Agency for Toxic Substances and Disease Registry
Polychlorinated Biphenyls (PCB) Toxicity
Biological Fate
Although PCBs are readily absorbed into the body, they are only slowly metabolized and excreted. Animal studies suggest that absorbed PCBs partition between the aqueous and lipid compartments of the body in a biphasic pattern. After first distributing preferentially to the liver and muscle tissue, PCBs are subsequently redistributed to the adipose tissue, skin, and other fat-containing organs.
The liver is the primary site of PCB metabolism, which occurs via hydroxylation and conjugation with glucuronic acid and sulfates. Glucuronide and sulfate conjugates are excreted mainly in the urine, whereas hydroxylated metabolites are excreted mainly in the bile.
The rate of individual congener metabolism depends on the number and position of chlorine atoms. In rats, the half-lives of PCB congeners range from 1 to 460 days, depending on the degree of chlorination. In general, less-chlorinated isomers are more readily metabolized than are more highly chlorinated congeners. As a result of this preferential metabolism, more highly chlorinated congeners tend to remain in the body longer than do less-chlorinated congeners. Highly chlorinated congeners therefore tend to become more concentrated in adipose tissues, where they are stored in solubilized form.
Excretion of PCBs is very slow, so bioaccumulation occurs even at low exposure levels. As long as exposure continues, a true steady state is never achieved. Background levels of PCBs in human sera are typically <20 ppb and residues measured in human milk have values ranging from 40 to 100 ppb. Reported levels in adipose tissue range from 1 to 2 ppm.
| 3. |
Explain why patients with Gilbert syndrome might be at increased risk for adverse effects due to PCB exposure. |
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