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Silver exposure

Bury, N.R., J.C. McGeer, and C.M. Wood. 1999b. Effects of altering freshwater chemistry on physiological responses of rainbow trout to silver exposure. Environ. Toxicol. Chem. 18 49-55. [Pg.575]

Toxicology. The primary effect of silver exposure is argyria, a gray-blue discoloration of the skin, eyes, nails, mucous membranes, and/or internal organs. [Pg.633]

For more information on criteria and standards for silver exposure, see Chapter 7. [Pg.25]

Hepatic Effects. A study that measured levels of several liver enzymes (alanine amino transferase, aspartate amino transferase, gamma glutamyl transferase, and alkaline phosphatase) found no significant differences between workers exposed to silver and insoluble silver compounds and those with no history of silver exposure (Pifer et al. 1989). [Pg.28]

Levels of silver exposure that have led to argyria in humans in the past are poorly documented, and it is not possible to establish minimum risk levels for this effect based on these data. Hill and Pillsbury (1939) in their review of cases of argyria report that total doses of silver that have resulted in argyria can be as low as a total of 1.4 grams of silver (as silver nitrate) ingested in small unspecified doses over several months. [Pg.55]

Immunological Effects. No studies were located that investigated toxic effects on the immune system in humans or animals exposed to silver, or that indicate that immune-related disease can be affected by silver exposure. Silver has been observed to elicit a mild allergic response (contact dermatitis) in humans following dermal exposure to various silver compounds. [Pg.55]

Several effects associated with silver exposure have been reported in humans which may be useful as biomarkers of effects. The significance of these biomarkers, however, is in doubt, because they do not appear consistently in exposed individuals and do not seem to correlate well with levels and duration of exposure. [Pg.63]

Low oxygen content in capillary blood, scattered thickening of lungs (as observed in chest radiograms), and upper respiratory irritation have been observed in studies of workers exposed intensely or chronically to molten silver or silver dusts (Forycki et al. 1983 Rosenman et al. 1979, 1987). Inhalation exposure also led to decreased red blood cell count and an increased mean corpuscular volume (Pifer et al. 1989). However, these potential hematologic biomarkers are not specific for silver exposure, and do not indicate or predict significant clinical sequelae. [Pg.63]

Populations that are unusually susceptible to toxic effects of silver exposure are those that have a dietary deficiency of vitamin E or selenium, or that may have a genetically based deficiency in the metabolism of these essential nutrients. Individuals with damaged livers may also be more susceptible to the effects of silver exposure. In addition, populations with high exposures to selenium may be more likely to develop argyria. Furthermore, some individuals may exhibit an allergic response to silver. [Pg.64]

As can be seen in Figure 2-2, very little information exists on the effects of dermal or inhalation exposure to silver in animals. Despite the need to evaluate NPL site exposure on a case by case basis, these routes are not expected to be significant sources of silver exposure. Furthermore, the oral exposure route has been examined primarily in regards to silver deposition in various tissues. The studies were not designed to examine other end points... [Pg.65]

Biomarkers of Exposure and Effect. Silver can be detected in blood, urine, feces, hair, and skin biopsy specimens. The best indictor of recent exposure to silver or silver compounds is detection of silver levels in feces and blood. Intermediate as well as long-term exposures are best monitored by measuring silver in blood or skin biopsy specimens. Argyria, the change in skin color associated with silver exposure, is also an indicator of chronic exposure. No other biomarkers for silver have been developed. Development of alternative biomarkers capable of detecting early exposure to low levels of silver would be useful in determining the possible toxic effects of this metal. [Pg.68]

Additional research into the comparative absorption, distribution, metabolism, and excretion of different silver compounds would allow a more accurate determination of the effects of silver exposure under specific environmental conditions. The current database primarily provides... [Pg.68]

Exposure Levels in Humans. Silver has been detected in the blood, tissues, urine, and feces of humans. The only biological monitoring studies located consisted of small numbers of worker populations in chemical manufacturing industries. Studies that better characterize important sources of general population exposure and define populations with potentially high exposure, such as those located near hazardous waste sites, would be helpful. More specific information concerning the chemical from of silver present at hazardous waste sites would also be useful. These data would assist in developing a more accurate estimate of the potential for silver exposure from hazardous waste sites contaminated with the metal. [Pg.110]

DiVincenzo et al. (1985) employed the GFAAS technique to evaluate human samples for biological monitoring of silver exposure levels in the workplace. The authors determined the total silver concentration in urine, blood, feces, and hair with detection limits of 0.005 pig/L, 0.5 pg/100 ml, 0.2 p gig, and 0.02 pg/g, respectively. [Pg.127]

Highly sensitive methods exist to measure silver concentrations in blood, urine, hair, and skin samples of individuals showing the few health effects that have been associated with silver exposure. These methods are also able to accurately measure background levels in the population. No additional analytical methods appear to be needed for the known biomarkers of effect. [Pg.129]

Morgan, T.P., C.M. Guadagnolo, M. Grosell, et al. 2005. Effects of water hardness on the physiological responses to ehronie waterborne silver exposure in early life stages of rainbow trout Oncorhynchus myldss). Aquat. Toxicol. 74 333-350. [Pg.239]

Fig. 47. Work function of the (110) facet of a tungsten field emitter at 300 K as a function of silver exposure. The authors interpret this data as follows Below an exposure treshold of about one ML, Ag adatoms migrate to the high-index facets that surround the W(llO) plane, and the emission properties are indistinguishable from those of the bare substrate. At 1 ML the adatoms invade the (110) plane, modifying the surface density of electron states and bringing about an abrupt increase in electron emission. Above 2 ML the additionally evaporated Ag atoms migrate again to the surrounding facets. From [95D]. Fig. 47. Work function of the (110) facet of a tungsten field emitter at 300 K as a function of silver exposure. The authors interpret this data as follows Below an exposure treshold of about one ML, Ag adatoms migrate to the high-index facets that surround the W(llO) plane, and the emission properties are indistinguishable from those of the bare substrate. At 1 ML the adatoms invade the (110) plane, modifying the surface density of electron states and bringing about an abrupt increase in electron emission. Above 2 ML the additionally evaporated Ag atoms migrate again to the surrounding facets. From [95D].

See other pages where Silver exposure is mentioned: [Pg.573]    [Pg.578]    [Pg.573]    [Pg.578]    [Pg.35]    [Pg.55]    [Pg.62]    [Pg.63]    [Pg.63]    [Pg.66]    [Pg.67]    [Pg.68]    [Pg.110]    [Pg.781]   
See also in sourсe #XX -- [ Pg.99 ]




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