Monday, June 28, 2010

Medical College of Georgia research shows long-term damage from low-levels of Gulf War chemicals

Written by Anthony Hardie

( - During today’s meeting of the Congressionally chartered Research Advisory Committee on Gulf War Veterans’ illnesses, Dr. Alvin V. Terry, Jr., Ph.D., gave a presentation entitled, “Organophosphate Exposure and Cognition: Novel Mechanisms of Neurotoxicity,” that covered his many years of research on the health effects of this class of chemicals.

Organophosphates (OPs) were first recognized as insecticides (pesticides) by German scientists in the 1930s. Their development as nerve agents came shortly thereafter.

During the 1991 Gulf War, OP pesticides were used to combat sand flies, fleas (including the unapproved but widely used flea collars), and other insects that carry diseases endemic to the region. [As an aside, the VA recently approved nine endemic diseases as presumptive for the purposes of service-connected disability claims.]

Gulf War troops were also exposed to varying levels of OP nerve agents following coalition air bombing of Iraqi chemical weapons production and storage facilities, and sarin and cyclosarin OPs (and probably mustard vesicant agent) as the result of the post-war demolition of Iraqi chemical warfare munitions at Khamisiyah, Iraq in early March 1991 that led to a plume containing the agents that drifted over troops in Iraq, Kuwait, and Saudi Arabia for at least a three-day period.

Health effects of OPs may be acute (close to the time of exposure) high-level exposures, or chronic and/or repeated low-level exposures.

The acute symptoms of exposure to high-levels of OPs have long been well understood are shown in Figure 1, below.

However, more recent studies have shown that even chronic or repeated low-level exposures are associated with anxiety, depression, psychotic symptoms, deficits in short-term memory, learning, attention, information processing, eye-hand coordination and reaction time, and other symptoms.

Terry’s published, peer-reviewed scientific research over many years on laboratory rodents has shown the scope and degree of OPs’ changes in and damage to neurons -- the functional cells of the brain -- and to axonal transport, part of the brain’s way of communicating.

Terry’s team found that exposure to OPs even at less than acute levels resulted in impairments in spatial learning, auditory startle response, and decreased brain proteins and axonal transport.

Terry’s team also found that there are differences between OPs, with low levels of pesticide-type OPs causing less damage than low levels of nerve agent OPs.  These findings are directly relevant to Gulf War illness research related to the chronic multi-symptom illness shown by a 2010 Institute of Medicine report to affect more than one-third (250,000) veterans of the 1991 Gulf War.

Terry is Professor of Pharmacology and Toxicology and Director of the Small Animal Behavior Core at the Medical College of Georgia.



Acute OP symptoms caused by Muscarinic (a neurotransmitter/brain chemical) stimulation (“DUMBBELS”)

  • Defecation
  • Urination
  • Miosis (constriction of the pupil in the eye)
  • Bradycardia (heart beating too slow)
  • Bronchospasm/Bronchorrhoea (excess production of mucus in the air passages of the lungs)
  • Emesis (vomiting)
  • Lacrimation (production, secretion, and shedding of tears)
  • Salivation (excess)

Acute OP symptoms caused by Nicotinic (another neurotransmitter/brain chemical) stimulation (“MATCH”)

  • Muscle weakness, fasciculations (spasming of small muscles)
  • Adrenal medulla activity increase
  • Tachycardia (heart beating too fast)
  • Cramping of skeletal muscle
  • Hypertension (high blood pressure)
Acute OP symptoms caused by Central receptor stimulation
  • Anxiety
  • Restlessness
  • Ataxia (gross lack of coordination of muscle movements)
  • Lethargy
  • Confusion
  • Coma
  • Seizure
  • Respiratory depression (hypoventilation,occurs when ventilation is inadequate)

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