PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Phosmet”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Photodegradation of phosmet in wool wax models and on sheep wool: determination of wool wax bound phosmet by means of isotope ratio mass spectrometry.

The photochemical reactions of phosmet, an organophosphorus insecticide used for plant protection and for control of ectoparasites on productive livestock, were studied in the presence of wool wax. Induced by UV light, phosmet features numerous degradation pathways as well as photoaddition reactions with lipid structure moieties. In model irradiation experiments of phosmet in mixtures of solvents (cyclohexane, cyclohexene, 2-propanol) and fatty acid methyl esters (methyl stearate, methyl oleate, 12-hydroxymethyl stearate), both adjusted to the hydroxyl and iodine values of wool wax, half-lives were determined to be approximately 7 and 16 h, respectively. Irradiation of phosmet on crude sheep wool resulted in a degradation rate of 65% after 24 h. In tracer studies with stable isotope labeled phosmet ([15N]phosmet) in commercial lanolin and on raw sheep wool, employing a sunlight simulator and natural sunlight, wool wax bound phosmet was formed. After extraction and measurement by elemental analyzer/isotope ratio mass spectrometry, delta15N values of the phosmet-free wool wax fractions were notably increased as compared to the value of natural lanolin. Calculated from the delta15N values, an average of 13.9/15.6% (sunlight simulator/natural sunlight) was bound to wool wax lipids after irradiation of thin films of commercial lanolin. In experiments with sheep wool, 13.2 and 15.4%, respectively, were detected as wax-bound.

Animals↗

Evaluation of chemical and photochemical oxidation processes for degradation of phosmet on lowbush blueberries (Vaccinium angustifolium).

Chemical and photochemical oxidation processes were evaluated for their ability to degrade residual phosmet on lowbush blueberries and for their role in the conversion of phosmet to phosmet oxon--a toxic metabolite of phosmet. Chemical processes included 1 ppm of aqueous ozone, 1% hydrogen peroxide, 100 ppm of chlorine, and UV, whereas photochemical processes included hydrogen peroxide/UV, chlorine/UV, and ozone/hydrogen peroxide/UV. Phosmet applied as Imidan 2.5EC under laboratory conditions resulted in a mean residual concentration of 44.4 ppm, which was significantly degraded (p < 0.05) by ozone and chlorine, yielding reductions of 57.7 and 46%, respectively. Interaction between phosmet (Imidan 2.5EC) and any chemical or photochemical treatment did not result in conversion to phosmet oxon. Residual analysis of commercially grown blueberries revealed mean phosmet (Imidan 70W) levels of 10.65 ppm and phosmet oxon levels of 12.49 ppm. Treatment of commercial blueberries resulted in significant reductions in phosmet regardless of treatment type; however, only UV, hydrogen peroxide/UV, and ozone treatments degraded phosmet (Imidan 70W) to less toxic metabolites and reduced phosmet oxon levels. Treatment-induced conversion of phosmet to phosmet oxon was noticeably influenced by variations between phosmet formulations. Acceleration of photochemical degradation by UV was not observed. Selective oxidation by ozone represents a significant postharvest process for degrading residual phosmet on lowbush blueberries.

Blueberry Plants↗

Photodegradation chemistry of the insecticide phosmet in lipid models and in the presence of wool wax, employing a 15N-labeled compound.

The organophosphorus insecticide phosmet is commonly used for plant protection as well as against pests on animals. Phosmet features numerous degradation pathways induced by UV irradiation. In this study, we focused on the reaction possibilities of phosmet in the presence of lipophilic substances with olefinic structure elements, as they are frequently found in animal fur lipids, especially in wool wax. In the first step, simple models were employed to characterize the structural types of formed photoaddition products. On irradiation in the presence of cyclohexene, three photoaddition products were identified, a (4pi + 2pi) cycloaddition product of phosmet and cyclohexene and two diastereoisomer carbinols. Likewise, in more sophisticated models employing fatty acid methyl esters for irradiation experiments, phosmet was readily photodegraded. In the presence of methyl oleate, also 1:1 photoaddition products could easily be identified by means of liquid chromatography-mass spectrometry, using a stable isotope-labeled phosmet (15N-phosmet, 50 at. %) for the photolysis experiments. To converge from models to the more complex natural environment of animal skin lipids, irradiation experiments of phosmet in the presence of wool wax were performed. After 24 h of irradiation, only a remnant of 1.4% of the initial phosmet was detectable. Phosmet-oxon was detected in concentrations up to 27.3 mol %.

Chromatography, High Pressure Liquid↗

Studies on the putative interactions between the organophosphorus insecticide Phosmet and recombinant mouse PrP and its implication in the BSE epidemic.

It has been suggested that exposure of cattle to the ectoparasiticide Phosmet in the 1980s caused a conformational change in the cellular prion protein (PrP(C)) to form the BSE prion (PrP(SC)), which initiated the epidemic of bovine spongiform encephalopathy (BSE). Recombinant mouse cellular prion (r[mouse]PrP(C)) was exposed to the organophosphorus pesticide Phosmet in vitro and the conformation of the prion before and after exposure was monitored using circular dichroism (CD) spectroscopy, utilizing synchrotron radiation at the Council for the Central Laboratory of the Research Councils (CLRC) facilities at Daresbury, UK. Metabolites of Phosmet, generated in situ by rat microsomes, were investigated in the same way, to determine whether they might initiate the conformational change due to their high chemical reactivity. Our studies showed that exposure of r[mouse]PrP(C) to Phosmet or microsomes-generated metabolites of Phosmet did not result in the conformational change in the protein from alpha-helix to beta-pleated sheet that is characteristic of the PrP(C) to PrP(SC) conversion and, therefore, Phosmet is very unlikely to have initiated the BSE epidemic by a simple direct mechanism of conformational change in the prion protein.

Animals↗

High-dose exposure to systemic phosmet insecticide modifies the phosphatidylinositol anchor on the prion protein: the origins of new variant transmissible spongiform encephalopathies?

Compulsory exposure of the UK bovine to exclusively high biannual doses of a 'systemic' pour-on formulation of an organo-phthalimido-phosphorus warblecide, phosmet, during the 1980s (combined with exposure to the lipid-bound residues of 'bioconcentrated' phosmet recycled back via the intensive feeding of meat and bone meal), initiated the 'new strain' modification of the CNS prion protein (PrP) causing the UK's bovine spongiform encephalopathy (BSE) epidemic. A lipophilic solution of phosmet was poured along the bovine's spinal column, whence it penetrated and concentrated in phospholipids of the CNS membranes, covalently modifying endogenous phosphorylation sites on phosphatidylinositols (PIs) etc., forming a 'toxic membrane bank' of abnormally modified lipids that 'infect' any membrane proteins (such as PrP) that are programmed to conjugate onto them for anchorage to the membrane. Thus, phosmet invokes a primary covalent modification on PrP's PI anchor which, in turn, invokes an overall diverse disturbance upon CNS phosphoinositide second messenger feed back cycle, calcium homeostasis and essential free radicals; thus initiating a self-perpetuating cascade of abnormally phosphorylated PI-PrP that invokes a secondary electrostatic and allosteric disturbance on the main body of PrP impairing tertiary folding. Chaperone stress proteins conjugate onto misfolded PrP blocking its sites of proteolytic cleavage. Fresh epidemiological evidence is presented and experimental evidence referenced that adds support to a multifactorial hypothesis which proposes that BSE is a hitherto unrecognized and previously unmanifested class of subtle chronic phosmet-induced delayed neuro-excitotoxicity in the susceptible bovine.

Animals↗

Photolysis experiments on phosmet, an organophosphorus insecticide.

The organophosphorus insecticide phosmet is used in plant protection as well as against parasites on animals. Phosmet showed numerous photoinduced reaction pathways, which first were studied in the presence of model environments for animal fur lipids (e.g., wool wax). The model solvents for saturated and unsaturated lipids were cyclohexane and cyclohexene, whereas methanol and 2-propanol were used as models for primary and secondary alcohol moieties of lipids. The measured degradation rates over an irradiation period of 7 h in all solvents used were very similar (49-55%). The obtained photoproducts generally included phthalimide, N-hydroxymethylphthalimide, and N-methoxymethylphthalimide. Furthermore, depending on the solvent used, additional degradation products were detectable as N-isopropoxy- and N-methylphthalimide in the presence of 2-propanol and cyclohexene, respectively. However, in the presence of cyclohexene, despite the similar turnover, distinctly lower concentrations of photoproducts were found, indicating further still unknown degradation pathways. Irradiations in methanol with increasing percentages of water led to higher degradation rates; however, the products were found to be the same. Irradiation experiments with pure phosmet on silica TLC plates and glass surfaces resulted in degradation rates of 19 and 32%, respectively, after 6 h. The results obtained clearly demonstrate for the first time that the photoinduced degradation of phosmet is strongly dependent on the chemical environment, affecting less the turnover than the photoproducts formed. The results additionally demonstrate the need to investigate the degradation behavior of phosmet on wool and in the presence of wool wax.

Insecticides↗

Sorption and degradation characteristics of phosmet in two contrasting Australian soils.

The organophosphate insecticide phosmet [phosphorodithioic acid, s-((1,3-dihydro-1,3-dioxo-2H-isoindol-2yl)methyl), o,o-dimethyl ester] is used to control red-legged earth mites (Halotydeus destructor), lucerne flea (Sminthurus viridis), and Oriental fruit moth (Cydia molesta) in horticulture and vegetable growing. This study was undertaken with two soils of contrasting properties to determine the extent to which sorption and degradation of the insecticide might influence its potential to leach from soil into receiving waters. Two soils were used: a highly organic, oxidic clay soil (Ferrosol) and a sandy soil low in organic matter (Podosol), sampled to 0.3 m depth. The extent of sorption and decomposition rate of a phosmet commercial formulation were measured in laboratory experiments. Sorption followed a Freundlich isotherm at all depths. The Freundlich coefficient K was significantly correlated (p = 0.005) with organic C content in the Podosol, and significantly correlated (p = 0.005) with organic C and clay content in the Ferrosol. K was highest (48.8 L kg-1) in the 0- to 0.05-m depth of the Ferrosol, but lowest (1.0 L kg-1) at this depth in the Podosol. Degradation followed first-order kinetics, with the phosmet half-life ranging from 14 h (0-0.05 m depth) to 187 h (0.2-0.3 m depth) in the Ferrosol. The half-life was much longer in the sandy Podosol, ranging from 462 to 866 h, and did not change significantly with depth. Soil organic C and to a lesser degree clay content influenced phosmet sorption and degradation, but the interaction was complex and possibly affected by co-solvents present in the commercial formulation.

Adsorption↗

Evaluation of an in vitro method for acaricidal effect. Activity of parathion, phosmet and phoxim against Sarcoptes scabiei.

An in vitro test to determine the acaricidal effect of organophosphorous insecticides (OP) is described. The effect of parathion, phoxim and phosmet against the pig mange mite Sarcoptes scabiei var. suis was evaluated. The test is based on the migration ability of mites on the surface of agar gels containing the acaricide. The mite activity is expressed as a migration index (MI) and compared with the OP concentration in the agar. Good dose-response data were obtained for all three OPs tested, although the instability of phosmet required special precautions concerning the analysis of the agar. The test was found to be accurate, sensitive, easy to carry out and applicable for routine determinations. However, the test requires that the actual concentrations of the OPs in the gel batches are determined. For the three OPs used analytical methods were developed. While the lower threshold for acaricidal effect in vitro was approximately 1-2 micrograms g-1 for all three OPs tested, a significant difference in the higher concentration range was seen between the dose-response curve for parathion and the curves for phoxim and phosmet. While the latter curves decreased only slightly at concentrations above 3-6 micrograms g-1 (corresponding to MI values around 5-10), the curve for parathion was linear down to an MI value of 1, corresponding to a parathion concentration of approximately 30 micrograms g-1. This discrepancy was ascribed to different rates of uptake through the cuticula due to differences in the lipophilicity of the OPs.

Animals↗

Phosmet induces up-regulation of surface levels of the cellular prion protein.

Chronic (2 day) exposure of human neuroblastoma cells to the organophosphate pesticide phosmet induced a marked concentration-dependent increase in the levels of PrP present on the cell surface as assessed by biotin labelling and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable and non-releasable forms of PrP were increased on the plasma membrane. These increases appear to be due to post-transcriptional mechanisms, since PrP mRNA levels as assessed by Northern blotting were unaffected by phosmet treatment. These data raise the possibility that phosmet exposure could increase the susceptibility to the prion agent by altering the levels of accessible PrP.

Cell Membrane↗

Exposure of farmers to phosmet, a swine insecticide.

OBJECTIVES: The goal of this study was to measure dermal and inhalation exposures to phosmet during application to animals and to identify what determinants of exposure influence the exposure levels. METHODS: Ten farmers were monitored using dermal patches, gloves, and air sampling media during normal activities of applying phosmet to pigs for insect control. Exposures were measured on the clothing (outer), under the clothing (inner), on the hands, and in the air. Possible exposure determinants were identified, and a questionnaire on work practices was administered. RESULTS: The geometric mean of the outer exposure measurements was 79 microg/h, whereas the geometric mean of the inner exposure measurements was 6 microg/h. The geometric mean for hand exposure was 534 microg/h, and the mean air concentration was 0.2 microg/m3. Glove use was associated with the hand and total dermal exposure levels, but no other determinant was associated with any of the exposure measures. The average penetration through the clothing was 54%, which dropped to 8% when the farmers wearing short sleeves were excluded. The farmers reported an average of 40 hours a year performing insecticide-related tasks. CONCLUSIONS: Farmers who applied phosmet to animals had measurable exposures, but the levels were lower than what has been seen in other pesticide applications. Inhalation exposures were insignificant when compared with dermal exposures, which came primarily from the hands. Clothing, particularly gloves, provided substantial protection from exposures. No other exposure determinant was identified.

Animal Husbandry↗

A comparative study of guanine N7-alkylation in mice in vivo by the organophosphorus insecticides trichlorphon, dimethoate, phosmet and bromophos.

Following intraperitoneal administration to male mice (strain AB Jena/Halle) of 14C-methyl-labelled trichlorphon, dimethoate, phosmet and bromophos, 10-20 Ci/mol, in dosages of 0.06-0.55 mmol/kg, DNA from liver and kidneys was analyzed for 14C in N-7 methylguanine (7-MeG). The extents of methylation were in the range of 5-10 mumol 7-MeG/mol guanine for trichlorphon and dimethoate and of 0.2-0.4 for phosmet and bromophos, for high doses, respectively Excretion half-lives of 7-MeG were differing between trichlorphon (5 hrs, high dose, and 15-17 hrs, low dose) and dimethoate (23-160 hrs, high dose). The extents of methylation at 0-6 of guanine were estimated to be around 0.01 mumol 0-6 MeG/mol guanine for high doses of organophosphates of sufficient water solubility. Factors associated with the partition of organophosphates in mammalian systems are useful for estimating DNA attack by organophosphates in mammals in vivo.

Alkylation↗

Pathophysiological studies of neuromuscular function in subacute organophosphate poisoning induced by phosmet.

A 51 year old man developed progressive cranial and proximal muscle weakness, hyperreflexia and mental change. The disorder progressed over 9 days following the fifth weekly spraying with the organophosphate (OP) insecticide, phosmet, with limited symptoms of acute toxicity. Marked decremental responses of 50-80% on slow and fast rates of stimulation were improved to 15% by edrophonium or neostigmine. Intracellular recordings at the endplate region of intercostal muscle revealed small miniature endplate potentials (mepps), reduced mean acetylcholine sensitivity and normal membrane potentials. Electronmicroscopy revealed degeneration and regeneration of the endplates. This study demonstrates that OP poisoning due to phosmet can produce a subacute postsynaptic neuromuscular syndrome without marked symptoms of acute toxicity.

Critical Care↗

Evaluation of phosmet for the control of the common scabies mite on cattle.

Thirty-four young range cattle heavily infested with the common scabies mite, Psoroptes ovis, were dipped in phosmet (O,O-dimethyl phosphorodithioate S-ester with N-(mercaptomethyl)phthalimide) in 15 trials. All concentrations from 0.15% to 0.25% that were applied once failed in at least one trial, but all concentrations from 0.075% to 0.20% were successful in eradicating mites when used twice at 7- to 10-day intervals. One single dip tried at 0.30% also was successful. Uninfested yearlings were dipped in 0.30% phosmet without apparent intoxication, but 2-year-old cattle treated in a spray-dip machine at 0.40% active ingredient became depressed and stiff gaited.

Administration, Topical↗

Mutagenic activity of phosmet, the active component of the organophosphorus insecticide Decemtione EK 20 in Salmonella and Saccharomyces assays.

Phosmet, the active component of the organophosphorus insecticide Decemtione EK 20, was shown to be mutagenic in the standard Ames Salmonella/mammalian microsome assay in the absence and presence of metabolic activation. It appears to be a direct mutagen inducing base substitution mutations (TA100) as well as a weak frameshift mutagen (TA97). This compound was genotoxic in the Saccharomyces cerevisiae D7 strain. It significantly increased reverse mutation, mitotic crossing-over and slightly, but not significantly, increased gene conversion at the highest concentration used.

Animals↗

Phosmet for the systemic control of pig mange in growing pigs.

A study of the effect of Sarcoptes scabiei var. suis on the performance of growing pigs under commercial conditions is described. Mange was endemic on the farm. Phosmet treatment controlled mange in growing pigs and resulted in a 12% increase in average daily liveweight gain over untreated mange-infected controls.

Animals↗

Phosmet residues in an orchard and adjacent recreational area.

Two cover sprays of phosmet were applied to an orchard adjoining a camping area and a bird sanctuary with a resident goose population. Insecticide residues were monitored on orchard leaves, orchard ground cover, ground cover in the camp-site and along the adjacent lakeshore. Despite attempts to minimize drift, significant spray residues were found outside the target area. Residues on ground cover and leaves were reduced by sprinkler irrigation subsequent to spray application.

Chromatography, Gas↗

Systemic activity of coumaphos, famphur, crufomate, ronnel, and phosmet given orally to hens for control of the northern fowl mite, Ornitbonyssus sulviarum (Canestrini and Fanzago).

Coumaphos (O-(3-chloro-4-methyl-2-oxo-2H-1-benzopyran-7-yl)O,O-diethyl phosphorothioate), famphur (O-[p-(dimethylsulfamoyl)phenyl] O,O-dimethyl phosphorothioate). crufomate (4-tert-butyl-2-chlorophenyl methyl methylphosphoramidate), ronnel (O,O-dimethyl O-(2,4,5-trichlorophenyl) phosphorothioate) and phosmet (O,O-dimethyl phosphorodithioate S-ester with N-(mercaptomethyl) phthalimide) were administered as systemic acaricides (either single or multiple oral doses or as feed additives) for control of the nortnern fowl mite, Ornithonyssus sylviarum (Canestrini and Fanzago), on caged White Leghorn hens. None of the treatments controlled the mites, but some hens were poisoned.

Animals↗

On the mechanism of acute toxicity of phosmet.

Rats were given single oral doses of phosmet (LD50 or 3/4 LD50). Changes of hematological parameters were studied in several time intervals; the main interest was paid to disturbances in blood clotting. Both light and electron microscopy were used to evaluate histopathological changes in selected organs (liver, lungs, spleen, stomach). Marked changes could be observed in all blood clotting parameters studied, other findings were not standard. The pathological picture was dominated by endothelial damage to the blood vessels and findings of thrombocytic clots in microcirculation of all organs examined. Together with hemocoagulation changes, they could be considered as reflecting the compensated stage of diffuse intravascular coagulopathy. In addition, damaged alveolar endothelium and interstitial edema could be observed in the lungs together with hepatic steatosis, damaged proximal renal tubuli, release of cellular elements from the splenic pulp and decomposition of megakaryocytes as well as serious exfoliation of the superficial layers of the gastric mucosa. The pathohistological alterations coincided with changes in organ weights.

Animals↗