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The attributable fraction is one of a class of measures used by epidemiologists to quantify the impact of an exposure or intervention on the occurrence of a disease or other outcome events in a population. These measures can be used, for example, to examine the impact of obesity on disease risk and the potential or expected impact of weight-reduction programs on disease rates. The origin of this concept is a measure proposed by a cancer epidemiologist, Morton Levin, in 1953. In describing the association between cigarette smoking and lung cancer, Levin (1953) offers the following definition of the new measure:

  • The third index (S) is the … maximum proportion of lung cancer attributable to smoking. This index is based on the assumption that smokers, if they had not become smokers, would have had the same incidence of lung cancer as that found among non-smokers. (p. 536)

Although Levin did not give this measure a name, many epidemiologists now call it the attributable fraction. It should be noted, however, that this term has several synonyms in the epidemiologic literature, including attributable risk, ∗ attributable proportion, excess fraction, etiologic fraction,∗ impact fraction,∗ and Levin's measure.

This article conceptually defines the attributable fraction and other impact measures, shows how they are estimated from population data, discusses how they are interpreted and sometimes misinterpreted, and demonstrates their use in public health practice. Before discussing these concepts in more detail, it is necessary to provide some background on the theory of causal inference in epidemiology.

Causal Inference in Populations

Measures of Effect and Counterfactuals

Much of epidemiologic research is aimed at making inferences about the net (causal) effect of one or more exposures on disease occurrence in a population. The dominant paradigm for defining such effects is the counterfactual or potential-outcomes model in which we contrast the frequency of disease (usually incidence) in the population under two or more exposure conditions such as everyone being exposed versus everyone being unexposed. Since individuals cannot be both exposed and unexposed simultaneously, at least one of those conditions is counter to fact or counterfactual. For example, suppose a group of Ne exposed persons at risk are followed without loss for a given period during which A new (incident) cases of the disease occur. Thus, therisk(Re)ofdisease in this exposed group is A=Ne. Thecentralcausal question is how many cases would have occurred during that period if no one in that population had been exposed. Suppose that counterfactual number is A0. Therefore, the counterfactual risk in the exposed group is A0/Ne, and the causal risk ratio (RRe), a measure of the exposure effect, is (A/Ne)= (A/0=Ne) = A= A0: If RRe > 1, the exposure is called acausalorpositive risk factor for the disease in that population; if RRe < 1, the exposure is called a protective or negative risk factor. It should be noted that without knowledge of biological mechanisms, this distinction between a causal and protective risk factor is generally arbitrary since exposure statuses can be reversed. For example, inferring that an active lifestyle is a protective risk factor for coronary heart disease is equivalent to inferring that a sedentary lifestyle is a causal risk factor.

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