Cobalt Compounds
Hazard Summary
Cobalt is a natural element found throughout the environment. Acute (short-term) exposure to high levels
of cobalt by inhalation in humans and animals results in respiratory effects, such as a significant decrease
in ventilatory function, congestion, edema, and hemorrhage of the lung. Respiratory effects are also the
major effects noted from chronic (long-term) exposure to cobalt by inhalation, with respiratory irritation,
wheezing, asthma, pneumonia, and fibrosis noted. Cardiac effects, congestion of the liver, kidneys, and
conjunctiva, and immunological effects have also been noted in chronically-exposed humans. Cobalt is
an essential element in humans, as a constituent of vitamin B . Human studies are inconclusive regarding
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inhalation exposure to cobalt and cancer, and the one available oral study did not report a correlation
between cobalt in the drinking water and cancer deaths. EPA has not classified cobalt for carcinogenicity.
Please Note: The main sources of information for this fact sheet are the Agency for Toxic Substances and Disease
Registry's (ATSDR's) Toxicological Profile for Cobalt (1) and California Environmental Protection Agency's Technical
Support Document for the Determination of Noncancer Chronic Reference Exposure Levels. (5)
Uses
•	Cobalt is used to make superalloys (alloys that maintain their strength at high temperatures approaching
their melting points) and in pigment manufacture. (1,5)
Sources and Potential Exposure
•	Cobalt is a natural element found throughout the environment; the general population may be exposed to
cobalt in the air, drinking water, and food. (1,5)
•	The average concentration of cobalt in ambient air in the United States is approximately 0.0004
micrograms percubjc meter (|jg/m ). However, higher levels have been detected; in one industrial area,
levels of 0.61 |jg/m were measured. (1)
•	A study found average cobalt levels in drinking water of 2 micrograms per liter (|jg/L), but values up to 1 07
|jg/L have been reported. (1)
•	The average daily intake of cobalt from food is estimated to be 5 to 40 |jg/d. (1)
•	Occupational exposure to cobalt may occur, particularly in workers in the hard metal industry. (1)
Assessing Personal Exposure
•	Cobalt can be measured in the urine and the blood, for periods up to a few days after the exposure. (1)
Health Hazard Information
Acute Effects:
•	Acute exposure to high levels of cobalt by inhalation in humans and animals results in respiratory effects,
such as a significant decrease in ventilatory function, congestion, edema, and hemmorhage of the lung. (1)
•	Acute animal tests in rats have shown cobalt to have extreme toxicity from inhalation exposure,
and moderate to high toxicity from oral exposure. (1,2)

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Chronic Effects (Noncancer):
. Cobalt is an essential element in humans and animals as a constituent of vitamin B . Cobalt has also been
l2
used as a treatment for anemia, because it stimulates red blood cell production. (1)
•	Chronic exposure to cobalt by inhalation in humans results in effects on the respiratory system, such as
respiratory irritation, wheezing, asthma, decreased lung function, pneumonia, and fibrosis. (1,5)
•	Other effects noted in humans from inhalation exposure to cobalt include cardiac effects, such as
functional effects on the ventricles and enlargement of the heart, congestion of the liver, kidneys, and
conjunctiva, and immunological effects that include cobalt sensitization, which can precipitate an asthmatic
attack in sensitized individuals. (1,3)
•	Cardiovascular effects (cardiomyopathy) were observed in people who consumed large amounts of beer
over several years time containing cobalt sulfate as a foam stabilizer. The effects were characterized by
cardiogenic shock, sinus tachycardia, left ventricular failure, and enlarged hearts. The beer drinkers
ingested cobalt at an average concentration of 0.04 milligrams per kilogram per day (mg/kg/d) to 0.1 4
mg/kg/d. (1,3)
•	Gastrointestinal effects (nausea, vomiting, and diarrhea), effects on the blood, liver injury, and allergic
dermatitis have also been reported in humans from oral exposure to cobalt. (1)
8 Animal studies have reported respiratory, cardiovascular, and central nervous system (CNS) effects,
decreased body weight, necrosis of the thymus, and effects on the blood, liver, and kidneys from inhalation
exposure to cobalt. (1,3)
" EPA has not established a Reference Concentration (RfC) or a Reference Dose (RfD) for cobalt.
s The California Environmental Protection Agency^CalEPA) has established a chronic reference exposure level
of 0.000005 milligrams per cubic meter (mg/m ) for cobalt based on respiratory effects in rats and mice.
The CalEPA reference exposure level is a concentration at or below which adverse health effects are not
likely to occur. It is not a direct estimator of risk, but rather a reference point to gauge the potential effects.
At lifetime exposures increasingly greater than the reference exposure level, the potential for adverse
health effects increases. (5)
3
•	ATSDR has established an intermediate inhalation minimal risk level (MRL) of 0.00003 mg/m based on
respiratory effects in rats. The MRL is an estimate of the daily human exposure to a hazardous substance
that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration of
exposure. (1)
Reproductive /Developmental Effects:
•	No information is available on the reproductive or developmental effects of cobalt in humans via inhalation
exposure. In one oral study, no developmental effects on human fetuses were observed following
treatment of pregnant women with cobalt chloride. (1)
•	Animal studies, via inhalation exposure, have reported testicular atrophy, a decrease in sperm motility, and
a significant increase in the length of the estrus cycle, while oral studies have reported stunted growth and
decreased survival of newborn pups. These effects on the offspring occurred at levels that also caused
maternal toxicity. (1,5)
Cancer Risk:
•	Limited data are available on the carcinogenic effects of cobalt. In one study on workers that refined and
processed cobalt and sodium, an increase in deaths due to lung cancer was found for workers exposed
only to cobalt. However, when this study was controlled for date of birth, age at death, and smoking
habits, the difference in deaths due to lung cancer was found to not be statistically significant. In another
study assessing the correlation between cancer deaths and trace metals in water supplies in the United
States, no correlation was found between cancer mortality and the level of cobalt in the water. (1)
•	In a study by the National Toxicology Program (NTP), cobalt sulfate heptahydrate exposure via inhalation
resulted in increased incidences of alveolar/bronchiolar tumors in rats and mice. (9)
•	In an animal study, inhalation of cobalt over a lifetime did not increase the incidence of tumors in
hamsters. (1,4)

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•	Cobalt, via direct injection under the muscles or skin, has been reported to cause tumors at the injection
site in animals. (1,4)
•	EPA has not classified cobalt for carcinogenicity.
Physical Properties
•	Cobalt usually occurs in the environment in association with other metals such as copper, nickel,
manganese, and arsenic. (1)
•	Pure cobalt is a steel-gray, shiny, hard metal that is insoluble in water. (1)
•	The chemical symbol for cobalt is Co, and the atomic weight is 58.93 g/mol. (1,5)
Conversion Factors:
3	3
To convert concentrations in air (at 2 5°C) from ppm to mg/m : mg/m = (ppm) x (molecular weight of the
compound)/(24.45). For cobalt: 1 ppm = 2.4 mg/m .
Health Data from Inhalation Exposure
Cobalt
6
1
£
5
1DDD
100
10
E
a
0.1
OjOI
0.001
OjOOOI
0.Q0001
OjOOOOOI
Healt h numbers"
Regulatory, advisory
numbers'*
LC^. (rat) (165 mg/nn3}
LQAEL11 Respiratory)
(0.3 mg/m3}
NIOSH IDLH (as Co) (20 rng/mfi
OSHA PEL faote It meta I dust a nd
fume, as Go). NIOSH REL tote It
carfconvL- oiite It hydros rtonyl,
asCoJ(0.l ring/mi2)
| NIOSH REL tote It metal
dust, andfun-e, asGo)
(0.05 mg/m3)
ACGIHTLV
LOAELd (respiratory)
(3.11 ring/ mPJ
AT SDR internreiliate MRL
. (3x1 o"5 mg/m3)
CalEF'A refererce
| | expsure level
(Sxio^ rng/rrft
Ref.
Ht
Hfil
Bet
8
(elemental
inorganic
mmpoundi
as Go)
(0.02 mg/rrtf
ACGIH TLV—American Conference of Governmental and Industrial Hygienists'threshold limit value expressed as a
time-weighted average; the concentration of a substance to which most workers can be exposed without adverse
effects.
LC (Lethal Concentration )—A calculated concentration of a chemical in air to which exposure for a specific
50	50

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length of time is expected to cause death in 50% of a defined experimental animal population.
LOAEL—Lowest-observed-adverse-effect level.
NIOSH IDLH —National Institute of Occupational Safety and Health's immediately dangerous to life or health limit;
NIOSH recommended exposure limit to ensure that a worker can escape from an exposure condition that is likely to
cause death or immediate or delayed permanent adverse health effects or prevent escape from the environment.
NIOSH REL—NIOSH's recommended exposure limit; NIOSH-recommended exposure limit for an 8- or 1 0-h time-
weighted-average exposure and/or ceiling.
OSHA PEL—Occupational Safety and Health Administration's permissible exposure limit expressed as a time-
weighted average; the concentration of a substance to which most workers can be exposed without adverse effect
averaged over a normal 8-h workday or a 40-h workweek.
The health and regulatory values cited in this factsheet were obtained in December 1 999.
a
Health numbers are toxicological numbers from animal testing or risk assessment values developed by EPA.
b
Regulatory numbers are values that have been incorporated in Government regulations, while advisory numbers
are nonregulatory values provided by the Government or other groups as advice. OSHA numbers are regulatory,
whereas NIOSH and ACGIH numbers are advisory.
c
^ The LOAEL is from the critical study used as the basis for the CalEPA reference exposure level.
The LOAEL is from the critical study used as the for the ATSDR intermediate MRL.
Summary created in April 1 992, updated in January 2000
Refe rences
1.	Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Cobalt. Public Health
Service, U.S. Department of Health and Human Services, Atlanta, GA. 1 992.
2.	U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical Substances (RTECS,
online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD.
1993.
3.	U.S. Department of Health and Human Services. Hazardous Substances Data Bank (HSDB, online database).
National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1 993.
4.	E.J. Calabrese and E.M. Kenyon. Air Toxics and Risk Assessment. Lewis Publishers, Chelsea, Ml. 1 991.
5.	California Environmental Protection Agency (CalEPA). Technical Support Document for the Determination of
Noncancer Chronic Reference Exposure Levels. Draft for Public Comment. Office of Environmental Health
Hazard Assessment, Berkeley, CA. 1 997.
6.	Occupational Safety and Health Administration (OSHA). Occupational Safety and Health Standards, Toxic
and Hazardous Substances. Code of Federal Regulations. 29 CFR 1 91 0.1 000. 1 998.
7.	American Conference of Governmental Industrial Hygienists (ACGIH). 1 999 TLVs and BEIs. Threshold Limit
Values for Chemical Substances and Physical Agents. Biological Exposure Indices. Cincinnati, OH. 1 999.
8.	National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to Chemical Hazards. U.S.
Department of Health and Human Services, Public Health Service, Centers for Disease Control and
Prevention. Cincinnati, OH. 1997.
9.	National Toxicology Program. Toxicology and Carcinogenesis Studies of Cobalt Sulfate Heptahydrate (CAS
No. 1 0026-24-1) in F344/N Rats and BSCSF^ Mice (Inhalation Studies). TR No. 471. U.S. Department of
Health and Human Services, Public Health Service, National Institutes of Health, Bethesda, MD. 1 998.

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