J Toxicol Environ Health A 2001 Apr 6;62(7):523-41
Effects of daily dermal application of DEET and epermethrin, alone and in combination, on sensorimotor performance, blood-brain barrier, and blood-testis barrier in rats.

Abou-Donia MB, Goldstein LB, Dechovskaia A, Bullman S, Jones KH, Herrick EA, Abdel-Rahman AA, Khan WA.

Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA. donia@acpub.duke.edu

DEET and permethrin were implicated in the development of illnesses in some veterans of the Persian Gulf War. This study was designed to investigate the effects of daily dermal application of these chemicals, alone or in combination, on the permeability of the blood-brain barrier (BBB) and blood-testes barrier (BTB) and on sensorimotor performance in male Sprague- Dawley rats. Groups of five rats were treated with a dermal daily dose of 4, 40, or 400 mg/kg DEET in ethanol or 0.013, 0.13, or 1.3 mg/kg permethrin in ethanol for 60 d. A group of 10 rats received a daily dermal dose of ethanol and served as controls. BBB permeability was assessed by injection of an iv dose of the quaternary ammonium compound [3H]hexamethonium iodide. While permethrin produced no effect on BBB permeability, DEET alone caused a decrease in BBB permeability in brainstem. A combination of DEET and permethrin significantly decreased the BBB permeability in the cortex. BTB permeability was decreased by treatment with DEET alone and in combination with permethrin. The same animals underwent a battery of functional behavior tests 30, 45, and 60 d after exposure to evaluate their sensorimotor abilities. All treatments caused a significant decline in sensorimotor performance in a dose- and time- dependent manner. These results show that daily dermal exposure to DEET, alone or in combination with permethrin, decreased BBB permeability in certain brain regions, and impaired sensorimotor performance. PMID: 11289702 [PubMed - indexed for MEDLINE]

Inj Prev 2001 Mar;7(1):4-9 Proposed explanations for excess injury among veterans of the Persian Gulf War and a call for greater attention from policymakers and researchers. Bell NS, Amoroso PJ, Wegman DH, Senier L. Social Sectors Development Strategies, Inc, Natick, Massachusetts 01760-1041, USA. BellSSDS@aol.com

INTRODUCTION: Death rates among US veterans of the Persian Gulf War were lower than rates among non-deployed veterans and the US population at large, with the exception of injury deaths; returning veterans were at significantly greater risk of injury mortality. Similar patterns of excess injury mortality were documented among US and Australian veterans returning from Vietnam. In spite of these consistent findings little has been done to explain these associations and in particular to determine whether or not, and how, war related exposures influence injury risk among veterans returning home after deployments.

HYPOTHESIZED PATHWAYS: Several potential pathways are proposed through which injury might be related to deployment. First, increases in injury mortality may be a consequence of depression, post-traumatic stress disorder, and symptoms of other psychiatric conditions developed after the war. Second, physical and psychological traumas experienced during the war may result in the postwar adoption of "coping" behaviors that also increase injury risk (for example, heavy drinking). Third, greater injury risk may be the indirect consequence of increased experiences of ill defined diseases and symptoms reported by many returning veterans. Fourth, veterans may experience poorer survivability for a given injury event resulting in greater mortality but not morbidity. Finally, the process that selects certain individuals for deployment may lead to a spurious association between deployment status and injury mortality by preferentially selecting individuals who are risk takers and/or exposed to greater hazards.

CONCLUSIONS: More research and attention from policymakers is needed to clarify the link between deployment and postwar increased risk of injury. PMID: 11289533 [PubMed - indexed for MEDLINE]