Lyme Disease - Scientists,resurrecting,use,of,silver,as,antiseptic

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Scientists,resurrecting,use,of,silver,as,antiseptic

BreastImplantAwareness.org

2006-06-24, 8:23 am

Scientists resurrecting use of silver as antiseptic

By Barnaby Feder The New York Times

WEDNESDAY, DECEMBER 21, 2005
Silver, one of humankind's first weapons against bacteria, is
receiving
new respect for its antiseptic powers thanks to the growing ability of
researchers to tinker with its molecular structure.

Doctors prescribed silver to fight infections at least as far back as
the days of ancient Greece and Egypt. Their knowledge was absorbed by
Rome, where historians like Pliny the Elder reported that silver
plasters caused wounds to close rapidly. More recently, in 1884, a
German doctor named C.S.F. Crede demonstrated that putting a few drops
of silver nitrate into the eyes of babies born to women with venereal
disease virtually eliminated the high rates of blindness among such
infants.

But silver's time-tested if poorly understood versatility as a
disinfectant was overshadowed in the latter half of the 20th century
by
the rise of antibiotics.

Now, with more and more bacteria developing resistance to antibiotic
drugs, some researchers and health care entrepreneurs have returned to
silver for another look. This time around, they are armed with
nanotechnology, a fast-developing collection of products and skills
that helps researchers deploy silver compounds in ways that maximize
the availability of silver ions - the element's most potent form.
Scientists also now have a better understanding of the weaknesses of
their microbial adversaries.

One of the urgent goals is to prevent bacterial infections that each
year strike 2 million hospital patients in the United States and kill
90,000, according to the Centers for Disease Control and Prevention.
Such infections are usually treated with large doses of antibiotics
and
sometimes with repeat surgeries. They cost the U.S. health care system
roughly $4.5 billion annually, and the challenge is growing with the
spread of drug-resistant microbes.
tood versatility as a disinfectant was overshadowed in the latter
half
of the 20th century by the rise of antibiotics....

http://www.iht.com/articles/2005/12...ce/snsilver.php

Will Ketcher

2006-06-24, 8:23 am

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=2E INTRODUCTION
2=2E METABOLISM AND DISPOSITION
2=2E1 ABSORPTION
2=2E2 DISTRIBUTION
2=2E3 METABOLISM
2=2E4 EXCRETION
3=2E NONCARCINOGENIC HEALTH EFFECTS
3=2E1 ORAL EXPOSURES
3=2E2 INHALATION EXPOSURES
3=2E3 OTHER ROUTES OF EXPOSURE
3=2E4 TARGET ORGANS/CRITICAL EFFECTS
4=2E CARCINOGENICITY
4=2E1 ORAL EXPOSURES
4=2E2 INHALATION EXPOSURES
4=2E3 OTHER ROUTES OF EXPOSURE
4=2E4 EPA WEIGHT-OF-EVIDENCE
4=2E5 CARCINOGENICITY SLOPE FACTORS
5=2E 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=2Ev. 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=2E 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=2E METABOLISM AND DISPOSITION
2=2E1. 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 =3D
0=2E5 =B5m) 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=2E2. 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=2E3. 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=2E4. 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=2E NONCARCINOGENIC HEALTH EFFECTS
3=2E1. ORAL EXPOSURES
3=2E1.1. Acute Toxicity
3=2E1.1.1. 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=2E1.1.2. 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=2E1.2. Subchronic Toxicity
3=2E1.2.1. 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=2E1.2.2. 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=2E1.3. Chronic Toxicity
3=2E1.3.1. 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=2E1.3.2. 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=2E1.4. Developmental and Reproductive Toxicity
3=2E1.4.1. Human
Information on the developmental and reproductive toxicity in humans
following inhalation exposure to silver was unavailable.

3=2E1.4.2. 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=2E1.5. Reference Dose
3=2E1.5.1. 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=2E1.5.2. 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=2Ev. 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=2E2. INHALATION EXPOSURES
3=2E2.1. Acute Toxicity
3=2E2.1.1. 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=2E2.1.2. 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=2E2.2. 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=2E2.2.1. Animal
Information on the subchronic inhalation toxicity of silver in animals
was unavailable.

3=2E2.3. Chronic Toxicity
3=2E2.3.1. 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-=DF-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=2E2.3.2. Animal
Information on the chronic inhalation toxicity of silver in animals was
unavailable.

3=2E2.4. Developmental and Reproductive Toxicity
Information on the developmental and reproductive toxicity in humans or
animals following inhalation to silver was unavailable.

3=2E2.5. Reference Concentration
Available data are not sufficiently quantified to permit calculation of
an RfC.

3=2E3. OTHER ROUTES OF EXPOSURE
3=2E3.1. Acute Toxicity
3=2E3.1.1. 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=2E3.1.2. 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=2E3.2. Subchronic Toxicity
3=2E3.2.1. 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=2E3.2.2. 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=2E3.3. Chronic Toxicity
3=2E3.3.1. 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=2E3.4. Developmental and Reproductive Toxicity
3=2E3.4.1. Human
Information on the developmental and reproductive toxicity in humans by
other routes of exposure to silver was unavailable.

3=2E3.4.2. 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=2E4. TARGET ORGANS/CRITICAL EFFECTS
3=2E4.1. Oral Exposures
3=2E4.1.1. 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=2E4.1.2. Other Target Organ(s)
1=2E Heart: Chronic exposure of rats caused enlargement of the left
ventricle of the heart.

2=2E Kidneys: Chronic exposure of rats caused a slight thickening of the
basement membranes of the renal glomeruli.

3=2E Central nervous system: Hypoactivity was observed in rats
subchronically exposed to silver.

3=2E4.2. Inhalation Exposures
3=2E4.2.1. Primary Target Organ(s)
1=2E Skin and mucous membranes: Argyria, both general and localized, is
the most common effect of chronic inhalation exposure to silver in
humans.

2=2E Respiratory tract: Occupational exposure to silver has caused upper
and lower respiratory tract irritation.

3=2E4.2.2. Other Target Organ(s)
1=2E Eyes: Impairment of night vision was reported in some workers
chronically exposed to silver.

2=2E 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=2E Gastrointestinal tract: Abdominal pain was one of the symptoms
recorded in workers exposed to silver.

4=2E CARCINOGENICITY
4=2E1. ORAL EXPOSURES
Information on the oral carcinogenicity of silver in humans or animals
is unavailable.

4=2E2. INHALATION EXPOSURES
Information on the carcinogenicity of inhaled silver in humans or
animals is unavailable.

4=2E3. OTHER ROUTES OF EXPOSURE

4=2E3.1. Human

4=2E3.2. 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. Schm=E4hl 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=2E4. 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=2E5. CARCINOGENICITY SLOPE FACTORS
None were calculated.

5=2E 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
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Mark Probert

2006-06-24, 9:22 pm

BreastImplantAwareness.org wrote:
> Scientists resurrecting use of silver as antiseptic
>
> By Barnaby Feder The New York Times
>
>
> WEDNESDAY, DECEMBER 21, 2005
> Silver, one of humankind's first weapons against bacteria, is
> receiving
> new respect for its antiseptic powers thanks to the growing ability of
> researchers to tinker with its molecular structure.
>
>
> Doctors prescribed silver to fight infections at least as far back as
> the days of ancient Greece and Egypt. Their knowledge was absorbed by
> Rome, where historians like Pliny the Elder reported that silver
> plasters caused wounds to close rapidly. More recently, in 1884, a
> German doctor named C.S.F. Crede demonstrated that putting a few drops
> of silver nitrate into the eyes of babies born to women with venereal
> disease virtually eliminated the high rates of blindness among such
> infants.
>
>
> But silver's time-tested if poorly understood versatility as a
> disinfectant was overshadowed in the latter half of the 20th century
> by
> the rise of antibiotics.
>
>
> Now, with more and more bacteria developing resistance to antibiotic
> drugs, some researchers and health care entrepreneurs have returned to
> silver for another look. This time around, they are armed with
> nanotechnology, a fast-developing collection of products and skills
> that helps researchers deploy silver compounds in ways that maximize
> the availability of silver ions - the element's most potent form.
> Scientists also now have a better understanding of the weaknesses of
> their microbial adversaries.
>
>
> One of the urgent goals is to prevent bacterial infections that each
> year strike 2 million hospital patients in the United States and kill
> 90,000, according to the Centers for Disease Control and Prevention.
> Such infections are usually treated with large doses of antibiotics
> and
> sometimes with repeat surgeries. They cost the U.S. health care system
> roughly $4.5 billion annually, and the challenge is growing with the
> spread of drug-resistant microbes.
> tood versatility as a disinfectant was overshadowed in the latter
> half
> of the 20th century by the rise of antibiotics....
>
>
> http://www.iht.com/articles/2005/12...ce/snsilver.php
>
>

No one questions the use of silver products as *topical* disinfectants.

The issue is the use of silver by swallowing it.

There is not proof that it is effective used that way.

BrentB

2006-06-26, 4:23 pm

BreastImplantAwareness.org wrote:
> Scientists resurrecting use of silver as antiseptic
>
> By Barnaby Feder The New York Times
>
>
> WEDNESDAY, DECEMBER 21, 2005
> Silver, one of humankind's first weapons against bacteria, is
> receiving
> new respect for its antiseptic powers thanks to the growing ability of
> researchers to tinker with its molecular structure.
>
>

Latest in vivo research from pubmed. remarkable that the patients
didn't die from silver toxicity.

Use of catheters with the AgION antimicrobial system in kidney
transplant recipients to reduce infection risk.

Loertzer H, Soukup J, Hamza A, Wicht A, Rettkowski O, Koch E, Fornara
P.

Department of Urology and Transplant Center of the Martin Luther
University, Halle, Germany. Hagen.Loertzer@medizin.uni-halle.de

Microbial blood infection represents a high risk for immuno-suppressed
patients. Of all catheter-related infections in the bloodstream, 90%
result from the use of central venous catheters, the main cause being
microbial colonization at the catheter's insertion point or the
catheter hub. Between January 2003 and December 2004, 102 patients
received a renal transplant including 57 who received a triple-lumen
central venous catheter (CVC) during the procedure. Two catheters were
used: a standard polyurethane catheter placed in the jugular veina or
the subclavian veina for group I, and polyurethane catheters with the
AgION antimicrobial system always placed in the subclavian veina for
group II. Care and maintenance of the CVCs was standardized in both
groups. After catheter removal, the tips were analyzed
microbiologically. Of 57 (43.9%) CVCs, 25 were found to be
contaminated. In the first group 24 out of 41 CVCs (58.5%) showed
bacterial growth, whereas in group II only one catheter (6.6%) had a
biofilm. The most common contaminant (18 out of 25, 72%) was
Staphylococcus epidermidis. In group II, two patients had positive
blood cultures yet a microbiologically sterile CVC. None of the
catheters with the AgION antimicrobial system had to be removed owing
to local infection or intolerance. The continuous release of silver
ions increases the protection against bacteria and fungi during the
entire time of catheterization. Use of catheters with the AgION
antimicrobial system lead to a marked reduction in catheter-associated
infections of the bloodstream.

PMID: 16647450 [PubMed - in process]