Neurological damage, lead exposure

Use of lead arsenate as a pesticide was also cancelled on most crops - the basis for the cancellation being two-fold -the irreversibility of neurological damage resulting from lead exposure of children and the potential for lead-induced renal tumors noted at high levels in rodents resulted in a requirement to reduce the total lead exposure from all soxirces, and secondly the occupational exposure data indicates the potential for human skin cancer resulting from arsenic exposure. 

Peripheral neuropathy wrist drop, due to radial nerve involvement, is a classic manifestation of chronic lead neurotoxicity. Clinical and experimental studies support the view that lead induces peripheral nerve lesions. Central nervous system the manifestations of saturnine encephalopathy include headache, irritability, insomnia, apprehension, confusion, nightmares and fits. High exposure levels (at least 200/ig Pb/lOOml in children and 500)Ltg Pb/lOOml in adults) are usually found. Recovery from encephalopathy is often incomplete, and residual neurological damage is frequent. 

Lead, emitted primarily from smelters and battery plants, enters the body in several different ways, including inhalation of lead in air, ingestion of lead in food, or consumption of lead in water. Lead can accumulate in the body over long periods of time and damage the kidneys, liver, and nervous system. Excessive exposure causes neurological damage, producing seizures, mental retardation, and other behavioral disorders. Fetuses, infants, and children are particularly sensitive. 

In cases of severe non-fatal episodes of lead encephalopathy, the neurological sequelae that occur are qualitatively similar to those often seen after traumatic or infectious cerebral injury, with permanent sequelae being more common in children than in adults. The most severe paediatric sequelae are cortical atrophy, hydrocephalus, convulsive seizures, and severe mental retardation (Mellins and Jenkins, 1955 Perlstein and Attala, 1966 Chisolm, 1968). Children who recover from acute lead encephalopathy but are re-exposed to lead almost invariably show evidence of permanent CNS damage (Chisolm and Harrison, 1956). Even if further lead exposure is minimized, 25 to 50% show severe permanent sequelae, such as seizure disorders, blindness, and hemiparesis (Chisolm and Barltrop, 1979). 

Because lead causes neurologic damage at doses that do not cause overt toxicity, blood lead levels are used to identify children with dangerous amounts of lead (see Chapter 1). Another measurement of body lead levels is the free erythrocyte protoporphyrin (EP or FEP) test, which measures the level of EP in the blood. The EP level reflects an impaired ability of the body to produce heme, the business end of the hemoglobin molecule, usually due to the presence of lead. Blood lead levels reflect a child s immediate past exposure to lead as well as lead previously absorbed by bone and now being released into the bloodstream. Thus a child may continue to have toxic levels of lead in his/ her blood long after a lead source has been removed. 

Human exposure to bromomethane is most likely to occur by inhalation or dermal contact (see Chapter 5). Inhalation exposure may cause neurological, respiratory and renal damage. Dermal contact may cause skin lesions while oral exposure leads to digestive tract mucosal membrane irritation (see Section 2.2). 

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