Summary
Cancer is a complex issue that has been the subject of observation and research for many disciplines which have investigated the different aspects of cancer aetiology. The predominant theory for the past 50 years has been that cancer is the result of cumulative mutations that alter specific locations in a cell’s DNA and which alter the proteins encoded by cancer-related genes. Susceptibility to mutation has been mainly researched with respect to people’s genetic make up and their lifestyles, which are largely dictated by behavioural patterns. However, a growing body of scientific evidence strongly implicates the environment in the causation of cancer. Findings from studies of wildlife, cancer trends, human migration, childhood cancer, twinning and industrial accidents suggest that concentrating solely on genetic origin and behavioural pattern as causes of DNA defects, and consequently the main causes of cancer, needs to be re-evaluated. There is now clear scientific evidence implicating exposure to radiation and man-made chemicals as major causes of mutation. In addition there is evidence that non-genotoxic mechanisms causing tissue dysgenesis might be a significant aetiological mechanism during development and this must become an element of any future re-evaluation.
DNA has a tremendous capacity for repair but if this fails for some reason, the DNA modified by carcinogen(s) may cause an abnormality in cell replication. The biological outcome cannot be predicted, as it is a result of the interaction of the exposure of an individual with his or her specific genome. Exposure of the individual to environmental carcinogens may start before birth, during critical periods of development, and this carries implications for the body’s natural defence system.
This paper applies the Bradford-Hill criteria for causation to the question of whether there is sufficient evidence to conclude in favour of the environment as a main cause of cancer in humans. The analysis shows that the current levels of pollution are more likely causally related to the rise of cancer incidence than they are not.
Different methodologies exist now to measure the impact of the environment on cancer. However, the quantification and evaluation of cancer risks in humans can only be performed on populations, e.g., as a consequence of environmental accidents. Furthermore, the idiosyncratic nature of individual human beings, associated with large random variations, makes such phenomena difficult to assess.
Policy on cancer and environmental exposure can be described both as simple and complex. Simple because the main target is to reduce exposure to carcinogens. Complex because of the economic and societal implications, and additionally because any benefits of imposing stricter controls cannot be immediately ascertained and are difficult to measure on a short-term basis. Therefore, policy to reduce exposure to carcinogens, and cancer in the long-term, shows increasing complexity in its principles, strategies and instruments. This concluding chapter overviews core issues in this cancer policy context: risk assessment, onus of proof and strict liability, a new authorisation policy for (potential) carcinogenic chemicals, economic instruments, communication and ethical aspects.
This should contribute to a revised, more effective cancer policy in the future, where more emphasis is put on involuntary exposure to carcinogens. Among them, carcinogenic environmental pollutants are of major importance.
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Nicolopoulou-Stamati, P., Howard, C.V., Gaudet, B.A.J. (2004). Re-Evaluation of Priorities in Addressing the Cancer Issue: Conclusions, Strategies, Prospects. In: Nicolopoulou-Stamati, P., Hens, L., Howard, C.V., Van Larebeke, N. (eds) Cancer as an Environmental Disease. Environmental Science and Technology Library, vol 20. Springer, Dordrecht. https://doi.org/10.1007/978-0-306-48513-8_9
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