Acute pesticide poisoning amongst adolescent girls and women in northern Tanzania.

BACKGROUND: Acute pesticide poisoning (APP) is reported to affect community health worldwide but its burden in Tanzania is unknown particularly in women. This study examines APP involving adult females and adolescent girls 10 to 19 years in 3 regions of Tanzania which are famous for coffee and vegetable production. METHODS: Over the period of 12 months, health facility-based surveillance for cases of APP was implemented in 10 Tanzanian healthcare facilities in 2006. RESULTS: The study identified 108 APP cases of whom 31 (28.7%) occurred amongst adolescent girls. Suicide was the leading poisoning circumstances (60.2%) and the most vulnerable women were 20-29 years old who comprised 38.4% of all cases with suicide as circumstance. Organophosphates (OPs), zinc phosphide, paraquat and endosulfan were common amongst known reported poisoning agents. The annual APP incidence, mortality and Case Fatality Rate for women were 5.1/100,000, 0.2/100,000 and 3.7/100, respectively. CONCLUSION: APP amongst women in Tanzania is common and this call for diverse preventive interventions to reduce poisoning incidents.

Endosulfan induced cardiac arrest treated with intravenous lipid emulsion.

OBJECTIVE: Endosulfan is an organochlorine pesticide with high lipophilic features that makes it a well-absorbed agent and penetrates easily to the site of action. Endosulfan toxicities may result in disastrous complications and have high rates of mortality. Several case reports and some researchs discuss the evidence supporting intravenous lipid emulsion (ILE) therapy as a rescue therapy in lipophilic agents' toxicity. CASE REPORT: A 33-years-old healthy woman with  a history of endosulfan ingestion of uncertain quantity in a suicide attempt six hours ago was admitted to our emergency department. Cardiac arrest ensued after one hour of admission. Cardiopulmonary resuscitation was initiated in accordance with advanced cardiac life support (ACLS) algorithm for asystole. During resuscitation, 2 mL/kg bolus of 20% intravenous lipid emulsion (ILE) was administered for three times at five-minute intervals in addition to ACLS guidance. Spontaneous circulation returned after twenty minutes of resuscitation. No additional antidotal or vasopressor therapies were required during the hospital course of the patient. To our knowledge, this is the first reported case with responded use of ILE treatment for endosulfan toxicity. CONCLUSION: This case report indicates that ILE treatment should be considered for life-threatening endosulfan intoxications.

Congenital scoliosis: an anomalous association with endosulfan.

Endosulfan is an organochlorine pesticide that is used extensively across the world to kill insects. Incidence of acute and chronic toxicity with endosulfan poisoning has been reported, and nearly 80 countries have banned its use. However, it is still being used in many low-income/middle-income countries. One of the most severe tragedies because of endosulfan poisoning has taken place in the Indian state of Kerala due to persistent aerial spraying of endosulfan. Even though there are reports of skeletal and other congenital abnormalities in humans and experimental animals following exposure to endosulfan, very few have been documented. We report two cases of congenital scoliosis in siblings living in a community affected by high levels of endosulfan in the environment. High index of suspicion is essential during the screening of school children exposed to endosulfan. Congenital scoliosis is a progressive deformity that leads to severe disability, unless detected and corrected at an early stage.

In-hospital outcomes and delayed neurologic sequelae of seizure-related endosulfan poisoning.

PURPOSE: This study investigated the predictive factors for progression from seizure-related endosulfan poisoning to status epilepticus (SE) and refractory SE (RSE). This study also investigated delayed neurologic sequelae in seizure-related endosulfan poisoning. METHODS: This retrospective, observational case series consisted of 73 patients who developed at least one seizure after endosulfan ingestion. RESULTS: The progression rates from seizure-related endosulfan poisoning to SE and from SE-related endosulfan poisoning to RSE were 78.1% and 54.4%, respectively. The SE and RSE fatality rates were 19.2% and 41.9%, respectively. No patients reported the development of delayed neurological sequelae at least six months after discharge. Glasgow coma scale (GCS) score were identified as an independent factor for progression from seizure-related endosulfan poisoning to SE and from SE-related endosulfan poisoning to RSE. Lorazepam administration was independently associated with preventing progression from SE-related endosulfan poisoning to RSE. CONCLUSION: Seizure-related endosulfan poisoning had higher progression rates to SE and RSE and higher fatality rates than other drug-induced seizures. However, delayed neurologic sequelae after discharge were not demonstrated. Due to the high progression rates from seizure-related endosulfan poisoning to SE and RSE and the absence of an established treatment for SE-related endosulfan poisoning, physicians should aggressively treat patients who experience a seizure after endosulfan poisoning and who present with decreased GCS score. Lorazepam should be considered a first-line anti-epileptic drug for controlling seizures in patients with endosulfan poisoning.

Endosulfan poisoning: An overview.

Endosulfan, an organochlorine (OC) insecticide, is a widely used agricultural pesticide, despite its life threatening toxic effects. In this review, the pharmacokinetics of endosulfan, mechanism of endosulfan toxicity, clinical presentations and management, histopathological findings, and toxicological analysis are described, in addition to its environmental toxicity. The toxic effects of endosulfan can affect many organs and systems presenting in a wide array of signs and symptoms. Although termed a restricted OC-classed pesticide, it continues to be used, especially in the developing world, owing to its beneficial effects on agriculture. Several cases of endosulfan poisoning have been reported from different regions of the world. Whether accidental or intentional, endosulfan ingestion proves to be fatal unless immediate, aggressive treatment is initiated. Management is mainly supportive as no antidote exists for endosulfan poisoning as yet. The use of endosulfan needs to be strictly regulated and eventually banned worldwide altogether to lower the current morbidity and mortality resulting from this pesticide. Additionally, monitoring biological samples, using non-invasive techniques such as breast milk sampling, can provide an effective method of observing the elimination of this environmentally persistent organic pollutant from the general population.

Endosulfan poisoning in canids and felids in the Calabria region of southern Italy.

Endosulfan, a highly toxic insecticide and acaricide, was globally banned under the Stockholm Convention in May 2011 because of its threats to human health and the environment. Despite the ban on its use, endosulfan is still present in the environment, causing poisoning events in domestic animals and wildlife. Toxicologic analysis of poisoned animals conducted by the Istituto Zooprofilattico Sperimentale del Mezzogiorno revealed that in the past 3 y, this pesticide has not disappeared in the regions of interest. More than 650 samples (baits and animal organs) collected from 2013 to 2015 were analyzed through solid-phase extraction followed by gas chromatography-electron capture detection. This methodology allowed us to identify 45 positive samples from the Calabria region of southern Italy (10.2 % of the total samples). Most were samples of gastric content (alpha-endosulfan range: 1.27-3,800 mg/kg) and baits (alpha-endosulfan range: 92-1,497 mg/kg). Lower concentrations of pesticide were found in samples of stomach (alpha-endosulfan: 6.7-118 mg/kg) and liver (alpha-endosulfan: 0.38-14.2 mg/kg).

Availability of intravenous lipid emulsion therapy on endosulfan-induced cardiovascular collapse.

Acute Endosulfan poisoning is associated with a high mortality rate in humans, and can exceed 30% [Moon JM, Chun BJ. Acute endosulfan poisoning: a retrospective study. Hum Exp Toxicol 2009;28:309-16]. Prophylactic anticonvulsant therapy for symptomatic patients and aggressive treatment for seizures may limit morbidity, but, no effective antidote is available [Moses V, Peter JV. Acute intentional toxicity: endosulfan and other organochlorines. Clin Toxicol (Phila) 2010;48:539-44]. However, endosulfan poisoning is often completely reversible with the appropriate management [Karatas AD, Aygun D, Baydin A. Characteristics of endosulfan poisoning: a study of 23 cases. Singapore Med J 2006;47:1030-2]. Intravenous lipid emulsion (ILE) may be a useful in treatment of lipophilic medication overdoses as an adjunct to antidotal therapy [Rothschild L, Berns S, Oswald S, et al. Intravenous lipid emulsion in clinical toxicology. Scand J Trauma Resusc Emerg Med 2010;18:51]. We believe that this is its first reported use in endosulfan toxicity.

Effects of endosulfan intoxication on pituitary functions.

CONTEXT: We investigated the effects of endosulfan intoxication on pituitary functions in three patients. METHODS: This is an observational case series including three patients with endosulfan intoxication. Patients were evaluated 3 months after the acute event. RESULTS: Based on the baseline hormonal values and dynamic endocrine tests, one patient had hypothalamo-pituitary-adrenal axis impairment and was diagnosed as ACTH deficiency (peak cortisol level was found 13.12 µg/dl after low dose ACTH stimulation test), and another one had GH-IGF-I axis impairment and was diagnosed as GH deficiency (peak GH level was found 1.06 µg/L after glucagon stimulation test). CONCLUSIONS: Endosulfan intoxication might cause pituitary hormone deficiencies after the acute phase. Therefore, patients with endosulfan toxicity should be followed for possible pituitary gland dysfunction.

Pesticide (endosulfan) levels in the bone marrow of children with hematological malignancies.

OBJECTIVES: (1) To confirm the presence of Pesticide (Endosulfan) residues in the bone marrow (BM) of children with acute hematological malignancies and compare them with controls. (2) To ascertain if children with Endosulfan in their marrow reside in areas sprayed with Endosulfan. STUDY DESIGN: Case control study SETTING: Pediatric oncology unit of a medical college teaching hospital in Dakshina Kannada district of Karnataka. SUBJECTS: 26 patients with proven hematological malignancy and 26 age matched controls suffering from benign hematological disease. METHODS: Endosulfan residues in the BM were estimated by gas chromatography mass spectrometry (Minimum detection limit 10ng/mL). The subjects geographical area of location (residence) was determined to see whether they belong to sprayed area or not. The Chi-square test was applied to see an association between exposure status and hematological malignancy. RESULTS: A total of 52 children were enrolled of which 26 were study cases and 26 were controls. Of the study and control groups, 84.7% ;and 73.1%, respectively were from exposed areas. The major (88.4%) illness in the study group was ALL, while ITP (50%) occurred most frequently in the control group. Six out of 26 study cases tested positive for endosulfan in the BM, against 1 out of 26 controls (P = 0.042). The Odds ratio was 7.5. All children who had endosulfan in the bone marrow originated from areas, where endosulfan is still being used. CONCLUSIONS: Children with hematological malignancy had raised levels of endosulfan in the bone marrow compared to those without. All the children with raised bone marrow Endosulfan levels were found to be from areas exposed to the pesticide.

Pesticide intoxications in Cukurova, Turkey: three years analysis.

In Cukurova region, pesticide poisonings still remain an unfortunate cause of death, which led to the present study. The autopsy records of Adana Branch of the Council of Forensic Medicine, between 2006 and 2008, were evaluated retrospectively. Deaths that were attributed to pesticide poisoning were included in the scope of the study to identify the type of pesticide, and etiology of intoxication. The frequency and distribution of intoxications were also analyzed in terms of sex and age. In the studied period, a total of 4199 autopsies were referred to the forensic toxicology laboratory for pesticide analysis. Seventy-two cases were positive for pesticide analysis. Of these, 42 (58.33%) were male and 30 (41.67%) were female, with a mean age of 38.8 ± 20.6 years. Among the inspected pesticides, endosulfan was found to be the most common with 47.2% of prevalence, followed by dichlorvos. This report showed that certain pesticides, endosulfan in particular, remains as common cause of poisonings in Cukurova region.

Acute intentional toxicity: endosulfan and other organochlorines.

INTRODUCTION: Organochlorine pesticides continue to be used in several developing countries despite concerns regarding their toxicity profile. Endosulfan is an organochlorine recognized as an important agent of acute toxicity. METHODS: In this retrospective study, the clinical features, course, and outcomes among patients with acute endosulfan poisoning requiring admission to the hospital during an 8-year period (1999-2007) were reviewed. RESULTS: Among 34 patients hospitalized during this study period for alleged organochlorine poisoning, 16 patients with endosulfan poisoning were identified. The majority (75%) received initial treatment at a primary or secondary center. Neurological toxicity predominated, particularly low sensorium (81%) and generalized seizures (75%), including status epilepticus (33%). Other features observed included hepatic transaminase elevation, azotemia, metabolic acidosis, and leukocytosis. Mechanical ventilation was required in 69% and vasoactive agents in 19%. In-hospital mortality was 19%. There were no gross neurological sequelae at discharge. In three other patients who presented with organochlorine poisoning, the compounds ingested were lindane, endrin, and dicofol (n = 1 each). The course and outcomes in these patients were unremarkable and all three patients survived. CONCLUSIONS: Endosulfan is capable of high lethality and significant morbidity. The commonest manifestations are neurological although other organ dysfunction also occurs. In the absence of effective antidotes, restriction of its availability, along with prompt treatment of toxicity, including preemptive anticonvulsant therapy are suggested.

Death in a toddler following endosulfan ingestion.

INTRODUCTION: Endosulfan, an organochlorine insecticide widely used in agriculture, is rapidly absorbed following ingestion, inhalation, or skin exposure. Poisonings rarely result in morbidity and mortality. Symptoms occur rapidly following exposure with CNS toxicity. Endosulfan has been banned in many countries; however, it is still used in the United States. CASE REPORT: A 2.5-year-old ingested an unknown amount of endosulfan from a 20-ounce soft drink bottle. He immediately developed generalized tonic-clonic seizure activity and became unresponsive. He was transferred to the local hospital and to a tertiary children's hospital where the seizures were refractory to treatment despite treatment with multiple anticonvulsants. He became hypotensive requiring vasopressors. On day 3, an MRI showed cerebral edema, and a nuclear medicine flow scan failed to show blood flow to the brain and he was pronounced dead. DISCUSSION: This is the first published pediatric death in the United States because of endosulfan. Central nervous system stimulation is frequently the presenting symptom with or without other organ dysfunction. Status epilepticus causes the highest morbidity and mortality, therefore prompt administration of anticonvulsant drugs is important although not always effective. The child is our case demonstrated the most severe features of endosulfan exposure. CONCLUSION: In summary, prevention of a potentially toxic exposure is critical. The presence of this substance in a soft drink bottle contributed to the toxic exposure in this child, thus emphasizing the need for poison prevention education. The severe toxicity to those exposed raises the question of the need of this compound on the U.S. market.

Acute endosulfan poisoning: a retrospective study.

Endosulfan is a widely used insecticide that is associated with a high fatality rate in humans when ingested accidentally or with the aim of suicide. However, the literature concerning human endosulfan exposure is limited to case reports. Thus, we sought to 1) describe the clinical features of patients with acute endosulfan poisoning and 2) identify independent factors to predict patients' outcome. Fifty-two patients who presented with acute endosulfan poisoning between January 2001 and January 2007 were enrolled in this retrospective study. Sixteen (30.7%) of the 52 patients died, and 48 patients experienced seizures. Endosulfan poisoning caused the hypotension and the abnormalities on electrocardiogram at presentation. Over half of the patients developed complications, such as rhabdomyolysis, hepatic toxicity, and hypotension. These complications resolved without sequelae in the survival group. Refractory status epilepticus was the most common cause of death in this series (75.0%). Amount ingested being greater than 35 g of endosulfan was the most found to be an independent variable that predicted patient mortality. Patients with this risk factor must be treated aggressively during the early stage of endosulfan poisoning.

Unintentional endosulfan poisoning.

Endosulfan is an organochloride insecticide, widely used in insect control. It is responsible for many severe intoxication and several deaths. We present a case series of endosulfan poisoning, admitted to our emergency department with different clinical courses. Two patients presented with status epilepticus and were successfully treated with thiopental sodium to control seizures. One patient required also hemodialysis. All patients were discharged following a complete recovery of their health. Endosulfan is a highly toxic insecticide that produces tonic-clonic convulsions, headache, dizziness and ataxia. It can cause also life threatening metabolic disturbances. Treatment is symptomatic and supportive (Tab. 2, Ref. 11). Full Text (Free, PDF) www.bmj.sk.

Determination of pesticides in postmortem blood and bone marrow of pesticide treated rabbits.

Forensic toxicological analyses have traditionally focused on the use of blood, body fluids, and certain organs in examinations of deaths due to intoxication. However, in some situations, putrefaction and contamination make proper sampling from tissues impossible, such as in exhumation cases. In these cases, bone marrow might be useful as an alternative specimen since it is a potential depot for drugs. This study aims to determine pesticides in postmortem and putrefied bone marrow of pesticide treated rabbits, so as to reveal the diagnostic value of toxicological analysis of bone marrow in exhumation cases. Out of thirteen rabbits, a 110 mg/kg dose of endosulfan was orally given to six through a gavage tool, and a 2500 mg/kg dose of diazinon was given to six using the same method. One rabbit was not treated with anything and served as a control sample. Venous blood, liver, lung, kidney, brain, and bone marrow samples were collected just after spontaneous death or cervical dislocation. After this, the rabbits were buried in soil. All of them were exhumed 1 month later, and putrefied viscera and bone marrow were sampled. Blood and tissue samples underwent solvent extraction and solid phase extraction, and then the samples were analyzed by GC-MS. Mean residue levels of diazinon in early postmortem samples were 85 mg/kg, 71 mg/kg, 23 mg/kg, 21 mg/kg, 19 mg/kg, and 0.4 mg/l in the liver, bone marrow, kidney, lung, brain, and blood, respectively. Mean residue levels of diazinon in the putrefied body were 3327 mg/kg in putrefied viscera and 1783 mg/kg in the bone marrow. Mean residue levels of endosulfan isomers and metabolites in early postmortem samples (blood, liver, lung, kidney, brain, and bone marrow) were 0.46 mg/kg (endosulfan sulfate), 0.32 mg/kg (alpha and beta isomers of endosulfan), and 0.14 mg/kg (endosulfan ether) while the same levels were 0.26 mg/kg (endosulfan sulfate), 0.24 mg/kg (alpha and beta isomers of endosulfan), and 0.1 mg/kg (endosulfan ether) in putrefied samples (putrefied bone marrow and putrefied viscera). Based on these experimental results, it can be concluded that cause of death can be determined as acute pesticide poisoning by toxicological analysis of samples from bone marrow and putrefied viscera in exhumation cases.