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20 February 2019 ..:: Cancer » State of the art ::..   Login
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Cancer accounted for more than 7 million deaths worldwide in 2000, and 10 million new cancer cases were diagnosed. More than 60% of cancer deaths occurred in the developing regions. Lung cancer was the most common, followed by cancers of the stomach, liver, colon and rectum, and breast. Cancer in all ages is a result of the interaction between genetic and environmental factors. Differences in lifestyle and environmental exposures have been assumed to be a major reason for the various geographical distribution of cancer. Genetic factors, and ethnic variations account for some part of regional differences (EEA report 10/2005).

Environmental factors are important in the pathogenesis of cancer, but if lifestyle-related environmental factors are excluded, the only environmental factor for which there is a proven connection to cancer development is ionising radiation: The carcinogenic effect of it arises through direct damage to DNA. The connection between non-ionising radiation and skin cancer is also well established: Approximately 80-90% of all skin cancers can be related to UV radiation.

There has been speculation, that long-term, low-dose exposure to both low and higher frequency electromagnetic fields can cause health effects. Indeed recent pooled studies showed a correlation between low frequency electromagnetic fields and childhood leukaemia. However, the mechanisms by which weak and low frequency electromagnetic fields could cause leukaemia are not understood, and so the evidence is not conclusive.

Some chemicals clearly cause cancers in some exposed groups, but the role of chemicals in overall cancer causation is unclear and disputed (Epstien, 1998). Any excess cancer mortality from a chemical pollutant is likely to be restricted to a section of the population, so mortality rates for entire populations can often be weak and insensitive indicators of environmental health effects from pollution. The other cause is, that people are exposed to many different substances and their breakdown products via indoor and outdoor pollution from several pathways, including air, water, food and passage through the skin. Furthermore, there are usually large gaps in time between an exposure to a chemical, the observation of possible ill effects, and a medical or scientific assessment about association and causation.

Air pollution includes carcinogenic chemicals such as benzene and polycyclic aromatic hydrocarbons (PAH). Several studies showed a positive association between local traffic density and childhood leukaemia. There are only a limited number of studies evaluating the potential risk of living nearby hazardous industrial sites, which may also be a source of carcinogenic chemicals. Fried and smoked food items may contain carcinogenic substances as well.

Cancer in European children younger than 15 years is in general terms rare but is still one of the most common causes of death in children in industrialised countries. The most common childhood cancers are leukaemia and brain tumours. A small but significant increase in childhood cancers has been noted since the mid- 1980s, which could have been explained by better diagnostic methods, but an additional component from environmental exposures cannot be excluded (EEA-WHO, 2002).

Children are particularly at risk from chemicals because of their greater biological sensitivity and greater exposure to environmental pollution relative to body weight (McConnell, 1992). Although no specific parental occupational exposure was definitely established as a cause of childhood cancer, several occupations have been found to be associated with it: increased risk of brain cancer has been related to maternal exposure to high levels of solvents; increased, but not dose-related risk of brain tumours has been related to paternal exposure to PAH; and epidemiological studies have reported associations between childhood cancer, and either parental or childhood exposure to pesticides. Many studies suggest that most cancers in children are initiated before birth. Greater susceptibility of the foetus and young child has physiological reasons since they are undergoing multiple processes of growth and differentiation and the potential for mutations to arise following exposure to a carcinogen is therefore much greater in the growing foetus and child. Chemical pollutants that may affect reproductive health and newborn children include certain metals (e.g. lead and methyl mercury), pesticides (e.g. DDT), and industrial chemicals (e.g. PCBs). In addition, exposure to exogenous carcinogens in childhood may have an important effect on cancer risk in adult life.

Recent epidemiological studies have demonstrated the important role of genetic susceptibility in cancer development. Individual susceptibility to cancer may result from several host factors including differences in metabolism, DNA repair, altered expression of protooncogenes and tumour suppressor genes, and nutritional status (Bartsch et al, 1996). Since most carcinogens require metabolic activation before binding to DNA, individual features of carcinogen metabolism may facilitate or help to block the development of environmental cancer.

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