Tobacco and Public Health - TCSC Indonesia

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TOBACCO AND CARDIOVASCULAR DISEASE
Hill 1950, 1952), and establishment, again with Doll, of the long-running cohort study
of smoking in British doctors (Doll et al. 1980, 1994). His criteria for assisting judgements
about the likelihood of causal relationships explaining associations seen in
observational data were published in 1965, with the original paper emphasizing that, as
a true experiment, a randomized controlled trial involving human subjects should
always provide the best evidence for answering such questions (Hill 1965). The criteria
are listed and briefly explained in Table 32.1. Various other individuals and groups
have proposed extensions and embellishments to the list of criteria, but Hill’s formulation
has the claim of simplicity as well as precedence, and therefore has been
adopted here.
In relation to diseases purportedly caused by tobacco, the weight of evidence available
by at least the early 1960s had made such experiments unethical, even if they were practical,
while experimental studies conducted in laboratory animals could contribute only
to Hill’s criterion of biological plausibility because the potential for between-species
differences limited their applicability to humans. Nevertheless, so-called ‘natural
experiments’, in which the incidence of cardiovascular and other diseases are tracked
as the smoking habits of a given population change, have contributed important
information bearing on the criteria of temporal sequence and reversibility. These
observations fall into a category known to epidemiologists as ‘ecological studies’
Table 32.1 The Bradford Hill criteria for judgements about causation
Criterion Test and its interpretation
Strength Is the statistical relationship strong? Does it show a dose–response relationship—is
a higher level of exposure to the putative cause associated with a greater risk of
the disease?
Consistency Is the relationship seen consistently in studies conducted at different historical
periods, in different places, in different people (for example, in men as well as in
women, in young people as well as in older ones, in different ethnic groups),
and using different epidemiological methods (such as case–control and
cohort studies)?
Temporal Do at least some of the studies provide incontrovertible evidence that exposure to
sequence the putative cause preceded development of the alleged effect?
Reversibility Is a reduction in exposure followed by a reduced risk of the disease of interest?
This question is best answered in data from individuals, but indicative
information may also be derived from studies of whole populations
Specificity Is exposure to the putative causal factor associated with development of an
outcome that is unique to that exposure?
Biological Is there supportive evidence from experimental studies in other species and from
plausibility laboratory work on relevant organs, tissues, and other physiological systems?
A systematic search for, and failure to find, evidence that would not support
a conclusion of biological plausibility can be very useful here in demonstrating
that the overall body of evidence is ‘coherent’.