Toxicity Profiles
Toxicity Summary for SILVER
NOTE:
Although the toxicity values presented in these toxicity profiles
were correct at the time they were produced, these values are subject to change.
Users should always refer to the
Toxicity Value Database
for the current toxicity values.
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- EXECUTIVE SUMMARY
- 1. INTRODUCTION
- 2. METABOLISM AND DISPOSITION
- 2.1 ABSORPTION
2.2 DISTRIBUTION
2.3 METABOLISM
2.4 EXCRETION
- 3. NONCARCINOGENIC HEALTH EFFECTS
- 3.1 ORAL EXPOSURES
3.2 INHALATION EXPOSURES
3.3 OTHER ROUTES OF EXPOSURE
3.4 TARGET ORGANS/CRITICAL EFFECTS
- 4. CARCINOGENICITY
- 4.1 ORAL EXPOSURES
4.2 INHALATION EXPOSURES
4.3 OTHER ROUTES OF EXPOSURE
4.4 EPA WEIGHT-OF-EVIDENCE
4.5 CARCINOGENICITY SLOPE FACTORS
- 5. REFERENCES
DECEMBER 1992
Prepared by: Rosmarie A. Faust, Ph.D., Chemical Hazard Evaluation and Communication Group,
Biomedical and Environmental Information Analysis Section,
Health and Safety Research Division, *, Oak Ridge, Tennessee.
Prepared for: Oak Ridge Reservation Environmental Restoration Program.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under
Contract No. DE-AC05-84OR21400.
EXECUTIVE SUMMARY
Silver is a relatively rare metal that occurs naturally in the earth's crust and is released to the
environment from various industrial sources. Human exposure to silver and silver compounds can
occur orally, dermally, or by inhalation. Silver is found in most tissues, but has no known physiologic function.
In humans, accidental or intentional ingestion of large doses of silver nitrate has produced
corrosive damage of the gastrointestinal tract, abdominal pain, diarrhea, vomiting, shock, convulsions, and death (U.S. EPA, 1985). Respiratory irritation was noted following acute inhalation
exposure to silver or silver compounds. Silver nitrate solutions are highly irritating to the skin,
mucous membranes, and eyes (Stokinger, 1981).
Ingestion, inhalation, or dermal absorption of silver may cause argyria, the most common indicator
of long-term exposure to silver or silver compounds in humans. Argyria is a gray or blue-gray,
permanent discoloration of the skin and mucous membranes that is not a toxic effect per se, but is
considered cosmetically disfiguring. Chronic inhalation exposure of workers to silver oxide and
silver nitrate dusts resulted in upper and lower respiratory irritation, deposition of granular silver-containing deposits in the eyes, impaired night vision, and abdominal pain (Rosenman et al., 1979).
Mild allergic responses have been attributed to dermal contact with silver (ATSDR, 1990).
In long-term oral studies with experimental animals, silver compounds have produced slight
thickening of the basement membranes of the renal glomeruli, growth depression, shortened
lifespan, and granular silver-containing deposits in skin, eyes, and internal organs (Matuk et al.,
1981; Olcott, 1948, 1950). Hypoactivity was seen in rats subchronically exposed to silver nitrate
in drinking water (Rungby and Danscher, 1984).
A Reference Dose (RfD) of 0.005 mg/kg/day for subchronic and chronic exposure was calculated
from a lowest-observed-adverse-effect level (LOAEL) of 0.014 mg/kg/day for argyria observed in
patients receiving i.v. injections of silver arsphenamine (U.S. EPA, 1992a,b). Data are presently
insufficient to derive a Reference Concentration (RfC) for silver (U.S. EPA, 1992a).
Data adequate for evaluating the carcinogenicity of silver to humans or animals by ingestion,
inhalation, or other routes of exposure were not found. Based on U.S. EPA guidelines, silver is
placed in weight-of-evidence group D, not classifiable as to human carcinogenicity (U.S. EPA,
1992a).
1. INTRODUCTION
Silver (Ag; CAS Reg. No. 7440-22-4) is a relatively rare element occurring naturally in the earth's
crust as a soft, silver colored metal. It can exist in several oxidation states, with elemental silver and
monovalent silver ion as the most common (ATSDR, 1990). Silver has a molecular weight of
107.868, a density of 10.5 g/cm3 at 20C, and a melting point of 961.93C (Weast et al., 1988). It
is insoluble in water and alkalis, but is soluble in nitric acid, hot sulfuric acid, and potassium
cyanide. Some of the more common silver compounds used in industry include nitrate, chloride,
bromide, acetate, oxide, sulfate, and cyanide (Stokinger, 1981).
The principal uses of silver and silver compounds are in photographic materials, electroplating,
electrical conductors, dental alloys, solder and brazing alloys, paints, jewelry, coins, and mirror
production. Silver is also used for cloud seeding, as an antibacterial agent, and has been used for
water purification. Silver may be discharged into surface waters by various industries and
accumulated in soils from the fallout emissions from coal-fired power plants. The increasing cost
of the metal, however, is spurring development of recovery practices (Nordberg and Gerhardsson,
1988; U.S. EPA, 1985).
2. METABOLISM AND DISPOSITION
2.1. ABSORPTION
Studies in humans and animals indicate that silver compounds are absorbed via the oral and
inhalation routes of exposure, with some absorption occurring through both intact and damaged skin
(ATSDR, 1990). East et al. (1980) reported that a patient with argyria (gray or blue-gray discoloration of the skin) absorbed approximately 18% of a single dose of orally administered silver.
Generalized argyria in a woman who repeatedly applied a silver nitrate solution to her gums
indicates absorption across the oral mucosa (Marshall and Schneider, 1977). Absorption from the
lung was documented in a case of accidental exposure to radiolabeled silver metal dust (Newton and
Holmes, 1966). Following intratracheal administration to beagle dogs, the absorption of metallic
silver particles appears to be extensive. Phalen and Morrow (1973) estimated that up to 90% of
silver (mean aerodynamic diameter = 0.5 µm) deposited in the lungs of dogs was absorbed into the
systemic circulation 6 hours after exposure. In humans, less than 1% of dermally applied silver
compounds are absorbed through the skin (Snyder et al., 1975).
2.2. DISTRIBUTION
Silver has been detected in 50% of the samples of 29 human tissues, but at lower levels than other
trace elements (U.S. EPA, 1985). Silver has no known physiological function in man, but its
accumulation leads to argyria when the body burden is > 1 g (Stokinger, 1981). Granular deposits
that contain silver have been observed in both pigmented and unpigmented skin of silver-exposed
humans and animals. Once absorbed, orally-administered silver undergoes a first-pass effect
through the liver, resulting in excretion into the bile, and thereby reducing the systemic distribution
to tissues (ATSDR, 1990). Following ingestion of silver nitrate and silver chloride, silver was
distributed widely in tissues of rats, with high concentrations seen in the tissues of the
reticuloendothelial system (liver, spleen, bone marrow, lymph nodes, skin, and kidney) (Olcott,
1948). Silver was confined mainly to the liver of a worker who had accidentally inhaled radiolabeled silver metal; a biological half-life of 52 days was estimated (Newton and Holmes, 1966).
Six hours after intratracheal administration of metallic silver to dogs, 96.9, 2.4, and 0.35% of the
initially deposited dose was detected in the lungs, liver, and blood, respectively. The remaining
silver was detected in the gall bladder and bile, intestines, and stomach. After 225 days, the
distribution in tissue type was similar, with most of the silver found in the liver (Phalen and Morrow,
1976).
2.3. METABOLISM
ATSDR (1990) reports that the deposition of silver in tissues is the result of the precipitation of
insoluble silver salts, such as silver chloride and silver phosphate. These insoluble silver salts are
then transformed into soluble silver sulfide albuminates, to bind or to form complexes with amino
or carboxyl groups in RNA, DNA, and proteins, or to be reduced by ascorbic acid or catecholamines.
The skin discoloration of humans with argyria may be caused by a photoreduction of silver chloride
to metallic silver. The metallic silver is then oxidized by tissue, subsequently forming black silver
sulfide.
2.4. EXCRETION
Following oral or inhalation exposure to silver compounds, humans excrete silver primarily in the
feces and only very minor amounts in the urine (East et al., 1980; Newton and Holmes, 1966). In
rats and mice, the cumulative recovery of silver in the feces was 98-99% on the second day after oral
exposure to silver; monkeys excreted 94% (U.S. EPA, 1985). Dogs excreted approximately 90%
of an inhaled dose of metallic silver particles in the feces within 30 days of exposure (Phalen and
Morrow, 1973).
3. NONCARCINOGENIC HEALTH EFFECTS
3.1. ORAL EXPOSURES
3.1.1. Acute Toxicity
3.1.1.1. Human
Accidental or intentional ingestion of large doses of silver nitrate caused corrosive damage to the
gastrointestinal tract, abdominal pain, diarrhea, vomiting, shock, convulsions, and death. The
estimated fatal dose of silver nitrate is 10 g, but recoveries have been reported following ingestion
of larger doses (U.S. EPA, 1985).
3.1.1.2. Animal
The acute toxicity of silver compounds appears to be high. Oral LD50 values for mice reported
for colloidal silver and silver nitrate are 100 mg/kg and 129 mg/kg, respectively; for silver cyanide,
the LD50 for rats is 125 mg/kg. An LDLO of 2820 mg/kg for rats is reported for the relatively
insoluble silver oxide (Venugopal and Luckey, 1978).
3.1.2. Subchronic Toxicity
3.1.2.1. Human
Argyria (see Section 3.1.3.1.) has been observed in individuals that have ingested both metallic
silver and silver compounds in small doses over periods of months to years (ATSDR, 1990).
Blumberg and Carey (1934) reported argyria in an emaciated female adult who had ingested an
estimated total dose 6.4 g silver nitrate over a 1-year period. Symptoms of argyria appeared in one
individual after the first 6 months of exposure to unknown quantities of silver acetate (East et al.,
1980).
3.1.2.2. Animal
One study indicated that female mice exposed to silver nitrate in drinking water for 4 months were
less active than controls. The mice also had granular silver-containing deposits in some areas of the
central nervous system, with highest concentrations in areas involved in motor control (Rungby and
Danscher, 1984).
3.1.3. Chronic Toxicity
3.1.3.1. Human
Argyria, a characteristic and irreversible gray or blue-gray discoloration of the skin and mucous
membranes, has been observed in individuals that have ingested both metallic silver and silver
compounds in small doses over periods of months or years. Argyria, both generalized or localized,
has resulted from such uses as antismoking lozenges containing silver acetate, breath mints coated
with silver, silver nitrate solutions for the treatment of gum disease, and silver nitrate capsules for
relief of gastrointestinal discomfort (ATSDR, 1990; Stokinger, 1981). Argyria is most noticeable
in areas of skin exposed to light (ATSDR, 1990) and blond individuals are considered more
susceptible to argyria than others (Nordberg and Gerhardsson, 1988). The pigmentation is not a
toxic effect per se, but can be considered a cosmetic disfigurement in some cases. Silver-containing
granules, particularly concentrated in basement membranes and elastic fibers surrounding sweat
glands, have been observed during histopathologic examination of the skin of these individuals
(ATSDR, 1990). When argyria is localized in the eyes, the conjunctiva is most frequently affected,
with silver deposition on the elastic fibers (Stokinger, 1981). The estimated total dose required to
induce argyria by ingestion is in the range of 1-30 g for soluble silver salts (Nordberg and
Gerhardsson, 1988).
3.1.3.2. Animal
Exposure of rats to 222 mg silver/kg/day in drinking water for 37 weeks resulted in growth depression and shortened lifespan. Also observed were granular silver deposits in the eyes (Matuk et al.,
1981).
Olcott (1948, 1950) reported enlargement of the left ventricle of the heart in rats receiving drinking
water containing 635-660 mg silver/day as either silver nitrate or silver chloride for life. Histologic
examination showed slight thickening of the basement membranes of kidney glomeruli in the
absence of severe renal lesions. Deposition of silver granules was observed in the skin, eyes, and
several internal organs.
3.1.4. Developmental and Reproductive Toxicity
3.1.4.1. Human
Information on the developmental and reproductive toxicity in humans following inhalation
exposure to silver was unavailable.
3.1.4.2. Animal
There was no decrease of fertility in male rats exposed for life to drinking water containing 635-660 mg silver/day as either silver nitrate or silver chloride (Olcott, 1948).
3.1.5. Reference Dose
3.1.5.1. Subchronic
ORAL RfD: 0.005 mg/kg/day (U.S.EPA, 1992b)
UNCERTAINTY FACTOR: 3
LOAEL: 0.014 mg/kg/day
COMMENT: The same study applies to the subchronic and chronic RfD. The study is described
in Section 3.3.2.1.
3.1.5.2. Chronic
ORAL RfD: 0.005 mg/kg/day (U.S.EPA, 1992a,b)
UNCERTAINTY FACTOR: 3
LOAEL: 0.014 mg/kg/day
CONFIDENCE:
Study: Medium
Data Base: Low
RfD: Low
VERIFICATION DATE: 7/18/91
PRINCIPAL STUDY: Gaul and Straud, 1935
COMMENTS: The LOAEL is based on argyria observed in humans administered i.v. injections
of silver arsphenamine over a 2- to 9-year period. The total i.v. dose of 1 g (as silver) was
converted to a total oral dose of 25 g (i.v. dose divided by 0.04, the assumed oral retention factor)
and dividing by 70 kg (adult body weight) and 25,500 days. The uncertainty factor is applied to
protect sensitive human subpopulations.
3.2. INHALATION EXPOSURES
3.2.1. Acute Toxicity
3.2.1.1. Human
Acute irritation of the respiratory tract can occur from inhalation of silver nitrate dust, but
generally only at concentrations that produce argyria (Stokinger, 1981). One case report described
severe respiratory effects in a worker who had become ill 14 hours after working with molten silver
ingots (Forycki et al., 1983).
3.2.1.2. Animal
Acute inhalation (2-8 hours) of an aerosol containing colloidal silver caused ultrastructural damage
and disruption of cells of the tracheal epithelium of rabbits (ATSDR, 1990).
3.2.2. Subchronic Toxicity
Because the available human inhalation studies do not permit a clear distinction between subchronic and chronic effects, the data are presented only in Section 3.2.3.1., Chronic Toxicity.
3.2.2.1. Animal
Information on the subchronic inhalation toxicity of silver in animals was unavailable.
3.2.3. Chronic Toxicity
3.2.3.1. Human
Generalized argyria has been reported in workers associated with manufacturing and packaging
of silver nitrate and in workers engaged in mining, smelting, polishing, and hammering of silver
(U.S. EPA, 1985). Argyria may be localized in the respiratory tract, with isolated areas of pigmentation occurring at the tracheobronchial junction and around the orifices of the smaller bronchi in more
severe cases (Stokinger, 1981). The estimated total dose required to induce argyria by inhalation
is in the range of 1-8 g for soluble silver salts (Nordberg and Gerhardsson, 1988).
Rosenman et al. (1979) reported that 25/30 workers exposed to silver nitrate and silver oxide dusts
for < 1 to > 10 years experienced respiratory irritation (sneezing, stuffiness, and running nose or sore
throat) at some time during their employment. Cough, wheezing, chest tightness, and abdominal
pain were reported in 20/30 workers. The abdominal pain was significantly correlated with blood
silver levels. Granular silver-containing deposits, observed in the conjunctiva and cornea of the eyes
of 20/30 workers, correlated with the duration of employment. Decreased night vision was recorded
in some workers. The exposure levels (8-hour time-weighted average), determined 4 months prior
to the study, ranged from 0.039 to 0.378 mg silver/m3.
Decreased night vision was also reported in a group of workers manufacturing metal silver powder
(Rosenman et al., 1987). Also seen was increased excretion of the kidney enzyme N-acetyl-ß-D-glucosaminidase and decreased creatinine clearance, suggestive of impaired kidney function.
However, the workers were also exposed to cadmium, a known nephrotoxic compound.
In a study with silver reclamation workers exposed to silver and insoluble silver compounds,
conjunctival and corneal argyria was seen in 21% and 25% of the workers, respectively (Pifer et al.,
1989). Many of the workers exhibited internal nasal-septal pigmentation. There were no significant
differences in the levels of several liver enzymes between exposed individuals and those with no
history of silver exposure.
3.2.3.2. Animal
Information on the chronic inhalation toxicity of silver in animals was unavailable.
3.2.4. Developmental and Reproductive Toxicity
Information on the developmental and reproductive toxicity in humans or animals following
inhalation to silver was unavailable.
3.2.5. Reference Concentration
Available data are not sufficiently quantified to permit calculation of an RfC.
3.3. OTHER ROUTES OF EXPOSURE
3.3.1. Acute Toxicity
3.3.1.1. Human
Silver nitrate solutions are highly irritating to the skin, mucous membranes, and eyes. Ocular
damage has been reported from application of solutions containing > 2% silver nitrate. Corneal
opacification may be so severe as to cause blindness. Application of silver nitrate to the gingiva
may result in necrotizing, ulcerative gingivitis (Stokinger, 1981).
3.3.1.2. Animal
Early studies reported effects on the nervous system, including weakness, rigidity of legs, loss of
voluntary movement, and respiratory paralysis following intravenous administration of high doses
of silver compounds to rats, dogs, and guinea pigs (U.S. EPA, 1985). Intravenous administration
of 25.2 mg/kg silver nitrate, 420 mg/kg colloidal silver, or 11.6 mg/kg silver proteinate resulted in
the death of rats within 24-48 hours (Dequidt et al., 1974).
3.3.2. Subchronic Toxicity
3.3.2.1. Human
Intravenous administration of an estimated total dose of 4-20 g silver arsphemamine over a 2- to
9.75-year period caused argyria in humans. Argyria developed after a total dose of 4-8 g in some
patients, while in others argyria did not develop until after a total dose of 10-20 g (Gaul and Straud,
1935).
3.3.2.2. Animal
Guinea pigs ceased to gain weight when a 0.239 molar solution of silver nitrate was applied to 3.1
cm2 of skin for 8 weeks (Wahlberg, 1965).
3.3.3. Chronic Toxicity
3.3.3.1. Human
Case histories indicate that dermal exposure to silver or silver compounds for extended periods can
lead to generalized skin discoloration similar to that seen after oral exposure. Also reported were
mild allergic responses attributed to dermal contact with silver or silver compounds. Sensitization
has resulted from contact with powdered silver cyanide, radiographic processing solutions
containing silver compounds, and to silver in dental amalgam (ATSDR, 1990).
3.3.4. Developmental and Reproductive Toxicity
3.3.4.1. Human
Information on the developmental and reproductive toxicity in humans by other routes of exposure
to silver was unavailable.
3.3.4.2. Animal
A single subcutaneous injection of 0.04 millimole/kg silver nitrate caused temporary
histopathological damage to testicular tissue of male rats (Hoey, 1966).
3.4. TARGET ORGANS/CRITICAL EFFECTS
3.4.1. Oral Exposures
3.4.1.1. Primary Target Organ(s)
Skin and mucous membranes: Argyria, both general and localized, is the most common effect of
chronic exposure to silver and silver compounds in humans. Granular silver-containing deposits
are seen in animals.
3.4.1.2. Other Target Organ(s)
1. Heart: Chronic exposure of rats caused enlargement of the left ventricle of the heart.
2. Kidneys: Chronic exposure of rats caused a slight thickening of the basement membranes of
the renal glomeruli.
3. Central nervous system: Hypoactivity was observed in rats subchronically exposed to silver.
3.4.2. Inhalation Exposures
3.4.2.1. Primary Target Organ(s)
1. Skin and mucous membranes: Argyria, both general and localized, is the most common effect
of chronic inhalation exposure to silver in humans.
2. Respiratory tract: Occupational exposure to silver has caused upper and lower respiratory tract
irritation.
3.4.2.2. Other Target Organ(s)
1. Eyes: Impairment of night vision was reported in some workers chronically exposed to silver.
2. Kidneys: An occupational study suggests impairment of kidney function as evidenced by
increased excretion of a kidney enzyme indicative of cellular damage and by decreased creatinine
clearance.
3. Gastrointestinal tract: Abdominal pain was one of the symptoms recorded in workers exposed
to silver.
4. CARCINOGENICITY
4.1. ORAL EXPOSURES
Information on the oral carcinogenicity of silver in humans or animals is unavailable.
4.2. INHALATION EXPOSURES
Information on the carcinogenicity of inhaled silver in humans or animals is unavailable.
4.3. OTHER ROUTES OF EXPOSURE
4.3.1. Human
4.3.2. Animal
Subcutaneous embedding of silver foil induced a 32% incidence of local fibrosarcomas in rats,
with a latency period of 275 days (Oppenheimer et al., 1956). Silver apparently produced fibrosarcomas earlier and more frequently than several other metal foils. Schmähl and Steinhoff (1960)
reported that colloidal silver injected subcutaneously into rats resulted in tumors in 8/26 rats that
survived longer than 14 months. In six of the eight rats, the tumors were at the injection site.
However, use of the subcutaneous route of exposure is questionable, because almost any implanted
solid may induce a fibrosarcoma at the site (Furst, 1981). In another study, no tumors were found
at the injection site of rats intramuscularly injected with silver (Furst and Schlauder, 1977).
4.4. EPA WEIGHT-OF-EVIDENCE
Classification D -- Not classifiable as to human carcinogenicity
Basis -- In animals, local sarcomas have been induced after implantation of foils and discs of
silver. However, the interpretation of these findings has been questioned due to the phenomenon
of solid-state carcinogenesis in which even insoluble solids such as plastics have been shown to
result in local fibrosarcomas (U.S. EPA, 1992a).
4.5. CARCINOGENICITY SLOPE FACTORS
None were calculated.
5. REFERENCES
ATSDR (Agency for Toxic Substances and Disease Registry). 1990. Toxicological Profile for
Silver. Prepared by Clement International Corporation, under Contract 205-88-0608. U.S. Public
Health Service. ATSDR/TP-90-24.
Blumberg, H. and T.N. Carey. 1934. Argyremia: Detection of unsuspected and obscure argyria by
the spectrographic demonstration of high blood silver. J. Am. Med. Assoc. 103: 1521-1524. (Cited
in U.S. EPA, 1991a)
Dequidt, J., P. Vasseur and J. Gromez-Potentier. 1974. Experimental toxicological study of some
silver derivatives. Bulletin de la Societe de Pharmacie de Lille 1: 23-25. (In French; cited in
ATSDR, 1990)
East, B.W., K. Boddy, E.D. Williams, et al. 1980. Silver retention, total body silver and tissue
silver concentrations in argyria associated with exposure to an anti-smoking remedy containing
silver acetate. Clin. Exp. Dermatol. 5: 305-311. (Cited in ATSDR, 1990)
Forycki, Z., W. Zegarski, J. Bardzik, et al. 1983. Acute silver poisoning through inhalation.
Bulletin of the Institute of Maritime and Tropical Medicine in Gdynia. 34: 100-203. (Cited in
ATSDR, 1990)
Furst, A. 1981. Bioassay of metals for carcinogenesis: Whole animals. Environ. Health Perspect.
40: 83-91.
Furst, A. and M.C. Schlauder. 1977. Inactivity of two nobel metals as carcinogens. J. Environ.
Pathol. Toxicol. 1: 51-57.
Gaul, L.E. and A.H. Staud. 1935. Clinical spectroscopy. Seventy cases of generalized argyria
following organic and colloidal silver medication. J. Am. Med. Assoc. 104: 1387-1390. (Cited in
U.S. EPA, 1991a)
Hill, W.R. and D.M. Pillsbury. 1939. Argyria, the Pharmacology of Silver. The Williams and
Wilkins Co., Baltimore, MD, 167 p.
Hoey, M.J. 1966. The effects of metallic salts on the histology and functioning of the rat testes.
J. Reprod. Fertil. 12: 461-471. (Cited in ATSDR, 1990)
Marshall, J.P., II, and R.P. Schneider. 1977. Systemic argyria: Secondary to topical silver nitrate.
Arch. Dermatol. 113: 1077-1079.
Matuk, Y., M. Gosh and C. McCulloch. 1981. Distribution of silver in the eyes and plasma proteins
of the albino rat. Can. J. Ophthalmol. 16: 145-150. (Cited in ATSDR, 1990)
Newton, D. and A. Holmes. 1966. A case of accidental inhalation of zinc-65 and silver-110m.
Radiat. Res. 29: 403-412.
Nordberg, G.F. and L. Gerhardsson. 1988. Silver. In: Handbook on Toxicity of Inorganic
Compounds, H.G. Seiler and H. Sigel, eds. Marcel Dekker, Inc., New York, pp. 619-623.
Olcott, C.T. 1948. Experimental argyrosis. IV. Morphologic changes in the experimental animal.
Am. J. Path. 24: 813-833.
Olcott, C.T. 1950. Experimental argyrosis. V. Hypertrophy of the left ventricle of the heart.
Archives of Pathol. 49: 138-149.
Oppenheimer, B.S., E.T. Oppenheimer, I. Danishefsky, et al. 1956. Carcinogenic effects of metals
in rodents. Cancer Res. 16: 439-441.
Phalen, R.F. and P.E. Morrow. 1973. Experimental inhalation of metallic silver. Health Physics
24: 509-518.
Pifer, J.W., B.R. Friedlander, R.T. Kintz, et al. 1989. Absence of toxic effects in silver reclamation
workers. Scand. J. Work Environ. Health 15: 210-221.
Rosenman, K.D., A. Moss and S. Kon. 1979. Argyria: Clinical implications of exposure to silver
nitrate and silver oxide. J. Occup. Med. 21: 430-435.
Rosenman, K.D., N. Seixas and I. Jacobs. 1987. Potential nephrotoxic effects of exposure to silver.
Br. J. Ind. Med. 44: 267-272.
Rungby, J. and G. Danscher. 1984. Hypoactivity in silver exposed mice. Acta Pharmacol. Toxicol.
55: 398-401.
Schmähl, D. and D. Steinhoff. 1960. Experimental carcinogenesis in rats with colloidal silver and
gold solutions. Z. Krebsforsch. 63: 586-591. (In German; cited in ATSDR, 1991; Stokinger, 1981)
Snyder, W.S., et al. 1975. Report of the Task Group on Reference Man. Pergamon Press, Oxford,
England, pp. 407-708. (Cited in ATSDR, 1990)
Stokinger, H.E. 1981. Silver. In: Patty's Industrial Hygiene and Toxicology, vol. 2A, G.D. Clayton
and E. Clayton, eds. John Wiley & Sons, New York, NY, pp. 1881-1894.
U.S. EPA. 1985. Drinking Water Criteria Document for Silver (Final Draft). Environmental
Criteria and Assessment Office, Cincinnati, OH. ECAO-CIN-026, PB86-118288.
U.S. EPA. 1992a. Integrated Risk Information System (IRIS). Environmental Criteria and
Assessment Office, Office of Health and Environmental Assessment, Cincinnati, OH.
U.S. EPA. 1992b. Health Effects Assessment Summary Tables. Annual FY-92. Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office,
Office, Cincinnati, OH, for the Office of Emergency and Remedial Response, Washington DC.
Venugopal, B. and T.D. Luckey. 1978. Metal Toxicity in Mammals: 2. Chemical Toxicity of
Metals and Metalloids, Chapter 1. Plenum Press, New York, pp. 32-36.
Wahlberg, J.E. 1965. Percutaneous toxicity of metal compounds. A comparative investigation in
guinea pigs. Arch. Environ. Health 11: 201-204.
Weast, R.C., J.A. Spadaro, R.O. Becker, et al. 1988-1989. Handbook of Chemistry and Physics,
69th ed. CRC Press, Inc., Boca Raton, FL., pp. (B)127-128.2
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