from the blood to the bones, where it can be stored -- like calcium is stored. (So someone with past exposure might have low blood levels but still have lead stored in their bones.)
Nutrition can affect how much leaves the body without getting absorbed . So two children with the same elevated blood lead level of 10, for example, might have different long term lead storage in their bodies; one might excrete more and one might absorb more into their bones and tissues. The malnourished child is more at risk of the lead not being excreted.
Also, this means that if exposure to lead stops, children with elevated blood levels should have blood lead levels that return to normal. They may still have lead stored in their bones, however. And there could be circumstances in their future that send the lead back out of their bones and into their blood.
From the CDC:
BLL= blood lead level
http://www.atsdr.cdc.gov/csem/csem.asp?csem=7&po=9
Although the blood generally carries only a small fraction of total lead body burden, it does serve as the initial receptacle of absorbed lead and distributes lead throughout the body, making it available to other tissues (or for excretion).
The half-life of lead in adult human blood has been estimated to be from 28 days (Griffin et al. 1975 as cited in ATSDR 2005) to 36 days. (Rabinowitz et al. 1976 as cited in ATSDR 2005)
(SNIP)
Blood lead is also important because the BLL is the most widely used measure of lead exposure.
These tests, however, do not measure total body burden—they are more reflective of recent or ongoing exposures.
(SNIP)
The bones and teeth of adults contain about 94% of their total lead body burden; in children, the figure is approximately 73% (Barry 1975 as cited in ATSDR 2005). Lead in mineralizing tissues is not uniformly distributed. It tends to accumulate in bone regions undergoing the most active calcification at the time of exposure.
(SNIP)
Because lead from past exposures can accumulate in the bones (endogenous source), symptoms or health effects can also appear in the absence of significant current exposure.
In most cases, toxic BLLs reflect a mixture of current exposure to lead and endogenous contribution from previous exposure.
An acute high exposure to lead can lead to high short-term BLLs and cause symptoms of lead poisoning.
It is important that primary care physicians evaluate a patient with potential lead poisoning, examine potential current and past lead exposures and look for other factors that affect the biokinetics of lead (such as pregnancy or poor nutrition).
https://www.lead.org.au/fs/Fact_sheet-Nutrients_that_reduce_lead_poisoning_June_2010.pdf
REDUCING LEAD ABSORPTION
For reducing lead absorption the key nutrients appear to be vitamin C, calcium, iron and, to
a lesser degree, zinc and phosphorus. Dietary deficiencies in any of these can increase lead
absorption, though supplementation of individuals with already high levels of these
nutrients in their diet may not have much impact on lead absorption. Further, since these
minerals compete with, or alter lead absorption during digestion, taking concentrated
supplements at one point of time, unless you are deficient in that particular nutrient, may
not affect continuing lead absorption, once the supplements have been processed through a
particular stage of digestion.
Vitamin D and folate (vitamin B9) can actually increase lead absorption, but have offsetting
advantages: vitamin D can play a role in decreasing the quantity of lead stored in the bone,
while folate seems to increases excretion more than it increases absorption.
INCREASING LEAD EXCRETION
For increasing lead excretion, two low toxicity B group vitamins have had widely
demonstrated impacts in animal studies: B1 (thiamine or thiamin), which specifically
increases excretion from the brain, and B9 (folate or folic acid); both are now compulsory
additives in non–organic bread inside Australia.
Vitamin B6 can increase lead excretion in animals,
= new reply since forum marked as read
