Orcas and PCBs

The dramatic population decline which has been predicted to affect killer whales (Orcinus orca) on a global scale by the end of this century is of concern, with the levels of polychlorinated biphenyls (PCBs) in tissues from free-ranging orcas having been estimated to be among the highest in the animal kingdom (1). As in other cetacean and non-cetacean “top predators”, in fact, lipophilic PCBs may heavily accumulate in killer whales’ subcutaneous blubber, thereafter undergoing ad hoc “biomagnification” processes. Since these bioaccumulation and biomagnification dynamics are shared by many other persistent environmental pollutants - either “classical” (i.e. DDTs, dioxins, heavy metals, etc.) or “emerging” (i.e. PBDEs, PFAS, micro- and nanoplastics, etc.) -, that almost unvariably form “mixtures” to which aquatic organisms are chronically exposed via the marine food web(s) (2), one could wonder how the biological effects of PCBs may be effectively “dissected” from those of the other contaminants present in the aforementioned mixtures. Furthermore, the “endocrine disrupting” and the additional pathogenic activities of PCBs on host’s reproductive and immune functions are also known to be exerted by other organochlorine (OC) pollutants, the entry of which into exposed animals’ cells is mediated by aryl hydrocarbon receptors (AHRs) (3). This implies that the susceptibility of a given species to PCBs and, more in general, to OC contaminants could “ideally” result from the “sum” of its trophic position and tissue expression level(s) of AHRs. Alternatively, if not complementarily, such an increased tendency to accumulate high PCB tissue burdens might depend upon a metabolic capacity toward OC xenobiotics that is less efficient in orcas as compared to other odontocete cetacean species. The prominent PCB immunotoxicity (3) has been also linked to an increased sensitivity toward infectious pathogens, as in the case of the dramatic Cetacean Morbillivirus (CeMV) epidemic which affected, between 1990 and 1992, the population of Western Mediterranean striped dolphins (Stenella coeruleoalba) (4). To the best of our knowledge, however, neither morbilliviral epidemics nor overt cases of morbilliviral infection have been hitherto reported in orcas, the susceptibility of which to CeMV is currently unknown. In this respect, should PCBs represent the major factor underlying the predicted killer whales’ population decline (1), one could reasonably expect a prevalence of “opportunistic” infections and/or neoplastic disease conditions (significantly) higher than in other cetacean and aquatic mammal species occupying a lower trophic level. Is this really the case? We are afraid that not enough, sufficiently reliable and robust data are available, thus far, to provide an affirmative or negative answer to the above query, considering also the “intrinsic” limitation due to the fact that an undefined number of orcas, similarly to their cetacean “heterospecifics”, will die in the open sea, with no possibility to perform a post mortem examination on them. Finally, the dramatically increasing pollution of global oceans and seas by plastics, micro- and nanoplastics would also deserve special concern, given that micro- and nanoplastics may act as “attractors and concentrators” for many chemical pollutants (including PCBs) (5), coupled with their long distance transfer across marine waters, as it has been recently described following the catastrophic tsunami in March 2011 along the Eastern coast of Japan (6). In conclusion, the herein dealt PCB-related alert (1), albeit of remarkable concern, appears to be influenced by a number of “environment”-dependent and “host”-related variables which should be carefully taken into account for an accurate evaluation of the effects of chronic PCB ingestion - and, more in general, exposure to OCs and other toxic pollutants - on killer whales’ health and conservation.