Poisoning early observations

Detoxication of Metals. Pectins or pectin derivatives have been proposed as antidotes for heavy metal poisoning for nearly 200 years. Kertesz (9) has reviewed the early work in this area. Pectin complexes lead so strongly as to quantitatively remove it from solution. Absorption 6f lead, arsenic, and selenium by several animal species has been reduced by pectin- or apple-containing diets. Use of pectin as a prophylactic agent in lead poisoning continues to be of interest. Bondarev (88) recently reported an increase in excretion and a decrease in bone accumulation of lead when rats fed 6 mg/day of lead also received 72-432 mg/day of low ester pectin. Paskins-Hurlburt et al. (89) achieved an 87% decrease in lead absorption by pectate fed rats. These studies bear out the early observations of Fellenburg (see 9, p. 572), who concluded that pectin of decreased ester content would have an enhanced ability to complex metals. 

The earliest records revealed, first, that lead was a human poison and, second, that it was a poison which affected some specific organs and systems and could eventually lead to fatal outcomes. Also present in these early observations was the conclusion that lead poisoning was a progressive disease with an increasingly dire prognosis attending continued (chronic) exposure. 

Renal Effects. Hemorrhage of the medullary layer of the kidneys was observed in an early report of three fatal cases of acute oral poisoning with endosulfan (Terziev et al. 1974). More recent studies have reported acute renal failure after ingestion of endosulfan as a major contributing cause of death in two individuals in both cases, postmortem examination showed extensive tubular necrosis (Blanco-Coronado et al. 1992 Lo et al. 1995). Neither case discussed the possible mechanism of endosulfan-induced acute renal failure, but in one case, the authors of the report indicate that the renal lesions may relate to sepsis and shock (Blanco-Coronado et al. 1992). Ingested doses were not determined in any of these cases, and it is not totally clear that the effects observed at autopsy were a direct result of endosulfan exposure, although based on results from acute animal studies, it seems likely. 

The product of the reaction in Entry 8 was used in the synthesis of the alkaloid pseudotropine. The proper stereochemical orientation of the hydroxy group is determined by the structure of the oxazoline ring formed in the cycloaddition. Entry 9 portrays the early stages of synthesis of the biologically important molecule biotin. The reaction in Entry 10 was used to establish the carbocyclic skeleton and stereochemistry of a group of toxic indolizidine alkaloids found in dart poisons from frogs. Entry 11 involves generation of a nitrile oxide. Three other stereoisomers are possible. The observed isomer corresponds to approach from the less hindered convex face of the molecule. 

An increase in plethora and focal dystrophic changes in the endocrine system matches clinical observations of changes in adrenal and thyroid function, as well as changes in local and general vascular dystonia, all detected in humans poisoned by OCP. Morphological changes in the brain s nerve cells conform to information on the disruption of reflex activity in the early stages of OCP exposure. 

Those early metallurgists who were clever enough to learn how to transform crude ores to shiny metals were prohahly also observant enough to discover that some of the materials being worked with could harm them. Some of the earliest written accounts of humans on earth provide evidence that the ancient Greeks and Romans were well aware of the poisonous properties of certain plants and metals. The case of the poisoning of Socrates with hemlock is only the most famous of the early references to the deliberate use of certain plants for suicidal or homicidal purposes. 

In the early years there was much interest in the amount of poison necessary to cause sickness and death of humans. From accidental cases of poisoning along the coast of California where catenella commonly blooms, Sommer and colleagues estimated that death of humans resulted from the consumption of about 20,000 HU of poison. However, along the St. Lawrence estuary and Bay of Fundy the Canadians observed death of persons with a consumption as low as 5000 MU. In these areas shellfish become poisonous by feeding on G. tamarensis. 

A complete separation of a carbonium ion from the hydride ion is very probably not necessary. It has been shown [73] by MO calculations that any attack by a charged species on an atom bonded to a carbon atom causes activation of the bonds from a /3-carbon atom to the substituents. In this way, the splitting of the Cp—Cy bond can be induced by adsorption of the alkane on a strongly acidic site. The preferential cracking of a saturated hydrocarbon chain in /3-positions to the position where a carbonium ion might be formed was observed early and named the /3-rule by Thomas [2], The question remains open as to which type of acidic centre is able to activate an alkane molecule. The fact that an aluminosilicate catalyst is poisoned for the cracking of alkanes by irreversibly adsorbed ammonia suggests a Lewis site [240], viz. 

As early as 1713, Bernardini Ramazzini, the father of occupational medicine, observed that artisans who worked with paints, stone, and metal had physical problems and short life expectancies. In modern times, it is suspected that van Gogh s craziness and Goya s illness may have been the result of lead poisoning. It is known that van Gogh used leaded yellow paint for his numerous sunflower paintings and was careless with his paints, leaving them open to dry and scatter into his environment. He could easily have ingested lead paint chips. 

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