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kristopher

(29,798 posts)
Sat May 12, 2012, 02:27 AM May 2012

dose-threshold analysis indicated no threshold - zero dose the best estimate of threshold

Ozasa, K., Shimizu, Y., Suyama, A., Kasagi, F., Soda, M., Grant, E. J., Sakata, R., Sugiyama, H. and Kodama, K.

"Studies of the Mortality of Atomic Bomb Survivors, Report 14, 1950–2003: An Overview of Cancer and Noncancer Diseases.
Radiat. Res. 177, 229–243 (2012)":

This is the 14th report in a series of periodic general reports on mortality in the Life Span Study (LSS) cohort of atomic bomb survivors followed by the Radiation Effects Research Foundation to investigate the late health effects of the radiation from the atomic bombs. During the period 1950–2003, 58% of the 86,611 LSS cohort members with DS02 dose estimates have died. The 6 years of additional follow-up since the previous report provide substantially more information at longer periods after radiation exposure (17% more cancer deaths), especially among those under age 10 at exposure (58% more deaths). Poisson regression methods were used to investigate the magnitude of the radiation-associated risks, the shape of the dose response, and effect modification by gender, age at exposure, and attained age. The risk of all causes of death was positively associated with radiation dose. Importantly, for solid cancers the additive radiation risk (i.e., excess cancer cases per 104 person-years per Gy) continues to increase throughout life with a linear dose–response relationship. The sex-averaged excess relative risk per Gy was 0.42 [95% confidence interval (CI): 0.32, 0.53] for all solid cancer at age 70 years after exposure at age 30 based on a linear model. The risk increased by about 29% per decade decrease in age at exposure (95% CI: 17%, 41%). The estimated lowest dose range with a significant ERR for all solid cancer was 0 to 0.20 Gy, and a formal dose-threshold analysis indicated no threshold; i.e., zero dose was the best estimate of the threshold. The risk of cancer mortality increased significantly for most major sites, including stomach, lung, liver, colon, breast, gallbladder, esophagus, bladder and ovary, whereas rectum, pancreas, uterus, prostate and kidney parenchyma did not have significantly increased risks. An increased risk of non-neoplastic diseases including the circulatory, respiratory and digestive systems was observed, but whether these are causal relationships requires further investigation. There was no evidence of a radiation effect for infectious or external causes of death.

http://www.ncbi.nlm.nih.gov/pubmed/22171960


The gray (symbol: Gy) is the SI derived unit of absorbed radiation dose of ionizing radiation (for example, X-rays), and is defined as the absorption of one joule of ionizing radiation by one kilogram of matter (usually human tissue).[1]
Named after the British physicist Louis Harold Gray, the SI unit replaces the traditional cgs unit, the rad (equivalent to 0.01 Gy), which remains common in industry in the United States, while "strongly discouraged" in the style guide for U.S. National Institute of Standards and Technology authors.[2]

http://en.wikipedia.org/wiki/Gray_(unit)



Paper published by Radiation Research* Studies of the Mortality of Atomic Bomb Survivors, Report 14, 1950–2003: An
Overview of Cancer and Noncancer Diseases


[Findings of this study]
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.

[Explanations]

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 [CI]: 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.

The Radiation Effects Research Foundation has studied A-bomb survivors in Hiroshima and Nagasaki for more than 60 years. RERF’s research achievements are considered the principal scientific basis for assessment of radiation risk by the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) and recommendations regarding radiation protection standards by the International Commission on Radiological Protection (ICRP).
Radiation Research, the official monthly journal of the US Radiation Research Society, publishes original and review articles dealing with radiation effects and related subjects in the areas of physics, chemistry, biology and medicine (impact factor in 2010: 2.578).
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caraher

(6,276 posts)
1. So this backs up the standard assumptions used for decades in radiation protection policymaking
Sat May 12, 2012, 10:51 AM
May 2012

Absent evidence of a threshold effect, let alone a protective effect, linear no-threshold models have always governed risk estimates. It's not surprising that this research backs up those models, since those models have always been based on earlier versions of this same research effort.

Failure to find a threshold and determining that a linear no-threshold model seems to work best surely undermines the claims of people who want to argue that linear no-threshold theories underestimate the hazards of low-dose radiation.

kristopher

(29,798 posts)
2. Typo?
Sat May 12, 2012, 11:16 AM
May 2012

Last edited Sat May 12, 2012, 12:23 PM - Edit history (1)

ETA: OK, I guess it isn't. I saw the conflict with the mainstream nuclear industry focus on DNA repair and the associated attempt to undermine LNT as most relevant - that goes to demonstrate our differing perspectives, eh?

"The estimated lowest dose range with a significant ERR for all solid cancer was 0 to 0.20 Gy, and a formal dose-threshold analysis indicated no threshold; i.e., zero dose was the best estimate of the threshold."


When I see "zero dose was the best estimate of the threshold" I can't help but think it is an unusually clear statement that was included in the paper for a specific reason, don't you think?

PamW

(1,825 posts)
3. Threshold Effect HAS been found!!
Mon May 14, 2012, 10:57 AM
May 2012

The most up to date research out of the national laboratories show that there is a threshold effect due to the DNA radiation damage repair mechanism. This research was published in the prestigious Proceedings of the National Academy of Sciences:

http://newscenter.lbl.gov/news-releases/2011/12/20/low-dose-radiation/

Researchers with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab), through a combination of time-lapse live imaging and mathematical modeling of a special line of human breast cells, have found evidence to suggest that for low dose levels of ionizing radiation, cancer risks may not be directly proportional to dose. This contradicts the standard model for predicting biological damage from ionizing radiation – the linear-no-threshold hypothesis or LNT – which holds that risk is directly proportional to dose at all levels of irradiation.

“Our data show that at lower doses of ionizing radiation, DNA repair mechanisms work much better than at higher doses,” says Mina Bissell, a world-renowned breast cancer researcher with Berkeley Lab’s Life Sciences Division.“This non-linear DNA damage response casts doubt on the general assumption that any amount of ionizing radiation is harmful and additive.

Costes and Bissell have published the results of their study in the Proceedings of the National Academy of Sciences in a paper titled “Evidence for formation of DNA repair centers and dose-response nonlinearity in human cells.” Also co-authoring the paper were Teresa Neumaier, Joel Swenson, Christopher Pham, Aris Polyzos, Alvin Lo, PoAn Yang, Jane Dyball, Aroumougame Asaithamby, David Chen and Stefan Thalhammer.

http://www.examiner.com/article/dna-repair-centers-fix-low-dose-radiation-damage

DNA repair centers fix low-dose radiation damage

PamW

kristopher

(29,798 posts)
4. Wrong way "Pam" strikes again - misrepresenting research.
Mon May 14, 2012, 02:20 PM
May 2012

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.




PamW

(1,825 posts)
5. BALONEY!!!
Tue May 15, 2012, 11:03 AM
May 2012

How do you study the low dose response when the study you are quoting is just extrapolating back from the large doses at Hiroshima and Nagasaki.

How can you claim, as you did in your first sentence above; that the results of very high doses at Hiroshima somehow constrains what happens at very low doses where one sees thresholds.

Hiroshima gave a ZERO data at low doses; because the Hiroshima doses were high.

So how can you then logically make the statement in your first sentence above. The scientific fact is you can't; it's unsupportable.

On my side, we have a study from top researchers at a top national lab, which was reviewed by the National Academy of Sciences and found worthy to publish in their Proceedings.

The study I'm referring to has the scientific pedigree as opposed to the "junk science" to which you refer.

PamW

kristopher

(29,798 posts)
6. Wrong way "Pam" strikes again - yet again misrepresenting research.
Tue May 15, 2012, 11:25 AM
May 2012

Specific to radiation studies it is difficult to get a more credentialed "scientific pedigree" than the journal "Radiation Research, the official monthly journal of the US Radiation Research Society, publishes original and review articles dealing with radiation effects and related subjects in the areas of physics, chemistry, biology and medicine (impact factor in 2010: 2.578).


As for the "scientific pedigree" of the authors originating the study:
"The Radiation Effects Research Foundation has studied A-bomb survivors in Hiroshima and Nagasaki for more than 60 years. RERF’s research achievements are considered the principal scientific basis for assessment of radiation risk by the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) and recommendations regarding radiation protection standards by the International Commission on Radiological Protection (ICRP)."


FBaggins

(26,696 posts)
7. You DO understand that a higher impact factor is better than a low one, right?
Tue May 15, 2012, 12:00 PM
May 2012

PNAS is usually in the high 9's and you're calling a 2.6 "difficult to get a more credentialed scientific pedigree" ???

As if IF is a measure of credentials in the first place.

kristopher

(29,798 posts)
8. Interesting how you cover your ass with that schizophrenic post.
Tue May 15, 2012, 12:14 PM
May 2012

Impact factor isn't a rating of the quality of a journal unless it is looked at in light of how large the specific field of research is that a given article relates to; and how broad the range of articles the publication handles.

Since the "impact factor" only rates citations, it cannot be used to draw a legitimate comparison between a journal dedicated to a very narrow field of research and a journal that is dedicated to a broad range of research interests.

You are starting to remind me of that old joke, "How do you know a lawyer is lying?"

The paper in the OP is questioned by no one except wild eyed nuclear supporters trying to stir up crap. It's antecedents are impeccable.

PamW

(1,825 posts)
9. Kris shows again he is NOT a SCIENTIST
Wed May 16, 2012, 12:15 AM
May 2012

Kris,

You have just shown again that you are not a scientist; because you don't know the ordering of the esteem to which journals are held.

The Proceedings of the National Academy of Science is THE most prestigious scientific journal in the USA.

What you are saying is akin to saying, "This order came from a lieutenant, but that one came from only an admiral" I consider this lieutenant's order to be much higher priority than that other order which only came from an admiral.

Keep going Kris - do post more. My scientist colleagues are LAUGHING themselves SICK at your failed attempts to be scientific.'

Why don't you give up attempting to be scientific, and stick with what you know; which is......????

PamW

kristopher

(29,798 posts)
10. Wrong way "Pam" with more misdirection (and evidence of his style of "science")
Wed May 16, 2012, 10:22 AM
May 2012

There is no conflict between the articles on the point you are claiming "Pam".

The NAS paper: “Our data show that at lower doses of ionizing radiation, DNA repair mechanisms work much better than at higher doses ... This non-linear DNA damage response casts doubt on the general assumption that any amount of ionizing radiation is harmful and additive.”


The Radiation Research paper: 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.


The NAS paper takes the implications of their findings too far. It might be what explains the concave curve, however it does not establish a lower threshold.

Your unending litany of misinformation and false claims are pathetic, "Pam".

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