Using reports of bee mortality in the field to calibrate laboratory-derived pesticide risk indices.

Mounting evidence suggests that pollinators worldwide are experiencing dramatic population declines, and exposure to pesticides is one of the factors that can account for this. By making use of a database containing more than two decades of honey bee (Apis mellifera) hive poisoning incidents from the United Kingdom (Wildlife Incident Investigation Scheme [WIIS]) and corresponding pesticide use surveys, we attempted to explain honey bee poisoning incidents in the field using models derived from pesticide use information, laboratory-generated bee toxicity data (defined as a hazard ratio; application rate divided by LD(50)), and physico-chemical properties of the applied pesticides. Logistic regression analyses were used to assess the relationship between honey bee poisoning incidents in the field and these parameters. In analyzing models with multiple dimensions, we selected the best model by the best subset method, an iterative method based on maximum likelihood estimation, and Akaike's information criterion. Results suggested that the size of the area treated and hazard ratios calculated from application rates and oral or contact toxicity (but the latter especially) can be used to predict the likelihood that honey bee mortality will occur. Model predictions also suggest that some insecticides carry an extreme risk for bees, despite the lack of documented incidents.

Using dried blood spots stored on filter paper to measure cholinesterase activity in wild avian species.

Birds of prey that are poisoned by cholinesterase inhibitors (e.g. organophosphate and carbamate insecticides) are often cared for at animal shelters, rehabilitation centres and wildlife diagnostic facilities. Plasma cholinesterase (ChE) activity is a recognized method of assessing exposure to these insecticides, but standard blood-handling protocols are difficult to follow in non-laboratory settings. The primary objective of this study was to expand upon a method for storing human blood on filter paper without the need for complicated equipment or refrigeration, and to test its utility for measurement of ChE activity in avian blood. ChE activity from whole blood, plasma, and dried blood spots was analysed from 169 wild birds and comparisons made among sample types. ChE activity measured in whole blood haemolysates and dried blood spots were significantly correlated (r = 0.74, p < 0.001), as was ChE activity measured in plasma and dried blood spots (r = 0.68, p < 0.001). This study demonstrated that monitoring pesticide exposure in birds could be conducted using elementary blood sampling, preserving and shipping techniques.

The energy budget of captive Siberian hamsters, Phodopus sungorus, exposed to photoperiod changes: mass loss is caused by a voluntary decrease in food intake.

Unlike most nonhibernating small mammals, Siberian hamsters (Phodopus sungorus) undergo a pronounced mass loss, almost exclusively as white adipose tissues, in response to a switch from long- to short-photoperiod exposure. This mass loss can be caused by an increase in the rate of energy expenditure, a decrease in the rate of energy intake, or a decrease in assimilation efficiency. In order to determine how they relate to photoperiod-induced mass loss, we measured these energy budget components every 2 wk on 12 captive Siberian hamsters exposed to 8 wk of long photoperiod followed by 12 wk of short photoperiod. Body mass decreased shortly after short-photoperiod exposure. This was accompanied by an immediate decrease in the rate of energy intake and, after a 2-wk delay, by a decrease in the rate of energy expenditure. The overall cumulative decrease in energy intake (376 kJ) could account for the mass loss (249 kJ) observed during short-photoperiod exposure. Regression analyses indicated that only the rate of energy intake was significantly related to the rate of mass change. Therefore, we conclude that photoperiod-induced mass loss in Siberian hamsters is caused by a decrease in the rate of food intake, rather than by changes in energy expenditure or in assimilation efficiency.