Appendix D Food Codes for NHANES - OEHHA
Appendix D Food Codes for NHANES - OEHHA
Appendix D Food Codes for NHANES - OEHHA
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Scientific Review PanelSRP Draft Version 2 February,June 2012<br />
PeCDD (1,2,3,7,8 Penta-CDD) is always found in the emissions from waste<br />
incinerators (USEPA, 1998). Early studies indicated that the presence of<br />
1,2,3,7,8-PeCDD with other PCDDs/PCDFs in human milk suggested that the<br />
major source of exposure came from waste incinerator emissions (Buser and<br />
Rappe, 1984; Rappe et al., 1985; Mukerjee and Cleverly, 1987). Note that these<br />
congeners are measurable in human milk currently (Sasamoto et al., 2006; Zhao<br />
et al., 2007; Raab et al., 2008).<br />
Levels of PCDFs in human milk tend to be lower than PCDDs. However, PCDFs<br />
dominate in particulates emitted by combustion sources, including hazardous<br />
waste incinerators, and are present in higher concentrations in the atmosphere<br />
than PCDDs (USEPA, 1998). HxCDDs/HxCDFs and HpCDDs/HpCDFs are<br />
prevalent in pentachlorophenol. Incineration of wood and other products<br />
impregnated with pentachlorophenol results in the <strong>for</strong>mation of these congeners<br />
and emissions of hexa- and hepta-CDDs/CDFs. Both 1,2,3,7,8 and 2,3,4,7,8-<br />
PeCDFs have been detected in human milk, but 90% of the PeCDFs is generally<br />
2,3,4,7,8-PeCDF. 1,2,3,4,7,8- , and 1,2,3,6,7,8- HxCDFs. 2,3,4,6,7,8-HxCDFs,<br />
and1,2,3,4,6,7,8-HpCDF are also prevalent.<br />
Several investigators have observed that dose, degree of chlorination, degree of<br />
lipophilicity, and molecular weight influence how much PCDD/F congener is<br />
absorbed through the lungs or gut, metabolized and transferred from blood to<br />
milk (Yakushiji, 1988; Abraham et al., 1998; Schecter et al., 1998; Kostyniak et<br />
al., 1999; Oberg et al., 2002; Wittsiepe et al., 2007).<br />
Numerous studies have attempted to correlate exposure to individual dioxins,<br />
furans and dioxin-like PCBs from ingestion of contaminated food with levels in<br />
human biological samples such as blood and milk. Transfer from intake sources<br />
to human milk has often been estimated in the context of accidental or<br />
occupational exposures or after a substantial decline in environmental<br />
concentrations (Liem et al., 1995; Pinsky and Lorber, 1998; Liem et al., 2000;<br />
Focant et al., 2002; Furst, 2006; Milbrath et al., 2009). Steady state conditions<br />
are not reached in these studies because the half-lives of these compounds are<br />
in years and exposure changed considerably over the period evaluated in each<br />
study.<br />
Others have attempted to model the relationship between maternal intake and<br />
concentration in mother’s milk using an indicator compound such as TCDD<br />
(Smith, 1987; Lorber and Phillips, 2002). Less understood is the relationship<br />
between modeled and measured transfer estimates of individual dioxins, furans<br />
and dioxin-like PCBs. The following sections describe the sources of data and<br />
methods <strong>for</strong> deriving estimates of transfer <strong>for</strong> an array of dioxins, furans and<br />
dioxin-like PCBs that have accounted to some extent <strong>for</strong> the non-steady state<br />
condition and other confounders.<br />
J-8