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Biomedical subjects

E P Radford

Publications and source records attributed to E P Radford.

At least 19 recordsLinked to original sources
PubMed1997

Estimating lung cancer mortality from residential radon using data for low exposures of miners.

Some recent estimates of lung cancer risk from exposure to radon progeny in homes have been based on models developed from a pooled analysis of 11 cohorts of underground miners exposed to radon. While some miners were exposed to over 10,000 working level months (WLM), mean exposure among exposed miners was 162 WLM, about 10 times the exposure from lifetime residence in an average house and about three times the exposure from lifetime residence at the "action level" suggested by the U.S. Environmental Protection Agency. The extrapolation of lung cancer risk from the higher exposures in the miners to the generally lower exposures in the home is a substantial source of uncertainty in the assessment of the risk of indoor radon. Using the pooled data for the miners, analyses of lung cancer risk were carried out on data restricted to lower exposures, either <50 WLM or <100 WLM. In the pooled data, there were 115 lung cancer cases among workers with no occupational WLM exposure and 2,674 among exposed miners, with 353 and 562 lung cancer cases in miners with <50 WLM and <100 WLM, respectively. Relative risks (RRs) for categories of WLM based on deciles exhibited a statistically significant increasing trend with exposure in each of the restricted data sets. In the restricted data, there was little evidence of departures from a linear excess relative risk model in cumulative exposure, although power to assess alternative exposure-response trends was limited. The general patterns of declining excess RR per WLM with attained age, time since exposure and exposure rate seen in the unrestricted data were similar to the patterns found in the restricted data. Risk models based on the unrestricted data for miners provided an excellent fit to the restricted data, suggesting substantial internal validity in the projection of risk from miners with high exposures to those with low exposures. Estimates of attributable risk for lung cancer (10-14%) in the U.S. from residential radon based on models from the unrestricted data were similar to estimates based on the data for miners receiving low exposures.

Air Pollutants, Radioactive↗
PubMed1995

Lung cancer in radon-exposed miners and estimation of risk from indoor exposure.

BACKGROUND: Radioactive radon is an inert gas that can migrate from soils and rocks and accumulate in enclosed areas, such as homes and underground mines. Studies of miners show that exposure to radon decay products causes lung cancer. Consequently, it is of public health interest to estimate accurately the consequences of daily, low-level exposure in homes to this known carcinogen. Epidemiologic studies of residential radon exposure are burdened by an inability to estimate exposure accurately, low total exposure, and subsequent small excess risks. As a result, the studies have been inconclusive to date. Estimates of the hazard posed by residential radon have been based on analyses of data on miners, with recent estimates based on a pooling of four occupational cohort studies of miners, including 360 lung cancer deaths. PURPOSE: To more fully describe the lung cancer risk in radon-exposed miners, we pooled original data from 11 studies of radon-exposed underground miners, conducted a comprehensive analysis, and developed models for estimating radon-associated lung cancer risk. METHODS: We pooled original data from 11 cohort studies of radon-exposed underground miners, including 65,000 men and more than 2700 lung cancer deaths, and fit various relative risk (RR) regression models. RESULTS: The RR relationship for cumulative radon progeny exposure was consistently linear in the range of miner exposures, suggesting that exposures at lower levels, such as in homes, would carry some risk. The exposure-response trend for never-smokers was threefold the trend for smokers, indicating a greater RR for exposure in never-smokers. The RR from exposure diminished with time since the exposure occurred. For equal total exposure, exposures of long duration (and low rate) were more harmful than exposures of short duration (and high rate). CONCLUSIONS: In the miners, about 40% of all lung cancer deaths may be due to radon progeny exposure, 70% of lung cancer deaths in never-smokers, and 39% of lung cancer deaths in smokers. In the United States, 10% of all lung cancer deaths might be due to indoor radon exposure, 11% of lung cancer deaths in smokers, and 30% of lung cancer deaths in never-smokers. This risk model estimates that reducing radon in all homes exceeding the U. S. Environmental Protection Agency's recommended action level may reduce lung cancer deaths about 2%-4%. These estimates should be interpreted with caution, because concomitant exposures of miners to agents such as arsenic or diesel exhaust may modify the radon effect and, when considered together with other differences between homes and mines, might reduce the generalizability of findings in miners.

Adult↗
PubMed1995

Radon and cancers other than lung cancer in underground miners: a collaborative analysis of 11 studies.

BACKGROUND: Exposure to the radioactive gas radon and its progeny (222Rn and its radioactive decay products) has recently been linked to a variety of cancers other than lung cancer in geographic correlation studies of domestic radon exposure and in individual cohorts of occupationally exposed miners. PURPOSE: This study was designed to characterize further the risks for cancers other than lung cancer (i.e., non-lung cancers) from atmospheric radon. METHODS: Mortality from non-lung cancer was examined in a collaborative analysis of data from 11 cohorts of underground miners in which radon-related excesses of lung cancer had been established. The study included 64,209 men who were employed in the mines for 6.4 years on average, received average cumulative exposures of 155 working-level months (WLM), and were followed for 16.9 years on average. RESULTS: For all non-lung cancers combined, mortality was close to that expected from mortality rates in the areas surrounding the mines (ratio of observed to expected deaths [O/E] = 1.01; 95% confidence interval [CI] = 0.95-1.07, based on 1179 deaths), and mortality did not increase with increasing cumulative exposure. Among 28 individual cancer categories, statistically significant increases in mortality for cancers of the stomach (O/E = 1.33; 95% CI = 1.16-1.52) and liver (O/E = 1.73; 95% CI = 1.29-2.28) and statistically significant decreases for cancers of the tongue and mouth (O/E = 0.52; 95% CI = 0.26-0.93), pharynx (O/E = 0.35; 95% CI = 0.16-0.66), and colon (O/E = 0.77; 95% CI = 0.63-0.95) were observed. For leukemia, mortality was increased in the period less than 10 years since starting work (O/E = 1.93; 95% CI = 1.19-2.95) but not subsequently. For none of these diseases was mortality significantly related to cumulative exposure. Among the remaining individual categories of non-lung cancer, mortality was related to cumulative exposure only for cancer of the pancreas (excess relative risk per WLM = 0.07%; 95% CI = 0.01-0.12) and, in the period less than 10 years since the start of employment, for other and unspecified cancers (excess relative risk per WLM = 0.22%; 95% CI = 0.08-0.37). CONCLUSIONS: The increases in mortality from stomach and liver cancers and leukemia are unlikely to have been caused by radon, since they are unrelated to cumulative exposure. The association between cumulative exposure and pancreatic cancer seems likely to be a chance finding, while the association between cumulative exposure and other and unspecified cancers was caused by deaths certified as due to carcinomatosis (widespread disseminated cancer throughout the body) that were likely to have been due to lung cancers. This study, therefore, provides considerable evidence that high concentrations of radon in air do not cause a material risk of mortality from cancers other than lung cancer. IMPLICATIONS: Protection standards for radon should continue to be based on consideration of the lung cancer risk alone.

Adult↗
PubMed1995

Radon concentrations in residential housing in Hiroshima and Nagasaki.

A measurement of indoor radon (222Rn) concentrations in Hiroshima and Nagasaki was carried out to assess the variability of exposure expected among atomic bomb survivors. Two hundred dwellings, mostly belonging to members of the fixed cohort of atomic bomb survivors under study by the Radiation Effects Research Foundations, were selected for this measurement. The geometric mean values of the radon concentrations for 100 dwellings in Hiroshima and 99 dwellings in Nagasaki measured by Track-Etch Type SF detectors were 56.8 Bq m-3 and 28.5 Bq m-3, respectively. No statistically significant difference was observed between lung cancer mortalities in the low-dose range in the two cities. However, apparent values of the mortality rate for low dose range in Hiroshima are consistently greater than those in Nagasaki. The exposure to radon and its progeny and the atomic bomb radiation effect might have some cooperative effects on the lung cancer incidence.

Air Pollutants, Radioactive↗
PubMed1995

Radon-exposed underground miners and inverse dose-rate (protraction enhancement) effects.

Recent models for radon-induced lung cancer assume that at high levels of cumulative exposure, as experienced historically by many underground miners of uranium and other ores, the risk of lung cancer follows an inverse dose-rate (protraction enhancement) pattern. That is, for equal total dose, a greater risk is incurred by those whose total dose is accumulated at a lower rate over a longer duration than at a higher rate over a shorter duration. This inverse dose-rate effect is hypothesized to be the consequence of multiple traversals of the nucleus of a target cell by alpha particles. It has recently been concluded, however, that for low total doses, as in most residential settings, the inverse dose-rate effect should diminish and perhaps even disappear, since at very low doses the probability that more than one alpha particle would traverse a cell is small and there would be no possibility for interactions from multiple hits. Pooling original data from 11 cohort studies of underground miners, including nearly 1.2 million person-y of observation and 2,701 lung cancer deaths, we evaluate the presence of an inverse dose-rate effect and its modification by total dose. An inverse dose-rate effect was confirmed in each cohort, except one, and overall in the pooled data. There also appears to be a diminution of the inverse dose-rate effect below 50 Working Level Months (WLM), although analyses were necessarily hampered by a limited range of exposure rates at low total WLM. These data support both the presence of an inverse dose-rate effect, as well as its diminution at low total dose. As a consequence, assessment of risks of radon progeny exposure in homes (on average 15-20 WLM for a lifetime) using miner-based models should not assume an ever-increasing risk per unit dose. Rather, it is more appropriate to apply risk models that take into account protraction enhancement and its diminution.

Humans↗
PubMed1995

Radon exposure and cancers other than lung cancer in Swedish iron miners.

Data are presented on the risks of cancers other than lung cancer in a cohort of iron miners from northern Sweden occupationally exposed to elevated levels of the radioactive gas radon. Compared with rates for the four northernmost counties of Sweden, mortality was increased for all cancers other than lung cancer (ratio of observed to expected deaths 1.21, 95% confidence interval 1.03-1.41), stomach cancer (ratio of observed to expected deaths 1.45, 95% confidence interval 1.04-1.98), and rectal cancer (ratio of observed to expected deaths 1.94, 95% confidence interval 1.03-3.31). Despite these overall increases, mortality was not significantly associated with cumulative exposure to radon, either for all cancers other than lung cancer or for any site of cancer other than lung cancer individually. However, the data from this cohort on its own have limited power; and for several sites of cancer the data in this study would be consistent with a radon-related increase. Further study of cancers other than lung cancer in populations exposed to radon is required.

Humans↗
PubMed1986

Evolution of attitudes toward occupational health in the U. S. A.

Attitudes toward ill-health associated with workplace are inevitably closely linked to attitudes toward disease occurring generally, and these have evolved remarkably slowly since the Middle Ages. By the nineteenth century in western countries, at least, people considered disease as a retribution for sins against God, or as a result of bad luck. Certainly this attitude was a factor in why the advent of the germ theory was followed only very slowly by measures aimed at preventing infections brought about from water, food, or airborne sources, even when methods for doing so were well understood. Today, attention is directed toward chronic degenerative diseases and cancer, with their long periods of development, and preventive approaches to these diseases are similarly slow to be applied. In part because the U. S. A. is a relatively young country, with a rapid influx of immigrant labor in this century, the contribution of occupations to injury, ill health and disease has been too seldom recognized. Doctors or nurses working in industries have usually focussed their attention on traditional health care techniques. In the U. S. A. there has recently been, however, a change, at least by ordinary citizens, toward recognizing the importance of prevention of disease. In the context of work-related illness, this recognition has been accelerated by recent legislation which makes employers legally responsible for detecting adverse effects on health of workers and the general public arising from their operations. Paradoxically the Occupational Safety and Health Act of 1970 has been less effective in bringing about a change of awareness of occupational disease than has the Toxic Substances Control Act of 1977.(ABSTRACT TRUNCATED AT 250 WORDS)

Accidents, Occupational↗
PubMed1985

Dietary vitamin A deficiencies and stomach cancer.

The hypothesis of vitamin A intake deficiencies serving as an antecedent factor in the development of stomach cancer was assessed employing a case-control design. Interviews of proxy informants for 111 cases and a pair-matched control group were conducted using a food frequency questionnaire from which an averaged vitamin A intake index was calculated. Stomach cancer cases showed a significantly higher proportion with lowered total vitamin A intake levels (odds ratio = 1.71) which remained constant across sex and socioeconomic status groupings. These results demonstrated a consistency with previous related studies vis-à-vis the strength and specificity of the putative association, a moderate (but statistically nonsignificant) dose-response curve, proper temporal association, and biologic plausibility.

Analysis of Variance↗
PubMed1985

Potential health effects of indoor radon exposure.

Radon-222 is a ubiquitous noble gas arising from decay of radium-226 normally present in the earth's crust. Alpha radiation from inhaled short-lived daughters of radon readily irradiates human bronchial epithelium, and there is now good evidence of excess risk of lung cancer in underground miners exposed to higher concentrations. In homes, radon levels are highly variable, showing approximately log-normal distributions and often a small fraction of homes with high concentrations of radon and radon daughters. Factors affecting indoor concentrations include type of bedrock under dwellings, house foundation characteristics, radon dissolved in artesian water, and ventilation and degree of air movement in living spaces. Despite much recent work, exposures to radon daughters by the general public are not well defined. From application of risk assessments in miners to home conditions, it appears that about 25% or more of lung cancers among nonsmokers over the age of 60, and about 5% in smokers, may be attributable to exposure to radon daughters at home. It may be necessary to take remedial action to reduce this hazard in those dwellings with elevated levels of radon, and new construction should take account of this problem.

Adult↗
PubMed1984

Lung cancer in Swedish iron miners exposed to low doses of radon daughters.

In a retrospective study, we investigated lung-cancer mortality from 1951 to 1976 in 1415 Swedish iron miners exposed to short-lived radioactive daughters of radon gas at concentrations leading to annual doses close to the currently accepted occupational limit. Fifty deaths from lung cancer were observed, as compared with 12.8 expected; expected rates were determined by a smoking-specific analysis based on data from a random sample of the Swedish male population. Among nonsmokers 18 deaths were observed, as compared with 1.8 expected; among current smokers and recent exsmokers 32 deaths were observed and 11.0 were expected. The effects of smoking and exposure to alpha radiation from radon daughters were nearly additive. Comparison of lung-cancer risk coefficients from this study and from other cohort studies of underground miners showed good agreement. Exposure to radon daughters is a major medical problem is underground metal mining, but our results also indicate that exposure to radon daughters at home accounts for an appreciable number of cases of lung cancer in the general population.

Adult↗
PubMed1983

Epidemiological bases for the current ambient carbon monoxide standards.

Carbon monoxide is widely distributed in the environment, and acute or chronic toxic effects may be of considerable public health significance. A review of the basis for current ambient standards is given. Mortality and morbidity studies have been negative or equivocal in relating carbon monoxide levels to health effects, but studies in human subjects with compromised coronary or peripheral circulation support an effect of acute exposure to CO at blood levels equivalent to about 20 ppm over several hours. It is possible that some of the cardiovascular effects of smoking may be related to the high levels of CO in cigarette smoke, but it has been difficult to isolate the contribution of CO independent of the effects of other smoke constituents.

Air Pollutants↗
PubMed1983

Epidemiology of radiation-induced cancer.

The epidemiology of radiation-induced cancer is important for theoretical and practical insights that these studies give to human cancer in general and because we have more evidence from radiation-exposed populations than for any other environmental carcinogen. On theoretical and experimental grounds, the linear no-threshold dose-response relationship is a reasonable basis for extrapolating effects to low doses. Leukemia is frequently the earliest observed radiogenic cancer but is now considered to be of minor importance, because the radiation effect dies out after 25 or 30 years, whereas solid tumors induced by radiation develop later and the increased cancer risk evidently persists for the remaining lifetime. Current estimates of the risk of particular cancers from radiation exposure cannot be fully evaluated until the population under study have been followed at least 40 or 50 years after exposure. Recent evidence indicates that for lung cancer induction, combination of cigarette smoking and radiation exposure leads to risks that are not multiplicative but rather nearly additive.

Breast Neoplasms↗
PubMed1981

Radiation dosimetry.

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Dose-Response Relationship, Radiation↗
PubMed1981

Sensitivity of health endpoints: effect on conclusions of studies.

The types of biological response to an environmental agent can depend on dose, thus in this case a family of widely different dose-response relationships would be expected. For those situations where the magnitude of the effect may be determined on probabilistic grounds as a function of dose ("stochastic" model), no particular dose-response relationship-may necessarily be inferred; the appropriate model still depends on the biological processes under consideration. Some examples of different conclusions concerning dose-response are given for studies of effects of lead and carbon monoxide at low doses. With increasingly sensitive measures of physiologic responses, these can be detected at exposures close to background, but for many cases the question remains whether an observed response really represents a true toxic effect. The application of epidemiologic data for regulatory purposes may depend on identification of the response to an agent appropriate for preventive measures. The conclusions one reaches about studies of health effects of environmental agents can be markedly influenced by the types of health endpoints under consideration.

Air Pollutants↗
PubMed1978

Occupational exposures to cyanide in Baltimore fire fighters.

A group of 479 fire fighters were investigated for routine exposure to hydrogen cyanide in the fire atmosphere using measurements of serum thiocyanate (SCN-). Our findings indicate that fire fighters were exposed to levels of hydrogen cyanide sufficient to raise their mean serum thiocyanate (SCN-) levels above that of controls. This elevation of serum SCN- occurred independently of smoking habits. Exposure to cyanide occurred much less frequently than previously studied exposures to carbon monoxide. Difficulties of correlating acute symptoms and the effectiveness of mask use with serum thiocyanate are discussed.

Air Pollutants↗