to organophosphates and related chemicals that inhibit cholinesterase is responsible for the three nervous system-based syndromes (Haley and Kurt, 1997). Each of the syndromes was associated with a distinct set of risk factors. The impaired cognition syndrome was found, through multiple logistic regression, to be associated with having a job in security and wearing flea-and-tick collars. The second syndrome, confusion–ataxia, was associated with self-reports of having been involved in a chemical weapons attack and with self-reports of having advanced adverse effects from pyridostigmine bromide (PB).16 Finally, the third syndrome, arthromyoneuropathy, was associated with higher scores on the scale of advanced adverse effects from PB, as well as with an index created by the investigators to enable veterans to self-report the amount and frequency of their use of government-issued insect repellent. The authors concluded that some Gulf War veterans had delayed, chronic nervous system syndromes as a result of exposure to combinations of neurotoxic chemicals (Haley and Kurt, 1997).

Another study by Haley and collaborators (1999) examined whether genetic susceptibility could play a role in placing certain veterans at risk for neurological damage from organophosphate chemicals. They hypothesized that neurological symptoms in ill veterans might be explained by their having genetic polymorphisms (genetic variations) in metabolizing enzymes. The polymorphism would impair their ability to rapidly detoxify organophosphates (e.g., sarin, soman, and certain pesticides). This study is described and assessed in Chapter 6. The investigators studied 45 veterans, 25 of whom had chronic neurological symptoms as identified through their earlier factor analysis study and 20 of whom were healthy controls from the same battalion. They measured blood levels of butyrylcholinesterase (BuChE) and two types, or allozymes, of paraoxonase/arylesterase 1 (PON1). The genotypes encoding the allozymes were also studied. Investigators found that veterans who were ill had levels of blood BuChE similar to control subjects; however, ill veterans had lower levels of type Q PON1, the allozyme that hydrolyzes sarin rapidly. They also were more likely to have the type R genotype, which encodes the allozyme with low hydrolyzing activity for sarin. The authors interpreted their findings as supporting their earlier studies that neurological symptoms in susceptible Gulf War veterans were caused by exposure to environmental chemicals (see discussion in Chapters 5 and 6). This work requires further investigation and independent confirmation.

A large study by Fukuda and colleagues (1998) used factor analysis and other methods to assess the health status of Gulf War veterans. By studying an Air Force National Guard unit from Pennsylvania and three comparison Air Force populations, the investigators aimed to organize symptoms into a case definition and to carry out clinical evaluations on a subset of veterans. Of 3,701 veterans surveyed, those deployed to the Gulf War experienced higher prevalence of chronic symptoms (33 of 35 symptoms with more than 6-month dura-


The scale for adverse effects of PB was developed by the investigators to measure less common adverse effects (e.g., excessive sweating, tearing, chest tightness, nausea, muscle twitching, muscle cramps, headache, pounding heartbeat).

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