Mercury: toxic effects

The toxic effects of mercury and mercury compounds as well as their medicinal properties have been known for many centuries. In the first century AD, Pliny indicated the use of mercuric sulfide (cinnabar or vermilion) in medicine and in cosmetics. This compound was probably known to the Greeks in the time of Aristotle (13). 

Heavy metals on or in vegetation and water have been and continue to be toxic to animals and fish. Arsenic and lead from smelters, molybdenum from steel plants, and mercury from chlorine-caustic plants are major offenders. Poisoning of aquatic life by mercury is relatively new, whereas the toxic effects of the other metals have been largely eliminated by proper control of industrial emissions. Gaseous (and particulate) fluorides have caused injury and damage to a wide variety of animals—domestic and wild—as well as to fish. Accidental effects resulting from insecticides and nerve gas have been reported. 

The hazards of chemicals are commonly detected in the workplace first, because exposure levels there are higher than in the general environment. In addition, the exposed population is well known, which allows early detection of the association between deleterious health effects and the exposure. The toxic effects of some chemicals, such as mercury compounds and soot, have been known already for centuries. Already at the end of the eighteenth century, small boys who were employed to climb up the inside of chimneys to clean them suffered from a cancer of the scrotum due to exposure to soot. This was the first occupational cancer ever identified. In the viscose industry, exposure to carbon disulfide was already known to cause psychoses among exposed workers during the nineteenth century. As late as the 1970s, vinyl chloride was found to induce angiosarcoma of the liver, a tumor that was practically unknown in ocher instances. ... 

Paracelsus, a Swiss physician of the sixteenth century, stated that everything is toxic, it is just the dose that matters. This statement still holds true 500 years after Paracelsus developed it to defend the use of toxic compounds such as lead and mercury in the treatment of serious diseases such as syphilis. Chemical compounds cause their toxic effects by inducing changes in cell physiology and biochemistry, and an understanding of cellular biology is a prerequisite if one wishes to understand the nature of toxic reactions. 

The toxic effects of mercury have long been known,and the use of HgCl, as a poison has already been mentioned. The use of mercury salts in the production of felt for hats and the dust generated in ill-ventilated workshops by the subsequent drying process, led to the nervous disorder known as hatter s shakes and possibly also to the expression mad as a hatter . 

Evidence suggests that lead exacerbates the toxic effects of mercury. In the rat, the administration of lead nitrate increased kidney and liver glutathione content and resulted in increased mercury deposition in the kidney, along with increased lethality in rats (Congiu et al. 1979). 

Penicillamine is reported to be more than 80% bound to plasma protein. The compound is metabolized in the liver. N-acetylpenicillamine is more effective than penicillamine in protecting against the toxic effect of mercury, presumably because it is even more resistant to metabolism [7,2]. 

Khera, K.S. 1979. Teratogenic and genetic effects of mercury toxicity. Pages 501-518 in J.O. Nriagu (ed.). The Biogeochemistry of Mercury in the Environment. Elsevier/North-Holland Biomedical Press, NY. 

Kirubagaran, R. and K.P. Joy. 1992. Toxic effects of mercury on testicular activity in the freshwater teleost, Clarias batrachus (L.). Jour. Fish Biol. 41 305-315. 

Ingestion Toxicity Data are available for the acute (single-dose) ingestion/oral toxicity of many toxic materials (National Institute for Occupational Safety and Health, Registry of Toxic Effects of Chemical Substances, 1983 Lewis, Sax s Dangerous Properties of Industrial Materials, 9th ed., 1996). However, very few data are available for prolonged ingestion or periodic doses of toxic materials. It is likely that metabolic processes would operate to increase the total burden required for toxic effects for such chronic exposures, except for some materials (such as mercury and lead) which apparently can accumulate in the body. 

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. 

The inhibition of amino-acid transport has been regarded as the main toxic effect of mercury compounds [82], The biochemical mechanism underlying the inhibition is unclear. In unfertilized sea-urchin eggs an interaction with the amino-acid carrier was found, whereas in fertilized eggs inhibition of amino-acid transport was indirect and might result from an elevation of the Na + content of the egg caused by the inhibition of the Na+ pump [83]. The action on the diffusional process could be mediated by an effect on membrane phospholipids or on membrane proteins, or by interaction with Ca2+ which stabilizes membrane structure. Mercuric chloride in skate liver cells inhibited amino acid transport, decreased Na + /K + -ATPase (adenosinetriphosphatase) activity, impaired volume regulatory mechanisms and increased the permeability of the plasma membrane to potassium [84]. It has been suggested that... 

The term heavy metals is rather broad, relative, and nonspecific. There are many heavy metals. In industrial toxicology, however, the term is used to describe certain heavy metallic substances that can be distinguished from other metals because of their particular toxic effects. Of these, the most common are arsenic, lead, and mercury. These are the ones that will be dealt with here. 

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. 

Trace metals (arsenic, cadmium, chromium, copper, nickel, lead, mercury, zinc) Industrial and municipal wastewaters runoff from urban areas and landfill erosion of contaminated soils and sediments atmospheric deposition Toxic effects including birth defects, reproductive failure, cancer, and systemic poisoning. 

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