EPA's Vessel General Permit and Small Vessel General

than EPA’s HC5 TLM for benzo(a)pyrene 0.28 ug/L. The services were unable to identify
information on the effects of PAH and MAH substances on aquatic vegetation.
In addition to survival and reproductive effects assessed by EPA, PAHs have been identified as
having immunotoxic (Reynaud and Deschaux 2006, Bravo et al. 2011) and neurodevelopmental
(Danion et al. 2011, He et al. 2011, He et al. 2012, Shi et al. 2012) effects in marine and
anadromous fish. A recent investigation of PAH implications for threatened and endangered
Chinook salmon reported mean PAH concentrations measured in some stomach content samples
from wild caught fish were near the threshold concentrations associated with variability and
immune dysfunction in juvenile salmonids (Yanagida et al. 2012). This study demonstrated that
dietary PAH exposure, rather than water column concentrations (which ranged from 0.001 to
0.005 ug/L), was the primary source of exposure for juvenile salmonids. Dietary threshold
concentrations calculated for pink salmon in EPAs BE were 38.7 and 71.7 mg/kg wet weight for
benzo(a)pyrene and benzene, respectively. However, these thresholds were for PAH induced
mortality alone and did not take into account other effects which may also lead to mortality, such
as effects on immune function. Mortality was 60% after 14 days among Chinook salmon fed
16.5 +/- 0.1 mg/kg total PAH and challenged with Listonella anguillarum. Mortality among
vaccinated PAH exposed fish was markedly lower (approximately 16%, read from figure). The
PAH exposure mixture which only contained about 0.72% benzo(a)pyrene, was formulated to
approximate the actual PAH profile observed in the stomach contents of juvenile wild Chinook
(Palm et al. 2003). Increased spinal curvature rates in rockfish embryos occurred after 7 days
exposure to ambient concentrations of benzo(a)pyrene as low as 0.126 ug/L. While statistically
significant, the difference between controls and embryos exposed to 0.126 ug/ml B(a)P appeared
to be less than 5% (read from figure). The incidence rate for spinal deformities was 80% at 1.26
ug/L B(a)P (He et al. 2011).
Information regarding PAH and MAH marine turtles is limited to tissue concentrations (Alam
and Brim 2000, Camacho et al. 2012) and much of the information on PAH and MAH for marine
mammals are tissue concentrations (Hellou et al. 1991, Fair et al. 2010, Godard-Codding et al.
2011). Tissue concentration information confirms exposure and uptake of PAHs by marine
turtles occurs, the ecological implications of such exposures are difficult to interpret. There are
also a few biomarker and in vitro studies for marine mammals. Two investigations establish
point of effect exposures by identifying DNA adducts or biomarkers of exposure/toxicant
metabolism for marine mammals (Wilson et al. 2005, Godard-Codding et al. 2011).
Environmental PAH concentrations and the presence of PAH DNA adducts have been of
implicated in the occurrence of cancer within the St. Lawrence population of beluga whale (Ray
et al. 1991, Beland et al. 1993, Martineau et al. 1994). One in vitro investigation demonstrated
cytolotoxic effects of benzo(a)pyrene in cell cultures from Northern Right Whale, with greatest
toxicity found for testis. Another investigation exposing harbor seal lymphoma cell lines to
benzo(a)pyrene identified genototic, but not immunotoxic effects (Frouin et al. 2010). While
data from biomarker and in vitro studies are difficult to interpret in ecological terms, they
identify the mechanisms by which pollutants can affect organisms.
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