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

Possible modes of transmission of Creutzfeldt-Jakob disease.

Creutzfeldt-Jakob disease (CJD) and kuru are subacute transmissible dementing encephalopathies characterized by spongiform changes in the brain. Scrapie is a similar slow viral encephalopathy which af

Transmissible virus dementia: evaluation of a zoonotic hypothesis.

Multiple Sclerosis in Italy

Multiple sclerosis (MS) appears to be more common in technically advanced countries than in underdeveloped regions and migration from one area to an-other at a young age affects the risk of acquiring MS. One way of explaining both the peculiar frequency distribution and the effect of migration while young is to postulate that an infection early in life decreases the chance of central demyelination. However, no specific infection has been implicated consistently. Alternatively, an aberrant host response to infection in childhood might induce central demyelination. Thus, the aberrant host response could be age-dependent. In seeking associations between age of infection and risk of MS, we observed a direct relationship: where childhood diseases were acquired early in life, the frequency of MS in that population was low; where childhood diseases tended to occur nearer adolescence, MS frequency in that population was high. Since immune responsiveness to antigenic challenges matures through early adolescence, we reason that early infection might be protective and delay in acquiring childhood infections might increase the risk of developing MS. Indeed, in experimental models, the chance of inducing chronic relapsing central demyelination is increased by using adolescent rather than newborn or mature animals. In this paper, epidemiologic evidence showing the strong association between age of infection and risk of MS is presented.

Zoreh Davanipour

Papers

Possible modes of transmission of Creutzfeldt-Jakob disease.

Transmissible virus dementia: evaluation of a zoonotic hypothesis.

Multiple Sclerosis in Italy

Does delay in acquiring childhood infection increase risk of multiple sclerosis

Creutzfeldt-Jakob Disease