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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a survey of occupationally acquired disease in workers at a pesticide plant, we found that 11 (11%) of 102 workers had been hospitalized for illness related to chemical exposures; highest hospitalization rates occurred in packaging (27%), production (22%), and maintenance (9%) workers. Commonest causes of hospitalization were intoxication by the carbamate pesticide methomyl [1-(methylthio)ethylideneamino methyl carbamate], a reversible cholinesterase inhibitor, and methemoglobinemia following exposure to 3,4-dichloroaniline. On clinical evaluation, five (46%) of 11 packaging workers, the group with the highest exposure to methomyl, had experienced blurred vision or pupillary constriction. Seventeen (61%) of 28 production workers with exposure to dichloroaniline and propanil (3'4'-dichloropropionanilide) had chloracne, an acne-form dermatosis caused by the contaminant tetrachlorazobenzene in propanil and dichloroaniline. The chloracnegenic potentials of propanil and dichloroaniline were verified by rabbit ear tests. These findings reemphasize the hazards inherent in the the manufacture and formulation of pesticides and herbicides.
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PMID:Propanil-chloracne and methomyl toxicity in workers of a pesticide manufacturing plant. 15 54

Pyridostigmine is known as a pre-treatment drug against intoxication with organophosphorus nerve agents. During the Persian Gulf war, we encountered a cluster of nine cases of pyridostigmine self-poisoning, of which three presented with mixed drug poisoning. The clinical and laboratory features of pyridostigmine toxicity are presented. Doses ranged between 390 and 900 mg. Pyridostigmine ingestion resulted in mild to moderate cholinergic symptoms such as abdominal cramps, diarrhea, emesis, nausea, hypersalivation, urinary incontinence, fasciculations, muscle weakness and blurred vision. No central nervous system manifestations were evident. The symptoms developed within several minutes and lasted up to 24 h. All patients underwent gastric emptying followed by administration of activated charcoal. Atropine (1-8 mg) was required in only three patients. Measurement of serum cholinesterase inhibition was found to be a reliable and sensitive diagnostic tool in pyridostigmine poisoning. No clear correlation was found between the extent of cholinesterase inhibition and the incidence or severity of the cholinergic signs. The clinical recovery was faster than the spontaneous recovery of the enzyme. Pyridostigmine intoxication is self-limited and well tolerated by young healthy adults.
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PMID:Acute pyridostigmine overdose: a report of nine cases. 175 42

Two men were accidentally exposed to vapors of sarin, a cholinesterase inhibitor and extremely toxic nerve gas. Diagnosis was confirmed by depressed cholinesterase activity, and fixed extremely miotic pupils. No other signs or symptoms developed and neither man required treatment. Recovery to normal cholinesterase activity was gradual over a 90-day period. Pupillary reflexes were not detectable until 11 days after exposure; the miotic pupils dilated slowly over a 30-45 day-period. Eye pain and blurred vision did not occur; visual acuity and amplitude of accommodation were improved for several weeks. Other functions not affected significantly were intraocular pressure, visual fields, color vision, heterophorias, and vergences.
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PMID:Accidental exposure to sarin: vision effects. 397 1

A group of 16 cauliflower workers poisoned by residues of the organophosphate insecticides mevinphos and phosphamidon was followed in weekly clinics with interviews and determinations of plasma and erythrocyte cholinesterase levels. None had preexposure baseline values. Although six had initial erythrocyte cholinesterase values within the laboratory normal range, subsequent testing showed their erythrocyte activity had been significantly inhibited. While the most severe symptoms of the 16 subjects resolved after 28 days, their erythrocyte cholinesterase levels did not reach a plateau until an average of 66 days after exposure, after which most patients continued to report blurred vision, headache, weakness or anorexia. These findings support the view that the diagnostic utility of single cholinesterase levels is limited in the absence of baseline values.
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PMID:Clinical management of field worker organophosphate poisoning. 401 66

Exposure to anticholinesterase pesticides has been associated with the development of ocular toxicity in humans and animals, ranging from blurred vision to degeneration of the optic nerve. Based on the concern for human safety, the US Environmental Protection Agency has recently required additional studies for this class of compounds, focusing on biochemical, functional and histopathological evaluation of the ocular system. This study was designed to determine the effects on the eye of ethyl parathion, a highly toxic organophosphate, when administered orally to 30 beagle dogs (five of each sex per group) at doses of 2.4, 7.9 or 794 micrograms kg-1day-1 for 6 months. Control animals received corn oil. Routine ophthalmoscopic and slit lamp examinations, refraction and intraocular pressure determinations and electroretinograms were performed as functional assessments at various intervals over the study. Plasma and erythrocyte cholinesterase were determined at weeks 1, 6, 14, 20 and 26, while brain, retinal and ocular muscle cholinesterase were measured at week 26 only. Histopathological examination of the retina, optic nerve, ocular muscle and ciliary body was conducted at termination. Plasma and erythrocyte cholinesterase was markedly depressed at 7.9 and 794 micrograms kg-1day-1 as early as week 1. Retinal cholinesterase was decreased (37-55%) from control values in the 794 micrograms kg-1day-1 group only. Ocular muscle cholinesterase was comparable in treated and control groups at termination. No functional impairment of the eye was noted over the 6-month study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of ocular toxicity in dogs during 6 months' exposure to a potent organophosphate. 802 10

On the day of the disaster, 641 victims were seen at St. Luke's International Hospital. Among those, five victims arrived with cardiopulmonary or respiratory arrest with marked miosis and extremely low serum cholinesterase values; two died and three recovered completely. In addition to these five critical patients, 106 patients, including four pregnant women, were hospitalized with symptoms of mild to moderate exposure. Other victims had only mild symptoms and were released after 6 hours of observation. Major signs and symptoms in victims were miosis, headache, dyspnea, nausea, ocular pain, blurred vision, vomiting, coughing, muscle weakness, and agitation. Almost all patients showed miosis and related symptoms such as headache, blurred vision, or visual darkness. Although these physical signs and symptoms disappeared within a few weeks, psychologic problems associated with posttraumatic stress disorder persisted longer. Also, secondary contamination of the house staff occurred, with some sort of physical abnormality in more than 20%.
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PMID:Sarin poisoning on Tokyo subway. 919 33

This paper investigates the acute effects of carbofuran in workers of two pesticide-formulating plants. Mean airborne carbofuran concentrations ranged from 0.025 to 1.115 mg/m3 in plant A and from 0.018 to 0.067 mg/m3 in plant B, respectively. In workers of plant A the post-shift blood cholinesterase activity was significantly reduced, compared to pre-shift values. No difference in blood cholinesterase activity was found between pre- and post-shift values in workers of plant B. During the investigation, 25 cases of acute carbofuran poisoning were diagnosed by their clinical picture and depressed cholinesterase activity in blood. Usual symptoms included dizziness, weakness, blurred vision, nausea and sweating. Pallor, epigastric pain, vomiting and chest tightness occurred only in a few cases. Myosis was recorded in 24 cases. Fasciculation of muscle gastrocnemius induced by percussion was found in 6 cases, and four of them had also fasciculation of muscle orbicularis oculi. Inhibition of cholinesterase activity in the blood was related with the clinical features; however, the inhibition was rapidly reversible. In most cases, recovery was complete within 2-3 hours, with or without atropine treatment, after the subjects were removed from exposure. Rapid onset, mild illness and quick recovery are typical characteristics of occupational acute carbofuran poisoning.
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PMID:Acute effects of carbofuran in workers of two pesticide plants. 1021 31

Chlorpyrifos is an extensively used organophosphate insecticide with numerous agricultural crop and urban pest control uses. Dow AgroSciences, one of the manufacturers of chlorpyrifos, convened a panel of toxicology and medical experts to consider the available scientific literature (both published papers and unpublished reports from Dow AgroSciences) on chlorpyrifos with respect to determining the acute and chronic toxicological reference doses (RfD) for chlorpyrifos. The most sensitive effect observed in the body of animal and human studies on chlorpyrifos is the inhibition of the various cholinesterases. In animal studies chlorpyrifos is not carcinogenic, teratogenic, or mutagenic. Reproductive toxicity studies indicate some effects on postnatal survival, but these effects were seen at doses higher than maternal toxic dose levels. There are no clinical signs of cholinergic toxicity below 70% inhibition of brain cholinesterase. Cognitive or behavioral defects are not observed until substantial brain cholinesterase inhibition occurs. There are no indications that chlorpyrifos caused delayed neurotoxicity at dose levels below twice the oral LD50. The panel members stated that plasma cholinesterase was an inappropriate endpoint for the RfD. They recommended that brain, erythrocyte cholinesterase depression and clinical signs were appropriate as endpoints for the RfD. Plasma cholinesterase should be used only as an indicator of exposure. After a thorough review of the experimental animal literature, it was determined that the chlorpyrifos repeated-exposure RfD based on application of a 100-fold uncertainty factor on the no observed adverse effects level (NOAEL) for brain cholinesterase inhibition or on a 10-fold uncertainty factor on the NOAEL for erythrocyte cholinesterase inhibition is 0.01 mg/kg/d. Based on the human volunteer studies, which indicate a repeated-dose NOAEL of 0.1 mg/kg/d for erythrocyte cholinesterase inhibition, and then using a 10-fold uncertainty factor, the RfD is again 0.01 mg/kg/d. In this human volunteer study on d 9 (last day) of administration, 1 individual in the 0.1 mg/kg/day dose group was removed from the study due to a "cold" (runny nose, blurred vision, and a feeling of faintness). He was asymptomatic 12 h later. To some degree this diagnosis is supported by the hematology, since lymphocyte counts were reduced and neutrophil counts were increased markedly, indicating a possible inflammatory reaction on d 8 of dosing, clearing by posttreatment d 5. In the absence of any indication of erythrocyte cholinesterase inhibition and with plasma cholinesterase inhibition being greater in two of the four other individuals treated at the same dose level, these signs and symptoms are unlikely to have been induced by cholinesterase inhibition. The panel concluded that the symptoms this individual displayed were not an appropriate endpoint for the RfD. The single-exposure reference dose can be based on the human data. No erythrocyte cholinesterase inhibition or clinical signs of toxicity were observed after a single oral dose of 0.5 mg/kg. Utilizing a 10-fold uncertainty factor, the single-dose RfD is 0.05 mg/kg.
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PMID:Determination of the reference dose for chlorpyrifos: proceedings of an expert panel. 1042 80

In order to clarify the later sequelae of sarin poisoning that occurred in Matsumoto City, Japan, on June 27, 1994, a cohort study was conducted on all persons (2052 Japanese people) inhabiting an area 1050 meters from north to south and 850 meters from east to west with the sarin release site in the center. Respondents numbered 1237 and 836 people when surveys were conducted at one and three years after the sarin incident, respectively. Numbers of persons with symptoms of sarin toxicity were compared between sarin victims and non-victims. Of the respondents, 58 and 46 people had symptoms associated with sarin such as fatigue, asthenia, shoulder stiffness, asthenopia and blurred vision at both points of the survey, respectively. The prevalences were low; some complained of insomnia, had bad dreams, difficulty in smoking, husky voice, slight fever and palpitation. The victims who had symptoms one year after the incident had a lower erythrocyte cholinesterase activity than did those who did not have symptoms at the early stage; such persons lived in an area with a 500 meter long axis north east from the sarin release site. The three-year cohort study clearly showed that the odds ratios of almost all of the symptoms were high in the sarin-exposed group, suggesting a positive relationship between symptoms and grades of exposure to sarin. These results suggest that symptoms reported by many victims of the sarin incident are thought to be sequelae related to sarin exposure.
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PMID:Sequelae of sarin toxicity at one and three years after exposure in Matsumoto, Japan. 1061 67

A 42-year-old pregnant woman (26 weeks of gestation, G(4)P(0+3)) presented at the emergency department with a two-hour history of dizziness, blurred vision and repeated vomiting. These symptoms started during the use of an undiluted insecticide liquid (diazinon 60 EC) while cleaning a small non-aired bathroom. After clinical and laboratory confirmation for organophosphate poisoning (plasma pseudocholinesterase levels 161 U/l), treatment with atropine and pralidoxime was started. She recovered within 7 days and delivered a healthy baby 12 weeks later (Apgar score 9 and 10) by elective cesarean section. The child showed no signs or symptoms of organophospate, atropine or pralidoxime exposure.
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PMID:Organophosphate poisoning in pregnancy: a case report. 1585 33


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