House wren (Troglodytes aedon), tree swallow (Tachycineta bicolor), and eastern bluebird (Sialia sialis) tissues collected in study areas (SAs) downstream of Midland, Michigan (USA) contained concentrations of polychlorinated dibenzofurans (PCDFs) and polychlorinated dibenzo-p-dioxins (PCDDs) greater than in upstream reference areas (RAs) in the region. The sum of concentrations of PCDD/DFs (ΣPCDD/DFs) in eggs of house wrens and eastern bluebirds from SAs were 4- to 22-fold greater compared to those from RAs, whereas concentrations in tree swallow eggs were similar among areas. Mean concentrations of ΣPCDD/DFs and sum 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (ΣTEQsWHO-Avian), based on 1998 WHO avian toxic equivalency factors, in house wren and eastern bluebird eggs ranged from 860 (430) to 1500 (910) ng/kg wet weight (ww) and 470 (150) to 1100 (510) ng/kg ww, respectively, at the most contaminated study areas along the Tittabawassee River, whereas mean concentrations in tree swallow eggs ranged from 280 (100) to 760 (280) ng/kg ww among all locations. Concentrations of ΣPCDD/DFs in nestlings of all studied species at SAs were 3- to 50-fold greater compared to RAs. Mean house wren, tree swallow, and eastern bluebird nestling concentrations of ΣPCDD/DFs and ΣTEQsWHO-Avian ranged from 350 (140) to 610 (300) ng/kg ww, 360 (240) to 1100 (860) ng/kg ww, and 330 (100) to 1200 (690) ng/kg ww, respectively, at SAs along the Tittabawassee River. Concentrations of ΣTEQsWHO-Avian were positively correlated with ΣPCDD/DF concentrations in both eggs and nestlings of all species studied. Profiles of relative concentrations of individual congeners were dominated by furan congeners (69–84%), primarily 2,3,7,8-tetrachlorodibenzofuran and 2,3,4,7,8-pentachlorodibenzofuran, for all species at SAs on the Tittabawassee and Saginaw rivers but were dominated by dioxin congeners at upstream RAs.Electronic supplementary materialThe online version of this article (doi:10.1007/s00244-009-9416-6) contains supplementary material, which is available to authorized users.

Avian reproduction studies for regulatory risk assessment are undergoing review by regulatory authorities, often leading to requests for statistical re-analysis of older studies using newer methods, sometimes with older study data that do not support these newer methods. We propose detailed statistical protocols with updated statistical methodology for use with both new and older studies and recommend improvements in experimental study design to set up future studies for robust statistical analyses. There is increased regulatory and industry attention to the potential use of benchmark dose (BMD) methodology to derive the endpoint to be used in avian reproduction studies for regulatory risk assessment. We present benefits and limitations of this BMD approach for older studies being re-evaluated and for new studies designed for with BMD analysis anticipated. Model averaging is recommended as preferable to model selection for BMD analysis. Even for a new study following the modified experimental design analyses, with BMD methodology will only be possible for a restricted set of response variables. The judicious use of historical control data, identification of outlier data points, increased use of distributions more consistent with the nature of the data collected as opposed to forcing normality-based methods, and trend-based hypothesis tests are shown to be effective for many studies, but limitations on their applicability are also recognized and explained. Updated statistical methodologies are illustrated with case studies conducted under existing regulatory guidelines that have been submitted for product registrations. Through the adoption of alternative avian reproduction study design elements combined with the suggested revised statistical methodologies the conduct, analyses, and utility of avian reproduction studies for avian risk assessments can be improved.

Transgenerational effects of stressors can have important implications for offspring fitness and the responses of offspring to future stressful conditions. Parental effects, a common type of transgenerational effect, are non-genetic influences on offspring phenotype that result from parental phenotypes or environments. Little is known, however, about how parental exposure to a stressor effects offspring responses to other stressors despite this type of multi-stressor scenario being common. To better understand the role that parental effects have on offspring contaminant tolerance, we raised freshwater snails, Biomphalaria glabrata, in the presence or absence of predator threat (crayfish + crushed snail) for 12 weeks. Predators are common stressors in aquatic systems and can co-occur with chemical contaminants. We then collected egg masses from parental snails and exposed their offspring to cadmium and malathion survival challenges. Snails raised in the presence of predator threat displayed indicators of stress, including increased time to first reproduction, lower production of egg masses per snail per day and fewer eggs per egg mass, and had smaller shell lengths at 6.5 weeks old compared to snails not exposed to predator threat. Parental exposure to predator threat increased the cadmium tolerance of offspring but did not affect malathion tolerance. These results may have important implications for understanding effects of multiple stressors and indicate that the parental environment can influence responses to contaminants in offspring. To our knowledge, this is the first study to demonstrate that a biotic stressor in the parental environment can significantly affect the contaminant tolerance of their offspring.

Previous field studies of hunter‐harvested mourning doves (Zenaida macroura) have reported the percentage of birds with ingested lead shot as 0.2–6.5%. To reduce the uncertainty concerning the number of doves that ingest shot, we conducted an experiment to test the proportion of mourning doves that ingested lead shot on the bare soil of a disked field (typical of a managed dove field) to simulate more natural feeding conditions. In each of 3 treatment groups of 80 birds, we exposed 35 birds to low‐density lead shot (1.5 million shot/ha), and35 birds to high‐density lead shot (29.5 million shot/ha), and 10 birds served as controls (no shot). We dosed 5 positive control birds with 2 lead shot each in trials 2 and 3. We scattered lead shot and mixed seed on the loosely packed soil of treatment cages and after 4 days of exposure, 2.9% of doves voluntarily ingested ≥1 lead shot. The proportion of birds that ingested shot when exposed to the high‐density shot treatment (4.9%) was not different (P = 0.098) from that of the low‐density shot treatment (1.0%). Lead concentrations in liver, kidneys, and blood reached maxima of 94.402 ppm, 346.033 ppm, and 13.883 ppm wet mass, respectively. Differences in delta‐aminolevulinic acid dehydratase (ALAD) activity, packed cell volume, and heterophil:lymphocyte ratio (H:L) were greater posttreatment in doves that had ingested shot than in those that did not. The risk posed to mourning doves from lead shot ingestion can be reduced by banning lead shot on management areas or dove fields or disking fields after hunting season to reduce shot availability. © 2011 The Wildlife Society.