Pesticides cholinesterase inhibition

See also Carbamate Pesticides Cholinesterase Inhibition Pesticides. 

At least for OP pesticides, cholinesterase Inhibition (AAChE) Is well established and accepted as a response criterion (. . ). although not without exception ( p. 133). 

ACETYLCHOLINESTERASE INHIBITING PESTICIDES Cholinesterase activity in red Discretionary 70% of individuals Ns... 

Mice that were exposed dermally to residues of methyl parathion in emulsifiable concentrate on foliage, and were muzzled to prevent oral intake, developed inhibition of plasma cholinesterase and erythrocyte cholinesterase after two 10-hour exposures (Skinner and Kilgore 1982b). For the organophosphate pesticides tested in this study, cholinergic signs generally were seen in mice with cholinesterase inhibition >50% results for this end point were not broken down by pesticide. 

Case Studies in Environmental Medicine Taking an Exposure History—The importance of taking an exposure history and how to conduct one are described, and an example of a thorough exposure history is provided. Other case studies of interest include Reproductive and Developmental Hazards Skin Lesions and Environmental Exposures Cholinesterase-Inhibiting Pesticide Toxicity and numerous chemical-specific case studies. 

ATSDR. 1993c. Case studies in environmental medicine - cholinesterase inhibiting pesticide toxicity. Agency for Toxic Substances and Disease Registry, Division of Toxicology, Atlanta, GA. 

The purpose of this chapter is not to discuss the merits, or lack thereof, of using plasma cholinesterase inhibition as an adverse effect in quantitative risk assessments for chlorpyrifos or other organophosphate pesticides. A number of regulatory agencies consider the inhibition of plasma cholinesterase to be an indicator of exposure, not of toxicity. The U.S. Environmental Protection Agency, at this point, continues to use this effect as the basis for calculating the reference doses for chlorpyrifos, and it is thus used here for assessing risks. 

L. Pogacnik and M. Franko, Optimisation of FIA system for detection of organophosphorus and carbamate pesticides based on cholinesterase inhibition. Talanta 54, 631-641 (2001). 

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... 

Presently available methods to diagnose and biomonitor exposure to anticholinesterases, e.g., nerve agents, rely mostly on measurement of residual enzyme activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in blood. More specific methods involve analysis of the intact poison or its degradation products in blood and/or urine. These approaches have serious drawbacks. Measurement of cholinesterase inhibition in blood does not identify the anticholinesterase and does not provide reliable evidence for exposure at inhibition levels less than 20 %. The intact poison and its degradation products can only be measured shortly after exposure. Moreover, the degradation products of pesticides may enter the body as such upon ingestion of food products containing these products. 

Disulfoton and its breakdown products can be measured in the blood, urine, feces, liver, kidney, or body fat of exposed people. In cases of occupational or accidental exposure to disulfoton, the breakdown products are often measured in the urine. The breakdown products are relatively specific for disulfoton and a few other similar organophosphate pesticides and can be detected in urine for up to one week after people were last exposed. Because disulfoton inhibits cholinesterase in blood and in blood cells, inhibition of this enzyme activity may also suggest exposure to disulfoton. Cholinesterase activity in blood and in blood cells may remain inhibited for as long as 1-2 weeks after the last exposure. Because other organophosphate pesticides also inhibit cholinesterase activity in blood and blood cells, this test is not specific for disulfoton. The measurement of cholinesterase in blood and blood cells and the amount of disulfoton breakdown products in the urine cannot always predict how much disulfoton you were exposed to. Your doctor can send samples of your blood or urine to special laboratories that perform these tests. Chapters 2 and 6 provide more information about medical tests. 

Hazards Skin Lesions and Environmental Exposures Cholinesterase-Inhibiting Pesticide Toxicity and numerous chemical-specific case studies. 

The WHO/FAO Joint Meeting of Experts on Pesticide Residues (JMPR) has given recommendations on interpretation of cholinesterase inhibition (FAO 1998, 1999), see Section 4.7.7.3.1. 

PSD. 1999. Methodology for the toxicological assessment of exposures from combinations of cholinesterase inhibiting compounds. Draft document. Medical and Toxicological Panel, Advisory Committee on Pesticides, Pesticides Safety Directorate, UK Ministry of Agriculture, Fisheries and Food, April 19,1999. 

AChEj induction correlated with the body burden of total pesticides in 15 pooled flounder livers at the Benelux tunnel (site 2) and Noordwijk (site 6) locations. The highest concentrations of several OCPs (total 150 00 o,g/kg lipid weight) were found in flounder from the Rotterdam transect (De Boer et ah, 2001). The Rotterdam transect (sites 6 to 2) is characterised by acethyl-cholinesterase inhibition (mainly brain), which may reflect contamination by pesticides in this transect. The concentrations of total OCPs in SPM varied in the Rotterdam and Amsterdam transects from below the detection limit to 1.8 mg kg and 1.6 mg kg respectively. Rotterdam showed relatively higher levels of OCPs from upstream, caused by one of the major sources of OCP residues in the rivers Meuse and Rhine. The eontamination might be classified as historical, or industrial centres might still be emitting these eompounds (Voorspoels et al., 2004). 

Kurt TL. 1988. Persistent symptoms of cholinesterase inhibiting pesticide toxicity (diazanon) [letter]. Vet Hum Toxicol 30(3) 268. 

This group of compounds is used as pesticides and nerve gases. The structure and therefore metabolism and potency varies. However, they all act in a similar manner. There are two toxic effects, cholinesterase inhibition and delayed neuropathy, but all OPs do not necessarily cause both. The cholinesterase inhibition results from the similarity between the organophosphorus compound and acetylcholine. The organophosphorus compound therefore acts as a pseudosubstrate but blocks the enzyme, in some cases, permanently. This is because the... 

F. Arduini, F. Ricci, I. Bourais, A. amine, D. Moscone and G. Palleschi, Extraction and detection of pesticides by cholinesterase inhibition in a two-phase system a strategy to avoid heavy metal interference, Anal. Lett., 48 (2005) 17003-17019. 

Convenient and rapid detection of cholinesterase inhibition by pesticides extracted from sheep wool... 

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