Toxicokinetics of PCBs and tissue-retainable PCB metabolites (hydroxylated (OH-PCB) and methylsulfonylated (MeSOィイD22ィエD2-PCB)) were studied in human blood, tissues of mammals as well as in laboratory animals exposed to PCBS.
(1) Single administration of each PCB (#105, #118, #126, #138, #146, #153, #167, #187) to rats resulted in the retention of selected OH-PCBs in blood, particularly of 4-OH-PCBs with 3,5-dichlorinated substitution. The levels of OH-PCBs in blood were higher than the parent PCB levels.
(2) Species difference in the biotransformation capacity of PCB to OH-PCBs and MeSOィイD22ィエD2-PCBs was investigated between rats, hamsters and guinea pigs dosed with Kanechlor-500 (PCB mixture). In blood, the selective retention of 3-OH-PCBs derived from #99 and #118 was observed in guinea pigs, although only 4-OH-PCB derived from #118 was retained in rats. In liver, the retention of 3- and 4-MeSOィイD22ィエD2-PCBs derived from e.g. #101 and #132 was largely dependent on the species.
(3) More than ten OH-PCBs and ten MeSOィイD22ィエD2-PCBs were isolated from human blood and tissues of mammals such as seals and cetaceans. The levels of OH-PCBs were 1/100 of total PCBs in human blood, whereas, MeSO2-PCBs were 1/10-1/20 in seals and 1/100 in dolphin liver and human blood.
(4) Administration of nine MeSOィイD22ィエD2-PCBS to rats resulted in the reduction of serum thyroxine hormone levels, indicating that these PCB metabolites act as an endocrine disruptor.
These results give us useful information on the metabolism and toxicokinetics of PCBs and their tissue-retainable PCB metabolites in human.