Lead toxicity symptoms

Reviews on the occurrence, biochemical basis, and treatment of lead toxicity in children (11) and workers (3,12,13) have been pubhshed. Approximately 17% of all preschool children in the United States have blood lead levels >10 //g/dL. In inner city, low income minority children the prevalence of blood lead levels >10 //g/dL is 68%. It has been estimated that over two million American workers are at risk of exposure to lead as a result of their work. PubHc health surveillance data document that each year thousands of American workers occupationally exposed to lead develop signs and symptoms indicative of... 

At neither site is there evidence of absorption of lead to the degree usually associated with clinical symptoms of lead poisoning, and the reported blood-lead levels are not high enough to make this likely. However, a public health concern exists, particularly in the RSR area, since 5 percent of these black children were found to have lead toxicity. 

Full Fanconi syndrome has been reported to be present in some children with lead encephalopathy (Chisolm 1968 Chisolm et al. 1955). According to the National Academy of Sciences (NAS 1972), the Fanconi syndrome is estimated to occur in approximately one out of three children with encephalopathy and PbB levels of approximately 150 pg/dL. Aminoaciduria occurs at PbB levels >80 pg/dL in children with acute symptomatic lead poisoning (Chisolm 1962). The aminoaciduria and symptoms of lead toxicity disappeared after treatment with chelating agents (Chisolm 1962). 

Neurotoxicity. There is a very large database on the neurotoxic effects of lead. The most severe neurobehavioral effect of lead toxicity in adults is lead encephalopathy (Kehoe 1961a Kumar et al. 1987 Smith et al. 1978). Early symptoms, which may develop within weeks of initial exposure, include dullness, irritability, poor attention span, headache, muscular tremor, loss of memory, and hallucinations. These symptoms worsen, sometimes abruptly, to delirium, convulsions, paralysis, coma, and death. 

Since only a few vitamins can be stored (A, D, E, Bi2), a lack of vitamins quickly leads to deficiency diseases. These often affect the skin, blood cells, and nervous system. The causes of vitamin deficiencies can be treated by improving nutrition and by administering vitamins in tablet form. An overdose of vitamins only leads to hypervita mi noses, with toxic symptoms, in the case of vitamins A and D. Normally, excess vitamins are rapidly excreted with the urine. 

The principles of toxicology, dose - response and individual sensitivity, are well illustrated by the metals. Historically, most of the interest and concern was with the obvious effects of metal toxicity such as colic from lead or symptoms of the Mad Hatter from mercury. The emphasis has changed to the more subtle and long-term effects and concern for potentially sensitive individuals. It is now well documented that children exposed to even low levels of lead will have a lowered IQ and other learning difficulties. This knowledge has resulted in significant changes in our use of metals. 

Another example is lead poisoning wherein acute toxicity symptoms are seen in the Gl tract. Chronic toxicity causes damage to blood cell formation and musculature and subtle decreases in mental ability. (See ASIDE 1) Frequent exposure to large doses can show both types of effects -this is called subacute. 

The toxic effects can be divided into three types as the accumulation of acetylcholine leads to symptoms that mimic the muscarinic, nicotinic, and CNS actions of acetylcholine. Muscarinic receptors for acetylcholine are found in smooth muscles, the heart, and exocrine glands. Therefore, the signs and symptoms are tightness of the chest, wheezing due to bronchoconstriction, bradycardia, and constriction of the pupils (miosis). Salivation, lacrimation, and sweating are all increased, and peristalsis is increased, leading to nausea, vomiting, and diarrhea. 

However, in no case have such studies informed us of the chemical bases for the toxic reactions. Examinations of lesions in the field can lead to the identification of newly polluted areas and new pollutants. Experiments in the greenhouse and laboratory can determine the dose response in terms of pollutant concentration and duration of exposure. Physiological studies of intact plants can correlate metabolic changes with the development of toxic symptoms. If we are to understand fully the effects of air pollutants on plants, however, it is essential that we elucidate the biochemical mechanisms of their action. 

In summary, acetylcholinesterase and butyr-ylcholinesterase are not the only proteins modified by OP exposure in humans. Neiuotoxicity from low doses of OPs may be explained by OP modification of heretofore imiden-tified proteins. Toxic symptoms from low-dose exposure to a particular OP are not identical to toxic symptoms from another OP, suggesting that the set of proteins modified by a particular OP does not overlap completely with the set of proteins modified by a different OP. Identification of new biomarkers of OP exposure could lead to new assays for OP exposure, and could lead to an understanding of the causes of low-dose toxicity. 

Continued dependence of salbutamol tablets taken in high doses (30 0 tablets daily and 48-64 mg day has lead to symptoms of toxic psychosis in one elderly woman and paranoid psychosis in a 52-year-old man. Up to 60-90 100 pg inhalations of salbutamol daily has been used by asthmatics who increased doses because they needed it and wanted to feel good . Long-term tolerance develops to bronchodilator action, tremor, tachycardia, prolongation of QTc interval, hyperglycemia, hypokalemia, and the vasodilator response. 

Note Sucralfate use can lead to symptoms of aluminium toxicity... 

Lead exposure mcreases urinary ALA and coproporphyrin-III excretion and causes accumulation of 2n-protoporphyrin in erythrocytes. The definitive test for lead toxicity is measurement of blood lead, but occasionally lead exposure is responsible for porphyria-like symptoms and may be an unexpected finding when investigating patients for suspected porphyria. ... 

Lead interferes with vitamin D metabolism, since it inhibits hydroxylation of 25-hydroxy-vitamin D to produce the active form of vitamin D. The effect has been reported in children, with blood levels as low as 10-15 pg/lOO cm3 (WHO, 1986). Measurements of the inhibitory effects of lead on heme synthesis are widely used in screening tests to determine whether medical treatment for lead toxicity is needed for children in high-risk populations who have not yet developed overt symptoms of lead poisoning. 

Cobalt toxicity symptoms in these patients included anorexia, nausea, vomiting, diarrhea, substernal aches, erythema, skin rashes, tinnitus, and neurogenic deafness. In some of the cobalt-treated patients paresthesias, numbness and other neurological signs developed, while others suffered optic nerve damage (Herndon etal. 1980). Erythema and several of the other symptoms can be directly attributed to the cobalt-induced stimulation of erythropoie-sis, leading to polycythemia. 

Pilocarpine is a tropane alkaloid. Toxic symptoms are characterized by muscarinic effects. Toxic effects include hypersecretion of saliva, sweat, and tears contraction of the pupils of the eyes and gastric pain accompanied with nausea, vomiting, and diarrhea. Other symptoms are excitability, twitching, and lowering of blood pressure. High doses may lead to death due to respiratory failure. A lethal dose in humans is estimated within the range of 150-200 mg. 

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