ABSTRACT
Aims: This study’s primary purpose was to determine whether earlier findings suggesting an association between sporadic Creutzfeldt-Jakob disease (sCJD), a transmissible spongiform encephalopathy of humans and specific dietary components could be replicated. The a priori hypotheses were that consumption of (i) foods likely to contain organ tissue and (ii) raw/rare meat are associated with increased sCJD risk. Study Design: Population-based case-control study. Place and Duration of Study: Department of Neurology, School of Medicine, Loma Linda University, Loma Linda, CA, USA; 4 years. Methodology: An 11-state case-control study of pathologically confirmed, definite sCJD cases, matched controls, and a sample of control-surrogates was conducted. Ninety-six percent (106/110) of the case data was obtained in 1991-1993, prior to variant CJD publicity. Results: Using control self-responses, consumption of hot dogs, sausage, pepperoni, kielbasa, "other" canned meat, poultry liver, any stomach/intestine, beef stomach/intestine, any organ tissue, and beef organ tissue was individually associated with increased sCJD risk; odds ratios (OR) ranged from 2.4 to 7.2 (0.003 <p<0.025). Rare/raw meat consumption was associated with sCJD (OR=2.0; p<0.05). Greater consumption of hot dogs, bologna, salami, sausage, pepperoni and kielbasa was associated with significantly higher risk. The OR for gizzard consumption was 7.6, p<0.04. Bologna, salami, any liver, beef liver and pork stomach/intestine were marginally associated with sCJD: ORs ranged from 1.7 to 3.7; 0.05 <p< 0.10. Brain consumption was not associated with an elevated risk. Analyses using control-surrogate data indicate that use of the control self-responses did not bias the results away from the null hypothesis. Conclusions: The a priori hypotheses were supported. Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.
ABSTRACT
Aims: To evaluate the hypothesis that sporadic Creutzfeldt-Jakob disease (sCJD) may be transmitted through ocular tonometry. Background: The infectious agent of sCJD may be present in the cornea prior to clinical symptoms. Cornea infectiousness has been documented by cornea transplants in guinea pigs and humans. sCJD is resistant to complete inactivity by conventional sterilization techniques. Thus contact tonometry equipment is not disinfected sufficiently to kill sCJD. We previously hypothesized that contact tonometry is a sCJD risk factor. Study Design: Population-based case-control study. Place and Duration of Study: Department of Neurology, School of Medicine, Loma Linda University, Loma Linda, CA, USA; 4 years. Methodology: An 11-state case-control study of pathologically confirmed definite sCJD cases, individually matched controls, and a sample of control surrogates was conducted. Ocular tonometry histories were obtained from case-surrogates, controls, and a sample of controlsurrogates. Results: The odds ratio (OR) for ever vs never having had an ocular tonometry test was statistically significant for matched and unmatched analyses for 15 through 3 years prior to disease onset, using both control self-responses and control surrogates: ORs were ∞ and 19.4 with 1-sided P-values <0.0001 and 0.003 and ORs=∞ and 11.1 with 1-sided P-values <0.003 and 0.02, respectively. ORs increased as the number of tonometry tests increased during this age period: trend test, 2-sided P-value < 0.0001. For ≥5 vs <5 tonometry tests, the OR was 5.8 (unmatched) and 3.7 (matched), 2-sided P-value<0.00005. Respondents generally could not specify the type of tonometry. There was no indication of increased tonometry testing among cases within 2 years of disease onset. Conclusions: The a priori hypothesis was supported. Contact tonometry, preferred by ophthalmologists, may be capable of transmitting sCJD. Consideration should be given to using disposable instrument covers after each use. The use the disposable covers or non-contact tonometry is preferable in the absence of effective disinfectant processes at this time.
ABSTRACT
Aims: This report is the first study of the possible relationship between extremely low frequency (50-60 Hz, ELF) magnetic field (MF) exposure and severe cognitive dysfunction. Earlier studies investigated the relationships between MF occupational exposure and Alzheimer’s disease (AD) or dementia. These studies had mixed results, depending upon whether the diagnosis of AD or dementia was performed by experts and upon the methodology used to classify MF exposure. Study Design: Population-based case-control. Place and Duration of Study: Neurology and Preventive Medicine, Keck School of Medicine, University of Southern California, 2 years. Methodology: The study population consisted of 3050 Mexican Americans, aged 65+, enrolled in Phase 1 of the Hispanic Established Population for the Epidemiologic Study of the Elderly (H-EPESE) study. Mini-Mental State Exam (MMSE) results, primary occupational history, and other data were collected. Severe cognitive dysfunction was defined as an MMSE score below 10. The MF exposure methodology developed and used in earlier studies was used. Results: Univariate odds ratios (OR) were 3.4 (P< .03; 95% CI: 1.3-8.9) for high and 1.7 (P=.27; 95% CI: 0.7-4.1) for medium or high (M/H) MF occupations. In multivariate main effects models, the results were similar. When interaction terms were allowed in the models, the interactions between M/H or high occupational MF exposure and smoking history or age group were statistically significant, depending upon whether two (65-74, 75+) or three (65-74, 75-84, 85+) age groups were considered, respectively. When the analyses were limited to subjects aged 75+, the interactions between M/H or high MF occupations and a positive smoking history were statistically significant. Conclusion: The results of this study indicate that working in an occupation with high or M/H MF exposure may increase the risk of severe cognitive dysfunction. Smoking and older age may increase the deleterious effect of MF exposure.