Sensory neuropathy associated with Dursban (chlorpyrifos) exposure

Kaplan, Jonathan; Kessler, John A.; Rosenberg, Nurit; Pack, Donna; Schaumburg, Herbert H.

doi:10.1212/wnl.43.11.2193

Cited by 106 publications

(56 citation statements)

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“…The study also provided important insight into the profile of neurotoxicity, which confirmed earlier findings and showed that there was a positive correlation between abnormal neurological tests and evidence of anxiety and depression in patients exposed to OP. In another study , the neuropathy profile confirmed earlier observations (Kaplan et al, 1993;Steenland et al, 1994;McConnell et al, 1994;Horowitz et al, 1999;Pilkington et al, 1999) that this neuropathy linked to LTLL exposure to OP, unlike OPIDN, was predominately involving the sensory nerve fibres and affected both small and large fibre populations. This neuropathy profile linked with LTLL exposure to OP was also compared with another one seen in chronic neurotoxicity following one or more acute cholinergic episodes ).…”

Section: Referencesupporting

confidence: 84%

“…Analysis of all the above 11 studies show that neither the incidence nor the severity of development of chronic neurotoxicity had any relation with either the number nor the severity of the acute cholinergic episodes. In some of the cases described, the acute episodes were so mild that they escaped clinical detection (Kaplan et al, 1993;Jamal et al, 2001). …”

Section: Copind Following Acute Cholinergic Episodesmentioning

confidence: 96%

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Low level exposures to organophosphorus esters may cause neurotoxicity

Hansen²,

2002

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A large number of published studies support the notion that long term, low level (LTLL) exposure to organophosphorus (OP) esters may cause neurological and neurobehavioral effects. In order to differentiate these from other effects of OP such as the acute cholinergic episodes, intermediate syndrome and organophosphate induced delayed neuropathy (OPIDN), the term Chronic Organophosphate Induced Neuropsychiatric Disorder (COPIND) will be used purely for the ease of reference. The question addressed in this particular review is whether LTLL exposure to OP may produce neurotoxicity. The profile and the degree of overlap of the various components of COPIND have been addressed elsewhere and description of the possible mechanisms for COPIND is outside the scope of this article. COPIND can be classified under two headings; those produced following one or more acute clinical cholinergic episodes, and those produced without such preceding attacks. With regards to the first group, there are a total of 11 studies, all of which support the existence of a positive link between exposure to OP and neurotoxicity; six of these studies comprise descriptions of large numbers of cases without controls while five additional studies employ controls. Appearance of neurotoxicity does not seem to be related to the number or the intensity of acute cholinergic attacks. With regards to the second group, three types of studies can be identified. Firstly, there are five studies using experimental animals, all of which showed a positive link between OP and neurotoxicity. Secondly, a total of seven case studies without controls, some involving large numbers of patients, concluded that there is a positive link between OP and neurotoxicity. Thirdly, 19 studies investigated such a link using cases and control groups. Of these, 15 studies (about 80%) showed a positive link and only four failed to identify any link between OP and neurotoxicity. Annotation of all the 19 studies according to ideal set of criteria showed that only a few of these comply with the rules of excellence and all of these few showed a positive link. Furthermore, the only study carried out blind without the identification of subjects or controls, showed a positive link between OP and neurotoxicity. This blind study estimated the overall incidence of a form of neurotoxicity in people exposed to OP to be about 40 times higher than in the general population. The type of neurological involvement was unique and different from OP induced syndromes previously described. The profile of the neurological involvement was similar to that in COPIND whether or not preceded by acute cholinergic episodes, thus providing further evidence that these two neuropathies probably share a similar mechanism. There is a characteristic pattern of involvement of 15 functional indices of the autonomic nervous system examined in our laboratory. There are, in addition, preferential anatomical sites of target organs affected, selective preservation of cholinergic function within the same neuropathy-po...

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Section: Referencesupporting

confidence: 84%

Section: Copind Following Acute Cholinergic Episodesmentioning

confidence: 96%

Low level exposures to organophosphorus esters may cause neurotoxicity

Hansen²,

2002

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“…Some organochlorine insecticides such as chlorpyrifos reportedly cause both chronic neurologic symptoms (114) and modulation of the IRA (112). Certain OP insecticides enhance the large-fiber distal axonopathy caused by other OPs such as chlorpyrifos (109,114). Recently reported studies of GulfWar veterans confirm earlier reports of a connection between a syndrome of neurologic damage and wartime exposure to pesticides and insecticides (115)(116)(117)(118).…”

Section: Individual Ids Descriptionsmentioning

confidence: 53%

“…This interference may also extend to polychlorinated biphenyls (PCBs) (75) and in general to organophosphate (OP) and organochlorine compounds (113). Some organochlorine insecticides such as chlorpyrifos reportedly cause both chronic neurologic symptoms (114) and modulation of the IRA (112). Certain OP insecticides enhance the large-fiber distal axonopathy caused by other OPs such as chlorpyrifos (109,114).…”

Section: Individual Ids Descriptionsmentioning

confidence: 99%

Integrated Defense System Overlaps as a Disease Model: With Examples for Multiple Chemical Sensitivity

Rowat¹

1998

Environmental Health Perspectives

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“…In other study, no or mild changes which are in association with cholinergic overstimulation were reported in the patients. [8] Pesticide spraying process is associated with increased risk of neurotoxic effects on peripheral nerves, and the severity of poisoning depends on the dose and the type of organophosphate exposure. Chronic low-level exposure in non-poisoned subjects has been associated with impaired neurological functions, as documented in some epidemiological studies.…”

Section: Introductionmentioning

confidence: 99%

Nerve conduction studies in cases with long-term unintentional exposure to pesticide spraying

Gawande¹,

Chalak²,

Banginwar³

et al. 2018

Natl J Physiol Pharm Pharmacol

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Background: Farm workers experience many work-related hazards, including exposure to organophosphorus (OP) compounds during the process of pesticide spraying during their crop season. The recurrent unintentional exposure to OP compounds may lead to motor and sensory nerve neuropathies and also have some delayed neurological sequels. Aims and Objectives: The aims of this study were (1) to find out the toxic effects of OP compound on motor nerve conduction velocity (MNCV) and (2) to compare the MNCV, in selected peripheral nerve (median nerve) of affected population with the normal population. Materials and Methods: A cross-sectional analytical study was conducted by recruiting 60 individuals matched with height, weight, and occupation matched (control group 30 and study group 30). Participants were selected randomly from the outpatient Department of Medical College Hospital with age group between 20 and 40 years, and both sexes were included. The MNCVs were recorded using multichannel polyrite machine. Results: MNCVs were evaluated on median nerves of both the sides. MNCV was recorded on distal stimulation. Our findings show that the motor abnormalities nerve velocities in case of exposed population were significantly less as compared to the controls in tested median nerve. This indicates the presence of abnormalities such as neuropathy in these patients. Conclusion: There was an evidence of peripheral neuropathy to some extent in peripheral nerves as evident by slow MNCVs in median nerve of those farmers who were exposed to the OP pesticide spraying in the farms and its consequent absorption through skin, inhalation, or ingestion as compared to the normal individuals.

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Sensory neuropathy associated with Dursban (chlorpyrifos) exposure

Cited by 106 publications

References 0 publications

Low level exposures to organophosphorus esters may cause neurotoxicity

Low level exposures to organophosphorus esters may cause neurotoxicity

Integrated Defense System Overlaps as a Disease Model: With Examples for Multiple Chemical Sensitivity

Nerve conduction studies in cases with long-term unintentional exposure to pesticide spraying

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