Organophosphate insecticide exposure and effects in a non-target bird species

Coturnix quail (Coturnix coturnix) were exposed to four different organophosphorus (OP) pesticides (dicrotphos (DCP), ethoprop (ETP), methamidophos (MMP), and naled (NLD)) either by oral gavage or by being enclosed upon a OP-sprayed simulated field of barley for 6 hours in controlled, replicated experiments. The selected OPs varied in solubility. Responses were measured as inhibition of cholinesterase (ChE) activity in plasma and brain. Oral doses were at one-third the estimated median lethal dose while the spray application rates used were expected to produce 60% inhibition of plasma ChE activity 24 hours following removal from the field. Oral doses caused significant inhibition of ChE activity in plasma (33-93%, p<0.001) and brain (17-61%, p<0.001), confirming that each OP was a ChE inhibitor and bioavailable via the oral route. Recovery from inhibition of ChE activity following oral doses was relatively uniform in plasma (17.6 hours ≤ half-life (t1/2) ≤ 24.5 hours) but slower and more variable in brain (64.8 hours ≤ t1/2 ≤ 128 hours). Responses to field exposures could not be explained by observations of consumption of contaminated feed. Responses to field exposures were inconsistent with those to oral doses with 3 of 4 OPs. The response to field exposures with MMP, the most hydrophilic OP, was generally consistent with the response to oral doses. ChE activity in both tissues was lower following field exposures than following oral doses, significantly so in brain (p<0.001), indicating the field dose was larger than the oral dose. Recovery from inhibition of ChE activity in plasma (t1/2=17.7 hours) and brain (t1/2=125 hours) following simulated field exposures were within the ranges observed following oral doses. The response to field exposures with DCP and NLD, the OPs of intermediate solubility, varied from the response to oral doses. ChE activity in plasma was significantly lower following field exposures than following oral doses (p ≤ 0.002), while the opposite significant relationship was observed in brain (p ≤ 0.009). Recovery from inhibition of ChE activity was prolonged in plasma (DCP, t1/2=41.3 hours; NLD, t1/2=34.7 hours) and brain (DCP, t1/2=34.7 hours) relative to recovery following oral doses. The response to field exposure to ETP, the most lipophilic OP, obviously differed from the response to oral doses. Field exposures produced only moderate inhibition of ChE activity in plasma and no significant inhibition of ChE activity in brain. The conclusion drawn was that the exposure of quail to the OPs on the simulated field was primarily via the dermal route and that quail skin served as a reservoir for storage and delayed release of the OPs, a reservoir effect that increased with increasing lipophilicity of the OP. Polynomial regression was used to investigate the extent to which inhibition of ChE activity in the brains of quail exposed for 6 hours on the simulated field could be predicted by log of the octanol:water partition coefficients (Kow) of the OPs. Quadratic polynomial curves were significantly fit to brain ChE activity inhibition data at both 24 (r2=0.888, p<0.001) and 72 hours (r2=0.871, p<0.001) post-exposure. These curves indicate that OPs having log Kow in the range of 0 to 1.5 will be those most rapidly absorbed and distributed under field conditions. A similar effort to predict the further inhibition of brain ChE activity in quail associated with the additional exposure to the pesticide spray itself yielded a significant quadratic polynomial curve at 24 hours post-exposure (r2=0.621, p=0.013). Comments are provided as to the utility and relevance of the findings in ecological risk assessment for pesticide registration. Quail were exposed to DCP and dehydration in controlled, crossed experiments to determine if dehydration could confound the diagnosis of OP exposure using inhibition of ChE activity in quail tissues. Measures of plasma osmolality (Posm) and hematocrit (Hct) quantified dehydration. DCP exposure caused significant inhibition of ChE activity in brain (38%, p<0.001) and plasma (26%, p<0.001). Dehydration caused a significant increase in plasma ChE activity (min. 55%, p<0.001). Variation in the change in plasma ChE activity in response to dehydration was significantly and positively correlated with dehydration-induced variation in both the change in Posm (r2=0.284, p<0.001) and the change in Hct (r2=0.081, p=0.018). The observed correlations suggest plasma ChE activity in quail is not limited to plasma but instead occupies some larger pool of body water. The effects of dehydration on plasma ChE activity masked the inhibitory effects of DCP. Combined dehydration and DCP exposure produced plasma ChE activity that was not significantly different from control values. A method to adjust plasma ChE activities for the confounding effects of dehydration and enable the diagnosis of OP exposure in dehydrated, DCP-exposed quail was developed. Quail received radio telemetry implants measuring body temperature and heart rate and were given sublethal oral doses of DCP, ETP, MMP, NLD, and vehicle alone. Observations were made before and after exposure and under thermoneutral and cold-stressed conditions. Significant hypothermia and tachycardia were observed under thermoneutral conditions following doses of DCP (1.20ºC, p<0.001; 98.4 beats per minute (bpm), p<0.001) and ETP (1.21ºC, p=0.004; 133 bpm, p