TOXICOLOGICAL PROFILE FOR
 

ANTIMONY AND COMPOUNDS
 

Agency for Toxic Substances and Disease Registry
 

U.S. Public Health Service
 

September 1992
 
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.
 
iii

FOREWORD
 

The Superfund Amendments and Reauthorization Act (SARA) of 1986
 

(Public Law 99-499) extended and amended the Comprehensive Environmental
 

Response, Compensation, and Liability Act of 1980 (CERCLA or Superfund). This
 

public law directed the Agency for Toxic Substances and Disease Registry
 

(ATSDR) to prepare toxicological profiles for hazardous substances which are
 

most commonly found at facilities on the CERCLA National Priorities List and
 

which pose the most significant potential threat to human health, as
 

determined by ATSDR and the Environmental Protection Agency (EPA). The lists
 

of the 250 most significant hazardous substances were published in the Federal
 

Resister on April 17, 1987; on October 20, 1988; on October 26, 1989; and on
 

October 17, 1990. A revised list of 275 substances was published on October
 

17, 1991.
 

Section 104(i)(3) of CERCLA, as amended, directs the Administrator
 

of ATSDR to prepare a toxicological profile for each substance on the
 

lists. Each profile must include the following content:
 

(A) An examination, summary, and interpretation of available
 

toxicological information and epidemiological evaluations on the
 

hazardous substance in order to ascertain the levels of significant
 

human exposure for the substance and the associated acute, subacute, and
 

chronic health effects.
 

(B) A determination of whether adequate information on the health
 

effects of each substance is available or in the process of
 

development to determine levels of exposure which present a
 

significant risk to human health of acute, subacute, and chronic
 

health effects.
 

(C) Where appropriate, an identification of toxicological testing
 

needed to identify the types or levels of exposure that may present
 

significant risk of adverse health effects in humans.
 

This toxicological profile is prepared in accordance with
 

guidelines developed by ATSDR and EPA. The original guidelines were
 

published in the Federal Register on April 17, 1987. Each profile will
 

be revised and republished as necessary.
 

The ATSDR toxicological profile is intended to characterize
 

succinctly the toxicological and adverse health effects information for
 

the hazardous substance being described. Each profile identifies and
 

reviews the key literature (that has been peer-reviewed) that describes
 

a hazardous substance's toxicological properties. Other pertinent
 

literature is also presented but described in less detail than the key
 

studies. The profile is not intended to be an exhaustive document;
 

however, more comprehensive sources of specialty information are
 

referenced.
 









1
 

1. PUBLIC HEALTH STATEMENT
 

This Statement was prepared to give you information about antimony and
 

to emphasize the human health effects that may result from exposure to it. The
 

Environmental Protection Agency (EPA) has identified 1,177 sites on its
 

National Priorities List (NPL). Antimony and its compounds have been found at
 

52 of these sites. However, we do not know how many of the 1,177 NPL sites
 

have been evaluated for antimony. As EPA evaluates more sites, the number of
 

sites at which antimony and its compounds are found may change. The
 

information is important for you because antimony may cause harmful health
 

effects and because these sites are potential or actual sources of human
 

exposure to antimony.
 

When a 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 chemical emission. This emission, which is also called a
 

release, does not always lead to exposure. You can be exposed to a chemical
 

only when you come into contact with the chemical. You may be exposed to it in
 

the environment by breathing, eating, or drinking substances containing the
 

chemical or from skin contact with it.
 

If you are exposed to a hazardous substance such as antimony, several
 

factors will determine whether harmful health effects will occur and what the
 

type and severity of those health effects will be. These factors include the
 

dose (how much), the duration (how long), the route or pathway by which you
 

are exposed (breathing, eating, drinking, or skin contact), the other
 

chemicals to which you are exposed, and your individual characteristics such
 

as age, sex, nutritional status, family traits, life style, and state of
 

health.
 

1.1 WHAT IS ANTIMONY?
 

Antimony is a silvery white metal of medium hardness that breaks easily.
 

Small amounts of antimony are found in the earth's crust. Antimony ores are
 

mined and then either changed into antimony metal or combined with oxygen to
 

form antimony oxide.
 

Antimony oxide is a white powder that does not evaporate. Only a small
 

amount of it will dissolve in water. Most antimony oxide produced is added to
 

textiles and plastics to prevent their catching on fire.
 

Antimony metal is too easily broken to be used much by itself. To make
 

it stronger, a little antimony is usually mixed with other metals such as lead
 

and zinc to form mixtures of metals called alloys. These alloys are used in
 

lead storage batteries, solder, sheet and pipe metal, bearings, castings, type
 

metal, ammunition, and pewter.
 

Antimony enters the environment during the mining and processing of its
 

ores and in the production of antimony metal, alloys, antimony oxide, and
 
2
 

1. PUBLIC HEALTH STATEMENT
 

combinations of antimony with other substances. Little or no antimony is mined
 

in the United States, Antimony ore and impure metals are brought into this
 

country from other countries for processing. Small amounts of antimony are
 

also released into the environment by incinerators and coal-burning power
 

plants. The antimony that comes out of the smoke stacks of these plants is
 

attached to very small particles that settle to the ground or are washed out
 

of the air by rain. It usually takes many days for antimony to be removed from
 

the air. Antimony attached to very small particles may stay in the air for
 

more than a month. Antimony cannot be destroyed in the environment. It can
 

only change its form or become attached to or separated from particles. Most
 

antimony will end up in the soil or sediment, where it attaches strongly to
 

particles that contain iron, manganese, or aluminum. For more information, see
 

Chapters 3, 4, and 5.
 

1.2 HOW HIGHT I BE EXPOSED TO ANTIMONY?
 

Antimony is found at very low levels in the environment, so low that we
 

often cannot measure it. You may be exposed to antimony by breathing air,
 

drinking water, and eating foods that contain it. You also may be exposed by
 

skin contact with soil, water, and other substances that contain antimony. The
 

analytical methods used by scientists testing for the presence of antimony in
 

the environment do not determine the specific form of antimony present.
 

Therefore, we do not always know what form of antimony persons may be exposed
 

to. Similarly, we do not know what forms of antimony are found in hazardous
 

waste sites. Much of the antimony found in sediment, soil, and rock is so
 

strongly attached to dust and dirt or buried in minerals that it cannot easily
 

affect your health. Some antimony in the environment is less tightly attached
 

to particles and may be taken up by plants and animals.
 

The concentration of antimony in air ranges from a very small part of a
 

nanogram (1 nanogram equals a billionth of a gram) in a cubic meter (m3

) of
 

air (ng/m3

) to about 170 ng/m3. However, near companies that change antimony
 

ores into metal or make antimony oxide, concentrations may be more than 1,000
 

ng/m3

. You may breathe high levels of antimony in dust if you live or work
 

near antimony mines or processing companies.
 

The concentration of antimony that is dissolved in rivers and lakes is
 

very low, usually less than 5 parts of antimony in 1 billion parts of water
 

(ppb) . We cannot measure such small amounts without special equipment.
 

Antimony does not appear to accumulate in fish and other aquatic animals. The
 

concentration of antimony dissolved in one polluted river where wastes from
 

antimony mining and processing had been dumped was as high as 8 ppb. Most of
 

the antimony in the river, however, was not dissolved, but was attached to
 

particles of dirt. Although antimony is used in solder for water pipes, it
 

does not seem to get into the drinking water.
 

Soil usually contains very low concentrations of antimony, less than 1
 

part of antimony in a million parts of soil (ppm). However, concentrations
 
3
 

1. PUBLIC HEALTH STATEMENT
 

close to 9 ppm have been found. The highest soil concentrations found at
 

hazardous waste sites on the NPL and at antimony-processing sites range from
 

109 to 2,550 ppm. High concentrations of antimony may be found in soil because
 

dust sent out during processing settles out from the air. Also, waste from
 

antimony-processing and other antimony-using industries is usually dumped onto
 

the soil. We do not know the form of antimony at these sites. However, we know
 

that much of the antimony in antimony-processing wastes is strongly attached
 

to soil. You may be exposed to this antimony by skin contact. Children may
 

also be exposed to this antimony by eating the dirt.
 

Food usually contains small amounts of antimony. You eat and drink
 

about 5 micrograms (5 millionths of a gram) of antimony every day. The
 

average concentration of antimony in meats, vegetables, and seafood is
 

0.2-1.1 ppb. The antimony oxide that is added to many materials for fire
 

protection is very tightly attached to these materials and does not expose
 

people to antimony.
 

You may also be exposed to antimony in the workplace. If you work in
 

industries that process antimony ore and metal or make chemicals that contain
 

antimony, such as antimony oxide, you may be exposed to antimony by breathing
 

dust or by skin contact.
 

For more information on how you may be exposed to antimony, see
 

Chapter 5.
 

1.3 HOW CAN ANTIMONY ENTER AND LEAVE MY BODY?
 

Antimony can enter your body when you drink water or eat food, soil, or
 

other substances that contain antimony. Antimony can also enter your body if
 

you breathe air or dust containing antimony. We do not know if antimony can
 

enter your body when it is placed on your skin.
 

A small amount of the antimony you eat or drink enters the blood after a
 

few hours. The amount and the form of antimony in the food or water will
 

affect how much antimony enters your blood. After you eat or drink very large
 

doses of antimony, you may vomit. This will prevent most of the antimony from
 

entering through the stomach and intestines into your blood. Antimony in your
 

lungs will enter your blood after several days or weeks. The amount of
 

antimony that will enter your blood from your lungs is not known.
 

After antimony enters your blood, it goes to many parts of your body.
 

Most of the antimony goes to the liver, lungs, intestines, and spleen.
 

Antimony will leave your body in feces and urine over several weeks. Further
 

information on how antimony enters and leaves your body is presented in
 

Chapter 2.
 
4
 

1. PUBLIC HEALTH STATEMENT
 

1.4 HOW CAN ANTIMONY AFFECT MY HEALTH?
 

Exposure to 9 milligrams per cubic meter of air (mg/m3

) of antimony for
 

a long time can irritate your eyes, skin, and lungs. Breathing 2 mg/m3

 of
 

antimony for a long time can cause problems with the lungs (pneumoconiosis)
 

heart problems (altered electrocardiograms), stomach pain, diarrhea, vomiting
 

and stomach ulcers. People who drank over 19 ppm of antimony once, vomited. We
 

do not know what other health effects would occur to people who swallow
 

antimony. We do not know if antimony can cause cancer or birth defects, or
 

affect reproduction in humans. Antimony can have beneficial effects when used
 

for medical reasons, It has been used as a medicine to treat people infected
 

with parasites. Persons who have had too much of this medicine or are
 

sensitive to it when it was injected into their blood or muscle have
 

experienced adverse health effects. These health effects include diarrhea,
 

joint and/or muscle pain, vomiting, problems with the blood (anemia) and heart
 

problems (altered electrocardiograms).
 

Rats and guinea pigs that breathed very high levels of antimony for a
 

short time died. Rats breathing high levels of antimony for several days had
 

lung, heart, liver, and kidney damage. Breathing very low levels of antimony
 

for a long time has resulted in eye irritation, hair loss, and lung damage in
 

rats. Dogs and rats that breathed low levels of antimony for a long period had
 

heart problems (changes in EKGs). Problems with fertility have been observed
 

in rats that breathed very high levels of antimony for a couple of months.
 

Lung cancer has been observed in some studies of rats breathing high
 

concentrations of antimony. Antimony has not been classified for cancer
 

effects by the Department of Health and Human Services, the International
 

Agency for Research on Cancer or the Environmental Protection Agency.
 

Dogs that drank very high levels of antimony for several weeks lost
 

weight and had diarrhea. Rats that drank very low levels of antimony for most
 

of their lives died sooner than rats not drinking antimony. Rats eating high
 

levels of antimony for a long time had liver damage and fewer red blood cells.
 

Rabbits that had very small amounts of antimony placed on their skin for
 

less than 1 day had skin irritation. Small amounts of antimony placed in
 

rabbit eyes resulted in eye irritation. Large amounts of antimony placed on
 

rabbit's skin resulted in death.
 

More information on how antimony can affect your health is presented in
 

Chapter 2.
 

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

TO ANTIMONY?
 

There are reliable and accurate ways of measuring antimony levels in the
 

body. Antimony can be measured in the urine, feces, and blood for several days
 

after exposure. High levels of antimony in these fluids will show that
 
5
 

1. PUBLIC HEALTH STATEMENT
 

you have been exposed to high levels of antimony. However, these measurements
 

can not tell you how much antimony you have been exposed to or whether you
 

will experience any health effects. For more information, see Chapters 2 and
 

6.
 

1.6 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO
 

PROTECT HUMAN HEALTH?
 

EPA has set a limit of 145 ppb in lakes and streams to protect human
 

health from the harmful effects of antimony taken in through water and
 

contaminated fish and shellfish. EPA has also set limits on the amount of
 

antimony that industry can release.
 

The Occupational Safety and Health Administration (OSHA) has set a limit
 

of 0.5 mg/m3

 of antimony in workroom air to protect workers during an 8-hour
 

work shift (40-hour workweek). The National Institute of Occupational Safety
 

and Health (NIOSH) also recommends that the concentration in workroom air be
 

limited to 0.5 mg/m3

 for antimony, averaged over an 8-hour work shift. Further
 

information on regulations and guidelines pertaining to antimony is provided
 

in Chapter 7.
 

1.7 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 provide you with information on the location of the
 

nearest occupational and environmental health clinic. Such clinics specialize
 

in recognizing, evaluating, and treating illnesses that result from exposure
 

to hazardous substances.
 

7
 

2. HEALTH EFFECTS
 

2.1 INTRODUCTION
 

The primary purpose of this chapter is to provide public health
 

officials, physicians, toxicologists, and other interested individuals and
 

groups with an overall perspective of the toxicology of antimony and a
 

depiction of significant exposure levels associated with various adverse
 

health effects. It contains descriptions and evaluations of studies and
 

presents levels of significant exposure for antimony based on toxicological
 

studies and epidemiological investigations.
 

Studies in which humans or animals are exposed to various antimony
 

compounds are discussed in this chapter. The antimony compounds include
 

organic forms (potassium antimony tartrate, sodium antimony tartrate, antimony
 

acetate), inorganic trivalent antimony (antimony trioxide, antimony
 

trichloride, antimony trisulfide, stibine), pentavalent inorganic antimony
 

(antimony pentoxide, antimony pentasulfide), antimony-containing drugs
 

(stibocaptate, stibophen), and metallic antimony. No limitations were placed
 

on the selection of compounds for inclusion in this toxicological profile.
 

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 information in this section is
 

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 (less than 15 days), intermediate (15­

364 days), and chronic (365 days or more).
 

Levels of significant exposure for each route and duration are presented
 

in tables and illustrated in figures. The points in the figures showing noobserved-adverse-effect levels (NOAELs) or lowest-observed-adverse-effect
 

levels (LOAELS) reflect the actual doses (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. They
 

should also help to determine whether or not the effects vary 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 in 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 may
 

be interested in levels of exposure associated with "serious" effects. Public
 

health officials and project managers concerned with appropriate actions to
 

take at hazardous waste sites may want information on levels of exposure
 

associated with more subtle effects in humans or animals (LOAEL) or exposure
 
8
 

2. HEALTH EFFECTS
 

levels below which no adverse effects (NOAEL) have been observed. Estimates of
 

levels posing minimal risk to humans (Minimal Risk Levels, MRLs) may be of
 

interest to health professionals and citizens alike.
 

Estimates of exposure levels posing minimal risk to humans (MRLs) have
 

been made, where data were believed reliable, for the most sensitive noncancer
 

effect for each exposure duration. MRLs include adjustments to reflect human
 

variability from laboratory animal data to humans.
 

Although methods have been established to derive these levels (Barnes et
 

al. 1988; EPA 1989a), uncertainties are associated with these techniques.
 

Furthermore, ATSDR acknowledges additional uncertainties inherent in the
 

application of the procedures to derive less than lifetime MRLs. As an
 

example, acute inhalation MRLs may not be protective for health effects that
 

are delayed in development or are acquired followLng repeated acute insults,
 

such as hypersensitivity reactions, asthma, or chronic bronchitis. As these
 

kinds of health effects data become available and methods to assess levels of
 

significant human exposure improve, these MRLs will be revised.
 

2.2.1 Inhalation Exposure
 

Health effects have been observed in humans and animals following
 

inhalation exposure to several antimony compounds. Health effects following
 

exposure to airborne stibine, antimony trisulfide, antimony trioxide, antimony
 

pentoxide, antimony trichloride, antimony pentasulfide, and metallic antimony
 

are discussed below. Of these, stibine (antimony hydride) is a naturally
 

occurring gas; for ease of comparison, its concentrations will be expressed in
 

units of mg/m3

 (1 ppm stibine = 5.1 mg/m3).
 

2.2.1.1 Death
 

No studies were located regarding death in humans after inhalation
 

exposure to antimony.
 

Guinea pigs exposed to approximately 37.9 mg antimony/m3

 as antimony
 

trioxide dust for 52-125 days (Dernehl et al. 1945) or guinea pigs and rats
 

exposed to 1,395 mg antimony/m3

 as stibine gas for 30 minutes (Price et al.
 

1979) died. In the Dernehl et al. (1945) study, four guinea pigs died, one
 

animal following each of 52, 90, 98, and 125 days of exposure. Pulmonary edema
 

was a contributing factor to the death of rats and guinea pigs exposed to
 

stibine (Price et al. 1979). None of the rats or guinea pigs exposed to 799 mg
 

antimony/m3 for 30 minutes died (Price et al. 1979). Lower concentrations of
 

antimony trisulfide or antimony trioxide did not affect the survival of rats
 

exposed for 1 year (Groth et al. 1986; Wong et al. 1979).
 

The highest NOAEL values and all reliable LOAEL values for death in each
 

species and duration are presented in Table 2-l and plotted in Figure 2-l.
 






15
 

2. HEALTH EFFECTS
 

2.2.1.2 Systemic Effects
 

The highest NOAEL values and all reliable LOAEL values for each systemic
 

effect in each species and duration are presented in Table 2-l and plotted in
 

Figure 2-1.
 

Respiratory Effects. Occupational exposure to antimony trioxide and/or
 

pentoxide dust (8.87 mg antimony/m3

 or greater) resulted in antimony
 

pneumoconiosis (inflammation of the lungs due to the irritation caused by the
 

inhalation of dust) (Cooper et al. 1968; Potkonjak and Pavlovich 1983; Renes
 

1953). Alterations in pulmonary function (airway obstruction, bronchospasm,
 

and hyperinflation) have been reported in workers exposed to airborne antimony
 

(Cooper et al. 1968; Potkonjak and Pavlovich 1983). Other respiratory effects
 

reported in workers include chronic bronchitis, chronic emphysema, inactive
 

tuberculosis, pleural adhesions, and irritation (Potkonjak and Pavlovich
 

1983). The respiratory irritation reported in the workers diagnosed as having
 

pneumoconiosis was characterized by chronic coughing, wheezing, and upper
 

airway inflammation. Respiratory irritation was not noted in workers exposed
 

to antimony trisulfide for 8 months to 2 years (Brieger et al. 1954). In the
 

reports of health effects associated with occupational exposure to antimony,
 

the workers inhaled a variety of compounds including antimony pentoxide,
 

arsenic oxide, iron oxide, hydrogen sulfide, and sodium hydroxide (Cooper
 

et al. 1968; Potkonjak and Pavlovich 1983; Renes 1953).
 

A variety of respiratory effects have been reported in animals exposed
 

to antimony. A majority of these effects are associated with the physiological
 

response to dust accumulation in the lung (pneumoconiosis). The effects
 

progress from pneumoconiosis and a proliferation of alveolar macrophages to
 

fibrosis.
 

Lung inflammation was noted in rabbits exposed to antimony trisulfide
 

for 5 days (Brieger et al. 1954).
 

Acute exposure to stibine gas also results in lung effects. Pulmonary
 

edema was observed in rats and guinea pigs exposed to a lethal concentration
 

of stibine for 30 minutes (Price et al. 1979).
 

A dose-related increase in the number of alveolar and/or intraalveolar
 

macrophages was observed in rats exposed to antimony trioxide for 13 weeks or
 

more (Bio/dynamics 1985, 1990). In rats exposed to 0.07 mg antimony/m3

 for 1
 

year or to 0.92 mg antimony/m3

 for 13 weeks, the proliferation of macrophages
 

was still present for 12 months or 28 weeks, respectively, after exposure
 

termination (Bio/dynamics 1985, 1990). Chronic interstitial inflammation was
 

also observed in rats exposed to 0.07 mg antimony/m3

 for 1 year with a 1 year
 

recovery.
 
16
 

2. HEALTH EFFECTS
 

The proliferation of macrophages is a normal physiological response to
 

the deposition of insoluble particulates in the lung. However, excessive
 

phagocytic activity prompted by extensive or repeated deposition of
 

particulates in the lung probably contributes to the development of fibrosis.
 

Because of the integral role the macrophages have in the progression to
 

fibrosis, nonreversible proliferation of macrophages is considered a less
 

serious adverse health effect.
 

More severe respiratory effects have also been reported in animals
 

exposed to antimony. Interstitial fibrosis and lipoid pneumonia have been
 

observed in rats exposed to antimony trisulfide or antimony trioxide for 1
 

year (Bio/dynamics 1990; Gross et al. 1952; Groth et al. 1986; Watt 1980,
 

1983; Wong et al. 1979). These effects have been reported at exposure levels
 

between 1.6 and 83.6 mg antimony/m3

. No respiratory effects were reported in
 

pigs exposed to 4.2 mg antimony/m3 as antimony trioxide for 1 year (Watt
 

1983).
 

Cardiovascular Effects. Increased blood pressure (greater than 150/90)
 

and altered EKG readings were observed in workers exposed to 2.15 mg
 

antimony/m3

 as antimony trisulfide for 8 months to 2 years (Brieger et al.
 

1954). Of the 75 workers examined, 37 showed changes in the EKG, mostly of the
 

T-waves; these workers had also been exposed to phenol formaldehyde resin
 

(Brieger et al. 1954). In another group of antimony workers, one out of seven
 

had altered EKG readings (Renes 1953). These limited data on cardiovascular
 

effects in humans are supported by the finding of cardiac effects following
 

parenteral administration of antimony to humans (see discussion of systemic
 

effects in Section 2.4).
 

Inhalation exposure to antimony trisulfide dust (the same dust the
 

factory workers were exposed to) resulted in degenerative changes in the
 

myocardium and related EKG abnormalities (elevation of the RS-T segments and
 

flattening of T-waves) in a variety of animal species (Brieger et al. 1954).
 

Five days of exposure to 19.94 mg antimony/m3

 as antimony trisulfide resulted
 

in EKG alterations in rabbits. The effective exposure levels resulting in
 

cardiovascular effects were at least four times lower (2-4 mg antimony/m3) in
 

rats, rabbits, and dogs exposed to airborne antimony for 6-10 weeks, as
 

compared to rabbits acutely exposed (Brieger et al. 1954). Dogs exposed to
 

3.81 mg antimony/m3

 as antimony trisulfide for 7 weeks (Brieger et al. 1954)
 

or pigs exposed to 4.2 mg antimony/m3

 as antimony trioxide for 1 year (Watt
 

1983) did not exhibit changes in EKG readings. The degenerative changes of the
 

myocardium observed in rats, rabbits, and dogs exposed to antimony trisulfide
 

consisted of hyperemia and swelling of myocardial fibers (Brieger et al.
 

1954). Myocardial damage was not observed in rats exposed to 17.48 mg
 

antimony/m3

 as antimony trioxide for 1 year (Groth et al. 1986; Watt 1980;
 

Wong et al. 1979).
 
17
 

2. HEALTH EFFECTS
 

Gastrointestinal Effects. A variety of gastrointestinal disorders have
 

occurred in factory workers engaged in activities including repeated prolonged
 

exposure to airborne antimony trichloride (Taylor 1966), antimony trisulfide
 

(Brieger et al. 1954) or antimony oxide (Renes 1953). These disorders include
 

abdominal pain, diarrhea, vomiting, and ulcers. A causal relationship to
 

antimony exposure has not been definitely established because workers were
 

exposed to a variety of other agents in addition to antimony that might cause
 

or contribute to gastrointestinal effects (e.g., hydrogen chloride, sodium
 

hydroxide). Furthermore, in all likelihood, both inhalation and oral exposure
 

to antimony occur at the workplace. Assuming that gastrointestinal effects are
 

related to antimony-exposure, site monitoring data indicate that effective
 

exposure levels may range from approximately 2 to 70 mg antimony/m3

.
 

Symptoms of gastrointestinal disturbances were not reported in animals,
 

and no histopathological alterations were observed in rats exposed to antimony
 

trioxide (4.2 mg antimony/m3

) for 1 year (Watt 1980).
 

Hematological Effects. No studies were located regarding hematological
 

effects in humans after inhalation exposure to antimony.
 

Toxicologically significant hematological effects have not been observed
 

in rats and pigs following long-term exposure to antimony aerosols ranging
 

from 4 to 20 mg antimony/m3

 as antimony trioxide (Bio/dynamics 1985, 1990;
 

Watt 1983). The only effects observed were small (but statistically
 

significant) changes in the hemoglobin concentration in the erythrocytes and
 

erythrocyte volume in rats exposed to 4.01 mg antimony/m3

 as antimony trioxide
 

(Bio/dynamics 1990).
 

Musculoskeletal Effects. No studies were located regarding
 

musculoskeletal effects in humans after inhalation exposure to antimony. No
 

histopathological alterations were noted in the musculoskeletal system in rats
 

exposed to 4.2 mg antimony/m3

 as antimony trioxide for 1 year (Watt 1980).
 

Hepatic Effects. No studies were located regarding hepatic effects in
 

humans after inhalation exposure to antimony.
 

Parenchymatous and fatty degeneration was observed in rabbits exposed to
 

19.94 mg antimony/m3

 as antimony trisulfide for 5 days (Brieger et al. 1954)
 

and in guinea pigs exposed to 37.9 mg antimony/m3

 as antimony trioxide for 30
 

weeks (Dernehl et al. 1945). The duration of exposure is unclear in the
 

Dernehl et al. (1945) study. No hepatic effects were observed in rats exposed
 

to antimony trioxide for 13 weeks (Bio/dynamics 1985) or after 1 year of
 

exposure to antimony trioxide or antimony trisulfide concentrations of 36 mg
 

antimony/m3

 or lower (Bio/dynamics 1990; Groth et al. 1986; Watt 1980; Wong et
 

al. 1979).
 
18
 

2. HEALTH EFFECTS
 

Renal Effects. No studies were located regarding renal effects in
 

humans after inhalation exposure to antimony.
 

Tubular dilation was observed in rats and guinea pigs exposed to stibine
 

gas for 30 minutes at a concentration of 799 mg antimony/m3

 (Price et al.
 

1979). Parenchymatous degeneration was observed in rabbits exposed to 19.94 mg
 

antimony/m3 as antimony trisulfide for 5 days (Brieger et al. 1954). No renal
 

effects were noted in rats exposed to 19.6 mg antimony/m3

 as antimony trioxide
 

for 13 weeks (Bio/dynamics 1985) or 17.5 mg antimony/m3 as antimony trisulfide
 

or up to 36 mg antimony/m3

 as antimony trioxide for 1 year (Bio/dynamics 1990;
 

Groth et al. 1986; Wong et al. 1979).
 

Dermal/Ocular Effects. Dermal and ocular effects have been reported in
 

humans. and animals. These effects (ocular conjunctivitis and dermatosis)
 

result from airborne antimony coming into contact with the skin and/or eyes
 

(Potkonjak and Pavlovich 1983; Renes 1953; Stevenson 1965).
 

The dermatitis associated with exposure to airborne antimony is
 

characterized as epidermal cellular necrosis with associated acute
 

inflammatory cellular reactions (Stevenson 1965). The dermatitis is seen more
 

often during the summer months and in workers exposed to high temperatures
 

(Potkonjak and Pavlovich 1983; Stevenson 1965). Stevenson (1965) concluded
 

that the dermatitis resulted from the action of antimony trioxide on the
 

dermis after dissolving in sweat and penetrating the sweat glands.
 

Transferring the worker to a cooler environment often resulted in the rash
 

clearing up within 3-14 days. Antimony trioxide is not a skin sensitizer in
 

humans following topical application (see Section 2.2.3.3).
 

Eye irritation has been observed in rats and guinea pigs exposed to
 

stibine gas (Price et al. 1979) and antimony trioxide (Bio/dynamics 1985).
 

Cataracts and chromodacryorrhea have been observed in rats exposed to antimony
 

trioxide for 1 year with a 1 year recovery period (Bio/dynamics 1990). The
 

authors suggest that the chromodacryorrhea may have been secondary to dental
 

abnormality, infectious disease, or xerosis.
 

Because these dermal and ocular effects may not be the result of
 

inhalation exposure, but rather dermal contact with airborne antimony, the
 

LOAEL values were not recorded in Table 2-l or Figure 2-l. Alopecia was noted
 

in rats exposed to 0.92 mg antimony/m3

 or greater as antimony trioxide for 13
 

weeks (Bio/dynamics 1985). Because high levels of antimony are measured in the
 

skin or hair of animals following nose-only exposure to antimony aerosols,
 

this effect may not be the result of dermal contact to airborne antimony
 

(Felicetti et al. 1974a, 1974b).
 

Other Systemic Effects. No studies were located regarding other
 

systemic effects in humans after inhalation exposure to antimony. Hyperplasia
 
19
 

2. HEALTH EFFECTS
 

of the reticuloendothelial cells in the peribronchiolar lymph nodes was
 

observed in rats exposed to 0.07 mg antimony/m3 antimony trioxide for 1 year
 

with a 1 year recovery period (Bio/dynamic 1990).
 

2.2.1.3 Immunological Effects
 

No studies were located regarding immunological effects in humans or
 

animals after inhalation exposure to antimony.
 

2.2.1.4 Neurological Effects
 

A causal relationship between exposure to airborne antimony and
 

neurological effects in humans has not been established. Nerve tenderness and
 

a tingling sensation were reported in workers exposed to antimony oxide at a
 

concentration of 10.07 mg antimony/m3

 (Renes 1953). However, the factory
 

workers were also exposed to arsenic, lead, copper, and possibly hydrogen
 

sulfide and sodium hydroxide. Thus, it is difficult to determine if this
 

effect was the result of antimony exposure.
 

No studies were located regarding neurological effects in animals after
 

inhalation exposure to antimony.
 

2.2.1.5 Developmental Effects
 

An increased incidence of spontaneous abortions, compared to a control
 

grow, were reported in women working at an antimony metallurgical plant. The
 

women were exposed to a mixture of antimony trioxide, antimony pentasulfide,
 

and metallic antimony (Belyaeva 1967). The level of airborne antimony and
 

presence of other compounds is not known. In addition, a description of the
 

control group was not given; thus, it is unclear if the controls had jobs
 

comparable to those of the exposed group.
 

A decreased number of offspring was born to rats exposed to 209 mg
 

antimony/m3

 as antimony trioxide prior to conception and throughout gestation.
 

No difference in fetal body weights was observed (Belyaeva 1967). This LOAEL
 

for developmental effects in rats is presented in Table 2-l and Figure 2-1.
 

2.2.1.6 Reproductive Effects
 

Disturbances in the menstrual cycle were reported in women exposed to
 

airborne metallic antimony, antimony pentasulfide, and antimony trioxide in a
 

metallurgical plant. No other details were provided (Belyaeva 1967).
 

In rats exposed to 209 mg antimony/m3 as antimony trioxide for 63 days,
 

67% failed to conceive. Metaplasia in the uterus and disturbances in the ovum-


maturing process were obsewed in the animals that failed to conceive,. These
 

effects were not observed in the rats that conceived (Belyaeva 1967).
 
20
 

2. HEALTH EFFECTS
 

This LOAEL value for reproductive effects in rats is presented in Table 2-l
 

and Figure 2-l.
 

2.2.1.7 Genotoxic Effects
 

No studies were located regarding genotoxic effects in humans or animals
 

after inhalation exposure to antimony.
 

Genotoxicity studies are discussed in Section 2.4.
 

2.2.1.8 Cancer
 

Inhalation exposure to 8.87 mg antimony/m3

 as antimony oxide did not
 

affect the incidence of cancer in workers employed for 9-31 years (Potkonjak
 

and Pavlovich 1983).
 

Antimony can be carcinogenic in rats. Lung tumors were observed in rats
 

exposed to 4.2 or 36 mg antimony/m3 as antimony trioxide (Groth et al. 1986;
 

Watt 1980, 1983; Wong et al. 1979) or 17.48 mg antimony/m3

 as antimony
 

trisulfide for 1 year (Groth et al. 1986; Wong et al. 1979). An increased
 

incidence of lung tumors was not observed in rats exposed to 4.01 mg
 

antimony/m3

 as antimony trioxide (Bio/dynamics 1990) or in pigs exposed to 4.2
 

mg antimony/m3

 as antimony trioxide (Watt 1983). The carcinogenic potential of
 

antimony may be related to the deposition and clearance of antimony from the
 

respiratory tract. Further discussion is presented in Section 2.4. The cancer
 

effect levels are recorded in Table 2-1 and
 

Figure 2-l.
 

2.2.2 Oral Exposure
 

Health effects have been observed in humans and animals following oral
 

exposure to a variety of antimony compounds. Adverse effects following
 

exposure to potassium antimony tartrate (an organic form of antimony),
 

antimony trichloride, antimony trioxide, and metallic antimony are discussed
 

below.
 

2.2.2.1 Death
 

No studies were located regarding death in humans after oral exposure to
 

antimony.
 

Mortality was not observed in rats following a single exposure to
 

188-16,714 mg antimony/kg or lower as inorganic antimony (Fleming 1982; Myers
 

et al. 1978; Smyth and Carpenter 1948; Smyth and Thompson 1945) or to a 7,000
 

mg antimony/kg dose of metallic antimony (Bradley and Frederick 1941).
 

However, a lower single dose of organic antimony (300 mg antimony/kg dose as
 

potassium antimony tartrate) resulted in death in rats (Bradley and Frederick
 

1941). Death was attributed to myocardial failure. These NOAELS and LOAELs
 
21
 

2. HEALTH EFFECTS
 

for death in animals suggest that organic antimony is more lethal than the
 

inorganic compounds, probably due to increased absorption of the potassium
 

antimony tartrate.
 

Chronic administration of a low dose of potassium antimony tartrate
 

(0.262 mg antimony/kg/day) resulted in decreased lifespan in rats (Schroeder
 

et al. 1970). No effect on longevity was observed in mice exposed to 0.35 mg
 

antimony/kg/day as potassium antimony tartrate (Kanisawa and Schroeder 1969;
 

Schroeder et al. 1968).
 

The highest NOAEL values for each antimony compound and all reliable
 

LGAEL values are presented in Table 2-2 and plotted in Figure 2-2.
 

2.2.2.2 Systemic Effects
 

Cardiovascular, gastrointestinal, hematological, hepatic, and other
 

systemic effects observed following oral exposure to antimony are presented
 

below. No studies were located regarding respiratory, musculoskeletal, renal,
 

or dermal/ocular effects in human and animals after oral exposure to antimony.
 

The highest NOAEL values and all reliable LOAELs for each systemic effect in
 

each species and duration are presented in Table 2-2 and plotted in Figure 2­

2.
 

Cardiovascular Effects. No studies were located regarding
 

cardiovascular effects in humans after oral exposure to antimony.
 

No effect on blood pressure or heart rate was observed in rats exposed
 

to antimony as antimony trichloride (Marmo et al. 1987) or antimony trioxide
 

(Gross et al. 1955). Pre- and postnatal exposure or only postnatal exposure
 

alone to 0.0748 mg antimony/kg/day as antimony trichloride appears to affect
 

the development of certain cardiovascular reflexes in rats that are important
 

for regulating systemic arterial blood pressure. In rats exposed to antimony
 

trichloride pre- and postnatally or postnatally, a decreased pressor response
 

to 1-noradrenaline and a decreased hypotensive response to 1-isoprenaline and
 

acetylcholine was observed (Marmo et al. 1987). The occurrence of the effect
 

is duration related.
 

Gastrointestinal Effects. Shortly after drinking an average of
 

10 ounces of lemonade contaminated with potassium antimony tartrate
 

(equivalent to 0.53 mg antimony/kg for a 70 kg man), workers began to vomit
 

(Dunn 1928). Gastrointestinal effects have also been reported in factory
 

workers after exposure to airborne antimony dust. As discussed in Section
 

2.2.1.2, the gastrointestinal effects probably resulted from
 

swallowing the antimony dust.
 

Vomiting and diarrhea have also been observed in animals following acute
 

exposure to antimony trioxide or potassium antimony tartrate (Houpt et al.
 




26
 

2. HEALTH EFFECTS
 

1984; Myers et al. 1978). Severe diarrhea was observed in dogs administered 84
 

mg antimony/kg/day as antimony trioxide for 32 days. No gastrointestinal
 

effects or gross abnormalities were noted in rats exposed to 501 mg
 

antimony/kg/day or less as antimony trioxide for 20 days (Fleming 1982).
 

Hematological Effects. No studies were located regarding hematological
 

effects in humans after oral exposure to antimony.
 

Mild hematological alterations are observed in animals exposed to
 

418 mg antimony/kg/day or greater. Increased red blood cell count was
 

observed in rats exposed to 894 mg antimony/kg/day as antimony trioxide for 30
 

days (Smyth and Thompson 1945). Exposure to metallic antimony resulted in
 

decreased hematocrit and hemoglobin levels and decreased plasma protein levels
 

in rats exposed to 500-1,000 mg antimony/kg/day for 12-24 weeks (Hiraoka 1986;
 

Sunagawa 1981). Decreased red blood cell count was observed in rats exposed to
 

418 mg antimony/kg/day as antimony trioxide for 24 weeks (Sunagawa 1981).
 

Hepatic Effects. No studies were located regarding hepatic effects in
 

humans after oral exposure to antimony.
 

Cloudy swelling of the hepatic cords has been observed in rats exposed
 

to 418 mg antimony/kg/day as antimony trioxide or 500 mg antimony/kg/day as
 

metallic antimony (Sunagawa 1981). Hepatic effects have not been observed at
 

lower concentrations of antimony trioxide or potassium antimony tartrate
 

(Fleming 1982; Schroeder et al. 1968).
 

Other Systemic Effects. No studies were located regarding other
 

systemic effects in humans after oral exposure to antimony.
 

Severe weight loss was observed in dogs administered
 

6,644 mg antimony/kg/day as antimony trioxide. Severe diarrhea and vomiting
 

were also observed in these dogs (Fleming 1982).
 

Increased serum cholesterol and decreased nonfasting serum glucose
 

levels were observed in rats exposed for a lifetime to low levels of potassium
 

antimony tartrate in drinking water (Schroeder et al. 1970). The toxicologic
 

significance of these effects is not known.
 

2.2.2.3 Immunological Effects
 

No studies were located regarding immunological effects in humans or
 

animals after oral exposure to antimony.
 

2.2.2.4 Neurological Effects
 

No studies were located regarding neurological effects in humans after
 

oral exposure to antimony.
 
 

27
 

2. HEALTH EFFECTS
 

Muscle weakness and difficulty in moving hind limbs were observed in a
 

dog exposed to 6,644 mg antimony/kg/day as antimony trioxide for 32 days
 

(Fleming 1982). This LOAEL value for neurological effects in dogs is recorded
 

in Table 2-2 and Figure 2-2.
 

2.2.2.5 Developmental Effects
 

No studies were located regarding developmental effects in humans after
 

oral exposure to antimony.
 

No developmental effects (differences in the number of newborn pups per
 

litter and macroscopic teratogenic effects) were observed in the offspring of
 

rats treated during gestation with 0.748 mg antimony/kg/day as antimony
 

trichloride (Rossi et al. 1987). As discussed in the cardiovascular effects
 

section, pre- and postnatal or postnatal exposure impaired the development of
 

certain cardiovascular reflexes that are important in regulating systemic
 

arterial blood pressure (Angrisani et al. 1988; Marmo et al. 1987; Rossi et
 

al. 1987). Because comparisons were not made between the hypotensive response
 

in pups exposed prenatally and the response in pups exposed postnatally, the
 

potential of antimony trichloride to produce developmental
 

cardiovascular effects cannot be assessed.
 

2.2.2.6 Reproductive Effects
 

No studies were located regarding reproductive effects in humans or
 

animals after oral exposure to antimony.
 

2.2.2.7 Genotoxic Effects
 

No studies were located regarding genotoxic effects in humans or animals
 

after oral exposure to antimony.
 

Genotoxicity studies are discussed in Section 2.4.
 

2.2.2.8 Cancer
 

No studies were located regarding cancer effects in humans after oral
 

exposure to antimony.
 

No change in the incidence of cancer was observed in rats (Schroeder
 

1970) or mice (Kanisawa and Schroeder 1969; Schroeder 1968) fed 0.262 or 0.35
 

mg antimony/kg/day, respectively, as potassium antimony tartrate for a
 

lifetime. The use of these studies to assess carcinogenicity is limited
 

because only one exposure level was used, which was below the maximum
 

tolerated dose.
 
28

2. HEALTH EFFECTS
 

2.2.3 Dermal Exposure
 

The dermal toxicity of antimony compounds is discussed below. Data were
 

located on the health effects following application of antimony trioxide,
 

antimony thioantimonate (a mixture of antimony trfsulfide, and antimony
 

pentasulfide) and antimony oxide to the skin or eye.
 

2.2.3.1 Death
 

No studies were located regarding death in humans after dermal exposure
 

to antimony.
 

Death was observed in rabbits following a single application of antimony
 

oxides at a level of 6,685 mg antimony/kg (Myers et al. 1978). The cause of
 

death was not reported. Two out of four rabbits died after 6-8 topical
 

applications of antimony trioxide paste. The antimony trioxide was combined
 

with a mixture formulated to resemble acidic sweat. The application area was
 

not occluded; thus, there is a possibility of oral ingestion of the paste
 

(Fleming 1982). Death was not reported in rabbits after 13 weeks of
 

application of a 5% solution of antimony thioantimonate (a mixture of antimony
 

trisulfide and antimony pentasulfide) (Horton et al. 1986). The highest NOAEL
 

and all reliable LOAEL values for death for rabbits for each duration are
 

recorded in Table 2-3.
 

2.2.3.2 Systemic Effects
 

Respiratory, cardiovascular, gastrointestinal, and dermal/ocular effects
 

following dermal or ocular exposure are presented below. No studies were
 

located regarding respiratory, gastrointestinal, hematological,
 

musculoskeletal, hepatic, or renal effects in humans and animals following
 

dermal exposure to antimony. The highest NOAEL for each antimony compound and
 

all reliable LOAEL values for each systemic effect for each species are
 

recorded in Table 2-3.
 

Respiratory Effects. No studies were located regarding respiratory
 

effects in humans following dermal exposure to antimony. Hyperemia in the
 

lungs was observed in two rabbits that died after 6-8 applications of an
 

antimony trioxide paste to shaven and abraded skin. The antimony trioxide
 

(concentration not reported) was combined with a mixture resembling acidic
 

sweat (Fleming, 1982). The application area was not occluded; thus, the
 

ingestion of the paste may have occurred.
 

Cardiovascular Effects. No studies were located regarding
 

cardiovascular effects in humans following dermal exposure to antimony.
 

Application of a 5% solution of antimony thioantimonate did not change EKG
 

readings or heart pathology in rabbits (Horton et al. 1986).
 


31
 

2. HEALTH EFFECTS
 

Gastrointestinal Effects. No studies were located regarding
 

gastrointestinal effects in humans following dermal exposure to antimony.
 

Hemorrhages in the cardiac portion of the stomach were observed in two rabbits
 

that died after 6-8 applications of an antimony trioxide-acidic sweat paste
 

(Fleming 1982). Because the application area was not occluded, ingestion of
 

the paste is possible.
 

Dermal/Ocular Effects. No studies were located regarding dermal/ocular
 

effects in humans following dermal exposure to antimony.
 

In rabbits, edema was noted in the area where an antimony trioxide patch
 

(6,685 mg antimony/kg) was applied for 1 day (Myers et al. 1978).
 

Instillation of 79-100 mg antimony.as antimony oxide or antimony
 

thioantimonate into the eyes of rabbits resulted in eye irritation (Horton et
 

al. 1986; Wil Research Laboratories). However, instillation of antimony
 

trioxide (34.5-83.6 mg antimony) did not result in eye irritation (Gross et
 

al. 1955; Myers et al. 1978).
 

Dermal and ocular effects have been observed in humans and animals
 

exposed to airborne antimony. The effects include ocular onjunctivitis, eye
 

irritation, and dermatosis. Further information on these effects is provided
 

in Section 2.2.1.2.
 

2.2.3.3 Immunological Effects
 

No studies were located regarding immunological effects in humans and
 

animals following dermal exposure to antimony.
 

2.2.3.4 Neurological Effects
 

No studies were located regarding neurological effects in humans after
 

dermal exposure to antimony.
 

Abnormal gait was observed in rabbits following application of a lethal
 

concentration of antimony trioxide (6,685 mg antimony/kg/day) (Myers et al.
 

1978). This LOAEL value for neurotoxicity in rabbits is recorded in Table 2-3.
 

No studies were located regarding the following effects in humans or
 

animals after dermal exposure to antimony:
 

2.2.3.5 Developmental Effects
 

2.2.3.6 Reproductive Effects
 

2.2.3.7 Genotoxic Effects
 

Genotoxicity studies are discussed in Section 2.4.
 
32
 

2. HEALTH EFFECTS
 

2.2.3.8 Cancer
 

No studies were located regarding cancer effects in humans or animals
 

after dermal exposure to antimony.
 

2.3 TOXICOKINETICS
 

2.3.1 Absorption
 

2.3.1.1 Inhalation Exposure
 

Quantitative data on the absorption of antimony from the lungs in humans
 

were not located. Elevated blood and urine antimony levels were observed in
 

workers exposed to antimony, suggesting that antimony is absorbed (Cooper et
 

al. 1968; Ludersdorf et al. 1987). However, there is a possibility that some
 

of the antimony detected in the urine and blood was swallowed.
 

The International Commission on Radiological Protection (ICRP 1981)
 

considers oxides, hydroxides, halides, sulfides, sulfates, and nitrates of
 

antimony to be class W chemicals. All other common compounds of antimony are
 

assigned to class D. Class W and D chemicals are considered to have
 

respiratory tract clearance rates of weeks and days, respectively. The ICRP
 

classifications are based on animal data (Felicetti et al. 1974a, 1974b;
 

Thomas et al. 1973). Data from deceased antimony smelter workers suggest that
 

the elimination half-time of some forms of antimony in the lungs may be longer
 

than weeks (Gerhardsson et al. 1982).
 

The absorption of antimony from the respiratory tract is a function of
 

particle size. Exposure to antimony tartrate with a particle size of 1.6 μm 

resulted in a greater deposition of antimony in the upper respiratory tract 

than exposure to 0.7 or 0.3 μm particles (Felicetti et al. 1974a; Thomas et 

al. 1973). Furthermore, the antimony deposited in the upper respiratory tract
 

was cleared after several hours via mucociliary clearance. Particles of the
 

two smaller sizes were relatively insoluble in the lung and were slowly
 

absorbed over several weeks (Thomas et al. 1973). No difference in the body
 

burden, 1 day after exposure to trivalent or pentavalent antimony tartrate,
 

was observed (Felicetti et al. 1974b). Although no information on differences
 

in absorption rates between antimony compounds was located, differences
 

related to solubility probably exist.
 

2.3.1.2 Oral Exposure
 

No quantitative data on the absorption of antimony from the
 

gastrointestinal tract in humans were located. However, results of studies in
 

animals suggest that at least certain forms of antimony are probably absorbed
 

from the gastrointestinal tract. Estimates of the absorption of antimony
 

tartrate and antimony trichloride in animals range from 2% to 7% (Felicetti et
 

al. 1974b; Gerber et al. 1982), suggesting that absorption of trivalent
 
33
 

2. HEALTH EFFECTS
 

antimony salts in humans is probably less than 10%. Gastrointestinal
 

absorption of antimony is likely to be affected by numerous factors, including
 

chemical form of the ingested antimony, particle size and solubility, age, and
 

diet. Although quantitative information on the absorption of antimony is not
 

available for all forms, ICRP (1981) has recommended 10% for antimony tartrate
 

and 1% for all other forms of antimony as reference values for
 

gastrointestinal
 

absorption in humans.
 

2.3.1.3 Dermal Exposure
 

No studies were located regarding absorption of antimony in humans
 

following dermal exposure.
 

Exposure to high levels of antimony trioxide or a mixture of antimony
 

trioxide and pentoxide resulted in death in rabbits (Myers et al. 1978). The
 

application area was occluded, suggesting that at least some forms of antimony
 

can be absorbed through the skin.
 

2.3.2 Distribution
 

Very low levels of antimony are found in unexposed humans. Autopsy data
 

on Japanese adults (Sumino et al. 1975) and other data on selected body fluids
 

are presented in Table 2-4. The mean body burden of antimony is 0.7 mg (Sumino
 

et al. 1975). The skin and hair had the highest levels of antimony. A somewhat
 

higher estimate of 7.9 mg for total body burden is reported by ICRP (1981).
 

ICRP (1981) has recommended'reference values of 5.9 mg of antimony in soft
 

tissue and 2.0 mg in skeletal tissue.
 

2.3.2.1 Inhalation Exposure
 

Information on the distribution of antimony in humans following
 

inhalation exposure was not located. Blood is the main vehicle for the
 

transport of absorbed antimony to various tissue compartments of the body. The
 

relative partitioning between erythrocytes and plasma is a function of
 

valency. Following exposure to trivalent antimony, erythrocyte levels are
 

elevated, compared to the elevated plasma antimony levels after inhalation
 

exposure to pentavalent antimony (Felicetti et al. 1974b). The clearance of
 

antimony from the blood appears to differ among animal species. Elevated blood
 

antimony levels persist longer in rats than in mice and dogs (Felicetti
 

et al. 1974a; Thomas et al. 1973).
 

Valence-state differences also exist in the distribution of antimony to
 

the rest of the body. In hamsters, the levels of trivalent antimony increase
 

more rapidly in the liver than pentavalent antimony. Skeletal uptake is
 

greater following exposure to pentavalent antimony than trivalent antimony
 

(Felicetti et al. 1974b). Outside of the respiratory tract, antimony
 

accumulates in the liver, thyroid, skeleton, and fur; with the largest burden
 

of antimony in the fur (Felicetti et al. 1974a, 1974b).
 

35
 

2. HEALTH EFFECTS
 

2.3.2.2 Oral Exposure
 

Data on the distribution of antimony in humans following oral exposure
 

to antimony were not located.
 

Following oral exposure in animals, the major sites of accumulation,
 

outside of the gastrointestinal tract, are the liver, kidney, bone, lung,
 

spleen, and thyroid. However, the rise in antimony levels in these tissues is
 

not dose-related (Sunagawa 1981). This lack of dose-responsiveness may be a
 

reflection of decreased absorption at higher antimony concentrations. Antimony
 

levels tend to reach a plateau in the livers and lungs of voles fed a diet
 

containing antimony trioxide (Ainsworth 1988).
 

Some species differences in animals exist in the elimination of antimony
 

from the tissues. In rats, antimony is cleared slowly from the thyroid, with
 

an elimination half-time of approximately 40 days (Gross et al. 1955);
 

however, more than 50% of liver, lung, and kidney antimony is removed after 15
 

days following exposure in voles (Ainsworth 1988).
 

Evidence is insufficient to determine if there are valency differences
 

in the distribution of orally administered antimony. Based on the inhalation
 

data and the fact that higher liver concentrations were found in rats fed
 

metallic antimony than those fed antimony trioxide (Sunagawa 1981), it is
 

assumed that there are differences.
 

Pregnancy results in a higher antimony body burden in mice. However,
 

transplacental transport of antimony appears limited. Exposure to antimony
 

during lactation results in high antimony levels in newborns (Gerber et al.
 

1982).
 

2.3.2.3 Dermal Exposure
 

No information on the distribution of antimony in humans or animals
 

following dermal exposure to antimony was located. However, judging from
 

studies of the distribution of antimony following inhalation, oral, and
 

parenteral exposure in animals, the major sites of accumulation are likely to
 

include the liver, kidney, skeleton, spleen, and fur.
 

2.3.2.4 Other Routes of Exposure
 

No information on the distribution of antimony in humans following
 

parenteral exposure was located. In animals, antimony is recovered primarily
 

in the liver, with smaller amounts in the spleen, heart, lungs, and muscle
 

(Gellhorn et al. 1946; Gerber et al. 1982).
 

Two hours after intraperitoneal injection of trivalent antimony, 95% of
 

the antimony in the blood is incorporated into the erythrocytes, mainly in the
 

hemoglobin fraction (Edel et al. 1983; Lippincott et al. 1947). Pentavalent
 
36
 

2. HEALTH EFFECTS
 

antimony is primarily distributed into the plasma fraction of blood (Edel et
 

al. 1983).
 

Following intraperitoneal administration of trivalent antimony, a larger
 

percentage of the administered dose is recovered in the liver than in the
 

spleen. However, a smaller difference in antimony levels between the liver and
 

spleen was observed when pentavalent antimony was administered (Gellhorn and
 

van Dyke 1946).
 

2.3.3 Metabolism
 

Antimony is a metal and, therefore, does not undergo catabolism.
 

Antimony can covalently interact with sulfhydryl groups and phosphate, as well
 

as numerous reversible binding interactions with endogenous ligands (e.g.,
 

proteins). It is not known if these interactions are toxicologically
 

significant. No information was located on the in vivo interconversion of
 

trivalent and pentavalent antimony.
 

2.3.4 Excretion
 

2.3.4.1 Inhalation Exposure
 

Increased levels of urinary antimony have been noted in workers exposed
 

to antimony trioxide (Cooper et al. 1968; Ludersdorf et al. 1987). In animals,
 

antimony is excreted via the urine and feces. Some of the fecal antimony may
 

represent unabsorbed antimony that is cleared from the lung via mucociliary
 

action into the esophagus to the gastrointestinal tract. Based on studies in
 

which antimony was parenterally administered to animals, the urine/feces ratio
 

of antimony depends on valence state. Antimony is excreted predominantly in
 

the urine following pentavalent antimony injection and in the feces after
 

trivalent antimony administration (Edel et al. 1983; Felicetti et al. 1974b).
 

In animals, whole-body clearance of trivalent antimony tartrate occurs
 

in two phases. Ninety percent of the initial body burden of antimony tartrate
 

was excreted within the first 24 hours. The half-life of the slow phase was 16
 

days (Felicetti et al. 1974b).
 

2.3.4.2 Oral Exposure
 

Information on the excretion of antimony in humans following oral
 

exposure was not located. However, information obtained from human and animal
 

studies in which antimony was administered parenterally provides some insight
 

regarding the routes and rates of excretion that can be anticipated after oral
 

exposure in humans. Animal studies have shown that ingested antimony is only
 

partially absorbed from the gastrointestinal tract (Felicetti et al. 1974b;
 

Gerber et al. 1982). Assuming that this is also true for humans, fecal
 

excretion is probably an important route of excretion of ingested antimony in
 
37
 

2. HEALTH EFFECTS
 

humans. Antimony absorbed from the gastrointestinal tract appears to be
 

excreted in the urine and feces to a variable degree, depending on the
 

chemical form. Pentavalent antimony injected parenterally into humans or
 

animals is excreted predominantly in the urine, whereas injected trivalent
 

antimony is excreted in the feces (Edel et al. 1983; Goodwin and Page 1943;
 

Rees et al. 1980).
 

2.3.4.3 Dermal Exposure
 

No information on the excretion of antimony following dermal exposure in
 

humans or animals was located. However, information obtained from human and
 

animal studies in which antimony was administered parenterally provides some
 

insight regarding the routes and rates of excretion that can be anticipated
 

after dermal exposure in humans. Antimony that is absorbed through the skin
 

will be excreted in urine and feces to a variable degree, depending on the
 

chemical species. Pentavalent antimony injected parenterally into humans or
 

animals is excreted predominantly in urine, whereas injected trivalent
 

antimony is excreted in feces (Edel et al. 1983; Goodwin and Page 1943; Rees
 

et al. 1980).
 

2.3.4.4 Other Routes of Exposure
 

Pentavalent antimony is rapidly excreted in humans following intravenous
 

or intramuscular administration, with greater than 50% excreted in the urine 6
 

hours after injection (Goodwin and Page 1943; Rees et al. 1980). Trivalent
 

antimony is predominantly excreted in the feces and not as rapidly excreted in
 

the urine as pentavalent antimony. Twenty-four hours after injection,
 

approximately 25% was excreted in the urine (Goodwin and Page 1943).
 

Twenty-four hours following intraperitoneal administration of trivalent
 

antimony in rats, 33% of the compound was excreted via the feces and 6% in the
 

urine. In contrast, 88% of the pentavalent antimony was excreted in the urine
 

and 1% in the feces (Edel et al. 1983j.
 

Following repeated intramuscular administration of trivalent antimony in
 

humans, approximately 15% was excreted per day at the beginning of treatment
 

and 25% at the end of treatment. Fecal antimony excretion ranged from 4% in
 

the beginning of treatment to 15.4% of the daily administered dose toward the
 

end of treatment (Lippincott et al. 1947).
 

The elimination of pentavalent antimony following intramuscular
 

injection fits into a two-compartment pharmacokinetic model. The half-life of
 

the rapid phase of elimination was 2 hours; the slower phase was 76 hours
 

(Chulay et al. 1988).
 
38
 

2. HEALTH EFFECTS
 

2.4 RELEVANCE TO PUBLIC HEALTH
 

Adverse health effects have been observed in humans and animals
 

following exposure to antimony and antimony compounds. Metallic antimony,
 

organic forms, and inorganic forms of antimony were included in this profile.
 

The organic forms of antimony discussed are potassium antimony tartrate,
 

sodium antimony tartrate, and antimony acetate. Also included are the
 

antimony-containing drugs stibocaptate (sodium antimony-2,3-meso-di-mercapto
 

succinate) also referred to as astiban, and stibophen (bis[4,5-dihydroxy- 1,3­

benzenedisulfonato(4)-O4

, O5]-antimonate (5-) pentasodium heptahydrate) also
 

called fuadin. Trivalent inorganic antimony compounds (antimony trioxide,
 

antimony trichloride, antimony trisulfide), pentavalent inorganic compounds
 

(antimony pentoxide, antimony pentachloride, and antimony pentasulfide), and
 

stibine are also discussed. The toxicity data for antimony and compounds have
 

been summarized across compounds; if differences in the
 

toxicity between the various antimony compounds are known, this information
 

will be presented in a compound specific discussion.
 

The toxicological effects of antimony in humans following inhalation or
 

oral exposure are pneumoconiosis, altered EKG readings, increased blood
 

pressure, abdominal distress, ulcers, dermatosis, and ocular irritation. No
 

effects were found in humans after dermal exposure to antimony. There are
 

several beneficial uses of antimony. Antimony and its compounds are among the
 

oldest known remedies in the practice of medicine. Currently, antimony
 

compounds are used to treat two parasitic diseases, schistosomiasis and
 

leishmaniasis. Toxic side effects in humans following intraperitoneal,
 

intravenous, or intramuscular injection of an antimony-containing drug have
 

been reported. These effects include altered EKG, anemia, vomiting, diarrhea,
 

joint and/or muscle pain, and death.
 

Similar toxicological effects have been reported in animals following
 

inhalation, oral, or dermal exposure to antimony. These effects include
 

fibrosis in the lung, altered EKG readings, myocardial damage, vomiting and
 

diarrhea in dogs, parenchymatous degeneration in the liver and kidney, muscle
 

weakness, difficulty in moving, developmental effects, and lung cancer. In
 

addition, degeneration of the myoneural junction has been observed in animals
 

following parenteral administration of antimony.
 

Inhalation and oral MRLs for antimony and compounds were not derived.
 

Damage to the lungs and myocardium has been observed in several species of
 

animals following acute, intermediate, and chronic inhalation exposure
 

(Brieger et al. 1954; Bio/dynamics 1985, 1990; Gross et al. 1952; Groth et al.
 

1986; Watt 1983). These effects have also been observed in humans chronically
 

exposed to airborne antimony (Brieger et al. 1954; Potkonjak and Pavlovich
 

1983). At the lowest exposure levels tested, the adversity of the effects was
 

considered to be serious. Thus, the data were inadequate for the derivation of
 

an acute-, intermediate-, and chronic-duration inhalation MKL values.
 
39
 

2. HEALTH EFFECTS
 

The lowest LGAEL for acute oral exposure is from-a human report (Dunn
 

1928). Gastrointestinal disturbances were reported in workers who drank
 

lemonade contaminated with potassium antimony tartrate. If the dose was
 

administered throughout the day rather than consumed as a bolus
 

administration, it is likely that the gastrointestinal disturbances would not
 

be observed. Thus, this study would not be an appropriate basis for an
 

acuteduration oral MRL. The intermediate-duration inhalation data suggest that
 

the myocardium is a target of antimony toxicity. The intermediate oral studies
 

did not examine sensitive end points (e.g., EKG) of myocardial damage. This
 

deficiency precludes derivation of an intermediate duration oral MRL. Two
 

chronic oral studies were identified (Schroeder et al. 1968, 1970). At the
 

lowest dose tested, decreased lifespan was observed in rats; this is not an
 

appropriate basis for a chronic-duration oral MRL.
 

Acute-, intermediate-, and chronic-duration dermal MRLs were not derived
 

for antimony due to the lack of an appropriate methodology for the development
 

of dermal MRLs.
 

Death. Death has not been reported in humans following inhalation,
 

oral, or dermal exposure to antimony. However, acute exposure to
 

approximately 2 mg antimony/kg/day as stibocaptate (a drug used to treat
 

parasitic disease) administered intramuscularly resulted in the death of an
 

adult and a child (Rugemalila 1980). Therefore, antimony may be lethal at
 

sufficiently high exposure levels. Animal studies have provided some
 

information about the relative lethality of various forms of antimony. Based
 

on data from studies on parenterally administered antimony, relative lethality
 

can be ranked as follows: antimony tartrate > metallic antimony > inorganic
 

trivalent antimony (Bradley and Frederick 1941).
 

Systemic Effects
 

Respiratory Effects. The respiratory tract is a target in humans
 

following inhalation exposure to antimony. Pneumoconiosis, impaired pulmonary
 

function (airway obstruction, bronchospasm, and hyperinflation) and
 

respiratory irritation (coughing and wheezing) have been observed in factory
 

workers exposed to antimony dust (Cooper et al. 1968; Potkonjak and Pavlovich
 

1983). A relationship between exposure level and effect cannot be established
 

from this data because the workers were also exposed to other compounds,
 

including arsenic oxide, iron oxide, hydrogen chloride, and hydrogen sulfide.
 

Information on the health effects in animals following inhalation
 

exposure to antimony supports the finding in humans that the respiratory tract
 

is a target. Most of the respiratory effects observed in animals are
 

associated with the physiological response to dust accumulation in the
 

respiratory tract. Because of the large amount of antimony that is deposited
 

in the lung during chronic inhalation, the proliferation of macrophages
 

observed in rats exposed to 0.07 mg antimony/m3

 or greater continues several
 
40
 

2. HEALTH EFFECTS
 

months after the exposure termination (Bio/dynamics 1990). This increase in
 

the number of alveolar macrophages may contribute to the development of
 

fibrosis. Fibrosis and lipoid pneumonia have been reported in rats chronically
 

exposed to 1.6 mg antimony/m3

 or higher as antimony trioxide or to 17.48 mg
 

antimony/m3 as antimony trisulfide (Bio/dynamics 1990; Gross et al. 1952;
 

Groth et al. 1986; Watt et al. 1980,1983; Wong et al. 1979). Respiratory
 

effects have not been reported in humans or animals following oral or dermal
 

exposure to antimony.
 

Although serious antimony-related lung disease has not been observed in
 

humans, antimony-induced pneumoconiosis is associated with serious lung
 

pathology in animals. Therefore, it is likely that, with sufficiently high or
 

prolonged exposures, serious lung disease would occur in humans. In addition,
 

the toxicity of inhaled antimony compounds may be greater for smaller particle
 

sizes.
 

Cardiovascular Effects. The heart is another target organ in humans.
 

Alterations in EKG readings and increased blood pressure have been reported in
 

workers exposed to airborne antimony trisulfide (Brieger et al. 1954). In
 

addition, altered EKG readings have been reported in individuals exposed to
 

repeated injections of antimony (Dancaster et al. 1966; Honey 1960; Pandey et
 

al. 1988). The antimony injections were part of a therapeutic treatment for
 

parasitic disease. In some of these individuals, the EKG did not return to
 

normal until 6 weeks after the last dose (Dancaster et al. 1966). Pentavalent
 

antimony appears to be less cardiotoxic than the trivalent form. Altered EKG
 

readings were observed after 4 days of trivalent antimony treatment (0.98 mg
 

antimony/kg/day) (Dancaster et al. 1966); however, a change in EKG readings
 

was not observed until after 3 weeks of pentavalent antimony injections (7.2
 

mg antimony/kg/day) (Pandey et al. 1988).
 

Altered EKG readings have also been observed in animals. In addition,
 

decreased blood pressure, increased heart rate, and decreased contractile
 

force have been observed following injection of trivalent antimony
 

(Bromberger-Barnea and Stephens 1965; Cotten and Logan 1966). The decreased
 

blood pressure contrasts with the increased blood pressure observed in humans
 

(Brieger et al. 1954). Studies on isolated dog hearts suggest that antimony
 

exerts its effect on the myocardium directly, and that the effect persists
 

after exposure is terminated (Bromberger-Barnea and Stephens 1965).
 

Gastrointestinal Effects. Historically, antimony has been known for its
 

emetic properties. Vomiting, diarrhea, gastric discomfort, and ulcers have
 

been reported in humans following inhalation or oral exposure to antimony.
 

Amounts as low as 0.529 mg antimony/kg have resulted in vomiting. The
 

gastrointestinal effects following inhalation exposure may have resulted from
 

antimony being swallowed. Gastrointestinal effects have also been observed in
 

humans receiving intramuscular injections of antimony (Harris 1956; Zaki et
 

al. 1964). Similar gastrointestinal effects have been reported in animals
 

following oral exposure to antimony.
 
41
 

2. HEALTH EFFECTS
 

Hematological Effects. Hematological effects in humans following
 

inhalation, oral, or dermal exposure to antimony have not been reported.
 

However, hematological parameters were not measured in the human studies.
 

Hemolytic anemia was reported in one subject following repeated injections of
 

fuadin (stibophen) (Harris 1956). Fuadin is an antimony-containing compound
 

used in the treatment of schistosomiasis. Alterations in hematological
 

parameters have not been reported in animals exposed to antimony via
 

inhalation or dermal routes. Decreased hemoglobin and hematocrit and altered
 

erythrocyte count were observed in animals following oral exposure to metallic
 

antimony or antimony trioxide (Smyth and Thompson 1945; Sunagawa 1981). The
 

potential of antimony to cause hematological effects in humans is not known.
 

Musculoskeletal Effects. Musculoskeletal effects have not been reported
 

in humans or animals following inhalation, oral, or dermal exposure to
 

antimony. However, muscle and/or joint pain was reported in 30-50% of subjects
 

injected with fuadin or astiban, which were administered as part of the
 

therapeutic treatment of schistosomiasis. The joint pain was more severe in
 

subjects receiving fuadin, although' the dose was four times less than the
 

astiban dose (Zaki et al. 1964). This suggests differences in the toxicity of
 

the different antimony compounds, which might explain why musculoskeletal
 

effects have not been observed in humans by the other routes of exposure.
 

Myoneural junction swelling was observed in mice following injection with
 

potassium antimony tartrate (Mansour and Reese 1965). A more complete
 

description of the myopathy observed in these mice is given in the
 

neurological section. Because of the limited human and animal data, it is
 

difficult to determine the significance of this effect to human health.
 

Hepatic Effects. Hepatic effects have not been observed in humans
 

exposed to antimony. Parenchymatous degeneration in the liver was observed in
 

rats and guinea pigs exposed to airborne antimony trioxide for 30 weeks or to
 

antimony trisulfide for 5 days (Brieger et al. 1954; Dernehl et al. 1945).
 

However, liver effects have not been observed in more recent intermediatechronic-duration inhalation studies (Bio/dynamics 1985, 1990; Groth et al.
 

1986; Watt 1983; Wong et al. 1979). Swelling of the hepatic cords has been
 

observed in rats orally exposed to metallic antimony or antimony trioxide
 

(Hiraoka 1986). Since hepatic effects have not been observed in humans and
 

animal data are inconsistent, it is not known if liver damage will occur in
 

humans exposed to antimony.
 

Renal Effects. Renal effects have not been reported in humans following
 

inhalation, oral, or dermal exposure to antimony. Tubular dilation and
 

degeneration of the tubular epithelium have been observed in rats, rabbits,
 

and guinea pigs acutely exposed to airborne antimony trisulfide or stibine gas
 

(Brieger et al. 1954; Price et al. 1979). Kidney effects have not been
 

reported in animals exposed to airborne antimony for an intermediate or
 

chronic duration (Bio/dynamics 1985, 1990; Groth et al. 1986; Watt 1983; Wong
 

et al. 1979). The kidneys were not examined in the oral and dermal exposure
 

studies. The relevance of this effect to human health is not known.
 
42
 

2. HEALTH EFFECTS
 

Dermal/Ocular Effects. Dermatosis and ocular irritation have been
 

reported in humans following exposure to airborne antimony and antimony via
 

injection (Potkonjak and Vishnijich 1983; R&es 1953; Stevenson 1965; Zaki et
 

al. 1964). The dermatitis associated with exposure to airborne antimony was
 

seen more often during the summer months and in workers exposed to high
 

temperatures. It is probably the result of antimony being dissolved in sweat
 

and penetrating the sweat glands (Stevenson 1965). Dermal and ocular exposure
 

to antimony has resulted in minimal skin and eye irritation in animals and the
 

formation of cataracts (Bio/dynamics 1985, 1990).
 

Other Systemic Effects. Hyperplasia of the reticuloendothelial cells in
 

the peribronchiolar lymph nodes was observed in rats chronically exposed to
 

airborne antimony (Bio/dynamics 1990). This effect is probably the result of
 

the clearance of antimony particles from the lungs, and thus it is an effect
 

that is likely to occur in humans.
 

Immunological Effects. Immunological effects have not been studied in
 

humans or animals following inhalation, oral, dermal, or parenteral exposure
 

to antimony.
 

Neurological Effects. Neurological effects have not been observed in
 

humans following inhalation, oral, dermal, or parenteral exposure to antimony.
 

Muscle weakness, difficulty in moving, and abnormal gait have been observed in
 

animals follotring oral and dermal exposure to antimony trioxide (Fleming
 

1982; Myers et al. 1978). Decreased motor efficiency and dystonic torsion of
 

the limbs were observed in mice receiving intraperitoneal injections of
 

potassium antimony tartrate (Mansour and Reese 1965). Degenerative changes in
 

the anterior horn cells of the lumbar cord, edema with hydropic degeneration
 

in the sciatic nerve, and swelling of the myoneural junction were also
 

observed in this mouse study. Because neurological effects have been observed
 

in three species of animals (dogs, rats, and mice), these effects may also
 

occur in humans exposed to high levels of antimony.
 

Developmental Effects. An increase in the number of spontaneous
 

abortions was observed in women exposed to airborne antimony in the workplace.
 

The exposure level was not reported in this study. No overt developmental
 

effects were observed in the children of these women (Belyaeva 1967). No gross
 

abnormalities were observed in the offspring of rats exposed to low levels of
 

antimony trichloride in the drinking water (Rossi et al. 1987). The likelihood
 

of antimony-induced developmental effects occurring in humans is not known.
 

Reproductive Effects. Human exposure to antimony dust in the workplace
 

has resulted in disturbances in menstruation (Belyaeva 1967). In animals, the
 

failure to conceive and metaplasia in the uterus have been observed following
 

inhalation exposure to antimony trioxide (Belyaeva 1967). No information on
 

the potential of antimony to cause reproductive effects in animals following
 
43
 

2. HEALTH EFFECTS
 

oral or dermal exposure was located. These data suggest a potential for
 

antimony to cause reproductive effects in humans.
 

Genotoxic Effects. No in vivo genotoxicity studies were located. The
 

results of in vitro genotoxicity studies are presented in Table 2-5. Positive
 

results for chromosome breakage in human leukocytes were found (Paton and
 

Allison 1972). Positive results were also found for DNA damage, viral
 

transformation, and chromosomal aberrations. Gene mutation and transformation
 

tests were negative. Because of the limited in vitro genotoxicity data and the
 

lack of in vivo tests, the genotoxicity of antimony in humans cannot be
 

determined.
 

Cancer. No information on the carcinogenic potential of antimony in
 

humans was located. Inhalation exposure to antimony trioxide or antimony
 

trisulfide produced lung tumors in rats (Groth et al. 1986; Watt 1980, 1983;
 

Wong et al. 1979). Lung tumors were not observed in the Bio/dynamics (1990)
 

study. The Watt (1980, 1983) and Bio/dynamics (1990) studies used similar
 

concentrations of antimony trioxide. However, lung cancer was observed only in
 

the Watt (1980, 1983) study. A possible explanation for the conflicting
 

results is differences in the amount of antimony that was deposited in the
 

lungs. Bio/dynamics (1990) asked the pathologist who examined the
 

histopathology slides from the Watt (1980, 1983) study to also examine the
 

slides from the Bio/dynamics (1990) study. The pathologist determined that the
 

degree of pigmentation in the lungs (indicative of the amount of antimony in
 

the lungs) was greater in the lungs of rats from the Watt (1980, 1983) study
 

compared to those from the Bio/dynamics study (1990). However, why there were
 

differences in antimony deposition and/or clearance between the studies is not
 

known. The deposition and clearance of antimony depends on particle size
 

(Felicetti et al. 1979b; Thomas et al. 1973). The smaller particles are
 

deposited in the lower respiratory tract and are slowly cleared from the lung.
 

The larger particles are deposited in the upper airways and are cleared more
 

efficiently from the lung. Thus, antimony with smaller particle sizes come
 

into contact with the lung tissue for a longer period of time; this may
 

influence the carcinogenic potential. Because of differences in the methods
 

used to assess particle size distribution between these two studies, a
 

comparison of particle size distribution between the studies can not be made.
 

The carcinogenicity of inhaled antimony also may vary with the chemical form
 

of antimony, which will affect the solubility of antimony and, thereby, lung
 

retention. The carcinogenicity of inhaled antimony is probably related to its
 

deposition in the respiratory tract and the resulting reactive processes
 

induced by its presence in the lung tissue. These include macrophage
 

infiltration and fibrosis, typical of pneumoconiosis. The lung carcinogenicity
 

of inhaled antimony may not, therefore, predict carcinogenic potential for
 

other routes of exposure. Antimony has not produced cancer in rats or mice
 

exposed by the oral route (Kanisawa and Schroeder 1969; Schroeder et al. 1968,
 

1970). There may be physiological differences in the deposition and clearance
 

of antimony from the lungs between humans and rats. Thus, it is
 

45
 

2. HEALTH EFFECTS
 

difficult to assess carcinogenic potential of antimony in humans. No
 

information of carcinogenic potential of antimony following dermal application
 

of antimony was located.
 

2.5 BIOMABKERS 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(s) or cell(s) 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(s) 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 substance (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,
 

and selenium). Biomarkers of exposure to antimony 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 antimony 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 substance. 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."
 
46
 

2. HEALTH EFFECTS
 

2.5.1 Biomarkers Used to Identify and/or Quantify Exposure to Antimony
 

Elevated blood, hair, urine, and fecal levels of antimony indicate high
 

exposure to antimony. A significant correlation exists between the level of
 

pentavalent antimony (N-methylglucamine antimonate) administered
 

intraperitoneally to humans and antimony levels in hair (Dorea et al. 1989).
 

However, Dorea et al. (1989) only tested two levels of antimony (10 and 20 mg
 

antimony/kg/day). Factory workers exposed to antimony trioxide (0.042-0.70 mg
 

antimony/m3) had elevated urine and blood antimony levels (Ludersdorf et al.
 

1987). Antimony levels in the urine and blood were 1.1 and 0.9-5.0 μg/L, 

respectively, compared to 0.6 μg/L urine levels and 0.4 μg/L blood levels in 

unexposed workers. Animal data suggest that urine and blood levels remain 

elevated several days after exposure (Felicetti et al. 1974b). 

No effect biomarkers that could be used to implicate exposure to
 

antimony were found.
 

2.5.2 Biomarkers Used to Characterize Effects Caused by Antimony
 

No toxic symptoms specific to antimony exposure have been identified.
 

Toxic effects that reportedly occur in humans include pneumoconiosis, altered
 

EKG readings, and gastrointestinal effects. No quantitative biomarkers
 

associated with these effects are known.
 

2.6 INTERACTIONS WITH OTHER CHEMICALS
 

No information on the influence of other compounds on the toxicity of
 

antimony was located.
 

2.7 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE
 

Individuals with existing chronic respiratory or cardiovascular disease
 

or problems would probably be at special risk, since antimony probably
 

exacerbates one or both types of health problems. Because antimony is excreted
 

in the urine, individuals with kidney dysfunction may be unusually
 

susceptible.
 

2.8 MITIGATION OF EFFECTS
 

This section will describe clinical practice and research concerning
 

methods for reducing toxic effects of exposure to antimony. However, because
 

some of the treatments discussed may be experimental and unproven, this
 

section should not be used as a guide for treatment of exposures to antimony.
 

When specific exposures have occurred, poison control centers and medical
 

toxicologists should be consulted for medical advice.
 
47
 

2. HEALTH EFFECTS
 

Adverse health effects in humans following antimony exposure appear to
 

target on the respiratory and cardiovascular systems. Eye and skin irritation
 

have also been noted.
 

Human exposure to antimony may occur by inhalation, ingestion, or by
 

dermal contact. Mitigation approaches to reduce absorption of antimony have
 

included general recommendations of separating contaminated food, water, air,
 

and clothing from the exposed individual. Externally, exposed eyes and skin
 

are flushed with a clean neutral solution such as water or normal saline.
 

Administration of water or milk and a cathartic such as magnesium sulfate has
 

been recommended by Stutz and Janusz (1988) for treatment following oral
 

exposure to antimony. This would reduce the concentration of antimony in the
 

stomach, but is not likely to affect its intestinal absorption.
 

Administration of activated charcoal following exposure to organic compounds
 

is thought to be effective in preventing absorption (Stutz and Janusz 1988).
 

Antimony may be found in the blood and urine several days after
 

exposure. It also can be found in the hair (Dorea et al. 1989). Pentavalent
 

antimony is rapidly excreted in humans following intravenous or intramuscular
 

administration, with greater than 50% excreted in the urine 6 hours after
 

injection (Goodwin and Page 1943; Rees et al. 1980). Trivalent antimony is not
 

as rapidly excreted in the urine and is primarily excreted in the feces over a
 

24 hour period of time as noted after intraperitoneal administration in
 

laboratory animals (Edel et al. 1983).
 

Chelation therapy with British anti-Lewisite (BAL) may be the most
 

effective mitigation approach following absorption of trivalent antimony
 

compounds into the blood stream (Ellenhorn and Barceloux 1988; Haddad and
 

Inchester 1990). Antimony can covalently bind with sulfhydryl groups. BAL, a
 

dithiol compound with two vicinal sulfur atoms, competes with the critical
 

binding sites that may possibly be responsible for the toxic effects. There is
 

no evidence that BAL is useful following stibine gas exposure (Ellenhorn and
 

Barceloux 1988).
 

Dialysis may be the most effective method for mitigation of pentavalent
 

antimony. Pentavalent antimony in the blood resides mainly in the plasma in an
 

easily dialyzable form (Edel et al. 1983); Dialysis treatment following
 

exposure to trivalent antimony may not be as effective. The majority of
 

trivalent antimony found in blood is incorporated into the red blood cell
 

fraction in a hard dialyzable form (Edel et al. 1983).
 

2.9 ADEQUACY OF THE DATABASE
 

Section 104(i)(S) of CERCLA as amended 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 antimony is available. Where adequate information is not
 

available, ATSDR, in conjunction with the National Toxicology Program (NTP),
 
48
 

2. HEALTH EFFECTS
 

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 antimony.
 

The following categories of possible data needs have been identified by
 

a joint team of scientists from ATSDR, NTP, and EPA. They are defined as
 

substance-specific informational needs that, if met, would reduce or eliminate
 

the uncertainties of human health assessment. In the future, the identified
 

data needs will be evaluated and prioritized, and a substance-specific
 

research agenda will be proposed.
 

2.9.1 Existing Information on Health Effects of Antimony
 

The existing data on health effects of inhalation, oral, and dermal
 

exposure of humans and animals to antimony are summarized in Figure 2-3. The
 

purpose of this figure is to illustrate the existing information concerning
 

the health effects of antimony. 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.
 

As seen in Figure 2-3, information on the health effects of antimony in
 

humans following inhalation, oral, or dermal exposure is limited. The
 

inhalation data consist of several reports of workers exposed to inorganic
 

forms of antimony. However, most of these studies are incomplete because the
 

workers were exposed to a variety of compounds or the exposure level was not
 

reported. One oral study involving accidental drinking of lemonade
 

contaminated with potassium antimony tartrate was located. The dermal data on
 

humans is limited to a study in which antimony was applied to the skin of
 

volunteers.
 

As compared to the human data, more complete information on the systemic
 

health effects of antimony in animals was located. Although there are several
 

reliable intermediate and chronic duration studies that examined numerous
 

toxicological end points following exposure to airborne inorganic trivalent
 

antimony (primarily antimony trioxide), most of the studies utilized rats. One
 

inhalation reproductive/developmental study was located. Several studies
 

that examined the toxicity of metallic antimony, antimony trioxide, antimony
 

trichloride, and potassium antimony tartrate via oral exposure were located.
 

Sensitive measurements of cardiovascular toxicity were not examined in most of
 

these studies. One developmental toxicity study in rats was located; internal
 

examination of pups was not located. The acute and intermediate toxicity of
 

dermally applied antimony trioxide, antimony oxide, and antimony
 

thioantimonate has been examined. However, these studies did not examine the
 

systemic toxicity of antimony; they were designed to assess the dermal and/or
 

ocular toxicity of antimony.
 

50
 

2. HEALTH EFFECTS
 

2.9.2 Data Needs
 

Acute-Duration Exposure. Information on the target organs of acute
 

exposure in humans to antimony is limited. Based on one human study, the
 

gastrointestinal tract appears to be a target following inhalation exposure to
 

antimony (Taylor 1966). Animal studies have shown that the respiratory tract
 

and cardiovascular, hepatic, and renal effects occur after exposure to
 

airborne antimony (Brieger et al. 1954; Price et al. 1979). The respiratory
 

and cardiovascular effects occur at a lower exposure levels than those
 

associated with gastrointestinal effects in humans. An acute inhalation MRL
 

could not be derived from this animal data because serious myocardial effects
 

were observed at the lowest exposure level tested. The gastrointestinal tract
 

also appears to be a target in humans following oral exposure to antimony.
 

This is based on a report of workers who accidentally drank lemonade
 

contaminated with potassium antimony tartrate (Dunn 1928). An acute oral MRL
 

could not be derived from this study. Acute animal data also suggest that the
 

gastrointestinal tract is a target system (Fleming 1982; Houpt et al. 1984;
 

Myers et al. 1978). However, two of the three acute animal studies did not
 

perform complete histological examinations, thus there may be other target
 

organs that have not been identified (Fleming 1982; Houpt et al. 1984; Myers
 

et al. 1978). There is no information on the target organs in humans following
 

dermal exposure to antimony. Application of antimony to the skin or eyes of
 

animals results in mild irritation (Gross et al. 1955; Horton et al. 1986;
 

Myers et al. 1978; Wil Research Lab 1979). A majority of the animal studies
 

only examined the skin or eyes following dermal/ocular exposure to antimony.
 

Toxicokinetic data that might allow route-to-route extrapolations of health
 

effects were not found. Knowledge about the acute toxicity of antimony is
 

important because people living near hazardous waste sites might be exposed to
 

antimony for brief periods. Information about the toxicity of different
 

antimony compounds, as well as differences in valence states, was not located.
 

Additional acute-duration studies by the inhalation, oral, and dermal routes
 

would provide information on differences in the potency of various antimony
 

compounds, as well as on the thresholds for systemic toxicity due to acute-


duration exposure to antimony.
 

Intermediate-Duration Exposure. Human target organs/systems following
 

exposure to airborne antimony include the respiratory tract and
 

gastrointestinal tract and skin (Brieger et al. 1954; Renes 1953; Stevenson
 

1965). No reports of health effects in humans following oral or dermal
 

exposure were located. Animal data suggest that the heart and respiratory
 

tract may be targets following inhalation exposure (Brieger et al. 1954;
 

Bio/dynamics 1985). Developmental and reproductive effects have also been
 

reported in animals (Belyaeva 1967). There is no information on human health
 

effects following oral exposure to antimony. Oral exposure of animals to
 

antimony has resulted in adverse health effects on the liver, cardiovascular
 

system, gastrointestinal tract, and mild hematological effects (Angrisani
 

1988; Fleming 1982; Hiraoka 1986; Marmo et al. 1987; Rossi et al. 1987; Smyth
 
51
 

2. HEALTH EFFECTS
 

and Thompson 1945; Sunagawa 1981). No reports of human health effects
 

following dermal exposure were located. No adverse health effects were
 

observed in animals following intermediate duration dermal exposure (Horton et
 

al. 1986). EKG readings are a sensitive indicator of myocardial damage;
 

however, in the oral and dermal intermediate-duration studies this end point
 

was not examined. Because the exposure levels tested were higher than the
 

threshold levels for respiratory tract effects, and/or because EKG readings
 

were not taken, inhalation and oral MKLs could not be derived. Toxicokinetic
 

data that might allow extrapolation of health effects across routes of
 

administration were not located. Information on the relative toxicity of the
 

different antimony compounds has not been assessed. Intermediate-duration
 

studies by inhalation, oral, and dermal routes would provide information on
 

the thresholds for systemic toxicity, as well as on the differences in the
 

potency of various antimony compounds. This information could be relevant to
 

human exposure because people living near hazardous waste sites may be exposed
 

to a variety of antimony compounds for an intermediate-duration.
 

Chronic-Duration Exposure and Cancer. There are several human and
 

animal chronic inhalation studies that indicate the targets appear to be the
 

respiratory tract, heart, eye, and skin (Brieger et al. 1954; Cooper et al
 

1968; Potkonjak and Pavlovich 1983). However, functional changes in the
 

cardiovascular system were not assessed in the animal inhalation studies
 

(Bio/dynamic 1990; Gross et al. 1952; Groth et al. 1986; Watt 1980, 1983; Wong
 

et al. 1979). A no-effect level (NOEL) for respiratory or cardiovascular
 

effects following exposure to antimony was not identified in the available
 

literature. The NOEL is an important level in evaluating the risk of exposure
 

to antimony, and it can be used along with protective uncertainty factors to
 

help determine the amount of antimony humans can be exposed to without
 

experiencing health effects. The chronic inhalation studies in animals
 

examined only the toxicologic effects in rats; thus, interspecies differences
 

could not be assessed. No target organs were identified in humans or animals
 

following oral exposure to antimony (Kanisawa and Schroeder 1989; Schroeder et
 

al. 1968, 1970). In addition, the data from the oral and inhalation studies
 

were insufficient for deriving a chronic MEL. There is no information on the
 

health effects in humans and animals following dermal exposure. Well-designed
 

oral experiments, using several exposure levels and measuring all sensitive
 

toxicological end points, would provide information on the health effects
 

associated with long-term exposure to antimony. Chronic toxicity information
 

is important because people living near hazardous waste sites might be exposed
 

to antimony for many years.
 

No studies were located regarding the carcinogenicity of antimony in
 

humans following inhalation, oral, or dermal exposure. Evidence for the
 

carcinogenicity of inhaled antimony in animals is mixed. Two studies reported
 

lung tumors in rats exposed to relatively low levels of antimony trioxide
 

(Groth et al. 1986; Watt 1983; Wong et al. 1979). A study using a similar
 

exposure level did not find evidence of carcinogenicity (Bio/dynamics 1990).
 
52
 

2. HEALTH EFFECTS
 

Differences in the amount of antimony deposited and/or cleared from the lungs
 

were reported. It is not known if the conflicting results were due to
 

differences in particle sizes. A study comparing the effects of different
 

particle sizes would determine if the particle size of the inhaled antimony
 

determines the carcinogenic potential of antimony. The increased incidence of
 

lung tumors appears to be route specific. There is no evidence of increased
 

incidence of cancer in humans as a result of oral exposure to antimony. The
 

oral cancer data in animals are limited to studies that used very low levels
 

of antimony (Kanisawa and Schroeder 1989; Schroeder et al. 1968, 1970). Oral
 

studies have shown that antimony tends to accumulate in the liver and
 

gastrointestinal tract (Ainsworth 1988; Sunagawa 1981); it is not known if
 

this results in cancer. No dermal cancer studies in humans or animals was
 

located. Oral and dermal studies in rodents using several exposure levels
 

including the maximum tolerated level would provide useful information because
 

prolonged exposure to antimony in humans may occur.
 

Genotoxicity. There are no in vivo genotoxicity studies in humans or
 

animals. In vitro studies using human leukocytes were positive for chromosome
 

breakage (Paton and Allison 1972). Results were mixed in in vitro studies
 

using mammalian cells (Casto et al. 1979; Tu and Sivak 1984), and positive for
 

DNA damage in Bacillus subtilis (Kanematsu et al. 1980). Additional in vitro
 

and in vivo genotoxicity studies would enable better estimation of the actual
 

genotoxic threat posed by antimony to people exposed in the environment.
 

Reproductive Toxicity. Women exposed to antimony in the workplace have
 

reported menstrual disturbances and a higher incidence of spontaneous
 

abortions as compared to nonexposed workers (Belyaeva 1967). From this report
 

it is unclear what the exposure level was, whether the women were exposed also
 

to other compounds, and whether the controls had comparable jobs. Reproductive
 

effects (failure to conceive, uterine metaplasia) have been observed in rats
 

exposed to airborne antimony (Belaeva 1967). In addition, studies on the
 

distribution of antimony following oral administration in animals have shown
 

high levels of antimony in the testes (Sunagawa 1981). It is not known whether
 

these high levels of antimony could result in functional changes. There are no
 

data on reproductive effects following oral or dermal exposure to humans and
 

animals. There are insufficient toxicokinetic data to make route-to-route
 

extrapolation. A well-designed study to assess the effects of orally or
 

dermally administered antimony on reproductive performance would provide
 

information on possible reproductive effects that
 

might be relevant to humans.
 

Developmental Toxicity. An increased number of spontaneous abortions was
 

observed in women exposed to antimony in the workplace (Belyaeva 1967).
 

However, there are several limitations to this study, as discussed above in
 

the reproductive toxicity section. No overt developmental effects were
 

observed in the offspring of these women. Developmental effects were not
 

observed in the offspring of rats exposed orally to antimony trichloride
 
53
 

2. HEALTH EFFECTS
 

(Rossi et al. 1987). An animal study has shown that antimony is not
 

efficiently transported across the placenta (Gerber et al. 1982). However,
 

there is evidence of high levels of antimony in unexposed newborn nursed by
 

exposed female mice (Gerber et al. 1982). A study in which animals are exposed
 

throughout gestation and lactation would provide information on the potential
 

of antimony to result in developmental effects in humans.
 

Immunotoxicity. Immunotoxicity following inhalation, oral, or dermal
 

exposure have not been studied in humans or animals. Immunological end points
 

should be examined in the intermediate or chronic studies, especially since
 

antimony has been shown to accumulate in the spleen (Sunagawa 1981).
 

Neurotoxicity. Neurotoxic effects have not been observed in humans
 

following inhalation, intramuscular, and intraperitoneal exposure to antimony.
 

Neuromuscular effects have been observed in animals following oral, dermal,
 

and intraperitoneal administration (Fleming 1982; Mansour and Reese 1965;
 

Myers et al. 1978). Furthermore, myopathy has been observed in mice exposed
 

via intraperitoneal injection (Mansour and Reese 1965). Although this effect
 

has not been observed by other routes of exposure there is no reason to
 

suspect that it would not occur. Sensitive tests of neurophysiological
 

function may detect early sign of neurotoxicity following inhalation, oral, or
 

dermal exposure to antimony.
 

Epidemiological and Human Dosimetry Studies. There are several
 

epidemiological occupational exposure studies (Brieger et al. 1954; Cooper et
 

al. 1968; Potkonjak and Pavlovich 1983; RBnes 1953; Stevenson 1965). However,
 

most of these studies are incomplete because the exposure level and/or
 

particle size of the airborne antimony was not reported and/or the workers
 

were often exposed to a variety of other compounds. In addition,
 

cardiovascular toxicity, a sensitive end point of antimony toxicity, was not
 

always assessed. No epidemiological or human dosimetry studies in which
 

individuals were exposed to antimony orally or dermally were located.
 

Epidemiological studies would be useful in order to determine the effects of
 

long-term exposure on humans, with particular attention paid to cardiovascular
 

and respiratory effects. If a cause/effect relationship was established
 

between antimony exposure and health effects in humans, monitoring of
 

individuals living near hazardous waste sites could be performed in order to
 

verify that exposure levels do not exceed recommended limits and that body
 

tissue and fluid levels remain below potentially hazardous levels.
 

Biomarkers of Exposure and Effect. Because antimony is not catabolized
 

in the body, metabolites could not be used as a biomarker. Thus, the only
 

biomarker of exposure would be measurement of antimony itself. Antimony levels
 

are increased in the blood, urine, and feces following exposure to antimony
 

(Cooper et al. 1968; Edel et al. 1983; Felicetti et al. 1974a, 1974b; Gerber
 

et al. 1982; Goodwin and Page 1943; Ludersdorf et al. 1987; Rees et al. 1980).
 

However, because antimony is poorly absorbed from the lung,
 
54
 

2. HEALTH EFFECTS
 

measurement of antimony levels in body fluids may not reflect the exposure
 

level of airborne antimony (Felicetti et al. 1974a, 1974b; Thomas et al.
 

1973). The relationship between exposure level and concentration of antimony
 

in various body fluids has not been established. Development of a biomarker
 

with more exposure/dose data would aid in future medical surveillance that
 

could lead to better detection of exposure.
 

No antimony-specific biomarkers of effects have been identified. Future
 

studies on the toxicity of antimony should use several antimony exposure
 

levels, this may lead to the identification of subtle biochemical or
 

physiological biomarkers of effects.
 

Absorption, Distribution, Metabolism, and Excretion. There is some
 

information on the toxicokinetic properties of antimony following oral or
 

inhalation exposure in humans and animals (Ainsworth 1988; Cooper et al. 1968;
 

Edel et al. 1983; Felicetti et al. 1974a, 1974b; Gerber et al. 1982;
 

Gerhardsson et al. 1982; Goodwin and Page 1943; Ludersdorf et al. 1987; Rees
 

et al. 1980; Sumino et al. 1975; Sunagawa 1981; Thomas et al. 1973). However,
 

there is limited comparative information on the absorption, distribution, and
 

excretion of different antimony compounds. Furthermore, the site and mechanism
 

of antimony absorption from the gastrointestinal tract has not been
 

elucidated. The influence of nutritional factors as well as the presence of
 

food in the gastrointestinal tract on absorption are not known. Information on
 

the absorption, distribution, or excretion of antimony following dermal
 

application is not known. In addition, a study on the effect of oxidation
 

state on the cellular uptake of antimony and the effect of water solubility of
 

an antimony compound on lung retention/absorption would provide useful
 

information on the toxicity of different antimony compounds. A study that
 

examined these aspects of antimony would be useful in assessing the potential
 

target organs following dermal exposure to antimony.
 

Comparative Toxicokinetics. Species differences in the toxicokinetics of
 

antimony have been identified (Ainsworth 1988; Felicetti et al. 1974a; Gross
 

et al. 1955; Thomas et al. 1973). However, the absorption, distribution, and
 

excretion of antimony following oral or inhalation exposure in humans is not
 

known. Thus, it is not possible to decide which animal species is the best
 

model for assessing the toxicity of antimony. Information on the behavior of
 

antimony in humans would be useful.
 

Mitigation of Effects. Chelation therapy with BAL has been shown to
 

effectively mitigate the toxicity of trivalent antimony compounds in humans
 

(Ellenhorn and Barceloux 1988; Haddad and Winchester 1990). Although BAL has
 

been found to form stable chelates in vivo with antimony, it is not known if
 

there are adverse side effects associated with the treatment. Studies
 

examining the effectiveness of chelating agents and possible side effects
 

would be helpful in determining the most effective treatment for antimony
 

toxicity. Antimony is widely distributed throughout the body. The hair and
 
55
 

2. HEALTH EFFECTS
 

skin contain the highest levels of antimony. The adrenal glands, lung, large
 

intestine, trachea, cerebellum, and kidneys also contain relatively high
 

levels of antimony (Muramatsu and Parr 1988; Sumino et al. 1975). No
 

information on methods of mitigating body stores were located. Studies that
 

examined such methods would be useful in the treatment of antimony toxicity.
 

2.9.3 On-going Studies
 

NTP (1990) has recently completed a 14-day drinking water study in which
 

groups of male and female Fischer 344 rats and B6C3Fl mice were given drinking
 

water containing potassium antimony tartrate. The doses in rats were 0, 16,
 

28, 59, 94, and 168 mg/kg/day; for mice, they were 0, 59, 98, 174, 273, and
 

407 mg/kg/day. In rats, the only effects observed were an increase in relative
 

liver and kidney (females only) weights in the high dose group. Focal areas of
 

ulceration with necrosis and inflammation of the squamous mucosa of the
 

forestomach were observed in the high dose mice. A final report
 

of this study is currently not available.
 

NTP (1990) has also completed a 13-week intraperitoneal injection study.
 

In this study, inflammation and/or fibrosis of the liver were observed in mice
 

dosed with 60 mg/kg potassium antimony tartrate every other day. Degeneration
 

was evident in the kidneys of male rats dosed with 24 mg/kg every other day. A
 

final report of this study is currently not available.
 

Genotoxicity tests were negative in Salmonella typhimurium strains
 

TAl00, TA1535, TA97, or TA98 for antimony potassium tartrate with and without
 

metabolic activation (NTP, 1990).
 

NIOSH is conducting an epidemiological study using a cohort of antimony
 

smelter workers to determine the possible association between exposure to
 

antimony and the risk of developing lung cancer (Federal Research in Progress
 

1989).
 

57

3. CHEMICAL AND PHYSICAL INFORMATION
 

There are many compounds, complexes, and alloys of antimony that occur
 

naturally or are man-made. The chemical identity and physical chemical
 

properties of all of these forms of antimony cannot be discussed in detail.
 

3.1 CHEMICAL IDENTITY
 

Antimony is in the fourth row of group 5A in the periodic table,
 

residing between arsenic and bismuth. It displays four oxidation states: Sb(­

3), Sb(0), Sb(+3), and Sb(+5). The +3 state is the most common and stable.
 

Antimony is sometimes referred to as a metalloid, indicating that it displays
 

both metallic and nonmetallic characteristics.
 

Metallic antimony is the only allotropic form of antimony that is stable
 

under normal conditions. Two unstable allotropes exist: yellow and black
 

amorphous forms (Herbst et al. 1985). Metallic antimony is a very brittle,
 

moderately hard metal (Herbst et al. 1985). It is occasionally found
 

uncombined in nature (Carapella 1978). Antimony has two stable isotopes with
 

mass numbers 121 and 123, with natural abundances of 57.25% and 42.75%,
 

respectively (Carapella 1978). One radioactive isotope, Sb125, is a fission
 

product released in nuclear explosions or nuclear fuel reprocessing plants and
 

has a half-life of 2.7 years (Weast 1988). Data on the chemical identity of
 

antimony, antimony pentasulfide, antimony pentoxide, antimony potassium
 

tartrate, antimony trichloride, antimony trioxide, antimony trisulfide, and
 

stibine are shown in Table 3-1.
 

3.2 PHYSICAL AND CHEMICAL PROPERTIES
 

The physical and chemical properties of antimony, antimony pentasulfide,
 

antimony pentoxide, antimony potassium tartrate, antimony trichloride,
 

antimony trioxide, antimony trisulfide, and stibine are given in Table 3-2.
 

Antimony metal is stable under ordinary conditions and is not readily attacked
 

by air or water (Herbst et al. 1985). It is a poor conductor of heat and
 

electricity (Weast 1988). Antimony is positioned after hydrogen in the
 

electrochemical series and therefore will not displace hydrogen ions from
 

dilute acids. It is not affected by cold, dilute acids (Windholz 1983). Simple
 

antimony cations (i.e., Sb+3 and Sb+5) do not occur in solution, but hydrolyzed
 

forms (e.g., Sb(OH)6

 ̄ ) are found. The dominant species in the pH range typical
 

of natural environments are Sb(OH)3 , in the case of trivalent antimony, and
 

Sb(OH)6

 ̄ for pentavalent antimony (Bodek et al. 1988). In oxidizing
 

environments, Sb(OH)6

 ̄

, is the dominant species for pH greater than 3, whereas
 

Sb(OH)3 is dominant under relatively reducing conditions. The concentration of
 

antimony is too low in natural water for Sb2O3 or Sb2O5 to precipitate out.
 

Antimony trioxide is dimorphic, existing as a cubic form, senarmontite,
 

and an orthorhombic form, valentinite. The cubic form is stable at
 

temperatures below 570°C (Freedman et al. 1978). Antimony trioxide is
 




62
 

3. CHEMICAL AND PHYSICAL INFORMATION
 

amphoteric; it is soluble in bases and hydrochloric and some organic acids,
 

but not dilute sulfuric or nitric acids (Cotton and Wilkinson 1966). Nitric
 

acid and other strong oxidizing agents convert antimony trioxide to antimony
 

pentoxide, Sb2O5, which is acidic (Carapella 1978; Cotton and Wilkinson 1966).
 

Antimony forms complex ions with organic and inorganic acids; one of the
 

best known is the tartrate. In the presence of sulfur, stable complexes such
 

as Sb2S4

2- may form (Bodek et al. 1988).
 

Stibine, SbH3, is a gaseous antimony compound in which antimony is in
 

the -3 valence state. It is formed by the action of acids on metal antimonides
 

or antimony alloys, reduction of antimony compounds, or the electrolysis of
 

acidic or basic solutions where antimony is present in the cathode. As such,
 

there is a danger of stibine being liberated from overcharged lead storage
 

batteries in which antimony is alloyed into the lead. Stibine slowly
 

decomposes into metallic antimony and hydrogen. It is readily, and sometimes
 

violently, oxidized by air to form antimony trioxide and water (Freedman et
 

al. 1978).
 
63
 

4. PRODUCTION, IMPORT, USE, AND DISPOSAL
 

4.1 PRODUCTION
 

Antimony, while not abundant, occurs in over 100 minerals; the more
 

important of these are sulfides and, to a lesser extent, oxides of Sb(III),
 

and combinations with lead, copper, and silver. Stibnite (Sb2S3) is the
 

predominant ore, followed in importance by valentinite (Sb2O3), senarmontite
 

(Sb2O3), stibiconite (Sb2O4.H2O), bindheimite (Pb2Sb2O7.nH2O), kermesite (Sb2S2O),
 

tetrahedrite (Cu2Sb2O7), and jamesonite (2PbS.Sb2S3). It also occurs uncombined
 

as the metal (Herbst et al. 1985; Miller 1973). The antimony content of
 

commercial ores ranges from 5% to 60% (Carapella 1978). The world's largest
 

concentrations of antimony are found in China, Bolivia, U.S.S.R., Republic of
 

South Africa, and Mexico (Miller 1973).
 

Between 1977 and 1984, the amount of antimony mined in the United States
 

ranged from 311 to 760 metric tons (Llewellyn 1988; Plunkert 1982). The low of
 

311 metric tons occurred in 1980, and was the result of an 8-month work
 

stoppage at the Sunshine Mine in the Coeur d'Alene district of Idaho. Data for
 

1985, 1986, and 1988 were withheld to avoid disclosing proprietary company
 

data (Anonymous 1989a, 1989b; Llewellyn 1988). This reflects the fact that
 

there were two or fewer active antimony mines in the United States. In 1987,
 

the Sunshine Mine was closed, and there was no antimony mined in the United
 

States. In recent years, the principal domestic ore producers have been the
 

Sunshine Mining Company in Idaho and the United States Antimony Corporation in
 

Montana. The Sunshine Mining Company principally mines tetrahedrite in
 

conjunction with silver mining, and the United States Antimony Corporation
 

principally mines stibnite. Antimony is also produced as a byproduct of the
 

smelting of primary lead ores.
 

The primary antimony output from smelters has generally been rising in
 

recent years; smelter outputs were 14,922, 16,309, 18,795, and 18,692 metric
 

tons in 1985, 1986, 1987, and 1988, compared with 11,644 metric tons in 1977
 

(Anonymous 1989a; Llewellyn 1988; Plunkert 1982). According to the U.S. Bureau
 

of Mines, nine companies produced primary antimony metal and metal oxide
 

products in the United States in 1987. These were ASARCO Incorporated, Omaha,
 

Nebraska; Amspec Chemical Corp., Gloucester City, New Jersey; Anzon America,
 

Laredo, Texas; Chemet Co., Moscow, Tennessee; Laurel Industries Inc., La
 

Porte, Texas; McGean Chemical Co., Inc., Cleveland, Ohio; M&T Chemicals Inc.,
 

Baltimore, Maryland; Sunshine Mining Co., Kellogg, Idaho; and U.S.
 

Antimony Corp, Thompson Falls, Montana (Llewellyn 1988). Most of the primary
 

antimony generated in the United States was generated as the oxide. In 1985
 

and 1986, 13,969 and 15,898 metric tons of antimony oxide were produced,
 

compared with 855 and 343 metric tons of metal, respectively. In 1987 and
 

1988, 18,758 and 18,226 metric tons of the oxide were produced, respectively;
 

production figures for the metal were withheld to maintain business
 

confidentiality (U.S. Bureau of Mines 1989a). In 1988, U.S. primary antimony
 

consumption was 12,060 metric tons, of which 2,121 metric tons were metal,
 

9,432 metric tons were oxide, and 42 metric tons were sulfide (U.S. Bureau of
 
64
 

4. PRODUCTION, IMPORT, USE, AND DISPOSAL
 

Mines 1989a). Consumption trends have generally paralleled those of
 

production. Table 4-l lists the number of facilities in each state that
 

produced, imported, processed, or used antimony and its compounds in 1987,
 

according to reports made to EPA under requirements of Section 313 of the
 

Emergency Planning and Community Right-to-Know Act of 1986 and subsequently
 

published in the Toxic Chemical Release Inventory (TRI). Companies are
 

required to report if they produced, imported, or processed 75,000 or more
 

pounds of antimony and its compounds or used more than 10,000 pounds. Also
 

included in Table 4-l is the maximum amount of antimony and its compounds
 

these facilities have on site and whether the antimony is produced, processed,
 

or used at the site. The quality of the TRI data must be viewed with caution
 

since 1987 data represent first-time, incomplete reporting by these
 

facilities. Not all facilities that should have reported have done so.
 

Almost as much antimony is produced from scrap as from ore. Antimony
 

produced from secondary sources is primarily derived from "old scrap,"
 

generally consisting of lead battery plates, type metal, and bearing metal.
 

"New scrap," which is derived from drosses and scrap generated during
 

fabrication, constituted 8.6% of the secondary antimony in 1987 (Llewellyn
 

1988). Secondary antimony is chiefly consumed as antimonial lead; a small
 

percentage goes into the production of other lead- and tin-based alloys.
 

Secondary antimony production has stabilized and recovered slightly after a
 

long decline; it was 27,780 metric tons in 1977, 12,886 metric tons in 1983,
 

and 13,635, 14,082, 15,189, and 16,172 metric tons in 1985, 1986, 1987, and
 

1988, respectively (U.S. Bureau of Mines.1989a; Llewellyn 1988; Plunkert
 

1982).
 

The method of treating antimony ore after mining depends on the type of
 

ore and its antimony content. High grade (45-602;) sulfide ore that is free
 

from lead and arsenic can be extracted by melting, a technique known as
 

liquation. In this process, the ore is heated to 550-660°C in a crucible or
 

reverberatory furnace in a reducing atmosphere. High-grade sulfide ores can
 

also be reduced to the metal by iron precipitation, a technique in which the
 

ore is heated with iron scrap, which replaces the antimony. High-grade oxide
 

ores are reduced with charcoal in a reverberatory furnace. An alkaline flux
 

is used to reduce volatilization losses, which may be as high as 12-20X. The
 

method of choice for low-grade (less than 20%) sulfide ores is volatilizing
 

roasting. In this process, the ore is heated to about 5OO"C, and the amount of
 

oxygen is controlled, so that the antimony trioxide formed is volatilized and
 

then recondensed. Intermediate-grade sulfide or oxide ores are generally
 

handled by smelting (Carapella 1978; Herbst et al. 1985). The impure metal may
 

be refined by pyrometallurgical techniques or electrolysis. For further
 

details on antimony mining, ore processing, recovery, and refining, see
 

Carapella (1978) or Herbst et al. (1985).
 

Antimony trioxide is produced by oxidizing antimony sulfide ore or
 

antimony metal in air at 600-800°C (Avento and Touval 1980).
 


67
 

4 . PRODUCTION, IMPORT, USE, AND DISPOSAL
 

4.2 IMPORT/EXPORT
 

The United States is not self-sufficient in antimony and depends heavily
 

on imports of both ore and metal. In 1987 and 1988, 24,248 and
 

30,027 metric tons of antimony, respectively, were imported into the United
 

States for consumption. Of this, 55.3% was as the metal, 31.9% as the oxide,
 

12.4% as ore and concentrate, and 0.4% as the sulfide in 1988 (U.S. Bureau of
 

Mines 1989a). The respective percentages for 1987 were 36.3, 42.4, 21.1, and
 

0.3. In 1987, China, Hong Kong, Mexico, and the Republic of South Africa
 

supplied over 72% of this antimony (U.S. Bureau of Mines 1989a). China is, by
 

far, our largest supplier of antimony, most of which is imported as antimony
 

metal. Importation of antimony has generally increased in recent years. In
 

comparison to the figures for 1987 and 1988 given above, imports ranged from
 

12,098 to 20,086 metric tons between 1977 and 1981 (Plunkert 1982). States
 

that have companies that imported more than 10,000 pounds of antimony and its
 

compounds in 1987 are indicated in Table 4-1.
 

The United States exported 624 metric tons of antimony metal, alloys,
 

and scrap and 1,227 metric tons of antimony oxide in 1988 (U.S. Bureau of
 

Mines 1989a). Canada is the largest recipient of these exports. No clear trend
 

in antimony exports was evident in the last decade (Llewellyn 1988; Plunkert
 

1982).
 

4.3 USE
 

Antimony is a brittle metal that is not readily fabricated and has no
 

significant use in its unalloyed state. It is alloyed with lead and other
 

metals to increase their hardness, mechanical strength, corrosion resistance,
 

and electrochemical stability or decrease their coefficient of friction. Some
 

antimony alloys expand slightly upon cooling, a valuable property for use in
 

type metal and other castings. Most primary antimony metal, 55% in 1988, as
 

well as most of secondary antimony, goes into antimonial lead, which is used
 

primarily in grid metal for lead acid storage batteries. In this application,
 

the antimony imparts fluidity and electrical stability, and increases the
 

fatigue strength and creep resistance of the lead (Carapella 1978). Other uses
 

in decreasing order of importance are solder, sheet and pipe, bearing metal,
 

and bearings, castings, and type metal. Antimony is also used in ammunition
 

and cable sheathing. Other uses, including nonantimonial lead alloys (e.g.,
 

pewter), accounted for 21.7% of 1988 metal consumption (U.S. Bureau of Mines
 

1989a). The level of antimony in grid metal ranges from 2.5% to 5% (Carapella
 

1978). Antimony levels in other antimony alloys range up to 23%. High-purity
 

antimony is used as a dopant in semiconductors. Intermetallic compounds of
 

antimony such as aluminum antimonide (AlSb), gallium antimonide (GaSb), and
 

indium antimonide (InSb) are used for thermoelectric devices such as infrared
 

detectors and diodes (Gudzovskij 1983; Herbst et al. 1985).
 
68
 

4 . PRODUCTION, IMPORT, USE, AND DISPOSAL
 

The most common end-use of antimony compounds is antimony trioxide for
 

fire retardation. In 1985, 15,500 metric tons of antimony oxides, amounting to
 

85% of production, were consumed for this use (Sutker 1988). Antimony trioxide
 

in a suitable organic solvent is used as a fire retardant for plastics,
 

textiles, rubber, adhesives, pigments, and paper (U.S. Bureau of Mines 1989a).
 

According to Bureau of Mine estimates, 56% of the end-use consumption of
 

primary antimony in the United States was for flame retardants, as opposed to
 

23% in metal products and 21% in nonmetal products (U.S. Bureau of Mines
 

1989a). Nonmetal products include enamels for plastics, metal, and ceramics,
 

decolorizing and refining agents in special optical glass and other
 

glasses, stabilizers in plastics, pigments in paints and ceramics,
 

vulcanization agents, ammunition primers, and fireworks (U.S. Bureau of Mines
 

1989a; Herbst et al. 1985; Ludersdorf et al. 1987). The number of companies in
 

each state that used more than 10,000 pounds of antimony and its compounds in
 

1987 is included in Table 4-l. The most common general use of antimony and its
 

compounds is as a formulation or article component.
 

Some trivalent organic antimony compounds (e.g., potassium or sodium
 

antimony tartrate) are used to treat bilharziasis (schistosomiasis)
 

(Swellengrebel and Sterman 1961).
 

4.4 DISPOSAL
 

Much of the antimony used in antimonial lead, most of which comes from
 

auto batteries, is recycled. This is evident from the large amount of
 

secondary antimony production. Little information concerning the disposal of
 

antimony and its compounds has been found in the literature. Wastes from
 

mining and smelting are generally disposed of in landfills. This is evident
 

from the amounts of releases to land from companies that produce antimony and
 

its compounds (Section 5.2.1). In addition, many companies transfer their
 

antimony wastes to publicly-owned treatment works or to off-site facilities
 

for disposal. Plastics and articles of clothing that contain small amounts of
 

antimony oxide flame retardants will generally be placed in landfills or
 

incinerated along with normal industrial or municipal trash.
 

Antimony and its compounds have been designated as priority pollutants
 

by EPA (1988). As such, persons who generate, transport, treat, store, or
 

dispose of antimony-containing material must comply with regulations of the
 

federal Resource Conservation and Recovery Act (RCRA). No limitations on the
 

disposal of antimony ore from mines and mills have been promulgated in the
 

Code of Federal Regulations (EPA 1988).
 
69
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5.1 OVERVIEW
 

Antimony and its compounds are naturally present in the earth's crust.
 

Releases to the environment occur from natural discharges such as windblown
 

dust, volcanic eruption, sea spray, forest fires, and biogenic sources, as
 

well as from anthropogenic activities. Therefore, it is important to consider
 

the background levels that are due to natural sources and distinguish these
 

from higher levels that may result from anthropogenic activities. According to
 

the SARA Section 313 TRI, an estimated total of 3,061,036 pounds of antimony
 

were released to the environment from manufacturing, processing, and antimony-


using facilities in the United States in 1987 (TRI 1989). Of these releases,
 

92.9% was to land, 4.4% was to air, 2.0% was to water, and 0.6% was to
 

underground injection. Table 5-1 lists releases of antimony to air, water, and
 

land from these facilities. Companies above a minimum size are required to
 

report if they produce, import, or process over 75,000 pounds of antimony and
 

its compounds or use in excess of 10,000 pounds. The quality of the TRI data
 

must be viewed with caution since the 1987 data represent first-time,
 

incomplete reporting of estimated releases from these facilities. Not all
 

sources of chemical waste are included, and not all facilities that should
 

have reported have done so.
 

Most antimony released to the atmosphere from anthropogenic sources
 

results from metal smelting and refining, coal-fired power plants, and refuse
 

incineration. Since antimony is a fairly volatile metal, it will volatilize
 

during combustion processes and subsequently condense on suspended particulate
 

matter that is predominantly less than 1 μm in size. Such fine particles are 

less efficiently trapped by pollution control devices than are larger 

particles. In the atmosphere, they tend to settle out slowly; they are also 

removed by dry and wet deposition. A model that relates particle size to 

volatility estimates average atmospheric half-lives of 1.9 and 3.2 days for 

antimony and antimony trioxide, respectively (Mueller 1985). Submicron 

particles may have atmospheric half-lives as long as 30 days (Schroeder et al. 

1987). The long atmospheric half-life and monitoring data indicate that 

antimony can be transported far from its source (Dutkiewicz et al. 1987; 

Hillamo et al. 1988). Antimony concentrations in air particulate matter in 

remote, rural, and U.S. urban areas are 0.00045-1.19, 0.6-7, and 0.5-171 

ng/m3

, respectively (Austin and Millward 1988; Schroeder et al. 1987). 

The speciation and physicochemical state of antimony are important to
 

its behavior in the environment and availability to biota. For example, the
 

antimony incorporated in mineral lattices is inert and unlikely to be
 

bioavailable. Most analytical methods for antimony do not distinguish the form
 

of antimony. While the total amount of antimony may be known, the nature of
 

the antimony compounds and whether they are adsorbed to other material are
 

not. This information, which is critical in determining antimony's lability
 

and availability, is apt to be site-specific.
 


72
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Antimony occurs in soil and rock in very low concentrations; the range
 

of concentration in soil ranges from less than 1 to 8.8 ppm, with a mean of
 

0.48 ppm (Shacklette and Boerngen 1984). This is the third lowest of 50
 

elements surveyed by the U.S. Geological Survey. The forms of antimony in
 

various soils and the transformations between these forms is poorly
 

understood. The available data indicate that the lability of antimony may vary
 

considerably according to its environment. In one study, three-quarters of the
 

soil near a smelter site was in a residual (extractible with aqua regia)
 

fraction (Ainsworth 1988). While the concentration of antimony was much lower
 

at control sites, it was in a more labile form; none of the antimony was in
 

the residual fraction. Little is known about the adsorption
 

of antimony to soil. Limited studies indicate that antimony may be fairly
 

mobile under diverse environmental conditions (Rai and Zachara 1984). Since
 

antimony forms anionic species, adsorption should be greatest under weakly
 

acidic conditions. Antimony's adsorption to soil and sediment is primarily
 

correlated with the iron, manganese, and aluminum content; it coprecipitates
 

with hydroxylated oxides of these elements.
 

As a natural constituent of soil, antimony is transported into streams
 

and waterways from natural weathering of soil as well as from anthropogenic
 

sources. Antimony has a low occurrence in ambient waters. In a survey of
 

dissolved antimony in ambient waters performed by the U.S. Geological Survey,
 

only 6% of 1,077 survey measurements were above the probable detection limit
 

of 5 ppb (Eckel and Jacobs 1989). Antimony concentrations in groundwater
 

appear to be similar to that in surface water. Mean antimony concentrations in
 

surface and groundwater at hazardous waste sites were 27 and 35 ppb,
 

respectively (CLPSD 1989). The forms of antimony and the chemical and
 

biochemical process that occur in the aquatic environment are not well
 

understood. Antimony in both aerobic freshwater and seawater is largely in the
 

+5 oxidation state, although antimony in the +3 oxidation state also occurs in
 

these waters. Trivalent antimony is the dominant oxidation state of antimony
 

in anaerobic water. Antimony can be reduced and methylated by
 

microorganisms in anaerobic sediment, releasing volatile methylated antimony
 

compounds into the water. Methylstibonic acid and dimethylstibonic acid occur
 

in natural water; the monomethyl species is the more abundant one (Andreae
 

1983; Andreae and Froelich 1984).
 

EPA has identified 1,177 NPL sites. Antimony and its compounds have been
 

found at 52 of the sites evaluated for the presence of these chemicals (View
 

1989). However, we do not know how many of the 1,177 NPL sites have been
 

evaluated for these chemicals. As more sites are evaluated by EPA, the number
 

may change. The maximum concentrations of antimony reported at these sites are
 

2,100 ppb in groundwater, 1,000 ppb in surface water, and 2,550 ppm in soil.
 

The frequency of these sites within the United States can be seen in Figure 5­

1.
 

The general population is exposed to low levels of antimony in ambient
 

air and food. The average intake of antimony from food and water is roughly
 

74
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5 μg/day (Iyengar et al. 1987). The intake from breathing air is generally a 

small fraction of that from ingestion. Exposure from antimony trioxide, which 

is used extensively in textiles and plastics as a fire retardant, is not 

expected to be significant. EPA estimates that approximately 4,000 workers may 

be exposed to antimony and antimony trioxide in production facilities and 

first-level processing facilities. These workers will have the highest levels 

of exposure to antimony. The highest air concentration of antimony reported in 

workplace surveys was 6.2 mg/m3

. 

5.2 RELEASES TO THE ENVIRONMENT
 

Most analytical methods for antimony in environmental samples do not
 

distinguish between antimony metal, antimony trioxide, or other compounds of
 

antimony. More sophisticated methods are required to determine the oxidation
 

state of antimony or the nature of its binding to soil and particulate matter;
 

therefore, it is generally impossible to say with certainty what forms of
 

antimony are released from natural and anthropogenic sources, what forms are
 

deposited or occur in environmental samples, and to what form of antimony
 

people are exposed. The form of antimony will have significant consequences as
 

far as its transport, transformations, and bioavailability are concerned.
 

5.2.1 Air
 

Antimony and its compounds are natural components of the earth's crust
 

and releases to the atmosphere result from natural as well as anthropogenic
 

sources. A recent assessment of natural sources of atmospheric trace metals
 

paid special attention to biologic origins of these metals. Nriagu (1989)
 

estimated that 41% of antimony emissions to the air are from natural sources.
 

The natural sources and their median percentage contribution are: wind-borne
 

soil particles, 32.5%; volcanoes, 29.6%; sea salt spray, 23.3%; forest fires,
 

9.2%; and biogenic sources, 12.1%. Previous assessments indicated that
 

natural inputs were minor compared with anthropogenic ones; in one estimate,
 

anthropogenic sources contributed 39 times more antimony than did natural
 

sources (Lantzy and Mackenzie 1979; Yocom 1983).
 

Anthropogenic sources of antimony releases to the atmosphere include
 

nonferrous metal mining, nonferrous metal primary and secondary smelting and
 

refining (Crecelius et al. 1974; Pacyna et al. 1984), coal combustion (Gladney
 

and Gordon 1978), and refuse and sludge combustion (Greenberg et al. 1978).
 

Table 5-1 lists the air releases by state from facilities that produce,
 

process, and use antimony and its compounds according to the 1987 TRI (1989).
 

Releases to air total 135,627 pounds. The highest annual release reported by a
 

single company is 29,900 pounds. The industries that contribute the bulk of
 

releases are those that produce antimony and antimony trioxide. Since the TRI
 

does not include emissions from power plants and refuse and sludge
 

incinerators, their estimate of antimony emissions is not complete. European
 

emissions of antimony were estimated at 380 tons for 1979 (Pacyna et al.
 

1984). Volatile elements and chalcophilic elements (those elements showing an
 
75
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

association with sulfur), like antimony, show large enrichment over crustal
 

abundances in particulate matter emitted from smelting, coal combustion, and
 

refuse combustion. The ranges of enrichment factors reported for these sources
 

are 10,300-l,000,000, 20-140, and 3,000-10,000, respectively (Gladney et al.
 

1978; Gordon and Sheffield 1986; Small et al. 1981). On a global basis, metal
 

smelting is estimated to make more than double the contribution to atmospheric
 

emissions as other sources, but long-term coal combustion is anticipated to be
 

a dominant factor in future tropospheric antimony levels (Austin and Millward
 

1988). The antimony that is associated with fine particles (less than 1 pm)
 

tends to result from combustion and other high temperature sources, while that
 

associated with large particles (greater than 10 pm) is likely to originate
 

from wind-blown soil and dust (Schroeder et al. 1987).
 

It is estimated that 3 g of antimony are released from copper smelters
 

for each ton of copper produced (Pacyna 1984). Typical concentrations of
 

antimony observed in plumes of five copper smelters ranged from 58 to 370
 

ng/m3

 versus an average background level of 2 ng/m3 in ambient air (Small et
 

al. 1981). It was found that most of the antimony deposited close to one
 

smelter originated from ground-level emissions (e.g., fugitive emissions)
 

rather than stack emissions (Ainsworth 1988). It was determined that between
 

57% and 66% of the antimony in the stack of a plant that recycled lead storage
 

batteries was in the vapor form (Craig et al. 1981). This antimony will
 

recondense onto small particles.
 

The antimony content of 166 American coal samples ranged from
 

0.1 to 8.9 ppm, with a mean content of 1.15 ppm (Sabbioni et al. 1983).
 

Therefore, it would be expected that coal-fired power plants are a significant
 

source of antimony emissions. A typical, modem coal-fired power plant emits
 

about 31 μg of antimony per kilogram of fuel burned, compared with 3.9 μg/kg 

for an oil-fired plant (Hasanen et al. 1986). Heavy fuel oil has an antimony 

content of about 0.067 ppm. Emissions from two units of the Columbia Station 

coal-burning power plant in Portage, Wisconsin, ranged from 220 to 1,300 ng 

antimony/m3

 when sampled over 1.5 years (Bauer and Andren 1988). Another 

investigator reported that a coal-fired power plant with pollution control had 

stack emissions of 6,800 ng antimony/m3

 (Lee et al. 1975). Antimony in these 

emissions tends to be associated with fine particles and the surface of 

particulate matter, consistent with their formation by volatilization and 

subsequent condensation (Hansen and Fisher 1980). In a modern coal plant, 69% 

of antimony emissions were associated with particles less than 3 μm in 

diameter (Sabbioni et al. 1984). Two other studies found that 34-52% of 

emissions from coal-fired power plants were associated with particles less 

than 2 μm, and that the mass medium diameter (MMD) of particles from a plant 

with pollution control devices was 0.6 μm (Gladney et al. 1978; Lee et al. 

1975). 

A study of emissions from two municipal incinerators in
 

Washington, D.C., showed that refuse incineration can account for the major
 
76
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

portion of antimony in urban aerosols (Greenburg et al. 1978). At least 90% of
 

this antimony is associated with respirable, fine particles that are less than 

or equal to 2 μm in diameter. The concentration range of antimony in suspended 

particles from these incinerators was 610-12,600 ppm, with a mean 

concentration of 2,400 ppm. In performance tests conducted under the Canadian 

National Incinerator Testing and Evaluation Program, 2.3 g antimony/ton of 

refuse was emitted under normal operating conditions. Under a range of 

operating conditions, the amounts ranged from 1.9 to 9.6 g antimony/ton (Hay 

et al. 1986). Respective stack antimony concentrations were 0.6 and 0.5-2.6 

mg/Nm3

 at 12% CO2, where Nm3 indicates standard cubic meter (1 atmosphere, 

25°C). A European study gave emission factors for refuse and sewage sludge 

incinerators as 4.55 and 1.9 g antimony/ton, respectively 

(Pacyna 1984). All of the antimony from the stack of a refuse-burning plant 

was in particulate rather than gaseous form (Braun et al. 1983). 

Antimony is a component of ammunition, and therefore antimony may be
 

emitted during the discharge of firearms. This source of emission is
 

inconsequential outdoors. However, in indoor firing ranges, it is a
 

significant source of antimony emission (Dams et al. 1988; Olmez et al. 1985).
 

An air monitoring study was conducted in 1982 at three sites surrounding
 

the Anaconda Minerals Company smelter facility in Montana. This company had
 

closed 2 years earlier after 8 decades of operation. The study was performed
 

under Superfund to ascertain whether the accumulated heavy metals released
 

during the smelting operations and from tailing ponds might become reentrained
 

by wind and pose a health hazard (Ives et al. 1984). While no antimony was
 

reported to have been produced at the Anaconda Minerals Company facility, many
 

of the metals that were extracted, (e.g., copper, lead, arsenic) are found in
 

association with antimony. The atmospheric levels of heavy metals were very
 

low, indicating that there was not any significant reentrainment of heavy
 

metals from tailing ponds or smelter deposits. The particulate matter examined
 

was generally crustal or carbonaceous in character. Antimony was detected on
 

only 3 of 85 air sampling filters at the three sites.
 

Stibine may be produced in lead acid battery plants during the formation
 

process. During this process, an electric current is passed through the
 

battery plates, reducing PbO to Pb at the negative plate, and oxidizing PbO to
 

PbO2 at the positive plate. Hydrogen gas is released that can react with the
 

antimony in the grid metal to form stibine (Jones and Gamble 1984). Stibine
 

may also be formed during remelting of mixed lead-calcium and lead-antimony
 

battery scrap, the former being used for starter batteries. In this process,
 

the intermetallic compound calcium antimonide may be produced in the dross or
 

scum. This compound releases stibine when it comes in contact with water
 

(Ayhan et al. 1982).
 
77
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

5.2.2 Water
 

Antimony is a natural constituent of soil and is transported into
 

streams and waterways in runoff either due to natural weathering or disturbed
 

soil. Much of this antimony is associated with particulate matter. In the EPA-


sponsored National Urban Runoff Program in which 86 samples of runoff from 19
 

cities throughout the United States were analyzed, antimony was found in 14%
 

of runoff samples at concentrations ranging from 2.6 to 23 ppb (Cole et al.
 

1984).
 

Estimated releases of antimony to water from facilities in the United
 

States that produced, processed, and used antimony in 1987 according to the
 

TRI are found in Table 5-1. These releases totaling 62,328 pounds are much
 

lower than those to air or land. A survey of raw and treated waste water from
 

20 industrial categories indicates that antimony is commonly found in some
 

waste waters. Those industries with mean effluent levels exceeding 1 ppm in
 

raw waste water were (industry [mean level in ppm]): foundries (l.l),
 

porcelain enameling (1.4), and nonferrous metal manufacturing (5.7) (EPA
 

1981). The maximum levels in discharges from these industries were 3.4, 22,
 

and 80 ppm, respectively. Additionally, four other industrial categories had
 

maximum concentrations exceeding 1 ppm. These were laundries (2.4 ppm),
 

inorganic chemical manufacturing (1.4 ppm), ore mining and dressing (3.8 ppm),
 

and paint and ink formulation (2.2 ppm). For treated waste water, only
 

porcelain enameling had mean antimony levels in excess of 1 ppm. The levels
 

reached 4.3 ppm.
 

Domestic waste water is a potential source of antimony in waterways.
 

Concentrations of antimony in influents to 11 municipal waste water treatment
 

plants (POTWs) (155 observations) ranged from 0.0003 to 2.1 ppm; the median
 

value was approximately 0.1 ppm (Minear et al. 1981). Antimony is not well
 

removed in POTWs, and releases from these facilities may contribute to
 

releases of antimony to water (Aulenbach et al. 1987; EPA 1981). The outfall
 

of a sewage treatment plant in Seattle, however, did not appear to make a
 

significant contribution to the antimony levels in the sediment of Puget Sound
 

(Crecelius et al. 1975).
 

Waste water generated from mining and smelting operations comes from
 

seepage, runoff from tailing piles, or utility water used for mine operation.
 

In addition to liquid effluent from smelting operations, slag may be dumped
 

directly into receiving waters (Crecelius et al. 1975). These discharges
 

largely contain insoluble silicates and sulfides which readily settle out.
 

Total antimony in effluent from a primary aluminum production facility was 40
 

ppb (Rawlings 1980). Sixty percent of this antimony was subsequently removed
 

by lime coagulation.
 

One of the potentially dangerous sources of chemical release at waste
 

sites is from leachate. Leachate from three municipal landfills in New
 

Brunswick, Canada, each contained 0.01 ppm of antimony (Cyr et al. 1987).
 
78
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

The antimony concentration in sediment at two sites below the leachate
 

outfalls was 23.9 ppm (dry weight) and nondetectable, respectively.
 

5.2.3 Soil
 

Most of the antimony released to the environment is released to land.
 

According to Table 5-1, which shows the estimated releases in 1987 of domestic
 

industries that produce, process, or use antimony, 2,845,131 pounds of
 

antimony are released to land, constituting 93% of environmental releases
 

reported to TRI (TRI 1989). The industries that release the largest amount of
 

antimony are the smelters that produce antimony and antimony trioxide. Much of
 

this release is slag, which is the residue from smelting operations. Other
 

releases to land include sludge from POTWs and municipal refuse.
 

An analysis of the concentration of antimony at hazardous waste sites at
 

the Contract Laboratory Program Statistical Database (CLPSD) shows that
 

antimony was reported in 153 of 1,307 soil samples, with geometric mean and
 

maximum levels in positive samples of 8.0 and 330 ppm, respectively (Eckel and
 

Langley 1988). An analysis of these data indicates that 7.3% of the CLPSD
 

samples exceed the number expected to be above the 95% upper confidence limit
 

for background U.S. soils (Eckel and Langley 1988). The CLPSD includes both
 

NPL and non-NPL data. A more recent update of the CLPSD reports a 12.8%
 

occurrence of antimony and a geometric mean concentration of 16.86 ppm (CLPSD
 

1989). No analysis was performed on these results to indicate what percentage
 

exceed the background levels of antimony normally found in soil.
 

5.3 ENVIRONMENTAL FATE
 

It is not always possible to separate the environmental fate processes
 

relating to transport and partitioning from those relating to transformation
 

for a metal and its various compounds and complexes. Part of this problem is
 

that the form of a metal is rarely identified. A change of mobility may result
 

from a transformation of a metal to a more or less soluble form. Adsorption
 

may be the result of the formation of strong bonds (transformation) as well as
 

weak bonds. Information regarding the deposition and general adsorption of
 

antimony is in Section 5.3.1 and information regarding the areas of
 

environmental fate where speciation is discussed is in Section 5.3.2.
 

5.3.1 Transport and Partitioning
 

Antimony is released to the atmosphere in the form of particulate matter
 

or adsorbed to particulate matter. It is dispersed by wind and removed by
 

gravitational settling and dry and wet deposition (Schroeder et al. 1987). The
 

removal rate and distance traveled from the source will depend on source
 

characteristics (e.g., stack height), particle size and density, and
 

meteorological conditions.
 
79
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Gravitational settling governs the removal of large particles (greater 

than 5 μm), whereas smaller particles are removed by the other forms of dry 

and wet deposition. Removal of coarse particles may occur in a matter of 

hours. Very small particles may have an atmospheric half-life as long as 30 

days (Schroeder et al. 1987). Antimony is predominantly associated with small, 

submicron particles (Stoessel and Michaelis 1986). This is frequently the case 

with the more volatile metals, such as antimony, that may volatilize during 

combustion and condense when cooled. A model which relates particle size to 

volatility estimates an average atmospheric half-life for antimony of 1.9 

days; for the more volatile antimony trioxide (see Table 3-2), the 

estimated half-life is 3.2 days (Mueller 1985). With such an atmospheric halflife, antimony may be transported far from its source. Evidence of this was 

reported by Animoto and Duce (1987), who stated that the antimony levels in 

aerosols at the Enewatak Atoll in the tropical North Pacific were higher than 

those expected from seawater or crustal material. 

Metal deposition is characterized by large temporal and spatial
 

variability. Estimated antimony deposition rates in urban areas are
 

0.006 and 0.004 kg/hectare/year (60 and 40 ng/cm2

/year) for dry and wet
 

deposition, respectively (Schroeder et al. 1987). For remote areas, bulk (wet
 

plus dry) deposition may be as little as 0.00016 kg/hectare/year (1.6
 

ng/cm2

/year). Rates of air-sea transfer of antimony are similar to the rates
 

of accumulation of antimony in sediment (Arimoto and Duce 1987).
 

The partitioning between dry and wet deposition depends on the intensity
 

and duration of precipitation, the element in question, its form in the
 

particulate matter, and its particle size. The ratio of wet to dry deposition
 

generally increases with decreasing particle size; therefore, a larger
 

proportion of antimony will be found in rain compared with most other metals.
 

A study of the wet and dry deposition over an 8-week period on an island in
 

the German Bight, which was presumably far from sources, found 87% of
 

deposited antimony dissolved in rain, 11% in particulate matter in rain, and
 

only 2% as dry deposition (Stoessel and Michaelis 1986). In other studies
 

conducted in areas removed from sources of antimony emissions, half of the
 

antimony deposition was in the form of wet deposition (Ainsworth 1988). The
 

total antimony deposition annualized from a B-month study in an industrial
 

area of England where a number of ferrous and nonferrous metal smelting and
 

manufacturing works were concentrated was 1,000 ng/cm2

-year (a factor of 20-40
 

above nonurban deposition rates) (Pattenden et al. 1982). Of this, 42%
 

represented wet deposition, of which 58% was dissolved antimony.
 

Antimony released into waterways is generally associated with
 

particulate matter; it is transported to and settles out in areas of active
 

sedimentation such as where a river empties into a lake or bay (Beijer and
 

Jernolov 1986). Similarities in the composition of suspended river sediment
 

and the sediment in bays indicate that the rivers transport the suspended
 

sediment and deposit it in the bottom sediment (Crecelius et al. 1975).
 

Additionally, when a river feeds into an estuary, the salinity changes that
 
80
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

are encountered may affect adsorption to sediment and particulate matter,
 

complexation, and coprecipitation.
 

Little is known of the adsorptive behavior of antimony, its compounds,
 

and ions. The binding of antimony to soil is determined by the nature of the
 

soil and the form of antimony deposited on the soil. Some forms of antimony
 

may bind to inorganic and organic ligands. On the other hand, a mineral form
 

would be unavailable for binding. Some studies suggest that antimony is fairly
 

mobile under diverse environmental conditions (Rai and Zachara 1984), while
 

others suggest that it is strongly adsorbed to soil (Ainsworth 1988; Foster
 

1989; King 1988). Since antimony has an anionic character (e.g., Sb(OH)i), it
 

is expected to have little affinity for organic carbon. No information could
 

be found about antimony's adsorption to clay minerals. It is not expected that
 

cation exchange, which generally dominates adsorption to clay, would be
 

important for anionic antimony. Antimony is known to form coprecipitates with
 

hydrous iron, manganese, and aluminum oxides in soil and sediment (Callahan et
 

al. 1978).
 

The capacity of soil to adsorb antimony and the nature of the bound
 

antimony were evaluated by incubating 200 ppm of antimony potassium tartrate
 

with 5 g samples of soils for 6 days (King 1988). Thirteen soils and subsoils
 

(21 samples) from the southeastern United States (10 mineral and 3 organic)
 

were included in the study. Antimony adsorbed strongly to most soils. The
 

amount of adsorbed antimony ranged from 50% in Lakeland surface soil to 100%
 

in several soils; the median percent adsorption was 93%. The percentage of
 

nonexchangeable (i.e., that not removed with KCl) antimony adsorbed paralleled
 

that of total antimony and ranged from 57% to 99%. Both sorbed and
 

nonexchangeable antimony were negatively correlated to sand content in mineral
 

soil. The soil/water partition coefficient (mmol/kg soil)/(mol/m3

) was 81 and
 

greater than 185 for organic and mineral soils, respectively. Several mineral
 

soils adsorbed 100% of the antimony and were excluded from the averaging. It
 

is not clear what species of antimony was adsorbed in this study. If it was
 

the antimony tartrate ion, the study may not be particularly relevant to other
 

forms of antimony. The mobility of antimony in clay, sandy loam, silt loam,
 

and sand soils was investigated using soil thin-layer chromatography (TLC)
 

(Foster 1989). The antimony was applied as antimony trioxide in a water or 1%
 

HCl suspension and developed with water in 8 hours or less. Despite
 

experimental difficulties, the results demonstrated that there is no general
 

mobility of antimony in any soil. The experimental problems and the fact that
 

small amounts of antimony were found in all zones is possibly due to an
 

unsuitable soil digestion (Ainsworth 1988).
 

A Superfund site study at a battery reclamation plant showed that while
 

soil and sediment contained high levels of antimony, an aquifer 3 m below the
 

surface contained 0.1 ppm of antimony; no antimony was detected in two deeper
 

aquifers (Trnovsky et al. 1988). Antimony adsorbs strongly to colloidal
 

material in soil. The partition coefficient of antimony to 0.05-0.003 μm 
81
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

colloids was 1,300. Antimony adsorbed to such material can be transported with
 

the colloids in groundwater (Buddenmeier and Hunt 1988).
 

Leaching experiments performed with river sediment samples from a mintng
 

district in Idaho indicated that Sb(V) was the major species released during
 

leaching (Mok and Wai 1990). The fraction of antimony leached from sediment
 

with deionized water after 10 days was highly correlated with the free iron
 

and manganese oxide content of the sediment (correlation coefficients of 0.90
 

and 0.75). Experiments were also performed in which the pH dependence of
 

leaching was determined. The release of antimony from the sediment increased
 

at low pH and increased sharply at high pH. The form of released antimony was
 

also sensitive to pH. At pH 2.7, the bulk of antimony released was as
 

Sb(II1); at pH 4.3, the concentrations of tri- and pentavalent antimony were
 

comparable; and at pH 6.3 and above, Sb(V) was the predominant species.
 

In order to evaluate the potential for leaching of elements from
 

landspread sewage sludge, Gerritse et al. (1982) studied the adsorption of
 

elements from water, salt solutions, and sludge solutions to sandy and sandy
 

loam top soils. They used metal levels that occur in the solution phase of
 

sewage sludge, lo-100 ppb in the case of antimony. The results indicate that
 

antimony is fairly mobile in these soils. The adsorption constants were
 

approximately 2-16 in the sandy soil and 20 in the sandy loam soil. Although
 

the presence of sludge increases the mobility of many trace elements because
 

of complexation with dissolved organic compounds or increased ionic strength,
 

this did not appear to be the case with antimony (Gerritse et al. 1982). It is
 

not easy to reconcile these results with those of Foster (1989), Ainsworth
 

(1988), Trnovsky et al. (1988), or Van der Sloot et al. (1982). These studies
 

indicated that antimony deposited on the soil surface accumulates primarily in
 

the surface layer, and that aquifers beneath antimony waste piles are not
 

grossly contaminated.
 

Mobilization of elements deposited on soil in fly ash is a potential
 

source of terrestrial and aquatic pollution. When the alkaline fly ash from a
 

coal-fired power plant was packed in a column and subject to leaching with
 

dilute sulfuric acid, antimony was partially dissolved and removed from the
 

upper layers of ash and deposited and retained on lower sections of ash in the
 

column (Warren and Dudas 1988). It was thought that extractable,
 

surfaceadsorbed antimony in the upper layers of ash was removed by the acid,
 

subsequently precipitated by iron oxyhydroxides, and retained lower down in
 

the column. Other column leaching and shake-flask experiments with coal ash
 

are too complex to summarize; they basically indicate that leaching of
 

antimony is low. Low concentrations of antimony found in groundwater beneath
 

precipitator ash ponds lend field confirmation to the laboratory results (Van
 

der Sloot et al. 1982).
 

When saline sediment is oxidized, such as when dredged sediment is
 

exposed to oxygen, the pH can become very low (pH 3.1 in a lab experiment),
 

and antimony and other toxic metals may be released (DeLaune and Smith 1985).
 
82
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

This occurs because sediments in estuaries often contain pyrite and other
 

readily oxidizable sulfur compounds; sulfuric acid may be produced and
 

overwhelm the buffering capacity of the sediment. An analogous pH decrease
 

following oxidation was not observed in a freshwater sediment.
 

Antimony does not appear to bioconcentrate appreciably in fish and
 

aquatic organisms. No detectable bioconcentration occurred during a 28-day
 

test in bluegills (EPA 1980). Only low levels of antimony have been reported
 

in fish and aquatic organisms collected off the coast of Africa, Australia,
 

and the Danube River in Austria (Callahan et al. 1978; Maher 1986).
 

Bioconcentration factors for antimony ranged from 0.15 to 390 (Acquire 1989;
 

Callahan 1978). A study of the distribution of antimony around a smelter site
 

indicated that antimony occurring in plants results from surface deposition.
 

Uptake from soil is minor and appears to be correlated with the amount of
 

available antimony (that which is soluble or easily exchangeable) (Ainsworth
 

1988). Antimony bioconcentration was measured in voles, shrews, rabbits, and
 

invertebrates around a smelter. Analysis of antimony in organs of the small
 

mammals, compared with estimates of their antimony intake from food, showed
 

that, although the amount of antimony in the organs was elevated, it was low
 

compared to the amount ingested. The results suggest that antimony does not
 

biomagnify from lower to higher trophic levels in the food chain.
 

5.3.2 Transformation and Degradation
 

5.3.2.1 Air
 

Little is known about the chemical forms and physical and chemical
 

transformations of trace elements in the atmosphere. This is primarily
 

because analytical methods provide information concerning the metal content
 

rather than the specific compounds or species. Studies at an antimony smelter
 

suggest that emissions consist of antimony oxide (Ainsworth 1988). In the
 

absence of specific information, it is generally assumed that elements of
 

anthropogenic origin, especially those emanating from combustion sources, are
 

present as the oxide. Windblown dust particles may contain antimony in mineral
 

species, such as sulfides and oxides, and are associated with silicates.
 

When released into the atmosphere as an aerosol, antimony is believed to
 

be oxidized to antimony trioxide by reaction with atmospheric oxidants.
 

Antimony trioxide particles do not undergo changes in chemical composition,
 

particle size, or morphology after emission; however, a surface coating of
 

sulfate may form (Ainsworth 1988).
 

5.3.2.2 Water
 

There is relatively little information available regarding the behavior
 

of antimony in the aquatic environment. Since the dissolved state is the phase
 

in which transfers to suspended matter, organisms, and sediment occur,
 
83
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

it is especially important to know the oxidation state and forms of the
 

antimony that is dissolved. This is particularly difficult for antimony
 

because the levels of total antimony in water are so low. Thermodynamically,
 

most dissolved antimony in natural waters under aerobic conditions should be
 

present in the +5 oxidation state as antimonate species. At 0.001 M total
 

antimony, the dominant species were Sb(OH)6 ̄ and Sb(OH)5 

0

 (Rai et al. 1984). A
 

small quantity of polymeric hydroxy species were found, but these will be less
 

significant when the total antimony concentration is low, such as in natural
 

water. While industrial inputs will commonly contain antimony in the +3
 

oxidation state (e.g., antimony trioxide), it is not known how fast antimonite
 

would oxidize to antimonate under natural conditions. Under reducing
 

conditions, trivalent species such as Sb(OH) 0

, Sb(OH)  ̄ , and Sb S 4-

3 4 2 4
 may be


significant (Andreae and Froelich 1984; Rai et al. 1984).
 

Antimony compounds may undergo photochemical reactions, but these do not
 

appear to be significant in determining their aquatic fate (Callahan et al.
 

1978). Antimony trioxide suspensions strongly absorb ultraviolet radiation
 

below 325 nm and darken. The process is reversible, and when the light is
 

removed, the white color slowly returns (Markham et al. 1958). The effect is
 

believed to be due to peroxide radical formation on the crystal surface. Both
 

water and oxygen seem to be necessary for the reoxidation of the reduced
 

antimony.
 

Antimony can be reduced and methylated by microorganisms in the aquatic
 

environment, similar to arsenic, and become mobilized (Andreae et al. 1983;
 

Austin and Millward 1988). This reaction is most likely to occur in reducing
 

environments, such as in bed sediment. In the case of arsenic, this reaction
 

may be mediated by fungi and bacteria (Beijer and Jernelov 1986), but it is
 

not known whether this is the case with antimony. The resulting
 

trimethylstibine is initially oxidized by atmospheric oxygen to a mixture of
 

trimethylstilbine oxide ((CH3 3 ) SbOH) and trimethylstibinic acid ((CH3 2 3
 ) SbO H),


and then to antimony oxides and insoluble polymers (Parris and Brinckman
 

1976). The rate constant is estimated to be of the order of 0.1 to 0.2 L/molsec. Trimethylstibine has a high vapor pressure, 103 mmHg at 25oC, and might
 

volatilize before it is completely oxidized. The oxidation product, (CH3)3SbO,
 

is much more soluble than trimethylstibine; therefore, oxidation will reduce
 

volatilization (Callahan et al. 1978). Oxidation of
 

trimethylstibine in the gas phase is very rapid; the rate is 0.11/mmHg-sec or
 

2000 L/mol-sec. Trimethylstibine has been shown to react with alkyl iodides
 

and bromides; this results in the formation of quaternary salts (Parris and
 

Brinckman 1975). Should antimony occur in a landfill with alkyl halides, the
 

formation of quaternary salts should greatly enhance antimony's mobility.
 

The chemical and biochemical transformations of antimony in natural
 

waters are not well understood. There are only a few studies that describe the
 

antimony species present in various systems and their transformations. A study
 

of the waters of the Ochlockonee River estuary revealed the presence of
 

Sb(III), Sb(V), methylstibonic acid, and dimethylstibonic acid (Andreae 1983).
 
84
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

The concentration of all four species increased with the salinity of the
 

water. For freshwater, the concentrations were about 18, 3.3, and 1 ng
 

antimony/L (ppt) for Sb(V), Sb(III), and methylstibonic acid, respectively;
 

dimethylstibonic acid was not detectable. The concentration of Sb(V) and
 

Sb(II1) increased linearly with salinity, reaching 135 and 11 ppt,
 

respectively, in the ocean. An analogous increase in the level of the
 

methylated forms with salinity was nonlinear, suggesting that these forms are
 

consumed in the estuary. In seawater, levels of methylstibonic acid and
 

dimethylstibonic acid were 12.5 and 1.5 ng antimony/L (ppt), respectively. It
 

was reported that the Sb(III) levels were approximately 2% that of Sb(V) in
 

samples of sea water and river water (Mok and Wai 1987). In a sample of river
 

water from the Kellogg mining district in Idaho, the contribution of Sb(III)
 

was only 0.4% (0.03 ppb compared with 7.03 ppb of Sb(V)). More recent studies
 

in Idaho indicated that 1-4% of antimony was in the trivalent form in a river
 

receiving mining leachate, while at a site on an unpolluted fork of the same
 

river, the fraction was 17% (Mok and Wai 1990).
 

The depth profile of antimony species in the Baltic sea showed that
 

Sb(V) was the most abundant species in the oxic zone, although Sb(III) was
 

detectable throughout the water column (Andreae and Froelich 1984). A maximum
 

for Sb(III) in the oxic zone was sometimes noted in the surface layer and is
 

believed to result from biological activity. There is evidence that
 

phytoplankton can reduce Sb(V) to the Sb(III). Sb(III) decreases to very low
 

levels at the base of the seasonal thermocline and remains low down to the
 

sediment where increasing levels are again observed. Sb(III) only accounts
 

for 44% of the inorganic antimony in the anoxic zone, and speciation in this
 

region is unclear. Thermodynamically, the antimony should be in the trivalent
 

state. Thiocomplexes are thought to account for some of the antimony in this
 

zone. Methylated antimony species existed throughout the water column and made
 

up 10% of total antimony. Monomethyl antimony species were more abundant in
 

surface waters and in the anoxic zone. There was no sharp increase in methyl
 

antimony near the sediment, which would be expected if these species were
 

formed biosynthetically. Since the highest antimony concentration is at
 

the surface, it is unlikely that antimony is taken up by phytoplankton, as is
 

the case with arsenic. A decrease in antimony concentration with depth
 

suggests scavenging by particulate matter and, at lower depths, by iron
 

hydroxyoxides.
 

Sea water samples off the Belgian coast were analyzed using oxidation,
 

UV irradiation, and anodic stripping voltammetry to distinguish bound antimony
 

and to identify its oxidation state (Gillian and Brihaye 1985). The
 

concentration of total antimony ranged from 0.05 to 0.38 ppb. The study showed
 

that antimony was mainly present as Sb(V), and the percentage complexed to
 

organic matter varied between 20% and 60%. This results is surprising because
 

antimony occurs as anionic species in water and these are not expected to
 

complex with organic matter. These results have not been confirmed by other
 

investigators. The concentration of Sb(II1) was below the detection
 

limit (0.005 ppb) at almost all sites. The exception was the coastal sites
 
85
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

where it ranged up to 0.039 ppb. Antimony found in rain and snow is
 

predominantly in the +5 oxidation state (Metzger and Braun 1986).
 

Information concerning the behavior of antimony in sediment is extremely
 

limited. Investigators would like to know how strongly antimony is bound in
 

sediment and what the potential is for long-term mobilization. A study was
 

conducted of sediments in Puget Sound, Washington, where a copper smelter
 

discharges large amounts of antimony (Crecelius et al. 1975). In 23
 

noncontaminated sediment samples, antimony concentrations correlated with
 

organic carbon and fine-grained particles; however, since these sediments are
 

also associated with hydrous-iron oxides, further investigations on the
 

association of antimony in sediment were conducted and showed that less than
 

10% of the antimony in both contaminated and uncontaminated sediment was bound
 

to readily oxidizable organic matter. Extraction with oxalate and
 

citratedithionite-bicarbonate suggested that roughly half of the antimony in
 

uncontaminated sediment and less than 20% of that in contaminated sediment was
 

bound to extractable iron or aluminum compounds. Most of the antimony in the
 

polluted water was bound to chemically stable slag.
 

Experiments were performed in which the forms of antimony in sediment
 

were evaluated after the sediment was incubated under anaerobic conditions for
 

45 days (Brannon and Patrick 1985). Ten dredged, contaminated sediments that
 

were obtained from various locations in the United States were used as is or
 

amended with 75 ppm antimony potassium tartrate. An extraction procedure was
 

used that identified the antimony in interstitial water and in "exchangeable,"
 

"easily reducible," and "moderately reducible" sediment fractions. Essentially
 

all antimony in the unamended sediment was in a "moderately reducible" phase
 

(oxalate extraction). The same was generally true for 7 of the 10 sediments
 

that were amended with potassium antimony tartrate. In the other three
 

sediments, the greatest proportion of antimony was in the "easily reducible"
 

fraction. A small fraction of the antimony-amended sediment (but none of the
 

unamended sediment) was contained in the more potentially mobile interstitial
 

water and "exchangeable" fraction. It should be stressed that since the
 

amended samples had higher antimony levels, small percentages in
 

different fractions were more readily detectable than for the unaziended
 

sediment. The high correlation of antimony with the "moderately reducible"
 

fraction indicates that hydrous iron and aluminum oxides were affecting the
 

fixation of antimony. These hydrous oxides are positively charged under
 

environmental conditions and bind the anionic antimony. The samples were
 

subjected to 6 months of aerobic leaching. Unamended samples released antimony
 

very slowly, compared with amended samples, indicating the higher amounts of
 

mobile antimony in the latter samples. Antimony-amended sediments lost from
 

3.6% to 32% of their antimony during leaching; unamended sediments lost from
 

0% to 23% of their antimony. The sediment/water distribution coefficient
 

ranged from 3.3 to 27.5 in amended sediments, compared with values
 

up to 1,183 in unamended sediments. The distribution coefficient correlated
 

with iron in both amended and unamended sediment; additionally, it correlated
 

with calcium carbonate in amended sediment. After aerobic leaching, there was
 
86
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

an increase in antimony in the "moderately reducible" phase and a decrease in
 

the "easily reducible" phase that paralleled changes in iron concentrations.
 

Volatile antimony compounds were formed in seven of the amended sediments but
 

in none of the unamended sediments; they escaped through the overlying water
 

independently of the redox state of the water (i.e., aerobic or anaerobic).
 

When 10 and 100 ppm antimony trioxide with added nutrients was incubated
 

with natural bottom sediment from Puget Sound under aerobic or anaerobic
 

conditions for up to 120 days, three organoantimony biotransformation products
 

were found in solution after 60 days (Martinson 1988). Two of these were
 

identified as methylstibonic acid and dimethylstibonic acid. No determination
 

of rate or conditions affecting the transformation was made. However, it was
 

estimated that much less than 0.1% of the antimony present was transformed.
 

Few data are available on the removal of antimony in the activated
 

sludge process used in water treatment plants. In one laboratory simulation,
 

mixture of metals at levels considered typical of industrial/domestic sewage
 

(0.1 ppm antimony) was continuously added to the influent of the treatment
 

system. No antimony removal was observed (Kempton et al. 1983).
 

5.3.2.3 Soil
 

Little is known about the behavior of antimony on soil during
 

weathering. In aerobic surface soils, oxidation generally occurs. Antimony
 

trisulfide in ore deposits is known to be oxidized by soil bacteria (Ainsworth
 

1988). Methylated antimony compounds, similar to those formed in sediment, may
 

be formed in waterlogged soil.
 

The form and availability of antimony in soil is determined by measuring
 

antimony's extractability with different solvents. A sequential extraction
 

procedure was used to determine the form of antimony in soil around a stibnite
 

smelter and to compare it with that found at a control site (Ainsworth 1988).
 

The extraction procedure used could identify the following fractions of
 

antimony: soluble or bound to ion-exchange sites and, therefore, available;
 

bound to carbonates; bound to manganese oxides that are easily reduced; bound
 

to iron oxides that are less easily reduced; bound to organic matter; and
 

residual antimony that was not incorporated into silicates (Ainsworth 1988).
 

Results of the study showed that the distribution pattern among the various
 

fractions was different at the smelter and control sites. Three quarters of
 

the total extracted antimony in surface (0-5 cm) soil near the smelter was in
 

the residual fraction; none of the antimony in the control site was in this
 

fraction. The remainder of antimony in soil from the smelter site was more or
 

less equally distributed among the other fractions. Higher proportions of the
 

antimony at the control site were in the readily available fraction, bound to
 

manganese oxides, or complexed with organic matter, compared to the smelter
 

site. Because of the low concentration of antimony in the control-site soil,
 

fractional determinations are less accurate than for sites near the smelter.
 

For subsoil (greater than 15 cm depth) from the smelter site, less antimony
 
87
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

was found in the residual fraction (62%), and more antimony was in the
 

available fraction, bound to carbonates, or bound to iron oxides than in the
 

surface sample. The factors determining the distribution of antimony between
 

fractions is unclear. The absence of any residual fraction at the control site
 

has been explained by assuming that antimony-containing mineral has been
 

completely broken down.
 

Near the smelter, antimony deposits have a different character than
 

further away since they are derived from fugitive emissions rather than stack
 

deposition. In a 3-month study of deposition of antimony from the smelter,
 

about one-third to one-half of the deposited antimony at the smelter site was
 

soluble, compared with about one-half to two-thirds at other sites. Since
 

antimony in rain near the smelter site was soluble, it appears that once
 

deposited on soil, antimony rapidly converts to more insoluble forms.
 

5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT
 

5.4.1 Air
 

There are insufficient data regarding antimony concentrations in the
 

atmosphere for representative general mean or median concentrations to be
 

reported. Antimony concentrations in air particulate matter in remote, rural,
 

and U.S. urban areas are 0.00045-1.19, 0.6-7, and 0.5-171 ng/m3

, respectively
 

(Austin and Millward 1988; Schroeder et al. 1987). No vapor-phase antimony has
 

been reported. Antimony concentrations over the North Atlantic and North
 

Pacific are 0.086 and 0.0037 ng/m3

, respectively (Arimoto and Duce 1987;
 

Austin and Millward 1988). Two values reported for antimony in aerosols in
 

clean continental and marine environments are 0.2 ng/m3

 at the Jungfraujoch in
 

the Swiss Alps and 0.00045 ng/m3

 at American Samoa (Austin and Millward 1988).
 

The mass median aerodynamic diameter of antimony-containing aerosols from a
 

range of areas remote from anthropogenic sources was 0.86 μm (Milford and 

Davidson 1985). The mass size distribution is bimodal, with the larger peak at 

about 0.6 μm and a smaller one at about 3 μm. An example of the size 

distribution of antimony-containing particles removed from anthropogenic 

sources was obtained in an 8-week study on an island in the German Bight. The 

concentration of antimony in a size fraction increased as the size decreased. 

The antimony concentration ranged from 0.03 ng/m3

 for particles greater than 

7.2 μm to 0.3 ng/m3

 for particles less than 0.5 μm (Stoessel and Michaelis 

1986). 

Several studies show that antimony can travel long distances, and that
 

ambient levels may reflect the origin of the air masses. The geometric mean
 

antimony concentration in aerosols at three rural/remote locations in New York
 

state was 1.0, 0.72, and 0.33 ng/m3

 (Dutkiewicz et al. 1987), and the
 

enrichment over crustal abundance ranged from 920 to 1,650. The enrichment
 

factor is smaller but similar to the mean enrichment factor of 1,880 for
 

antimony in 29 cities (Gladney et al. 1984). The high enrichment indicates
 

that the antimony is of anthropogenic origin. An analysis of the New York
 
88
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

State data using backward-in-time air trajectories is consistent for the
 

Midwest being the dominant source of antimony. An analysis of European sources
 

and wind trajectories further illustrate that antimony may be transmitted over
 

long distances. The average concentration at a city in southern Norway was
 

0.54 ng/m3

 when the air masses came from the United Kingdom, and 0.07 ng/m3
 

when they came from over the Atlantic (Hillamo et al. 1988).
 

Twenty-four-hour samples collected at 10 locations in Washington, D.C.,
 

yielded average antimony concentrations ranging from 1.1 to 3.0 ng/m3
 

(Kowalczyk et al. 1982). As a result of a chemical element balance analysis,
 

the three major contributing sources in order of decreasing significance are
 

believed to be refuse incineration, motor vehicles, and coal combustion. In a
 

Houston study, the range of antimony concentrations in fine (0.1-2.5 μm) 

aerosols was 0-12 ng/m3

, whereas that in particles greater than 2.5 μm was 0-4 

ng/m3

 (Johnson et al. 1984). Median, mean, and maximum concentrations of 

antimony in aerosols at three sites in Quebec, Ontario, and Nova Scotia were 

0.05-0.10, 0.11-0.23, and 0.37-2.17 ng/m3

, respectively (Hopper and Barrie 

1988). According to the Texas Air Control Board, the first- and secondhighest 

annual average antimony concentration in Texas between 1978 and 1982 was 452 

and 50 ng/m3 at Laredo and Dallas, respectively. The statewide 1978-1982 

average was below the minimum detectible mean of 90 mg/m3

 (Wiersema et al. 

1984). 

Concentrations of antimony in 24-hour air samples at Kellogg, Idaho,
 

which is the site of a large and active nonferrous metal industry, ranged from
 

5.21 to 1,210 ng/m3

 with a mean of 146 ng/m3 (Ragaini et al. 1977). Air
 

particulate matter in Tacoma, Washington, 40 km downwind of a copper smelter
 

often have antimony concentrations in excess of 300 ppm (Crecelius et al.
 

1974). The 6-month average concentration of antimony in air in an industrial
 

area of England where a number of ferrous and nonferrous metal smelting and
 

manufacturing works were concentrated was 40 ng/m3

. This is a factor of 50
 

higher than that found in rural areas (Pattenden et al. 1982). Antimony was
 

reported in air at one site on the NPL (View 1989). The maximum concentration
 

at the site was 69 ng/m3

.
 

The mean monthly concentration of antimony in precipitation at Birkenes
 

in southern Norway ranged from 0.2 to 2.3 ppb with a mean of 0.6 ppb (Pacyna
 

et al. 1984). During the same period, the respective air concentrations were
 

0.19-0.80 and 0.43 ng/m3

. Rain samples were collected during two storms upwind
 

and downwind of a copper smelter in Tacoma, Washington. Antimony in rainwater
 

originated primarily from the smelter. The mean total antimony concentration
 

in rainwater downwind from the smelter was 1.3 ppb; the concentration upwind
 

was 0.03 ppb (Vong et al. 1988). Eighty percent of the antimony in rainwater
 

was dissolved (i.e., passed through a 0.45 μm filter). 

Antimony is almost entirely found in the particulate, as opposed to the
 

dissolved fraction of snow (Landsberger et al. 1983). The antimony content of
 
89
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

snow particulate matter in samples from Montreal, Canada, ranged from
 

4 to 145 ppm. A more recent sampling of snow around Montreal found total
 

antimony concentrations of l-8.7 ppb and enrichment factors of 39-590
 

(Zikovsky and Badillo 1987).
 

Antimony is a component of ammunition, and studies have been performed
 

to ascertain the elemental concentrations of antimony in the air of indoor
 

shooting ranges. Antimony might be expected in such situations because it is
 

alloyed with lead in bullets, and lead stibnite and antimony sulfides are used
 

as primers (Dams et al. 1988). After an intensive 3-hour shooting exercise,
 

levels of antimony reached 119 μg/m3

 or four orders of magnitude over ambient 

levels (Vandecasteele et al. 1988). An instructor at the shooting range had a 

time-weighted average (TWA) inhalable antimony concentration of 12.0 μg/m3

, 

compared with the threshold limit value (TLV) of 500 μg/m3

. An American study 

conducted at the National Guard Armory in Washington, D.C., during 

routine daytime and gun club use, had antimony concentrations ranging from 57 

to 216 μg/m3

 versus background air ranging from 1.5 to 2.3 μg/m3, an enrichment 

of 9,900 over District of Columbia air) (Olmez et al. 1985). More than 60% of 

the antimony was associated with respirable particles with an aerodynamic 

diameter less than 3.5 pm. 

5.4.2 Water
 

Antimony has a low occurrence in ambient waters, and there are few
 

monitoring data with which one can establish a mean value of antimony in
 

surface waters. Eckel and Jacob (1989) gathered water monitoring data from the
 

Water Resources Division of the U.S. Geological Survey covering the period
 

from about 1960 to September, 1988, and found that all but 70 of 1,077 entries
 

for dissolved antimony were below 5 ppb, which was the probable detection
 

limit. The geometric mean and standard deviation of the 70 values above 5 ppb
 

were 12 and 1.93 ppb, respectively. By applying a technique known as
 

censoring, and assuming a log normal distribution for the monitoring data,
 

these investigators determined the population geometric mean and standard
 

deviation for antimony to be 0.25 and 7.16 ppb, respectively. The
 

concentration of dissolved antimony in other rivers reported in the literature
 

include: St. Lawrence River at Massena, New York, 1.62 nM (0.197 ppb); Yukon
 

River 2.73 nM (0.332 ppb); and European rivers less than 0.03-4.43 nM (0.004­

0.539 ppb) (Andreae and Froelich 1984). Few rivers have dissolved antimony
 

concentrations below 1 nM (0.120 ppb) (Andreae and Froelich 1984).
 

The major antimony mining area in the United States was the Kellogg
 

district in northern Idaho, and mining and smelting wastes have been dumped
 

into the South Fork of the Coeur d'Alene River for over 80 years (Mok and Wai
 

1990). The South Fork joins with the North Fork of the river to form the Main
 

Stem of the Coeur d'hlene River somewhat below Kellogg. Mean and maximum total
 

dissolved antimony concentrations at two sites on the South Fork are 4.3 and
 

8.2 ppb, respectively. Mean and maximum concentration at six stations on the
 

Main Stem ranged from 0.6 to 1.0 and 0.8 to 1.9 ppb, respectively.
 
90
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Those at a station on the unpolluted North Fork were 0.09 and 0.2 ppb,
 

respectively.
 

The concentration of dissolved antimony in a polluted estuary in
 

Portugal was found to increase with salinity up to 30 parts per thousand and
 

then rapidly decrease (Andreae et al. 1983). The total antimony content of
 

seawater samples off the Belgian coast ranged from 0.05 to 0.38 ppb (Gillain
 

and Brihaye 1985). Filtered and unfiltered coastal marine waters from the
 

North Adriatic contained 0.31 and 45 ppb, respectively (Strohal et al. 1975).
 

Little information is available concerning the concentration of antimony
 

in groundwater. The range of antimony concentrations reported for antimony in
 

groundwater in Switzerland (0.3-1.0 ppb) was essentially the same as that
 

reported for the nearby Glatt River (0.5-1.2 ppb) (von Gunten and Ku11 1986).
 

The concentration of antimony in groundwater under four retention-recharge
 

basins receiving urban runoff water in Fresno, California, were all less than
 

the 1 ppb detection limit (Nightingale 1987).
 

Antimony was found in 5.7% and 8.5% of surface waters and groundwaters
 

at hazardous waste sites on the CLPSD (CLPSD 1989). The geometric means of
 

antimony found in positive samples of these media were 40 and 50 ppb,
 

respectively (CLPSD 1989). The CLPSD includes both NPL and non-NPL sites.
 

Since antimony is used in solder, there has been interest as to whether
 

antimony will leach from pipes soldered with antimony-containing solder into
 

drinking water. Leaching of antimony from tin/antimony (Sn/Sb) solder when it
 

comes in contact with water with pH of 5.2-8.6 was evaluated using loops of
 

pipe containing 20 solder joints (Murrell 1987). Antimony was undetectable
 

(less than 4 ppb) in the water at first, but rose to 10 ppb after 4 days and
 

68 ppb (at pH 7.4) after 4 weeks. A study was conducted at the University of
 

Washington to evaluate the potential for leaching of metals into drinking
 

water from 95/5 Sn/Sb solder (Herrera et al. 1982). After a series of static
 

and continuous-flow laboratory tests and evaluation of field samples from
 

university buildings, it was concluded that increases in antimony
 

concentration as a result of corrosion and leaching were minimal and would not
 

contribute significantly to dietary antimony intake. Only one of the field
 

samples of standing water from university buildings containing Sn/Sb solder
 

joints was above the detection limit of 0.6 ppb. The sample contained 2 ppb of
 

antimony, one-half of which was dissolved. Examination of the solder joints
 

indicated that a double passivation film of tin monoxide (SnO) and tin dioxide
 

(SnO2) forms and inhibits leaching.
 

Sediment is a significant sink for antimony. No information was found on
 

the levels of antimony in pristine sediment. Background antimony
 

concentrations in sediment cores from open water of Lake St. Clair ranged from
 

0.032 to 0.098 ppm with a mean concentration of 0.061 and 0.068 ppm in sand
 

and silty-clay sediment, respectively (Rossmann 1988). The range of antimony
 

levels in 10 sediments obtained from all over the United States by workers
 
91
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

engaged in research on contaminated, dredged sediment was 0.5-17.5 ppm, and
 

the median concentration was 2.9 ppm (Brannon and Patrick 1985). Sediment
 

samples taken from Puget Sound in Washington (the site of a copper smelter)
 

were analyzed for antimony. This was the only known anthropogenic source of
 

antimony in the area. While the antimony concentration in sediment from
 

noncontaminated areas ranged from 0.3 to 1.0 ppm, these levels rose to 2-3
 

times background within 8-15 km of the smelter, and up to 12,500 ppm within 1
 

km of the smelter where considerable amounts of slag were dumped (Crecelius et
 

al. 1975). One hundred and seven core samples of sediment were collected in
 

the delta area of the Coeur d'Alene river in northern Idaho, a primary
 

antimony mining and smelting area in the United States. The sediment was
 

mostly fine silt, which is typical of mine tailings. The top layer of sediment
 

contained 270-900 ppm of antimony with a mean of 512 ppm (Maxfield et al.
 

1974). More recent monitoring data reported antimony concentrations in
 

sediment of 137, 49-72, and 1.9 ppm on the South Fork, Main Stem, and North
 

Fork of the Coeur d'Alene River, respectively (Mok and Wai 1990). The South
 

Fork receives mining and smelting wastes, and the North Fork is essentially
 

uncontaminated. A sediment profile on one sample showed that the antimony
 

concentration decreased with depth and was between 2 and 3 ppm between 8.5 and
 

21.5 cm depth.
 

5.4.3 Soil
 

A survey of soils throughout the conterminous United States conducted by
 

the U.S. Geological Survey showed that antimony concentrations ranged from
 

less than 1 to 8.8 ppm with an average concentration of 0.48 ppm. This was the
 

third lowest concentration of the 50 elements surveyed (Shacklette and
 

Boerngen 1984). In this survey, samples were taken at a depth of 20 cm at
 

1,318 sampling sites. Soils not derived from ore-bearing rock or close to
 

industrial sources do not generally contain more than 1 ppm of antimony.
 

Antimony concentrations in igneous rock, shales, limestone, and sandstone have
 

been reported to be 0.2, 1.5, 0.2, and 0.05 ppm, respectively (Ainsworth
 

1988). Antimony concentrations in 57 sludge-treated soils in an agricultural
 

area west of Toronto in Ontario, Canada, ranged from 0.16 to 0.37 ppm (dry
 

weight) (Webber and Shamess 1987).
 

A study of the effects of an antimony smelter on soil found that
 

antimony levels exceeding 50 ppm were found only within 2 km of the smelter
 

(Ainsworth 1988); the background antimony concentration was 6.9 ppm. Antimony
 

concentrations in surface soil near the Kellogg Valley, Idaho, the site of one
 

of the nation's largest and richest mining districts, were considerably
 

elevated at seven contaminated sites, with mean and maximum levels of 111 and
 

260 ppm, respectively (Ragaini et al. 1977). These values represent an
 

enrichment of 1,000 or more over crustal antimony levels. The concentration
 

profiles in core samples sharply decreased with depth. This indicates that the
 

antimony contamination resulted from air deposition. Soil samples taken in
 

Tacoma, Washington, 40 km downwind of a copper smelter, often
 
92
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

had antimony concentrations in the range of 11-109 ppm (dry weight). Natural
 

levels are believed to be 3-5 ppm (Crecelius et al. 1974).
 

The range of maximum antimony concentration in soil at sites on the NPL
 

was 0.084-2,550 ppm (View 1989). The geometric mean and the maximum
 

concentration of antimony found in soil at hazardous waste sites on the CLPSD
 

is 8.0 and 330 ppm, respectively (Eckel and Langley 1988). Thirteen percent of
 

sites on an updated version of CLPSD contain antimony in soil (CLPSD 1989).
 

The geometric mean of positive samples is 17 ppm. The CLPSD includes both NPL
 

and non-NPL sites. The concentration of antimony in surface soil at the Sapp
 

Battery Superfund site in northern Florida, which housed a facility for
 

recovering lead from auto batteries from 1970 to 1980, ranged from 0.46 to
 

857.0 ppm (Trnovsky et al. 1988).
 

A New Zealand study showed that the mean level of antimony in street
 

dust was comparable to that in soil (4.69 ppm versus 5.94 ppm) (Fergusson et
 

al. 1986). The antimony content of household dust, however, was enriched
 

approximately two-fold to 10.0 ppm.
 

5.4.4 Other Environmental Media
 

A determination of nutrients in a human diet was conducted by the U.S.
 

Food and Drug Administration (FDA) using mixed diet composites representative
 

of the intake of a 25- to 30-year-old U.S. male. The average concentration of
 

antimony in the diet was 9.3 ppb (dry weight). This corresponds to a daily
 

dietary intake of 4.6 μg of antimony assuming a 3,075 g diet/day (wet weight 

with a total dry matter of 16.2%) (Iyengar et al. 1987). Another study of 

antimony in food using a highly sensitive neutron activation procedure found 

that the average antimony concentration in 12 table-ready foods ranged from 

0.22 to 2.81 ppb (Cunningham 1987). The food items used in the study were
 

primarily prepared for FDA's Total Diet Studies program in Kansas City and
 

included meats, vegetables, and seafood. The mean concentration ranges of
 

antimony in meats, seafoods, and vegetables were 0.46-1.15, 0.22-1.81, and
 

1.09-2.81 ppb, respectively. The results of an earlier investigation of trace
 

elements in food in an FDA basket survey reported that median levels of
 

antimony in eight food groups were less than 10 ppb (wet weight) (Tanner and
 

Friedman 1977). In a separate study, the concentration of antimony in pooled
 

human milk was 13 ppb (dry weight) (Iyengar et al. 1982).
 

In a comprehensive survey of the presence of heavy metals in sewage
 

sludge, 30 sludge samples from 23 American cities were analyzed (Mumma et al.
 

1984). The antimony concentration in the sludge samples ranged from 1.3 to
 

55.7 ppm (dry weight) and had a median value of 7.35 ppm. The highest
 

concentration of antimony was in a sludge sample from Baltimore. This level
 

was more than double that of the second highest sludge sample analyzed. In
 

comparison with the above values, the concentration of antimony in cow manure
 

was 0.43 ppm.
 
93
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

The concentration of antimony in grass from representative sites in the
 

Kellogg Valley, Idaho (the site of the heavy-metal industry), ranged from 6.2
 

to 111 ppm. Grass from background sites in the valley that were located 3.3
 

and 7.8 miles from a smelter contained from 3.5 to 4.5 ppm of antimony
 

(Ragaini et al. 1977). Similar results were found around an antimony smelter
 

in England. The antimony content of grass close to the smelter was 50-300 ppm.
 

The content at control sites ranged from 0.1 to 0.3 ppm (Ainsworth 1988). In
 

comparison with the above values, the concentration of antimony in forage
 

crops was about 0.1 ppm (Ragaini et al. 1977).
 

Concentrations of antimony in selected species of algae, mollusc tissue,
 

crustacean tissue, and fish muscle from southeastern Australia were 0.094­

0.193, 0.031-0.060, 0.018-0.116, and less than 0.009-0.010 ppm (dry weight),
 

respectively. The water collected at the site contained 0.17 ppm of antimony
 

(Maher 1986).
 

A French study of the metallic content in soaps, shampoos, body oils,
 

and cosmetics found that of all products tested only lacquer contained
 

significant amounts of antimony (1.7 ppm) (Demanze et al. 1984). Antimony was
 

found in high concentrations in certain composite resins used in dentistry.
 

Two materials analyzed in England had mean antimony levels of 288 and 403 ppm
 

(Molokhia and Lilley 1986).
 

5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE
 

Antimony occurs naturally in the earth's crust, and the general
 

population is exposed to low levels of antimony in ambient air and food. The
 

average daily intake of antimony from food or water was estimated at 100
 

μg/day (Wiersema et al. 1984). According to the recent results of Iyengar 

(1987), the average daily dietary intake is 4.6 μg, ,and, because of the low 

antimony levels in water, the average daily intake of antimony (by ingestion) 

is probably not much greater than 5 pg. Laredo, Texas, has the highest annual 

average concentration of antimony in ambient air (452 ng/m3

). If a person is 

assumed to inhale 20 m3 of air/day, this would amount to an average antimony 

intake of 9.0 μg/day. For a city such as Washington, D.C. (average antimony 

concentration about 2 ng/m3

), the inhalation intake would be 0.04 μg/day. Only 

in an extreme situation would the amount of antimony inhaled compare to the
 

amount that is ingested; the amount inhaled is generally much less. Those
 

people who reside near industrial sources of antimony such as smelters,
 

coalfired power plants, and refuse incinerators are exposed to higher levels
 

of atmospheric antimony. People who spend time in shooting galleries are also
 

exposed to higher antimony levels.
 

EPA does not believe that the antimony found in such consumer products
 

as car batteries and flame retardants in plastics and textiles results in
 

significant consumer exposure (EPA 1983a). When antimony oxide is used as a
 

fire retardant, it is tightly bound into the material; release and subsequent
 

exposure during use is unlikely (EPA 1983a). No antimony leached from several
 
94
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

glass containers used for injectable solutions into distilled water, saline,
 

sodium bicarbonate solution, or hydrochloric acid (Pradeau et al. 1988). This
 

glass contained up to 5 ppm of antimony, and the detection limit for the
 

analytical procedure was 10 ppb. In another study, no antimony was detected in
 

water (pH 3, 7, or 10) kept in a canteen for 24 hours (Augustson 1976).
 

A National Occupational Exposure Survey (NOES) conducted by NIOSH from
 

1981 to 1983 estimated that 373,460 workers were potentially exposed to
 

antimony (molecular formula unknown) in the United States in 1981-1983 (NIOSH
 

1989). The number of workers exposed to antimony trioxide, antimony sulfide,
 

antimony oxide, antimony pentoxide, antimony dialkyldithiocarbamate, and other
 

antimony compounds is estimated to be 226,645. The total estimated number of
 

workers exposed to antimony and all of its compounds is 486,347. Since all of
 

the data for trade-name products that may contain antimony have not been
 

analyzed, this estimate is preliminary. The NOES was based on field surveys of
 

4,490 facilities. It was designed as a nationwide survey based on a
 

statistical sample of virtually all workplace environments in the United
 

States where eight or more persons are employed in all standard industrial
 

codes (SIC) except mining and agriculture. The NOES database does not contain
 

information on the frequency, concentration, or duration of exposure of
 

workers to any of the chemicals listed therein. These surveys provide only
 

estimates of the number of workers potentially exposed to chemicals in the
 

workplace. EPA states that the NOES figures substantially overestimate
 

occupational exposure to antimony and compounds (EPA 1983a). Most antimony in
 

this country is either smelted from imported ore or impure metallic antimony
 

or recycled from antimony scrap. According to EPA, "mining, hauling, and
 

crushing of ore will be of minor consequence," because ore crushing is done in
 

closed systems, and ore processing is done under wet conditions to minimize
 

dust (EPA 1983a). Following a membership survey, the Antimony Oxide Industry
 

Association (AOIA) reported that 230-240 production workers and l,000-2,000
 

workers using antimony were exposed to antimony (EPA 1983a). This represented
 

the entire population.of workers potentially exposed to antimonial substances.
 

An independent survey of the three facilities producing and processing
 

antimony metal in 1979 estimated that 2,249 workers were exposed to antimony
 

(EPA 1983a). This estimate included producers and first-level processors of
 

antimony metal into products such as batteries and alloys. Alloys usually
 

contain small amounts of antimony that are most often combined with much
 

larger amounts of lead. Occupational exposure controls that are employed to
 

mitigate lead exposure also protect workers from antimony. Much of the
 

estimated exposure to antimony metal may actually be to antimony oxide; fumes
 

formed when heating the metal (e.g., for carting) are oxidized. The survey
 

also estimated that 1,710-1,880 workers were employed at facilities that
 

manufacture and process antimony trioxide. EPA believes that 200-2,000 workers
 

may be exposed to stibnite, which is used in small quantities in smokes and in
 

priming mixtures for igniting explosives (EPA 1983a). This stibnite is
 

expected to form antimony trioxide during use, and exposure will be primarily
 

to the oxide.
 
95
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

There have not been any systematic and representative surveys of
 

occupational exposure levels to antimony in industry; however, some data are
 

available from walk-through surveys of selected companies conducted by NIOSH
 

and other investigators. In some of these surveys, only a few samples were
 

analyzed. In a facility where antimony oxide was produced from the sulfide
 

ore, breathing-zone samples from five antimony oxide production workers ranged
 

from 0.21 to 3.2 mg antimony/m3

; four of these samples were above 0.5 mg
 

antimony/m3

. Air samples from the bagging area ranged from 0.43 to 0.83 mg
 

antimony/m3

 (Cassady and Etchison 1976). In another facility that produced
 

antimony and antimony oxide from ore, breathing-zone samples from 55 employees
 

ranged from 0.05 to 6.21 mg antimony/m3

, and area air samples ranged from 0.14
 

to 2.12 mg antimony/m3 (Donaldson 1976). The mean exposure for the antimony
 

oxide operation was 2.23 mg/m3

, and this was the highest in the plant. Two
 

personal air samples in a third antimony oxide production facility were 2.7
 

and 5.0 mg antimony/m3

, and general area samples ranged from 1.8 to 5.6 mg
 

antimony/m3

 (Donaldson and Gentry 1975). In a secondary lead smelter where
 

scrap batteries were reclaimed, breathing zone samples in 2 of 21 workers
 

were quantifiable; these TWAs were 0.037 and 0.051 mg/m3

 (Craig et al. 1981).
 

TWA antimony concentrations in the compounding area of a rubber company ranged
 

from 0.01 to 0.15 mg/m3, and the mean in an iron foundry was 0.00015 mg/m3
 

(Salisbury 1980; Zhang et al. 1985). Antimony levels in a glass production
 

facility were 0.005 mg/m3

, and this represents 1% of the NIOSH-recommended
 

maximum level (Burroughs and Horan 1985). Antimony may also be released during
 

injection molding of ignitionresistant polystyrene in which fire retardant
 

additives that contain antimony are used. In one such study, antimony levels
 

ranged from less than the detection limit of 0.0003 to 0.2 mg/m3

 (Willetts et
 

al. 1982).
 

Since antimony trioxide is used in many materials as a fire retardant,
 

it is likely that antimony will be released during fires. Antimony was present
 

in soot and in tracheal specimens of people who perished in fires (Willetts et
 

al. 1982). In 18 cases that were analyzed, soot antimony concentrations ranged
 

from 0.1 to 543 ppm, and 50% of tracheal antimony concentrations exceeded the
 

normal range of 0.1-124.0 ppm. These results indicate that firemen and other
 

people at fires may be exposed to increased antimony levels in smoke.
 

Stibine may be produced in lead-acid battery plants during the formation
 

process (Jones and Gamble 1984). In a study involving five battery plants,
 

stibine concentrations ranged from not detectable to 2.5 mg/m3

. In three other
 

surveys of battery plants, stibine concentrations ranged from not detectable
 

to 0.35 mg/m3

 (Young 1979a), 0.007 mg/m3 (Young 1979b), and 0.031 mg/m3 (Young
 

et al. 1979). Stibine was also reported in a company that manufactured glass
 

for hypodermic syringes at levels up to 0.5 mg/m3 (Burroughs and Horan 1985).
 

Antimony trioxide is used in the glass industry as a refining agent and
 

colorant. In an exposure assessment in the German glass industry, TWA
 
96
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

antimony levels were as high as 0.351 mg/m3

 (Ludersdorf et al. 1987). Urine 

and blood antimony levels of exposed workers were enhanced. The median and 

maximum urine antimony levels in spot urine samples were 1.9 and 15.7 μg/L, 

respectively, compared with 0.4 and 0.7 μg/L for controls. Median and maximum 

blood levels for workers were 1.0 and 3.1 μg/L, respectively, versus 0.3 and 

1.7 μg/L, respectively, for unexposed persons. 

Nail samples from 71 Americans contained an average of 0.41 ppm of
 

antimony. Averages for residents of four other countries ranged from
 

0.28 to 0.70 ppm (Takagi et al. 1988). In an analogous study, the mean
 

concentration of antimony in hair samples from 55 men and women from Scranton,
 

Pennsylvania, contained 0.096 ppm of antimony. The hair samples of populations
 

from cities in four other countries contained mean antimony levels between
 

0.11 and 0.86 ppm (Takagi et al. 1986). These hair levels can also be compared
 

to those in a Japanese national study in which the geometric mean
 

concentration and standard deviation of antimony in washed hair samples from
 

234 healthy individuals were 0.078 and 2.5 ppm, respectively. No significant
 

differences between different sexes or age groups were noted (Ohmori et al.
 

1981). In another Japanese study, hair and nail samples taken from workers at
 

an antimony refinery, nearby residents, and a control group were analyzed
 

before and after washing with a nonionic, surface-active agent in an
 

ultrasonic cleaner (Katayama and Ishide 1987). The concentration of antimony
 

in the nails of the three groups before and after washing was 730, 2.46, 0.19
 

ppm and 230, 0.63, and 0.09 ppm, respectively. The concentration of antimony
 

in the hair of workers before and after washing was 222 and 196 ppm, compared
 

with 0.21 and 0.15 ppm for controls. Exposure to antimony, therefore, greatly
 

increases the antimony levels in nails and hair. The concentration in nails in
 

exposed people is largely surficial.
 

A group of 21 workers from northern Sweden who were employed in
 

nonferrous metal smelting and refining industries had median antimony
 

concentrations‘ in their lungs of 0.30 ppm (wet weight). Controls from an
 

unpolluted area had 0.029 ppm in their lungs (Hewitt 1988). Antimony
 

concentrations in the lung tissues of eight British coal miners ranged from
 

0.19 to 0.59 ppm (dry weight); the levels in two controls were
 

0.47 and 0.62 ppm (Hewitt 1988).
 

5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES
 

In discussing exposure to antimony, it is important to consider what
 

form of antimony a person is exposed to and what is its availability. Such
 

information is seldom available. Although high concentrations of antimony may
 

be found in contaminated soil and sediment, the few studies that have been
 

conducted indicate that much of the antimony may be embedded in a crystalline
 

matrix or bound to hydrated iron, aluminum, and manganese oxides. In water,
 

the pentavalent state is predominant, although significant levels of trivalent
 

antimony and methylated antimony compounds exist. People who live or work near
 

sources of antimony such as smelters, coal-fired power plants, and refuse
 
97
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

incinerators may be exposed to high levels of antimony in airborne dust, soil,
 

and vegetation. People who live near or work at waste sites that receive slag
 

from smelters or fly ash from power plants and refuse incinerators may also be
 

exposed to higher than background levels. Exposure routes would include either
 

inhalation of contaminated air or ingestion of contaminated soil or
 

vegetation. Similarly, people who are exposed to soot and smoke in fires, such
 

as firemen, may be exposed to high levels of antimony. Occupational exposure
 

to antimony appears to be highest for those involved in the production and
 

processing of antimony and antimony oxide. Workers in battery-forming areas of
 

lead-storage battery plants may be exposed to high levels of stibine.
 

5.7 ADEQUACY OF THE DATABASE
 

Section 104(i)(5) of CERCLA as amended 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 antimony 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 antimony.
 

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 Data Needs
 

Physical and Chemical Properties. It is apparent from the physical and
 

chemical properties of antimony and antimony trioxide shown in Table 3-2, that
 

there are discrepancies in the literature values for the boiling points of
 

antimony, antimony trichloride, and antimony trioxide (Freedman et al. 1978;
 

Herbst et al. 1985; Weast 1988; Windholz 1983). This may be due to different
 

levels of impurities in the samples tested. The fact that no numerical value
 

exists for the water solubility of antimony trioxide, antimony pentoxide, and
 

antimony pentasulfide is of no special significance. For inorganic salts, the
 

solubility product coupled with stability constants for the ionic species in
 

solution are the factors determining how much of the compound.goes into
 

solution; the solubility in terms of the number of milligrams of the parent
 

compound in solution, as used for organic compounds, is not meaningful. We do
 

not know whether all the solubility products and stability constants for
 

antimony and its compounds, required for determining the antimony species in
 

natural water and their concentrations, are available. Other physical and
 
98
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

chemical properties in Table 3-2 for which there are no data are generally not
 

well defined for antimony and its compounds or are not useful in determining
 

their environmental fate.
 

Production, Import/Export, Use, and Disposal. Information on the
 

production, import, and use of antimony and antimony trioxide is readily
 

available (Carapella 1978; Llewellyn 1988; Plunkert 1982; U.S. Bureau of Mines
 

1989a). However, information on the production, import, and use patterns of
 

other antimony compounds is not available, and is needed to assess human
 

exposure to these compounds. Except for the recycling of batteries, little
 

information is available concerning the disposal of antimony and its
 

compounds.
 

Much of the antimony released to the environment is transferred to
 

offsite locations for disposal (probably landfills) (TRI 1989). Most of the
 

waste products from mining and smelting operations are discarded on land in
 

large tailing piles; many of these are now abandoned (TRI 1989). Acid
 

conditions are often created in these tailing piles by the oxidation of
 

pyrites contained in the tailings that increase the potential for leaching
 

(DeLaune and Smith 1985). Information concerning antimony leaching from slag
 

heaps is important in assessing antimony releases to the environment. More
 

detailed information regarding the form of antimony that is disposed of and
 

the disposal methods is necessary to assess the potential exposure to these
 

compounds.
 

According to the Emergency Planning and Community Right-to-Know Act of
 

1986, 42 U.S.C. Section 11023, industries are required to submit chemical
 

release and off-site transfer information to the EPA. The Toxic Release
 

Inventory (TRI), which contains this information for 1987, became available in
 

May of 1989 (TRI 1989). This database will be updated yearly and should
 

provide a list of industrial production facilities and emissions. Releases
 

according to this database are shown in Table 5-l.
 

Environmental Fate. In assessing human exposure, the form (valence
 

state, compound, adsorption, coprecipitation, particle size) of antimony and
 

its availability must be considered. This information is apt to be
 

sitespecific. Data concerning the forms of antimony in air, soil, water, and
 

sediment are limited. Information regarding the transformations that may
 

occur, the rates of transformation, and the conditions that facilitate the
 

transformations is also lacking. For example, we do not know whether antimony
 

is methylated in soil as is arsenic and as antimony itself may be methylated
 

in the aquatic environment (Andreae et al. 1983; Austin and Millward 1988).
 

Information relating to the adsorption of antimony and its compounds by soil
 

and sediment is limited. This information should cover a range of soil types,
 

soil components (e.g., clay), and conditions.
 
99
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Bioavailability from Environmental Media. Antimony is poorly absorbed
 

following inhalation and oral exposure (Felicetti et al. 1979a, 1979b; Gerber
 

et al. 1982; Thomas et al. 1973). Dermal exposure to high levels of antimony
 

trioxide resulted in death in rabbits (Myers et al. 1978). The application
 

area was occluded, suggesting that at least some forms of antimony can be
 

absorbed through the skin. Although there is no information on the absorption
 

efficiency of antimony from environmental media in humans, there is evidence
 

in animals that it is absorbed. The vegetation and soils at sites near
 

antimony smelters are heavily contaminated with antimony. Elevated levels of
 

antimony in various tissues were observed in animals living near the smelter
 

(Ainsworth 1988). An animal study designed to measure the rate of absorption
 

of antimony from environmental media would be useful in assessing the
 

toxicological significance of levels of antimony in the air and soil near
 

hazardous waste sites.
 

Food Chain Bioaccumulation. Extensive studies at a smelter site
 

indicate that the uptake of antimony from soil in grass and subsequent
 

translocation in shoots is slight (Ainsworth 1988). At a polluted site, most
 

of the antimony on plants resulted from atmospheric deposition. These studies
 

additionally showed that there was no bioaccumulation of antimony in small
 

mammals compared with their food. Other studies on fish and aquatic organisms
 

indicate that the bioconcentration of antimony is low (Callahan et al. 1978;
 

EPA 1980; Maher 1986). Accordingly, there is little indication that antimony
 

would bioconcentrate in the food chain and in humans. It should be pointed
 

out that data on the biconcentration of antimony in fish and biomagnification
 

in higher trophic levels of animals is limited. Monitoring data on the levels
 

of antimony in plants and animals is minimal. A larger database of information
 

covering more sites and species is desirable. This would establish whether
 

antimony might accumulate in some species or in the presence of some forms of
 

antimony.
 

Exposure Levels in Environmental Media. Although some data on the
 

levels of antimony in ambient air are available, these data are not
 

representative and recent enough to estimate the current exposure levels to
 

antimony by the U.S. population via inhalation (Austin and Millward 1988;
 

Hopper and Barrie 1988; Johnson et al. 1984; Kowalczyk et al. 1982; Schroeder
 

et al. 1987; Wiersema et al. 1984). While the levels of antimony in water are
 

generally very low (Eckel and Jacob 1989), the data for ambient water are
 

marginally adequate; data for drinking water and groundwater are virtually
 

nonexistent. Similarly data regarding the levels of antimony in the various
 

food classes and diet are fragmentary (Cunningham 1987; Syengar et al. 1987;
 

Tanner and Freedman 1977). Reliable and recent monitoring data for antimony in
 

air, water, and foods are essential for estimating the extent of exposure from
 

each of these sources. While the levels of antimony in surface and groundwater
 

at hazardous waste sites are elevated above ambient levels (CLPSD 1989), the
 

elevation is not very great. Since it is not clear whether the levels reported
 

at waste sites are for dissolved antimony as are the ambient
 
100
 

5. POTENTIAL FOR HUMAN EXPOSURE
 

levels, the difference between antimony concentrations at waste sites and
 

ambient sites may be lower. Antimony concentrations in soil at some hazardous
 

waste sites are high (CLPSD 1989; Eckel and Langley 1988; View 1989), and
 

there is a potential of exposure from ingesting soil at these sites. The
 

leaching potential of these soils appears to be low (Ainsworth 1988; Foster
 

1989; King 1988; Trnovsky et al. 1988). The exposure potential from antimony
 

at these sites from antimony reentrained by wind also appears to be low
 

(Ainsworth 1988).
 

Exposure Levels in Humans. The levels of antimony in the hair, nails,
 

and breast milk of a sample of the U.S. population are known (Iyengar et al.
 

1982; Takagi et al. 1986, 1988). While the tissue levels of antimony in
 

Japanese people are available (Sumino et al. 1975), analogous levels for
 

Americans were not found. In particular, no reliable data regarding the levels
 

of this element in the blood and urine of unexposed U.S. residents are
 

available. Such data may be helpful in establishing the background exposure
 

levels of antimony. Levels of antimony in hair, nails, lung, blood, and urine
 

of some exposed workers are available, but the amount of data is small (Hewitt
 

1988; Katyama and Ishidi 1987; Ludersdorf et al. 1987). None of these data
 

refer to populations living around the hazardous waste sites containing
 

elevated levels of antimony. Such data may be significant in assessing the
 

exposure levels of this component of the population.
 

Exposure Registries. No exposure registries for antimony and its
 

compounds were located. Antimony and its compounds do not currently have a
 

subregistry established in the National Exposure Registry. They will be
 

considered in the future when chemical selection is made for subregistries to
 

be established. The information that is amassed in the National Exposure
 

Registry facilitates the epidemiological research needed to assess adverse
 

health outcomes that may be related to the exposure to the compound.
 

5.7.2 On-going Studies
 

Remedial investigations and feasibility studies conducted at the 52 NPL
 

sites known to be contaminated with antimony will add to the available
 

database on exposure levels in environmental media, exposure levels in humans,
 

and exposure registries, and will increase the current knowledge regarding the
 

transport and transformation of antimony in the environment. NIOSH is updating
 

its estimates of occupational exposure by including exposure to antimony and
 

its compounds in trade name chemicals (NIOSH 1989). No other ongoing
 

research studies pertaining to the environmental fate of antimony or to
 

occupational or general population exposures to antimony were identified.
 
101
 

6. ANALYTICAL METHODS
 

The purpose of this chapter is to describe the analytical methods that
 

are available for detecting and/or measuring and monitoring antimony 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 antimony. 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 antimony 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 groups such as the Association of
 

Official Analytical Chemists (AOAC) and the American Public Health Association
 

ww - 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
 

Methods for the analytical determination of antimony in biological
 

materials are basically the same as those used for the environmental samples
 

that are discussed below. The most commonly used methods determine the total
 

antimony content of the sample, not the particular antimony compound or
 

oxidation state that is present. Methodological differences are a function of
 

the level of antimony in the sample, digestion procedures required to
 

solubilize the sample, and the level of potentially interfering substances in
 

the type of sample. Antimony occurs at very low levels in biological samples.
 

The accurate determination of trace levels of antimony in these samples may
 

require special methods (e.g., neutron activation) that are both sensitive and
 

selective. Atomic absorption spectroscopy and inductively coupled plasmaatomic
 

emission spectroscopy, with or without preconcentration or separation
 

steps, are the most commonly employed methods. Atomic absorption has three
 

variants: direct aspiration into a flame, atomization in an electrically
 

heated carbon rod, or generation of stibine that is then passed into a heated
 

silica tube.
 

Instrumental neutron activation analysis (INAA), with or without
 

chemical separation, has very good sensitivity and selectivity for antimony,
 

and it has the advantage of being able to measure many elements
 

simultaneously. However, it is slow, costly, and requires special facilities.
 

INAA is favored for surveys where trace levels of many elements are to be
 

determined. It is often required for measuring antimony in tissues in which
 

the antimony level is very low. The neutron activation analysis of antimony
 

requires an exposure to neutron fluxes for 6 hours to 2 days. After the
 

exposure period, the samples are kept for several days before counting, This
 

allows the activity of short half-lived isotopes to decline, and thus improves
 

accuracy of the analysis (Iyengar et al. 1978). Nondestructive INCA can be
 

used to measure concentrations to levels somewhat below 1 ppm. Nondestructive
 

methods are not only advantageous because of reduced sample handling, but also
 
102
 

6. ANALYTICAL METHODS
 

because they are independent of the sample matrix and of the efficiency of the
 

digestion or extraction procedure. While this is generally adequate for
 

antimony determinations in hair and lung tissues, the antimony levels in blood
 

serum and kidney tissues are usually too low to measure without
 

preconcentration (Iyengar et al. 1978). Detection limits may be limited by
 

interferences from matrix elements such as sodium, potassium, phosphorus, and
 

bromine. Lower detection limits (approximately 0.006 ppm) can be obtained by
 

digestion and solvent extraction to eliminate these interferences (Mok and Wai
 

1988).
 

Analytical methods and detection limits for antimony in biological
 

materials are given in Table 6-1. Antimony contained in other biological
 

materials such as hair and nails can be determined by using the same
 

analytical techniques as for blood and tissue, but suitable procedures for
 

dissolving the sample matrix must be used (Takagi et al. 1986, 1988).
 

6.2 ENVIRONMENTAL SAMPLES
 

Analytical methods for antimony in environmental samples generally
 

determine the total antimony content of the sample; determining specific
 

antimony compounds is difficult. Some methods can be used to determine
 

antimony in different oxidation states, but these methods are only used in
 

special circumstances.
 

The most common methods used for environmental samples are atomic
 

absorption spectrometry (AAS) (either flame or graphite furnace) and
 

inductively coupled plasma-atomic emission spectroscopy (ICP-AES). Before the
 

widespread use of AAS, calorimetric methods were used for the determination of
 

antimony; the best known of these methods is the rhodamine B method (APHA
 

1972). The basis for the method is the formation of a pink complex when
 

pentavalent antimony reacts with rhodamine B in the presence of an excess of
 

chloride ions. The complex is extracted into an organic solvent and the
 

absorbance measured at 565 nm. Trivalent antimony must be oxidized to the
 

pentavalent state with nitric, sulfuric, and perchloric acids.
 

Water and waste water samples can be analyzed for antimony by EPA Test
 

Methods 220.1 (atomic absorption, direct aspiration), 220.2 (atomic
 

absorption, furnace technique), or 200.7 (inductively coupled plasma-atomic
 

emission spectroscopy) (EPA 1983b). These methods are suitable for
 

groundwater, surface water, and domestic and industrial effluents. In open
 

ocean water and in other water samples with a low antimony concentration, a
 

preconcentration and/or separation procedure involving coprecipitation,
 

chelation, selective adsorption, or hydride formation is required before
 

analysis (Andresen and Salbu 1982; Apte and Howard 1986; Maher 1986; Sturgeon
 

et al. 1985). The atomic absorption wavelength used for antimony is 217.6 nm.
 

In the presence of lead concentrations of the order of 1 g/L, however, a
 

spectral interference may occur at this resonance line, and the line at
 

231.1 nm should be used instead. When using direct aspiration, the spectral
 

104
 

6. ANALYTICAL METHODS
 

absorption of antimony is reduced when the concentration of acid increases.
 

Therefore, it is important to match the concentration of acid in standards and
 

samples (EPA 1983b). Background correction of nonspecific absorption is
 

advisable for some samples, such as those containing sulfuric acid (Ainsworth
 

1988). Analytical methods and detection limits for antimony in environmental
 

media are given in Table 6-2. If the determination of dissolved antimony is
 

required, samples should be filtered using a 0.45 μm membrane filter. 

Acid digestion to assure release of antimony from the sample matrix is a
 

crucial step in the analysis of environmental samples. Unless the particular
 

type of sample has been well studied, it is usually important to experiment
 

with different digestion procedures. For the release of antimony from soil,
 

hydrogen fluoride mixed with perchloric acid or another strong acid is
 

generally required. Aqua regia, however, has been found to be suitable. For
 

plant and animal tissue, a combination of sulfuric and nitric acids is most
 

satisfactory (Ainsworth 1988).
 

Antimony forms a volatile hydride under reducing conditions, and hydride
 

generation has been interfaced with different analytical procedures for
 

enhanced sensitivity and selectivity. The most popular reagent used for this
 

reduction is sodium borohydride (Andreae 1983). It is necessary to add KI to
 

the reaction medium to completely reduce Sb(II1). In atomic absorption,
 

increased sensitivity can be achieved by using hydride generation because the
 

efficiency of atomization is greater for stibine than for antimony solutions
 

introduced into the flame. Another advantage of hydride generation is that
 

separati.on is achieved from nonhydride-forming elements, thereby eliminating
 

interferences. Antimony reduction is pH dependent, possibly because neutral
 

and cationic species (but not anionic ones) are subject to reduction by
 

negatively charged borohydride ions. By exploiting the pH dependence of the
 

reduction, it is possible to separately determine Sb(III) and Sb(V) in natural
 

waters (Andreae 1983; Apte and Howard 1986). Other methods that distinguish
 

Sb(II1) from Sb(V) rely on selective extraction techniques in which Sb(II1) is
 

extracted into an organic solvent and analyzed. After analysis, Sb(V) is
 

reduced and extracted (Abbasi 1989; Mok and Wai 1987). When very high
 

sensitivity is required, such as that necessary for the analysis of antimony
 

in food, neutron activation analysis is often employed. X-ray fluorescence
 

(XRF) and anodic stripping voltammetry (ASV) are other analytical methods that
 

are frequently used (Costantini et al. 1985; Gillain and Brihaye 1985; Ives
 

et al. 1984; Johnson et al. 1984).
 

In the determination of trace metals, major concerns include
 

contamination and loss. Contamination can be introduced from impurities in
 

reagents and containers and from laboratory dust. Losses may also occur due
 

to adsorption of the analyte onto container walls. In the case of antimony, a
 

common source of loss is volatilization during acid digestion or ashing in an
 

AAS furnace.
 

106
 

6. ANALYTICAL METHODS
 

6.3 ADEQUACY OF THE DATABASE
 

Section 104(i)(5) of CERCLA as amended 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 antimony 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 antimony.
 

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.
 

6.3.1 Data Needs
 

Methods for Determining Biomarkers of Exposure and Effect. Methods for
 

determining antimony in biological materials are well developed, and there are
 

methods available to most laboratories that are satisfactory for testing
 

biological samples that naturally contain high concentrations of antimony or
 

for occupational exposure testing (Anonymous 1977; NIOSH 1985). Since
 

antimony occurs at very low levels in many biological materials, methods such
 

as INAA that require special facilities must often be used to achieve adequate
 

sensitivity (Iyengar et al. 1978). Standardized methods are available from
 

NIOSH and other sources to measure antimony in blood, urine, and tissue (NIOSH
 

1985). Several authors have reported that antimony concentrations in hair,
 

nails, blood, or urine are elevated in exposed individuals; therefore,
 

antimony levels in these samples can be used as a biomarker for exposure to
 

antimony (Katayama and Ishidi 1987). Available analytical methods are capable
 

of determining the levels of antimony in these media in both normal and
 

occupationally exposed persons (Bakagi et al. 1986, 1988; Iyenger et al.
 

1988). Methods with sufficient sensitivity (e.g., INAA), however, are not
 

available in most laboratories.
 

No biomarkers that could be used to characterize effects of antimony
 

have been identified, Should subtle biochemical or physiological changes
 

unique to antimony be identified, methods to analyze for these changes could
 

possibly be developed if they don't already exist.
 

Methods for Determining Parent Compounds and Degradation Products in
 

Environmental Media. Methods for determining antimony in environmental media
 

are well developed and adequate. Standardized methods are available from EPA,
 

NIOSH, and other sources (APHA 1972; Cunningham 1987; DeDonker et al. 1983;
 
107
 

6. ANALYTICAL METHODS
 

EPA 1983a, 1986; NIOSH 1987). Since most analytical methods measure total
 

antimony, the methods for analyzing for the parent compound and degradation
 

product are identical.
 

6.3.2 On-going Studies
 

Analytical methods for antimony and antimony compounds are currently
 

being developed at EPA's Environmental Monitoring Systems Laboratory in
 

Cincinnati, Ohio (EPA 1989b). No on-going studies regarding new analytical
 

methods for measuring antimony in biological materials were located In the
 

available literature.
 

109
 

7. REGULATIONS AND ADVISORIES
 

National and international guidelines and state regulations pertinent to
 

human exposure to antimony and compounds are summarized in Table 7-1.
 

Antimony compounds are regulated by the Clean Water Effluent Guidelines
 

for the following industrial point sources: nonferrous metal manufacturing,
 

steam electric, asbestos, timber products processing, mineral mining, paving
 

and roofing, paint formulating, ink formulating, gum and wood, carbon black,
 

and nonferrous metal forming (EPA 1988). Antimony compounds are also
 

regulated by the Clean Air Act.
 



____________________ 

113
 

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*Von Guten HR, Ku11 TP. 1986. Infiltration of inorganic compounds from the
 

Glatt River, Switzerland, into a groundwater aquifer. Water Air Soil Pollut.
 

*Warren CJ, Dudas M.J. 1988. Leaching behavior of selected trace elements in
 

chemically weathered alkaline fly ash. Sci Total Environ 76:229-246.
 
131
 

8. REFERENCES
 

*Watt WD. 1980. Chronic inhalation toxicity of antimony trioxide:
 

Validation of the T.L.V.-progress report-summary of results. OTS206195.
 

*Watt WD. 1983. Chronic inhalation toxicity of antimony trioxide:
 

Validation of the threshold limit value. Dissertation, Wayne State
 

University.
 

*Weast RC. 1988. Handbook of chemistry and physics. 69th ed. Boca Raton,
 

FL: CRC Press, B-8, B-72 to B-73.
 

*Webber MD, Shamess A. 1987. Heavy metal concentrations in Halton Region
 

soils: An assessment for future municipal sludge utilization. Can J Soil Sci
 

67:893-903.
 

*Wiersema JM, Wright L, Rogers B, et al. 1984. Human exposure to potentially
 

toxic elements through ambient air in Texas. Proc Air Pollut Contr Assoc
 

1:84-1.2.
 

*Wil Research Laboratories, Inc. 1979. Acute eye irritation study in rabbits
 

with antimony oxide. Sponsored by PPG Industries Inc., Pittsburgh, PA.
 

*Willetts P, Anderson RA, Farmer JG, et al. 1982. Inorganic elements in the
 

tracheas of fire fatalities. Fire Mater 6:32-37.
 

*Windholz M, ed. 1983. The Merck index. 10th ed. Rahway, NJ: Merck and
 

co.
 

Woessner WM, Shapley. 1985. Effects of U.S. antimony's disposal ponds on an
 

alluvial aquifer and Prospect Creek, western Montana.
 

*Wang LCK, Winston JM, Hagensen J, et al. 1979. Study of carcinogenicity and
 

toxicity of inhaled antimony trioxide, antimony ore concentrate and thallic
 

oxide in rats. Prepared for National Institute for Occupational Safety and
 

Health, Cincinnati, OH, U.S. Department of Health. OTS0511065.
 

*Yocom JE. 1983. Industrial sources of metals. NeuroToxicology 4:91-102.
 

*Young M. 1979a. Walk-through survey report of General Battery and Ceramic
 

Corporation, Dallas, Texas. Cincinnati, OH: Division of Surveillance, Hazard
 

Evaluations, and Field Studies, Industry-wide Studies Branch, Industrial
 

Hygiene Section, National Institute for Occupational Safety and Health.
 

*Young M. 1979b. Walk-through survey report of Standard Industries, Inc.
 

(Reliable Battery Company), .San Antonio, Texas. Cincinnati, OH: Division of
 

Surveillance, Hazard Evaluations, and Field Studies, Industry-wide Studies
 

Branch, Industrial Hygiene Section, National Institute for Occupational Safety
 

and Health.
 
132
 

8. REFERENCES
 

*Young M, Beaumont J, Brown D, et al. 1979. Walk-through survey report of
 

Electric Storage Battery, Inc., Dallas, Texas. Cincinnati, OH: Division of
 

Surveillance, Hazard Evaluations, and Field Studies, Industry-wide Studies
 

Branch, Industrial Hygiene Section, National Institute for Occupational
 

Safety and Health.
 

*Zaki MH, Shookhoff HB, Sterman M, et al. 1964. Astiban in schistosomiasis
 

mansoni: A controlled therapeutic trial in a nonendemic area. Am J Trop Med
 

Hyg 13:803-810.
 

*Zhang J, Billiet J, Dams R. 1985. Elemental composition and source
 

investigation of particulates suspended in the air of an iron foundry. sci
 

Total Environ 41:13-28.
 

*Zikovsky L, Badillo M. 1987. An indirect study of air pollution by neutron
 

activation analysis of snow. J Radioanal Nucl Chem 114:147-153.
 
133
 

9. GLOSSARY
 

Acute Exposure -- Exposure to a chemical for a duration of 14 days or less, as
 

specified in the Toxicological Profiles.
 

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.
 

Bioconcentration Factor (BCF) -- The quotient of the concentration of a
 

chemical in aquatic organisms at a specific time or during a discrete time
 

period of exposure divided by the concentration in the surrounding water at
 

the same time or during the same period.
 

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.
 

Carcinogen -- A chemical capable of inducing cancer.
 

Ceiling Value -- 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.
 

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 life span of the organism.
 

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.
 

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.
 
134
 

9. GLOSSARY
 

Immediately Dangerous to Life or Health (IDLH) -- The maximum environmental
 

concentration of a contaminant from which one could escape within 30 min
 

without any escape-impairing symptoms or irreversible health effects.
 

Intermediate Exposure -- Exposure to a chemical for a duration of 15-364 days
 

as specified in the Toxicological Profiles.
 

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.
 

Lethal Concentration (LC (Lo) Lo
) -- The lowest concentration of a chemical in


air which has been reported to have caused death in humans or animals.
 

Lethal Concentration (LC ) (50) 50
 -- A 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 experimental animal population.
 

Lethal Dose (LD (Lo) 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 (LD (50) 50
) -- The dose of a chemical which has been calculated to


cause death in 50% of a defined experimental animal population.
 

Lethal Time (LT (50) 50
) -- A calculated period of time within which a specific


concentration of a chemical is expected to cause death in 50% of a defined
 

experimental animal population.
 

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.
 

Malformations -- Permanent structural changes that may adversely affect
 

survival, development, or function.
 

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.
 
135
 

9. GLOSSARY
 

Mutagen -- A substance that causes mutations. A mutation is a change in the
 

genetic material in a body cell. Mutations can lead to birth defects,
 

miscarriages, or cancer.
 

Neurotoxicity -- The occurrence of adverse effects on the nervous system
 

following exposure to chemical.
 

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.
 

Octanol-Water Partition Coefficient (KOW) -- The equilibrium ratio of the
 

concentrations of a chemical in n-octanol and water, in dilute solution.
 

Permissible Exposure Limit (PEL) -- An allowable exposure level in workplace
 

air averaged over an 8-hour shift.
 

q1* -- The upper-bound estimate of the low-dose slope of the dose-response
 

curve as determined by the multistage procedure. me 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). 

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.
 

Reportable Quantity (RQ) -- The quantity of a hazardous substance that is
 

considered reportable under CERCLA. Reportable quantities are (1) 1 lb or
 

greater or (2) for selected substances, an amount established by regulation
 

either under CERCLA or under Sect. 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.
 
136
 

9. GLOSSARY
 

Short-Term Exposure Limit (STEL) -- The maximum concentration to which workers
 

can be exposed for up to 15 min continually. No more than four excursions are
 

allowed per day, and there must be at least 60 min between exposure periods.
 

The daily TLV-TWA may not be exceeded.
 

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.
 

Teratogen -- A chemical that causes structural defects that affect the
 

development of an organism.
 

Threshold Limit Value (TLV) -- A concentration of a substance to which most
 

workers can be exposed without adverse effect. The TLV may be expressed as a
 

TWA, as a STEL, or as a CL.
 

Time-Weighted Average (TWA) -- 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 experimental animal population.
 

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 LCAEL data rather than NOAEL data.
 

Usually each of these factors is set equal to 10.
 
A-1
 

APPENDIX A
 

USER'S GUIDE
 

Chapter 1
 

Public Health Statement
 

This chapter of the profile is a health effects summary written in
 

nontechnical language. Its intended audience is the general public especially
 

people living in the vicinity of a hazardous waste site or substance release.
 

If the Public Health Statement were removed from the rest of the document, it
 

would still communicate to the lay public essential information about the
 

substance. The major headings in the Public Health Statement are useful to
 

find specific topics of concern. The topics are written in a question and
 

answer format. The answer to each question includes a sentence that will
 

direct the reader to chapters in the profile that will provide more
 

information on the given topic.
 

Chapter 2
 

Tables and Figures for Levels of Significant Exposure (LSE)
 

Tables (2-1, 2-2, and 2-3) and figures (2-l and 2-2) are used to summarize
 

health effects by duration of exposure and endpoint and to illustrate
 

graphically levels of exposure associated with those effects. All entries in
 

these tables and figures represent studies that provide reliable, quantitative
 

estimates of No-Observed-Adverse-Effect Levels (NOAELs), Lowest-ObservedAdverse-Effect Levels (NOAELs) for Less Serious and Serious health effects, or
 

Cancer Effect Levels (CELs). In addition, these tables and figures illustrate
 

differences in response by species, Minimal Risk Levels (MRLs) to humans for
 

noncancer end points, and EPA's estimated range associated with an upper-bound
 

individual lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. The LSE
 

tables and figures can be used for a quick review of the health effects and to
 

locate data for a specific exposure scenario. The LSE tables and figures
 

should always be used in conjunction with the text.
 

The legends presented below demonstrate the application of these tables and
 

figures. A representative example of LSE Table 2-l and Figure 2-1 are shown.
 

The numbers in the left column of the legends correspond to the numbers in the
 

example table and figure.
 

LEGEND
 

See LSE Table 2-l
 

(1). Route of Exposure One of the first considerations when reviewing the
 

toxicity of a substance using these tables and figures should be the
 

relevant and appropriate route of exposure. When sufficient data exist,
 
A-2
 

APPENDIX A
 

three LSE tables and two LSE figures are presented in the document. The
 

three LSE tables present data on the three principal routes of exposure,
 

i.e., inhalation, oral, and dermal (LSE Table 2-1, 2-2, and 2-3,
 

respectively). LSE figures are limited to the inhalation (LSE Figure 2-l)
 

and oral (LSE Figure 2-2) routes.
 

(2). Exposure Duration Three exposure periods: acute (14 days or less); 

intermediate (15 to 364 days); and chronic (365 days or more) are 

presented within each route of exposure. In this example, an inhalation 

study of intermediate duration exposure is reported. 

(3). Health Effect The major categories of health effects included in 

LSE tables and figures are death, systemic, immunological, 

neurological, developmental, reproductive, and cancer. NOAELs and 

LOAELs can be reported in the tables and figures for all effects but 

cancer. Systemic effects are further defined in the "System" column of 

the LSE table. 

(4). Key to Figure Each key number in the LSE table links study information 

to one or more data points using the same key number in the 

corresponding LSE figure. In this example, the study represented by key 

number 18 has been used to define a NOAEL and a Less Serious LOAEL (also 

see the two "18r" data points in Figure 2-l). 

(5). Species The test species, whether animal or human, are identified in 

this column. 

(6). Exposure Frequency/Duration The duration of the study and the weekly and 

daily exposure regimen are provided in this column. This permits 

comparison of NOAELs and LOAELs from different studies. In this case 

(key number 18), rats were exposed to [substance x] via inhalation for 

13 weeks, 5 days per week, for 6 hours per day. 

(7). System This column further defines the systemic effects. These systems 

include: respiratory, cardiovascular, gastrointestinal, hematological, 

musculoskeletal, hepatic, renal, and dermal/ocular. "Other" refers to 

any systemic effect (e.g., a decrease in body weight) not covered in 

these systems. In the example of key number 18, one systemic effect 

(respiratory) was investigated in this study. 

(8). NOAEL A No-Observed-Adverse-Effect Level (NOAEL) is the highest exposure 

level at which no harmful effects were seen in the organ system studied. 

Key number 18 reports a NOAEL of 3 ppm for the respiratory system which 

was used to derive an intermediate exposure, inhalation MR.L of 0.005 

ppm (see footnote "cm). 

(9). LOAEL A Lowest-Observed-Adverse-Effect Level (LOAEL) is the lowest 

exposure level used in the study that caused a harmful health effect. 

LOAELS have been classified into "Less Serious" and "Serious" effects. 

These distinctions help readers identify the levels of exposure at which 

adverse health effects first appear and the gradation of effects with 

increasing dose. A brief description of the specific end point used to 
A-3
 

APPENDIX A
 

quantify the adverse effect accompanies the LOAEL. The "Less Serious"
 

respiratory effect reported in key number 18 (hyperplasia) occurred at a
 

LOAEL of 10 ppm.
 

(10). Reference The complete reference citation is given in Chapter 8 of the
 

profile.
 

(11). CEL A Cancer Effect Level (CEL) is the lowest exposure level associated
 

with the onset of carcinogenesis in experimental or epidemiological
 

studies. GELS are always considered serious effects. The LSE tables and
 

figures do not contain NOAELs for cancer, but the text may report doses
 

which did not cause a measurable increase in cancer.
 

(12). Footnotes Explanations of abbreviations or reference notes for data in
 

the LSE tables are found in the footnotes. Footnote "c" indicates the
 

NOAEL of 3 ppm in key number 18 was used to derive an MRL of 0.005 @pm.
 

LEGEND
 

See LSE Figure 2-1
 

LSE figures graphically illustrate the data presented in the corresponding LSE
 

tables. Figures help the reader quickly compare health effects according to
 

exposure levels for particular exposure duration.
 

(13). Exposure Duration The same exposure periods appear as in the LSE table.
 

In this example, health effects observed within the intermediate and
 

chronic exposure periods are illustrated.
 

(14). Health Effect These are the categories of health effects for which
 

reliable quantitative data exist. The same health effects appear in the
 

LSE table.
 

(15). Levels of Exposure Exposure levels for each health effect in the LSE
 

tables are graphically displayed in the LSE figures. Exposure levels are
 

reported on the log scale "y" axis. Inhalation exposure is reported in
 

mg/m3

 or ppm and oral exposure is reported in mg/kg/day.
 

(16). NOAEL In this example, 18r NOAEL is the critical end point for which an
 

intermediate inhalation exposure MRL is based. As you can see from the
 

LSE figure key, the open-circle symbol indicates a NOAEL for the test
 

species (rat). The key number 18 corresponds to the entry in the LSE
 

table. The dashed descending arrow indicates the extrapolation from the
 

exposure level of 3 ppm (see entry 18 in the Table) to the MRL of 0.005
 

ppm (see footnote "b" in the LSE table).
 

(17). CEL Key number 38r is one of three studies for which Cancer Effect
 

Levels (CELs) were derived. The diamond symbol refers to a CEL for the
 

test species (rat). The number 38 corresponds to the entry in the LSE
 

table.
 
A-4
 

APPENDIX A
 

(18). Estimated Upper-Bound Human Cancer Risk Levels This is the range
 

associated with the upper-bound for lifetime cancer risk of 1 in 10,000
 

to 1 in 10,000,000. These risk levels are derived from EPA's Human
 

Health Assessment Group's upper-bound estimates of the slope of the
 

cancer dose response curve at low dose levels (q1*).
 

(19). Key to LSE Figure The Key explains the abbreviations and symbols used in
 

the figure.
 


A-7
 

APPENDIX A
 

Chapter 2 (Section 2.4)
 

Relevance to Public Health
 

The Relevance to Public Health section provides a health effects summary based
 

on evaluations of existing toxicological, epidemiological, and toxicokinetic
 

information. This summary is designed to present interpretive, weight-ofevidence discussions for human health end points by addressing the
 

following questions.
 

1. 	 What effects are known to occur in humans?
 

2. 	 What effects observed in animals are likely to be of concern to
 

humans?
 

3. 	 What exposure conditions are likely to be of concern to humans,
 

especially around hazardous waste sites?
 

The section discusses health effects by end point. Human data are presented
 

first, then animal data. Both are organized by route of exposure (inhalation,
 

oral, and dermal) and by duration (acute, intermediate, and chronic). In vitro
 

data and data from parenteral routes (intramuscular, intravenous,
 

subcutaneous, etc.) are also considered in this section. If data are located
 

in the scientific literature, a table of genotoxicity information is included.
 

The carcinogenic potential of the profiled substance is qualitatively
 

evaluated, when appropriate, using existingtoxicokinetic, genotoxic, and
 

carcinogenic data. ATSDR does not currently assess cancer potency or perform
 

cancer risk assessments. MRLs for noncancer end points if derived, and the end
 

points from which they were derived are indicated and discussed in the
 

appropriate section(s).
 

Limitations to existing scientific literature that prevent a satisfactory
 

evaluation of the relevance to public health are identified in the
 

Identification of Data Needs section.
 

Interpretation of Minimal Risk Levels
 

Where sufficient toxicologic information was available, MRLs were derived.
 

MRLs are specific for route (inhalation or oral) and duration (acute,
 

intermediate, or chronic) of exposure. Ideally, MRLs can be derived from all
 

six exposure scenarios (e.g., Inhalation - acute, -intermediate, -chronic;
 

Oral - acute, -intermediate, - chronic). These MRLs are not meant to support
 

regulatory action,but to aquainthealth professionals with exposure levels at
 

which adverse health effects are not expected to occur in humans. They should
 

help physicians and public health officials determine the safety of a
 

community living near a substance emission, given the concentration of a
 

contaminant in air or the estimated daily dose received via food or water.
 

MRLs are based largely on toxicological studies in animals and on reports of
 

human occupational exposure.
 
A-8
 

APPENDIX A
 

MRL users should be familiar with the toxicological information on which the
 

number is based. Section 2.4, "Relevance to Public Health," contains basic
 

information known about the substance. Other sections such as 2.6,
 

"Interactions with Other Chemicals" and 2.7, "Populations that are Unusually
 

Susceptible" provide important supplemental information.
 

MRL users should also understand the MRL derivation methodology. MRLs are
 

derived using a modified version of the risk assessment methodology used by
 

the Environmental Protection Agency (EPA) (Barnes and Dourson, 1988; EPA
 

1989a) to derive reference doses (RfDs) for lifetime exposure.
 

To derive an MRL, ATSDR generally selects the end point which, in its best
 

judgement, represents the most sensitive human health effect for a given
 

exposure route and duration. ATSDR cannot make this judgement or derive an MRL
 

unless information (quantitative or qualitative) is available for all
 

potential effects (e.g., systemic, neurological, and developmental). In order
 

to compare NOAELs and LOAELs for specific end points, all inhalation exposure
 

levels are adjusted for 24hr exposures and all intermittent exposures for
 

inhalation and oral routes of intermediate and chronic duration are adjusted
 

for continuos exposure (i.e., 7 days/week). If the information and reliable
 

quantitative data on the chosen end point are available, ATSDR derives an MRL
 

using the most sensitive species (when information from multiple species is
 

available) with the highest NOAEL that does not exceed any adverse effect
 

levels. The NOAEL is the most suitable end point for deriving an MRL. When a
 

NOAEL is not available, a Less Serious LOAEL can be used to derive an MRL, and
 

an uncertainty factor (UF) of 10 is employed. MRLs are not derived from
 

Serious LOAELs. Additional uncertainty factors of 10 each are used for human
 

variability to protect sensitive subpopulations (people who are most
 

susceptible to the health effects caused by the substance) and for
 

interspecies variability (extrapolation from animals to humans). In deriving
 

an MRL, these individual uncertainty factors are multiplied together. The
 

product is then divided into the adjusted inhalation concentration or oral
 

dosage selected from the study. Uncertainty factors used in developing a
 

substance-specific MRL are provided in the footnotes of the LSE Tables.
 
B-l
 

APPENDIX B
 

ACRONYMS, ABBREVIATIONS, AND SYMBOLS
 

ACGIH	 American Conference of Governmental Industrial Hygienists
 

ADME	 Absorption, Distribution, Metabolism, and Excretion
 

ATSDR	 Agency for Toxic Substances and Disease Registry
 

BCF	 bioconcentration factor
 

BSC	 Board of Scientific Counselors
 

CDC	 Centers for Disease Control
 

CEL	 Cancer Effect Level
 

CERCLA	 Comprehensive Environmental Response, Compensation, and
 

Liability Act
 

CFR	 Code of Federal Regulations
 

CLP	 Contract Laboratory Program
 

cm	 centimeter
 

CNS	 central nervous system
 

DHEW	 Department of Health, Education, and Welfare
 

DHHS	 Department of Health and Human Services
 

DGL	 Department of Labor
 

ECG	 electrocardiogram
 

EEG	 electroencephalogram
 

EPA	 Environmental Protection Agency
 

EKG	 see ECG
 

FAO	 Food and Agricultural Organization of the United Nations
 

FEMA	 Federal Emergency Management Agency
 

FIFRA	 Federal Insecticide, Fungicide, and Rodenticide Act
 

f1	 first generation
 

fpm	 feet per minute
 

ft	 foot
 

FR	 Federal Register
 

G	 gram
 

GC 	chromatography
 

Ha	 hectare
 

HPLC	 high performance liquid chromatography
 

hr	 hour
 

IDLH	 Immediately Dangerous to Life and Health
 

IARC	 International Agency for Research on Cancer
 

ILO	 International Labor Organization
 

in	 inch
 

Kd	 distribution ratio (soil/water)
 

Kg	 kilogram
 

Koc	 organic carbon partition coefficient
 

Kow	 octanol-water partition coefficient
 

L	 liter
 

LC	 liquid chromatography
 

LCLo	 lethal concentration low
 

LC50	 lethal concentration 50 percent kill
 

LDLo
 lethal dose low

B-2 

APPENDIX B 

LD50 lethal dose 50 percent kill 

LOAEL lowest-observed-adverse-effect level 

LSE Levels of Significant Exposure 

m meter 

M molar 

mg milligram 

min minute 

mL milliliter 

mm millimeters 

mmo1 millimole 

mppcf millions of particles per cubic foot 

MRL Minimal Risk Level 

MS mass spectrometry 

NIEHS National Institute of Environmental Health Sciences 

NIOSH National Institute for Occupational Safety and Health 

NIOSHTIC NIOSH's Computerized Information Retrieval System 

nm nanometer 

nM nanomolar 

NHANES National Health and Nutrition Examination Survey 

nmol nanomole 

NOAEL no-observed-adverse-effect level 

NOES National Occupational Exposure Survey 

NOHS National Occupational Hazard Survey 

NPL National Priorities List 

NRC National Research Council 

NTIS National Technical Information Service 

NTP National Toxicology Program 

OSHA Occupational Safety and Health Administration 

PEL permissible exposure limit 

pg picogram 

pmo1 picogram 

PHS Public Health Service 

PMR proportional mortality ratio 

ppb parts per billion 

ppm parts per million 

ppt parts per trillion 

REL recommended exposure limit 

RfD Reference Dose 

RTECS Registry of Toxic Effects of Chemical Substances 

sec seconds 

SCE sister chromatid exchange 

SIC Standard Industrial Classification 

SMR standard mortality ratio 

STEL short-term exposure limit 

STORET STORAGE and RETRIEVAL 

TLV threshold limit value 

TSCA Toxic Substance Control Act 
B-3 

APPENDIX B
 

TRI Toxics Release Inventory
 

TWA time-weighted average
 

U.S. United States
 

UF uncertainty factor
 

WHO World Health Organization
 

> greater than 

≥ greater than or equal to 

= equal to 

< less than 

≤ less than or equal to 

5 percent 

α alpha 

β beta 

δ delta 

γ gamma 

μm micron 

μg microgram 
C-l
 

APPENDIX C
 

PEER REVIEW
 

A peer review panel was assembled for antimony. The panel
 

consisted of the following members: Dr. William Buck, University of
 

Illinois, Urbana, Illinois; Dr. George Cherian, University of Western
 

Ontario, London, Ontario, Canada; Dr. Ernest Foulkes, University of
 

Cincinnati, Cincinnati, Ohio; Dr. Derek Hodgson, University of
 

Wyoming, Laramie, Wyoming; and Dr. Maryce Jacobs, American Institute
 

for Cancer Research, Washington, DC. These experts collectively have
 

knowledge of antimony'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 Comprehensive Environmental Response,
 

Compensation, and Liability Act of 1986, Section 104.
 

Scientists from the Agency for Toxic Substances and Disease
 

Registry (ATSDR) have reviewed the peer reviewers comments and
 

determined which comments will be included in the profile. A listing
 

of the peer reviewers comments not incorporated in the profile, with a
 

brief explanation of the rationale for their exclusion, exists as part
 

of the administrative record for this compound. A list of databases
 

reviewed and a list of unpublished documents cited are also included
 

in the administrative record.
 

The citation of the peer review panel should not be understood to
 

imply its approval of the profile's final content. The responsibility
 

for the content of this profile lies with the ATSDR.