Review of health consequences from high-, intermediate- and low-level exposure to organophosphorus nerve agents

Is Gulf War Illness a prolonged early phase tauopathy?

“…These symptoms reflect decrements in musculoskeletal, gastrointestinal and Central Nervous System (CNS) functioning. CNS symptoms include diminished short‐term memory, poor attention/concentration, chronic headaches, and impaired sleep, and are consistent with CNS symptoms found in people with chronic exposure to neurotoxicants, including organophosphate (OP) pesticides and nerve agents (Brown & Brix, 1998; Landrigan, 1997; Proctor et al, 2006; Winkenwerder, 2003). OPs and carbamates, two subsets of pesticides used during the GW, are known to produce chronic health and cognitive symptoms at sufficient exposure levels (Rauh et al, 2012; Rowe et al, 2016).…”

Is Gulf War Illness a prolonged early phase tauopathy?

“…These symptoms reflect decrements in musculoskeletal, gastrointestinal and Central Nervous System (CNS) functioning. CNS symptoms include diminished short‐term memory, poor attention/concentration, chronic headaches, and impaired sleep, and are consistent with CNS symptoms found in people with chronic exposure to neurotoxicants, including organophosphate (OP) pesticides and nerve agents (Brown & Brix, 1998; Landrigan, 1997; Proctor et al, 2006; Winkenwerder, 2003). OPs and carbamates, two subsets of pesticides used during the GW, are known to produce chronic health and cognitive symptoms at sufficient exposure levels (Rauh et al, 2012; Rowe et al, 2016).…”

(-)-Phenserine Attenuates Soman-Induced Neuropathology

“…Neuronal cell death is a major consequence of nerve agent exposure that leads to long-term cognitive and behavioral deficits in individuals surviving initial exposure [12] , [40] , [41] – [45] . In the present study, fluorojade C staining was employed to evaluate phenserine-induced neuroprotection against soman-induced neuropathology, in accordance with its prior use to quantify soman-induced brain damage [33] , [46] .…”

Reaction of Cresyl Saligenin Phosphate, the Organophosphorus Agent Implicated in Aerotoxic Syndrome, with Human Cholinesterases: Mechanistic Studies Employing Kinetics, Mass Spectrometry, and X-ray Structure Analysis

“…Aerotoxic syndrome is assumed to be caused by exposure to low doses of TOCP . Organophosphate-induced delayed neuropathy (OPIDN) is known to be caused by exposure to high doses of TOCP. ,− High doses of TOCP result in paralysis of the legs, whereas low doses do not cause delayed paralysis.…”

Is Gulf War Illness a prolonged early phase tauopathy?

“…These symptoms reflect decrements in musculoskeletal, gastrointestinal and Central Nervous System (CNS) functioning. CNS symptoms include diminished short‐term memory, poor attention/concentration, chronic headaches, and impaired sleep, and are consistent with CNS symptoms found in people with chronic exposure to neurotoxicants, including organophosphate (OP) pesticides and nerve agents (Brown & Brix, 1998; Landrigan, 1997; Proctor et al, 2006; Winkenwerder, 2003). OPs and carbamates, two subsets of pesticides used during the GW, are known to produce chronic health and cognitive symptoms at sufficient exposure levels (Rauh et al, 2012; Rowe et al, 2016).…”

(-)-Phenserine Attenuates Soman-Induced Neuropathology

“…Neuronal cell death is a major consequence of nerve agent exposure that leads to long-term cognitive and behavioral deficits in individuals surviving initial exposure [12] , [40] , [41] – [45] . In the present study, fluorojade C staining was employed to evaluate phenserine-induced neuroprotection against soman-induced neuropathology, in accordance with its prior use to quantify soman-induced brain damage [33] , [46] .…”

Reaction of Cresyl Saligenin Phosphate, the Organophosphorus Agent Implicated in Aerotoxic Syndrome, with Human Cholinesterases: Mechanistic Studies Employing Kinetics, Mass Spectrometry, and X-ray Structure Analysis

“…Aerotoxic syndrome is assumed to be caused by exposure to low doses of TOCP . Organophosphate-induced delayed neuropathy (OPIDN) is known to be caused by exposure to high doses of TOCP. ,− High doses of TOCP result in paralysis of the legs, whereas low doses do not cause delayed paralysis.…”

Is Gulf War Illness a prolonged early phase tauopathy?

“…These symptoms reflect decrements in musculoskeletal, gastrointestinal and Central Nervous System (CNS) functioning. CNS symptoms include diminished short‐term memory, poor attention/concentration, chronic headaches, and impaired sleep, and are consistent with CNS symptoms found in people with chronic exposure to neurotoxicants, including organophosphate (OP) pesticides and nerve agents (Brown & Brix, 1998; Landrigan, 1997; Proctor et al, 2006; Winkenwerder, 2003). OPs and carbamates, two subsets of pesticides used during the GW, are known to produce chronic health and cognitive symptoms at sufficient exposure levels (Rauh et al, 2012; Rowe et al, 2016).…”

(-)-Phenserine Attenuates Soman-Induced Neuropathology

“…Neuronal cell death is a major consequence of nerve agent exposure that leads to long-term cognitive and behavioral deficits in individuals surviving initial exposure [12] , [40] , [41] – [45] . In the present study, fluorojade C staining was employed to evaluate phenserine-induced neuroprotection against soman-induced neuropathology, in accordance with its prior use to quantify soman-induced brain damage [33] , [46] .…”

Reaction of Cresyl Saligenin Phosphate, the Organophosphorus Agent Implicated in Aerotoxic Syndrome, with Human Cholinesterases: Mechanistic Studies Employing Kinetics, Mass Spectrometry, and X-ray Structure Analysis

“…Aerotoxic syndrome is assumed to be caused by exposure to low doses of TOCP . Organophosphate-induced delayed neuropathy (OPIDN) is known to be caused by exposure to high doses of TOCP. ,− High doses of TOCP result in paralysis of the legs, whereas low doses do not cause delayed paralysis.…”