TOPICS 3: Types of Dose Effects
Lets take a little deeper look into the different types of dose effects.
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We mentioned Somatic Effects when we talked about the atomic bomb survivors. Somatic Effects are effects to cells of the body that are non-reproductive cells. When a cell becomes damaged, one of four things can happen to that cell:
- The cell can repair itself and continue on normally. The cells in the body are constantly being damaged by natural means. As long as the damage is not too severe, the cell has an effective method of repairing itself. This is the most common occurrence after damage.
- The cell does not repair itself but lives its normal life and then dies. However, in the meantime, it may alter function of the cell.
- The cell dies immediately.
- The cell mutates and then reproduces. The result of this could be a pre-cancerous cell that could develop into cancer.
A somatic effect happens to the body of the irradiated individual only. It cannot be passed on to that person’s children or any other future generations. For example, if you accidentally lost a finger, your children would not be born without that finger. Somatic effects would be things like skin reddening, hair falling out or cataracts.
A somatic effect is not an effect to an embryo or fetus. They have their own category that we will present later.
Patients that are undergoing radiation therapy for cancer are experiencing somatic affects when their hair falls out or they experience diarrhea.
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People have been mining for centuries, and it has been known for a long time that their incidence of lung disease, including cancer, is higher than normal. These are internal exposures, from breathing in mine dust. But lung cancer is also associated with external irradiation from the gamma-rays in the natural materials. No study has been able to differentiate between the internal and external exposures in miners.
But internal cancers can be created by external exposures. Again, x-rays was commonly used for medical treatments in the 1930s – 1950s. Enlarged thymus glands in children were irradiated with up to 300 rem (partial body) to successfully shrink the tissue. Due to the proximity, the thyroid was also irradiated. A higher incidence of tumors was observed for this group of exposed children much later in life. Children were also similarly treated for ringworm of the scalp. Over 10,000 immigrant children were treated in Israel. The dose was high enough to cause temporary loss of hair. Again, the sensitive thyroid was also irradiated as collateral damage. The incidence of malignant thyroid tumors was 6 times greater than normal in this group as they aged. Over 2,000 people were also treated in New York using the same method resulting in excess brain cancer, leukemia, and benign thyroid tumors, but no excess in thyroid cancer, possibly due to differences in the treatment techniques.
As we have seen, thyroid cancer had been well-documented in children who underwent x-ray treatment for enlarged thymus glands, acne, and ringworm of the scalp. There were also cases due to internal exposures from inhalation of fallout from atomic bomb testing in some populations but not in all. The latency period is on the order of years. An increase in thyroid cancers was also observed in Ukrainians exposed as children to the radioactive materials drifting and settling after the Chernobyl accident.
Life-shortening effects have been experimentally observed in animals. Basically animals irradiated at high acute doses may recover and eventually die for the same reasons, as normally expected, but sooner than expected. At low doses, radiation-induced life shortening is simply the result of increases in leukemia and cancer. No definitive life-shortening has been observed in human populations, including the atomic bomb survivors.
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Radiation can also damage the chromosomes causing breaks and incorrect repairs, which can be detected in blood samples through a microscope. The types and frequencies of these chromosome problems give us an estimate of the severity of radiation dose. When a chromosome breaks it reunites in most cases, but not all cases. In a small fraction of cases, the broken fragments may be lost and insufficient information is carried forward during cell division. Or, broken chromosomes may exchange fragments resulting in abnormal chromosomes. These abnormal or aberrant chromosomes have impaired reproductive capacity and other problems.
We know that biological repair mechanisms are effective at low doses and dose rates, but there is evidence that they can be overwhelmed at high dose rates.
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Genetic Effects are effects that are passed on from one generation to another. We know that radiation damage to cells interferes with the normal development process. The main effects of in utero irradiation are prenatal death, growth retardation, and congenital malformations (teratogenesis). An embryo that is not yet implanted in the uterine lining is most sensitive to radiation and will develop no further. But an embryo is less likely to have other effects if it survives the early irradiation (0-9 days post conception). From 10 days to 6 weeks post-conception, the organs are forming and the embryo is most susceptible to teratogenic effects if it is exposed to radation. The fetal stage is from 6 weeks to term. The highest degree of permanent growth retardation is found due to irradiation during this stage of development.
Inherited genetic effects of radiation have not been observed in humans. This is possibly due to the fact that there would be nothing unique about them that could be distinguished from the mutations and chromosomal aberrations that happen normally. Consequently, the theoretical risk factors for hereditary effects are even smaller than for cancer.
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About 270,000 people have been monitored in the surviving population from the atomic bombings. Their doses range from background to several hundred rad. Numerous genetic indicators have been investigated, but nothing has been found to distinguish the atomic bomb survivors from non-exposed individuals. The Japanese atomic bomb victims exposed to high radiation doses have had more than 80,000 children and grandchildren. Under extreme monitoring of these and 27,000 non-exposed persons in a comparison group, there have been no detectable increases in hereditary damage that could be used to define a risk factor.
The Nagasaki and Hiroshima atomic bombs created in-utero effects on unborn babies of some adult survivors. It is not genetic in nature, since the deformities did not result from genetic damage to reproductive cells, and those victims do not pass on their deformities to their offspring. For bomb victims exposed in utero, the risk of small head size and mental retardation increased with increasing dose. The risk of mental retardation is greatest when the exposure occurred between 8 and 17 weeks post conception. This is when the number of neurons is rapidly increasing and moving to their permanent locations in the developing brain. For those exposed earlier than 8 weeks or later than 25 weeks post conception, no mental retardation was observed.
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Genetic Effects
Mutations can be induced in any cell but those induced in reproductive cells are the only ones that could be passed on to future generations. Radiation does not produce unique mutations, but can increase the occurrence of known mutations in a population. The mutations we are talking about are changes to genes that reside in chromosomes within the nucleus of a cell. Genes are segments of DNA that determine traits, structures, and functions of the body. Mutations occur naturally all the time, mostly from chemical actions and only about 5% of the time from natural radiation. Damage to a single base pair of the DNA molecule can result in a point mutation (point meaning a single gene). But remember, most of the time the DNA can repair itself.