AbstractIngestion 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>pree