In comparison with the non-exposed Japanese population, so far no statistically significant increase in the frequency of hereditary diseases has been observed in the children and grandchildren of atomic bomb survivors. For risk estimation, the effects of relatively strong irradiations thus have to be investigated in animal experiments and the effects of low radiation doses on humans, which cannot be recorded statistically up to now, have to be inferred from these results.
The International Commission on Radiological Protection ICRP assumes that the the parental radiation exposure to a single acute gonadal dose of 1 gray Gy leads to one additional severe disease caused by radiation-induced mutations in births. This genetic risk may last for up to two generations. Chronic radiation exposure may persist over several generations.
In this case it is assumed that, with a gonadal dose of 1 Gy one additional mutation, which causes a severe disease, occurs in births. When estimating the genetic radiation risk, a doubling dose of 1 Gy is assumed in the case of chronic exposure. In the case of acute radiation exposure the doubling dose is 0. Ionizing radiation-induced mutagenesis. Cancer 57 6—18 CrossRef Google Scholar.
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Ultraviolet and laser safety. Kranert, T. Mutation induction in V79 Chinese hamster cells by very heavy ions. J Radial. Stoll, U. Barth, N. Scheerer, E. Schneider, J. Schmidt, E. Hei, T. Mutagenic effects of a single and an exact number of a particles in mammalian cells. Backer H. Biostack, a study of the biological effects of HZE galactic cosmic radiation.
Google Scholar. ICRP Recommendations of the International Commission on Radiological Protection. ICRP 21 , No. Crompton, N. Increased mutant induction by very low dose-rate-irradiation.
Naturwissenschaften 72, — CrossRef Google Scholar. Barth, J. Inverse dose rate effect for the induction of 6-thioguanine 60 resistant mutants in V79S Chinese hamster cells by Co-rays. Lack of dose-rate effect for mutation by -rays in human TK6 cells. A build-up of this type of mutation can cause melanoma. Cosmic rays also fall on us from space but on earth they are insignificant in terms of causing cancer.
For astronauts this becomes a considerable problem. Chernobyl and accidental or otherwise leaks from radioactive sources damages DNA. At certain levels this type of radiation can produce double strand breaks see graphic 12 in the DNA molecule. Double strand breaks are difficult for the cell to repair. It can seep upwards into buildings constructed above the rocks. Some lung cancers are associated with radon gas but in the worst affected areas building regulations require that buildings are specially ventilated below floor level.
Public Health England has information and excellent maps about radon distribution. Graphic Problems can start when a chemical in tobacco smoke binds with part of the DNA to produce an adduct structure. Smoke from open solid fuel fires used for cooking can also generate mutagenic chemicals.
This is a cause of lung cancer in some countries. Fortunately a vaccine against HPV is available and is now offered to young women and perhaps, soon, to young men.
Bacteria that are foreign to humans can also alter the microenvironment around cells. An inflammatory site presents a good ecological niche which is conducive to cancer cells developing, and where they can keep dividing. Stomach cancer is an example of this. Helicobacter pylori bacteria create the inflamed microenvironment.
The preservatives in some foodstuffs can contribute to the formation of some types of cancer. This is mainly through chemicals in food reacting with chemicals in the gut, and their effect on specific genes.
Sodium nitrite for example is included in processed meats to preserve them. Unfortunately sodium nitrite reacts with acids in the stomach to form carcinogenic chemicals called nitrosamines.
Eating too much red meat increases the level of haem protein containing iron in the body. In people with a deleted APC gene, an increase in haem level switches on a specific wnt signalling pathway and this results in uncontrolled cell division. Charred food such as that produced on a smoky barbeque, can also produce mutagenic chemicals.
An example of this is the chemical aflatoxin which binds to DNA and prevents normal replication. Aflatoxin is produced by a mould growing on peanuts.
The workplace can contain mutagenic and carcinogenic substances and factors that are associated with cancer development. Mutagenic substances and factors can cause mutations alterations in the DNA code. Carcinogenic substances and factors are also associated with cancer, but do not directly cause mutations.
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