No reports of chronic toxicity related to human PB exposure in clinical or military populations are available. The suggestions by Haley and Kurt, 1997 of a unique manifestation of organophosphate-induced delayed polyneuropathy associated with PB exposure alone or in combination with other wartime exposures, in the absence of acute symptoms of organophosphate toxicity, requires further investigation.
Although Haley and colleagues provide evidence that chronic neurological changes are present in a small number of ill Gulf War veterans compared to a small number of well veterans from the same unit, the validity and causal nature of this association are uncertain due to the large potential for selection and information biases in this study population and the lack of a nondeployed comparison group.
In addition, the evidence that some types of chronic neuropsychological changes may be linked to acute responses to administration of PB, also suggested by Haley and Kurt (1997), is limited by the lack of consistency with results from toxicological and clinical studies; uncertainty about the selection, administration, and interpretation of the neuropsychological tests employed; the highly select nature of the small number of Gulf War veterans studied; and the lack of comparable studies in a nondeployed comparison group.
The epidemiologic data do not provide evidence of a link between PB and chronic illness in Gulf War veterans. Most epidemiologic studies of Gulf War veterans focused on whether a unique Gulf War syndrome exists and on defining its characteristics. Only two epidemiologic studies specifically investigated the possible association of PB use and chronic symptoms among Gulf War veterans (Haley and Kurt, 1997; Unwin et al., 1999). The limitations of the small, selected population studied by Haley have been noted. With regard to PB, Haley’s factor-derived syndromes were not associated with taking PB or with the dose of PB. Two of the three syndromes showed an association with self-reported symptoms that are consistent with adverse effects of PB. This finding may result from reporting bias for adverse health syndromes and adverse effects of PB, and provides an inadequate basis for concluding that an association exists. The other epidemiologic study was of U.K. servicemen (Unwin et al., 1999), and all exposures studied (PB, diesel or petrochemical fumes, oil fire smoke, viewing dismembered bodies, etc.) showed an association of similar magnitude with adverse symptoms. Recall and reporting bias may also explain this finding. Thus, neither of these two studies provides a basis for determining that a specific association between PB and chronic adverse health effects exists.
The committee concludes that there is inadequate/insufficient evidence to determine whether an association does or does not exist between PB and long-term adverse health effects.