mixed evidence of a relationship between environmental lead exposure, as judged by current BLL, and impaired cognitive performance in adults. However, when bone lead was used as the measure of lead dose, the Normative Aging Study found significant associations with impaired neurocognitive performance. Bone lead measurements capture both long-term cumulative exposure and past high lead exposure, which may be more important than current BLL.

In contrast, EPA noted that occupational lead exposure measured by BLL, CBLI, and bone lead was associated with decreased cognitive and psychomotor performance, diminished peripheral sensory nerve function, slowing in visual evoked potentials and brainstem auditory evoked potentials, and abnormalities in postural sway. Evidence in support of EPA’s conclusion included onset of diminished cognitive function and diminished psychomotor speed at a BLL of 18 μg/dL (Schwarz et al. 2001). However, in some studies, it was not the current BLL (under 30 μg/dL) but the measures of CBLI or bone lead concentration that were associated with poorer neurobehavioral performance (Lindgren et al. 1996; Bleecker et al. 1997; Hänninen et al. 1998; Bleecker et al. 2005a). The same relationship was found for peripheral sensory nerve studies most commonly associated with CBLI (Chia et 1996a,b; Kovala et al. 1997; Yokoyama et al. 1998). Changes in sensory nerve function occurred at BLLs of 28-30 μg/dL (Chuang et al. 2000; Bleecker et al. 2005b). Visual evoked potentials, measuring speed of conduction in the optic nerves, were prolonged beginning at BLLs of 17-20 μg/dL (Abbate et al. 1995). Slowed brainstem auditory evoked potentials were found to be associated with CBLI or weighted average BLL (Discalzi et al. 1992, 1993, Bleecker et al. 2003). A calculated benchmark dose for postural sway (measure of balance) was a current BLL of 14 μg/dL (Iwata et al. 2005).

EPA identified a few publications that reported an increased risk of amyotrophic lateral sclerosis (ALS) and motor neuron disease associated with past occupational lead exposure (Roelofs-Iverson et al. 1984; Armon et al. 1991; Gunnarsson et al. 1992; Chancellor et al. 1993; Kamel et al. 2002). The presence of the delta-aminolevulinic acid dehydratase (ALAD) 2 allele (ALAD2) increased that risk (odds ratio [OR] = 1.9; 95% confidence interval [CI]: 0.60, 6.3) (Kamel et al. 2003). Essential tremor, another neurodegenerative disorder, was associated with low concurrent BLL (3 μg/dL) caused by exposure to environmental lead (Louis et al. 2003), but there was no information about past exposures, which might have been higher. The presence of the ALAD2 allele increased the odds of essential tremor by a factor of 30 compared with subjects that had only the ALAD1 allele (Louis et al. 2005).

Environmental Protection Agency 2012 Integrated Science Assessment for Lead (Second External Review Draft)

Neurobehavioral and Mood Effects

EPA (2012) reviewed epidemiologic evidence of associations between environmental lead exposure and neurobehavioral outcomes primarily from two



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