Neurology -- Correspondence for Bleecker et al., 69 (5) 470-476

Correspondence published:

Impact of cognitive reserve on the relationship of lead exposure and neurobehavioral performance: Inka Milewski (18 October 2007)

Reply from the authors: Margit L. Bleecker, MD, PhD, D. Patrick Ford, MD, MPH (18 October 2007)

Impact of cognitive reserve on the relationship of lead exposure and neurobehavioral performance 18 October 2007

Inka Milewski,
Conservation Council of New Brunswick
180 St. John Street, Fredericton, New Brunswick, E3B 4A9, Canada
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Re: Impact of cognitive reserve on the relationship of lead exposure and neurobehavioral performance

milewski{at}nbnet.nb.ca Inka Milewski

Bleecker et al conclude that lead smelter workers with lower cognitive reserves (CR) were more susceptible to the effects of lead on cognitive performance tests than workers with higher CR. [1] The authors do not mention why some workers had a lower CR.
One hypothesis is that some workers—as children—may have been exposed disproportionately to high levels of lead. Antenatal and postnatal exposure to environmental lead has been shown to result in cognitive deficits that persist into later childhood and adulthood. [2,3]
The smelter’s work force was drawn from the community (Belledune, New Brunswick) where the smelter was located and from surrounding communities. [Personal communications with retired smelter workers] Many smelter workers were children or not yet born when the smelter began operating (1966). The smelter was built less than one kilometer from the school and church. Dust testing in 1968 by investigators with the Department of National Health and Welfare, Occupational Health Division showed lead levels were 2000 ppm in the school and 5200 ppm in the playground. [4] Lead discharges to the atmosphere were 2.2 mt per day. [4] In 1972, the school was moved 6 km upwind of the smelter and, in 1975, emissions dropped to 0.5 mt per day.
Early childhood exposure to lead and other factors could help to explain why some workers had a lower CR than others. Regardless of the cause, the findings of this study suggest that individuals with low CR continue to be vulnerable as adults to the effects of further lead exposure.
References
1. Bleecker ML, Ford DP, Celio MA, Vaughn, CG, Lindgren KN. Impact of cognitive reserve on the relationship of lead exposure and neurobehavioral performance. Neurology 2007;69:470-476.
2. Tong S, Baghurst P, McMichael A, Sawyer M, Mudge J. Lifetime exposure to environmental lead and children’s intelligence at 11-13 years: the Port Pirie cohort study. British Medical Journal 1996;312:1569-1575.
3. Stokes L, Letz R, Gerr F, et al. Neurotoxicity in young adults 20 years after childhood exposure to lead: the Bunker Hill experience. Occupational and Environmental Medicine 1998;55:507-516.
4. Ross CR, deVilliers AJ, Monkman JL. Investigation of the lead hazards at East Coast Smelting and Chemical Company Limited, Belledune, N.B. Report of the Department of National Health and Welfare, Occupational Health Division.1968; 9 pages plus test results and figures.
Disclosure: Inka Milewski is the Science Advisor for the Conservation Council of New Brunswick and author of the 2006 report, Dying for Development: The legacy of lead in Belledune.

Reply from the authors 18 October 2007

Margit L. Bleecker, MD, PhD,
Center for Occupational and Environmental Neurology
2 Hamill Road, Suite 225, Baltimore, MD 21210-1815,
D. Patrick Ford, MD, MPH
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Re: Reply from the authors

coen{at}msn.com Margit L. Bleecker, MD, PhD, et al.

We thank the author for commenting on our recent article. [1] It is possible that low cognitive reserve (CR) in our study participants may have been the persistence of cognitive deficits acquired from antenatal and postnatal lead exposure.
Unfortunately, the additional environmental data provided does not help us test that hypothesis. Without personal lead exposure data for each participant during that period, the only thing we can conclude is that during the years 1966-1975 residents of Belledune living in the vicinity of the smelter were more likely to have higher environmental lead exposure than either before or after that period. We can offer two types of indirect evidence which suggest that childhood lead poisoning was not a cause of the cognitive deficits in our participants with low CR.
Since peak susceptibility to childhood lead poisoning occurs from birth to four years, we identified all study participants born during 1962 through 1975 (i.e., those who were at peak age susceptibility to lead toxic effects during the period when environmental lead exposure was most likely to be at its highest). We found no significant difference between their mean Wide-Range Achievement Test – reading (WRAT) score and that of the remaining participants. The lack of difference persisted when we used more stringent criteria for the period of childhood susceptibility and under multi-variable analyses controlling for our covariates and exposure measure.
In addition, only three percent of the 112 workers were born in Belledune and by the time of the study that had only increased to 11 percent. Moreover, all of the workers born in Belledune were hired as adults when the smelter began operating in 1966.
Finally, blood lead levels obtained at the time of hire (pre-exposure) were comparable in both the loCR and hiCR groups. While our evidence is only indirect it may argue against childhood lead poisoning as the cause of low CR.
Disclosure: The authors report no conflicts of interest.