Abstract
Primary prevention is based on the incontrovertible logic that a most efficient way to decrease the risk for a disease is to avoid, or reduce to minimal attainable levels, exposures to agents that can cause the disease or contribute to an increase in risk for the disease. This notwithstanding, the adoption of primary prevention measures has often encountered serious obstacles and unjustifiable delays. The success of primary prevention has also been limited by the combined effect of: (a) the inefficient and/or incomplete use of the cumulated etiological knowledge: (b) the spectrum of target organs for human carcinogens which does not include some of the most common cancer sites, a limitation that may be related to a disregard of epidemiological results and case reports that provide evidence that is less than sufficient of a causal relationship between an exposure and human cancer: (c) the pressure that powerful economic interests may have exerted in a variegated way to interfere or delay implementation of preventive measures that could have decreased their profit, and (d) the decreased acceptance of the ability of experimental results to predict similar effects in humans, in spite of the evidence that positive carcinogenicity results in experimental animals have often preceded and could indeed have predicted similar results in humans.
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