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The chemical elements gallium, indium, and thallium belong to group IIIA in the periodic table. Unlike other metals, such as lead and arsenic, which have been featured prominently in toxicologic folklore since antiquity, they are relative newcomers, discovered from 1861 to 1876. Since then, thallium has developed a well‐deserved reputation for its toxic properties and is recognized as a potent accidental, occupational, and environmental poison, with incidence in cases of homicide and suicide. Although gallium and indium are not as toxic as thallium, their production and industrial use represent an important source of exposure, particularly in the increasing manufacture of semiconductor electronic devices. Gallium compounds particularly produce pulmonary toxicity. Indium compounds induce pulmonary toxicity and also nephrotoxicity, hepatotoxicity, and developmental toxicity, whereas thallium compounds act as general poisons. Some compounds are also capable of altering various cellular defense mechanisms involved in carcinogenesis. However, many aspects of the toxicity of individual compounds in human beings, including toxicokinetics, mechanisms of action, teratogenic potential, and the best treatment, remain to be elucidated.
The chemical elements gallium, indium, and thallium belong to group IIIA in the periodic table. Unlike other metals, such as lead and arsenic, which have been featured prominently in toxicologic folklore since antiquity, they are relative newcomers, discovered from 1861 to 1876. Since then, thallium has developed a well‐deserved reputation for its toxic properties and is recognized as a potent accidental, occupational, and environmental poison, with incidence in cases of homicide and suicide. Although gallium and indium are not as toxic as thallium, their production and industrial use represent an important source of exposure, particularly in the increasing manufacture of semiconductor electronic devices. Gallium compounds particularly produce pulmonary toxicity. Indium compounds induce pulmonary toxicity and also nephrotoxicity, hepatotoxicity, and developmental toxicity, whereas thallium compounds act as general poisons. Some compounds are also capable of altering various cellular defense mechanisms involved in carcinogenesis. However, many aspects of the toxicity of individual compounds in human beings, including toxicokinetics, mechanisms of action, teratogenic potential, and the best treatment, remain to be elucidated.
The chemical elements gallium, indium, and thallium belong to group IIIA in the periodic table. Unlike other metals, such as lead and arsenic, which have been featured prominently in toxicological folklore since antiquity, these are relative newcomers, discovered from 1861 to 1876. Since then, thallium has developed a well‐deserved reputation for its toxic properties and is recognized as a potent accidental, occupational, and environmental poison, with incidence in cases of homicide and suicide. Although gallium and indium are not as toxic as thallium, their production and industrial use represent an important source of exposure, particularly in the increasing manufacture of semiconductor electronic devices. Gallium compounds particularly produce pulmonary toxicity. Indium compounds induce pulmonary toxicity and also nephrotoxicity, hepatotoxicity, and developmental toxicity, whereas thallium compounds act as general poisons. Some compounds are also capable of altering various cellular defense mechanisms involved in carcinogenesis. However, many aspects of the toxicity of individual compounds in human beings, including toxicokinetics, mechanisms of action, teratogenic potential, and the best treatment, remain to be elucidated.
Achondroplasia was induced in chicken embryos by in ovo application of 0.6 mg/egg thallium sulfate. The critical (sensitive) period for production of achondroplasia began on day 5 of incubation and ended at the start of HH stage 35 (8.5 days). The end of the critical period was accurately timed and found to be 205-207 hours of incubation and to coincide with a 66% decrease in growth rate of the embryos. Treatment resulted in reduced tibial growth one day later, tibial angulation two days later, and chrondrocytic necrosis four days later. The last was therefore not the cause of the angulation. Tibias were taken from thallium-treated and control donor embryos of various ages and grafted to the chorioallantoic membranes of treated and control host embryos of various ages during and outside the critical period and achondroplastic changes induced in grafted tibias exposed to thallium while on the chorioallantoic membrane. The critical period was extended into day 10 of incubation in such grafted tibias. Tibias maintained for seven days in organ culture were achondroplastic if pretreated with thallium at seven or eight days of incubation but not at ten days. Exposure of as little as 0.5 hour was sufficient to elicit micromelia when the tibias were grafted or organ cultured. Thallium therefore rapidly binds to skeletal tissues during a critical period of embryonic development but this critical period may be extended when tibias are removed from the embryo.
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