Lead, neurobehavioral impairment

Several studies have reported no association between neurobehavioral impairment and low levels of lead exposure. Cooney et al. (1989a) reported that PbB levels of approximately 10 pg/dL had little or no effect on neurobehavioral development at age 4. Harvey et al. (1988) concluded that the effects of lead (mean PbB, 13 pg/dL) were small and generally not significant. Likewise, Emhart et al. (1988), Lansdown et al. (1986), and Pocock et al. (1989) found no effect of lead on intelligence. 

Although most of the early reports of lead concentrations in humans were limited to individuals suffering from acute lead toxicity, there have been studies within the past several decades that have focused on defining the sublethal effects of lead toxicity. A notable series of studies by Needle-man and others have demonstrated neurobehavioral impairment in children... 

The main toxic effect of lead in males and females is impairment of neurobehavioral test performance. Available evidence indicates that the LOAEL for long-term exposed subjects should be around 400 tg L (Scientific Committee 2000). 

Blood lead levels are less than 5 mcg/dL in populations without occupational or specific environmental exposure. Levels between 5 (or lower) and 25 mcg/dL have been associated with subtle decreases in intelligence and impaired neurobehavioral development in children exposed in utero or in early childhood, but these levels are generally without demonstrable effects in adults. 

Council Directive 98/24/EC of 1998. The SCOEL recommends a BLL of 30 tig/dL to prevent adverse neurobehavioral effects and signs of male reproductive toxicity that occur at BLLs of 40 pg/dL and higher. The SCOEL could not identify a threshold for impairment of cognitive development in newborns and infants and indicated that exposure of fertile women to lead should. .. be minimised (SCOEL 2002, p. 13). 

In addition to providing advanced measures of both the lead dose and the toxic response portions of dose—neural response relationships, these prospective approaches helped to resolve interpretive questions not answered in earlier cross-sectional studies. For example, the inherent stability of the exposure measure is more discernible and quantifiable with serial measures of PbB or combined measures of blood and bone than isolated PbB measures done concurrently. One can also employ different statistical expressions of the exposure metric, e.g., average PbB, peak PbB, concurrent PbB, or lifetime integrated expression of exposure to estimate relative robustness of dose—response. Second, the potential confounding of dose—response relationships by any reverse causality is more reliably addressed. Reverse causality would hold that the dose term is elevated because of the higher likelihood of Pb exposures due to existing impairment of neurobehavioral function in other words, PbB levels rise with a higher frequency of abnormal hand-mouth activity because of neurobehaviors unrelated to Pb exposures. 

Inhalation, ingestion. Acute poisoning leads to acute encphalopathy, renal failure and severe GI distress. Chronic poisoning leads to central nervous system problems, impaired neurobehavioral function, diminished gross and line motor development in children, kidney disease, hypertension, anemia, and other hematologic effects. 

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