<< In February of 1995 (Yes, I know that was a long time ago, but I am a very slow typist) Cecil wrote
<<Although the data is unclear, many believe the relationship between smoking
and disease is linear: the more you smoke the greater your risk, but any
smoking presents some risk>
Actually the effect is non-linear, with larger than expected effects occurring at low doses. There has been a lot of discussion of this non-linearity in medical journals, because breathing secondhand smoke is like being a smoker of low amounts of cigarettes.
An article entitled “Environmental Tobacco Smoke Exposure and Ischaemic Heart Disease: an Evaluation of the Evidence” in the October 18 1997 issue of the British Medical Journal says
<<Risk of smoking one cigarette per day
Figure 2 shows the dose-response relation in each of the five studies of smoking and ischaemic heart disease (age standardised to age 65). The risk of ischaemic heart disease increases continuously with daily cigarette
consumption, but in all five studies linear extrapolation of the regression
line back to zero dose (no cigarettes per day) does not yield the expected
relative risk estimate of 1.0. The estimates from the five individual studies
of the risk at low dose are consistent with each other, and the weighted
average relative risk at one cigarette per day (defining risk in non-smokers
as 1.0) was 1.39 (1.18 to 1.64; P<0.001). At 20 cigarettes per day this risk
was 1.78>>
In other words, smoking one cigarette per day raises the risk of heart
attack by 39%.
The entire article can be found at:
http://www.bmj.com/cgi/content/full/315/7114/973
The reason for the very large effect at small doses is that the effect on
clotting abnormalities has a very non-linear behavior. Very low doses are almost as potent as large doses in doing this. The following is from the Harvard Study in the May 20 1997 issue of CIRCULATION (a scientific journal of the American Heart Association)
<<Several potential mechanisms have been identified through which passive
smoking may increase the risk of coronary heart disease. These include
carboxyhemoglobinemia, increased platelet aggregation, damage to the arterial
endothelium, and reduced HDL cholesterol. In one experiment, the sensitivity
of platelets to the antiaggregetory action of exogenous prostacyclin (PG2)
was compared in smokers and non-smokers before and after they sat in a room
for 20 minutes where cigarettes had been smoked just before the experimental
subjects had entered. No change in platelet sensitivity was detected among
smokers; however a significant change occurred among the platelets of
non-smokers such that their sensitivity to the anti-aggregatory action of PG2
was not discernably different from the smokers>>