Tobacco and Public Health - TCSC Indonesia

492
SMOKING AND LUNG CANCER
Associations of this strength are likely to reflect a causal relationship and the
likelihood is increased when a dose–response relationship can be demonstrated.
Evidence of dose–response also supports the biological coherence of the association.
In regard to lung cancer, several cohort studies have illustrated dose–response in several
ways; in terms of the daily amount smoked, the duration of smoking, the age at onset
of smoking, and the cumulative amount smoked. For example, in terms of number of
cigarettes smoked, the mortality ratio compared with non-smokers for those who
smoked 25 or more a day exceeded 25 for men and 29 for women in the British
Physician’s Study (Doll and Hill 1950). For age at onset less than 15 years the mortality
ratio exceeded 16 for men in the ASC 25 state study (Hammond 1966) and 18 for men
in the US Veteran’s study (Rogot and Murray 1980).
The specificity of the association
As mentioned already, the specificity criterion for causality is a relict from Koch’s
postulates with respect to causal agents for infectious diseases. The specificity criterion,
however, only reinforces a causal hypothesis and is not considered a necessary criterion
(USPHS 1964; Hill 1966). Although tobacco smoke is measured epidemiologically as
a single exposure, it is a complex mixture of carcinogenic chemicals that act together in
a variety of ways to cause cancers in several organs and tissues. Of all the cancer types
that can be at least partly attributed to smoking, the specificity for lung cancer is the
greatest as evidenced by the strength of the association already noted above. The relative
risks observed for smoking and lung cancer are much larger than those observed for
cancers occurring in other organs, especially for cancers in tissues that are not directly
exposed to tobacco smoke such as the kidney and the uterine cervix.
The temporal relationship of the association
Obviously, to be causally associated with the disease the suspect aetiological exposure
has to antedate the diagnosis. One reason why the findings from major prospective
cohort studies have been most useful in establishing a causal relationship between
smoking and lung cancer is because the exposure to smoking was measured in advance
of diagnosis in thousands of subjects who were free of disease at entry to the studies.
The coherence of the association
The coherence criterion links the epidemiological observations with other knowledge
in regard to the biology and natural history of the disease. This takes into account
other criteria, for example those of temporal sequence and dose–response relationship
discussed above. Another piece of supportive evidence is the diminution of risk after
smoking cessation, which shows a negative dose–response relationship with increasing
time since quitting. In the British Physician’s Study after quitting for 15 years or more
the mortality ratio was 2 compared with 16 in those who had quit for less than 5 years
(Doll and Peto 1976). This was similar to the mortality ratio for US Veterans who had