Urine mercury excretion

Unithiol and succimer increase urine mercury excretion following acute or chronic elemental mercury inhalation, but the impact of such treatment on clinical outcome is unknown. Dimercaprol has been shown to redistribute mercury to the central nervous system from other tissue sites, and since the brain is a key target organ, dimercaprol should not be used in treatment of exposure to elemental or organic mercury. Limited data suggest that succimer, unithiol, and N- acetyl-L-cysteine (NAC) may enhance body clearance of methylmercury. 

Bell ZG, Lovejoy HB, Vizena TR. 1973. Mercury exposure evaluations and their correlations with urine mercury excretion 3. Time-weighted average (TWA) mercury exposures and urine mercury levels. 

Lovejoy HB, Bell ZG, Vizena TR. 1974. Mercury exposure evaluations and their correlation with urine mercury excretion. J Occup Med 15 590-591. 

Levy M, Schwartz S, Dijak M, Weber JP, Tardif R, Rouah F (2004) ChUdhood urine mercury excretion dental amalgam and fish consumption as exposure factors. Environ Res 94 283-290... 

Not all agents can be readily metabolized. The toxic metals lead and mercury are elements that cannot be degraded but must still be removed from the body. Another important mechanism of detoxification is the attachment or binding of another compound to a toxic chemical to make it easier for the kidney to filter the compound out of the blood and excrete it in the urine. A primary purpose of the kidney is to screen the blood for waste products and concentrate them in the urine for excretion, as occurs, for example, with mercury. Caffeine is excreted in the urine at approximately the same concentration as the blood because the kidney cannot concentrate caffeine. Vitamins, however, are readily concentrated and excess quickly eliminated in the urine. 

Phenylmercuric acetate is mainly excreted through urine. The excretion of phenylmercuric acetate in humans was reported to exhibit two phases. The first phase showed a transient increase in urinary mercury concentration followed by a second slower phase. 

Data are limited on elimination of metallic and inorganic mercury in animals. Initial excretion of mercury is predominantly in the fecal matter following inhalation of metallic mercury vapor, but as mercury concentrations increase in the kidneys, urinary excretion increases (Rothstein and Hayes 1964). After inhalation, approximately 10-20% of the total excreted metallic mercury is by exhalation (Rothstein and Hayes 1964). Mercury is excreted in the urine of mice exposed orally to mercuric sulfide ( 8-200 mg Hg/kg) (Yeoh et al. 1986, 1989). The amount of mercury in the urine of the treated group was 4.5-15-fold greater than the control levels. Urinary rates of mercury excretion were 1.6-2.2 ng/hour. Neonatal rats (1, 8, and 15 days old) eliminated mercury slower than older rats (22 and 29 days old) given mercuric chloride subcutaneously (Daston et al. 1986). 

Organic Mercury. The fecal (biliary) pathway is the predominant excretory route for methylmercury, with less than one-third of the total mercury excretion occurring through the urine, following oral and inhalation exposure (Norseth and Clarkson 1970). In humans, nearly all of the total mercury in the feces after organic mercury administration is in the inorganic form. The conversion of methylmercury to inorganic mercury is a major step that is dependent on the duration of exposure and/or the duration after cessation of exposure. 

An association between urine mercury levels and performance on memory tests and verbal intelligence tests has been established. Abnormal results on memory tests were reported for 9 workers exposed to mercury in the production of thermometers urinary mercury excretion levels were 7-1,101 g/24 hours (Vroom and Greer 1972). The short-term memory span of 26 workers was examined by Smith et al. (1983) and found to decrease with increasing urine mercury levels. The range of mercury found in the urine of these workers was 0-510 g/L. A significant linear relationship was reported between subjects 50% memory threshold spans and 12-month urinary mercury concentrations. Disturbances on tests of verbal intelligence and memory were more frequent among individuals with mercury blood levels above 1.5 g/100 mL and mercury urine levels above 56 g/L in 36 male chloralkali workers (Piikivi et al. 1984). 

The mechanism of mercury excretion in the bile is unknown. Binding to glutathione and cysteine has been demonstrated in rodents (Refsvik and Norseth, 1975). The excretion through the intestinal mucosa may be related to the plasma protein turnover. The relative importance of the main excretory routes - by feces and by urine - is dose-dependent -with higher doses, a larger portion is excreted by urine (Lomholt, 1928). 

Res. Commun. Chem. Pathol. Pharmacol. 5 673 Jakubowski M, Piotrowski J, Trojanowska B (1970) Binding of mercury in the rat studies using HgCl2 and gel filtration. Toxicol. Appl. Phajnnacol. 16 743 Joselow MM, Ruiz R, Goldwater LJ (1968) Absorption and excretion of mercury in man XIV. Salivary excretion of mercury and its relationship to blood and urine mercury. Arch. Environ. Health 17 35... 

The half-lives of toxic metals vary over an enormous range and the value for a given toxic metal depends upon the site at which it is deposited. Thus the half-life of mercury in the whole blood of men following exposure to mercury vapor was found to be 3.1 days for a fast phase and 18 days for a slow phase. In this same study the half-life for the mercury in the urine was found to be 40 days (Barregard et al. 1992). In a similar study of a more severe human exposure a half-life of 45 days was estimated (Bluhm et al. 1992). In this latter group of workers the administration of DMSA produced a threefold increase in the amount of mercury excreted in the urine, while the administration of A-acetyl-D,L-penicillamine produced a twofold increase. The half-life of mercury in the human brain may be much longer than this (Cavanagh 1988). The half-life of elements which deposit in the bone, such as lead, can be of the order of many years (Rabinowitz et al. 1976). 

The (n)-enantiomer of penicillamine is used clinically in man either as the hydrochloride or as the free amino acid [1], although the (L)-enantiomer also forms chelation complexes. Penicillamine is an effective chelator of copper, mercury, zinc, and lead, and other heavy metals to form stable, soluble complexes that are readily excreted in the urine [2,3]. 

The major part of absorbed mercuric mercury is excreted in urine and faeces in about equal parts in rat [49] and man [2, 50]. Since absorption rates from the lung or gastrointestinal tract do not vary greatly from one animal species... 

Exposure is also affected by absorption. Even though we may come into contact with an agent, if little is taken up into the body (or absorbed), there is little effect. For example, the metallic mercury from a broken thermometer, if swallowed, is very poorly absorbed by the gut and will be excreted in the feces. However, if this same amount of mercury were allowed to evaporate and be inhaled, there would be very serious health consequences. This example shows that metabolism and excretion modify absorption. What is not absorbed (and even some of what is absorbed) may be excreted from the body by various routes, including the urine, feces, and sweat or through exhalation. Excretion reduces the effect because it lowers the amount of toxicant in the body, thus reducing exposure to sensitive organs. 

Mercury is eliminated from the body in the urine and feces, with the latter being the major route. Thus, with methyl mercury, 90% is excreted into the feces. Methyl mercury is secreted into the bile as a cysteine conjugate and undergoes extensive enterohepatic recirculation. 

Excretion of inorganic mercury occurs through the urine and feces. The mechanisms by which excretion occurs are not well understood. 

Drugs that alter the pH of urine can significantly affect the renal excretion of other drugs. Acid urine increases the effectiveness of mercurial diuretics. It also accelerates the excretion of basic drugs such as meperidine, tricyclic antidepressants, amphetamines, and antihistamines. Acidic drugs, such as aspirin, streptomycin, phenobarbital, sulfonamides, nalidixic acid, and nitrofurantoin have been shown to increase renal clearance in alkaline urine (61). The possible effects of urine pH on the renal excretion of drugs has been illustrated by the observation that if urine is rendered sufficiently alkaline, the excretion of amphetamine is markedly delayed and effective blood levels, after a single dose, can be maintained for several days (62). 

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