Page 871 - The Toxicology of Fishes

Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals 851

TABLE 21.2
Mortality Thresholds and LD 50 Values for 2,3,7,8-Tetrachlorodibenzo-
p-Dioxin (TCDD) in Early Life Stages of Lake Trout
NOAEL LOAEL LD 50
(pg/g) (pg/g) (pg/g) Exposure Ref.
— 40 40–80 I Walker et al. (1991)
— — 47 I Guiney et al. (1997)
30 — 44 EI Guiney et al. (1996)
34 — 53 EI Guiney et al. (1996)
23 50 58 MT Walker et al. (1994)
41 — 65 EI Guiney et al. (1996)
34 40 69 EI Walker et al. (1994)
45 — 69 EI Guiney et al. (1996)
— — 74 I Walker et al. (1996)
44 55 80 I Walker et al. (1994)
20 40 81 I Wright (2006)
— — 85 EI Zabel et al. (1995c)
Note: Exposure routes were by egg injection (I) or egg immersion (EI) during
water hardening or by maternal transfer (MT).

The risk evaluation component missing from historic analyses of the effects of HAHs on lake trout
populations has been an accurate model for the exposure assessment. Analytical methods for HAHs were
improving during the last two decades of the 20th century, but accurate, reliable methods for quantification
of HAHs were not consistently applied to this problem until the 1990s. Separation technologies for
analytical clean-up, most notably carbon-based enrichment of the planar PCBs, PCDDs, and PCDFs, were
developed in the 1980s (Kuehl et al., 1984; Smith, 1981) and only became routinely used in the Great
Lakes in the 1990s (Echols et al., 1995; Feltz et al., 1995; O’Keefe et al., 1990). So, the ability to accurately
measure HAHs in lake trout only became common after the concentrations of HAHs had severely dropped
in the Great Lakes. These improved analytical methods have been applied to archived samples of lake
trout to examine historic trends in contaminant concentrations, but archived samples of lake trout collected
prior to 1970 are generally not available; therefore, an accurate exposure assessment of HAHs in lake
trout in the first half of the 20th century has been the limiting factor in our ability to critically evaluate
HAH impacts on lake trout populations and recruitment. The retrospective risk analysis of HAH on lake
trout from Lake Ontario conducted by Cook and colleagues (2003) offers the most complete exposure
assessment available combined with examination of the consistency between the predicted lake trout
early-life-stage mortalities and actual lake trout population changes during the 20th century.

Lake Trout Exposure History Assessment for
PCBs, PCDDs, and PCDFs in Lake Ontario
The retrospective analysis of HAH impacts on lake trout in Lake Ontario conducted by Cook et al.
(2003) used the ecological risk assessment model of the USEPA (1998) and the recommendations for
application of TEFs to fish and wildlife. The tissue and life stage targeted for the exposure model were
lake trout eggs, as the developing embryos are known to be the most sensitive life stage, and maternal
deposition of the HAHs into developing oocytes is the major route of exposure to the eggs (Walker et
al., 1991; Zabel et al., 1995). The concentrations of HAHs in lake trout eggs had to be estimated for
many of the years in question, because egg samples were unavailable for analysis prior to 1978. The
authors used sediment concentrations of HAH congeners from core samples, along with biota-sediment
accumulation factors (BSAFs), to estimate concentrations in lake trout eggs (Ankley et al., 1992). Lipid-
normalized egg concentrations (C ) were estimated from organic carbon-normalized sediment concen-
egg
trations (C ) of HAHs by the formula:
soc
C = (C )(BSAF )
egg
soc
egg