No abstract

Advances in both sensitivity and specificity of analytical chemistry have made it possible to quantify substances in human biological specimens, such as blood, urine, and breast milk, in specimen volumes that are practical for collection from individuals. Research laboratories led by the Centers for Disease Control and Prevention (CDC) in its series National Report on Human Exposure to Environmental Chemicals [Centers for Disease Control and Prevention (CDC), 2005. Third National Report on Human Exposure to Environmental Chemicals. NCEH Pub. No. 05-0570.] are dedicating substantial resources to designing and conducting human biomonitoring studies and compiling biomonitoring data for the general population. However, the ability to quantitatively interpret the results of human biomonitoring in the context of a health risk assessment currently lags behind the analytical chemist's ability to make such measurements. The traditional paradigm for human health risk assessment of environmental chemicals involves comparing estimated daily doses to health-based criteria for acceptable, safe, or tolerable daily intakes (for example, reference doses [RfDs], tolerable daily intakes [TDIs], or minimal risk levels [MRLs]) to assess whether estimated doses exceed such health screening levels. However, biomonitoring efforts result in measured chemical concentrations in biological specimens (the result of absorption, distribution, metabolism and excretion of administered doses) rather than estimated intake doses. Quantitative benchmarks of acceptable or safe concentrations in biological specimens (analogous to RfDs, TDIs, or MRLs) needed to interpret these levels exist for very few chemicals of environmental interest. This paper discusses issues inherent in converting existing health screening benchmarks based on intake doses to screening levels for evaluating biomonitoring data, and presents methods and approaches that can be used to derive such screening levels (termed ''Biomonitoring Equivalents,'' or BEs) for a range of chemicals and biological media.

No abstract

No abstract

No abstract

No abstract

No abstract

Elimination half-life estimates for several polychlorinated dibenzodioxins/furans (PCDD/F) were calculated by modeling the blood and breast milk concentrations in two breast-fed human infants as reported by Abraham et al. (1996, 1998). Our analysis differs from that of other investigators in that we analyzed individual dioxin and furan congeners while the other studies considered TCDD only and we determined the half-lives in infants, rather than simply predicting body burdens in infants and older children. The average half-life values for each consistently measurable congener were determined to be less than about 6 mo and did not vary substantially between the two infants studied. The average elimination half-life values for 2,3,7,8-tetraCDD, 1,2,3,7,8-pentaCDD, 1,2,3,6,7,8-hexaCDD, 1,2,3,4,6,7,8-heptaCDD, and octaCDD were 0.40, 0.32, 0.39, 0.32, and 0.46 yr, respectively, and 0.27 yr for 2,3,4,7,8-pentaCDF. These values are in stark contrast with the 7 to 15+ yr values reported for these congeners in human adults (Michalek et al., 1996). These much shorter half-life values, likely attributable to rapid growth of the adipose tissue volume and enhanced fecal excretion of dioxins for breast-fed infants, explain why the much higher daily dioxin intake during breastfeeding does not translate to proportionately higher tissue concentrations. Thus, the shorter half-life of dioxins during breastfeeding needs to be considered when evaluating the dioxin hazard to children.