Abstract-There is increasing concern that birds in terrestrial ecosystems may be exposed to spent lead shot. Evidence exists that upland birds, particularly mourning doves (Zenaida macroura), ingest spent lead shot and that raptors ingest lead shot by consuming wounded game. Mortality, neurological dysfunction, immune suppression, and reproductive impairment are documented effects of exposure to lead in birds. An ecological risk assessment on the impact of lead shot exposure in upland birds was conducted and is presented in the context of the new United States Environmental Protection Agency's Ecological Risk Assessment Paradigm. A considerable amount of spent lead shot is released into the environment each year from shooting and hunting. Doves collected from fields that are cultivated to attract mourning doves for hunting activities show evidence of ingestion of spent lead shot. Because lead can cause both acute and chronic toxicity if ingested by birds, and because there is evidence of widespread deposition of lead shot in terrestrial ecosystems, concern for impacts on upland game birds and raptors seems warranted. Although this ecological risk assessment does not clearly define a significant risk of lead shot exposure to upland game birds, this issue merits continued scrutiny to protect our upland game bird and raptor resources.
Ingestion of contaminated food is considered the primary route of exposure in birds to agricultural chemicals. Routes of exposure other than ingestion are not often considered in risk assessments of agricultural chemicals to avian wildlife. However, recent studies demonstrated anorexic or avoidance behaviors in birds exposed to organophosphate (OP) insecticides. These behaviors would tend to limit exposure if ingestion alone were considered. The contribution, if any, of dermal, preening, and respiratory pathways to the exposure of birds to pesticides under field conditions is unknown. In addition, oral exposures are currently assessed in artificial environments that do not reflect real‐life exposure scenarios. To determine the relative contribution of these pathways and to assess exposures under ecological conditions, 270 northern bobwhite (Colinus virginianus) were exposed to simulated aerial crop applications of methyl parathion in an environmentally controlled wind tunnel. The wind tunnel environment consisted of a 25‐cm cotton plant canopy, a 5‐cm‐thick floor of silt‐loam, a temperature of 25°C, 50% RH, UV intensity similar to summer sunlight, and a wind speed of 3.2 km/h. Inhalation, preening, and dermal routes were isolated in groups of birds exposed to each application. Five birds from each group were collected at 1, 4, 8, 24, and 48 h post‐spray to determine cholinesterase (ChE) response to the exposures. Contaminated and uncontaminated darkling beetle (Tenebrio molitar) larvae were presented to free‐ranging sprayed birds in the wind tunnel to assess oral uptake. ChE response was determined at 4, 8, 24, and 48 h postspray. All exposures were replicated. All four routes contributed to the inhibition of brain ChE at different post‐spray periods. Dermal uptake and preening were major contributors to the overall dose and toxic response of birds to methyl parathion. Inhalation was the major route of exposure at 1 h post‐spray. At 4 h post‐spray, uptake through preening caused the greatest inhibition of brain ChE activity. Oral ingestion resulted in less than 20% inhibition of brain ChE during the test. Routes of uptake in order of contribution to toxicologic response from 8 to 48 h post‐spray were dermal > preening ≥ oral > inhalation.
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