Models of Causal Relationships
Drawing upon the concepts presented earlier in the chapter, this section introduces models of disease causation. Relationships between suspected disease-causing factors and outcomes fall into two general categories: not statistically associated and statistically associated.15 Among statistical associations are non-causal and causal associations. Possible types of associations are formatted in Figure 9–2.
We have already considered the role of statistical significance in evaluating an association and noted that evaluation of statistical significance is used to rule out the operation of chance in producing an observed association; a nonstatistically associated (independent) relationship is shown in box A of the diagram (left side).
FIGURE 9–2 Map of possible associations between disease-causing factors and outcomes.
Source: Data from B MacMahon and TF Pugh, Epidemiology Principles and Methods. Boston, MA: Little, Brown and Company; 1970.
As shown in Figure 9–2, a statistical association may be either noncausal or causal. What is meant by a noncausal (secondary) association? Suppose factor C is related to disease outcome A. The association may be due to the operation of a third factor B that is related to both C and A. Thus, the association between C and A is secondary to the association of C with B and C with A. For example, periodontal disease (C) is associated with chronic obstructive pulmonary disease (A).16 One possible explanation for this association is the secondary association
of smoking (B) with both periodontal disease (C) and chronic obstructive pulmonary disease (A). This model suggests that the increased risk of chronic obstructive pulmonary disease associated with periodontal disease is related to the role that smoking may play as a cofactor in both conditions. Here is a map of a secondary association: C ← B → A.1
With respect to causal associations, the relationship between factor and outcome may be indirect or direct. An indirect causal association involves the operation of an intervening variable, which is a variable that falls in the chain of association between C and A. An illustration of an indirect association is the postulated relationship between low education levels (C) and obesity (A) among men.17 Men who have lower education levels tend to be more obese than those who have higher education levels. It is plausible that the relationship between C and A operates through the intervening variable of lack of leisure time physical activity (B). An indirect association involves an intervening variable in the association between C and A. This relationship may be formatted as follows: C → B → A.1 Note that the arrow between C and B has been reversed in contrast with an indirect noncausal association.
Multiple Causality
The foregoing section provided models of causality that employ more than one factor. As stated earlier in this chapter, the measure risk difference implies multivariate causality ...
Models of Causal RelationshipsDrawing upon the concepts presente.docx
1. Models of Causal Relationships
Drawing upon the concepts presented earlier in the chapter, this
section introduces models of disease causation. Relationships
between suspected disease-causing factors and outcomes fall
into two general categories: not statistically associated and
statistically associated.15 Among statistical associations are
non-causal and causal associations. Possible types of
associations are formatted in Figure 9–2.
We have already considered the role of statistical significance
in evaluating an association and noted that evaluation of
statistical significance is used to rule out the operation of
chance in producing an observed association; a nonstatistically
associated (independent) relationship is shown in box A of the
diagram (left side).
FIGURE 9–2 Map of possible associations between disease-
causing factors and outcomes.
Source: Data from B MacMahon and TF Pugh, Epidemiology
Principles and Methods. Boston, MA: Little, Brown and
Company; 1970.
As shown in Figure 9–2, a statistical association may be either
noncausal or causal. What is meant by a noncausal (secondary)
association? Suppose factor C is related to disease outcome A.
The association may be due to the operation of a third factor B
that is related to both C and A. Thus, the association between C
and A is secondary to the association of C with B and C with A.
For example, periodontal disease (C) is associated with chronic
obstructive pulmonary disease (A).16 One possible explanation
for this association is the secondary association
of smoking (B) with both periodontal disease (C) and chronic
obstructive pulmonary disease (A). This model suggests that the
increased risk of chronic obstructive pulmonary disease
associated with periodontal disease is related to the role that
2. smoking may play as a cofactor in both conditions. Here is a
map of a secondary association: C ← B → A.1
With respect to causal associations, the relationship between
factor and outcome may be indirect or direct. An indirect causal
association involves the operation of an intervening variable,
which is a variable that falls in the chain of association between
C and A. An illustration of an indirect association is the
postulated relationship between low education levels (C) and
obesity (A) among men.17 Men who have lower education
levels tend to be more obese than those who have higher
education levels. It is plausible that the relationship between C
and A operates through the intervening variable of lack of
leisure time physical activity (B). An indirect association
involves an intervening variable in the association between C
and A. This relationship may be formatted as follows: C → B →
A.1 Note that the arrow between C and B has been reversed in
contrast with an indirect noncausal association.
Multiple Causality
The foregoing section provided models of causality that employ
more than one factor. As stated earlier in this chapter, the
measure risk difference implies multivariate causality by
isolating the effects of a single exposure from the effects of
other exposures. The example on NSAIDs examined the
difference between risk of peptic ulcer among users and
nonusers of NSAIDs, where the risk difference was 12.5 per
1,000 person-years. The risk of peptic ulcer caused by other
exposures was 4.2 per 1,000 person-years.
The issue of disease causality is exceedingly complicated. To
describe exposure–disease relationships, epidemiologists have
developed complex models of disease causality. These models
acknowledge the multifactor causality of diseases, even those
that seem to have “simple” infectious agents. Often, these
models involve an ecologic approach by relating disease to one
or more environmental factors. “The requirement that more than
3. one factor be present for disease to develop is referred to
as multiple causation or multifactorial etiology.”18(p
27) Examples of several influential models are the:
· •• epidemiologic triangle
· •• web of causation
· •• wheel model
· •• pie model
Web of causation
The web of causation is “… a popular METAPHOR for the
theory of sequential and linked multiple causes of diseases and
other health states.”1 The web of causation implicates broad
classes of events and represents an incomplete portrayal of
reality.15 Although the web of causation for most diseases is
complex, one may not need to understand fully the causality of
any specific disease in order to prevent it. An example of the
web of causation of avian influenza is provided in Figure 9–3.
Follow the infection of the human host from the virus reservoir
in wild birds. As of 2007, the virus had not mutated into a form
that could be spread readily from person to person.
Wheel model
The wheel model is similar to the epidemiologic triangle and
web of causation with respect to involving multiple causality
(Figure 9–4). Observe that the model explains the etiology of
disease by calling into play host and environment interactions.
Environmental components are biologic, social, and physical.
The circle designated as “host” refers to human beings or other
hosts affected by a disease. The circle called “genetic core”
acknowledges the role that genetic factors play in many
diseases. The wheel model de-emphasizes specific agent factors
and, instead, differentiates between host and environmental
factors in disease causation. The biologic environment is
relevant to infectious agents, by taking into account the
environmental dimensions that permit survival of microbial
agents of disease.
4. FIGURE 9–3 The web of causation for avian influenza.
A wheel model may be used to account for the occurrence of
childhood lead poisoning.18 In this example, preschool children
are typical hosts. The physical environment provides many
opportunities for lead exposure from lead-based paint in older
homes, playground equipment, candy wrappers, and other
sources. Some children ingest paint chips from peeling surfaces
as a result of pica, the predilection to eat nonfood substances.
Because lead-based paints often are located in poorer
neighborhoods that have substandard housing, the social
environment is associated with childhood poisoning. Limited
access to medical care in such communities may restrict
screening of preschool children for lead exposure. Elimination
of childhood lead poisoning requires visionary public
health leadership to advocate for detection of lead-based paints
and other sources of environmental lead exposure as well as the
implementation of screening programs. Such efforts will help to
protect vulnerable children against the sequelae of lead
poisoning.
Pie model
Another model of multiple causality (multicausality) is the
causal pie model.19 As Figure 9–5 shows, the model indicates
that a disease may be caused by more than one causal
mechanism (also called a sufficient cause), which is defined as
“a set of minimal conditions and events that inevitably produce
disease.”19(p S144) Each causal mechanism is denoted in
Figure 9–5 by the numerals I through III. An example of
different causal mechanisms for a disease is provided by the
etiology of lung cancer: lung cancer caused by smoking; lung
cancer caused by exposure to ionizing radiation; and lung
cancer caused by inhalation of carcinogenic solvents in the
workplace.
FIGURE 9–5 Three sufficient causes of disease.
5. Source: From KJ Rothman and S Greenland, Causation and
causal inference in epidemiology, Am J Public Health, 2005;
vol 95, p S145. Reprinted with permission from the American
Public Health Association.
Rothman and Greenland note that, “A given disease can be
caused by more than one causal mechanism, and every causal
mechanism involves the joint action of a multitude of
component causes.”19(p S145) The component causes, or
factors, are denoted by the letters shown within each pie slice.
A single letter indicates a single component cause. A single
component could be common to each causal mechanism (shown
by the letter A that appears in each pie); in
other cases, the component causes for each causal mechanism
could be different for each mechanism (shown by the letters that
differ across the pies). Returning to the lung cancer example, a
common factor that could apply to all causal mechanisms for
lung cancer is a genetic predisposition for cancer. Several other
component causes might be different for each causal mechanism
involved in the etiology of lung cancer.
In models of multicausality, most of the identified component
causes are neither necessary nor sufficient causes (defined in
the section on absolute effects). Accordingly, it is possible to
prevent disease when a specific component cause that is neither
necessary nor sufficient is removed; nevertheless, when the
effects of this component cause are removed, cases of the
disease will continue to occur.
Conclusion
This chapter covered two new measures of effect—absolute and
relative effects—that may be used as aids in the interpretation
of epidemiologic studies. In addition, the chapter presented
guidelines that should be taken into account when one is
interpreting an epidemiologic finding. Absolute effects, the first
variety of which is called risk differences, are determined by
finding the difference in measures of disease frequency between
exposed and nonexposed individuals. A second type of absolute
6. effect, called population risk difference, is found by computing
the difference in measures of disease frequency between the
exposed segment of the population and the total population.
Relative effects are characterized by the inclusion of an
absolute effect in the numerator and a reference group in the
denominator. One type of relative effect, the etiologic fraction,
attempts to quantify the amount of a disease that is attributable
to a given exposure. The second type of relative effect, the
population etiologic fraction, provides an estimate of the
possible impact on the population rates of disease that can be
anticipated by removal of the offending exposure. With respect
to interpretation of epidemiologic findings, one should be
cognizant of the influence of sample size upon the statistical
significance of the results. Large sample sizes may lead to
clinically unimportant, yet statistically significant, results;
small sample sizes may yield statistically nonsignificant results
that are clinically important. Therefore, we presented a series of
five questions that should be asked when one attempts to
interpret an epidemiologic observation. The chapter closed with
a discourse on causal models, which may be particularly
instructive when trying to interpret epidemiologic data.
DATAProductAgeGenderEducationMarital
StatusUsageFitnessIncomeMilesTM19518Male14Single3429562
112TM19519Male15Single233183675TM19519Female14Partner
ed433069966TM19519Male12Single333297385TM19520Male13
Partnered423524747TM19520Female14Partnered333297366TM
19521Female14Partnered333524775TM19521Male13Single3332
97385TM19521Male15Single5435247141TM19521Female15Par
tnered233752185TM19522Male14Single333638485TM19522Fe
male14Partnered323524766TM19522Female16Single433638475
TM19522Female14Single333524775TM19523Male16Partnered3
13865847TM19523Male16Partnered334093275TM19523Female
14Single2334110103TM19523Male16Partnered433979594TM19
523Female16Single4338658113TM19523Female15Partnered223
10. 1) Download a clean copy of the file CardioGoodFitness.xlsx to
your computer.Remember, don’t try to work on it by just
clicking on the file name from Blackboard. You need to save it
first.
2) Years ago the company did an analysis of their entire
customer base and found that the average income for their
customers was $50,000. They believe that incomes of their
current customers are significantly higher than that. Test at the
10% significance level, showing all steps of the hypothesis
testing procedure (see the text, page 307). Be sure to include a
practical statement indicating how the company could use the
results you’ve found. HINT: here are the steps to follow…
· Write your Ho and H1
· Make note of your alpha (level of significance)
· Determine your test statistic (that is, find the proper formula
to use)
· Find the critical value of the test statistic from the table, and
define your rejection region
· Find your sample mean and standard deviation using the
proper Excel formulas. Compute the value of the test statistic
(that is, do the number crunching in the formula you identified
in the third step)
· Make the statistical decision and interpret in practical form
3) Years ago about 30% of purchases were for the TM 798 (the
“high end” expensive treadmill), however since those data were
collected we’ve gone through a recession, and a lot of people’s
finances haven’t really recovered. Has the proportion of people
purchasing the TM 798 dropped significantly? Test at the 5%
level of significance. Be sure to include a practical statement
indicating how the company could use the results you’ve found.
That’s it! The final case (for chapter 13) will use the same data
set but will focus on relationships between variables.