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CASRN 7440-22-4



Silver; CASRN 7440-22-4  

Health assessment information on a chemical substance is included in IRIS only 
after a comprehensive review of chronic toxicity data by U.S. EPA health 
scientists from several Program Offices and the Office of Research and 
Development.  The summaries presented in Sections I and II represent a 
consensus reached in the review process.  Background information and 
explanations of the methods used to derive the values given in IRIS are 
provided in the Background Documents. 


File On-Line 01/31/1987

Category (section)                           Status      Last Revised
-----------------------------------------    --------    ------------

Oral RfD Assessment (I.A.)                   on-line       12/01/1996

Inhalation RfC Assessment (I.B.)             no data     

Carcinogenicity Assessment (II.)             on-line       06/01/1989



Substance Name -- Silver
CASRN -- 7440-22-4
Last Revised -- 12/01/1996

The oral Reference Dose (RfD) is based on the assumption that thresholds exist 
for certain toxic effects such as cellular necrosis. It is expressed in units 
of mg/kg-day.  In general, the RfD is an estimate (with uncertainty spanning 
perhaps an order of magnitude) of a daily exposure to the human population 
(including sensitive subgroups) that is likely to be without an appreciable 
risk of deleterious effects during a lifetime.  Please refer to the Background 
Document for an elaboration of these concepts.  RfDs can also be derived for 
the noncarcinogenic health effects of substances that are also carcinogens.  
Therefore, it is essential to refer to other sources of information concerning 
the carcinogenicity of this substance.  If the U.S. EPA has evaluated this 
substance for potential human carcinogenicity, a summary of that evaluation 
will be contained in Section II of this file. 


Critical Effect         Experimental Doses*          UF     MF       RfD
--------------------    -----------------------    -----   ---     ---------
Argyria                 NOEL: None                     3     1       5E-3
2- to 9-Year            LOAEL: 1 g (total dose);
Human i.v. Study        converted to an oral
                        dose of 0.014 mg/kg/day
Gaul and Staud, 1935

*Conversion Factors:  Based on conversion from the total i.v. dose to a
total oral dose of 25 g (i.v. dose of 1 g divided by 0.04, assumed oral
retention factor; see Furchner et al., 1968 in Additional Comments
section) and dividing by 70 kg (adult body weight) and 25,500 days (a
lifetime, or 70 years).


Gaul, L.E. and A.H. Staud.  1935.  Clinical spectroscopy.  Seventy cases of 
generalized argyrosis following organic and colloidal silver medication.  J. 
Am. Med. Assoc.  104: 1387-1390. 

The critical effect in humans ingesting silver is argyria, a medically benign 
but permanent bluish-gray discoloration of the skin.  Argyria results from the 
deposition of silver in the dermis and also from silver-induced production of 
melanin.  Although silver has been shown to be uniformly deposited in exposed 
and unexposed areas, the increased pigmentation becomes more pronounced in 
areas exposed to sunlight due to photoactivated reduction of the metal.  
Although the deposition of silver is permanent, it is not associated with any 
adverse health effects.  No pathologic changes or inflammatory reactions have 
been shown to result from silver deposition.  Silver compounds have been 
employed for medical uses for centuries.  In the nineteenth and early 
twentieth centuries, silver arsphenamine was used in the treatment of 
syphillis; more recently it has been used as an astringent in topical 
preparations.  While argyria occurred more commonly before the development of 
antibiotics, it is now a rare occurrence.  Greene and Su (1987) have published 
a review of argyria. 

Gaul and Staud (1935) reported 70 cases of generalized argyria following 
organic and colloidal silver medication, including 13 cases of generalized 
argyria following intravenous silver arsphenamine injection therapy and a 
biospectrometric analysis of 10 cases of generalized argyria classified 
according to the quantity of silver present.  In the i.v. study, data were 
presented for 10 males (23-64 years old) and for two females (23 and 49 years 
old) who were administered 31-100 i.v. injections of silver arsphenamine 
(total dose was 4-20 g) over a 2- to 9.75-year period.  Argyria developed 
after a total dose of 4, 7 or 8 g in some patients, while in others, argyria 
did not develop until after a total dose of 10, 15 or 20 g.  In the 
biospectrometric analysis of skin biopsies from 10 cases of generalized 
argyria, the authors confirmed that the degree of the discoloration is 
directly dependent on the amount of silver present.  The authors concluded 
that argyria may become clinically apparent after a total accumulated i.v. 
dose of approximately 8 g of silver arsphenamine.  The book entitled "Argyria.  
The Pharmacology of Silver" reached the same conclusion, that a total 
accumulative i.v. dose of 8 gm silver arsphenamine is the limit beyond which 
argyria may develop (Hill and Pillsbury, 1939).  However, since body 
accumulates silver throughout life, it is theoretically possible for amounts 
less than this (for example, 4 g silver arsphenamine) to result in argyria.  
Therefore, based on cases presented in this study, the lowest i.v. dose 
resulting in argyria in one patient, 1 g metallic silver (4 g silver 
arsphenamine x 0.23, the fraction of silver in silver arsphenamine) is 
considered to be a minimal effect level for this study. 

Blumberg and Carey (1934) reported argyria in an emaciated chronically ill 
(more than 15 years) 33-year-old female (32.7 kg) who had ingested capsules 
containing silver nitrate over a period of 1 year.  The patient reported 
ingesting 16 mg silver nitrate three times a day (about 30 mg silver/day) for 
alternate periods of 2 weeks.  Spectrographic analysis of blood samples 
revealed a blood silver level of 0.5 mg/L 1 week after ingestion of silver 
nitrate capsules ceased, and there was only a small decrease in this level 
after 3 months.  The authors noted that this marked argyremia was striking 
because even in cases of documented argyria, blood silver levels are not 
generally elevated to this extent.  Normal levels for argyremic patients were 
reported to range from not detected to 0.005 mg Ag/l blood.  Heavy traces of 
silver in the skin, moderate amounts in the urine and feces, and trace amounts 
in the saliva were reported in samples tested 3 months after ingestion of the 
capsules stopped; however, despite the marked argyremia and detection of 
silver in the skin, the argyria at 3 months was quite mild.  No obvious dark 
pigmentation was seen other than gingival lines which are considered to be 
characteristic of the first signs of argyria.  The authors suggested that this 
may have been because the woman was not exposed to strong light during the 
period of silver treatment.  This study is not suitable to serve as the basis 
for a quantitative risk assessment for silver because it is a clinical report 
on only one patient of compromised health.  Furthermore, the actual amount of 
silver ingested is based on the patient's recollection and cannot be 
accurately determined. 

In a case reported by East et al. (1980), argyria was diagnosed in a 47-year-
old woman (58.6 kg) who had taken excessively large oral doses of anti-smoking 
lozenges containing silver acetate over a period of 2.5 years.  No information 
was provided as to the actual amount of silver ingested.  Symptoms of argyria 
appeared after the first 6 months of exposure.  Based on whole body neutron 
activation analysis, the total body burden of silver in this female was 
estimated to be 6.4 (plus or minus 2) g.  Both the total body burden and 
concentration of silver in the skin were estimated to be 8000 times higher 
than normal.  In a separate 30-week experiment, the same subject retained 18% 
of a single dose of orally-administered silver, a retention level much higher 
than that reported by other investigators.  East et al. (1980) cited other 
studies on this particular anti-smoking formulation (on the market since 1973) 
which demonstrated that "within the limits of experimental error, no silver is 
retained after oral administration."  However, this may not hold true for 
excessive intakes like that ingested by this individual.  As with the study by 
Blumberg and Carey (1934), this study is not suitable to serve as the basis 
for a quantitative risk assessment.  It is a clinical report on only one 
patient and the actual amount of silver ingested can only be estimated. 


UF -- An uncertainty factor of 3 is applied to account for minimal effects in 
a subpopulation which has exhibited an increased propensity for the 
development of argyria.  The critical effect observed is a cosmetic effect, 
with no associated adverse health effects.  Also, the critical study reports 
on only 1 individual who developed argyria following an i.v. dose of 1 g 
silver (4 g silver arsphenamine).  Other individuals did not respond until 
levels five times higher were administered.  No uncertainty factor for less 
than chronic to chronic duration is needed because the dose has been 
apportioned over a lifetime of 70 years. 

MF -- None


In the study by East et al. (1980) (see section 1.A.2.), one human was found 
to retain 18% of a single oral dose.  However, the authors acknowledge that 
this high level of retention is not consistent with data published in other 
laboratories.  For ethical reasons, the experiment could be not repeated to 
determine the validity of the results. 

Humans are exposed to small amounts of silver from dietary sources.  The oral 
intake of silver from a typical diet has been estimated to range from 27-88 
ug/day (Hamilton and Minski, 1972/1973; Kehoe et al., 1940).  Tipton et al.  
(1966) estimated a lesser intake of 10-20 ug/day in two subjects during a 30-
day observation period.  Over a lifetime, a small but measurable amount of 
silver is accumulated by individuals having no excessive exposure.  Gaul and 
Staud (1935) estimated that a person aged 50 years would have an average 
retention of 0.23-0.48 g silver (equivalent to 1-2 g silver arsphenamine).  
Petering et al. (1991) estimated a much lower body burden of 9 mg over a 50-
year period based on estimated intake, absorption, and excretion values; 
however, it is not clear how the final estimate was calculated.  Furchner et 
al. (1968) studied the absorption and retention of ingested silver (as silver 
nitrate, amount not specified) in mice, rats, monkeys and dogs.  In all four 
species, very little silver was absorbed from the GI tract.  Cumulative 
excretion ranged from 90 to 99% on the second day after ingestion, with <1% of 
the dose being retained in <1 week in monkeys, rats and mice.  Dogs had a 
slightly greater retention.  The authors used the data from the dog to 
estimate how much silver ingested by a 70 kg human would be retained.  An 
"equilibrium factor" of 4.4% was determined by integrating from zero to 
infinity a retention equation which assumes a triphasic elimination pattern 
for silver with the initial elimination of 90% coming from the dog data.  The 
first elimination half-time of 0.5 days was used "arbitrarily"; subsequent 
half-times of 3.5 days and 41 days were taken from a metabolic study by 
Polachek et al. (1960).  Furchner et al. (1968) considered their calculated 
equilibrium factor of 4.4% to be a conservative estimate for the amount of 
silver which would be retained by a 70 kg human.  This figure was rounded to 
4% and was used in the dose conversion (i.v. dose converted to oral intake) 
for the calculation of the RfD. 

In addition to silver arsphenamine, any silver compound (silver nitrate, 
silver acetate, argyrol, Neosilvol and Collargol, etc.), at high dose, can 
cause argyria.  Another important factor predisposing to the development of 
argyria is the exposure of the skin to light. 

Argyria, the critical effect upon which the RfD for silver is based, occurs at 
levels of exposure much lower than those levels associated with other effects 
of silver.  Argyrosis, resulting from the deposition of silver in the eye, has 
also been documented, but generally involves the use of eye drops or make-up 
containing silver (Greene and Su, 1987).  Silver has been found to be 
deposited in the cornea and the anterior capsule of the lens.  The same 
deposition pattern was seen in the eyes of male Wistar rats following 
administration of a 0.66% silver nitrate solution to the eyes for 45 days 
(Rungby, 1986).  No toxicological effects were reported. 

Toxic effects of silver have been reported primarily for the cardiovascular 
and hepatic systems.  Olcott (1950) administered 0.1% silver nitrate in 
drinking water to rats for 218 days.  This exposure (about 89 mg/kg/day) 
resulted in a statistically significant increase in the incidence of 
ventricular hypertrophy.  Upon autopsy, advanced pigmentation was observed in 
body organs, but the ventricular hypertrophy was not attributed to silver 

Hepatic necrosis and ultrastructural changes of the liver have been induced by 
silver administration to vitamin E and/or selenium deficient rats (Wagner et 
al., 1975; Diplock et al., 1967; Bunyan et al., 1968).  Investigators have 
hypothesized that this toxicity is related to a silver-induced selenium 
deficiency that inhibits the synthesis of the seleno-enzyme glutathione 
peroxidase.  In animals supplemented with selenium and/or vitamin E, exposures 
of silver as high as 140 mg/kg/day (100 mg Ag/L drinking water) were well-
tolerated (Bunyan et al., 1968). 


Study -- Medium
Data Base -- Low
RfD -- Low

The critical human study rates a medium confidence.  It is an old study (1935) 
which offers fairly specific information regarding the total dose of silver 
injected over a stated period of time.  One shortcoming of the study is that 
only patients developing argyria are described; no information is presented on 
patients who received multiple injections of silver arsphenamine without 
developing argyria.  Therefore, it is difficult to establish a NOAEL.  Also, 
the individuals in the study were being treated for syphilis and may have been 
of compromised health. 

Confidence in the data base is considered to be low because the studies used 
to support the RfD were not controlled studies.  For clinical case studies of 
argyria (such as Blumberg and Carey, 1934; East et al., 1980), it is 
especially difficult to determine the amount of silver that was ingested. 

Confidence in the RfD can be considered low-to-medium because, while the 
critical effect has been demonstrated in humans following oral administration 
of silver, the quantitative risk estimate is based on a study utilizing 
intravenous administration and thus necessitates a dose conversion with 
inherent uncertainties. 


Source Document -- This assessment is not presented in any existing U.S. EPA 

Other EPA Documentation -- None

Agency Work Group Review -- 10/09/1985, 02/05/1986, 04/18/1990, 02/20/1991, 07/18/1991 

Verification Date -- 07/18/1991 


Please contact the Risk Information Hotline for all questions concerning this 
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX) 
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).

Substance Name -- Silver
CASRN -- 7440-22-4

Not available at this time.


Substance Name -- Silver
CASRN -- 7440-22-4
Last Revised -- 06/01/1989

Section II provides information on three aspects of the carcinogenic 
assessment for the substance in question; the weight-of-evidence judgment of 
the likelihood that the substance is a human carcinogen, and quantitative 
estimates of risk from oral exposure and from inhalation exposure. The 
quantitative risk estimates are presented in three ways.  The slope factor is 
the result of application of a low-dose extrapolation procedure and is 
presented as the risk per (mg/kg)/day.  The unit risk is the quantitative 
estimate in terms of either risk per ug/L drinking water or risk per ug/cu.m 
air breathed.  The third form in which risk is presented is a drinking water 
or air concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1 
in 1,000,000.  The rationale and methods used to develop the carcinogenicity 
information in IRIS are described in The Risk Assessment Guidelines of 1986 
(EPA/600/8-87/045) and in the IRIS Background Document.  IRIS summaries 
developed since the publication of EPA's more recent Proposed Guidelines for 
Carcinogen Risk Assessment also utilize those Guidelines where indicated 
(Federal Register 61(79):17960-18011, April 23, 1996).  Users are referred to 
Section I of this IRIS file for information on long-term toxic effects other 
than carcinogenicity. 



Classification -- D; not classified 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 plastic have been shown to result in local 


    No evidence of cancer in humans has been reported despite frequent 
therapeutic use of the compound over the years. 


    Inadequate.  Local sarcomas have been induced after subcutaneous (s.c.) 
implantation of foils and discs of silver and other noble metals.  Furst 
(1979, 1981), however, cited studies showing that even insoluble solids such 
as smooth ivory and plastic result in local fibrosarcomas and that tin when 
crumbled will not.  He concluded that i.p. and s.c. implants are invalid as 
indicators of carcinogenicity because a phenomenon called solid-state 
carcinogenesis may complicate the interpretation of the cause of these tumors.  
It is difficult to interpret these implantation site tumors in laboratory 
animals in terms of exposure to humans via ingestion.  Within these 
constraints there are two studies given below in which silver per se appeared 
to induce no carcinogenic response. 

    Schmahl and Steinhoff (1960) reported, in a study of silver and of gold, 
that colloidal silver injected both i.v. and s.c. into rats resulted in tumors 
in 8 of 26 rats which survived longer than 14 months.  In 6 of the 8, the 
tumor was at the site of the s.c. injection.  In about 700 untreated rats the 
rate of spontaneous tumor formation of any site was 1 to 3%.  No vehicle 
control was reported. 

    Furst and Schlauder (1977) evaluated silver and gold for carcinogenicity 
in a study designed to avoid solid-state carcinogenesis.  Metal powder was 
suspended in trioctanoin and injected monthly, i.m., into 50 male and female 
Fischer 344 rats per group.  The dose was 5 mg each for 5 treatments and 10 mg 
each for 5 more treatments for a total dose of 75 mg silver.  The treatment 
regimen included a vehicle control (a reportedly inert material), and cadmium 
as a positive control.  Injection site sarcomas were found only in vehicle 
control (1/50), gold (1/50) and cadmium (30/50); no tumors (0/50) appeared at 
the site of injection in the silver-treated animals.  A complete necropsy was 
performed on all animals.  The authors mentioned the existence of spontaneous 
tumors in Fischer 344 rats, but reported only injection site tumors.  They 
concluded that finely divided silver powder injected i.m. does not induce 


    Further support for the lack of silver's ability to induce or promote 
cancer stems from the finding that, despite long standing and frequent 
therapeutic usage in humans, there are no reports of cancer associated with 
silver.  In a recent Proceedings of a Workshop/Conference on the Role of 
Metals in Carcinogenesis (1981) containing 24 articles on animal bioassays, 
epidemiology, biochemistry, mutagenicity, and enhancement and inhibition of 
carcinogenesis, silver was not included as a metal of carcinogenic concern. 

    No evidence of the mutagenicity of silver was shown in two available 
studies.  Demerec et al. (1951) studied silver nitrate for the possible 
induction of back-mutations from streptomycin dependence to nondependence in 
Eschericha coli.  Silver nitrate was considered nonmutagenic in this assay.  
Nishioka (1975) screened silver chloride with other chemicals for mutagenic 
effects using a method called the rec-assay.  Silver chloride was considered 
nonmutagenic in this assay. 


    Not available.


    Not available.



Source Document -- U.S. EPA, 1988

The 1988 Drinking Water Criteria Document for Silver has received Agency 


Agency Work Group Review -- 09/22/1988

Verification Date -- 09/22/1988


Please contact the Risk Information Hotline for all questions concerning this 
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX) 
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).


Substance Name -- Silver
CASRN -- 7440-22-4
Last Revised -- 12/01/1991


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(20): 1521-1524.

Bunyan, J., A.T. Diplock, M.A. Cawthorne and J. Green.  1968.  Vitamin E and 
stress.  8. Nutritional effects of dietary stress with silver in vitamin E-
deficient chicks and rats.  Br. J. Nutr.  22(2): 165-182.

Diplock, A.T., J. Green, J. Bunyan, D. McHale and I.R. Muthy.  1967.  Vitamin 
E and stress.  3. The metabolism of D-alpha-tocopherol in the rat under 
dietary stress with silver.  Br. J. Nutr.  21(1): 115-125. 

East, B.W., K. Boddy, E.D. Williams, D. MacIntyre and A.L.C. McLay.  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. 

Furchner, J.E., C.R. Richmond and G.A. Drake.  1968.  Comparative metabolism 
of radionuclides in mammals - IV. Retention of silver - 110m in the mouse, 
rat, monkey, and dog.  Health Phys.  15: 505-514. 

Gaul L.E. and A.H. Staud.  1935.  Clinical spectroscopy.  Seventy cases of 
generalized argyrosis following organic and colloidal silver medication 
including a biospectrometric analysis of ten cases.  J. Am. Med. Assoc.  
104(16): 1387-1390. 

Greene, R.M. and W.P.D. Su.  1987.  Argyria.  Am. Fam. Phys.  36: 151-154.

Hamilton, E.I. and M.J. Minski.  1972/1973.  Abundance of the chemical 
elements in man's diet and possible relations with environmental factors.  
Sci. Total Environ.  1: 375-394.

Hill, W.R. and D.M. Pillsbury.  1939.  Argyria.  The pharmacology of silver.  
Williams and Wilkins Company, Baltimore, MD.

Kehoe, R.A., J. Cholar and R.V. Story.  1940.  A spectrochemical study of the 
normal ranges of concentration of certain trace metals in biological 
materials.  J. Nutr.  19: 579-592. 

Olcott, C.T.  1950.  Experimental argyrosis.  V. Hypertrophy of the left 
ventricule of the heart in rats ingesting silver salts.  Arch. Pathol.  49: 

Petering, H.G. and C.J. McClain.  1991.  Silver.  In: Metals and Their 
Compounds in the Environment: Occurrence, Analysis, and Biological Relevance, 
E. Merian, Ed.  VCH, Weinheim.  p. 1191-1201. 

Polachek, A.A., C.B. Cope, R.F. Williard and T. Enns.  1960.  Metabolism of 
radioactive silver in a patient with carcinoid.  J. Lab. Clin. Med.  56:

Rungby, J. 1986.  The silver nitrate prophylaxis of crede causes silver 
deposition in the cornea of experimental animals.  Exp. Eye Res.  42: 93-94. 

Tipton, I.H., P.L. Stewart and P.G. Martin.  1966.  Trace elements in diets 
and excretia.  Health Phys.  12: 1683-1689. 

Wagner, P.A., W.G. Hoeskstra and H.E. Ganther.  1975.  Alleviation of silver 
toxicity by selenite in the rat in relation to tissue glutathione 
peroxidase.  Proc. Soc. Exp. Biol. Med.  148(4): 1106-1110.




Demerec, M., G. Bertani and J. Flint.  1951.  A survey of chemicals for 
mutagenic action on E. coli.  Am. Nat. 85(821): 119-136. 

Furst, A.  1979.  Problems in metal carcinogenesis.  In: Trace Metals in 
Health and Disease, N. Kharasch, Ed.  Raven Press, New York.  p. 83-92. 

Furst, A.  1981.  Bioassay of metals for carcinogenesis: Whole animals.  
Environ. Health Perspect.  40: 83-92.

Furst, A. and M.C. Schlauder.  1977.  Inactivity of two noble metals as 
carcinogens.  J. Environ. Pathol. Toxicol.  1: 51-57. 

Nishioka, H.  1975.  Mutagenic activities of metal compounds in bacteria.  
Mutat. Res.  31: 185-189. 

Proceedings of a Workshop/Conference on the Role of Metals in Carcinogenesis.  
1981.  Environ. Health Perspect.  40: 252. 

Schmahl, D. and D. Steinhoff.  1960.  Versuche zur Krebserzeugung mit 
kolloidalen Silber-und Goldlosungen an Ratten.  Z. Krebsforsch.  63: 586-591. 

U.S. EPA.  1988.  Drinking Water Criteria Document for Silver.  Prepared by 
the Office of Health and Environmental Assessment, Environmental Criteria and 
Assessment Office, Cincinnati, OH for the Office of Drinking Water, 
Washington, DC.  ECAO-CIN-026.  Final Draft.


Substance Name -- Silver
CASRN -- 7440-22-4

--------   --------   --------------------------------------------------------
Date       Section    Description
--------   --------   --------------------------------------------------------
03/01/1988   I.A.4.     Text revised
03/01/1988   I.A.7.     Secondary contact changed
06/30/1988   I.A.7.     Primary contact changed
06/01/1989   II.        Carcinogen summary on-line
06/01/1989   VI.        Bibliography on-line
08/01/1989   VI.A.      Oral RfD references added
03/01/1991   I.A.       Oral RfD summary noted as pending change
08/01/1991   I.A.       Withdrawn; new oral RfD verified (in preparation)
08/01/1991   VI.A.      Oral RfD references withdrawn
12/01/1991   I.A.       Oral RfD summary replaced; RfD changed
12/01/1991   VI.A.      Oral RfD references replaced
01/01/1992   IV.        Regulatory actions updated
12/01/1996   I.A.7.     Secondary contact removed


Substance Name -- Silver
CASRN -- 7440-22-4
Last Revised -- 06/01/1989


Last updated: 5 May 1998
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