Exposure to Elemental Mercury

Occupational exposure to mercury vapor occurs in a variety of industries such as chloralkali plants, thermometer factories, gold extraction process, and mercury mining. Dentists and dental assistants are also exposed to mercury vapor during insertion, polishing, and removal of amalgam fillings. 

Mercury vapor is well absorbed through inhalation (about 80%), while liquid mercury is poorly absorbed by the gastrointestinal tract (about 0.01%). Due to its high lipophilicity and diffusibility, mercury vapor is readily transferred across the cell membranes. When mercury vapor is inhaled, it efficiently enters the blood stream through the alveolar membrane and is quickly distributed between the plasma and red blood cells (RBCs). Little is known about the efficiency of elemental mercury absorption through the skin. 

In blood, dissolved mercury vapor enters the RBCs and oxidizes to the divalent ionic form (Hg ). The catalase-H202 complex (compound I) is responsible for this oxidation (see below). Oxidized mercury readily reacts with SH groups of protein or glutathione. 

Until recently, little information has been available concerning detailed distribution of mercury in the brain after mercury vapor exposure. However, a recent improvement in the staining method permitted the detection of mercury deposits in the brains of animals exposed to rather lower concentrations of mercury vapor (Moller-Madsen 1992 Warfvinge et al. 1992). Mercury was found primarily in the neocortex, thalamus, pons, ependyma, choroid plexuses, cerebellar Purkinje cells, and vessel walls in the brain of rats exposed to mercury vapor. 

Distribution of mercury in fetal and neonatal tissues has been extensively investigated in guinea pigs exposed to mercury vapor in utero (Yoshida et al. 1987, 1990). Though mercury vapor easily crosses the placental barrier, mercury concentration in the fetal or neonatal brain is lower than that in the maternal brain after in utero exposure. On the contrary, much higher concentrations of mercury were found in the fetal liver than in the maternal liver. Most of the mercury in the fetal liver was found in the fraction of MT in the cytosol. The hepatic concentration of MT is known to increase drastically in the late gestational and early neonatal period. It seems likely that mercury vapor which entered the fetus is readily oxidized in the fetal liver, then trapped by the abundant MT, thus resulting in a lower distribution of mercury to the other fetal tissues. 

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Mercury exists in the environment in three main chemical forms elemental mercury (Hg°), inorganic mercurous (Hg+) and mercuric (Hg2+) salts, and organic methylmer-cury (CH3Hg) and dimethylmercury (CH3HgCH3) compounds. Elemental mercury, in the form of mercury vapor, is almost completely absorbed by the respiratory system, whereas ingested elemental mercury is not readily absorbed and is relatively harmless. Once absorbed, elemental mercury can cross the blood-brain barrier into the nervous system. Most exposure to elemental mercury tends to be from occupational sources. 

Boogaard PJ, Houtsma AT, Journee HL, Van Sittert NJ. Effects of exposure to elemental mercury on the nervous system and the kidneys of workers producing natural gas. Arch Environ Health 1996 51(2) 108-15. 

Smith PJ, Eangolf GD, Goldberg J. Effects of occupational exposure to elemental mercury on short term memory. Brit J Ind Med 1983 40 413-9. 

Cherian MG, Clarkson TW. 1976. Biochemical changes in rat kidney on exposure to elemental mercury vapor Effect on biosynthesis of metallothionein. Chem Biol Interact 12 109-120. 

Molin M, Schutz A, Skerfving S, et al. 1991. Mobilized mercury in subjects with varying exposure to elemental mercury-vapor. Int Arch Occup Environ Health 63(3) 187-192. 

Orloff KG, Ulirsch G, Wilder L, et al. 1997. Human exposure to elemental mercury in a contaminated residential building. Arch Environ Health 52(3) 169-72. 

Taueg C, Sanfilippo DJ, Rowens B, et al. 1992. Acute and chronic poisoning from residential exposures to elemental mercury. J Toxicol Clin Toxicol 30(l) 63-67. 

Yoshida M. 1985. Relation of mercury exposure to elemental mercury levels in the urine and blood. Scand J Work Environ Health 11 33-37. 

Mercury poisoning may be acute or chronic and is related to exposure to elemental mercury vapour, inorganic salts or organic forms such as methyl-mercury. Metallic mercury is relatively non-toxic if ingested, hut mercury vapour can give rise to acute toxicity. The symptoms are respiratory distress and a metallic taste in the mouth. 

For a toxicological assessment of an exposure to elemental mercury, a strict distinction must be made between the route of intake, whether the inhalation of mercury vapor, ingestion of liquid metallic mercury, rectal (from broken thermometers), or by injection of liquid mercury. 

Animal studies reveal that pulmonary edema and asphyxiation result from acute high-dose exposure to elemental mercury vapor (EPA 1997). After 2 hours of exposure to 30 mg m mercury vapor, 20 of 32 rats died. Histological lesions such as alveolar edema, hyaline membranes and sometimes fibrosis were observed (Livardjani et al. 1991). 

Exposure to elemental mercury vapour may cause effects on the central nervous system, with a change of personality and tremor (cf. Skerfving and Vostal, 1972). Also, mercury may affect the kidney this may occur as a tubular (BarregSrd et al.. 1987) and/or glomerular (cf. Berlin, 1986 WHO, 1991) malfunction. Further, mercury may provoke hypersensitivity with skin manifestations. 

Health problems are documented for gold miners who worked mainly underground with litUe exposure to elemental mercury in Australia, North America, South America, Europe, and Africa. Major problems examined included life expectancy, cancer frequency, and pleural diseases. Health problems of miners who worked mainly on the surface and with extensive exposure to elemental mercury owing to its use in amalgamating and extracting gold are reported extensively in Chapter 19. 

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