Inorganic mercury, toxic effects

Toxicity. Inorganic mercury compounds, aryl mercury compounds, and alkoxy mercurials are generahy considered to be quite similar in their toxicity. Alkyl mercury compounds are considered to be substantiahy more toxic and hazardous. Mercury and its compounds can be absorbed by ingestion, absorption through the skin, or by inhalation of the vapor. The metal itself, however, rarely produces any harmful effects when ingested (16). 

Methylation of divalent inorganic mercury salt has been shown in vivo in rat intestine [61] and in vitro in human intestine [62], yet it is seldom followed by toxic effects. MeHg has been found in hen tissues [63 ] and probably in rat brain [64] after ingestion of divalent mercuric salts. 

Information concerning the effects of selenium in man is lacking and it is doubtful whether administration of selenium in man has any effect on the toxicity of mercuric mercury. However, mercury and selenium were found in the cellular lysozomes in renal tubular cells in two patients with inorganic mercury poisoning [143]. 

The RfDs and TDIs are often used to establish regulatory standards. Such standards usually specify a limit on the allowable concentration of a chemical in an environmental medium. The process is not difficult to understand. The RfD and its related estimates of population thresholds is a dose, typically expressed in mg/(kg b.w. day), that is considered to be without significant risk to human populations exposed daily, for a lifetime. Consider mercury, a metal for which an RfD of 0.0003 mg/(kg b.w. day) has been established by the EPA, based on certain forms of kidney toxicity observed in rats (Table 8.4). These are not the only toxic effects of mercury, but they are the ones seen at the lowest doses. Note also that we are dealing with inorganic mercury, not the methylated form that is neurotoxic. 

Mercury exists in three forms elemental, inorganic, and organic with different toxic effects. Elemental mercury is absorbed as a vapor and may enter the CNS and cause toxicity there. Inorganic mercury is poorly absorbed, but the cysteine conjugate of mercury is concentrated in the kidney by active transport. The kidney is the main target organ (also gastrointestinal tract if exposure by that route). 

Mercury (11) is a frequent component of industrial wastewaters, remarkably toxic at concentrations higher than 0.005 mg The World Health Organization (2006) and national environmental agencies recommend a limit of 0.006 mg of inorganic mercury in drinking water. The health hazards due to the toxic effect of mercury at Minamata, Japan, and Iraq are very well known (Bockris, 1997). 

The association between metal exposure and renal failure can be approached from two points of view. On the one hand environmental/industrial exposure to heavy metals, more particularly, lead, cadmium and mercury and other inorganic substances such as silicon has been linked to a reduced renal function and/or the development of acute or chronic renal failure [1]. This issue has been dealt with in other chapters of this book. On the other hand patients with chronic renal failure, especially those treated by dialysis are at an increased risk for trace element disturbances (Figure 1). Indeed in these subjects the reduced renal function, the presence of proteinuria, metabolic alterations associated with renal insufficiency, the dialysis treatment, medication etc. all may contribute to either accumulation or deficiency of trace metals. With regard to aluminum intensive research on the element s toxic effects has been performed in the past. Recently, new metal-containing medications have been introduced of which the potential toxic effects should be considered and put in a justified context. 

Potassium dichromate and atrazine may increase the toxicity of mercury, although these effects have been noted only with metallic and inorganic mercury. Ethanol increases the toxicity of methylmercury in experimental animals. Vitamins D and E, thiol compounds, selenium, copper, and possibly zinc are antagonistic to the toxic effects of mercury. 

The bulk of the information regarding toxicity resulting from oral exposure to inorganic mercury comes from studies of mercuric chloride. However, a few studies are also available on the effects of oral exposure to mercuric acetate, mercurous chloride (calomel), and mercuric sulfide (cinnabar). Discussion of these compounds has not been separated in this section, but the specific inorganic compound responsible for any effect is noted both in the text and in Table 2-2 and Figure 2-2. 

Mechanisms for the toxic effects of inorganic and organic mercury are believed to be similar. It has been suggested that the relative toxicities of the different forms of mercury (e g., metallic, monovalent, and divalent cations and methyl- and phenylmercury compounds) are related, in part, to its differential accumulation in sensitive tissues. This theory is supported by the observation that mercury rapidly accumulates in the kidneys and specific areas of the central nervous system (Rothstein and Hayes 1960 Somjenetal. 1973). 

---