Acute Organophosphate Pesticide Poisoning Research Articles

Prevalence and management outcomes of organophosphorus poisoning in emergency departments: systematic review

Organophosphorus poisoning (OPP) is a significant public health concern in various regions, with its prevalence and outcomes influenced by diverse sociodemographic factors. This systematic review aimed to collate and analyze data from multiple studies to provide a comprehensive understanding of the prevalence, risk factors, and management outcomes of OPP in emergency departments. A systematic search was conducted in October 2023, adhering to the PRISMA guidelines, primarily using PubMed. Studies were selected based on specific inclusion and exclusion criteria, with a focus on those that investigated OPP prevalence and management outcomes in emergency departments. Out of 87 initial studies, 9 met the inclusion criteria, encompassing a total of 1,469 participants from countries like Nepal, India, Korea, China, and Turkey. The studies predominantly included the younger to middle-aged demographic, with a significant male representation indicating that young males. Key findings highlighted the role of pesticides, especially organophosphorus compounds, in intentional poisonings, which can be seen more in young and unmarried females. Additionally, the therapeutic efficacy of treatments like plasma exchange has proven to be another promising tool for management. Finally, the importance of specific prognostic indicators such as D-CRP and the sequential organ failure assessment (SOFA) score, when combined with lactate levels (SOFA-Lac), are superior predictors of mortality in patients with acute organophosphate pesticide poisoning. The insights from this review emphasize the need for targeted interventions, both therapeutic and preventive, to address the challenges posed by OPP, especially in high-risk populations.

Clinical Profile of Adult Organophosphorus Compound Poisoning in a Tertiary Care Hospital

Despite the apparent benefits of organophosphate compounds (OPCs) acute organophosphate (OP) pesticide poisoning is an increasing problem worldwide. In a country like Bangladesh, where agriculture is a major component of the economy, these compounds are readily available to the general public. There is paucity of evidence from Bangladesh showing the pattern of organophosphate poisoning (OPP) in healthcare facilities. The aim of this study is to see the clinical profile of organophosphorus compound poisoning in admitted patients of tertiary care hospital.
 Methods: This observational cross-sectional study was carried out over all admitted patient with OPC poisoning in the department of Medicine, Cumilla Medical college, Cumilla from July 2019 to January 2020. A total of 100 cases were enrolled in the study. Patients having history of poisoning with OPC compound were stabilized by ABC care system and then assessed according to detailed history, physical examination and paradeniya organophosphorus poisoning (POP) scale.
 Results: The mean age was found 25.0±8.0 years and male to female ratio was 1:1.2, were mostly married (78.0%) and most of them from poor family (86%). The commonest manner of poisoning was suicidal (90.0%) with oral ingestion. More than eighty (84.0%) percent patients came from rural area. Commonest symptoms were abdominal pain (88.0%), vomiting (63.0%), excessive sweating (58.0%), salivation (35.0%), breathlessness (34.0%) and lacrimation (27.0%). Total hospitalization period was more than one week and less than two weeks in majority of cases (73%) and mortality rate was 2.0%.
 Conclusion: Due to increasing numbers of organophosphorus poisoning cases in younger age groups strict legislature on the availability of organophosphate compounds, preventive measures and appropriate health education should be introduced to decrease the incidence.
 Central Medical College Journal Vol 5 No 2 Jul 2021 PP 76-83

Changes of attention-related brain activity over 6 months after acute organophosphate pesticide poisoning: a prospective follow-up study

Context Ingestion of organophosphate (OP) pesticides is a common method of self-harm in developing countries. Apart from acute cholinergic effects, limited evidence implicates OP poisoning in long-term neurocognitive deficits. However, prospective neurophysiological evidence of long-term deficits is scarce in humans. We aimed to determine long-term cognitive changes of acute OP pesticide self-poisoning in a prospective follow-up study, using event-related potentials (ERPs), an electroencephalographic index of cognitive functioning. Methods We recruited 203 patients (147 men) hospitalised with OP pesticide ingestion (OP group; all had significant erythrocyte cholinesterase inhibition) and 50 patients (23 men) with paracetamol overdose (control group) as a means of self-harm. We recorded their ERPs and behavioural performance in a selective attention task at three post-exposure time points: on discharge from hospital (around 14 days post-ingestion), 6 weeks and 6 months post-ingestion. We compared the reaction time and ERP components of the two groups at each time point, adjusting for sex, age, education and comorbid depression in multiple regression models. Results OP group had significantly slower reaction times than the control group on discharge and at 6 weeks, but not at 6 months. On discharge, the OP group also showed significantly prolonged latency of the parietal P3b component, signifying delayed attentional processing. P3b amplitudes were also significantly smaller in the OP group on discharge and at 6 months. Within the OP group, greater clinical severity of poisoning was associated with smaller P3b amplitudes. Early pre-attentive cortical processing (as indexed by N1 ERP component) showed no significant intergroup differences. Conclusions Acute OP pesticide poisoning was associated with impaired behavioural and neurophysiological indices of selective attention. These deficits outlast the cholinergic phase of intoxication. The neurobehavioral impairment disappears over months, but neurophysiological deficits seem to last even after 6 months. This impairment could potentially compromise the performance and safety of patients for months following clinical recovery.

Serum High-sensitivity C-reactive Protein Level and Corrected QT Interval in Agricultural Workers in Myanmar Exposed to Chronic Occupational Organophosphate Pesticides.

Although acute organophosphate (OP) pesticide poisoning is associated with the risk cardiovascular diseases (CVD), the association between chronic occupational OP pesticide exposure and CVD risk is limited. We investigated serum high-sensitivity C-reactive protein (hs-CRP) levels and QTc intervals in 45 agricultural workers who were chronically exposed to OP pesticides and 45 non-exposed subjects. Serum hs-CRP level was determined by enzyme-linked immunosorbent assay (ELISA) and a level >1.0 mg/l was regarded as CVD risk. The QT interval was measured by routine 12-lead Electrocardiogram (ECG) with Lead II rhythm, and QTc was calculated. The median value of the serum hs-CRP level [1.20 (0.67-2.38) vs 0.74 (0.41-1.17) mg/l, P <0.05] and the mean QTc interval (422.71 ± 23.73 vs 396.27 ± 18.48 ms, P <0.0001) was significantly higher in the OP pesticide exposed subjects. Pesticide exposure was significantly associated with CVD risk (Chi-Square χ2 = 6.480, P = 0.011) and QTc interval prolongation (χ2 = 13.846, P <0.001). A higher risk of CVD (odds ratio = 3.030; 95% confidence interval = 1.276 - 7.197) was observed in the OP pesticide exposed subjects. This study suggested that OP pesticide exposure should be considered as one of the significant risk factors for CVDs.

Subacute and chronic neuropsychological sequalae of acute organophosphate pesticide self-poisoning: a prospective cohort study from Sri Lanka

Context Some epidemiological evidence implicates acute organophosphate (OP) pesticide poisoning in long-term neurocognitive deficits. However, no study has prospectively followed up poisoned patients long-term from the time of intoxication. We aimed to determine whether clinically significant acute OP self-poisoning leads to subacute and chronic neurocognitive deficits, in a prospective follow up study. Methods Employing Mini Mental State Examination, Digit Span and Cambridge Neuropsychological Test Automated Battery (CANTAB), we compared multiple cognitive functions in 222 patients hospitalized with acute OP pesticide self-poisoning with a control group of 52 patients hospitalized with paracetamol overdose, at three time points: on discharge following clinical recovery, 6 weeks and 6 months post-ingestion. Intergroup comparisons at each time point were done in multiple regression models, adjusting for sex, age, education and psychiatric comorbidities. OP within-group analysis was done to determine a dose–response relationship. Results After adjusting for covariates, the OP poisoned group had significantly poorer working memory (Digit Span) and episodic memory (CANTAB Paired Associates Learning); impaired spatial planning (CANTAB Stocking of Cambridge); and slower response speed in the sustained attention task (CANTAB Rapid Visual Information Processing), in the post-discharge assessment. Only working memory and episodic memory measures were impaired in the OP group at 6 weeks, whereas no significant intergroup differences were observed at 6 months. The OP subgroup who had complete red cell acetylcholinesterase inhibition on admission had poorer episodic memory when tested post-discharge than those who had partial inhibition, but no significant subgroup differences were observed at 6 weeks or 6 months. Discussion Acute OP pesticide poisoning may cause neuropsychological impairment that outlasts the cholinergic phase on a subacute time scale; but does not cause measurable chronic neuropsychological deficits.

Xuebijing injection induces anti-inflammatory-like effects and downregulates the expression of TLR4 and NF-κB in lung injury caused by dichlorvos poisoning

BackgroundThe mechanism in lung injury caused by acute organophosphate pesticide poisoning (AOPP) and an effective treatment remains unclear. We aim to clarify how the inflammatory lung injury caused by AOPP might be modulated by Xuebijing (XBJ) injection. MethodsAOPP-induced lung injury model was induced by dichlorvos (DDVP) subcutaneous administration in rats and XBJ injection was administered by intraperitoneal injection after DDVP challenge. The effects of XBJ injection were assessed by lung histopathological analysis and lung injury scores, lung wet-to-dry weight ratios (WDR) and oxygenation, differential immune cell count in bronchoalveolar lavage fluid (BALF), IL-6 and TNF-α levels in blood, the levels of TLR4 and NF-κB proteins in lung tissue and blood acetylcholinesterase (AChE) activity. ResultsDDVP administration resulted in damage of lung histopathology and lower PaO2/FiO2 ratios (P < 0.05), which were notably attenuated by XBJ injection (P < 0.05). Total cell, macrophage, and neutrophils count in BALF and TNF-α and IL-6 levels in blood were significantly increased after DDVP exposure (P < 0.05), which were notably ameliorated by XBJ injection (P < 0.05). TLR4 and NF-κB protein in lung tissue expression after DDVP challenge were markedly increased (P < 0.05), and they were substantially downregulated by XBJ injection (P < 0.05). In addition, blood AChE activity was significantly decreased by DDVP administration (P < 0.05), however, there was no significant improvement after XBJ injection. ConclusionXBJ injection prevents DDVP poisoning induced lung injury by attenuating the inflammatory response. The protective effect appears to be mediated through downregulation of the TLR4 and NF-κB expression.

Evaluation of MR perfusion abnormalities in organophosphorus poisoning and its correlation with SPECT.

Aim:Acute organophosphate (OP) pesticide poisoning causes substantial morbidity and mortality worldwide. Many imaging modalities, such as computerized tomography (CT), magnetic resonance imaging (MRI), and single photon emission computed tomography (SPECT) of the brain, have been used for quantitative assessment of the acute brain insult caused by acute OP poisoning. Perfusion defects on SPECT in acutely poisoned patients with OPs have been described, however, MR perfusion abnormalities have not been described in the literature. MR perfusion Imaging has the advantage of having higher spatial resolution, no radiation, and better availability.Materials and Methods:In this prospective study, 20 patients who ingested OP compounds were included. All the patients underwent brain SPECT on a dual head SPECT gamma camera and MRI brain on a 1.5T MR system. Neurocognitive tests were performed for all patients.Results:SPECT showed perfusion defects in 7 patients and total number of perfusion defects were 29. On MR perfusion, based on the cut-off values of normalized cerebral blood volume (nCBV) ratios and normalized cerebral blood flow (nCBF) ratios, the total number of patients showing perfusion defects were 6 and 8; and the total number of perfusion defects were 29 and 45, respectively. There was significant difference of the nCBV ratios and nCBF ratios between the control group (n = 20) and positive patients group (n = 6 and n = 8, respectively) (P > 0.05). All the defects seen on SPECT were well appreciated on nCBF maps (MRI perfusion) suggestive of 100% correlation.Conclusion:MR perfusion imaging can be used as an effective modality for evaluation in acute OP poisoning.

Exposure to organophosphate (OP) pesticides and health conditions in agricultural and non-agricultural workers from Maule, Chile

The objective was to evaluate the characteristics of exposure to OP pesticides and health status in Chilean farm workers from the Maule Region. An occupational health questionnaire was administered in 207 agricultural and non-agricultural workers. For the group of agricultural workers, we asked about specific occupational exposure history and symptoms of OP pesticide poisoning. The main health problem of the exposed group was previous OP pesticide poisoning (p < 0.001). Fifty-six percent of agricultural workers reported symptoms consistent with acute OP pesticide poisoning. The use of respiratory personal protective equipment and younger age were protective against these symptoms, and number of years of OP pesticide exposure was positively associated with reporting symptoms of poisoning. Of the pesticide applicators 47 % reported using chlorpyrifos. The regulations regarding use and application of pesticides should be strengthened, as should training and intervention with workers to improve the use of personal protective equipment.

P102 – 2305: Long-term neurodevelopmental and behavioural outcomes of acute organophosphate poisoning in South African children

Objective Organophosphate poisoning (OPP) is a significant cause of mortality in resource-poor countries, especially in economies such as that of South Africa where agricultural activity remains an important contributor to the economy. Long-term neurobehavioural sequelae of OPP have been reported in adults, but little is known about the neurodevelopmental outcomes of children who survive acute organophosphate pesticide poisoning, including that from domestic exposure. This study aimed to determine the performance of South African children surviving acute episodes of OPP on a standardized neurobehavioural battery compared to a control group of children previously admitted to hospital with paraffin poisoning. Methods Children were included who were 3–12 years with a previous admission for OPP to the Red Cross Children's Hospital, Cape Town. The control group comprised children admitted for paraffin poisoning and were matched to the index group for age, gender, home language, admission date and illness severity. All children were assessed for neurodevelopmental function. Caregivers were administered a questionnaire-based behavior rating scale, Achenbach System of Empirically Based Assessment. The neurodevelopmental performance and behaviour of OPP children was compared to that of the controls. Results A total of 91 children were tested, 46 OPP and 45 control children. No between group differences were found on any measures. Conclusion Although there were no significant differences between the children with OPP and those with acute paraffin exposure on preliminary analysis, possible explanations for this include sample size too small to detect subtle differences, exclusion from the study of children who had severe neurodisability or who had died due to OPP. Between group effects of these children may also have been masked by high prevalence risk factors in South Africa for poor development such as low socio-economic status, HIV exposure, maternal alcohol and smoking during pregnancy and poor maternal mental health.

Phase II study of magnesium sulfate in acute organophosphate pesticide poisoning

Background. Acute organophosphorus (OP) poisoning is relatively common and a major cause of death from poisoning in developing countries. Magnesium has been shown to be of benefit in animal models. Methods. We conducted a phase II study of bolus doses of (MgSO4) in 50 patients with acute organophosphate poisoning. Patients eligible for inclusion had ingested OP and had cholinergic symptoms consistent with moderate or severe poisoning. All patients received standard care of atropinization titrated to control muscarinic symptoms and pralidoxime. The trial was run in 4 sequential groups of patients. Participants in each group received a different total dose of MgSO4 (20%) administered as intermittent bolus doses infused over 10–15 min or placebo. There was one control patient for every 4 patients who received MgSO4. Group A (16 patients) received a total of 4 gm MgSO4 as a single bolus, group B (8 patients) received 8 gm (in two 4 gm doses q4H), group C (8 patients) received 12 gm (in three 4 gm doses q4H) group D (8 patients) received 16 gm (in four 4 gm doses q4H) and control (10 patients) received placebo). Patients were closely monitored for any adverse reaction like significant clinical neuromuscular disturbance and respiratory depression. Results. No adverse reactions to magnesium were observed. The 24 hour urinary magnesium concentration were statistically different between 16 gm (234.74 ± 74.18 mg/dl) and control (118.06 ± 30.76 mg/dl) (p = 0.019), while it was much lower than the 80% of the intravenous magnesium load. Six patients died in control group compared to 3 in 4 gm, 2 in 8 gm and 1 in 12 gm group. There was no mortality in 16 gm group. Conclusion. Magnesium was well tolerated in this study. Larger studies are required to examine for efficacy.

Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery

BackgroundThe principal toxicity of acute organophosphate (OP) pesticide poisoning is the disruption of neurotransmission through inhibition of acetylcholinesterase (AChE). However, other mechanisms leading to persistent effects and neurodegeneration remain controversial and difficult to detect. Because Caenorhabditis elegans is relatively resistant to OP lethality—particularly through the inhibition of AChE—studies in this nematode provide an opportunity to observe alterations in global gene expression following OP exposure that cannot be readily observed in less resistant organisms.ResultsWe exposed cultures of worms in axenic, defined medium to dichlorvos under three exposure protocols. In the first, worms were exposed continuously throughout the experiment. In the second and third, the worms were exposed for either 2 or 8 h, the dichlorvos was washed out of the culture, and the worms were allowed to recover. We then analyzed gene expression using whole genome microarrays from RNA obtained from worms sampled at multiple time points throughout the exposure. The worms showed a time-dependent increase in the expression of genes involved in stress responses. Early in the exposure, the predominant effect was on metabolic processes, while at later times, an immune-like response and cellular repair mechanisms dominated the expression pattern. Following removal of dichlorvos, the gene expression in the worms appeared to relatively rapidly return to steady-state levels.ConclusionThe changes in gene expression observed in the worms following exposure to dichlorvos point towards two potential mechanisms of toxicity: inhibition of AChE and mitochondrial disruption.

Oximes for acute organophosphate pesticide poisoning

Acute organophosphorus pesticide poisoning causes tens of thousands of deaths each year across the developing world. Standard treatment involves administration of intravenous atropine and oxime to reactivate inhibited acetylcholinesterase. The clinical usefulness of oximes, such as pralidoxime and obidoxime, has been challenged over the past 20 years by physicians in many parts of the world. To quantify the effectiveness and safety of the administration of oximes in acute organophosphorus pesticide-poisoned patients. We searched both English and Chinese databases: Cochrane Injuries Group Specialised Register, Cochrane Central Register of Controlled Trials (The Cochrane Library), MEDLINE (Ovid SP), EMBASE (Ovid SP), ISI Web of Science: Science Citation Index Expanded (SCI-EXPANDED), ISI Web of Science: Conference Proceedings Citation Index-Science (CPCI-S) and the Chinese language databases CNKI and WANGFANG. All searches were run in September 2009. Articles that could possibly be RCTs were retrieved to determine if they were randomised. The published methodology of three RCTs was not clear. We contacted the principal authors of these, but did not obtain further information. Seven pralidoxime RCTs were found. Three RCTs including 366 patients studied pralidoxime vs placebo and four RCTs including 479 patients compared two or more different doses. These trials found quite disparate results with treatment effects ranging from benefit to harm. However, many studies did not take into account several issues important for outcomes. In particular, baseline characteristics were not balanced, oxime doses varied widely, there were substantial delays to treatment, and the type of organophosphate was not taken into account. Only one RCT compared the World Health Organization (WHO) recommended doses with placebo. This trial showed no clinical benefits and a trend towards harm in all sub-groups, despite clear evidence that these doses reactivated acetylcholinesterase in the blood. Current evidence is insufficient to indicate whether oximes are harmful or beneficial. The WHO recommended regimen (30 mg/kg pralidoxime chloride bolus followed by 8 mg/kg/hr infusion) is not supported. Further RCTs are required to examine other strategies and regimens. There are many theoretical and practical reasons why oximes may not be useful, particularly for late presentations of dimethyl OP and those with a large excess of OP that simply re-inhibits reactivated enzymes. Future studies should screen for patient sub-groups that may benefit and may need flexible dosing strategies as clinical effectiveness and doses may depend on the type of OP.

Monocrotophos toxicity and bioenergetics of muscle weakness in the rat

Acute organophosphate pesticide poisoning is a common medical emergency with high fatality in agricultural communities of Asia. Organophosphate compounds inhibit acetylcholinesterase and prolonged neuromuscular weakness is a major cause of morbidity and mortality of poisoning. Organophosphate pesticide induced muscle weakness may not only arise from inhibition of acetylcholinesterase but also from non-cholinergic pathomechanisms, particularly mitochondrial dysfunction, affecting the production of sufficient ATP for muscle function. This study examined whether muscle weakness in rats subject to monocrotophos toxicity (0.8LD 50) was caused by inhibition of ATP synthesis, by oxidative phosphorylation and glycolysis, in addition to inhibition of muscle acetylcholinesterase. Severe muscle weakness in rats following monocrotophos administration was associated with inhibition of muscle acetylcholinesterase (30–60%) but not with reduced ATP production. The rats rapidly recovered muscle strength with no treatment. The ability of rats to spontaneously reactivate dimethyoxy phosphorylated acetylcholinesterase and efficiently detoxify organophosphates may prevent severe inhibition of muscle acetylcholinesterase following acute severe monocrotophos poisoning. This may protect rodents against the development of prolonged muscle weakness induced by organophosphates.

Chronic, Intermittent Exposure to Chlorpyrifos in Rats: Protracted Effects on Axonal Transport, Neurotrophin Receptors, Cholinergic Markers, and Information Processing

Persistent behavioral abnormalities have been commonly associated with acute organophosphate (OP) pesticide poisoning; however, relatively little is known about the consequences of chronic OP exposures that are not associated with acute cholinergic symptoms. In this study, the behavioral and neurochemical effects of chronic, intermittent, and subthreshold exposures to the OP pesticide, chlorpyrifos (CPF), were investigated. Rats were injected with CPF s.c. (dose range, 2.5-18.0 mg/kg) every other day over the course of 30 days and then were given a 2-week CPF-free washout period. In behavioral experiments conducted during the washout period, dose-dependent decrements in a water-maze hidden platform task and a prepulse inhibition procedure were observed, without significant effects on open-field activity, Rotorod performance, grip strength, or a spontaneous novel object recognition task. After washout, levels of CPF and its metabolite 3,5,6-trichloro-2-pyridinol were minimal in plasma and brain; however, cholinesterase inhibition was still detectable. Furthermore, the 18.0 mg/kg dose of CPF was associated with (brain region-dependent) decreases in nerve growth factor receptors and cholinergic proteins including the vesicular acetylcholine transporter, the high-affinity choline transporter, and the alpha(7)-nicotinic acetylcholine receptor. These deficits were accompanied by decreases in anterograde and retrograde axonal transport measured in sciatic nerves ex vivo. Thus, low-level (intermittent) exposure to CPF has persistent effects on neurotrophin receptors and cholinergic proteins, possibly through inhibition of fast axonal transport. Such neurochemical changes may lead to deficits in information processing and cognitive function.

The importance of electrodiagnostic studies in acute organophosphate poisoning

Six patients with acute organophosphate pesticide poisoning in whom electrodiagnostic studies influenced or supported specific decisions in management are described. One patient was admitted to hospital with a diagnosis of acute alcoholic intoxication. Electrodiagnostic studies revealed single stimulus induced repetitive responses and decrement–increment responses at 30 and 50 Hz repetitive nerve stimulation, findings that are indicative of a depolarization block due to inactivation of acetylcholinesterase at the motor end-plate. The patient was subsequently treated as a case of acute organophosphate poisoning. The administration of edrophonium (0.1 mg) to another patient with normal neuromuscular transmission studies unmasked the latent electrophysiological abnormalities. Three instances are described in which electrodiagnostic studies were useful in predicting whether pralidoxime administration was likely to be useful and for how long was pralidoxime therapy to be continued. Phrenic nerve conduction study in one patient with impending respiratory failure revealed an unstimulable phrenic nerve. The potential role of phrenic nerve conduction studies and neuromuscular transmission studies in influencing decisions like intubation and mechanical ventilation is discussed.

Chronic neurological sequelae to organophosphate pesticide poisoning.

This work was undertaken to determine whether there are any chronic neurological sequelae to acute organophosphate pesticide poisoning. California surveillance data were used in a study of neurological function among 128 men poisoned by organophosphate pesticides in California from 1982 to 1990 and 90 referents. Tests included a neurological physical examination, 5 nerve conduction tests, 2 vibrotactile sensitivity tests, 10 neurobehavioral tests, and 1 postural sway test. After correcting for confounding, the poisoned group performed significantly worse than the referent group on two neurobehavioral tests (sustained visual attention and mood scales). When the data were restricted to men with documented cholinesterase inhibition (n = 83) or to men who had been hospitalized (n = 36), the poisoned subjects also showed significantly worse vibrotactile sensitivity of finger and toe. Significant trends of increased impairment were found with increased days of disability on a wide spectrum of tests of both central and peripheral nerve function. While these findings are limited by low response rates and by small sample sizes for specific pesticides, this study was based on a large surveillance database and is the largest study to date of the chronic effects of organophosphate pesticide poisoning. The evidence of some long-term effects of poisoning is consistent with two prior studies.

Elevated quantitative vibrotactile threshold among workers previously poisoned with methamidophos and other organophosphate pesticides.

To evaluate chronic effects of acute organophosphate pesticide poisoning, quantitatively determined vibrotactile thresholds were measured as an index of peripheral neuropathy among agricultural workers in Nicaragua. Thirty-six male workers were evaluated between 10 and 34 months after hospitalization for acute organophosphate poisoning and compared to an age- and sex-matched community reference group. Vibrotactile thresholds were measured quantitatively in right and left index fingers and right and left great toes. Study subjects were stratified into three groups: 1) never poisoned; 2) poisoned with organophosphates other than methamidophos, agents which have not been reported to cause peripheral neuropathy; and 3) poisoned with methamidophos, a peripheral neurotoxin. For all digits, there was a statistically significant trend of increasing age- and height-adjusted thresholds across these three exposure categories. Over one fourth of patients previously poisoned with methamidophos we studied had abnormal vibrotactile thresholds. These results suggest that previously reported cases of organophosphate-induced delayed polyneuropathy may represent only the worst disease in a spectrum of impairment, a sequela of exposure that may be much more common than previously thought.

Chronic neurological sequelae of acute organophosphate pesticide poisoning.

To evaluate the latent neurological effects of organophosphate pesticide poisoning, this epidemiologic study examined 100 matched-pairs of individuals with previous acute organophosphate pesticide poisoning and nonpoisoned controls. No significant difference between poisoned subjects and controls was found on audiometric tests, ophthalmic tests, electroencephalograms, or the clinical serum and blood chemistry evaluations. Of the more than 50 scores from the neurological examination, abnormalities were demonstrated among the cases only on measures of memory, abstraction, and mood, and on one test of motor reflexes. Differences between the two cohorts were much more apparent in the neuropsychological tests. The differences occurred on tests of widely varying abilities including intellectual functioning, academic skills, abstraction and flexibility of thinking, and simple motor skills. Twice as many cases as controls (24 vs. 12) had Halstead-Reitan Battery summary scores in the range characteristic of individuals with cerebral damage or dysfunction. Results from the Minnesota Multiphasic Personality Inventory and the Patient's and Relative's Assessment of Patient Functioning Inventories also revealed greater distress and complaints of disability for the poisoned subjects.