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At least 19 recordsLinked to original sources

PubMed1978

Single case study. Possible organophosphate-induced parkinsonism.

A case of possible organophosphate-induced parkinsonism is presented. The patient was a crop duster with numerous episodes of acute organophosphate intoxication and chronic organophosphate exposure. The etiology of parkinsonism is discussed in terms of a balance hypothesis between cholinergic and dopaminergic neurotransmission in the striatum. A possible relationship between chronic organophosphate exposure and alterations in central cholinergic or dopaminergic activity is suggested. The course of this patient raises the possibility that agricultural workers may be at risk for the late development of parkinsonism.

Humans↗

PubMed1979

Myopathy of chronic organophosphate poisoning: a clinical entity?

The acute aspects of organophosphate poisoning are well understood. Persistent weakness and muscular wasting in some cases have been attributed to neuropathic effects resulting in muscular atrophy from denervation. Recently, necrosis of skeletal muscle has been induced by chronic inhibition of cholinesterase with organic phosphates in a reproducible experimental model. The literature on organophosphate poisoning in man alludes to cases in which it appears plausible to postulate this mechanism as a cause of a residual myopathy. A new case in which chronic organophosphate intoxication may be implicated in the etiology of a proximal myopathy is presented. Reports of additional cases, followed up from the onset of symptoms, are needed to determine whether primary myopathic effects are a clinically significant complication of chronic organophosphate poisoning.

Adult↗

PubMed1976

Behavioral effects of organophosphate in man.

Increasingly widespread application of organophosphate pesticies has underscored the importance of studying their effects on human behavior. Clinical reports and laboratory investigations have generally supported the assumption that neurobehavioral manifestations of organophosphate toxicity are attributable to accumulation of acetylcholine at central and peripheral synapses as a result of cholinesterase inhibition. Despite methodologic shortcomings in many of the published studies, investigators generally agree on the presence of several behavioral sequelae of organophosphate poisoning: (a) impaired vigilance and reduced concentration, (b) slowing of information processing and psychomotor speed, (c) memory deficit, (d) linguistic disturbance, (e) depression, and (f) anxiety and irritability. The few studies of asymptomatic workers at risk for repeated exposure to organophosphate pesticides have produced only equivocal findings concerning the presence of less severe or latent forms of these behavioral abnormalities.

Anxiety↗

PubMed1978

Organophosphate pesticide poisoning.

A total of 118 workers from a 120-person grape picking crew became ill in early September 1976. Of these (108 men and 10 women), 85 received medical attention and three of the 85 were admitted to hospital. The symptoms were typical for organophosphate poisoning. Average plasma and red cell cholinesterase values for the affected workers were depressed more than 60 percent. Most were treated with atropine and some were also treated with 2-PAM (pralidoxime). The exposure to residues of the organophosphate pesticides dialifor (Torak((R))) and phosalone (Zolone((R))) occurred in one grower's vineyards near Madera, California. It appeared that workers had been allowed into recently-treated areas before the expiration of the required 30-day safety interval for dialifor, and that excessive skin exposure to residues of this pesticide had resulted. The clinical management of these cases and the occupational surveillance of the workplace became quite complex. The grower sustained significant losses of grapes during the period in which some of his vineyards were under quarantine and he had to pay substantial medical expenses as well as a fine for violating state regulations concerning the proper use of pesticides. Organophosphate pesticides decay more slowly under hot, dry weather conditions than they do when rainfall is frequent. California has imposed a number of specific safety intervals to be observed after the application of these pesticides to certain crops. If, in violation of these regulations, workers are permitted to enter fields too soon, poisoning can occur.

Adult↗

PubMed1977

Evaluation of hazards involved in treating cattle with pour-on organophosphate insecticides.

Eighteen veterinarians regularly practicing organophosphate pour-on treatment of cattle for grub infestations were examined in the course of the 1975-1976 application season for symptoms and signs as well as enzymologic and chemical evidence of organophosphate absorption. Some subjects reported headache, nausea, and irritation of the face and throat during chemical applications in poorly ventilated buildings. Organophosphate absorption was not sufficient to depress blood cholinesterase activities, and only occasionally generated measurable amounts of alkyl phosphate meatbolites in urine of exposed veterinarians.

Animals↗

PubMed1976

Probable progress in the therapy of organophosphate poisoning: extracorporeal hemodialysis and hemoperfusion.

Whether or not extracorporeal hemodialysis or hemoperfusion with coated activated charcoal might be used in eliminating organophosphates following poisoning with nitrostigmine, demeton-S-methyl sulfoxide, or dimethoate was here examined. Nitrostigmine could not be hemodialysed. The other two organophosphates, on the other hand could be well eliminated from the blood by hemodialysis. The clearance rates for demeton-S-methyl sulfoxide and dimethoate were 52.98 ml/min and 59.07 ml/min respectively, at a blood flow rate of 100 ml/min. The clearance values for hemoperfusion with coated activated charcoal were higher under the same trial conditions, the values being 83.70 ml/min for demeton-S-methyl sulfoxide and 87.84 ml/min for dimethoate. Nitrostigmine, too, could be eliminated from the blood by hemoperfusion, its clearance being 59.20 ml/min.

Adult↗

PubMed1979

Arrhythmias in organophosphate poisonings.

168 cases of organophosphate poisonings are reviewed with special respect to frequent arrhythmias. In 134 cases toxic repolarisation with QT prolongation, ST- and T- anomalies were present. 56 patients had arrhythmias and the prevalence of ventricular arrhythmias was impressive. In five patients a transient picture of myocardial infarction was seen. The great incidence of ECG alterations and arrhythmias necessitate the permanent monitoring of patients with organophosphate poisoning in an intensive care unit.

Adolescent↗

PubMed1977

[Routine chemical-toxicological examination in fata poisoning through organophosphates].

The authors describe in their work methods of isolation of organophosphate insecticides from biological material--the isolation of the effective substance proper as well as of the solvent. They detect organophosphates by means of chromatography on a thin leyer and in one instance also by gas chromatography. In conjunction with chromatography on a thin leyer they discuss methods of detection according to the chemical structure of the substances searched for and submit their own modification of detection based on inhibition of acetylcholine esterase. They detect the solvent in insecticides in biological materials by means of gas chromatography.

Chromatography, Gas↗

PubMed1978

Binding of the organophosphates parathion and paraoxon to bovine and human serum albumin.

Binding of parathion and paraoxon to bovine serum albumin (BSA) and human serum albumin (HSA) was studied by using equilibrium dialysis. The concentration of unbound organophosphate was determined from its anticholinesterase activity. Binding of parathion to BSA was shown to be reversible. The organophosphates interact with only one type of binding sites in BSA and HSA. The affinity constants at pH 7.2 and 4 degrees C for the interaction of BSA or HSA and parathion were found to be 2.7 X 10(6) and 1.5 X 10(6) M-1, respectively. The affinity constants for the interaction of the serum albumins and paraoxon were considerably lower, 6.0 X 10(3) and 1.6 X 10(4) M-1, respectively. Lowering the pH from 7.2 to 4.8 did not significantly affect the binding parameters. The great difference of affinity of the serum albumins to parathion and paraoxon is discussed with respect to the fate of parathion in the body.

Animals↗

PubMed1976

Enzymatic hydrolysis of organophosphate insecticides, a possible pesticide disposal method.

A crude cell extract from a mixed bacterial culture growing on parathion, an organophosphate insecticide, hydrolyzed parathion (21 C) at a rate of 416 nmol/min per mg of protein. This rate of enzymatic hydrolysis, when compared with chemical hydrolysis by 0.1 N sodium hydroxide at 40 C, was 2, 450 times faster. Eight of 12 commonly used organophosphate insecticides were enzymatically hydrolyzed with this enzyme preparation at rates ranging from 12 to 1,360 nmol/min per mg of protein. Seven pesticides were hydrolyzed at rates significantly higher (40 to 1,005 times faster) than chemical hydrolysis. The pH optimum for enzymatic hydrolysis of the eight pesticides ranged from 8.5 to 9.5, with less than 50% of maximal activity expressed at pH 7.0. Maximal enzyme activity occurred at 35 C. The crude extract lost its activity at the rate of only 0.75%/day when stored at 6 C. Eight organic solvents, ranging from methanol to hexane, at low concentrations stimulated enzymatic hydrolysis by 3 to 20%, whereas at higher concentrations (1,000 mg/liter) they inhibited the reaction (9 to 50%). Parathion metabolites p-nitrophenol, hydroquinone, and diethylthiophosphoric acid, at up to 100-mg/liter concentrations, did not significantly influence enzyme activity.

Bacteria↗

PubMed1977

Correlation between organophosphate poisoning, acetylcholinesterase inhibition, and increased cyclic GMP levels in malathion-treated insects.

Organophosphate poisoning with malathion caused large increases (up to 125 and 440%, respectively) in the level of cyclic GMP in larvae of Mamestra configurata Wlk. and in the fly Sarcophaga bullata Parker. Cyclic AMP was little affected. The malathion-induced increase in cyclic GMP was time and dose dependent. Time-course studies with the head and thorax of S. bullata demonstrated that the increase in cyclic GMP level occurred precipitously after a lag period of about 1 h, during which time the activity of acetylcholinesterase (EC 3.1.1.7) was progressively inhibited. The abrupt increase in cyclic GMP began when acetylcholinesterase activity had been inhibited to a sufficient extent to permit accumulation of acetylcholine. It is suggested that the accumulation of acetylcholine in the malathion-poisoned insects caused cyclic GMP levels to rise. Cyclic GMP may have a role in cholinergic transmission in normally functioning insect neural tissue. Increased levels of cyclic GMP induced by organophosphate and organocholorine (Bodnaryk, R. P. (1976) Can. J. Biochem. 54, 957-962) insecticides appear to be a vital and previously unrecognized biochemical lesion in insects poisoned by these compounds.

Animals↗

PubMed1978

Effects of organophosphate insecticides on the cholinergic receptors of frog skeletal muscle.

The organophosphates octamethyl pyrophosphoramide, Bidrin, and phosphoric acid 2,2-dichlorovinyl dimethyl ester inhibit the membrane voltage response of frog sartorius muscles to carbamylcholine in a manner expected of either a slowly reversing competitive inhibitor or a noncompetitive inhibitor. The inhibition reverses with a time course of minutes, depending upon the temperature. The inhibition by these compounds is reduced by d-tubocurarine but is unaffected by hexamethonium. This may indicate that the organophosphate binding sites are near the cholinergic binding site since both d-tubocurarine and hexamethonium are competitive inhibitors of cholinergic agonists and d-tubocurarine is the larger compound.

Acetylcholine↗

PubMed1978

Organophosphate poisoning in Rhodesia. A study of the clinical features and management of 105 patients.

A series of 105 patients with organophosphate poisoning admitted to Harari Hospital during the past 4 years is described. Poisoning with organophosphate compounds is being seen more frequently in hospital practice in Rhodesia. Many of the cases are attempted suicides, but frequently there is no positive history of contact with the poison. The majority of patients exhibit the classic clinical features of parasympathetic overactivity, but diagnosis may be obscured by atypical presentation. Rapid diagnosis and utilization of the treatment regimen outlined in this article should reduce the mortality to less than 15%.

Adolescent↗

PubMedDate not supplied

A controlled field trial of physiological responses to organophosphate residues in farm workers.

Blood acetylcholinesterase (ACHE) and pseudocholinesterase (PCHE) activity and urinary dialkyl phosphate (DAP) excretion were measured in a group of 15 male agriculture field workers during a five-day thinning operation in a Northern California peach orchard. Eight men were randomly assigned to work in a Guthion-treated plot, and seven men to work in an adjoining plot free from organophosphate residues. Foliage samples were taken to measure dislodgeable and total Guthion residues. The daily mean percent change in the ACHE and in the PCHE activity was less than -10.0 percent of baseline values for each group of men. Mean ACHE activity of workers in the Guthion treated plot was different from that of workers in the control plot on the fifth exposure day. The mean PCHE activity of workers in the Guthion treated plot was not different from that of workers in the control plot. Daily group-mean urinary metabolite excretion levels for workers exposed to Guthion residues were highly correlated with their daily group-mean percent change in ACHE activity. No urinary metabolites were detected in workers in the control plot. Decay in Guthion residues was markedly slower in this trial than in a comparable study conducted one year previously, emphasizing the difficulty in setting re-entry intervals based on time elapsed from pesticide application. Suggestions were made to extend the time interval of future studies on the human health effects of organophosphate residue exposure, and to further refine urinary metabolite surveillance methods toward the goal of establishing a threshold level of metabolites which would correspond to meaningful exposure to these pesticides residues.

Acetylcholinesterase↗

PubMed2026

Comprehensive source-risk assessment of organophosphate esters in surface water of the Dianchi Lake Basin, Yunnan, China.

Organophosphate esters (OPEs), widely used as flame retardants and plasticizers, have been increasingly detected in aquatic environments. However, investigations of their distribution in high-altitude plateau lakes remain scarce. Identifying and quantifying the sources and associated risks of OPEs are crucial for subsequent water environment management. In this study, an integrated source-risk analysis approach was employed by combining the Positive Matrix Factorization (PMF) model, the Geodetector (GD) model, and risk quotient (RQ). Analysis of 14 OPEs in surface waters of the Dianchi Lake Basin (DLB) revealed 12 detectable compounds, with total OPEs concentrations (ΣOPEs) ranging from not detected (ND)-64.6 ng/L during the wet season and ND-35.8 ng/L during the dry season. Elevated ΣOPEs were primarily observed at inflow sites in the northern part of the lake and in urban rivers. Source apportionment indicated four major contributing sources: agricultural films containing flame-retardant and plasticizer additives, traffic-related particulate emissions, releases from household and personal care products, and industrial production and applications of flame retardants in plastics, electronics, and related products (the predominant source). The ecological impact caused by OPEs ranges from no risk to low risk, with tris(2-chloroethyl) phosphate emitted from industrial source being the primary driver of potential environmental risk. These findings highlight the necessity of prioritizing industrial sources in future management strategies. Overall, this study provides a methodological framework for source apportionment and risk assessment of OPEs and offers scientific evidence to support environmental management of OPEs in the DLB.

Environmental Monitoring↗

PubMed1977

Core/targetoid fibres and multiple cytoplasmic bodies in organophosphate neuropathy.

From correlated histochemical and ultrastructural investigations of biopsy specimens of a rare case with delayed-onset neuropathy due to organophosphate (Dipterex) intoxication, several pathological characteristics were recognized in the muscle fibres. Most striking was concurrence of core/targetoids and multiple cytoplasmic bodies in the same fibres. Foci of markedly reduced or absent oxidative enzyme activity were revealed in 71.6% of type I fibres and in 3.4% of type II fibres. Most of those foci were two-zoned core/targetoids. Cytoplasmic bodies were also revealed selectively in type I fibres contrary to the previous reports. Targets, targetoids, cores and multicores were suggested to be strongly related to each other pathogenetically and to be due to the disturbance of some neurotrophic influences. In the biopsy specimen taken 220 days after exposure to the drug, numerous sarcoplasmic masses were revealed, and they were very likely to represent special forms of regeneration.

Biopsy↗

PubMed2025

Prenatal organophosphate ester exposure and epigenetic changes at birth: a characterization of the methylome in the ECHO cohort.

BACKGROUND: Prenatal exposure to organophosphate esters (OPEs) affects multiple child health domains. Alterations to the DNA methylome are a plausible mechanism through which these changes occur. This study characterized DNA methylation signatures at birth associated with prenatal OPE biomarkers. METHODS: We included 736 mother-infant pairs from 7 sites in the Environmental influences on Child Health Outcomes (ECHO) Cohort. Five OPE biomarkers were quantified in maternal urine samples collected during the second and third trimesters and modeled as log2-transformed continuous variables. Using covariate-adjusted linear regression, we tested associations between OPE biomarkers and locus-specific, regional, and global cord blood DNA methylation changes measured by Illumina 450 K and EPIC arrays, and gestational epigenetic age measured by the Knight gestational age epigenetic clock generated with measures from the 27 K, 450 K, and EPIC arrays. When feasible, we examined relationships by sex. FINDINGS: Global hypomethylation at multiple regions was associated with BDCPP concentrations (p = 0.003 to 0.02, coef = -0.002). Differentially methylated regions annotated to PCDHGB1 and SLC43A2 were associated with BDCPP and DPHP concentrations, respectively (FDR q < 0.05). In sex-specific analyses, global hypomethylation was associated with prenatal BDCPP (p = 0.006 to 0.03, coef = -0.0003 to -0.0002) and DBUP_DIBP (p = 0.01, coef = -0.0007 to -0.0006) concentrations in females; and global hypermethylation was associated with DBUP_DIBP concentrations in males (p < 0.05, coef = 0.0004). BCETP concentrations were significantly associated with decelerated epigenetic aging at birth in females (p < 0.05, coef = -0.05). INTERPRETATION: Prenatal exposure to OPEs impacts child methylation at birth, suggesting a potential mechanism for the association between prenatal OPE exposure and child health outcomes.

Humans↗

PubMed1979

The influence of 2-/o-cresyl/-4 H-1 : 3 : 2-benzodioxa-phosphorin-2-oxide (CBDP) on organophosphate poisoning and its therapy.

The aim of the experiments was to obtain more information on the toxicity of organophosphates and protection against them. Pretreatment of mice with CBDP increased the s.c. toxicity of soman 19.1-fold, and its i.p. toxicity 17.8-fold. The protective effect of atropine and the oximes HS-3, HS-6 and HI-6 in soman poisoning was much greater in CBDP pretreated than in control animals. Atropine + HI-6 raised the s.c. LD50 of soman in the CBDP pretreated animals from 6.8 micrograms/kg to 166 micrograms/kg (PI = 24.3), but in control animals the i.p. LD50 was only raised from 370 micrograms/kg to 608 micrograms/kg (PI = 0.6). CBDP inhibited blood and brain AChE activity, but had no effect on aliesterase (AE) activity in plasma, liver and brain of mice in vivo. CBDP increased s.d. toxicities of sarin 11-fold, of tabun 5-fold and of VX 0.24-fold. The protective index of atropine + HS-3 in sarin poisoning, as in the case of soman poisoning, was much higher in CBDP pretreated than in control animals (20.1 : 13.6), only slightly higher in tabun poisoning (4.3 : 3.4) and in the case of VX poisoning lower in CBDP pretreated than in control animals (32 : 47). The results indicate that CBDP potentiates soman, sarin and tabun toxicities mainly by blocking their binding to non-specific sites in the body.

Acetylcholinesterase↗