SCIENTIFIC RESEARCH GROUP
NEWSLETTER
No. 1 1712187
For further information, please contact:
Dr Sharon Boyse
Corporate R & D Department
British-American Tobacco Co. Ltd
Westminster House
7 Millbank
London
SWIP UE
BATCo document for Province of British Columbia 23 April 1999
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1. PASSIVE SMOKING
J Peto & R Doll-(1986) Passive Smoking. Br. J. Cancer 54: 381-383
This editorial highlights the controversy that is currently raging on the
subject of passive smoking. Sir R;chard 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: 1501-1504
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 misclassification (eg smokers saying that they are
non-smokers) could be remedied, the apparent risk should be much lower if
not zero.
P N Lee (1986) Passive Smoking and Lung Cancer: Association a result of
bias?
This is a paper which Peter Lee is attempting to have published. expanding
on his arguments in the above letter to the BMJ.
P R J Burch (1986). Br. Ned. Journal 293: 1503
Professor Burch does not believe that smoking causes 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 Ur,
R A Jones (1986) Individual differences in nicoting sensitivity.
Addictive Behaviours II: 435-438
It has been suggested (ea C D Frith, 1971. Psychopharnacolosia 19:188-192)
that smokers smoke 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 snaking 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
suuestins regulation of nicotine intake.
4. A strict nicotine regulation model is not consistent with several
other findings in the literature.
Dr Jones suggests that evidence may be more consistent with some smokers
using smoking as a means of maintaining their emotional equilibrium in %-O
specific situations. Individual differences in sensitivity to nicotine Lpli
exist that are stable over time. Dr Jones believes. therefore, that not --J
all smokers are addicted to nicotine.
NJ
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3. SMOKING, OESIBO EN AND ENDOMETRIAL CANgER
Lancet, December 20-2i MM): 1433
The evidence that smoking reduces the risk of endometrial cancer is
discussed (ie cancer of the body of the uterus). This may 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.
J J Michnovicz et al (1986) Increased 2-hydroxylation of oestradiol as a
Possible mechanism for the anti-estrogenic effect of cigarette smoking.
New England J. Ned. 315: 1305-1309
The study suggests that smoking activates the 2-hydroxylation pathway of
oestradial metabolism. which leads to decreased bio-availability of
oestrogen at target tissues. The subject group was premenopausal women
who smoked more than 20 cigarettes daily.
4. SMOKING AND ALZHEIMER'S/PARKINSON'S DISEASE
J A Baron (1986) cigarette smoking and Parkinson's Disease.
Neurology 36: 1490-1496
This is a review of the evidence suggesting that smoking may 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.
L I Golbe, R A Cody, R C Duvoisin (1986) Smoking and Parkinson's Disease.
Searching for a dose-response relationship. Arch. Neurol. 43: 774-778
This paper reports a study that does not agree with the hypothesis that
cigarette smoking say protect against Parkinson's Disease. However. the
deficiencies of the self-report questionnaire design must be taken into
consideration. We hope to have a critique on methodology available soon
from an independent scientific consultant.
S. HEART DISEASE
D G Cogk et al (1986) Giving up smoking and the risk of he&E& attacks,
The Lancet, December 13e 1376-79
This study claim 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. -J
of heart disease. _Cb-
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J H MacDounall et al (1986) Individual differences in cardiovascular
reactions to stress and cigarette saakii 5: 531-544
This study investigated (in 30 sale smokers) the extent to which
cardiovascular reactions (ie 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 way constitute a risk factor for coronary
heart disease.
M S Green, E Jucha. Y Luz (1986) Blood pressure in smokers and
non-smokers* evideniologic findings. An. Heart J. 111: 232-940
The major finding of this study is that the proposed role of smoking as a
risk factory for hypertension (high blood pressure) is not 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 es relative weight, ethnic origin, alcohol and
coffee intake, and participation in sports.
6. RESPIRATORY/LUNG DISEASE
R B Bridnes. R J Wyatt and S R Rehm (1986) Fff&q1s_Qf smQkLn&_qn
inflamatory mediators tbeit relationship to Pulmonary dysfunction.
Eur. J. ResRir. Dis. 69 (AMppi 146): 145-152
It is claimed that smokers (male; mean age 37.0 years. mean 24 pack-years)
have significant impairment of lung function as indicated by elevations in
inflammatory mediators (total blood leukocytes, neutrophils, lymphocytes,
monocytes, eosinophils, and phase-reactive proteins). The data were
claimed to be supportive of suggestions that a low-grade inflammatory
reaction is induced in smokers; and diseases are associated with pulmonary
dysfunction. Duration of smoking or cumulative smoking history were the
most important factors in predicting pulmonary dysfunction.
7. SMOKING AND MENTAL IMNESS
A K Gopalaswamy And R Morgan (1986) Smoking in chronic lchizophre
Br. J. Psych, 149: 523
With reference to the recent SRG meeting where the correlation between
smoking and mental illness was discussed, a letter is now enclosed
commenting an the association.
%O
8. GENETlC KARKERS IN HYPERTENSION
Dr Nick Carter, whose project on genetic markers in hypertension the SRG
is supporting. provided us with the two enclosed relevant abstracts when
we visited him recently. A note an this visit is also enclosed.
BATCo document for Province of British Columbia 23 April 1999