Feather lead concentrations and (207)Pb/(206)Pb ratios reveal lead exposure history of California Condors (Gymnogyps californianus).

Lead poisoning is a primary factor impeding the survival and recovery of the critically endangered California Condor (Gymnogyps californianus). However, the frequency and magnitude of lead exposure in condors is not well-known in part because most blood lead monitoring occurs biannually, and biannual blood samples capture only approximately 10% of a bird's annual exposure history. We investigated the use of growing feathers from free-flying condors in California to establish a bird's lead exposure history. We show that lead concentration and stable lead isotopic composition analyses of sequential feather sections and concurrently collected blood samples provided a comprehensive history of lead exposure over the 2-4 month period of feather growth. Feather analyses identified exposure events not evident from blood monitoring efforts, and by fitting an empirically derived timeline to actively growing feathers, we were able to estimate the time frame for specific lead exposure events. Our results demonstrate the utility of using sequentially sampled feathers to reconstruct lead exposure history. Since exposure risk in individuals is one determinant of population health, our findings should increase the understanding of population-level effects from lead poisoning in condors; this information may also be helpful for other avian species potentially impacted by lead poisoning.

Detection of depleted uranium in urine of veterans from the 1991 Gulf War.

American soldiers involved in "friendly fire" accidents during the 1991 Gulf War were injured with depleted-uranium-containing fragments or possibly exposed to depleted uranium via other routes such as inhalation, ingestion, and/or wound contamination. To evaluate the presence of depleted uranium in these soldiers eight years later, the uranium concentration and depleted uranium content of urine samples were determined by inductively coupled plasma mass spectrometry in (a) depleted uranium exposed soldiers with embedded shrapnel, (b) depleted uranium exposed soldiers with no shrapnel, and (c) a reference group of deployed soldiers not involved in the friendly fire incidents. Uranium isotopic ratios measured in many urine samples injected directly into the inductively coupled plasma mass spectrometer and analyzed at a mass resolution m/delta m of 300 appeared enriched in 235U with respect to natural abundance (0.72%) due to the presence of an interference of a polyatomic molecule of mass 234.81 amu that was resolved at a mass resolution m/delta m of 4,000. The 235U abundance measured on uranium separated from these urines by anion exchange chromatography was clearly natural or depleted. Urine uranium concentrations of soldiers with shrapnel were higher than those of the two other groups, and 16 out of 17 soldiers with shrapnel had detectable depleted uranium in their urine. In depleted uranium exposed soldiers with no shrapnel, depleted uranium was detected in urine samples of 10 out of 28 soldiers. The median uranium concentration of urines with depleted uranium from soldiers without shrapnel was significantly higher than in urines with no depleted uranium, though substantial overlap in urine uranium concentrations existed between the two groups. Accordingly, assessment of depleted uranium exposure using urine must rely on uranium isotopic analyses, since urine uranium concentration is not an unequivocal indicator of depleted uranium presence in soldiers with no embedded shrapnel.

Low cumulative manganese exposure affects striatal GABA but not dopamine.

The introduction of the anti-knock methylcyclopentadienyl manganese (Mn) tricarbonyl (MMT) in gasoline has raised concerns about the potential for manganese neurotoxicity. Because subpopulations such as the elderly in the early stages of neurodegenerative disease may be at increased risk for manganese toxicity, a pre-Parkinsonism rat model was used to evaluate whether sub-chronic manganese exposure can aggravate the neurochemical and behavioral dysfunctions characteristic of Parkinsonism. Sub-threshold levels of dopamine depletion of 3.5, 53 and 68% were generated via intrastriatal unilateral 6-hydroxydopamine (6-OHDA) doses. A sub-chronic dosing regimen of low cumulative manganese exposure (4.8 mg Mn/kg body weight, 3 i.p. injections per week x 5 weeks) was started 4 weeks after 6-OHDA treatments. Neurochemical and neuromotor (functional observational battery (FOB)) measures were evaluated. Manganese produced significant (P < 0.05) reductions of 30-60% in motor function. This effect was exacerbated in the presence of a pre-Parkinsonism condition [Neurotox. Teratol. 22 (2000) 851]. Manganese did not affect striatal dopamine, but resulted in significant increases in striatal y-aminobutyric acid (GABA) of 16 and 22% (P < 0.01) in both striati and a borderline non-significant 4% increase in frontal cortex (P = 0.076). Manganese treatment produced increased aspartate (P < 0.01) in the manganese and 6-OHDA treated striatum. In light of previous studies predominantly showing dopamine depletion with elevated manganese exposures, the significant effects of manganese on striatal GABA but not on striatal dopamine at the low cumulative exposure administered here suggest a progression in manganese toxicity with increasing cumulative dose, whereby GABA levels are adversely affected before striatal dopamine levels. Because these neurochemical disruptions were accompanied by motor dysfunction that was exacerbated in the presence of a pre-Parkinsonism condition, an increased environmental burden of manganese may have deleterious effects on populations with sub-threshold neurodegeneration in the basal ganglia (e.g. pre-Parkinsonism).

Lead isotopes as a supplementary tool in the routine evaluation of household lead hazards.

The advent of magnetic sector inductively coupled plasma-mass spectrometry (ICP-MS) allows rapid, accurate, and precise measurement of lead isotopes in environmental and biological samples at a lower cost than traditional methods. This may increase the feasibility of including lead isotope measurements as a routine tool to identify household sources of lead exposure to children. Here, we present three household case studies to illustrate how lead hazard evaluations by an environmental specialist could be supplemented with routine lead isotope analyses of potential lead sources and blood. Sampling for lead isotopes was undertaken following the U.S. Department of Housing and Urban Development regulatory guidelines for the evaluation of lead hazards in housing, and with the consideration of minimizing the additional costs associated with lead isotope measurements. The range of isotopic ratios within a single residence was large enough to allow the characterization of different lead sources, particularly when both major (e.g., (207)Pb/(206)Pb) and minor (e.g., (206)Pb/(204)Pb) isotope ratios were considered. These cases illustrate the utility of the lead isotope method to identify main source(s) of lead exposure to the child; discard unlikely sources of exposure to the child; point to sources of lead to dust; and substantiate or refine the environmental assessment based exclusively on lead concentrations and loadings. Thus, a more effective evaluation of household lead hazards would likely benefit from considering a) lead concentrations and loadings in and around the household environment; b) all isotopic ratios of potential lead sources within that environment; and c) information about behavioral habits, as well as an evaluation of viable pathways of exposure to the child.

The neurobehavioral effects of subchronic manganese exposure in the presence and absence of pre-parkinsonism.

Recent studies have implicated chronic elevated exposures to environmental agents, such as metals (e.g., manganese, Mn) and pesticides, as contributors to neurological disease. In particular, there is a concern that sensitive subpopulations such as the aged may be at increased risk for the onset of neurologic disorders because elevated exposures to Mn is associated with increased incidence of parkinsonism. Here, we utilized a rat model of pre-parkinsonism to investigate the effects of Mn exposure on neurotoxicity and the exacerbation of parkinsonism. A pre-parkinsonism state was induced using a unilateral intrastriatal injection of 6-hydroxydopamine (6-OHDA), followed 4 weeks later by Mn exposure (4.8 mg Mn/kgx3 intraperitoneal injections/week) for 5 weeks. Female Sprague-Dawley rats (n=44) were divided among the following treatments: (A) control, saline/vehicle; (B) Mn only; (C) 6-OHDA only; and (D) 6-OHDA+Mn. Brain Mn levels were measured by ICP-MS. Neurobehavioral function was assessed following Mn exposure using a functional observational battery (FOB) consisting of 10 neurobehavioral tests. Unilateral 6-OHDA lesions produced significant ipsilateral vs. contralateral striatal dopamine depletions (60-70%), but no measurable impairment of neurobehavioral function, thereby substantiating this pre-parkinsonism (i.e., subthreshold) model. In contrast, Mn exposure resulted in significant impairment of neurobehavioral function for eight of the 10 FOB tests. No effects of Mn exposure on striatal dopamine depletion were detected, despite the 3.4-fold increase in brain Mn levels over controls. Notably, Mn exposure in the presence of a pre-parkinsonism state significantly exacerbated the neurobehavioral impairment in the reactivity to handling (P<.049) and hopping contralateral rear limb (P<.033) FOB tests. While the persistence and Mn dose-response relationship of these neurobehavioral effects were not evaluated here, these results nonetheless suggest that chronic Mn exposure may increase the risk of neurobehavioral impairment in subpopulations that are in a pre-parkinsonism state.