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.

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.

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.

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.

Do targeted bans of insecticides to prevent deaths from self-poisoning result in reduced agricultural output?

BACKGROUND: The pesticides monocrotophos, methamidophos, and endosulfan were a very common cause of severe poisoning in Sri Lanka during the 1980s and early 1990s, before they were banned in 1995 and 1998. Now, the most commonly used insecticides are the less toxic World Health Organization Class II organophosphorus pesticides and carbamates. These bans were followed by a large reduction in both fatal poisonings and suicide in Sri Lanka. OBJECTIVE: We aimed to see if these bans adversely affected agricultural production or costs. METHODS: We used data from the World Resources Institute to compare the yields of the main crop groups in Sri Lanka with those from surrounding South Asian countries for 1980-2005. We also examined data from the Sri Lankan Department of Census and Statistics to examine the yields of 13 specific vegetable crops and rice for 1990-2003, along with the costs of rice production. RESULTS: We found no drop in productivity in the years after the main bans were instituted (1995, 1998). We observed substantial annual fluctuation in estimated yields in all data sources, but these did not coincide with the bans and were no larger than the fluctuations in other countries. Also, there was no sudden change in costs of rice production coinciding with bans. CONCLUSIONS: Countries aiming to apply restrictions to reduce deaths from pesticide poisoning should evaluate agricultural needs and develop a plan that encourages substitution of less toxic pesticides. If farmers have an affordable alternative for pest control for each crop, there is no obvious adverse effect on agricultural output.

Endosulfan poisoning with intravascular hemolysis.

We describe a 26-year-old female patient, who had attempted suicide with Endosulfan, and who presented to the Emergency Department with status epilepticus. She subsequently developed hypotension refractory to inotropes, intravascular hemolysis, disseminated intravascular coagulation (DIC), metabolic acidosis and, finally, cardiac arrest and death. Endosulfan is a chlorinated insecticide that causes central nervous system hyperstimulation. It is absorbed from the gastrointestinal tract, skin, and respiratory tract, and leads to nausea, vomiting, paraesthesia, giddiness, convulsion, coma, respiratory failure, and congestive cardiac failure. Hepatic, renal and myocardial toxicity, agranulocytosis, aplastic anemia, cerebral edema, DIC, thrombocytopenia, and skin reaction also have been reported. Management includes decontamination of skin and gastrointestinal tract, supportive care including treatment of status epilepticus, dysrhythmias, and mechanical ventilation. Mortality and morbidity rates are very high and there is no specific antidote. Atropine and catecholamines should be avoided.

Two cases of acute endosulfan toxicity.

BACKGROUND: Endosulfan is widely used in insect control and is absorbed by both humans and animals through the intestinal tract, the lungs, and the skin. Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide, with several deaths. A 9-year analysis by one of Turkey's poison control centers reported that pesticide intoxications accounted for 8.8% of 25,572 poisoning calls, with 80.3% of them relating to insecticides and 19.7% concerning rodenticides. CASE REPORTS: We present two cases of unintentional exposure to endosulfan, one of which presented with neurological manifestations, liver toxicity, and required mechanical ventilation and emergent hemodialysis; the other had only neurological manifestations and liver toxicity. CONCLUSION: In cases of endosulfan poisoning, physicians must be aware of neurological manifestations, seizures, and severe metabolic acidosis. If severe metabolic acidosis is present, we suggest that hemodialysis may be an important intervention and should be performed early.

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 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).

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.

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.

Characteristics of endosulfan poisoning: a study of 23 cases.

INTRODUCTION: Organochloride insecticides are chlorinated cyclic hydrocarbons having molecular weights in the range of 300-550 Da. Case series of endosulfan poisoning are extremely rare in the literature. We report 23 cases of endosulfan poisoning. METHODS: This retrospective study enrolled patients with endosulfan poisoning presenting to our emergency department from January to December 2005. The data were collected from clinical records and laboratory files. RESULTS: On admission, initial symptoms were nausea and vomiting in 17 patients (73.9 percent), seizures in five patients (21.7 percent), and dizziness in one patient (4.3 percent). Symptoms began within one hour after ingestion in 12 patients (52.2 percent), in the second hour in nine patients (39.1 percent), and in the third hour in two patients (8.7 percent). Seizure types were generalised tonic-clonic in 16 patients (84.2 percent), and focal seizures in three patients (15.8 percent). 19 patients were observed for one day, two patients were observed for two days, and one patient was followed-up for ten days in the emergency department. One patient was transferred for liver transplantation on the fifth day to another centre. All patients were treated symptomatically by intravenous diazepam for controlling seizures. CONCLUSION: Endosulfan poisoning can be suspected in the presence of primary central nervous system manifestations including seizures, with or without clinical or laboratory evidence of other organ dysfunction such as liver failure.

Effect of endosulfan on male reproductive development.

There is experimental evidence of adverse effects of endosulfan on the male reproductive system, but there are no human data. Therefore, we undertook a study to examine the relationship between environmental endosulfan exposure and reproductive development in male children and adolescents. The study population was composed of 117 male schoolchildren (10-19 years of age) of a village situated at the foothills of cashew plantations, where endosulfan had been aerially sprayed for more than 20 years, and 90 comparable controls with no such exposure history. The study parameters included recording of clinical history, physical examination, sexual maturity rating (SMR) according to Tanner stages, and estimation of serum levels of testosterone, luteinizing hormone (LH), follicle-stimulating hormone, and endosulfan residues (70 study and 47 control subjects). Mean +/- SE serum endosulfan levels in the study group (7.47 +/- 1.19 ppb) were significantly higher (p < 0.001) than in controls (1.37 +/- 0.40 ppb). Multiple regression analysis showed that SMR scoring for development of pubic hair, testes, penis, and serum testosterone level was positively related to age and negatively related to aerial exposure to endosulfan (AEE; p < 0.01). Serum LH levels were significantly positively related to AEE after controlling for age (p < 0.01). The prevalence of congenital abnormalities related to testicular descent (congenital hydrocele, undescended testis, and congenital inguinal hernia) among study and controls subjects was 5.1% and 1.1%, respectively, but the differences were statistically nonsignificant. Our study results suggest that endosulfan exposure in male children may delay sexual maturity and interfere with sex hormone synthesis. Our study is limited by small sample size and nonparticipation.

Selective involvement of basal ganglia and occipital cortex in a patient with acute endosulfan poisoning.

We report a teenage girl with acute endosulfan poisoning who developed psychosis, generalized tonic-clonic seizures, myoclonic jerks, cortical blindness and limb rigidity. Serial magnetic resonance imaging (MRI) showed bilateral reversible lesions localized to caudate nucleus, putamen and occipital cortex; internal capsule and thalamus were spared. This selective involvement may have a bearing on mechanisms underlying endosulfan toxicity.

Endosulfan intoxication: Blood glucose, electrolytes, Ca levels, ascsorbic acid and glutathione in rats.

Endosulfan-induced changes in blood glucose, plasma electrolytes, and blood and brain ascorbic acid, hexokinase and glutathione have been investigated following acute and subacute administration in 12 h fasted male rats. After a single oral dose of endosulfan (40 mg/kg) a significant increase in blood glucose, blood ascorbic acid, and blood and brain glutathione was observed. The maximum increase in blood was observed at 2 h (36%). Increase in blood and brain glutathione was highly significant at 4 h (50 and 43%, respectively). The blood ascorbic acid slowly increased by 19% over control during the treatment period. No significant change in brain hexokinase was observed. Repeated oral administration of endosulfan (0.625 to 20 mg/kg) for 7 weeks had no effect on plasma sodium and potassium. At the highest dose (20 mg/kg), blood glucose was slightly increased (16%). Plasma Ca was significantly decreased, the maximum fall (35%) being observed at 4 h.

Endosulfan poisoning in Northern India: a report of 18 cases.

Eighteen cases of endosulfan poisoning by accidental overexposure during spray, admitted between October 1995 to September 1997, were observed and analyzed. These accounted for approximately one third of the total number of poisoning cases admitted in our unit during this period. Nausea, vomiting abdominal discomfort, tonic and clonic convulsions, confusion, disorientation, and muscular twitchings were cardinal manifestations. None of the patients succumbed to their illness. Analysis of various incriminating factors revealed that accidental overexposure was due to failure to adhere to the instructions for spray either due to ignorance or due to illiteracy. All the patients avoided preventive measures and developed toxicity both due to inhalation and absorption through skin. Endosulfan (a chlordiene derivative) poisoning is gaining up momentum in this part of world and has become an important matter for public health in India.

Refractory status epilepticus following self-poisoning with the organochlorine pesticide endosulfan.

We describe a case of refractory status epilepticus presenting to a rural general hospital in Sri Lanka. This patient's condition was precipitated by intentional self-poisoning with the organochlorine insecticide endosulfan. Although rarely seen in developed countries, pesticide poisoning particularly with endosulfan is an important cause of difficult-to-manage seizures in Asian countries. In this case report, we discuss the management of status epilepticus and refractory status epilepticus. Further, we specifically discuss the clinical pharmacology and toxicology of endosulfan.

Death caused by ingestion of endosulfan.

This paper reports the autopsy and toxicological findings of a death caused by ingestion of endosulfan dispersed in a colorless liquid containing about 55% of xylene (w/v). For isolation of endosulfan, the biological material was homogenized and the drug was isolated by extraction with ether. Quantitative determinations were carried out by gas chromatography. The following concentrations of endosulfan were found: Blood 30 mg/L Gastric contents 0.5 g in the total 50 mL Liver 20 mg/kg Kidney 2.0 mg/kg Brain 0.3 mg/kg Xylene (solvent) was detected only in stomach contents (0.4 g in the total 50 mL).

Three cases of recurrent epileptic seizures caused by Endosulfan.

To commit suicide, three young adults swallowed a relatively small amount of a widely used insecticide containing endosulfan. They developed recurrent epileptic seizures. After hospitalization they were treated and recovered without any sequel. These seizures were classified as acute symptomatic or provoked seizures. We suggest that if one faces acute repetitive seizures, especially in the rural areas, an intoxication such as endosulfan intoxication should be considered when the etiology is uncertain even in the absence of any signs of intoxication.