home edit2 whole TSD November 2002 PDF format - OEHHA

immunotoxicity, reproductive toxicity, thymic atrophy, decreased body weight gain, increased
cytochrome P450-dependent activity, cell proliferation and liver damage. The current working
hypothesis for the mechanism of the origin of the disease state associated with exposure to
PCDD/PCDF is the required binding of the PCDD or PCDF congener to a specific receptor protein
(the Ah receptor) followed by the expression of various endpoints (CDHS, 1986; NATO/CCMS,
1988a,b; US EPA, 1989). While continued research on the toxicities associated with each of the 210
congeners, including dose-response assessments, would lead to important toxicologic information, the
cost and time would lead to delays in addressing the public health concerns associated with exposures
to these mixtures. Hence, a means for expressing exposure related health risk of PCDD/PCDF
mixtures needs to be developed in the absence of a complete data base.
Toxicity Equivalency Factors
Toxicity equivalency factors (TEFs) are numerical factors that express the toxicity of an individual
PCDD or PCDF relative to the toxicity of TCDD, the highly toxic and best studied among the 210
congeners. TEFs are used in risk assessment to calculate the potential for health effects from a mixture
of PCDDs and PCDFs. The total "2,3,7,8-TCDD" equivalents - referred to as TCDD equivalents - in
a sample (e.g. air, soil, food) is estimated by multiplying the concentration of each congener in the
sample by its appropriate TEF and summing all TCDD equivalents. The total TCDD equivalents (TEQ)
is then used in conjunction with a cancer potency or reference exposure level to estimate cancer risk or
noncancer hazard index, respectively.
Although analytical methods are currently available to reliably quantify the amount of the various
congeners in a sample, not all congeners of PCDD and PCDF possess equal biologic activity. Such
differences may be a reflection of different toxicokinetic properties. For example, congeners that lack
the 2,3,7,8-configuration of chlorine groups, do not appear to bioaccumulate, as do the 2,3,7,8-
congeners. Within the group of 2,3,7,8-congeners, biologic activity is variable, and this property is
probably due to differences in dose-response relationships. A basic premise of the TEF methodology is
the presence of a common biologic end-point or in the case of multiple end-points, a common
mechanism of action. A second assumption is additivity of effects. These assumptions are inherent in all
TEF-schemes, and the accuracy of all TEF-schemes will be affected by situations where such
assumptions are not applicable.
California TEFs (CTEFs)
TEF schemes for PCDDs and PCDFs have been developed or adopted by many governmental
institutions throughout the industrialized world (NATO/CCMS, 1988). Among the schemes was one
developed by the CDHS, based on carcinogenicity data (CDHS, 1986) and adopted for use in the
California Toxic Air Contaminant Program and in the California Air Toxics "Hot Spots" Program
(CAPCOA, 1992). This scheme is referred to as the CTEF. Due to lack of data on the 2,3,7,8-pentaand
hepta- congeners of PCDD, the carcinogenic potencies of the penta-congeners were considered
equal to that of TCDD (1.0) and that of the hepta-congeners equal to that of hexaCDD (0.03), relative
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