Appendix D Food Codes for NHANES - OEHHA

Scientific Review PanelSRP Draft Version 2 February,June 2012
Although exposure to lead can come from many sources, ambient air
contaminated from combustion sources has been a significant source of
exposure in the U.S. population and European countries (U.S. EPA 1998). The
relationship between air lead and blood lead has been studied extensively in both
field studies and experimental chamber studies. OEHHA evaluated studies
conducted prior to 1997 in their health risk assessment of inorganic lead under
the toxic air contaminant program (OEHHA, 1997).
Briefly, in the OEHHA report, the contribution of airborne lead to blood lead levels
was examined using several different methods – disaggregate, aggregate,
uptake biokinetic, and physiologically based pharmaco-kinetic models (OEHHA,
1997). Findings were evaluated for linearity over a wide range of air and blood
lead levels and are expected to apply to some exposure scenarios under the Hot
Spots program. Most of these studies were conducted prior to 1985 when both
air and blood lead levels were much higher than they are now. For example, the
level of lead in the air used in chamber studies was 3.2 µg/m 3 representing low
exposure and 10.9 µg/m 3 representing high exposure, while background air was
typically between 7 µg/m 3 and 8 µg/m 3 in the city of Los Angeles during similar
time-periods – late 1960s / early 1970s. Lead in Los Angeles air is 100-fold lower
today (Ospital et al., 2008).
The relationship between air lead concentration and blood lead is not linear.
Higher slopes are observed at lower air lead concentrations. However, the
aggregate model was chosen because it implicitly incorporates all air-related
pathways (i.e. soil, dust, water, contaminated food, etc.) and has averaged
slopes estimated from a wide range of air concentrations. Using this model
OEHHA estimated that an average change of 1.8 µg/dL in adult blood lead levels
(µg/m 3 ) per µg/m 3 air lead concentration with current ambient air levels in
California
As part of our effort to estimate a lactational transfer factor for lead (Tco), we
searched for studies that examined slope factors in other populations or were
conducted subsequent to our 1997 report (OEHHA, 1997).
In addition to the kinetics of lead in the general adult population, recent studies
have observed that - under similar exposure conditions - plasma lead rises by
about 20% – 80% during lactation (Gulson et al., 1997; Gulson et al., 1998b;
Gulson et al., 1999; Rothenberg et al., 2000; Tellez-Rojo et al., 2002). Findings
from these and other investigations suggest that, in addition to daily
environmental sources of exposure, breast milk levels of lead also reflect lead
released from lead accumulated in the lactating woman’s bones.
We were not able to locate studies that measured both long-term exposure to
ambient air lead and lead levels in breast milk. Therefore, we calculated
estimates of transfer from blood to human milk from separate study populations
to combine with estimates of lead transfer from air to blood.
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