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MERCURY 449<br />

5. POTENTIAL FOR HUMAN EXPOSURE<br />

(15.2 ppm) were from Nome, Alaska where the population consumes large amounts of fish <strong>and</strong> marine<br />

mammals (Lasora <strong>and</strong> Citterman 1991) <strong>and</strong> from Florida (15.6 ppm), where measurements were made only<br />

in adults that consumed wildlife from the Everglades area, a region where high mercury levels in wildlife<br />

have been reported (Fleming et al. 1995). Most recently, Davidson et al. (1998) reported the results of the<br />

Seychelles Child Development Study at 66 months (5.5 years) post-parturition. These researchers reported<br />

that there were no adverse neurodevelopmental outcomes observed in mother-child pairs, with mean<br />

maternal <strong>and</strong> mean child hair total mercury concentrations of 6.8 ppm <strong>and</strong> 6.5 ppm, respectively, in the<br />

Seychelles Isl<strong>and</strong> study.<br />

Oral Tissues. Mercury concentrations as high as 380 µg/g (ppm) have been found in oral tissues in<br />

contact with amalgam fillings. In individuals with more than six amalgam fillings, a mean value of 2.3 µg/g<br />

(ppm) was found in tissue without direct contact with amalgam fillings (Björkman et al. 1997). In some<br />

European countries, health authorities recommend that sensitive or susceptible individuals in higher risk<br />

groups (i.e., pregnant women <strong>and</strong> individuals with kidney disease) avoid treatment with dental amalgam<br />

(Björkman et al. 1997).<br />

Occupational Exposure. Workplace environments presenting the largest potential sources of<br />

occupational exposure to mercury include chloralkali production facilities, cinnabar mining <strong>and</strong> processing<br />

operations, <strong>and</strong> industrial facilities involved in the manufacture <strong>and</strong>/or use of instruments containing liquid<br />

mercury (Stokinger 1981). According to NIOSH (1973), the principal route of occupational exposure to<br />

mercury is vapor phase inhalation from workplace atmospheres. Studies by Barregard et al. (1992) <strong>and</strong> by<br />

Langworth et al. (1992b) revealed increased total mercury levels in blood <strong>and</strong> urine of exposed chloralkali<br />

workers. These results are summarized in Table 5-19. Personal air sampling of workers in a mercury<br />

recycling plant in Germany showed mercury levels ranging from 115 to 454 µg/m 3 (Schaller et al. 1991).<br />

Human tissues that are routinely monitored as evidence of exposure to mercury are urine, blood, <strong>and</strong> hair.<br />

Urine is most frequently monitored as an indicator of human body burden following chronic exposure to<br />

mercury vapor, particularly in occupational settings; approximately 95% of all urine samples contain less<br />

than 20 µg /L (ppb) (EPA 1984b). A comparison of mercury content in the urine of Swedish workers<br />

exposed to high levels of mercury, dentists, occupationally unexposed workers, <strong>and</strong> unexposed workers<br />

without dental amalgams gave values of 15, 1.7, 0.8, <strong>and</strong> 0.3 µmol/mol creatinine, respectively<br />

(corresponding mercury plasma levels were 35, 9.4, 5.3, <strong>and</strong> 2.8 nmol/L [7.19, 1.89, 1.06, <strong>and</strong> 0.56 ppt],<br />

respectively) (Molin et al. 1991). Blood <strong>and</strong> urine monitoring may be useful <strong>for</strong> groups of workers subject

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