Exposure, definition blood lead

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. ... 

While there is disagreement about what exposure levels are needed to produce the earliest symptoms, most experts agree that symptoms definitely can occur at blood lead levels of 60 ng/dl whole blood and therefore recommend a 40 ng/dl maximum. The central nervous system effects frequently are not reversible following discontinued exposure or chelation therapy and when improvement does occur, it is almost always only partial. 

The measurement of bone lead is the most definitive indicator but is quite difficult to assess and interpret. Consequently the blood lead level (BLL) is used as the principal indicator of exposure. It is usually expressed in micrograms per decilitre of blood and can be measured from finger prick samples as a first order screen or from drawn blood samples. 

Lead exposure Not a substitute for effective abatement of lead exposure. Neutropenia Mild to moderate neutropenia has been observed in some patients receiving succimer. While a causal relationship to succimer has not been definitely established, neutropenia has been reported with other drugs in the same chemical class. Obtain a complete blood count with white blood cell differential and direct platelet counts prior to and weekly during treatment. Withhold or discontinue therapy if the absolute neutrophil count (ANC) is below 1200/mcL and follow the patient closely to document recovery of the ANC to above 1500/mcL or to the patient s baseline neutrophil count. There is limited experience with reexposure in patients who have developed neutropenia. Therefore, rechallenge such patients only if the benefit of succimer therapy clearly outweighs the potential risk of another episode of... 

The definition of neurotoxicity also indicates a potential difference between the developing and the mature nervous system, to underscore the fact that developmental neurotoxicity is an important aspect of neurotoxicology. Most known human neurotoxicants are indeed developmental neurotoxicants.4 In most, but not all cases, the developing nervous system is more sensitive to adverse effects than the adult nervous system, as indicated, for example, by the most deleterious effects of ethanol, methylmercury, or lead when exposure occurs in utero or during childhood. Furthermore, the blood-brain barrier (BBB), which protects the mature nervous system from the entry of a number of substances, appears to be poorly developed at birth and during the first few years of life.6... 

The definitive test for establishing lead toxicity is an assay that measures the amount of lead in the blood in micrograms per decilitre (mcg/dl). This is the most universally accepted marker for lead exposure. Further tests include a blood film (looking for punctate basophilia) and X-ray fluorescence which helps to quantify the total body burden. Needless to say, complete... 

In summary, lead affects peripheral nerves by damaging Schwann cells and myelin sheaths, by damaging some axons (though not definitely their precursor cells), and by influencing the permeability of blood vessels within nerves. The primary site of damage is not known, nor is it known what effects, if any, may be seen at levels of exposure comparable to those found in the contemporary urban environment. 

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