Carbamate measuring exposure

Antidotes are administrated to patients after there has been exposure to OPs. They are also sometimes given as a protective measure when there is a risk of exposure, for example, to troops fighting in the Gulf War. Of the two types of antidote mentioned earlier, only atropine is effective against carbamate poisoning. 

The measurement of inhibition of brain AChE is a valuable biomarker assay for OPs and carbamates and is not jnst an index of exposure. Being an assay based on... 

Occupational exposure to carbamate insecticides may be monitored by measuring RBC-ACHE and/or PCHE. However, given the low cholinesterase inhibition levels and the short time duration of this effect, ACHE inhibition can generally be used as a biomarker of exposure only when exposure levels are high. Three sequential samples are recommended to establish an individual baseline before exposure. In exposed workers, blood sampling and analysis should be carried out soon after the end of exposure (WHO, 1986). 

Pharmacologically, carbofuran inhibits cholinesterase, resulting in stimulation of the central, parasympathetic, and somatic motor systems. Sensitive biochemical tests have been developed to measure cholinesterase inhibition in avian and mammalian brain and plasma samples and are useful in the forensic assessment of carbamate exposure in human and wildlife pesticide incidents (Bal-lantyne and Marrs Hunt and Hooper 1993). Acute toxic clinical effects resulting from carbofuran exposure in animals and humans appear to be completely reversible and have been successfully treated with atropine sulfate. However, treatment should occur as soon as possible after exposure because acute carbofuran toxicosis can be fatal younger age groups of various species are more susceptible than adults (Finlayson et al. 1979). Carbofuran labels indicate that application is forbidden to streams, lakes, or ponds. In addition, manufacturers have stated that carbofuran is poisonous if swallowed, inhaled, or absorbed through the skin. Users are cautioned not to breathe carbofuran dust, fumes, or spray mist and treated areas should be avoided for at least 2 days (Anonymous 1971). Three points are emphasized at this juncture. First, some carbofuran degradation... 

Edmiston, C.E., Jr., Goheen, M., Malaney, G.W., and Mills, W.E. Evaluation of carbamate toxicity acute toxicity in a culture of Paramecium multlmlcronucleatum upon exposure to aldicarb, carbaryl, and mexacarbate as measured by a Warburg respirometry and acute plate assay. Environ. Res., 36(2) 338-350, 1985. 

In view of the various possible pathways for nitrosation of amines as well as of amine derivatives (amides, ureas, carbamates, etc. ), it is not unexpected then for N-nitroso compounds to be found in many different areas of the human environment (11). It is possible that N-nitroso compounds may represent a carcinogenic exposure which most people experience on a daily basis. The list of items that have now been demonstrated to have measurable levels of various N-nitroso compounds present within them has grown considerably over the past decade (, 11, 12). A portion of this list would include air, water, soil, cheese, meats, fish, eggs. 

While the depression of plasma and/or RBC cholinesterase may be detected after exposure to very large amounts of carbamates, enzyme activity usually recovers rapidly--within minutes to hours. Hence these tests can be misleading unless one of the rapid methods for testing cholinesterase activity has been employed. A more sensitive and specific absorption test for several of the carbamate pesticides is the measurement of their metabolites in the urine within 48 hours of exposure. Carbamate pesticides are sufficiently acutely toxic that those attending the victim must avoid contact with contaminated apparel or vomitus, and should wear rubber gloves during decontamination of hair and skin of the victim. 

Assessment of exposure to carbamate pesticides can be a complex matter for a variety of reasons. Measurement of cholinesterase depression can be difficult in the case of carbamates. 

Exposure to a toxic dose of OP results in inhibition of acetylcholinesterase and butyrylcholinesterase activities. The most common method to measure OP exposure is to assay acetylcholinesterase and butyrylcholinesterase activities in blood using a spectrophotometric method (EUman et al, 1961 Wilson et al, 2005 Worek et al, 1999). The drawbacks of activity assays are that they do not identily the OP. They show that the poison is a cholinesterase inhibitor but do not distinguish between nerve agents, OP pesticides, carbamate pesticides, and tightly bound, noncovalent inhibitors like tacrine and other anti-Alzheimer drugs. In addition, low-dose exposure, which inhibits less than 20% of the cholinesterase, carmot be determined by measuring acetylcholinesterase and butyrylcholinesterase activity because individual variability in activity levels is higher than the percent inhibition. 

Clinical diagnosis is relatively simple and is based on medical history, circumstances of exposure, and the presence of clinical symptoms of poisoning. Confirmation of diagnosis can be made by measurement of red blood cell AChE or plasma ChE. Activities of these enzymes are accepted as biomarkers of exposure and/or toxicity of OPs and carbamates. Red blood cell AChE is identical to the enzyme present in the target synapses and its levels are assumed to reflect the effects in target organs. Thus, red blood cell AChE is regarded as a biomarker of toxicity of these compounds. However, it must be kept in mind that the above assumption is only correct when the inhibitor has equal access to blood and synapses. It is difficult to know... 

An enzyme-based Pz biosensor for the detection of organophosphorous and carbamate pesticides has also appeared [176]. The assay was based in the inhibitory effect of the pesticides on immobilised acetylcholinesterase. After exposure of the enzyme to the pesticides, the substrate 3-indoyl acetate was added. This was enzymatically converted to an insoluble product, the concentration of which was determined by the resulting frequency change. The rate and amount of conversion was due to the concentration of the active immobilised enzyme, which was dependent on the amount of pesticide present. The system was very similar to that used by Ebersole and Ward in their AMISA [66]. The authors measured paroxon to 5 x 10 M and carbaryl to 1 X 10- M. 

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