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Based on earlier work by several groups, in 1989 Selkoe and colleagues [1,2] suggested that amyloid beta (A beta) found in cerebral blood vessels, skin tissue, and elsewhere might come from a peripheral source and might contribute to the Alzheimer's disease (AD) pathogenesis. Independently, using four clinical series and four different types of controls, Sobel et al. [3,4] found that having a primary occupation likely to have resulted in medium-to-high extremely low frequency (ELF) electromagnetic field (EMF) exposure significantly increases the risk of AD. The means by which EMF (or any other) exposure might precipitate the Alzheimer pathogenesis are currently unknown. One possibility is that EMF exposure might affect the peripheral or neuronal processing of the amyloid precursor protein. We outlined a cascade of events as a hypothesis of how EMF exposure may be associated with AD onset.
Epidemiologic findings: Workers with primary occupations likely to have resulted in medium-to-high ELF EMF exposure are at increased risk of AD.
In two published papers, Sobel et al. [3,4] found elevated risk of AD associated with having a primary occupation likely to have resulted in medium-to-high EMF exposure. The four clinical series examined were widely separated by time or distance and the data were collected without any consideration of EMF exposure.
(Table 1) provides information about patients and control subjects and the ascertainment period for each series. The total number of AD patients in the four series was 713 and the total number of control subjects was 627. Surrogate-derived data were used for all patients and for control subjects from Finnish Series 1 and the Rancho Los Amigos Medical Center (RLAMC), Los Angeles, series because these subjects were demented. Following standard practice, we defined high EMF exposure as averaging above 10 milligauss (mG) or often above 100 mG and medium EMF exposure as averaging between 2 and 10 mG or often above 10 mG. We classified all other EMF exposures as low. The …
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