ETIOLOGIC EVIDENCE AND PRIMARY PREVENTION OF CANCER

Abstract

For many decades, primary prevention of cancer was implemented on the basis of evidence for a causal relationship between exposure and human cancer that took into consideration biological plausibility, but did not depend on the degree of understanding of the underlying mechanisms. One of the credos of public health is that primary prevention can be implemented before reaching a complete understanding of mechanisms that could confirm/explain causality. Measures of primary prevention are taken on the basis of what is recognized as causative factors of human cancer. The most authoritative lists of recognized human carcinogens are those compiled from the evaluations of carcinogenic risk carried out by the International Agency for Research on Cancer (IARC) and the evaluations that the U.S. National Toxicology Program (NTP) publishes in its periodical Report on Carcinogens. Knowledge of mechanisms is accumulating at a fast pace, and although it has not yet led to the definition of an efficient strategy for primary prevention for the majority of cancer cases, it may drive the scientific establishment toward a high-risk approach to prevention. The most reasonable and socially acceptable development of primary prevention should be the blending of a population approach; that is, the shifting of the distribution of risk factors across an entire population in a favorable direction (e.g., a general decrease of the levels of exposure to environmental carcinogens) with the high-risk approach that will concern individuals with extreme values of genetically determined weaknesses in the interactions with the environment.