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R C Clelland

Publications and source records attributed to R C Clelland.

At least 19 recordsLinked to original sources
PubMed1983

Radiation hormesis, public health, and public policy: a commentary.

Public policy affecting public health regarding effects of low-level ionizing radiations has been, and is being, determined by effects estimates based on linear or other monotonic extrapolation from high-level radiation dose-response data to presumed ecologically realistic low-level exposure effects. Such predictive, unmeasured estimates are very possibly in serious error; they are incompatible with observed low-level dose-response data that indicate a negative correlation between low-level radiation data and health effects, such as cancer mortality rates. Observed negative correlations with low-level radiation data are to be expected on the basis of evidence supporting the validity of the hormesis phenomenon. Hormesis theory, derived in part from evolutionary biology, asserts that while high levels of exposure to an agent such as ionizing radiation are indeed hazardous, ecologically realistic low levels can be stimulatory and largely beneficial. Stimulation of activities of DNA and other repair mechanisms may be involved. Although evidence of the reality of radiation hormesis has been reported in about 1000 scientific publications over the last century, this effect has been largely unrecognized. Moreover, this widespread non-acceptance of hormesis as a real-world phenomenon is usually but not always present in the case of chemical hormesis; the oversight appears systematic. The ignoring of the hormesis phenomenon seems to constitute a very serious error in modern biomedical science and in preventive medicine. A mathematical model is offered that describes the general shape of certain dose-response functions when radiation hormesis at low-level exposure is taken into consideration along with the well-known detrimental effects of high-level radiation.

Background Radiation↗
PubMed1980

Epidemiological studies of chronic disease: maladjustment of observed mortality rates.

Age adjustment of observed mortality and morbidity rates is not a substitute for age-specific analysis. Measures of association between potential causal factors and adjusted mortality rates are functions of the particular adjustment procedure and the choice of reference population. We exhibit here the wide variation in simple correlation statistics that occurs with eight adjustment methods and three reference populations. We then generalize these results to the multivariate situation showing an example in which there is coherent structure for the associations between predictors and mortality. This is contrasted with another example in which no such meaningful pattern exists. Studies are cited that could have been improved by greater attention to the underlying structure of age-adjusted rates. Age adjustment of total observed rates yields meaningless numbers that are useful for comparative purposes only. Total observed rates have substantive meaning but provide useful etiological clues primarily when supported by analyses of appropriate age-specific data.

Adolescent↗
PubMed1979

Essential hormones as carcinogenic hazards.

Recently, the Occupational Safety and Health Administration (OSHA) proposed regulations regarding lists of environmental substances that allegedly pose potential occupational carcinogenic risk. Known carcinogens such as bis(chloromethyl) ether, along with natural substances such as estradiol, estriol, estrone, progesterone, tannic acid, maltose, and lactose, were included in the general OSHA list. Clear distinction between true hazards and essential endogenously formed biochemicals was not made. A major reappraisal of the OSHA list is essential. The revised document should indicate the conditions under which various classes of substances constitute human health hazards -- including dosage levels and routes of entry.

Animals↗
PubMed1978

Maternal smoking, birth weight, infant death, and the self-selection problem.

Several aspects of the relationship between maternal smoking and birth weights of infants are discussed. No satisfactory explanation for Yerushalmy's results has been given other than that low birth weight appears to relate more to the smoker than to the smoking. Recent studies by Silverman support this position. The possibility that nicotine may induce a physiologic response that serves to alleviate bioenergetic deficiency in some individuals should not be overlooked. In this view, both smoking and low birth weight are symptoms of deficient maternal bioenergetic systems.

Birth Weight↗