IN 1974, the International Radiation Protection Association (IRPA) formed a working group on non-ionizing radiation (NIR), which examined the problems arising in the field of protection against the various types of NIR. At the IRPA Congress in Paris in 1977, this working group became the International Non-Ionizing Radiation Committee (INIRC). In cooperation with the Environmental Health Division of the World Health Organization (WHO), the IRPA/INIRC developed a number of health criteria documents on NIR as part of WHO’s Environmental Health Criteria Programme, sponsored by the United Nations Environment Programme (UNEP). Each document includes an overview of the physical characteristics, measurement and instrumentation, sources, and applications of NIR, a thorough review of the literature on biological effects, and an evaluation of the health risks of exposure to NIR. These health criteria have provided the scientific database for the subsequent development of exposure limits and codes of practice relating to NIR. At the Eighth International Congress of the IRPA (Montreal, 18–22 May 1992), a new, independent scientific organization—the International Commission on Non-Ionizing Radiation Protection (ICNIRP)—was established as a successor to the IRPA/INIRC. The functions of the Commission are to investigate the hazards that may be associated with the different forms of NIR, develop international guidelines on NIR exposure limits, and deal with all aspects of NIR protection. Biological effects reported as resulting from exposure to static and extremely-low-frequency (ELF) electric and magnetic fields have been reviewed by UNEP/ WHO/IRPA (1984, 1987). Those publications and a number of others, including UNEP/WHO/IRPA (1993) and Allen et al. (1991), provided the scientific rationale for these guidelines. A glossary of terms appears in the Appendix.

Guidelines for limiting exposure to time-varying electric, magnetic, and electromagnetic fields (up to 300 GHz)

Objective. —To examine more closely the association between apolipoprotein E (APOE) genotype and Alzheimer disease (AD) by age and sex in populations of various ethnic and racial denominations. Data Sources. —Forty research teams contributed data onAPOEgenotype, sex, age at disease onset, and ethnic background for 5930 patients who met criteria for probable or definite AD and 8607 controls without dementia who were recruited from clinical, community, and brain bank sources. Main Outcome Measures. —Odds ratios (ORs) and 95% confidence intervals (Cls) for AD, adjusted for age and study and stratified by major ethnic group (Caucasian, African American, Hispanic, and Japanese) and source, were computed forAPOEgenotypes ∈2/∈2,∈2/∈3,∈2/∈4,∈3/∈4 and ∈4/∈4 relative to the ∈3/∈3 group. The influence of age and sex on the OR for each genotype was assessed using logistic regression procedures. Results. —Among Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for people with genotypes ∈2/∈4 (OR=2.6, 95% Cl=1.6-4.0), ∈3/∈4 (OR=3.2, 95% Cl=2.8-3.8), and ∈4/∈4 (OR=14.9, 95% CI=10.8-20.6); whereas, the ORs were decreased for people with genotypes ∈2/∈2 (OR=0.6, 95% Cl=0.2-2.0) and ∈2/∈3 (OR=0.6, 95% Cl=0.5-0.8). TheAPOE∈4-AD association was weaker among African Americans and Hispanics, but there was significant heterogeneity in ORs among studies of African Americans (P Conclusions. —TheAPOE∈4 allele represents a major risk factor for AD in all ethnic groups studied, across all ages between 40 and 90 years, and in both men and women. The association betweenAPOE∈4 and AD in African Americans requires clarification, and the attenuated effect ofAPOE∈4 in Hispanics should be investigated further.

https://jamanetwork.com/journals/jama/articlepdf/418446/jama_278_16_041.pdf

Effects of Age, Sex, and Ethnicity on the Association Between Apolipoprotein E Genotype and Alzheimer Disease: A Meta-analysis

Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6105 individuals with previous stroke or transient ischaemic attack

Objective To estimate the current incidence and prevalence in the United States of 12 neurologic disorders. Methods We summarize the strongest evidence available, using data from the United States or from other developed countries when US data were insufficient. Results For some disorders, prevalence is a better descriptor of impact; for others, incidence is preferable. Per 1,000 children, estimated prevalence was 5.8 for autism spectrum disorder and 2.4 for cerebral palsy; for Tourette syndrome, the data were insufficient. In the general population, per 1,000, the 1-year prevalence for migraine was 121, 7.1 for epilepsy, and 0.9 for multiple sclerosis. Among the elderly, the prevalence of Alzheimer disease was 67 and that of Parkinson disease was 9.5. For diseases best described by annual incidence per 100,000, the rate for stroke was 183, 101 for major traumatic brain injury, 4.5 for spinal cord injury, and 1.6 for ALS. Conclusions Using the best available data, our survey of a limited number of disorders shows that the burden of neurologic illness affects many millions of people in the United States.

How common are the “common” neurologic disorders?

Summary The uneven distribution of multiple sclerosis (MS) across populations can be attributed to differences in genes and the environment and their interaction. Prevalence and incidence surveys could be affected by inaccuracy of diagnosis and ascertainment, and prevalence also depends on survival. These sources of error might play a part in the geographical and temporal variations. Our literature search and meta-regression analyses indicated an almost universal increase in prevalence and incidence of MS over time; they challenge the well accepted theory of a latitudinal gradient of incidence of MS in Europe and North America, while this gradient is still apparent for Australia and New Zealand; and suggest a general, although not ubiquitous, increase in incidence of MS in females. The latter observation should prompt epidemiological studies to focus on changes in lifestyle in females. New insights into gene–environment and gene–gene interactions complicate interpretations of demographic epidemiology and have made obsolete the idea of simple causative associations between genes or the environment and MS.

The Changing Demographic Pattern of Multiple Sclerosis Epidemiology

The authors present analyses of data from three independent clinical series and controls indicating an association between working in occupations with probable medium to high exposure to extremely low frequency ( 10 mG intermittently) to high (> 10 mG or > 100 mG intermittently) exposed cases were seamstress, dressmaker, and tailor. The results appear to be independent of education, and the sex-combined odds ratios for the three series are quite homogeneous: 2.9, 3.1, and 3.0. The odds ratio for the three series analyzed together is 3.0 (p < 0.001), with a 95% confidence interval of 1.6-5.4. The odds ratio for women is 3.8 (p < 0.001), with a 95% confidence interval of 1.7-8.6. The most obvious, possibly etiologically relevant exposure is that of electromagnetic fields, which may have biologic plausibility because they may adversely influence calcium homeostasis and/or inappropriately activate immune system cells such as microglial cells, initiating events that result in neuronal degeneration.

Occupations with Exposure to Electromagnetic Fields: A Possible Risk Factor for Alzheimer's Disease

No association between Alzheimer's disease (AD) and apolipoprotein E type epsilon 4 (ApoE epsilon 4) phenotype was found among centenarians in Finland (N = 179). The data are based on ascertainment of all centenarians in Finland in 1991. All examinations were conducted during 1991. The diagnoses of dementia and AD were based on clinical grounds, conforming to DSM-III-R and NINCDS-ADRDA criteria. The percentage of ApoE epsilon 4 alleles among the centenarians was 8.7% (31 of 358 alleles). This is significantly lower than percentages found in younger Finnish populations. Thirty (16.8%) of the 179 centenarians were epsilon 4 allele carriers. One hundred fifty-one (84.4%) of the centenarians were women. Twenty-eight (18.5%) of the women had at least one epsilon 4 allele, as did two (7.1%) of the men. The prevalence of clinically diagnosed AD was 26.8%; 44% of the subjects were cognitively normal, 23% had signs of cognitive decline or at most mild dementia (with no differential diagnosis), and 6% had a dementia clinically diagnosed as being due to some cause other than AD. For AD cases versus cognitively normal subjects, the odds ratio associated with being a carrier of the epsilon 4 allele was 1.34 (p = 0.64; 95% CI = [0.5, 3.3]). Among women, the odds ratio was 0.99 (p = 1.0; 95% CI = [0.4, 2.6]). There were fewer, but not significantly so, epsilon 4 carriers among subjects with cognitive decline or at most mild dementia (12.2%) than there were among the cognitively normal subjects (16.5%). The AD patients had no evidence of difficulty standing on a flat stationary surface unless the surface suddenly moved.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of association of apolipoprotein E allele ϵ4 with late‐onset Alzheimer's disease among Finnish centenarians

We investigated the seasonal pattern of stroke using the Lehigh Valley Stroke Register. This register includes all patients hospitalized with stroke or transient ischemic attack (TIA) from among the 600,000 Lehigh Valley residents. Meterological data were obtained from the National Oceanic and Atmospheric Administration. The study, which uses 18 months of data, included 1,944 cases. Using single harmonic regression analysis, the seasonal pattern of TIA and infarction, but not hemorrhage, fit a sine-cosine wavefunction with a 12-month period (R2 = 41% and 36%, respectively). For infarction, the strongest seasonal pattern was exhibited for women of all ages and for both sexes in the age groups 65-74 and 75-84, but only the sine component was significant. The peak months for TIA were June-August, while the peak months for infarcts were February-April. Correlations between ambient temperature and each type of stroke were computed. A significant positive correlation for TIA was found (r = 0.57, p = 0.01). After adjusting for a 2-month lag between the low for infarction and the peak for temperature, a significant negative correlation was found (r = -0.64, p = 0.01). No significant correlation was found for hemorrhage. Possible reasons for the opposite relations of TIA and infarct are discussed.

Stroke in the Lehigh Valley: seasonal variation in incidence rates.

To explore possible risk factors in the past medical history of patients with Creutzfeldt-Jakob disease (CJD), we conducted a case-control study among 26 cases and 40 matched controls. Statistically significant odds ratios were obtained for intraocular pressure testing; injury to or surgery on the head, face, or neck; and trauma to other parts of the body. The odds ratios were nearly significant for head trauma and procedures requiring sutures. These data suggest that the CJD agent may be acquired by inoculation through injury or during surgery, and perhaps on certain absorbable sutures of animal origin. The tonometer used for glaucoma testing may also be a vehicle of transmission.

Creutzfeldt‐Jakob disease: Possible medical risk factors

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.

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 …

Zoreh Davanipour

Papers

Occupations with Exposure to Electromagnetic Fields: A Possible Risk Factor for Alzheimer's Disease

Lack of association of apolipoprotein E allele ϵ4 with late‐onset Alzheimer's disease among Finnish centenarians

Stroke in the Lehigh Valley: seasonal variation in incidence rates.

Creutzfeldt‐Jakob disease: Possible medical risk factors

Electromagnetic field exposure may cause increased production of amyloid beta and eventually lead to Alzheimer's disease