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Exposure Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
In EPA’s Food Quality Protection Act, the Office of Pesticide Programs (OPP) determined in 1999 to choose the 99.9th percentile of exposure as the regulatory target for single-day acute dietary exposure to pesticides.21 This was an interim choice because OPP recognized that individuals might be exposed to more than one pesticide with a common mechanism of action. For example, chlorpyrifos and methamidophos are both organophosphate pesticides that act by inhibition of an enzyme called cholinesterase that has important functions in regulating neuromuscular transmission and brain activity in mammals.22,23 In 2006, OPP withdrew the guidance that stipulated use of the 99.9th percentile in favor of a cumulative risk assessment approach.24,25
Organophosphorus Compound-Induced Mitochondrial Disruption
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Changes in mitochondrial structure following acute exposure to OPs have also been observed at the ultrastructural level by electron microscopy (Satar et al., 2004). For this study methamidophos alone or with counter OP poisoning treatments (atropine and pralidoxime), were administered to male Wistar rats. Methamidophos was given by gavage at the median LD50 concentration and cholinergic signs started to appear within 5 minutes, at which point the OP-only treated rats were sacrificed for analysis. Treatments were administered either at the first signs of cholinergic symptoms (5 min) or when all cholinergic signs were exhibited (8 min) and rats sacrificed after signs had subsided. In the livers of rats exposed to OP without atropine and pralidoxime treatment, there was evidence of ultrastructural changes. Interestingly, there was evidence of vacuolation in the mitochondrial matrix and accumulation of lipid droplets and glycogen granules, consistent with disruption of mitochondria and metabolism. However, quantitative data with respect to these changes were not presented. No such changes were observed in liver samples from either of the pharmacological treatments or in the vehicle control, suggesting that they were induced rapidly by acute exposure to this OP and that the effects were reversible following therapy with atropine and pralidoxime. However, since the treated animals were kept alive until all symptoms disappeared, the possibility that the effects of initial OP administration on mitochondria were time related rather than treatment related cannot be ruled out completely. However, ultrastructural changes to rat liver mitochondria, typically swelling and blebbing, have also been observed following 12 weeks chronic exposure) to the OP pesticide dichlorvos (Binkumar et al., 2010) suggesting that sub-acute effects on mitochondrial structure can be cumulative.
Indoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Organophosphate-induced delayed polyneuropathy (OPIDP) is a rare toxicity resulting from exposure to certain OP esters. It is characterized by distal degeneration of some axons of both the peripheral and central nervous systems (CNSs) occurring 1–4 weeks after single or short-term exposures. Cramping muscle pain in the lower limbs, distal numbness, and paresthesia occur, followed by progressive weakness, depression of deep tendon reflexes in the lower limbs and, in severe cases, in the upper limbs. Signs include high-stepping gait associated with bilateral foot drop and, in severe cases, quadriplegia with foot and wrist drop as well as pyramidal signs. In time, there might be significant recovery of the peripheral nerve function but, depending on the degree of pyramidal involvement, spastic ataxia may be a permanent outcome of severe OPIDP. Human and experimental data indicate that recovery is usually complete in the young. At onset, the electrophysiological changes include reduced amplitude of the compound muscle potential, increased distal latencies and normal or slightly reduced nerve conduction velocities. The progression of the disease, usually over a few days, may lead to nonexcitability of the nerve with electromyographical signs of denervation. Nerve biopsies have been performed in a few cases and showed axonal degeneration with secondary demyelination. Neuropathy target esterase (NTE) is thought to be the target of OPIDP initiation. The ratio of inhibitory powers for acetylcholinesterase and NTE represents the crucial guideline for the etiological attribution of OP-induced peripheral neuropathy. In fact, premarketing toxicity testing in animals selects OP insecticides with cholinergic toxicity potential much higher than that to result in OPIDP. Therefore, OPIDP may develop only after very large exposures to insecticides, causing severe cholinergic toxicity. However, this was not the case with certain triaryl phosphates (TAPs) that were not used as insecticides but as hydraulic fluids, lubricants, and plasticizers and do not result in cholinergic toxicity. Several thousand cases of OPIDP as a result of exposure to tri-ortho-cresyl phosphate have been reported, whereas the number of cases of OPIDP as a result of OP insecticide poisoning is much lower. In this article “Organophosphate-induced delayed polyneuropathy”, they mainly discuss OP pesticide poisoning, particularly when caused by CPF, dichlorvos, isofenphos, methamidophos, mipafox, trichlorfon, trichlornat, phosphamidon/mevinphos, and by certain carbamates. They also discuss case reports where neuropathies were not convincingly attributed to fenthion, malathion, omethoate/dimethoate, parathion, and merphos. Finally, several observational studies on long-term, low-level exposures to OPs that sometimes reported mild, inconsistent, and unexplained changes of unclear significance in peripheral nerves are briefly discussed.
Interactions of organophosphorus pesticides with solute carrier (SLC) drug transporters
Published in Xenobiotica, 2019
Lisa Chedik, Arnaud Bruyere, Olivier Fardel
OPs, rhodamine 123, verapamil, probenecid, amitriptyline, fluorescein, 4′,6′-diamidino-2-phenylindole (DAPI), and tetra-ethylammonium bromide (TEA) were provided by Sigma-Aldrich (Saint-Quentin Fallavier, France). [1-14 C]-TEA (sp. act. 3.5 mCi/mmol), [6,7-3 H(N)]-estrone-3-sulfate (E3S) (sp. act. 51.8 Ci/mmol) and 3,4-[Ring-2,5,6-3 H]-dihydroxyphenylethylamine (dopamine) (sp. act. 46 Ci/mmol) were purchased from Perkin-Elmer (Boston, MA). Stocked solutions of chemicals were commonly prepared in dimethyl sulfoxide (DMSO); final concentrations of solvent in transport assay medium did not exceed 0.2% (vol/vol). The chemical structures of the 13 OPs analyzed in the study are shown in Supplementary Figure S1. Six of these OPs, i.e. dichlorvos, fenamiphos, metasystox, methamidophos, monocrotophos, and profenofos, were organophosphate pesticides, with a central phosphorus atom with double-bonded oxygen (P = O). The remaining OPs (n = 7), i.e. fenitrothion, malathion, methyl parathion, parathion, phosmet, propetamphos and temephos, were organothiophosphates compounds, with a central phosphorus atom with double-bonded sulfur atom (P = S). These thion OPs have to be metabolized in oxon metabolites by cytochrome P-450 enzymes, for inhibiting acetylcholinesterase (Elersek & Filipic, 2011). According to the PubChem database (U.S. National Library of Medicine, Bethesda, MA), all OPs tested in the study were predicted to be water-soluble at 100 µM, which was the OP concentration retained for initially screening their potential inhibitory effects towards SLC transporter activities.
Fumigant toxicity of three Satureja species on tomato leafminers, Tuta absoluta (Meyrick) (Lepidoptera: Gelechiidae)
Published in Toxin Reviews, 2021
Chemical control was considered as the first method of management against T. absoluta. The insecticides used against this pest have been very diverse including organophosphates, pyrethroids, cartap, thiocyclam, and chemicals with new sites of action such as abamectin, spinosad, fipronil, chlorantraniliprole, flubendiamide, tebufenozide, acylurea insect growth regulators and chlorfenapyr (Desneux et al. 2010, Khani et al. 2020, Kumar et al. 2020, Mohanny et al. 2020). Generally, the feeding behavior of larvae (leaf mining) causes problems in the chemical control effectiveness (Lietti et al. 2005). Moreover, resistance to insecticides may be the most important reason of control failure. The primary reports of insecticide resistance were seen in South American countries such as Chile, Brazil, and Argentina. In these countries, different levels of resistance to organophosphates (e.g. methamidophos), pyrethroids (e.g. permethrin and deltamethrin), cartap, and abamectin, have been evaluated (Salazar and Araya 1997, Siqueira et al. 2000, Lietti et al. 2005). In addition, resistance to pyrethroid, indoxacarb, diamide and spinosyn spinosad has been reported in South America and Europe (Silva et al. 2011, Guedes and Siqueira 2012, Gontijo et al. 2013, Roditakis et al. 2013, Campos et al. 2015, Roditakis et al. 2015). In addition to insecticide resistance which may cause control failure, insecticides have adverse effects on non-target organisms such as beneficial arthropods either through direct acute toxicity in short-term and/or sublethal effects in entire organism life (Martinou et al. 2014).
Differences between organophosphates in respiratory failure and lethality with poisoning post the 2011 bans in Sri Lanka
Published in Clinical Toxicology, 2020
Chanika Alahakoon, Tharaka L. Dassanayake, Indika B. Gawarammana, Vajira S. Weerasinghe, Nicholas A. Buckley
Self-poisoning using organophosphorus pesticides (OP) is a common clinical problem in many developing countries [1–4]. These poisonings are commonly fatal and also have high morbidity, with prolonged ventilation needed for many patients [1–3,5–7]. Initial attempts to address this problem relied heavily on the WHO classification of extremely/highly hazardous (Class I) OP, which in turn was largely based on rat lethal doses (LD50). In Sri Lanka in the 1980s there was an epidemic of poisoning with highly hazardous OP such as monocrotophos, methamidophos and methylparathion. All these Class I agents were banned in late 1990s and case fatality declined sharply [8–10]. Other Class II (moderately hazardous based on LD50) OP replaced these in Sri Lanka. However, fatal poisoning and respiratory failure (RF) remained common with a 10% case-fatality and 24% requiring ventilation post these initial bans [11,12]. As better human toxicity data became available, the Pesticide Technical and Advisory Committee of Sri Lanka, implemented progressive bans on several Class II OP. Dimethoate and fenthion were phased out between the years 2008–2011 due to their high human toxicity [13,14]. From 2011 onwards chlorpyrifos, profenofos and diazinon were increasingly used. In 2014, chlorpyrifos was also banned due to concerns over chronic toxicity. Since then profenofos, an S-alkyl compound, has acquired a large share of the OP market [15]. Along with these regulatory changes, the pattern of OP poisonings have changed, but no studies have examined how those changes have altered the risk of major complications from acute OP poisoning. Therefore, we conducted this prospective cohort study to describe the RF and case-fatality of the OPs that were in use from 2013–2016 in Sri Lanka.