SMOKING AND HEALTH INFORMATION
BULLETIN
No. 1 17L2AL7
For further information. please contact:
Dr Sharon Boyse
Corporate R & D Department
British-American Tobacco Co. Ltd
Westminster House
7 Millbank
London
SW1P ME
L.14
__j
Ln
BATCo document for Province of British Columbia 23 April 1999

1. PASSIVE SHOKING
J Peto & 8 Doll (1986i Passive Smoking. Br. J. Cancer 54: 381-383
This editorial highlights the controversy that is currently raging on the
subject of passive smoking. Sir Richard Doll and his colleagues believe
that non-smokers who are exposed to environmental tobacco smoke must also
be significantly exposed to the risk of lung cancer, since they will be
exposed to the same chemicals as smokers. These authors hold the view
that there is no safe threshold for carcinogens.
P N Lee (1986). Br. Med. Journal 293: 1503-1504
Peter Lee has suggested that a major reason why passive smoking risks
appear to be so high is due to misclassification of the subjects in the
studies. If this misciassification (es smokers saying that they are
non-smokers) could be remedied, the apparent risk should be such lower if
not zero.
P R J Burch (1986). Br. Ned, Journal 293: 1503
Professor Burch does not believe that smoking pauses lung cancer. although
he does not deny that the two are associated. He believes in a genetic
interpretation ie people are genetically predisposed, or not, to lung
cancer.
2. THEORIES OF ADDICTION, DEPENDENCY ETC
R A Jones (1986) Individual differences in nicotine sensitivity.
Addictive Behaviours II: 435-438
It has been suggested (es C D Frith, 1971. Psychopharmacologia 19:188-192)
that smokers snake because they are 'addicted' to nicotine. One of the
major reasons that nicotine has been considered by some investigators to
be addictive. is the suggestion that smoking serves to regulate the level
of nicotine in the body. Dr Jones provides the following
counter-arguments;
1. Regulation of nicotine intake bys smoking is not very precise, even
among heavy smokers.
2. Regulation of nicotine intake may not- occur at all for light smokers.
3. Difficulties have been observed in replicating earlier studies
suggesting regulation of nicotine intake.
4. A strict nicotine regulation model is not consistent with several
other findings in the literature.
N%0
11.0
Lr4
-1-4
BATCo document for Province of British Columbia 23 April 1999

2
3. SMOKING, OZATROGEN AND ENDOMETRIAL CANCER
Lancet, December 20-27 (1986): 1433
The evidence that smoking reduces the risk of endometrial cancer is
discussed (ie cancer of the body of the uterus). This way be to be due to
its ability to increase the metabolism of (and thereby reduce the
availability of) oestrogen, the hormone associated with the development of
this cancer.
4. SMOKING AND ALZUAMER'S/RARKINSON'S DISEASE
J A Baron (19&61-f"arette smoking and Parkinson's Disease.
Neurology 36: 1490-1496
This is a review of the evidence suggesting that smoking way be a
protective factor against Parkinson's disease which is a progressive
disease of motor function. Epidemiological studies suggest a negative
association between smoking and the disease. Animal data suggests that
nicotine may stimulate brain cells that would normally be stimulated by
the neurotransmitter dopamine which is known to be depleted in Parkinson's
disease.
5. HEART DISEASE
D G Cook et al (1986) Giving up smoking and the risk of heart attacks.
The Lancet, Degember 13: 1376-79
This. study claims that both current and ex-smokers have a risk of
ischaemic heart disease more than twice that of men who had never smoked
cigarettes. (The population consisted of middle-aged males "randomly
selected" from general practice and studied for 6.2 years). Men who had
given up smoking for over 20 years still had an increased risk. The total
number of smoking years was stated to be the clearest indicator of risk.
of heart disease.
H MacDougall et al (1986) Individual differences in cardiovasc"Aar
reactions to stress and cigarette smoking. Health Psychology 5: 531-544
This study investigated (in 30 male smokers) the extent to which
cardiovascular reactions Ue heart rate and blood pressure) to stress were
predictive of cardiovascular reactions to smoking. The study shows wide
and stable (over 7 weeks) individual differences in the above measures.
For blood pressure (but not heart rate) reactions to stress were modestly
correlated with reactions to smoking. The authors conclude that level of
reactivity to cigarette smoking may constitute a risk factor for coronary
heart disease. N-0
L^j
__4
-V.IU
BATCo document for Province of British Columbia 23 April 1999

3
M S Gregn. E Jucha. Y Luz (1986) Blood Pressure in smokers and
non-smokers: evidemioiogic findings, Am. Heart J. III: 932-940
The major finding of this study is that the proposed role of smoking as a
risk factory for hypertension (high blood pressure) is = supported by
the epidemiological evidence. The data were suggestive, if anything, of
lower blood pressure among smokers compared with non-smokers, whereas
ex-smokers had blood pressure similar to non-smokers. The differences
could not be explained by various potentially confounding factors that may
also affect blood pressure eg relative weight, ethnic origin, alcohol and
coffee intake. and participation in sports.
7.
C=)
%-O
J
_Ara
_991b
co
BATCo document for Province of British Columbia 23 April 1999
1 1