The chemical environment was recognized as a threat to health early in history.
Well-documented outbreaks of occupational mercury and lead "poisonings" had been recorded and preventive measures implemented by 200 BC.
In the Middle Ages, arsenic poisoning was used as a political weapon.
In more recent times, industrial toxins, "accidental poisoning" in childhood, purposeful overdoses in adults, adverse reactions to drugs, medication mix-ups in hospitals, and environmental hazards increasingly have been recognized.
The patient's metabolic and genetic variability determine the impact of a given molecule in hereditary disorders such as phenylketonuria, glucose-6-phosphate dehydrogenase deficiency, and others.
[...] Arsenic poisoning also has resulted from using certain herbal preparations, from ingesting illegal (moonshine) whiskey, from burning arsenate-treated wood, and from administering arsenic-containing folk and prescription medicines. In contrast to mercury, organic arsenic is far less toxic to humans than the inorganic form. Etiology For coastal inhabitants who consume large amounts of shellfish (e.g., clams, oysters, mussels), urinary excretion of arsenic may be elevated to three to four times normal values, but the arsenic is typically organic and not an important risk. [...]
[...] In the Middle Ages, arsenic poisoning was used as a political weapon. Definition In more recent times, industrial toxins, "accidental poisoning" in childhood, purposeful overdoses in adults, adverse reactions to drugs, medication mix-ups in hospitals, and environmental hazards increasingly have been recognized. The patient's metabolic and genetic variability determine the impact of a given molecule in hereditary disorders such as phenylketonuria, glucose-6-phosphate dehydrogenase deficiency, and others. Etiology New analytical techniques can identify poisonings promptly and completely and have uncovered the causes of diverse entities such as Minamata disease (teratogenesis consequent to methyl mercury), an outbreak of ascending paralysis affecting more than 4000 with more than 400 deaths in Iraq (also caused by methyl mercury), the "gray syndrome" in premature infants (caused by chloramphenicol), mesotheliomas induced by asbestos, and an epidemic of angiosarcoma of the liver among industrial workers (caused by vinyl chloride). [...]
[...] Thereafter, other signs of mercury poisoning may appear, including amblyopia, polyneuropathy, erythroderma, acrodynia, joint pains, swollen gums with a blue line around the teeth, sialorrhea, and paresthesias. Clinical Manifestations and Treatment The major manifestation of chronic mercury vapor exposure may be renal damage, including nephrotic syndrome. The wide range of clinical findings after elemental mercury exposure seems to relate in part to the rate of oxidation of mercury to its salts and the rapidity of their subsequent excretion through the kidneys, saliva, and urine. [...]
[...] The interval between lodging of the bullet and clinical evidence of lead poisoning has ranged from 2 days to 40 years. Etiology Lead poisoning also has occurred in adults who have eaten fowl and inadvertently ingested lead pellets. Children have been poisoned by swallowing lead household objects, such as lead curtain weights, that are retained in the gastrointestinal tract for a prolonged time. Gasoline sniffing can produce lead poisoning; the organic tetraethyl lead seems to have a proclivity for the nervous system. [...]
[...] Clinical Manifestations Tetraethyl lead (organic lead) poisoning causes euphoria, nervousness, insomnia, hallucinations, convulsions, and frank psychosis. Peripheral nerve involvement is seen more often in adults than in children. Wristdrop and footdrop occur most often; the former, depending on type of occupation, may be asymmetrical, and there may be paresthesias. Clinical Manifestations The spinal cord also may be involved, with manifestations having some similarity to those of amyotrophic lateral sclerosis. Since the 1980s, increasing evidence has arisen of subtle brain damage in the absence of clinical evidence of encephalopathy. [...]
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