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How and Why are PCBs Absorbed?
The main source of background human exposure to persistent lipophilic organic pollutants, such as PCBs is diet.[1]
To learn how PCBs and other lipophilic toxics gain access and are transported throughout the body click here.
Inside the body, PCBs will eventually be stored in the fat cells where they will be released slowly over prolonged length of time. Some of the PCBs are broken down into metabolites which may be eliminated in the feces or urine within a few days or stored in the fat. Higher chlorinated PCBs predominant route of excretion is via the feces while lower chlorinated PCBs leave in the urine. PCB metabolites may behave differently than unchanged PCBs and accumulate in specific tissues due to solubility differences as well as tissue binding.
Mobilization of PCBs from fat stores will release PCBs into the bloodstream, where they will associate with proteins by non-covalent binding. Likewise, metabolites will also bind to proteins in the bloodstream based on structure and affinity.
PCBs and Ah receptors
Studies have shown that PCBs with a coplanar configuration bind to the Ah receptor. After binding to the Ah receptor, the PCB is then transported into the nucleus where it subsequently changes gene expression of the cell.[2] Thus PCBs with a planar configuration and affinity for Ah receptors are the most toxic. Altering hepatic enzyme production, PCBs produce body weight wasting, muscle atrophy, and inhibition of immunological responces.[1]
PCBs and Ah independent receptors
Other PCB-induced effects not linked to Ah receptors include neurological effects involving changes in brain dopamine levels, changes in brain cell calcium homeostasis and related signal transmitting processes, and thyroid disruptions. PCBs can mimic or block the action of hormones from the thyroid and other endocrine glands.[1]
Sources:
[1] http://www.atsdr.cdc.gov/toxprofiles/tp17-c3.pdf
