Faculty Bibliography

The literature is briefly summarized as to how several nutrients affect immune function, susceptibility to infection, and cancer susceptibility or progression. Nutritional deficiencies can impair immunity and so influence susceptibility to infectious agents, including ones that are common and relatively virulent in acquired immune deficiency syndrome (AIDS) patients. A variety of nutrients affect several of the immune functions that are defective in human immunodeficiency virus (HIV)-infected individuals. For example, beta-carotene increased the number of CD4+ cells; vitamin E decreased the number of CD8+ cells and increased the CD4+/CD8+ ratio; vitamin D decreased the CD4+/CD8+ ratio; and iron increased the number of peripheral lymphocytes in humans receiving supplementation. Furthermore, nutritional deficiencies can influence gastrointestinal function, while infectious diseases can influence nutrient requirements by altering the efficiency of absorption and the rate of tissue metabolism. Malnutrition, depressed serum zinc levels, and intestinal nutrient malabsorption have been found in AIDS patients. The above findings suggest that dietary manipulations might diminish the immune defects in HIV infection and enhance resistance to opportunistic infections. However, dietary alterations in immune defects are generally not well quantified and may be small relative to the magnitude of the defects observed in AIDS patients. Because conflicting or adverse effects have been reported for some nutrients, recommendations for dietary supplementation in HIV-infected individuals are premature and possibly hazardous. Further studies are much needed to relate dietary nutrient intakes to clinical outcomes

The various types of electromagnetic radiation differ considerably in their ability to induce cancer. The potential of radiofrequency or microwave radiation and low-frequency electromagnetic radiation to alter DNA is very limited, because their energy is too low to produce substantial ionizations. They are therefore unlikely to be carcinogenic by any direct mechanism. Epidemiologic studies of the carcinogenicity of microwave radiation are basically negative. Studies of workers with relatively high exposures to low-frequency electromagnetic fields have suggested that such persons may be at somewhat elevated risk for leukemia, especially of the acute myeloid type, but the studies have had methodologic weaknesses and mixed results. The association is not proven at this point, but neither can it be ruled out. For ionizing radiation, which is clearly carcinogenic, major questions pertain to how to define the magnitude of risk from low doses and low dose rates, how to identify subgroups of people who are especially susceptible to the effects of ionizing radiation, and how to minimize radiation exposure. When fortuitous radiation exposure from manmade sources, such as radioactive releases from nuclear power plants, are examined in the context of the total exposure people receive from natural sources, medical irradiation, etc., they are almost always found to be small by comparison. Quantitatively, two sources of radiation provide the greatest opportunities for exposure reduction: abatement of radon levels in homes, and reduction in medical radiation exposures

National statistics show that the burden of occupational foot problems is large. For example, over 20 per cent of work-related injuries occur in the lower extremities. However, to date few epidemiologic studies have been undertaken to document the nature, frequency, and causes of occupational foot problems. More are clearly needed. The results of such studies could profitably be disseminated among occupational health professionals to increase their awareness of this relatively neglected aspect of worker health

An industry-wide retrospective cohort mortality study was conducted on 6,152 chemical workers (2,460 exposed and 3,692 nonexposed) engaged in chloromethyl ether manufacture at 7 major U.S. companies between 1948 and 1980. A previous study at 6 companies from 1948 through 1972 reported excess respiratory cancer (RC) mortality and significant exposure-response relationships in exposed workers at 1 company (company 2). The present study, which extended follow-up of an additional 7 years for companies 1-6 and included company 7 for follow-up from 1953 through 1980, found excess RC mortality in exposed workers at company 2 [observed (Obs) = 32, standardized mortality ratio (SMR) = 430] and company 7 (Obs = 9, SMR = 603). External comparisons of RC mortality at both companies showed significant exposure-response relationships with respect to cumulative time-weighted exposure. At company 2, where the greatest number of RC deaths occurred, external comparisons showed that RC risk remained constant in relation to age at first exposure and decreased with increasing time since last exposure. With the use of Mantel-Haenszel and relative risk (RR) regression methods, internal comparisons at company 2 demonstrated significant findings of increasing RR with cumulative duration of exposure and cumulative time-weighted exposure and with decreasing time since last exposure. No association was found between RR and age at first exposure. An interesting finding was a significant negative interaction between cumulative time-weighted exposure and age at risk. The best-fitting logistic regression model for the exposed group predicted RR at 2.79 (95% confidence interval = 1.66-4.69) for workers with the mean cumulative exposure score of the 32 RC deaths (lagged by 6 yr) compared with those with negligible exposure (assuming mean age at risk of the RC deaths, 51 years old, and time since last exposure held constant). Qualitative assessment of the results suggests that chloromethyl ether exposure affects both an early as well as a late stage of a putative multistage respiratory malignant process.

Acute postpartum mastitis (APM) is an inflammatory-infectious condition of the breast, occurring commonly at childbirth or during lactation. A series of 601 women who received x-ray therapy for APM during the 1940's or 1950's have been followed up by mail questionnaire, with medical verification of pertinent conditions, to ascertain their incidences of breast cancer. Control subjects consisted of a series with APM who did not receive irradiation, plus the female siblings of both the APM groups, for a total of 1,239 controls. The groups have been followed up to 45 years; the average was 29 years. The relative risk (RR) for breast cancer, adjusted for age and interval since irradiation (or an equivalent entry definition for controls), was 3.2 for the irradiated breasts; the 90% confidence interval (CI) was 2.3-4.3. For a linear multiplicative model, the risk increased by 0.4% per rad (90% Cl of 0.2-0.7). The dose-response curve appeared to be essentially linear, except for a diminution of risk at high doses (greater than or equal to 700 rad). The fact that there were no treated breasts with doses between 0 and 60 rad, however, means that it was not possible to evaluate the curvature with the maximum contrast between low and high doses. The dose fractionation analyses showed that neither the number of dose fractions, the number of days between fractions, nor the dose per fraction had any apparent effect on breast cancer risk when the variables were analyzed separately. Similarly, when the fractionation variables were considered jointly in a Cox regression analysis, none was significant once total breast dose was controlled for. Analyses of age at irradiation did not show appreciable differences between age groups, although the numbers were too small to be clear-cut (only 64 women greater than 34 yr old at irradiation). Other studies have shown diminished risk associated with an older age at irradiation. The lack of diminished risk in this study may occur because during pregnancy and lactation the breasts are under increased proliferative stimulation by hormones, by comparison with the normal condition of breasts at older ages. An analysis of the temporal relationship of radiation to breast cancer showed that the RR did not vary systematically with interval since irradiation, but the absolute risk increased over time. This finding agrees with other studies that have also suggested a better fit for the multiplicative model