444
cytotoxicity and genotoxicity of Corexit 9527 and Corexit 9500, the two dispersant
chemicals used during the DWH spill, to sperm whale skin cells has been demonstrated in a laboratory setting (Wise et al. 2014). These findings were consistent
with cytotoxicity and cell survival studies using Corexit 9500 in human and rat cells
(Bandele et al. 2012; Zheng et al. 2014); however, Corexit 9527 was found to be less
cytotoxic to whale cells than reported for other species’ cells. Cytotoxicity may lead
to acute effects, while genotoxicity is expected to lead to delayed effects associated
with genetic mutations in somatic and/or germ cells. Mutations in somatic cells
from toxic exposure may be associated with cancer in exposed marine mammals
(Gauthier et al. 1999), while mutations in germ cells are inherited by offspring.
Effects of dispersants on sea turtles are largely unknown, but dispersants have the
potential to interfere with lung function, digestion, and salt gland function
(Shigenaka 2003). In an exposure study that investigated the effects of crude oil,
dispersant, and a crude oil/dispersant combination on loggerhead hatchlings, significant differences between treatment and nonexposed controls were detected in
multiple blood chemistry parameters (Harms et al. 2014). Electrolyte imbalances
and hydration challenges were worst in the combined oil/dispersant group, and the
failure to gain weight was noted in dispersant and combined exposed hatchlings
(Harms et al. 2014). Only one heavily oiled Kemp’s ridley showed evidence of
DOSS at detectable concentrations (Ylitalo et al. 2017). Recent studies have demonstrated that DOSS degrades more rapidly in surface conditions than under deepwater conditions (Campo et al. 2013; Batchu et al. 2014), suggesting that DOSS
exposure was minimized in surface-pelagic turtles (Ylitalo et al. 2017).
26.4.5 Mortality Events
The 2010 marine mammal UME which began prior to the DWH spill complicated
measurement of the fatalities from the DWH event itself. It is now thought that the
UME was not caused by the spill but was aggravated and potentially prolonged and
expanded by the event (Venn-Watson et al. 2015; Antonio et al. 2011). An exponential increase in sea turtle and cetacean mortality was reported beginning 38 days
after the initial blowout (Antonio et al. 2011). The relationship between observed
strandings and unobserved offshore mortality is difficult to assess, but it has been
estimated that strandings accounted for at most 6.2% of the total dead marine mammals in the GOM following the DWH oil spill, depending upon the species (Williams
et al. 2011). This study relied on highly uncertain population estimates and mortality rates but strongly suggests that stranded carcass counts are not an adequate
means to estimate the total mortality. Similarly, sea turtle carcass stranding rates
likely represent a fraction of total at-sea mortality, as carcasses are likely to sink
prior to detection (Epperly et al. 1996). Winds, surface currents, and sea temperatures can bias stranding sites with respect to offshore source mortality locations
(Nero et al. 2013).
K. E. Frasier et al.
cytotoxicity and genotoxicity of Corexit 9527 and Corexit 9500, the two dispersant
chemicals used during the DWH spill, to sperm whale skin cells has been demonstrated in a laboratory setting (Wise et al. 2014). These findings were consistent
with cytotoxicity and cell survival studies using Corexit 9500 in human and rat cells
(Bandele et al. 2012; Zheng et al. 2014); however, Corexit 9527 was found to be less
cytotoxic to whale cells than reported for other species’ cells. Cytotoxicity may lead
to acute effects, while genotoxicity is expected to lead to delayed effects associated
with genetic mutations in somatic and/or germ cells. Mutations in somatic cells
from toxic exposure may be associated with cancer in exposed marine mammals
(Gauthier et al. 1999), while mutations in germ cells are inherited by offspring.
Effects of dispersants on sea turtles are largely unknown, but dispersants have the
potential to interfere with lung function, digestion, and salt gland function
(Shigenaka 2003). In an exposure study that investigated the effects of crude oil,
dispersant, and a crude oil/dispersant combination on loggerhead hatchlings, significant differences between treatment and nonexposed controls were detected in
multiple blood chemistry parameters (Harms et al. 2014). Electrolyte imbalances
and hydration challenges were worst in the combined oil/dispersant group, and the
failure to gain weight was noted in dispersant and combined exposed hatchlings
(Harms et al. 2014). Only one heavily oiled Kemp’s ridley showed evidence of
DOSS at detectable concentrations (Ylitalo et al. 2017). Recent studies have demonstrated that DOSS degrades more rapidly in surface conditions than under deepwater conditions (Campo et al. 2013; Batchu et al. 2014), suggesting that DOSS
exposure was minimized in surface-pelagic turtles (Ylitalo et al. 2017).
26.4.5 Mortality Events
The 2010 marine mammal UME which began prior to the DWH spill complicated
measurement of the fatalities from the DWH event itself. It is now thought that the
UME was not caused by the spill but was aggravated and potentially prolonged and
expanded by the event (Venn-Watson et al. 2015; Antonio et al. 2011). An exponential increase in sea turtle and cetacean mortality was reported beginning 38 days
after the initial blowout (Antonio et al. 2011). The relationship between observed
strandings and unobserved offshore mortality is difficult to assess, but it has been
estimated that strandings accounted for at most 6.2% of the total dead marine mammals in the GOM following the DWH oil spill, depending upon the species (Williams
et al. 2011). This study relied on highly uncertain population estimates and mortality rates but strongly suggests that stranded carcass counts are not an adequate
means to estimate the total mortality. Similarly, sea turtle carcass stranding rates
likely represent a fraction of total at-sea mortality, as carcasses are likely to sink
prior to detection (Epperly et al. 1996). Winds, surface currents, and sea temperatures can bias stranding sites with respect to offshore source mortality locations
(Nero et al. 2013).
K. E. Frasier et al.