Radiation exposure: cancer risk in middle age

November 04, 2010 04:50 pm | Updated 04:51 pm IST

Stark reminder: The Atomic Bomb Dome is silhouetted in the sky beside the Peace Memorial Park in Hiroshima. Researchers reanalyzed the Japanese A- bomb survivor data and assumed two different pathways through which radiation exposure can lead to cancer.

Stark reminder: The Atomic Bomb Dome is silhouetted in the sky beside the Peace Memorial Park in Hiroshima. Researchers reanalyzed the Japanese A- bomb survivor data and assumed two different pathways through which radiation exposure can lead to cancer.

Study of the data on A-bomb survivors continues to throw surprises.

An interesting analysis published in the Journal of the National Cancer Institute (25 October 2010) revealed that contrary to common assumptions, the risk of cancer associated with radiation exposure in middle age may not be lower than the risk associated with exposure at younger ages. The study is important as most of the diagnostic studies and occupational radiation exposures occur at middle age. However, if all radiation exposures are As Low As Reasonably Achievable (ALARA), there is no reason to worry.

Latent period

Children are more sensitive than adults to the effects of radiation as the cells in the body are dividing rapidly. Generally, cancer is induced after a latent period. Since children have longer life than adults, they have a greater chance of developing radiation-induced cancer than adults. Some data also suggest that, in general, the older a person is when exposed to radiation, the lower their risk of developing a radiation-induced cancer.

Recent analysis of the statistical evidence from long-term studies of atomic bomb survivors in Japan indicates that for radiation exposure after about age 30, the risk of developing radiation-induced cancer does not continue to decrease. This was not consistent with earlier studies.

Two pathways

Dr.David J. Brenner, at Columbia University in New York, and colleagues reanalyzed the Japanese A- bomb survivor data; they assumed two different pathways through which radiation exposure can lead to cancer.

Firstly, there may be the initiation of gene mutations that convert normal stem cells to premalignant cells that could eventually lead to cancer.

Second pathway

The second pathway assumes the existence of radiation induced promotion, or expansion, of the number of existing premalignant cells in the body. Researchers believe that the initiation effect is more likely to play a role in children than in adults; because cells initiated at an early age have a longer time available to proliferate and progress to cancer.

The promotion effect is more likely to be important for radiation exposures in middle age, because the adult body already contains larger numbers of premalignant cells.

Researchers developed a model based on these biological effects and applied it to the Japanese atomic bomb survivor data. The model reproduced the cancer risk patterns associated with age at radiation exposure observed in these survivors.

They applied the same model to predict cancer risks as a function of age in the U.S. population and found that the cancer risks predicted by the model were consistent with the data in the age range from about 30 to 60.

The authors argued that cancer risk after exposure in middle age may increase for some tumour types; this was contrary to what was known earlier.

Dr John D. Boice of the International Epidemiology Institute, Rockville, Md., and Vanderbilt University, Nashville, cautioned that there are uncertainties in generalizing the Japanese data to a U.S. population (Editorial in JNCI). According to him other data and other models contradict the results of this study.

Provocative hypotheses

He conceded that this biology-based model “raises provocative hypotheses and conclusions that, although preliminary, draw attention to the continued importance of low-dose radiation exposures in our society.”

Dr Brenner and colleagues concluded that overall, the weight of the epidemiological evidence suggests that for adult exposures, radiation risks do not generally decrease with increasing age at exposure, They noted that the mechanistic underpinning described here provides this conclusion with some biological plausibility.

Dr Brenner's papers may appear controversial; In 2003, he along with 14 eminent radio-biologists and epidemiologists concluded thus: “Given that it is supported by experimentally grounded, quantifiable, biophysical arguments, a linear extrapolation of cancer risks from intermediate to very low doses currently appears to be the most appropriate methodology.

This linearity assumption is not necessarily the most conservative approach, and it is likely that it will result in an underestimate of some radiation-induced cancer risks and an overestimate of others” ( Proceedings of the National Academy of Sciences, 2003 ).

The JNCI paper throws fresh light on the topic.

K.S. PARTHASARATHY

Raja Ramanna Fellow, Department of Atomic Energy

( ksparth@yahoo.co.uk )

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