3.5 Water Column Compartment
47
LC50 ∞ is the intrinsic toxicity value, which is assumed to correspond to 96 h
LC50 values for each component group (Johansen et al. 2005). ε is a coefficient which
expresses the exposure time dependency of the toxicity. It depends on the KOW for
the given component by the equation log ε = 1.47–0.414 log KOW (French-McCay
2002).
The dose-response curve used is a log-normal Species Sensitivity Distribution
(SSD) curve developed by Nilsen et al. (2006) (logarithmic SD = 0.32). The LC5
value derived from the SSD curve is used to represent LC50 for a particularly sensitive
species (5th percentile most sensitive), which is used as the effect limit for dissolved
components.
Based on the QSARs, the Critical Body Residue (CBR) is calculated by CBRj
= BCFj × LC50j for each component group j, Bioconcentration Factor (BCF) is
related to KOW (Brönner and Nordtug 2015). To calculate the actual body residue at
each time step for each component, the body concentration is a result of uptake and
elimination. The uptake rate is proportional to the environmental concentration C A ,
while the elimination rate is proportional to the body concentration (body residue)
C B . The uptake rate is related to the size of the organism (Hendriks et al. 2001) and
the lipophilic properties of the compounds which are related to the octanol/water
partitioning constant (Log Kow). See Brönner and Nordtug (2015) for equations
OSCAR uses to calculate this, referring to De Hoop et al. (2013) and McCarty and
Mackay (1993). From the calculated body residue (CB) at the given timestep, a
potential mortality is calculated by the SSD curve developed by Nilsen et al. (2006)
and implemented as:
Potential mortality, P = (x, 0, σ )
where is the cumulative normal distribution with argument x, mean value 0 and
standard deviation (slope) σ, x = log(C B /CBR) or log ((C B,j /CBR j ) (where j is
component) and standard deviation is = 0.32. This dose-response curve is used to
compute potential mortality in each grid cell at each time-step. The accumulated
maximum mortality over all time steps is reported as “fraction killed” in the cell
which is then used as input to ERA Acute. The maximum is a maximum of the
whole water column, which may be conservative in some water layers.
This second approach in ERA Acute involves access to detailed modelling of
input of potential mortality and an oil spill model that has composition information
on component groups. It bears some similarities with calculation of mortalities of
early life stages of fish in SYMBIOSES (SYsteM for BIOlogy-based asSESsments),
which consists of several coupled models where OSCAR provides the oil spill input
on component composition at each time step to LARMOD, which in turn calculates toxicity using chemical uptake kinetics and elimination rates for a given life
stage. The fish ecotoxicology module calculates mortality assuming additive effects
between mortalities caused by individual pseudo-components (Carroll et al. 2014,
2018).
47
LC50 ∞ is the intrinsic toxicity value, which is assumed to correspond to 96 h
LC50 values for each component group (Johansen et al. 2005). ε is a coefficient which
expresses the exposure time dependency of the toxicity. It depends on the KOW for
the given component by the equation log ε = 1.47–0.414 log KOW (French-McCay
2002).
The dose-response curve used is a log-normal Species Sensitivity Distribution
(SSD) curve developed by Nilsen et al. (2006) (logarithmic SD = 0.32). The LC5
value derived from the SSD curve is used to represent LC50 for a particularly sensitive
species (5th percentile most sensitive), which is used as the effect limit for dissolved
components.
Based on the QSARs, the Critical Body Residue (CBR) is calculated by CBRj
= BCFj × LC50j for each component group j, Bioconcentration Factor (BCF) is
related to KOW (Brönner and Nordtug 2015). To calculate the actual body residue at
each time step for each component, the body concentration is a result of uptake and
elimination. The uptake rate is proportional to the environmental concentration C A ,
while the elimination rate is proportional to the body concentration (body residue)
C B . The uptake rate is related to the size of the organism (Hendriks et al. 2001) and
the lipophilic properties of the compounds which are related to the octanol/water
partitioning constant (Log Kow). See Brönner and Nordtug (2015) for equations
OSCAR uses to calculate this, referring to De Hoop et al. (2013) and McCarty and
Mackay (1993). From the calculated body residue (CB) at the given timestep, a
potential mortality is calculated by the SSD curve developed by Nilsen et al. (2006)
and implemented as:
Potential mortality, P = (x, 0, σ )
where is the cumulative normal distribution with argument x, mean value 0 and
standard deviation (slope) σ, x = log(C B /CBR) or log ((C B,j /CBR j ) (where j is
component) and standard deviation is = 0.32. This dose-response curve is used to
compute potential mortality in each grid cell at each time-step. The accumulated
maximum mortality over all time steps is reported as “fraction killed” in the cell
which is then used as input to ERA Acute. The maximum is a maximum of the
whole water column, which may be conservative in some water layers.
This second approach in ERA Acute involves access to detailed modelling of
input of potential mortality and an oil spill model that has composition information
on component groups. It bears some similarities with calculation of mortalities of
early life stages of fish in SYMBIOSES (SYsteM for BIOlogy-based asSESsments),
which consists of several coupled models where OSCAR provides the oil spill input
on component composition at each time step to LARMOD, which in turn calculates toxicity using chemical uptake kinetics and elimination rates for a given life
stage. The fish ecotoxicology module calculates mortality assuming additive effects
between mortalities caused by individual pseudo-components (Carroll et al. 2014,
2018).