Self-reported exposure to neurotoxic chemical combinations in the Gulf War. A cross-sectional epidemiologic study.
OBJECTIVE
To identify risk factors of factor analysis-derived Gulf War-related syndromes.


METHODS
A cross-sectional survey.


METHODS
A total of 249 Gulf War veterans from the Twenty-fourth Reserve Naval Mobile Construction Battalion.


METHODS
Participants completed standardized booklets measuring self-reported wartime exposures and present symptoms.


METHODS
Associations of factor analysis-derived syndromes with risk factors for chemical interactions that inhibit butyrylcholinesterase and neuropathy target esterase.


RESULTS
Risk of syndrome 1 ("impaired cognition") was greater in veterans who reported wearing flea collars during the war (5 of 20, 25%) than in those who never wore them (7 of 229, 3%; relative risk [RR], 8.7; 95% confidence interval [CI], 3.0-24.7; P<.001). Risk of syndrome 2 ("confusion-ataxia") increased with a scale of advanced adverse effects from pyridostigmine bromide (chi2 for trend, P<.001), was greater among veterans who believed they had been involved in chemical weapons exposure (18 of 108, 17%) than in those who did not (3 of 141, 2%; RR, 7.8; 95% CI, 2.3-25.9; P<.001), and was increased in veterans who had been in a sector of far northeastern Saudi Arabia on the fourth day of the air war (6 of 21, 29%) than in those who had not been (15 of 228, 7%; RR, 4.3; 95% CI, 1.9-10.0; P=.004). Effects of perceived chemical weapons exposure and advanced adverse effects from pyridostigmine were synergistic (Rothman S, 5.3; 95% CI, 1.04-26.7). Risk of syndrome 3 ("arthro-myo-neuropathy") increased with an index of frequency and amount of government-issued insect repellent containing 75% DEET (N,N-diethyl-m-toluamide) in ethanol applied during the war (chi2 for trend, P<.001) and with advanced adverse effects from pyridostigmine (chi2 for trend, P<.001).


CONCLUSIONS
Some Gulf War veterans may have delayed, chronic neurotoxic syndromes from wartime exposure to combinations of chemicals that inhibit butyrylcholinesterase and neuropathy target esterase.
Haley
R W
RW
Epidemiology Division, Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 75235-8874, USA.
Kurt
T L
TL
D000328:Adult; D001259:Ataxia / Q000139:chemically induced; D002265:Carboxylic Ester Hydrolases / Q000037:antagonists & inhibitors*; D002618:Chemical Warfare; D002800:Cholinesterase Inhibitors / Q000506:poisoning*; D003072:Cognition Disorders / Q000139:chemically induced; D003430:Cross-Sectional Studies; D003671:DEET / Q000506:poisoning*; D004781:Environmental Exposure / Q000009:adverse effects*; D006801:Humans; D007302:Insect Repellents / Q000506:poisoning*; D016015:Logistic Models; D008875:Middle Aged; D009135:Muscular Diseases / Q000139:chemically induced; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000453:epidemiology; D018923:Persian Gulf Syndrome / Q000175:diagnosis / Q000453:epidemiology; D011729:Pyridostigmine Bromide / Q000506:poisoning*; D012307:Risk Factors; D013315:Stress, Psychological; D014481:United States / Q000453:epidemiology; D014728:Veterans
D002800:Cholinesterase Inhibitors; D007302:Insect Repellents; D003671:DEET; D002265:Carboxylic Ester Hydrolases; C021859:neurotoxic esterase; D011729:Pyridostigmine Bromide