Samples collected from harlequin ducks in oiled areas of PWS have been collected and analyzed for P450-CYP1A induction since the 1990’s. For the first time in 2013, and confirmed in 2014, these samples indicated the ducks are no longer being exposed to lingering oil.
A demographic model built in 2010, using data on survival and movements collected from radio-marked harlequin ducks in the Spill area, estimated that population recovery would occur approximately 24 years post-Spill, in 2013 (Iverson and Esler, 2010).
For the sea otter population, mortality patterns and abundance returned to pre-Spill conditions between 2010 and 2013 (Ballachey et al. 2014a). To evaluate sea otter demography and recovery status, aerial surveys were conducted annually from 1993-2011 (except for 2001, 2006 and 2010) in western PWS to quantify abundance. Carcasses that washed up on beaches were collected to document the age-class structure of otters that die each year (Bodkin et al., 2012). At northern Knight Island, an area heavily impacted by the Spill, abundance was depressed until the three most recent surveys, 2011 to 2013, where the numbers became similar to the pre-spill estimate of 165 sea otters (Ballachey et al, 2014a). Overall, in the western PWS, which includes oiled areas, aerial survey results indicate an increase in sea otter abundance which has nearly doubled since the time of the Spill.
Based on the scientific findings above, the Council declared the sea otter and harlequin duck populations recovered, in the 2014 Update on the Status of Injured Resources and Services.
A 2015 report presents the timelines and mechanisms of population recovery of wildlife from the Spill, and a synthesis of the findings of numerous reports funded by the Council. The report addresses variation in recovery times across species, and presents recent data for two species - harlequin ducks and sea otters - whose delayed recovery was related to exposure to lingering oil. The report describes long-term, or chronic, effects on wildlife including direct and delayed toxic effects, demographic lags, and indirect effects such as immune suppression, genetic damage, organ systems damage, and oxidative stress (Esler, 2015b).