weight, and the dominant risk factors seem
to be the mother's age and the mother's socioeconomic class. Even those studies which show a correlation between maternal smoking and low birth weight speak of weight differences in grams, not ounces, and one ounce = 28.35
grams.
Risk factors associated with low birth weight (in rank order):
• 1. Mother's age (too young or too old) • 2. First pregnancy
• 3. More than two previous stillbirths • 4. Lower birth weight of older siblings • 5. Small stature and weight of mother • 6. Fewer examinations during pregnancy • 7. Smoking by mother or father
0360. Department of Public Health. Jichi Medical School (Japan). Nagai. M.; Yanagawa. H.; Kawaguchi, T. et al. "A Study of the Factors Associated With low Birth Weight. A Case-Control Study in Togichi Prefecture Apr. 1982-Dec. 1984.
"Women who smoke during pregnancy have full-term babies which, on the average are 5-6 grams [a fraction of an ounce] smaller than full-term babies born to nonsmoking mothers."
0755. University of Colorado. Health Sciences Centre. Moore. L.C. "Maternal O2 Transport During Pregnancy at High Altitude " [emphasis added]
• 1. Birth weight lower in the smoking group, but the incidence of smoking was higher in • young, unmarried women of lower socioeconomic status. Perinatal death was also higher • among young, unmarried, low income women.
• 2. "No differences in antepartum hemorrhage or congenital anomalies between the groups" • 3. "Hypertension and postpartum hemorrhage were lower in smokers [emphasis added]." 0045. University of Tasmania, ( Queen Alexandra Hospital, Dept. of Obstetrics & Gynaecology. Correy, J.;
Newman. N.: Currarn, J "An Assessment of Smoking in Pregnancy." Method: Since I974, this study was conducted on ALL patients in Tasmania (smoking data was collected since Jan.1981 ). Details of alcohol ingestion and drug use were also included. By 1984 information available on 90% of patients on average birth weight of infants, incidence of low birth weight (less than 2,500 grams), incidence of prematurity, congenital abnormalities, perinatal death antepartum hemorrhage and hypertension in pregnancy.
"The proportion of complications of pregnancy and delivery were similar in smokers and nonsmokers."
University of Oslo (Norway). Dalaher, K.; Grunfeld, B.; Jansen, A.
"Data do not confirm the suggestion that changes in cord blood vessels similar to those of
arteriosclerosis are brought about by maternal smoking during pregnancy. Pathological changes in the cord at term may be found in infants of healthy, nonsmoking mothers..."
0184. Universitat Freiburg, Anatomische: Institut (Germany). Staubesand, J.; Seydewitz, V.; Hugod, C. et al. "Effects of Maternal Smoking on the Neonatal Umbilical Cord."
Parental Smoking, ETS and Children
"...excess influenza virus infection was found for black infants and infants with at least one sibling (especially those with school-age siblings), and rhinovirus infection rates were highest among girls attending daycare. No convincing differences for viral infection or respiratory illness were seen with parental smoking as an isolated factor..." [emph. added]
1462. Baylor College of Medicine, Influenza Research Centre (Texas). Gardner, G.C.; Frank, A.L.; Taber, L.H. "Effects of Social and Family Factors on Viral Respiratory Infection and Illness in the First Year of Life." A
longitudinal study,1975 - 1980. This study was published in the Journal of Epidemiology and Community Health 39 (1); 42-48, March, 1984.
"The correlation matrix revealed that maternal education was the variable most significantly
inversely correlated with infection... Its statistical significance persisted in the presence of other added factors." "Maternal education appeared to have played a highly significant role in the health of the children studied." [emphasis added]
0878. University of Kansas, College of Health Sciences. Holmes. G.E.; Hassanein, K.M.; Miller. H.C. "Factors Associated with Morbidity Among Breast Fed and Formula Fed Babies." The incidence of infection in babies was studied with regard to a number of factors, including maternal smoking.
Nicotine and Smoking: Benefits
Though the risks of smoking are highly publicized, the medical benefits of smoking are rarely mentioned. The greatest risks of smoking come from the tars released during the combustion of tobacco, and these tars are
implicated in lung cancer and other breathing disorders, though even the t ar apparently has some beneficial effects in protecting the lungs from some noxious particulate matter (e.g. asbestos). According to many studies, the chief medical benefits of smoking are from the nicotine, which occurs naturally in tobacco as well as in certain vegetables such as tomatoes, potatoes, and red peppers, though in much smaller amounts. Interestingly, these three plants
originated in the Americas so nicotine was essentially a "New World" substance. Native Americans were well aware of the curative properties of tobacco, and used it both medicinally and ceremonially.
Numerous studies have shown the protective effects of smoking with regard to Parkinson's Disease and ulcerative colitis, and an increasing body of research indicates it also helps protect against Alzheimer's Disease and colo-rectal cancer. Since these effects are so well known, wehave not listed them below but have focused instead on a few more obscure medical benefits culled from the 1984-85 CDC bibliography. Brief documentation of the beneficial effects of smoking with regard to Parkinson's, ulcerative colitis, Alzheimer and colo-rectal cancer will appear in an attached appendix of some relevant studies from the 1991 CDC bibliography.
• 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."
0574. 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 "
"In general, motor performance in all groups improved after smoking."
0530. London University, Institute of Psychiatry. O'Connor, K.P "Individual Differences in Psychophysiology of Smoking and Smoking Behaviour "
"Smokers in general are thinner than nonsmokers, even when they ingest more calories." [Numerous studies, but only two are listed below]
0885. 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 prevalence rate among smokers was 3.94 percent; among nonsmokers the rate was 4.90 percent."
0146. Shanghai Institute of Cardiovascular Diseases. Chen, H.Z.; Pan, X.W.; Guo, G. et al. "Relation Between Cigarette Smoking and Epidemiology of Hypertension.
AND
"Hypertension and postpartum hemorrhage were lower in smokers."
0045. University of Tasmania (Australia). Correy, J.; Newman, N. Curran, J. "An Assessment of Smoking in Pregnancy."
"RBCs [red blood cells] from cigarette smokers contain more glutathione and catalase and protect lung endothelial cells against O2 [dioxide] metabolites better than RBCs from nonsmokers." [emphasis added]
0759. University of Colorado. Refine, J.E.; Berger, E.M.; Beehler, C.J. et al. "Role of RBC Antioxidants in Cigarette Smoke Related Diseases." Jan 1980 - continuing.
(A number of studies in the 1991 CDC bibliography describe the apparent protective effect of smoking with regard to mouth ulcers).
APPENDIX Following are studies listed in the Centres for Disease control's Bibliography on Smoking and Health, 1991. Many newer studies appear in this more recent CDC bibliography which support the earlier studies listed in the foregoing selected bibliography, including a lower risk of breast cancer, lower risk of endometrial cancer in smoking women; the improvement of fine motor control for smokers; lower incidence of
overweight in smokers; lower incidence of high blood pressure among smokers. Below are selected studies which demonstrate the protective effect of smoking in Parkinson's Disease and ulcerative colitis.
"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."
1102. 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.
"These results indicate that in sufficient doses chronic treatment with nicotine may be considered in the pharmacological treatment of Parkinson's disease. It remains to be demonstrated whether these protective actions can be extended to include also other injured neurons..."
1190. Janson, A.M.; Fuxe, K.; Agnati, L.F. Jansson, A. et al. "Protective effects of chronic nicotine treatment on lesioned nigrostriatal dopamine neurons in the male rat." Pub. in Progress in Brain Research 79:257-65, 1989.
"Several studies have reported an apparent protective effect of cigarette smoking for the risk of idiopathic Parkinson's disease (IPD). These observations are supported by neurochemical studies..." These findings suggest that the inverse association between smoking and IPD may apply to NIP [neuroleptic-indiced parkinsonism]."
4014. Decina, P.; Caracci, G.; Sandik, R.; Berman, W. et al. "Cigarette smoking and neuroleptic- induced parkinsonism." In Biological Psychiatry 28(6):502-8, Sept. 15, 1990
"There is a low prevalence of smoking in ulcerative colitis. The disease often starts or relapses after stopping smoking."
4101. Prytz, H.; Benoni, C.; Tagesson, C. "Does smoking tighten the gut?" In Scandinavian Journal of Gastroenterology 24(9):1084-8, Nov. 1989.
"These results indicate that nonsmokers and especially ex-smokers of cigarettes have greater risk of UC [ulcerative colitis] and thus confirm the results of other studies."
4134. Lorusso, D.; Leo, S.; Miscianga, G.; Guerra, V. "Cigarette smoking and ulcerative colitis. A case control Study." Hepato-Gastroenterology 36(4): 202-4, Aug. 1989.
Documentation for the protective effect of smoking on Alzheimer's may be found in the 11 studies reviewed in the International Journal of Epidemiology, 1991. There is also documentation for lower incidence of colorectal cancer in JAMA in the early 1980s
ADDITIONAL BIBLIOGRAPHY Forces Canada wishes to thank Martha Perske for providing the following bibliography:
"...particular attention is paid to the consumption of ethanol [alcohol] which has a major impact on the incidence of human cancer"
91-2046. Doll, R. Lifestyle: An overview. Cancer detection and prevention. 14(6): 589-94, 1990
" There is little direct evidence that cancer prevention has led to any major reduction in cancer incidence or mortality."
91-2068. Claysdon, D.B. " An overview of current and anticipated methods for cancer prevention." Cancer Letters. 50(1):3-9, April 9, 1990.
"...the prevalence of mild and moderate disease [oesophageal cancer] was found to be positively associated with the consumption of burning hot beverages (odds ratio = 4.7), the prevalence of esophagitis among siblings (O.R. = 4.4) and family history (O.R. = 1.8) ... Weaker associations were seen for cigarette smoking and the use of cottonseed oil..."
91-2069. Chang-Claude, J.C.; Wahrendorf, J. et al. " An epidemiological study of precursor lesions of oesophageal cancer among young persons in a high risk population in Hulxian, China." Cancer Research 50(8):2266-74, April 15, 1990.
" The incidence of these cancers appear to be increasing rapidly in response to the increasing level of alcohol consumption in Denmark."
91-2130. Miller, H. "Changing incidence of cancer of the tongue, oral cavity, and pharynx in Denmark." Journal of Oral Pathology and Medicine. 18(4): 224-9, Apr. 1989.
" Cancers of the mouth or pharynx and oesophagus were independently and strongly related to alcohol consumption..."
91-2147. Ferraroni, M.; Negri, E. et al. " Socioeconomic indicators, tobacco and alcohol in the aetiology of digestive tract neoplasms." International Journal of Epidemiology. 18(3): 556-62, Sep 1989.
"...Linxian, a rural country in North Central China with one of the world,s highest mortality rates for these tumours. Cancer rates tended to raise with increasing intake of wheat or corn... Few persons reported drinking alcoholic beverages. Smoking was reported by 61% of the male cases and was a mild risk factor, related more to cancer of the cardia than of the oesophagus. The risk was increased by 70% among those whose parents had oesophageal or stomach cancer..."
91-2180. Li, J.Y.; Brshow, A.G.; et al [including Blot, W.J.]. "A case-control study of cancer of yhe oesophagus and gastric cardia in Linxian [China]." International Journal of Cancer. 43(5) : 755-61, May 15, 1989.
Odds ratios for oesophageal cancer: Current smokers: 3.8 - Heavy drinkers: 6.0
91-2199 Franceschini, S.; Talamini, R., et al. "Smoking and drinking in relation to cancers of the oral cavity, pharynx, larynx, and oesophagus in Northern Italy." Cancer Research. 50(20) :6502-7, Oct. 15, 1990.
"Highly significant associations with frequent intake of Maize emerged for oral cancer, pharyngeal cancer, and oesophageal cancer (OR = 3.3, 3.2, and 2.8, respectively). The risk elevation could not be explained in terms of difference in education, occupation, tobacco use, or consumption of fresh fruits and vegetables. The unfavourable effect of Maize... was evident only in those individuals who reported heavy drinking... The present findings agree with previous observations from Africa, China, the U.S., and Italy."
91-2202. Franceschini, S.; Bidoli, E.; et al. "Maize (corn) and risk of cancer in the oral cavity, pharynx, and oesophagus in Northeastern Italy." Journal of the National Cancer Institute. 82(17) :1407-11, Sept. 5, 1990.
"The three risk factor showed a strong tendency to be related to cancer only in combination, adding new evidence to the theory that risk factors in cancer act in a synergistic fashion."
91-2322. Grossart-Maticek, R.; Eysenck, H.J. "Personality, smoking, and alcohol as synergistic risk factors for cancer of the mouth and pharynx." Phycological Reports. 67 (3 Pt. 1) : 1024-6, Dec. 1990.
Source: Bibliography On Smoking and Health, 1991. Centres for Disease Control and Prevention.
SMOKERS HAVE REDUCED RISKS OF ALZHEIMER'S AND PARKINSON'S DISEASE Patients with Alzheimer's disease (AD) have a considerably decreased life expectancy, with the entire course of the disease taking an average of about eight years. AD is defined by a specific combination of neuropathologic features that
include neuronal loss in particular regions of the brain and a high density of senile plaques and neurofibrillary tangles. It is hard to distinguish during life because of other damage and dementias. As many as 80% of the
cases may be unrecognized by general practitioners.
Acute administration of low doses of nicotine improved mental processes and may be protective in AD. This possibility was first put forward by Appel, who noted that only 6 out of 30 patients had smoked at any time in their
lives. Since that time, nineteen case control studies have been published and are considered here. The overall from these showed a clear negative association, 15 out of 18 studies reporting a lower risk of AD in men and women who had smoked.
Of the 19 studies, 15 found a reduce risk in smokers, and none found an increased risk. And smoking is clearly associated with a reduced risk of Parkinson's disease, another disease in which nicotine receptors are reduced. The fact that acute administration of nicotine improves attention and information processing in AD patients adds further plausibility to the hypothesis.
"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 from the same family."
(Conelia M. van Duljn MSC Albert Hoffman Md., Erasmus Univ. Md. School) STUDIES AND PUBLICATIONS
Amaducci LA, et al. A case-controlled study of an Italian population. Neurology, 1986, 36:922-931.
Barclay L, Kheyfets S. Tobacco used in Alzeimer's disease. Prog. Clin. Bho. Res 0989, 317:189-194.
Brenner DE, et al. Relationship between cig. smoking and Alz. disease. Neurology 1993, 43:293-300.
Broe GA et al. A case -controlled study of alz. in Australia. Neurology 1990, 40:1698-1707.
Chandra V. et al. Case study of the late on-set 'probable Alz. disease'. Neurology 1987, 37:1295-1300.
Dewey ME, et al. Risk factors for Dementia. Liverpool, Int. Geriatric Psychiatry 1988, 3:245-249.
Ferini-Strambi, et al. Clinical Aspect of Alz. Disease with pre-senile on-set. Neuro Epidem 1990, 9:34-49.
French LR, et al. Case-control study of dementia of Alz. type. Am J Epidemiol 1985, 121:414-421.
Grossberg, GT, et al. Smoking as a risk factor for Alz disease. Am. Geriatric Soc. 1989, 37:819.
Hebert LE, et al. Relation of smoking and alcohol to Alz disease. Amer. J Epidemiol 1992, 135:347-355.
Heyman A, et al. Alz disease: a study of epidem aspects. Am Neurol 1984, 15:335-341.
Hofman A, van Duijn. Alz disease, Parkinson's disease, and smoking. Neurobiol Aging 1990, 11:295.
Jones GMM, et al. Smoking and dementia of Alz type. Neurol Neurosurg Psychiatry 1987, 50:1383.
Joya CJ, et al. Risk factors in clinically-diagnosed Alz disease. SA Neuroniol Aging 1990, 11:296.
Katzman R, et al. Develop of dementing ill. in 80 yr. old volunteer cohort. Am Neurol 1989, 25:317-324.
Kondo, K Yamashita I. Case study of Alz in Japan. Biol & Social advances. Excerpta Medica 1990, 49-53.
Shalat SL, et. al. Risk factors for Alz. disease. Neurology 1987, 37:1630-1633.
Soininen H, et al. Clinical and etiological aspects of senile dementia. Eur Neurol 1982, 21:401-410.
Korten AE, et al. Control informant agr. in case control studies of Alz. Int. J Epidie. 1992, 21:1121-1131.
Breteler MMB, et al. Epidemiology of Alz disease. Epidemiol Review 1992, 14:59-82.
Lee PN Statistics, Sutto, UK.
ALZHEIMER'S DISEASE IS ASSOCIATED WITH NON-SMOKING
Graves' pooled reanalysis found, "A statistically significant inverse relation between smoking and Alzheimer's disease was observed at all levels of analysis, with a trend towards decreasing risk with increasing consumption (p=0.0003). A propensity towards a stronger inverse relation was observed among patients with a positive family
history of dementia."
Only three studies have ever linked smoking with AD. The reanalysis, in which the author of one participated, noted, "Since veterans may be expected to smoke more than the general population, and since smokers have been found to respond less frequently to questionnaires than non-smokers, the positive result observed for this study may
Contrary to a claim that smokers got AD at a younger age, there was no difference in men. Female smokers were younger among both cases and controls, which proved it to be spurious.
Over 4 million people suffer from AD, and annual costs are over $88 billion. There may be 73,000 excess cases per year among non-smokers, with $17.5 billion in excess costs.
Ferini-Strambi L, Smirne S et al.Clinical and epidemiological aspects of Alzheimer's disease with presenile onset: a case-control study.Neuroepidemiol 1990;9:39-49. 63 ADs, ever/never 0.47 (0.23-0.94).
Li G, Shen YC et al.A case-control study of Alzheimer's disease in China. Neurol 1992 Aug;42(8):1481-1488. 70 ADs, >10y 0.92 (0.45-1.87), >20y 0.87 (0.35-2.16).
Hebert LE, Scherr PA et al.Relation of smoking and alcohol consumption to incident Alzheimer's disease.Am J Epidemiol 1992;135(4):347-355. 76 ADs, ever/never 0.7 (0.3-1.4), 40 pyrs 0.8 (0.6-1.1).
Jones GMM, Reith M et al.Smoking and Dementia of Alzheimer type (letter). J Neurol Neurosurg Psychiatry 1987;50:1383. 81 ADs. ever/never 0.63 (from Graves: NON-smokers 1.58).
Grossberg GT, Nakra R et al.Smoking as a Risk Factor for Alzheimer's Disease (letter). J Am Geriatr Soc 1989;37:822. 144 ADs ever/never 0.33 unmatched OR (p<0.01) (from Graves). Reported that female smokers had onset 2 years earlier, non-significant.
Brenner DE, Kukull WA et al.Relationship between cigarette smoking and Alzheimer's disease in a population-based case-control study.Neurol 1993; 43(2):293-300. 152 e/n 0.61 (0.37-0.99).
Graves AB, van Duijn CM et al., for the EURODEM Risk Factors Research Group.Alcohol and tobacco consumption as risk factors for Alzheimer's disease: A collaborative reanalysis of case-control studies. Int J Epidemiol 1991;20(2 Suppl 2):S48-S57. All 8 studies, 899 cases: ever/never 0.78 (0.62-0.98 with Shalat), 0.72 (0.56-0.92 without); <1p 0.84 (0.75-0.92), >1p 0.81 (0.53- 1.27) with. 4 studies with pack-year data, adjusted for education: <15 py 0.68 (0.46-1.01), 15.5-37.0 py 0.58 (0.37-0.89), >37.0 py 0.49 (0.30-0.78).
The 8 studies:
Broe GA et al. Neurol 1990;40:1698-1707. 168 ever/never 0.79 (0.47-1.31).
Chandra V et al. Neurol 1987;37:1295-1300. 63 ever/never 0.57 (0.24-1.36)
French LR et al. Am J Epidemiol 1985;121(3):414-421. 78 ever/never 0.50 (0.15-0.66).
Graves AB et al. Ann Neurol 1990;28:766-774. 129 ever/never 0.73 (0.43-1.23).
Heyman A et al. Ann Neurol 1984;15:335-341. 46 ever/never 0.97 (0.45-2.13).
Hofman A et al. Neurobiol Aging 1990;11:295. 197 ever/never 0.73 (0.45-1.17).
Shalat SL et al. Neurol 1987;37:1630-1633. 102 ever/never 1.53 (0.74-3.17). NOT SHOWN ON GRAPH:
Appel SH.Alzheimer's disease. In: Brain Neurotransmitters and Receptors in Aging and Age-Related Disorders(Aging, Vol 17). SJ Enna et al, eds. New York: Raven Press 1981. pp 203-207. Observed that only 6/30 patients ever smoked.
Barclay L, Kheyfets S.Tobacco use in Alzheimer's disease. In: Alzheimer's Disease and Related Disorders.Alan R Liss 1989. pp 189-194. 39 ADs vs spouse controls: ever 64.1%/69.2%.
Hirayama T.Health effects of active and passive smoking. In: Smoking and Health 1987. Proc 6th World Conf of Smoking and Health, Tokyo, 9-12 Nov, 1987. Amsterdam, The Netherlands: Elsevier Science Pub, pp. 75-86. Rate ratio 39 male 1.53, 13 female 1.72; 1-14 cigs 1.5, 15-19 2.1, 20+ 2.4. Number of non-smokers not given.
Joya CJ, Pardo CA, Londono JL. (abstr)Risk factors in clinically diagnosed Alzheimer's disease: a case-control study in Colombia (South America).Neurobiol Aging 1990;11:296. 43 ADs. "Tobacco use (>20 cigarettes/day)... tended to be more frequent among cases of AD than controls; however differences were not significant." No detail.
Katzman R, Aronson M et al. Development of dementing illnesses in an 80-year-old volunteer cohort. Ann Neurol 1989;25:317-324. 32 incident ADs/controls: 28.1%/51.1% ex, 0.0%/10.9% current. Prospective: "In this [75-85 yr old] study population, the incidence of dementia exceeded that of stroke and equalled that of presumed heart attacks."
Mayeux R, Ottman R et al.Genetic susceptibility and head injury as risk factors for
Alzheimer's disease among community-dwelling elderly persons and their first-degree relatives. Ann Neurol 1993;33(5):494-501. 138 ADs; "smoking was more frequent in control subjects than in patients," no
detail.
PARKINSON'S DISEASE IS ASSOCIATED WITH NON-SMOKING (Studies listed by size)
Duvoisin RC, Eldridge R et al. Twin study of Parkinson disease. Neurol 1981;
31:77-80. 12 pairs. 1.0 ever/never; 0.4 current; all nonsignificant.
Ho SC, Woo J, Lee CM. Epidemiologic study of Parkinson's disease in Hong Kong. Neurol 1989;39:1314-1318. 34 PDs; ever/never 0.6 (0.2-1.3).
Tanner CM, Chen B et al. Environmental factors in the etiology of Parkinson's disease. Can J Neurol Sci 1987;14:419-423. 35 PDs; ever/never 0.67 not significant. Bharucha NE, Stokes L et al. A case-control study of twin pairs discordant for Parkinson's disease: A search for environmental risk factors. Neurol 1986;
36:284-288. 41 PDs; ever 0.4, p<0.05; current 0.4 p<0.05. Statistically significant less cigarette smoking by PDs.
[*] Doll R, Peto R. Mortality in relation to smoking: 20 years' observations on male British doctors. Br Med J 1976;25:1525-1536. 51 men; current/non 0.36
p<0.01.
Ngim C-H, Devathasan G. Epidemiologic study on the association between body burden mercury level and idiopathic Parkinson's disease.
Neuroepidemiol 1989;8:128-141. 54 PDs ever 0.61 (0.18-2.03).
Hertzman C, Wiens M et al. Parkinson's disease: A case-control study of occupational and environmental risk factors. Am J Ind Med 1990;17:349-355.
57 cases. Age-adj logistic regression ever s 0.40 (0.19-0.86).
[*] Grandinetti A, Morens DM et al. Prospective study of cigarette smoking and the risk of developing idiopathic Parkinson's disease. Am J Epidemiol
Butterfield PG, Valanis BG et al. Environmental antecedents of young-onset Parkinson's disease. Neurol 1993;43(6):1150-1158. 63 PDs <50y; s p/d 15y prior
0.32 (0.15-0.67).
Hofman A, Collette HJA et al. Incidence and risk factors of Parkinson's disease in the Netherlands. Neuroepidemiol 1989;8:296-299. 86 PDs ever 0.6 (0.3-1.0),
current 0.7 (0.4-1.4).
[*]Sasco AJ, Paffenbarger RS. Smoking and Parkinson's disease. Epidemiology
1990;1:460-465. C-c in 50k Harvard cohort, 96 PDs; smoked at college 1.0; adult current cig 0.51 (0.26-1.0). Most eventual smokers did not smoke at college.
Cazzato G, Capus L et al. Abitudine al fumo e morbo di Parkinson.Rivista di Neurologia 1985;55:79-87. 100 PDs; ever/never 0.4 sig. (Baron's calculation).
Rajput AH, Offord KP et al. A case-control study of smoking habits, dementia, and other illnesses in idiopathic Parkinson's disease. Neurol
1987;37:226-232. 118 PDs; ever 0.7 (0.4-1.2). Reanalysis of subjects of 1984 study, with linear logistic regression.
[*] Hammond EC.Smoking in relation to the death rates of one million men and women. In: Haenszel W, ed. USDHEW NCI Monograph 19, 1966. 123 PDs; ever/
never RR 0.76 ages 45-64.
Barbeau A, Pourcher E. New data on the genetics of Parkinson's disease. Can
J Neurol Sci 1982;9(1):53-60. 124 early onset PD; ever/never OR 0.4 (Baron's Calculation).
Jimnez-Jimnez FJ, Mateo D, Gimnez-Roldan S. Premorbid smoking, alcohol consumption, and coffee drinking habits in Parkinson's disease: A case-control study. Movement Dis 1992;7(4):339-344. 128 PDs; 11+c, p<0.005. [Mean of Table 1, 0.63 11+/never].
Semchuk KM, Love EJ, Lee RG. Parkinson's disease: A test of the
multifactorial etiologic hypothesis. Neurol 1993;43(6):1173-1180. 130 PDs; ever smokers 0.58 (0.33-1.02) adj; 0.48 (0.29-0.80) crude.
Stern M, Dulaney E et al. The epidemiology of Parkinson's disease. A case-control study of young-onset and old-onset patients. Arch Neurol
1991;48:903-907. 149 PDs; 0.5 (0.3-0.9).
Mayeux R, Tang M-X, Marder K, Ct LJ, Stern Y. Smoking and Parkinson's disease. Movement Disorders 1994 Mar;9(2):207-212. 150 PDs. Ever s adj for age & sex
0.8 (0.4-1.5); <30py 0.8 (0.4-1.5), >30py 0.6 (0.3-1.2).
Tanner CM, Koller WC et al. (abstr)Cigarette smoking, alcohol drinking and Parkinson's disease: cross-cultural risk assessment. Movement Disorders
1990; 5(suppl 1):11. US: 150 PDs OR 0.2 p<0.0001.
Kondo K. Epidemiological clues for the etiology of Parkinson's disease. Adv Neurol 1984;40:345-351. 166 PDs; ever/never, female 0.6 sig, male 0.4 sig (Baron's calculation).
Nefzger MD, Quadfasel FA, Karl VC. A retrospective study of smoking in Parkinson's disease. Am J Epidemiol 1968;88(2):149-158. 198 PDs; ever/never 0.44 sig.
Kessler II. Epidemiologic studies of Parkinson's disease. Am J Epidemiol
1972;96(4):242-254. 228 PDs; ever/never,female 0.56 p>0.05, male 0.38 p<0.001.
Baumann RJ, Jameson HD et al. Cigarette smoking and Parkinson disease: 1. A comparison of cases with matched neighbors. Neurol 1980;30:839-843; and
Haack DG, Baumann RJ et al. Nicotine exposure and Parkinson disease. Am J Epidemiol 1981;114(2):191-200. 237 PDs. ever/never both sexes 0.46 p<0.001.
Godwin-Austen RB, Lee PN et al. Smoking and Parkinson's disease. J Neurol
Neurosurg Psychiatry 1982;45:577-581. 350 PDs; ever 0.52, current 0.40; dose-response 1-19=ref., 20+ 0.76 cur.
[*] Hellenbrand W et al. Smoking and Parkinson's disease: a case control study in Germany. Int J Epidemiol 1997 Apr;26(2):328-339. 380 PD pts. Ever s 0.5
(0.3-0.7), P<0.00005; current s 0.2 (0.1-0.4), versus never. Dose-response.
[*] Kahn HA.The Dorn study of smoking and mortality among U.S. veterans: report on eight and one-half years of observation. In: Haenszel W, ed.
USDHEW NCI Monograph 19, 1966. 400 PDs; ever RR 0.36, current RR 0.30, vs. never.
Marttila R, Rinne UK. Smoking and Parkinson's disease. Acta Neurol Scand
1980; 62:322-325. 443 PD; ever/never 0.7 significant (Baron's calculation).
Kessler II, Diamond EL. Epidemiologic studies of Parkinson's disease. Am J
Epidemiol 1971;94(1):16-25. 468 PDs; both sexes ever/never 0.66, p<0.05.
Busenbark KL, Huber SJ et al. Olfactory function in essential tremor. Neurol 1992 Aug;42:1631-1632. yes/no 1/15 PDs, 3/13 normal controls.
