To the EditorThis paper highlights an impressive finding that polychlori-nated biphenyls (PCBs) exposures above background (0.9–1.5ppb)(Haase et al., 2009) may accelerate cognitive impairments inadults affecting memory, executive functioning and motorperformance. Although the results of several subtests of executivefunction and motor performance as reported are differentfrom those reported elsewhere with lower or higher PCBsexposure (e.g., Schantz and Widholm, 2001; Fitzgerald et al.,2008; Lin et al., 2008), it is important tohave this information thatincreased exposures to those toxins can affect cognitive decline inadults.This study used a set of 18 neuropsychological tests and founddeclines in logical and visual memoryafteradjustment forage andeducation. Further, the authors reported effects on other variablesby predicted extrapolation in Fig.1 with a threshold level of 2ppb.This analysis utilized several statistical analyses, using SPLINEregression models, LISREL methods, and factor analyses to revealeffects of PCBs exposure in Native Americans who had consumedwildlife and fish as well as contaminated crops for a long time. Bythese statistical analyses, tests on memory, dexterity of motorperformance, and motor steadiness, in both dominant and non-dominant side, were shown to be associated with exposure.However, in this study, age was considered as an effectmodifier in assessing a disproportionate cognitive deteriorationin addition to age-related expectations. Most researchers considerage as a confounder and adjust for age in the analysis. In thecontext of assessing several types of environmental toxicants(DDE, dieldrin, lead, mercury, PCBs, and derivates of PCDF, whichis more toxic to cognitive functioning), it seems inappropriate toconsider age a modifier modifying the complexity of pharmaco-kinetics and other factors in an epidemiological study. Thelipophilicity and long half-life of PCBs (around 7–8 years) givesthis toxin both a linear or non-liner decay (Tee et al., 2003), whichdepends partly on the body mass index (BMI) and is also related tothe lipid content of organs such as the brain. Investigations arealso needed on the associations between the cognitive assess-ments and PCB metabolites as well as concentrations in organs, inaddition to the covariates utilized in this study as well as theimpact of the aging process.We have examined the long-term consequences of PCBexposure in a population involved in the Yucheng incident ofPCBs exposure in 1979, with more than 2000 people in Taiwan. In316 elderly Taiwanese people (age X60 years) with heavyexposure to PCBs (3–732ng/g, mean 78.3) we found similarmemory deficits, but we did not find effects on motor andexecutive functioning (Lin et al., 2008) to this paper (Haase et al.,2009). It is acknowledged that memory domains are moresensitive to toxic exposures, in both epidemiological and animalstudies (Newman et al., 2006; Schantz et al., 2001). Motorperformance, relating to several cortical and sub-cortical regions,was not affected even by the heavy exposures in the Yuchengstudy, based on our studies, which is in contrast to the finding inthis study. These differences could result from difference inclinical assessment as well as in statistical analyses. The findingby Haase et al. (2009) is based upon statistical extrapolation,which is less persuasive than our findings of direct evidencewith Lin et al. (2008). It is advisable to have real data foranalysis rather than using a population without knowing thelongitudinal information on actual early exposures of toxicoki-netics over time.
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