Assuntos
Inseticidas/intoxicação , Paration/intoxicação , Adolescente , Criança , Pré-Escolar , Humanos , Peru , PesquisaRESUMO
Este artículo resume los hechos de las tres intoxicaciones masivas con plaguicidas ocurridas en Colombia hasta 1998. La primera ocurrió en Chiquinquirá (Boyacá) en 1967 e involucró a más de 500 personas, de los cuales 165 requirieron tratamiento hospitalario y 63 murieron. La segunda ocurrió en Puerto López (Meta) en 1970 y tuvo 190 intoxicados, de los cuales 157 requirieron tratamiento médico y 7 murieron. El tercer caso ocurrió en Pasto (Nariño) en 1977 y tuvo como consecuencia más de 300 intoxicados, con 120 hospitalizados y 15 muertos. En los casos de Chiquinquira y Pasto los plaguicidas que provocaron la intoxicación fueron metil-paratión y paratión respectivamente, mientras que en el caso de Puerto López solo se conoce que fue un plaguicida organofosforado. Los 3 casos de intoxicación masiva ocurrieron por consumo de alimentos contamidados. Estos casos se analizaron y se compararon con las principales intoxicaciones ocurridas en el mundo. Se propone una discusión en torno a las consecuencias que tuvieron estos hechos en las políticas de salud pública nacionales, la capacidad de hacer frente a situaciones de este tipo en el país, la capacitación de personal para la prevención y manejo de estas situaciones y la educación de los profesionales de la salud en epidemiología, toxicologia y otras disciplinas involucradas en el campo de la salud ambiental
Assuntos
Humanos , Praguicidas/toxicidade , Metil Paration/intoxicação , Paration/intoxicaçãoRESUMO
In a fatal case of acute parathion ingestion, paranitrophenyl sulphate, the paranitrophenyl glucuronide and free paranitrophenol excretion on day 3 were quantitated using a HPLC reverse method with a C18 column following sample preparation using a C18 mini-column and methanol elution. Paranitrophenyl sulphate amounted to about 81% of the total conjugates excreted. The results were confirmed by collecting the fractions identified by high-performance liquid chromatography, hydrolysing them with concentrated hydrochloric acid and quantitating paranitrophenol by gas chromatography. Total paranitrophenol excretion was also determined. The excreted paranitrophenol was equivalent to 76 mg parathion (lethal dose in humans between 20 and 100 mg). No changes in the concentrations of paranitrophenol or its conjugates were seen in the urine on storage, frozen over a one year period.
Assuntos
Nitrofenóis/urina , Paration/intoxicação , Doença Aguda , Adulto , Cromatografia Gasosa , Cromatografia Líquida de Alta Pressão , Evolução Fatal , Feminino , Humanos , Intoxicação/urinaAssuntos
Paration/intoxicação , Adulto , Chile , Feminino , Hospitais Rurais , Humanos , Dose Letal MedianaAssuntos
Adulto , Humanos , Feminino , Paration/intoxicação , Hospitais Rurais , Chile , Dose Letal MedianaRESUMO
This study shows our clinical and therapeutical experience in 48 cases of infant COFA intoxication admitted in the Intensive Care Unit of "Emilio Civit Children Hospital", Mendoza, Argentina in a periode of seven years. They were investigated to determine the presence of Parathion in blood and gastric washing with the sodium hydroxide qualitative method, and also cholinesterase was detected in blood with a colorimetric method (the monotest cholinesterase). Age range from one to ten years with predominance from 3 to 4 years; 27 were males and 21 females. In almost all the cases (90%) the toxic ingressed through several ways, and from 10 to 30 minutes appeared the characteristic signs: miosis and bronchorrhea. Clinically in 30 cases the intoxication was considered dangerous and mild in the others. The data obtained by laboratory techniques were diagnostic only in half of the cases. Atropine's sulphate was done to all cases until their recuperation, in doses from 2.5 mg to 20 mg. The evolution was highly satisfactory, only two died and two remained with seizures. Always had thanklessness and carelessness with the child from living together adults, who playing handle and waste the toxic. In two occasions the intoxication was familiar by contaminated food.
Assuntos
Paration/intoxicação , Criança , Pré-Escolar , Feminino , Humanos , Lactente , Masculino , Paration/metabolismoAssuntos
Malation/intoxicação , Paration/intoxicação , Inibidores da Colinesterase/farmacologia , Reativadores da Colinesterase/uso terapêutico , Feminino , Humanos , Lactente , Malation/farmacologia , Masculino , Cloreto de Obidoxima/uso terapêutico , Paration/farmacologia , Compostos de Pralidoxima/uso terapêuticoRESUMO
A case of 38 year old man who worked with organochlorinated and Parathion during 5 years is reported. His follow-up was up to 2 years. The onset of the disease was characterized by cholinergic signs, headache, loss of weight, trembling, miokimias, fasciculations, ataxia, myotonic phenomena (in hands only) and motor sensitive peripheral polyneuropathy (affecting the lower limbs symmetrically). Low concentrations of blood cholinesterases confirmed the etiology. Myotonic phenomena disappeared spontaneously 6 months after the initial observation. One year later, the concentration of erythrocyte acetylcholinesterase was found to be low and plasma cholinesterase was normal, suggesting that the patient was carrier of a congenital deficiency of acetylcholinesterase. In literature relationship between myotonia and intoxication due to organophosphorus was not found. The whole clinical picture, cholinergic symptoms, transitory phenomena and spontaneous motor activity could be explained by an excess of acetylcholine. Electromyography (EMG) in the first observation showed neuromuscular transmission blocking characterized by deficiency or absence of voluntary activity, unexcitability of fibular nerves, with fibrillations and positive peaks as described previously with Mipafox (another organophosphorus agent). During 2 years of observation numerous end-plates potentials of muscular fibres persisted in the EMG. A progressive increase in voluntary activity showed by unit motor potential of almost normal amplitude and very increased duration was observed. No potentials of reinnervation were noted. The results of EMG were explained as disturbances of neuromuscular transmission associated with moderate signs of denervation. The Eaton-Lambert's test and the stimulation of a single unit motor potential confirmed disorder of neuromuscular synapses. The histochemistry of brachial biceps showed scattered atrophic and angulated type I and II fibres. Teased-fibres preparations showed nerve fibres with B, C, and G alterations as defined by Dyck et al. indicating axonal degeneration. These results were according to velocity of sensitive conduction. The conduction velocity of fibular nerves was strongly delayed during all the evolution indicating serious disorders of motor nerves myelin.(ABSTRACT TRUNCATED AT 400 WORDS)
Assuntos
Colinesterases/sangue , Doenças Neuromusculares/induzido quimicamente , Paration/intoxicação , Acetilcolina/sangue , Adulto , Eletromiografia , Humanos , Masculino , Músculos/patologia , Condução Nervosa , Nervo Sural/patologiaAssuntos
Convulsões/etiologia , Negro ou Afro-Americano , Bahamas , Serviços de Saúde Comunitária , Eletroencefalografia , Alucinações/etiologia , Serviços de Saúde do Indígena , Humanos , Masculino , Pessoa de Meia-Idade , Paration/intoxicação , Convulsões/induzido quimicamente , Convulsões/psicologia , Síncope/etiologiaRESUMO
Enzyme determinations and hepatic histological studies were carried out in normal rats and in rats intoxicated with the organophosphorus pesticide parathion. No significative evidence of hepatocellular damage was seen in parathion -- intoxicated rats as responsible of the impaired bile flow and sulfobromophthalein biliary excretion that were previously reported. On the contrary, the isolated perfused rat liver from normal and intoxicated rats showed a similar behavior when the perfusate flow through the liver was maintained at a similar rate. We conclude that altered hepatic blood flow may be a factor determinant of an impairment of bile flow and of biliary excretion of several organic anions like sulphobromopthalein that were observed in parathion -- intoxicated rats.
Assuntos
Fígado/fisiologia , Paration/intoxicação , Alanina Transaminase/análise , Animais , Aspartato Aminotransferases/análise , Bile/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/enzimologia , Fígado/patologia , Fígado/fisiopatologia , Circulação Hepática/efeitos dos fármacos , Masculino , Ratos , Sulfobromoftaleína/metabolismoRESUMO
In January 1976, 79 persons in Jamaica were acutely poisoned by the organophosphorus insecticide parathion. Seventeen died. Cases occurred in three episodes at separate locations, but all patients had consumed wheat flour from a single lot consisting of 5264 cotton bags. Parathion in concentrations of less than 1 to 9900 ppm was identified in flour from six bags in this lot; three had splash marks. The flour had been milled in Western Europe from European wheat, carried in trucks to a dockside warehouse, and loaded aboard ship after 2-5 days' storage. In Jamaica, the flour had moved from quayside to outbreak locations along separate routes through two import houses. Site inspections and review of shipping records suggested that the likely point of contamination was the European port, where foodstuffs and insecticides were stored in the same warehouse.
Assuntos
Farinha , Contaminação de Alimentos , Paration/intoxicação , Adolescente , Adulto , Criança , Pré-Escolar , Surtos de Doenças , Métodos Epidemiológicos , Feminino , Farinha/análise , Humanos , Lactente , Jamaica , Masculino , Paration/análiseRESUMO
In January 1976, 79 persons in Jamaica were acutely poisoned by the organophosphorous insecticide parathion. Seventeen died. Cases occurred in three episodes at separate locations, but all patients had consumed wheat flour from a single lot consisting of 5264 cotton bags. Parathion in concentrations of <1 to 9900 ppm was identified in flour from six bags in this lot: three had splash marks. The flour had been milled in Wertern Europe from European wheat, carried in trucks to a dockside warehouse, and loaded aboard ship after 2-5 days' storage. In Jamaica, the flour had moved from quayside to outbreak locations along separate routes through two import houses. Site inspections and review of shipping records suggested that the likely point of contamination was the European port, where foodstuffs and insectisides were stored in the same warehouse (AU)