Long-term Neurobehavioral Effects of Mild Poisonings with Organophosphate and n-Methyl Carbamate Pesticides among Banana Workers

Universidad Nacional, Heredia, Costa Rica.
International journal of occupational and environmental health (Impact Factor: 1.1). 01/2002; 8(1):27-34. DOI: 10.1179/oeh.2002.8.1.27
Source: PubMed

ABSTRACT Organophosphate poisoning has been associated with chronic neurobehavioral dysfunction, but no epidemiologic data exist with regard to long-term consequences from carbamate poisoning. This cross-sectional study evaluated the neurobehavioral performances of 81 banana workers who, on average 27 months earlier, had received medical attention not requiring hospitalization for mild occupational poisoning by either an organophosphate or a carbamate pesticide. These performances were compared with those of 130 banana workers who had never sought medical attention for pesticide poisoning. Poisoned subjects did less well than controls on tests measuring psychomotor and visuomotor skills, language function, and affect, the differences being significant for coding skills on the Digit-Symbol test and two tests of neuropsychiatric symptoms. These deficits, in particular a marked increase of neuropsychiatric symptoms, occurred among the organophosphate-poisoned subjects, but small deficits in performance were also seen in the carbamate-poisoned subjects. The performances of the previously poisoned subjects who had had contact with cholinesterase inhibitors within three months before testing were particularly poor. These findings in workers with mild poisoning are consistent with previous findings of persistent damage to the central nervous system from organophosphate poisoning. The possibility of persistent neurobehavioral effects associated with poisonings by nmethyl carbamate insecticides cannot be excluded. Workers with histories of poisoning may be more susceptible to neurobehavioral effects with subsequent exposures.


Available from: Linda Rosenstock, Jun 03, 2015
1 Follower
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Organophosphate (OP) compounds, including paraoxon (POX), are similar to nerve agents such as sarin. There is a growing concern that OP agents could be weaponized to cause mass civilian causalities. We have developed a rodent survival model of POX toxicity that is being used to evaluate chronic morbidity and to screen for medical countermeasures against severe OP exposure. It is well known that the survivors of nerve gas and chronic OP exposure exhibit neurobehavioral deficits such as mood changes, depression, and memory impairments. In this study we investigated whether animals surviving severe POX exposure exhibited long-term neurological impairments. POX exposure produced overt signs of cholinergic toxicity. Rats were rescued using an optimized atropine, 2-PAM and diazepam therapy. Surviving rats were studied using established behavioral assays for identifying symptoms of depression and memory impairment 3-months after POX exposure. In the forced swim test, POX rats exhibited increased immobility time indicative of a despair-like state. In the sucrose preference test, POX rats consumed significantly less sucrose water indicating anhedonia-like condition. POX rats also displayed increased anxiety as characterized by significantly lower performance in the open arm of the elevated plus maze. Further, when tested with a novel object recognition paradigm, POX rats exhibited a negative discrimination ratio indicative of impaired recognition memory. The results indicate that this model of survival from severe POX exposure can be employed to study some of the molecular bases for OP-induced chronic behavioral and cognitive comorbidities and develop therapies for their treatment.
    NeuroToxicology 09/2014; 44. DOI:10.1016/j.neuro.2014.08.008 · 3.05 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: There is limited evidence about whether background exposure to organochlorine pesticides is related to impairment of cognitive function in general populations. This study was performed to investigate cross-sectional associations between serum concentrations of organochlorine pesticides and cognitive function, a predictor of dementia, among U.S. elders without overt dementia. Study subjects were 644 elders aged 60–85, participating in the National Health and Nutrition Examination Survey 1999–2002. We selected 6 organochlorine pesticides (p,p′-dichlorodiphenyltrichloroethane (DDT), p,p′-dichlorodiphenyldichloroethylene (DDE), trans-nonachlor, oxychlordane, heptachlor epoxide, and β-hexachlorocyclohexane) which were commonly detected in current general population. Cognitive function was assessed with the Digit-Symbol Substitution Test. All 6 compounds showed statistically significant or marginally significant inverse associations with cognitive score after adjusting for covariates including education levels. The strongest association was observed with p,p′-DDT. With the outcome of low cognitive score defined as < 25th percentile, elders in the highest quartile of p,p′-DDT, p,p′-DDE, and β-hexachlorocyclohexane had 2 to 3 times higher risks than those in the lowest quartile. In particular, when their concentrations were further divided with the cutoff points of 90th and 95th percentiles, p,p′-DDT in the highest 5th percentile showed 6.5 (95% confidence interval: 2.6–16.3) times higher risk of low cognitive score. On the other hand, non-persistent pesticides like organophosphates or pyrethroid showed little association with this cognitive score. The potential role of background exposure to organochlorine pesticides in the development of dementia should be explored in future prospective studies and in-vitro/in-vivo experimental studies.
    Environment International 11/2014; DOI:10.1016/j.envint.2014.11.003 · 5.66 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Organophosphates (OP) are highly toxic compounds that cause cholinergic neuronal excitotoxicity and dysfunction by irreversible inhibition of acetylcholinesterase, resulting in delayed brain damage. This delayed secondary neuronal destruction, which arises primarily in the cholinergic areas of the brain that contain dense accumulations of cholinergic neurons and the majority of cholinergic projection, could be largely responsible for persistent profound neuropsychiatric and neurological impairments such as memory, cognitive, mental, emotional, motor, and sensory deficits in the victims of OP poisoning. The therapeutic strategies for reducing neuronal brain damage must adopt a multifunctional approach to the various steps of brain deterioration: (i) standard treatment with atropine and related anticholinergic compounds; (ii) anti-excitotoxic therapies to prevent cerebral edema, blockage of calcium influx, inhibition of apoptosis, and allow for the control of seizure; (iii) neuroprotection by aid of antioxidants and N-methyl-d-aspartate (NMDA) antagonists (multifunctional drug therapy), to inhibit/limit the secondary neuronal damage; and (iv) therapies targeting chronic neuropsychiatric and neurological symptoms. These neuroprotective strategies may prevent secondary neuronal damage in both early and late stages of OP poisoning, and thus may be a beneficial approach to treating the neuropsychological and neuronal impairments resulting from OP toxicity.
    Canadian Journal of Physiology and Pharmacology 09/2014; DOI:10.1139/cjpp-2014-0113 · 1.55 Impact Factor