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SESSl〇N I[[

L〇W-D〇S ERADI ATl〇N EFFECTS
TUESDAY, AUGUST24

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3.1 I〇NIZING RADIATI〇N I N 2 l ST CENTURY
Zbigniew Jaworowski-

CentralLaboratoryfor RadiologicalProtection CLOR,Warsaw,Poland

Trying to assess the risk of ionizing radiation from a 2 1 S t centuryperspective we may start by
1ooking at what weleamed from the world's greatest nuclearaccident that occurred almost20
years ago:the Chemobylcatastrophe.For myselfit was a dramatic personalexperience,adifficult exam,which I am not sure I passed. For many people,but not a11,engaged inradio1ogicalprotection,it was a watershed that changed their view on the paradigm on which
the present safety regulations are based,the holy mantra ofLNT-1inear no thresholdassumption,according to which even the1owest,near zero doses ofradiation may cause
cancer and genetic harm.For everybody it might serve as a yardstick for comparison ofradiation risks from naturaland man made sources(Figure1).It also shedslight on how
easiiy the g1obalcommunitymayleave therealm ofrationalityfacing an imaginarylemergency.
The LNT assumption is in direct contradiction
I l EaRoa a n
with a vast sea ofdata on the beneficialeff el cts of
1ow doses ofradiation.When in1980,as a「1●l 二● liillll
chairman ofthe United Nations ScientificCommittee on the Effects ofAtomic Radiation(UNSCEAR),I tried to convince its members that
we should not ignore but rather peruse and assess
these data,published in the scientific.The LNT
assumption is in direct contradiction with a vast
sea of data on the beneficialeffects of 1ow doses
ofradiation. When in1980,as a chairman ofthe
United Nations Scientific Committee on the
Eff el cts ofAtomic Radiation(UNSCEAR),I tried
to convince its members that we should not ignore
but rather peruse and assess these data,publishedin the scientificliterature since the end of 19th
century,everybody in the Committee was against
it.In eaoh ofthe next seven years I repeated the
proposa1,to no avai1. Fina11y,the Chemoby1
appeared to be an eye opener two years after theaccident,in1988,the Comnittee saw thelightand decided to study radiation hormesis,i.e.,the,:l ・ :'
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adaptive and beneficialeff el cts of 1owlevels ofradiation.Six years ofthe Committee's work
Figurel.Average individualradiationd?tiveand hot discussionslater,Annex B Adapti
Exposure to world population and in
Re? onses to radiation i n ce11s an d o rganlsms
Chemobylregion(Based on data inyears fromUNSCEAR,1988and2000)
appeared in theUNSCEAR1994Report,fourteen

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years after my originalproposa1.The A n nex started a virtualrevolution in radiation protection,
now infu11speed.
The LNT/hormesis controversy is notlimited to radiation. It poses problems for practica11y ali
noxious ph ysicai.chen i ical a nd bio1ogical agents whlch we meet inlife[1]. lo n i 1ii n g radlat1onwas discoverecl ral herla lely, at the end ofthe19tl' cen lury. bu1.as most ol l he;se other agents,
it has been with us since time immemoria1.
Chemobylaccident was a radiation event unique in human history,but not in the1ong history
ofthe biosphere,in which increased radiationlevels occurred at much greater scales[2 4]. In
terms ofhuman1osses it was a minor event as compared with many other man madecatastrophes[5].But its politica1,economic,socialand psycho1ogicalimpact was enormous.
Let's have a1ook at what happened--

Lessons of Chernobyl
About9a.m.on Monday28Apri1 1986at the entrance of CLOR in Warsaw I was greeted by
my assista11t with a statc、m e l l t; ' 'i o o i, ( i / 7. f )0 u 'e r t't'ei l ' t i / ( 1 i e/e.t /;'f J 用 M i'o/(l/il momfor 加gstaf lon stjv1 f lg fんat f/1e ra t f1o a t,ff ,//v ( f t fr i, f/1ere i 5 0 f1f1a / 加e,i f l lgf le ' f f la 1 a t4t0' f ) tf Jr t'. イ
simila r increase lf(ound i n the a i rf ilter fr om the st,ation i n our backyard,and the p avementin
fi・on/ o/ ;i' 1e instiiliie i. ilig hly r a dioaciil ,e''.Soon,to ourreliet we fou nd t hal th elsotopic
com position of r1lldioactive dust was not from anuclearexplosion,but rather from a nuclear
reactor.Reports inflowing successively from our140 monitoring stations suggested that aradioactive c1oud over Poland traveled westwards and that itarrived from the Soviet Union,
but it was only about6p.m.that weleamed from BBC radio that its source was in Chemoby1.

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This was a terrible psychologicalshock.The air over the whole countrywas fiiled with theradioactive m a ierial.at evels hundrcds ofthousands times higherthan anything we
experienced in the past. even in1(1163. a record yearoffa1lout fr( ) m nuc leartest c xp1os1o ns.It
is curiousl h;1l i a1lmy atte, ntion was conccntrated onthis enorm ous i ncrease in air radioactlvity,
although I knew that on this first day of Chemobylin Poland ,the dose rate of extema1
radiation penetrating our bodies reached30µ R per hour,or2.6mSv peryear,i.e.,wasonly bya factor of 3higher than a day before.This dose rate was four times1ower than I would
experience visiting places in Norway,where the naturalextemalradiation(up to11.3
mSv/year[6])from the rocks is higher than over CentralEuropean plane.It was also some
100 times1ower than in an Iranian resortRamsar,where in a house the annualdose reaches
about250 mSv per year[7],or more than300 times1ower than at the Brazilian beaches(790mSv per year)[8]or in South West France(up to870 mSv per year)[9]. No adverse healthefliects among the peopleliving in thoseareaswith high naturalbackground radiation,wereever reported.

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But in 1986the impact of a dramatic increase in atmospheric radioactivitydominated thethinking ofmyselfand ofeverybody.This state ofmindled to immediate serious
conseq uenccs in Pol 1nd. [ n the Soviet t lnio n, tl l ro Ll ghout t he l .urope. :a ndlat,irallover the
g1obe. First were di fferen l l1oc l ic actio l1 s.such as tlt/ i1( 1 t coi ning otdit1lerc1l t prl1lciples andemergency cou1l[crmea s u 1 e s.w]11c]1 sens l◆ and ILluality vaslagging 「ar beh ind the exce11ent
measuring techniques and monitoring systems.An example ofthis was the radionuclide
concentrationlimits in food implemented few days after the accident by various countries andintemationa1organizations,which were varying by a factor ofup to50,000[10].The base of、-- 140 --J A E R I Conf-

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some of theselimits was not scientific,but reflected the emotionalstate of the decision
makers,and also politicaland mercantile factors.For example,Sweden a11owed for30 times
more activityin imported vegetables than in the domestic ones,and Israelimposed1ower
1imits for radioactivityin food imported from Eastem than 1lirom Westem Europe[10].The
limit ofcesium 137concentration in meat of 6 B q/kg was accepted in Philipines and6000
Bq/kg in Norway[10].

--The monetarycosts of such restrictions were estimated in Norway. A t first the cesium 137
1imit for meat was accepted there as600 Bq/kg,which from a health physics point ofview ismeaningless[11],as consumption of l k g ofsuch a meat would correspond to a dose of
0.0078mSv.Ifsomebody would eat 0.25kg ofthis meat each day forlyearthe intema1
radiation dose would reach 0.7mSv. Thislimit was often surpassed in mutton,and thefarmers received compensation for destroying the meat,and for specialfodder they wereforced to feed the sheep for months before slaughtering.Such a1owlimit could havedestroyed theliving of Lapps whose economy depends on reindeer,an animalhaving a specia]
food chain based onlichens.Due to this chain the reindeer meat contained in1986highconcentrations ofcesium 137,reaching up to40,000 Bq/kg. I n November1986Norwegianauthorities introduced alimit of 6000 Bq/kg ofreindeer meat and game.0rdinaryNorwegian
diet includes only about 0.6kg ofreindeer meat per year[11],thus thislimit was aimed toprotect Norwegians against a radiation dose of0.047mSv/year.In1994the costs ofthis
protection were evaluated:they reached over$51mi11ion[12].

-Sweden was not better.When the farmers near Stockholm discovered that the Chemoby1
accident contaminated the milk oftheir cows with cesium 137above thelimit of 300 Bq per
1iter imposed by Swedish authorities,they wrote to them andasked iftheir milk could not be
diluted with uncontaminated milk from other regions,untilthelimit were attained,forinstance by mixing11iter ofcontaminated milk with101iters ofclean m通k.To the farmers'
surprise the answer was no,and the milk wasto be discarded.This wasstrange,as it always
waspossible to do so for other pollutants in foodstuffs,and we also dilute the fumesf l・om
fireplaces or ovens with the atmospheric air.Authorities explained that even though one could
reduce the individualrisk by diluting the milk,at the same time,one would increase thenumber of consumers,and thus the risk would remained the same,although now spread over a
1arger population[13].This was apracticalapplication ofthe LNTassumption,and of its
off 1spring,the concept ofthe co11ective dose (i.e.reaching terrifyinglygreat numbers ofman sieverts ,by multiplying tiny innocuous individualradiation doses by alarge number of
exposed people).I believe that in an earlier paper I demonstrated thelack of sense andnegative consequences both ofthisassumption and ofthe concept[l4].This practicalapplication made that the costs ofthe Chemobylaccident might probably exceed in Westem
Europe$100 bi11ion[15].

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The most nonsensicalaction,however,was the evacuation of 336000 peoplefrom the regions
ofthe former Soviet Union,where during the years1986-1995the Chemobylfa11out
increased the average naturalradiation dose(ofabout2.5mGy per year)by 0.8to1.4mSv per
year,i.e.by about30%to50%[8].The evacuation was based on radiationlimits
recommended by IntemationalCommission for Radio1ogicalProtection(ICRP)for the eventof m可or radiation accidents [16]and on recommendations for protection of genera1
population[17,18],which were tens to hundreds oftimes1ower than naturaldoses in many
countries[19].In the streets of the ghost town ofPripyat,from which about50 000 people
were re1ocated,and where nobody can enter without specialpermission,the radiation dose
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rate measured by a Polish team in May2001was 0.9 m S v per year[20],i.e.the same as in
Warsaw,and five times1ower than at the Grand CentralStation in New York.The evacuation
1ed to deve1opment ofmass psychosomatic disturbances,great economica1losses,andtraumatic socialconsequences.0bviously,ICRPw加 never accept responsibilityfor thedisastrous effects ofpracticalapplication of its easy chair elucubrations,which make that thepresent system of rad iationprotection becom e a healthhazard''[13].

-In Poland,to save the populationfrom effects of exposure to iodine 131,the govemmenl,
upon my instigation,administered during three days(starting on Apri129th ) a sing,le dose ofiodine to about18.5mi1lion people,thegreatest prophylactic action in the historyofmedicine
performed in such shorta time.My medicalcolleagues and the Minlstryof l lealth wererightly proud ofthe ingenious and innovative way they implemented thls countermeasure.
Recently severalcountries,including the USA, planned to fo11ow in our flight[21 23].
However,now I see this actionasnonsensica1.We endeavored to save Polish childrenfrom
developing thyroid cancers by protecting themf l:・om a radiation dose of 50 mSv to the thyroid
gland[24].At this dose ICRP recommended implementation of stable iodine prophylaxis[16].
But in studies ofmore than34000 Swedish patients whose thyroid glands received radiation
doses reaching up to40 000 mSv from iodine 13l,tliere was no statistica11y significant
increase in thyroid cancers in adults or children,who had not already been thought to havecancer before treatment with iodine 131.In fact,an opposite eff e1 ct was observed:there was a
38%decrease inthyroid cancer incidenceascompared with the non irradiatedpopulation[25,26].In a smaller British study of 7417adult hyperthyroid patients whose thyroids received
average radiation dosesfrom iodine 131of 300 000 m S v , a 1 7 % d eficit in incidence of a11
studied cancers was found[27].Without the stable iodine prophylaxis and milk restrictions
the maximum thyroid dose would reach about1000 mSv in about5%ofPolish children[24].
A11what I would now expectfi:・om this dose is a zero eff el ct.
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Fourteen years after the Chemobylaccident in the highly contaminatedareas o f the former
Soviet Union,no increase in incidence in solid cancers andleukemia was observed,except forthyroid cancers.In its2000 ReportUNSCEAR stated that the population need n o11 live i nfeear tf se ・1ot s healtk con、1i・equenees ,and gen era11ypos1ltive prospectsfor thefi出 irehealthh?mostindi ,tduais sholddprevaif'[8].No epidemics ofcancers in the N o11hem Hemisphere,
direly predicted from the LNTassumption to reach tens and hundreds ofthousands,or evenmi11ions ofcases,has ever occurred.

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The n umber of 1800 new thyroid cancers registered among the children from Belarus,Russia
and Ukraine should be viewed in respect to extremely high occurrence ofthe occult thyroid
cancers in normalpopulations[28 31].The occult cancers,not presenting adverse clinicalefflects,are detected at post morte m,or by USG examinations.Their incidence ranges firom
5 % i n Co1ombia,to9%in Poland,13%in the U S A , a n d 3 5 % i n Finland[29]. In Finland
occult thyroid cancers appear i n 2.4%ofchildren 0 to15yearold[28].In Minsk,Belanls thenormalincidence ofoccult thyroid cancers is9.3%[32].Thegreatest incidence ofChemoby1 thyroid cancers in children under15years old,of0.027%,was registered in1994
in the Bryansk region of Russia,which wasless by a factor ofabout90 than the norma1
incidence ofoccult thyroid cancers among the Finish children.The Chemoby1 thyroid
cancers are ofthe sametype and similarly invasive as the occult cancers[30].The firstincrease ofthese cancers was registered in1987in the Bryansk region,Russia,one year after
the accident.Since1995the number ofregistered cancers tends to decline.This is not inagreement with what we know about radiation induced thyroid cancers,the risk ofwhich

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increases unti1 15 - 29years after exposure[8].In the United States the incidence rate ofthyroid tumors detected between1974-1979during a screening program was21times higher
than before the screening[33],an increase similarto that observed in three former Soviet
countries.I believe that the increased registration ofthyroid cancers in contaminated parts o fthese countries is a classic screening effect,i.e.,a consequence ofmass thyroid examinations
and ofthe use ofmodem diagnostic equipment,in the countries where before1986such
examinations were rather scarce.
Besides the28fatalities caused by veryhigh doses of radiation among rescue workers and the
emp1oyees ofthe power station,and3deaths in thisgroup due to other reasons,the only rea1
adverse health consequence ofthe Chemobylcatastrophe among about five mi11ion people
1iving in the contaminated regions is the epidemics ofpsychosomatic diseases[8].Thesediseases were not due to irradiation with Chemobylfa11out,but were caused by radiophobia,
induced by years ofpropaganda before and after the accident,and aggravated by improper
administrative decisions.These decisions caused that severalmillion people in three countries
has been la1)l e1le das, andpercelive themse1lves as, actua1〇r potential victims of
C hernobyf '[34].This was the main factor behind the economic1osses caused by the
Chemobylcatastrophe,estimated for Ukraine to reach$148bi11ion unti12000,and$235
bi11ion unti12016for Belarus[34].

In1986most of my professionalco11eagues and myself,the authorities, and the public in
Poland and elsewhere were pre conditioned for irrationalreactions.Victims ofthe LNT
dogma,we a11wished to protect people even against the1owest,near zero doses ofionizing
radiation.The dogma influenced behavior of everybody,1eading to a mass psychosis,in fact tothegreatest psycho1ogicalcatastrophe in history[5],into which the accident in Chernoby1,with the efficient help ofmedia[10],and nationaland intemationalauthorities,quickly
evolved.It seems that professionals,intemationaland nationalinstitutions,and the system ofradio1ogicalprotection did not meet the cha11enge ofthe Chemobylcatastrophe.

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The fol1owing mainlessons can be deduced from this accident.
(1) Ionizing radiation ki11ed only a few occupationa11y exposed people.The Chemobylfa11out
did not expose the generalpopulation to hannfulradiation doses.Thearea covered by thedangerous radioactive fa1lout,where the radiation dose rate reachedlGy per hour,was
1imited to about 0.5km2 in an uninhabited1ocation,reaching a distance o f 1.8km 1lirom theburning nuclear reactor.Severalhundred meters outside t h e l G y isoline the dose rate dropped
bytwo orders ofmagnitude,to a safeleve1of0.01to 0.001Gy per hour(Figure2).This is asituation completely diff el rent from a surface explosion of a 1 0 Mt nuclearbomb,when the1
Gy per hour isoline can reach a distance of440km[35],and thelethalfallout can cover tens
ofthousandskm2,and endanger thelife ofmi11ions ofpeople.

(2)Radionuclides were i11ljected high into the stratosphere,atleast up to 15kmaltitude[36],what made possible its1ong distance migration in the whole Northem Hemisphere,and apenetration over the Equator down to the South Pole[37]. With a unique,extremely
sophisticated radiation monitoring systems,implemented in a11deve1oped countries,even themost tiny debris 16rom the Chemobylreactor was easily detected al1over the world. No such
system exists for any other potentia11y harmfulenvironmentalagent.Ironica11y,this exce11ence
ofradio1ogicalprotection ignited the mass anxiety,with its disastrous consequences in thefor mer Soviet Union,and strangulation ofnuclear energydeve1opment elsewhere.
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Figure2. Measured radiation exposure rates in air on26ApriI
1986in the1ocalarea ofthe Chemobylreactor.Units ofisolines、 are Gy per hour.(AfterUNSCEAR,2000).
(3)Psycilosomatic disorders and the screening eff el cts werethe only detectable healthconsecl uences among thc generalpopulatiol l . l 'ig hting the panic and mass hysteria could be
regarded l hc most importa n t countermeasure to protcct the public against the efl lects o f asimilaraccident should it occur again.
「(4)This was the worsl possible ca lastroph e, o f a badly constructcd nuclear reac i or,in which
two tasks were mixed: production ofelccl ric power with prod ,u ction of militarygrade
plutonium.The accident caused a complete meltdown ofthe reactor core,followed by the ten
dayslong completely free emlssion ol、radionuclides into the atmosphere.Nothing worse could
happen.It l ,esulted i n a comparatively minute occupationaldeath to1l,amo l l nting to a t)out halfof that ofeach weekend 's traffic in PolaJ ld, and tens orhundred s times」ower tha n that ofmany other i ndusl rlalcatastrophes,and no fatalities among the public.In the centu l・ies tocome,the Chemobyi catastropl le wi11be seen as a proofthat n Lに1ear power is a sa fel means of-Beneficialradiation and regulations

After ionizing radiation and radioactivitywere discovered at the end of the 19th century,theirsocialperce1̲)tioa has alternaled betwecn enthusiastic acceptance and r可ection.This stemmed
from recog ln ltion otth eir three basic、 asplicts:
1) usefulness llor medica1 app!ical ions and for technicaland scientific aims;
2 ) bcneficlaleffects o「theirlowlcvels:and3 ) harmfuleff el cts ofhighlevels.

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In the first part of the20th centuryacceptance prevailed,in the second rejection. The change
ot l he p 1Ll blic moocl wh ich had occurred ratherabf uptly after the World War II was not due todiscove、ry of some new dangcr o「ral」iatio ll.but w:as c1;l used by politicaland socialreasons,u nrelaled to L he actuale ffec is of radiai ion[l4] .
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The possibilities that ionizing radiation off el red for medicaldiagnostics were first
demonstrated by W.K.Roentgen,one month after his discovery,by publishing in N ature in
January1896an x ray photograph ofthe hand o f h i s wife.The first therapeutic application ofhigh doses o f x rays for pain release,rheumatic diseases and chronic bronchitis wasannounced in1897[38].In1902Pierre Curie,together with two physicians:C.Balthazard
and V.Bonchard,discovered that radium rays are usefulin cancer therapy.

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The beneficialor hor metic efliects of 1ow doses of ionizing radiation were found two years
after Roentgenannounced the discoveryofionizing radiation.First observed eff el ct was anincreasedgrowth rate of bluegreen algae exposed to x rays[39].During the next decades,thisobservation was fo11owed bythousands ofpublications on hormetic effects at a11bio1ogica1
levels(see e.g.[40 43]),including human epidemio1ogy(Table1).

--That ionizing radiation can be hazardous for man was firstannounced in 1896in the German
MedicalWeekly[44].The early students and users ofradiation voluntarily or unknowingly
exposed themselves to high radiation doses.Among the pioneers ofradiation and radioactivity
from23countries,scientists,physicists,medicaI doctors,nurses,and x ray technicians,about
100 persons died by1922,and406died unti11992,with afflictions that could be related toradiation.The names ofa1lthese victimsare recorded in the"Book ofHonour ofRoentgenologists ofAllNations"[45].This experience sounded an alarm,and the need forprotection against high doses ofradiation wasrealised quite early.

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The radio1ogicalprotection deve1oped since the 1920s,and reached high standards after theWorld War II.Due to this deve1opment,the totalnumber of persons exposed worldwide
between1945and2001to significant radiation doses was only2044.Among them134
persons died;probably70%ofthese fatalities occurred in medicalapplications ofradiation[46].This record includes the Chernobylvictims,and is unusua11y1owascompared with otherhuman activities.This testifiestwo facts:(1)exce1lency ofradio1ogicalprotection(but see
below the criticism of exaggerated standards);and(2)a1ow noxiousness of ionizing radiation.
In the 1920s the concept of "tolerance dose"wasintroduced,defined as afraction of the dosethat caused skin reddening.Thisfraction corresponded origina11y to an annualdose(inmodem units)of700 mSv.In1936it was reduced to350 mSv,and in1941to70 mSv.The
concept oftolerance dose,which was effectively a statement ofthreshold,servedasthe basis
for radiation protection standards for three decades[47]unti11959,when the Intemational
Commission on Radio1ogicalProtection based its recommendations on thelinearno thresholdassumption(LNT)[48].Introducing LNT to radio1ogicalprotection was stimulated by undue
concem in the1950s with the allegedly disastrous genetic eff el cts on the human population ofionizing radiation produced by man.In theliterature on ionizing radiation at that time,one
could often see the fo11owing statements of geneticists:" w e have reache d a stage w here
human mist,a kes can have a more d isastrouseffet ct than ever bef(ore i n our h isto y becatisesuch mistakes may drastica11y c hange t he course ofm an's bio1ogica1evolution"[49].In theyears that fo11owed,even in the progeny of survivors ofnuclearattacks on Hiroshima andNagasaki no radiation induced genetic disorders were detected[50].Also from other genetic
studies it became clear that this concern was an overreaction,intune with strong emotions,evoked by the menace ofnuclearwar. However,emotionsare not a good basis for regulations
Professor W.V.Mayneord,thelate chairman ofthe ICRPCommittee IV,a highly respectedscholar and humanist,made the fo11owing comment on using LNT as aregulatorybasis:" Ihave always feelt that the argumen t that because a t higher values of d ose a n o bse?ed eflfeect 1ls

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proportio na1l to dose, then at ve ry lio w doses t here is necessar iiy som e 'ef fect' of d ose, howevers m au, is nonsense"[51].Mayneord's concem about the values applied in ICRP
recommendations was in '' the w eaknessof the bio1'ogica1 a n d m edicalf(o,undations coupledwith a most impressive n um er ica lfcaf ade" .This numericalfagade,however,is now regarded
as epistemo1ogica11y unacceptable to interpret a bio1ogicalreality[52].An outsider oftheradiation protection community,thelate professor E.T. Jaynes,presented as a classica1
example for a common scientific errorjudging the effects ofradiation by assuming alinear
response without threShold(LNT).He stated that to analyse one 's d,ata i n terms of a mo de1
w h ichdoes not a11o w even t hep ossibili??a t hresholdeffecti is topreJtidge the ilssue m a waythat can 1lead tof(a lse conclusions, howe )er goodthe data .Thef :ia lse prem ise built into a
mo del w h i c hils never q uest1o nedcannot be removed by a? a mountof ne w data . Failse
conclusions of j ust thiskind are n ow not only causi ng mafor economic waste, but a1lso
creating unnecessary dangers topublic health an d saffe?. Sociely has onlyfi n ite reso urces todea1 withsuchproblems, ,so any eがortexpen ded o n lm aginarydang,e rs m eans that the rea1
da ngers are going u nattended [53].

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For the past f le w decades the main support of LNT assumption in radio1ogywastheinterpretation ofepidemio1ogicaldatafrom Japanese A bomb survivor Life Span Study.This
population was exposed to extremely high dose rates,as the duration ofradiation pulse during
nuc!ear exp1osion was abou110 3 second.This dose rate waslarger b y 2 x 1 0 l 5 than the
Chemobyldose rate in the US(0.0046mSv over50 years).Using LNTassumption based onsuch an enormous diff el rence ofthe dose rates to calculate exactly53400 cancer death tol1,is
not only unacceptable scientifically[14].Indeed,Lauriston Tay1or,the former president ofthe
US NationalCounci1on RadiologicalProtection and Measurements,deemed such
、 . Recently,a meticu1ous
extrapolations to be deep1;y i m mora1 use of o ur sc ientjfic heritage
revision ofthe cancer andleukemia incidence datafrom Hiroshima demonstrated that theyare
consistent with the threshold 1ike dose response mode1[54].

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During the past severaldecades there was a tendency to decrease thelevels of dose applied instandards ofradiation protection tolower and1ower values. I n the1980s and the1990s these
became20 mSv per yearfor occupationa11y exposed people,andlmSv per year for thegeneralpopulation.For an individualwho receives no direct benefit 1lirom a source ofradiation,a maximum dose of 0.3mSv in a yearhas been recently proposed[55],and for some instances
an exemptionleve1of0.01mSv per year[56]. Justification for such1owlevels is difficult toconceive,as no one hasever been identifiably in1ured by radiation while standards set by the
ICRPin the1920s and the1930s were in force,involving doselevels hundreds or thousands
oftimeshigher[57,58].Thelife expectancy ofthe survivors ofnuclearattacks on Hiroshima
and Nagasakiwasfound to be higher than that in the controlgroups[59],no adverse genetic
eff el cts were found in the progeny ofsurvivors[50].There is also ample evidence ofbeneficia1
eff el cts of 1ow doses ofradiation in people occupationa11y,medica11y or natura11y exposed todoses much higherthan the current radiation protection standards(see e.g.[60],and Table1).

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To adhere to regulations based on standards involving suchlow doselimits,the societyis
paying hundreds ofbillions ofdo11ars,with no detectable benefit.Each humanlife
hypothetica11y saved by implementing the present regulations costs about$2.5bi11ion[70].
Such spending is mora11y questionable,as:(1)thelimited resources ofthe society are spent on
prevention of an imaginaryharm,instead of achieving realprogress in health care,and(2)because1ow radiation doses are beneficialfor the individua1. For these two reasons,suchexpenditures may have actually an adverse effect on the population.
-

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Table 1. Deficit of mortalityinlarge human populations exposed to1ow radiation doses
ulations.
(u to500 mSv . m com r ison with unex osed
De
fi
c
i
t
(
%
)
a
n
d
causesReferences
Population

High backgroundarea,USA

15%

cancers *[61]

High background area,China
Nuclear industryworkers, Canada
Nuclear shipyard workers,USA

15%
68%
24%
58%
9%

cancers
leukemia
a11cancers
leukemiacancers

[62]
「63 l
[64]

78%
32%
29%
36%
29%

leukemia
a11cancers
cancers
non cancers
leukemia[67]

lung cancers
cancers
cancers

[68]
「69]
[26]

Nuclearworkers,combined Hanford,
ORNL,Rocky Flats,USA
British medicalradio1ogists after1955
1979-

Plutonium workers,Mayak
Eastem Ura1, Russia
High residentialradon,USA
35%
39%
Accident in Eastern Ura1,Russia
38%
Swedish patients diagnosed withiodine 131 * ** incidence; **thyroid doses 0 257,000 mGy

-

[65]

[66]

-

-

Naturalradioactivityand nuclear wastes
Whenlife began some three and half biiiion years ago,the natura11evelof ionizing radiation
at the planet's surface was about three to five times higher than presently[71].At that time,
the1ong 1ived potassium 40,uranium 238,and thorium 232had not yet decayed to theircurrentlevels.Their content in the contemporaryEarth's crust is sti11quite high,and it is
responsible for the highest radiation exposure ofeveryliving being. 0 n e ton ofaverage soi1
contains about1.3x106 Bq ofpotassium 40,thorium 232and uranium 238and theirdaughters.This corresponds t o 3 . 6 x 1 0 15 Bq per cubic ki1ometer(Table2).Decay ofthesenaturalradionuclides present inlkilometer thick soi11ayer produces8000 ca1ories per square
meter annua11y[2].

-

-

-

-

-

-

,

-

-

-

-

We can compare the natural,extremelylon g 1ived activityofpotassium 40(T'/2 = 1.28x 109
years),thorium 2 3 2 ( Ty2 = 1 . 4 x 1 01 o years)and uranium 238(T'/2 = 4.47x109 years)in soi1,
with the activityofmuch shorter 1ived radioactive wastesfrom the nuclearpower cycle(Table
2).In2002the totalannualproduction ofelectricityin nuclear reactors was285.4GW(e)[8,80].The g1obalproduction ofradioactive wastes from this source amounts t o 3 x 1 015 Bq per
year,with the1ongestlived plutonium 244(T½ = 8 . 2 6 x 1 07 years).Such amount ofaveragenaturalactivityis contained in a relatively smallb1ock of soilfrom high activityareas 0.17by
0.17kmwide and2kmdeep.None ofthe man made component ofthese wastes hasappreciably higher radiotoxicity(expressed as Sv/Bq)than the naturalthorium 232[81].

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Table2. Activity of naturalradionuclides in the terrestrialcrust and totalactivityof wastes
from nuclearpower.(After「72l .corrected)
Naturalradioaetivi
Number of radionuclides in chain
Concentration ofparent in soi i, B q /g
MedianMax
Concentration o f series in soi1, Bq/g
MedianMax
Activityof series i n l k m' o f soil
(2 .7E15g),Bq
MedianMax
Activityofseries in terrestrialcrust( l 7.3E24g b), Bq
MedianWastes from nuclear nl]-w cr
ILW and LLWfrom electricity
productionin2002, Bq C
Wastes accumulated until2000 firom thewhole civilian nuclear fuelcycle after
500 years ofstorage for coo]ing,Bq d
aA

-

-

-

-

-

K 40
1

R b 87
1

Th 232
l l

U 235
l2

U 238
14

0.40

0.08

0.030
0.360

0.00160.0160

0.035
0.900

0.08

0.33
3.96

0.019
0.192

0.49
12.60

1.32
19.95

1.1E15
8.6E152.2E14

8.9E14
1.1E16

5.1E13
5.2E14

1.3E15

3 .4E16

3 .6E15
5.4E16

6.9E24

1.4E245 .7E24

3 .3E23

8.5E24

2.3E25

3 .20
0.40

3 .20

Total

3.0E15 e
5.8E18 'fter ref. [8],[73],and[74];f [74];C 285.4GWe ,after ref.[75],andassuming20%nuclearpower station efficiency;and10,000
GBq/GW(e)y 1 for conditioned solid intermediatelevelwastes(ILW),and500 GBq/GW y 1
1owlevelwastes(LLW)after ref.[76];d 200,000 tones of heavymeta1 wastes after ref.[77];decay rate of fission products andactinides from 〇RIGEN after ref.[78]and[79];e Corresponds to median naturalactivityin 0.8 3 k m 3 of soil,i.e.in a b1ock of 0.64x 0 . 6 4 x 2km;or in 0.0 6 k m 3 of soilwith maximum concentration ofnaturalradionuclides,i.e.in ab1ock ofabout 0.17x 0.1 7 x 2 k m .
f Corresponds to activityinl611km3 of soilwith median concentration ofnaturalradionuclides,i.e.in a b1ock ofabout28.4x28.4 x 2 k m ; o r i n l 0 7 k m3 of soilwith
maximum concentration ofnaturalradionuclides,i.e.in a b1ock of a b o u t 7 . 3 x 7 . 3 x 2 k m .
b A量er re--

The activityof wastes accumulated untilthe end of 2000f l:・om the whole g1obalcivilian
nuclearfuelcycle is much greater.It amounts to200 000 tones of "heavymetals".Disposa1of
highlevelwastes and spentfuelin geo1ogic repositories may result in doses to population that
do not begin to accum Lllate untilwe11after500 years[82].After500 years activityofa1lhigh
1evelwastes wi11decreaseto about5.8x10 l9 Bq[83],correspondingto naturalactivity
contained in a b1ock ofsoilfrom high activityareas about7.3by7.3kmwide and2kmdeep.
N o specialbarriers prevent the naturalradionuclides from migrationfrom,say,a depth of 2
kmto the surface ofthe ground. They can be transported by mechanicalaction,or move insolution.Thorium is not susceptible toleaching under most geologicalconditions and its
148

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principalmode o f occurrence is in refractoryminerals. Uranium is highly mobiie,and may
migrate with ground water to distances ofseveraltens ofki1ometres or more. Radium is mobile
in sulphate free neutra1or acidic solutions. The average volcanic injections ofalpha emitting
2lOPo into the g1obalatmosphere during non eruptive activity amount to a b o u t 5 x 1 0 15 Bq peryear[84],i.e.,almost twice as much as the2002production ofradioactive wastesfi・omnuclear
power reactors(Table2). Geochemicaldif flerences between uranium , thorium and radium may
1ead to drastic changes in their radioactive equilibrium[85] .

-

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In contrast,for man made radioactive wastes many ef fiictive,sophisticated barriers areprovided in deep underground depositories.At a first glance,one can see in Table2that it
would take few bi11ion years o f such a globalproduction ofwastesfrom nuclear powerreactors as in2002,to double the totalactivity ofnaturalradionuclides in the Earth's
continentalcrust.
Conclusions

Man's contribution to the content and flo w o f radionuclides and of radiation energy in theparticular compartments ofthe environment consist but a tinyfraction ofthe natura1
contribution. In some areas in the world the naturalradiation doses to man and to other biota
are many hundreds times higher than the currently accepted doselimits for the genera1
population. No adverse health effects were found in humans,animals and plants in these areas.
In thefuture reconstruction ofthe edifice ofradiation protection which now stands on the
abstract LNT foundations,a down to earth approach willbe necessary,taking into account theapparently safe chronic doses in high naturalradiation areas. It seems,therefore,that studies ofthese areas deserve specialattention and support in the coming years.

- --The twentieth centurywitnessed the dawn ofman made ionizing radiation and radioactivity,
the use ofthehighest human knowledge toki11people in Hiroshima and Nagasaki,and thegreatest nuclear catastrophe in Chernoby1. This catastrophe claimed only31fata1occupationa1
victims and probably none among the public,ultimatelyproving that nuclear energy is acomparatively save means ofpower production. It was also found that high sem i acute doses
ofradiation can cure cancers,and that smal1 chronic doses ofradiation are beneficialfor health
It seemsthat the discoveryof "new"radiation and ofradioactivitywhich opened the gate to an
unlimited energy resource,has a significance to humankind similar to that ofthe discoveryof
fire some500 000 years ago. Fire made us the most ubiquitous species and enabled expansion
oflife outside the Earth's biosphere. 0 u r ancestors had many thousands ofyears to menta11y
adapt to fire,sometimes even deifying it. It seems that one centuryhas not been1ong enoughto adapt menta11y in the same manner to ionizing radiation and radioactivity. But everything
now seems to proceed faster than before. Perhaps21 ' centurywi11suffice for this adaptation.
,

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Magi11, J ., Nuclides 2000 An ectromc Chartofthe Nuclides. 1999,Eureopean Commission
Joint Research Centre. Institute for Transuranium Elements.
1A EA, Nuclea r p owerstatus a r ol lndthe wo r ld lAEA Bu11etin,2002. 44(2):p . 59.
UNSCEAR, Sources, Elfftects a n d Risk s ofio nlzing Radiation .1988,United Nations Scientifi c
Committee on the Effects ofAtomic Radiation.New York:New York. p . 1 647.
1onstration of safie allsposa1of spe ntfue1 a n d
Semenov,B. and M.Be11. Pro,gress to1, ノards the de,″hlgh leve1
11 radloactlve 1,,,aste.・ Acritical issuefot r nucle ar p ow er. in G eo1loglcalDisposa1of Spen t
F ue1l an d Hlgh Leve1l andAlpha Bea ring Wastes.1993 . Antwerp,Belgium:IntemationalAtomic
EnergyAgency,Vienna,Austria.
Be11,M., 〇Rf GE N - the 〇RNL lsotope generation a n d depletion code. 1973 .
Croff,G ., 〇RIG EN 2 A versattle computer codef i:or ca lculating the n uclide composition a n dc haractertstics ( lf n uclear m a terials Nuclear Techno1ogy,1983.62(September):p. 335.

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80.
81.

82.

83.
84 .
85.

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UNSCEAR, ,Exp osu resfr om ma n m a de sources of radiation. 2000,United NationsScientificCommittee on the Effect ofAtomic Radiation. p. 1 155.
t tyStandards f(
o r Protection agains1o nlzing Radiation a ndfi
or
]AEA, i n ternationalBasic S afe
S afet tyof Radiatio 1 Source.s・. S a fwetySeries No.115. 1996,Vienna:IntemationalAtomic Energy-,

Agency.353.
〇ECD, R a d i o11 ogica11mpac t s of Spen t N u c lear F ue11 Ma nagemen t 〇ptions A Compara t iv e Study
2000,0rganisation for Economic Co operation and Deve1opment,Nuclear EnergyAgency:Paris. p .

--Chwaszczewski,S., The ma nagemen t of the spentfuelf om p ow er reactors - 1lechnotogies,
econo m y an d env ironm ent PolitykaEnergetyczna,1999. 2(1 2):p. 6 5 80.
Jaworowski,Z., Nlatura1 a n d ma n ma de radionuclides i n t he g1loba1atmosphere. ]AEABulletin,
1982.24(2):p. 3 5 39.
Jaworowski,Z., Sources and the g 1lo ball cyc le of radium, i n The enviro nm entatbehav1o u r ofradium. 1990,IAEA:Vienna . p. 1 2 9 142.

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3.2 M D I〇PH〇BIA:A SERI〇US BUT CURABLE MENTAL DIS〇R D E R
Klaus Becker
Radiation Science&Health
Boothstr.27. D 12207Berlin,e mailpr,uI .ur. K l ;au s.oe t st・rl(i lt online . de

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Symptoms,some consequences a n d treatments of radiophobia
The radiophobia syndrome is the excessive acute or chronicalfear of sma11
radiation doses in the range of naturalbackground fluctuations be1ow about50
mSv/y. It may be considered and treated as a mentaldisorder. It is caused primarily
by anti nuclear activists and"green"politicalparties,as we11as by fear mongering
sensation oriented media,and is endemic in severalindustrialized countries.
The consequences are serious. Best known is thelack ofpublic acceptance forclean,safe,and economicalnuclear power. In extreme forms,e.g. in Germanyl,it can
1ead to quasi terrorist actions against transports of nuclear materials,purely politica11y
motivated b1ocking of an almost completed high 1evelwaste repositoryin the Gorlebensalt stock,and the premature phasing out o f some ofthe world's safest and most reliablenuclear powerplants. At high costs for industry1,electricity consumers and tax payers,
they are intended to be replaced by many vastly more expensive and controversia1
wind millparks,or even more uneconomic photovoltaic facilities in order tofu11filthe
German C 02 reduction commitments according to the Kyoto Protoco1. Less obvious
are other side effects,such as excessive costs o f decommissioning and waste disposa1,
unnecessary but very expensive radon remediation programs in former uranium
m ining areas, private residences, etc., reluctance of patients to accept vita1
radiodiagnostic or radiotherapeutic measures, administrative obstacles curbing the useof radioactive sources in industry and research,and complications for some industries
involving increased naturalradiationlevels.
ong the relatively new aspects is that of terrorist threat with dirty bombs
based on the distribution of radioactive materialsfrom stolen or orphan sources.
Although such devices would create only minor realradio1ogicaldamage, such
Weapons of Mass Disruption could,ifcleverly pIaced,easily create tremendous costs
and chaos among uninformed populations and authorities.
The therapeutic approach for treating radiophobia must include atleast two

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measures:(1) Changes in the regulations should abolish the LNT hypothesis and the co11ective
dose concept. The doselimits should be increased to the1owerlevelfor observable
detrimentalhealth effects, or to the fluctuations of natura11evels including the
hig h 1evelareas in the world. New radiobio1ogicaland epidemio1ogical data canaccelerate this process.
(2) C1osely connected are improvements in information and education regarding
1ow 1evelradiation effects and the risk benefit situation,for example by pointing out
beneficialradiation effects,e.g. in the wide spread and successfillradon therapy forarthritic/rheumatic diseases and Morbus Bechterew. Such efforts should initia11y be

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focussed on public opinion makers and multiplicators,namely the media (journalists)and politicians,progressing to teachers on a111evels,physicians,clerics,community
organizations, etc. Both approaches are difficult and time consuming, but recent
deve1opments show that encouraging progress has already been made.

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In a historicalview,unti11940 50s1ow dose radiation was generaliy associated with
beneficialhealth effects. Since the Japanese A bombs disaster and g1obaltest fa11out
i n l 9 4 0 50s increasing worries arose about genetic disorders. After the1950s,theantinuclear Green/altemative movements increased in some countries. Since1986,vast--

exaggerations ofChemobyleff el cts stimulated intense anti-nuclear,mostly ideo1ogica11y
motivated media and politicalcampaigns in severalrich nations. A fte r 1 9 9 0 , t h edivergence between accumulating scientific evidence and overcautious regulations
increased,causing rapidly increasing costs for waste management,decommissioning,etc., a n d negative effects on society(inexpensive clean energy,reluctance of medica1
radiation uses,etc. )The Current Situation

Discrepancies betweenlarge fluctuations of naturalexposures and the restrictive
1imits for "artificial'' population doses became increasingly problematic for thecredibility ofradiation protection. I n Germany, f o r instance,there are currently release
1imits for radioactive materials corresponding to 0.01mSv/y population exposure(<0 . 5 % o f average annualnaturaldose),and requirements for the safe fiinalstorage ofradioactive waste for one mi11ion years perhaps exceeding the survivalexpectancy o fhomosapiens(and the U. S. requirements by a factor of 100).
The risk/benefit assessment of such measures becomes particularly serious when
economic problems are not any more restricted toless deve1oped countries,but alsointerfere with socialstructures(emp1oyment,socialservices,education,etc. ) , a n d
become a serious burden for the taxpayer in formerly a ffluent countries.Radiation
protection in not aluxury which only a few rich countries can afford.
For example. currently in Germany for dose reduction down to individualdoses of
0.5 % o f average natura1 exposure (0.01 mSv p. a. ), 100,000 ECU/Sv (about
US$135,000)are being spent. This results in direct expenses,e.g., i n Germany,, ofabout
1,500 mi11.ECU in the remediation offormer U mining areas,about5,000 mi11. ECU onradiation protection measures in decommissioning and waste programs,and about200
mi11. ECU for destruction o f agriculturalproducts after Chernoby1,etc. It is important
to note that indirect economic and socialcosts amount to a muchlarger amount o f at
1east1,000 mi11. ECU annualiy.

--Some Expertopinions
According to the study o f U. S . Congress/GeneralAccounting Office,a question
has been presented as to the scientific basis ofthe present radiation standard as fo11ows

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2005-001(released July14,2000):"A disagreement between federalagencies over whatlevelof radiation exposure issafe was not based on scientific evidence and could cost the taxpayer bi11ions in
unnecessary spending. Current standards assume there is no safelevelfor radiation
exposure,but many scientists say that radiation exposure is harmless be1ow a certain
threshold. Current standards of acceptable radiation exposure are based on
extrapolationsfrom studies on much higher exposure.The question is,is it justified tospend money i f y o u are not sure that there is some benefit derivedfi・o m spending thatmoney?"
There are many relevant statements of experts,e. g. at5th Intemat. Conference on
High Levels o f Radiation and Radon Areas, Dose and Health Eff el cts,
IAEA/WH0/EU/BMU/BIS /UNSCEAR,Munich Sept. 4 7,2000):" We are swimming in a sea ofuncertainties and contradictions. We cannotlive witha consistent system for naturaland artificialradiation. The cleanup industrymakes a1ot
o f money and tries to maximize pro fits. " (Gonzalez,IAEA,Director,Radiation and
Wlaste Safely Div. )--- "There are no conclusive datafrom epidemio1ogicalstudies The risk fro m radiation.

is muchless than currently estimated. The costs for decommissioning and remediation
arenot acceptable. "( A. C. S . Amara1,Director,Inst. Radiat. Protect.,Brazi1)-- "Radiation protection should avoid splendid isolation i a self- inflected ghetto Whyn.

w o 町 , a t a cost of 100,000 E U R 0 for one Sievert avoided down to aleve1of0. 01mSv/y,and1ook awayfrom peopleliving a t 1 0 m Sv/ y?" ( W. Burkart,IAEA Dep. Direct.
Gen. )
一一 "We should not extrapolatefrom high tolowlevels,because the bio1ogica1

effiects are basica1ly different. "(L. Wei,Ministry ofHealth,China)
Naturaland '' artificial" dose limits

There are no detrimentalhealth eff el cts up to atleast10mSv/y in high natura1
radiation areas,e.g. in Kerala/India,China,or,Germany.However,ifcurrentlimits for"artificia1"radiation(1mSv/ y)are applied also to naturalradiation,1arge parts ofmany
countries would have to be evacuated,and many industries(minerals,phosphate,coa1,oi1)have to be c1osed down. The extreme expenses could seriously aff el ct whole national
economies.
Possible solutions could be:
1 . To apply very different standards for naturaland artificialradiation,or
2. to adjust regulatorylimits for artificialradiation to a much higherleve1

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2005-001-(by a factor10 100),which would also correspond with the approx. 1:10fluctuations, this obvious solution seems to be not politica11y
in naturalexposure. Unfortunately.
acceptable at present.
High naturalradon concentration measured i n Germany:
Residentialradon:Some basements ofolder houses in Saxony with more than
100,000 Bq/m3
Air in overground industrial facilities:In the HoffBavaria Public Water Works ca.
750,000 Bq/m3,
Air in radon spa sources:Up to180,000 Bq/m3
Air in U mines around Schneeberg/Saxony(ca. l946 1950):more than2,000,000
Bq/m3.

-The Schneeberg area of Saxony/Germany,12%of a11homes are above15000 Bq/m3(maximum around115000 Bq/m3 ). Since1990,about3 .000 mi11. U S $ h a v e beenspent on overground radon assessment and remediation programs,however,in1998
there has been the officialreopening ofnew radon therapyfacilities in the same area.

Radon Therapy as an Example of BeneficialRadiation Effects
Radon therapy has a1ong historydating back to the ancient Romans. Afterthe1903/04discoveryofTh/Ra(ca11ed emanation)in the U.K.and Germany1,first spa
studies were made in Gastein/ Austria. S ystematic investigations ofRnsources
fo1lowed inAustria,Bohemia,Germany,and first scientific studies in Germany.
There was a widespread use ofRa/Rn"emanators",and rapidly deve1oping radon spas,
e.g. Joachimsta1(43patients in1906,373in1920,2476in1913,withthe Radium
Palace Hote1opening in19l2). In Russia,since ca.1910 there was increasing radon
therapy with up to one mi11ion annualpatient treatments,and in1993the first clinica1
proofofradon effects in randomized double blind studies started Germany. Atota1ofmore than1,000 publications appeared in scientific/medica1 joumals onRntherapy
since1904.

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As iio r radon spas,there are currently >30 in Russia,7in Germany., 3 i n Austria,and
others in the Czech Republic,in Bulgaria,in Italy, Japan,Poland,and USA. Patientsare treated mostly for rheumatic arthritis and spondilytis anky1osans(M.Bechterew),e.g. 75,000 p.a.in Germanyand Austria. Severalexplanations forthe effectiveness o fradon treatments have been investigated, e.g.stimulation of the immune system,
improved ce1lular repair capacityl , o r promotion o f hormone and radicalscavenger
production.
The New ICRP2005Draft

However,ICRPinsists that even1ow and very1ow radiation doses are dangerous.
The proposedlimits remainlargely unchanged w i t h l m S v /y for the population dose,and 0.0 1 m S v/yrelease constrains.For radon,it is up to600 Bq/m3 in residences,1,000

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Bq/m3 at the working place(nationalregulations are in many cases much1ower,e.g.
150 250 Bq/m3 for residentialradon,and a recently proposedlimit o f 100 Bq/m3 inGermany,, w h i c h would cause costs of about1 .000 ECU). The weighting factor(RBE)
for alphas remains at20,and LNT the basic principle. The inconsistent consideration o f
natura1(NORM,etc. ),medica1,and artificia1"exposure also remains unchanged.
ong the new topics are c1oudy stakeholder and ethica1 phi1osophica1
considerations. and an increasing concern about the radiation protection o f n o n humanspecies. There are slight indications o f improvements in co11ective dose andlung risk
assessment, but without any action. Remarkable is the increasing influence o f
non scientific politica1 and public opinion factors in the formulation o f ICRP

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recommendation.
Conclusions

The current consensus o f (almost)a11radiation protection and radiation bio1ogy
experts may be summarized as fo11ows:
1.
For economica1 (cost/benefit), ethica1 and politica1 (e.g. nuclear energy
acceptance)reasons,1ow dose ef flects are ofutmost interest.
2.
Radiobio1ogicaland epidemio1ogicalevidence demonstrates that the LNT
hypothesis and co11ective dose concept are invalid for1ow and very1ow doses,but
perhaps sti11oflimited administrative value. In particular the co11ective dose concept
frequently produces,by multiplication of very sma11doses withlarge populations,obviously absurd results.
3.
TheRBE ofhigh LET(alpha,neutron)radiation should be reducedfrom20 to amore realistic value around5 10.

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Current populationlimits o f l m S v /y(individuals)and ˜0 .0 1 m S v /y(1arge
groups)are,considering research results,e.g.effects ofnaturalbackground fluctuations,much too1ow and should be revised.

Re m ar k.・ These are r1o tes f (o r a lecture1 , and not a caref u11y polished sc ientjfi c paper
R eferences an d add前o na1l irf(o r mation may bereq uestedf rom the author:

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3.3 Evidence for beneficiallowlevelradiation effects

and radiation hormesis
L.E.Feinendegen--

Heinrich Heine University Dusseldorf,Germany;
Brookhaven NationalLaboratory,Upton,NY,USA
Abstract

Low doses in the mGy range cause a dualefliect on celiular DNA. One effect concems arelatively1ow probabilityofDNA damage per energy deposition event and it increases
proportionalwith dose,with possible bystander effects operating. T h i s damage at backgroundradiation exposure is orders ofmagnitudes1ower than that from endogenous sources,such as
ROS. The other effect at comparable doses brings an easily observable adaptive protection
against D N A damage from any,mainly endogenous sources,depending on ce11type,species,
and metabolism.Protective responses express adaptive responses to metabolic perturbations
and also mimic oxygen stress responses.Adaptive protection operates in terms o f D N A
damage prevention and repair,and ofimmune stimulation.It deve1ops with a delay ofhours,
maylast for days to months,and increasingly disappears at doses beyond about100 to200
mGy.Radiation induced apoptosis and terminalce11diff el rentiation occurs also at higher
doses and adds to protection by reducing genomic instability and the number ofmutated ce11s
in tissues.At1ow doses,damage reduction by adaptive protection against damage fromendogenous sources predictably outweighs radiogenic damage induction.The analysis ofthe
consequences ofthe particular1ow dose scenario shows that thelinear no threshold(LNT)
hypothesis for cancer risk is scientifica11y unfounded and appears to be invalid in favor o f athreshold or hormesis. This is consistent with databothfrom animalstudies and humanepidemio1ogica1observations on1ow dose induced cancer.The LNT hypothesis should beabandoned and be replaced by a hypothesis that is scientifica11yjustified. The appropriate
modelshould include terms for bothlinearand non 1inearresponse probabilities.Maintaining
the LNT hypothesis as basis for radiation protection causes unreasonable fear and expenses.

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Ionizing radiation and endogenous toxins atlow doses

A11agree that ce11ular responses to1ow values of absorbed doses of ionizing radiation are notreadily predictable by extrapolation ofresponses observed at high doses. One reason for this-unpredictability is in the physics ofenergy distribution in1ow dose exposed tissues.In caseofpenetrating radiation,particle tracks arise stochastica11y throughout the exposed tissue withthe relatively1ow density at1ow doses[l]. These tracks generate on the one hand unevenly

distributed ionizations and excitations ofconstituent molecules a1ong the track path,as we11as

bursts ofreactive oxygen species(R〇S)[2]. In case ofexposureto intemalemitters,thedistribution ofparticle tracks is determined by the distribution ofthe emitter in tissue[3].
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The1ower the radiationfluence or number ofparticle emitters in a given tissue mass,thelesscrowded are the particles in the exposed mass and with them the more heterogeneous is the
distribution of ionized molecules and o f R O S bursts.
The other reason is the presence of compounds that may aggravate or reduce radiation eff el cts;
there is especia11y the abundant and constant metabolic generation o f R O S and ofother-endogenous toxins,on top ofwhich1ow dose radiation acts[2, 4]. The quotient between therates of endogenous and radiogenic ROS production at background radiation exposurestrongly favors the forme r . I n fact,the average production rate of endogenous DNA double
strand breaks(DSB)per ce11per day in the body is about103 times higher than that of-radiogenic DSB from background irradiation assumed overwhelmingly to be1ow LET type.

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However,at1ow LET irradiation the probabilityofradiation induced DSB per primary DNA
alteration ofany type is about105 times higher than that caused endogenously[5]. This data

set attests not only that endogenous DNA damage faroutweighs radiation induced DNA

damage at backgroundlevelexposure,but also that irradiation is far more effective in causing
DSB thanare endogenous ROS.

Ratio of DNA damage and cancer probabilities
Radiation induced DNA damage increases with absorbed dose[6]. Such ce1lular effects comethrough direct energy deposition events from traversing particle tracks by which DNA

damage rises proportionalwith dose.Dependent ofthe amount ofenergy deposited per ce11,-

bystander effects in non irradiated neighboring ce11s may add to this damage in tissue at1ow
doses[7, 8]. By measuring damage in multicellularsystems,values ofdamage per exposed

ce11or defined micromass are calculated averages.This implies that any bystander
phenomenon that may have occurred is coregistered and expressed in the oberved values from-which these calculations were m a d e [ 91. A dose o f l m G y of1ow LET radiation,such as100-

kVp x rays,causes on average the fo11owing eff el cts per potentia11y oncogenic stem ce11withan average mass of lnanogram:1particle track;about150 R O S ; 2 D N A alterations ofany-

kind;10-2 DSB;10 4 chromosomalaberrations;and the probability of an oncogenic-transformation ofthe hit ce11withletha1outcome is about10-13 to10 14 [10, 11, l 2 ]. In otherwords,the ratio ofthe probabilities for radation inducedlethalcancer and the corresponding-

DSB is about10-11 to10 l 2 . T h i s means that the statement ofeven one DSB to pose a risk of

causing alethalcancer to deve1op from the afliected cellis unrealand,in fact,scientifica11y
unfounded.
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Adaptive Responses, Protection-

A sudden suprabasalyet non 1ethalrise of toxin concentration in a biologicaltarget tends toelicit stress responses and to stimulate adaptation usually in terms ofprotective mechanisms

in the sense ofhormesis[l3]. Increasing evidence in theliterature over the past25years

indicates that adaptive protection responses occur in mammalian ce11s i n vivo and i n v前ro-after single as we11asprotracted exposures to X or γ一radiation at1ow doses.Not only theoccurrence of adaptive protection but also the nature of some biochemicalmechanisms
involved have been reported[4, l l, l 2, l 4, 15, 16, 17]. There appearto betwo principal

types of adaptive protection,one is to prevent and repair D N A damage and in doing so tokeep ce11s alive andfunctioning properly. The other is to remove damaged ce11s from tissue

by inducing apoptosis,terminaldiff el rentiation,and immune responses and thus to reduce
genomic instability in the tissue system and eliminate mutated cells.
Contraryto the imnediate begin of repair after DNA damage hasoccurred,adaptive
protection deve1ops as adaptive response relatively s1owly within a few hours,maylast forseveralweeks to months,and resemble physio1ogicalstress responses that protect against

accumulation o f D N A damage in tissue. T h i s damage may befrom any source such asfrom

metabolica11y generated or environmentaltoxins orrenewed irradiation[l8]. Such protective
responses occur in various ways.They appearto depend on mammalian species,individua1

genomes,ce11types,cellcycle,and cellmetabolism.Adaptive protection categories after--

singlelow dose,1ow LET irradiationare as fo1lows:

Da mage p revention
Stimulation ofthe radicaldetoxification system that appears to reach a maximum at about4

hours after irradiation andlasts for severalhours to even weeks,depending on tissue and ce11

type. I n mouse bone marrow m vivo,there wasa delayed and temporaryreduction oftheincorporation o f D N A precursors and ofthymidine kinase activityto some70%ofcontro1
with a concomitant rise offree glutathione;the eff el ct s1owly declined over a period ofabout6-

hours. [ l 0, l 9, 20, 2 l ]. In otherlow dose irradiated rodent tissues,increasedlevels ofsuperoxide dismutase(SOD)occurred in para11elwith decreasedlipid peroxidationlasting forweeks[22,23]and an elevatedleve1ofglutathione up by a factor ofc1ose to five in spleen

ce11s was involved in an increase in naturalki11er cellactivity[24]. ROS detoxification was-

alsolinked to gene activation.Thus,mRNAs for glutathione synthesis related proteins in the- 1 6 1 --

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intrace11ularglutathione caused by1ow-dose inRAW264.7cells had its maximum between3
and6hours after exposure;this eff ect was mediated by transcriptionalregulation ofthe
gamma- glutamylcysteine synthetase gene,predominantly through the AP -1binding site in its

mouseliver became elevated after Iow dose gamma irradiation[25]. The increase inlpromoter[26].

Damage r epair-

Protection against high dose induced chromosomalaberrations in humanlymphocytes--

increased to a maximum about4hours after a conditioning1ow dose1ow LET irradiation;theprotection also operated against other DNA damaging agents[27, 28]. This protection-

covered up to about30%ofthe damage seen in non conditioned controls and varied between
individuals and ce11s types;it was absent in some individuals and is probably determined

genetically[29, 30]. Where it operates,it appears tolast up to about3days,as reported forvarious human cells i n vivo aswe11as in culture[l5]. This adaptive response probably-

involves a severa1 fold enhancement ofthe DNA repair rate[31, 32lwiththe s1ow component-

o f D S B repair being much faster at 0.5Gy x rays than that seen at2Gy[33]. Anotheradaptive response ofthistype appeared regarding micronuclei formation in human fibroblasts[34]. Inthese ce11s,conditioning doses f r o m l t o 5 0 0 mGy were equa1ly eff el ctive;this also

indicated that at the1owest dose,when approximately40%ofthe cells did not experience anenergy deposition event,a bystander efliect was involved in causing the adaptive protection[35]. A similarset ofdatain fibroblasts showed constancy ofthe adaptive protection over a-d o s e f r o m l t o 1 0 0 mGy gamma rays using the micronucleus assay[36]. The degree of

inhibition ofDNA synthesis and ce11growth in rat glialce11s in culture by a highdose o f x-rays was reduced by about one fourth to one third at severalhours fol1owing a conditioning-

1ow dose exposure,when the ce1ls were obtainedfrom young rats.The adaptive response-

decreased with age ofthe donor rats.This adaptive response involvedprotein kinase C

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(PCK),DNA dependent protein kinase(DNA P K),and phosphatidylinosito13 kinase(PI3K),-

as we11as the activity ofthe ataxia telangiectasia gene(ATM)[37].

-Damage removalbyapoptosisDamaged ce11s may be induced into apoptosis by intra and-interce1lularce1lular signaling.Apoptosis also may occur within hours after high dose--

irradiation.Low dose induced apoptosis ofpre damaged ce11swith replacement by healthy
cells may be a major route of mvivo remova1of oncogenica11y transformed ce1ls[38, 39, 40,-

41, 42,43,44]. Low dose induced apoptosis is assumed to operate also through intercellular
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signalingfrom normalce11s,which may also be activated by transformed celis in culture [45,

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46]. N o n growing human fibroblasts in culture with DSBs 1lirom1ow dose1ow LET-

irradiation readily1ost this damage to theleve1ofDSBs in non irradiated controlce11s after-

induction ofproliferation;this damage removalwas mainly due to apoptosis[47]. Low dose

induced enhancement of DNA repair may be responsible for the observation in rat thymocytes,-

where the incidence ofradiation induced apoptosis first declined at1ow doses and only rosewith higher doses[48l. The induction ofapoptosis apparently requires a certainlevelofDNA
damage.

Stimulation cfimmune response-

Remova1ofdamaged cells occurred i n v ivo by way ofa1ow dose induced immune

competence[49, 50l. This was,in another study,associated witha reduction in the incidence
ofcancer metastases toless than one third of controlconcomitantly with an increased number

ofcirculating cytotoxiclymphocytes[5l]. Such response had its maximum ln v ivo at about-

0.2Gy[52l. Low dose induced immune competence maylast fio rseveralweeks[53].
Protection an d ce11 cycle

Damaged ce11s also may exit the system by premature diff el rentiation and maturation tosenescence[54]. This was observed to occur also via bystander effect in microbeam
experiments directed to single ce11s in complex tissue[55]. The various mechanisms ofprotection may be directly or indirectlylinked to transient changes in the activityofthe G1
ce1lcycle checkpoint[56]. Another mechanism in this categoryofdamage removalis known-

to occur in a number oftissue culture ce11types by way ofhypersensitivity to1ow doseradiation that disappears at higher doses[57, 58]. This hypersensitivityin some ce11s was

1inked to the ce11cycle[59, 60]and it disappeared in a number ofculture ce11swithin about4

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hours,but not immediately,after a single1ow dose,1ow LET irradiation[6l]. Radiation-induced predisposition to genetic instability in culture ce11s also declined fo11owing1ow dose-

irradiation[62].These data indicate prevention ofdamage removalby way of1ow dose

induced DNA repair.

Reductionof carcinogenes is
The coordinated action ofthese protective responses,in one form or another may be

responsible for the observation ofareduction ofspontaneously occurring cancers. In fact,-

single1ow doses of 1ow LET radiation in tissue culture ce1ls initiated with a delay of lday,
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but not immediately,a significant reduction of spontaneous c1onogenic transformation to-about one third ofcontro1[63, 64, 65].There is indication that this1ow dose suppression of

oncogenic transformation is not in response to ce11ularglutathione[66l. It can involve-

bystander phenomenalikely through extra ce11ular signaling exchange[67l. In mice--heterozygous for the Trp 53gene,a single1ow dose of low LET radiation given at the age ofabout2months significantly delayed the appearance of spontaneous 1ymphoma and spina1-

osteosarcomalater inlife[68]. A review ontumor development fo11owing1ow dose,1ow-

LET irradiation in rodents showed the existence o f a threshold dose[69]. This is supported

by a recently published study ofinduction of lymphomas,solid tumors,and ovarian tumors in
BC3Flfemale mice that at the age of lmonth or3months received single whole body doses-

up to32cGy of1ow LET radiation;the threshold dose was4cGy[70]. Severalhumanepidemio1ogicalstudies also indicate either a threshold or a reduced cancer incidence below-

controlfollowing a single1ow dose irradiation[5, l 5, l 6, 40].

-

Low dose lnduced changes i n gene expression
The abovelisted categories ofadaptive protection involve changes in gene expression[4,25,

26,37, 71l. Anexample for D N A repair gene activation refers to the telangiectasia gene[37].

Human fibroblasts in culture showed DNA repair in the course of adaptive protection against-

micronucleus formation fo11owing acute high dose irradiation;the repair was more effectivein the gene poor chromosome than in the gene rich chromosome ofthe ce11s[72]. Anotherdata set showed that exposure ofhuman skin fibroblasts in culture to a single dose o f 2 0 mGy

γ一radiation caused more than100 genes to change their expression within2hours.This genegroup included stress response genes and was differentfrom the group ofgenes in para11e1
cultures that concomitantly responded to500 mGy[73]. A similarpattem ofexpression

amongst a tota1of 1574genes deve1oped in theγ一irradiated mouse brain more at30 min.than
at4hours, w i t h 3 0 % o f t h e genes exclusively aff el cted by 0.1Gy[74l.

A common patter nDespite the disparity ofthe examined systems and responses,there appears to be a common-

pattem in the data. I n fact,adaptive protection following1ow doses of1ow LET radiation

appears to be the consequence ofchanged ce1lular signaling and to be ubiquitous.
Adaptive protection is a physio1ogicalexpression ofce11ularcapabilities to maintain integrity
oftissue structure andfunction in the face ofvarious exposures to potentia11y toxic agentsincluding ROS,be they from endogenous sources orfrom ionizing radiation[5,75,76]. 0 n e- 1 6 4 -

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JAERI Conf-

2005 001

might speculate that DNA damage accumulationfrom any source eventua11y conditions a celi
to become susceptible to apoptosis induced bylow doses including thatfrom backgroundradiation exposure[2]. In this sense,background radiation exposure comes into focusasa

possible trigger for maintaining tissue homeostasis.

Regardingtheir dependence on absorbed dose,the abovelisted categories of adaptive

protectionare schematically summarized in Figure1.Except for apoptosis and terminalcel1
diflierentiation,a11the above protective responses to single exposures tend to be expressed-

maxima1lyafterlessthan 0.1and notaftermore than 0.5Gy X orγ一radiation[10, 77, 78]
and to increasingly failwithhigher doses depending ontype ofadaptive protection in a given
ce11systemassummarized previously[5, l 0 , 1 l, l 2 ] ; i n most mammalian ce11s so far
examined,the expression ofadaptive protectionhad a maximum above5mGy and below
about200 mGy.

-

Fig.1:
Singlelow dose induced adaptive responses have a protectingfunctionthroughvarious
mechanisms.Note that mechanisms ofDNA damage prevention and repair andthe l mmune
stimulation decreaseafter amaximum at doses between 0.1 0.2Gy,in contrast to apoptosis
incidencethat increaseswith dose.Absorbed dose is in Gy andalso in terms of
microdosimetry,inthatthe mean energy deposition per particle traversalper defined
micomass(specific energy i1 )(ICRU1983)is multiplied bythe number of such events(NH )inthe number ofexposed micomasses(NE).

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Regarding the duration of their eff el ctiveness,Figure2gives a schematic summaryof
available published data.The time scales ofduration ofadaptive protection ofvarious kinds

are crucia1ly important fortheassessment ofdose rate effects[79]. Depending on radiation

type and dose rate,energy deposition events per defined miocromass such as a cellhappen atcertain average time intervals.The time intervalbetween repetitive energy deposition eventsin a defined bio1ogicaltarget at a given dose rate may determine to what degree damage oradaptive protection prevails.

-

Fig.2:
Singlelow dose inducedadaptive responses have diflierent times ofduration depending onprotective mechanisms,that beginwitha delay of severalhours and maylast for up to months
regarding immune response.Notethat repair in response to radiation damage begins
immediately afterdamage hasoccurred.

-

Since DNAdamage and cancer in mammalsarise mainlyfrom non radiogenic sources,it is--justified to relatethelow dose induced variousadaptive protection mechanism mainly to nonradiogenic,i.e., spontaneous DNA damage and cancer in addition totheir potentialef liectagainst radiogeneicdamage and cancer,aspresented in more detailin a modelelsewhere[5,l 1, l 2, l 7 ]. A summarizing graphicaldisplay applyingthe mode1of risk evaluationafter--

singlelow dose irradiation is shown in Figure3.It illustrates in principlethat1ow doses
induce adaptive protectionagainst DNAdamage and itsaccumulation in tissue,mainly 16rom

endogenous,i.e., spontaneous sources andthus counterbalances effects from radiation
-

166 -

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JAERI Conf

2005 -0 0 l-

exposure. The net risk of cancer,then,becomeslower than predicted by the LNT hypothesis,-

or even negative with more benefit than damage to the1ow dose exposed system.

-

Fig.3:The dualefliect of single1ow dose irradiation is schematically analyzed according to asimplified model(see also text).This encompassesasafunction ofdose D,i.e.ofNH/NE for agiven radiation quality,t1・l,e following probabilities: a) of DNA damage induction per energy
deposition event il (see Fig.1),plnd,witha potentialcontributionfrom bystander eff el ct,in
red;thisfunction appearslinearwithdose beyondthe contributionfrom bystander effect;b)ofthe net protection provided by dose dependent mechanisms,ppr。t(fNH),plusof apoptosis
papo, bothagainst spontaneous cancerwiththe probabilitypspo per af liected cel1,ingreen.
The net cancerrisk derivesf l:omthe diflierence between cancer induction and prevention at
由e variousdoselevels;the solid curve ofnet cancer risk i s w ithout protectionfrom apoptosis,
andthe dotted curve ofnet cancer risk iswithprotectionfi'om apoptosis.

-

Summaryl)Ionizing radiation causes DNAdamage in mammalian cells proportionalwithdosewith
additionalpossible bystander effects. 2 ) A t background radiation exposurelevels,DNA-damage comes overwhelminglyfrom non radiation sources.3)The probabilityofradiationinduced adaptive protection measurably outweighs that ofdamagefrom doses we1lbe1ow200-

mGylow LET radiation.4)The delayed and temporaryadaptive protection at1ow doses
involves damage prevention,damage repair,and immune responses.They appearto operate- 1 6 7 -

JAERI-Conf-2005 001-

primarily against D N A damage from non radiation sources. Moreover,apoptosis andterminalcelldifferentiation also occur at higher doses and tend to remove susceptible-

damaged ce11sasdoes the1ow dose induced stimulation ofthe immune system.Ce11remova1
reduces genomic instabilityand mutated cellsfrom tissue. 5 ) A t higher absorbed doses intissue,ce11and DNA damage appearincreasingly to overmle,negate,or annihilate the more
subtle signaling ef lfects seen afterlow doses thatlead to adaptive protection,whereas- -apoptosis and terminalce1ldifferentiation continue tofunction.6)Thelinear dose riskb c t i o n appears invalid and should be replaced by afunction that includes bothlinearand-non 1inearterms.Basic researchdataand human epidemiologicaldata conform to threshold-or hormesis inthelow dose range.

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JAERI C o n f 2 0 0 5 0 0 l

3.4 Health Effects of Low Dose Radiation
低線量放射線の健康影響

Sohei K O N D 0
近藤宗平
Emeritus Professor of OsakaUniversity

大阪大学名誉教授〒583 - 0864羽曳野市羽曳が丘6 - 2- 1 3-

E mai1:skondo@taurus.bekkoame.ne.jp

Abstract
Studies of 30,000 children born to atomic bomb survivors exposed to an average of 400 mSv
revealed no statistica11y significant increase in the genetic indicators when compared with40,000
controlchildren. Nevertheless,UNSCEAR reports in2001gave estimates of hereditaryef fects ofradiation using experimentaldata on mice.Four cases(peopleliving at a highbackground radiation
area in China,British radio1ogists,European airline pi1ots and children in Belarus exposed to high1eve1of radioactive fal1out from the Chemobylaccident)of epidemio1ogic data are presented toshow that cancer incidences after chronic exposure to radiation at theleve1of a few mSv to100
mSv are not higher than those after exposure to the norma11eve1of naturalradiation. Radiation,
when given at a1ow dose,is safe.

はじめに
20世紀の科学文明発展の基礎を支えた物理学の分野におけるノ ー ベル 賞は、 4 0 % が 放 射線関連分野の研究に与えられている。 放 射 線 は 科 学 的 に 最 も よ く 研 究 さ れ た 対 象 で あ る 。

し か し な が ら 、 広島・長崎の原爆災害が余りにも甚大であったので、 原爆災害の主因は、
よ く し ら れ て い る 爆 風 や 熱 線 で あ っ た 4 ) に も か か わ ら ず 、 放射線という魔物の作用であった と 信 じ て い る 人 が 多 い 。 さ ら に 、 人工放射線の一般人 へ の 被 ば く は 1 m S v 以 下 に 限 る よ
うに法的に厳しく規制されている。このため、一般には、放射線は1mSvでも浴びると危
険 だ と 誤 解 さ れ て い る 。 人類は数百万年前に地上に誕生して以来、 昼 も 夜 も 自 然 放 射 線 を

浴 び な が ら 毎 日 暮 ら し て き た 。 そ う し て 、 現在では平均寿命70年の長寿を享受している。

自然放射線の年間の量は1mSvを少し上回る。 数百万年も浴び続けたこの程度の放射線が人体に危険であるはずはない。 な ぜ な ら 、 人類はこの自然放射線による人体影響に対しては、 数百万年問の進化の過程で、 防衛機能を獲得しているに違いないからである 4 ) 。 しかし 、数mSvの放射線の被ばくが健康に危険か否は、科学的課題であるから、低線量放射線

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うな調査結果の実例を引用して、 この問題を総括的に検討する。

1. 原爆放射線の遺伝的影響 4・6)
原爆被ばく者の=世の人たちに対するアンケ ト調査によれば、 4 人 に 1 人 が 差 別 を 受ー

け て き た と い う こ と で あ る 。 被 ば く 二 世 の 多 く が 、 親の原爆被ばくの遺伝的悪影響が自分たちに異常として現れるかも知れないと心配して暮らしているということである。

原爆放射線の遺伝的影響の調査は、広島のAtomic Bomb Casualty Co mmission (ABCC)
で1948年最重要項日として取り上げられ、 1975年に、 ABCCがRERF(Radiation Effects

Research Foundat ion:放射線影響研究所) と 組 織 替 え さ れ て か ら も 、 継 続 さ れ 、 約40年にわ た り 追 跡 調 査 が な さ れ 、 人類遺伝学史上で最大規模の調査である 4 , - 6) 。
原 爆 放 射 線 の 遺 伝 的 影 響 の 調 査 は 、 被 ば く 者 の 子 、 「 被 ば く 二 世 」 す な わ ち 、 Exposed F l(F 1 = f i r s t filialgeneration)と被ばくしていない対照者の子「対照二世」(ControlF 1 )との間で、 適当な遺伝的指標 (genet ic indicator ) に 関 す る 異 常 頻 度 の 比 較 で な さ れ た 。

Table1に調査結果を総括して示す 4・6) 。

Table1 Genetic effects of atomic bomb radiationa ) ; comparison of abnormality
frequencies between children(F1)ofcontrolparents a n d F1 of exposed parents b)
原 爆 放 射 線 a ) の遺伝的影響;対照二世と被ばく二世の間の異常頻度の比較 b)

Genetic
indicators

Trans1ocationsof chromosomes

遺伝的指標

転座;染色体異常
0.31%(25/7976)
0.2 2 %
(18/8322)

ControlF1

=

対照

世

Exposed F1
被ばく二世

Sex chromosome
abnormalities
性染色体数の異常
0.30%(24/7976)
0.23%(19/8322)

Mutations i n blood
proteins
血液蛋白質の変異
0.00064%(3/(4. 7x105))0.00045%(3/(6.7x105))

Congenitaldefects Childhooda n d stillbirths
deaths発生異常と死産
遺伝的指標
小児期の死亡4. 9 9 %0.05%
7. 3 8 %ControlF1
対照 二世(21/41,069)(2,257/45,234)(2,451/33,361)
5
%
0
.
0
5
%
7
.08%
Exposed F1
被ばく二世(503/10,069)(989/13,969)(16/31,159)a ) Average value of parentalexposure doses w a s 0. 4 S vb) A w a et a l ( 1 9 8 9 ) , N e e l e t a l ( 1 9 8 8 ) , Ylo shimoto et a 1 ( 1 9 9 1 ) , 0 t a k e et a l ( 1 9 9 0 )Yoshimoto et a l (1991)
Genetic
Indicators

Childhoodleukemia
小児白血病

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染色体の異常が遺伝的異常の指標としては一番分りやすい。 Table1 に 示 す よ う に 、
常染色体の転座の頻度では被ばく二世の値0.2 2 % は 対 照 二 世 の 値 0 . 3 1 % よ り 小 さ く 、 性染'色体の数の異常頻度では、 被 ば く 二 世 の 値 0 .23%は対照二世の値0. 3 0 % よ り 小 さ い ) 。
血液細胞で生産される蛋白質を生産する遺伝子に被ばく二世または対照二世で突然変異が発生すると、 蛋白質の特性が異常として現れる場合が少なくない。 こ の よ う な 異 常 特 性 を検出するため、 被ばく二世と対照二世の各人について、 血球細胞の蛋白質30種類の特性が生化学的に調査された 6 ) 。 被 ば く 二 世 で は 、 調査された遺伝子の述べ総数67万個当たり3個に変異蛋白質が検出されたので、 1 個 の 遺 伝 子 当 た り の 変 異 頻 度 は 0 . 0 0 0 4 5 % で あ り 、

対照二世の血液蛋白質生産遺伝子の変異頻度の0 . 0 0 0 6 4 % よ り 小 さ い ( T a b l e 1 参 照 ) 。 親 の
放 射 線 被 ば く の た め 、 その子でがん頻度が増えている可能性がある。 2 0 歳 ま で に 発 生 し'た白血病頻度では、被ばく二世も対照二世も0.05%で両者間に差がなかった o) ( T a b l e 1 ) 。
親 の 被 ば く が 原 因 で 、 子 供 に 「 発 生 異 常 ・ 死 産 」 7)

る可能性がある。いずれの調査でも被ばく='または「小児期の死亡」 o) が増加す

世と対照二世とで頻度に有意の差はなかった。.

2 . 自然放射線の高い地区と対照地区のがん死亡率の比較 4 , 9 )中国広束省陽江県には自然放射線が普通地区(ControlArea)より約3倍高い地区(HBRA:High Background RadiationArea) が あ る 。 両地区の年間がん死亡率の比較をTable2に示す。この地区の調査は1970年に開始され、現在も調査は継続されている。統計的に有意差はないが、 自 然 放 射 線 線 量 率 が 3 倍 高 く て も が ん リ ス ク は 高 く な い 。

Table2Comparison of cancer death rates in controland high background radiation areas i n
China a)
中国の自然放射線の高い地区 (HBRA) と対照地区のがん死亡率の比較
Radiation dose b) Cancer death rates Relative cancer death
rates
rates
がん死亡率
がん死亡率相対比
自然放射線線量率1
ControlArea
6.8x10 - 4 / e a r
0.7mSv/year
対照地区
HBRA
0.96(0.8˜1.2)
2.2mSv/year
5.7x10 - 4 /yeara) W e i , L.X. a n d Sugahara,T. . J . Radiat. Supp1. V;ol.41(2000)b) Externalnaturalradiation dose only;外部自然放射線線量のみy-

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3 . 英国放射線科医と一般臨床医の死亡率の比較 2)
英国の放射線科医として1955年 ˜ 1979年の間に初めて登録した医師の1955˜ 1 9 9 7 年 間の死亡数〇と放射線を臨床現場で使用しない一般臨床医の期待死亡数Eの比〇/EをSMR(standardized mortality ratio標準化死亡比)という。 期待死亡数は次式によって求める:E = n lp1 十 n2p2 十 ' ' ' 十 nkpk

(1)

こ こ に 、 nl は放射線科医集団のi番目の年齢階級の人数、 P 1 は一般臨床医のi番目の年齢

階級の死亡率、 kは調査集団で採用した年齢階級数である。

Table3に放射線科医の観察死亡数、一般臨床医の期待死亡数、標準化死亡比を示す。

T a b l e 3 0 b s e r v e d ( 0 ) d e a t h s i n British radjologists a n d expected d e a t h s ( E ) i n medical
practitioners a n d SMR(standardized mortality ration)stratified by cause of death a)
英国における放射線科医と一般臨床医の死亡率の標準化した相対比SMR
Cause of death 死因
0 観察死数 l0l 期待死数 S M R 標準化死亡比
32
45.03
0.71
Allcancers 全がん
0.64* * *77
120.66
A li n o n cancer diseases
がん以外の病気* * *f 0 . 0 0 1) Berrington,A. et al. B r J Radiol74:507 519(2001)
The death rates given i n this table are for radio1ogists,who entered the profession during
1 9 5 5 a n d 1 9 7 9 , a n d have been annually exposed to a n estimated dose of 5 m Sv.
この表は、 1955˜1979年に放射線医になり、年間5mSvを浴び続けた放射線医のデ一夕。

--

Table3 によれば、 放射線科医のがん死率は一般臨床医のがん死亡率にく ら べ 0. 7 1 で 、 2 9 %
低いが統計的に有意の低下ではない。 他方、 がん以外の病気死亡率のでは、 放射線医の値は 一 般 臨 床 医 の 値 に 比 べ 0 . 6 4 と 低 く 、 この値は統計的に有意の低下である 。 放射線科医は.

毎年約5mSvのX線など人工放射線を被ばくしたと推定されている。

4 . 欧州の定期航空便パイロッ トの宇宙線被ばく量と死亡数の標準化死亡比との関係 5)
定期航空便のパイロットは毎年数mSvの宇宙線を高度飛行のために浴びている。 この宇宙線被ばく量が地上の一般人の宇宙線被ばく量より増加しているため、 がん死が地上の一般人より高い可能性が重要な関心事になっている。欧州7ケ国の飛行機パイロットの調査
結果をTable4に示す。

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T a b l e 4 S t a n d a r d i z e d mortality r a t i o s ( S M R ) s t r a t i f i e d by cumulative dose of cosmic
radiation i n European airline pilots a)
欧州の定期航空便パイロットの標準化死亡相対比SMRと累積宇宙線被ばく量の関係
0˜4.9
5˜14.91 5 ˜24.9
25.0+
Cumulative dose(mSv)
累積線量(mSv)

S M R for allcause deaths

0.97
0.66
0.64
0.46
全原因死に対するSMR(0.89˜1.06) (0.58˜0.74) (0.57˜0.72)(0.39˜0.53)
S M R for a11cancer deaths
0.91
0.67
0.71
0.6
がん死に対する S M R(0.72˜1.09) (0.53 ˜0.87) (0.58˜0.91)(0.45˜ 0.77)a) Langner,I. et al.:Radiat Environ Biophys42:247 - 256(2004)
Pilots were exposed to annualcosmic radiation doses of 2˜5 m Sv .
パイロットは年間2˜5mSvの宇宙線を浴びた。

Table4は、欧州の定期航空便パイロ ッ ト を 、 宇 宙 線 被 ば く 累 積 線 量 の 大 き さ に し た が って 4 群 に 分 割 し て 、 各 亜 群 ご と に 、 全原因死亡またはがん死亡に対するSMR値を、 地上の一 般 国 民 の 死 亡 率 と 比 較 し て 示 し た も の で あ る 。 例えばがん死亡に対するS M R 値 は 、宇 宙 線 被 ば く 量 が 4. 9 m S v 以 下 の 亜 群 で は 0 . 9 1 で あ り 、 地上の一般国民の死亡率と統計的に有意差はない . 。 他 方 、 宇 宙 線 被 ば く 量 が 2 5 m S v 以 上 の 亜 群 で は 、 が ん 死 亡 の S M R 値
は 0 . 6 と 大 き く 低 下 し 、 この値は統計的に有意の低下である。すなわち、放射線は25m S v を 越 す 程 度 に な る と 、 放射線を浴びた方が、 がん死亡率を低下させる有益効果があることが示唆されている。

5 . 原爆放射線被ばく量と小児白血病頻度の関係 8)
原爆放射線被ばくによるがんでは、 小児の白血病が被ばく後一番早く発病し、 し か も誘発頻度も高い。原爆ひばく時に15歳以下であって、被ばく後6˜ 10年間に急性リンパ性白血病(ALL:acutelymphoblasticleukemia)を発病した人に対する線量とALL発病率の関係をTable5に示す。
T a b l e 5 は 、 被 ば く 量 が 0 . 0 3 ˜ 0.3Svの低線量域では、急性リンパ性白血病の年間発病率は、 非被ばく群の発病率0.3x10 - 5 / 年 に く ら べ 、 1 ˜ 1.3x10 - 5 / 年 と 微 増 し た こ と を 示 す 。

被ばく量が1Gy以上になるとは血病の発病率は桁違いに激増する ( T a b l e 5 ) 。 小児の白血病の頻度は線量0.03Sv付近では増加しないで、 し き い 値 が る こ と が 示 唆 さ れ る が 、 Table

5 の デー タ で は 、 数 値 を 額 面 通 り と れ ば 、 し き い 値 が 3 0 m S v 付 近 に あ る こ と は 断 定 で き

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ない。放射線誘発小児白血病にしきい値があるか否かは、もっと多数の小児の低線量被ばく の デー タ を 調 査 し な け れ ば 結 論 を だ す こ と は で き な い 。

-

Table5Incidence rates of acutelymphoblasticleukemia(ALL)in children 0 15years
old at the time of atomic bombings stratified by dose of atomic bomb radiation a)
原爆放射線被ばく量と小児の急性リンパ性白血病発生率の関係

Atomic bomb radiation dose
(Sv)
原爆放射線被ばく線量

0

0.03

0.3

1

t 1.5

0.3

1

1.3

23

149

(Sv)

Incidence rates(10 -5/year)
白血病の発病率 (10 - 5/年)
a)--Tomonaga,M et a l : R E R F TR 9 91,RER ]1l1, Hiroshima(1993)
Leukemia incidence rates given are average rates d u r i n g 6 ˜ 1 0 yearsafter the atomic
bombings.
白血病発生率は原爆被ばく後6˜10年間の平均値。

6 . チ ェルノブイリ事故による放射性降下物高濃度汚染地域の小児白血病の発病率 3)

べ ラ ル ー シ国では、 1 9 8 2 年 以 降 1 5歳未満の小児の白血病発病は登録が義務になっている 。 この国には、チ ェルノブイリ事故による放射性降下物が高濃度で汚染した地域がある。

例 え ば G o m e 1 付 近 は 、 放 射 性 C s137の高濃度汚染地であり、平均値が370kBq/m 2 であった。この地区の15歳未満の男の子16万人における白血病の年間発生率は、1982年

˜1 9 9 4 年 の 間 で は T a b l e 6 の よ う な 変 動 を し た 。
Table6によれば、 チ ェルノブイリ事故が発生した 1986年の前と後の年間白血病発病率の平均値は(3.98±1.94)x10 - 5 と(4.45±2.09)x10 - 5 で あ り 、 両者の間に有意の差はない。
従 つ て 、 チ ェルノブイリ事故で放出された放射性C s 1 3 7 に よ る 汚 染 に よ る 線 量 率 約 4

mSv/年の放射線を被ばくした男の子(女の子の場合も、白血病発病率は1986年の前と後で統計的有意の差なし) には白血病の有意の上昇は起こらなかった。 すなわち、 放射線による小児白血病の誘発は線量率約4mSv/年では起こらない証拠がえられた。

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Table6 Annualchildhoodleukemia incidence rates for boys aged <1 5 y e a r s i n Gomel,
Belarus plotted against calendar years a )べラルー シ国 ゴメルのおける男の子 ( 1 5 歳 未 満 ) の自血病の年間発病率の経年変化 a)
Calendar year

1 9 8 2 8 3 84

85

86

87

88 89 90 9 1

1.4

6.8

6

3.4

92

93 94

白血病を調査した年

Incidence(10 -5/year)

4.5

5

5

3 6.4 3.5 7.3 1

5

発 病 率 ( 1o- 5/年)-

a ) I v a n ov, E P et a1:Radiat Environ Biophys35:75 80(1996)b ) T h e average of leukemia incidence rates for the period before a n d after the year of
Chernobylaccident(1986)is(3.98±1.94)x10 - 5 and(4.45±2.09)x10 - 5 ,respectively
G o m e l w a s polluted with radioactive Cs 1 3 7 a t c a . 3 7 0 kBq/m2 (=4mSv/year)
ゴメル地区の放射性Cs - 137 汚染濃度≒37万Bq/m 2 (= 4mSv/年)-

むすび
原爆放射線を平均約400 m S v 被 ば く し た 人 た ち の 子 供 さ ん 達 に は 、 遺伝的異常頻度の統計的に有意な上昇は見られなかった。 この結果は、 3 万 人 の 被 ば く 二 世 と 4 万 人 の 対
照=世 を 4 0 年 問 追 跡 調 査 し た 大 規 模 の 研 究 に よ っ て え ら れ た も の で あ る 。 この調査結果は、 一 般 に は あ ま り し ら れ て い な く て 、 知識人にもこの調査結果の意義はほとんど理解されていない。

放 射 線 は 、 年 間 数 m S v 程 度 の 被 ば く で あ る な ら 、 安 全 で 発 が ん の 危 険 は な く て 、 しば

しば健康に有益である。この結論は、英国の放射線科医、欧州の定期航空便パイロット、チ ェルノブイリ事故で放出された大量の死の灰からの放射線を浴びたBelarus国の小児について、 がん死または白血病発病の疫学的調査を行つた結果からえられたものである。

放射線は少しなら害がない証拠が、 上述の例のように多数存在するのに、 国際放射線防護委員会や文部科学省の当局は、 こ の よ う な 実 例 を 無 視 し 、 微量放射線の管理を強めて い る 。 この結果、 教育の現場では、 放射線はどんなに微量でも危険だという考えが普及し 、 放射線を正しく怖がる科学的な教育は無視されている。

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References参考文献
1)Awa,A.A.et a1.(1989):Cytogenetic Study of the O ffspring ofAtomic Bomb urvivors,
Hiroshima a n d Nagasaki.RERF T R 2 1 - 88,Radiation Effects Research
Foundation,Hiroshima,pp. 1 20.
2)Berrington,A. e t a1(2001)100 years of observation on British radio1ogists:mortality
from cancer a n d other causes1897 - 1997 . Br. J . Radiol. 74:507- 519.
3)Ivanov,l E . P.et al.(1996)Childhoodleukemia i n Belarus before a n d after the
Chernobylaccident. Radiat.Environ. Biophys.35:75 80.
4 ) 近 藤 宗 平 ( 1 9 9 8 ) 「人は放射線になぜ弱いか」 ブル ー バックス 、 講談社、 東京
5 ) L a n g n e r , I . e t al(2004)Cosmic radiation a n d cancer mortality among airline pi1ots:
results from European cohort study(EECAPE). Radiat. Environ.Biophys.
,

-

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42:247 256.
6)Neel, J .V. e t a1. (1988)Search for mutations altering protein charge and/or function
i n children of atomic bomb survivors:finalreport.Am. J . H u m. Genet. 4 2 : 6 6 3 - 676.

7 ) 0 t a k e , M . e t al(1990)Congenitalmalformations,sti1lbirths a n d early mortality
Among the children of atomic bomb survivors:reanalysis. Radiat. Res. 1 2 2 : 1 11.
8)Tomonaga,M. et a l.(1993)DifferentialEffects ofAtomic Bomb Irradiation
i n Inducing Major Leukemia的pes:Analysis of Open City Cases Including the LifeS p a n Study Cohort Based upon Updated Diagnostic Systems a n d the Dosimetry
System1986(DS86),RERF TR9 91.Radiation Effects Research Foundation,
Hiroshima9 ) W e i , L .X. and Sugahara,T.(Eds)(2000)High Background RadiationArea. J . Radiat.
R e s. Suppl V,oI. 4 1 , p p . 1 76.
10)Yoshimoto, Y et a l.(1991)Mortality among the O ffspring(F1)ofAtomic Bomb
Survivors,1946- 8 5 ( R E R F T R 1- 91)Radiation Effects Research Foundation,
Hiroshima,pp . 1 27.

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3.5 Recent Advances in Research on Radiation Adaptive Responses
放射線適応応答に関する最近の研究から
Kazuo SAKAI
酒井一夫

Low Dose Radiation Research Center,CentralResearch Institute of Electric Power Industry
電力中央研究所・低線量放射線研究センター〒201 -8511東京都狛江市岩戸北2 -11 -1 E -mai1:kazsakai@criepi.denken.or.jp

The radiation adaptive responses have been typicaliy demonstrated as an acquired resistanceinduced by a l o w dose ofradiation to alarge(cha11enge)dose administered after some interval. The
responses have been demonstrated in various types of cultured ce11s; the endpoints include
micronucleus formation,sister chromatid exchange,mutation induction, /'n vltlr o transformation,and
ce1ldeath. The adaptive response has been also demonstrated in the whole body system;mice
irradiated with a sma11dose developed a resistance against alethalirradiation.The response was also
demonstrated in terms ofradiation and carcinogen induced tumors.
The adaptive responses seem to work in a protective way against radiation damage andcontradicts what is assumed in the current radiation protection system:radiation is harmfu1,no matter
how1ow the dose is.
,

1.はじめに放射線はどんなに微量であっても有害であると言われる。一般の人々はこれが放射線防護のための仮定であることを認識せず、 あたかも事実のように受け止めている場合が多い。 これが放射線に対する恐怖感の一因ともなり、 中学校、 高校の教科書や一般向けの書籍の中には放射線を危険なもの'の代表として取り扱い、恐怖感をあおるような記述すら見られる。 )高線量の放射線が有害であることは様々な事例が示す通りであるが、高線量での障害のイメー ジもこのような誤解の原因のひとっと考えられる。高線量の場合の影響に目が奪われていたためか、 低線
量域の放射線の生物作用に関する研究の歴史はまだ浅い。しかし、低線量放射線の生物作用が詳細に調べられるようになるに っれ、その様相が高線量の場合とは大きく異なることが明らかとなりっつある 。 その代表的な例が放射線適応応答 2 ) である。

2.放射線適応応答とは放射線適応応答とは、予め低線量の放射線を照射しておくと、その後の高線量照射に対して抵抗性を示す現象のことを指す。代表的な解析の手順

O hallenge
Dose
Priming Dose
Adapting Dose
Conditioning Doseは図1に示すとおりである。まず、わずかな線量をAnalysis for
Endooints

図1:放射線適応応答の解析法

照射し、時間をおいた後で予め照射する低い線量を priming dose、adaptirig d o s e 、 あ る い は
conditioning doseなどとよぶ。これに対し、その後に照射する高い線量はcha11enge doseとよばれる。

Fig.1:Typicalprotocolto demonstrate radiation
adaptive responses

183

184 --JAERI Conf

2005 -001(1)細胞レベルで見られる適応応答
放射線によってDNAに切断が生じこれが修復されずに残つてしまうと、本来の細胞核のほかに、DNA の断片を含む小さな核と類似の構造体が残る。このような構造を「小核」あるいは「微小核」とよび、修復されずに残つてしまったDNA切断の指標とされている(図2)。さて、V79という培養細胞に3GyのX
線を照射したところ、20 % 余りの細胞に小核が生じた。これに対して3Gyの照射の4時間前に0.1Gyの照射をしておくと、小核を持つ細胞の割合は約 17 % に、0.2Gyの照射をしておいた場合には約15 % に低下した。0 . 1 G y の み あ る い は 0 .2Gy のみの場合は、照射しなかった場合(0Gy)とほとんど差がなかった(図3)。ここでは4時間という間隔が重要で、0.1Gyあるいは0.2Gyの照射の直後に3Gyを照射しても小核形成の低下は見られない。
このことから、0.1Gyあるいは0.2Gyの事前照射が細胞内で4時間の間にDNA切断が後に残らな
いような仕組み、おそらくはDNAの損傷を修復する機能の増強を引き起こしたものと考えられる。

(2)マウスの急性死を指標とした適応応答

T

0 Gy
0.1 G y0.2Gy

3Gy
0.1 G y + 4 hr + 3 G y
0 2 Gy+4 hr + 3 G y

5

0

10

20

15

25

Micronudei(%)--

図3:小核形成を指標とした適応応答

Fig3:Adaptive response i n terms of
micronucleus formation.

20

25

-

︑

・
・︑

、

e
o
o
u
u

7Gy Only l ,,

0
2

n

S

った。ここでも2週間の間隔をあけることが

、
ti

:

と、7Gy照射1ヵ月後の生存率は80 % であ

ii

0
4

照射の2週間前に0.5Gyの照射をしておく、

lrradiatedwith 0.5Gy
2Weeks before7Gyt6

いる割合は10 % であった。ところが、7Gyの'0
6のX線を照射すると、1ヵ月後に生き残つて

Ol

l

0
8

C57BL/6Nという系統のマウスに7Gyほど'

u 一一︵ ︶一 ﹂﹀i4:米澤らの結果をもとに筆者が作成)。

-.

一生存率を指標とした例が典型的である') (図

100

yo

個体レベルの適応応答としてはマウスの獲得は見られない。つまり、0.5Gyという線'

続いて7Gy を照射した場合には抵抗性の

5

10

15

Days after7Gylrradiation-

重要であり、間隔をあけずに0.5Gyに引き

30(Yonezawa1996)

量がマウスの体の中で何らかの変化を引き起こし、2 週間の間に次第に抵抗性が獲得されたと考えられる。また、ここで獲得された

図 4 : マ ウ ス の 放 射 線 感 受 性 を 指 標 と した適応応答

Fig.4 : R a d i a t i o n adaptive response i n terms ofradiosensitivityofmice

抵抗性はいつまでも続くわけではない。 このことは、0.5Gy照射後 1カ月たってから7Gyの照射をしても抵抗性の獲得が見られないことからわか

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る。

(3)発がんを指標とした適応応答
マウスに放射線を週に 1 回の割合で4 回照射すると胸腺リンパ腫と呼ばれるある種のがんが生ずることが知られている。C57BL/6Nという系統のマウスに1.8GyのX線を4回照射した場合には90 % の
マウスに胸腺リンパ11重が発症した。これに対して、1.8Gyの照射の6時間前に0.075Gyを照射すると胸腺リンパ腫の発症は約70 % にとどまった 2)。このことは、0.075Gyの事前照射が1.8Gyの照射による胸

一
一
一
一 一o
一﹂
一
一︶ 一
一
一
．

腺リンパ腫の発生を抑えたことを示してい︵oo。また、がん抑制遺伝子p53に異常を

一﹂﹂

．．

持つマウスにおいて自然に生ずるリンパ︐腫や骨肉腫の発症の時期が低線量照射

60
40
20
0

d

5)

ao

u

6︑
f リンパ ︵9●︶ー-は他の系統のマウスでも報告されている

u
o
E
e

る。 同様の、 胸腺リンパ腫の発症の抑制

0

100

200

300

400

500
Days

によって遅れるという報告がある6 )。

X- rays, 1 .8 Gy x 4 二 7.2Gy(4)低線量率長期照射による発がん抑制

出以上の結果はいずれも、「事前照射」(0.075Gy + 6hr + 1 . 8 G y ) X 4,b.

500 Daysを短時間のうちに与えた場合に観察されたものであるが、同様の現象が微量の放図 5 : 胸 腺 リ ンパ腫の発生を指標と した放射線適応応答

射線を長期間にわたって照射した場合

Fig5:Adaptive response i n t e r m s of thymiclymphoma
inductionsにも起こるかどうかを化学発がんの場合に っいて調べた。

-

マ ウ ス ( I C R 系 統 ) に 3 . 5 、 1 .2、あるいは
0
0

o
M
o

P
a
u

、

1 .2mGy/hr

ll
l

n
E
o

0
2

l
3 e
﹀一
一

0- -

n
E
n

〇

低下が認められた。1.2mGy/hr照射群

3. 5mGy/hr

04

が、3.5mGy照射群では若干発がん率の0.35mGy/hr

、

、、

0
6

照射群ではほとんど差が見られなかった:の 場 合 に は 9 4 % であった。 0.35mGy/hr̲

0
8

日後までの累積発がん率は、 非照射群

Non lrradiated

︶
﹂
一
．

い、腫瘍が生ずるまで観察を続けた。216-基発 生率 ︵% ︶累積l-それぞれの線量率で引き続き照射を行一

その後そけい部にメチルコラントレンと呼ばれる化学発癌剤を投与した。投与後は︵ ︶ -一︶ ou
一﹂

0.35mGy/hrの線量率で35日間照射し、

0

)

100

150

200

250

;)ays after Carcinogenlnjection
発がん剤投与後の日数ではさらに低下が見られ、 発がん率は

図6:低線量率照射による発がんの抑制

74 % であった7 )。

Fig.6:Suppression ofcarcinogenesis by1ow dose rateirra diation

5.まとめ
放射線適応応答の機構の解明は現在も進行中の研究分野である。詳細は今後の研究の進展を待たなければならないが、活性酸素を除去する機能、DNAの損傷を修復する機能、体内に生じた変異細胞を排除する仕組み(アポトー シ ス ) 、 あるいは免疫機能などいわゆる「生体防御機能」の活性化がpress.

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起こっているものと考えられている。別の見方をすれば、生体には微量の放射線に対する絶妙な応答の機構が備わっていると言えよう。
放射線適応応答は生物学の題材として興味深いだけでなく、 放射線の影響というものを正しく理解する上で非常に重要な現象である。 今後人類と放射線との関わりがますます深まる中で、次の世代には放射線に対する生き物の応答のおもしろさと生物影響に対する正しい知識を伝えることが大事であ
ろう。

引用文献
lン s・ No.588,60-62
1. 松 浦 辰 男 「 学 校・社会における放射線教育の重要性とその在り方」 fsotope Nel,:(2003)
2.

G.01ivieri, J.Bodycote,and S.Wolff:Adaptive response ofhumanlymphocytes to1ow concentrations ofradioactive thymidine. Sa1'ence 223,594-597(1984)

3.

M.Yonezawa, J.Misonoh and Y.Hosokawa:Two types of X-ray-induced radioresistance in micepresence o f 4 d o s e rangeswith distinct bio1ogicaleffects. Mutat. .Res.358:237 -243(1996)

4.

Y.Ina,T.Yamada,H.Tanooka,and K.Sakai:Suppression ofThymic Lymphoma Induction by Life-Long
Low Dose-Rate Irradiation Accompanied by Immune Activation in C57BL/6Mice. ,Rladilat. ,Res.(2005)In

5. D.Bhattacharjee:Role of radioadaptation on radiation-induced thymiclymphoma in mice.
358, 231-235(1996)
6.

Mutat.Res.

R . E . J.Mithel, J . S . Jackson,D.P.Morrison,and S . M . C a r lisle:Low doses of radiation increase the1atency of spontaneouslymphomas and spina1osteosarcomas in cancer-prone,radiation-sensitive Trp53
heterozygous mice. Radiat Res.159:320-327(2003)

7. K. Sakai e t aj. Suppression of Carcinogenic Processes in Mice by Chronic Low Dose Rate
Gamma-Irradiation, h t. J. Low ftadjat 1:142(2003)
'

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3.6 Concerns on the health effects of low dose ionizing radiations

from naturally occurring radioactive materials(N〇R M )MaryN. Mohankumar
Radio1ogicalSafety Division,Indira Gandhi Centre for Atomic Research,
Kalpakkam603102,India
Abstract
It is a widely knownfact that man evolved in a natura11y radioactive environment.Even todaylife
exists in an atmosphere of cosmic and terrestrialradiation.Radionuclides are found natura11y in air,water and soi1.They are even found in u s , w e being the products of our environment.Every day,weingest and inhale radionuclides in our air and food and the water. Nattl ralradioactivity is common in
the rocks and soilthat makes up ourplanet,in water and oceans,and in ourbuilding materials andhomes.There is nowhere on earththat onecannot find naturalradioactivity.Radioactive materials
which occur natura11y and expose people to radiation occur widely,and areknown by the acronym
NORM(Natura11y O ccurring Radioactive Materials). Besides,aroundthe g1obe there are some areas
with an elevatedbackground radiation.These areas includeparts ofBrazi1,Iran,India and China. T h esourcesof radiation inthese areas include monazite containing beach sands and radiumfio m hot
springs. 〇 n the southwestcoast ofIndia,there arelarge deposits ofthorium bearing monazite sandsthat contribute to an extemalradiation dose ofabout5 6 m G y/ yr,but in some parts doses up to32.6
mGy/yrhave been reported. Nevertheless,most generalpublic associate ionising radiations only with
the nuclear industry . Antinuclear activists often failto accept the fact that coa1- fi redpower stations
and the o i l a n d gas exploration operations may emit more radioactivity than an operating nuclear
reactor.Another N〇RM issue relates to radonexposure in homes,particularly those built on granite
grounds.The solid airbome R n-222progeny,particularly Po-218,Pb -214and B i-214are of healthimportance because they can be inspiredand retained in t h e l u n g c a u s ing cancer. Man madeope11a tionslike oiland gas production and processing operations result in techno1ogica11y enhanced
natura11y occurring radioactive materials(TEN〇RM)to accumulate at elevatedconcentI:ations in byproduct waste streams. Theconcem arises because ofthe verylarge amounts ofTEN〇RMneeding
recycling or disposalfrom many sources.Thelargest TENORMwaste stream is coalash.In India andAustraliamining of beachminerals is a profitable industry. The beach sands along the south Indiancoast arerich sources ofminerals such as ilmenite,rutile,zircon,silimanite and gamet. Thetailings
obtained after the extraction o f t h e above minerals get enriched with monazite,a thorium bearing
mineralthat is radioactive.Recent studies show that the activities in the tailings are somewhat morethanthe naturalbackgroundlevels in some parts of south India . Studies on health effects(cancer)
from doses arising from theselevels ofnaturalradiation exposure are contradictory,some reporting
adverse effects,others nulland a few others beneficialhormetic effects.Systematic andlarge-scale
epidemio1ogicalstudiesandlaboratory investigations are ca11ed for in order to resolve this issue.
Concerns on bio1ogicaleffects ofradiationsfrom NORMare growing and efforts are on to implement
radiation protection standards in TENORMindustries in the same way as inthe nuclear industry .

--Introduction
Radiation is ubiquitous. It is natura1lypresent in our environment and hasbeen since the birthof this planet.In factlife has evolvedin an environment which had significantlevels of ionizing
radiation. It comes from outer space(cosmic),the ground(terrestria1),and even from within our own
bodies. It is present inthe air we breathe,the food w e e a t t h e water we drink,and in the construction
materials usedto build our homes. Foodstuflislike bananas and ice creams contain significant amounts
ofradioactive potassium.
The major radionuclidescontributing to N〇RM are uranium,thorium,and potassium.Theseradioactive elements are found in granite,sandstone,cement,1imestoneconcrete,sandstone

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concrete,drywa11board,and gypsum by product.Another source of radiation exposure in dwe1ling
places is radon gas,which may be present in the soilbeneath the dwe1ling.This gascan diffuse into abuilding and together with its radioactive decay products(polonium 2 l 4 a n d po1onium 218),cause
1arge radiation doses to thelungs of the occupants.This is especia11y true in c1osed or poorly
ventilated indoorareas.Radon hasbeen identi fied by the E P A a s t h e secondleading cause of lungcancer.(1)Radon in domestic water supplies can be released into the air within a home.Water
obtained from we11s a rid other groundwater sources can contain high radon concentrations. Besides,
due to the presence of large deposits ofthorium bearing sandspeople residing in some parts of India,
Braziland China are exposed to more naturalradiation than thoseliving in other parts ofthe globe.
lmproper ventilation in homes and mines and more recently the radioactive mineralcontent in tailings
ofbeach sand mining hasraised concems on elevating naturalbackground radiationlevels.

--

TechnoIogicaIIy Enhanced naturaliy 〇ccurring Radioactive MateriaIs(TEN〇RM)--

Uranium 238,radium 226,and other members of the uranium decay seriesare present invarying amounts in nearly a11rocks,soils,and water.Sometimes human activities,suchasmining andmi11ing of ores,extraction ofpetroleum and naturalgasresources,use of groundwater for domestic
purposes may alter the naturalbackground radiation environment,either by moving N〇RMs frominaccessiblelocations to places where humansare present or by concentrating them. Situations due toanthropogenic activities causing an enhancement ofN〇RMresult in TENORM.
Mining and processing of phosphate for fertilizer is another major source of TEN〇RM.The
currently used process generateslarge piles ofphosphogypsum,in which naturally occurring radium isconcentrated.N〇RMis also technologica1ly enhanced in the course of producing and processing oi1
and gas.Although in the early'70sthere were concems about radioactive materialassociated with oil
and gasoperations,a series of investigations resulted in a conclusion that radioactivitywas not aserious health threat thus,any concem about it dissipated untilthe1980s. I n the early1980s,it was
discovered thatlarge production facilities in the North Sea were generating concentrated quantities of
N〇RMwastes that required specialmanagement techniques.In1986,NORMwasidentified intubing
in a Mississippi wellby Chevron during routine maintanance(2).Ra 226,an alpha emitter,is apotentialintemaI hazard to workersfrom the inhalation and ingestion of the dust produced during
descaling or pipe cleaning operations.Thelargest TEN〇RMwaste strearn is coalash,with280
mi11ion tonnesarising g1oba1ly each year,and carrying uranium 238and a11its non gaseous decay
productsaswellas thorium 232and its progeny.Most coalcontains uranium and thorium,as wellaspotassium 40,1ead 2 10,and radium 226.
Radon exposuresfrom NORM also include visit to caves and spas.In a recent study,theannualexposure ofcave tour guides was estimated to fallbetween3and10 mSv,which is the range
ofactionlevels recommended by the ICRP(3).
In India and Australia mining ofbeach minerals is a profitable industry. The south Indiancoastbeach sandsarerich sources ofminerals suchasilmenite,rutile,zircon,silimanite and gamet.
The tailing obtained after the extraction ofthe above minerals get enriched with monozite,a thorium
bearing mineralthat is radioactive. Recent studies show that the activities in the tailingsare somewhat
more than the naturalbackgroundlevels(4).

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Regulations and RegulatoryIssues:
Due to strict measures,radiation exposures to workers are stringently measured and kept far
below the perm issiblelimits in the nuclearindustry. H o w e v e r a s a result ofTEN〇RMindustries andcertain tourism related activities a new group of radiation workers in the non nuclear industrynow
emerge.These include maintenance workers in the oiland gasindustry,miners,cave tour guides andspa workers. Americansliving nearcoal fired power plantsare exposed to higher radiation doses,
particularly bone doses,than thoseliving near nuclearpower plants that meet government regulations(5).
The Marina11study revealed t h a t a s a result of the activities discharged and the higher
biologicaleffiectiveness ofalpha radiation,phosphate and oilproduction currentlyare the major--

18 1il- 189 --JAERI Conf

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contributors to co11ective dose to the population of the European Union from industrialactivities(6).
Nevertheless,in many European countries double standards operate for radiation doses emitted fromnon nuclear operations compared to those from nuclear industries. I n these countries 0.3to1.0 mSv/yr
individualdose constraint is applied to o i l a n d gasrecyclables,and 0 . 0 l m S v/yr for release ofmaterials with the same kind of radiationfrom the nuclear industry.Decommissioning expertsare
increasingly concemed about these double standards(7).
It is now being strongly felt among radiation protectionists that radionuclides must be
regulated in a uniform and consistent manner on the basis ofthe fo11owing:-

If a radionuclide is a hazard at a given concentration,it is a hazard regardless ofthe
regulatoryenviron ment;
I f a n atom ofuranium poses a hazard at alicensed site,then the atom of uranium poses the same
hazard at an alumina or rare earth production site"(8).

Fo11owing radiation measurements in TENORMindustries,radiation protection agencies
worldwideare now implementing similarguidelines to workers in the TENORMindustries .Table1
is an example ofthe type ofcontrolmeasures proposed to be implemented in the European Union.
Table 1.ControlBands for Radiation Protection(9)Normal
<1mSv/

yLowerlevelregulation
H igherlevelregulation

Process not peml itted
u n less dose can be
reducedIn India,the Atomic Energy RegulatoryBoard's(AERB)recommendationsare based on ICRPforboth occupationaland public exposure categories. A stringent watch is also maintained on the beachsand mineralindustryand controlbandsare currently being worked out-

Health effects of low dose ionising radiations

Atypicalbreakdown between naturalbackground radiation andartificialsources ofradiationis shown in the pie chartbe1ow. I t shows naturalradiation contributes about82%ofthe annualdose to
the population while medicalprocedures contribute most of the remaining18%.Both naturaland
artificialradiations affect us in the same way.
Althoug11 mutations are the basis for cancer initiation,theassociation between radiation
exposure and the deve1opment of cancer hasbeen we11established only with bigh dose exposures(>
0.5Gy).Cancersassociated with such high aose exposure includeleukemia,breast,bladder,co1on,liver,lung,esophagus,ovarian,multiple myeloma,and stomach cancers(10). Reports on the health
eff el cts of low dose ionising radiationsare contradictory.The EPA hasidenti fied radonasthe major
cause o f lung cancer among non smokers and based on current exposure and risk estimates,radon
exposure in single family houses may be a cause ofasmany as20,000lung cancer fatalities each year(1).Besides,a dose response relationship between chromosome aberrations and increased levels ofradon hasbeen reported among miners(11).Although the presence ofchromosomalaberrations is a

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biomarker ofeffect,the potentialrange ofchemicals which could cause this effect is so great that it
would not necessarily be considered radon speci fic.

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Fig.1.Sources of Radiation Exposures (NCRP93)

For1owlevels of radiation exposure,the bio1ogicaleffects are so smal i they may not be
detected.The body has repair mechanisms against damage induced by radiation as we11as bychemicalcarcinogens.Consequently,inJured or damaged cells can repair themselves,resulting in noresidualdamage,some may die,muchlike mi11ions ofbody ce1ls do everyday,being replaced throughnormalbiologicalprocesses.Sometimes,ce11s incorrectly repairthemselves resulting in mutations.
Extensive studies have been undertaken on populations residing in areaswith high natura1
background radiation and among nuclearemp1oyees. W h i l e thereare a few reports that relate cancer
incidence and mortality to background radiation and occupationalexposures(12,13),most surveys
have frequently indicated decreased rates in cancer mortality(14,15,16,17).0thers show no adverse
bio1ogicaleffects(18,19).
Reportsfrom ourlaboratory(20,21)and elsewhere(22,23,24)show that DNA repair
capacities are enhanced when humanlymphocytes are exposed to1ow doses ofgamma radiations andthis phenomenon popularly termedasradio adaptive response(RAR)is though to occur via error free
repair mechanism.However,compared to gamma rays,the penetrating power ofalpha particles is1ow
and ifalpha emitters are inhaled,ingested or absorbed into the b1ood stream,sensitiveliving tissue canbe exposed to alpharadiation.Also,due to the highlinear energy transfer(LET),alpharadiation may
have a adverse biologicaleffect at1ow doses.
Taking into considerations these controversies, the radiation protection community
conservativelyassumes that any amount of radiation may pose some risk for causing cancer andhereditaryeffect,and that the risk is higher for higher radiation exposures. A l i n e a r , n o threshold(LNT)dose response relationship is used to describe the relationship between radiation dose and theoccurrence of cancer.This dose response modelsuggests that any increase in dose,no matter how
small,results in an incrementalincrease in risk.However,contenders to the LNT hypothesisare those
supporting hormesis and adaptive responses on one hand and those who support an inverse dose/rate
effect claiming disproportionately higher risks at1ower doses on the other(Fig2).
The studies conducted so faron the Indian population residing inHNBRA for over1000 years
indicate that highlevelnaturalradiation hasno discemible impact on the health of population and infact may provide valuable input to understand the bio1ogicalmechanism of response to radiation at
1ow dose rates.Cytogenetic studies were done using cord b1ood samplesfrom nearly23,000 newboms.
Rate of constitutionalanomaly wasaround 0 . 5 % w h i c h is comparable to the intemationalvalue.
Cytogenetic preparations from over10,000 children were also screened for detection of chromosoma1
aberration.Frequency ofaberration wasl.87/10,000 ce1ls for dicentrics,3.42/10,000 cells

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for stable aberrations and7.72/10,000 ce11s for totalchromosomaltype aberrations(25).These figures
are comparable to those in publishedliterature from other parts ofthe world.

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a Linear m odelc Disproportionatelylower risksb Th reshoIdeffectd Disproportionatelyhigherrisks

Fig2.The1ow dose controversy
In summary,none of these approaches has provided unambiguous evidence of cancer
induction at1ow doselevels,and the issue remains highly controversia1.Moreover,the complexity ofthe biologicaleffects induced by alpha emitting radionuclides poses aproblem in estimating risks due
to1ow dose radiation.
Long term systematic studies on occupationa1ly exposed personneland epidemio1ogica1
surveys of areas with high naturalbackground radiation together withlaboratoryinvestigations are
therefore required before meaningfulconclusions could be drawn and infl uence current radiation
protection standards. T h e existence of inter individualdifferences in radiation sensitivity govemed bygeneticfactors making some individuals more sensitive to radiation induced damage remains a
confounding factor in relaxing radiation protection norm s(26).Although it may be not too early to
accept the beneficia1or nu11biologicaleffects of 1ow doses of ionising radiation,it is certainly so to
set standards and threshold doses for purposes of cancer risk estimates and radiation protection.
If1owlevels ofradiation tum out to have athreshold be1ow where there really is no risk to speak of,thenlaws may be1oosened.However,if1owlevels ofradiation actua1lyare proven to be carcinogenic,or have mutagenic,teratogenic,or some other detrimentaleffects,then current regulatoryefforts may
fa1lshort ofprotecting the public and workers.Untilthen it may be prudent to fo11ow the LNT modeI
for purposes ofradiation protection for those engaged in both nuclear and non nuclear industries.
Regarding NORM and TENORM we are in the enviable position,given that a potentialhealthconcem is being identi fied ahead of any visible problem among workers. B y recognizing a potential
problem,it is now possible for industries with someleve1ofrisk to protect their workers using fairly
simple,1ow cost methods.

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References:
1. EnvironmentalProtection Agency.Technicalsupport document forthe1992citizen's guideto radon.EPA publication400 R 92 011.Washington,D.C(1992).
2 . Bu11etin on ManagementofNaturally Occurring Radioactive Materia1(NORM)in〇iland GasProduction, American Pe tro1leu m I n s t Bld1. E2,1st ed.,Apr.1992
3 . Papachristodou1ou C.A.,Ioannides K.G.,Stamoulis KC.,Patiris D.L.,Pavlides SB.Radon
activitylevels and effiective doses in the Perama Cave,Greece.Health Phys.(2004)86:619

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Suresh K . , A j o y K.C.,Dhanasekaran A . , B a l a Sundar S.,Santhanam R.,Gajendiran.V.,
Meenakshisundaram V.Investigation ofradiationlevels in beach sand mineralindustries - A
preliminarystudy.Radiation Protection and Environment(2003)26:478 - 481.
McBride J.P.,Moore R.E.,Witherspoon J.P.,Blanco R.E.Radio1ogicalimpact ofairbome
effluents ofcoaland nuclearplants.Science(1978)202:1045.
Pi1ot Study for the update ofthe MAR工N AProject on the radio1ogicalexposure ofthe
European Community from radioactivityin North European marine waters.FinalReport:
December1999,!l
1i tud(l 1tp ・1/ w ,t. eurol1)里二j11u . inllco m m le11:elrl !v . n u cl,iaj;1 ・ad ro. pdf)
Nucleonics W e e k 4 3 ( 1 7 ) A pri125,2002.
Scott L.M.N〇RM in the Non Nuclear Industries in the USA,in:Proceedings ofN〇RM II
Second IntemationalSymposium,Novemberl0 13,l998,Krefeld,Ger many,paper V/4,

、 、、、

7.
8.

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Simmons2000.NORMin Europe A Regulation Perspective.Charles Simmons.The
N〇RMReportFa1l99/Winter 00.Peter Gray,Editor.Fort Smith,AK.
10.UNSCEAR(1994).Sources and effects ofionising radiation,United nations reportto thegeneralassembly with scienti fic annexes.
11.Smerhovsky Z.,Landa K.,Rossner P., Juzova D.,Brabec M.,Zudova Z.,HolaN.,Zarska H.,
Nevsimalova E.Increased risk of cancer in radon exposed miners with elevatedfrequency ofchromosomalaberrations.Mutat Res.(2002)514:165 176.
12.Baum J.W Population heterogeneityhypothesis on radiation induced cancer.Health Phys.
(1973)25:97 104.
13.Kneale,G.W.,StewartA.,Mancuso T.F(1978).Reanalysis ofDatarelating tothe Hanford
study ofthe cancer risks ofradiation workers.Proceedings ofthe intemationalsymposium on
thelate effects ofionising radiation.Vo11.IAEA,Vienna,STI/PUB/489.
l4.Frigerio N A . , S h o w e R S(1976).Carcinogenic and genetic hazardfrom backgroundradiation.In Bio1ogicaland Environment Effects ofLow LevelRadiation,IAEA,2,385 393.
1 5 . L i u S Z(1989).Radiation hormesis A new concept in radio1ogicalscience.Chinese Med. J.
1032:750 755.
16.Wei L.(1990).Epidemio1ogicalinvestigations of radiological effects in high backgroundradiation areas,YangJiang,China. J.Radiat.Res:119 136.
1 7 . Z o u J.,Sun Q.,Akiba S.,Yuan Y.,Zha Y.,Tao Z.,Wei L.,SugaharaT.A case controlstudyof nasopharyngealcarcinoma in the high background radiation areasofYangjiang,China. J
Radiat Res(2000)41Supp1:53 62.
18.Savitz DA.,Zuckerm an DL.Childhood cancer in the Denver metropolitanarea1976 1983.
Cancer(1987)59:1539 1542.
19.Nambi,K.S.V and Soman,S.D(1987).Environmentalradiation and cancer in India.HealthPhys.52:653 658.
20.Mohankumar,M.N.,PaulS.F.D.,Venkatachalam P., Jeevanram R.K.Influence of in vitro
low levelgamma radiation on the UV Induced DNA repair capacityof humanlymphocytes
analysed by unscheduled DNA synthesis (UDS) and cometassay, Radiat. Environ.
Biophysics(1998)37:267 - 275.
21.Mohankumar,M.N, Venkatachalam P.,Prabhu B.K., Jeevanram R.K.,Comparison of UV
induced unscheduled DNA synthesis inlymphocytes exposed to1ow doses of ionisingradiation in vivo and in vitro,MutationRes(2000)447,199 207.
22.Ikushima T.,Aritomi H.,Morisita J.Radioadaptive response:Efficient repair of radiationinduced DNA damage in adapted cells Mutation Res(1996)358,l93 198.
2 3 . W o l ff S The adaptive response in radiobio1ogy: Evolving insights and implications.
Environ.Health.Perspectives(1998)106:277 283(supp1).
24.A.Wojick,C.Streffer.Adaptive response to ionising radiation in mammalian ce1ls a review,
Bio1ogisches Zentralblatt(1994)113:4l7 434.
9.

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25.Cheriyan VD.,Kurien CJ.,DasB.,Ramachandran EN.,Karuppasamy CV.,ThampiMV.,
George KP.,Kesavan PC.,Koya PK.,Chauhan PS.Genetic monitoring of the humanpopulation from high levelnaturalradiationareasofKerala on the southwest coast o f India.
II.Incidence of numericaland structuralchromosomalaberrations in thelymphocytes ofnewboms.Radiat Res.(1999)152(6SuppI):S154 158.
26.MohankumarMN,Prabhu B.K:,.Jeevanra m R.K(2000)Adaptive response to ionizin長radial l on and its role in influencmg radttttion protection standal:tLs .Proceedings of lile 1 0
IntemationalCongress of Radiation Protection(IRPA10), Japan P 2b 74.
,

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3.7 Ramsar Hot Springs:How Safe is to Live in an Environment

with High Levelof NaturalRadiation
S . M . J. Mortazavi

MedicalPhysics Department,Rafsanjan UniversityofMedicalSciences,Rafsarljan,Iran
Abstract
Ramsarin northem ]1ran is among the world's we11 known areas with highestlevels ofnaturalradiation. A n nualexposurelevels i n a r e a s w i t h elevatedlevels of natura1
radiation in Ramsarare up to260 mGy y-1 and average exposure ratesare about10
mGy y 1 for a population of about2000 residents. Due to thelocalgeo1ogy,which
includes highlevels of radium in rocks,soils,and groundwater,Ramsarresidentsare
also exposed to highlevels of alpha activityin the form of ingested radium and radium
decay progenyaswe1las veryhigh radonlevels(over1000 MBq m-3 ) i n their dwe11ings.
In some cases,the inhabitants oftheseareas receive doses much higher than the current
ICRP 60 doselimit of 20 mSv y l . A s the bio1ogicalef lfects of 1ow doses of radiation
are notfu11y understood,the current radiation protection recommendationsare based on
the predictions ofanassumption on thelinear,no threshold(LNT)relationship between
radiation dose and the carcinogenic effects.Considering LNT,areashaving suchlevelsof naturalradiation must be evacuated or atleast require immediate remedialactions.
Inhabitants of the highlevelnaturalradiationareas(HLNRAs)of Ramsararelargely
unaware of naturalradiation,radon,or its possible health eff el cts,and the inhabitants
have not encountered any harmfuleffects due toliving in their patemalhouses.In thisregard,it is often difficult to ask the inhabitants of HLNRAs of Ramsarto carryout
remedialactions.Despite the fact that considering LNT and ALARA,public health in
HLNRAslike Ramsaris best served by re1ocating the inhabitants,the residents'healthseems unaffected and re1ocation is upsetting to the residents.Based on the findings
obtained by studies on the health effiect ofhighlevels ofnaturalradiation in Ramsar,as
we11asother HLNRAs,no consistent detrimentaleff el ct hasbeen detected so far.
However,more research is needed to clarify i f t h e regulatoryauthorities should set
1imiting regulations to protect the inhabitants against elevatedlevels ofnaturalradiation.

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Te1; +98 39 ] 8220097
Fax:+98 391 8220092
E mail:iamo」 」 f 4u 1 ycos ,com

Address for Correspondence;
S M J Mortazavi,Ph.D
Vice Chancel1or for Education andResearchRafsanjan Universityof MedicalSciences
Imam Ali Blvd.
Rafsanj an
Iran

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l. Introduction
Humans,animals and plants have been exposed to cosmic radiation since the beginningof l i f e . T h e l e v e l o f cosmic radiation varies in dif lferent parts of the world due todifferences in elevation and the geomagneticlatitude,and ofterrestrialradiation due togeochemicaldiversity. A b o u t 4 b 加ion years ago,when theliving organisms appearedon the Earth,theleve1of naturalradiation was about3 5times higher than its current
1eve1(Jaworowski1997,Karam1999,Karam2001).The annua11eve1ofradiation fromintemalpotassium 40 has decreased to1/8while the extemalradiation from geo1ogic
materials hasdecreased from about1.6mGy to 0.66mGy since the beginning of life.
Thus,the annualbackground radiation exposure from these two sources has decreased
from about7.0 to1.35mGy(Karam and Leslie1999).The annualper caput effective
dosefrom naturaland man made sources for the world's population is currently about
2 . 8 m S v . N e a r l y 8 5 % o f this dose(2.4mSv)comes from naturalbackground radiation(UNSCEAR2000).People wholive in high altitudeareas such as Tibet in China,Andes

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in SouthAmerica,or citieslike Denver,Co1orado,are exposed to higherlevels of
cosmic radiation due to a thinner atmosphere than peopleliving inareas at sealeve1.
Also astronauts,pi1ots and cabin crew are exposed to higher than norma11evels of
cosmic radiation.The study o f these population groups may revealinformation on
adaptive responses(AR)induced by exposure to higher than norma11evels of natura1
radiation.
Whenliving organismsare exposed to a varietyofDNA damaging stresses suchasUV,
alkylating or oxidizing agents and heat,adaptive responses(AR)are induced whichcause resistance to the agent(Samson and Caims1977).The early investigations of
01ivieri and his co11eagues(1984)showed that cultured humanlymphocytes,whichwere exposed to a 1 o w dose of ionizing radiation had fewer chromatid aberrations
induced by a subsequent high doseascompared to thelymphocytes that have not been
exposed to a1ow dose.Since1984,many investigators have demonstrated A R in plantce11s(Cortes et al.1990),insects(Fritz Niggli and Schaeppi Buechi1991),Chinese
hamster V79ce11s(Ikushima1987),cultured humanlymphocytes(Wiencke et a1.1986,
Shadley and Wolff 1987, Wolff et a1. 1988, Shadley and Wiencke 1989,
Sankaranarayanan et a1.1989),human embryonic and HeLa ce11s(Ishii and Watanabe
1996),occupationa11y exposed persons(Barquinero et a1.1995,Gourabi and Mozdarani
1998),cultured anima11ymphocytes(F1ores et a1. 1996),and i n v ivo studies on
1aboratoryanimals(Wojcik and Tusch11990,Cai and Liu1990,Liu et al.1992,Farooqi
and Kesavan1993).Mortazavi et al.(2003c)have recently reported that the interindividualvariabilityof adaptive response in humans is much greater than what is
usually expected.Recent dataon diflierent aspects of adaptive response,obligate us toreevaluate the current conservative radiation protection regulations(Po1lycove andFeinendegen2001,Mortazavi et a1.2002,Mortazavi2002). In this paper,studies on
adaptive responses related to naturalradiationleVelsare shortly reviewed.

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2. Adaptation after Exposure to Cosmic and TerrestrialRadiation
2.l. Underground Studies
Early experiments carried out on single ce11organisms shielded against backgroundradiation showed that at thelevels of naturalradiation1ower than norma1,theproliferation of these organisms can be inhibited.Interestingly,this inhibitoryeffectdisappeared when shielded ce11s were exposed to very1ow doses of gamma radiation

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c1ose to backgroundlevels(Planelet a1. 1987).Later it was shown that yeast celis
cultured in a1ow background environment wereless protected from mutationaldamage
induced by methylmethane sulfonate than the cells grown in a normalbackgroundradiation environment(Sattaet al. 1995).The results of a recent study on mammaliance11s showed an increase in both the basal hprt mutationfrequency and sensitivityto themutagenic eflliects ofgamma rays in ce11s grown in an undergroundlaboratory,comparedto the ce11s grown in alaboratorywith naturalradiation environment(Sattaet a1.2002).
2.2. High Altitude Areas
The people wholive in Tibet, the roof of the world ,are exposed to highlevels of
cosmic radiation.At the mean elevation of about4000 meters above the sealevel,theatmosphere isless thick,and the residents are exposed to extemalannualradiation doses
up to2.12mSv(Shouzhi2000).This dose is3.5times higher than that at the sealeve1.
Recently the Glycophorin A based somatic mutation assay wascarried out on theresidents of high altitude areas and on those wholived a t l o w altitude.Thelife time
cumulative doses for the high altitude and1ow altitudeareas were111mSv and27mSv
respectively.This study showed no significant diff el rence between the Glycophorin A
based somatic mutation frequencies in these two populations(Jensen et a1.1997).An
epidemio1ogica1 study on mortalitydue to cancer(Xin I983) showed tha t thestandardized mortalityo「cancer(56.26xl0 5) i n the high altitude area of Tibet was
1owerthan those ofthe wllole country(66.92x10 5).The meanannualdose ecl uivalent
for high altitude area w a s 1 . 8 m S v that is a few times higher than that of areas at sea
1evel.The mortalityfromleukemia in the high altitudearea was1ower than those ofthe
whole countryeither.
In an old paper,Frigerio and Stowe(1976)reported that in the United States they founda consistent and continuous inverse relationship betweenlevels of naturalbackgroundradiation and cancer mortality rates i n 5 0 states.Again in the Unites States a negative
correlation ofnormalbackground radiation with overallcancer death was observed in amore recent study. I n RockyMountain States,where theleve1ofnaturalradiation is3.2
times higher than that in GulfStates,the age a(ij usted overa11cancer death w a s 7 9 % o fthat in GulfStates(Jagger1998).

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2.3. Flights and Space Journeys
Zwingmann et a1. (1998)recently measured the DNA damages in23flight engineers.
Despite that oxidative DNA damage inflight engineers was higher than the contro1
ground personne1,it was observed that DNA damage inflight engineers who had arelatively1onger flight t i m e (>7,500hr)and a higher cumulative radiation dose(53.6
mSv)wasless than that of the flight engineers with a shorterflight history(<7,500hr)
and alower cumulative radiation dose(30.7mSv).They also observed that frequencies
o f hprt mutations and micronuclei also tend to be higher inflight engineers with ashorter flight history.These findingsare in keeping with the results of another study thatwas performed on flight crew using the chromosomalaberrations as the end point(Zwingmann et a1 l. 1998).It was indicated that pi1ots and stewardesses with a flighthistoryof only1 6years had more chromosome aberrations compared to crew withmore than20 years ofintercontinental flights. The frequency of chromosome aberrationsin the pilots and stewardesses who were exposed to cosmic radiation for a1ong term, i .e.

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more than20 years of intercontinentalflights、 and those who had been flying o n l y l 6
yearswere1.4x10 3 a n d 3 . 2 x 1 0 3 , respectively.
In a recent study on thefrequency of chromosome aberrations in eighteen supersonicConcorde pilots(Heimers2000),it wasindicated that the dicentric yield in pilots who
were emp1oyed over28years wasabout50%ofthat observed in pilots w i t h l 6 26yearsof occupation(1.3士0 . 5 x 1 0 3 and2.9士0 . 5 x 1 0 3 respectively).Also the frecl uency of
ce11s with trans1ocations in pi1ots with28 34years offlight occupation was78%ofthat
in pi1ots w i t h 1 6 26years of flight occupation(2.8士0 . 7 x l 0 3 and3.6士0 . 6 x 1 0 3
respectively).Despitethe factthatthere are statisticaluncertainties inthese data,thiskind of adaptive response hasbeen we11documented in eukaryotes suchasyeast.

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Deorukhakarand Rao(1995)investigated the radiation induced genetic damage in yleastby culturing the ce11s continuously at a radiationlevelof 0.383-1.275µ Sv h byselecting appropriate concentrations of tritiated water in the growth medium.It was
shown that ce11s which were incubated at higher radiationlevels and for1onger duration
had a higher conversionfrequency.However,when subculturing continued beyond900h,
the gene conversionfrequency reverted back to nor malvalue.Such a response could not
be detected when the cells were exposed to an acute highdose.The authors concluded
that chronic exposure ofyeast to1ow dose radiation might induce an A R .
In a recent study on6061male cockpit personnelwhich yielded105,037person yearsof observation it wasshown that cockpit crew h a d a l o w overa11and cancer mortality(Zeeb et al.2002).This result is consistentwith the results obtainedfrom previous
studies on Canadian(Band et a1.1996)and British Air Ways pilots(]lrwin et a1.1999).
Thatthis is not a healthy worker effiect,suggests mortality from a11cancers,which incabin crew who received5 14.99mSv cumulative radiation dose,was1owerthan inthose who received either 0 4.99or15 2 9.99mSv(Zeeb et a1.2002).
Results of a cytogenetic study on22cosmonauts who stayed on average4 6months in
MIR station shows thattheafter mission percentage of chromosomalaberrations i n 6
cosmonauts isless than that ofthe scoredfrequency before the mission(Fedorenko et al.
2001).Also the after missionfrequency ofthe ce11s with dicentrics and centric rings infour cosmonauts wasless than that ofbefore mission. ]lnterestingly,in one case,the after
missionfrequency of chromosomalaberrations wasabout1/3of the before mission
value.

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2.4. VeryHigh Levels of NaturalTerrestrialRadiation
People in someareasaround the worldlive in dwe1lingswithradiation and radonlevels
asmuch as100 times the g1obalaverage.Inhabitedareaswith highlevels of natura1
radiationare found in differentareasaround the world including Yangjiang,China;
Kerala,India;Guarapari,Braziland Ramsar,Iran.(Figure.1).

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Figure 1.Ramsarhot springsWhite colored sediments at the streams'bed have highconcentrations ofRadium 226. ]ln some cases,residents ofthese hotareas have usedthe
residue ofthe hot springsasbuilding materials to constructtheir houses.

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Ramsarin northem ]lran is amongthe world's weli knownareaswithhighestlevels ofnaturalradiation. Annualexposurelevels inareaswithelevatedlevels of natura1
radiation in Ramsarare up to260 m( i y y l and average exposure ratesare aboutl0 mGyy l for apopulation ofabout2000 residents.
'-

BiologicalFindings on HLNRAs of Ramsar
Chromosome Aberrations. Preliminary results showed no significant
dif lierence even i n t h e case of the inhabitantswholived in houseswith
extraordinarily elevatedlevels ofnaturalradiation.
Dose Effect Relationship.There is agreat controversy aboutthe dose efliect
relationship in published reports on thefrequency of chromosome aberrations
induced by chronic exposure to elevated environmentallevels ofradiation.This
controversy existsin studies of residents inareaswithelevatedlevels ofnturald
画iationaswe11asthe residents ofareascontaminated by nuclear accidents.
Using chromosomalabenationsas 1the main endpoint,an experiment toassess
出e dose eff el ct relationship inthe residents ofhighlevelnaturalradiation areasofRamsarwas ca med out.A cytogeneticalstudy wasperformed on21healthy
inhabitants ofthe highlevelnaturalradiationareasandl4residents of a nearby
controlarea.Preliminaryresultsshowed no positive correlation betweenthe?equency of chromosome aberrations a n d the cumulative dose of theaabitants.
●
HematologicalAlterations. It hasbeenreportedthat in mice and rats totalbody
exposure to moderate doses decreasesthe number of circulating erythrocytes,
platelets,granu1ocytes,lymphocytes etc.However,data on hematopoiesesasa
result of exposure to verylow doses of ionizing radiationare scarce.
Hematologicalparameterssuchascounts of leukocytes(WBC),lyrnphocytes,
monocytesgranulocytes,red blood cells(RBC),hemog1obin(Hb),hematocrit(Ht),MCV,MCH,MCHCRDW,PLT,and MPV were studied ina11ofthe
individuals.The results ofthis study indicatedthatthere wasno any statistically

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significant alteration in hemato1ogicalparameters of the inhabitants of HLNRAsof Ramsar compared to those ofthe neighboring controlarea.
ImmunologicalChanges. It is we11known that high doses ofionizing radiation
suppress the activityof the immune system. 0 n the other hand,the1ow 1eve1
whole body irradiation(WBI)can enhance the immuno1ogicalresponse.To
assess whether relatively high doses o f naturalradiation can alter humora1
imnune parameters,an experiment was conducted on the inhabitants of
HLNRAs of Ramsar,permanentlyliving in houses with elevatedlevels ofnaturalradiation.]lmmuno1ogicalfactors such as the concentration of serum
immunoglobulins ofIgA,IgG,IgM and C3,C4components ofthe complement
system in healthy donorsfrom HLNRAs and a neighboring NBRA were studied.
Preliminary findings indicate that there is a slight increase in IgA and IgGlevels
ofthe inhabitants ofHLNRAs compared to those ofmatched controls.IgM,C3,
and C4complements were in the nor ma l r a n g e . I n spite of the fact that theincrease in IgA and IgG were not so marked to show probable enhanced
immuno1ogicalcapability,it can be concluded that relatively high doses o fnaturalradiationare not immunosuppressive.More research is needed to clarif
的e immuno1ogicalalterations induced by differentlevels ofnaturalradiation. yRadioadaptive Response It has been shown that in highlevelnaturalradiation
areas(HLNRAs)of Ramsar,the b1ood ce11s of inhabitants whose cumulative
radiation doses were170 times higher than of thoseliving in a nearby controlarea(2,550 mSv and15mSv respectively)were significantly more radioresistant
to chromosomaldamage when subjected to1.5Gy cha11enge dose(Ghiassi nejad
et a1.2002,Mortazavi et a1.2002,Mortazavi2002). The relationship between
the degree of AR(asindicated by the k value2) a n d cumulativelifetime dose is
an important finding.The A R of the residents of Iranian HLNRAs is more
pronounced at higher cumulative doses, except for 2 residents, whose
cumulative dosesare much higher than those o f t h e others(Mortazavi et a1.

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The results of the adaptive responses observed in the residents of highlevelnaturalradiation areasof Ramsarare summarized here:●

Individuals whose cumulative radiation doses were up to950 mGy,showed asignificant A R after exposure of their culturedlymphocytes t o 1 . 5 G y gamma
radiation.These dosesare much higher thanthose received byastronauts during
a six month space mission that has been reported to b e 9 0 mGy absorbed doseand180 mSv equivalent dose.The radiation dose oftheseastronauts ranged95
455mGy(Testard et a1.1996).

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The k value is the coefficient of induced adaptive response(k)that shows themagnitude ofthe adaptive response and can be calculatedasthe ratio ofthe observed
frequency to the expectedfrequency of chromosome aberrations.
2

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There is a controversy over the induction of A R in resting cells(Cai and Liu
1990,Shadley et a1.1987,Azzam et a1.1992).Ramsarresults showed that highlevels of naturalradiation might enhance radiation resistance in non cycling
lymphocytes.Since the m可orityof thelymphocytes in the bodyare in theresting phase ofthe ce11cycle(Go),any implication of A R strongly depends on
the possibilityof induction o f A R in Go stage.
●
ARs have been usua11y observed in experiments by exposing the ce11s to a1ow
dose radiation in the range of 10 100 mGy.These dosesare considerably1ower
than thelifetime doses that induced A R in the inhabitants of HLNRAs ofRamsar.
●
It was suggested that aging could cancelthe AR(Gadhia1998). This is contrary
to findings in Ramsarpopulation which show that aging does not influence theinduction' ofAR.
The cumulative doses and the magnitudes of the induced adaptive response in cultured
1ymphocytes ofresidents of Ramsar HLNRAsare shown in Figure2.
●

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2.5. PotentialImplications of Radioadaptation in Radiation Protection
It was genera11y believed that the presence of A R does not mean that the1ow doseradiation is beneficialtoliving organisms(Sagan1989,Wolff1989).Even in its1994
report on adaptive responses to radiation in ce11s and organisms(UNSCEAR1994),
after reviewing experimentaland epidemio1ogicalstudies showing increased1ongevity
and1ower than expected incidence of tumorsUNSCEAR stated that it would bepremature to conclude that cellularadaptive response could convey possible beneficial
effects to the organism that would outweigh the detrimentalefliects of exposure to1ow
doses of 1ow LETradiation However,more recent worldwide studies on the diff el rent
aspects of AR,havelead to recognition of its positive health effects,and to a more
realistic assessment of therisk of radiation.The preliminarystudies of the Ramsar
residents(Mortazavi et a1.2001),suggest that the induced A R might have considerable
implications for radiation protection,and that the chronic1ow dose radiation may beprotective against accidentalhigh dose radiation(Po11ycove and Feinendegen2001).

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2.6. Radioadaptation and Deep Space Manned Missions
Based on Ramsar findings,it has been recently reportedthat adaptive response studies
may have implications in radiation protection.It wasproposed that individuals who
failed to show an adaptive response would not be goodcandidates for space trave1(Mortazavi et a1.2003a,Mortazavi et a1.2003b).These authors suggested that a1l
potentialcrew members for a deep space mission hadtheir adaptive response measured.
The space crew should show a high magnitude of adaptive response.The chronic
exposure to elevatedlevels of space radiation during a1ong term mission canconsiderably decrease their radiation susceptibilityand protect them against theunpredictable exposure to sudden and dramatic increase i n f l u x dueto s01ar flares andcoronalmass ejections.

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