Late (Delayed) 

Effects of Radiation Effects of Radiation

10/25/2010
Contents

General

Late Effects (Delayed Effects)Types of Late EffectsImportant References

Stochastic Effects

GeneralThe Nature of Cancer

Deterministic (non stochastic) Effects

General
Contents

Somatic Stochastic Effects

Hiroshima and Nagasaki Life Span StudyMathematical Model of RiskAdditive (absolute) Risk ModelMultiplicative (relative) Risk ModelDose Response RelationshipThe “Standard” Extrapolation ApproachThe Standard Extrapolation ApproachAn “Anti-nuke” Extrapolation ApproachA “Pro-nuke” Extrapolation ApproachDose and Dose Rate Effectiveness FactorRisks to WorkersPrimary Cancers Induced by RadiationLeukemiaBreast Cancer
Contents

Somatic Stochastic Effects continued

Lung CancerCancer of the Digestive TractUNSCEAR 1988 Risk EstimatesUNSCEAR 2000 Risk EstimatesUNSCEAR 2006 Risk EstimatesBEIR V Risk EstimatesBEIR V Risk EstimatesBEIR VII Risk EstimatesNCRP 126 Risk EstimatesICRP 60 Risk EstimatesICRP 103 Risk Estimates
Contents

Somatic Deterministic Effects

GeneralCataracts

Hereditable Effects

GeneralBEIR Risk EstimatesBEIR Risk EstimatesBEIR V Risk EstimatesBEIR VII Risk EstimatesUNSCEAR 2001 Risk EstimatesICRP 60 Risk EstimatesICRP 103 Risk Estimates
Contents

Fetal (in utero) Effects

GeneralCancerMental RetardationDecreased IQMalformations

Appendix A: Ways to Express Risk

Relative Risk (RR)Excess Relative Risk (ERR)Excess Absolute Risk (EAR)

Appendix B: ICRP Detriment

General

Appendix C: Loss of Life Expectancy

General
General
General

Late Effects (Delayed Effects)

Delayed effects are usually considered to be thothat appear more than 2 months (in many casesafter the exposure.Depending upon the effect they can be produce

.

Depending upon the effect, they can be produceacute or chronic exposures.One type of delayed effect is considered possible with the smallest of exposures. The other types ooccurs if the dose exceeded a threshold value
Radiation da

cell goes unmost importasuch damagto be chromo

Cell Death

Mainly due to DNA double strand breaks and 

l i h l b i C ll i h

Cell L

Damage insufficie

ll b li i 

resulting chromosomal aberrations. Cells might 

survive but are nonfunctional (fibrotic).

cell metabolism im

divides and producmalfunctioning cel

Late Stoch

Early Effect

Death of cells with short cell cycle. The more rapidly the cells divide, the shorter the latent period.

Late Effect 

Deterministic 

Death of slowly dividing cells. Cells survive longer since a longer time passes before cell divides. This creates a long latent period.
General

Types of Late Effects (Delayed Effects)

Late effects are classified as: Somatic

Hereditable (geneFetal (in utero)Fetal (in utero)

They can also be classified as: Stochastic

Deterministic 
General

Types of Late Effects (Delayed Effects)

Somatic Effects

These occur in the exposed individual. 

Hereditable (genetic) Effects

These occur in the offspring of the exposed ind

Fetal (in utero) Effects

These effects occur in those who were expose
General

Types of Late Effects (Delayed Effects)

Somatic Effects might be: Stochastic

Deterministic

Hereditable (genetic) Effects are: Stochastic onlyFetal (in utero) Effects might be: Stochastic

Deterministic
General

Important ReferencesBEIR VII. Health Risks from Low Levels of Ionizing (2005) .ICRP Publication 103. The 2007 Recommendations International Commission on Radiological ProtectioInternational Commission on Radiological Protectio

NCRP No.126. Uncertainties in fatal Cancer Risk Eused in Radiation Protection. 1997.NCRP No. 136. Evaluation of the Linear-NonthreshResponse Model for Ionizing Radiation. 2001.
General

Important ReferencesUNSCEAR 2001 Report. Hereditary effects radiatioUNSCEAR 2006 Report Volume I. Effects of IonizinRadiation. Annexes A and B.UNSCEAR 2006 Report Volume II. Effects of IoniziRadiation. Annexes C,D and E.
Stochastic Effects
Stochastic Effects

GeneralThe only stochastic somatic effect is cancer. Stochastic effects are those whose probability of ocincreases with dose. We cannot say that a stochastwill definitel

y occur or not occur, we can onl

y

give th

y , yg

probability of such an effect occurring.The greater the dose, the greater the number of ex

cells and the greater the chance one of them will suultimately result in cancer. This is why the probabiliteffects is related to dose.
Stochastic Effects

GeneralFor the purpose of radiation protection, stochastic eassumed to be possible at the smallest of doses. In other words, stochastic effects are not assumed thresholds, i.e. doses below which the effects will nWhether or not this assumption is valid is not knowThe severity of a stochastic effect is not increased bdose. The severity of a stochastic effect (i.e. cancedepends on its location and type, something that is independent of the dose. 
Stochastic Effects

GeneralSince the exposed cell must survive for these effecthe probability of stochastic effects decreases abovat which cell killing becomes significant. This dose the order of 300 to 400 rads. At such high doses, aceffects are a more immediate concern than cancer.The U.S. regulatory agencies limit the possibility of effects for workers by restricting the annual total effdose equivalent to 5 rem (0.05 Sv). The ICRP recommendation is to limit exposures to rems) over five years which more or less equates to per year.
Stochastic Effects

The Nature of CancerCancer is a non-contagious disease involving maligtissues of potentially unlimited growth. These tissueform discrete masses called tumors. In the case of a special type of cancer, no tumors are formed.Approximately one in five will die of cancer. Roughl

that many develop cancer. The older someone is, the more likely they are to dcancer.Not all types of cancer appear to be induced by radWhen a cancer has been induced by radiation, thernothing unique about it that identifies radiation as th
Stochastic Effects

The Nature of CancerCancer is a non-contagious disease involving maligtissues of potentially unlimited growth. These tissueform discrete masses called tumors. In the case of a special type of cancer, no tumors are formed.Approximately one in five will die of cancer. Roughl

that many develop cancer. The older someone is, the more likely they are to dcancer.Not all types of cancer appear to be induced by radWhen a cancer has been induced by radiation, thernothing unique about it that identifies radiation as th
Deterministic 

(Non

-Stochastic) Effects Stochastic) Effects
Deterministic (Non-Stochastic) E

GeneralDeterministic (non-stochastic) effects are those whoseverity, but not probability, increases with dose. Deterministic effects primarily result from cell killingdela

ys in cell division, cell sterilization, severe chany , ,

function, replacement of functional cells with fibrotic and damage to the supporting blood vessels can alimportant role. The result is the gradual atrophy of the tissue. In sothe loss of function may eventually reverse, e.g., a in glandular secretion may only be temporary if the tissue can be replaced by fully functional cells.
Deterministic (Non-Stochastic) E

GeneralDeterministic effects have a threshold dose below wwill not occur. In other words, it is possible to say theffect will definitely not occur at doses below the thand the effect will definitely occur above a certain dThis “threshold” is the dose (or range of doses) abothe severity of the effect is large enough to be diagnFor example, the severity of cataracts depends on number of cells in the lens of the eye that are killed

might killed below the threshold, but if not enough h

for cataracts to be observed we say that the effect hoccurred. 
Deterministic (Non-Stochastic) E

GeneralEarly (acute) effects are non-stochastic because thpimarily brought about by cell death. Late (delayed effects) can be deterministic or stochDeterministic late effects involve the death of slowl

y y 

cells, e.g. those in the liver.The U.S. regulatory agencies prevent deterministic workers by restricting the annual dose equivalent to tissue to 50 rem. The dose equivalent to the lens of restricted to 15 mrem. The ICRP does not employ deterministic limits.
Deterministic (Non-Stochastic) E

General

Frequency

of Diagnosis

%

Dose

Threshold

100

0

Severity

Dose

Seve

fo

0

Variation 

among 
Somatic Stochastic Effect
Somatic Stochastic Effects

Hiroshima and Nagasaki Life Span StudyOur current risk estimate of developing and/or dying due to an external exposure is primarily based on sthe survivors of those exposed at Hiroshima and Nai.e., the life span study (LSS). In the year 2000, 45% of the 86,611 survivors were Of the 10,127 deaths due to solid cancers, 479 werestimated to be due to radiation.Of the 296 deaths due to leukemia, 93 were estimadue to the radiation exposure.
Somatic Stochastic Effects

Hiroshima and Nagasaki Life Span StudyThe advantages of the LSS include:

• The large number of individuals (in the tens of th• The study group represents a typical population

and female young and old healthy and infirmand female, young and old, healthy and infirm

• We have excellent information concerning the m

history of the exposed individuals, i.e., what theand when.
Somatic Stochastic Effects

Hiroshima and Nagasaki Life Span StudySources of uncertainty in the LSS include:

• The individuals were exposed to large doses in 

time (acute exposures). Typical exposures to wothe public are much lower and delivered over a 

• Many of the exposed individuals experienced se

physical and mental trauma, disease and malnu

• There is some uncertainty concerning the individ

doses.

• The study is not complete (the entire study grou

die) before the study can be completed.
Somatic Stochastic Effects

Hiroshima and Nagasaki Life Span StudySources of uncertainty in the LSS include:

• The possibility that the risks observed to the Jap

population are different than those that would apother ethnic groups.The table on the next slide indicates the annual per 100,000 people in three countries (Shull 199these are baseline risks that do not involve radiaexposure.The major contributor to the differences is undolifestyle (e.g., diet, smoking, etc.), but a genetic contribution cannot be ruled out. 
Somatic Stochastic Effects

Hiroshima and Nagasaki Life Span Study

Cancer Sex Japan United Kingdom 

Bladder

Male 3.1 13.2 

Female 1.4 1.4 

Breast

Male --

Female 9.0 52.3 

Colon

Male 11.3 21.1 

Female 11.1 24.3 

Leukemia

Male 5.4 7.8 

Female 3.8 6.5 

Liver

Male 20.0 1.9 

Female 6.3 0.8 

Lung

Male 40.6 100.6 

Female 14.6 41.9 

Rectum

Male 8.5 2.8 

Female 5.8 10.0 

Stomach

Male 50 22.7 

Female 29.0 14.7 
Somatic Stochastic Effects

Mathematical Model of RiskThe total risk of developing or dying of a particular a cancer is the baseline risk (zero exposure) plus the risk.The excess risk is the risk due to the radiation expoThe excess risk is the risk due to the radiation expo

R = R

0 + Excess Risk

R is the total risk (e.g., cancer deaths/rem)R

0 is the baseline risk
Somatic Stochastic Effects

Mathematical Model of RiskWe sometimes estimate the risk of cancer at a speci.e. during a particular year or years:

R(a) = R(a)

0 + Excess Risk

R(a) is the total risk of the specific cancer at R

0 is the baseline risk of the cancer at age a
Somatic Stochastic Effects

Mathematical Model of RiskThere are many mathematical ways to model risk. Isimplest form they fall into two broad categories:

1. Absolute Risk Model

(aka time

-constant absolute or time

-constant ad

(aka time constant absolute or time constant ad

2. Relative Risk Models 

(aka time-constant relative or time-constant mul

This is the preferred model.
Somatic Stochastic Effects

Additive (absolute) Risk ModelThe excess risk (risk at age a) does not change, e.gfollowing an exposure at age 30, the excess risk is at ages 50 and 70 even though the baseline risk is age 70. No excess risk is attributed during a defined latent (often 10 years). Mathematically, the excess risk is product of the dose and a risk factor:

R(a) = R

0(a) + D x RISK FACTOR

D is the dose, e.g. rad, Gy Risk factor is the risk of cancer per unit dose, e.g. 
Somatic Stochastic Effects

Multiplicative (relative) Risk ModelThe excess risk increases with age in the same wabaseline risk increases with age. Therefore, the baseline risk R

0(a), is a component o

excess risk term in the following linear equation:excess risk term in the following linear equation:

R(a) = R

0(a) + R

0(a) x D x RISK FACTOR

This is the basic structure of the linear equation. The risk factor can depend on the sex (s), age at ex(e) and attained age (a).
Somatic Stochastic Effects

Multiplicative (relative) Risk ModelThe linear quadratic version of this equation might something the following: 

R(a) = R

0(a) + R

0(a) [

" D + 

$

D

2] 

Where the risk factors are indicated by 

" and 

$.

If we want to account for cell killing or sterilization adoses, the following linear quadratic exponential eqemployed:

R(a) = R

0(a) + R

0(a) [

" D + 

$

D

2] e

(

D
Somatic Stochastic Effects

Total Risk

R(a)

Latent

Period

Excess Risk Baseline 

R

0(a

Additive 

Risk Model

Age (a)

Latent

Period

Baselin

R

0(

Age (a)

Total Risk

R(a)

Multiplicative

Risk Model
Somatic Stochastic Effects

Dose Response RelationshipIn the atomic bomb survivor life span studies (LSS) statistically significant increase in deaths was obseabove 0.1 Gy (10 rads) or so. An increase in deaths was observed below 0.1 Gy An increase in deaths was observed below 0.1 Gy 

is no consensus as to whether or not they were stasignificant.The plot on the next slide is intended to convey the we are faced with when interpreting the data seen aHiroshima and Nagasaki – it is not based on real da
Excess 

Cancers

Somatic Stochastic EffectsDose Response Relationship

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7

Dose (Gy)

We are primarily interested in the risk at low doses 0.05 Gy), but there is no statistically significant data 

This forces us to extrapolate the risks at high doses dose region. How we do this depends on our “politi
Somatic Stochastic Effects

The “Standard” Extrapolation ApproachThe standard approach preferred by regulatory ageadvisory bodies (e.g., ICRP) is to employ the linear threshold approach. For some cancers (e.g., leukemlinear quadratic approach provides a better fit.

Excess 

Cancers

Dose 

Excess 

Cancers

Dos

Linear No Threshold (LNT) Linear - Qu
Somatic Stochastic Effects

An “Anti-nuke” Extrapolation ApproachAn anti-nuke might prefer to extrapolate using the smodel. In this case, the risk, which is the slope of th(deaths/Gy) , is greater at the low doses to which thexposed than it is at the higher doses seen at HirosNagasaki.

Excess 

Cancers

Dose 

Supralinear 
Somatic Stochastic Effects

A “Pro-nuke” Extrapolation ApproachA pro-nuke might prefer to extrapolate as follows. Abelow some value (usually unspecified) the numbedeaths goes negative. In other words, at low dosesexposures reduce the risk of cancer. This is known radiation hormesis.

Excess 

Cancers

Dose 

radiation hormesis.

Radiation Hormesis 
Somatic Stochastic Effects

Dose and Dose Rate Effectiveness FactoUnless corrections are made, the linear dose-respoassumes that the risk per unit dose (e.g., excess derem) is the same at low doses as at the high doses rates seen at Hiroshima and Nagasaki.There is reason to believe the cellular repair mechamore efficient at low doses and dose rates. If true, tunit dose is lower at low doses. To account for this, and more accurately estimate thlow doses, it is common to divide the risk observed span study (LSS) by the dose rate effectiveness fac(DREF). 
Somatic Stochastic Effects

Dose and Dose Rate Effectiveness FactoThe ICRP prefers to call this correction factor the ddose rate effectiveness factor (DDREF). The DDREF (or DREF) is the magnitude of the risk overestimate at low doses. ICRP Report 60 recommvalue of 2 (ICRP 60, p.18). The more recent ICRP continues to employ a DDREF of 2. The BEIR VII rprefers a value of 1.5.Unless stated otherwise, risks presented in the liter

not been adjusted with the DDREF. It is left to the redecide whether or not to divide the stated risk by th
Somatic Stochastic Effects

Dose and Dose Rate Effectiveness FactoThe DDREF is intended to be used with low LET ra(e.g., gamma rays, x-rays, beta particles and electrhigh LET radiation (e..g., neutrons). What constitutes the low doses and dose rates at wWhat constitutes the low doses and dose rates at w

DDREF can be applied? 

The ICRP considers a dose under 0.2 Gy (20 radand they consider low dose rates to be those undGy/hr (10 rads per hour). The BEIR VII report considers low doses to be tho0.1 Sv (10 rems). 
Somatic Stochastic Effects

Dose and Dose Rate Effectiveness FactoThe use of the linear-quadratic dose response relata model automatically assigns a lower risk per unit low doses. The DDREF should not be used with such a modelThe DDREF should not be used with such

a model
Somatic Stochastic Effects

Risks to WorkersThe risks to radiation workers tend to be 50 - 60% othe general public. The main reason is that the workforce has a smallerepresentation of the most s representation of the most sensitive ensitive age group, tho

age group, tho

20. In addition, the working population is healthier general population (healthy worker effect).As a result, the risks to the public are estimated sepfrom the risks to workers. 
Somatic Stochastic Effects

Primary Cancers Induced by RadiationThe LSS of the survivors of Hiroshima and Nagasaobserved an excess in a wide range of cancers. Nevertheless, the overall increased risk is primarily excess of four types of cancer: excess of four types of cancer:

• Leukemia• Breast cancer• Lung cancer• Cancer of the digestive system
Somatic Stochastic Effects

Leukemia Leukemia is a malignant disease of the blood formiIt involves a large increase in the population of leuk(granulocytes and lymphocytes). There is also a sureduction in the number of erythrocytes and plateleleads to an increased risk of hemorrhage and anemDespite the increase in the white blood cells, there increased susceptibility to infection. Leukemia is unique in that it doesn't involve the prosolid tumors. The baseline incidence is ca. seven per thousand i
Somatic Stochastic Effects

LeukemiaThe excess risk of leukemia begins to rise approximyears after the exposure. It peaks around 5 years after the exposure and theAfter 25 years or so, the rate of leukemia becomes for exposed and unexposed populations. The short latent period and the significant decrease with time following the exposure are not typical of ocancers. 
Somatic Stochastic Effects

LeukemiaAcute myeloid leukemia, the most commonly occurin the general population, is the most likely to result radiation exposures. On the other hand, chronic lymleukemia has never been associated with radiation Assuming a linear-quadratic dose response relationBEIR V committee estimated an excess risk probabapproximately 1 x 10-4 per rem. In other words, an e

of one rem carries a risk of approximately one in tethousand of developing a fatal case of leukemia. 
Somatic Stochastic Effects

LeukemiaThe UNSCEAR 2006 report estimates the risk of dea fatal case of radiation induced leukemia at two doranges:At a dose of 0.1 Sv: 3 to 5 x 10-3 Sv-1 (0.3

-0.5% 

At

a dose of 0.1 Sv:

3 to

5

x 10 Sv (0.3 0.5% 

10 rems: 3 to 5 x 10-5 rem-1

At a dose of 1 Sv: 6 to 10 x 10-3 Sv-1 (0.6-1.0

100 rems: 6 to 10 x 10-5 rem-1

These estimates have implicitly accounted for the D
Somatic Stochastic Effects

Breast CancerBreast cancer is the most common type of cancer iApproximately one in nine develop it, although it rain women younger than twenty-five.One concern with breast cancer is the possibility thmetastasize to another part of the body. Breast canespecially prone to spreading to the skeleton. The latent period for radiation induced breast canceestimated at 10 years with the rate of incidence pea20 years after the exposure. The time at which the of death peaks is 20 to 25 years after the exposureperiod, there is a slow decline in the risk. 
Somatic Stochastic Effects

Breast CancerThe BEIR V committee estimated the risk for those under the age of 20 to be four times the risk to thos20 and 40 and roughly ten times the risk to women age of 40. Women who have borne children and those who exlate menarche or early menopause are at lower riskThe BEIR V report estimated the excess risk at 0.7 

rem (0.7% Sv-1) while the UNSCEAR 88 report put 

0.6 x 10-4 per rem (0.6% Sv-1).
Somatic Stochastic Effects

Lung CancerLung cancer is a common form of cancer that can bby any number of chemical or physical irritants. It anever occurs in those under forty.Approximately 1.1% of male and 0.6% of female nosmokers die of lung cancer. For male smokers the risk is 12.3% and for female is 5.8%. If caught in the very early stages, the tumor might bsuccessfully removed with surgery. 
Somatic Stochastic Effects

Lung CancerRegarding radiation-induced lung cancer the age ais not a major factor. The risk decreases with time exposure, however. BEIR V estimated the risk at 1.9 x 10-4 per rem (1.9 BEIR

V estimated the risk at 1.9

x 10 per rem (1.9

for males and 1.5 x 10-4 per rem (1.5 % Sv-1) for femThe UNSCEAR 1988 average risk for males and fe1.5 x 10-4 per rem (1.5 % Sv-1).
Somatic Stochastic Effects

Cancer of the Digestive TractThe baseline incidence of stomach cancer appears influenced by both lifestyle and genetics. Diets rich smoked, pickled and salted foods predispose one tcancer. After leukemia, it showed the largest excess among survivors of Hiroshima and Nagasaki. ICRP 60 estimated the risk of fatal stomach cancer 10-4 per rem (1.1% Sv-1). The excess relative risk a

(1 Sv) is estimated at 0.23 and the corresponding ris 1.2.
Somatic Stochastic Effects

Cancer of the Digestive TractColon cancer can be characterized by anemia, loss and changes in bowel habits. It is most commonly oin those over forty. Roughly twice the incidence of ccancer was observed among the survivors of HirosNagasaki as among the control population. ICRP 6Nagasaki as among the control population. ICRP 6

estimated the excess risk for colon cancer at 0.85 x 

rem (0.85% Sv-1).

ICRP 60 estimated the risk for all components of thsystem to be 2.25 x 10-4 per rem (2.25% Sv-1). The 

report estimated the risk at 1.7 x 10-4 and 2.9 x 10-4 for males and females respectively, with an average 2.3 x 10-4 (2.3% Sv-1). 
Somatic Stochastic Effects

UNSCEAR 1988 Risk EstimatesThe overall risk of fatal cancer is 11 x 10-4 per rem 

Sv). This does not account for a decreased risk at l

UNSCEAR 2000 Risk Estimates

Male solid tumor fatalities: 9 x 10-4 per rem (9

Male leukemia fatalities: 1 x 10-4 per rem (1

Female solid tumor fatalities: 13 x 10-4 per rem (13

Female leukemia fatalities: 1 x 10-4 per rem (1

For chronic exposures, they stated that the estimatbe reduced by 50%. In other words, the DDREF waapplied to the indicated risks.
Somatic Stochastic Effects

UNSCEAR 2006 Risk EstimatesThe following fatal cancer risks, averaged over both are provided for two dose ranges. They are based oquadratic models so that an application of the DDRappropriate:

Acute Exposure of S( ) 0.1 

Sv 

(10 rems

)

Solid tumor: 3.6 to 7.7 x 10-4 rem-1 (3.6 to 7.7% 

Leukemia: 0.3 to 0.5 x 10-4 rem-1 (0.3 to 0.5% 

Acute Exposure of 1 Sv (100 rems):

Solid tumor: 4.3 to 7.2 x 10-4 rem-1 (4.3 to 7.2% 

Leukemia: 0.6 to 1.0 x 10-4 rem-1 (0.6 to 1.0% 
Somatic Stochastic Effects

BEIR V Risk EstimatesFor a mixed population and an acute exposure, BEestimated the risk of dying of radiation induced canabout 8 x 10-4 per rem (0.8% per 0.1 Sv). 

“For low LET radiation, accumulation of the same d

For low LET radiation, accumulation of the same d

weeks or months, however, is expected to reduce trisk appreciably, possibly by a factor of 2 or more.” 
Somatic Stochastic Effects

BEIR V Risk EstimatesMales

The risk for all cancers: 7.7 x 10-4 per rem (7.7% 

Broken down, the risk for leukemia was 1.1 x 10-

and for non leukemia cancers was 6 6 x 10-4 and for non

-leukemia cancers was

6.6

x 10-4 per 

per 

Females

The risk for all cancers: 8.1 x 10-4 per rem (8.1% 

Broken down, the risk for leukemia was 0.8 x 10-

and for non-leukemia cancers was 7.3 x 10-4 per 
Somatic Stochastic Effects

BEIR VII Risk EstimatesSolid cancer mortality averaged for both sexes (DD

5.1 x 10-3 per 0.1 Gy (5.1 x 10-4 per rad)

Leukemia mortality averaged for both sexes (DDRE

6.1 x 10-4 per 0.1 Gy (0.61 x 10-4 per rad)
Somatic Stochastic Effects

BEIR VII Risk EstimatesMales

Solid cancer mortality (DDREF of 1.5)

4.1 x 10-3 per 0.1 Gy (4.1 x 10-4 4.1

x 10 per 0.1 Gy (4.1

x 10 per rad) per rad)

2.9 x 10-3 per 1 mGy/y for life (2.9 x 10-3 per 100 

Leukemia mortality (DDREF of 1.5)

6.9 x 10-4 per 0.1 Gy (6.9 x 10-5 per 1 rad)

4.7 x 10-4 per 1 mGy/y for life (4.7 x 10-4 per 100 
Somatic Stochastic Effects

BEIR VII Risk EstimatesFemales

Solid cancer mortality (DDREF of 1.5):

6.1 x 10-3 per 0.1 Gy (6.1 x 10-4 6.1

x 10 per 0.1 Gy (6.1

x 10 per rad) per rad)

4.6 x 10-3 per 1 mGy/y for life (4.6 x 10-3 per 100 

Leukemia mortality (DDREF of 1.5):

5.2 x 10-4 per 0.1 Gy (0.52 x 10-4 per rad)

3.8 x 10-4 per 1 mGy/y for life (3.8 x 10-4 per 100 
Somatic Stochastic Effects – BEIR VII Risk Estim
Somatic Stochastic Effects – BEIR VII Risk Estim
Somatic Stochastic Effects

NCRP No. 126 Risk EstimatesThe following risk estimates identified in NCRP 126 same as in NCRP No. 116. These, in turn, are basrisk estimates of ICRP 60. They incorporate a DDR

5 x 10-2 Sv-15

x 10 Sv for a population of all ages for

a population of all ages

4 x 10-2 Sv-1 for adult workers

NCRP 126 discusses the uncertainties in these estsome detail.
Somatic Stochastic Effects

ICRP 60 Risk EstimatesICRP 60 rounded the UNSCEAR 88 and BEIR V es10 x 10-4 per rem (10% Sv-1) for high dose/ high do

When calculating the risk to the general population 

doses and low dose rates, ICRP 60 used a DDREF doses and low dose rates, ICRP 60 used

a DDREF 

This produced an overall risk of 5 x 10-4 per rem (5 

Sv) . For workers, the estimated risk was somewhat lowe

per rem (4 x 10-2 per Sv) . 
Somatic Stochastic Effects

ICRP 103 Risk EstimatesICRP 103 provides its risk estimates in terms of the (see Appendix B) rather than the risk of fatal cancerisks are higher than the risk of mortality alone becadetriment factors in cancer incidence and hereditabPopulation Exposure

5.5 x 10-2 per Sv (5.5 x 10-4 per rem) 

Worker Exposure

4.1 x 10-2 per Sv (4.1 x 10-4 per rem) 
Somatic Stochastic Effects

ICRP 103 Risk Estimates“It is therefore the recommendation of the Commissthe approximated overall fatal risk coefficient of 5% which current international radiation safety standardbased continues to be appropriate for the purpose oradiological protection. radiological protection.

”
Somatic Deterministic Effec
Somatic Deterministic Effects

GeneralAt the doses commonly experienced by radiation wthe public, the severity of non-stochastic effects is sto make them undetectable.
Somatic Deterministic Effects

GeneralThe following table is taken from ICRP 60.

Threshold for Selected Non-Stochastic Effects (rad

Tissue/Effect Single (acute) Ex

posure

Ann

E

Pro

p

m

Male Temporary sterility 15 

Permanent sterility 350 - 600 

Female Permanent sterility 250 - 600 

Lens of Eye

Detectable opacities 50 - 200 

Visual impairment 

(cataracts) 500 

Bone marrow Decrease in blood cell count 50 
Somatic Deterministic Effects

CataractsCataracts are one of the most important of the non-(deterministic) effects in man. Cataracts induced by radiation tend to develop on tposterior surface of the lens of the eye (posterior subcapsular) while the cataracts associated with oldiabetes, etc., tend to occur on the anterior surfacePosterior subcapsular cataracts can be induced by causes however, e.g., trauma.They might appear as soon as 10 months after an aexposure of 200 rads (2 Gy) or chronic exposures orads (10 Gy) from low LET radiation. 
Somatic Deterministic Effects

CataractsThe threshold is lower for high LET radiation: 75 raGy) or so.Neutrons, fast neutrons in particular, are especially at inducin

g cataracts.

The relative risk for radiation induced cataracts decwith age.
Hereditable Effects
Hereditable Effects

GeneralHereditable effects are those effects that occur in thdescendants of the exposed individual. The are alsto as genetic effects but hereditable is better since radiation effects are "genetic" in that they involve efthe genetic material in the chromosomes. the genetic material in the chromosomes.

The radiation damage, mutations or chromosomal aberrations, takes place in the reproductive cells of exposed individual. By reproductive cells we primarthe oocytes, spermatogonia and sperm cells. Heredeffects could occur if this damage is passed on to sgenerations. 
Hereditable Effects

GeneralChromosomal aberrations (rings, dicentrics, acentrfragments and inversions) in the reproductive cells type of DNA damage that is the most likely to result apparent abnormalities in the offspring. Effects due to mutations (genetic aberrations) that adominant or X-linked recessive mostly occur in the generations. Recessive mutations (unless X-linked) have almost in the first two generations but lead to an overall incthe genetic damage in the gene pool.
Hereditable Effects

GeneralWhile animal studies have indicated that genetic daradiation exposures can be passed on to subsequegenerations, there are no similar human studies.None of the offspring of survivors of Hiroshima and have shown effects that could be linked to the radiaexposures of their parents. Perhaps the best evidence that radiation induced mcan be passed on to subsequent generations in hupresented in a report in the journal Science (DubrovA gradual decrease in mutations was observed in sgenerations of the offspring of those who lived near Semipalatinsk nuclear test site in Kazakhstan. 
Hereditable Effects

GeneralIt has been reported that the children of radiation wthe Sellafield nuclear facility in England have an incrisk of leukemia. Caution must be used when assesreports because childhood cancer is rare and it only few cases to give the appearance of a greatly increfew cases to give the appearance of

a greatly incre

It is possible that the increased leukemia rate, if reaan increase in viral infections created by large scale immigration to the area. When large facilities like nuplants are built, the area experiences a wave of immand an concurrent increase in viral infections, a phethat has shown a link to the rate of leukemia.
Hereditable Effects

BEIR Risk EstimatesExcept for their risk estimates for congenital abnormwhich are based on mouse data, the BEIR committthe doubling dose concept to come up with their BEBEIR VII risk estimates.The doubling dose is the radiation dose that doubleof mutations. In both reports, it was assumed to be rads).Unlike the ICRP, they limit their risk projections to thgenerations.
Hereditable Effects

BEIR Risk EstimatesMultifactorial diseases are those that have a geneticomponent but are not “inherited” according to clasMendelian genetics. They occur because of a comgenetics and the environment (e.g., diet). Examples di b t d h t di di

a

b

e

tes an

d

hear

t disease.

Congenital abnormalities are those that are presen
Hereditable Effects

BEIR V Risk Estimates

Risk per Gray per Million Progeny at

Disease Class Baseline Frequency 

per Million Live Births

First 

Generation

Mendelian

Autosomal dominant 10,000 600 to 3500 

X-linked

Autosomal recessive

400 <100 

2,500 <100 

Chromosomal 4,400 <600 Multifactorial

Congenital abnormalitiesHeart diseaseCancerSelected others

20,000 to 30,000 1000 

600,000 NE300,000 NE300,000 NE 
Hereditable Effects

BEIR VII Risk Estimates

Risk per Gray per Million Progeny at

Disease Class Baseline Frequency per Million Live Births First Generation 

Mendelian

Autosomal dominant 

d X li k d

16,500 750 to 1500 

an

d

X

-li

n

k

e

d

Autosomal recessive

,

7,500 0 

Chromosomal 4,000

b

Multifactorial

Chronic multifactorialCongenital abnormalities

650,000

c 250 to 1200 

60,000 2000 

d 

Total 738,000 3000 to 4700 Total risk of baseline per gray as percent 0.41 to 0.64 
Hereditable Effects

BEIR VII Risk EstimatesNotes to previous table:a. Risk to second generation includes that of the f

generation

b.

Assumed to be subsumed in part under the risk 

autosomal dominant and X-linked diseases and under congenital (condition present at birth) abn

c. Frequency in the populationd. Calculated using mouse data on developmenta

abnormalities without using the doubling dose m
Hereditable Effects

BEIR VII Risk EstimatesThe risk estimate equation used in BEIR VII is:

Risk per unit dose = P x (1/DD) x MC x 

P i th b li f f th di l P is the 

baseline 

frequency o

f the disease class

DD is the doubling dose MC is the mutation component for that disease PRCF is the potential recoverability correction facto
Hereditable Effects

BEIR VII Risk EstimatesAutosomal Dominant and X-Linked

P = 16,500/10

6

DD = 1 GyMC

= 0 3 for first generation and 0 51 for the sec

0.3 for first generation and

0.51 for the sec

PRCF = 0.15 to 0.30

Chronic Diseases

P = 650,000/10

6

DD = 1 GyMC = 0.02PRCF = 0.02 to 0.09
Hereditable Effects

UNSCEAR 2001 Risk EstimatesUNSCEAR 2001 estimates the risk of hereditable eusing the same doubling dose approach and equatBEIR VII. They even use exactly the same values fdoubling dose, baseline frequency, mutation comppotential recoverability correction factor! potential recoverability correction factor!Quoting the report: “For a population exposed to raone generation only, the risks to the progeny of the radiation generation are estimated to be 3,000 to 4per gray per one million progeny; this constitutes 0.to 0.6 per cent of the baseline frequency of those din the human population.”
Hereditable Effects

ICRP 60 Risk EstimatesICRP 60 estimated the detriment for all generations x 10-4 per rem. Dominant and X-linked mutations ar

to be responsible for 80% of these effects.

The detriment for multifactorial effects was estimateThe detriment for multifactorial effects was estimate

10-4. Multifactorial effects have a genetic componen

not occur unless certain environmental conditions eTherefore, the total risk estimate for the general po1 x 10-4 per rem. 

When the ICRP took into account the years of life lo

descendants, the risk increased to 1.3 x 10-4. 
Hereditable Effects

ICRP 103 Risk EstimatesAs was the case with somatic effects, ICRP 103 prothese risk estimates in terms of the detriment (see AB) which factors in cancer incidence as well as canmortality. ICRP 103 uses the same mathematical aestimating the risks as BEIR VII and UNSCEAR 20estimating the risks as BEIR VII and UNSCEAR 20Population Exposure

0.2 x 10-2 per Sv (0.2 x 10-4 per rem) 

Worker Exposure

0.1 x 10-2 per Sv (0.1 x 10-4 per rem) 
Hereditable Effects

ICRP 103 Risk EstimatesThe ICRP 103 risk estimates for hereditable effects factor of 6-8 lower than those of ICRP 60.The reduced genetic risk has resulted in a significareduction in the tissue weighting factors for the gonreduction in the tissue weighting factors for the gon
Fetal (in utero) Effects
Fetal (in utero) Effects

GeneralIn order to minimize the risk to the fetus, the U.S. NRegulatory Commission limits the dose during the epregnancy to 0.5 rems (5 mSv).This section considers the following risks due to a fThis section considers the following risks due to a f

exposure:

CancerMental RetardationDecreased IQMalformations
Fetal (in utero) Effects

CancerAs noted in the BEIR VII report, “In the case of in u

exposures (exposures to the fetus during pregnanccancers can be detected at doses as low as 10 mS

Based on the atomic bomb life span study, they notBased on the atomic bomb life span study, they not

excess relative risk (ERR) per Sv was 2.1. Of the tindividuals in the LSS exposed in utero who develo

cancer, nine were female. Summarizing medical exposure data, UNSCEAR 1that there was a statistically significant increased risleukemia and a 40% increase in the risk of childhooat doses of 10 to 20 mSv (1 to 2 rem). 
Fetal (in utero) Effects

Mental RetardationThe evidence from the LSS indicates that the risk omental retardation is extremely small for exposures first seven weeks after fertilization. The observed risk was greatest during the 8 - 15 wfollowing fertilization when the CNS neurons are raincreasing in number. During the 16 - 25 week period, the risk of mental rstill exists but has been substantially reduced. After 26 weeks the CNS continues to develop but nincreased risk was observed for those exposed durperiod. 
Fetal (in utero) Effects

Mental RetardationICRP 90 noted that the LSS data indicated a threshmental retardation of at least 300 mGy (30 rads) whexposure was in the most sensitive stage, i.e., the 8 week period post conception.
Fetal (in utero) Effects

Decreased IQTreating mental retardation as an either/or phenoma threshold of 20 to 40 rads (0.2 to 0.4 Gy) can be misleading in that it might be taken to imply that dothis threshold cannot have effects on intelligence. With regard to the risk of a decreased IQ, ICRP 103 “even in the absence of a true dose threshold, any IQ following in-utero doses under 100 mGy [10 radsbe of no practical significance.” They also noted thaIQ losses estimated at around 25 points per Gy [10more difficult to interpret.”
Fetal (in utero) Effects

MalformationsAt birth approximately 3% of children exhibit some significant malformation. Over time, two to three timnumber demonstrate some type of abnormality. The most common malformation observed in humaThe most common malformation observed in huma

prenatal exposures to radiation is microcephaly (dehead size). Almost all microcephalic children will alsseverely mentally retarded. Other observed malformations include growth retarabnormalities of the eye (cataracts and retinal pigmchanges), and genital and skeletal malformations. 
Fetal (in utero) Effects

MalformationsThe lowest dose at which malformations have been to a prenatal exposure is approximately 0.05 Gy (5 Quoting ICRP 103 “there are age-dependent patterutero radiosensitivity with m utero radiosensitivity with maximum sensitivity bein

sensitivity bein

expressed during the period of major organogenesbasis of animal data, it is judged that there is a true threshold of around 100 mGy [10 rads] for the inducmalformations; therefore for practical purposes, the Commission judges that risk of malformation after iexposure to doses well below 100 mGy [10 rads] aexpected.”
Appendix A

Ways to Express Risk Ways to Express Risk
Ways to Express Risk

Relative Risk (RR)The relative risk is the ratio of the total risk to thbaseline risk at a specified dose, usually 100 raTo say that the relative risk is 2 at 100 rad is to sthe total risk due to a 100 rad exposure is twice the total risk due to

a 100 rad exposure is twice 

baseline risk.
Ways to Express Risk

Excess Relative Risk (ERR)The excess relative risk (ERR) is the rate of the effeconsideration in the exposed population divided by an unexposed population minus 1.To say that the relative excess is 1.0 at 100 rads mthe excess risk is the same as the baseline risk. If the excess relative risk is 1.0, the relative risk is 2
Ways to Express Risk

Excess Absolute Risk (EAR)The excess absolute risk (EAR) is the rate of the efexposed population minus the rate in the unexposepopulation.
Appendix B

ICRP D t i t ICRP

D

e

t

rimen

t
ICRP Detriment

GeneralThe detriment is a risk approach wherein the risk of detrimental occurrences are reported rather than th

of deaths. 

It is an attempt to recognize that there is more to thIt is an attempt to recognize that there is more to th

radiation than just the risk of death. The detriment tries to factor in the loss of life expecalso the number and severity of non-fatal cancers iradiation. Non-fatal cancers are not given equal wefatal cancers.
ICRP Detriment

GeneralThe following table is from ICRP 60. It is intended texplain the concept of the detriment. The first column indicates the probability of fatal caTh d l h th i k f h dit bl The second column shows the risk of hereditable e

The third column calculates the relative length of lifeach cancer type: the years of life lost for the canceby the average years of life lost for all cancer typesThe fourth column calculates the relative contributionon-fatal cancers by subtracting the lethality fractiocancer from 2. 
ICRP Detriment

ICRP 60 Data
ICRP Detriment

GeneralThe product of these is the detriment. 

Detriment = risk x relative life lost x non-fatal c

The total ICRP 60 detriment is 7.25 x 10-4/rem (7.25

The current ICRP 103 detriment is 5.7 x 10-4/rem (5

Note that the detriment is a little higher than the risk 

cancers, but not much. The ICRP uses these detriments for the individual ctypes to calculate the tissue weighting factors.
Appendix C

Loss of Life Expectancy Loss of Life Expectancy
Loss of Life Expectancy (LLE)

While it is most common to express the stochastic radiation as the number of cancer deaths per unit dpossible to express the risk as the average number of life lost (due to cancer). The following table (ICRP 60 data) shows for varioThe following table (ICRP 60 data) shows, for vario

cancer, the fraction that prove fatal and the average life lost per death. 
Loss of Life Expectancy

The average years of life lost for all cancers (l) is 15. The years of life lost because of exposure to the gonads refers to resulting deaths in the offspring.
Loss of Life Expectancy (LLE)

If we take the risk per rem of dying of cancer and mby the average years of life lost per cancer death (1obtain the loss of life expectancy per rem:

For acute exposures

10 x 10-4 10

x 10

4/rem x 15 years/death = 5 5 days lost

/rem

x 15 years/death

=

5.5 days lost

For chronic exposures (assuming a DDREF of 2) 

5 x 10-4 /rem x 15 years/death = 2.75 days los
Loss of Life Expectancy (LLE)

In Regulatory Guide 8.29 the U.S. NRC estimates:15 days of life would be lost due to an occupationaof 0.3 rems/y (3 mSv/y) from age 18 to 65 51 days of life would be lost due to an occupationaof 1 rems/

y ( y) g 10 mSv/y) from a

ge 18 to 65 

They also note that:

6 years of life would be lost because of smoking 20 

cigarettes a day2 years of life would be lost due to being 15% overw1 year is lost due to the average U.S. consumption