TOXICOLOGICAL PROFILE FOR
 

THORIUM
 

Agency for Toxic Substances and Disease Registry
 

U.S. Public Health Service
 

In collaboration with:
 

U.S. Environmental Protection Agency
 

October 1990
 
ii
 

DISCLAIMER
 

The use of company or product name(s) is for identification only and
 

does not imply endorsement by the Agency for Toxic Substances and Disease
 

Registry.
 










1
 

1. PUBLIC HEALTH STATEMENT
 

The purpose of this statement is to provide you with information about
 

thorium and to emphasize the human health effects that may result from
 

exposure. At this time, thorium has been found at above background levels
 

at 16 out of 1177 National Priorities List (NPL) hazardous waste sites. We
 

do not know how many of the 1177 NPL sites have been evaluated for thorium.
 

As EPA evaluates more sites, the number of sites at which thorium is found
 

at above background levels may change. Because these sites are potential or
 

actual sources of human exposure to thorium and because thorium may cause
 

harmful health effects, this information is important for you to know.
 

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 emission. This emission, which is
 

also called a release, does not always lead to exposure. You are exposed
 

only when you come into contact with the radioactive chemical. You can come
 

into contact with it in the environment through breathing air, eating,
 

drinking, or smoking substances containing the radioactive chemical.
 

Exposure may also result from skin contact with the radioactive chemical
 

alone, or with a substance containing it. Exposure can also occur by being
 

near radioactive chemicals in concentrations that may be found at hazardous
 

waste sites or at industrial accidents.
 

If you are exposed to a hazardous chemical, several factors determine
 

whether harmful effects will occur and the type and severity of those health
 

effects. These factors include the dose (how much), the duration (how
 

long), the pathway by which you are exposed, the other chemicals to which
 

you are exposed, and your individual characteristics such as age, sex,
 

eating habits, family traits, and state of health.
 

1.1 WHAT IS THORIUM?
 

Thorium is a naturally-occurring, radioactive metal. Small amounts of
 

thorium are present in all rocks, soil, above-ground and underground water,
 

plants, and animals. These small amounts of thorium contribute to the weak
 

background radiation for such substances. Soil commonly contains an average
 

of about 6 parts of thorium per million parts (ppm) of soil. Rocks in some
 

underground mines may also contain thorium in a more concentrated form.
 

After these rocks are mined, thorium is usually concentrated and changed
 

into thorium dioxide or other chemical forms. Thorium-bearing rock that has
 

had most of the thorium removed from it is called "depleted" ore or
 

tailings.
 

More than 99% of natural thorium exists in the form (isotope)
 

thorium-232. Besides this natural thorium isotope, there are more than 10
 

other different isotopes that can be artificially produced. In the
 

environment, thorium-232 exists in various combinations with other minerals,
 

such as silica. Most thorium compounds commonly found in the environment do
 

not dissolve easily in water and do not evaporate from soil or water into
 

the air.
 
2
 

1. PUBLIC HEALTH STATEMENT
 

The thorium isotope-232 is not stable. It breaks down into two parts.
 

This process of breaking down is called decay. The decay of thorium-232
 

produces a small part called "alpha" radiation and a large part called the
 

decay product. The decay product of thorium-232 also is not stable. Like
 

thorium-232, it in turn breaks down to an unstable isotope and the process
 

continues until a stable product is formed. During these decay processes,
 

the parent thorium-232, its decay products, and their next decay products
 

produce a series of new substances (including radium and radon), alpha and
 

beta particles, and gamma radiation. The alpha particles can travel only
 

very short distances through most materials and cannot go through human
 

skin. The gamma radiation can travel farther and can easily go through
 

human skin. The decay of thorium-232 into its decay products happens very
 

slowly. In fact, it takes about 14 billion years for half the thorium-232
 

to change into new forms. Fourteen billion years is called the radioactive
 

half-life of thorium-232.
 

Due to the extremely slow rate of decay, the total amount of natural
 

thorium in the earth remains almost the same, but it can be moved from place
 

to place by nature and people. For example, when rocks are broken up by
 

wind and water, thorium or its compounds becomes a part of the soil. When
 

it rains, the thorium-containing soil can be washed into rivers and lakes.
 

Also, activities such as burning coal that contains small amounts of
 

thorium, mining or milling thorium, or making products that contain thorium
 

also release thorium into the environment. Smaller amounts of other
 

isotopes of thorium are produced usually as decay products of uranium-238,
 

uranium-235, and thorium-232, and as unwanted products of nuclear
 

reactions.
 

Thorium is used to make ceramics, lantern mantles, and metals used in
 

the aerospace industry and in nuclear reactions. Thorium can also be used
 

as a fuel for generating nuclear energy. More than 30 years ago thorium
 

oxides were used in hospitals to make certain kinds of diagnostic x-ray
 

photographs. Further information on the properties and uses of thorium can
 

be found in Chapters 3 and 4 of this profile.
 

1.2 HOW MIGHT I BE EXPOSED TO THORIUM?
 

Since thorium is found almost everywhere, you will be exposed to small
 

amounts of it in the air you breathe and in the food and water you eat and
 

drink. Scientists know, roughly, the average amounts of thorium in food and
 

drinking water. Most people in the United States eat some thorium with
 

their food every day. Normally, very little of the thorium in lakes,
 

rivers, and oceans gets into the fish or seafood we eat. The amounts in the
 

air are usually so small that they can be ignored.
 

There may be more thorium than normal near an uncontrolled hazardous
 

waste site in which thorium has not been disposed of properly, Consequently,
 

you may be exposed to slightly more thorium if you live near
 
3
 

1. PUBLIC HEALTH STATEMENT
 

one of these sites because you could breathe windblown dust containing
 

thorium or eat food grown in soil contaminated with thorium. Children
 

playing near a waste site could get thorium into their bodies if they eat
 

contaminated soil. You could also be exposed to more thorium than normal if
 

you work in an industry that mines, mills, or manufactures products
 

containing thorium, or work in a research laboratory performing experiments
 

with thorium. Larger-than-normal amounts of thorium might also enter the
 

environment through accidental releases from thorium processing plants.
 

Further information on the potential for exposure to thorium can be found in
 

Chapter 5 of this profile.
 

1.3 HOW CAN THORIUM ENTER AND LEAVE MY BODY?
 

Only a small amount of the thorium that you breathe or swallow in food,
 

water, or soil enters your blood. One animal study has shown that thorium can
 

enter the body if it is placed on the skin. After breathing thorium, you will
 

usually sneeze, cough, or breathe out some of it within minutes. Some forms of
 

thorium can stay in your lungs for long periods of time. However, in most
 

cases, the small amount of thorium left in your lungs will leave your body in
 

the feces and urine within days. After you eat or drink thorium, almost all of
 

it leaves your body in the feces. The small amount of thorium left in your
 

body may enter your bones from the blood and stay there for many years. The
 

main way thorium will enter your body is by
 

breathing dust contaminated with thorium. For further information on how
 

thorium can enter and leave your body, see Chapter 2.
 

1.4 HOW CAN THORIUM AFFECT MY HEALTH?
 

Studies on thorium workers have shown that breathing thorium dust may
 

cause an increased chance of developing lung disease and cancer of the lung
 

or pancreas many years after being exposed. Changes in the genetic material
 

of body cells have also been shown to occur in workers who breathed thorium
 

dust. Liver diseases and effects on the blood have been found in people
 

injected with thorium in order to take special x-rays. Many types of cancer
 

have also been shown to occur in these people many years after thorium was
 

injected into their bodies. Since thorium is radioactive and may be stored
 

in bone for a long time, bone cancer is also a potential concern for people
 

exposed to thorium. Animal studies have shown that breathing in thorium may
 

result in lung damage. Other studies in animals suggest drinking massive
 

amounts of thorium can cause death from metal poisoning. The presence of
 

large amounts of thorium in your environment could result in exposure to
 

more hazardous radioactive decay products of thorium, such as radium and
 

thoron, which is an isotope of radon. Radium and radon are the subjects of
 

separate toxicological profiles prepared by ATSDR. Thorium is not known to
 

cause birth defects or to affect the ability to have children. For further
 

information on the health effects of thorium, see Chapter 2.
 
4
 

1. PUBLIC HEALTH STATEMENT
 

1.5 WHAT LEVELS OF EXPOSURE HAVE RESULTED IN HARMFUL HEALTH EFFECTS?
 

Thorium is odorless and tasteless, so you cannot tell if you are being
 

exposed to thorium. As shown in Tables l-l through l-4, we know very little
 

about specific exposure levels of thorium that result in harmful effects in
 

people or animals. High levels of exposure have been shown to cause death
 

in animals, but no direct cause of death could be determined and no other
 

health effects have been reported. For more information, see Chapter 2.
 

1.6 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO
 

THORIUM?
 

Special tests that measure the level of radioactivity from thorium or
 

thorium isotopes in your urine, feces, and air you breathe out can determine
 

if you have been exposed to thorium. These tests are useful only if run
 

within several days to a week after exposure. The tests cannot, however,
 

tell you if your health will be affected by the exposure. The tests can be
 

run only with special equipment and are probably not available at your local
 

clinic or hospital. For more information, see Chapters 2 and 6.
 

1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO PROTECT HUMAN
 

HEALTH?
 

The Environmental Protection Agency (EPA) requires that the Federal 

Government be notified if more than 1 millicurie (3.7x107

 Becquerels) of 

radioactivity from natural thorium is released into the environment. The 

Nuclear Regulatory Commission has issued Maximum Permissible Concentrations 

(MPC) in air and water for workplace exposure to thorium. For more 

information on government regulations and guidelines, see 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.
 




9
 

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
 

thorium. Its purpose is to present levels of significant exposure for
 

thorium 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
 

thorium and (2) a depiction of significant exposure levels associated with
 

various adverse health effects.
 

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
 

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.
 

Thorium is a relatively reactive, metallic radioactive element.
 

Because thorium is a radioactive element, evaluation of adverse health
 

effects due to exposure to thorium requires a slightly different approach
 

than with chemicals. Radiation is a health risk because radioactive
 

elements can emit energetic particles or electromagnetic radiation that can
 

damage cells. Radioactive elements are those that undergo spontaneous
 
10
 

2. HEALTH EFFECTS
 

disintegration (decay) in which energy is released (emitted) either in the
 

form of particles, such as alpha or beta particles, or rays, such as gamma
 

or x-rays. 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 (non-radiative) state
 

is reached (see Appendix B for more information). The rate of emission of
 

alpha particles from thorium is low, and the rate of emission of gamma rays
 

is very low (see Chapter 3). Alpha particles are unable to deeply penetrate
 

skin, but can travel short distances in the body (about 4 to 6 cell
 

diameters) if they are emitted from within the body. The intensity and
 

energy of alpha particles emitted depends on the particular isotope of
 

thorium in question. Several isotopes of thorium exist. By mass, the most
 

predominant ones in the environment are thorium-230 (a decay product of
 

uranium-238) and natural thorium (thorium-232) (see Chapter 3). The number
 

of particles emitted is related to the radioactive half-life of the isotope,
 

which is about 14 billion years for natural thorium (thorium-232). The
 

other type of radiation hazard is from gamma rays, which can penetrate the
 

body and pass through the air. However, natural thorium has a very low
 

gamma activity, which means there is little danger from this type of
 

radiation from natural thorium. Daughter products of thorium, however, may
 

emit more gamma radiation than natural thorium (see Chapter 3).
 

When thorium emits alpha particles, it disintegrates into other
 

daughter radionuclides (radioactive materials), such as radium-226 and
 

radon-222 (from thorium-230 in the uranium-238 decay series) or radium-228
 

and thoron (radon-220 from thorium-232 in the thorium decay series). It
 

eventually decays to stable lead-208 or -206, which is not radioactive.
 

More information about the decay of thorium can be found in Chapter 3. The
 

toxicological characteristics of radon, radium, and lead are the subject of
 

separate ATSDK Toxicological profiles.
 

The decay rate or activity of radioactive elements has traditionally 

been specified in curies (Ci). The curie is approximately 37 billion 

disintegrations (decay events) per second (3.7x1010 dps). In discussing 

thorium, a smaller unit,1x10-l2 Ci. the picocurie (pCi) is used, where pCi is 

equal to In international usage, the S.I. unit (the International 

System of Units) for activity is the Becquerel (Bq), which is equal to 

1 disintegration per second or about 27 pCi. (Information for conversion 

between units is given in Appendix B.) Measurements of radioactivity, 

expressed as nCi (nanocurie), in the environment are more sensitive than 

units of mass. For this reason, amounts of thorium are expressed in pCi 

units in Chapter 5. In animal studies, the exposure levels were usually 

reported in mg (milligrams), but have been converted to activity units (nCi 

and Bq) for presentation in Chapter 2. The absorbed dose from radiation can 

be expressed in units of rads or it can be stated in terms of dose 

equivalent, which includes a modification to reflect the quality of the 

radiations, for radiation protection purposes, and is expressed in terms of 

rems. For alpha radiations a quality factor, Q, of 20 is used to convert 

absorbed dose to dose equivalent. 
11
 

2. HEALTH EFFECTS
 

Both large and small amounts of radiation are damaging to health.
 

Current scientific consensus is radiation can also increase the probability
 

of cancer, and a conservative assumption is no threshold level exists below
 

which there is no additional risk of cancer. There is considerable debate
 

about how great the cancer risks are when people are chronically exposed to
 

very low levels of radiation. Since everyone is environmentally exposed to
 

a small amount of radiation, the minimum amount of additional radiation that
 

may constitute a health hazard is not well known.
 

The following sections summarize the health effects associated with
 

thorium. Evidence exists that most, if not all, effects of thorium may be
 

due to its radiological, and not chemical, effects. The mechanism of
 

toxicity for all effects are not well understood. For more information
 

about radiation, see Appendix B.
 

2.2.1 Inhalation Exposure
 

2.2.1.1 Death
 

Two epidemiology studies have examined mortality among thorium workers
 

neither found significant excess mortality. The standard mortality ratio
 

(SMR) for all causes of death in a cohort of 3039 male workers in a thorium
 

processing plant was 1.05 in comparison to United States white males
 

(Polednak et al. 1983). The estimated radiation levels to the workers for
 

inhalation intake ranged from 0.003-0.192 nCi/m3

 (0.001-0.007 Bq/m3) for a 

period of l-33 years. No evidence of overt industrial disease was found in 

a cohort of 84 workers at a thorium refinery exposed to <0.045-450 nCi/m3 

(<0.002-0.02 Bq/m3) for <l-20 years (Albert et al. 1955). In both studies, 

the workers were exposed to other toxic compounds (uranium dust) as well as 

other radioactive materials (thoron, uranium daughters, thorium daughters, 

cerium). 

No compound-related mortality was found in mice exposed to 114-330 

Mg/m3

(12.54-36.3 nCi/m3 = 464-1343 Bq/m3) thorium nitrate intermittently 

for 18 weeks (Patrick and Cross 1948). No compound-related mortality was 

found in rats, guinea pigs, rabbits, or dogs exposed intermittently for 1

3 3 3 year to 5 mg thorium/m (0.550 nCi/m = 20 Bq/m ) as thorium dioxide (Hodge
 

et al. 1960). These NOAEL values are reported in Table 2-l and plotted in
 

Figure 2-l.
 

2.2.1.2 Systemic Effects
 

Respiratory Effects. Although the SMR for respiratory diseases was
 

1.31 among workers at a thorium refinery (Polednak et al. 1983), the
 

increase may have been attributable in part to smoking. Exposure level


3 estimates for inhalation intakes ranged from 0.003-0.192 nCi/m (0.001-0.007
 

Bq/m ) for a period of 1-33 years. Because the workers were exposed to
 3



15
 

2. HEALTH EFFECTS
 

other toxic compounds (uranium dust) as well as other radioactive metals,
 

toxic effects cannot necessarily be attributed to thorium. Therefore, no
 

quantitative information from the study is reported in Table 2-l or
 

Figure 2-l.
 

Progressive cirrhosis of the lungs was found in a subchronic inhalation
 

study in rats (Likhachev et al. 1973a). Rats were exposed intermittently for
 

6-9 months to an inert aerosol (control), to the inert aerosol enriched with
 

10% or 49% insoluble thorium dioxide, or to thorium dioxide (100%) alone. The
 

severity of the lung cirrhosis was directly related to the radiation dose and
 

the amount of thorium dioxide. Cirrhosis of the lungs became evident in 3-6
 

months in the 100% thorium dioxide group, in 9-12 months in the 49% thorium
 

dioxide group, in 12-15 months in the 10% thorium dioxide group, and in 18-24
 

months in the inert aerosol control group. At lung exposures of up to 150 rad,
 

reticulosarcoma was found, while at lung exposures of 100-2700 rad, glandular
 

cancerous tumors were found (see Section 2.2.1.8). The tumors may have been
 

caused by thorium dioxide; the exact amount of thorium administered was not
 

clear from the report, so the results of the study do not appear in Table 2-l
 

or Figure 2-l.
 

No histopathological effects on the lungs were found in rats, guinea 

pigs, rabbits,or dogs exposed intermittently for 1 year to 5 mg thorium/m3 

(0.550 nCi/m3 = Bq/m3) as thorium dioxide (Hodge et al. 1960). This 

NOAEL value is presented in Table 2-l and plotted in Figure 2-l. 

Hematological Effects. A complete blood count (CBC) was done on a
 

cohort of 273 male monazite sand refinery workers to determine the effect
 

of thorium on the hematological system. The measured body burden
 

(calculated from in vivo detection of external gamma rays emitted by
 

daughter products of thorium still in the subject's body and from thoron in
 

expired air) of thorium was higher in those workers exposed for a longer
 

time period, but the blood count did not correlate with the body burden of
 

thorium (Conibear 1983). A correlation was found, however, between the
 

blood count and cigarette smoking habits. Exposure level estimates for
 

inhalation intakes of nicotine or thorium were not reported, and the
 

external gamma-ray exposure rate was between 0.5 and 5.0 mR/hour. Because
 

the workers were exposed to other toxic compounds (silica, yttrium, acid and
 

alkali fumes) as well as other sources of radioactivity, toxic effects
 

cannot necessarily be attributed to thorium. Therefore, the results of the
 

study do not appear in Table 2-l or Figure 2-l.
 

Effects on hematological parameters (abnormal forms of monocytes,
 

lymphocytes and granulocytes, hypoplastic bone marrow, red cell count
 

depression, macrocytosis, increase in immature granulocytes) were found in
 

dogs exposed 6 hours/day, 5 days/week to various chemical forms of thorium:


3 3 thorium nitrate tetrahydrate for 60 days (4 nCi/m = 150 Bq/m ); thorium

3 3 dioxide for 60 days (4.8 nCi/m = 180 Bq/m ); thorium tetrafluoride for 304


3 3 3 days (0.9 nCi/m = 33 Bq/m ); thorium oxalate for 270 days (1.4 nCi/m = 52
 

Bq/m ) (Hall et al. 1951). Differences in the degree of toxicity of the
 3
16
 

2. HEALTH EFFECTS
 

various chemical forms of thorium on hematological parameters could not be
 

determined from this study, although gagging, retching, and occasional
 

vomiting were found periodically in the dogs exposed to thorium nitrate


3 tetrahydrate. The lowest LOAEL, thorium tetrafluoride (0.9 nCi/m = 33
 

3 Bq/m ), is reported on Table 2-l and plotted on Figure 2-l.
 

No effects on hematological parameters, blood nonprotein nitrogen
 

(NPN), or the histopathology of the spleen were found in rats, guinea pigs,


3 3 rabbits, or dogs exposed for 1 year to 5 mg/thorium m (0.550 nCi/m = 20
 

3 Bq/m ) as thorium dioxide (Hodge et al. 1960). This NOAEL value is
 

presented in Table 2-l and plotted in Figure 2-l.
 

Musculoskeletal Effects. No studies were located regarding the
 

musculoskeletal effects in humans after inhalation exposure to thorium.
 

Upon histopathological examination, no effects in the femur were found


3 In rats, guinea pigs, rabbits, or dogs exposed for 1 year to 5 mg thorium/m


3 3 (0.550 nCI/m = Bq/m ) as thorium dioxide (Hodge et al. 1960). This
 

NOAEL value is presented in Table 2-l and plotted in Figure 2-l.
 

Hepatic Effects. The levels of aspartate aminotransferase, globulin,
 

and total bilirubin in sera of a cohort of 275 former workers in a thorium
 

refinery were correlated with body burdens of radioactivity (Farid and
 

Conibear 1983). The levels of aspartate aminotransferase and total
 

bilirubin were significantly higher (p<O.OOOl and p=O.O43, respectively) in
 

thorium-exposed workers, as compared to U.S. white males. Globulin levels
 

also increased with increasing levels of body burden, but not significantly.
 

Although the enzymatic levels tested were elevated, they were still within
 

the normal range. No effects on albumin, total protein, or alkaline
 

phosphatase were seen. The correlation of hepatic function tests with body
 

burden of radioactivity may suggest a radiotoxic effect, but this was not
 

proven by the authors. No exposure concentrations were reported.
 

No histopathological effects in the liver were found in rats, guinea


3 3 3 pigs, rabbits, or dogs exposed to 5 mg thorium/m (0.550 nCi/m = 20 Bq/m )
 

for 1 year as thorium dioxide (Hodge et al. 1960). This NOAEL value is
 

presented in Table 2-l and plotted in Figure 2-l.
 

Renal Effects. No studies were located regarding renal effects in
 

humans after inhalation exposure to thorium.
 

No histopathological effects in the kidneys were found in rats, guinea


3 3 3 pigs, rabbits, or dogs exposed to 5 mg thorium/m (0.550 nCi/m = 20 Bq/m )
 

for 1 year as thorium dioxide (Hodge et al. 1960). This NOAEL value is
 

presented in Table 2-l and plotted in Figure 2-l.
 
17
 

2. HEALTH EFFECTS
 

2.2.1.3 Immunological Effects
 

No studies were located regarding immunological effects in humans
 

after inhalation exposure to thorium. No histopathological effects in the
 

lymph nodes were found in rats, guinea pigs, rabbits, or dogs exposed to 5 mg


3 3 3 thorium/m (0,550 nCi/m = 20 Bq/m ) for 1 year as thorium dioxide (Hodge et
 

al. 1960). Since no parameters of immune function were examined, this value
 

does not appear as a NOAEL for immunological effects in Table 2-l or Figure 2­

l.
 

No studies were located regarding the following health effects in
 

humans or animals after inhalation exposure to thorium.
 

2.2.1.4 Neurological Effects
 

2.2.1.5 Developmental Effects
 

2.2.1.6 Reproductive Effects
 

2.2.1.7 Genotoxic Effects
 

Hoegerman and Cummins (1983) assessed the frequency of chromosome
 

aberrations in the lymphocytes of 47 male workers in a thorium processing
 

plant. The workers were divided into three groups based on their body
 

burdens of radioactivity: low (0 nCi/kg), moderate (0.003 nCi/kg = 0.11
 

Bq/kg) and high (0.015 nCi/kg = 0.56 Bq/kg) body burden groups. An
 

increased frequency of chromosomal aberrations (dicentric ring chromosomes)
 

were found in the high burden groups (combined high and moderate burden
 

groups) compared to the low burden group and historical controls. No
 

significant differences were found in the frequency of two-break chromosome
 

aberrations. A positive correlation was not established between the
 

frequency of chromosomal aberrations and duration of employment. The
 

observed aberration frequency was generally compatible with that found in
 

patients injected with thorium dioxide colloid (Thorotrast) (see Section
 

2.2.4.7). Costa-Ribeiro et al. (1975) also reported a statistically
 

significant (p<O.O5) increase in the number of chromosomal aberrations
 

(dicentrics) in 240 monazite sand millers, as compared to controls. No
 

significant differences in the incidence of translocations were observed.
 

No exposure concentrations were reported in either study.
 

No studies were located regarding genotoxic effects in animals after
 

inhalation exposure to thorium.
 

2.2.1.8 Cancer
 

A statistically significant excess of deaths from pancreatic cancer was
 

seen in a cohort of 3039 former thorium workers employed for 1 year or more (6
 

observed vs. 1.3 expected) but not in workers employed for a shorter time
 
18
 

2. HEALTH EFFECTS
 

(3 observed vs. 2.7 expected) (Stehney et al. 1980). The workers were


3 3 exposed to 0.003-0.192 nCi/m (0.001-0.007 Bq/m ). Although a correlation
 

between smoking and pancreatic cancer has not been established, the excess
 

mortality may be due, in part, to the fact that a higher proportion of
 

smokers was found in the worker population when compared to U.S white males
 

(ratio of 1.3 observed smokers/expected smokers). A second study compared
 

the SMR of workers in a thorium processing plant to the mortality rates for
 

U.S. white males and determined that the SMRs in the workers were high for
 

deaths due to lung cancer (SMR=1.44; 95% confidence limit 0.98 and 2.02) and
 

pancreatic cancer (SMR=2.01; 95% confidence limit 0.92 and 3.82) (Polednak
 

et al. 1983). In a subgroup of men in jobs with the highest exposure to
 

thorium, the SMR for lung cancer was 1.68 and the SMR for pancreatic cancer
 

was 4.13. Exposure level estimates for inhalation intakes ranged from


3 3 0.003-0.192 nCi/m (0.0001-0.007 Bq/m ) for a period of l-33 years. The
 

authors indicated that smoking may be a confounding factor in the increased
 

rates of cancer and that the workers were exposed to other potentially
 

carcinogenic agents, such as thoron (radon-220). Consequently, the evidence
 

for a causal relationship between thorium exposure and cancer is not
 

convincing and no concentrations are reported in Table 2-l or plotted in
 

Figure 2-l.
 

A significantly (p<O.O5) increased incidence of malignancies in the
 

lymphatic and hematopoietic tissues of uranium mill workers (cohort of 662
 

males) was found by Archer et al. (1973). The radioactivity in the
 

tracheobronchial lymph nodes of the workers was found to be primarily the
 

result of alpha emissions from thorium-230 and not from uranium-234 or
 

uranium-238. Consequently, the authors suggested that the increased
 

incidence of malignancies may have been a result of thorium-230 exposure and
 

not uranium exposure. Exposure levels of thorium were not reported;
 

therefore, the results of the study are not reported on Table 2-l or plotted
 

in Figure 2-l.
 

Rats were exposed to various concentrations of thorium dioxide for
 

6-9 months, and the frequency and histological type of lung tumors were
 

determined following observation for up to 21 months (Likhachev et al.
 

1973b; Likhachev 1976). The authors concluded that the incidence and
 

histological type of lung tumors that developed were dependent on the
 

radiation dose to the lungs. At lung doses of up to 150 rad (3000 rems),
 

primarily reticulosarcoma was found (in 16% of the animals), while at total
 

doses of 1000-2700 rads (20,000-54,000 rems), glandular cancerous tumors
 

(adenomatosis and squamous cell carcinoma) were found in all of the exposed
 

animals, and the reticulosarcoma was no longer observed.
 

2.2.2 Oral Exposure
 

2.2.2.1 Death
 

No studies were located regarding lethal effects in humans after oral
 

exposure to thorium.
 
19
 

2. HEALTH EFFECTS
 

A single gavage administration of 1000 mg thorium/kg body weight/day
 

(110 nCi/kg/day = 4070 Bq/kg/day) as thorium nitrate resulted in the death
 

of 4/20 mice, while a single amount of 760 mg thorium/kg body weight/day (84
 

nCi/kg/day = 3100 Bq/kg/day) resulted in no mortality. Occasional
 

intestinal hemorrhage was noted at autopsy in the mice that died, but it was
 

not reported if the hemorrhage was the cause of death in the animals. No
 

effects were found following administration of a 10% sodium nitrate
 

solution, suggesting that the adverse effects were due to thorium and not to
 

nitrate (Patrick and Cross 1948). Following 4 months of continuous exposure
 

to 123 mg thorium/kg body weight/day (13.6 nCi/kg/day = 503 Bq/kg/day) as
 

thorium nitrate in the drinking water, 50% of the treated mice and 10% of
 

the control mice died (Patrick and Cross 1948). No cause of death was
 

reported in either the acute or the 4-month studies. In rats, 4 months of
 

exposure to 3043 mg thorium/kg body weight/day (335 nCi/kg/day = 12,400
 

Bq/kg/day) as thorium nitrate resulted in death, but the deaths may have
 

been due to the poor nutritional state of the animals since the treated
 

animals ate much less of the treated food and, therefore, lost weight (Downs
 

et al. 1959).
 

Death occurred following four daily administrations of ≥2130 mg 

thorium/kg body weight/day (234 nCi/kg/day = 8657 Bq/kg/day) as thorium 

nitrate in the food to a single dog (Patrick and Cross 1948). No immediate 

deaths were reported following a single administration of 121 mg thorium/kg 

body weight/day (13 nCi/kg/day = 481 Bq/kg/day) by gavage as thorium 

nitrate to dogs (Sollman and Brown 1907). Death was not found following 

exposure of a single dog to food containing 426 mg thorium/kg body 

weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium nitrate for 46 days 

(Downs et al. 1959). No deaths were reported following a single gavage 

administration of thorium nitrate (483 mg thorium/kg body weight/day = 53 

nCi/kg/day = 1960 Bq/kg/day) in rabbits (Sollman and Brown 1907). The 

number of treated and control animals (dogs and rabbits) was not reported in 

the Sollman and Brown (1907) study. 

All reliable NOAEL and LOAEL values are reported in Table 2-2 and
 

plotted in Figure 2-2. Values from the Sollman and Brown (1907) study are
 

not reported in the table and figure since the number of animals in the
 

study were not reported. The LOAEL value for death in rats from the Downs
 

et al. (1959) study is not reported since the deaths may have been due to
 

the poor nutritional state of the animals and not to thorium toxicity, and
 

the NOAEL and LOAEL values for the death of dogs in the Downs et al. (1959)
 

and the Patrick and Cross (1948) studies, respectively, are not reported
 

since they were pilot studies and only one animal was used.
 

2.2.2.2 Systemic Effects
 

Respiratory Effects. No studies were located regarding the
 

respiratory effects in humans after oral exposure to thorium.
 


22
 

2. HEALTH EFFECTS
 

No histopathological changes in the lungs were found in rats treated
 

for 4 months with 3043 mg thorium/kg body weight/day (335 nCi/kg/day =
 

12,400 Bq/kg/day) or in one dog treated for 46 days with 426 mg thorium/kg
 

body weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium nitrate in the
 

food (Downs et al. 1959). These NOAEL values for rats are reported in Tab
 

2-2 and plotted in Figure 2-2. The NOAEL value for the effects in dogs is
 

not reported since this was a pilot study and only one animal was used.
 

Cardiovascular Effects. No studies were located regarding the
 

cardiovascular effects in humans after oral exposure to thorium.
 

No histopathological changes in the heart were found in rats treated
 

for 4 months with 3043 mg thorium/kg body weight/day (335 nCi/kg/day =
 

12,400 Bq/kg/day) or in one dog treated for 46 days with 426 mg thorium/kg
 

body weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium nitrate in the
 

food (Downs et al. 1959). These NOAEL values for rats are reported in Tab
 

2-2 and plotted in Figure 2-2. The NOAEL value for the effects in dogs is
 

not reported since this was a pilot study and only one animal was used.
 

Gastrointestinal Effects. No studies were located regarding the
 

gastrointestinal effects in humans after oral exposure to thorium.
 

No histopathological changes in the stomach and intestines were found
 

in rats treated for 4 months with 3043 mg thorium/kg body weight/day (335
 

nCi/kg/day = 12,400 Bq/kg/day) or in one dog treated for 46 days with 426 mg
 

thorium/kg body weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium
 

nitrate in the food (Downs et al. 1959). These NOAEL values for rats are
 

reported in Table 2-2 and plotted in Figure 2-2. The NOAEL value for the
 

effects in dogs is not reported since this was a pilot study and only one
 

animal was used.
 

Occasional intestinal hemorrhages were reported in mice that died
 

following a single gavage exposure to thorium nitrate (Patrick and Cross
 

1948). It was not reported whether the intestinal hemorrhage was the cause
 

of death in the mice. The level at which this occurred was not reported.
 

The possibility that intestinal damage resulted from improper gavage
 

technique cannot be ruled out; therefore, these data are not presented in
 

Table 2-2 or plotted in Figure 2-2.
 

Hematological Effects. No studies were located regarding the
 

hematological effects in humans after oral exposure to thorium.
 

No histopathological changes in the spleen were found in rats treated
 

for 4 months with 3043 mg thorium/kg body weight/day (335 nCi/kg/day =
 

12,400 Bq/kg/day) or in one dog treated for 46 days with 426 mg thorium/kg
 

body weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium nitrate in the
 

food (Downs et al. 1959). These NOAEL values for rats are reported in
 

Table 2-2 and plotted in Figure 2-2. The NOAEL value for the effects in
 
23
 

2. HEALTH EFFECTS
 

dogs is not reported since this was a pilot study and only one animal was
 

used.
 

Hepatic Effects. No studies were located regarding the hepatic effects
 

in humans after oral exposure to thorium.
 

No histopathological changes in the liver were found in rats treated
 

for 4 months with 3043 mg thorium/kg body weight/day (335 nCi/kg/day =
 

12,400 Bq/kg/day) or in one dog treated for 46 days with 426 mg thorium/kg
 

body weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium nitrate in the
 

food (Downs et al. 1959). These NOAEL values for rats are reported in Table
 

2-2 and plotted in Figure 2-2. The NOAEL value for the effects in dogs is
 

not reported since this was a pilot study and only one animal was used.
 

Renal Effects. No studies were located regarding the renal effects in
 

humans after oral exposure to thorium.
 

No histopathological changes in the kidneys were found in rats treated
 

for 4 months with 3043 mg thorium/kg body weight/day (335 nCi/kg/day =
 

12,400 Bq/kg/day) or in one dog treated for 46 days with 426 mg thorium/kg
 

body weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium nitrate in the
 

food (Downs et al. 1959). These NOAEL values for rats are reported in Table
 

2-2 and plotted in Figure 2-2. The NOAEL value for the effects in dogs is
 

not reported since this was a pilot study and only one animal was used.
 

Other Systemic Effects. Weight loss was found in rats treated for
 

4 months with 3043 mg thorium/kg body weight/day (335 nCi/kg/day = 12,400
 

Bq/kg/day) and in one dog treated for 46 days with 426 mg thorium/kg body
 

weight/day (47 nCi/kg/day = 1740 Bq/kg/day) as thorium nitrate in the food
 

(Downs et al. 1959). The weight loss was attributed to a decrease in intake
 

of the treated food; therefore, these values are not reported in Table 2-2
 

or Figure 2-2.
 

No studies were located regarding the following health effects in
 

humans or animals after oral exposure to thorium.
 

2.2.2.3 Immunological Effects
 

2.2.2.4 Neurological Effects
 

2.2.2.5 Developmental Effects
 

2.2.2.6 Reproductive Effects
 

No studies were located regarding reproductive effects in humans after
 

oral exposure to thorium.
 

No histopathological changes in the gonads (exact tissues examined were
 

not reported) were found in male and female rats treated for 4 months with
 
24
 

2. HEALTH EFFECTS
 

3043 mg thorium/kg body weight/day (335 nCi/kg/day = 12,400 Bq/kg/day). No
 

histopathological changes in the testes were found in one dog treated for 46
 

days with 426 mg thorium/kg body weight/day (47 nCi/kg/day - 1740 Bq/kg/day)
 

as thorium nitrate in the food (Downs et al. 1959). The value of 335
 

nCi/kg/day for rats is reported in Table 2-2 and plotted in Figure 2-2.
 

2.2.2.7 Genotoxic Effects
 

No studies were located regarding genotoxic effects in humans or
 

animals after oral exposure to thorium.
 

2.2.2.8 Cancer
 

No studies were located regarding carcinogenic effects in humans or
 

animals after oral exposure to thorium.
 

2.2.3 Dermal Exposure
 

2.2.3.1 Death
 

No studies were located regarding lethal effects in humans after
 

dermal exposure to thorium.
 

Tandon et al. (1975) reported no lethality in rats following dermal
 

application of 529 mg thorium/kg body weight (58 nCi/kg = 2146 Bq/kg), daily
 

for 15 days, to the lateroabdominal and scrotal skin. Prior to treatment,
 

the hair was clipped. The area remained uncovered for the duration of
 

treatment. The thorium was administered as thorium nitrate. This NOAEL
 

value is reported in Table 2-3.
 

2.2.3.2 Systemic Effects
 

Hepatic Effects. No studies were located regarding hepatic effects in
 

humans after dermal exposure to thorium.
 

Tandon et al. (1975) reported no histopathological effects on the liver
 

of rats following dermal application of 529 mg thorium/kg body weight/day (58
 

nCi/kg/day - 2146 Bq/kg/day) for 15 days to the lateroabdominal and scrotal
 

areas. Prior to treatment, the hair was clipped. The area remained uncovered
 

for the duration of treatment. The thorium was administered as thorium
 

nitrate. This NOAEL value for hepatic effects in rats is reported in Table 2­

3.
 

Renal Effects. No studies were located regarding renal effects in
 

humans after dermal exposure to thorium.
 

26
 

2. HEALTH EFFECTS
 

Tandon et al. (1975) reported no histopathological effects on the
 

kidneys of rats following dermal application of 529 mg thorium/kg body
 

weight/day (58 nCi/kg/day = 2146 Bq/kg/day) for 15 days to the
 

lateroabdominal and scrotal areas. Prior to treatment, the hair was
 

clipped. The area remained uncovered for the duration of treatment. The
 

thorium was administered as thorium nitrate. This NOAEL value for renal
 

effects in rats is reported in Table 2-3.
 

Dermal/Ocular Effects. No studies were located regarding
 

dermal/ocular effects in humans after dermal exposure to thorium.
 

Tandon et al. (1975) applied daily dermal applications of 132.5 mg
 

thorium/kg body weight/day (15 nCi/kg/day = 555 Bq/kg/day), 265 mg
 

thorium/kg body weight/day (29 nCi/kg/day = 1073 Bq/kg/day), or 529 mg
 

thorium/kg body weight/day (58 nCi/kg/day = 2146 Bq/kg/day) to the
 

lateroabdominal and scrotal areas of rats for 15 days. The thorium was
 

administered to skin (hair was clipped) as thorium nitrate, and the area
 

remained uncovered for the duration of treatment. Mild hyperkeratinization
 

of the lateroabdominal skin was found at all exposure levels. At the
 

highest exposure level, mild acanthosis and thickening of the epithelial
 

lining of the lateroabdominal skin were seen. At this level, mild
 

acanthosis, swollen collagen fibers, and foamy dermis were found in the
 

scrotal skin. The value of 15 nCi/kg/day is a less serious LOAEL, and the
 

exposure level of 58 nCi/kg/day is a serious LOAEL for dermal effects in the
 

rat. These values are reported in Table 2-3.
 

No studies were located regarding the following health effects in
 

humans or animals after dermal exposure to thorium.
 

2.2.3.3 Immunological Effects
 

2.2.3.4 Neurological Effects
 

2.2.3.5 Developmental Effects
 

2.2.3.6 Reproductive Effects
 

No studies were located regarding reproductive effects in humans after
 

dermal exposure to thorium.
 

Tandon et al. (1975) applied daily dermal applications of 132.5 mg
 

thorium/kg body weight/day (15 nCi/kg/day = 555 Bq/kg/day), 265 mg
 

thorium/kg body weight/day (29 nCi/kg/day = 1073 Bq/kg/day), or 529 mg
 

thorium/kg body weight/day (58 nCi/kg/day = 2146 Bq/kg/day) to the
 

lateroabdominal and scrotal skin of rats for 15 days. The thorium was
 

administered to skin (hair was clipped) as thorium nitrate, ,and the area
 

remained uncovered for the duration of treatment. Mild edema of the
 

seminiferous tubules and the interstitium was seen at all exposure levels.
 

At the highest exposure level, some desquamation of sperm and giant
 
27
 

2. HEALTH EFFECTS
 

spermatid-type cells were found. The percentage of sperm affected by
 

thorium treatment was not reported. It was not clear whether these
 

reproductive changes were due to chemical or radiation effects, although
 

they were more likely the result of chemical toxicity because of the short
 

time required to produce the effects. The level of 15 nCi/kg/day is a less
 

serious LOAEL and 58 nCi/kg/day is a serious LOAEL for the reproductive
 

effects of thorium in rats. These values are reported in Table 2-3.
 

2.2.3.7 Genotoxic Effects
 

No studies were located regarding genotoxic effects in humans or
 

animals after dermal exposure to thorium.
 

2.2.3.8 Cancer
 

No studies were located regarding carcinogenic effects in humans or
 

animals after dermal exposure to thorium.
 

2.2.4 Other Routes of Exposure
 

Most of, the literature deals with the carcinogenic effects of thorium
 

as a result of intravenous injection of Thorotrast, a colloid consisting of
 

approximately 25% thorium-232 dioxide and stabilized with dextran. Thorotrast
 

was used as a radiographic contrast medium between the years 1928 and 1955. It
 

was estimated that 50,000-100,000 patients worldwide received Thorotrast
 

(Harrist et al. 1979; Isner et al. 1978). Generally, l0-75 mL of Thorotrast
 

was injected and toxic effects were found at all exposure -levels.It has been
 

reported that the thorium-232 in Thorotrast has an activity of 24.2 nCi/mL
 

(Steinstrasser 1981); therefore, the injected amounts of l-75 mL correspond to
 

3.5-26 nCi/kg body weight (129-962 Bq/kg). The toxic effects include formation
 

4-6 years after exposure of "Thorotrastomas," granulomas at the site of
 

injection resulting from the extravasation of the injected Thorotrast (Frank
 

1980; Grampa 1971). Blood disorders (hemolytic and aplastic anemia,
 

myelofibrosis, and leukemia) appeared 20 years following injection, and
 

hemangiosarcoma of the liver was found 25-30 years post-exposure (Frank 1980).
 

A relationship was found between the amount of the Thorotrast injected and the
 

incidence of liver tumors (cholangiocarcinoma, angiosarcoma, hepatic cellular
 

carcinoma) (Wesch et al. 1983; Van Kaick et al. 1983). A decrease in the time
 

to tumors was also found with increased injected volume of Thorotrast (Van
 

Kaick et al. 1983). The use of Thorotrast ceased when the potential toxic
 

effects were recognized.
 

2.2.4.1 Death
 

No studies were located regarding acute lethal effects in humans after
 

other routes of exposure to thorium. Death from various types of cancer,
 

however, was found 20-30 years after intravenous injection of Thorotrast.
 
28
 

2. HEALTH EFFECTS
 

After a period of 15 months, no increased mortality was seen from a
 

single intravenous injection of 0.5 mL of Thorotrast (403 nCi/kg = 14909
 

Bq/kg) in mice (Guimaraes et al. 1955).
 

2.2.4.2 Systemic Effects
 

Respiratory Effects. No studies were located regarding respiratory
 

effects in humans after other routes of exposure to thorium.
 

No degenerative changes in the pulmonary parenchyma were found, but
 

7/20 mice that died 15 months after intravenous injection of Thorotrast
 

(Guimaraes et al. 1955) and 8/20 mice that were sacrificed 5-12 months after
 

injection of Thorotrast (Guimaraes and Lamerton 1956) had lung adenomas.
 

There was no significant difference in survival between the treated and
 

control animals in either study. In a few cases, an association between the
 

presence of Thorotrast deposits in the lungs and the proliferation of
 

bronchioles and alveoli was found.
 

Cardiovascular Effects. Myocardial infarction, severe coronary
 

luminal narrowing, and internal alteration of the carotid artery were found
 

in two patients injected 21-30 years before with an unreported amount of
 

Thorotrast (Isner et al. 1978). The authors concluded that the vascular
 

effects were the result of chronic alpha irradiation. The patients were
 

injected in the carotid artery, and thorotrastoma (see Other Systemic
 

Effects, below) was found in both patients.
 

Lipchik et al. (1972) reported no significant acute changes in cardiac
 

output, pulse rate, pressure or left ventricle volumes, or clotting time in
 

dogs injected intravenously with up to 1 mL of Thorotrast/kg (1.9 nCi/kg =
 

70 Bq/kg.
 

Eleven months after intratracheal and intraperitoneal injection of
 

thorium dioxide in rats, a sharp and persistent fall in blood pressure was
 

found (Syao-Shan 1970). The fall in blood pressure could not be directly
 

attributed to the chemical or radiological effects of thorium.
 

Hematological Effects. Aplastic anemia, leukemia (erythroleukemia,
 

acute myelogenous leukemia), myelofibrosis, and splenic cirrhosis were among
 

the hematological effects commonly found in patients after injection of
 

Thorotrast (Dejgaard et al. 1984; Kamiyama et al. 1988; Kato et al. 1983;
 

Rao et al. 1986; Summers and Chung 1986; Van Kaick et al. 1983). The
 

appearance of the leukemia commonly occurred 20 years after injection (see
 

Section 2.2.4.8).
 

No studies were located regarding hematological effects in animals
 

after other routes of exposure to thorium.
 

Hepatic Effects. Severe cirrhosis of the liver was one of the primary
 

systemic effects seen following injection of Thorotrast in humans (Baxter
 
29
 

2. HEALTH EFFECTS
 

et al. 1980a,b; Faber 1979; Kato and Kido 1987; Kato et al. 1983; Mori
 

et al. 1979, 1983a,b; Rao et al. 1986; Van Kaick et al. 1983). Cases of
 

fibrosis, veno-occlusive disease, and blood-filled cavities were also found
 

in the livers of Thorotrast patients (da Silva Horta 1967a; Dejgaard et al.
 

1984). The latency period for the appearance of the cirrhosis was not
 

clear, but was probably comparable to the latency period for liver tumors
 

(25-30 years) since the two effects were often found together.
 

Degenerative liver changes (necrosis, fibrosis, cirrhosis) were found
 

in mice and rats treated with a single dose of Thorotrast and allowed to
 

survive up to 15 months after treatment (Guimaraes et al. 1955; Guimaraes
 

and Lamerton 1956; Wegener et al. 1983). The authors of the mouse study
 

(Guimaraes et al. 1955; Guimaraes and Lamerton, 1956) concluded that
 

radiation was responsible for the cellular proliferation that led to the
 

degeneration and hepatic tumors.
 

Following intravenous injection of O-2.8 μCi/kg (104,000 Bq/kg) 

thorium-227 in a solution of citric acid-sodium citrate buffer in dogs, an 

increase in serum alkaline phosphatase measurements and hypoalbuminemia and 

hyperglobulinemia were observed (Stevens et al. 1967). No effects on the 

levels of serum glutamic pyruvic transaminase (SGPT) or serum glutamic 

oxaloacetic transaminase (SGOT) were found. 

Renal Effects. No studies were located regarding renal effects in
 

humans or animals after other routes of exposure to thorium, but tumors of
 

the kidney have been reported after intravenous administration of thorium in
 

humans (see Section 2.2.4.8).
 

Other Systemic Effects. Localized fibrosis infiltrated with
 

macrophages was often found surrounding deposits of Thorotrast at the point
 

of intravenous injection. These granulomas were termed Thorotrastoma and
 

resulted from fibroblastic proliferation due to the extravascular deposition
 

of Thorotrast (Coorey 1983; Stanley and Calcaterra 1981; Stougaard et al.
 

1984; Wustrow et al. 1988). Histologically, the Thorotrastoma consisted of
 

dense, hyalinized connective tissue with Thorotrast found both free and in
 

the cytoplasm of macrophages (Grampa 1971). The Thorotrastoma most commonly
 

occurred in the neck after a cerebral angiography and appeared 4-6 years
 

after intravenous injection (Frank 1980).
 

2.2.4.3 Immunological Effects
 

Fibrosis of the lymph nodes, which occluded the lymph vessels, and of
 

the spleen were found in patients injected intravenously with unknown
 

quantities of Thorotrast (da Silva Horta 1967a; Wegener et al. 1976; Wegener
 

and Wesch 1979). No malignancies were found in the lymph nodes, but
 

hemangioendothelioma of the spleen was reported in 2/14 patients examined by
 

da Silva Horta (1967a).
 
30
 

2. HEALTH EFFECTS
 

No degenerative changes were observed in the spleen of mice injected
 

intravenously with Thorotrast, but one animal had a malignant
 

hemangioendothelioma (Guimaraes et al. 1955). Michael and Murray (1970)
 

found a suppression in immune response following administration of
 

Thorotrast to mice. The suppression was found to appear sooner (within
 

1 hour after treatment) and last for a longer period of time (up to 3 days)
 

when Thorotrast was administered intraperitoneally rather than
 

intravenously. Thorotrast was found to affect lymphoid cells involved in
 

antibody formation, as well as the blockade of phagocytic cells in certain
 

organs of the reticuloendothelial system (Michael and Murray 1970).
 

No studies were located regarding the following health effects in
 

humans or animals after other routes of exposure to thorium:
 

2.2.4.4 Neurological Effects
 

2.2.4.5 Developmental Effects
 

2.2.4.6 Reproductive Effects
 

2.2.4.7 Genotoxic Effects
 

The intravenous injection of Thorotrast resulted in radiation-induced
 

chromosomal aberrations in patients (Fischer et al. 1967; Kemmer 1979;
 

Kemmer et al. 1971, 1979; Sadamori et al. 1987; Sasaki et al. 1987). A
 

positive correlation was found between the chromosomal aberration rate and
 

the administered amount of Thorotrast (Buckton and Langlands 1973; Fischer
 

et al. 1967; Kemmer et al. 1971, 1973).
 

No studies were located regarding the genotoxic effects in animals
 

after intravenous injection or other routes of exposure to thorium.
 

2.2.4.8 Cancer
 

The primary effects of intravenously injected Thorotrast in humans are
 

liver tumors (cholangiocarcinoma, angiosarcoma, hepatic cellular carcinoma)
 

and blood disorders (aplastic anemia, erythroleukemia, acute myelogenous
 

leukemia) (BEIR IV 1988; Ito et al. 1988; Kamiyama et al. 1988; Kato and
 

Kido 1987; Kojirs et al. 1985; Levy et al. 1986; Van Kaick et al. 1983;
 

Yamada et al. 1983). Two groups of former Thorotrast patients were examined
 

(one group was 93 autopsy cases from the "Annual of Pathological Autopsy
 

Cases" in Japan and the other was a group of 78 autopsy cases from the
 

Japanese literature). Cholangiocarcinoma was found in 55-58%, angiosarcoma
 

was found in 24-25%, and hepatocellular carcinoma was found in 17-21% of
 

these cases (Yamada et al. 1983). The mean latency period for all tumor
 

types was between 25 and 30 years (Frank 1980). The mean value of absorbed
 

dose to the liver was calculated to be 876 rads for hepatocellular carcinoma
 

and 1053 rads for cholangiocarcinoma (Mori et al. 1983b). It was determined
 

that angiosarcoma developed later (33.5-year mean latency period) than
 
31
 

2. HEALTH EFFECTS
 

cholangiocarcinoma (27.8 years) (Yamada et al., 1983). Blood-filled
 

cavities in the tumors were common (Visfeldt and Poulsen 1972). Kato et al.
 

(1983) reported that malignant hepatic tumors accounted for 63% of all
 

Thorotrast-related deaths, and as the dose rate increased (<15 to ≥45 

rad/year;<0.15 to ≥0.45 Gy/year), the severity of the liver effects 

increased and the latency period decreased. A dose-effect relationship was 

found between the amount of Thorotrast injected and the incidence of liver 

tumors in humans (Van Kaick et al. 1983). The radiation dose to the liver 

from l-10 mL injected was 10 rad/year (0.10 Gy/year), 11-20 mL was 18 

rad/year (0.18 Gy/year), and >20 mL was 30 rad/year (0.30 Gy/year). 

The latency period for leukemia was about 20 years, which was 5-10
 

years shorter than the liver tumors (Frank 1980). The primary forms of
 

leukemia found were erythroleukemia and acute myelogenous leukemia (da Motta
 

et al. 1979; Kamiyama et al. 1988; Mori et al. 1983b). Kamiyama etal.
 

(1988) reported that the damage from Thorotrast may have been due to effects
 

on the hematopoietic stem cell level.
 

Fifteen cases of bone tumors resulting from intravenous Thorotrast
 

injection have been reported (9 of which were osteosarcoma). The mean
 

latency period was 26 years and the latency period and injected amount of
 

Thorotrast were inversely related (Harrist et al. 1979). The mean dose rate
 

to bone was 16 rads/year (0.16 Gy/year) per 25 mL of injected Thorotrast
 

(Van Kaick et al. 1983).
 

Tumors of the kidneys, spleen, and pancreas have also been reported
 

(Christensen et al. 1983; Guimaraes et al. 1955; Kauzlaric et al. 1987; Levy
 

et al. 1986; Mori et al. 1979; Van Kaick et al. 1983; Westin et al. 1973).
 

Christensen et al. (1983) determined that transitional cell carcinoma of
 

the kidneys have a significantly longer latency period (35.8 years; p<0.005)
 

compared to carcinoma of other histological types (27.6 years). A few
 

cases of meningioma and gliosarcoma were found (da Silva Horta 1967b; Kyle
 

et al. 1963; Sussman et al. 1980; Wargotz et al. 1988).
 

The literature suggests that the toxic effects of Thorotrast are due to
 

the alpha radiation effects of thorium and not to the chemical effects of
 

thorium or of the.colloid (Faber 1973; BEIR IV 1988; Taylor et al. 1986;
 

Wesch et al. 1983). Wesch et al. (1983) injected Thorotrast enriched with
 

thorium-230 into rats and found a linear relationship between radiation
 

level and tumor incidence. At a constant radioactive level, an increase in
 

the injected colloidal volume had little influence on the number of liver
 

tumors, but resulted in a decrease in tumor appearance time and, therefore,
 

a decrease in lifespan. The larger colloidal volume may result in a more
 

diffuse organ dose and a less "hot spot" distribution, Injection of the
 

nonradioactive colloid resulted in no appreciable incidence of liver tumors.
 

It is not known whether the colloidal particles induce the liver tumors when
 

given in combination with the radioactive thorium, or if the colloid only
 

accelerates the expression of the radiation-induced tumors. However,
 
32
 

2. HEALTH EFFECTS
 

studies in mice reported by Taylor et al. (1986) suggest that the induction
 

of liver cancer can be accounted for by the radiation alone.
 

Thorotrast studies in rats found a positive correlation between the
 

administered amount and the number of liver and splenic tumors (Johansen
 

1967; Wesch et al. 1983).
 

2.3 TOXICOKINETICS
 

2.3.1 Absorption
 

2.3.1.1 Inhalation Exposure
 

The absorption of thorium from the lungs is dependent upon the
 

chemical nature of the isotope and the size of the aerosol particle (Boecker
 

1963; Boecker et al. 1963; Moores et al. 1980; Newton et al. 1981; Sunta
 

et al. 1987; Syao-Shan 1970a). Increasing the particle size (>2 μm) 

increases deposition in the respiratory tract of mice, but decreases 

deposition in the alveolar region. A linear relationship was found between 

aerosol dosage of thorium-232 and the amount deposited in the alveolar 

region (Moores et al. 1980). Approximately twice as much thorium-234 is 

absorbed from the lungs of rats exposed to soluble thorium citrate (33%) 

compared to soluble thorium chloride (19%) (Boecker et al. 1963). However, 

following the initial difference in absorption, thorium shows the same 

distribution and excretion pattern, regardless of absorbed compound. SyaoShan (1970b) determined that 1.5-5.0% of the administered amount to rats is 

absorbed from the lungs 1 day after intratracheal administration of 

insoluble thorium-232 dioxide. Deposited thorium dioxide tends to remain in 

the lungs for long periods of time; 68-73% of thorium-232 dioxide remained 

in the lungs after 1 day, while 15-30% remained after 21 months. Thorium is 

removed primarily by ciliary clearance and is excreted in the feces 

(Wrenn et al. 1981). ICRP (ICRP 1979) assumes a total of 5% absorption of 

inhaled thorium.is transferred to the blood. However, the solubilities of 

the thorium compounds appear to be an important biological factor, as 

evidenced by differences in toxicity: LD5Os after 30 days following 

intraperitoneal injection in mice were 370.8 mg thorium/kg for soluble 

thorium-232 nitrate and 589.1 mg thorium/kg for soluble thorium-232 

chloride, while 2000 mg thorium/kg for insoluble thorium-232 dioxide 

resulted in deaths of only 2/18 mice (Syao-Shan 1970b). 

Lung levels of thorium (230 and 232) in workers occupationally exposed
 

to thorium (miners and millers) are significantly higher than those not
 

occupationally exposed (Gilbert et al. 1985; Singh et al. 1981; Vocaturo
 

et al. 1983; Wrenn et al. 1985). In a review of the epidemiological
 

evidence, Wrenn et al. (1981) concluded that the major route of exposure was
 

inhalation. Though intake of thorium through the air may account for less
 

than 1% of the total intake, absorption through the lungs accounts for
 

approximately 2/3 of the ultimate uptake in the body. This is due primarily
 
33
 

2. HEALTH EFFECTS
 

to the low gastrointestinal absorption rate (0.02%) in humans (Maletskos
 

et al. 1969; Sullivan et al. 1983).
 

2.3.1.2 Oral Exposure
 

ICRP has recommended a human gastrointestinal absorption value of 0.02%
 

for all forms of thorium (ICRP 1979). In a recent review of the literature by
 

Johnson and Lamothe (1989), a human gastrointestinal absorption value of 0.1
 

to 1% was calculated. Absorption of thorium in the form of thorium nitrate is
 

40-fold higher in neonatal rats (l.l-1.2%) (Sullivan et al.1980b, 1983) than
 

in adult rats (0.028-0.5%) (Sullivan et al. 1980a; Traikovich 1970).
 

Absorption of thorium in adult mice was 0.065% (Sullivan et al. 1983). These
 

data suggest that infants may be a susceptible population for exposure. In
 

other studies of actinide elements (including thorium), little variation in
 

gastrointestinal absorption was found between rats, guinea pigs, or dogs.
 

Solubility factors and particle size were found to be the determinants of
 

absorption (Sullivan 1980a). The absorption of various forms and isotopes of
 

thorium in rats was compared by Pavlovskaia (1973). It was found that the rate
 

of absorption of thorium-EDTA by the gastrointestinal tract was 60 times
 

greater than that of thorium dioxide. Thorium nitrate had a 4 times greater
 

absorption rate than thorium dioxide, and the absorption rate of thorium
 

chloride was 10 or 20 times greater than thorium dioxide, depending on
 

concentration. The absorption differences are attributable to different
 

solubilities of the various chemical forms.
 

2.3.1.3 Dermal Exposure
 

No studies were located regarding the rate and extent of absorption of
 

thorium following dermal exposure of humans or animals. Absorption of
 

thorium through the skin of animals can be inferred, however, because
 

testicular effects were seen in rats following application of thorium
 

nitrate directly to the lateroabdominal and scrotal skin (Tandon et al.
 

1975).
 

2.3.2 Distribution
 

2.3.2.1 Inhalation Exposure
 

The median concentrations of thorium-232, thorium-230, and thorium-228
 

in bone and various soft tissues of autopsy samples of a control population
 

from Grand Junction, CO, and Washington, DC are presented in Table 2-4
 

(Ibrahim et al. 1983; Wrenn et al. 1981; Singh et al. 1983). The maximum
 

concentration of all three thorium isotopes was found in the
 

tracheobronchial lymph nodes, with lungs and bones containing the next
 

highest activity of thorium isotopes. The high activity in the lymph nodes
 

implies that some of the thorium is cleared from the lungs by the lymphatic
 

system and deposited in the lymph nodes (Mausner 1982; Wrenn et al. 1981).
 

One possible explanation for the higher activity of thorium-228 than
 

35
 

2. HEALTH EFFECTS
 

thorium-232 in bone is that a major portion of the thorium-228 may be from
 

intake of radium-228 (radium appears to be absorbed from the
 

gastrointestinal tract to a greater extent than thorium); radium-228
 

concentrates in bones and decays to thorium-228 (Wrenn et al. 1981).
 

Studies in mice have shown that thorium-227, injected intraperitoneally,
 

distributes directly to the bone (Miiller et al. 1978); therefore, there may
 

be other explanations for the higher levels of thorium-228 than thorium-232
 

in the bone. More thorium-232 is retained in the lungs and lymph nodes
 

than thorium-230, suggesting that the solubilization of thorium-230 may be
 

faster than that of thorium-232 in the lungs. This may be due to thorium230 being inhaled in smaller particles than thorium-232. Consequently,
 

thorium-230 is removed more quickly from the lungs and is transported to
 

bone. The low content of thorium in the reticuloendothelial system (liver,
 

spleen, bone marrow) is in contrast to the distribution following
 

intravenous injection of thorotrast (Th02 colloid), where the vast majority 

of the thorium is taken up by the macrophages of the reticuloendothelial 

system. 

The dose rates to various organs in humans from environmental thorium
 

were estimated to be: 2.2-4.5, 0.41-0.44, 0.19-0.23, 0.057-0.071, and
 

0.071-0.072 mrad/year in the lymph nodes, bone, lungs, liver, and kidneys,
 

respectively (Wrenn et al. 1981). The dose rates to organs tended to be
 

higher in subjects living in the vicinity of uranium mine tailings, and the
 

dose rates to the organs in miners were even higher (4.8-10.5 mrad/year in
 

the lymph nodes and 1.2-1.5 mrad/year in the lungs) (Wrenn et al. 1981).
 

2.3.2.2 Oral Exposure
 

Autopsy data of persons environmentally exposed to thorium indicated
 

that pulmonary lymph nodes contained the highest levels of thorium (mean
 

53.4 μg/kg), followed by the lungs (mean of 5.4 μg/kg, ranging from 

1.5-16 μg/kg) and bones (mean of 0.55 μg/kg, ranging from 0.2-9.0 μg/kg) 

(Sunta et al. 1987). This study estimated that the daily intake of thorium 

through food, water, and inhalation was 2.29 μg /day, with the majority from 

food and water ingestion (2.27 μg/kg). However, it was determined that, 

since absorption through the gastrointestinal tract is so low (0.02%),
 

twothirds of the body burden of thorium results from inhalation exposure.
 

Neonatal rats retained 50% of the absorbed amount of thorium (1.1% of
 

the administered amount) in the skeleton (Sullivan et al. 1983). In the
 

same study, adult mice retained 75% of the absorbed amount of thorium
 

(0.065% of the administered amount) in the skeleton. Traikovich (1970)
 

found that about 75% of the absorbed amount (0.5% of the administered
 

amount) of thorium-232 nitrate was located in the bones of rats.
 

2.3.2.3 Dermal Exposure
 

No studies were located regarding the rate and extent of distribution
 

of thorium following dermal exposure of humans or animals.
 
36
 

2. HEALTH EFFECTS
 

2.3.2.4 Other Routes of Exposure
 

The majority of thorium studies concern the injection of colloidal
 

thorium-232 dioxide (Thorotrast) into patients as a radiographic contrast
 

medium. Approximately 97% of intravenously injected Thorotrast is taken up
 

by the reticuloendothelial system (RES) and distributed to the liver (59X%),
 

spleen (29%), and bone marrow (9%) (BEIR IV 1988; Kaul and Muth 1978; Kaul
 

and Noffz 1978; Parr et al. 1968; Wegener et al. 1976). Thorium is also
 

deposited in the lymph nodes throughout the body after being transported
 

from the liver and the spleen via the lymph ducts (Wegener et al. 1976).
 

The distribution is inhomogeneous in all tissues and organs since thorium,
 

which is complexed with transferrin in the serum (Peter and Lehmann 1981),
 

is taken up by the macrophages of the RES (Hallegot and Galle 1988;
 

Odegaard et al. 1978). Thorotrast tends to remain in the RES, but some of
 

the radium-228 and radium-224, produced by decay of their parent nuclides,
 

escapes from Thorotrast deposits, possibly as a result of the recoil energy
 

created from decay, and migrates to bone (Kaul and Noffz 1978; Parr et al.
 

1968). The dose rate to the organs of the RES is dependent upon the
 

nonuniform deposition of Thorotrast aggregates (clumping of the colloid
 

within the organ), the self-absorption of alpha particles in the aggregate
 

itself (alpha particles are absorbed by the aggregate and not by the
 

surrounding tissue), and the characteristic metabolic behavior of thorium
 

daughters (Kato et al. 1979; Kaul and Noffz 1978). Kaul and Noffz (1978)
 

determined that, as the concentration of Thorotrast increases in an organ,
 

alpha self-absorption is increased so that the effective alpha dose to the
 

tissue may be reduced. Kato et al. (1979) found that the value for
 

selfabsorption in fibrous tissue was higher than for nonfibrous tissue and was
 

dose dependent. Mean annual radiation doses from the intravenous injection of
 

30 mL of Thorotrast were: 30 rads/year in liver, 80 rads/year in spleen, 10
 

rads/year in red bone marrow, 4.5 rads/year in lungs, and 15 rads/year in the
 

cells on the bone surface. The dose to compact bone was 3.3 rads/year and the
 

dose to cancellous bone was 4.8 rads/year (Kaul and Muth 1978). Due to the
 

uneven distribution of thorium within the colloid, however, these mean annual
 

doses must be considered estimates. The fact that toxic effects rarely
 

appeared in the spleen following Thorotrast injection regardless of the high
 

radiation dose was unexplained, but implies that the liver is more susceptible
 

than the spleen to the effects of radiation and/or Thorotrast. Mays (1978)
 

determined the dose rate to the endosteum (the sensitive cells for the
 

induction of bone sarcoma may lie within 10 μm of bone surfaces) to be about 

16 rad/year (7 rad/year from radium-224 [5.1], thorium-228 [1.5], and radium228 [0.4] translocated from Thorotrast to calcified bone and 9 rad/year from 

Thorotrast on bone surfaces [5.9] and in red marrow [3.1]). Kaul and Noffz 

(1978) estimated that the alpha dose 30 years after injection of 25 mL of 

Thorotrast would be: 750 rad in liver, 2100 rad in spleen, 270 rad in red bone 

marrow, 18 rad in total calcified bone, 13 rad in the kidneys, and 60-620 rad 

in various parts of the lungs. 
37
 

2. HEALTH EFFECTS
 

The distribution pattern of intravenously-injected Thorotrast in
 

animals is similar to the pattern in humans; most of the Thorotrast is
 

taken up by the RES (Guimaraes et al. 1955; McNeil1 et al. 1973;
 

Reidel et al. 1979). Reidel et al. (1979) determined that the average
 

percent distribution of Thorotrast in the liver was within one order of
 

magnitude in mice, rats, rabbits, dogs, and humans. The amount of thorium
 

in the spleen of all species, except mice, was clearly below that in
 

humans. Only 50% of the thorium in rats was retained in the liver and
 

spleen, while approximately 85% was retained in humans. Direct comparison
 

of the species is difficult, since the data were taken from other authors
 

and analyzed by Reidel et al. (1979). The study concluded that the
 

biological behavior of colloids was similar in humans and animals. Kaul and
 

Heyder (1972) reported an extremely low rate of clearance of the colloid
 

form from the blood about 1 hour after intravenous injection in rabbits.
 

Subsequently, an increase in the rate of disappearance from the blood of the
 

colloid form (biological half-life of 90 minutes) and of the soluble form
 

(biological half-life of 75 minutes) was found. After 3, 6, or 12 hours,
 

23, 45, or 60% of the injected amount, respectively, was located in the
 

liver.
 

Maletskos et al. (1969) found that, following intravenous injection in
 

humans, thorium-234 citrate generally was retained in the skeleton and soft
 

tissues rather than in the RES, as found with Thorotrast. A similar
 

distribution pattern was found in dogs injected intravenously with thorium228 citrate (Stover et al. 1960). Intravenous exposure studies in rats and
 

guinea pigs, however, showed a distribution of thorium-234 sulfate similar
 

to Thorotrast: 60-68% in the liver, 3-7% in the spleen, 0.4-l% in the
 

kidneys, and about 10% in the remaining carcass, including bone (Scott
 

et al. 1952). Peter-Witt and Volf (1985) determined that the mass of
 

thorium-234 intravenously injected (carrier-free) in rats dictated the
 

pattern of distribution. A "critical" concentration of thorium in the


-7 -6 extracellular space was found to be between 10 and 10 ; above this
 

concentration thorium hydrolizes, becomes colloidal, and distributes
 

primarily to organs of the reticuloendothelial system; below this
 

concentration, thorium is distributed primarily to bone. The exposure
 

levels in the human and animal studies cannot be compared since the
 

concentration injected was not reported in the human study.
 

2.3.3 Metabolism
 

Transferrin plays a major role in the transport and cellular uptake of
 

thorium (Peter and Lehmann 1981). Thorium can be displaced from
 

transferrin by an excess of iron, but it is not known whether thorium and
 

iron bind to the same sites on the transferrin molecule. It has also been
 

determined that thorotrast (Th02 colloid) blocks the uptake of labelled 

protein by the RES in female rabbits and in both male and female rats (Hyman 

and Paldino 1967). The mechanism of the blockade is not clear. Sex 

differences were found in rabbits but not in rats. The particle size of the 
38
 

2. HEALTH EFFECTS
 

Thorotrast colloid influences its effect on the uptake of protein; only 

particles larger than 1 μm will interfere with uptake of protein by the RES. 

2.3.4 Excretion
 

2.3.4.1 Inhalation Exposure
 

After inhalation exposure, the primary route of excretion is in the
 

feces following ciliary clearance from the lungs to the gastrointestinal
 

tract (Wrenn et al. 1981). Fecal excretion may account for as much as 97%
 

of total excretion (Fisher et al. 1983). Higher levels of thorium-230 were
 

excreted in the feces by active crushermen (uranium mill workers exposed to
 

uranium ore dust in the crusher building) compared to retired workers or
 

controls (Fisher et al. 1983). Levels of thorium-230 in the urine were
 

comparable to those of retired workers, and the levels in both were
 

significantly greater than controls.
 

The biological half-lives of thorium-232 and thorium-230 in the lungs
 

of subjects living in the vicinity of uranium mine tailings (Grand Junction,
 

CO) were 5.3 and 1.4 years, respectively. The biological half-lives for
 

subjects in a non-mine area (Washington, DC) were 2.6 and 1.0 years for
 

thorium-232 and thorium-230, respectively (Wrenn et al. 1981). Since
 

biological half-lives in humans should be the same regardless of where
 

people live, the differences at the two locations may reflect the duration
 

of exposure, the time between exposure and sampling, or the inhalation of
 

larger particle size dust in Grand Junction compared to Washington, DC. The
 

232 isotope from nature apparently is retained in the lungs longer than the
 

230 isotope.
 

In a subject who had accidentally inhaled thorium-228 dioxide (alpha
 

emitter, radioactive half-life of 1.9 years), the biological half-life for
 

long-term clearance of thorium-228 from the body was at least 14 years as a
 

result of skeletal deposition (Newton et al. 1981). The early lung
 

clearance of thorium-228 was found to be on the order of approximately 50
 

days, thereby designating thorium dioxide a class W compound (biological
 

half-life in weeks) as opposed to the class Y (biological half-life in
 

years) designation recommended by ICRP (ICRP 1979). Davis (1985), however,
 

concluded that both thorium-232 nitrate and thorium-232 dioxide were class Y
 

compounds by determining the solubility in simulated lung fluid. The near
 

equilibrium of thorium-230, uranium-234, and uranium-238 in the lungs of
 

former uranium miners suggests that the elimination rates of these nuclides
 

are similar (Singh et al. 1987; Wrenn et al. 1985). In dogs, the thorium230/uranium-234 ratio increases with time, suggesting that uranium is
 

cleared faster than thorium from dog lungs (Singh et al. 1986). The
 

effective half-life of inhaled thorium-227 nitrate (radioactive half-life of
 

18.7 days and biological half-life of about 20 days) in the lungs of rats
 

was found to be about 10 days (Müller et al. 1975). Pavlovskaia et al.
 

(1974a) determined that the excretion of intratracheally-administered
 

thorium-228 (as thorium dioxide or thorium chloride) in the feces occurred
 
39
 

2. HEALTH EFFECTS
 

in two phases in the rat: in the first phase, up to 60% of the thorium-228
 

contained in the body was eliminated, and in the second phase, the rate of
 

thorium-228 excretion in the feces averaged 0.25% of the body burden daily.
 

2.3.4.2 Oral Exposure
 

It was determined in several species of animals (mice, rats, rabbits)
 

that more than 95% of the ingested amount is excreted in the feces within
 

several days (approximately 2-4 days) (Patrick and Cross 1948; Scott et al.
 

1952; Sollmann and Brown 1907). Sollmann and Brown (1907) concluded that,
 

since very little thorium was excreted in the feces following intravenous or
 

intramuscular injection, and since very little thorium was excreted in the
 

urine following ingestion, appreciable amounts of thorium were neither
 

absorbed nor excreted from the gastrointestinal tract.
 

2.3.4.3 Dermal Exposure
 

No studies were located regarding the rate and extent of excretion of
 

thorium following dermal exposure of humans or animals.
 

2.3.4.4 Other Routes of Exposure
 

A very small percentage of injected thorium-232 dioxide (Thorotrast) in
 

humans was excreted (more in the feces than urine) (Kaul and Muth 1978;
 

Molla 1975). Jee et al. (1967) found that a patient excreted 0.7% of the
 

injected amount of Thorotrast in the 17 days between injection and the death
 

of the patient (mode of excretion not reported). Kemmer (1979) determined
 

that the amount of thoron (radon-220) exhaled by the lungs in humans
 

correlated to the amount of Thorotrast intravenously injected. The thoron
 

(radon-220) correlated with a "radium-224 equivalent value."
 

In contrast to the thorium from Thorotrast (a thorium dioxide and
 

dextran suspension) after intravenous injection, a higher percentage of
 

thorium from more soluble thorium compounds is excreted. Following
 

intravenous injection of thorium-234 citrate in humans, there is a
 

relatively rapid but small (7%) amount of excretion within the first 20
 

days. A urine/feces ratio of 12 for male subjects and 24 for female
 

subjects was determined. About 93% of the injected thorium-234 was retained
 

at 100 days after injection, with a biological half-time of more than 5
 

years (Maletskos et al. 1969).
 

Less than 5% of thorium was excreted in the urine up to 42 days after
 

intravenous injection of thorium-234 sulfate in rats and guinea pigs (Scott
 

et al. 1952). After intravenous injection, the amount of thorium excreted
 

in the feces was 0.7-24.5% of the level administered for 14-42 days in
 

rats, 0.6 and 14.6% for 2 and 5 days in guinea pigs, and 0.9% for 7 days in
 

rabbits. In dogs injected with thorium-228 citrate, urinary excretion
 

dominated initially, but after 2.5 years, the fecal to urinary ratio
 

approximated 1.0 (Stover 1981; Stover et al. 1960). Thomas et al. (1963)
 
40
 

2. HEALTH EFFECTS
 

reported the excretion of thorium citrate administered as thorium-234
 

tracer plus thorium-232 carrier in rats. No differences were found in the
 

rate and route of excretion following various routes of administration
 

(intravenous, intraperitoneal, intratracheal, and intramuscular). In the
 

first 2 days, 25-30% of the thorium was excreted. Most of the thorium was
 

excreted in the feces and not in the urine. At a high exposure level, the
 

feces/urine ratio was 45 and at a low level, it was 1.6. This indicates
 

that at the high level, thorium was hydrolyzed, became insoluble, was taken
 

up by the RES and quickly cleared from the blood. The higher fecal levels
 

of thorium in the high exposure level animals suggest greater biliary
 

excretion.
 

2.4 RELEVANCE TO PUBLIC HEALTH
 

Very little data exist on health effects due to inhalation, oral, or
 

dermal exposure of thorium in humans or animals. The existing health
 

effects data suggest that thorium may pose a potential health threat to an
 

exposed population. Some evidence of respiratory disease and increased
 

incidence of pancreatic, lung, and hematopoietic cancers in humans was found
 

following inhalation exposure (Archer et al. 1973; Polednak et al. 1983;
 

Stehney et al. 1980). These effects were seen in thorium workers exposed to
 

many toxic agents, so that the effects cannot be attributed directly to
 

thorium exposure, but a causal effect cannot be discounted. High incidences
 

of malignancies found in patients injected intravenously with colloidal
 

thorium (Thorotrast) demonstrates the carcinogenic potential of thorium.
 

Subchronic animal studies have shown pneumocirrhosis and increased
 

incidences of lung cancer following inhalation exposure (Likhachev et al.
 

1973a). No studies regarding the health effects to humans from oral or
 

dermal exposure were reported in the literature. Animal studies of oral
 

exposure to thorium showed death at high exposure levels, but no other
 

systemic effects were observed (Patrick and Cross 1948). Animal
 

pharmacokinetic data suggest that, while soluble forms are absorbed to a
 

greater extent than insoluble forms, no chemical form of thorium is absorbed
 

appreciably from the gastrointestinal tract (Pavlovskaia 1973; Sullivan
 

et al. 1980a, 1980b, 1983). Dermally-administered thorium nitrate in
 

animals showed effects on the skin, the testes, and sperm morphology when
 

administered directly on the scrotum, but no other systemic effects were
 

observed (Tandon et al. 1975).
 

The chemical form of thorium (soluble or insoluble) inhaled,,ingested,
 

or injected determines the absorption distribution and excretion of thorium
 

into the body and, consequently, the toxic effects. Thirty-three percent of
 

inhaled thorium citrate and 19% of inhaled thorium chloride was absorbed
 

from the lungs of rats (Boecker et al. 1963), while 1.5-5.0% of insoluble
 

thorium dioxide was absorbed following intratracheal administration in rats
 

(Syao-Shan 1970b). Following ingestion of thorium, soluble chemical forms
 

were absorbed 4 (thorium nitrate), l0-20 (thorium chloride) or 60
 

(thorium-EDTA) times greater than insoluble thorium dioxide (Pavlovskaia
 

1973). The fact that the LD5Os of these thorium compounds increase with 
41
 

2. HEALTH EFFECTS
 

solubility in a similar pattern, thorium dioxide <<< thorium nitrate <
 

thorium chloride (Syao-Shan, 1970b), indicates that solubility and acute
 

toxicity are closely related. The less soluble forms of thorium, however,
 

are of greater radiological concern because they remain in the body for long
 

periods of time. Thorium dioxide is retained in the body for long periods
 

of time after inhalation (Newton et al., 1981>, and the long-term radiation
 

effects from thorium dioxide, as evidenced by the induction of cancer by
 

intravenously injected Thorotrast, are apparently of greater concern than
 

from the more soluble (and readily excreted) forms of thorium.
 

The organ distribution of the thorium isotopes was similar in humans
 

and dogs, with the skeleton having the highest levels of thorium (Singh
 

et al. 1988). In both humans and dogs, the level of thorium-232 > thorium230 > thorium-228 in the lungs. The average skeletal activity of thorium228 was 30-50 times greater than thorium-232 in dogs, but the difference was
 

only 4- to 5-fold in humans. The higher levels of thorium-228 in dogs
 

compared to humans may be due to a higher intake of radium-228 in their
 

diet (Singh et al. 1988). Radium-228 will translocate to bones and decay to
 

thorium-228. In this study, dogs had been exposed in the food, water, and
 

air to simulate human exposure. Wrenn et al. (1983) reported that thorium230, uranium-234, and uranium-238 were in close equilibrium in the lungs of
 

humans, while they were in disequilibrium in the lungs of dogs (thorium230/uranium-234 ratio averaged 6.3). The data suggest that, under these
 

experimental conditions, uranium is cleared faster than thorium from dog
 

lungs (Wrenn et al. 1983). These species differences have been proven not
 

to be due to radiochemical methods (Singh et al. 1986), but may be due to
 

time factors or to a particle size difference, as the experimental animals
 

and the uranium miners inhaled aerosols of different composition and size.
 

The vast majority of the human thorium data deal with the effects of
 

Thorotrast (colloidal thorium-232 dioxide) administered intravenously to
 

patients as a radiologic contrast medium. The literature suggests that the
 

toxic effects of Thorotrast are due to the alpha radiation effects of
 

thorium and not to the chemical effects of thorium or of the colloid (BEIR
 

IV 1988; Taylor et al. 1986). Cirrhosis of the liver, hepatic tumors, and
 

blood dyscrasias were the most common effects of intravenously injected
 

Thorotrast. Because Thorotrast is no longer used in this capacity, the
 

introduction of new health risks from injection of Thorotrast is not
 

considered a prob.lem. Although the pharmacokinetic behavior of
 

intravenously injected Thorotrast in the body is vastly different from the
 

behavior of inhaled or ingested thorium, and the injected Thorotrast was
 

sometimes enriched with a higher proportion of more radioactive isotopes of
 

thorium (e.g., thorium-230 or thorium-228) than is generally found in the
 

environment, the effects from Thorotrast in patients suggest that thorium
 

could be a potential carcinogen (BEIR IV 1988).
 

The main issue regarding thorium is its potential radiological effect.
 

Since thorium is an alpha-emitting bone-seeker, the small amount of thorium
 

that enters the body migrates to bone surfaces. The carcinogenic potential
 
42
 

2. HEALTH EFFECTS
 

of thorium is most likely a result of its radiological properties. 

Different isotopes of thorium have different radioactive half-lives: 

thorium-232 (natural thorium) is a long-lived alpha emitter (half-life of 

1.4x1010 years), thorium-230 is a relatively long-lived alpha-emitter that 

is a member of the uranium decay series (half-life of 8x104

 years), thorium228 is a short-lived alpha-emitter that is a member of the thorium series 

(half-life of 1.9 years), and thorium-234 is a short-lived beta-emitter that 

is a member of the uranium series (half-life of 24.1 days). 

For short-term experiments, thorium-232 is considered radiologically
 

inert since its half-life is so long. Therefore, the chemical toxicity of
 

thorium was tested using this isotope. The low chemical toxicity of
 

thorium was evidenced by the lack of initial systemic effects in patients
 

injected with Thorotrast and in occupationally exposed workers. Animal
 

studies also showed low toxicity (Guimaraes et al. 1955; Patrick and Cross
 

1948). Natural thorium (thorium-232) is toxic only after a latency period
 

of 20-30 years, when the radiological effects are manifested.
 

The radiological effects of thorium were examined by testing isotopes
 

with shorter radioactive half-lives than thorium-232. No increased
 

mortality was found in mice injected intravenously with 0.5 mL Thorotrast
 

(3660 mg thorium-232/kg) (Guimaraes et al. 1955), or in dogs after
 

intraarterial injection of thorium nitrate (476 mg thorium-232/kg), but the
 

LD50 for intravenously-injected thorium-230 in rats was 42.7 mg thorium/kg 

(Boone et al. 1958). The toxic effects of thorium were attributed to 

radiological and not chemical effects (Boone et al. 1958). 

The removal of thorium from the body has been achieved by the use of
 

chelating agents, primarily ethylenediaminetetraacetic acid (EDTA) and
 

diethylenetriaminepentaacetic acid (DTPA) (Fried and Schubert 1961; Peter-


Witt and Volf 1984, 1985; Young and Tebrock 1958). In animals, DTPA was
 

about 10 times as effective at removing thorium from the body as EDTA, and
 

Ca-DTPA was more effective than Zn-DTPA (Fried and Schubert 1961; Peter-Witt
 

and Volf 1985). The total percentage of thorium removed from the body using
 

chelation therapy was not reported. Thorium administered in the monomeric
 

form (single molecule) was cleared more effectively from the body than when
 

given in the polymeric form (colloidal). The polymeric form was deposited
 

primarily in the liver and the level was only lowered when massive, nearlethal
 

amounts of. chelating agent were given (Fried and Schubert 1961). The
 

chelating agents were most effective shortly after thorium dosing (Young and
 

Tebrock, 1957).
 

Death. No deaths in humans resulting from acute inhalation, oral, or
 

dermal exposure to thorium have been reported. Deaths from various forms of
 

cancers have been observed (liver tumors, leukemia, bone tumors), however,
 

in patients injected intravenously with Thorotrast (Thorotrast was enriched
 

with more active forms of thorium than are environmentally available) (BEIR
 

IV 1988). The toxicity of thorium depends on the specific isotope (dose
 

rate effect: isotopes with shorter radioactive half-lives and higher energy
 
43
 

2. HEALTH EFFECTS
 

are more toxic after intravenous injection [Boone et al. 19581) and the
 

chemical form of thorium (total dose effect: soluble compounds are more
 

toxic than insoluble compounds after intraperitoneal injection [Syao-Shan
 

1970b]). Intravenous and intraperitoneal injections, however, are not
 

normal routes of environmental exposure. No deaths were reported in animals
 

following inhalation exposure, and high exposure levels were necessary to
 

produce death in animals following oral exposure, since gastrointestinal
 

absorption is very small (0.02%). The acute exposure levels required to
 

cause death in humans are not known and cannot be predicted based on the
 

animal data.
 

Systemic Effects. There is evidence in the literature of an increase
 

in respiratory disease (SMR=1.31) (Polednak et al. 1983) and hepatic effects
 

(increase in serum levels of aspartate aminotransferase, globulin, and total
 

bilirubin) (Farid and Conibear 1983) in individuals occupationally exposed
 

to thorium. The individuals, however, were occupationally exposed to other
 

toxic substances (uranium dust) as well as other sources of radioactivity,
 

so that these effects cannot be attributed directly to thorium. Both
 

studies suggest that the observed effects may have resulted from
 

radiological toxicity. Progressive cirrhosis of the lungs was observed in
 

rats subchronically exposed by inhalation to thorium dioxide (Likhachev
 

et al. 1973a). The severity of the lung cirrhosis was related directly to
 

the radiation dose and treatment, but the exact radiation exposure level was
 

not reported. Effects on hematological parameters, suggestive of
 

radiological toxicity, were found in dogs subchronically exposed by
 

inhalation to various chemical forms of thorium (Hall et al. 1951). No
 

other systemic effects were observed in animals exposed by inhalation, and
 

no systemic effects were found in orally or dermally exposed animals.
 

Following intravenous injection of Thorotrast, cirrhosis of the liver
 

was the primary systemic effect in humans and animals. Hematological
 

disorders (aplastic anemia, leukemia, myelofibrosis, and splenic cirrhosis),
 

cardiovascular effects (myocardial infarction, severe coronary luminal
 

narrowing and internal alteration of the carotid artery), and Thorotrastoma
 

(localized fibrosis surrounding deposits of Thorotrast) were also found in
 

patients injected with Thorotrast. The effects of Thorotrast were a result
 

of the radiological toxicity of thorium.
 

The existing data indicate that, in humans, respiratory and hepatic
 

effects result from inhalation exposure and that the liver, hematopoietic
 

system and cardiovascular system are the target organs following intravenous
 

injection of Thorotrast. Studies in animals have not reported effects in
 

these tissues, with the exception of the liver, further supporting the
 

concern that the humans were exposed to other toxic agents, thereby
 

preventing an accurate assessment of the systemic toxicity of thorium.
 

Immunological Effects. Studies in humans or animals were not located
 

regarding the immunological effects of thorium following oral and dermal
 

exposure. No histopathological effects were found in the lymph nodes of
 
44
 

2. HEALTH EFFECTS
 

animals exposed by inhalation to thorium dioxide (Hodge et al. 1960).
 

Following injection of Thorotrast in humans, fibrosis of the lymph nodes and
 

the spleen were observed (da Silva Horta 1967a; Wegener and Wesch 1979;
 

Wegener et al. 1976). A suppression of immune response was found in mice
 

following intravenous and intraperitoneal injection of Thorotrast (Michael
 

and Murray 1970). Thorotrast affected lymphoid cells involved in antibody
 

formation and blockaded phagocytic cells in organs of the RES. In the
 

absence of data via relevant routes of exposure, the immunotoxic potential
 

of thorium cannot be fully assessed.
 

Neurological Effects. There have been no human or animal studies
 

specifically designed to determine the neurological effects of thorium.
 

Neurological effects, such as narcosis, ataxia, or cholinergic signs, have
 

not been reported in any of the inhalation or oral studies in animals. It
 

is not known whether humans would experience major neurological deficits
 

from exposure to thorium.
 

Developmental Effects. There have been no human or animal studies
 

regarding the developmental effects of thorium following any relevant route
 

of exposure (inhalation, oral, dermal). Since information regarding
 

developmental effects in animals are not known, conclusions regarding the
 

potential for developmental effects in humans are not known.
 

Reproductive Effects. No studies were located regarding reproductive
 

effects in humans or animals following inhalation or oral exposure to thorium.
 

When thorium was applied directly to the scrotum of rats, mild edema of the
 

seminiferous tubules and the interstitium and desquamation of sperm and giant
 

spermatid-type cells were observed (Tandon et al. 1975). Since information is
 

limited to one study in one species and one sex, and since no information on
 

the effect of thorium on reproductive function was located, conclusions
 

regarding the potential for humans to develop these effects are not known.
 

Genotoxic Effects. Chromosomal aberrations have been found in the
 

lymphocytes of Thorotrast patients and occupationally exposed workers
 

(Fischer et al. 1967; Hoegerman and Cummins 1983; Kemmer et al. 1971, 1979).
 

A study by Nishioka (1975) screened thorium chloride (0.05 M) as a potential
 

mutagen by determining whether it inhibited bacterial growth. Since
 

bacterial growth was not inhibited, thorium was not further tested for
 

mutagenicity. Thorium chloride (10%) was shown to have no effect on the
 

survival of Klebsiella oxvtoca or Klebsiella pneumoniae (Wong 1988). Based
 

on the limited human data, thorium appears to be a genotoxic agent.
 

Cancer. Increased incidences of lung, pancreatic, and hematopoietic
 

cancers were observed in individuals occupationally exposed to thorium
 

(Archer et al. 1973; Polednak et al. 1983; Stehney et al. 1980). The
 

individuals were occupationally exposed to other toxic substances (uranium
 

dust) as well as other sources of radioactivity; hence, the higher
 

incidences of cancer cannot be attributed directly to thorium. The follow­
45
 

2. HEALTH EFFECTS
 

up period in the studies ranged from 17-35 years, and the latency periods of
 

the various types of cancer were not reported. In rats chronically exposed
 

by inhalation to thorium as thorium dioxide, lung tumors were found that
 

correlated with the total radioactivity in the lungs (Likhachev 1976;
 

Likhachev et al. 1973b). The exact amount of administered radioactivity was
 

not reported. No studies in humans were located regarding oral or dermal
 

exposure to thorium. No malignancies were reported following oral or dermal
 

exposure of rats to thorium, but these studies were of relatively short
 

duration (oral study, 4 months; dermal study, 15 days) and were not designed
 

to detect an increase in the incidence of neoplasms.
 

Following intravenous injection of Thorotrast in humans and animals,
 

various malignancies were found, primarily liver cancers (latency period of
 

25-30 years), leukemia (latency period of 20 years), and bone cancers
 

(latency period of about 26 years). Short-lived daughter products of
 

thorium also resulted in the induction of bone sarcoma because of their
 

short radioactive half-lives. Intravenous injection of thorium-228 resulted
 

in dose-dependent induction of bone sarcoma in dogs (Lloyd et al. 1985; Mays
 

et al. 1987; Stover 1981; Wrenn et al. 1986). At the highest administered
 

level, the animals died from systemic radiological effects (e.g., radiation
 

induced blood dyscrasia and nephritis) before the bone sarcoma could develop
 

(Stover 1981; Taylor et al. 1966). A relationship was found between the
 

amount of thorium-227 (half-life of 18.7 days) injected intraperitoneally
 

and the incidence of bone sarcoma in mice (Luz et al. 1985; Miiller et al.
 

1978).
 

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 of
 

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
 

half-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 mineral nutrients such as copper, zinc
 
46
 

2. HEALTH EFFECTS
 

and selenium). Biomarkers of exposure to thorium 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 epithelial 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
 

thorium 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 Thorium
 

Exposure to thorium can be determined by measurement of radioactive
 

thorium and/or daughters in the feces, urine, and expired air. The primary
 

route of excretion of thorium is in the feces following either inhalation or
 

oral exposure. Fecal excretion is essentially complete in a matter of
 

several days (Patrick and Cross 1948; Scott et al. 1952; Sollman and Brown
 

1907; Wrenn et al. 1981). The measurement of external gamma rays emitted
 

from thorium daughters present in the subject's body and of thoron in the
 

expired air many years following exposure can be used to estimate the body
 

burden of thorius'(Conibear 1983).
 

No tissue concentrations in humans were found that correlated with
 

health effects, but about 20 pCi was found in the lungs of an exposed worker
 

suffering from lung fibrosis. However, it was not clear if the fibrosis was
 

due to thorium or to rare-earth-containing fumes and dusts (Vocaturo et al.
 

1983).
 

Blood levels of thorium following oral exposure of humans to simulated
 

radium dial paint demonstrated that approximately 0.02% of the ingested
 

amount was absorbed by the gastrointestinal tract (Maletskos et al. 1969).
 

This study was the basis for the ICRP (1979) recommendation of an oral
 

absorption factor of 0.02% for thorium.
 
47
 

2. HEALTH EFFECTS
 

2.5.2 Biomarkers Used to Characterize Effects Caused by Thorium
 

Occupational and experimental studies have shown that the lung, liver,
 

and hematopoietic system are the target organ systems following inhalation
 

exposure to thorium. No relationship was found, however, between the
 

measured body burden of thorium in exposed workers and complete blood count
 

parameters (e.g., hemoglobin, red and white blood cell) (Conibear 1983).
 

Target organs systems have not been identified for oral or dermal exposure
 

to thorium. For further information on the health effects of thorium, see
 

Section 2.2 of Chapter 2.
 

2.6 INTERACTIONS WITH OTHER CHEMICALS
 

Thorium is commonly found in combination with other actinide elements,
 

with organic and inorganic chemicals, and with acids and bases during
 

occupational exposure. The health effects of occupational exposures to
 

thorium on humans, therefore, cannot necessarily be attributed to thorium.
 

The daughter products of thorium have unique properties that also add to the
 

radiological toxicity of thorium. For further information, see the
 

toxicological profiles on uranium, radon, and radium.
 

The injection of tetracycline either before or simultaneously with
 

injection of thorium-228 markedly reduced the deposition of thorium-228 in
 

rat bone to about 60% of control values (Taylor et al. 1971). The effects
 

of tetracycline injection following injection of thorium-228 were not
 

reported. Studies with a similar actinide element, plutonium, suggest that
 

a thorium-tetracycline complex may be formed, which is excreted rapidly
 

through the kidneys. Similarly, chelating agents such as EDTA and DTPA can
 

remove some thorium from the body (see Section 2.4).
 

2.7 POPUIATIONS THAT ARE UNUSUALLY SUSCEPTIBLE
 

Neonatal animals have been found to absorb 20-40 times more thorium
 

through the gastrointestinal tract than adult animals (Sullivan et al.
 

1980a, 1980b, 1983) indicating that children may be more susceptible to
 

both the chemical and radiological effects of thorium than adults.
 

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 thorium 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 thorium.
 
48
 

2. HEALTH EFFECTS
 

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
 

substancespecific research agenda will be proposed.
 

2.8.1 Existing Information on Health Effects of Thorium
 

The existing data on health effects of inhalation, oral, and dermal
 

exposure of humans and animals to thorium are summarized in Figure 2-3. The
 

purpose of this figure is to illustrate the existing information concerning
 

the health effects of thorium. 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.
 

The effects of thorium in humans have been well studied following
 

intravenous exposure, but not following any relevant routes of exposure
 

(inhalation, oral, dermal). Several case studies exist on the effects on
 

thorium millers, especially on the genotoxic and carcinogenic effects of the
 

agent. No studies on the effects of pure thorium on humans have been found
 

by any route of exposure (the thorium miners were exposed to many toxic
 

agents in addition to thorium, and it is impossible to directly attribute
 

effects to thorium). The effects of thorium in animals following
 

intravenous injection have been well studied, but very few studies have
 

been done by a relevant route of exposure. Figure 2-3 reflects the few
 

studies regarding oral and dermal exposure of animals to thorium located in
 

the existing literature.
 

2.8.2 Identification of Data Needs
 

Acute-Duration Exposure. No studies were located regarding the effects
 

of thorium in humans following acute exposure by any relevant route.
 

Intravenous injection of thorium as an x-ray contrast medium into people
 

resulted in death from various malignancies 20-30 years following injection.
 

Animals studies were limited to determining dose levels resulting in death
 

following inhalation and oral exposure, and in dermal and reproductive
 

effects following dermal administration to the lateroabdominal and scrotal
 

skin, Inhalation-based pharmacokinetic data indicate that the lymph nodes,
 

lungs, and bone may be the target organs of thorium toxicity. Oral
 

pharmacokinetic data indicate that bone may be the target organ of toxicity
 

following ingestion of thorium. The acute toxicity of thorium in animals
 

has also been tested by routes of exposure (intravenous, intraperitoneal,
 

intratracheal) that are difficult to interpret, and it would be useful to
 

compare these toxic levels to toxic levels found after administration by a
 

relevant route (inhalation, oral, dermal). Knowledge about the acute
 

toxicity of thorium is important because people living near hazardous waste
 

sites might be exposed for brief periods.
 

50
 

2. HEALTH EFFECTS
 

Intermediate-Duration Exposure. No studies were located regarding the
 

effects of thorium in humans following intermediate-duration exposure by any
 

route of exposure. Two animal studies were reported: one inhalation study in
 

rats showing lung damage and one oral study in mice resulting in death.
 

Intermediate-duration dermal studies in animals were not located. The lungs
 

appear to be the target organs following intermediate-duration inhalation
 

exposure to thorium. Oral pharmacokinetic data indicate that bone may be the
 

target organ of toxicity following ingestion of thorium. More extensive
 

studies by all relevant routes (inhalation, oral, dermal) would be useful in
 

assessing both the chemical and radiological toxicity of thorium.
 

Intermediate-duration toxicity information is important because people
 

living near hazardous waste sites might be exposed for corresponding time
 

periods.
 

Chronic-Duration Exposure and Cancer. Several studies have been
 

reported regarding the toxic effects on workers occupationally exposed to
 

thorium or monazite sand found in refinery dust. In these studies, effects
 

on the lungs and chromosomes and an increased cancer incidence were
 

reported. Because the workers were exposed to many toxic agents, however,
 

effects cannot be attributed directly to thorium. Epidemiology studies
 

investigating workers exposed primarily to thorium (e.g., during the
 

production of gas lamp mantles) would be useful. No human studies were
 

located regarding chronic oral or dermal exposure. Many studies on longterm
 

radiological effects of thorium have been reported following
 

intravenous injection of thorium dioxide in the form of Thorotrast in both
 

humans and animals. Effects reported in these studies included cirrhosis of
 

the liver, hematological disorders, and various malignancies. Studies have
 

shown that the lungs and the hematological system are the target organ
 

systems for thorium toxicity. Oral pharmacokinetic data indicate that bone
 

may be the target organ of toxicity following ingestion of thorium. Chronic
 

studies by relevant routes of exposure, inhalation and oral, are important
 

because people living near hazardous waste sites might be exposed to thorium
 

for years.
 

Studies in workers occupationally exposed to thorium have reported an
 

increase in the incidence of pancreatic, lung and hematopoietic cancers.
 

These effects were observed in workers exposed to many toxic agents, so they
 

cannot be attribu.ted directly to thorium. Intermediate duration inhalation
 

exposure of rats to thorium dioxide resulted in lung tumors. No data were
 

located regarding the carcinogenic effects of oral or dermal thorium
 

exposure in humans or animals. Further chronic exposure studies by all
 

relevant routes of exposure (inhalation, oral, dermal) using wider exposure
 

level ranges and a number of species of animals may be useful in assessing
 

the carcinogenic potential of thorium in humans.
 

Genotoxicity. Occupationally exposed workers as well as patients
 

injected with Thorotrast show chromosomal abnormalities in their
 

lymphocytes. No in vivo genotoxicity studies in animals or in vitro studies
 
51
 

2. HFALTH EFFECTS
 

in bacterial strains were located, but these studies may be useful in
 

determining whether thorium has the potential to cause gene mutations in
 

addition to chromosomal abnormalities.
 

Reproductive Toxicity. No studies were located regarding the
 

reproductive effects of thorium in humans following exposure by any route.
 

Neither inhalation nor oral reproduction studies in animals were located.
 

Pharmacokinetic data following inhalation or oral exposure were not located
 

to allow the prediction of possible reproductive effects. One dermal rat
 

study found testicular effects after administration directly onto the
 

scrotal skin. Additional inhalation, oral, and dermal reproduction studies
 

and multigenerational studies would be helpful in assessing the potential
 

risk to humans.
 

Developmental Toxicity. No studies were located regarding the
 

developmental effects of thorium in humans or animals following exposure by
 

any route. Also, pharmacokinetic data do not exist that may predict
 

whether thorium crosses the placental barrier. Further developmental
 

studies in animals by all relevant routes of exposure may clarify the
 

potential developmental effects of thorium in humans.
 

Immunotoxicity. No studies were located regarding the immunological
 

effects of thorium in humans or animals following any relevant route of
 

exposure (inhalation, oral, dermal). One report, however, showed
 

intraperitoneal and intravenous injection of thorium dioxide in mice
 

resulted in a suppression of the immune response. Studies on the
 

immunotoxic effects of thorium, both histopathological and effects on the
 

immune response, by all relevant routes of exposure in animals may
 

determine the potential immunotoxic effects in humans.
 

Neurotoxicity. No studies were located regarding the neurological
 

effects of thorium in humans or animals following exposure by any route.
 

Other metals, such as lead, however, have been shown to have more severe
 

neurological effects on children than adults; therefore, it is possible that
 

children may be more susceptible than adults to the effects of thorium.
 

Studies on the neurological effects of thorium, both histopathological and
 

effects on behavior by all relevant routes of exposure in animals, may
 

determine the potential neurological effects in humans.
 

Epidemiological and Human Dosimetry Studies. Epidemiology studies have
 

investigated the relationship between long-term exposure to thorium and
 

systemic effects, genotoxic effects, and cancer in humans. The authors of
 

these studies found increases in respiratory disease and certain types of
 

cancer (lung, pancreatic, hematopoietic) in exposed thorium workers, but the
 

findings were not definitive. The existing epidemiological studies are often
 

weakened by not sufficiently accounting for smoking habits or exposure to
 

other chemicals and by relying too heavily on the accuracy of death
 

certificates. Increased incidences of chromosomal abnormalities were found in
 

exposed workers (approximately 4% dicentric in controls vs. 20% in
 
52
 

2. HEALTH EFFECTS
 

exposed workers) as well as in patients injected intravenously with
 

colloidal thorium dioxide (Thorotrast) (l-25 dicentric per 100 cells). The
 

occupational studies focus primarily on adult males. It would be useful to
 

study groups that include women, children, and neonates that have been
 

exposed to greater than normal levels of thorium to determine their level of
 

susceptibility. Epidemiology studies investigating workers exposed
 

primarily to thorium (e.g., during the production of gas lamp mantles) would
 

also be useful. Further studies assessing the cause/effect relationship
 

between thorium exposure and human health effects would be helpful in
 

monitoring individuals living near a hazardous waste site.
 

Biomarkers of Exposure and Effect. The major route of excretion of
 

inhaled or ingested thorium is in the feces. Exposure to thorium can be
 

determined by measurement of thorium and/or its daughters in the feces,
 

urine, blood, or expired air. The body burden of thorium may be estimated
 

by the measurement of external gamma rays emitted from thorium daughters in
 

the body. Further studies correlating thorium exposure with thorium and/or
 

thorium daughters in the urine, feces, blood, and expired air would be
 

helpful in more accurately quantifying thorium exposure.
 

No relationship was found between the measured body burden of thorium
 

and complete blood count parameters (e.g., hemoglobin, red and white blood
 

cells) in humans occupationally exposed to thorium (see Section 2.2.1.2).
 

Further studies may reveal thorium-specific biomarkers that may alert health
 

professionals to thorium exposure before toxicological effects occur.
 

Absorption, Distribution, Metabolism and Excretion. The absorption of
 

thorium from the lungs and the gastrointestinal tract and the tissue
 

distribution of thorium have been studied in both humans and animals.
 

Inhalation was found to be the major route of exposure with gastrointestinal
 

absorption being very low (see Section 2.3.1). The data in humans correlate
 

well with the animal data. The excretion of systemic thorium in humans has
 

not been extensively studied, especially the partition between feces and
 

urine, and work in this area in both humans and animals would be helpful.
 

No studies were located regarding the pharmacokinetics in humans or animals
 

following dermal exposure to thorium. Studies on the dermal route of
 

exposure may be helpful in determining whether thorium is a human health
 

hazard by this route.
 
53
 

2. HEALTH EFFECTS
 

2.8.3. On-going Studies
 

No on-going studies were located relating to the toxicity of thorium in
 

humans or animals.
 

55
 

3. CHEMICAL AND PHYSICAL INFORMATIONS
 

3.1 CHEMICAL IDENTITY
 

Data pertaining to the chemical identity (that is, the common terms or
 

smbols used for the identification of the element) of thorium are listed in
 

Table 3-1.
 

3.2 PHYSICAL AND CHEMICAL PROPERTIES
 

The physical and chemical properties of elemental thorium and a few
 

rpresentative water soluble and insoluble thorium componds are presented
 

in Table 3-2. Water soluble thorium compounds include the chloride,
 

fluoride, nitrate, and sulfate salts (Weast 1983). These compounds dissolve
 

fairly readily in water. Soluble thorium compounds, as a class, have
 

greater bioavailability than the insoluble thorium compounds. Water
 

Insoluble thorium compounds include the dioxide, carbonate, hydroxide,
 

oxalate, and phosphate salts. Thorium carbonate is soluble in concentrated
 

sodium carbonate (West 1983). Thorium metal and several of its compounds
 

are commercially available. No general specifications for commercially
 

prepared thorium metal or compounds have been established. Manufactures
 

prepare thorium products according to contractual specifications (Hedrick
 

1985)
 

Thorium is a metallic element of the actinide series. It exists in
 

several isotopic forms. The isotope thorium-232 is a naturally occuring
 

element that is radioactive. Ti decays through the emission of a series of
 

alpha and beta particles, gamma radiation, and the formation of daughter
 

products, finally yielding the stable isotope of lead, lead-208. The decay
 

series of thorium-232, together with that of uranium-238 and uranium-235,
 

are shown in Figure 3-1. It can be seen from Figure 3-1 that the isotopes
 

thorium-234 and thorium-230 are produced during the decay of naturally
 

occuring uranium-238, the isotope thorium-228 diring the decay of thorium-232,
 

and the isotopes thorium-231 and thorium-227 during the decay of
 

naturally occuring uranium-235. Of these naturally produced isotopes of
 

thorium, only thorium-232, thorium-230, and thorium-228 have long enough
 

half-lives to be environmentally significant. More than 99.99% of natural
 

thorium is thorium-232; the rest is thorium-230 and thorium-228.
 

Including artifically produced isotopes, there are 12 isotopes of
 

Thorium with atomic masses ranging from 223 to 234. All are radioactive and
 

Decay with the emission of alpha or beta particles and/or gamma radiation
 

(West 1983). The percent occurrence and the energies of the major alpha
 

and beta particles emitted by these isotopes are shown in Table 3-3. In
 

general, the alpha particles are more intensely ionizing and less penetrating
 

than the beta particles. The gamma radiation is the most
 

penetrating of the three, but it has the least ionizing intensity. Alpha
 

particles do not penetrate external skin to a sufficient depth to produce
 

biological damage due to the protective effect of the epidermis. However,
 

alpha particles emitted from thorium deposited in the lung are able to
 

penetrate lung tissue and produce adverse biological damage since the
 





61
 

3. CHEMICAL AND PHYSICAL INFORMATION
 

protective coating of the lung tissue is very thin. In turn, beta
 

particles are able to penetrate the skin to a sufficient depth to cause
 

biological effects in the skin just below the epidermis. Likewise, they
 

penetrate lung tissues to a greater depth. Gamma rays can generally pass
 

through all tissue and interact with tissue at any depth.
 

Alpha particles give up all of their energy in a very short distance
 

and, hence, produce ionization. Beta particles produce less dense
 

ionization, and gamma rays produce less yet. In general, the severity of
 

biological effects of exposures to ionizing radiations is proportional to
 

the density of the ionization produced by their passage through tissue.
 

Finely divided thorium metal is pyrophoric in air, and thorium ribbon
 

burns in air to give the oxide. The metal also reacts vigorously with
 

hydrogen, nitrogen, the halogens, and sulfur. Thorium compounds are stable
 

in +4 oxidation state (Katzin 1983). Details of thorium chemistry are given
 

by Katzin (1983).
 

63
 

4. PRODUCTION, IMPORT, USE, AND DISPOSAL
 

4.1 PRODUCTION
 

The principal source of thorium is monazite (phosphate of rare earth
 

metals, usually with thorium), a mineral produced as a by-product of mineral
 

sands mined for titanium and zirconium. Thorium compounds are extracted
 

from monazite by acid and alkali treatment processes (Hedrick 1985).
 

Associated Minerals, a subsidiary of the Australian-owned firm Associated
 

Minerals Consolidated Ltd., was the only commercial operation in the United
 

States to produce purified monazite in 1987. This company produced monazite
 

as a by-product of mineral sands mined for titanium and zirconium minerals
 

at Green Cove Springs, FL. The monazite produced in the United States was
 

exported. Thorium products used domestically were obtained from imported
 

material, existing company stocks, and thorium nitrate previously released
 

from the National Defense Stockpile (Hedrick 1987). In 1984, the mine
 

production capacity for thorium in the United States was 20 metric tons of
 

thorium oxide equivalent (Hedrick 1985). Actual mine production data have
 

not been released over the years to avoid disclosure of proprietary
 

information. Nevertheless, the domestic mine production volume of monazite
 

or other thorium ore is expected to be approximately the same as the United
 

States export volume. The principal processors of thorium-containing ores
 

in the United States during 1987 were W.R Grace & Co. in Chattanooga, TN,
 

and Rhone-Poulenc Inc. in Freeport, TX (Hedrick 1987). United States
 

companies that have thorium processing and fabricating capacities are listed
 

in Table 4-1.
 

4.2 IMPORT
 

Imports of thorium into the United States in metric tons of thorium
 

oxide equivalent were 45.8 in 1983, 45.4 in 1984, 69.3 in 1985, 19.7 in
 

1986, and 30.7 in 1987. Additionally, concentrated monazite containing 350­

550 tons of Th02 has been imported annually (Hedrick 1987). Imports of 

thorium by the United States may decrease as a result of increased costs of 

processing thorium. These increased costs are primarily due to increasing 

concerns about the radiological risks of handling, storing, and disposing of 

thorium, thereby encouraging the search for nonradioactive substitutes 

(Hedrick 1987). Exports of thorium metal, waste, and scrap from the United 

States in metric tons of thorium oxide equivalent were 1.1 in 1983, 1.0 in 

1984, 1.6 in 1985, 17.0 in 1986, and 20.4 in 1987 (Hedrick 1987). 

4.3 USE
 

Thorium can be used as fuel in the generation of nuclear energy.
 

However, there is currently only one plant in the United States that is
 

using thorium for the production of energy (Hedrick 1987). In 1983, 3
 

metric tons of thorium oxide equivalent were used for energy uses in the
 

United States (Hedrick 1985). Nonenergy uses accounted for almost all of
 

the thorium used in the United States during 1987. The 1987 use pattern
 

for thorium was as follows: refractory applications (57%); lamp mantles
 

(18%); aerospace alloys (15%); welding electrodes (5%); nuclear weapon
 

65
 

4. PRODUCTION, IMPORT, USE, AND DISPOSAL
 

production; and other applications including ceramics and special use
 

lighting (5%). Specific applications include production of investment molds
 

for casting high-temperature metals and alloys, crucibles and alloys of
 

special shapes for use in high-temperature vacuum or oxidizing furnaces.
 

Other special applications include production of core-retention beds used in
 

nuclear reactors to contain and possibly diffuse heat generated by
 

accidental core meltdown; magnesium-thorium alloys for strategic aircraft
 

such as military jet fighters and bombers; mantles for incandescent lanterns
 

such as those used on camping trips; thoriated tungsten electrodes used to
 

join stainless steels and other alloys which require controlled weld
 

applications; special lighting such as airport runway lighting; computer
 

memory components; photoconductive film; and target material for x-rays
 

(Hedrick 1985). Natural thorium is also used in ceramic tableware glaze and
 

in flints for lighters (UNSCEAR 1977). Domestic nonenergy thorium
 

consumption was estimated to be 39.4 metric tons of thorium oxide equivalent
 

in 1987, a decrease of 33 metric tons from 1986 usage. The drop in
 

consumption was primarily the result of reduced demand for thorium oxide in
 

high-temperature refractory molds, because suitable substitutes had been
 

developed (Hedrick 1987).
 

4.4 DISPOSAL
 

Disposal of radioactive wastes is a serious environmental problem for
 

which there is, as yet, no completely satisfactory solution. Intensive
 

research is being conducted by both government and industry for the disposal
 

of this type of waste. Small amounts of low-level wastes containing
 

radioisotopes can be diluted with an inert material sufficiently to reduce
 

its activity to an acceptable level for further storage or disposal. At one
 

nuclear waste disposal site, high-level reactor wastes are stored in
 

concrete tanks lined with steel which are buried under a foot of concrete
 

and 5-6 feet of soil. Use of compressed alumina (corundum) containers has
 

been recommended, since this material remains impervious to water
 

indefinitely. The Department of Energy has recommended disposal in deep
 

geologic formations. Disposal in salt formations is being considered since
 

they are self-sealing and free from water (Hawley 1981). The Department of
 

Defense Authorization Act, 1987 (Public Law 99-661) authorized 4536 kg
 

(10,000 pounds) of thorium nitrate for disposal in fiscal year 1987.
 

Further information regarding the amount of thorium disposed of in the
 

United States was not located. Regulations established by the
 

Environmental Protection Agency regarding release limits which apply to the
 

storage and disposal of spent nuclear fuel, high-level radioactive wastes,
 

and transuranic radioactive wastes can be found in 40 CFR 191 and
 

40 CFR 192.
 

67
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5.1 OVERVIEW
 

Thorium is ubiquitous in our environment. Release of thorium to the
 

atmosphere can occur both from natural and anthropogenic sources, and
 

emissions from the latter sources can produce locally elevated atmospheric
 

levels of thorium over the background. Windblown terrestrial dust and
 

volcanic eruptions are two important natural sources of thorium in the air
 

(Fruchter et al. 1980; Kuroda et al. 1987). Uranium and thorium mining,
 

milling and processing, tin processing, phosphate rock processing and
 

phosphate fertilizer production, and coal fired utilities and industrial
 

boilers are the primary anthropogenic sources of thorium in the atmosphere
 

(Hu and Kandaiya 1985; McNabb et al. 1979; Nakoaka et al. 1984; Sill 1977).
 

The major industrial releases of thorium to surface waters are effluent
 

discharges from uranium and thorium mining, milling and processing, tin
 

processing, phosphate rock processing and phosphate fertilizer production
 

facilities (Hart et al. 1986; McKee et al. 1987; Moffett and Tellier 1978;
 

Platford and Joshi 1988). The primary sources of thorium at the Superfund
 

sites are perhaps from the processing and extraction of thorium, uranium,
 

and radium from ores and concentrates (EPA 1988a). At this time, elevated
 

levels (higher than background) of thorium have been found at 16 out of 1177
 

National Priority List (NPL) hazardous waste sites in the United States
 

(VIEW Database 1989). The frequency of these sites within the United States
 

can be seen in Figure 5-l.
 

Data regarding the fate and transport of thorium in the air are
 

limited. Wet and dry deposition are expected to be mechanisms for removal
 

of atmospheric thorium. The rate of deposition will depend on the
 

meteorological conditions, the particle size and density, and the chemical
 

form of thorium particles. Although atmospheric residence times for thorium
 

and compounds were not located, judging from residence times of other
 

metals (e.g., lead) and their compounds, they are likely to be a few days.
 

Thorium particles with small aerodynamic diameters (<10 micron aerodynamic
 

diameter) will travel long distances from their sources of emission. In
 

water, thorium will be present in suspended matters and sediment and the
 

concentration of soluble thorium will be low (Platford and Joshi 1987).
 

Sediment resuspension and mixing may control the transport of particlesorbed
 

thorium in water. The concentration of dissolved thorium in some
 

waters may increase due to formation of soluble complexes with carbonate,
 

humic materials, or other ligands in the water (LaFlamme and Murray 1987).
 

Thorium has been found to show significant bioconcentration in lower trophic
 

animals in water, but the bioconcentration factors decrease as the trophic
 

level of aquatic animals increases (Poston 1982; Fisher et al. 1987). The
 

fate and mobility of thorium in soil will be governed by the same principles
 

as in water, In most cases, thorium will remain strongly sorbed to soil and
 

its mobility will be very slow (Torstenfelt 1986). However, leaching into
 

groundwater is possible in some soils with low sorption capacity and the
 

ability to form soluble complexes. The plant/soil transfer ratio for
 

thorium is less than 0.01 (Garten 1978), indicating that it will not
 

bioconcentrate in plants from soil. However, plants grown at the edge of
 

69
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

impoundments of uranium tailings containing elevated levels of thorium had
 

a plant/soil concentration ratio of about 3 (Ibrahim and Whicker 1988).
 

The atmospheric mass concentration of thorium ranged from 0.2-1.0 

ng/m3

, with a mean value of 0.3 ng/m3 in air samples collected from 250 

sites in the United States (Lambert and Wilshire 1979). In another study, 

the mean activity concentrations of thorium-228, thorium-230, and thorium232 in New York City air were 36 aCi/m3 (aCi = l0-l8 Ci), 36 aCi/m3

, and 37 

aCi/m3

, respectively (Wrenn et al. 1981). The average population-weighted 

concentrations of thorium-232 and thorium-230 in United States community 

water supplies derived both from surface and groundwater were less than 0.01 

pCi/L and less than 0.04 pCi/L, respectively (Cothern 1987; Cothern et al. 

1986). The maximum concentration of thorium-232 in several fruits, 

vegetables and other type of foods from New York City was reported to be 

less than 0.01 pCi/g (Fisenne et al. 1987). The daily intakes of thorium230 and thorium-232 for residents of New York City were estimated to be 0.17 

and 0.11 pCi, respectively. Significant exposure to thorium requires 

special exposure scenarios (Fisenne et al. 1987). People who consume foods 

grown in high background areas, reside in homes with high thorium background 

levels, or live near radioactive waste disposal sites may be exposed to 

higher than normal background levels of thorium. Workers in uranium, 

thorium, tin, and phosphate mining, milling, and processing industries, and 

gas mantle manufacture may also be exposed to higher than normal background 

levels of thorium (Bulman 1976; Hannibal 1982; Hu et al. 1984; Kotrappa et 

al. 1976; Metzger et al. 1980). 

5.2 RELEASES TO THE ENVIRONMENT
 

5.2.1 Air
 

Releases of thorium to the atmosphere can occur from both natural and
 

anthropogenic sources. The release of thorium in volcanic ash containing as 

much as 0.116 pCi/g (1.06 μg/g) of thorium-232 was reported by Fruchter 

et al. (1980). Increased concentrations of thorium in rain water following 

a volcanic eruption have also been observed (Kuroda et al. 1987). Since 

the average level of thorium in soil is about 6 μg/g of thorium (Harmsen and 

De Haan 1980), windblown terrestrial dust is also a likely natural source of 

thorium in the atmosphere. Since coal contains 0.5-7.3 μg/g thorium 

(Nakaoka et al. 1984), burning of coal for power generation produces thorium 

in the fly ash and is a manmade source of this chemical in the atmosphere. 

The amount of thorium in the fly ash from coal-burning power plants depends 

on the nature of coal burned and the emission control devices of the plant, 

but concentrations usually range from 4.5-37 μg/g (Abel et al. 1984; Coles 

et al. 1979; Tadmor 1986; Weissman et al. 1983). However, the concentrations 

of all natural radioactive isotopes in (including thorium isotopes) the stack 

effluents from coal-fired power plants are usually much lower than those from 

the natural background concentrations of these radionuclides (Nakaoka et al. 

1984; Roeck et al. 1987). Similarly, fly ash 
70
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

from oil- and peat-fired power plants can also be atmospheric sources of
 

thorium (Mustonen and Jantunen 1985).
 

Thorium-230 has been detected in air dust from uranium ore processing
 

and mill tailings. These concentrations of thorium-230 (a decay product of
 

uranium-238) may be particularly high in ore crushing areas (Sill 1977).
 

Similarly, processing of thorium ores is expected to be an atmospheric
 

source of thorium. Elevated levels of thoron (thoron or radon-220
 

originating from thorium-232) daughters, such as bismuth-212 and polonium216, were present at a former thorium and rare-earth extraction facility
 

waste site, although the concentrations of thorium in air particulate
 

samples were not significant (Jensen et al. 1984). Since phosphate ores
 

usually contain thorium-230, phosphate-ore processing plants are also
 

atmospheric sources of thorium-230 (Metzger et al. 1980; McNabb et al.
 

1979). The by-products obtained during processing of tin ores usually
 

contain thorium-232. Therefore, tin processing industries are sources of
 

atmospheric thorium-232 emissions (Hu et al. 1981, 1984; Hu and Kandaiya
 

1985).
 

EPA (1984) estimated that about 0.2 Ci of thorium-230 is annually
 

emitted into the air from uranium mill facilities, coal-fired utilities and
 

industrial boilers, phosphate rock processing and wet-process fertilizer
 

production facilities, and other mineral extraction and processing
 

facilities. About 0.084 Ci of thorium-234 from uranium fuel cycle
 

facilities and 0.0003 Ci of thorium-232 from underground uranium mines are
 

emitted into the atmosphere annually (EPA 1984).
 

5.2.2 Water
 

The acidic leaching of uranium tailing piles in certain areas is a
 

source of thorium-230 in surface water and groundwater (Moffett and Tellier
 

1978; Platford and Joshi 1988). The contamination of surface waters and
 

benthic organisms by thorium-230 (a decay product of uranium-238) from
 

uranium mining and milling operations and from radium and uranium recovery
 

plants has been reported (Hart et al. 1986; McKee et al. 1987). Similarly,
 

effluents from thorium mining, milling, and recovery plants are expected to
 

be sources of thorium in water. Other industrial processes that are
 

expected to be sources of thorium contamination into water are phosphorus
 

and phosphate fertilizer production and processing of some tin ores. Since
 

both phosphate rocks and the tailings from tin ore processing contain
 

thorium mainly as thorium-230 and thorium-232, respectively (see Section
 

5.2.1), discharges of processed or unprocessed effluents and leaching from
 

tailing piles can be sources of thorium in water. Leaching from landfill
 

sites containing uranium and thorium may result in the contamination of
 

surface water and groundwater with thorium (Cottrell et al. 1981).
 
71
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5.2.3 Soil
 

Thorium occurs naturally in the earth's crust at an average 

lithospheric concentration of 8-12 μg/g (ppm). The typical concentration 

range of naturally-occurring thorium in soil is 2-12 μg/g, with an average 

value of 6 μg/g (Harmsen and De Haan 1980). Manmade sources of thorium 

contamination in soil are mining, milling and processing operations and 

uranium, thorium, tin and phosphate fertilizer production (Chong et al. 

1985; Hu and Kandaiya 1985; Joshi 1987; McNabb et al. 1979; Sill 1977). The 

two principal processes that can contaminate soil from these industries are 

precipitation of airborne dusts and land disposal of uranium or 

thoriumcontaining 

wastes. 

According to EPA (1988a), the primary sources of thorium at the
 

Superfund sites are processing and extraction of thorium, uranium and radium
 

from ores or ore-concentrates. The following radioactive waste Superfund
 

sites have been found to contain one or more isotopes of thorium (VIEW
 

1989): Shpack and adjacent landfills, Norton, MA; Maywood Chemical Co.,
 

Sears Property, Maywood, NJ; W.R.Grace and Co., Wayne, NJ; West Chicago
 

Sewage Treatment Plant, W. Chicago, IL; Reed-Keppler Park, West Chicago, IL;
 

Kerr-McGee (Residential Areas), W. Chicago, IL; Kress Creek and the West
 

Branch of the DuPage River, W. Chicago, IL; United Nuclear Corp., Church
 

Rock, NM; Homestake Mining Co., Milan, NM; Kearsarge Metallurgical Corp.,
 

Conway, NH; Naval Air Engineering Center, Lakehurst, NJ: Teledyne Wah Chang,
 

Albany, OR; Woodland Route 72 Dump, Woodland Township, NJ; Weldon Spring
 

Quarry, St. Charles City, MO; Monticello Radioactivity-Contaminated
 

Properties, Monticello, UT; Uravan Uranium Project, Montrose City, CO.
 

Disposal of incandescent lights and lanterns containing thorium-232 will be
 

an additional source of thorium at waste disposal sites.
 

5.3 ENVIRONMETAL FATE
 

Thorium occurs in nature in four isotopic forms, thorium-228, thorium230, thorium-232, and thorium-234. Of these, thorium-228 is the decay
 

product of naturally-occurring thorium-232, and both thorium-234 and
 

thorium-230 are decay products of natural uranium-238. To assess the
 

environmental fate of thorium, these isotopes of thorium with the exception
 

of thorium-234 which has short half-life (24.1 days), should be considered.
 

5.3.1 Transport and Partitioning
 

Data regarding the transport and partitioning of thorium in the
 

atmosphere are limited. Release of atmospheric thorium from mining,
 

milling, and processing operations of thorium will mainly consist of
 

thorium-232 particulate matter. Emissions from mining, milling, and
 

processing of uranium and the airblown dust from uranium tailing piles wil
 

contribute to the presence of thorium-230 as an atmospheric particulate
 

aerosol. The aerodynamic diameters of both thorium-230 and thorium-232 in
 

atmospheric aerosols are greater than 2.5 μm. The aerodynamic diameter of 
72
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

thorium-228, however, is less than 1.6 pm (Hirose and Sugimura 1987) and may
 

travel longer distances than both thorium-230 and thorium-232. Like other
 

particulate matter in the atmosphere, thorium will be transported from the
 

atmosphere to soil and water by wet and dry deposition.
 

The deposition of thorium through snow and rain water has been observed
 

(Jiang and Kuroda 1987). Dry deposition of thorium through impaction and
 

gravitational settling has also been observed (see Section 5.2.3). The
 

atmospheric residence time of thorium depends on the aerodynamic diameter of
 

the particles. Those with small diameters are likely to be transported longer
 

distances. For example, high thorium-228/thorium-232 activity ratios observed
 

in surface air of the Western North Pacific Ocean are thought to be due to
 

long distance transport of small particles of thorium-228 (Hirose and Sugimura
 

1987).
 

The dry deposition velocity of lead-212, a thoron (thoron or radon-220
 

itself originating from thorium-232) decay product has been reported to be
 

in the range 0.03-0.6 cm/set (Bigu 1985; Rangarajan et al. 1986). These
 

low deposition velocities indicate that the thoron daughter, stable lead,
 

may have a long residence time in the atmosphere with respect to dry
 

deposition.
 

Thorium discharged as Th02 into surface waters from mining, milling, 

and processing will be present as suspended particles or sediments in water 

because of the low solubility of thorium in water (Platford and Joshi 1986). 

Other soluble thorium ions will hydrolyze at pH above 5 forming Th(OH)4 

precipitate or hydroxy complexes, e.g., Th(OH)2+2, Th2(0H)2

+6, Th3(OH)5+7 

(Bodek et al. 1988; Hunter et al. 1988; Milic and Suranji 1982). The 

hydroxy complexes will be adsorbed by particulate matter in water, e.g., 

goethite (alpha-FeOOH), with the result that most of the thorium will be 

present in suspended matter or sediment, and the concentration of soluble 

thorium in water will be low (Hunter et al. 1988; Sheppard 1980). The 

adsorption of thorium to suspended particles or sediment in water depends un 

the particle size, and the adsorption and subsequent removal from aqueous 

phase is expected to be higher for finer grained particles (Carpenter et al. 

1987). The residence times for thorium with respect to removal by 

adsorption onto particles were reported to be shorter in nearshore waters 

than in deeper waters, probably because of the availability of more 

adsorbents (particulate matter). The residence time may vary from 1 day to 

70 days (Cochran 1984). The scavenging rate varied seasonally and was 

inversely related to the sediment resuspension rate. Therefore, the removal 

rate was found to be dependent on both sediment resuspension rate and the 

concentration of iron and manganese compounds (good adsorption properties) 

in water (Cochran 1984). 

The transport of thorium in water is principally controlled by the
 

particle flux in the water, i.e., most of the thorium will be carried in the
 

particle-sorbed state (Santschi 1984), and sediment resuspension and mixing
 

may control the transport of particle-sorbed thorium in water (Santschi
 
73
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

et al. 1983). Although the concentration of dissolved thorium is low in
 

most waters, its value could be higher in some waters. For example, the
 

concentration of dissolved thorium in an alkaline lake was up to 4.9 dpm/L
 

(2.21 pCi/L) compared to about 1.3x10-5 dpm/L (O.59x10-5 pCi/L) in sea water 

(LaFlanune and Murray 1987). The dissolved thorium concentration can 

increase by the formation of soluble complexes. The anions or ligands 

likely to form complexes with thorium in natural water are C03

-2 and humic 

materials, although some of the thorium-citrate complexes may be stable at 

pH above 5 (LaFlamme and Murray 1987; Miekeley and Kuchler 1987; Platford 

and Joshi 1986; Raymond et al. 1987; Simpson et al. 1984). 

The transport of thorium from water to aquatic species has been 

reported. The bioconcentration factor (concentration in dry 

organism/concentration in water) (dry weight basis) in algae may be as high 

as 975x10+4, but the maximum value in zooplankton (calanoids and 

cyclopoids) may be 2x104

 (Fisher et al. 1987). Fisher et al. (1987) 

suggested that sinking plankton and their debris may account for the 

sedimentation of most of the thorium from oceanic surface waters. The 

highest observed thorium bioconcentration factor in the whole body of 

rainbow trout (Salmo gairdneri) was 465 (Poston 1982). The succeedingly 

lower bioconcentration factors in higher trophic animals indicates that 

thorium will not biomagnify in the aquatic environment. It was also noted 

that the majority of thorium body burden in fish is in the gastrointestinal 

tract (Poston 1982). 

The mobility of thorium in soil will be governed by the same principles 

as in water. In most soil, thorium will remain strongly sorbed onto soil and 

the mobility will be very slow (Torstenfelt 1986). The presence of ions or 

ligands (C03

-2, humic matter) that can form soluble complexes with thorium 

should increase its mobility in soil. The contamination of groundwater through 

the transport of thorium from soil to groundwater will not occur in most 

soils, except soils that have low sorption characteristics and have the 

capability to form soluble complexes. Chelating agents produced by certain 

microorganisms (Pseudomonas aeruginosa) present in soils may enhance the 

dissolution of thorium in soils (Premuzic et al. 1985). 

The transport of atmospherically deposited thorium from soil to plants 

is low. The soil to plant transfer coefficients (concentration in dry plant 

to concentration in dry soil) were estimated to be 10-4 to 7x10-3

 by Garten 

(1978) and 0.6x10-4 for thorium-232 by Linsalata et al. (1989). The root 

systems of grasses and weeds adsorb thorium from the soil but the transport 

of thorium from the root to the aboveground parts of the plant is not very 

extensive, as indicated by l00-fold higher concentrations of all three 

isotopes (thorium-228, thorium-230, and thorium-232) in the root than in the 

aboveground parts of the plant (Taskayev et al. 1986). However, Ibrahim and 

Whicker (1988) showed that under certain conditions, vegetation can 

accumulate thorium-230, as indicated by the plant/soil concentration ratio 

(dry weight) of 1.9-2.9 for mixed grasses, mixed forbs and sagebrush plants 
74
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

grown at the edge of uranium tailings impoundments. Vegetation
 

concentration ratios for thorium-232 (a concentration ratio of about 0.1)
 

and thorium-228 (a maximum concentration ratio of about 0.4) were lower than
 

that of thorium-230. It was postulated that the acidity and wet conditions
 

at this site enhanced the solubility of thorium in soil and that the
 

difference in solubility was responsible for the difference in plant uptake
 

of the three thorium isotopes (Ibrahim and Whicker 1988). However, it is
 

possible that the observed difference in the uptake of the three isotopes by
 

plants is due to a difference in the chemical compounds formed by the
 

isotopes, making one more leachable than the other (therefore more available
 

for uptake) under the prevailing local conditions (also see Section 5.6).
 

5.3.2 Transformation and Degradation
 

5.3.2.1 Air
 

Thorium may change from one chemical species to another in the 

atmosphere (such as Th02 to Th(S04)2) as a result of chemical reactions, but 

nothing definitive is known about the atmospheric chemical reactions of 

thorium. The chemical forms in which thorium may reside in the atmosphere 

are also not known, but it is likely to be present mostly as Th02. 

5.3.2.2 Water
 

The principal abiotic processes that may transform thorium compounds in
 

water are complexation by anions/organic ligands and hydroxylation. The
 

increase in the mobility of thorium through the formation of soluble


-2 complexes with C03 , humic materials, and other anions or ligands and the 

decrease in the mobility due to formation of Th(OH)4 or anionic 

thoriumhydroxide complexes were discussed in Section 5.3.1.2. In a model 

experiment with seawater at pH 8.2 and freshwater at pH 6 and pH 9, it was 

estimated that almost 100% of the thorium resides as hydroxo complexes 

(Boniforti 1987); 

5.3.2.3 Soil
 

No published data were located referencing biotic transformation of
 

thorium in soil. Abiotic transformation processes that can convert
 

immobile thorium in soil into mobile forms through the formation of
 

complexes were discussed in Section 5.3.1.3.
 

5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT
 

5.4.1 Air
 

The level of thorium in air have not been measured as frequently as it 

has for uranium. The concentration of thorium in the atmosphere of the 

South Pole measured in 1970 ranged between 18 and 83 fg/m3

, with a mean 

value of 59 fg/m3

 (1 fg = l0-l5 g). The origin of thorium in the polar 
75
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

atmosphere was speculated to be either crustal weathering or the ocean water 

(Zoller et al. 1974). The thorium level in the air of Algonquin Park, 

Ontario, Canada was reported to be 7.1 pm3

 (Sheppard 1980). The level of 

thorium measured in 1969 in East Chicago, IN, a heavily polluted industrial 

area, was 1.3 ng/m3

 compared to a value of 0.27 ng/m3 at a rural location in 

Michigan (Niles, MI) (Dams et al. 1970). The air particulate samples 

collected from 250 sites in the United States by the National Air 

Surveillance Network (NASN) of EPA during 1975 and 1976 were analyzed for 

thorium-232 by neutron activation analysis. The measured concentrations at 

250 urban and nonurban sites in the United States ranged from 0.2-1.0 ng/m3 

, 

with a mean concentration of 0.3 ng/m3

 (Lambert and Wilshire 1979). The 

mean concentrations of thorium-228, thorium-230 and thorium-232 in New York 

City air (sample collected on the roof above the 14th floor) were 36 aCi/m3 

(aCi = 10-l8 Ci), 36 aCi/m3, and 37 aCi/m3, respectively (Wrenn et al. 

1981). 

The air concentrations of thorium and other airborne radioactivity near 

a former thorium and rare-earth extraction facility in the United States were 

measured. The maximum radioactivity due to all three isotopes of 

thorium at a site about 450 feet from the primary waste pile was 0.66 

fCi/m3

. Although the background thorium radioactivity was not reported, the 

total radioactivity at a site about 4000 feet south of the waste pile was 

about 3.5 times lower than a site 450 feet from the pile (Jensen et al. 

1984). 

The concentration of thorium in rainwater over Fayeteville, AR, ranged
 

from 2.8-123 fCi/L for thorium-228, 1.7-123 fCi/L for thorium-230, and 0.8­

118 fCi/L for thorium-232. The peak values in thorium concentrations
 

correlated well with the 1980 eruption of Mount St. Helen and the 1982
 

eruption of El Chichon (Jiang et al. 1986; Jiang and Kuroda 1987; Salaymeh
 

and Kuroda 1987).
 

The natural decay of uranium-238 and thorium-232 will produce radon-222
 

and thoron (radon-220). The indoor air levels of radon (radon-222) and
 

thoron (radon-220) daughters arising from some building materials and the
 

soil, have been reported by several authors. It was generally believed that
 

the effective dose equivalent from radon-220 (thoron) daughters (originating
 

from thorium-232) might average about one-fifth of that due to radon-222
 

daughters (originating from uranium-238) in the temperate regions (Schery
 

1985). However, more recent measurements at varied indoor locations within
 

the United States and Germany have shown that the potential alpha energy
 

concentrations from radon-220 daughters may be as high as 60% of that
 

originating from radon-222. It has also been shown that the concentrations
 

of thoron (radon-220) and radon-222 daughters in the indoor air are
 

dependent on the air exchange rate in the dwellings and that the indoor
 

concentrations are about 3-4 times higher than the outdoor concentrations
 

(Keller and Folkerts 1984; Schery 1985).
 
76
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5.4.2 Water
 

Compared to uranium, relatively less information was located on the
 

levels of thorium in natural waters. The concentrations of dissolved
 

thorium in water with high pH (more than 8) are expected to be very low, and
 

the concentration may increase with the decrease of pH (Harmsen and De Haan
 

1980). Cothern et al. (1986) reported thorium-232 concentrations rarely
 

exceed 0.1 pCi/L in natural waters, but that the concentrations of thorium230, a progeny of uranium-238, may be as high as 0.4 pCi/L. In a natural
 

surface water in Austria, the concentration of thorium (isotope undefined)
 

was reported to be 1.24-2.90 μg/L (Harmsen and De Haan 1980). The 

concentration of thorium (isotope undefined but probably thorium-230) in 

water under low pH conditions which may occur from the leaching of uranium 

tailings may be as high as 38 mg/L (Harmsen and De Haan 1980). The 

individual concentrations of thorium-228, -230, and -232 in an area of Great 

Bear Lake in Canada contaminated with mine wastes (silver and uranium mines) 

were less than 0.5 pCi/L (Moore and Sutherland 1981). The concentrations of 

thorium-228, -230, and -232 in a highly alkaline (pH of about 10) lake (Mono 

Lake) in California have been reported to be as high as 1.02, 1.41, and 0.7 

pCi/L, respectively (Anderson et al. 1982; Simpson et al. 1982). 

The concentrations of thorium in seawater at various depths and
 

locations have been reported by several authors. Because of the very low
 

concentrations of thorium and the differences in location and the varying
 

characteristics of the water, the reported results are different. The
 

concentration of total thorium in seawater ranges from 4x10-5 to less than
 

0.5 μg/kg (Greenberg and Kinston 1982; Sheppard 1980) and the world average 

concentration in seawater is 0.05 μg/L (Harmsen and De Haan 1980). The 

concentrations of the individual isotopes thorium-232, thorium-230, and 

thorium-228 in seawater have been reported to range from 0.00023-0.032, 

0.014-0.72, and 0.023-3.153 fCi/L, respectively (Anderson et al. 1982; 

Hirose 1988; Huh and Bacon 1985; Livingston and Cochran 1987; Simpson et al. 

1982). The concentrations of thorium in sediments are much higher than in 

seawater. In several sediments, concentrations of thorium-232, thorium-230, 

and thorium-228 ranged from 0.52-1.96, 1.01-30.77, and 0.36-1.93 pCi/g,
 

respectively (Huh et al. 1987; Yang et al. 1986).
 

Thorium has also been detected in groundwaters. In groundwater in 

Austria, concentrations ranged from 0.5-2.90 μg/L (Harmsen and De Haan 

1980). Briny groundwater from a well in Palo Duro Basin, WA, contained 

0.009, 0.1, and 0.59 pCi/L of thorium-232, thorium-230, and thorium-228, 

respectively (Laul et al. 1987). In a California well, thorium-230 was 

detected at a concentration as high as 1.3 pCi/L (Aieta et al. 1987). The 

average population-weighted concentrations of thorium-232 and thorium-230 in 

United States community water supplies derived from both surface water and 

groundwater are less than 0.01 pCi/L and less than 0.04 pCi/L, respectively 

(Cothern 1987; Cothern et al. 1986). 
77
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5.4.3 Soil
 

The typical concentration range of thorium in soil is 2-12 μg/g (ppm), 

with an average value of 6 μg/g (Harmsen and De Haan 1980). The thorium 

content of soil normally increases with an increase in clay content of soil 

(Harmsen and De Haan 1980). The thorium contents in most soils from the 

Superfund sites listed in Section 5.2.3 were above background levels. The 

soil concentrations of thorium-232 at the Reed-Keppler Park, W. Chicago, IL, 

site and the Kerr-McGee Residential areas in W. Chicago, IL, were 11,000 and 

16,000 pCi/g, respectively (EPA 1988a). Soils near processing and milling 

operations, and concentrations of uranium and thorium ores, phosphate ores, 

and tin ores may contain thorium at concentrations higher than the 

background levels. Higher concentrations of thorium in soils near uranium 

ore crushing facilities have been reported (Jensen et al. 1984; Sill 1977). 

5.4.4 Other Media
 

Because concentrations of thorium in foods are very low, very few data
 

exist. The thorium-232 content in fresh fruits, vegetables, and tea was
 

determined (in pCi/g), and the values are listed in Table 5-l. Vegetables
 

grown in an area of high natural activity in Brazil had the following
 

concentrations of thorium (μg/g in dry sample) (Linsalata et al. 1987): 

brown beans, 0.011; potato, 0.0019; zucchini, 0.011; corn, 0.0022; carrot, 

0.0074; and sweet potato, 0.0027. These authors did not observe rapid 

transport of thorium-232 from soil to the edible parts of the plants. 

The concentrations of thorium in both hard and soft tissues of humans
 

have been determined by a few authors. The concentration of thorium-232 in
 

the blood of normal populations (not occupationally or otherwise known to be
 

exposed to levels higher than background level of thorium) in the United
 

Kingdom was 2.42 μg/L. The thorium-232 level in the urine of the same 

population was below the detection limit of 0.001 μg/L, although the 

concentration in the urine of exposed workers ranged from less than 

0.001-2.24 μg/L. The highest value (2.24 μg/L) was found in a worker in the 

thorium nitrate gas mantle industry (Bulman 1976; Clifton et al. 1971).
 

The thorium-232 concentration in rib bones from several control humans
 

from the United States ranged from less than 0.1-72 ng/g (ppb) and were
 

found to increase-with age (Lucas et al. 1970). A similar increase in
 

thorium concentration with age was seen in bones (primarily vertebral
 

wedges) of a Colorado population (Wrenn et al. 1981). The level of thorium232 in rib bones of individuals in the United Kingdom not occupationally
 

exposed to thorium ranged from 0.8-163.8 ng/g, with a mean value of 28.7
 

ng/g in dry ash (Clifton et al. 1971). The concentration of thorium in the
 

fibula of a Thorotrast patient was reported to be 2.0 μg/g (ppm) (Edgington 

1967). Singh et al. (1985) reported more recent measurements of isotopic 

concentrations of thorium in different human bones from the general 

population of Colorado and Pennsylvania. These values are shown in Table 

5-2. The authors concluded that the concentrations of thorium-230 in ribs 


80
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

of the Colorado population were significantly higher (statistically),
 

probably because of exposure to uranium tailings, than those from the
 

Pennsylvania population.
 

The levels of thorium in the tissues of a hard-rock miner, a uranium
 

miner, and the levels in two uranium millers (thorium-230 is a decay product
 

of uranium-238, and thorium-238 and thorium-232 are impurities in uranium)
 

were compared with the levels in the 50th percentile for the general
 

population (Singh et al. 1987; Wrenn et al. 1981). These data are given in
 

Table 5-3. The levels of thorium-230 in the hard-rock miner were about 10
 

times higher than the median levels in most tissues of the general
 

population. In the case of the uranium miner and millers, the values were
 

more than two orders of magnitude higher than the median tissues levels in
 

the general population.
 

Wrenn et al. (1981) determined the median concentrations of thorium228, thorium-230, and thorium-232 in the lungs of smokers and nonsmokers;
 

the respective values were 0.22, 0.56, and 0.43 pCi/kg for smokers and 0.37,
 

0.84, and 0.60 pCi/kg for nonsmokers. The investigators concluded that
 

cigarette smoking had no effect relative to increasing the concentration of
 

thorium isotopes in lungs.
 

5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE
 

The general population will be exposed to thorium through the
 

inhalation of air and ingestion of food and drinking water containing trace
 

amounts of the chemical. Because the concentration of thorium is normally
 

very low in air, drinking water, and foods (see Section 5.4), few studies
 

were located that determined the daily human intake of thorium. According
 

to Cothern (1987), the estimated daily intakes of thorium-230 in the United
 

States population through inhalation of air and ingestion of drinking water
 

are 0.0007 and less than 0.06 pCi, respectively. The corresponding values
 

for thorium-232 are 0.0007 and less than 0.02 pCi. Cothern (1987) assumed
 

that the intake from food would be negligible. Based on these values, the
 

total daily intakes of thorium-230 and thorium-232 are expected to be less
 

than 0.06 and less than 0.02 pCi, respectively. However, other authors
 

estimated the contribution of food to the total human thorium intake may not
 

be negligible and may be the most significant. Based on a survey of the
 

levels of thorium in air, water, and food, Fisenne et al. (1987) estimated
 

the daily intake of thorium-230 and thorium-232 by New York City residents.
 

The daily dietary, water, and inhalation intake of thorium-230 was estimated
 

to be 0.164, 0.005, and 0.0003 pCi, respectively, giving a total daily
 

intake of 0.17 pCi. The corresponding estimated values for thorium-232 are
 

0.110, 0.002, and 0.0002 pCi, with a total daily intake being 0.112 pCi.
 

From the measured values of thorium in feces and the assumed values for
 

uptake and elimination rates, Linsalata et al. (1985) estimated a daily
 

ingestion intake of thorium-232 for New York residents to be about 0.08 pCi
 

or 0.7 μg. This value is considerably smaller than the value estimated by 

Fisenne et al. (1987). The value from Linsalata et al. (1985) is again 

82
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

considerably smaller than the daily dietary, water, and inhalation intakes 

of 2.24, 0.02, and 0.02 μg, respectively, as estimated for residents of 

Bombay, India (Dang et al. 1986). It can be concluded from the above 

discussion that the total intake of thorium by the United States population 

may vary depending on the thorium content in the consumed food and that no 

firm United States average thorium intake value is yet available. The 

importance of the intake of thorium from foods is overshadowed by the 

relative absorption of thorium by lung compared with its uptake by gut (see 

Chapter 2). 

Occupational exposures to higher levels of thorium isotopes occur
 

primarily to workers in uranium, thorium, tin, and phosphate mining,
 

milling, and processing industries, radium dial workers, and gas lantern
 

mantle workers. From the measurement of airborne thorium concentrations in
 

workplaces of the uranium and thorium industry, it was concluded that
 

radioactive dust, particularly from crushing areas, represents an important
 

route of exposure (Hannibal 1982; Kotrappa et al. 1976). It has also been
 

reported that exposure of workers in the fertilizer industry to natural
 

radioactivity may increase by 100% over normal background (Metzger et al.
 

1980). Measuring external gamma radiation dosages to a person working 8
 

hours/day has shown that monazite and xenotime storage rooms of Amang
 

upgrading plants (tin processing) on the west coast of Malaysia exhibited
 

exposure rates exceeding the ICRP recommended maximum value of 5 rem/year
 

(Hu et al. 1984). From the radioactivity released by a burning gas mantle
 

(contains thorium), it was concluded that the user would be at minimal risk
 

unless the person was in a small unventilated room (Leutzelschwab and
 

Googins 1984). However, workers in the gas mantle manufacturing industry
 

are expected to be exposed to higher concentrations of radioactivity than
 

the normal population.
 

Workers are exposed to higher levels of thorium and other radionuclides
 

in certain thorium industries, as indicated by the measured exhaled breath and
 

tissue levels of these chemicals. The significantly higher level of radon-220
 

(a decay product of thorium-232) in the exhaled breath of some thorium plant
 

workers (Mayya et al. 1986) is indirect evidence of higher thorium intakes.
 

Similarly, other authors have found higher tissue and body fluid levels
 

(compared to background) of thorium in workers in the thoriumprocessing
 

industry (Clifton et al. 1971; Mausner 1982; Twitty and Boback 1970), workers
 

in the radium dial industry (Keane et al. 1986), in uranium mill crushermen
 

(Fisher et al. 1983), and in uranium and hard rock miners and uranium millers
 

(Singh et al. 1987; Wrenn et al. 1981).
 

Thorium-doped glass is also used in the production of some camera
 

lenses (Waligorski et al. 1985). A relatively recent measurement has shown
 

that the external dose rate from exposure to a camera lens can be 10 times
 

higher (as high as 9.25 mrem/hour at the front glass surface of the lens)
 

than previously reported (Waligorski et al. 1985). Therefore, professional
 

photographers and workers in the thorium-doped photographic lens
 
83
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

manufacturing industry may be at slightly higher risk of exposure to thorium
 

and its daughter products from inhalation and/or external radiation.
 

5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURE
 

The three groups of the general population that have the potential of 

exposure to thorium and its decay products at levels higher than background 

are people who consume large amounts of foods grown in high background 

areas, people who reside in homes built with high thoron (radon-220)­

emitting building materials and constructed on soil with high background 

levels of thorium, and people who live near radioactive waste disposal 

sites. Linsalata et al. (1987) analyzed vegetables grown in two areas near 

Sao Paulo, Brazil, that contained high natural radioactivity, and found the 

thorium is not bioaccumulated in the vegetables but maintained a mean 

concentration ratio (concentration in dry vegetable/concentration in dry 

soil) of 10-4. Root vegetables (e.g., carrots and potatoes) showed lower 

concentration ratios than zucchini and beans. Therefore, it can be 

concluded that vegetables grown in these soils would contain more thorium 

than vegetables grown in soil with normal background levels. 

Linsalata et al. (1985) 1 a so estimated that the intake of thorium by
 

populations residing in these parts of Brazil was 6-10 times higher than
 

the population in New York City, as indicated by the analysis of human bones
 

from the two areas. The concentration of thorium in human bones was found
 

to be 100 times higher in high background monazite areas in India than in
 

areas with normal thorium concentration in soils (Pillai and Matkar 1987).
 

The building construction materials that contain higher levels of
 

thorium-232 are granite, clay bricks and certain kinds of concrete blocks
 

and gypsum, particularly the materials in which waste products from uranium
 

mining and milling industry are used (Beretka and Mathew 1985; Ettenhuber
 

and Lehmann 1986; Hamilton 1971). Ettenhuber and Lehmann (1986) reported
 

that the indoor gamma radiation dose equivalent in buildings made from
 

bricks and concrete is mainly due to radon-222 (originating from uranium)
 

and radon-220 (originating from thorium-232), and can be over 7 times higher
 

than outdoors.
 

The effect of soil on the level of thorium and its decay products in
 

indoor air has been discussed by Gunning and Scott (1982). Homes near the
 

Elliot Lake (Canada) uranium mines were suspected to contain higher than
 

normal levels of thoron (radon-220) and its daughters, because of higher
 

levels of thorium in the surface soil and building materials used in the
 

town. The ratio of the concentration of decay products of thoron (radon220) to radon-222 found in these homes was 0.3. Therefore, the
 

concentrations of thoron in decay products originating from thorium-232
 

inside the homes were lower than radon-222 decay products originating from
 

uranium-238, and the levels were insignificant compared with the remedial
 

action limit of 20 mWL (1 WL is the concentration of short-lived radon decay
 
84
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5 products that will result in 1.3x10 MeV of potential alpha energy per liter
 

of air) (Gunning and Scott 1982).
 

The concentrations of thorium-232 in soil from several residential lots
 

near the Kerr-McGee ore processing facilities in W. Chicago, IL, have been
 

determined to be up to 16,000 pCi/g (EPA 1988a). Therefore, homes built on
 

such lots or homes that are close to other radioactive disposal sites may
 

be sources of higher thorium exposure.
 

Both cigarette tobacco and its smoke contain thorium (Munita and
 

Mazzilli 1986; Neton and Ibrahim 1978) (see Section 5.2.1). However, the
 

effect of cigarette smoking on potential thorium exposure remains unclear.
 

Joyet (1971) analyzed the lungs of 10 autopsied smokers and two nonsmokers.
 

In 5 of 10 smokers, the lungs contained significantly higher levels of
 

thorium than the nonsmokers, and the thorium levels in the residual five
 

were not significantly different from the nonsmokers. Limited data suggest
 

that cigarette smoking has no effect on the concentration of thorium
 

isotopes in the lungs (Wrenn et al. 1981).
 

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 thorium 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
 

thorium.
 

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. Some of the physical and chemical 

properties (i.e., Kow, Koc and Henry's law constant) that are often used in 

the estimation of environmental fate of organic compounds are not useful or 

relevant for most inorganic compounds including thorium and its compounds, 

Relevant data concerning the physical and chemical properties, such as 

solubility, stability, and oxidation-reduction potential of thorium salts 

and complexes have been located in the existing literature.Production, Use, 

Release, and Disposal. In the absence of experimental or estimated population 

exposure data, information concerning 
85
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

production volume, uses, release, and disposal are sometimes useful
 

indicators of potential population exposure. For example, if the production
 

volume of a chemical is high, it is likely that the release of the chemical
 

in the workplace and in the environment will be high. The exposure of
 

population groups to a certain substance is dependent on its use pattern.
 

The frequency of general population exposure will be high for substances
 

that have widespread uses in homes. The production volumes and their past
 

and future trends of the commercially important thorium compounds are
 

known. The use pattern of thorium and compounds is well described in the
 

literature. It is also known that occupational groups are most susceptible
 

to thorium exposure. Data regarding the amounts of thorium disposed in the
 

past, the present rates of disposal, and future disposal trends in the
 

United States were not located. These data would be helpful in determining
 

the potential for and extent of general population exposure to thorium. The
 

current disposal and storage methods for thorium or its byproducts must be
 

efficient in order to meet the NRC and EPA guidelines and regulations
 

regarding their release into the accessible environment and exposure of the
 

general population.
 

According to the Emergency Planning and Community Right-to-Know Act
 

are of 1986 (EPCRTKA), (§313), (Pub. L. 99-499, Title III, §313), industries
 

required to submit release information to the EPA. The Toxics Release
 

Inventory (TRI), which contains release information for 1987, became
 

available in May of 1989. This database will be updated yearly and shou
 

provide a more reliable estimate of industrial production and emission.
 

Id
 

Environmental Fate. It can be concluded from the transport
 

characteristics that surface water sediment will be the repository for
 

atmospheric and aquatic thorium. Normally, thorium compounds will not
 

transport long distances in soil. They will persist in sediment and soil.
 

There is a lack of data on the fate and transport of thorium and its
 

compounds in air. Data regarding measured particulate size and deposition
 

velocity (that determines gravitational settling rates), and knowledge of
 

the chemical forms and the lifetime of the particles in air would be
 

useful.
 

Bioavailability from Environmental Media. The absorption and
 

distribution of thorium as a result of inhalation and ingestion exposures
 

have been discussed in Sections 2.3.1 and 2.3.2. However, quantitative data
 

relating physical/chemical properties, such as particle size, chemical form
 

of thorium, and degree of adsorption with the bioavailability of thorium in
 

inhaled air particles and inhaled and/or ingested soil particles are
 

lacking. Such studies would be useful in assessing potential thorium
 

toxicity to people living near a hazardous waste site.
 

Food Chain Bioaccumulation. Information about bioaccumulation in fish
 

and food exists, as does information on the levels of thorium in various
 

foods. Existing data in the literature indicate that thorium does not
 

biomagnify in predators due to consumption of contaminated prey organisms.
 
86
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Exposure Levels in Environmental Media. Because of the paucity of data
 

on the levels of thorium in air, water, and food, there are conflicting
 

reports on the importance of each medium to the total human dietary intake
 

of this substance. Data on the levels of thorium in foods grown in
 

contaminated areas, particularly in the vicinity of hazardous waste sites,
 

are limited, and further development of these data will be useful. There is
 

also a lack of air monitoring data around hazardous waste sites.
 

Exposure Levels in Humans. Although some data on the levels of thorium
 

in human tissues exists, neither consensus values of the background levels
 

for thorium in human tissues nor its levels in tissues of populations
 

residing in the vicinity of hazardous waste sites were located. Conflicting
 

data also exist regarding the level of thorium in the lungs of smokers and
 

nonsmokers. Further research would be useful to provide conclusive evidence
 

regarding the effect of cigarette smoking on thorium content in the lung.
 

In addition, there are no reliable data on urinary and fecal excretion of
 

thorium in general populations in the United States. The skeleton is the
 

main organ for the accumulation of thorium, yet there are also no reliable
 

data on macro and micro distribution of thorium in human bone necessary to
 

quantify its body burden.
 

Exposure Registries. No exposure registries for thorium 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 exposure to this
 

compound.
 

5.7.2 On-going Studies
 

According to the Federal Research in Progress Database, Perry and Tsao
 

at the Lawrence Berkeley Laboratory are studying the chemical species and
 

transport of thorium in soil. In other on-going projects, Krey et al. at
 

Environmental Measurements Laboratory in New York are studying the daily
 

intake of thorium, and McInroy et al. at Los Alamos National Laboratory are
 

studying the tissue levels of thorium in the general population and
 

occupationally exposed individuals.
 
87
 

6. ANALYTICAL METHODS
 

The purpose of this chapter is to describe the analytical methods
 

available for detecting and/or measuring and monitoring thorium 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 thorium. 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 thorium 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
 

Some of the methods commonly used for the determination of thorium in
 

biological materials are given in Table 6-1. The calorimetric methods are
 

not capable of isotope-specific determination of thorium isotopes. Alpha
 

spectrometric and neutron activation analysis are useful in the
 

quantification of isotope-specific thorium and thorium-232, respectively,
 

and have better sensitivities than calorimetric methods. Alpha spectrometry
 

is the commonly used isotope-specific analysis for the determination of
 

thorium-232 and the thorium-230 derived from the decay of uranium-238 (Wrenn
 

et al. 1981). Standard reference materials (SRMs) containing thorium in
 

human liver (SRM-4352) and human lung (SRM-4351) necessary for the
 

determination of absolute recovery in a given sample are available from the
 

National Institute of Standards and Technology (Inn 1987).
 

In vitro monitoring methods for the analysis of thorium in urine,
 

feces, hair, and nails have been used to show that none of these biological
 

media is a good indicator of thorium uptake, and hence thorium exposure in
 

the human. In vivo monitoring with large NaI detectors are probably good
 

methods for determining thorium lung burdens. In one method, thoron (radon220) is determined in exhaled air as a measure of thorium lung burden. The
 

exhaled air is passed to a delay chamber where the positively-charged decay
 

products of thoron (e.g., polonium-216 and lead 212) are collected
 

electrostatically and the collection electrode is measured in an alpha
 

scintillation counter. The method has the required sensitivity to be used
 

as an indicator of thorium uptake. However, because of lack of information
 

regarding the thoron escape rate from the thorium particles in the lungs,
 

the method is not accurate for indicating lung uptake of thorium (Davis
 

1985). Several authors have measured the levels of exhaled thoron or its
 

decay products in human breath (Keane and Brewster 1983; Mayya et al.
 

1986).
 


90
 

6. ANALYTICAL METHODS
 

6.2 ENVIRONMENTAL SAMPLES
 

Some of the commonly used methods for the determination of thorium in
 

environmental samples are shown in Table 6-2. Standard reference materials
 

(SRMs) for thorium in river and freshwater lake sediment (SRM-4350B and SRM4354), soils (SRM-4355 and SRM-4353), coal (SRM-1632), and fly ash (SRM
 

1633) are available from the National Institute of Standards and Technology
 

(formerly National Bureau of Standards) (Inn 1987; Ondov et al. 1975).
 

Neither calorimetric nor atomic absorption/emission methods are suitable for
 

the determination of thorium-specific isotopes; these methods are also not
 

sensitive enough for the quantification of trace amounts of thorium, e.g.,
 

in seawater. The filtration of particulate phases by inert polypropylene
 

fiber filter and adsorption of solution phase thorium onto Mn02-coated fiber 

or preconcentration of thorium on XAD-2 resin by adsorption of thoriumXylenol Orange complexes and quantitation by alpha spectrometry or neutron 

activation analysis are two of the better methods for the quantification of 

low levels of thorium in water (Hirose 1988; Huh and Bacon 1985; Livingston 

and Cochran 1987). The isotope dilution-mass spectrometric method provides 

the most accurate and sensitive thorium quantification (Arden and Gale 1974) 

but is rarely used because of the specialized nature and the cost of the 

analytical technique. The beta counting of thorium deposited on counting 

discs is useful for the determination of thorium-234 derived from uranium238 (Velten and Jacobs 1982). The direct gamma radiation counting with a 

Ge planer detector has been used for the quantification of thorium-228 in 

grass samples (Joshi 1987). The recoveries of thorium from soil and 

sediment samples are usually poor (Singh and Wrenn 1988) and special 

attention should be given to sample treatment during their analysis. 

6.3 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 thorium 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
 

thorium.
 

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.
 


93
 

6. ANALYTICAL METHODS
 

6.3.1 Identification of Data Needs
 

Methods for Determining Biomarkers of Exposure and Effect. A few
 

authors have found elevated levels of thorium in tissues of thorium workers
 

and these studies have been discussed in Sections 2.6 and 5.4.4. However,
 

there are no data in the literature that correlate the concentrations of
 

thorium in any human tissue or body fluid with its level of exposure. If a
 

biomarker for thorium in human tissue or fluid were available, the level of
 

the biomarker in a tissue could be used as an indicator of exposure to
 

thorium. Analytical methods with satisfactory sensitivity are available to
 

determine the levels of thorium in most human tissues and body fluids of
 

exposed and background population, but the recovery of thorium by these
 

methods needs further refinement.
 

No studies were located that identified biomarkers specific to
 

thorium-induced disease states. If a biomarker for thorium-induced effect
 

in humans were found, this effect could also be used as an indicator of
 

exposure to thorium. Therefore, there is a need to develop biomarkers that
 

will serve as indicators of exposure and effect from exposure to uranium.
 

It may be necessary to develop analytical methods of satisfactory
 

sensitivity and precision for the quantification of thorium-induced effects
 

in humans.
 

Methods for Determining Parent Compounds and Degradation Products in
 

Environmental Media. Analytical methods with required sensitivity and
 

precision are available for the quantification of thorium in most
 

environmental samples. However, some of the more sensitive analytical
 

methods have not always been used for the determination of thorium
 

concentrations in drinking water and food. Knowledge of the levels of
 

thorium compounds in environmental media can be used to indicate human
 

exposure to thorium through inhalation of air and ingestion of drinking
 

water and foods containing these compounds. The concentration of thorium is
 

usually very low in drinking water and food and the more sensitive methods
 

may not always have been used for quantification. Because of this, there is
 

controversy in the literature about the relative importance of drinking
 

water and food in contributing to the total dietary daily intake of thorium.
 

It will be helpful to reevaluate the concentrations of thorium in drinking
 

water and food by using the more sensitive analytical methods.
 

In the environment, thorium and its compounds do not degrade or
 

mineralize like many organic compounds, but instead speciate into different
 

chemical compounds and form radioactive decay products. Analytical methods
 

for the quantification of radioactive decay products, such as radium, radon,
 

polonium and lead are available. However, the decay products of thorium are
 

rarely analyzed in environmental samples. Since radon-220 (thoron, a decay
 

product of thorium-232) is a gas, determination of thoron decay products in
 

some environmental samples may be simpler, and their concentrations may be
 

used as an indirect measure of the parent compound in the environment if a
 

secular equilibrium is reached between thorium-232 and all its decay
 
94
 

6. ANALYTICAL METHODS
 

products. There are few analytical methods that will allow quantification
 

of the speciation products formed as a result of environmental interactions
 

of thorium (e.g., formation of complex). A knowledge of the environmental
 

transformation processes of thorium and the compounds formed as a result is
 

important in the understanding of their transport in environmental media.
 

For example, in aquatic media, formation of soluble complexes will increase
 

thorium mobility, whereas formation of insoluble species will enhance its
 

incorporation into the sediment and limit its mobility.
 

6.3.2 On-going Studies
 

Under the sponsorship of the National Science Foundation and in
 

collaboration with scientists in New Zealand, Burnett of Florida State
 

University is attempting to develop a chemical separation technique for
 

uranium, thorium, and their daughter products (Federal Research in Progress
 

1990). Other than this research, no studies are in progress for improving
 

the method for the quantification of thorium and daughter products in
 

biological and environmental samples.
 
95
 

7. REGULATIONS AND ADVISORIES
 

International and national regulations and guidelines pertinent to
 

human exposure to thorium and its radiations are summarized in Table 7-l.
 

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
 

1987). This guidance for occupational exposure supercedes 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 (EPA
 

1987), guides for Annual Limits on Intake (ALIs) and Derived Air
 

Concentrations (DACs) have been calculated (EPA 1988b). The AL1 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 1988b; ICRP 1979) (see Appendix B).
 

The DAC is defined as "the concentration of radionuclide in air which, if
 

breathed by Reference Man (ICRP 1975) for a work-year, would result in the
 

intake of one AL1 (EPA 1988b). The ALIs and DACs refer to occupational
 

situations but may be converted to apply to exposure of persons in the
 

general population by application of conversion factors (Table 7-l).
 





____________________________ 

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131
 

9. GLOSSARY
 

Absorbed Dose -- The mean energy imparted to the irradiated medium, per unit
 

mass, by ionizing radiation. Units: gray (Gy), rd.
 

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 imparts 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=Ioeμx, Io is the initial intensity, I the intensity 

of the beam after passage through a thickness of the material x, and μ

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 μ/p, where μ 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.)
 

Activity Median Aerodynamic Diameter (AMAD) -- The diameter of a unitdensity
 

sphere with the same terminal settling velocity in air as that of
 

the aerosol particulate whose activity is the median for the entire aerosol.
 
132
 

9. GLOSSARY
 

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.
 
133
 

9. GLOSSARY
 

Background Radiation -- Radiation arising from radioactive material other
 

than that 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 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 +l 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 α or β

-

decay, 64Cu or undergo β

-,β+

, 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 "K-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.
 
134
 

9. GLOSSARY
 

Cataract -- A clouding of the crystalline lens of the eye which obstructs
 

the passage of light.
 

Ceiling 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 3.7x1010 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 (3.7x104 disintegrations per 

set) . Abbreviated μCi. 
135
 

9. GLOSSARY
 

Millicurie -- One-thousandth of a curie (3.7x107

 disintegrations per 

set) . Abbreviated mCi. 

Nanocurie -- One-billionth of a curie. Abbreviated nCi.
 

Picocurie -- One-millionth of a microcurie (3.7x10-2 disintegrations 

per second or 2.22 disintegrations per minute). Abbreviated pCi; 

replaces the term μμc. 

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 λ). (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; λ is the symbol for decay 

constant in the equation N=Noe-λ

t, where No 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.)
 
136
 

9. GLOSSARY
 

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.
 

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=l 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 (MID) -- 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 LD50. 

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.
 
137
 

9. GLOSSARY
 

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.
 

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 ±1.6O210x10-19 C (Coulombs) and a rest mass equal to 9.1091x10-31 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.
 

eV, 1 eV=1.6x10-12 erg,)
 

(Abbreviated:
 

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.
 
138
 

9. GLOSSARY
 

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.
 

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.
 
139
 

9. GLOSSARY
 

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 sum of the electrical charges on all ions of one sign
 

produced in air when all electrons liberated by photons in a volume element
 

of 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 onehalf
 

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.
 
140
 

9. GLOSSARY
 

Immunologic Toxicity -- The occurrence of adverse effects on the immune
 

system that may result from exposure to environmental agents such as
 

chemicals.
 

In 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.
 

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.
 
141
 

9. GLOSSARY
 

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.
 

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(LO) (LC LO) -- 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 50% of a defined laboratory animal population. 

Lethal Dose(LO) (LD LO) -- 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. 
142
 

9. GLOSSARY
 

Lethal Time(50) (LT50) -- A calculated period of time within which a 

specific concentration of a chemical is expected to cause death in 50% 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 gamma
 

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.
 

Lowest-Observed-Adverse-Effect 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.
 
143
 

9. GLOSSARY
 

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.
 

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 (9.1091x10-31 kg) and
 

having an equal but positive charge (+1.6O210x10-1g 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.
 
144
 

9. GLOSSARY
 

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.
 

ql* -- The upper-bound estimate of the low-dose slope of the dose-response
 

curve as determined by the multistage procedure. The ql* can be used to
 

calculate an estimate of carcinogenic potency, the incremental excess cancer
 

risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/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."
 

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 td electromagnetic 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.
 
145
 

9. GLOSSARY
 

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.
 

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.
 
146
 

9. GLOSSARY
 

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
 

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., rnd)
 

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 CERCIA. 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.
 
147
 

9. GLOSSARY
 

Roentgen (R) -- A unit of exposure for photon radiation. One roentgen


-4 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 associated with intense acute exposure to ionizing
 

radiations. The rapidity with which symptoms develop is a rough measure OE
 

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.
 
148
 

9. GLOSSARY
 

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.
 

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


3 nucleus (Symbol: H or T).
 

218 Unattached Fraction -- That fraction of the radon daughters, usually Po
 

(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.
 


151
 

APPENDIX A
 

PEER REVIEW
 

A peer review panel was assembled for thorium. The panel
 

consisted of the following members: Dr. Marvin Goldman,
 

Radiological Sciences and Toxicology, University of California;
 

Dr. Raymond Lloyd, Radiology Division, University of Utah: Dr.
 

Ingeborg Harding-Barlow, private consultant, Palo Alto,
 

California; and Dr. George Angleton, Collaborative Radiology
 

Health Laboratory, Colorado State University. These experts
 

collectively have knowledge of thorium'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 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.
 

153
 

APPENDIX B
 

OVERVIEW OF BASIC RADIATION PHYSICS, CHEMISTRY, AND BIOLOGY
 

Understanding the basic concepts in radiation physics, chemistry, and
 

biology is important to the evaluation and interpretation of radiationinduced
 

adverse health effects and to the derivation of radiation protectiol
 

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 naturallyoccurring
 

radionuclides throughout life. This background radiation is the
 

major source of radiation exposure to man and arises from several sources.
 
154
 

APPENDIX B
 

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 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
 

156
 

APPENDIX B
 

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:
 

10 1 curie (Ci) = 3x710 disintegrations (transformations)/second (dps) or
 

1 2.22x10 2 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, TE, 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:
 

-0 A = Aoe ·693t/Trad 

where A is the activity in dps, Ao 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
 

8 curies/gram = 1.3x10 /(Trad)(atomic weight) 

where Trad 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 (Tbiol) which is the time required for 
157
 

APPENDIX B
 

biological 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 = Tbiol X Trad)/(Tbiol + Trad). 

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 (Xrays
 

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
 

159
 

APPENDIX B
 

number by two, thereby changing the parent to a different element. The
 

alpha particle is identical 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 alphaemitting
 

radionuclides may result in the emission of several different alp1
 

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 radionuclidc
 

is ingested, inhaled, or otherwise absorbed).
 

B.2.4.2. Beta Emission. Nuclei which are excessively neutron rich 

decay by β-decay. A beta particle (β) is a high-velocity electron ejected 

from a disintegrating nucleus. The particle may be either a negatively 

charged electron, termed a negatron (β-) or a positively charged electron, 

termed a positron (β+). Although the precise definition of "beta emission" 

refers to both β- and β+, common usage of the term generally applies only to 

the negative particle, as distinguished from the positron emission, which 

refers to the β+ particle. 

B.2.4.2.1 Beta Negative Emission. Beta particle (β-) 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 (β+) 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 β emitters of equal 

energy. 
160
 

APPENDIX B
 

B.2.4.2.3 Gamma Emission. Radioactive decay by alpha, beta, positron
 

emission or electron capture often leaves some of the energy resulting from
 

these changes in the nucleus. As a result, the nucleus is raised to an excited
 

level. None of these excited nuclei can remain in this high-energy state.
 

Nuclei release this energy returning to ground state or to the lowest possible
 

stable energy level. The energy released is in the form of gamma radiation
 

(high energy photons) and has an energy equal to the change in the energy
 

state of the nucleus. Gamma and X-rays behave similarly but differ in their
 

origin; gamma emissions originate in the nucleus while X-rays originate in the
 

orbital electron structure.
 

B.3 ESTIMATION OF ENERGY DEPOSITION IN HUMAN TISSUES
 

Two forms of potential radiation exposures can result -- internal and
 

external. The term exposure denotes physical interaction of the radiation
 

emitted from the radioactive material with cells and tissues of the human
 

body. An exposure can be "acute" or "chronic" depending on how long an
 

individual or organ is exposed to the radiation. Internal exposures occur
 

when radionuclides, which have entered the body (e.g., through the
 

inhalation, ingestion, or dermal pathways), undergo radioactive decay
 

resulting in the deposition of energy to internal organs. External
 

exposures occur when radiation enters the body directly from sources located
 

outside the body, such as radiation emitters from radionuclides on ground
 

surfaces, dissolved in water, or dispersed in the air. In general, external
 

exposures are from material emitting gamma radiation, which readily
 

penetrate the skin and internal organs. Beta and alpha radiation from
 

external sources are far less penetrating and deposit their energy primarily
 

on the skin's outer layer. Consequently, their contribution to the absorbed
 

dose of the total body dose, compared to that deposited by gamma rays, may
 

be negligible.
 

Characterizing the radiation dose to persons as a result of exposure to
 

radiation is a complex issue. It is difficult to: (1) measure internally
 

the amount of energy 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
 

biologically triggered effects, that are an indirect consequence of the
 

primary interaction event.
 

B.3.1 Dose Units
 

B.3.1.1 Roentgen. The roentgen (R) is a unit of exposure related to
 

the amount of ionization caused in air by gamma or x-radiation. One


-4 roentgen equals 2.58x10 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.
 
161
 

APPENDIX B
 

B.3.1.2 Absorbed Dose and Absorbed Dose Rate. Since different typesof
 

radiation interact differently with any material through which they pass, any
 

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


5 will result in the emission of 1.3x10 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.


5 In this case, 1.3x10 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
 

(WIJf). 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
 
162
 

APPENDIX B
 

through the tract, or a combination of both. The fraction of a radioactive
 

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 interaction 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
 
163
 

APPENDIX B
 

a given dose of radiation. Factors related to the exposure include the dose
 

rate, the energy of the radiation, and the temporal pattern of the exposure.
 

Biological considerations include factors such as species, age, sex, and tile
 

portion of the bodjr 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) t 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
 

Bergoni-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 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
 
164
 

APPENDIX B
 

the rapid renewal system, organ injury results from the direct destruction
 

of highly radiosensitive cells, such as the stem cells in the bone marrow.
 

Injury 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 stage, 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 bloodforming
 

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 (BEIR 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
 
165
 

APPENDIX B
 

use of Thorotrast (colloidal thorium dioxide) resulted in increases in the
 

incidence of cancers of the liver, bone, 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
 

i-ncreases 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 199Oc). 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. Radiationinduced
 

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), BETR 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, 0 r
 

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 radionuclidcs (ATSDR)
 

139Oc, 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 teratogcnicity 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 atonic bomb provide evidence that
 
166
 

APPENDIX B
 

radiation may produce 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=DxQxN.
 

The quality factor is a dimensionless quantity that depends in part on the
 

stopping power for charged particles, and it accounts for the differences il
 

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
 


169
 

APPENDIX B
 

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.
 

The effective dose equivalent, Hg, is
 

Hg = (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.
 


172
 

APPENDIX B
 

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