Toxicological
Profile
for
RADON
U.S. DEPARTMENT OF HEALTH & HUMAN SERVICES
Public Health Service
Agency for Toxic Substances and Disease Registry
TP-90-23
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TOXICOLOGICAL PROFILE FOR
RADON
Prepared by:
Clement International Corporation
Under Contract No. 205-88-0608
Prepared for:
Agency for Toxic Substances and Disease Registry
U.S. Public Health Service
In collaboration with:
U.S. Environmental Protection Agency
December 1990
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ii
DISCLAIMER
The use of company or product narae(s) is for identification only
and does not imply endorsement by the Agency for Toxic Substances and
Disease Registry.
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iii
FOREWORD
The Superfund Amendments and Reauthorization Act (SARA) of 1986
{Public Law 99-499) extended and amended the Comprehensive Environmental
Response, Compensation, and Liability Act of 1980 (CERCLA or Superfund).
This public law directed the Agency for Toxic Substances and Disease
Registry (ATSDR) to prepare toxicological profiles for hazardous
substances which are most commonly found at facilities on the CERCLA
National Priorities List and which pose the most significant potential
threat to human health, as determined by ATSDR and the Environmental
Protection Agency (EPA). The lists of the 250 most significant hazardous
substances were published in the Federal Register on April 17, 1987, on
October 20, 1988, on October 26, 1989, and on October 17, 1990.
Section 104(i)(3) of CERCLA, as amended, directs the Administrator of
ATSDR to prepare a toxicological profile for each substance on the list.
Each profile must include the following content:
(A) An examination, summary, and interpretation of available
toxicological information and epidemiological evaluations on the
hazardous substance in order to ascertain the levels of significant
human exposure for the substance and the associated acute, subacute,
and chronic health effects,
(B) A determination of whether adequate information on the health
effects of each substance is available or in the process of
development to determine levels of exposure which present a
significant risk to human health of acute, subacute, and chronic
health effects, and
(C) Where appropriate, an identification of toxicological testing
needed to identify the types or levels of exposure that may present
significant risk of adverse health effects in humans.
This toxicological profile is prepared in accordance with guidelines
developed by ATSDR and EPA. The original guidelines were published in the
Federal Register on April 17, 1987. Each profile will be revised and
republished as necessary, but no less often than every three years, as
required by CERCLA, as amended.
The ATSDR toxicological profile is intended to characterize succinctly
the toxicological and adverse health effects information for the hazardous
substance being described. Each profile identifies and reviews the key
literature (that has been peer-reviewed) that describes a hazardous
substance's toxicological properties. Other pertinent literature is also
presented but described in less detail than the key studies. The profile
is not intended to be an exhaustive document; however, more comprehensive
sources of specialty information are referenced.
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iv
Foreword
Each toxicological profile begins with a public health statement,
which describes in nontechnical language a substance's relevant
toxicological properties. Following the public health statement is
information concerning significant health effects associated with exposure
to the substance. The adequacy of information to determine a substance's
health effects is described. Data needs that are of significance to
protection of public health will be identified by ATSDR, the National
Toxicology Program (NTP) of the Public Health Service, and EPA. The focus
of the profiles is on health and toxicological information; therefore, we
have included this information in the beginning of the document.
The principal audiences for the toxicological profiles are health
professionals at the federal, state, and local levels, interested private
sector organizations and groups, and members of the public.
This profile reflects our assessment of all relevant toxicological
testing and information that has been peer reviewed. It has been reviewed
by scientists from ATSDR, the Centers for Disease Control, the NTP, and
other federal agencies. It -has also been reviewed by a panel of
nongovernment peer reviewers and Is being made available for public
review. Final responsibility for the contents and views expressed in this
toxicological profile resides with ATSDR.
t\
(x)llwv\ U:
William L. Roper, Hj)., M.P.H.
Administrator
Agency for Toxic Substances and
Disease Registry
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V
CONTENTS
FOREWORD iii
LIST OF FIGURES ix
LIST OF TABLES xi
1. PUBLIC HEALTH STATEMENT 1
1.1 WHAT IS RADON? 1
1.2 HOW MIGHT I BE EXPOSED TO RADON? 2
1. 3 HOW CAN RADON ENTER AND LEAVE MY BODY 2
1.4 HOW CAN RADON AFFECT MY HEALTH? 3
1.5 WHAT LEVELS OF EXPOSURE HAVE RESULTED IN
HARMFUL HEALTH EFFECTS? 3
1.6 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE
BEEN EXPOSED TO RADON? 3
1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL
GOVERNMENT MADE TO PROTECT HUMAN HEALTH? 3
1.8 WHERE CAN I GET MORE INFORMATION? 8
2. HEALTH EFFECTS 9
2.1 INTRODUCTION 9
2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 11
2.2.1 Inhalation Exposure 12
2.2.1.1 Death 12
2.2.1.2 Systemic Effects 18
2.2.1.3 Immunological Effects 22
2.2.1.4 Neurological Effects 22
2.2.1.5 Developmental Effects 22
2.2.1.6 Reproductive Effects 22
2.2.1.7 Genotoxic Effects ... 23
2.2.1.8 Cancer 23
2.2.2 Oral Exposure 27
2.2.2.1 Death 27
2.2.2.2 Systemic Effects 27
2.2.2.3 Immunological Effects 27
2.2.2.4 Neurological Effects 27
2.2.2.5 Developmental Effects 27
2.2.2.6 Reproductive Effects 27
2.2.2.7 Genotoxic Effects 27
2.2.2.8 Cancer 28
2.2.3 Dermal Exposure 28
2.2.3.1 Death 28
2.2.3.2 Systemic Effects 28
2.2.3.3 Immunological Effects 28
2.2.3.4 Neurological Effects 28
2.2.3.5 Developmental Effects 28
2.2.3.6 Reproductive Effects 28
2.2.3.7 Genotoxic Effects 28
2.2.3.8 Cancer 28
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2.2.4 Other Routes of Exposure 29
2.2.4.1 Death 29
2.2.4.2 Systemic Effects 29
2.2.4.3 Immunological Effects 30
2.2.4.4 Neurological Effects 30
2.2.4.5 Developmental Effects 30
2.2.4.6 Reproductive Effects 30
2.2.4.7 Genotoxic Effects 30
2.2.4.8 Cancer 30
2.3 TOXICOKINETICS 30
2.3.1 Absorption 31
2.3.1.1 Inhalation Exposure 31
2.3.1.2 Oral Exposure 32
2.3.1.3 Dermal Exposure 33
2.3.1.4 Other Routes of Exposure 33
2.3.2 Distribution 33
2.3.2.1 Inhalation Exposure 33
2.3.2.2 Oral Exposure 34
2.3.2.3 Dermal Exposure 34
2.3.2.4 Other Routes of Exposure 34
2.3.3 Metabolism 35
2.3.4 Excretion 35
2.3.4.1 Inhalation Exposure 35
2.3.4.2 Oral Exposure 35
2.3.4.3 Dermal Exposure 36
2.3.4.4 Other Routes of Exposure 36
2.4 RELEVANCE TO PUBLIC HEALTH 37
2.5 BIOMARKERS OF EXPOSURE AND EFFECT 42
2.5.1 Biomarkers Used to Identify or
Quantify Exposure to Radon 43
2.5.2 Biomarkers Used to Characterize
Effects Caused by Radon 44
2.6 INTERACTIONS WITH OTHER CHEMICALS 44
2.7 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 46
2.8 ADEQUACY OF THE DATABASE 47
2.8.1 Existing Information on Health Effects
of Radon 47
2.8.2 Identification of Data Needs 49
2.8.3 On-going Studies . • • 54
3. CHEMICAL AND PHYSICAL INFORMATION 57
3.1 CHEMICAL IDENTITY 57
3.2 PHYSICAL AND CHEMICAL PROPERTIES 57
4. PRODUCTION, IMPORT, USE, AND DISPOSAL 63
4.1 PRODUCTION 63
4.2 IMPORT 63
4.3 USE 63
4.4 DISPOSAL 64
5. POTENTIAL FOR HUMAN EXPOSURE 65
5.1 OVERVIEW 65
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5.2 RELEASES TO THE ENVIRONMENT 67
5.2.1 Air 67
5.2.2 Water 68
5.3.3 Soil 68
5.3 ENVIRONMENTAL FATE 68
5.3.1 Transport and Partitioning 68
5.3.2 Transformation and Degradation 71
5.3.2.1 Air 71
5.3.2.2 Water 71
5.3.2.3 Soil 71
5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 72
5.4.1 Air 72
5.4.2 Water 73
5.4.3 Soil 73
5.4.4 Other Media 74
5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 75
5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 77
5.7 ADEQUACY OF THE DATABASE 78
5.7.1 Identification of Data Needs 78
5.7.2 On-going Studies 80
6. ANALYTICAL METHODS 81
6.1 BIOLOGICAL MATERIALS 81
6.2 ENVIRONMENTAL SAMPLES 82
6.3 ADEQUACY OF THE DATABASE 88
6.3.1 Identification of Data Needs 88
6.3.2 On-going Studies 89
7. REGULATIONS AND ADVISORIES 91
8. REFERENCES 97
9. GLOSSARY 117
APPENDIX A -- PEER REVIEW 135
APPENDIX B -- OVERVIEW OF BASIC RADIATION PHYSICS,
CHEMISTRY AND BIOLOGY 137
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LIST OF FIGURES
2-1 Levels of Significant Exposure to Radon - Inhalation 16
2-2 Existing Information on Health Effects of Radon 48
3-1 Uranium and Thorium Isotope Decay Series Showing
the Sources and Decay Products of the Three
Naturally-Occurring Isotopes of Uranium 62
5-1 Frequency of Sites with Radon Contamination 69
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2
3
4
1
2
1
2
3
1
2
1
4
5
6
7
13
40
58
59
61
83
85
92
xi
LIST OF TABLES
Human Health Effects from Breathing Radon
Animal Health Effects from Breathing Radon
Human Health Effects from Eating or Drinking Radon
Animal Health Effects from Eating or Drinking Radon
Levels of Significant Exposure to Radon - Inhalation
Genotoxicity of Radon In Vivo
Chemical Identity of Radon
Physical and Chemical Properties of Radon
Radioactive Properties of Radon-222 and Its Short-lived Progeny
Analytical Methods for Determining Radon in Biological Samples
Analytical Methods for Determining Radon in Environmental Samples
Regulations and Guidelines Applicable to Radon-222
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1. PUBLIC HEALTH STATEMENT
This Statement was prepared to give you information about radon and to
emphasize the human health effects that may result from exposure to it. The
Environmental Protection Agency (EPA) has identified 1,177 sites on its
National Priorities List (NPL). Radon has been found above background levels
at five of these sites. However, we do not know how many of the 1,177 NPL
sites have been evaluated for radon. As EPA evaluates more sites, the number
of sites at which radon is found may change. The information is important for
you because plutonium may cause harmful health effects and because these sites
are potential or actual sources of human exposure to radon.
When a radioactive chemical is released from a large area such as an
industrial plant, or from a container such as a drum or bottle, it enters the
environment as a radioactive chemical. This emission, which is also called a
release, does not always lead to exposure. You can be exposed to a chemical
only when you come into contact with the chemical. You may be exposed to it
in the environment by breathing, eating, or drinking substances containing the
chemical or from skin contact with it.
If you are exposed to a hazardous substance such as radon, several
factors will determine whether harmful health effects will occur and what the
type and severity of those health effects will be. These factors include the
dose (how much), the duration (how long), the route or pathway by which you
are exposed (breathing, eating, drinking, or skin contact), the other
chemicals to which you are exposed, and your individual characteristics such
as age, sex, nutritional status, family traits, life style, and state of
health.
1.1 WHAT IS RADON?
Radon is a naturally occurring colorless, odorless, tasteless radioactive
gas that is formed from the normal radioactive decay of uranium. Uranium is
present in small amounts in most rocks and soil. It slowly breaks down to
other products such as radium, which breaks down to radon. Some of the radon
moves to the soil surface and enters the air, while some remains below the
soil surface and enters the groundwater (water that flows and collects
underground). Uranium has been around since the earth was formed and has a
very long half-life (4.5 billion years), which is the amount of time required
for one-half of uranium to break down. Uranium, radium, and thus radon, will
continue to exist indefinitely at about the same levels as they do now.
Radon also undergoes radioactive decay and has a radioactive half-life of
about 4 days. This means that one-half of a given amount of radon will be
changed or decayed to other products every 4 days. When radon decays, it
divides into two parts. One part is called radiation, and the second part is
called a daughter. The daughter, like radon, is not stable; and it also
divides into radiation and another daughter. Unlike radon, the daughters are
metal and easily attach to dust and other particles in the air. The dividing
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1. PUBLIC HEALTH STATKMKNT
of daughters continues until a stable, nonrad i «a<: t i v. daught <-r is formed.
During the decay process, alpha, beta, and gamma null ,-.t ions arc released.
Alpha particles can travel only a short distance and cannot go through your
skin Beta particles can penetrate your skin, but tlu-y cannot. go all the way
through your body. Canuna radiation, however, can go all the way through your
bodv Thus there are several types of decay products that result from radon
decav You will find more information about the physical and chemical
properties of radon in Chapter 3, about: its uses in Chapter . ami about your
potential for exposure in Chapter r>.
1.2 HOW MIGHT I BE EXPOSED TO RADON?
Since radon is a gas and radon daughters are often attached to dust, you
are exposed to them primarily by breathing them in. They are present in
nparlv all air However, background levels of radon in outdoor air are
generally quite low, about 0.003 to 2.6 picocuries of radon per liter of air
A oicocurie is a very small amount of radioactivity equal to one quintlllxonth
a/1018) of an ounce of radon. In indoor locations, such as homes, schools,
or office buildings, levels of radon and daughters are generally higher than
outdoor levels Indoor radon levels are generally about 1.', picocuries radon
liter of air Cracks in the foundation or basement ol your home may allow
increased amounts of radon to move into your home. You may also be exposed to
radon and daughters by drinking water obtained from wells that contain radon.
Average levels of radon in groundwater are about Jj() p i cocu r, es of radon per
liter of water However, most radon in water is rapidly released into the air
^nd can be breathed in. In some areas of the country the amount of uranium
and radium in some rock types, such as phosphate or granite is high. In
these areas radon levels in outdoor air or in groundwater will generally be
higher. You will find more information on exposure to radon in Chapter 5.
1.3 HOW CAN RADON ENTER AND LEAVE MY BODY?
Radon and its radioactive daughters can enter your body when you breathe
them in or swallow them. By far, the greater amounts are breathed in. Most
of the radon is breathed out again. However, some radon and most of the
daughters remain in your lungs and undergo radioactive decay. The radiation
released during this process passes into lung tissue and is the cause of lung
damage Some of the radon that you swallow with drinking water passes through
the walls of your stomach and intestine. After radon enters your blood stream
most (greater than 901) of the radon goes to the lungs where you breathe most
of it out This occurs very shortly after it is taken in. Any remaining
radon undergoes decay. Radon that does not go to the lungs goes to other
ns and fat where it may remain and undergo decay. There is very limited
information on whether radon gas can penetrate the skin, but some radon may be
ble to pass through the skin when you bat-he in water containing radon. You
will find more information on behavior of radon in the body in Chapter 2.
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1. PUBLIC HEALTH STATEMENT
1.4 HOW CAN RADON AFFECT MY HEALTH?
Long-term exposure to radon and radon daughters in air increases your
chances of getting lung cancer. When exposures are high, noncancer diseases
of the lungs may occur, such as thickening of certain lung tissues. While
noncancer health effects may occur within days or weeks after exposure to
radon, it will be several years before cancer effects become apparent. This
is known from studies of workers exposed to radon in mines, primarily uranium
miners, and from tests on laboratory animals. Although radon is radioactive,
it gives off little gamma radiation. Therefore, harmful health effects from
external exposure (when the chemical does not come into direct contact with
your body) are not likely to occur. In addition, it is not known if radon
causes health effects other than to the lung. Also, the effects of drinking
water or eating food containing radon are not known. You will find more
information on the health effects of radon in Chapter 2.
1.5 WHAT LEVELS OF EXPOSURE HAVE RESULTED IN HARMFUL HEALTH EFFECTS?
In studies of uranium miners, workers exposed to radon levels of 50 to
150 picocuries of radon per liter of air for about 10 years have shown an
increased frequency of lung cancer. Although there is some uncertainty as to
how much exposure to radon increases your chances of getting lung cancer, the
greater your exposure to radon, the greater your chance of developing lung
cancer. Even small exposures may increase your risk of developing lung
cancer, especially if you smoke cigarettes. Tables 1-1 and 1-2 were derived
from animal and human data for short-term or long-term exposure, as described
in Chapter 2 and in Table 2-1. This information provides a basis for
comparison to radon levels that you might encounter in the air. As seen in
Tables 1-3 and 1-4, there is no information on the effects of radon if you
drink water or eat food containing radon.
1.6 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO
RADON?
Radon in human tissues is not detectable by routine medical testing.
However, several of its decay products can be detected in urine and in lung
and bone tissue. These tests, however, are not generally available to the
public and are of limited value since they cannot be used to accurately
determine how much radon you were exposed to, nor can they be used to predict
whether you will develop harmful health effects. You will find more
information on methods used to investigate levels of radon in Chapters 2 and
6.
1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO PROTECT
HUMAN HEALTH?
EPA recommends that all homes should be monitored for radon. If testing
shows levels less than 4 picocuries radon per liter of air, then no action is
necessary. For levels above this, follow-up measurements should be taken. If
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1. PUBLIC HEALTH STATEMENT
TABLE 1-1. Human Health Effects from Breathing Radon*
Short-term Exposure;
(less than or equal to 14 days)
Levels in Air
l.enpth of Exposure
Description of Effects
The health effects
resulting from short-
term exposure of humans
to air containing
specific levels of
radon tire not known.
Long-term Exposure
(greater than 14 clays)
Levels in Air (pCi/L)
100
Lene.t,h of Exposure
Occupational
(10 years)
Description o( Effects**j
Severe lunj> damagp
*See Section 1.2 for a discussion of exposures encountered in daily life.
**These effects are listed at the lowest level at which they were first
observed. They may also be seen at higher levels.
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1. PUBLIC HEALTH STATEMENT
TABLE 1-2. Animal Health Effects from Breathing Radon
Short-term Exposure
(less than or equal to 14 days)
Levels in Air
(vCi/U
Length of Exposure Description of Effects*
2.2x10®
1 day Death in mice
Long-term Exposure
(greater than 14 days)
Levels in Air
(nCi/L)
Lenpth of Exposure Description of Effects*
2.6xl05
5.5x10s
4.8xl06
Life Damage to lung tissue
in hamsters.
50 days Lung damage in dogs.
Life Abnormal growth of cells
in lung in rats.
*These effects are listed at the lowest level at which they were first
observed. They may also be seen at higher levels.
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1. PUBLIC HEALTH STAT KM KMT
TABLE 1-3. Human Health Effects from Eating or Drinking Radon*
Short -1 v rrn Exposure
(less than or equal to \h days}
Levels in Food
Length of Exposure
J)t;s< i i i_> t i on of Ef fee ts
The hea I t h e f f ec ts
)'<¦ su 11 i ng from short-
H'liii exposure of humans
t o i ood coniaining
.Spec i I i <• ] cvi'l s of
radon arc not known.
I Levels in Water
The health e i i ec t. s
result i tij', (rom short-
t e rrn exposure of humans
to water containing
speci I i c 1 eve]s of
l'adon are not known.
Long- t t-.rm Exposure
(greater than ] h days)
T.eveIs in Food
Length oi Expos
;til'c
of Effects
Levels in Water
Uv.se LiiLLioLL
The health effects
resulting from long-
term exposure of humans
to 1ood containing
spec i i i c 1 eve 1s of
radon are not known.
The hea1t h ef f ec ts
lesul t i ng from long-
term exposure of humans
to wa t e r cont ai ning
spec i t i c 1 eve Is of
radon are not. known.
*See Section 1.2 for a discussion of exposures encountered In daily life.
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1. PUBLIC HEALTH STATEMENT
TABLE 1-4. Animal Health Effects from Eating or Drinking Radon
Short-term Exposure
(less than or equal to 14 days)
Levels in Food Length of Exposure Description of Effects
The health effects
resulting from short-
term exposure of
animals to food con-
taining specific levels
of radon are not known.
Levels in Water
The health effects
resulting from short-
term exposure of
animals to water con-
taining specific levels
of radon are not known.
Long-term Exposure
(greater than 14 days)
Levels in Food Length of Exposure Description of Effects
The health effects
resulting from
long-term exposure of
animals to food con-
taining specific levels
of radon are not known.
Levels in Water
The health effects of
long-term exposure of
animals to water con-
taining specific levels
of radon are not known.
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1. PUBLIC HEALTH STATEMENT
follow-up levels are 20 plcocuries radon per liter of air or higher, the home
owner should consider some type of procedure to decrease indoor radon levels.
The Mine Safety and Health Administration (MSHA) uses a standard of A Working
Level Months (WLM) per year for people who work in mines. (Working Level
Months combine the amount with length of exposure.) You will find more
information ori guidelines and standards in Chapter 7.
1.8 WHERE CAN I GET MORE INFORMATION?
If you have any more questions or concerns not covered here, please
contact your State Health or Environmental Department or:
Agency for Toxic Substances and Disease Registry
Division of Toxicology
1600 Clifton Road, E-29
Atlanta, Georgia 30333
This agency can also give you information on the location of the nearest
occupational and environmental health clinics. Such clinics specialize in
recognizing, evaluating, and treating illnesses that result from exposure to
hazardous substances.
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2. HEALTH EFFECTS
2 .1 INTRODUCTION
This chapter contains descriptions and evaluations of studies and
interpretation of data on the health effects associated with exposure to
radon. Its purpose is to present levels of significant exposure for radon
based on toxicological studies, epidemiological investigations, and
environmental exposure data. This information is presented to provide public
health officials, physicians, toxicologists, and other interested individuals
and groups with (1) an overall perspective of the toxicology of radon and (2)
a depiction of significant exposure levels associated with various adverse
health effects.
Radon is a relatively inert noble gas that does not readily interact
chemically with other elements. However, radon is a radioactive element and
evaluation of the adverse health effects due to exposure to radon requires a
slightly different approach than other chemicals. Radioactive elements are
those that undergo spontaneous transformation (decay) in which energy is
released (emitted) either in the form of particles, such as alpha and beta
particles, or photons, such as garroiia or X-ray. This disintegration or decay
results in the formation of new elements. some of which may themselves be
radioactive, in which case they will also decay. The process continues until
a stable (nonradioactive) state is reached (See Appendix B for more
information).
The decay rate or activity of radioactive elements has traditionally been
specified in curies (Ci). The activity defines the number of radioactive
transformations (disintegrations) of a radionuclide over unit time. The curie
is approximately 37 billion disintegrations (decay events) per second
(3.7xl010 transformations per second). In discussing radon, a smaller unit,
the picocurie (pCi) is used, where 1 pCi is equal to IxlO"12 Ci. In
international usage, the S.I. unit (the International System of Units) for
activity is the Becquerel (Bq), which is equal to one disintegration per
second or about 27 pCi. (Information for conversion between units is given in
Chapter 9.) In the text of this profile, units expressed in pCi are followed
by units in Bq contained in parentheses. The activity concentration of radon
or another radionuclide in air is expressed in Ci/liter (L) of air (Bq/m3) .
The activity concentration is a description of the exposure rather than the
dose. In radiation biology the term dose refers specifically to the amount of
radiant energy absorbed in a particular tissue or organ and is expressed in
rad (or grays).
When radon decays, it and its daughters (decay products) emit alpha and
beta particles as well as gamma radiation. However, the health hazard from
radon does not come primarily from radon itself, but rather from the
radioactive products formed in the decay of radon. These products, called
"radon daughters" or "radon progeny," are also radioactive (See Chapter 3 for
more information on the chemical and physical properties of radon). Unlike
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2. HEALTH EFFECTS
radon, Che radon daughters are heavy metals and readily attach themselves to
whatever they contact. The main health problems arise when radon daughters or
dust particles carrying radon daughters are inhaled. Radon daughter particles
attach to lung tissue and decay, resulting in the deposition of radiation (in
the form of alpha particles) in the lung tissue.
Because it was not feasible to routinely measure the individual radon
daughters, a unit termed the "Working Level" (WL) was introduced by the U.S.
Public Health Service. The WL unit is a measure of the amount of alpha
radiation emitted from the short-lived radon daughters (polonium-218,
polonium-214, and lead-214) and represents any combination of short-lived
radon progeny in one liter of air that will release 1.3x1.0^ million electron
volts (MeV) of alpha energy during decay. One WL is equivalent to 2.08x10s
joules per cubic meter of air (J/m3) .
To convert between units of radon 222 radioactivity (Ci or Bq) and the
potential alpha energy concentration (WL or J/m3), the equilibrium between
radon gas and radon daughters must be known (See Chapter 9 for conversion
formula). When radon is in equilibrium with its progeny, that is, when each
of the short-lived radon daughters is present at the same activity
concentration in air as radon-222, then 1 WL equals 100 pCi radon-222/L of
air. However, when removal processes other than radioactive decay are
operative, such as with ventilation, the concentration of short-lived
daughters will be less than the equilibrium amount. In .such cases an
equilibrium factor (F) is applied. For example, if the equilibrium factor is
0.5, then 200 pCi radon-222/L of air is equivalent to 1.0 WL; if the
equilibrium factor is 0.3, then 1 WL corresponds to 333 pCi radon-222/L of
air.
An additional unit of measurement used to describe, human exposure to
radon and radon progeny is the Working Level Month (WLM), which expresses both
the intensity and duration of exposure. One WLM is defined as the exposure of
a person to radon progeny at a concentration of 1.0 WL for a period of 1
working month (WM). A working month is assumed to be 170 hours. The S.I.
unit for WLM is joule-hour per cubic meter of air (J-h/m3); 1 WLM is equal to
3.6xl03 J-h/m3.
The WL and the WLM have been used to describe human exposure in
occupational settings for uranium and other hard rock miners. Since the WLM
represents both the intensity and duration of exposure, it alone does not
provide enough information to determine the actual activity concentrations of
radon in the air. For example, exposure to radon and radon daughters at 1 WL
(100 pCi radon-222/L of air) for 100 working months (WM) results in a
cumulative dose of 100 WLMs; exposure to 100 WL (10,000 pCi radon-222/L of
air) for 1 WM also results in a cumulative dose of 100 WLMs.
For both human and animal studies, exposures expressed in WLs were
converted to pCi radon-222/L of air. The unit of activity, the curie (or
Becquerel) , is the appropriate unit to describe radon levels in the
-------
11
2. HEALTH EFFECTS
environment. Unless otherwise stated by the authors of the studies reviewed,
the equilibrium factors assumed for the conversion of WLs to pCi were 1.0 for
animal studies and 0.5 for occupational epidemiological studies. For several
of the epidemiological studies, exposure categories were expressed in WLMs
without specific information concerning duration of radon exposure; therefore,
for these studies dose conversions were not made, In this text and in the
Supplemental Document, whenever possible radon levels are expressed in
activity concentrations of pCi/L of air, pCi/kg of body weight, or pCi/L of
water (along with the corresponding units in Becquerels).
Radon-222 is a direct decay product of radium-226, which is part of the
decay series that begins with uranium-238 (see Chapter 3, Figure 3-1).
Thorium-230 and thorium-234 are also part of this decay series. Uranium,
thorium, and radium are the subject of other ATSDR Toxicological Profiles.
Other isotopes of radon, such as radon-219 and radon-220, are formed in other
radioactive decay series. However, radon-219 usually is not considered in the
evaluation of radon-induced health effects because it is not abundant in the
environment (Radon-219 is part of the decay chain of uranium-235, a relatively
rare isotope) and has an extremely short half-life (4 seconds). Radon-220 is
also usually not considered when evaluating radon-related health effects.
While the average rate of production of radon-220 is about the same as radon-
222, the amount of radon-220 entering the environment is much less than that
of radon-222 because of the short half-life of radon-220 (56 seconds). All
discussions of radon in the text refer to radon-222.
2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE
To help public health professionals address the needs of persons living
or working near hazardous waste sites, the data in this section are organized
first by route of exposure -- inhalation, oral, and dermal -- and then by
health effect -- death, systemic, immunological, neurological, developmental,
reproductive, genotoxic, and carcinogenic effects. These data are discussed
in terms of three exposure periods -- acute, intermediate, and chronic.
Levels of significant exposure for each exposure route and duration (for
which data exist) are presented in tables and illustrated in figures. The
points in the figures showing no-observed-adverse-effect levels (NOAELs) or
lowest-observed-adverse-effect levels (LOAELs) reflect the actual levels of
exposure used in the studies. LOAELs have been classified into "less serious"
or "serious" effects. These distinctions are intended to help the users of
the document identify the levels of exposure at which adverse health effects
start to appear, determine whether or not the intensity of the effects varies
with dose and/or duration, and place into perspective the possible
significance of these effects to human health.
The significance of the exposure levels shown on the tables and figures
may differ depending on the user's perspective. For example, physicians
concerned with the interpretation of clinical findings in exposed persons or
with the identification of persons with the potential to develop such disease
-------
12
2. HEALTH EFFECTS
may be interested in levels of exposure associated with "serious" effects.
Public health officials and project managers concerned with response actions
at Superfund sites may want information on levels of exposure associated with
more subtle effects in humans or animals (LOAEL) or exposure levels below
which no adverse effects (NOAEL) have been observed.
For certain chemicals, levels of exposure associated with carcinogenic
effects may be indicated in the figures. These levels reflect the actual
doses associated with the tumor incidences reported in the studies cited.
2.2.1 Inhalation Exposure
Levels of significant exposure for the inhalation route for acute,
intermediate, and chronic exposure duration (for which data exist) are
presented in Table 2-1 and illustrated in Figure 2-1.
2.2.1.1 Death.
No deaths in humans have been reported as the result of acute radon
exposure. However, several epidemiological studies of individuals exposed
over long periods have reported significant increases in early mortality due
to cancer and nonneoplastic (noncancer) diseases (see Section 2.2.1.8 for a
discussion on cancer). Descriptions of cancer mortality were presented by
exposure categories, i.e., WLM categories; however, deaths due to noncancer
respiratory effects were generally reported for the total cohort. Increased
mortality as a result of nonneoplastic respiratory diseases, such as emphysema
and pulmonary fibrosis, has been reported in United States uranium miners
exposed to radon and radon daughters at concentrations in the range, of 100 to
10,000 pCi radon-222/L of air (3,700 to 370,000 Bq/m3) (Lundin et al. 1971;
Waxweiler et al. 1981). The concentration of radon and radon daughters in
mine air was reported to result in cumulative exposures of from 50 WLM to
levels equal to or greater than 3,720 U1M. The incidence of mortality from
respiratory diseases other than cancer and tuberculosis has been reported for
uranium miners and related to cumulative exposure expressed in WLMs (Archer et
al. 1976). As exposure increased, the number of cases per 1,000 individuals
exposed also increased. However, there are a number of confounding factors to
consider in all of these studies, including exposure to other agents,
ethnicity, smoking history, and work experience. The cases of nonneoplastic
respiratory diseases reported in these miners cannot be attributed solely to
radon or radon daughters but may be due to exposure to silica, to other mine
pollutants, to smoking, or to other causes.
In a more recent study (Roscoe et al. 1989) mortality from nonmalignant
respiratory disease was reported for a cohort of white nonsmoking uranium
miners. Deaths from these diseases were twelve times higher in uranium miners
than in nonsmoking United States veterans. Causes of death in the cohort
included silicosis, chronic obstructive pulmonary disease, fibrosis, and
emphysema. However, the exposure history of the individuals having these
-------
TABLE Z-l. Levels of Significant Exposure to Radon - Inhalation
Exposure LOAEL (Effect)
Figure Frequency/ HOAEL Less Serious Serious
Key Species Duration Effect (pCi/L) (pCi/L) (pCi/L) Reference
ACUTE EXPOSURE
Death
1 Mouse
Id
5-
5
X
tn
n
hi
Systemic
? Rat
8 Mouse
lifespan Resp
2d/wk Other
90hr/wk
Lifespan Resp
150hr/wk Hemato
Other
>.exX06 (dec bw)
4.8x10s (metaplasia)6
4.2x10s (metaplasia)
4.2xlQ5 (dec lymphocytes)
4.2xl05 (dec bw)
Palmer et al.
1973
Morken and Scott
1966
-------
TABLE 2-1 (Continued)
Figure
Key Species
Exposure
Frequency/ NOAEL Less Serious
Duration Effect (pCi/L) (pCi/L)
Serious
CpCi/L)
Reference
10
11
Mouse
Hamster
Dog
lifespan Resp
2d/wk Other
90hr/wk
lifespan Resp
2d/wk Other
90hr/wk
l-50d Resp
5d/wk
20hr/d
*.8*106 (dec bw)
4.8xl06 (dec bw)
*.8xl06 (fibrosis)
<». 8x10® (metaplasia)
5.5xl05 (fibrosis)c
Palmer et al.
1973
Palmer et al.
1973
Morken 1973
Cancer
12
13
14
Rat
Rat
Rat
CHRONIC EXPOSURE
Death
15 Hamster
Systemic
16 Human
17
Hamster
2.5-8wk
4d/v»k
3-6hr/d
25-115 d
4-5hr/d
4-6mo
2d/wk
lhr/d
lifespan
5d/wk
6hr/d
>lmo-18yr Resp
(occup)
lifespan Resp
5d/wk Hemato
6hr/d Other
3.lxlO5
3.1xl05
3.0xl05 (CEL-lung)
7.5xlG5 (CEL-lung)
3.0xl03 (CEL-lung)
>1.0xl02 (tuberculosis)
2.6*105 (hyperplasia)0
Chameaud et al.
1982
Chameaud et al
1974
Chameaud et al.
1984,
2.6xl05 (dec bw)
Pacific
Scrthwfest
Laboratory 1978
Waxveiler et al.
1981
Pacific
Northwest
Laboratory 1976
:r
re
>
t*3
-------
TABLE 2-1 (Continued)
Figure
Key
Species
Exposure
Frequency/ NOAEL
Duration Effect (pCi/L)
Less Serious
(pCi/L)
LOAEL (Effect)
Serious
(pCi/L)
Reference
Cancer
18
19
20
21
22
23
24
25
26
27
28
Human
Human
Human
Human
Human
Human
Human
Human
Human
Human
Human
0.5-23yr
(occup)
(occup)
O-Hyr
(occup)
>29yr
(occup)
>lyr->20yr
(occup)
48wk/yr
48hr/wk
(occup)
>10yr
(occup)
>2-30yr
(res)
(occup)
>lmo-18yr
(occup)
>lmo-30yr
(occup)
3.4xl02 (CEL-lung)
Z.OxlO2 (CEL-Lung)
l.OxlO2 (CEL-lung)*
6-OxlO1 (CEL-lung)
5.0x10* (CEL-lung)
S.OxlO1 (CEL-lung)
>3.0x10* (CEL-lung)
1.5x10° (CEL-lung)
2.4xl02 (CEL-lung)
l.OxlO2 (CEL-lung)
4.0xl02 (CEL-lung)
Gottlieb and
Husen 1982
Morrison et al. 1981
Solli et al.
1985
Edling and
Axelson 1983
Damber and
Larsson 1985
Howe et al.
1987
Snihs 1974
Svensson et al.
1987
Fox et al. 1981
Waxweiler et al.
1981
Roscoe et al.
1989
X
w
>
r
H
x
w
m
o
H
va
Ui
*2.2x10® presented in Table 1-2,
b4.8xl0* presented in Table 1-2.
C5.5acl05 presented in Table 1-2.
d2.6xl05 presented in Table 1-2.
*100 presented in Table 1-1.
NQAEL^o-observed-adverse-eff ect level; LOAEL«lowest-observed-adverse-effect level; pCi/L=picocurie per liter; d=day; hr=hour; wk=week;
mo-month; CEL^ancer Effect Level; yr=year; hemato=hematological; resp»respiratory; occup=occupational; dec^decreased; bw=body weight;
res=residential
-------
ACUTE
(<14 Days)
(pCi/L)
1,000,000,000
100,000,000 \-
10,000,000
1,000,000
100,000
10,000
1,000
100
10
1
/ /
£
|1m
3'
INTERMEDIATE
(15-364 Days)
'a
h0s#9m #7r
#11d fern (J8m
X9
d1
®9m ®7r
®8m
J?
+13r
~ l2r
+ Mr
EC
m
>
t-1
H
rc
M
~n
n
H
C/3
- - 1
Key
r Rat
¦
LC50
m Mouse
•
LOAEL for serious effects (animals)
s Hamster
»
LOAEL tor less serious effects (animals)
d Dog
O
NOAEL (animals)
~
CEL-Canoer Effect Level
The number next to each point corresponds lo entries in Table 2-1
FIGURE 2-1. Levels of Significant Exposure to Radon - Inhalation
-------
(pCi/L)
1,000,000,000 r
100,000,000
10,000,000
1,000,000
100,000
10,000
1.000
100
10
1
CHRONIC
(> 365 Days)
r1
H
EC
m
T!
~n
m
n
H
C/}
~25
Key
$ Hamster 9
LOAEl tor serious effects (animals)
3
LOAEL for less serious effects (animals)
O
NOAEL (animals)
A
LOAEL tor serious effect (humans)
~
CEL-Cancer Effect Level (humans)
The number next lo each point corresponds to entries in Table 2-1.
FIGURE 2-1 (Continued)
-------
18
2. HEALTH EFFECTS
diseases was not reported. Excepting cigarette smoking, this study has 0£
the confounding factors mentioned previously.
Mortality due to nonneoplastic respiratory diseases was not significantly
elevated in other uranium mining cohorts including miners in Czechoslovakia
(Sevc et al. 1988) or Ontario, Canada (Muller et al. 1985). Although
environmental radon levels were not reported in either the Czechoslovakia or
Canadian studies, cumulative occupational exposure to radon and radon
daughters were estimated at levels up to about 600 WLMs. A statistically
significant excess of mortality due to chronic nephritis and renal sclerosis
was also reported in the United States uranium miner cohort, although it xs
unclear whether this was related to exposure to radon, uranium ore, or other
mining conditions or to nonmining factors (Waxweiler et aL. 1981).
The acute lethal effects of radon and radon daughters have been studied
in mice. A 30-day LD50 was estimated based on single exposures via inhalation
to radon and radon daughters at a concentration of 2.2xl.0H pCi/L (S.lxlO9
Bq/m3) for 5 to 40 hours (Morken 1955). After 40 hours of exposure, 100% Qf
the exposed mice died within 2 weeks (cause of death was not reported), while
no deaths occurred within 60 days following an exposure of 26 hours or less.
Significant decreases in the lifespan of laboratory animals exposed to
high doses of radon and radon daughters were reported by several investigators
(Cross 1987; Morken 1973; Morken and Scott 1966; Palmer et al. 1973).
Respiratory system insult contributed to the death of treated animals in these
studies, although the actual cause of death was not reported. The lifespan of
male and female mice (median lifespan of controls was 79 and 98 weeks) was
reduced by 55% and 42%, respectively, as a result of continuous exposure (150
hours/week) to 4.2xl05 pCi radon-222/L of air (1.6xl07 Bq/m3) for up to 47
weeks (Morken and Scott 1966). Emaciation, reddening of the ears, and
abnormal grooming was observed preceding death. Pseudoparalysis was observed
in mice which died a few days after exposure (Morken and Scott 1966). A
similar decrease in lifespan was observed in rats and hamsters following
exposure to 4.8xl06 pCi radon-222/L of air (1.8x10® Bq/m3) for 90 hours/week
(Palmer et al. 1973). All animals in the Palmer et al. (1973) study died by
the fourth month of treatment, while all treated animals in the Morken and
Scott (1966) study died by the eleventh month. At lower concentrations (3,000
pCi radon-222/L of air fl.lxlO5 Bq/m3] f°r 2 hours/week, 6 months) the
lifespan of rats was not decreased (Chameaud et al. 1984).
2.2.1.2 Systemic Effects
No studies were located regarding carcUovascular, gastrointestinal,
musculoskeletal, hepatic, dermal, or ocu ar effects in humans or animals after
inhalation exposure to radon and radon aughters.
Respiratory Effects. Adverse respiratory effects have been observed in
humans under occupational conditions an m laboratory animals exposed to
-------
19
2. HEALTH EFFECTS
radon and radon daughters. Epidemiology studies of miner cohorts report an
increased frequency of chronic, nonneoplastic lung diseases, such as emphysema
and pulmonary fibrosis, among uranium miners in the United States (Lundin et
al. 1971; Roscoe et al. 1989; Waxweiler et al. 1981) and among Cornish tin
miners (Fox et al. 1981), and chronic interstitial pneumonia among Canadian
uranium miners (Muller et al. 1985). Chronic lung disease was reported to
increase with increasing cumulative exposure to radiation and with cigarette
smoking (Archer 1980) . In addition, nonsmoking uranium miners were also
reported to have increased deaths from nonmalignant repiratory disease
compared to a nonsmoking United States veteran cohort (Roscoe et al. 1989).
Alterations in respiratory function in United States uranium miners have
been reported (Archer et al. 1964; Samet et al. 1984a; Trapp et al. 1970).
Analyses among United States uranium miners indicated a loss of pulmonary
function with increasing cumulative exposure (Archer et al. 1964) and with the
duration of underground mining (Samet et al. 1984a). Evaluations of these
respiratory end points did not permit assessment of the effects of each of the
other possible mine pollutants, such as ore dust, silica, or diesel-engine
exhaust. The individual contributions of these factors to the observed
adverse respiratory effects are not defined.
No studies were located regarding the respiratory effects of radon and
radon daughters in laboratory animals following acute exposure. Respiratory
toxicity occurred in mice, hamsters, dogs, and rats following exposure to
radon and radon daughters for intermediate exposure durations. Chronic
inflammation (radiation-induced pneumonitis), pneumonia, and/or fibrosis of
varying degrees in the alveolar region occurred in most animals exposed to
radon and radon daughters (4.2xl05 to 4.8xl06 pCi radon-222/L of air [1.6xl07
to 1.8xl08 Bq/m3]) for 4 to 150 hours/week for 10 to approximately 45 weeks
(Chaumeaud et al. 1974; Morken 1973; Morken and Scott 1966; Palmer et al.
1973). In these studies, the relationship of dose, temporal dosing pattern,
and length of exposure to onset of effects is unclear since the time of onset
of effects was rarely reported or effects were reported only when animals died
or were sacrificed.
In Palmer et al. (1973), rats, mice, and hamsters, were exposed to radon
[4.8x10® pCi radon/L of air (1.8x10s Bq/m3)] via inhalation for approximately
90 hours per week, in two continuous 45-hour periods. These animals were
allowed to die, or were sacrificed when moribund, after which they were
histopathologically examined. At four months of exposure, only one of the
rodents remained alive. The radiation effects observed in these animals,
which included interstitial pneumonitis or septal fibrosis, were found at
post-mortem examination. Therefore the onset of respiratory effects could not
be determined.
In a study conducted by Morken and Scott (1966), mice were to be exposed
to 4. 2xl05 pCi radon/L of air (1.6xl07 Bq/m3) 150 hours/week for life.
However, by week 15 of the experiment the median lifetime of the animals had
been decreased by 50%. However, the cause of this decreased lifespan was not
-------
20
2. HEALTH EFFECTS
reported. The authors then sacrificed the remaining animals (15 treated mice
and 3 control mice) for purposes of histopathological examination. Tracheal
effects, including thickening of the mucous membrane, inflammation of the
mucous glands, and destruction of cells lining the trachea, were observed.
However, the onset of these effects could not be determined. In Morken
(1973), mice and dogs were exposed to radon for intermediate periods of time
and then sacrificed at designated times post-exposure. In mice exposed to
5.5xl05 pCi radon/L of air (2.0xl07 Bq/m3) for 10, 15, 20, or 25 weeks,
lesions of the trachea and bronchi were observed immediately post-exposure,
but by eight weeks post-exposure tissues appeared normal. However, with
increasing time post-exposure, the epithelial lining of the terminal
bronchiole became flattened or disappeared. At long intervals after exposure
to radon for 25 weeks, non-specific pulmonary effects, including small foci of
interstitial fibrosis, were observed in mice. In dogs exposed to radon for
one to 50 days (5.5xl05 pCi of radon/L of air (2.0xl07 Bq/m3)], no significant
effects were observed in treated dogs immediately post-exposure compared to
untreated controls. At one and two years post-exposure, there was a "probable
increasing relation" to dose of small foci of chronic inflammation. At three
years post-exposure, this relation had disappeared in dogs exposed to low
doses of radon up to 800 WLM, but was still considered "probable" for the
larger doses. However, a definite time of onset of respiratory effects in
either mice or dogs could not be determined from the results of this study.
Respiratory effects similar to those observed following intermediate
exposure have also been observed in laboratory animals following chronic
exposure to radon and radon daughters. Respiratory lesions, mainly squamous
metaplasia, were observed in the bronchioa veolar region of hamsters 8 months
following initiation of lifetime exposure to 2.6xl05 pCi radon-222/L of air
(9.6xl06 Bq/m3) for 30 hours/week (Pacific Northwest Laboratory 1978).
Pulmonary fibrosis in rats, hamsters, dogs and emphysema in hamsters
and dogs occurred following exposure to ra °n and radon daughters and uranium
ore dust (Cross et al. 1984, 1985, 1986, acific Northwest Laboratory 1978)
In hamsters emphysema was produced as a ot exposure to uranium ore
alone, diesel exhaust alone, and radon an radon daughters alone; however,
emphysema was not observed in hamsters at cumulative doses of radon of less
than 7,000 WLM (Pacific Northwest Laboratory 1978). Fibrosis occurred in
hamsters following exposure to radon an ^ °n daughters at a cumulative dose
of 8,000 WLM in combination with uranium and dlesel exhausti but not wlth
radon and radon daughters alone at cumu a e exposure at approximately 7,000
WLM. However, the incidence of bronchia do^erPlasia was significantly
greater in hamsters receiving radon an ^ daughters alone. In dogs the
combination of uranium ore dust and ra<^°n radon daughters produced more
severe emphysema and fibrosis than uranl ^ re dust alone; however, radon and
radon daughters alone were not tested i*1 o^sS (Pacific Northwest Laboratory
1978). Fibrosis, but not emphysema, waSogs Grved in rats
exposed to radon and
radon daughters and uranium ore dust ( et 1985). These studies
are discussed further in Section 2.6.
-------
21
2. HEALTH EFFECTS
Renal Effects. A statistically significant increase in mortality due to
kidney disease, characterized by chronic nephritis and renal sclerosis, was
reported among United States uranium miners (Waxweiler et al. 1981) and in
Canadian miners at the Eldorado mines (Muller et al. 1985). Kidney toxicity
has been induced experimentally in animals exposed to uranium (ATSDR 1990a).
Kidney disease was not reported among other mining cohorts and no studies were
located regarding renal effects in laboratory animals following inhalation
exposure to radon. It is not clear whether the kidney effects observed by
Waxweiler were due to radon, uranium ore, or other mining and nonmining
factors.
Hematological Effects. No studies were located regarding hematological
effects in humans after inhalation exposure to radon.
Hematological effects have been observed in mice following acute and
chronic exposure to radon and radon daughters. The extent and severity of the
hematological effects in mice were exposure related. Effects following acute
exposure, either a single or multiple exposures, were transient. Recovery to
control values occurred within a shorter time post-exposure after a single
acute exposure than with multiple exposures. Chronic exposure of mice to
radon-222 resulted in dose-related alterations to the hematological system.
Following a single exposure to mice of 1.76x10® pCi radon-222/L of air
(6.5xl09 Bq/m3) , transient decreases in erythrocytes, reticulocytes,
platelets, and white blood cells were observed immediately post-exposure
(Morken 1961). Platelets and white blood cells returned to control levels by
50 days post-exposure, and reticulocytes increased 50% to 100% over controls
within 2 to 3 weeks, but returned to normal about one year after exposure.
Erythrocyte counts remained depressed for one-year post-exposure (Morken
1961). In mice exposed 2 or 4 times at concentrations of 2.11x10s pCi radon-
222/L of air (7.8xl09 Bq/m3), erythrocyte counts remained depressed compared
to controls, while platelets and neutrophils rapidly decreased and then
recovered within 2 weeks (Morken 1964). After multiple exposures, lymphocyte
counts remained lower for longer periods of time compared to single exposures,
indicating that recovery was affected by larger or repeated doses (Morken
1964). These effects are based on results observed in small numbers of
animals.
In mice, lifetime exposure to 4.2xl05 pCi radon-222/L of air (1.6xl07
Bq/m3), 150 hours/week resulted in mild, progressive anemia in male mice and a
decrease in lymphocyte count in male and female mice, which was linearly
related to cumulative dose as expressed in working level months (WLMs) (Morken
and Scott 1966). However, no hematological effects were observed in hamsters
exposed to 3.lxlO5 pCi radon-222/L of air (l.lxlO7 Bq/m3) (Pacific Northwest
Laboratory 1978).
Other Systemic Effects. Exposure to radon and radon daughters at
concentrations ranging from 2.6xl05 to 4.8xl06 pCi radon-222/L of air (9.6xl06
-------
22
2. HEALTH EFFECTS
to 1.8x10s Bq/m3), 30 to 150 hours/week, resulted in a significant: decrease in
body weight in hamsters (Pacific Northwest Laboratory 1978), mice (Morken and
Scott 1966; Palmer et al. 1973), and rats (Palmer et al. 1973). There was no
explanation given for these weight losses and food consumption was not
reported in any of the studies.
2.2.1.3 Immunological Effects
No studies were located regarding immunological effects in humans and
animals after inhalation exposure to radon.
2.2.1.4 Neurological Effects
No studies were located regarding neurological effects in humans after
inhalation exposure to radon. Two guinea pigs exposed to approximately
4.7xl010 to 5. 8xl010 pCi (1.7xl09 to 2.15xl09 Bq) radon for 1 to hours
became drowsy, their respiration increased, and after several hours, they died
(Proescher 1913). Autopsy showed that both animals died from respiratory
paralysis caused by central nervous system failure. The study has many
limitations, such as the use of only two animals and the possibility that
oxygen deprivation contributed to the respiratory failure. A causal
relationship between central nervous system failure and radon exposure was not
established.
2.2.1.5 Developmental Effects
No studies were located regarding developmental effects in humans and
animals after inhalation exposure to radon.
2.2.1.6 Reproductive Effects
No maternal or fetal reproductive effects in humans have been attributed
to exposure to radon and radon daughters. However, a decrease in the
secondary sex ratio (males:females) of the children Df male underground miners
may be related to exposure to radon and radon daughters (Dean 1981; Muller et
al. 1967; Wiese and Skipper 1986). The secondary sex ratio of the first born
children of uranium miners was decreased wltn cumulative exposure to radon and
radon daughters in miners whose median age at the time of conception was less
than 25 years of age but was increased with cumui^^ exposure tQ radon and
radon daughters in miners whose median ag® a the time of conception was
greater than 25 years of age (Waxweiler and RoScoe 1981), This age effect was
also observed when the miners were analyze according to race
No studies were located regarding reproductive effects animals
following inhalation exposure to radon an a on daughters.
-------
23
2. HEALTH EFFECTS
2.2.1.7 Genotoxic Effects
Some epidemiologic studies have indicated that radon and radon daughters
may produce genotoxic effects in persons exposed in occupational and
environmental settings. Brandom et al. (1978) reported a higher incidence of
chromosomal aberrations among uranium miners exposed to radon and radon
daughters at cumulative exposures ranging from <100 to >3,000 WLM, as compared
to their matched controls. A clear exposure - related increase was observed for
the groups exposed to 770 to 2,890 WLM with a sharp decrease at the highest
dose group (>3,000 WLM). The cause of the reversal in exposure-response at
the highest dose is unclear. Increases in chromosomal aberrations were also
reported among spa-house personnel and in area residents in Badgastein,
Austria, who were chronically exposed to radon and radon decay products
present in the environment (Pohl-Ruling and Fischer 1979, 1982; Pohl-Ruling et
al. 1976). A study by Tuschl et al. (1930) indicated a stimulating effect of
repeated low-dose irradiation on DNA-repair in lymphocytes of persons
occupationally exposed to radon (3,000 pCi/L of air [1.1x10s Bq/m3]). The
study further indicated higher DNA-repair rates in juvenile cells than in
fully differentiated cells.
Evidence of chromosomal aberrations was equivocal in an animal study.
Rabbits exposed to high natural background levels of radon-222 (12 WLM) for
over 28 months displayed an increased frequency of chromosomal aberrations
(Leonard et al. 1981). However, when a similar study was conducted under
controlled conditions (10.66 WLM), chromosomal aberrations were not found.
According to the authors, the increased chromosomal aberrations in somatic
cells of rabbits exposed to natural radiation were mainly due to the gamma
radiation from sources other than radon.
Exposure of Sprague-Dawley male rats to radon at cumulative doses as low
as 100 WLM resulted in an increase in sister chromatid exchanges (SCEs) in
bone marrow by 600 days post-exposure (Poncy et al. 1980). At 750 days post-
exposure, the number of SCEs reached 3.21 per cell. The SCEs in the 500 and
3,000 WLM groups reached constant values of 3.61 and 4.13 SCEs per cell. In
the high-dose group (6,000 WLM), SCEs continued to increase from 100 to 200
days after exposure, reaching a mean value of 3.5 SCE per cell. In controls
SCEs were constant with age (2.4 per cell).
2.2.1.8 Cancer
Significant excesses in deaths from lung cancer have been identified in
epidemiology studies of uranium miners and other hard rock miners.
Statistically significant excesses in lung cancer deaths have been reported in
uranium miners in the United States (Archer et al. 1973, 1976, 1979; Gottlieb
and Husen 1982; Hornung and Meinhardt 1987; Lundin et al, 1971; Roscoe et al.
1989; Samet et al. 1984b, 1989; Wagoner et al. 1964; Waxweiler et al. 1981),
Czechoslovakia (Sevc et al. 1988), and Canada (Howe et al. 1986, 1987; Muller
et al. 1985).
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¦?n
2. HEALTH KKFKCTS
The results of these studies ate consistent and demonst rate that the
frequency of respiratory cancer mortality increased wit}, increasing exposure
to radiation (cumulative WLMs). Statistically significant excesses in lung
cancer deaths were present after cumulat ive exposures of less than 50 WLKs in
the Czechoslovak!an cohort (Sevc et a], 1988) and at cumulat ive exposures
greater than 100 WLMs in the cohorts from the United States and Ontario
Canada (Muller et al. 1985; Samet et a1. 3989; Waxweiler et al. 1981) These
studies indicate that lung cancer mortality was influenced by the total
cumulative radiation exposure, by the age at first exposure, and by the time-
course of the exposure accumulation. Most, deaths from respiratory cancers
occurred 10 or more years after the individual began uranium mining (Lundin et
al. 1971). Among uranium miners, epidermoid, small cell undifferentiated and
adenocarcinoma were present with increased freipu-ney, while large-cell
undifferentiated and other morphological type?; of lung cancer were seen less
frequently (Archer et al.. 1974).
The evidence for radon daughter - i ndweed lung, cancer is further supported
by epidemiological studies conducted among, uonuranium hard rock miners The
lung cancer mortality rate was also statistically higher in iron ore miners i
Sweden (Damber and Larsson 1982; Edling and Axel son 1 ); lorgensen 1984- °
Radford and Renard 1984; Snihs 1974); metal miners in the United States
(Wagoner et al. 1963); zinc-lead miners in Sweden (Axelson and Sundell 1978)-
tin miners in England (Fox et al . 1.981); phosphate miners in Florida
(Checkoway et al. 1985; Stayner et al. 1985); in a niobium mine (Solli et al
1985); and Newfoundland fluorspar miners (Morrison el al. I and greater
(Snihs et al. 1974). Since exposure was for at least 10 years, the cumulati
exposure to workers was approximately "if, WIJTs or greater. This excess Ca 6
mortality occurred at cumulative exposures as low as 5 Wins (Howe et al 1987"*
but generally at cumulative doses greater than 100 WI.M.S.
In a subcohort of 516 white nonsmoking uranium miners (drawn from a
larger cohort of United States uranium miners), mean exposure was reportedl
720 WLM. For this cohort the mortality risk for lung cancer was found to be
12-fold greater than that of nonsmoking, noninining United States veterans w
lung cancer deaths were found in nonsmoking miners who had exposure less th °
465 WLMs (Roscoe et al. 1989). Unlike the nonmining cohort, the miners in th
subcohort may have been exposed to other mining pollutants, e.g., diesel
exhaust and silica dusts. The contribution of these factors was not
considered in the analysis.
Several case-control studies have examined the association between lune
cancer and housing construction materials, or between lung cancer and
residential radon exposure. The majority of these have been conducted in
Sweden (Axelson and Edling 1980, Axelson eL al. 1979, 1981; Edling 1984-
Svensson 1987, 1989). The Axelson studies examined the- association between
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25
2. HEALTH EFFECTS
housing type and lung cancer risk. Residences of cases (having died from lung
cancer) and controls (having died from noncancer causes) were classified into
three categories: having lived in wooden house without basements; brick,
concrete, or granite houses with basements; and a mixed category (all other
types of houses). No radon measurements were taken in these homes. However,
previous studies in Sweden had shown that, in general, the wooden structures
had lower radon levels than brick or concrete structures. Axelson reported a
statistically significant trend for increased lung cancer deaths associated
with residence in mixed category houses or in stone houses with basements
(Axelson and Edling 1980, Axelson et al. 1979). These studies were adjusted
for age and sex, but not for smoking history. An additional study based on
the same approach (lung cancer associated with type of residence) did measure
radon levels in residences of interest (Edling et al. 1984). Wooden houses
without basements had mean levels of 1.1 pCi/L (42 Bq/m3), wooden houses with
a basement on radiation producing ground or plaster houses had mean levels of
4.6 pCi/L (170 Bq/m3), while all other types of houses had mean levels of 1.5
pCi/L (57 Bq/m3). Again, the association of incidence of lung cancer,
adjusted for age and sex, and additionally for smoking, with type of residence
and with radon levels, showed a significantly increasing trend (Axelson et al.
1981, Edling et al. 1984). All of the above studies have one or more
methodological limitations, such as small cohort size and limited or no
measurement of radon levels in homes.
Another study of a Swedish cohort has also reported significant
correlation between incidence of lung cancer, type of residence, and radon
exposure, although only 10% of residences were monitored for radon. In
addition, it correlates levels of exposure with particular types of lung
cancer. Association of exposure with lung cancer, adjusted for smoking, age,
and degree of urbanization, was strongest for small cell carcinoma of the lung
(Svensson et al. 1989). This particular type of lung tumor has also been
reported in cohorts of United States uranium miners.
A study of lung cancer in adult white residents in Maryland reported an
association of lung cancer with age, sex, and smoking. Lung cancer rates were
highest in houses which had concrete walls and in houses without basements but
with concrete slabs, but this association was very slight (Simpson and
Comstock 1983).
Identification of specific cancer effect levels, i.e., the environmental
concentration of radon and radon daughters, was not feasible for all of the
epidemiological studies because of the quality of the exposure information
provided. Environmental levels of radon and radon daughters, expressed in pCi
radon-222/L of air, present in mines were measured at various times; however,
actual measurements of radon and radon daughter levels were not available for
every mine and for every year of exposure. Rather, actual measurements along
with estimates of radon daughter levels based on extrapolations from actual
measurements were then combined with individual work histories to derive
estimates of cumulative radon daughter exposure for each individual, reported
in WLMs. Workers were then classified into cumulative WLM exposure
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26
2. HF.ALTH KFFKCTS
categories. For example, in the llni t.ed Stales uranium mining, cohort radon and
radon daughter levels in mines were measured from to and ranged from
>100 to >10,000 pCi radon-222/L of air (> J./:¦:]')' to i./xlo' Bq/ur) (>0.5 to
>50 WLs) across various mines and year;;. Miner.-; were employed in the mines
for 4 to 28 years with an average length of employment of 1'> years (Saccomanno
et al. 1988). The resulting exposure categories ranged from -120 Wl,M to
>3,720 WLMs . Only a few of the epidemiological s t ml i provided enough
exposure information to express exposures in pC i radon • of air. However,
the quality of the exposure measurement s does not aitei t he conclusion that,
based on the epidemiology studies, exposures to radon and radon daughters at
cumulative doses greater than 100 WLMs resulted in excesses in lung cancer
mortality, with the exception of the nonsmoking, cohort jeported hv Roscoe et
al. (1989), which reported excesses in lung cancel at higher doses.
No studies were located regarding cancer- in laboratory animals following
acute exposure to radon and radon daughters. Lung tumors have been observed
in rats following intermediate exposure at concent rat ions as low as 3,000 pCi
radon-222/L of air (1.1x10s Bq/in3) 2 hours/week for 4 months (Chairieaud et al.
1984) and up to 3xl06 pCi radon-222/L of air (1.1x10" Bq/m\) 12 hours/week for
21A weeks (Chameaud et al . 1974, 1982a, 19K21>). The mean time to death with
tumor in the Chameaud et al. (1984) study was appro.-: i ma t <• 1 y 112 weeks, which
is close to the normal lifespan for a rat (104 weeks). In chameaud et al.
(1980), lung cancers were not observed in rats until the 24th month of the
study. These studies would indicate that the latency petiod for radon-induced
lung tumors is long. No treatment-related cancels were observed in dogs,
mice, or rats following exposure to radon and radon progeny alone [5.5x10s to
lxlO6' pCi radon-222/L of air (2.0xl07 to 3.7x10' Bq/m1)], 25 to 150 hours/week
(Morken 1973). In this study, dogs were exposed for 1 to 50 days, mice (three
separate experiments) for 8 weeks to life, and rats f or 24 weeks. However,
the dog study was terminated at 3 years; the rat study only reported results
through the twelfth month of the study; and two of the mouse studies had
lifespan shortening. Some of the changes observed may have been
preneoplastic. However, based on the results f rom t lie Chameaud et al . (1980,
1984) studies, lifespan shortening or the early termination of experiments nay
have precluded the development of tumors. In the remaining mouse study
reported by Morken (1973), mice were sacrificed beginning at 60 weeks of age,
following exposure to radon for 10, 15, 20, or 2 5 weeks, at 10 week intervals
until all of the mice were killed (110 weeks). No t reat.merit - related cancers
were reported. However, reviewers of this study (Cross 198'/) report that
laboratory room air containing dusts and oil and water droplets may be a
confounding factor in this study. The influence of these confounding factors
is uncertain, but may have led to a more rapid solubilization of radon progeny
causing a decrease in observed lung effects.
In other studies in which a significant increase in the incidence of lung
cancer was not reported, the respiratory lesions that, were observed following
exposure to radon and radon daughters alone were considered by the authors to
be "precancerous" (Morken and Scott 1966; Pacific Northwest. Laboratory 1978;
Palmer et al. 1973). In the Morken and Scott (1966) study, destructive
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27
2. HEALTH EFFECTS
hyperplastic and metaplastic lesions were observed in the trachea and
bronchioles of mice following exposure to 4.2xl05 pCi radon-222/L of air
(1.6xl07 Bq/m3) 150 hours/week for life, but no carcinomas were observed.
However, there was a significant shortening of lifespan in the study, with
many of the animals dead at 35 weeks of age. Because of this lifespan
shortening, the animals may not have lived long enough to develop tumors. In
a study reported by Palmer et al. (1973), no treatment-related cancers were
observed in mice, rats, or hamsters exposed to 4.8xl06 pCi radon-222/L of air
(1.8x10s Bq/m3), but precancerous respiratory effects were observed in mice
and rats, such as hyperplasia. The lack of cancer may be attributed to the
fact that all of the animals but one were dead by the fourth month of the
study. However, the cause of death was not reported. In a separate study,
"precancerous" respiratory effects (fibrosis) were observed in dogs exposed to
1.1x10s pCi radon-222/L of air (4.1xl06 Bq/m3) (Pacific Northwest Laboratory
1978). The lack of cancer observed in dogs may be due to lifespan shortening
(4 years in treated versus 7 years in the normal dog), although the lifespan
of untreated controls in this study was comparable.
Following chronic exposure to radon and radon daughters alone, no
statistically significant increase in the incidence of any type of tumor was
observed in hamsters exposed to 3.lxlO5 pCi radon-222/L of air (l.lxlO7
Bq/m3), 30 hours/week for life, although pulmonary fibrosis and bronchial
hyperplasia were observed (Pacific Northwest Laboratory 1978). Hamsters may
be resistent to alpha radiation-induced lung cancer since no lung tumors were
produced in hamsters exposed to another alpha-emitter, plutonium (ATSDR
1990b).
Lung cancer was reported in laboratory animals by Chameaud et al. (1974),
Cross et al. (1982a, 1982b, 1984), and Stuart et al. (1970) following chronic
administration of radon and radon daughters in conjunction with air
pollutants, such as cigarette smoke, uranium ore dusts, or diesel exhaust (see
Section 2.6).
2.2.2 Oral Exposure
No studies were located regarding the following health effects in humans
or animals after oral exposure to radon and radon daughters.
2.2.2.1 Death
2.2.2.2 Systemic Effects
2.2.2.3 Immunological Effects
2.2.2.4 Neurological Effects
2.2.2.5 Developmental Effects
2.2.2.6 Reproductive Effects
2.2.2.7 Genotoxic Effects
An increase in chromosomal aberrations in lymphocytes was observed in 18
Finnish people of different ages chronically exposed to radon in household
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28
2. HEALTH EFFECTS
water at concentrations of 2.9x10" to 1.2x10* pCi radon-222/L of wat;cr of
(l.lxlO3 to 4.4x10'' Bq/L) compared with people "who did not have a histo
exposure to high radon levels (Stenstrand et. al. 1979). This study a s°
indicated that the frequencies of chromosomal aberrations and multiple
chromosomal breaks were more common in older people than In younger p< °P ^
exposed to radon. Although the radori was in household water, it is Pr
that much of this radon volatilized and was available to he inhaled.
Therefore, this route of exposure includes both oral and inhalation route.
2.2.2.8 Cancer
Limited information was located regarding cancer in humans after e*^Qg
to radon and radon daughters in water. Radon levels were measured in 2,
public and private wells in 14 counties in Maine (Hess et: al . 1'38 3) • g
county averages were compared to cancer rate by county to determine any c b
of correlation. Significant correlation was reported for all lung cancel
all cancers combined, when both sexes were combined, and for lung tumors
females. The authors note that correlation does not demonstrate causation
that confounding factors (e.g., smoking) exist. In addition, expo-sure fr°m^
radon, in these water supplies could have been by the inhalation route as ^e
as the oral route.
No studies were located regarding cancer in animals after oral exposure
to radon and radon daughters.
2,2,3 Dermal Exposure
No studies were located regarding the following health effects in humans
or animals after dermal exposure to radon and radon daughters
2.2.3.1 Death
2.2.3.2 Systemic Effects
2.2.3.3 Immunological Effects
2.2.3.4 Neurological Effects
2.2.3.5 Developmental Effects
2.2.3.6 Reproductive Effects
2.2.3.7 Genotoxic Effects
2.2.3.8 Cancer
A statistically significant increase in the incidence of basal cell skin
cancers (103.8 observed vs. 13.0 expected) was observed in uranium miners
exposed occupationally for 10 years or more to approximately 3.08 pCi/L of air
(1.74x10' Bq/m3) resulting in 6.22 pCi (0.23 Bq) radon-222/cm2 skin surface
area (Sevcova et al. 1978). The authors believe that the causal aBent may be
exposure to radon and radon daughters. However, they acknowledge that
exposure to other agents in the uranium raining environment, as well as minor
traumas of the skin, may also play a role in the incidence of skin cancer.
Increased incidences of skin cancer have not been reported in other uranium
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29
2. HEALTH EFFECTS
miner cohorts or for workers in other types of mining, such as metal or coal
mines.
No studies were located regarding cancer in animals after dermal exposure
to radon and radon daughters.
2.2.4 Other Routes of Exposure
2.2.4.1 Death
A single intravenous injection of 1.6xl010 pCi (6.0x10® Bq) radon-222/kg
body weight in equilibrium with its decay products resulted in a 56% decrease
in the average lifespan of mice (Hollcroft et al. 1955). This decrease was
believed to be due to radiation-induced renal failure as indicated by
inflammatory lesions and atrophy of the renal cortex as seen in most of the
radon treated animals. The study by Hollcroft et al. (1955) has
methodological deficiencies including an erratic schedule for sacrifice of
animals and the failure to examine animals that died from acute radiation
injury. Many other causes of such renal effects are known and the relevance
of these effects is questionable following near lethal doses of radon.
2.2.4.2 Systemic Effects
No studies were located regarding respiratory, cardiovascular,
gastrointestinal, musculoskeletal, hepatic, or dermal/ocular effects in humans
or animals after exposure to radon and radon daughters by other routes of
exposure.
Hematological Effects. No studies were located regarding
hematological effects in humans after exposure to radon and radon daughters by
other routes.
A single intravenous injection of 1.6xl010 pCi (6.0xl08 Bq) radon-222/kg
body weight in equilibrium with its decay products in mice resulted in a
decrease in red blood cell count within 2 weeks, which remained depressed
until death of the mice at about 150 to 180 days (Hollcroft et al. 1955). The
anemia observed was associated with the observed renal failure in these
animals. White blood cell counts were decreased immediately post-exposure,
but soon returned to normal levels. (See Section 2.2.4.1 for limitations of
Hollcroft et al. 1955.)
Renal Effects. No studies were located regarding renal effects in humans
after exposure to radon and radon daughters by other routes.
A decrease in kidney weight, extreme shrinkage of the cortex, and
infiltration of fat into the lining of the renal tubules and eventual renal
failure occurred in mice given a single intravenous injection of 1.6xl010 pCi
(6.0xl08 Bq) radon-222/kg body weight in equilibrium with its decay products
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30
2. HEALTH EFFECTS
(Hollcroft et al. 1955). Renal failure may have caused the observed anemia
(see Hematological Effects), weight loss (see Other Effects), and decrease in
lifespan observed in these mice. (See Section 2.2.4.1 for limitations of
Hollcroft et al. 1955.)
Other Effects. A single intravenous injection of radon at a
concentration of 1.6xl010 pCi (6.0x10s Bq) radon-222/kg body weight in
equilibrium with its decay products resulted in a decrease in body weight in
mice, possibly due to renal failure (Hollcroft et al. 1955). (See Section
2.2.4.1 for limitations of Hollcroft et al. 1955.)
No studies were located regarding the following effects in humans or
animals after exposure to radon and radon daughters by other routes.
2.2.4.3 Immunological Effects
2.2.4.4 Neurological Effects
2.2.4.5 Developmental Effects
2.2.4.6 Reproductive Effects
2.2.4.7 Genotoxic Effects
2.2.4.8 Cancer
2. 3 TOXICOKINETICS
In radiation biology the term dose has a specific meaning. Dose refers
to the amount of radiation absorbed by the organ or tissue of interest and is
expressed in rad (grays) . Estimation of this radiation dose to lung tissue or
specific cells in the lung from a given exposure to radon and radon daughters
is accomplished by modeling the sequence of events involved in the inhalation,
deposition, clearance, and decay o ^adon daughters within the lung. While
based on the current understanding o 1^ng morphometry and experimental data
on radon and radon daughter toxico inetiCS) different models make different
assumptions about these ProcesSeS^esceffby resulting in different estimates of
dose and risk. These models are escr bed in numerous reports including Bair
(1985), BEIR IV (1988), EPA (1988a;, ICRp (1978)_ James (1987) NEA (19g3)
and NCRP (1984).
In this section the toxic0¥^Vhan °f radon is described based on the
available experimental data rat lates Ascriptions derived from models. The
toxicokinetics of radon, as it re f the development of adverse health
effects in exposed populations, i er complicated by the transformation
of radon to radon daughters. alon7 may be Present with radon in the
environment and inhaled or ing® the *8 with radon and/or they may be formed
in situ from the transformation radon absorbed in the body.
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31
2. HEALTH EFFECTS
2.3.1 Absorption
2.3.1.1 Inhalation Exposure
The primary route of exposure to radon and its progeny is inhalation.
The degree of deposition and the subsequent absorption of inhaled radon and
progeny is determined by physiological parameters, such as respiration rate
and tidal volume; and physical properties, such as the particle size
distribution of the carrier aerosols and of the unattached fraction, the
equilibrium state, and solubility coefficients (Crawford-Brown 1987; Holleman
et al. 1969; Jacobi 1964).
Since radon is an inert gas, its movement across membranes is driven by
solubility coefficients (Crawford-Brown 1987) and it may be readily absorbed
by crossing the alveolar membrane. Most inhaled radon will be exhaled before
it can decay and deposit a significant radiation dose to the lung tissue, due
to the relatively long half-life of radon gas (McPherson 1980).
The radioactive decay of radon results in the formation of long- and
short-lived daughter products which may attach to the surface of aerosol
particles and, when inhaled, deposit on the mucus lining of the respiratory
tract through impaction, sedimentation, or diffusion (Altshuler et-al. 1964).
It is assumed that the short-lived daughters, polonium-218, lead-214, and
bismuth-214, remain in the mucus layer (James 1987); however, absorption of
deposited radon daughters from the lung into the blood stream also may occur
(Jacobi 1964; Morken and Scott 1966). The deposited radon daughters appear to
act as soluble substances and are released from the dust particles after they
undergo solvation (ICRP 1966). The long-lived radon daughter products (lead-
210, bismuth-210, and polonium-210) contribute little to the radiation dose to
lung tissue because they have a greater likelihood of being physically removed
by ciliary action or absorbed by macrophages before they can decay and deliver
a significant radiation dose (McPherson 1980). The absorption characteristics
and rates of mucus clearance in various parts of the respiratory tract are
uncertain (James 1987).
The total respiratory deposition of radon daughters in human subjects has
been determined experimentally by George and Breslin (1967, 1969), Holleman et
al. (1969), and Shapiro (1956) to range from 18% to 51% of the inhaled amount
and to be dependent on tidal volume, particle size, and breathing rate. In
general, deposition increases with increasing tidal volume, with smaller
particle size, and with changes in normal breathing rates. Respiratory
deposition has also been measured in casts of the human larynx and trachea by
Chamberlain and Dyson (1956) who determined an average deposition of about 22%
of the inhaled, uncombined radon activity at a breathing rate of 20 L/minute.
The important sites for deposition of aerosols were determined by the use of
casts of the human tracheobronchial tree to be at or near the first
bifurcations of the bronchi (Cohen 1987; Martin and Jacobi 1972). According
to Cohen (1987), the nonuniform deposition for bifurcations as compared with
airway lengths suggests that the dose from radon daughter deposition will be
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32
2. HEALTH EFFECTS
about 20% greater than estimated for uniform deposition. Estimation of dose
to the respiratory tract has been extensively studied using models (BEIR IV
1988; EPA 1989a; Harley and Pasternak 1982). Both the studies of human lung
casts and the information derived from models indicate that most deposition
occurs in the tracheobronchial region of the lung; other regions
(nasopharyngeal and pulmonary) receive much smaller doses (BEIR IV 1988)
From a study in rats, Cohn et al. (1953) were able to conclude that the
radiation exposure per unit area is greater for the bronchi than for any other
lung tissue and, that the radiation dose to the respiratory tract from the
progeny was 125 times greater than from radon alone.
2,3.1.2 Oral Exposure
Exposure to radon by the oral route occurs from dissolution of radon in
drinking water and, of the total radon dissolved in wat;eri 30% to 79% may be
lost by aeration and would be available for inhalation (Dundulis et al 1984-
Holoway and Turner 1981). Another study reported a loss of 15% to 25% radon'
to the air from drinking (Suomela and Kahlos 1972). Based on the time-course
of radon elimination in expired air, it appears that the majority of radon
absorption following ingestion in water occurs in the stomach and small
intestine, and only 1% to 3% of the ingested radon remains to enter the large
intestine to be available for absorption (Dundulis et al 1984) Studies with
other inert gases indicated that the small intestine plays a major role in
gastrointestinal uptake of these inert gases (Tobias et al 1949)
The rate of absorption of radon from the'gastrointestinal tract depends
on the stomach contents and the vehicle m which it j_s dissolved
Experimental data from humans who ingested radon dissoLved in water indicate
that radon is rapidly absorbed from the stomach and small intestines and that
greater than 90% of the absorbed dose is eliminated by exhalation in'less than
1 hour (Hursh et al. 1965). Absorption of radon also may occur in the x
intestine. This is based on experimental data where exhalation of radon
continues at lower concentrations for a lo^ time af(_er administration when
radon dissolved in drinking water is ingested on a full stomach as compared to
ingestion of radon on an empty stomach (Meyer 1937). The absorption of radon
following ingestion of a meal high in fat is delayed (Vaternahm 1922). Radon
is present in exhaled air at higher concentrations and at later times after
ingestion of oil or fat emulsions contain ng radon contai
radon (Vaternahm 1922) .
Ingested radon progeny may not contr^^ s^gnificantiy to the radiation
dose to the stomach as they may not pene e the Unl to a t
extent (Von Dobeln and Lindell 1964). P ^tion of daughter products in
situ, following absorption of radon in c . gastr°intestinal tract, will
primarily result in a radiation dose to &ast^intestinal wall (Von Dobeln
and Lindell 1964). The ingestion of int ** also result in exposure to lung
tissue due to absorption from the gastr tmal tract with transport hy way
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33
2. HEALTH EFFECTS
of the systemic circulation to the lung with subsequent decay to daughter
products occurring in the lung (Crawford-Brown 1987).
2.3.1.3 Dermal Exposure
Data regarding the absorption of radon following dermal exposure are very
limited. Dermal absorption of radon has been measured in subjects after
bathing in a radon-water spa (Furuno 1979; Pohl 1965) or after application of
a radon-containing ointment to the intact skin (Lange and Evans 1947). After
bathing for 5 to 15 minutes, radon-222 concentrations in expired air reached
approximately 0.9% of that in the water and ranged from 17.9 to 49.1 pCi
radon-222/L of air (662 to 1817 Bq/m3) compared to pre-bath levels of less
than 1 pCi radon-222/L of air (37 Bq/m3). Radon concentrations in the water
were reported by the authors as 5,800 pCi (215 Bq) radon-222/kg. However, the
relative contributions of the dermal and inhalation routes cannot be
determined (Furuno 1979). Radon concentrations in blood reached 0.85% to 1%
of the radon concentration in the bath water, which was 1.8xl05 pCi (4.9xl06
Bq) radon-222/L of water, after 30 to 40 minutes of bathing while breathing
compressed air (Pohl 1965). Approximately 4.5% of the radon applied in
ointment to intact skin was measured in expired air within 24 hours following
application (Lange and Evans 1947).
2.3.1.4 Other Routes of Exposure
No studies were located regarding absorption of radon or its progeny in
humans and laboratory animals after exposure by other routes.
2.3.2 Distribution
2.3.2.1 Inhalation Exposure
The distribution of radon once it is absorbed or deposited in the lung is
a function of its physical properties. Radon progeny, especially the long-
lived daughters, that have been deposited in the lungs are partially removed
by the mucociliary blanket, which then carries the particles to the trachea
and the gastrointestinal tract. Following chronic exposure in humans, lead-
210, a stable daughter product, has been found in bone (Black et al. 1968;
Blanchard et al. 1969; Cohen et al. 1973; Fry et al. 1983) and in teeth
(Clemente et al. 1982, 1984). After prolonged exposure, radon concentrations
in body organs can reach 30% to 40% of inhaled concentrations (Pohl 1964).
Fat appears to be the main storage compartment in rats following
inhalation exposure. In rats following an acute exposure to radon,
concentrations of radon and radon daughters were much higher in the omental
fat than in any of the other tissues examined, followed by the venous blood,
brain, liver, kidney, heart, muscle tissues, and testes (Nussbaum and Hursh
1957). Radon reached equilibrium in the fat in about 6 hours compared to 1
hour in all other tissues. This may be due to the nonuniformity of blood
perfusion within this tissue.
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2. HKAI.TH KFKKC'n
2.3.2.2 Oral Exposure
After radon enters the gastrointestinal t ract , it is absorbed into the
blood stream and then distributes to different organs and tissues (Crawford-
Brown 1987). This transfer from the gastrointestinal tract to the blood was
dependent upon the emptying patterns of the stomach into the upper intestine
stomach content, fat content of meals, and time of meal in relation to radon*
ingestion (Hursh et al. 1965; Suoraela and Kahlos 14/2; Vaternahm 1922' Von
Dobeln and Lindell 1964). No age - dependent differences in radon distribution
from the gastrointestinal tract should be evident due to rapid equilibration
in the body (Crawford-Brown 1983). However, changes in the mass of fatty
tissue would be expected to affect distribution pi <»•<•?;;;»•:; since radon is more
soluble in fat than in other tissues (Crawford-Hrown 1 'iH/).
According to Hursh et al . (196b), in humans greater than (*<>X of ingested
radon is distributed to the lung where it is rapidly exhaled Of the
remaining administered dose of radon, bX is distributed to the liver, 1 62 to
the kidneys, and 2% to lung tissue (Holoway and Turner ](/8]). Acute exposure
of human subjects to 1. 3xl05 to 2.83x10'' pCi (A.'lxK)' to l.ObxlO2 Rq) radon-
222/L of water resulted in a whole body accumulation of ].4xlOJ to 1.22x10*
pCi (70 to 450 Bq) bismuth-214, a radon decay product. The biological half-
life of radon in these individuals ranged from 30 to bo minutes (Suomela and
Kahlos 1972).
From a chronic study in laboratory animals where 3.6 pCi (0.13 Bq) of
radon was administered daily for 1 year, a body accumulation of 5 pCi (0 19
Bq) lead- 210/g of tissue, 0.08 pCi (3.0x10 J Bq) po 1 on i urn -'? 10/g of tissue, and
0.003 pCi (l.lxlO"4 Bq) bismuth-210/g of tissue was reported (Fernau and
Smereker 1933). Radon is very soluble in far with its distribution
coefficient in fat greater than in any other organ or tissue (Nussbaum and
Hursh 1957). This storage of radon in body fat is a constant; source of lead-
210, polonium-210, and other progeny (Djuric et al. 1964), The presence of
lead-210 and polonium-210 are not unique to radon exposure and are also found
in cigarette smoke and food (NCRP 1984b).
In addition to the available data on distribut ion in huinans and
laboratory animals, many different models exist, which estimate distribution 1
humans (EPA 1988a; ICRP 1978). n
2.3.2.3 Dermal Exposure
No studies were located regarding distribution in humans or laboratory
animals after dermal exposure to radon or its progeny.
2.3.2.4 Other Routes of Exposure
No studies were located regarding distribution of radon or its progeny in
humans or laboratory animals after exposure by other routes.
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35
2. HEALTH EFFECTS
2.3.3 Metabolism
Radon is an inert noble gas that does not readily interact chemically
with cellular macromolecules. Radon does not undergo metabolism in biological
systems.
2.3.4 Excretion
2.3.4.1 Inhalation Exposure
Most of the inhaled radon will be eliminated by exhalation before it can
decay and deposit a significant radiation dose to the lung tissue. The long-
lived radon progeny are, to some extent, physically removed before they can
decay and deposit a radiation dose (McPherson 1980). The biological half-time
for radon daughters in the pulmonary region has been reported to range from 6
to 60 hours and in the tracheobronchial region to range from 10 minutes to 4.8
hours (Altshuler et al. 1964; Jacobi 1964, 1972), The biological half-time in
fat tissue has two components, a fast component of 21 minutes and a slow
component of 130 minutes (Nussbaum and Hursh 1957).
Long-lived radon progeny (lead-210) have been reported to be excreted in
the urine of uranium miners at 1 to 18 years following exposure. This
excretion of lead-210 results from a slow release of the daughters from bone.
Concentration of lead-210 in bone has been shown to correlate with cumulative
exposure to radon and radon daughters in WLM (Black et al. 1968).
Experiments in rats and mice indicated that polonium-214 may be retained
in the lung following inhalation exposure. The retention efficiency of
polonium-214, a stable daughter product, in the lung was 2% and 2.2% of the
administered activity in rats and mice, respectively, immediately following
acute inhalation exposure (Doke et al. 1973).
2.3.4.2 Oral Exposure
Following ingestion of radon dissolved in water, greater than 90% of the
absorbed radon was eliminated by exhalation within 100 minutes. By 600
minutes, only 1% of the absorbed amount remained in the body (Hursh et al.
1965). The biological half-time for removal of radon from the body ranges
from 30 to 70 minutes depending on whether the stomach is empty or full and on
fat content in the diet (Hursh et al. 1965; Suomela and Kahlos 1972; Vaternahm
1922) . The presence of food in the stomach may result in a marked delay in
the removal of radon from the body due to an increased emptying time of the
stomach during which time a portion of the radon may decay (Hursh et al.
1965). The biological half-life in the blood of humans has been reported to
be 18 minutes for 95% of the administered dose and 180 minutes for the
remaining 5% (Hursh et al. 1965). The longer half-life for the remaining 5%
may be due to storage and subsequent removal from tissues. The effective
half-life for removal of radon was reported as 30 minutes (Andersson and
Nilsson 1964).
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36
2. HEALTH EFFECTS
The transfer rate of radon from the gastrointestinal tract and subsequent
elimination from the respiratory tract was found to be dependent on the
pattern of emptying of the stomach into the small intestines (i.e., with or
without a meal), and the accompanying vehicle (i.e., water or fat). After
ingestion of radon dissolved in drinking water on an empty stomach, radon in
exhaled air rapidly increased reaching a maximum concentration in exhaled air
5 to 10 minutes after ingestion (Meyer 1937). With ingestion of radon in
drinking water with or after a meal, radon elimination in expired air is
delayed and varies in concentration with time, reflecting absorption from the
small intestines as it receives a portion of the stomach contents (i.e., with
stomach emptying patterns) (Meyer 1937). After ingestion of radon dissolved
in olive oil on an empty stomach, elimination in expired air reached a maximum
concentration 50 minutes post-ingestion, then declined; however, when
administered in olive oil after a meal, radon in expired air remained constant
from 10 minutes to 5 hours after ingestion (Vaternahn 1922). These data
suggest that radon is eliminated in expired air more rapidly from a water
vehicle than a fat or oil vehicle and this elimination occurs over a longer
period of time when ingested with a meal than on an empty stomach.
When radon dissolved in water was ingested on a full stomach, the
exhalation of radon reached a maximum at 5 to 15 minutes then declined. This
was then followed by a second peak about 20 minutes after ingestion. When
ingestion of radon occurred "some time" after a meal, the second radon peak in
exhaled air was delayed and was followed by further peaks (Meyer 1937). These
subsequent peaks were explained by the absorption of radon from the intestine
after it has received portions of the stomach content (Meyer 1937).
2.3.A.3 Dermal Exposure
Information on the excretion of radon and its progeny following dermal
exposure is very limited. Within 24 hours, 4.5% of the radon, which was
applied as a salve to intact human skin, was eliminated by exhalation, while
10% was exhaled after applic^tion the radon to an open wound (Lange and
Evans 1947). Bathers breathing compressed air while immersed in radon-
containing water had exhaled approximately
one-third of radon measured in
blood immediately after bathing ( ° 1 1965). By 6 to 8 minutes after bathing,
these persons were exhaling one" ^ of the amounts exhaled immediately after'
bathing. The author stated that e remaining radon which distributed to
fatty tissue was excreted i*°re slowly.
2.3.4.4 Other Routes of E*P°sure
Experiments in animals have reported the retention of radon after
exposure by the intraperic°"ea^ ^travenous routes. After intravenous
administration, 1.6% to 5- m*nistered activity was retained in the
animals after 120 minutes ,° an Lorenz 1949). Retention was greatest
after intraperitoneal adminlstra minutes, but by 240 minutes it was
nearly the same for both 't'^U^ej0n r.e^m^n^"stration. These authors also
reported that the amount °* ra aine^ tissues was greater in obese
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37
2. HEALTH EFFECTS
mice than in normal mice, especially after intraperitoneal administration
(Hollcroft and Lorenz 1949). Radon retention has also been studied in dogs
after intravenous administration of radium-226. The amount of radon in bone
was found to increase with increasing time after injection (Mays et al. 1975).
2.4 RELEVANCE TO PUBLIC HEALTH
Growing concern in the late 1940s that the inhalation of radon and radon
daughters was contributing to the adverse health effects observed in
underground miners stimulated the conduct of epidemiological investigations
and initiated animal studies with radon and radon daughters. Earlier
inhalation studies had been conducted with radon only, but evidence from radon
dosimetry studies indicated the involvement of radon daughters rather than
just radon (Bale 1951). Epidemiological studies further suggested that the
major health effects observed in miners might be attributed to radon
daughters. Both human and animal studies indicate that the lung and
respiratory system are the primary targets of radon daughter-induced toxicity.
The evidence indicates that inhalation of radon decay products results in
radiation damage to tissues in which these products are deposited.
Nonneoplastic respiratory disease and lung cancer have been reported in humans
and animals exposed to radon and radon daughters by inhalation.
Death. No deaths in humans following acute exposure to radon have been
reported. Following long-term exposure, significant increases in early
mortality due to nonneoplastic respiratory diseases have been reported among
uranium miners. Because mortality due to nonneoplastic diseases is not
generally reported by exposure categories (i.e., WLM categories), it is not
clear what exposure concentration or duration of exposure in these mining
cohorts is associated with this increased mortality. In addition, these
nonneoplastic respiratory deaths cannot be attributed solely to radon but may
result from exposure to other mine air pollutants. Reduction in lifespan due
to respiratory disease as a result of exposure to high levels of radon or
radon daughters has been reported in various animal studies. Based on the
evidence in animals, it is apparent that death due to respiratory disease may
result after exposure to radon at very high levels. However, it is unclear to
what extent low-level environmental exposure to radon and radon daughters may
increase the risk of death due to nonneoplastic respiratory disease.
Respiratory Effects. Respiratory disease characterized as emphysema,
fibrosis, or pneumonia has been reported in both humans and animals with
inhalation exposure to high levels of radon and radon daughters. In addition
to deaths due to nonneoplastic respiratory disease, some studies have reported
reductions in respiratory function. In all of the occupational cohorts,
miners were concomitantly exposed to other mine pollutants, such as ore dust,
other minerals, or diesel-engine exhaust. The contribution of these
pollutants, as well as cigarette smoking, to the induction of nonneoplastic
respiratory disease is unclear. As reported in Section 2.6, Interactions With
Other Chemicals, the combination of radon and radon daughters along with ore
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38
2. HKALTH EFFKCTS
dust or other pollutants enhanced the incidence and severity of adverse
respiratory effects in laboratory animals as compared to either toxicant
alone. Induction of this type of respiratory disea.se may occur primarily at
doses that exceed those commonly found in the environmental .setting; however,
the radiation dose that would result in either pulmonary dysfunction or
pulmonary disease is not known. The adverse respiratory effects observed
appear to be consistent with alpha radiation damage that may occur at high
doses in slower regenerating tissues such as the lung (see Appendix B) . That
being the case, production of respiratory tissue damage in the lungs may not
be immediately apparent, especially at low environmental exposures.
Hematological Effects. No information on the hematological effects of
radon in humans was located in the available literature. Alterations in
hematological parameters following exposure to radon have been reported in
animals. The extent and severity of the hematological effects were related to
the level of exposure and the exposure duration, and reel blood cells appear to
be more sensitive to the effects of radon than white blood cells. Following
acute exposure by the inhalation or intravenous routes, decreases in the
number of red blood cells and white blood cells occurred immediately post-
exposure. Red blood cells remained depressed for the remaining life of the
treated animals, while white blood cells returned to normal levels post-
exposure. Following repeated exposures, white blood cell counts remained
depressed for longer periods of time and, with chronic exposure, depression in
white blood cell counts was linearly related to the cumulative exposure. The
animal studies indicate chronic exposure of humans to radon may result in
similar alterations in the hematopoietic system.
Renal Effects. Evidence of kidney disease has been reported in United
States uranium miners (Waxweiler et al. 1981), In that survey, chronic and
unspecified nephritis was elevated after a 10-year latency. The
nephrotoxicity of soluble uranium in animals has been documented (ATSDR
1990a). Due to their relatively short half-lives, the alpha-emitting radon
daughters present in the lung undergo radioactive decay before they move to
other organs, in contrast to other alpha-emitting radionuclides, such as
uranium or plutonium (ATSDR 1990a, 1990b), which may translocate from the lung
to irradiate other tissues. Nevertheless, direct evidence of renal
dysfunction or impairment resulting from inhalation or oral exposure to radon
and radon daughters alone is lacking.
Neurological Effects. No information on neurological effects in humans
exposed to radon was located in the available literature. Only one animal
study attributed the toxic effects observed to the action of radon on the
central nervous system. This study reported respiratory paralysis due to
central nervous system depression; however, the study has numerous flaws (see
Section 2.2.1.4) that limit its usefulness and render the reported results
questionable.
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39
2. HEALTH EFFECTS
Reproductive Effects. Recent epidemiological studies have raised
speculation that inhalation exposure to radon and radon daughters during
uranium mining may be associated with effects on reproductive outcome. A
decrease in the secondary sex ratio (the ratio of male to female children) of
children of underground miners following employment in uranium mines was
reported (Dean 1981; Muller et al. 1967). Waxweiler and Roscoe (1981),
however, found the secondary sex ratio to increase in older men but to
decrease in younger men. If the father is exposed to radiation, an increase
in the number of male children might be expected due to the relative
resistance of the Y chromosome as compared to the X chromosome (Waxweiler and
Roscoe 1981). In a preliminary study, Wiese and Skipper (1986) reported a
decrease in the secondary sex ratio, although not statistically significant,
in children born to underground uranium and potash workers. No other
information exists on reproductive effects in other epidemiological
investigations or animal studies. Therefore, these observations of
alterations in secondary sex ratios are suggestive of possible effects but are
not conclusive evidence that radon can produce reproductive toxicity in
persons environmentally exposed to radon.
Genotoxic Effects. Increases in chromosomal aberrations have been
reported among uranium miners and among personnel employed at a radon spa in
Austria following inhalation exposure. Increases in chromosomal aberrations
were also reported in a small group of people living in an area with high
radon concentrations in their water supply. As stated in Section 2.3 on
toxicokinetics, radon rapidly escapes from water; therefore, the probable
major route of exposure in this cohort also was inhalation. In addition,
increased DNA-repair rates in lymphocytes were observed in another
occupational cohort. The increased DNA repair rates may reflect increases in
DNA damage. DNA repair enzymes may be induced in response to DNA damage. The
implications of this information for environmental exposures are unclear. In
the case of the miner occupational cohorts, cumulative exposures were greater
than 100 WLM and ranged up to 6,000 WLM. Also, the animal data are
inconclusive and do not clearly establish a link between genotoxicity and
radon exposure. A summary of the genotoxicity studies is given in Table 2-2.
Cancer. Numerous epidemiological studies have demonstrated a causal
association between lung cancer mortality and exposure to radon in combination
with radon daughters. The majority of these epidemiological data have been
collected from occupational cohorts exposed to radon and radon daughters
during mining operations. Despite the variety of conditions reported for the
mines (including dust concentrations, type of ore mined, and ventilation
rates) and differences in the cohorts (including levels of exposure, length of
follow-up, smoking habits, and ages of exposure), exposure to radon in mining
operations is clearly directly associated with lung cancer mortality.
Some of these studies indicate that lung cancer mortality was influenced
by the total cumulative radiation exposure, by the age at first exposure, and
by the time-course of the exposure accumulation. The length of the induction
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AO
2. 1IKALTH F.FFFXTS
TABLE 2-2. Genotoxicity of Radon-222 In Vivo
End Point
MAMMALIAN SYSTEMS
Chromosomal
aberrations
DNA repair
Sister
chromatid
exchanges
Human (peripheral
lymphocytes)
Human (whole body
lymphocytes)
Rabbit (somatic cells)
Human (lymphocyte.';)
Rat (bone marrow cells
Species (Test System) Result
Rcf erenee
i'oh 1 - Ri'U ing et al .
1 <)/<>, 198 7; Pohl-
Ri'tl in)', and Fischer
1') /'), 198?, 1983;
Brandon) et al. 1972,
1') /H
Stenstrnnd et al.
19/9
Leonard et al. 1981
Tusi'h 1 et al . 1980
I'm icy et al . 1980
INVERTEBRATE SYSTEMS
Dominant lethal Drosophila
melanop.aster
O)
Spc i 1 i ch et al. 1967
+ - positive result
- - negative result
(+) - positive or marginal result
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41
2. HEALTH EFFECTS
latency, that is, the time from the start of mining to the development of
cancer, is strongly dependent on the age at which a man starts mining (Archer
1981). The data indicate that the older a man is when he starts mining, the
shorter his induction-latency period will be. The Czechoslovakian data
indicate that the frequency of attributable lung cancer mortality rises
steeply with increasing age at the start of mining, corresponding to
decreasing induction-latency periods (Sevc et al. 1988). There is evidence
that the induction-latency period is also dependent on the exposure rate and
total radiation exposure, that is, the lower the exposure rate, the longer a
group must be followed to evaluate the lung cancer risk (Archer et al. 1979).
According to Sevc et al. (1988) lung cancer mortality for the same cumulative
WLMs was greater in the subcohort with higher exposures early in their work
history, compared to those with nearly equal yearly exposure or the subcohort
with lower initial exposure which increased to higher levels in later years.
Additional support for the role of radon as a causative agent in lung cancer
is provided by the results of the studies of nonuranium hard rock miners,
which also showed an increased mortality rate from lung cancer.
Some of these studies also indicated that underground miners who were
cigarette smokers had a higher incidence of radiation-induced lung cancer
mortality than did miners who were nonsmokers, and that the induction-latency
period was substantially shorter for smokers than for nonsmokers (Archer
1981). A study of a nonsmoking cohort of uranium miners clearly indicated an
increased mortality risk for lung cancer for the cohort (Roscoe et al. 1989).
In addition, increases in lung cancer among American Indian uranium miners,
who had a low frequency of lung cancer in the nonexposed general population
compared to rates in the white United States population and a low frequency of
cigarette smoking, support the conclusion that radiation is the primary cause
of lung cancer among uranium miners (Gottlieb and Husen 1982; Samet et al.
1984b; Sevc et al. 1988). A comprehensive evaluation of risk estimates from
various mining cohorts can be found in BEIR IV (1988).
Several studies of residential exposure to radon and radon daughters also
indicate an increased risk of lung cancer (Axelson and Edling 1980; Axelson et
al. 1971, 1981; Edling et al. 1984; Svennson et al. 1987, 1989). These
studies are primarily case-control studies that involve a small number of
subjects and have exposure estimates that are limited or based on surrogates.
A more recent study has reported on a much larger cohort and has provided some
exposure information (Svennson et al. 1989). These studies support the
evidence obtained from the occupational cohorts. Radon concentrations in
environmental settings are not expected to be at levels as high as those
encountered in mining operations nor would they be expected to be combined
with dusty conditions or diesel exhaust exposure, two features of the exposure
of several of the examined cohorts. However, the BEIR IV (1988) Committee
indicated that the risk from occupational or residential exposure to radon is
the same per unit dose.
Studies in animals confirm and support the conclusions drawn from the
epidemiological data. When all animal data are combined and reviewed, four
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2. HEALTH EI-TKCTS
variables surface which appear t o i nf 1 uence the <• t f i c i ency of radon daughters
to produce lung cancer in laboratory animal:; (Cross et al. 1H ^) . These
variables include: cumulative exposure to radon and radon daughters, exposure
rate to radon and radon daughters, unattached fraction of radon daughters, and
disequilibrium of radon daughters. Another factor which may influence the
tumorigenic potential of radon and radon daughter;; is exposure in conjunction
with other pollutants, such as uranium ore dust or cigarette smoke (see
Section 2.6 for a discussion of interactions of radon with other chemicals).
The ability of radon daughters, alone or in conjunction with uranium ore
dusts, to produce lung tumors in laboratory animals appears to increase with
an increase in exposure until lifespan shortening reverses the trend, wLth a
decrease from high exposure rate to low exposure rate, and with increasing
unattached fraction and disequilibrium.
In general, the pattern of results from the epidemiological studies and
animal experiments clearly indicates a risk due to radon and radon daughter
exposure. Although individual studies have particular shortcomings that may
make that conclusion less supportable for the individual study, the pattern
over all the studies is convincing. Posit ive assoriat ions between exposure to
radon daughters and lung cancer have been found in occupat ional settings for
various types of mining operations, in various ethnic groups around the world,
and under various concomitant exposure conditions. in some of these
occupational settings, concomitant exposure to other pollutants, such as ore
dust, diesel engine exhaust, or other minerals, such as silica, may have
occurred. The possible impact of these other pollutants on radon daughter-
induced lung cancer is unclear (see Section ¦?.(>).
2.5 BIOMARKERS OF EXPOSURE AND EFFECT
Biomarkers are broadly defined as indicators signaling events in biologic
systems or samples. They have been classified as markers ot exposure, markers
of effect, and markers of susceptibility (NAS/NRC 1989).
A biomarker of exposure is a xenobiotic substance or its metabolite(s) or
the product of an interaction between a xenobiotic agent and some target
molecule or cell that is measured within a compartment of an organism (NAS/NRC
1989). The preferred biomarkers of exposure are generally the substance
itself or substance-specific metabolites in readily obtainable body fluid or
excreta. However, several factors can confound the use and interpretation of
biomarkers of exposure. The body burden of a substance may be the result of
exposures from more than one source. The substance being measured may be a
metabolite of another xenobiotic (e.g., high urinary levels of phenol can
result from exposure to several different aromatic compounds). Depending on
the properties of the substance (e.g., biologic hnlf-life) and environmental
conditions (e.g., duration and route of exposure), the substance and all of
its metabolites may have left the body by the time biologic samples can be
taken. It may be difficult to identify individuals exposed to hazardous
substances that are commonly found in body tissues and fluids (e.g., essential
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43
2. HEALTH EFFECTS
mineral nutrients such as copper, zinc and selenium). Biomarkers of exposure
to radon are discussed in Section 2.5,1.
Biomarkers of effect are defined as any measurable biochemical,
physiologic, or other alteration within an organism that, depending on
magnitude, can be recognized as an established or potential health impairment
or disease (NAS/NRC 1989). This definition encompasses biochemical or
cellular signals of tissue dysfunction (e.g., increased liver enzyme activity
or pathologic changes in female genital epithelium cells), as well as
physiologic signs of dysfunction such as increased blood pressure or decreased
lung capacity. Note that these markers are often not substance specific.
They also may not be directly adverse, but can indicate potential health
impairment (e.g., DNA adducts). Biomarkers of effects caused by radon are
discussed in Section 2.5.2.
A biomarker of susceptibility is an indicator of an inherent or acquired
limitation of an organism's ability to respond to the challenge of exposure to
a specific xenobiotic. It can be an intrinsic genetic or other characteristic
or a preexisting disease that results in an increase in absorbed dose,
biologically effective dose, or target tissue response. If biomarkers of
susceptibility exist, they are discussed in Section 2.7, "POPULATIONS THAT ARE
UNUSUALLY SUSCEPTIBLE."
2.5.1 Biomarkers Used to Identify or Quantify Exposure to Radon
Biomarkers of exposure to radon and its progeny include the presence of
radon progeny in several human tissues and fluids, including bone, teeth,
blood, hair, and whiskers, and can be measured by methods which are both
specific and reliable (Blanchard et al. 1969; Clemente et al. 1984; Gotchy and
Schiager 1969). Although the presence of radon progeny in these tissues and
fluids indicate exposure to radon, exposure to uranium or radium may also
result in the presence of these decay products. Polonium-210 may also be
found in tissues after exposure to cigarette smoke. Levels of lead-210 in
teeth have been associated with levels of radon in the environment in an area
with high natural background levels of radon and radon daughters (Clemente et
al. 1984). In addition, Black et al. (1968) reported correlation of radiation
exposure and lead-210 levels in bone from uranium miners. However, cumulative
exposure to these individuals was estimated. Biomarkers of radon or radon
progeny exposure may be present after any exposure duration (e.g., acute,
intermediate, chronic). Because of the relatively short half-lives of most
radon progeny, with respect to a human lifetime, the time at which the
biological sample is taken related to time of exposure may be important.
However, for the longer lived progeny the time factor is less critical.
Models are available which estimate exposure to radon-222 from levels of
stable radon daughter products, lead-210 and polonium-210, in bone, teeth, and
blood (Blanchard et al. 1969; Clemente et al. 1982, 1984; Eisenbud et al.
1969; Gotchy and Schiager 1969; Weissbuch et al. 1980). However, these models
make numerous assumptions, and uncertainties inherent in all models are
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44
2. HEALTH FFFKCTS
involved in these estimates. Therefore, at present , these estimated levels of
biomarkers of exposure are not useful for quantifying exposure to radon and
progeny. Quantification of exposure to radon is furtiur complicated by the
fact that radon is an ubiquitous substance and background levels of radon and
radon progeny are needed to quantify higher than "average" exposures.
2.5.2 Biomarkers Used to Characterize Effects Caused by Radon
The principal target organ identified in both human and animal studies
following exposure to radon and progeny is the lung. Alterations in sputum
cytology have been evaluated as an early indicator of radial ion damage to lung
tissue. The frequency of abnormalities in sputum cytology, which may indicate
potential lung cancer development, increased with increasing cumulative
exposures to radon and radon daughters (Band et al. 1980; Saccomanno et al.
1974). Although abnormal sputum cytology may lie observed following radon
exposure, this effect is also seen following exposure to other xenobiotics
such as cigarette smoke. In addition, even though increases in the frequency
of abnormal sputum cytology can be measured, they may not provide a reliable
correlation between levels in human tissues or fluids with health effects in
exposed individuals.
A dose - response relationship between chromosome aberrations and increased
environmental levels of radon has been reported (I'ohl-Ruling and Fischer 1983;
Pohl-Ruling et al. 1976, 1987). Although the presence of chromosome
aberrations is a biomarker of effect, the potential range of chemicals which
could cause this effect is so great that it: would not necessarily be
considered radon-specific.
Additional biomarkers of effect for radon and radon progeny exposure may
exist; however, these were not located in the reviewed literature. For more
information on biomarkers for effects of the immune, renal, and hepatic
systems see ATSDR, CDC Subcommittee Report on Biological Indicators of Organ
Damage (1990c) and for biomarkers of effect for the neurological system see
OTA (1990). For more information on health effects following exposure to
radon and radon daughters see Section 2.2.
2.6 INTERACTIONS WITH OTHER CHEMICALS
The interaction of cigarette smoke with radon and the possible effect on
radon-induced toxicity is a complex one and is still an issue under
consideration. Cigarette smoke appears to interact with radon and radon
daughters to potentiate their effects. In general, epidemiological studies
have reported synergistic, multiplicative, or additive effects of cigarette
smoke in lung cancer induction among miners exposed to radon and radon
daughters (US DHHS 1985). Studies by Lundin et al. (1969, 1971) reported 10
times more lung cancer among United States uranium miners who smoked. In a
case-control study of United States uranium miners, Archer (1985) reported
that smoking miners with lung cancer had significantly reduced latency-
induction periods than nonsmokers. Cigarette smoking also appeared to shorten
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45
2. HEALTH EFFECTS
the latency period for lung cancer among Swedish lead-zinc miners (Axelson and
Sundell 1978), and Swedish iron miners (Damber and Larsson 1982). Miners who
smoke cigarettes may be at higher risk because of the possible synergistic or
additive effect between radon and radon daughters and cigarette smoking
(Klassen et al, 1986). However, an antagonistic relationship between
cigarette smoking and lung cancer in humans may exist according to Sterling
(1983). His hypothesis is that smokers may have a lower potential retention
of deposited radon daughter particles due to enhanced mucociliary clearance.
Other investigators have reported that nonsmoking miners exhibited a higher
incidence of lung cancer than smokers, although the latency of cancer
induction was shorter in nonsmokers than for smokers (Axelson 1980; Axelson
and Sundell 1978). Again, the theories put forth to explain this phenomenon
include increased mucus production and alterations in mucociliary clearance in
smokers resulting in the increased mucus thickness.
Some animal studies support the theory that cigarette smoke potentiates
the effects of radon and radon daughters alone or in conjunction with uranium
ore dust. A study by Chameaud et al. (1982b) reported an increase in the
incidence of lung cancer, as well as a decrease in the cancer latency period
in rats exposed to radon and then to cigarette smoke, compared to rats exposed
to radon and radon daughters alone. This study did not include untreated
controls. Alterations in normal blood parameters, including carboxyhemoglobin
levels and leukocyte counts, were observed in dogs exposed to cigarette smoke
followed by exposure to radon daughters plus uranium ore dust, compared to
animals exposed to only radon daughters plus uranium ore (Filipy et al. 1974).
In contrast, some studies suggest an antagonistic interaction between smoking
and radon daughter-induced lung cancer. Dogs exposed daily to cigarette smoke
followed immediately by exposure to radon and radon daughters and uranium ore
dust exhibited a decrease in the incidence of lung tumors, compared to dogs
exposed to radon and radon daughters plus uranium ore dust (Cross et al.
1982b). Cross (1988) reported that this was possibly due to a thickening of
the mucus layer as a result of smoking and, to a lesser extent, a stimulatory
effect of cigarette smoke on mucociliary clearance, although no empirical
evidence was collected during the experiment to test these possibilities.
In rats administration of chemicals present in cigarette smoke after
exposure to radon and radon daughters resulted in a decrease in the lung
cancer Latency period when compared to the time-to-tumor induction in animals
treated with radon alone. This effect was seen with 5,6-benzoflavon (Queval
et al. 1979) and with cerium hydroxide (Chameaud et al. 1974).
Other airborne irritants, as well as ore dust and diesel exhaust, may act
synergistically with radon and radon daughters to increase the incidence of
adverse health effects. Epidemiological studies report the presence of other
airborne irritants in mining environments, including arsenic, hexavalent
chromium, nickel, cobalt (Sevc et al. 1984), serpentine (Radford and Renard
1984), iron ore dust (Damber and Larsson 1982; Edling and Axelson 1983;
Radford and Renard 1984), and diesel exhaust (Damber and Larsson 1982; Sevc et
al. 1984).
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46
2. HEALTH EFFECTS
Cross and colleagues at Pacific Northwest; Laboratory have conducted
extensive experiments involving exposure of dogs, mice, rat.s, and hamsters to
radon and its progeny in conjunction with uranium ore dust and/or diesel
exhaust (Cross 1988; Cross et al. 1981, 1982b, 1984; Pacific Northwest
Laboratory 1978; Palmer et al. 1973). Studies in hamsters, mice, and rats
have shown that exposure to uranium ore dust and/or diesel exhaust increases
the pulmonary effects of radon. Radon and combinations of uranium ore dust
and/or diesel exhaust produced greater incidences of pulmonary emphysema and
fibrosis in hamsters than radon and radon daughters alone (Cross 1988).
Exposure to uranium ore dust or diesel exhaust alone caused significant
bronchial hyperplasia, but not as great an effect as combining either of these
with radon and radon daughters. The incidence of .severe lesions of the upper
respiratory tract (nasal passages and trachea) of mice and rats was increased
following exposure to radon and uranium ore dust, compared to animals exposed
to radon and radon daughters alone (Palmer et al. 1973). An increased
incidence of thoracic cancer (40%) was observed in rats treated with asbestos
(mineral dust) after inhalation of radon and radon daughters, compared with
animals exposed to radon alone (Bignon et al. 1981). However, these tumors
may have been due to asbestos rather than to an interaction between agents.
This experiment did not include a group exposed only to mineral dusts.
Inhalation exposure to radon and radon daughters in conjunction with silicon
dioxide increased the incidence of nodular fibrosis of the lungs in rats
(Kushneva 1959).
2.7 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE
Children may be more susceptible to the effects of radon and radon
daughters. Differences in lung morphometry and breathing rates in children
result in higher estimated doses that may make children more susceptible to
the effects of radon than adults (Samet et al. 1989). In calculating the
inhaled dose of radon, Hofmann et al. (1979) reported that dose was strongly
dependent on age, with a maximum value reached at about the age of 6 years.
Risk of cancer from exposure to low levels of ionizing radiation during
childhood are estimated to be twice that of adults (BE'IR V 1990). Risk of
lung cancer in children resulting from exposure to radon may be almost twice
as high as the risk to adults exposed to the same amount of radon (NCRP
1984a).
Populations that may be more susceptible to the respiratory effects of
radon and radon daughters are people who have chronic respiratory disease,
such as asthma, emphysema, or fibrosis. People with chronic respiratory
disease often have reduced expiration efficiency and increased residual
volume; i.e., greater than normal amounts of air left in the lungs after
normal expiration (Guyton 1977). Therefore, radon and its progeny would be
resident in the lungs for longer periods of time, increasing the risk of
damage to the lung tissue. In addition, persons who have existing lung
lesions may be more susceptible to the tumor-causing effects of radon (Morken
1973) .
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47
2. HEALTH EFFECTS
2.8 ADEQUACY OF THE DATABASE
Section 104(i)(5) of CERCLA directs the Administrator of ATSDR (in
consultation with the Administrator of EPA and agencies and programs of the
Public Health Service) to assess whether adequate information on the health
effects of radon is available. Where adequate information is not available,
ATSDR, in conjunction with the National Toxicology Program (NTP), is required
to assure the initiation of a program of research designed to determine the
health effects (and techniques for developing methods to determine such health
effects) of radon.
The following categories of possible data needs have been identified by a
joint team of scientists from ATSDR, NTP, and EPA. They are defined as
substance-specific informational needs that, if met, would reduce or eliminate
the uncertainties of human health assessment. In the future, the identified
data needs will be evaluated and prioritized, and a substance-specific
research agenda will be proposed.
2.8.1 Existing Information on Health Effects of Radon
The existing data on health effects of inhalation, oral, and dermal
exposure of humans and animals to radon and radon daughters are summarized in
Figure 2-2. The purpose of this figure is to illustrate the existing
information concerning the health effects of radon. Each dot in the figure
indicates that one or more studies provide information associated with that
particular effect. The dot does not imply anything about the quality of the
study or studies. Gaps in this figure should not be interpreted as "data
needs" information.
Figure 2-2 graphically describes whether a particular health effect end
point has been studied for a specific route and duration of exposure. Most of
the information on health effects in humans caused by exposure to radon and
radon progeny was obtained from epidemiological studies of uranium and other
hard rock miners. These studies of chronic occupational exposure to radon via
inhalation provide information on cancer and lethality, and limited insight
into reproductive and genetic effects. Limited information is also available
regarding cancer following dermal exposure to radon and radon daughters. No
information on the health effects of radon and radon daughters in humans was
available following acute or intermediate exposure by any route. No
information on the health effects of radon and radon daughters in animals
following acute, intermediate, or chronic oral or dermal exposure was located.
The only information available from animal studies was by the inhalation route
of exposure which provides data on systemic and genetic effects, as well as
cancer.
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48
2. HEALTH EFFECTS
SYSTEMIC
/ J?/ J
Inhalation
Oral
Dermal
HUMAN
SYSTEMIC
£
Inhalation
Oral
Dermal
ANIMAL
Existing Studies
FIGURE 2-2. Existing Information on Health Effects of Radon
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49
2. HEALTH EFFECTS
2.8.2 Identification of Data Needs
Acute-Duration Exposure. No information exists regarding the health
effects to humans following their acute exposure to radon and radon daughters
by any route. Single dose studies are available for laboratory animals that
have been exposed by the inhalation and parenteral routes. No information is
available on acute oral exposure in laboratory animals. Information is
available on lethality following acute inhalation exposure to high doses.
However, this study did not provide information on target organs, sensitive
tissues, or cause of death. No information is available on effects in humans
or animals following acute exposure to lower levels of radon. This
information is needed in order to assess the toxicity of radon.
Intermediate-Duration Exposure. No information regarding health effects
following intermediate-duration exposure to humans by any route was clearly
identified in the available literature. Epidemiological studies in general
focused on cohorts exposed to radon and radon daughters for durations longer
than one year. Animal studies demonstrate that intermediate exposure to high
levels of radon and radon daughters resulted in chronic respiratory toxicity
and lung cancers. This is an indication of the potential for such effects in
exposed human populations. The relationship between the nature and severity
of the respiratory toxicity and the amount of radon exposure is not clearly
defined; nor is there any information on toxicity to other organs, other than
the respiratory tract following intermediate-duration exposure. Additional
research on the dose - duration-response relationship between radon exposure and
the type and permanence of resulting toxicity would provide pertinent
information. Carefully designed studies in which laboratory animals are
exposed to levels that are similar to high environmental levels for partial
lifetime and observed for life could provide important information. These
studies would facilitate the estimation of cancer risk to persons living in an
area with high natural levels for only a portion of their life. These animal
studies should address both the effect of total dose and dose-rate on
development of adverse health effects. This information may also be useful in
situations in which the time lapse between identifying the presence of radon
and any remediation effort is of an intermediate duration.
Chronic-Duration Exposure and Cancer. Knowledge of the adverse health
effects in humans following chronic radon and radon daughter exposure is based
primarily on studies in adult male underground miners. These studies describe
predominantly respiratory end points, such as emphysema, fibrosis, and cancer.
To a large extent other health effects have not been studied. Epidemiological
studies in general report only the cause of death for each member of the
cohort; therefore, there is insufficient information on whether other adverse
effects were identified other than the ones listed as cause of death. Little
or no information exists on cardiovascular, gastrointestinal, renal,
musculoskeletal, immunological, or dermal/ocular effects in humans or animals.
In addition, these miners also may have been simultaneously exposed to other
pollutants (e.g., long-lived radioactive dusts (uranium), diesel-engine
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50
2. HEALTH EFFECTS
exhaust, cigarette smoke, and external gamma radiation). Several of these
factors have been implicated independently as causative agents of lung cancer
and respiratory diseases and the excess lung cancers in cigarette smokers have
been well documented. Thus, the data currently used to characterize a human
health hazard with regard to respiratory toxicity represent a composite
response to other factors as well as to radon daughters.
Chronic exposure to radon and radon daughters in laboratory animals also
results in respiratory lesions. In laboratory animals exposed to radon and
radon daughters in combination with uranium ore dust, pulmonary fibrosis and
emphysema have resulted. Further research of the interaction of radon and
radon daughters with other environmental pollutants, especially cigarette
smoke, is needed. This information could be used to clarify uncertainties in
the extrapolation of the data in miners to describe the potential hazard to
human health from environmental radon daughter exposures. Well-defined
studies that examine both pathological and functional changes in other organ
systems are necessary to clarify these issues.
Radon dissolved in drinking water is a source of human exposure. Studies
are needed which describe the absorption and translocation of radon gas and
the effects of alpha radiation emitted by radon daughters at the site of
entry, the gastrointestinal tract. While translocation of radon daughters
from the portal of entry to other sites in the body may be limited (due
primarily to the short half-life of most alpha emitting radon daughters),
radon gas may distribute to other organs and, thereby, provide an internal
source of radon daughter alpha radiation.
Epidemiological studies have demonstrated a causal association between
exposure to radon and radon daughters and lung cancer mortality. The number
of lung cancer mortality cases in these cohorts was influenced by the total
cumulative radiation exposure, by the age at first exposure, and by the time-
course of the exposure duration. Significant increases in lung cancer that
were demonstrated in chronic studies in mice, rats, and dogs resulted from
exposure of these animals to radon and radon daughters in combination with one
or more other pollutants, such as uranium ore dust, diesel-engine exhaust, or
cigarette smoke. Chronic studies in hamsters (Pacific Northwest Laboratories
1978) in which animals were exposed to radon and radon daughters alone did not
demonstrate a significant carcinogenic response; however, the hamster may be
resistant to radiation-induced lung cancer. Hamsters did not develop lung
tumors when exposed to another alpha-emitter, plutonium (ATSDR 1990b).
Evidence from animal studies indicates that factors such as the unattached
fraction and disequilibrium of radon daughters influence lung cancer
production. Other air pollutants may interact synergistically with radon
daughters in lung tumor induction. Long-term studies designed to evaluate the
potential interaction of radon daughters with other pollutants would provide
information necessary to determine the toxicity of radon and radon daughters.
Factorial studies, i.e., studies that test radon and radon daughters alone and
radon and radon daughters with only one other confounding factor are needed
because much of the cancer information to date is from studies with several
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51
2. HEALTH EFFECTS
confounding factors. These studies could help elucidate the extent of
interaction between radon and each confounding factor.
Genotoxlcity. Studies of miners and other populations exposed to radon
and radon daughters showed an increased occurrence of chromosomal
abnormalities. However, because exposure - effect relationships have not yet
been established and the biological significance of these chromosomal effects
is uncertain, further studies should be performed. In vitro studies using
human cell lines could help determine a dose - response for exposure to radon
and radon daughters and increased chromosomal abnormalities. Such
relationships may be difficult to establish because of possible interactions
with other substances, i.e., uranium ore dust. There are no in vivo animal
data to support the observed increase in chromosomal abnormalities in human
populations. Further observations in laboratory animals are needed to explain
these effects.
Reproductive Toxicity. Recent epidemiological studies have suggested
that exposure to radon and radon daughters during uranium mining may be
associated with adverse reproductive outcomes (Dean 1981; Muller et al. 1967;
Wiese and Skipper 1986). While the evidence of the possible reproductive
effects of uranium mining is largely descriptive, reports of alterations in
the secondary sex ratio among offspring of uranium miners merits further
study. Currently there are no experimental data that evaluate the
reproductive toxicity of radon and radon progeny exposure by any route.
Controlled experiments that are designed to evaluate reproductive toxicity and
that attempt to correlate the amount of alpha radiation to germ cells could
provide an explanation of the effects that have been observed in the
epidemiology studies.
Developmental Toxicity. Recent data indicate that mental retardation may
result from low-level exposure of children to radiation during their
development in utero (Otake and Schull 1984). While this effect may have
resulted from external radiation rather than internally delivered radiation
dose, the potential of ionizing radiation to induce developmental toxicity is
generally accepted. No experimental data currently exist that evaluate the
developmental toxicity of radon and radon progeny by any route. Controlled
experiments that are designed to evaluate developmental toxicity and that
attempt to correlate the amount of alpha radiation available to the fetus
could show whether the effects observed following exposure to other forms of
radiation also may occur following exposure to radon and progeny.
Immunotoxicity. No information currently exists on humans or laboratory
animals regarding adverse effects on the immune system following exposure by
any route to radon or radon progeny. However, data indicate that acute
exposure to radon in laboratory animals results in a transient decrease in
lymphocytes. Although these effects were transient, it is possible that the
immune system may be compromised during this time. In addition, some
epidemiological studies have reported increased chromosomal abnormalities
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52
2. HEALTH EFFECTS
following exposure to radon and radon daughters. Depending upon the target
cells in which these chromosomal changes occurred, adverse effects on the
immune system could result. A battery of immunological tests administered to
members of a nonminer cohort, such as radon spa workers or people exposed to
high background levels, is needed to clarify whether immunological effects
occur following exposure to radon or radon progeny. Animal studies designed
to evaluate immune competence also are necessary to provide information on
subtle alterations in immune function. In addition, lymphocytes and lymphatic
tissues are sensitive to the radiation-induced damage caused by other alpha-
emitting radionuclides (ATSDR 1990b). Although lymphocytopenia observed in
dogs exposed to plutonium is not seen following exposure to radon and radon
daughters or uranium ore dust, other tests for immunocompetence have not been
conducted (ATSDR 1990a, 1990b).
Neurotoxicity. Cells and tissues in the nervous system may be less
radiosensitive, due to a lack of cell turnover or cellular regeneration, than
faster regenerating cells of the gastrointestinal tract or pulmonary
epithelium. Consequently, neuronal impairment as a result of radon alpha
emissions is not expected. Therefore, studies which specifically or directly
measure either pathological or functional damage to the nervous system
following exposure to radon do not appear to be necessary at this time.
Epidemiological and Human Dosimetry Studies. Epidemiological studies of
uranium and hardrock miner cohorts in the United States, Czechoslovakia, and
Canada have demonstrated an increase in lung cancer deaths. A similar
increase in lung cancer deaths also has been reported in epidemiological
studies of iron ore, zinc-lead, tin, phosphate, niobium, and fluorspar miners.
Many of the persons included in the various mining cohorts began work in
underground mines prior to 1969 when recommendations for the maximum radon
daughter levels were established in United States mines or prior to 1972 when
yearly exposure levels (4 WLM) for United States miners were proposed (MSHA
1989). (The WLM represents a cumulative exposure; see Section 2.1,
Introduction or Appendix B.) Since institution of these guidelines, radon
daughter levels in United States mines have decreased. For example, the
average radon and radon daughter levels in United States uranium mines were as
high as 10,000 pCi/L of air (3.7xl05 Bq/m3) in the early 1950s but dropped to
less than 100 pCi radon-222/L of air (3.7xl02 Bq/m3) by 1968 (Lundin et al.
1971). Among the Colorado uranium miner study group, only a relatively small
number of persons who have been exposed to low levels of radiation have had a
long follow-up (Archer 1980) . A continuation of the follow-up on this group
is needed to contribute to the evaluation of health hazards at levels at or
below the current exposure standard for radon daughters or at the levels
present in the environment. Continuation of the follow-up of epidemiological
studies of New Mexico uranium miners is also necessary because smoking is less
frequent in this group than in other groups studied. Continuation of studies
of underground miners exposed to radon daughters to cover the full lifetimes
of the cohort members would generate useful information. Additional
information on the smoking habits of these cohorts is required to provide some
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53
2. HEALTH EFFECTS
insights on the complex interaction between radon daughters and cigarette
smoking with regard to the induction of lung cancer. If exposure warrants,
new population studies could be initiated or additional information could be
gathered on previously defined populations.
The exact duration and level of exposure in human studies involving
underground miners are not adequately characterized. Generally, approximate
exposure is used based on environmental measurements of radon and radon
daughters in the mines and individual work histories. The relationship
between WLM and dose to the respiratory tract can differ in the occupational
and environmental settings primarily due to differences in type and quantity
of dust levels or ventilation rates. Additional evaluation of radon daughter
dosimetry in various settings is needed to provide a better basis for
estimating adverse health effects and correlating these effects with
environmental exposures.
As with some of the chronic animal studies, exposures in most of the
occupational miner cohorts consist of exposure to radon and radon progeny in
the presence of other contaminants such as uranium ore dust, diesel-engine
exhaust, or other mine pollutants. Only a few studies of lung cancer
associated with environmental exposures to radon and radon daughters have been
reported. These studies are primarily case-control or case-referent studies
that involve a small number of subjects and have exposure estimates that are
based on either surrogates for measurements or limited measurements.
Additional studies of the extent of the hazard associated with environmental
radon daughter exposures would provide useful information since radon is an
ubiquitous substance, especially as they compare to estimates of the human
health hazard based on the occupational setting.
Biomarkers of Exposure and Effect. Potential biomarkers of exposure may
include the presence of radon progeny in urine, blood, bone, teeth, or hair.
Although the detection of radon progeny in these media is not a direct
measurement of an exposure level, estimates may be derived from mathematical
models. Quantification of exposure to radon is further complicated by the
fact that radon is an ubiquitous substance and background levels of radon and
radon progeny are needed to quantify higher than "average" exposures. It has
been reported (Brandom et al. 1978; Pohl Ruling et al. 1976) that chromosome
aberrations in the peripheral blood lymphocytes may be a biological dose-
response indicator of radiation exposure. In addition, the frequency of
abnormalities in sputum cytology has been utilized as an early indicator of
radiation damage to lung tissue (Band et al. 1980). However, more extensive
research is needed in order to correlate these effects with radon exposure
levels and subsequent development of lung cancer or other adverse effects.
Absorption, Distribution, Metabolism, and Excretion. Some quantitative
information is available on the absorption, distribution, and excretion of
radon and radon daughters following inhalation and oral exposure, but
information following dermal exposure is inadequate. Additional information
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54
2. HEALTH EFFECTS
on the deposition patterns in airways for radon daughters and the relationship
of these deposition patterns to the onset of respiratory disease is needed to
enhance understanding of the disease process and delineate health protective
measures to reduce deposition. In particular, further study of the role of
ultra fine particles on lung doses is needed. More information on chronic
exposure to low levels of radon in air and water is also necessary since this
is the most common type of exposure for the majority of people who are exposed
environmentally. Although absorption of radon via the oraL route is known to
occur, dosimetry of the gastrointestinal tract wall and the radiosensitivity
of the wall is poorly understood. This information would be important in
assessing the impact of oral exposure. Information on the storage of radon
and radon daughters in fat tissue, especially following chronic exposure, is
necessary to determine whether steady-state conditions can be achieved and the
possibility of long-term bioaccumulation of radon daughters in body tissues.
No information is available on the rate or extent of bioaccumulation of the
long-lived radon daughter products such as lead-210 or polonium-210. This
information is needed so that past exposures to radon may be quantified.
Comparative Toxicokinetics. Very little information is known about the
comparative toxicokinetics of radon and radon daughters among animals and
humans. However, similar target organs have been identified in both humans
and laboratory animals exposed to radon and radon progeny. More information
on respiratory physiology, target cells, lung deposition, and absorption of
radon and radon daughters in different animal species is needed to clarify
observed differences in species-sensitivity and tumor types. For example,
rats generally develop lung tumors in the bronchioalveolar region of the lung
while humans develop lung tumors in higher regions (tracheobronchial area).
These studies could identify the appropriate animal model for further study of
radon-induced adverse effects, although differences in anatomy and physiology
of the respiratory system between animals and humans require careful
consideration. Most of the information available on the toxicokinetics of
radon and progeny has been obtained from studies of inhalation exposure.
Studies on the transport of radon and progeny following oral and dermal
exposures are needed to compare different routes of exposure.
2.8.3 On-going Studies
In recent years, concern over exposure to radon in both occupational and
residential settings has increased. Consequently, numerous institutions have
become involved in radon-related activities, partly to investigate the adverse
health effects of radon. The following discussion is intended to be a
representative sample of on-going research and is not an exhaustive list of
the work in this area.
Several epidemiological studies pertaining to radon in homes and lung
cancer incidence are underway. Comprehensive case-control studies of lung
cancer among nonsmoking women are under investigation by M. Alavanja (NCI) in
Missouri, Z. Hrubec (NCI) in Stockholm, Sweden, and New Jersey, J. Boice (NCI)
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55
2. HEALTH EFFECTS
in Shenyang, China, J.H. Stebbings (Argonne National Laboratory), and G.W.
Collman (National Institute of Environmental Health Sciences). All studies
involve residential exposure to radon. Epidemiological studies of New Mexico
uranium miners and tin miners are being conducted by J.M. Samet (University of
New Mexico School of Medicine) and J.H. Lubin (NCI), respectively. C. Eheman
(Centers for Disease Control) has been working with the National Park Service
in assessing past and current radon exposure of employees who work in caves
for the possibility of an epidemiology study of park service employees exposed
to radon at home and in caves.
F.T. Cross (Pacific Northwest Laboratories) is studying the exposure-rate
effect in radon daughter-induced carcinogenesis, and the role of oncogenes and
the involvement of growth factors and receptors in radon-induced
carcinogenesis. Similar studies on the influence of dose and dose-rate on
carcinogenesis and other biological effects are being conducted by M.
Terzaghi-Howe (Oak Ridge National Laboratories). F.T. Cross (Pacific
Northwest Laboratories) is also continuing a series of animal experiments, in
particular studies in rats with exposure to low cumulative doses of radon
(more than 20 WLM). R.S. Caswell (National Institute for Standards and
Technology) is developing a mechanistic model of the interaction of the alpha
particles of radon and its daughters with the cells at risk in the lung.
L.A. Braby (Pacific Northwest Laboratories) is studying the malignant
transformation of mammalian cells exposed to alpha particles that pass through
the cell nuclei in an attempt to elucidate the mechanisms of action of
radiation. The mechanisms of cell killing by alpha particles (M. Raju, Los
Alamos Laboratories), cell neoplastic transformation from alpha particles
(S.B. Curtis, Lawrence Berkeley Laboratory), and pulmonary tissue injury from
radon/radon daughter exposure (T.M. Seed, Argonne National Laboratory) are
also under investigation.
Radon-induced genotoxicity is another subject of interest under
investigation. D.J. Chen (Los Alamos National Laboratories) is investigating
the mechanistic basis for gene mutation induced by ionizing radiation in
normal human fibroblasts. J.E. Turner (Oak Ridge National Laboratories) is
examining the early physical and chemical changes produced by energetic alpha
particles to elucidate the mechanisms involved in DNA damage. F.T. Cross
(Pacific Northwest Laboratories) is studying the effects of exposure to radon
on DNA and DNA-repair processes. M.N. Cornforth (Los Alamos National
Laboratory) is attempting to provide quantitative data concerning both dose-
response and repairability of cytogenetic damage to human cells caused by
ultra low doses of ionizing radiation. The types and yields of damage
produced in mammalian-cell DNA by radon (J.F. Ward, University of California,
La Jolla); radon-induced mutation in mammalian cells, utilizing a recombinant
shuttle plasmid containing a target gene (S. Mitra, Oak Ridge National
Laboratories); and cytotoxic, mutagenic, and molecular lesions induced in
mammalian cells differing in DNA repair capabilities by low rates of radon and
radon daughters (H.H. Evans, Case Western Reserve University) are under
investigation. The direct effect of radon progeny and other high-LET alpha
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2. HEALTH EFFECTS
radiation on DNA damage in respiratory epithelial cells (D.G. Thomassen,
Lovelace Inhalation Toxicology Research Institute) and the biological
consequences of high-LET alphas from radon on chromosomal and episomal DNA in
human cells (J.E. Cleaver, University of California, San Francisco) are under
investigation. Alteration in the DNA content of critical cells in the
respiratory tract following exposure to radon and other aspects of radiation-
induced damage to DNA is the current topic of study by many other
investigators, such as N.F. Johnson (Lovelace Inhalation Toxicology Research
Institute) and J.L. Schwarz (University of Chicago Medical Center).
Interaction of radon and radon progeny with other pollutants is another
area of investigation. J.M. Daisey (University of California, Berkeley) and
Y-S. Cheng (Los Alamos National Laboratories) are independently studying the
complex interactions between radon and its progeny with other gaseous indoor
pollutants. Further, F.J. Burns (New York University Medical Center) also is
conducting experiments on rats to study lung cancer risk from inhalation of
radon alone or in combination with other pollutants commonly found in the home
environment. Interaction of radon and cigarette smoke in causing lung tumors
in rats is being studied by S.H. Moolgavkar (Fred Hutchinson Cancer Research
Center). The induction/promotion relationships associated with radon and
cigarette smoke mixtures also are being studied by F.T. Cross (Pacific
Northwest Laboratories).
Another factor that influences radon toxicity is the toxicokinetics of
radon and radon progeny. Target regions of the lung for inhaled radon and
radon progeny are being studied independently by R.R. Mercer (Duke University)
and R.G. Cuddihy (Lovelace Inhalation Toxicology Institute) to determine the
sensitivity of cell types located In the target regions. H-C. Yeh (Lovelace
Inhalation Toxicology Research Institute) is quantifying radon deposition in
the respiratory tract of humans, based on the mode of breathing, body size
and aerosol characteristics. B.S. Cohen (New York University Medical Center)
is also conducting a similar study on humans and laboratory animals. A
comparative morphometric study between dogs and humans is being conducted by
E.S. Robbins (New York University Medical Center). W. Castleman, Jr.
(Pennsylvania State University) is investigating the chemical and physical
processes associated with radon distribution and effects. This would aid in
assessing the mechanisms governing distribution, fate, and pathways of entry
into biological systems. More studies related to the above topics are in
progress by R.G. Cuddihy (Lovelace Inhalation Toxicology Research Institute)
D.R. Fisher (Pacific Northwest Laboratory), N.H. Harley (New York University'
Medical Center), and D.L. Swift (Johns Hopkins University).
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57
3. CHEMICAL AND PHYSICAL INFORMATION
3.1 CHEMICAL IDENTITY
The chemical formula and identification numbers for radon are listed in
Table 3-1.
3.2 PHYSICAL AND CHEMICAL PROPERTIES
Important physical and chemical properties of radon are listed in
Table 3-2. The radioactive properties of the important, short-lived daughters
of radon-222 are listed in Table 3-3. The radon-222 decay series is depicted
in Figure 3-1.
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58
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-1. Chemical Identity of Radon
Value
Reference
Chemical name
Isotopes
Trade name
Chemical formula
Chemical structure
Identification numbers:
CAS Registry
NIOSH RTECS
EPA Hazardous Waste
OHM/TADS
DOT/UN/NA/IMCO Shipping
HSDB
NCI
Radon
Radon-222 (Radon)
Radon-220 (Thoron)
Radon-219 (Actinon)
No data
Rn
Not applicable
14859-67-7 (radon-222)
22481-48-7 (radon-220)
14835-02-0 (radon-219)
No data
No data
No data
No data
No data
No data
Windholz 1983
Cothern 1987a
EPA 1989
CAS - Chemical Abstract Service; NIOSH - National Institute for Occupational
Safety and Health; EPA - Environmental Protection Agency; OHM/TADS - Oil and
Hazardous Materials/Technical Assistance Data System; DOT/UN/NA/IMCO -
Department of Transportation/United Nations/North America/International
Maritime Dangerous Goods Code; HSDB - Hazardous Substance Data Base; NCI -
National Cancer Institute
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59
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-2. Chemical and Physical Properties of Radon
Property
Value
Reference
Molecular weight
Color
Physical state
Melting point
Boiling point
Density at 20°C
Odor
Odor threshold
Solubility:
Water at 20°C
Organic solvents
Partition coefficients:
Log octanol/water
Log Koe
Vapor pressure at -71°C
Henry's Law constant
Autoignition temperature
Flash point
Flammability limits
Half-life
Radon-222
Radon-220
Radon-219
Decay modes and energy, MeV
Radon-222
Radon-220
Radon-219
222(radon), 220(thoron),
219(actinon)
Colorless
Gas
-71°C
- 61.8°C
9.96xl0~3
Odorless
No data
Cothern 1987a
gm/cm3
230 cm3/L
Organic liquid, slightly
soluble in alcohol
No data
No data
395.2 mmHg
No
No
No
No
data
data
data
data
3.823 days
55 seconds
4 seconds
«,
Y-
«,
a,
o,
a,
5.4897
0.512
6.29
6.42
6.55
6.82
Specific activity (Ci/gm)
Radon-222 3.6x10*
Radon-220 9.3x10s
Radon-219 1.3xl010
Cothern
Cothern
Cothern
Cothern
Cothern
Cothern
1987a
1987a
1987a
1987a
1987a
1987a
NCRP 1988
Weast 1980
Cothern 1987a
Cothern 1987a
Cothern 1987a
Cothern 1987a
US DHEW 1970
US DHEW 1970
US DHEW 1970
US DHEW 1970
US DHEW 1970
US DHEW 1970
-------
60
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-2 (Continued)
Property
Value
Reference
Decay products
Radon-222
Radon-220
Radon-219
Polonium-218
Lead-214
Bismuth-214
Polonium-214
Lead-210
Bismuth-210
Polonium-210
Lead-206
Polonium-216
Lead-212
Bismuth-212
Polonium-212
Thallium-208
Lead-208
Polonium-215
Lead-211
Bismuth-211
Thallium-207
Lead-207
Cothern 1987a
Cothern 1987a
Cothern 1987a
MeV - Million electron volts
-------
61
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-3. Radioactive Properties of Radon-222
and Its Short-lived Progeny"
Decay Specific
Historical Principal Energies Activity
Element Symbol Radiation(s) (MeV) Half-Life (Ci/gm)
Radon-222
Rn
a
5.5
3.82 days
3.6xl0A
Polonium-218b
RaA
a
6.0
3.05 min
2.8x10s
Lead-214
RaB
y >
&
1.0
26.8 min
3.3xl07
Bismuth-214
RaC
Y,
£
3.3
19.7 min
4.5xl07
Polonium-214b
RaC'
a
7.7
164 jisec
3.2X101*
"Source: BEIR IV 1988; US DHEW 1970.
bIsotopes of primary radiological interest due to the potential for retention
in the lung and subsequent alpha decay.
MeV = million electron volts
min = minutes
max — maximum
psec — microseconds
-------
Np
Ttx
fcn
Uraniua*23S Series
239
U
45E9
J™
234
-n>
24 d»y\
Pb
234
P«
1 2 mm
234
U
2.5E5
%V> .
230
Th
B.0E4
7M
226
fU
1600 m
FX j
J 62 dijvj
Thoriiui-232 Series
232
Th
1 4E10
vis
228
Th
1 91 yn
*
1
226 /
Ac
6 13 hn
1
229 '
' Ri
j<-sy»
i
Fj
3 64 d»ys
1
Uraniua-235 Series
235
U
7.1E9
yn
I
'5IT '
Th
2S5hi<
231
Pi
3 2E4
1
zFT' *
Ac
21 6 y:i
227
Tli
19 2 day-
1
223
Fi
! 4 d»v \
i |
! ? C5 rr.i:.!
i 1?? dif:
/
l ; & 1
:S">m.r
l#—
:u
rt
26 S mm
23?
n
:ir>
j-
20S
Pb
«ub!e
¦-A-
i " 1
3 1 mm
j I
1 "
-.»r;p
/
I Tl
I4 79 run
J i!ph»dfc»y /* fcfuiifciy
FIGURE 3-1. Uranium and Thorium Isotope Decay Series Showing the Sources
and Decay Products of the Three Naturally-Occurring Isotopes of Uranium
d
pr
K
s
~-—i
n
>
lr.
^:
Adapted from Atta er ad w
-------
63
4. PRODUCTION, IMPORT, USE, AND DISPOSAL
4.1 PRODUCTION
Ration is a naturally occurring radionuclide. The largest source of radon
in the environment is due to the ambient levels produced by the widespread
distribution of uranium and its decay products in the soil. Radon is a decay
product of radium and part of the uranium decay chain (see Figure 3-1). Every
square mile of surface soil, to a depth of 6 inches, contains approximately 1
gram of radium, which releases radon in small amounts to the atmosphere (Weast
1980). The ambient outdoor radon level goes through a daily cycle of
concentrations ranging from 0.03 to 3.50 pCi radon-222/L (1.11 to 130 Bq/m3)
of air with the average level in the United States being about 0.3 pCi radon-
222/L (11.1 Bq/m3) of outdoor air (Martin and Mills 1973).
The amount of naturally occurring radon released to the atmosphere is
increased in areas with uranium and thorium ore deposits and granite
formations, which have a high concentration of natural uranium. It is the
presence of granite formations that has greatly increased radon concentrations
in eastern Pennsylvania and parts of New York and New Jersey. Sources of
radon in the global atmosphere include natural emanation from radium in soil
and water, uranium tailings, phosphate residues, coal, and building materials
(NCRP 1984a). In a few locations, tailings have been used for landfills and
were subsequently built on, resulting in possible increased exposure to radon
(Eichholz 1987). There is also an increased radon concentration in spring
water due to the deposition of radium isotopes in the sinter areas about hot
springs, where it is coprecipitated with calcium carbonate or silica (NCRP
1975).
Radon has been produced commercially for use in radiation therapy but for
the most part has been replaced by radionuclides made in accelerators and
nuclear reactors. Radiopharmaceutical companies and a few hospitals pump the
radon from a radium source into tubes called "seeds" or "needles" which may be
implanted in patients (Cohen 1979). Research laboratories and universities
produce radon for experimental studies.
4.2 IMPORT
Radon is not imported into the United States.
4.3 USE
Medical uses of radon in the United States began as early as 1914.
Treatments were primarily for malignant tumors. The radon was encapsulated in
gold seeds and then implanted into the site of malignancy. During the period
of 1930 to 1950, radon seeds were used for dermatological disorders, including
acne.
-------
64
4. PRODUCTION, IMPORT, USE, AND DISPOSAL
Radon therapy is still being studied and applied (Morken 1980). In many
places in the world, water or air containing naturally high levels of radon-
222 is used for therapeutic treatment of various diseases (Pohl-Rilling et al
1982). These diseases include obliterative. arteritis and atherosclerosis of
lower extremities. In a few places, "radon mines" (caves with a high radon
concentration in the air) are used as a health treatment. By law, these
facilities cannot advertise; therefore, the number of people involved is quite
small (Cohen 1979). A few of these caves are located in old Montana mines.
Thousands of people seek medical cures through exposure to radon gas for
ailments ranging from arthritis, asthma, and allergies to diabetes, ulcers,
and cancer (Dobbin 1987). Radon "spas" are used in Europe for the treatment
of hypertension and a number of other disorders. In the U.S.S.R., about
25,000 radon baths are prescribed daily by the National Health System, and in
Badgastein, Austria, every year 1 million radon thermal baths are taken
(Usunov et al. 1981).
The prediction of earthquakes is fairly new technology that uses radon
(Cothern 1987b). The emanation of radon from soil and the concentration
measured in groundwater appear to be good indicators of crustal activity.
Other uses of radon include the study of atmospheric transport, and the
exploration for petroleum or uranium (Cothern 1987b).
4.4 DISPOSAL
Disposal of radon would only be applicable to those facilities producing
and/or using it for medical or experimental purposes where its release may be
controlled. Regulations regarding the land disposal of radionuclides are set
forth in 10 CFR 61 (NRC 1988); however, there appear to be no regulations
specific to radon. See Chapter 7 for a listing of regulations concerning
radon. Radioactive effluents from facilities operating under a Nuclear
Regulatory Commission (NRC) license are regulated by 10 CFR 20 (NRC 1988).
The NRC effluent regulations and also disposal regulations regarding uranium
tailings are listed in Table 7-1. Since radon is relatively short lived, it
may be compressed and stored in tanks until it decays or, if the quantity is
small, it may be adsorbed on activated charcoal (Cember 1983). Particulate
matter may be removed from the gas by a variety of different devices including
detention chambers, adsorbent beds, and liquefaction columns. After
filtration, the remaining radioactive particulates are. discharged into the
atmosphere for dispersion of the nonfilterable low levels of activity (Cember
1983) .
Low-level radioactive waste produced as a result of using radon medically
or experimentally include paper towels, protective clothing, rags, animal
excreta, and animal carcasses. This waste is often accumulated in containers
Combustible waste is incinerated and the activity is concentrated by burning
away the substrate in which activity is held. The ashes are then either
dispersed to the atmosphere or packaged for disposal into the sea or into the
ground.
-------
65
5. POTENTIAL FOR HUMAN EXPOSURE
5.1 OVERVIEW
Radon is a product of the natural radioactive decay of uranium, which
occurs naturally in the earth's crust, to radium and then to radon. As radium
decays, radon is formed and is released into small air or water-containing
pores between soil and rock particles. If this occurs near the soil surface,
the radon may be released to ambient air. Radon may also be released into
groundwater. If this groundwater reaches the surface, most of the radon gas
will quickly be released to ambient air, but small amounts may remain in the
water. By far, the major source of radon is its formation in and release from
soil and groundwater, with soil contributing the greater amount. Smaller
amounts of radon are released from the near surface water of oceans, tailings
from mines (particularly uranium and phosphate mines), coal residues and
combustion products, natural gas, and building products, such as concrete and
brick.
The ultimate fate of radon is transformation through radioactive decay.
Radon decays only by normal radioactive processes, that is, an atom of radon
emits an alpha particle resulting in an atom of polonium, which itself
undergoes radioactive decay to other radon progeny. There are no sinks for
radon; therefore, small amounts of radon are lost to the stratosphere.
In soil, radon is transported primarily by alpha recoil and mechanical
flow of air and water in the soil. Alpha recoil is the process by which
radon, when it is formed by radium emitting an alpha particle, actually
recoils in the opposite direction from the path of particle ejection. After
radon is released into the pore spaces, its ultimate release to ambient air is
a function of the soil porosity and meteorological factors, such as
precipitation and atmospheric pressure. Once radon is released to ambient
air, its dispersion is primarily determined by atmospheric stability,
including vertical temperature gradients and effects of wind.
Transport of radon in indoor air is almost entirely controlled by the
ventilation rate in the enclosure. Generally, the indoor radon concentrations
increase as ventilation rates decrease.
In groundwater, radon moves by diffusion and, primarily, by the
mechanical flow of the water. Radon solubility in water is relatively low
and, with its short radioactive half-life of 3.8 days, much of it will decay
before it can be released from groundwater.
Radon levels in ambient air vary with the type of soil and underlying
bedrock of the area. Available measurements indicate that the mean value for
atmospheric radon in the contiguous United States is approximately 0.25 pCi
radon-222/L of air (9 Bq/m3). However, measurements of air from the Colorado
Plateau show radon levels up to 0.75 pCi radon-222/L of air (30 Bq/m3).
Studies of indoor radon levels indicate an average concentration of from 1.5
-------
66
5. POTENTIAL FOR HUMAN EXPOSURE
to 4.2 pCi radon-222/L of air (55 to 157 fiq/m3) (Alter and Oswald 1987; Nero
et al 1986) .
Groundwater supplies in the United States have been surveyed for radon
levels. In larger aquifers, average radon concentrations were reported to be
240 nCi (8.8 Bq) radon-222/L of water, while in smaller aquifers and wells
average levels were considerably higher (780 pCl radon-222/L of water; 28.9
Bc/L) (Cothern et al. 1986). These differences in radon levels between large
and small groundwater supplies are a reflection of the type of rock which
surrounds them.
Measurements of radon in soil are expressed in terms of levels in soil-
gas However, these measurements do not directly relate to rates of radon
released to the atmosphere. Factors which affect radon soil-gas levels
include radium content, soil porosity, moisture content, and density.
Technically, measurement of soil-gas is difficult and there are few studies
which report such data.
Delivered dose of radon and its progeny can only be estimated by complex
mathematical models. Therefore, exposure, both occupational and
environmental, will be discussed, primarily in terms o£ radon levels in the
air. However, some estimates of daily intake have been made. Daily intake of
radon originating outdoors is estimated to be 970 pCi (36 Bq) radon-222/day
(Cothern et al 1986). Exposure from indoor radon is higher due to
concentration of levels from lack of ventilation and other factors. Total
daily intake of radon originating indoors is estimated as 8,100 pCi (300 Bq)
radon-222/day, assuming a breathing rate of 20 m3/day. However, daily intake
is dependent on time spent in and outdoors and on breathing rate (Cothern et
al. 1986).
Radon releases to the environment (primarily indoor levels) from
groundwater also contribute to environmental exposures. The daily intake of
radon originating from drinking water only is estimated at 100 to 600 pCi (3.7
to 22 2 Bq) radon-222/day both from ingestion of drinking water and inhalation
of radon released from drinking water (Cothern et al. 1986). Radon releases
from building materials contribute little to potential exposure.
Occupational exposure to radon results from employment in uranium and
other hard rock mining, or in phosphate mining. Persons engaged in uranium
mining are believed to receive the largest exposures, although the number of
arsons employed in uranium mining has steadily decreased in the past 9 years.
Measurements of radon progeny in these mines from 1976 to 1985 showed annual
mean concentrations of 0.11 to 0.36 WL (22 to 72 pCi radon-222/L of air; 800
9 f.(,L Rn/m3! (NIOSH 1987). However, levels in phosphate mines measured
.V' the same period showed a larger range of mean levels (0.12 to 1.20 UL;
M « 2M pCi r^oL222/L of air; 888 to 8.880 *,/„=>. Radon exposure in
underground mines is continually being reduced due to improved engineering
controls (NIOSH 1987).
-------
67
5. POTENTIAL FOR HUMAN EXPOSURE
5.2 RELEASES TO THE ENVIRONMENT
5.2.1 Air
Because of the extended half-lives of uranium and radium and their
abundance in the earth's surface, radon is continually being formed in soil
and released to air. This normal emanation of radon from radium-226 in soils
is the largest single source of radon in the global atmosphere (NCRP 1984a).
Using average emanation rates from available measurements, Harley (1973)
estimated soil emanation of radon to be on the order of 2xl09 Ci (7.4xl019 Bq)
radon-222/year. This estimation is equivalent to 1,600 pCi (60 Bq/cmz)
radon/cm2 soil/year (Harley 1973). The emanation rate at a particular
location is highly variable and is affected by many factors, including
barometric pressure, composition of soil, and soil moisture and temperature.
Usually, less than 10% of radon in upper soil layers is released to the
atmosphere (Vilenskiy 1969). Some radon is released by plants through
evapotranspiration. However, the amount released has not been estimated
(Taskayev et al. 1986).
Groundwater that is in contact with radium-containing rock and soil will
be a receptor of radon emanating from the surroundings. When the groundwater
reaches the surface by natural or man-made forces, this radon will be released
to air. Although most of the radon present in groundwater will decay before
reaching the surface, groundwater is still considered to be the second largest
source of environmental radon and is estimated to contribute 5x10® Ci
(1.85xl019 Bq) radon-222/year to the global atmosphere (NCRP 1984a). Radon is
also released from oceans, but only from the near surface water, and in
amounts that are an order of magnitude less than that from groundwater.
Radium in oceans is largely restricted to the sediments where it cannot affect
atmospheric levels of radon (Harley 1973).
Tailings from uranium mines and residues from phosphate mines both
contribute to global radon in the approximate amount of 2 to 3xl06 Ci
(7.4xl016 to l.llxlO17 Bq) radon-222/year. Although these sites are not
numerous (in 1984 there were 50 sites containing uranium tailings), emanation
rates to air may be substantial. It is estimated that 20% of the radon formed
in tailings is released and that emanation rates can be as high as 1,000 pCi
(37 Bq) radon/m2/second (NCRP 1984a).
Coal residues and combustion products, as well as natural gas, each
contribute to atmospheric radon levels to a minor extent (NCRP 1984a). Coal
and natural gas, at the time of combustion, release radon to air. Coal
residues, such as fly ash, contribute very small amounts to atmospheric radon.
Some building materials release very small amounts of radon. However,
the major source of radon in single family dwellings is the soil directly
under the building (NCRP 1984b).
-------
68
5. POTENTIAL FOR HUMAN EXPOSURE
According to the VIEW database, 14 NPL sites reportedly contain radon
above background levels (VIEW 1989). The frequency of these sites within the
United States can be seen in Figure 5-1. Quantification of the levels found
is not available. However, the majority of the radon released would be to
air.
5.2.2 Water
The amount of radon released to groundwater is a function of the chemical
concentration of radium-226 in the surrounding soil or rock and in the water
itself. High radon activity is associated with groundwater surrounded by
granitic rock. The physical characteristics of the rock matrix are important
also since it is believed that much of the radon released diffuses along
microcrystalline imperfections in the rock matrix (Hess et al. 1985). Radon
is rarely found in surface water due to the fact that it is rapidly released
to the air when the water reaches surface levels (Michel 1987).
In a reanalysis of published data, Hess et al. (198b> reported a
geometric population average of 187 pCi (6.9 Bq) radon-222/L of water in over
6,000 samples of groundwater supplies for public use. In contrast, samples of
surface water supplies indicated that the average level of radon was 1 pCi
(0.037 Bq) radon-222/L of water.
5.2.3 Soil
As stated in Section 5.2.1, soil is the primary source of" radon. As
such, radon is not released to soil but is the result of radioactive decay of
radium-226 within the soil. The radon concentration in the soil is a function
of the radium concentration, the soil moisture content, the soil particle
size, and the rate of exchange of air with the atmosphere (Hopke 1987). Hopke
(1987) states that normal soil-gas radon measurements are in the range of 270
to 675 pCi radon-222/L of air (10,000 to 25,000 Bq/m3) . However, levels
exceeding 10,000 pCi radon-222/L of air (370,000 Bq/m3) have been documented
5.3 ENVIRONMENTAL FATE
5.3.1 Transport and Partitioning
Emanation is the process by which radon is transported from a solid to a
gas or liquid medium. At the soil particle level, radon gas is transferred
from soil particles into pore spaces (gas- or 1iquid-filled spaces between
soil particles) primarily by alpha recoil. Alpha recoil occurs after radium
decays by emitting an alpha particle. After the particle is ejected, the
resulting radon atom actually recoils in the opposite direction. Alpha recoil
results in breaking of chemical bonds in the solid, physically moving the atom
to a different position, and damaging the crystal structure. The radon atom
may recoil to a position from which it will not be released (embedded in the
same particle or in another particle) or may recoil into the pore space from
-------
-RtQUENCY 11 I II I I 1 SITE BHfflffifflffl 3 SITES ¦¦¦ 6 SITES
FIGURE 5-1. FREQUENCY OF SITES WITH RADON CONTAMINATION
-------
70
5. POTENTIAL FOR HUMAN EXPOSURE
which it may move by diffusion or convection toward the soil surface. If the
pore space is filled with liquid, any radon atoms which recoi L into it will
travel slower than those that recoil into air-filled spaces (Michel 1987).
Although alpha recoil is believed to be the major process of radon release
from solids, diffusion from very small pores near the particle surfaces and
along imperfections of the crystalline structure of the particle also occurs.
Once radon enters the pore space, it is transported by diffusion,
convection, and flow of rain and groundwater. The diffusion constant for
radon is approximately 10~2 cm2 per second in air and 10 5 cm2 per second in
water (WHO 1983). These constants indicate that diffusion of radon is a
relatively slow process and that its movement is, therefore, primarily
accomplished by mechanical transport of air and water in the pore space.
The actual release of radon from the pore space or soil-gas to ambient
air is called exhalation. The rate of this process is a function of many
variables including the concentration of radon in the soil-gas, the soil
porosity, and meteorological factors such as precipitation and variations in
atmospheric pressure (WHO 1983).
Behavior of radon at the interface between soil and ambient air is not
well understood. However, once radon reaches a height of approximately 1
meter above the soil surface, its dispersion is predominantly determined by
atmospheric stability (Cohen 1979). This stability is a function of vertical
temperature gradient, direction and force of the wind, and turbulence.
Temperature inversions in the early morning act to produce a stable atmosphere
which keeps radon concentrations near the ground. Solar radiation breaks up
the inversion, leading to upward dispersion of radon which reverses with
radiant cooling in late afternoon (Gesell 1983). In addition, general trends
in air turbulence lead to maximum levels in air in the early autumn and early
winter (when turbulence is generally less) and lower levels in air in the
spring due to increased turbulence (Michel 1987). In the absence of these
factors, radon levels in air decrease exponentially with altitude (Cohen
1979). This phenomenon has been studied by sampling and many models have been
derived to fit the data (WHO 1983).
Sources of indoor radon include entry of amounts released beneath the
structure, entry in utilities such as water and natural gas, and release from
building materials. The greatest contribution is that from radon released
from soil or rock (Nero 1987). Entry occurs primarily by bulk flow of soil-
gas driven by small pressure differences between the lower part of the house
interior and the outdoors. The pressure differences are primarily due to
differences in indoor/outdoor temperature and the effects of wind (Nero 1987)
Transport of radon in indoor air is primarily a function of the
ventilation rate of the enclosure. Under most conditions, the indoor radon
concentration increases in direct proportion to the decrease in ventilation
rates (WHO 1983). However, in some indoor radon studies, radon concentrations
showed greater variability than could be accounted for by ventilation rates.
-------
71
5. POTENTIAL FOR HUMAN EXPOSURE
This was said to suggest that the strength of the radon source was the main
cause of the wide range in observed indoor radon levels (Nero 1987). Behavior
of radon in enclosed areas has also been extensively studied and predicted by
modeling (Eichholz 1987; Jonassen 1975).
Transport of radon daughters indoors has also been extensively modeled.
Transport is primarily a function of the rate of attachment of radon daughters
to particles, the concentration and size of the particles, and the rate of
deposition. A major complication of modeling both radon and radon daughter
transport indoors is that the ventilation rate acts both to increase flow of
radon into the structure and to remove radon and radon daughters from the
structure (Nero 1987) . Ventilation rate also acts on the movement of air
indoors causing variations in radon concentrations from room to room, as well
as within a room.
Mechanisms for transport of radon in groundwater are much less complex
than those for other media. In fact, transport of radon in groundwater is
accomplished by diffusion and, primarily, by the mechanical flow of
groundwater. As previously stated, the diffusion coefficient of radon in
water is sufficiently low so that diffusion is only important for movement in
very small spaces (such as pore spaces). The solubility of radon in water is
relatively low (230 cm3 radon-222/L of water at 20°C) and, due to radon's
relatively short half-life, much of it will have decayed before the
groundwater reaches the surface. However, that remaining in solution will be
quickly released to ambient air once it is encountered. In areas where
groundwater has high levels of radon, release from groundwater may
significantly affect ambient air levels.
5.3.2 Transformation and Degradation
5.3.2.1 Air
Regardless of the surrounding media, radon is transformed or degrades
only by radioactive decay. There are no sinks for radon, and it is estimated
that only negligible amounts escape to the stratosphere (Harley 1973).
Therefore, degradation proceeds by alpha-emission to form polonium-218. As
stated in Table 3-2, the half-life of radon is 3.82 days. The half-lives of
the progeny are much shorter, ranging from approximately 0.0002 seconds for
polonium-214 to 30 minutes for lead-214.
5.3.2.2 Water
See Section 5.3.2.1.
5.3.2.3 Soli
See Section 5.3.2.1.
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72
5. POTENTIAL FOR HUMAN KXI'OSIJKK
5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT
5.4.1 Air
The most comprehensive compilation ot data on radon levels in outdoor air
was reported by Gesell (1983). Measurements were taken over the continental
United States, Hawaii, and Alaska. The highest concentrations were found in
the Colorado Plateau, which is a region containing high levels of uranium as
well as mines and uranium tailings. Measurements in this region ranged from
0 5 to 0.75 pCi radon-222/L of air (18.5 to 30 Bq/m3). Average values from
the continental United States ranged from 0.12 to O.i pCi radon-222/L of air
(4 4 to 11 Bq/m3) Based on these and other data, Michel (108 7) states that
the mean value for atmospheric radon in normal geological areas of the
contiguous United States is approximately 0.2b pCi radon-2,2/L of air (9
Bq/m3) with a range of 0. 1 to 0.4 pCi radonA <>' -"r ('« to J 5 Bq/m ).
Data reported by Fisenne (1987) indicate variability of radon levels with
time In continuous data (9 years of hourly nu.-asum.u-ni.s) , both diurnal and
seasonal patterns were observed. Diurnal variations showed an early morning
peak and a drop in the afternoon. Seasonally, levels were highest in early
autumn and lowest in early spring.
Radon concentrations in air decrease with height from the soil surface.
Several investigators have measured radon levels in the troposphere. Machta
and Lucas (1962) measured 0.007 pCi radon-222/L of air Bq/m ) at 25,000
feet. Comparable measurements have been taken over Alaska and the
southwestern United States (Harley 1973).
Although there are many studies which undertake to quantity radon in
indoor air the work of Nero et al. (1986) is the most comprehensive and the
most often'cited This study reanalyzed up to 38 small data sets, of which 22
were considered unbiased. Biased data were those collected from areas where
hieh radon concentrations were expected. On the basis of the unbiased data,
the geometric mean of indoor radon levels was reported to be approximately 0.9
nri radon-222/L of air (33 Bq/m3). These data implied an arithmetic average
concentration of 1.5 pCi radon-222/L of air (56 Bq/m3). Distribution studies
of household levels indicated that from 1% to 3X of single - family houses may
exceed 8 pCi radon-222/L of air (296 Bq/m3). In th is study many of Che
measurements were made in main-floor living rooms or average living areas
(Nero et al. 1986).
Indoor radon levels were measured in homes located in the Reading Prong
of Pennsylvania This area has an unusual abundance of homes with high
radon concentrations that is presumed to be from geologically produced
Hnn of radon Indoor levels of radon in this area ranged from 4 to 20
fiCi/L (150 to 740 Bq/m3) in 291 of the homes to >80 pCi/L (3,000 Bq/m3) in IX
of\he homes (Fleischer 1986).
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73
5. POTENTIAL FOR HUMAN EXPOSURE
Other studies of indoor radon levels were summarized in NCRP (1987). The
median levels ranged up to 18.9 pCi radon-222/L of air (700 Bq/m3) in homes in
Butte, Montana (Israeli 1985). A study by Cohen (1986) reported results from
453 indoor sites in 42 states and showed a mean of 1.62 pCi radon-222/L of air
(60 Bq/m3) with a median of 1.08 pCi radon-222/L of air (40 Bq/m3).
5.4.2 Water
In a nationwide survey by the EPA, almost 2,500 public drinking water
supplies were sampled (nonrandom) with most of these serving greater than
1,000 people. Results of this survey were used to estimate the mean
population-weighted radon levels in public groundwater systems by state
(Cothern et al. 1986). Average concentrations for United States groundwater
were estimated to be 240 pCi radon-222/L of water (8.8 Bq/L) for larger
systems (>1,000 persons served), and for smaller systems 780 pCi radon-222/L
of water (28.9 Bq/L). The nationwide average for all groundwater samples
tested was 351 pCi radon-222/L of water (13 Bq/L). When surface water
supplies were taken into consideration, due to the fact that their radon
levels are essentially zero, the average radon concentration in all community
water supplies was estimated to range from 54 to 270 pCi radon-222/L of water
(2 to 10 Bq/L) (Michel 1987). The highest levels reported were in smaller
groundwater systems in Maine which averaged 10,000 pCi radon-222/L of water
(370 Bq/L); lowest average levels were found in larger systems in Tennessee
with levels of 24 pCi radon-222/L (8.9 Bq/L).
This same relationship, i.e., radon concentrations in groundwater
increasing with decreasing system size, was previously reported by Hess et al.
(1985). This correlation is believed to reflect a relationship between system
size and aquifer composition. Those rock types that are associated with high
radon levels (granitic rock) do not form aquifers large enough to support
large systems. However, smaller systems may tap into such aquifers.
Crystalline aquifers of igneous and metamorphic rocks generally have
higher radon levels than other aquifer types with granites consistently
showing the highest levels. Average radon levels in water from granite
aquifers are usually 2,703 pCi radon-222/L of water (100 Bq/L) or greater
(Michel 1987). This is indicated in the data of Cothern et al. (1986) which
report the following trends in groundwater radon levels: in New England and
the Piedmont and Appalachian Mountain Provinces, where igneous and metamorphic
rocks form the aquifers, concentrations are in the range of 1,000 to 10,000
pCi radon-222/L of water (37 to 370 Bq/L); in the sandstone and sand aquifers
which extend from the Appalachian Mountains west to the Plains, concentrations
are generally less than 1,000 pCi radon-222/L of water (37 Bq/L).
5.4.3 Soil
Because radon is a gas, its occurrence in soil is most appropriately
referred to as its occurrence in "soil-gas," which is in the gas or water-
filled space between individual particles of soil. Factors that affect radon
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74
5. POTENTIAL FOR HUMAN KXPOSURK
soil-gas levels include radium concent and distribution, soil porosity,
moisture, and density. However, soil as a source of radon is seldom
characterized by radon levels in soil-gas, but is usually characterized
directly by emanation measurements or indirectly by measurements of members of
the uranium-238 series (National Research Council 1981). Radon content is not
a direct function of the radium concentration of the soil, but radium
concentration is an important indicator of the potential for radon production
in soils and bedrock. However, Michel (1987) states that average radium
content cannot be used to estimate radon soil-gas levels, primarily due to
differences in soil porosity.
Despite such caveats, theoretical rates of radon formation in soil have
been estimated as demonstrated by the following:
"Consider a cube which is 1 meter in each dimension. Using rounded
numbers, if the average density of the soil is 2.0 grams per cubic-
centimeter and the average radium-226 concentration is 1.0 pCi/g
(0.037 Bq/g), the cube will contain 2 million grams of soil and
2xl0"6 Ci (7.4x10* Bq) of radium-226. This corresponds to the
production of 7.4x10'' radon atoms per cubic-meter per second and the
escape of 7,400 atoms per square meter per second, in rough
correspondence to the average measured value." (Nevissi and Bodansky
1987).
For a discussion of uranium-238 and radium-226 levels in soil, see the
ATSDR Toxicological Profiles for Uranium and Radium (ATSDR 1990a, 1990d).
Only two soil-gas measurements for United States locations were found in
the literature: one from Spokane, Washington, with soil-gas radon from 189 to
1,000 pCi radon-222/L of air (7,000 to 37,000 Bq/m3) in soils formed from
coarse glacial outwash deposits with 2.3 ppm uranium, and the other from
Reading Prong, New Jersey, with soil-gas radon levels from 1,081 to 27,027 pCi
radon-222/L of air (40,000 to 1,000,000 Bq/m3) (Michel 1987). Hopke (1987)
states that normal soil-gas radon measurements are in the range of 270 to 675
pCi radon-222/L of air (10,000 to 25,000 Bq/m3). It is reported that radon-
222 levels increase with soil depth, reaching a probable maximum at about 800
cm below ground level (Jaki and Hess 1958).
5.4.4 Other Media
Limited information exists to indicate that plants absorb both radium-226
and radon-222 from the soil layer and that these compounds are translocated to
above ground plant parts (Taskayev et al. 1986). However, there is little
information on the quantitative contribution of this process to exposure from
ingestion of plant crops or of emanation rates from these plants. One
measurement of emanation rates from field corn was located in the literature
Radon-222 release from leaves was reported to be 2.47x10 pCi (9.15x10 6 Bq)/
cm2/sec. This emanation rate was 1.8 times greater Lhan the emanation rate
from local soil (Pearson 1967).
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75
5. POTENTIAL FOR HUMAN EXPOSURE
5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE
In the following section, exposure to radon is discussed in terms of
environmental levels not in terms of actual or estimated dose. The estimation
of whole body or target tissue dose of radionuclides is extremely complex and
must be accomplished by mathematical models for the specific radionuclide.
Although such models are available to estimate whole body and target tissue
dose for radon, discussion of these lies outside the scope of this document.
For a discussion of these models the reader is referred to NCRP (1984a) or
BEIR IV (1988) .
The general population is exposed to radon by inhalation both outdoors
and indoors. Outdoor levels, also referred to as ambient or background
levels, are the result of radon emanating from soil. These levels vary widely
with geographical location, depending on factors such as the radium content of
soil and soil porosity and moisture content. However, a reasonable average
for near ground level is suggested by Eichholz (1987) to be on the order of
0.150 pCi radon-222/L of air (5.55 Bq/m3) . Michel (1987) states that the mean
value for atmospheric radon in the contiguous United States is approximately
0.24 pCi radon-222/L of air (8.88 Bq/m3) with a range of 0.11 to 0.41 pCi
radon-222/L of air (4.07 to 15.2 Bq/m3). Cothern et al. (1986) report a daily
intake of radon originating outdoors of approximately 1,000 pCi (36 Bq) radon-
222/day based on data derived from the United Nations Scientific Committee on
the Effects of Atomic Radiation (1982) and assuming an inhalation rate of 20
m3/day of air containing 0.05 pCi/L (1.8 Bq/m3) radon-222. Because of the
gaseous nature of radon, radon levels will decrease with increasing height
from the soil surface. Studies of this vertical gradient indicate that a
child who is 0.5 m tall would be exposed to 16% more radon than an adult who
is 1.5 m tall (Michel 1987).
In contrast to the average ambient levels of radon, which are usually
quite low, levels indoors are found to be greater than ambient outdoor levels.
This is due to enhancement and it is believed to be a function of the
following: movement of radon from underlying soil and rock through the
foundation of the building, release of radon from water and utility use, radon
emanation from radium-containing structural materials, and rate of ventilation
(NCRP 1984b) . The contribution of each of these to the overall indoor radon
level is difficult to assess, except qualitatively. It has been determined
that elevated indoor radon levels are primarily due to radon emanation from
underlying soil (Eichholz 1987). The actual indoor levels are greatly
affected by other parameters such as composition of the foundation materials
and the ventilation rate of the enclosed area. Two of the largest indoor
monitoring efforts in the United States reported arithmetic mean levels
ranging from 1.5 to 4.2 pCi radon-222/L of air (55 to 157 Bq/m3) (Alter and
Oswald 1987; Nero et al. 1986). The data from Alter and Oswald (1987) are
limited in that the dwellings do not represent a random sample and individual
measurement values were reported rather than average concentrations from a
residence. Cothern et al. (1986) report daily intake of radon originating
indoors of 8,100 pCi (300 Bq) radon-222/day based on data derived from the
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76
5. POTENTIAL FOR HUMAN KXl'OSURK
.c. „ -w-*¦<¦>*> nn the Ft feets of Atomic Radiation (1982)
cars rvs.
, fiTMZ
release of ra performed an analysis which combined information on
Nazarof f et (1987;) *e rto^ ^ hQusp voluncSi and
water use, fo determine the impact on indoor radon levels. Their
w"lino0f0radon0lnCgro'n pd <<..3 to 12.6,10- Hi,) radon-
be in the range or v.t to y
222/kg/second (Michel 1987).
Persons who are occupational^ exposed to radon are those employed in
• („r „rT»arUv" ining of uranium and hard rock (NIOSH 1187). NIOSH reports
mining, p „01.kers „ere employed in metal and no,.metal mines in the
,V ¦: A ct.r.i However the number of underground uranium mines has steadily
United States 16 ln 1984. ln tur„. the number of employees t„
decreased from JW ln decreased from 9,000 in 1979 (3,400 of whom
underground L 448in 1986 (N10SH 1987).
worked un er&toyx ' progeny concentrations in these mines iron. 1976 to 1985
MrSTZual geomftric mfan'concentrations in uranium mines of 0.11 to 0.36
showed annual g.o»etr^ ^ radon.222/L of air (800 to 2,664 Bq/nr>]
WLS^ineVan equilibrium factor of 0.5), with 95th percentile levels ranging up
r}? UL <^6 pCi radon-222/L of air; 20,202. Bq/nr') . Annual geometric mean
to 2.73 VJL (546 poi same od were () 1? to ! 20 UL (24 to 240
levels m p osp a ^ ^ g g8() Bq/m3]} with 9bth percentile levels as
pCi radon-222/ radon-222/L of air; 12,506 Bq/m3). Measurements in
uranium/vanadium mines showed annual geometric mean concentrations similar to
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77
5. POTENTIAL FOR HUMAN EXPOSURE
those in uranium mines. However, 95th percentile levels ranged up to 4.80 WL
(960 pCi radon-222/L of air [3.6x10'' Bq/m3]), which was the highest annual
concentration reported among the different types of mines (NIOSH 1987).
Estimates of annual cumulative radon progeny exposures indicated that of the
1,405 underground uranium miners working in 1984, 28% had exposures greater
than 1.0 WL (200 pCi radon-222/L of air; 7,400 Bq/m3).
Radon exposure in underground mines has been vastly reduced by
installation of improved engineering controls. In New Mexico mines the median
annual exposure in 1967 of 5.4 WLM was reduced to 0.5 WLM by 1980 due to this
technique (Eichholz 1987).
Several researchers have attempted to correlate levels of lead-210 in
bone with cumulative radon daughter exposure. Eisenbud et al. (1969) employed
in vivo techniques to measure lead-210 in the skull of nonoccupationally
exposed and occupationally exposed individuals. Exposure for miners was
derived from mine records and compared to that estimated from a model. Their
results showed that the amount of lead-210 deposited, regardless of temporal
considerations, will be within a factor of two of that deposited if exposure
is assumed to be uniform over time. In addition, they reported that a burden
of 2,000 pCi (74 Bq) is equivalent to a calculated cumulative exposure of
approximately 800 WLM.
Blanchard et al. (1969) reported a positive correlation between the log
of lead-210 concentration in post-mortem derived bone and the log of estimated
miners' cumulative exposure. However, more lead-210 was observed in bone than
was predicted by the model utilized. Furthermore, a linear correlation was
observed between lead-210 levels in blood and that in bone; however, for both
of these analyses sample numbers were small (n=ll to 22). Another study
(Clemente et al. 1984) has analyzed the correlation between lead-210 in human
teeth and environmental radon levels in various countries. This analysis
reported that for the incremental increase in lead-210 in teeth, a value of
3.24xl0~3 pCi (1.2x10"'' Bq) radon-222/gm of tissue has been associated with a
lifetime exposure to 1 WLM. All of these studies are limited by the
difficulty in estimating exposure to individuals on the basis of mine levels
and worker histories (often related by next of kin). Such estimates, although
unavoidable, introduce considerable uncertainty into these analyses. In
addition, lead-210 can be introduced in cigarette smoke, food, and ambient
air, thus confounding results of studies (NCRP 1984b).
5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES
Populations with potentially high exposures include those occupationally
exposed as previously described (see Section 5.5). In addition, certain
populations are exposed to elevated environmental levels, such as those
resulting from emanation from soil in the Reading Prong area of Pennsylvania
(soil-gas of up to 27,000 pCi [l.OxlO3 Bq] radon-222/L soil-gas) and from
release from groundwater in certain areas in Maine (levels up to 180,000 pCi
[6.7xl03 Bq] radon-222/L of water) (Hess et al. 1983). Communities that are
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78
5. POTENTIAL FOR HUMAN EXPOSURE
very near uranium or phosphate mill tailing piles may have increased
environmental radon levels. In addition, in some areas mill tailings have
been used for landfills and were subsequently developed (for example, Grand
Junction, Colorado). Persons in these communities could be exposed to levels
of radon exceeding normal background levels.
5.7 ADEQUACY OF THE DATABASE
Section 104(i)(5) of CERCLA directs the Administrator of ATSDR (in
consultation with the Administrator of EPA and agencies and programs of the
Public Health Service) to assess whether adequate information on the health
effects of radon is available. Where adequate information is not available,
ATSDR, in conjunction with the NTP, is required to assure the initiation of a
program of research designed to determine the health effects (and techniques
for developing methods to determine such health effects) of radon.
The following categories of possible data needs have been identified by a
joint team of scientists from ATSDR, NTP, and EPA. They are defined as
substance-specific informational needs that, if met would reduce or eliminate
the uncertainties of human health assessment. In the future, the identified
data needs will be evaluated and prioritized, and a substance-specific
research agenda will be proposed.
5.7.1 Identification of Data Needs
Physical and Chemical Properties. Information is available on the
physical and chemical properties of radon, and parameters that influence the
behavior of radon in the environment have been determined. Therefore, no data
needs are identified concerning physical and chemical properties of radon.
Production, Use, Rel©ase. and Disposal. The production of radon occurs
directly from a radium source either in the environment or in a laboratory
environment. The disposal of gaseous radioactive effluents has been
documented. Increased radon concentrations have been detected in waste
generated by uranium and phosphate mining; therefore, these sites should be
monitored on a continual basis. Although there are regulations for disposal
of radionuclides in general, there are none that specifically address disposal
of radon contaminated materials. Further research on the disposal of radon
attached to charcoal, which is used in radon monitoring indoors, would be
beneficial.
Environmental Fate. ^formation is available on the environmental fate
of radon in air and water and on tfte transport of radon in environmental
media. Factors which af£ect the partitioning of radon from soil or water to
air have been identified. however, rates of flux from one media to another
are rarely reported. The e""aUation rate of radon from soil is uncertain.
Additional information on the behavior of radon at the soil-air interface, as
well as soil-gas measuren»ents, would facilitate a better understanding of the
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79
5. POTENTIAL FOR HUMAN EXPOSURE
emanation rate of radon from soil. Movement of radon into and within homes
and the influence of meteorological conditions on this movement should be
investigated. Study of radon movement would enhance understanding of
potential indoor exposures. Transformation of radon has been adequately
characterized. There is limited information on the uptake of radon by plants.
Additional research of this phenomenon is needed in order to determine the
effects of exposures which might be incurred from ingestion of food.
Bioavailability from Environmental Media. Radon and radon progeny are
known to be absorbed from air and water and information is available which
characterizes the relative contribution of various media to levels of radon in
air and water. Further studies of bioavailability are not necessary at this
time.
Food Chain Bioaccumulation. Information on bioaccumulation of radon and
radon daughters in the food chain is not available. Therefore, the potential
for bioconcentration in plants, aquatic organisms or animals, or for
biomagnification in the food chain is unknown. However, due to the short
half-life of radon, it would not tend to bioaccumulate. Studies of the
bioaccumulation of radon in the food chain are not necessary at this time.
Exposure Levels in Environmental Media. Some information is available on
exposure levels in environmental media, however, most of this information is
from areas with higher than average levels of radon. Although levels in
groundwater, primarily for public water supplies, have been more
comprehensively reported than levels in ambient air, on-going monitoring
efforts for both media are necessary for quantification of human exposure.
Comprehensive data on levels of radon in ambient air are needed in order to
assess potential human exposure.
Exposure Levels in Humans. There is a lack of comprehensive information
associating radon and radon progeny levels monitored in the environment and
exposure of the general population. Although levels of radon may be measured
in exhaled air, the relationship of that amount exhaled to the exposure level
can be estimated only by use of mathematical models. Concentrations of radon
progeny are measurable in urine, blood, bone, teeth, and hair; however, these
levels are not direct measurements of levels of exposure. These estimates
also may be derived through use of mathematical models. Studies are needed to
characterize the utility of these biomarkers of exposure.
Exposure Registries. No exposure registries for radon were located.
This compound is not currently one of the compounds for which a subregistry
has been established in the National Exposure Registry. The compound will be
considered in the future when chemical selection is made for subregistries to
be established. The information that is amassed in the National Exposure
Registry facilitates the epidemiological research needed to assess adverse
health outcomes that may be related to the exposure to this compound. The
Hanford Environmental Foundation in Richland, Washington, maintains a registry
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80
5. POTRNTIAL FOR HUMAN KXI'OSURK
of United States uranium miners and millers. lhe data in thc> legistry are
derived from autopsy material and include exposure i ni orm.i t. i oti.
Since uranium decays to radon, this exposure registry on minors and millers
may provide information on radon exposure.
5.7.2 On-going Studies
S D Schery (New Mexico Institute of Mining and Technology) is studying
the fundamental processes influencing release of radon isotopes from porous
media and the physical properties of radon isotopes which affect their
behavior in enclosed environments. The hypothesis that, plant functions
increase soil-radon flow to the atmosphere, thus measurably reducing the flow
into subsurface areas is under investigation by F.W. Whicker (Colorado State
University) A B. Tanner (U.S. Department of Interior) is completing a
qualitative study on the range and variability of diffusive and
advective/convective transport of radon and its controlling factors at
selected areas. Further, a study designed to provide information on the
transport pathway of radon and radon progeny, their charge state, and the
effect of clustering on decay products is being conducted by M.G. Payne (Oak
Ridge National Laboratories). Computer models are also being developed in an
attempt to simplify studies on radon transport within and from soils into the
atmosphere and structures (P.C. Owczarski, Pacific Northwest Laboratories) and
to unify theories of radon emanation and transport in the -oil (K..K. Nielson,
Rogers and Associates Engineering Corporation).
Investigations of factors which influence transport or mobility of radon
and its progeny from rocks/soils to the environment or homes are underway by
K K. Turekian (Yale University), D. Thomas (University oi Hawaii at Manoa),
R H Socolow (Center for Energy and Environmental Studies, Princeton
University) and C.S. Dudney (Oak Ridge National Laboratories). The study by
Dudney included New Jersey and the Tennessee Valley arc-as with high background
levels The influence of season, heating fuel, tobacco smoking, and building
characteristics on indoor air pollutant levels is being studied by R.H. Rainey
(Office of Power, Tennessee Valley Authority). Research Triangle Institute
(Research Triangle Park, North Carolina) is presently studying both modeling
and measurement of radon in houses,
One aspect of radon mobility, in relation to groundwater, is being
studied by 0 S Zepecza (U.S. Geological Survey). He is determining the
factors which control radionuclide transport and fate in groundwater in the
Newark basin and southern coastal plains of New Jersey, and the mechanism of
release of radionuclides to groundwater or retention in aquifer solids.
G Harbottle (Brookhaven National Laboratories) is studying the mobility
and chemical behavior of radium in the soli and the processes involved in the
emanation of radon. The dynamic behavior of radon and radon daughters will be
studied in controlled laboratory environments (J.S. Johnson, Lawrence
Livermore National Laboratory)¦
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6. ANALYTICAL METHODS
The purpose of this chapter is to describe the analytical methods that
are available for detecting and/or measuring and monitoring radon in
environmental media and in biological samples. The intent is not to provide
an exhaustive list of analytical methods that could be used to detect and
quantify radon. Rather, the intention is to identify well-established methods
that are used as the standard methods of analysis. Many of the analytical
methods used to detect radon in environmental samples are the methods approved
by federal agencies such as EPA and the National Institute for Occupational
Safety and Health (NIOSH). Other methods presented in this chapter are those
that are approved by a trade association such as the Association of Official
Analytical Chemists (AOAC) and the American Public Health Association (APHA).
Additionally, analytical methods are included that refine previously used
methods to obtain lower detection limits and/or to improve accuracy and
precision.
6 .1 BIOLOGICAL MATERIALS
Urine analysis and whole body counting are most frequently performed to
monitor exposure to radon. Tooth enamel and bone are also used as indicators
of radon exposure. The longer-lived radioactive isotopes, lead-210 and
polonium-210, are generally used as a means of estimating exposure to the
short-lived radon-222 decay products. It is generally known that lead-210 is
deposited primarily in bone with a relatively long biological half-life, which
enables it to reach transient radioactive equilibrium conditions with its
descendant, polonium-210 (Clemente et al. 1984). The short half-lives of
radon and the daughters, polonium-218 through polonium-214, preclude their
detection through normal bioassay techniques which typically require a day or
more after the sample has been collected before counting can commence (Gotchy
and Schiager 1969).
Direct measurements of emerging gamma rays typically use the gamma rays
from lead-210 and rely on decays occurring in lung or bone tissues. This
method utilizes a system of either sodium iodide or germanium detectors placed
over the body in a well-shielded room (Crawford-Brown and Michel 1987). For
past exposures, the lead-210 and polonium-210 concentrations in the urine are
determined by counting the number of decays on a sodium iodide system or by
use of liquid scintillation.
Applying these concentrations to estimate the exposure an individual
might have received introduces large uncertainties. Pharmacokinetic metabolic
models are used to detail the movement of the radionuclides within the organs
and tissues of the body (EPA 1988a; ICRP 1978). Several additional models are
described in BEIR IV (1988). The uncertainties involved make it unlikely that
these approaches can yield estimates of exposure to within better than a
factor of four to five, particularly when values specific to individuals
(rather than populations) are required (Crawford-Brown and Michel 1987).
Analytical methods for determining radon in biological samples are given in
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82
6. ANALYTICAL METHODS
Table 6-1. These methods provide indirect measurements of radon; i.e., the
activity emitted from radon and radon progeny is detected and quantified.
6.2 ENVIRONMENTAL SAMPLES
Radon has been recognized as a health hazard for many years, primarily
for uranium miners. Recently, unusually high radon concentrations have been
found in several areas of the country, particularly Northeast Pennsylvania.
This has prompted nationwide concern and interest in the measurement of radon.
To aid in the effort in standardizing procedures for making accurate and
reproducible measurements and to ensure consistency, the EPA has issued two
reports recommending measurement techniques and strategies. The 1986 report,
"Interim Radon and Radon Decay Product Measurement Protocols," provides
procedures for measuring radon-222 concentrations with continuous monitors,
charcoal canisters, alpha-track detectors and grab techniques (EPA 1986). The
second report, "Interim Protocols for Screening and Follow-up Radon and Radon
Decay Product Measurements" (EPA 1987a), outlines the recommendations for
making reliable, cost effective radon measurements in homes (Ronca-Battista et
al. 1988).
There are several generalizations about the measurement of radon which
apply regardless of the specific measurement technique used. Radon
concentrations in the same location may differ by a factor of two over a
period of 1 hour. Also, the concentration in one room of a building may be
significantly different than the concentration in an adjoining room.
Therefore, the absolute accuracy of a single measurement is not critical, but
improvements in sampling methodology would be helpful. Since radon
concentrations vary substantially from day to day, single grab-type
measurements are generally not very useful, except as a means of identifying a
potential problem area, and indicating a need for more sophisticated testing.
An initial screening for radon can be made with activated charcoal.
After a potential problem is identified, more accurate measurements can be
made using additional techniques.
There are three main methods of determining the air concentration of
radon: an instantaneous measurement, or grab sample, a continuous readout
monitor which continually registers the concentration, and a time averaged
concentration where the sample is obtained over a relatively long period of
time and yields a single average concentration for an extended time period
from a tew days to a week or more.
*:eciinl^ues ®easure air concentrations are outlined by Breslin
i dnn 999 Ih S tecl'r}iques for measuring radon use the fact that both
"Jl i . j j ye dauShters are alpha-emitting nuclides. The
sample is collected and taken back to the laboratory for "alpha-counting" or
an alpha-detector is taken tn rhe f{Di^ f . J ttj-pud cuuni-iiig
field for on-site measurement. There are
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83
6. ANALYTICAL METHODS
TABLE 6-1. Analytical Methods for Determining
Radon in Biological Materials
Sample
Matrix
Sample
Preparation
Analytical
Method
Sample
Detection
Limit
Accuracy Reference
Tooth Clean and dry tooth;
dry overnight and
grind to fine powder;
separate enamel from
dentin and compress
into pellets; coat
with titinium nitride
PIXE for
PB-210
content
No 0.5 Anttila
data ppm 1987
Urine Wet ash in HN03-NC10A,
electrostatic
precipitation
Blood Wet ash
Blood Wet ash and plate
on disk
Alpha
spectometry
Alpha
spectrometry
Autoradio-
graphy of
tracks, using
nuclear
emulsion
0.1 pCi
(3. 7xlO~3
Bq)
0.1 pCi
(3.7xlO~3
Bq)
No
data
85%
85%
No
data
Gotchy and
Schiager
1969
Gotchy and
Schiager
1969
Weissbuch
et al.
1980
Bone Extract fat with
anhydrous benzene;
wet ash
Scintillation No No
counter data data
Blanchard
et al.
1969
Bone
In vivo
Tissue Place in tared test
tube
Whole body No No Eisenbud
counting gamma data data et al.
spectroscopy 1969
Scintillation No No
counter data data
Nussbaum
and Hursh
1957
PIXE - proton induced X-ray emission analysis
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6. ANALYTICAL METHODS
several ways to measure alpha decay. A scintillation flask is one of
oldest and most commonly used methods. The flask is equipped with valves
which are lined with a phosphor (silver-activated zinc sulfide) and emit light
flashes when bombarded with alpha particles. Other methods draw the air
through a filter (or filters) for a variety of time intervals and then count
the number of alpha-decays occurring on the filter. EPA (1986) and NCRP
(1988) reports provide more in-depth discussions of these methods.
EPA (1986) outlines the most common procedures for making measurements
and describes conditions that should exist at the time of the measurement.
The simplest, least expensive method of radon measurement is with charcoal-
adsorption. One side of the container is fitted with a screen to keep the
charcoal in and allow the radon to diffuse into the charcoal. The adsorbed
radon subsequently decays, depositing decay products in the charcoal. After
exposure for 3 to 7 days the canister is sealed and sent to the laboratory
where the charcoal is placed directly into a gamma detector.
For continuous monitoring of an indoor environment, a common method is
the scintillation cell method. The monitor pumps air into a scintillation
cell after passing it through a particulate filter that removes dust and radon
decay products. As the radon in the cell decays, the decay products plate out
on the interior surface of the scintillation cell. The alpha particles
emitted by radon and radon daughters strike the coating on the inside of the
cell causing scintillations to occur. These scintillations are detected by a
photomultiplier tube in the detector and an electrical signal is generated.
Another widely used method is solid state nuclear track detection. In
the case of radon, an alpha track detector is used. It consists of a small
piece of plastic enclosed in a container with a filter-covered opening. Alpha
particles in the air strike the plastic and produce submicroscopic damage
tracks. At the end of the measurement period the plastic is placed in a
caustic solution that accentuates the damage tracks. The tracks are then
counted using a microscope or automated counting system.
Radon daughter aerosols may also be measured by using electrets. These
are uniformly charged surfaces which provide a collection medium with a built-
in electrostatic force to attract the aerosols, therefore avoiding use of a
pump (Khan and Phillips 1984). Deposition is quantified with an alpha
counter.
There are two primary methods for measuring radon in aqueous samples, the
radon bubbler/alpha scintiHati°n cell method and the liquid scintillation
counting method. There are problems associated with sample collection for the
radon bubbler/alpha scintillat*-on method. One problem is that the sample in
the field must be collected in a glass bubbler flask that must then be
transported to the lab. Due ^ transport an(j handling problems, sample
results may be compromised. T erefore, the liquid scintillation counting
method is more commonly used. A description of the liquid scintillation
counting method is given in ^ The greatest analytical uncertainty of
-------
85
6. ANALYTICAL METHODS
TABLE 6-2. Analytical Methods for Determining
Radon in Environmental Samples
Sample
Matrix
Sample
Preparation
Analytical
Method
Sample
Detection
Limit
Accuracy Reference
Air
Radon
Adsorb onto Gamma
activated charcoal, spectro-
2 to 7 days scopy
Adsorb onto activated Liquid
charcoal; extract with scintil-
toluene; gently shake lation
1.3 pCi/m3 No data
(0.048 Bq/m3)
Cohen and
Nason 1986
0.21-0.37
pCi/m3
(0.007-
0.014 Bq/m3)
0.094 of Prichard and
true con- Marlen 1983
centration
Scintillation Cell
Allow air to enter ZnS(Ag)
detection chamber scintil-
through millipore lation/
filter until equili- photomulti-
brated, or collect plier tube
sample in bag (Mylar
or Tedlar), transfer
to chamber ASAP
0.1 pCi/m3 No data
(0.004 Bq/m3)
Crawford-
Brown and
Michel 1987
Diffuse through filter
into detector housing;
collections with
electret
TLD chip
89 pCi/
3 (3.30
Bq/m3)
m
0.95-1.08 Maiello and
of true Harley 1987
concen-
tration
Two-Filter Method
Draw air into fixed
length tube with
entry and exit filters;
monitor exit filter
activity
ZnS(Ag) 0.011 pCi/
scintil- m3 (<0.001
lation/ Bq/m3)
photomulti -
plier tube
90%
Schery
et al.
1980
-------
86
6. ANALYTICAL METHODS
TABLE 6-2 (Continued)
Sample
Sample Sample Analytical Detection
Matrix Preparation Method Limit Accuracy Reference
Solid State Nuclear
Track Detector
Diffuse through a fil-
ter into a cup con-
taining alpha track
material (cellulose
nitrate film) for up
to 1 year; etch in
acidic or basic solu-
tion operated upon by
an alternating electric
field
Micro-
scopic
examina-
tion of
damaged
material
14 pCi/m3
(0.519
Bq/m3)
No data
NCRP 1988
Radon progeny
Draw air through Gross
filter for a sampling alpha
time of 5 to 10 counting
minutes
1.1 pCi/m3
(0.041
Bq/m3)
No data NCRP 1988
Draw air through Alpha
filter at a known spectro-
flow rate for metry
specified time
(10 m to 1 hr)
Charge surface electro- Alpha
statically to attract spectro-
aerosols metry
1.1 pCi/m3
(0.041
Bq/m3)
1.lpCi/m3
(0.041
Bq/m3)
70%
NCRP 1988
70%
NCRP 1988
Soil
Dry in 55°C oven for Scintil-
24 hours; place 5 grams lation
in 20 ml borosilicate counter
glass scintillation.
Cover with 10 ml dis-
tilled water; allow soil
to become wet; add 5 ml
high-efficiency mineral
oil; allow to age 30 days
No data
No data
Rangarajan
and Eapen
1987; Wadach
and Hess
1985
-------
87
6. ANALYTICAL METHODS
TABLE 6-2 (Continued)
Sample
Sample Sample Analytical Detection
Matrix Preparation Method Limit Accuracy Reference
None
Track No data
etch detec-
tor buried
30 cm deep
No data
Rangarajan
and Eapen
1987
Water
Radon
Pass carrier gas Scintil-
through samples in a lation
bubbler flask to purge counter
out dissolved radon;
transfer radon to eva-
cuated scintillation cell
1.4 pCi/L
(52 Bq/m3)
90%
Crawford-
Brown and
Michel 1987
Inject into glass vial Liquid
containing liquid scintil-
scintillation solution; lation
shake vigorously counter
Direct measurement
Gamma
ray
spectro-
scopy
10 pCi/L
(370 Bq/m3)
10 pCi/L
for 1 L
sample
(370 Bq/m3)
No data
Crawford-
Brown and
Michel 1987
No data Yang 1987
TLD = Thermoluminescent Dosimeter
-------
88
6. ANALYTICAL METHODS
these methods is due to sampling. Since radon is a gas, care must bo taken to
prevent its escape from the sample (Crawford-Brown and Michel 1987). A
discussion of measurement techniques in water may be found in the report, by
Crawford-Brown and Michel (1987).
There has been little attempt to standardize a method for measuring radon
in soil. However, a method which utilizes liquid scintillation counting for
determining concentration is given by Wadach and Hess (1985). A description
of this method may be found in Table 6-2.
The accuracy of any measurement will depend upon the calibration of the
instrument used. The calibration of an instrument determines its response to
a known amount or concentration of radioactivity. This allows a correlation
to be made between the instrument reading and the actual amount or
concentration present. A range of activities of radium-?26 standard reference
materials (SRM) is available from the U.S. Department of Commerce, National
Bureau of Standards (NBS) as solutions for calibrating detection systems.
Also, an elevated radon atmosphere may be produced in a chamber, and samples
drawn and measured in systems previously calibrated by radon emanation from an
NBS radium-226 SRM. Other radon detectors may then be filled from or exposed
in the chamber and standardized based on this "secondary" standard (NCRP
1988). Analytical methods for measuring radon in environmental samples are
given in Table 6-2. These methods provide indirect measurements of radon;
i.e., the activity emitted from radon and radon progeny is detected and
quantitied.
6.3 ADEQUACY OF THE DATABASE
Section 104(i)(5) of CERCLA directs the Administrator of ATSDR (in
consultation with the Administrator of gpA and agencies and programs of the
Public Health Service) to assess whether adequate information on the health
effects of radon is available. Wfaere adequate information is not available,
ATSDR, in conjunction with the NTP, is required to assure the initiation of a
program of research designed to determine the health effects (and techniques
for developing methods to deterwine such health effects) of radon.
The following categories of Possible data needs have been identified by a
joint team of scientists from ATSDr. NTp, and EPA. They are defined as
substance-specific informational rieeds that, if met would reduce or eliminate
the uncertainties of human heal^ aSseSsment. In the future, the identified
data needs will be evaluated arid P loritized, and a substance - specific
research agenda will be propose0 -
6.3.1 Identification of Data Nee<^
Methods for Determining Bi
-------
89
6. ANALYTICAL METHODS
the majority of these methods are unknown ar.d should be determined so that
exposure to radon may be quantified. In addition, measurement of radon gas in
expired air should be possible by methods such as gas chromatography.
However, descriptions of any such methods have not been found in the
literature.
The frequency of abnormalities in sputum cytology has been utilized as a
possible early indicator of radiation damage to lung tissue (Band et al. 1980;
Brandom et al. 1978; Saccomanno et al. 1974). The accuracy and precision of
this measurement is not known.
Methods for Determining Parent Compounds and Degradation Products in
Environmental Media. Analytical methods are available which allow for the
quantification of radon in air, water, and soil. However, methods for the
measurement of radon concentrations in soil-gas are limited. The ability to
accurately measure soil-gas is needed to provide a better understanding of the
emanation rate of radon gas from soil.
6.3.2 On-going Studies
Although several analytical methods for measuring and determining radon
and radon progeny from environmental media or biological tissues exist,
several on-going studies have been identified in the Federal Radon Activities
Inventory. There are a mwiber of animal studies underway. Occupationally
exposed individuals are continually monitored in order to obtain more accurate
models and better measurement techniques.
R. Cole (National Institute for Standards and Technology (NIST)) is
currently upgrading the primary radon measurement system which constitutes the
national radon measurement standard. D.R. Fisher (Pacific Northwest
Laboratories) is attempting to develop analytical methods which will aid in
calculating microdosimetry within the tracheobronchial epithelium after
inhalation of radon and radon progeny. Also, R.S. Caswell (NIST) is working
on a related investigation but with cells at risk in other parts of the lung
and adjacent areas.
J.R. Duray (Chem Nuclear Geotech, formerly United Nuclear Corporation
Geotech) is testing instruments and devices in order to develop accurate and
reliable measurements of annual indoor and outdoor levels of radon and radon
daughters. I. Pomerantz (EPA) is investigating analytical techniques to
measure certain radionuclides, which would aid in monitoring radon levels in
drinking water; whereas K. Fox (EPA) is working on radon removal techniques
for community water supplies in New Hampshire. Another area of concern is the
development of analytical methods for measuring radon in buildings.
C. Arnolts (Department of Housing and Urban Development) is investigating
techniques builders can use to identify the presence of radon in a given
building, ar.d T. Peake (EPA) is working on methodology which would identify
areas with a high potential for radon exposure. M. Ronca-Battista (EPA)
-------
90
6. ANALYTICAL METHODS
reports the steps that are being taken to revise EPA radon measurement
protocols and includes a new method for measuring indoor radon and radon
progeny concentrations.
-------
91
7. REGULATIONS AND ADVISORIES
International and national regulations and guidelines pertinent to human
exposure to radon are summarized in Table 7-1. Recommendations for radiation
protection for people in the general population as a result of exposure to
radiation in the environment are found in the Federal Radiation Guidance (FRC
1960) and ICRP No. 26 (ICRP 1977). National guidelines for occupational
radiation protection are found in the "Federal Radiation Protection Guidance
for Occupational Exposure" (EPA 1987b). This guidance for occupational
exposure supersedes recommendations of the Federal Radiation Council for
occupational exposure (FRC 1960). The new guidance presents general
principles for the radiation protection of workers and specifies the numerical
primary guides for limiting occupational exposure. These recommendations are
consistent with the ICRP (ICRP 1977).
The basic philosophy of radiation protection is the concept of ALARA (As
Low As Reasonably Achievable). As a rule, all exposure should be kept as low
as reasonably achievable and the regulations and guidelines are meant to give
an upper limit to exposure. Based on the primary guides, guides for Annual
Limits on Intake (ALIs) have been calculated (EPA 1988a; ICRP 1979). The ALI
is defined as "that activity of a radionuclide which, if inhaled or ingested
by Reference Man (ICRP 1975), will result in a dose equal to the most limiting
primary guide for committed dose" (EPA 1988a) (see Appendix B),
-------
92
7. REGULATIONS AND ADVISOR IKS
TABLE 7-1. Regulations and Guidelines Applicable to Radon-222
Agency
Description
Vali
Reference
Guidelines
WHO
WHO
WHO
ICRP
ICRP
Internat i ona1
Remedial action should be con-
sidered if exceeded in building
Remedial action should be con-
sidered without long delay if
exceeded in building
Should not be exceeded before
remedial action
Maximum cumulative occupational
exposure
Annual limit for intake by
inhalation
National
Regulations
a. Air
Environmental and indoor
EPA
EPA
Average annual atmospheric
release rate from residual radio-
active material from inactive
uranium processing sites
Annual average concentration
should not be increased by more
than this due to inactive
uranium processing sites
2,700 pCi/I.
(99,900 Bq/m')
EER
Suess 1988
10,800 pCi/L Suess 1988
( 399 , C00 Bq/m-')
EER
5.Ax10* pCi
yr/L (2.00x106
Bq yr/m3) EER
Suess 1988
4 . 8 WI-M/yr
0.02 Joules/yr TCRP 1977
Bodansky
et al. 1987
20 pCi/m2/sec
(0.74 Bq/m2/
sec)
0.5 pCi/L
(18.5 Bq/m3)
EPA 1988b
(40 CFR 190
192.02)
EPA 1988b
(40 CFR 190
192.02)
-------
93
7. REGULATIONS AND ADVISORIES
TABLE 7-1 (Continued)
Agency
Description
Value
Reference
EPA
EPA
NRC
Maximum average annual radon
decay product concentration
(including background) as a
result of inactive uranium
processing sites, in any
occupied or habitable building
Maximum radon decay product
concentration (including back-
ground) as a result of inactive
uranium processing sites, in any
occupied or habitable building
Maximum permissible concentration
in air released to unrestricted
areas
0.02 WL
0.03 WL
3xl0"09 nCi/
cm3 (l.lxlO-4
Bq/cm3)
EPA 1988b
(AO CFR 190
192.12)
EPA 1988b
(40 CFR 190
192.12)
NRC 1988a
(10 CFR 20)
Mine and cave
0SHA
Individual exposure limit
4.0 WLM/yr
0SHA 1988
(41 CFR
57.5038)
OSHA
Monitor workspace at least
once yearly
0.1 \JL
OSHA 1988
(41 CFR
57.5087)
OSHA
Monitor workspace quarterly
0.1 - 0.3 WL
OSHA 1988
(41 CFR
57.5037)
OSHA
OSHA
Monitor workspace weekly and > 3.0 WL
maintain exposure records on
all exposed employees
Immediate corrective action to 1.0 WL
lower the concentration
OSHA 1988
(41 CFR
57.5037)
OSHA 1988
(41 CFR
57.5041)
MS HA
Maximal cumulative dose
4.0 WLM/yr
MSHA 1989
(30 CFR 57)
-------
94
7. REGULATIONS AND ADVISORIES
TABLE 7-1 (Continued)
Agency
Description
Value
Re ference
MSHA
Instantaneous maximum
1.0 WL
b. Drinking water
NRC Maximum permissible concentration
in water released to unrestricted
areas
c. Food
d. Nonspecific media
EPA Reportable quantity
Radon-220
Radon-222
Guidelines
a. Air
ANSI/ Annual average concentration of
ASHRAE indoor radon
EPA Upper level of exposure in home
EPA Desired target concentration in
the home
EPA Action within several months
EPA Remedial action must be under-
taken
EPA Occupational ALI for inhalation13
NCRP Remedial action level
NIOSH Recommended exposure limit
No data
No data
CI (Bq )
0.1 (3.7xl09)
0.1 (3.7xl09)
0.01 WL
4 pCi radon-
222/L of air
(148 Bq/m3)
0.02 WL
0.1 WL
8 pCi radon-
222/L of air
(300 Bq/m3)
4 WLM
2 WLM/yr
1.0 WLM/yr
MSHA 1989
(30 CFR 57)
EPA 1989b
40 CFR 302
Natl. Res.
Council 1981
Deluca and
Castronovo
1988
Bodansky
et al. 1987
Bodansky
et al. 1987
Deluca and
Castronovo
1988
EPA 1988a
NCRP 1984b
NIOSH 1987
-------
95
7. REGULATIONS AND ADVISORIES
TABLE 7-1 (Continued)
Agency
Description
Value
Reference
NIOSH Average work shift concentration
limit
b. Drinking water
c. Food
Regulations and Guidelines
a. Air
State
Alaska Regulated hazardous substance
New Immediate corrective action or
Mexico withdraw workers
New Withdraw workers until corrective
Mexico action is taken or until reduced
to 1,0 WL or less
New Maximal cumulative exposure
Mexico to workers
New Instantaneous maximum to
Mexico workers
New Exposure records should be kept
Mexico for employees entering areas
with this concentration
New Respiratory devices to prevent
Mexico inhalation of radon daughters
should be worn by workers
New Respiratory devices to prevent
Mexico inhalation of radon gas and
daughters should be worn by
workers
0.083 WL
No data
No data
NIOSH 1987
No.data
1.0 - 1.4 WL
> 1.4 WL
4.0 WLM/yr
1.0 WL
0.3 WL
1.0 WL
10 WL
Alaska 1988
New Mexico
1981
(NMMSC 11)
New Mexico
1981
(NMMSC 11)
New Mexico
1981 (SIM
Rule 76-1)
New Mexico
1981 (SIM
Rule 76-1)
New Mexico
1981 (SIM
Rule 71-2)
New Mexico
1981 (SIM
Rule 78-l(2a)
New Mexico
1981 (SIM
Rule 78-l(2a)
-------
96
7. REGULATIONS AND ADVISORIES
TABLE 7-1 (Continued)
Agency Description Value Reference
b. Water/Drinking water
Maine
Rhode
Island
10,000 pCi/L FSTRAC 1988
(3 . 7xl05 Bq/in1)
10,000 pCi/L FSTRAC 1988
(3.7xl05 Bq/m3)
aThe Nuclear Regulatory Commission limits in 10 CFR 20 are in the process of
revision.
bThe ALI recommended by the EPA is numerically identical, to that recommended
by the ICRP Publication 30 (ICRP 1979).
ALI — Annual Limit of Intake
ANSI/ASHRAE - American National Standards Institute/American Society of
Heating, Refrigerating and Air Conditioning
EER — Equilibrium Equivalent Radon
EPA - Environmental Protection Agency
FSTRAC = Federal-State Toxicology and Regulatory Alliance Committee
ICRP = International Commission on Radiological. Protection
MSHA - Mine Safety and Health Adminstration
NCRP - National Council for Radiation Protection and Measurements
NRC = Nuclear Regulatory Commission
NIOSH — National Institute for Occupational Safety and Health
NMMSC - New Mexico Mine Safety Code
OSHA - Occupational Safety and Health Administration
SIM - State Inspector of Mines, New Mexico
WHO - World Health Organization
WL - Working Level
WLM — Working Level Month
-------
97
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9. GLOSSARY
Absorbed Dose -- The mean energy imparted to the irradiated medium, per unit
mass, by ionizing radiation. Units: gray (Gy), rad.
Absorbed Fraction -- A term used in internal dosimetry. It is that fraction
of the photon energy (emitted within a specified volume of material) which is
absorbed by the volume. The absorbed fraction depends on the source
distribution, the photon energy, and the size, shape and composition of the
volume.
Absorption -- The process by which radiation mparts some or all of its energy
to any material through which it passes.
Self-Absorption -- Absorption of radiation (emitted by radioactive atoms)
by the material in which the atoms are located; in particular, the
absorption of radiation within a sample being assayed.
Absorption Coefficient -- Fractional decrease in the intensity of an
unscattered beam of x or gamma radiation per unit thickness (linear absorption
coefficient), per unit mass (mass absorption coefficient), or per atom (atomic
absorption coefficient) of absorber, due to deposition of energy in the
absorber. The total absorption coefficient is the sum of individual energy
absorption processes. (See Compton Effect, Photoelectric Effect, and Pair
Production.)
Linear Absorption Coefficient -- A factor expressing the fraction of a beam
of x or gamma radiation absorbed in a unit thickness of material. In the
expression I-t0e"|,x, ID is the initial intensity, I the intensity of the
beam after passage through a thickness of the material x, and p is the
linear absorption coefficient.
Mass Absorption Coefficient -- The linear absorption coefficient per cm
divided by the density of the absorber in grams per cubic centimeter. It
is frequently expressed as \i/p, where p is the linear absorption
coefficient and p the absorber density.
Absorption Ratio, Differential -- Ratio of concentration of a nuclide in a
given organ or tissue to the concentration that would be obtained if the same
administered quantity of this nuclide were uniformly distributed throughout
the body.
Activation -- The process of inducing radioactivity by irradiation.
Activity -- The number of nuclear transformations occurring in a given
quantity of material per unit time. (See Curie.)
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9. GLOSSARY
Activity Median Aerodynamic Diameter (AMAD) -- The diameter of a unit-density
sphere with the same terminal settling velocity in air as that of the aerosol
particulate whose activity is the median for the entire aerosol.
Acute Exposure -- Exposure to a chemical for a duration of 14 days or less, as
specified in the toxicological profiles.
Acute Radiation Syndrome -- The symptoms which taken together characterize a
person suffering from the effects of intense radiation. The effects occur
within hours or weeks.
Adsorption Coefficient (Koc) -- The ratio of the amount of a chemical adsorbed
per unit weight of organic carbon in the soil or sediment to the concentration
of the chemical in solution at equilibrium.
Adsorption Ratio (Kd) -- The amount of a chemical adsorbed by a sediment or
soil (i.e., the solid phase) divided by the amount of chemical in the solution
phase, which is in equilibrium with the solid phase, at a fixed solid/solution
ratio. It is generally expressed in micrograms of chemical sorbed per gram of
soil or sediment.
Alpha Particle -- A charged particle emitted from the nucleus of an atom. An
alpha particle has a mass charge equal in magnitude to that of a helium
nucleus; i.e., two protons and two neutrons and has a charge of +2.
Annihilation (Electron) --An interaction between a positive and a negative
electron in which they both disappear; their energy, including rest energy,
being converted into electromagnetic radiation (called annihilation radiation)
with two 0.51 Mev gamma photons emitted at an angle of 180° to each other.
Atomic Mass -- The mass of a neutral atom of a nuclide, usually expressed in
terms of "atomic mass units." The "atomic mass unit" is one-twelfth the mass
of one neutral atom of carbon-12; equivalent to 1.6604X10"24 gm. (Symbol: u)
Atomic Number -- The number of protons in the nucleus of a neutral atom of a
nuclide. The "effective atomic number" is calculated from the composition and
atomic numbers of a compound or mixture. An element of this atomic number
would interact with photons in the same way as the compound or mixture.
(Symbol: Z)
Atomic Weight -- The weighted mean of the masses of the neutral atoms of an
element expressed in atomic mass units.
Auger Effect -- The emission of an electron from the extranuclear portion of
an excited atom when the atom undergoes a transition to a less excited state.
Background Radiation -- Radiation arising from radioactive material other than
that under consideration. Background radiation due to cosmic rays and natural
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9. GLOSSARY
radioactivity is always present. There may also be background radiation due
to the presence of radioactive substances in building materials.
Becquerel (Bq) -- International System of Units unit of activity and equals
one transformation (disintegration) per second. (See Units.)
Beta Particle -- Charged particle emitted from the nucleus of an atom. A beta
particle has a mass and charge equal in magnitude to that of the electron.
The charge may be either +1 or -1.
Biologic Effectiveness of Radiation -- (See Relative Biological
Effectiveness.)
Bone Seeker -- Any compound or ion which migrates in the body preferentially
into bone.
Branching -- The occurrence of two or more modes by which a radionuclide can
undergo radioactive decay. For example, radium C can undergo a or decay,
64Cu can undergo , £+, or electron capture decay. An individual atom of a
nuclide exhibiting branching disintegrates by one mode only. The fraction
disintegrating by a particular mode is the "branching fraction" for that mode.
The "branching ratio" is the ratio of two specified branching fractions (also
called multiple disintegration).
Bremsstrahlung The production of electromagnetic radiation (photons) by the
negative acceleration that a fast, charged particle (usually an electron)
undergoes from the effect of an electric or magnetic field, for instance, from
the field of another charged particle (usually a nucleus).
Cancer Effect Level (CEL) -- The lowest dose of chemical in a study, or group
of studies, that produces significant increases in the incidence of cancer (or
tumors) between the exposed population and its appropriate control.
Capture, Electron - - A mode of radioactive decay involving the capture of an
orbital electron by its nucleus. Capture from a particular electron shell is
designated as MK-electron capture," "L-electron capture," etc.
Capture, K-Electron -- Electron capture from the K shell by the nucleus of the
atom. Also loosely used to designate any orbital electron capture process.
Carcinogen -- A chemical capable of inducing cancer.
Carcinoma -- Malignant neoplasm composed of epithelial cells, regardless of
their derivation.
Cataract -- A clouding of the crystalline lens of the eye which obstructs the
passage of light.
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9. GLOSSARY
Celling Value (DL) -- A concentration of a substance that should not be
exceeded, even instantaneously.
Chronic Exposure -- Exposure to a chemical for 365 days or more, as specified
in the Toxicological Profiles.
Compton Effect -- An attenuation process observed for x or gamma radiation in
which an incident photon interacts with an orbital electron of an atom to
produce a recoil electron and a scattered photon of energy less than the
incident photon.
Containment -- The confinement of radioactive material in such a way that it
is prevented from being dispersed into the environment or is released only at
a specified rate.
Contamination, Radioactive -- Deposition of radioactive material in any place
where it is not desired, particularly where its presence may be harmful.
Cosmic Rays -- High-energy particulate and electromagnetic radiations which
originate outside the earth's atmosphere.
Count (Radiation Measurements) -- The external indication of a
radiation-measuring device designed to enumerate ionizing events. It may
refer to a single detected event to the total number registered in a given
period of time. The term often is erroneously used to designate a
disintegration, ionizing event, or voltage pulse.
Counter, Geiger-Mueller -- Highly sensitive, gas-filled radiation-measuring
device. It operates at voltages sufficiently high to produce avalanche
ionization.
Counter, Scintillation -- The combination of phosphor, photmultiplier tube,
and associated circuits for counting light emissions produced in the
phosphors by ionizing radiation.
Curie -- A unit of activity. One curie equals 3.7xl010 nuclear
transformations per second. (Abbreviated Ci.) Several fractions of the curie
are in common usage.
Megacurie -- One million curies. Abbreviated MCi.
Microcurie -- One-millionth of a curie (3.7xl04 disintegrations per sec).
Abbreviated |iCi.
Millicurie -- One-thousandth of a curie (3.7xl07 disintegrations per sec).
Abbreviated mCi.
Nanocurie -- One-billionth of a curie. Abbreviated nCi.
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9. GLOSSARY
Picocurie -- One-millionth of a microcurie (3.7xl0~2 disintegrations per
second or 2.22 disintegrations per minute), Abbreviated pCi; replaces the
term mic.
Decay, Radioactive -- Transformation of the nucleus of an unstable nuclide by
spontaneous emission of charged particles and/or photons.
Decay Chain or Decay Series -- A sequence of radioactive decays
(transformations) beginning with one nucleus. The initial nucleus, the
parent, decays into a daughter nucleus that differs from the first by whatever
particles were emitted during the decay. If further decays take place, the
subsequent nuclei are also usually called daughters. Sometimes, to
distinguish the sequence, the daughter of the first daughter is called the
granddaughter, etc.
Decay Constant -- The fraction of the number of atoms of a radioactive nuclide
which decay in unit time. (Symbol X). (See Disintegration Constant).
Decay Product, Daughter Product -- A new isotope formed as a result of
radioactive decay. A nuclide resulting from the radioactive transformation of
a radionuclide, formed either directly or as the result of successive
transformations in a radioactive series. A decay product (daughter product)
may be either radioactive or stable.
Delta Ray -- Energetic or swiftly moving electrons ejected from an atom during
the process of ionization. Delta rays cause a track of secondary ionizations
along their path.
Developmental Toxicity -- The occurrence of adverse effects on the developing
organism that may result from exposure to a chemical prior to conception
(either parent), during prenatal development, or postnatally to the time of
sexual maturation. Adverse developmental effects may be detected at any point
in the lifespan of the organism.
Disintegration Constant -- The fraction of the number of atoms of a
radioactive nuclide which decay in unit time; X is the symbol for the decay
constant in the equation N-NQe~lt, where N0 is the initial number of atoms
present, and N is the number of atoms present after some time, t. (See Decay
Constant.)
Disintegration, Nuclear -- A spontaneous nuclear transformation
(radioactivity) characterized by the emission of energy and/or mass from the
nucleus. When large numbers of nuclei are involved, the process is
characterized by a definite half-life. (See Transformation, Nuclear.)
Dose -- A general term denoting the quantity of radiation or energy absorbed.
For special purposes it must be appropriately qualified. If unqualified, it
refers to absorbed dose.
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9. GLOSSARY
Absorbed Dose -- The energy imparted to matter by ionizing radiation per
unit mass of irradiated material at the place of interest. The unit of
absorbed dose is the rad. One rad equals 100 ergs per gram. In SI units,
the absorbed dose is the gray which is 1 J/kg. (See Rad.)
Cumulative Dose (Radiation) -- The total dose resulting from repeated or
continuous exposures to radiation.
Dose Assessment --An estimate of the radiation dose to an individual or a
population group usually by means of predictive modeling techniques,
sometimes supplemented by the results of measurement.
Dose Equivalent (DE) - - A quantity used in radiation protection. It
expresses all radiations on a common scale for calculating the effective
absorbed dose. It is defined as the product of the absorbed dose in rad
and certain modifying factors. (The unit of dose equivalent is the rem.
In SI units, the dose equivalent is the sievert, -which equals 100 rem.)
Dose, Radiation -- The amount of energy imparted to matter by ionizing
radiation per unit mass of the matter, usually expressed as the unit rad,
or in SI units, 100 rad-1 gray (Gy). {See Absorbed Dose.)
Maximum Permissible Dose Equivalent (MPD) -- The greatest dose equivalent
that a person or specified part thereof shall be allowed to receive in a
given period of time.
Median Lethal Dose (MLD) -- Dose of radiation required to kill, within a
specified period, 50 percent of the individuals in a large group of animals
or organisms. Also called the LDS0.
Threshold Dose -- The minimum absorbed dose that will produce a detectable
degree of any given effect.
Tissue Dose -- Absorbed dose received by tissue in the region of interest,
expressed in rad. (See Dose and Rad.)
Dose, Fractionation -- A method of administering radiation, in which
relatively small doses are given daily or at longer intervals.
Dose, Protraction -- A method of administering radiation by delivering it
continuously over a relatively long period at a low dose rate.
Dose-distribution Factor - - A factor which accounts for modification of the
dose effectiveness in cases in which the radionuclide distribution is
nonuniform.
Dose Rate -- Absorbed dose delivered per unit time.
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9. GLOSSARY
Dosimetry -- Quantification of radiation doses to individuals or populations
resulting from specified exposures.
Early Effects (of radiation exposure) -- Effects which appear within 60 days
of an acute exposure.
Electron -- A stable elementary particle having an electric charge equal to
±1.60210xl0~19 C (Coulombs) and a rest mass equal to 9.1091xl0~31 kg. A
positron is a positively charged "electron." (See Positron.)
Electron Volt -- A unit of energy equivalent to the energy gained by an
electron in passing through a potential difference of one volt. Larger
multiple units of the electron volt are frequently used: keV for thousand or
kilo electron volts; MeV for million or mega electron volts. (Abbreviated:
eV, 1 eV=l. 6xlCT12 erg.)
Embryotoxicity and Fetotoxicity -- Any toxic effect on the conceptus as a
result of prenatal exposure to a chemical; the distinguishing feature between
the two terms is the stage of development during which the insult occurred.
The terms, as used here, include malformations and variations, altered growth,
and in utero death.
Energy -- Capacity for doing work. "Potential energy" is the energy inherent
in a mass because of its spatial relation to other masses. "Kinetic energy"
is the energy possessed by a mass because of its motion; MKSA unit: kg-m2/sec2
or joules.
Binding Energy -- The energy represented by the difference in mass between
the sum of the component parts and the actual mass of the nucleus.
Excitation Energy -- The energy required to change a system from its ground
state to an exited state. Each different excited state has a different
excitation energy.
Ionizing Energy -- The average energy lost by ionizing radiation in
producing an ion pair in a gas. For air, it is about 33.73 eV.
Radiant Energy -- The energy of electromagnetic radiation, such as radio
waves, visible light, x and gamma rays.
Enriched Material -- (1) Material in which the relative amount of one or more
isotopes of a constituent has been increased. (2) Uranium in which the
abundance of the 235U isotope is increased above normal.
EPA Health Advisory --An estimate of acceptable drinking water levels for a
chemical substance based on health effects information. A health advisory is
not a legally enforceable federal standard, but serves as technical guidance
to assist federal, state, and local officials.
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9, GLOSSARY
Equilibrium, Radioactive - - In a radioactive series, the state which prevails
when the ratios between the activities of two or more successive members of
the series remains constant.
Secular Equilibrium -- If a parent element has a very much longer half-life
than the daughters (so there is not appreciable change in its amount in the
time interval required for later products to attain equilibrium) then,
after equilibrium is reached, equal numbers of atoms of all members of the
series disintegrate in unit time. This condition is never exactly
attained, but is essentially established in such a case as radium and its
series to Radium D. The half-life of radium is about 1,600 years; of
radon, approximately 3.82 days, and of each of the subsequent members, a
few minutes. After about a month, essentially the equilibrium amount of
radon is present; then (and for a long time) all members of the series
disintegrate the same number of atoms per unit time.
Transient Equilibrium -- If the half-life of the parent is short enough so
the quantity present decreases appreciably during the period under
consideration, but is still longer than that of successive members of the
series, a stage of equilibrium will be reached after which all members of
the series decrease in activity exponentially with the period of the
parent. An example of this is radon (half-life of approximately 3.82 days)
and successive members of the series to Radium D.
Equilibrium, Radiation -- The condition in a radiation field where the energy
of the radiations entering a volume equals the energy of the radiations
leaving that volume.
Equilibrium Fraction (F) --In radon-radon daughter equilibrium, the parents
and daughters have equal radioactivity, that is, as many decay into a specific
nuclide as decay out. However, if fresh radon is continually entering a
volume of air or if daughters are lost by processes other than radioactive
decay, e.g., plate out or migration out of the volume, a disequilibrium
develops. The equilibrium fraction is a measure of the degree of
equilibrium/disequilibrium. The working-level definition of radon does not
take into account the amount of equilibrium. The equilibrium fraction is used
to estimate working levels based on measurement of radon only.
Excitation -- The addition of energy to a system, thereby transferring it from
its ground state to an excited state. Excitation of a nucleus, an atom, or a
molecule can result from absorption of photons or from inelastic collisions
with other particles. The excited state of an atom is a metastable state and
will return to ground state by radiation of the excess energy.
Exposure -- A measure of the ionization produced in air by x or gamma
radiation. It is the stun of the electrical charges on all ions of one sign
produced in air when all electrons liberated by photons in a volume element of
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9. GLOSSARY
air are completely stopped in air, divided by the mass of the air in the
volume element. The special unit of exposure is the roentgen.
Fission, Nuclear -- A nuclear transformation characterized by the splitting of
a nucleus into at least two other nuclei and the release of a relatively large
amount of energy.
Gamma Ray -- Short wavelength electromagnetic radiation of nuclear origin
(range of energy from 10 keV to 9 MeV).
Genetic Effect of Radiation -- Inheritable change, chiefly mutations, produced
by the absorption of ionizing radiation by germ cells. On the basis of
present knowledge these effects are purely additive; there is no recovery.
Gray (Gy) -- SI unit of absorbed dose. One gray equals 100 rad. (See Units.)
Half-Life, Biological -- The time required for the body to eliminate one-half
of any absorbed substance by regular processes of elimination. Approximately
the same for both stable and radioactive isotopes of a particular element.
This is sometimes referred to as half-time.
Half-Life, Effective -- Time required for a radioactive element in an animal
body to be diminished 50% as a result of the combined action of radioactive
decay and biological elimination.
Effective half-life: - Biological half-life x Radioactive half-life
Biological half-life + Radioactive half-life
Half-life, Radioactive -- Time required for a radioactive substance to lose
50% of its activity by decay. Each radionuclide has a unique half-life.
Immediately Dangerous to Life or Health (IDLH) -- The maximum environmental
concentration of a contaminant from which one could escape within 30 minutes
without any escape-impairing symptoms or irreversible health effects.
Immunologic Toxicity -- The occurrence of adverse effects on the immune system
that may result from exposure to environmental agents such as chemicals.
Tn Vitro -- Isolated from the living organism and artificially maintained, as
in a test tube.
In Vivo -- Occurring within the living organism.
Intensity -- Amount of energy per unit time passing through a unit area
perpendicular to the line of propagation at the point in question.
Intermediate Exposure -- Exposure to a chemical for a duration of 15 to 364
days as specified in the Toxicological Profiles.
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9. GLOSSARY
Internal Conversion -- One of the possible mechanisms of decay from the
metastable state (isomeric transition) in which the transition energy is
transferred, to an orbital electron, causing its ejection from the atom. The
ratio of the number of internal conversion electrons to the number of gamma
quanta emitted in the de-excitation of the nucleus is called the "conversion
ratio."
Ion -- Atomic particle, atom, or chemical radical bearing a net electrical
charge, either negative or positive.
Ion Pair -- Two particles of opposite charge, usually referring to the
electron and positive atomic or molecular residue resulting after the
interaction of ionizing radiation with the orbital electrons of atoms.
Ionization -- The process by which a neutral atom or molecule acquires a
positive or negative charge.
Primary Ionization -- (1) In collision theory: the ionization produced by
the primary particles as contrasted to the "total ionization" which
includes the "secondary ionization" produced by delta rays. (2) In counter
tubes: the total ionization produced by incident radiation without gas
amplification.
Specific Ionization -- Number of ion pairs per unit length of path of
ionizing radiation in a medium; e.g., per centimeter of air or per
micrometer of tissue.
Total Ionization -- The total electric charge of one sign on the ions
produced by radiation in the process of losing its kinetic energy. For a
given gas, the total ionization is closely proportional to the initial
ionization and is nearly independent of the nature of the ionizing
radiation. It is frequently used as a measure of radiation energy.
Ionization Density -- Number of ion pairs per unit volume.
Ionization Path (Track) -- The trail of ion pairs produced by ionizing
radiation in its passage through matter.
Isobars -- Nuclides having the same mass number but different atomic numbers.
Isomers -- Nuclides having the same number of neutrons and protons but capable
of existing, for a measurable time, in different quantum states with different
energies and radioactive properties. Commonly the isomer of higher energy
decays to one with lower energy by the process of isomeric transition.
Isotones -- Nuclides having the same number of neutrons in their nuclei.
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127
9. GLOSSARY
Isotopes -- Nuclides having the same number of protons in their nuclei, and
hence the same atomic number, but differing in the number of neutrons, and
therefore in the mass number. Almost identical chemical properties exist
between isotopes of a particular element. The term should not be used as a
synonym for nuclide.
Stable Isotope -- A nonradioactive isotope of an element.
Joule -- The unit for work and energy, equal to one newton expended along a
distance of one meter (lJ-lNxlm).
Labeled Compound -- A compound consisting, in part, of labeled molecules.
That is molecules including radionuclides in their structure. By observations
of radioactivity or isotopic composition, this compound or its fragments may
be followed through physical, chemical, or biological processes.
Late Effects (of radiation exposure) -- Effects which appear 60 days or more
following an acute exposure.
Lethal Concentration^} (LC^o) -- The lowest concentration of a chemical in
air which has been reported to have caused death in humans or animals.
Lethal Concentration(50) (LC50) -- The calculated concentration of a chemical
in air to which exposure for a specific length of time is expected to cause
death in 50X of a defined laboratory animal population.
Lethal Dose(L0) (LDlq) -- The lowest dose of a chemical introduced by a route
other than inhalation that is expected to have caused death in humans or
animals.
Lethal Dose(50) (LD50) -- The dose of a chemical which has been calculated to
cause death in 50% of a defined laboratory animal population.
Lethal Tlme(50) (LT50) -- A calculated period of time within which a specific
concentration of a chemical is expected to cause death in 50X of a defined
laboratory animal population.
Linear Energy Transfer (LET) -- The average amount of energy transferred
locally to the medium per unit of particle track length.
Low-LET -- Radiation characteristic of electrons, x-rays, and ganuna rays.
High-LET -- Radiation characteristic of protons or fast neutrons.
Average LET -- is specified to even out the effect of a particle that is
slowing down near the end of its path and to allow for the fact that
secondary particles from photon or fast-neutron beams are not all of the
same energy.
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128
9. GLOSSARY
Lowest-Observed-Adverse-Effeet Level (LOAEL) -- The lowest dose of chemical in
a study, or group of studies, that produces statistically or biologically
significant increases in frequency or severity of adverse effects between the
exposed population and its appropriate control.
Linear Hypothesis -- The assumption that a dose-effect curve derived from
data in the high dose and high dose-rate ranges may be extrapolated
through the low dose and low dose range to zero, implying that,
theoretically, any amount of radiation will cause some damage.
Malformations -- Permanent structural changes in an organism that may
adversely affect survival, development, or function.
Mass Numbers -- The number of nucleons (protons and neutrons) in the
nucleus of an atom. (Symbol: A)
Minimal Risk Level --An estimate of daily human exposure to a chemical
that is likely to be without an appreciable risk of deleterious effects
(noncancerous) over a specified duration of exposure.
Mutagen -- A substance that causes mutations. A mutation is a change in
the genetic material in a body cell. Mutation can lead to birth defects,
miscarriages, or cancer.
Neurotoxicity -- The occurrence of adverse effects on the nervous system
following exposure to chemical.
Neutrino -- A neutral particle of very small rest mass originally
postulated to account for the continuous distribution of energy among
particles in the beta-decay process.
No-Observed-Adverse-Effect Level (NOAEL) -- The dose of chemical at which
there were no statistically or biologically significant increases in
frequency or severity of adverse effects seen between the exposed
population and its appropriate control. Effects may be produced at this
dose, but they are not considered to be adverse.
Nucleon -- Common name for a constituent particle of the nucleus. Applied
to a proton or neutron.
Nuclide -- A species of atom characterized by the constitution of its
nucleus. The nuclear constitution is specified by the number of protons
(Z), number of neutrons (N), and energy content; or, alternatively, by the
atomic number (Z), mass number A-(N+Z), and atomic mass. To be regarded
as a distinct nuclide, the atom must be capable of existing for a
measurable time. Thus, nuclear isomers are separate nuclides, whereas
promptly decaying excited nuclear states and unstable intermediates in
nuclear reactions are not so considered.
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129
9. GLOSSARY
Octanol-Water Partition Coefficient (Kow) -- The equilibrium ratio of the
concentrations of a chemical in n-octanol and water, in dilute solution.
Pair Production --An absorption process for x and gamma radiation in which
the incident photon is annihilated in the vicinity of the nucleus of the
absorbing atom, with subsequent production of an electron and positron pair.
This reaction only occurs for incident photon energies exceeding 1.02 MeV.
Parent -- A radionuclide which, upon disintegration, yields a specified
nuclide--either directly or as a later member of a radioactive series.
Photon -- A quantity of electromagnetic energy (E) whose value in joules is
the product of its frequency (v) in hertz and Planck constant (h). The
equation is: E-hv.
Photoelectric Effect --An attenuation process observed for x- and gamma-
radiation in which an incident photon interacts with an orbital electron of an
atom delivering all of its energy to produce a recoil electron, but with no
scattered photon.
Positron -- Particle equal in mass to the electron (9.1091xl0~31 kg) and
having an equal but positive charge (+1.60210xl0~19 Coulombs). (See
Electron).
Potential Ionization -- The potential necessary to separate one electron from
an atom, resulting in the formation of an ion pair.
Power, Stopping -- A measure of the effect of a substance upon the kinetic
energy of a charged particle passing through it.
Progeny -- The decay products resulting after a series of radioactive decays.
Progeny can also be radioactive, and the chain continues until a stable
nuclide is formed.
Proton -- Elementary nuclear particle with a positive electric charge equal
numerically to the charge of the electron and a rest mass of 1.007277 mass
units.
qx* -- The upper-bound estimate of the low-dose slope of the dose-response
curve as determined by the multistage procedure. The qx* can be used to
calculate an estimate of carcinogenic potency, the incremental excess cancer
risk per unit of exposure (usually \xg/L for water, mg/kg/day for food, and
Hg/m3 for air).
Quality -- A term describing the distribution of the energy deposited by a
particle along its track; radiations that produce different densities of
ionization per unit intensity are said to have different "qualities."
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130
9. GLOSSARY
Quality Factor (QF) -- The linear-energy-transfer-dependent factor by which
absorbed doses are multiplied to obtain (for radiation protection purposes) a
quantity that expresses - on a common scale for all ionizing radiation - the
effectiveness of the absorbed dose.
Rad -- The unit of absorbed dose equal to 0.01 J/kg in any medium. (See
Absorbed Dose.)
Radiation -- (1) The emission and propagation of energy through space or
through a material medium in the form of waves; for instance, the emission and
propagation of electromagnetic waves, or of sound and elastic waves. (2) The
energy propagated through space or through a material medium as waves; for
example, energy in the form of electromagnetic waves or of elastic waves. The
term radiation or radiant energy, when unqualified, usually refers to electro-
magnetic radiation. Such radiation commonly is classified, according to
frequency, as Hertzian, infra-red, visible (light), ultra-violet, X-ray and
gamma ray. (See Photon.) (3) By extension, corpuscular emission, such as
alpha and beta radiation, or rays of mixed or unknown type, as cosmic
radiation.
Annihilation Radiation -- Photons produced when an electron and a positron
unite and cease to exist. The annihilation of a positron-electron pair
results in the production of two photons, each of 0.51 MeV energy.
Background Radiation -- Radiation arising from radioactive material other
than the one directly under consideration. Background radiation due to
cosmic rays and natural radioactivity is always present. There may also be
background radiation due to the presence of radioactive substances in other
parts of the building, in the building material itself, etc.
Characteristic (Discrete) Radiation -- Radiation originating from an atom
after removal of an electron of excitation of the nucleus. The wavelength
of the emitted radiation is specific, depending only on the nuclide and
particular energy levels involved.
External Radiation -- Radiation from a source outside the body -- the
radiation must penetrate the skin.
Internal Radiation -- Radiation from a source within the body (as a result
of deposition of radionuclides in body tissues).
Ionizing Radiation -- Any electromagnetic or particulate radiation capable
of producing ions, directly or indirectly, in its passage through matter.
Monoenergetic Radiation -- Radiation of a given type (alpha, beta, neutron,
gamma, etc.) in which all particles or photons originate with and have the'
same energy.
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131
9. GLOSSARY
Scattered Radiation -- Radiation which during its passage through a
substance, has been deviated in direction. It may also have been modified
by a decrease in energy.
Secondary Radiation -- Radiation that results from absorption of other
radiation in matter. It may be either electromagnetic or particulate.
Radioactivity -- The property of certain nuclides to spontaneously emit
particles or gamma radiation or x radiation following orbital electron capture
or after undergoing spontaneous fission.
Artificial Radioactivity -- Man-made radioactivity produced by particle
bombardment or electromagnetic irradiation, as opposed to natural
radioactivity.
Induced Radioactivity -- Radioactivity produced in a substance after
bombardment with neutrons or other particles. The resulting activity is
"natural radioactivity" if formed by nuclear reactions occurring in nature,
and "artificial radioactivity" if the reactions are caused by man.
Natural Radioactivity -- The property of radioactivity exhibited by more
than 50 naturally occurring radionuclides.
Radioisotopes -- A radioactive atomic species of an element with the same
atomic number and usually identical chemical properties.
Radionuclide -- A radioactive species of an atom characterized by the
constitution of its nucleus.
Radiosensitivity -- Relative susceptibility of cells, tissues, organs,
organisms, or any living substance to the injurious action of radiation.
Radiosensitivity and its antonym, radioresistance, are currently used in a
comparative sense, rather than in an absolute one.
Reaction (Nuclear) --An induced nuclear disintegration, i.e., a process
occurring when a nucleus comes in contact with a photon, an elementary
particle, or another nucleus. In many cases the reaction can be represented
by the symbolic equation: X+a-Y+b or, in abbreviated form, X(a,b) Y. X is the
target nucleus, a is the incident particle or photon, b is an emitted particle
or photon, and Y is the product nucleus.
Reference Dose (RfD) --An estimate (with uncertainty spanning perhaps an
order of magnitude) of the daily exposure of the human population to a
potential hazard that is likely to be without risk of deleterious effects
during a lifetime. The RfD is operationally derived from the NOAEL (from
animal and human studies) by a consistent application of uncertainty factors
that reflect various types of data used to estimate RfDs and an additional
modifying factor, which is based on a professional judgment of the entire
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132
9. GLOSSARY
database on the chemical. The RfDs are not applicable to nonthreshold effects
such as cancer.
Relative Biological Effectiveness (RBE) -- The RBE is a factor used to compare
the biological effectiveness of absorbed radiation doses (i.e., rad) due to
different types of ionizing radiation. More specifically, it is the
experimentally determined ratio of an absorbed dose of a radiation in question
to the absorbed dose of a reference radiation required to produce an identical
biological effect in a particular experimental organism or tissue. NOTE:
This term should not be used in radiation protection. (See Quality Factor.)
Rem - - A unit of dose equivalent. The dose equivalent in rem is numerically
equal to the absorbed dose in rad multiplied by the quality factor, the
distribution factor, and any other necessary modifying factors.
Reportable Quantity (RQ) -- The quantity of a hazardous substance that is
considered reportable under CERCLA. Reportable quantities are (1) 1 lb or
greater or (2) for selected substances, an amount established by regulation
either under CERCLA or under Section 311 of the Clean Water Act. Quantities
are measured over a 24-hour period.
Reproductive Toxicity -- The occurrence of adverse effects on the reproductive
system that may result from exposure to a chemical. The toxicity may be
directed to the reproductive organs and/or the related endocrine system. The
manifestation of such toxicity may be noted as alterations in sexual behavior,
fertility, pregnancy outcomes, or modifications in other functions that are
dependent on the integrity of this system.
Roentgen (R) -- A unit of exposure for photon radiation. One roentgen equals
2.58x10"* Coulomb per kilogram of air.
Short-Term Exposure Limit (STEL) -- The maximum concentration to which workers
can be exposed continually for up to 15 minutes. No more than four excursions
are allowed per day, and there must be at least 60 minutes between exposure
periods. The daily TLV-TWA may not be exceeded.
SI Units -- The International System of Units as defined by the General
Conference of Weights and Measures in 1960. These units are generally based
on the meter/kilogram/second units, with special quantities for radiation
including the becquerel, gray, and sievert.
Sickness, Radiation -- (Radiation Therapy): A self-limited syndrome
characterized by nausea, vomiting, diarrhea, and psychic depression following
exposure to appreciable doses of ionizing radiation, particularly to the
abdominal region. Its mechanism is unknown and there is no satisfactory
remedy. It usually appears a few hours after irradiation and may subside
within a day. It may be sufficiently severe to necessitate interrupting the
treatment series or to incapacitate the patient. (General): The syndrome
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133
9. GLOSSARY
associated with intense acute exposure to ionizing radiations. The rapidity
with which symptoms develop is a rough measure of the level of exposure.
Sievert -- The SI unit of radiation dose equivalent. It is equal to dose in
grays times a quality factor times other modifying factors, for example, a
distribution factor; 1 sievert equals 100 rem.
Specific Activity -- Total activity of a given nuclide per gram of an element.
Specific Energy -- The actual energy per unit mass deposited per unit volume
in a given event. This is a stochastic quantity as opposed to the average
value over a large number of instance (i.e., the absorbed dose).
Standard Mortality Ratio (SMR) -- Standard mortality ratio is the ratio of the
disease or accident mortality rate in a certain specific population compared
with that in a standard population. The ratio is based on 200 for the
standard so that an SMR of 100 means that the test population has twice the
mortality from that particular cause of death.
Stopping Power -- The average rate of energy loss of a charged particle per
unit thickness of a material or per unit mass of material traversed,
Surface-seeking Radionuclide -- A bone-seeking internal emitter that is
deposited and remains on the surface for a long period of time. This
contrasts with a volume seeker, which deposits more uniformly throughout the
bone volume.
Target Organ Toxicity -- This term covers a broad range of adverse effects on
target organs or physiological systems (e.g., renal, cardiovascular) extending
from those arising through a single limited exposure to those assumed over a
lifetime of exposure to a chemical.
Target Theory (Hit Theory) -- A theory explaining some biological effects of
radiation on the basis that ionization, occurring in a discrete volume (the
target) within the cell, directly causes a lesion which subsequently results
in a physiological response to the damage at that location. One, two, or more
"hits" (ionizing events within the target) may be necessary to elicit the
response.
Teratogen -- A chemical that causes structural defects that affect the
development of a fetus.
Threshold Limit Value (TLV) --An allowable exposure concentration averaged
over a normal 8-hour workday or 40-hour workweek.
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134
9. GLOSSARY
Toxic Dose (TD50) -- A calculated dose of a chemical, introduced by a route
other than inhalation, which is expected to cause a specific toxic effect in
50% of a defined laboratory animal population.
Transformation, Nuclear -- The process by which a nuclide is transformed into
a different nuclide by absorbing or emitting a particle.
Transition, Isomeric -- The process by which a nuclide decays to an isomeric
nuclide (i.e., one of the same mass number and atomic number) of lower quantum
energy. Isomeric transitions, often abbreviated I.T., proceed by gamma ray
and/or internal conversion electron emission.
Tritium -- The hydrogen isotopes with one proton and two neutrons in the
nucleus (Symbol: 3H or T).
Unattached Fraction -- That fraction of the radon daughters, usually 218Po
(Radium A), which has not yet attached to a particle. As a free atom, it has
a high probability of being retained within the lung and depositing alpha
energy when it decays.
Uncertainty Factor (UF) -- A factor used in operationally deriving the RfD
from experimental data. UFs are intended to account for (1) the variation in
sensitivity among the members of the human population, (2) the uncertainty in
extrapolating animal data to the case of human, (3) the uncertainty in
extrapolating from data obtained in a study that is of less than lifetime
exposure, and (4) the uncertainty in using LOAEL data rather than NOAEL data.
Usually each of these factors is set equal to 10.
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135
9. GLOSSARY
Units, Radiological --
UniCs
Equivalents
Becquerel*
Curie
Gray*
Rad
Rem
Sievert*
1 Bq -1 disintegration per second - 2.7xlO~n Ci
1 Ci - 3.7xl010 disintegrations per second - 3.7xl010 Bq
1 Gy - 1 J/kg - 100 rad
1 Rad - 100 erg/g - 0.01 Gy
1 Rem - 0.01 Sievert
1 Sv - 100 rem
¦^International Units are designated (SI) .
Working Level (WL) -- Any combination of short-lived radon daughters in 1
liter of air that will result in the ultimate emission of 1.3x10s MeV of
potential alpha energy.
Working Level Month (WLM) -- Inhalation of air with a concentration of 1 WL of
radon daughters for 170 working hours results in an exposure of 1 WLM.
X-rays -- Penetrating electromagnetic radiations whose wave lengths are
shorter than those of visible light. They are usually produced by bombarding
a metallic target with fast electrons in a high vacuum. In nuclear reaction,
it is customary to refer to photons originating in the extranuclear part of
the atom as X-rays. These rays are sometimes called roentgen rays after their
discoverer, W.C. Roentgen.
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137
APPENDIX A
PEER REVIEW
A peer review panel was assembled for radon. The panel consisted of the
following members: Dr. Victor E. Archer, University of Utah Medical Center;
Dr. Douglas J. Crawford-Brown, University of North Carolina; Dr. Richard
Gerstle, private consultant; and Dr. John Spengler, Harvard School of Public
Health. These experts collectively have knowledge of radon's physical and
chemical properties, toxicokinetics, key health end points, mechanisms of
action, human and animal exposure, and quantification of risk to humans. All
reviewers were selected in conformity with the conditions for peer review
specified in the Section 104(i)(13) of the Comprehensive Environmental
Response, Compensation, and Liability Act, as amended.
A joint panel of scientists from ATSDR and EPA has reviewed the peer
reviewers' comments and determined which comments will be included in the
profile. A listing of the peer reviewers' comments not incorporated in the
profile, with a brief explanation of the rationale for their exclusion, exists
as part of the administrative record for this compound. A list of databases
reviewed and a list of unpublished documents cited are also included in the
administrative record.
The citation of the peer review panel should not be understood to imply
its approval of the profile's final content. The responsibility for the
content of this profile lies with the Agency for Toxic Substances and Disease
Registry.
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139
APPENDIX B
OVERVIEW OF BASIC RADIATION PHYSICS, CHEMISTRY AND BIOLOGY
Understanding che basic concepts in radiation physics, chemistry, and
biology is important to the evaluation and interpretation of radiation-
induced adverse health effects and to the derivation of radiation
protection principles. This appendix presents a brief overview of the
areas of radiation physics, chemistry, and biology and is based to a large
extent on the reviews of Mettler and Moseley (1985), Hobbs and McClellan
(1986), Eichholz (1982), Hendee (1973), and Early et al. (1979).
B.l RADIONUCLIDES AND RADIOACTIVITY
The substances we call elements are composed of atoms. Atoms in turn
are made up of neutrons, protons, and electrons; neutrons and protons in
the nucleus and electrons in a cloud of orbits around the nucleus.
Nuclide is the general term referring to any nucleus along with its
orbital electrons. The nuclide is characterized by the composition of its
nucleus and hence by the number of protons and neutrons in the nucleus.
All atoms of an element have the same number of protons (this is given by
the atomic number) but may have different numbers of neutrons (this is
reflected by the atomic mass or atomic weight of the element). Atoms with
different atomic mass but the same atomic numbers are referred to as
isotopes of an element.
The numerical combination of protons and neutrons in most nuclides is
such that the atom is said to be stable; however, if there are too few or
too many neutrons, the nucleus of the atom is unstable. Unstable nuclides
undergo a process referred to as radioactive transformation in which
energy is emitted. These unstable atoms are called radionuclides; their
emissions are called ionizing radiation; and the whole property is called
radioactivity. Transformation or decay results in the formation of new
nuclides some of which may themselves be radionuclides, while others are
stable nuclides. This series of transformations is called the decay chain
of the radionuclide. The first radionuclide in the chain is called the
parent; the subsequent products of the transformation are called progeny,
daughters, or decay products.
In general there are two classifications of radioactivity and
radionuclides: natural and man-made. Naturally-occurring radionuclides
exist in nature and no additional energy is necessary to place them in an
unstable state. Natural radioactivity is the property of some naturally
occurring, usually heavy elements, that are heavier than lead.
Radionuclides, such as radium and uranium, primarily emit alpha particles.
Some lighter elements such as carbon-14 and tritium (hydrogen-3) primarily
emit beta particles as they transform to a more stable atom. Natural
radioactive atoms heavier than lead cannot attain a stable nucleus heavier
than lead. Everyone is exposed to background radiation from naturally-
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140
APPENDIX B
occurring radionuclides throughout life. This background radiation is the
major source of radiation exposure to man and arises from several sources.
The natural background exposures are frequently used as a standard of
comparison for exposures to various man-made sources of ionizing
radiation.
Man-made radioactive atoms are produced either as a by-product of
fission of uranium atoms in a nuclear reactor or by bombarding stable
atoms with particles, such as neutrons, directed at the stable atoms with
high velocity. These artificially produced radioactive elements usually
decay by emission of particles, such as positive or negative beta
particles and one or more high energy photons (gamma rays). Unstable
(radioactive) atoms of any element can be produced.
Both naturally occurring and man-made radioisotopes find application
in medicine, industrial products, and consumer products. Some specific
radioisotopes, called fall-out, are still found in the environment as a
result of nuclear weapons use or testing.
B.2 RADIOACTIVE DECAY
B.2.1 Principles of Radioactive Decay
The stability of an atom is the result of the balance of the forces of
the various components of the nucleus. An atom that is unstable
(radionuclide) will release energy (decay) in various ways and transform
to stable atoms or to other radioactive species called daughters, often
with the release of ionizing radiation. If there are either too many or
too few neutrons for a given number of protons, the resulting nucleus may
undergo transformation. For some elements, a chain of daughter decay
products may be produced until stable atoms are formed. Radionuclides can
be characterized by the type and energy of the radiation emitted, the rate
of decay, and the mode of decay. The mode of decay indicates how a parent
compound undergoes transformation. Radiations considered here are
primarily of nuclear origin, i.e., they arise from nuclear excitation
usually caused by the capture of charged or uncharged nucleons by a
nucleus, or by the radioactive decay or transformation of an unstable
nuclide. The type of radiation may be categorized as charged or uncharged
particles (electrons, neutrons, neutrinos, alpha particles, beta
particles, protons, and fission products) or electromagnetic radiation
(gamma rays and X-rays). Table B-l summarizes the basic characteristics
of the more common types of radiation encountered.
B.2.2 Half-Life and Activity
For any given radionuclide, the rate of decay is a first-order process
that depends on the number of radioactive atoms present and is
characteristic for each radionuclide. The process of decay is a series of
random events; temperature, pressure, or chemical combinations do not
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141
APPENDIX B
TABLE B~l. Characteristics of Nuclear Radiations
Radiation
Rest Mass
Charge
Typical
Energy Range
Path Length
(Order of Magnitude)
Air Solid
General Comments
(negatron)
4 .00 amu
5.48x10'* amu
0.51 MeV
Positron 5.48xl0~4 amu
(B positive) 0.51 MeV
Proton
938.26 MeV
1.0073 amu
2+ 4-10 MeV
0-4 MeV
5-10 cm 25-40 |im
0-1 m 0-1 cm
0-1 m
0-1 era
Identical to ionized He
nucleus
Identical to electron
Identical to electron
except for charge
Neutron
1.0036 amu
939.55 MeV
0-15 MeV
0-100 m 0-100 cm Free half life: 16 min
(e.m. photon)
(e.m. photon)
eV-100 keV
0.1-10 m* 0-1 m*
10 KeV-3 MeV 0.1-10 m* 1 nm-1 m
Photons from electron
transitions
Photons from nuclear
transitions
'Exponential attenuation in the case of electromagnetic radiation.
a » alpha
8 - beta
X - X-ray
Y* gamma
amu " atomic mass unit
MeV - Mega electron volts
KeV - Kiloelectron volts
cm " centimeter
m " meter
lim ¦ micrometer
nm " millimeter
e.m. " electromagnetic
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142
APPENDIX B
effect the rate of decay. While it may not be possible to predict exactly
which atom is going to undergo transformation at any given time, it is
possible to predict, on the average, how many atoms will transform during any
interval of time.
The source strength is a measure of the rate of emission of radiation.
For these radioactive materials it is customary to describe the source
strength in terms of the source activity, which is defined as the number of
disintegrations (transformations) per unit time occurring in a given quantity
of this material. The unit of activity is the curie (Ci) which was originally
related to the activity of one gram of radium, but is now defined as:
1 curie (Ci) - 3.7xl010 disintegrations (transformations)/second (dps) or
2.22xl012 disintegrations (transformations)/minute (dpm).
The SI unit of activity is the becquerel (Bq); 1 Bq - 1 transformation/second.
Since activity is proportional to the number of atoms of the radioactive
material, the quantity of any radioactive material is usually expressed in
curies, regardless of its purity or concentration. The transformation of
radioactive nuclei is a random process, and the rate of transformation is
directly proportional to the number of radioactive atoms present. For any
pure radioactive substance, the rate of decay is usually described by its
radiological half-life, TR, i.e., the time it takes for a specified source
material to decay to half its initial activity.
The activity of a radionuclide at time t may be calculated by:
A - A p-0.693t/T
rad
where A is the activity in dps, A0 is the activity at time zero, t is the time
at which measured, and Trad is the radiological half-life of the radionuclide.
It is apparent that activity exponentially decays with time. The time when
the activity of a sample of radioactivity becomes one-half its original value
is the radioactive half-life and is expressed in any suitable unit of time.
The specific activity is the radioactivity per unit weight of material.
This activity is usually expressed in curies per gram and may be calculated by
curies/gram - 1.3xl08/(^rad)(atomic weight)
where Tiad is the radiological half-life in days.
In the case of radioactive materials contained in living organisms, an
additional consideration is made for the reduction in observed activity due to
regular processes of elimination of the respective chemical or biochemical
substance from the organism. This introduces a rate constant called the
biological half-life (Tblol) which is the time required for biological
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143
APPENDIX B
processes to eliminate one-half of the activity. This time is virtually the
same for both stable and radioactive isotopes of any given element.
Under such conditions the time required for a radioactive element to be
halved as a result of the combined action of radioactive decay and biological
elimination is the effective half-life:
Teff ~ (TmoL ^ "^"rad)/("^biol ^*rad) •
Table B-2 presents representative effective half-lives of particular interest.
B.2.3 Interaction of Radiation with Matter
Both ionizing and nonionizing radiation will interact with materials,
that is, it will lose kinetic energy to any solid, liquid or gas through which
it passes by a variety of mechanisms. The transfer of energy to a medium by
either electromagnetic or particulate radiation may be sufficient to cause
formation of ions. This process is called ionization. Compared to other
types of radiation that may be absorbed, such as ultraviolet radiation,
ionizing radiation deposits a relatively large amount of energy Into a small
volume.
The method by which incident radiation interacts with the medium to cause
ionization may be direct or indirect. Electromagnetic radiations (X-rays and
gamma photons) are indirectly ionizing; that is, they give up their energy in
various interactions with cellular molecules, and the energy is then utilized
to produce a fast-moving charged particle such as an electron. It is the
electron that then secondarily may react with a target molecule. Charged
particles, in contrast, strike the tissue or medium and directly react with
target molecules, such as oxygen or water. These particulate radiations are
directly ionizing radiations. Examples of directly ionizing particles include
alpha and beta particles. Indirectly ionizing radiations are always more
penetrating than directly ionizing particulate radiations.
Mass, charge, and velocity of a particle all affect the rate at which
ionization occurs. The higher the charge of the particle and the lower the
velocity, the greater the propensity to cause ionization. Heavy, highly
charged particles, such as alpha particles, lose energy rapidly with distance
and, therefore, do not penetrate deeply. The result of these interaction
processes is a gradual slowing down of any incident particle until it Is
brought to rest or "stopped" at the end of its range.
B.2.4 Characteristics of Emitted Radiation
B.2.4.1 Alpha Emission. In alpha emission, an alpha particle consisting
of two protons and two neutrons Is emitted with a resulting decrease in the
atomic mass number by four and reduction of the atomic number by two, thereby
changing the parent to a different element. The alpha particle is identical
-------
144
APPENDIX B
TABLE B-2 Half-Lives of Some Radionuclides in Adult Body Organs
Half-Life"
Crit^al Orean
Physical
Biological
Effective
RaHlnnuclide
Hydrogen-3b
Whole body
12.3 y
12 d
11.97d
(Tritium)
Iodine-131
Thyroid
8 d
138 d
7.6 d
Strontium-90
Bone
28 y
50 y
18 y
Plutonium-239
Bone
24,400 y
200 y
198 y
Lung
24,400 y
500 d
500 d
Cobalt-60
Whole body
5.3 y
99.5 d
9.5 d
Iron-55
Spleen
2.7 y
600 d
388 d
Iron-59
Spleen
45.1 d
600 d
41.9 d
Manganese-54
Liver
303 d
25 d
23 d
Cesium-137
Whole body
30 y
70 d
70 d
®d - days, y - years.
bMixed in body water as tritiated water.
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145
APPENDIX B
to a helium nucleus consisting of two neutrons and two protons. It results
from the radioactive decay of some heavy elements such as uranium, plutonium,
radium, thorium, and radon. Alpha particles have a large mass as compared to
electrons. Decay of alpha-emitting radionuclides may result in the emission
of several different alpha particles. A radionuclide has an alpha emission
with a discrete alpha energy and characteristic pattern of alpha energy
emitted.
The alpha particle has an electrical charge of +2. Because of this
double positive charge, alpha particles have great ionizing power, but their
large size results in very little penetrating power. In fact, an alpha
particle cannot penetrate a sheet of paper. The range of an alpha particle,
that is, the distance the charged particle travels from the point of origin to
its resting point, is about 4 cm in air, which decreases considerably to a few
micrometers in tissue. These properties cause alpha emitters to be hazardous
only if there is internal contamination (i.e., if the radionuclide is
ingested, inhaled, or otherwise absorbed).
B.2.4.2. Beta Emission. Nuclei which are excessively neutron rich decay
by S-decay. A beta particle (S) is a high-velocity electron ejected from a
disintegrating nucleus. The particle may be either a negatively charged
electron, termed a negatron (fi-) or a positively charged electron, termed a
positron (6+). Although the precise definition of "beta emission" refers to
both S- and £+, common usage of the term generally applies only to the
negative particle, as distinguished from the positron emission, which refers
to the £+ particle.
B.2.4.2.1 Beta Negative Emission. Beta particle (&-) emission is
another process by which a radionuclide, usually those with a neutron excess,
achieves stability. Beta particle emission decreases the number of neutrons
by one and increases the number of protons by one, while the atomic mass
remains unchanged. This transformation results in the formation of a
different element. The energy spectrum of beta particle emission ranges from
a certain maximum down to zero with the mean energy of the spectrum being
about one-third of the maximum. The range in tissue is much less. Beta
negative emitting radionuclides can cause injury to the skin and superficial
body tissues but mostly present an internal contamination hazard.
B.2.4.2.2 Positron Emission. In cases in which there are too many
protons in the nucleus, positron emission may occur. In this case a proton
may be thought of as being converted into a neutron, and a positron (6+) is
emitted, accompanied by a neutrino (see glossary). This increases the number
of neutrons by one, decreases the number of protons by one, and again leaves
the atomic mass unchanged. The gamma radiation resulting from the
annihilation (see glossary) of the positron makes all positron emitting
isotopes more of an external radiation hazard than pure 6 emitters of equal
energy.
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146
APPENDIX B
09123 Gamma Emission. Radioactive decay by alpha, beta positron
• caoture often leaves some of the energy resulting from
emission or electron capture ot^ ^ ^ .fi raised to an
these changes inN of theSe excited nuclei can remain in this high-energy
sSte Nuclei release this energy returning to ground state or to the lowest
cihle stable energy level. The energy released is m the form of ganuna
Hnfhieh energy photons) and has an energy equal to the change in the
radiation ( g nucleus Gamma and X-rays behave similarly but differ in
energy state of the nucleus while X-rays originate
their origin; gamma emissions originate
in the orbital electron structure.
B.3 ESTIMATION OF ENERGY DEPOSITION IN HUMAN TISSUES
Two forms of potential radiation exposures can result - - Jnternai and
r.rnal The term exposure denotes physical interaction of the radiation
^Sd from the radioactive material with cells and tissues of the human
bodv An exposure can be "acute" or "chronic" depending on how long an
body• An exp . r the radiation. Internal exposures occur
individual or h have entered the body (e.g., through the inhalation,
*ges"oi"nor derail pathways) . undergo radioactive decay renting in the
ingestion, 01 r , oreans External exposures occur when
body directly from sources Located outside the body, such
as radiation emitters from radionuclides on ground surfaces. dissolved in
later or dispersed In the air. In general, external exposures are from
^t^ial emitting gamma radiation, which readily penetrate the skin and
internal organs. Beta and alpha radiation l-
Consequently? their contribution tftL .bsorLd dose of the total Wy dose,
compared to that deposited by gamma rays, may be negligibl .
Characterizing the radiation dose to persons as a result of exposure to
radiation is a e0mgplex issue. It is difficult to: (1) measure internally the
:!t Qf enerEV actually transferred to an organic material and to correlate
any observed effects with this energy deposition, and (2) account for and
predict secondary processes, such as collision effects or biologica y
triggered effects, that are an indirect consequence of the primary interaction
event.
B.3.1 Dose Units
8 3 11 Roentgen. The roentgen (R) is a unit of exposure related to the
amount' of ionization caused in air by gamma or x-radiation. One roentgen
^uals 2 58xl0~4 Coulomb per kilogram of air. In the case of gamma radiation,
over the'commonly encountered range of photon energy, the energy deposition in
tissue for a dose of 1 R is about 0.0096 joules(J)/kg of tissue.
» 0 1 ? Absorbed Dose and Absorbed Dose Rate. Since different types of
radiation interact differently with any material through which they pass, any
-------
147
APPENDIX B
attempt to assess their effect on humans or animals should take into account
these differences. The absorbed dose is defined as the energy imparted by the
incident radiation to a unit mass of the tissue or organ. The unit of
absorbed dose is the rad; 1 rad - 100 erg/gram - 0.01 J/kg in any medium. The
SI unit is the gray which is equivalent to 100 rad or 1 J/kg. Internal and
external exposures from radiation sources are not usually instantaneous but
are distributed over extended periods of time. The resulting rate of change
of the absorbed dose to a small volume of mass is referred to as the absorbed
dose rate in units of rad/unit time.
B.3.1.3 Working Levels and Working Level Months. Working levels are
units that have been used to describe the radon decay-product activities in
air in terms of potential alpha energy. It is defined as any combination of
short-lived radon daughters (through polonium-214) per liter of air that will
result in the emission of 1.3xl05 MeV of alpha energy. An activity
concentration of 100 pCi radon-222/L of air, in equilibrium with its
daughters, corresponds approximately to a potential alpha-energy concentration
of 1 WL. The WL unit can also be used for thoron daughters. In this case,
1.3xl05 MeV of alpha energy (1 WL) is released by the thoron daughters in
equilibrium with 7.5 pCi thoron/L. The potential alpha energy exposure of
miners is commonly expressed in the unit Working Level Month (WLM). One WLM
corresponds to exposure to a concentration of 1 WL for the reference period of
170 hours.
B.3.2 Dosimetry Models
Dosimetry models are used to estimate the internally deposited dose from
exposure to radioactive substances. The models for internal dosimetry
consider the quantity of radionuclides entering the body, the factors
affecting their movement or transport through the body, distribution and
retention of radionuclides in the body, and the energy deposited in organs and
tissues from the radiation that is emitted during spontaneous decay processes.
The models for external dosimetry consider only the photon doses to organs of
individuals who are immersed in air or are exposed to a contaminated ground
surface. The dose pattern for radioactive materials in the body may be
strongly influenced by the route of entry of the material. For industrial
workers, inhalation of radioactive particles with pulmonary deposition and
puncture wounds with subcutaneous deposition have been the most frequent. The
general population has been exposed via ingestion and inhalation of low levels
of naturally occurring radionuclides as well as man-produced radionuclides
from nuclear weapons testing.
B.3.2.1 Ingestion. Ingestion of radioactive materials is most likely to
occur from contaminated foodstuffs or water or eventual ingestion of inhaled
compounds initially deposited in the lung. Ingestion of radioactive material
may result in toxic effects as a result of either absorption of the
radionuclide or irradiation of the gastrointestinal tract during passage
through the tract, or a combination of both. The fraction of a radioactive
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148
APPENDIX B
material absorbed from the gastrointestinal tract is variable, depending on
the specific element, the physical and chemical form of the material ingested
and the diet, as well as some other metabolic and physiological factors The'
absorption of some elements is influenced by age usually with higher
absorption in the very young.
B.3.2.2 Inhalation. The inhalation route of exposure has long been
recognized as being of major importance for both nonradioactive and
radioactive materials. The deposition of particles within the lung is largely
dependent upon the size of the particles being inhaled. After the particle is
deposited, the retention will depend upon the physical and chemical properties
of the dust and the physiological status of the lung. The retention of the
particle in the lung depends on the location of deposition, in addition to the
physical and chemical properties of the particles. The converse of pulmonary
retention is pulmonary clearance. There are three distinct mechanisms of
clearance which operate simultaneously. Ciliary clearance acts only in the
upper respiratory tract. The second and third mechanisms act mainly in the
deep respiratory tract. These are phagocytosis and absorption. Phagocytosis
is the engulfing of foreign bodies by alveolar macrophages and their
subsequent removal either up the ciliary "escalator" or by entrance into the
lymphatic system. Some inhaled soluble particulates are absorbed into the
blood and translocated to other organs and tissues. Dosimetric lung models
are reviewed by James (1987) and James and Roy (1987).
B.3.3 Internal Emitters
The absorbed dose from internally deposited radioisotopes is the energy
absorbed by the surrounding tissue. For a radioisotope distributed uniformly
throughout an infinitely large medium, the concentration of absorbed energy
must be equal to the concentration of energy emitted by the isotope. An
infinitely large medium may be approximated by a tissue mass whose dimensions
exceed the range of the particle. All alpha and most beta radiation will be
absorbed in the organ (or tissue) of reference. Gamma-emitting isotope
emissions are penetrating radiation and a substantial fraction may travel
great distances within tissue, leaving the tissue without interacting. The
dose to an organ or tissue is a function of the effective retention half-time
the energy released in the tissue, the amount of radioactivity initially '
introduced, and the mass of the organ or tissue.
B.4 BIOLOGICAL EFFECTS OF RADIATION
When biological material is exposed to ionizing radiation, a chain of
cellular events occurs as the ionizing particle passes through the biological
material. A number of theories have been proposed to describe the interactio
of radiation with biologically important molecules in cells and to explain the
resulting damage to biological systems from those interactions. Many factors
may modify the response of a living organism to a given dose of radiation
Factors related to the exposure include the dose rate, the energy of the
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149
APPENDIX B
radiation, and the temporal pattern of the exposure. Biological
considerations include factors such as species, age, sex, and the portion of
the body exposed. Several excellent reviews of the biological effects of
radiation have been published, and the reader is referred to these for a more
in-depth discussion (Hobbs and McClellan 1986; ICRP 1984; Mettler and Moseley
1985; Rubin and Casarett 1968).
B.4.1 Radiation Effects at the Cellular Level
According to Mettler and Moseley (1985), at acute doses up to 10 rad (100
mGy), single strand breaks in DNA may be produced. These single strand breaks
may be repaired rapidly. With doses in the range of 50 to 500 rad (0.5 to 5
Gy), irreparable double-stranded DNA breaks are likely, resulting in cellular
reproductive death after one or more divisions of the irradiated parent cell.
At large doses of radiation, usually greater than 500 rad (5 Gy), direct cell
death before division (interphase death) may occur from the direct interaction
of free-radicals with essentially cellular macromolecules. Morphological
changes at the cellular level, the severity of which are dose-dependent, may
also be observed.
The sensitivity of various cell types varies. According to the Bergoni6-
Tribondeau law, the sensitivity of cell lines is directly proportional to
their mitotic rate and inversely proportional to the degree of differentiation
(Mettler and Moseley 1985). Rubin and Casarett (1968) devised a
classification system that categorized cells according to type, function, and
mitotic activity. The categories range from the most sensitive type,
"vegetative intermitotic cells," found in the stem cells of the bone marrow
and the gastrointestinal tract, to the least sensitive cell type, "fixed
postmitotic cells," found in striated muscles or long-lived neural tissues.
Cellular changes may result in cell death, which if extensive, may
produce irreversible damage to an organ or tissue or may result in the death
of the individual. If the cell recovers, altered metabolism and function may
still occur, which may be repaired or may result in the manifestation of
clinical symptoms. These changes may also be expressed at a later time as
tumors or mutations.
B.4.2 Radiation Effects at the Organ Level
In most organs and tissues the injury and the underlying mechanism for
that injury are complex and may involve a combination of events. The extent
and severity of this tissue injury are dependent upon the radiosensitivity of
the various cell types in that organ system. Rubin and Casarett (1968)
describe and schematically display the events following radiation in several
organ system types. These include: a rapid renewal system, such as the
gastrointestinal mucosa; a slow renewal system, such as the pulmonary
epithelium; and a nonrenewal system, such as neural or muscle tissue. In the
rapid renewal system, organ injury results from the direct destruction of
highly radiosensitive cells, such as the stem cells in the bone marrow.
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150
APPENDIX B
Iniury may also result from constriction of the microcirculation and from
edema and inflammation of the basement membrane (designated as the
histohematic barrier - HHB) , which may progress to fibrosis. In slow renewal
and nonrenewal systems, the radiation may have little effect on the
parenchymal cells, but ultimate parenchymal atrophy and death over several
months result from HHB fibrosis and occlusion of the microcirculation.
B.4.3 Acute and Chronic Somatic Effects
B.4.3.1 Acute Effects. The result of acute exposure to radiation is
commonly referred to as acute radiation syndrome. This effect is seen only
after exposures to relatively high doses (>50 rad), which would only be
expected to occur in the event of a serious nuclear accident. The four stages
of acute radiation syndrome are prodrome, latent stage, manifest illness
staee recovery or death. The initial phase is characterized by nausea,
vomiting malaise and fatigue, increased temperature, and blood changes. The
latent stage is similar to an incubation period. Subjective symptoms may
subside, but changes may be taking place within the blood-forming organs and
elsewhere which will subsequently give rise to the next stage.^ The manifest
illness stage gives rise to symptoms specifically associated with the
radiation injury. Among these symptoms are hair loss, fever, infection,
hemorrhage, severe diarrhea, prostration, disorientation, and cardiovascular
collapse. The symptoms and their severity depend upon the radiation dose
received.
B 4 3.2 Delayed Effects. The level of exposure to radioactive
pollutants that may be encountered in the environment is expected to be too
low to result in the acute effects described above. When one is exposed to
radiation in the environment, the amount of radiation absorbed is more likely
to produce long-term effects, which manifest themselves years after the
original exposure, and may be due to a single large over-exposure or
continuing low-level exposure.
Sufficient evidence exists in both human populations and laboratory
animals to establish that radiation can cause cancer and that the incidence of
cancer increases with increasing radiation dose. Human data are extensive and
include epidemiological studies of atomic bomb survivors, many types of
radiation-treated patients, underground miners, and radium dial painters.
Reports on the survivors of the atomic bomb explosions at Hiroshima and
Nagasaki Japan (with whole-body external radiation doses of 0 to more than
200 rad)'indicate that cancer mortality has increased (Kato and Schull 1982).
Use of X-rays (at doses of approximately 100 rad) in medical treatment for
ankylosing spondylitis or other benign conditions or diagnostic purposes, such
as breast conditions, has resulted in excess cancers in irradiated organs
CRT7TR 1980 1990: UNSCEAR 1977, 1988). Cancers, such as leukemia, have been
observed in children exposed in utero to doses of 0.2 to 20 rad (BEIR, 1980,
1990- UNSCEAR 1977, 1988). Medical use of Thorotrast (colloidal thorium
dioxide) resulted in increases in the incidence of cancers of the liver, bone,
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APPENDIX B
and lung (ATSDR 1990a; BEIR 1980, 1990; UNSCEAR 1977, 1988). Occupational
exposure to radiation provides further evidence of the ability of radiation to
cause cancer. Numerous studies of underground miners exposed to radon and
radon daughters, which are alpha emitters, in uranium and other hard rock
mines have demonstrated increases in lung cancer in exposed workers (ATSDR
1990b). Workers who ingested radium-226 while painting watch dials had an
increased incidence of leukemia and bone cancer (ATSDR 1990c). These studies
indicate that depending on radiation dose and the exposure schedule, ionizing
radiation can induce cancer in nearly any tissue or organ in the body.
Radiation-induced cancers in humans are found to occur in the hemopoietic
system, the lung, the thyroid, the liver, the bone, the skin, and other
tissues.
Laboratory animal data indicate that ionizing radiation is carcinogenic
and mutagenic at relatively high doses usually delivered at high dose rates.
However, due to the uncertainty regarding the shape of the dose-response
curve, especially at low doses, the commonly held conservative position is
that the cancer may occur at dose rates that extend down to doses that could
be received from environmental exposures. Estimates of cancer risk are based
on the absorbed dose of radiation in an organ or tissue. The cancer risk at a
particular dose is the same regardless of the source of the radiation. A
comprehensive discussion of radiation-induced cancer is found in BEIR IV
(1988), BEIR V (1990), and UNSCEAR (1982, 1988).
B.4.4 Genetic Effects
Radiation can induce genetic damage, such as gene mutations or
chromosomal aberrations, by causing changes in the structure, number, or
genetic content of chromosomes in the nucleus. The evidence for the
mutagenicity of radiation is derived from studies in laboratory animals,
mostly mice (BEIR 1980, 1988, 1990; UNSCEAR 1982, 1986, 1988). Evidence for
genetic effects in humans is derived from tissue cultures of human lymphocytes
from persons exposed to ingested or inhaled radionuclides (ATSDR 1990c,
1990d). Evidence for mutagenesis in human germ cells (cells of the ovaries or
testis) is not conclusive (BEIR 1980, 1988, 1990; UNSCEAR 1977, 1986, 1988).
Chromosome aberrations following radiation exposure have been demonstrated in
man andn in experimental animals (BEIR 1980, 1988, 1990; UNSCEAR 1982, 1986,
1988).
B.4.5 Teratogenic Effects
There is evidence that radiation produces teratogenicity in animals. It
appears that the developing fetus is more sensitive to radiation than the
mother and is most sensitive to radiation-induced damage during the early
stages of organ development. The type of malformation depends on the stage of
development and the cells that are undergoing the most rapid differentiation
at the time. Studies of mental retardation in children exposed in utero to
radiation from the atomic bomb provide evidence that radiation may produce
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152
APPENDIX B
teratogenic effects in human fetuses (Otake and Schull 1984). The damage to
the child was found to be related to the dose that the fetus received.
B.5 UNITS IN RADIATION PROTECTION AND REGULATION
B.5.1 Dose Equivalent and Dose Equivalent Rate. Dose equivalent or rem
is a special radiation protection quantity that is used to express the
absorbed dose in a manner which considers the difference in biological
effectiveness of various kinds of ionizing radiation. The ICRU has defined
the dose equivalent, H, as the product of the absorbed dose, D, the quality
factor, Q, and all other modifying factors, N, at the point of interest in
biological tissue. This relationship is expressed as follows:
H - D x Q x N.
The quality factor is a diraensionless quantity that depends in part on the
stopping power for charged particles, and it accounts for the differences in
biological effectiveness found among the types of radiation. By definition it
is independent of tissue and biological end point and, therefore, of little
use in risk assessment now. Originally Relative Biolotical Effectiveness
(RBE) was used rather than Q to define the quantity, rem, which was of use in
risk assessment. The generally accepted values for quality factors for
various radiation types are provided in Table B-3. The dose equivalent rate
is the time rate of change of the dose equivalent to organs and tissues and is
expressed as rem/unit time or sievert/unit time.
B.5.2 Relative Biological Effectiveness. The term relative biologic
effectiveness (RBE) is used to denote the experimentally determined ratio of
the absorbed dose from one radiation type to the absorbed dose of a reference
radiation required to produce an identical biologic effect under the same
conditions. Gamma rays from cobalt-60 and 200 to 250 KeV X-rays have been
used as reference standards. The term RBE has been widely used in
experimental radiobiology, and the term quality factor used in calculations of
dose equivalents for radiation protection purposes (ICRP 1977; NCRP 1971;
UNSCEAR 1982) . The generally accepted values for RBE are provided in Table
B-4.
B.5.3 Effective Dose Equivalent and Effective Dose Equivalent Rate. The
absorbed dose is usually defined as the mean absorbed dose within an organ or
tissue. This represents a simplification of the actual problem. Normally
when an individual ingests or inhales a radionuclide or is exposed to external
radiation that enters the body (gamma), the dose is not uniform throughout the
whole body. The simplifying assumption is that the detriment will be the same
whether the body is uniformly or nonuniformly irradiated. In an attempt to
compare detriment from absorbed dose of a limited portion of the body with the
detriment from total body dose, the ICRP (1977) has derived a concept of
effective dose equivalent.
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153
APPENDIX B
TABLE B-3. Quality Factors (QF)
1. X-rays, electrons, and. positrons of any specific ionization
QF - 1.
2. Heavy ionizing particles
Average LET in Water
(MeV/cm^ QF.
35 or less 1
35 to 70 1 to 2
70 to 230 2 to 5
230 to 530 5 to 10
530 to 1750 10 to 20
For practical purposes, a QF of 10 is often used for alpha particles® and
fast neutrons and protons up to 10 MeV. A QF of 20 is used for heavy
recoil nuclei.
"The ICRP (1977) recommended a quality factor of 20 for alpha particles.
LET - Linear energy transfer
MeV/cm - Megaelectron volts per centimeter
MeV - Megaelectron volts
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154
APPENDIX B
TABLE B-4. Representative LET and RBE Values*
Radiation
Energy
fMeV)
Av. LET
(keV/u)
RBE
Quality
Factor
X-rays, 200 kVp
0.01-0.2
3.0
1.00
1
Gamma rays
1.25
0.3
0.7
1
4
0.3
0.6
1
Electrons (15)
0.1
0.42
1.0
1
0.6
0.3
1.3
1
1.0
0.25
1.4
_ _
Protons
0.1
90.0
6
2.0
16.0
2
10
5.0
8.0
2
10
Alpha particle
0.1
260.0
5.0
95.0
10-20
10
Heavy ions
10-30
-150.0
-25
20
Neutrons
thermal
4-5
3
1.0
20.0
2-10
10
*These values are general and approximate. RBE and QF values vary widely with
different measures of biological injury.
MeV - Megaelectron volts
KeV/ji - Kiloelectron volts per micron
RBE - Relative biological effectiveness
kVp - Kilovolt potential
LET - Linear energy transfer
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155
APPENDIX B
The effective dose equivalent, HE, is
He - (the sum of) Wt Ht
where Ht is the dose equivalent in the tissue, Wt is the weighting factor,
which represents the estimated proportion of the stochastic risk resulting
from tissue, T, to the stochastic risk when the whole body is uniformly
irradiated for occupational exposures under certain conditions (ICRP 1977).
Weighting factors for selected tissues are listed in Table B-5.
The ICRU (1980), ICRP (1984), and NCRP (1985) now recommend that the rad,
roentgen, curie and rem be replaced by the SI units: gray (Gy), Coulomb per
kilogram (C/kg), becquerel (Bq), and sievert (Sv), respectively. The
relationship between the customary units and the international system of units
(SI) for radiological quantities is shown in Table B-6.
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156
APPENDIX B
TABLE B-5. Weighting Factors for Calculating
Effective Dose Equivalent for Selected Tissues
Tissue
Gonads
Breast
Red bone marrow
Lung
Thyroid
Bone surface
Remainder
Weighting Factor
0.25
0.15
0.12
0.12
0.03
0.03
0.30
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157
APPENDIX B
TABLE B-6. Comparison of Common and SI Units
for Radiation Quantities
Quantity
Customary
Units
Definition
SI Units Definition
Activity (A)
Absorbed Dose (D)
Absorbed Dose
Rate (D)
Dose Equivalent
(H)
Dose Equivalent
Rate (H)
Linear Energy
Transfer (L.)
Curie (Ci)
rad per
second
(rad s"1)
rem (rem)
rem per
second
(rem s"1)
kiloelectron
volts per
micrometer
3. 7xl010
transforma-
tions s"1
rad (rad)
10"2Jkg"1s"1
10~2Jkg~
10~2Jkg *s 1
becquerel
(Bq)
= -i
10"2Jkg_1 gray (Gy)Jkg
-l
gray per
second
(Gy s"1)
Jkg xs
lo-l
-1
(keVuM"1)
sievert (Sv) Jkg
sievert per Jkg"1s"1
second
(Sv s"1)
1. 6O2xlO~10Jm~1 kiloelectron 1. 602xlO-10Jnf1
volts per
micrometer
(keVjim"1)
S"1 — per second
Jkg"1 - Joules per kilogram
Jkg'1s'1 - Joules per kilogram per second
Jnf1 - Joules per meter
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158
APPENDIX B
References
ATSDR 1990a Toxicological profile for thorium. U.S. Department of Health
and Human Services. Public Health Service. Agency for Toxic Substances and
Disease Registry. Atlanta, GA.
ATSDR 1990b Toxicological profile for radium. U.S. Department of Health
and Human Services. Public Health Service. Agency for Toxic Substances and
Disease Registry. Atlanta, GA.
ATSDR 1990c Toxicological profile for radon. U.S. Department of Health
and Human Services. Public Health Service. Agency for Toxic Substances and
Disease Registry. Atlanta, GA.
ATSDR 1990d Toxicological profile for uranium. U.S. Department of Health
and Human Services. Public Health Service. Agency for Toxic Substances and
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