3
Introduction
Compounds that concentrate in the food chain can provide a much higher dose
of toxic chemicals than may be apparent from the initial release to the environment.
Bioconcentration is a process by which an organism living in water develops a chemical concentration higher than that of the water. This is the result of the intake or
absorption of the chemical from the water being higher than the rate of excretion and
metabolism of the chemical. This occurs when a toxin remains unchanged as it moves
up the food chain. For example, although mercury is only present in small amounts in
seawater, it is absorbed by algae (generally as methyl mercury). Mercury is efficiently
absorbed but only very slowly excreted by organisms (Croteau, Luoma, and Stewart
2005). Mercury builds up in the adipose (fatty) tissue of successive levels in the food
chain. At each level, mercury in the tissue of organisms that are eaten accumulates
in the tissue of the animals until they in turn are eaten by organisms at the next level,
who then add to their own mercury contamination. The higher the level in the food
chain, the higher the concentration of mercury is in the fish. This process explains
why predatory fish such as swordfish and sharks or birds like osprey and eagles have
higher concentrations of mercury in their tissue than could be accounted for solely
by direct exposure. For example, herring contain mercury levels at approximately
0.01 part per million (ppm), whereas sharks contain mercury levels at greater than
1 ppm. In Chapter 9, bioconcentration data are used to develop a bioconcentration
adjustment factor, to be integrated into the toxicity factor for each TRI chemical.
A nervous radio interviewer once asked John Dillinger, “Why do you rob banks?”
His well-known answer was, “Because that is where the money is.” Similarly, if our
goal is to keep track of and reduce use or exposure to toxic chemicals, we should measure and report not just volumes released, but rather quantify the chemical release in
units that account for the mass released, the toxicity (toxicity factor), mobility (mobility
factor), persistence (persistence factor), and ability to bioconcentrate (bioconcentration
adjustment factor). Chapter 10 presents one method for integrating these factors to
estimate the relative impact of TRI chemical release (effective toxicity factor/toxicity
units), with the goal of developing a rational method of prioritizing toxic chemicals
for reduction. As this is an initial proposed approach, we welcome suggestions on how
to improve our analysis or use the same or additional toxicity data to rank chemicals
differently. The important point to keep in mind is that the objective of this approach
was not to come up with an absolute number that we claim to represent the actual and
fixed toxic impact of a chemical. Rather, the proposed methodology was developed
solely for the purposes of coming up with a logical means of applying published and
routinely used toxicological data to then develop chemical-specific “toxicity” factors.
In this way, we can conduct an apples-to-apples comparison across chemicals and
rank the potential effect among various toxic chemicals such that reduction in the use
of toxic chemicals can be targeted and managed accordingly.
The problem with basing programs on total poundage of chemicals is that reduction efforts may end up being concentrated on high-volume, low-toxicity release.
One could conceivably reduce total volume of a chemical by replacing a low-toxicity
compound with a smaller volume of a much more toxic compound. Chapter 11
reviews programs that concentrate on reducing the release of chemicals with the
greatest adverse toxic impact.
Introduction
Compounds that concentrate in the food chain can provide a much higher dose
of toxic chemicals than may be apparent from the initial release to the environment.
Bioconcentration is a process by which an organism living in water develops a chemical concentration higher than that of the water. This is the result of the intake or
absorption of the chemical from the water being higher than the rate of excretion and
metabolism of the chemical. This occurs when a toxin remains unchanged as it moves
up the food chain. For example, although mercury is only present in small amounts in
seawater, it is absorbed by algae (generally as methyl mercury). Mercury is efficiently
absorbed but only very slowly excreted by organisms (Croteau, Luoma, and Stewart
2005). Mercury builds up in the adipose (fatty) tissue of successive levels in the food
chain. At each level, mercury in the tissue of organisms that are eaten accumulates
in the tissue of the animals until they in turn are eaten by organisms at the next level,
who then add to their own mercury contamination. The higher the level in the food
chain, the higher the concentration of mercury is in the fish. This process explains
why predatory fish such as swordfish and sharks or birds like osprey and eagles have
higher concentrations of mercury in their tissue than could be accounted for solely
by direct exposure. For example, herring contain mercury levels at approximately
0.01 part per million (ppm), whereas sharks contain mercury levels at greater than
1 ppm. In Chapter 9, bioconcentration data are used to develop a bioconcentration
adjustment factor, to be integrated into the toxicity factor for each TRI chemical.
A nervous radio interviewer once asked John Dillinger, “Why do you rob banks?”
His well-known answer was, “Because that is where the money is.” Similarly, if our
goal is to keep track of and reduce use or exposure to toxic chemicals, we should measure and report not just volumes released, but rather quantify the chemical release in
units that account for the mass released, the toxicity (toxicity factor), mobility (mobility
factor), persistence (persistence factor), and ability to bioconcentrate (bioconcentration
adjustment factor). Chapter 10 presents one method for integrating these factors to
estimate the relative impact of TRI chemical release (effective toxicity factor/toxicity
units), with the goal of developing a rational method of prioritizing toxic chemicals
for reduction. As this is an initial proposed approach, we welcome suggestions on how
to improve our analysis or use the same or additional toxicity data to rank chemicals
differently. The important point to keep in mind is that the objective of this approach
was not to come up with an absolute number that we claim to represent the actual and
fixed toxic impact of a chemical. Rather, the proposed methodology was developed
solely for the purposes of coming up with a logical means of applying published and
routinely used toxicological data to then develop chemical-specific “toxicity” factors.
In this way, we can conduct an apples-to-apples comparison across chemicals and
rank the potential effect among various toxic chemicals such that reduction in the use
of toxic chemicals can be targeted and managed accordingly.
The problem with basing programs on total poundage of chemicals is that reduction efforts may end up being concentrated on high-volume, low-toxicity release.
One could conceivably reduce total volume of a chemical by replacing a low-toxicity
compound with a smaller volume of a much more toxic compound. Chapter 11
reviews programs that concentrate on reducing the release of chemicals with the
greatest adverse toxic impact.