Lead toxicity direct exposure

Many neurotoxic chemicals easily cross the blood-brain barrier, leading to direct exposure of brain regions to toxic chemicals carried in the blood. 

Abstract Delivery of nicotine in the most desirable form is critical in maintaining people s use of tobacco products. Interpretation of results by tobacco industry scientists, studies that measure free-base nicotine directly in tobacco smoke, and the variability of free-base nicotine in smokeless tobacco products all indicate that the form of nicotine delivered to the tobacco user, in addition to the total amount, is an important factor in whether people continue to use the product following their initial exposure. The physiological impact of nicotine varies with the fraction that is in the free-base form and this leads to continued exposure to other toxic tobacco contents... 

Other approaches to induce gastrointestinal discomfort have far more serious toxic effects. The chemical colchicine stops cell division (an antimitotic), producing severe nausea, vomiting, and dehydration, which can lead to delirium, neuropathy, and kidney failure. On the other hand, colchicine is used in the treatment of gout and has been studied as an anticancer agent because it stops cell division. Most toxic of all are plants that produce lectins, and the most toxic of these is the chemical ricin produced by castor beans. Only 5 to 6 seeds are necessary to kill a small child. Fortunately, following oral consumption much of the ricin is destroyed in the stomach. Ricin is extremely effective at stopping protein synthesis, so much so that direct exposure to only 0.1 pg/kg can be fatal. 

The exact mechanisms of MIC toxicity are not known, however, carbamylation of globin and other blood proteins have been speculated to contribute to MIC-induced toxicity. Acute exposure via inhalation of MIC vapors is known to cause irritation to the respiratory tract causing severe pulmonary edema and injury that can lead to death. It is also corrosive to the eyes causing severe corneal damage. Survivors of acute exposures may exhibit long-term respiratory and ocular effects. Direct skin contact of MIC in the liquid or gaseous form causes irritation of the skin. 

Other critical endpoints of lead toxicity include toxicity to the nervous system and the kidneys. Based on experimental findings, it seems plausible that lead has no direct genotoxic effects, which argues for establishing a practical threshold limit value for lead toxicity. Thus, an occupational exposure limit (OEL) based on avoiding functional CNS alterations is expected also to protect versus toxicity to the peripheral nervous system and the kidney, including possibly the development of renal cancer. 

Once the possibility for lead exposure is raised, the focus can then be directed toward eliciting information from the medical history, physical exam, and finally from laboratory data to evaluate the worker for potential lead toxicity. 

Special problems are, of course, created by the general use of particularly toxic elements, such as antimony, arsenic, beryllium, cadmium, lead, mercury and thallium, in our society. The production and use of these elements and their compounds is inevitably associated with some release into the environment and there are public health problems in factories and laboratories arising at the initial stage of dispersion. Such problems may be regarded as primary problems of environmental pollution. They are often acute since they may involve direct exposure to a highly toxic element, or one of its compounds, before it has been substantially diluted in the environment. For example. 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

Toxic substances can interfere with normal neurotransmission in a variety of ways, either directly or indirectly, and cause various central effects. For example, cholinesterase inhibitors such as the organo phosphate insecticides cause accumulation of excess acetylcholine. The accumulation of this neurotransmitter in the CNS in humans after exposure to toxic insecticides leads to anxiety, restlessness, insomnia, convulsions, slurred speech, and central depression of the respiratory and circulatory centers. 

Endocrine and Reproductive Effects. Because the male and female reproductive organs are under complex neuroendocrine and hormonal control, any toxicant that alters any of these processes can affect the reproductive system (see Chapters 17 and 20). In addition metals can act directly on the sex organs. Cadmium is known to produce testicular injury after acute exposure, and lead accumulation in the testes is associated with testicular degeneration, inhibition of spermatogenesis, and Leydig-cell atrophy. 

Lead Blood lead Biomarker to toxic effect in humans biomarker to external dose in humans Biomarker results can be used directly for estimation of human risk exposure apportionment and intervention possible... 

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