While inhalation absorption data are insufficient to determine absorption rates, inhalation is considered a major route of occupational exposure to PCBs.4 Additionally, there is indirect evidence suggesting absorption of PCBs via inhalation from observational studies of humans in occupational settings where air concentrations have been measured. These studies detected individual PCB congeners in both tissue and in body fluids.
Oral exposure through the consumption of food is believed to be the predominant route of exposure to PCBs for the general population. Contaminated water and soil impose an additional threat of PCB exposure on those near hazardous waste sites. 1994 estimates of PCB exposure for the contemporary UK claimed that approximately 97% of PCB exposure for the general population was due to food consumption. PCB contaminated fish, milk and dairy products, vegetables, and meat and animal fat accounted for 32, 26,18, and 16% of this exposure respectively. Vegetables are believed to account for most of the lower chlorinated PCBs while fish, dairy products, and meat contribute most of the higher chlorinated PCBs.
While not a major concern for the general population, dermal absorption is recognized as important to the accumulation of PCBs in adipose tissue of workers in the capacitor manufacturing industry. Wipe samples taken from the face and hands of employees at a private utility company yielded PCB levels from 0.05-5mg/cm2. Assuming 100% absorption, these exposure levels would account for up to 20% of the adipose PCB levels seen among capacitor manufacturing workers.
Data regarding the distribution of PCBs in human tissues and body fluids come mainly from studies of people exposed to PCBs in an occupational setting or from studies of those who have ingested contaminated food. Generally speaking, the main exposure routes in occupational settings are inhalation and dermal routes, while the main exposure routes for the general population is oral.
Metabolism of PCBs is the rate limiting step in the elimination of the toxic compounds so the biological half life of a congener depends on the bodys ability to metabolize it. The liver is the primary site of PCB metabolism, which occurs by hydroxylation and conjugation with glucuronic acid and sulfates. Generally, PCBs with more than five chlorines and para-chlorine atoms are less susceptible to hydroxylation and show the longest half lives. These PCBs can bioaccumulate withing the body. PCBs with chlorine-unsubstituted meta-para-carbons are more susceptible to hydroxylation with PCBs of greater than five chlorines being relatively less susceptible. Typically, the metabolism of xenobiotics yields polar compounds that can be cleared from the body, but several PCB metabolites are retained in the body displaying biotransformation into a secondary class of environmental toxicants. A better look at the mechanism of hydroxylation will help to clarify this (SEE FIGURE BELOW).
from the Handbook of Environmental Chemistry vol 3. part K, pg320, 2000 29
Hydroxylated metabolites are the predominant products with hydroxylation occurring at unsubstituted para and meta positions. Hydroxylation can occur via direct insertion in a meta position or by formation of an arene oxide intermediate, a process mediated by the cytochrome P450 system (CYPs). The arene oxide intermediate then rearranges to a hydroxy group. Some OH-PCBs (formed either by direct insertion or by arene oxide intermediate) are persistent within the body and are retained in the blood. Other OH-PCBs can be further metabolized in a conjugation reaction with glucoruonic acid or sulfate. This conjugation increases the water solubility of these compounds and facilitates excretion in bile.
In addition to forming OH-PCBs, arene oxide intermediates can undergo further metabolism to form methyl sulfone PCBs (MeSO2-PCBs) which can accumulate in adipose or specific tissue. Both MeSO2-PCBs and OH-PCBs can accumulate in specific tissue such as the lung and fetus. The flow chart below summarizes the biological fate of typical PCBs within the human body.
Excretion of PCBs is dependent on the rate of metabolism to polar products. Most PCB congeners display biphasic elimination; The initial half life is short, but the later half life is long and structure dependent. The rate of metabolism for each congener depends on the number and position of chlorine atoms. As stated, highly chlorinated PCBs with para-chlorines remain in the body longer than less chlorinated congeners with chlorine-unsubstituted meta-para-carbons. Metabolites of all congeners are eliminated primarily through bile and fecies. However, a small degree of elimination (<5%) can occur through urine for less chlorinated congeners.