The ongoing toll from Hiroshima and Nagasaki disputes your interpretation of that laboratory work. Finding a repair mechanism that is behaving differently than expected doesn't mean the reality of an observed no lower threshold. In fact the two studies seem completely congruent:
The linear dose-response relationship provided the best fit for the ERR data across the entire dose range, but a concave curve was the best fit for data restricted to dose < 2 Gy. This resulted because risk estimates for exposure to around 0.5 Gy were lower than those in the linear model.
But we are fortunate, aren't we? I mean now we have another real world laboratory provided by the nuclear industry in NE Japan that has a much greater sample size. We can follow these population groups for the next 100 years and count how many die and re-re-reconfirm what is already glaringly obvious.
"Excess relative risk (ERR) for all solid cancer mortality showed a linear dose-response relationship over the entire dose range, with no threshold observed, with the lowest dose range with significant risk for all solid cancers 0 to 0.20 Gy. The risk of all solid cancer mortality at the age of 70 years after exposure to 1 Gy at age 30 was 42% higher than that for unexposed individuals, increasing by about 29% per decade decrease in age at exposure. With regard to site-specific cancers, significant increase in cancer risk was observed for stomach, lung, liver, colon, breast, gallbladder, esophagus, bladder, and ovary, whereas rectum, pancreas, uterus, prostate, and kidney parenchyma did not have significantly increased risk. Increased risks of non-cancer diseases including those of the circulatory, respiratory and digestive systems were observed, but whether there was a causal relationship with radiation requires further investigation."
We followed the Life Span Study cohort during the period from 1950 through 2003 and elucidated effects of A-bomb radiation on mortality and causes of death using the DS02 dosimetry system. Excess relative risk (ERR) for all solid cancer mortality showed a linear dose-response relationship over the entire dose range, with no threshold observed, with the lowest dose range with significant risk for all solid cancers 0 to 0.20 Gy. The risk of all solid cancer mortality at the age of 70 years after exposure to 1 Gy at age 30 was 42% higher than that for unexposed individuals, increasing by about 29% per decade decrease in age at exposure. With regard to site-specific cancers, significant increase in cancer risk was observed for stomach, lung, liver, colon, breast, gallbladder, esophagus, bladder, and ovary, whereas rectum, pancreas, uterus, prostate, and kidney parenchyma did not have significantly increased risk. Increased risks of non-cancer diseases including those of the circulatory, respiratory and digestive systems were observed, but whether there was a causal relationship with radiation requires further investigation.
1) This report covers an additional six years of follow-up since the 13th LSS report was published in 2003. This is the first time the DS02 dosimetry system has been used for estimating individual dose and comprehensively analyzing radiation risk by cause of death. The subject population consisted of 86,611 directly exposed A-bomb survivors with individual dose estimates available, from among the LSS cohort of about 120,000 people. During the follow-up period, 50,620 people died, a number representing 58% of the original population, including 10,929 solid cancer deaths.
2) ERR* at the age of 70 years after exposure at age 30 was 0.42/Gy (95% confidence interval : 0.32, 0.53), while excess absolute risk** was 26.4 persons/Gy /10,000 person-year.
3) Excess cancer deaths attributable to radiation exposure are estimated to account for more than half of all solid cancer deaths in the dose range of 2 Gy or greater, with the same being the case for about one-fourth in the range of 0.5 Gy-1 Gy and about one-twentieth in the range of 0.1-0.2 Gy.
4) The linear dose-response relationship provided the best fit for the ERR data across the entire dose range, but a concave curve was the best fit for data restricted to dose < 2 Gy. This resulted because risk estimates for exposure to around 0.5 Gy were lower than those in the linear model.
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