Methylene blue can act as an antidote to pesticide poisoning of bumble bee mitochondria.

The population of bumble bees and other pollinators has considerably declined worldwide, probably, due to the toxic effect of pesticides used in agriculture. Inexpensive and available antidotes can be one of the solutions for the problem of pesticide toxicity for pollinators. We studied the properties of the thiazine dye Methylene blue (MB) as an antidote against the toxic action of pesticides in the bumble bee mitochondria and found that MB stimulated mitochondrial respiration mediated by Complex I of the electron transport chain (ETC) and increased respiration of the mitochondria treated with mitochondria-targeted (chlorfenapyr, hydramethylnon, pyridaben, tolfenpyrad, and fenazaquin) and non-mitochondrial (deltamethrin, metribuzin, and penconazole) pesticides. MB also restored the mitochondrial membrane potential dissipated by the pesticides affecting the ETC. The mechanism of MB action is most probably related to its ability to shunt electron flow in the mitochondrial ETC.

Identification of cattle poisoning by Bifenthrin via earwax analysis by HS/GC-MS.

The use of pyrethroids has increased over recent years, and corresponds to a higher exposure of animals to pesticide residues in the environment and diet. Here, an outbreak of pyrethroid poisoning in beef cattle was reported occurring in Midwestern Brazil. After veterinary evaluation, it was observed that the bovines presented common pyrethroid intoxication symptoms. Aiming to identify the cattle poising by pyrethroid, earwax samples were collected from two groups: exposed and nonexposed animals from the same farm. Blind earwax analyses of the bovines were carried out using headspace/gas chromatography-mass spectrometry (HS/GC-MS). The HS/GC-MS analysis detected the presence of bifenthrin in the earwax analysis of the exposed animals, confirmed by the comparison of its MS fragments with a bifenthrin standard, and also by its retention time relative to the internal standard. In summary, HS/GC-MS analysis of earwax emerges as a tool that can be used in the detection and monitoring of bifenthrin poisoning in cattle, as a useful veterinary diagnosis that ensures animal health and the safety of their products.

[A case report of death from acute emamectin·chlorfenapyr poisoning].

To analyze the clinical data of a case of acute emamectin·chlorfenapyr poisoning in Guangzhou 12th People's Hospital in 2019. The patient developed high fever and night sweats, and gradually became unconscious. The patient died after 5 days of treatment. The toxicity and mortality of emamectin·chlorfenapyr were high. For acute poisoning patients, in addition to conventional symptomatic treatment, early blood purification treatment should be actively carried out.

Mediation of oxidative stress toxicity induced by pyrethroid pesticides in fish.

Organophosphate and organochlorine pesticides are banned in most countries because they cause high toxicity and bioaccumulation in non-target organisms. Pyrethroid pesticides have been applied to agriculture and aquaculture since the 1970s to replace traditional pesticides. However, pyrethroids are approximately 1000 times more toxic to fish than to mammals and birds. Fish-specific organs such as the gills and their late metabolic action against this type of pesticide make fish highly susceptible to the toxicity of pyrethroid pesticides. Oxidative stress plays an important role in the neurological, reproductive, and developmental toxicity caused by pyrethroids. Deltamethrin, cypermethrin, and lambda-cyhalothrin are representative pyrethroid pesticides that induce oxidative stress in tissues such as the gills, liver, and muscles of fish and cause histopathological changes. Although they are observed in low concentrations in aquatic environments such as rivers, lakes, and surface water they induce DNA damage and apoptosis in fish. Pyrethroid pesticides cause ROS-mediated oxidative stress in fish species including carp, tilapia, and trout. They also cause lipid peroxidation and alter the state of DNA, proteins, and lipids in the cells of fish. Moreover, changes in antioxidant enzyme activity following pyrethroid pesticide exposure make fish more susceptible to oxidative stress caused by environmental pollutants. In this review, we examine the occurrence of pyrethroid pesticides in the aquatic environment and oxidative stress-induced toxicity in fish exposed to pyrethroids.

Clinical effects from household insecticide: pyrethroid or organophosphate toxicity?

A 54-year-old man with a history of schizophrenia presented to the emergency room for weakness with associated lacrimosis, drooling, nausea, emesis, diarrhoea, diplopia and burning sensation on his skin that began 6 hours after spraying five cans of Raid on his carpet. He was noted to have miotic pupils and hyperactive bowel sounds. Given the clinical presentation, the patient was diagnosed with organophosphate (OP) toxicity. After being admitted, he developed symptoms associated with his OP toxicity and was successfully treated with atropine and pralidoxime. Most Raid products contain pyrethroids; however, both OPs and pyrethroids are available in commercial pesticides and patients may misidentify ingestions. There are limited data reporting the toxicity of pyrethroid overdose in humans and to guide its subsequent treatment. It is crucial to keep a low threshold for diagnosing and treating patients with acute onset of symptoms suspicious for an OP or pyrethroid toxidrome.

Pyrethroid intoxication: A rare case report and literature review.

Synthetic pyrethroid cypermethrin is commonly used in agriculture, veterinary, and household insects management. It has been found to be a newer insectiside poisoning reported in Turkey. Acute severe poisoning of cypermethrin is a rare event. Here we report a case of a 25-year-old woman presented with features of cypermethrin poisoning in intensive care unit. Management of acute rare poisoning is discussed in this case with literature review.

A Study on Deliberately Self-Poisoned In-Hospital Patients in a Tertiary Health Care Center in Northeast India: A Cross-Sectional Review.

BACKGROUND: The nature and profile of different modes of poisoning vary significantly in different parts of India. The assessment of the magnitude of suicidal poisoning is an area of paramount importance not only for appropriate management but also for raising social awareness and framing government policies for the prevention of same. OBJECTIVES: We aimed to determine the pattern of poisoning, the sociodemographic profile of patients who poison themselves, and the in-hospital outcome of self-poisoned patients over a 1-year period. METHODS: This was a cross-sectional observational study conducted between May 2015 and April 2016 that included 492 patients >12 years of age who were admitted to our hospital after consuming poison with the intention of deliberate self-harm. Relevant history with respect to the nature and amount of poison ingested were taken and recorded, and the patients' sociodemographic profiles and outcome (as either discharge or death) were noted. RESULTS: Most of the patients were 13-28 years of age (69%). Males (n = 293 [59.55%]) predominated over females and the majority were farmers (n = 193 [39.23%]). Rural cases (n = 373 [75.81%]) outnumbered urban cases. The major causes of deliberate self-harm attempts were impulsive actions (n = 442 [89.84%]). Pesticides (n = 393 [79.88%]) were the most commonly consumed poison. The overall mortality rate was 12%, with paraquat (94.74%) topping the list of fatal substances. CONCLUSION: Young adults and males constitute majority of the population in this study. Agricultural poisons made up the bulk of the cases, mostly taken by rural population. Paraquat, an herbicide banned in several countries, had the highest mortality rate in this study.

Short-term glucose dysregulation following acute poisoning with organophosphorus insecticides but not herbicides, carbamate or pyrethroid insecticides in South Asia.

BACKGROUND: Ingestion of organophosphorus (OP) insecticides is associated with acute hyperglycaemia. We conducted a prospective study to determine whether glucose dysregulation on admission associated with ingestion of OP insecticides or other pesticides is sustained to hospital discharge or to 3-12 months later. METHODS: We recruited participants to two similar studies performed in parallel in Anuradhapura, Sri Lanka, and Chittagong, Bangladesh, following hospitalisation for OP insecticide, herbicide or other pesticide self-poisoning. Two-hour 75 g oral glucose tolerance testing (OGTT) was performed after recovery from the acute poisoning, at around the time of discharge. In Sri Lanka, a four time-point OGTT for area-under-the-curve (AUC), C-peptide and homeostatic modelling of insulin resistance (HOMA-IR) was undertaken, repeated after 1 year. In Bangladesh, a 2-h OGTT for glucose was undertaken and repeated after 3 months in participants with initial elevated 2-h glucose. We compared glucose homeostasis by poison group and adjusted findings for age, BMI and sex. FINDINGS: Seventy-three Sri Lankan and 151 Bangladeshi participants were recruited. We observed higher mean [SD] fasting (4.91 [0.74] vs. 4.66 [0.46] mmol/L, p = .003) and 2-h glucose (7.94 [2.54] vs. 6.71 [1.90] mmol/L, p < .0001) in OP-poisoned groups than pyrethroid, carbamate, herbicide or 'other poison' groups at discharge from hospital. In Sri Lanka, HOMA-IR, glucose and C-peptide AUC were higher in OP than carbamate or herbicide groups. Adjusted analyses remained significant except for fasting glucose. Follow-up analysis included 92 participants. There was no significant difference in OGTT results between OP-poisoned and other participants at follow-up (mean [SD] 2-h fasting glucose 4.67 [0.92] vs. 4.82 [0.62], p = .352; 2-h glucose 6.96 [2.31] mmol/L vs. 6.27 [1.86] mmol/L, p = .225). CONCLUSION: We found in this small prospective study that acute OP insecticide poisoning caused acute glucose dysregulation that was sustained to hospital discharge but had recovered by 3-12 months. Acute glucose dysregulation was related to defects in insulin action and secretion. This study did not address long-term risk of diabetes following acute OP insecticide poisoning, but could provide the data for a power calculation for such a study.

Bifenthrin Fatality in a Canine: A Case Report with Postmortem Concentrations.

A case of canine intoxication and fatality with the pyrethroid insecticide bifenthrin is described. A 5-year-old female spayed Pit Bull Terrier was off leash and unsupervised at home for 15-20 min prior to discovery by her owner. The patient was in lateral recumbency, having what the owner described as a seizure. The patient was transported to an emergency veterinary hospital where she presented with tachycardia, tachypnea and intractable tremors/seizures. Despite aggressive medical intervention, the patient went into respiratory and cardiac arrest and died at 28 h after presentation. A postmortem liver sample screened positive for bifenthrin by gas chromatography-mass spectrometry (GC-MS). During the screening procedure, four additional bifenthrin-metabolic products were also observed. Concentrations for bifenthrin were determined for fat, kidney, liver and urine by GC-MS-MS. This is the first reported case of a canine fatality resulting from bifenthrin.

Delayed hyperthermia from chlorfenapyr overdose.

We describe the hospital course of a 42-year-old patient who presented to the Emergency Department following an ingestion of an unknown quantity of chlorfenapyr, an organochlorine pesticide that acts as a mitochondrial uncoupler (MU). There is limited data on chlorfenapyr toxicity in humans, but reports indicate a 100% mortality rate after a 7-10 day quiescent period.3-6 Our patient was admitted for a 5-day asymptomatic observation period before becoming critically ill. Supportive care, antioxidant therapy, and late hemodialysis (HD) proved futile. The patient expired from complications due to uncontrollable hyperthermia on hospital day 6. This case represents the first reported fatality due to chlorfenapyr in North America, and illustrates: 1) its potency as a human toxin, 2) the futility of extracorporeal decontamination once late toxicity has set in; 3) the potential need for early and aggressive decontamination in the ED; and 4) the need for a better understanding of this unique poison.

Validación de un método para la determinación del ácido 3-fenoxibenzoico en orina por QuEChERS, microextracción líquido-líquido dispersiva y cromatografía líquida de alta resolución-arreglo de diodos / Validation of a method for the determination of 3-phenoxybenzoic acid in urine using QuEChERS, microextraction liquid-liquid dispersive and high-performance liquid chromatography-diode array

Los piretroides son insecticidas ampliamente usados no sólo en el ámbito agropecuario y doméstico sino también en salud pública. Una vez absorbidos, son rápidamente metabolizados a compuestos polares eliminados por vía renal. Uno de los metabolitos común a un gran número de piretroides es el ácido 3-fenoxibenzoico (3-PBA) el cual es utilizado como marcador de exposición. Se presenta en este trabajo, la validación de una metodología analítica para la determinación del 3-PBA utilizando QuEChERS acoplado a microextracción líquido-líquido dispersiva con tricloroetileno como disolvente extractivo y cromatografía líquida de alta resolución con detector de foto-arreglo de diodos. La validación se realizó con muestras aisladas de orina de voluntarios adultos de ambos sexos sin exposición conocida y orina sintética. El método resultó lineal en el intervalo 9 μg L-1-79 μg L-1; los límites de detección y cuantificación fueron de 3 μg L-1 y 9 μg L-1, respectivamente. No se observaron señales de interferentes a los tiempos de retención del 3-PBA y del ácido 2-fenoxibenzoico (2-PBA), estándar interno, en las muestras de orina blanco. Las señales cromatográficas en las muestras enriquecidas fueron espectralmente homogéneas. Las precisiones intradiarias (RSDr%) (n= 5) para 9 μg L-1 estuvieron comprendidas entre 9,3%-9,9% y para 27 μg L-1 entre 5,9%-10,6%. Las precisiciones interdiarias (RSDint%) (n=15) para los mismos niveles de concentración fueron de 11,8% y 9,1%, respectivamente. El rango de porcentajes de recuperación para 9 μg L-1 fue de 87%-119% y para 27 μg L-1 de 70%-91%. Se evaluó la estabilidad del analito en la muestra y en el extracto. El analito resultó estable a -20 °C durante 7 días en la muestra y durante 1 día en el extracto. Los valores de incertidumbre relativa e incertidumbre expandida fueron evaluados mediante la ecuación de Horwitz, los resultados obtenidos fueron para el nivel 9 μg L-1 de 33% y 65% y para el nivel 27 μg L-1 de 28% y 55%. La aplicabilidad del método validado fue evaluada con muestras reales de personas sin exposición laboral conocida, quienes declararon haber usado insecticidas piretroides. El método resultó sensible y selectivo.

Pyrethroid insecticides are used not only in the agricultural and domestic environment, but also in public health. Once absorbed, they are rapidly metabolized into polar compounds eliminated by the kidneys. One of the metabolites common to many pyrethroids is 3-phenoxybenzoic acid (3-PBA) which are used to evaluate exposure. We present in this paper the validation of an analytical methodology for the determination of 3-PBA using QuEChERS coupled to dispersive liquid-liquid microextraction with trichloroethylene as an extractive solvent and high-performance liquid chromatography with a photodiode array detector. Validation was carried out with isolated samples of urine from adult volunteers of both sexes without exposure and synthetic urine. The method was linear in the interval 9 μg L-1-79 μg L-1; the limit of detection and quantitation were 3 μg L-1 and 9 μg L-1, respectively. Interfering signals were not observed in the blank urine samples and the chromatographic signals in the enriched samples were spectrally homogeneous. The within-run precision (RSDr%) (n = 5) for 9 μg L-1 were between 9.3%-9.9% and for 27 μg L-1 between 5.9%-10.6%. The between-run precision (RSDint%) (n = 15) for the same concentration levels were 11.8% and 9.1%, respectively. The recovery for 9 μg L-1 ranged from 87%-119% and for 27 μg L-1 from 70%-91 %. The stability of the analyte was evaluated in the sample and in the extract. The analyte in the sample was stable at -20 °C for 7 days and in the extract was stable for 1 day. The values of relative uncertainty and expanded uncertainty obtained by the Horwitz equation were 33% and 65% for 9 μg L-1, and 28% and 55% for 27 μg L-1. The applicability of the validated method was evaluated with real samples of people without known occupational exposure, who declared having used pyrethroid insecticides. The method was sensitive and selective.

Seizures in patients with acute pesticide intoxication, with a focus on glufosinate ammonium.

The incidence and clinical aspects of seizures remain to be elucidated in patients with acute pesticide intoxication. The present study included subjects who ingested pesticide with the intention of committing suicide and were treated at Soonchunhyang University Hospital (Cheonan, Korea) between January 2011 and December 2014. We analyzed the incidence and characterized the type and frequency of seizure, from the medical records of 464 patients with acute pesticide intoxication, according to the pesticide class. The effect of seizure on the clinical outcome was assessed. The incidence of seizure was 31.5% in patients who ingested glufosinate ammonium {2-amino-4-[hydroxyl (methyl) phosphinoyl] butyrate; ammonium DL-homoalanin-4-yl (methyl) phosphinate}, followed by those who ingested pyrethroid (5.9%) or glycine derivatives (5.4%). All of the seizures developed between 12 and 24 h of pesticide ingestion and had ceased by 72 h after seizure initiation, following treatment with antiseizure medication. Generalized tonic-clonic seizures were the most commonly observed (85.7% of the cases). Multivariable logistic regression analysis showed that the effect of seizure on mortality was not statistically significant. In conclusion, glufosinate ammonium herbicide is the most common seizurogenic pesticide class. Seizure itself was not a risk factor for mortality in patients with acute glufosinate ammonium intoxication.

Complex suicide involving pyrethroid ingestion (mosquito coils) and fatal self-wounding by sharp force.

"Complex suicide" is a term referring to the suicidal pattern in which more than one suicidal method is applied in the purpose of inducing death. The present paper aims to review complex suicide literature shortly and investigate an unusual planned complex suicide incident, the rarity of which is attributable to the combination of suicide methods as well as the type and quantity of substances applied to induce poisoning. A 33-year-old man with a history of psychotic depression was found dead in his bedroom lying within a large quantity of blood. He had already committed two previous suicide attempts and he was under treatment with antidepressants. The forensic examination revealed the use of the following successive suicide methods: benzodiazepine and alcohol intake, pyrethroid poisoning due to ingestion of mosquito coils, wrist cutting, and a fatal cut in the victims neck. Death occurred due to hemorrhagic shock. Furthermore, the authors extensively discuss the use of sharp force in suicide and the discrimination "tools" between suicide and homicide.

Pesticide poisoning in Chitwan, Nepal: a descriptive epidemiological study.

BACKGROUND: Globally, there is a growing concern over pesticides use, which has been linked to self-harm and suicide. However, there is paucity of research on the epidemiology of pesticides poisoning in Nepal. This study is aimed at assessing epidemiological features of pesticides poisoning among hospital-admitted cases in selected hospitals of Chitwan District of Nepal. METHODS: A hospital-based quantitative study was carried out in four major hospitals of Chitwan District. Information on all pesticides poisoning cases between April 1 and December 31, 2015, was recorded by using a Pesticides Exposure Record (PER) form. RESULTS: A total of 439 acute pesticides poisoning cases from 12 districts including Chitwan and adjoining districts attended the hospitals during the 9-month-long study period. A majority of the poisoned subjects deliberately used pesticides (89.5%) for attempted suicide. The total incidence rate was 62.67/100000 population per year. Higher annual incidence rates were found among young adults (111.66/100000 population), women (77.53/100000 population) and individuals from Dalit ethnic groups (98.22/100000 population). Pesticides responsible for poisoning were mostly insecticides (58.0%) and rodenticides (20.8%). The most used chemicals were organophosphates (37.3%) and pyrethroids (36.7%). Of the total cases, 98.6% were hospitalized, with intensive care required for 41.3%. The case fatality rate among admitted cases was 3.8%. CONCLUSIONS: This study has indicated that young adults, females and socially disadvantaged ethnic groups are at a higher risk of pesticides poisoning. Pesticides are mostly misused intentionally as an easy means for committing suicide. It is recommended that the supply of pesticides be properly regulated to prevent easy accessibility and misuse. A population-based study is warranted to reveal the actual problem of pesticides exposure and intoxication in the community.

Immunological and genotoxic effects of occupational exposure to α-cypermethrin pesticide.

OBJECTIVES: The aim of this work has been to find out the occupational oxidative stress, immunological and genotoxic health hazards among α-cypermethrin (CYP) pesticide-exposed workers. MATERIAL AND METHODS: A cross-sectional study was performed including 200 workers divided into 3 groups according to the level of exposure: highly exposed group (50 workers), moderately exposed group (50 workers) and unexposed group (100 workers). All workers were subjected to detailed laboratory investigation for gene P53 mutations, immunological parameters as a cluster of differentiation into 3 percentage (CD3%), CD4% and CD8% in addition to peripheral blood total leukocytic and platelet counts that were measured. Spectrophotometer technique was used for detection of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx). Air samples were collected with a High Volume Small Surface Sampler for measurement of α-cypermethrin level. RESULTS: A highly exposed group to the α-cypermethrin had lower CD4/CD8 as compared to an unexposed group with statistically significant difference. As regards gene mutation, exons 5a and 6 were more frequent among the highly exposed group as compared to no mutation among moderately exposed and unexposed groups with significant difference. As regards antioxidants; SOD, CAT, GSH and GPx were higher among the unexposed group as compared to the highly and moderately exposed group with statistically significant difference. Significant negative correlation was found between working years and antioxidant parameters. CONCLUSIONS: Repeated exposure to α-CYP may lead to gene mutations, immunological disturbances and oxidative stress. Strict safety precautions are required not only for workers but also for public users. Int J Occup Med Environ Health 2017;30(4):603-615.

Chemical components, antioxidant potential and hepatoprotective effects of Artemisia campestris essential oil against deltamethrin-induced genotoxicity and oxidative damage in rats.

In the present study, we evaluated the antioxidant potential of Artemisia campestris essential oil (ACEO) and the possible protective effects against deltamethrin induced hepatic toxic effects. The ACEO showed radical scavenging activity with IC50 = 47.66 ± 2.51 µg/ml, ferric reducing antioxidant power (FRAP) potential (EC50 = 5.36 ± 0.77 µg/ml), superoxide scavenging activity (IC50 = 0.175 ± 0.007 µg/ml) and ˙OH scavenging activity (IC50 = 0.034 ± 0.007 µg/ml). The obtained results of phenolic profile demonstrated that phenolic compounds are the major contributor to the antioxidant activity of ACEO. GC-MS analysis revealed the presence of 61 components in which monoterpene hydrocarbons constitute the major fraction (38.85%). In in vivo study, deltamethrin exposure caused an increase of serum AST, ALT and ALP activities, hepatic malondialdehyde (MDA) (measured as TBARS) and conjugated dienes markers of lipid peroxidation (LPO), while antioxidant enzyme activities (SOD, CAT and GPx) decreased significantly. Furthermore, it induces DNA damage as indicated by DNA fragmentation accompanied with severe histological changes in the liver tissues. The treatment with vitamin E or ACEO significantly improved the hepatic toxicity induced by deltamethrin. It can be concluded that vitamin E and ACEO are able to improve the hepatic oxidative damage induced by deltamethrin. Therefore, ACEO is an important product in reducing the toxic effects of deltamethrin.

Poisoning suicide with ingestion of the pyrethroids alpha-cypermethrin and deltamethrin and the antidepressant mirtazapine: A case report.

This case report describes a death attributed to the intake of the pyrethroid insecticides, alpha-cypermethrin and deltamethrin, and the antidepressant mirtazapine. The autopsy findings showed absence of external traumatic injuries and internal generalized visceral congestion, edema and cyanosis. The toxicological results revealed the presence of a toxic concentration of mirtazapine (12.5mg/L and 10.7mg/L in blood and urine, respectively) and high concentrations of pyrethroids (2.46mg/L alpha-cypermethrin and 2.40mg/L deltamethrin in blood, and 0.41mg/L alpha-cypermethrin and 0.46mg/L deltamethrin in urine, respectively). Blood ethanol concentration was 0.75g/L. All the evidence - from autopsy, police investigation and toxicology - was consistent with the intentional self-harm of the deceased. The current case was determined and recorded as a poisoning suicide. Cause of death of the deceased was reported as the synergistic toxicity of the ingested pyrethroids and mirtazapine. The presence of a significant blood ethanol concentration was considered a secondary contributory factor to the fatal outcome. The case presented herein is the first death attributed to poisoning from ingestion of pyrethroids in combination with mirtazapine, with the intention of the victim to cause self-harm, with corresponding toxicology results.

Who is the real killer? Chlorfenapyr or detergent micelle-chlorfenapyr complex?

1. Chlorfenapyr [4-bromo-2-(4-chlorophenyl)-1-(ethoxymethl)-5-(trifluoromethyl)-1H-pyrrole-3-carbonitrile] is a commonly employed pesticide throughout the world. The mechanism of chlorfenapyr action is to uncouple oxidative phosphorylation in the mitochondria. The characteristic features of chlorfenapyr intoxication are high fever, rhabdomyolysis and neurologic symptoms that gradually get worse until death. 2. In recent years, suicide attempt cases using commercial chlorfenapyr pesticide were reported. Even small doses of commercial chlorfenapyr pesticide intoxication caused human fatality. However, world health organization (WHO) has classified chlorfenapyr as class 2-moderately hazardous chemical. Animal studies using technical grade (94.5%; AC 7504-59A) chlorfenapyr in 0.5% carboxy methyl cellulose as the vehicle, single dose through oral route in male rats were well tolerated. 3. We planned a therapeutic strategy for suicidal chlorfenapyr intoxication, therefore we evaluated the three different toxic doses of chlorfenapyr (10% chlorfenapyr and 90% detergent) through oral route in male rats for human extrapolation. The major difference between the technical grade chlorfenapyr and commercial grade chlorfenapyr was the vehicle. In the technical grade chlorfenapyr study, 0.5% carboxy methyl cellulose was used as a vehicle, whereas in the present study 90% detergent acted as a vehicle. The LD50 of commercial grade chlorfenapyr-40.63 mg/kg bw, which was approximately tenfold decrease than technical grade chlorfenapyr, LD50 - 441 mg/kg bw. 4. The combination of chlorfenapyr and detergent, a deadly cocktail to form micelle complex that can greatly influence bioavailability by attaching to biological membranes in vivo. To conclude, the enhanced bioavailability of chlorfenapyr by the detergent causes the fatality in suicidal attempts using chlorfenapyr.

The use of self-reported symptoms as a proxy for acute organophosphate poisoning after exposure to chlorpyrifos 50% plus cypermethrin 5% among Nepali farmers: a randomized, double-blind, placebo-controlled, crossover study.

BACKGROUND: Previous studies stating a high prevalence of occupational acute pesticide poisoning in developing countries have mainly relied on measurements of the rather non-specific self-reported acute pesticide poisoning symptoms. Only a few studies have measured the biomarker plasma cholinesterase (PchE) activity, in addition to the symptoms, when assessing occupational acute pesticide poisoning. This study evaluated self-reported symptoms as a proxy for acute organophosphate poisoning among Nepali farmers by examining self-reported acute organophosphate poisoning symptoms and PchE activity in response to occupational acute organophosphate exposure. METHODS: We performed a randomized, double-blind, placebo-controlled, crossover trial among 42 Nepali commercial vegetable farmers. The farmers were randomly assigned (ratio 1:1) to a 2-h organophosphate (chlorpyrifos 50% plus cypermethrin 5%: moderately hazardous) spray session or a 2-h placebo spray session, and after 7 days' washout, the farmers were assigned to the other spray session. Before and after each spray session farmers were interviewed about acute organophosphate poisoning symptoms and PchE activity was measured. Analyses were conducted with a Two Sample T-test and Mann Whitney U-test. RESULTS: We found no difference in the symptom sum or PchE activity from baseline to follow up among farmers spraying with organophosphate (symptom sum difference -1, p = 0.737; PchE mean difference 0.02 U/mL, p = 0.220), placebo (symptom sum difference 9, p = 0.394; PchE mean difference 0.02 U/mL, p = 0.133), or when comparing organophosphate to placebo (symptom p = 0.378; PchE p = 0.775). However, a high percentage of the farmers reported having one or more symptoms both at baseline and at follow up in the organophosphate spray session (baseline 47.6%, follow up 45.2%) and placebo spray session (baseline 35.7%, follow up 50.0%), and 14.3% of the farmers reported three or more symptoms after the organophosphate spray session as well as after the placebo spray session. CONCLUSION: We found a general presence of acute organophosphate symptoms among the farmers regardless of organophosphate exposure or poisoning. Thus, self-reported acute organophosphate symptoms seem to be a poor proxy for acute organophosphate poisoning as the occurrence of these symptoms is not necessarily associated with acute organophosphate poisoning. TRIAL REGISTRATION: ClinicalTrials.gov, NCT02838303 . Registered 19 July 2016. Retrospectively registered.

Myelopathy following Cypermethrin Poisoning.

Cypermethrin is a synthetic pyrethroid and pyrimethrin analogue. Cypermethrin poisoning produces neurological manifestations due to its primary target on sodium channels.1 Neuropathy following cypermethrin poisoning is common. But myelopathy is rare and not reported so far. We report a 17 year old healthy male who developed myelopathy following cypermethrin ingestion. The possible mechanism for the myelopathy in this patient is discussed.