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That research was discussed at a major conference on low-level lead toxicity convened by U.S. EPA and NIEHS in North Carolina in October 1973 and subsequently published in Environmental Health Perspectives (Low-Level Lead Toxicity 1974).
Low-level lead toxicity is not confined to childhood.
We found that the impact of low-level lead toxicity varied by race and ethnicity.
Research in the centers has made important contributions to understanding of the environmental causes of asthma, neurobehavioral disorders, endocrine dysfunction, autism and low-level lead toxicity.
We also found that, for about one in six children, failure in reading or math is attributable to low-level lead toxicity.
Although it is noteworthy that toxicity levels of lead and copper in G. obscurus DSM 43160T by comparison with the results displayed by Gtari et al. [ 11] were much different from each other.
Lead concentrations were far below the toxicity levels observed in PBMC at concentrations above 500 μM [ 81].
In addition, this study suggests that measurement of urinary lead might be useful as a proxy for plasma lead levels in studies of lead toxicity.
Although this finding conflicts with the widely held belief that 2-year (or peak) blood lead levels are the most salient measure of lead toxicity, there is increasing evidence that lifetime mean blood lead and concurrent blood lead levels are stronger predictors of IQ in older children (Baghurst et al. 1992; Canfield et al. 2003; Dietrich et al. 1993; Factor-Litvak et al. 1999).
Wu et al. (2003) postulated that lead toxicity became apparent at a lower exposure level for Msp-2 carriers than for Msp 1-1 persons.
Implicit in the log-lead specification is that change in health effect with change in BPb at higher levels is small, save when lead toxicity associated with pathologic organ damage is reached.
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