Showing papers by "Duncan Thomas published in 1986"

The rare-disease assumption revisited. A critique of "estimators of relative risk for case-control studies".

Abstract: The extension of case-control methods to the study of common outcomes has led to the development of several design and analysis techniques which do not employ the rare-disease assumption. Unfortunately, the principles underlying valid application of these techniques are more subtle than those first considered by Cornfield in the rare-disease setting, and appear to be easily misunderstood. We especially wish to caution that: The unrestricted inclusion of prevalent cases in the control group (as described by Hogue et al. for estimation of the risk ratio) will not make the odds ratio an unbiased estimate of the risk ratio (or anything else). In their response to our article, following, Hogue et al. describe restrictions on prevalence and duration necessary for the odds ratio from a case-exposure design to unbiasedly estimate the risk ratio in a stable population; these conditions were not mentioned in their original article, and in their new paper Hogue et al. do not provide mathematical proof that the conditions are sufficient to guarantee unbiasedness. Exclusion ("decontamination") of incident cases from the control group (as recommended by Hogue et al. for testing and test-based interval estimation) will result in improperly narrow risk-ratio confidence intervals whether or not the population is stable, and, in unstable populations, will generally lead to an invalid test. Methods that replace the rare-disease assumption with the stable-population assumption (such as case-exposure designs applied to open populations) will not yield unbiased results when the source population is a fixed cohort. (Of course, this will not be an issue for methods that are not based on either assumption, such as the case-base design applied to fixed cohorts, and the matched density design.) As each case-control design has certain practical implications for selection and interviewing, in choosing a design one should carefully consider practical issues (such as vulnerability to recall bias and ease of control selection) in addition to the statistical issues discussed here. In general, however, one should be wary of methods of studying incidence that involve the use of prevalent cases (such as the approach of Hogue et al.): prevalence is influenced by factors related to treatment, recovery, and fatality, and thus any etiologic study employing prevalent cases may be biased by such factors.(ABSTRACT TRUNCATED AT 400 WORDS)

Contribution of metals to respiratory cancer.

Abstract: This paper reviews studies on the adverse health effects of exposure to metals, using arsenic and cadmium as examples. The carcinogenic potential of arsenic has been studied in various settings. Inhalation is clearly related to the development of lung cancer in (copper) smelting and arsenical pesticide manufacturing, and also in heavily exposed wine merchants who had an additional source of exposure by ingestion. Animal studies have shown cadmium to be a lung carcinogen, while a study by Thun et al. provides the best evidence to date that cadmium inhaled as CdO particles may be a human lung carcinogen. On the basis of this latter study, EPA estimates the risk due to cadmium at 1.8 X 10(-3) cases/micrograms/m3, which results in more than 100,000 excess lung cancers (lifetime). For arsenic, the risk estimate of 4.29 cases/1,000 micrograms/m3, based on epidemiologic data also results in more than 100,000 lung cancers (lifetime). This paper reviews the bases for these estimates and presents recommendations for further research. Lung cancer risks also exist for other metals such as nickel, chromium, and beryllium. Further study is required before a definitive conclusion can be reached about the significance and magnitude of environmental exposures to metals as a cause of lung cancer.

Contribution of radon and radon daughters to respiratory cancer.

Abstract: This article reviews studies on the contribution of radon and radon daughters to respiratory cancer and proposes recommendations for further research, particularly a national radon survey. The steady-state outdoor radon concentration averages 200 pCi/m3, and indoor levels are about 4 times higher. The primary source of radon in homes is the underlying soil; entry depends on multiple variables and reduced ventilation for energy conservation increases indoor radon levels. Occupational exposures are expressed in units of radon daughter potential energy concentration or working level (WL). Cumulative exposure is the product of the working level and the time exposed. The unit for cumulative exposure is the working level month (WLM). The occupational standard for radon exposure is 4 WLM/year, and 2 WLM/year has been suggested as a guideline for remedial action in homes. Epidemiologic studies show that miners with cumulative radon daughter exposures somewhat below 100 WLM have excess lung cancer mortality. Some 3% to 8% of miners studied have developed lung cancer attributable to radon daughters. All of the underground mining studies show an increased risk of lung cancer with radon daughter exposure. All cell types of lung cancer increased with radon exposure. If radon and smoking act in a multiplicative manner, then the risk for smokers could be 10 times that for nonsmokers. The potential risk of lung cancer appears to be between 1 and 2 per 10,000/WLM, which yields a significant number of lung cancers as some 220 million persons in the United States are exposed on average to 10 to 20 WLM/lifetime.