Radiation Risk is Linear with Dose at Low Doses Essay

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Introduction

The research hypothesis presented by Chadwick and Leenhouts (p 8) was chronic exposure to low dose radiation induces cancer through breaking up the double stranded DNA and thus produces cellular mutations. The second research hypothesis was the dose-effect relationship for low dose radiation exposure is linear in pattern.

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Scientists and their assumptions about cancer

Brenner and colleagues (p 13761) pointed two questions as regards radiation induced cancer; first what is the minimum radiation dose required to induce cancer. The second question, what apt methods to use known facts as a starting point to draw inferences about radiation-induced cancers. They assumed that we still need large epidemiological studies.

Aurengo and colleagues (p 1-4), at the French National Academy of Medicine stated that epidemiological studies, even those carried on large populations, failed to show statistical significance in the rate of radiation induced cancer for doses lower than 100 mSv. They assumed, therefore, that cancer risks are low and considered that case controlled, and follow up studies might not provide the answer. They suggested that studies comparing geographical regions with high and low radiation exposure level with similar living conditions (as those under course in Kerala-India and in China) could provide the answer.

Cohen (p 1137) provided a simple explanation for the linear hypothesis of radiation induced cancer at low doses. The author assumed that if 100 rad of radiation exposure result in cancer risk, hypothetically assumed, R, then exposure to one percent of the dose should produce cancer risk of one per cent R. Thus, cancer risk 0 can never occur whatever small is the exposure dose. This argumentative evidence is questioned by recent radiobiological evidence, the bases of which are: 1- there is a constant probability that cellular mutation might take place whatever the dose or dose rate. 2- The carcinogenic process evolves similarly after initiation irrespective of the number of the number of DNA molecular effects in the nearby cells or tissue (Aurengo and others, p 1-4). The questions now are; do cells recover from radiation effects, does chronic exposure to small doses of radiation carry the risk of carcinogenesis and does the linear theory have enough support.

Recent radiobiological studies suggest that cells react to the accumulating effect of radiation by different methods (Aurengo and others, p 1-4):

  1. Combating the reactive oxygen species produced by radiation.
  2. Getting rid of injured cells by: A) apoptosis: It is one kind of cell death meant to make room for regenerated cells and to get rid of cells with damaged DNA to the point at which cancerous change becomes a possibility. Alternatively, B) Cell death at the time of mitosis, in case no cell repair occurs for radiation injury.
  3. Response of DNA repair on exposure to doses of 10 mSv or slightly higher.

Immune screening (immune-surveillance) cells as monocytes and lymphocytes are capable of getting rid of clones of transformed cells as evidenced in tumor cell transplants and in immune-therapy of some tumors.

However, this is not always the case as there is cumulative evidence in the literature demonstrating that exposure to radiation is related to increase cancer risk. In addition, this risk relates to period of exposure (chronological exposure) and dose of exposure. Moreover, there is neither a safe dose nor safe dose rate (Valentin p 1-3).

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Brenner (p 253), explained the purpose of the linear no threshold hypothesis. It is to estimate cancer risk on exposure to doses of radiation and obtain a secure fix point from which data can be inferred linearly down to the lowest dose desired. Besides, in contrast to Aurengo and others, Brenner assumed that, as we cannot quantify cellular mechanisms of repair and recovery from radiation effects or the immune surveillance mechanisms, the linear hypothesis stand as a tool to estimate cancer risk although those risks may be lower than predicted.

The Health Physics Society (p 1) report summarized the current situation. First, there is no need for quantitative assessment of health risks at exposure levels of 5 rem per year (1 rem equals 10mSv) or 10 rem per life time above that of exposure from natural sources. The Health Physics Society defined exposure from natural sources in USA as 5 rem for the first 17 years of life and 25 rem for lifetime (up to age 80 years old). Exposure to doses similar to naturally exposed to should receive qualitative assessment and close follow up. The society’s report stated that whereas there is considerable health risk with exposure to high dose radiation, health risk at doses between 5-10 rem (50 -100 mSv), which includes environmental and occupational exposure, are too small to consider.

Prophylaxis remains always a golden rule; in this context, the basic radiation safety measures of the University of North Carolina (p 5) stand suitable for nurses and perhaps radiation technicians. The basis of these measures is to keep radiation exposure as low as reasonably achievable, abbreviated as ALARA. Radiation exposure can be reduced by shortening exposure times, doubling the distance from a radiation source (this simply means reducing the dose to on fourth), and use of proper shielding.

Conclusion

There is evidence that radiation exposure predisposes to increased cancer risk. The dose- effect is generally linear-quadratic. In low dose radiation, the dose effect relationship is claimed to be linear, as there is still a debate as to the evidence supporting or opposing this hypothesis. The difficulties in determining the effect of low dose radiation is lack of quantification of the cellular defensive mechanisms to repair radiation effect as well as lack of conclusive epidemiological evidence. More large-scale epidemiological studies are essential to investigate the effect of low dose radiation exposure. Radiobiology research is still to provide an understanding to the effects of low dose radiation on the molecular and cellular levels. In the quest for that, a differentiation between the effects of low doses (less than 100 mSv) and very low doses (less than 10 mSv) is necessary. More attention to public health issues and to prophylaxis is indispensable. I cannot say that I agree with Chadwick and Leenhouts as conclusive evidence is lacking and there is still a debate on the linear hypothesis of the dose effect of low dose irradiation.

Works Cited

Chadwick K H and Leenhouts H P. “Radiation risk is linear with dose at low doses”. British Journal of Radiology. Vol. 78. 2005. p. 8-10.

Brenner, D J., Doll, R., Goodhead, D.T et al. “Cancer risks attributable to low doses of ionizing radiation: Assessing what we really know”. Proceedings of the National Academy of Sciences of the United States of America. Vol. 100 (24). 2003. p. 13761-13766.

Aurengo, A, Averbaeck, D, Bonnin, A et al. “Dose-effect relationships and estimation of the carcinogenic effects of low doses of ionizing radiation.” French National Academy of Medicine. 2005. Web.

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Cohen, B.L. “Cancer Risk from Low-Level Radiation”. American Journal of Roentgenology. Vol. 179. 2002. p. 1137-1143.

Valentin, J (Ed.). “The 2007 Recommendations of the International Commission on Radiological Protection.” Annals of the ICRP. Vol. 37 (2-4). 2007. p. 1-332.

Brenner, D.J and Sachs, R.K (2006). Estimating radiation-induce cancer risks at very low doses: rationale for using a linear no-threshold approach. Radiation Environ Biophys, 44, 253-256.

University of North Carolina Health Care System. “Radiation Safety Manual For Nursing Staff.” Web.

Burk, R. J (Ed.). “Radiation Risk In Perspective: Position Statement of The Health Physics Society”. 2004. Health Physics Society. Web.

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