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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The accurate determination of exposure to environmental tobacco smoke is notoriously difficult. There have been to date two approaches to determining this exposure in the study of association of passive smoking and lung cancer: the biochemical approach, using cotinine in the main as a marker, and the epidemiological approach. Typically results of the former have yielded much lower relative risk than the latter, and have tended to be ignored in favour of the latter, although there has been considerable debate as to the logical basis for this. We settle this question by showing that, using the epidemiologically based meta-analysis technique of Wald et al. (1986), and misclassification models in the EPA Draft Review (1990), one arrives using all current studies at a result which is virtually identical with the biochemically-based conclusions of Darby and Pike (1988) or Repace and Lowry (1990). The conduct of this meta-analysis itself raises a number of important methodological questions, including the validity of inclusion of studies, the use of estimates adjusted for covariates, and the statistical significance of estimates based on meta-analysis of the epidemiological data. The best estimate of relative risk from spousal smoking is shown to be approximately 1.05-1.10, based on either of these approaches; but it is suggested that considerable extra work is needed to establish whether this is significantly raised.
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PMID:Lung cancer and passive smoking: reconciling the biochemical and epidemiological approaches. 141 10

A recent report by the National Academy of Sciences estimates that the radiation dose to the bronchial epithelium, per working level month (WLM) of radon daughter exposure, is about 30% lower for residential exposures than for exposures received in underground mines. Adjusting the previously published BEIR IV radon risk model accordingly, the unit risk for indoor exposures of the general population is about 2.2 x 10(-4) lung cancer deaths (lcd)/WLM. Using results from EPA's National Residential Radon Survey, the average radon level is estimated to be about 1.25 pCi/L, and the annual average exposure about 0.242 WLM. Based on these estimates, 13,600 radon-induced lcd/yr are projected for the United States. A quantitative uncertainty analysis was performed, which considers: statistical uncertainties in the epidemiological studies of radon-exposed miners; the dependence of risk on age at, and time since, exposure; the extrapolation of risk estimates from mines to homes based on comparative dosimetry; and uncertainties in the radon daughter levels in homes and in the average residential occupancy. Based on this assessment of the uncertainties in the unit risk and exposure estimates, an uncertainty range of 7000-30000 lcd/yr is derived.
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PMID:An analysis of the uncertainties in estimates of radon-induced lung cancer. 150 75

This paper provides an easy-to-use screening methodology to estimate potential excess lifetime lung cancer risk resulting from indoor radon exposure. The methodology was developed under U.S. EPA Office of Policy, Planning, and Evaluation sponsorship of the agency's Integrated Environmental Management Projects (IEMP) and State/Regional Comparative Risk Projects. These projects help policymakers understand and use scientific data to develop environmental problem-solving strategies. This research presents the risk assessment methodology, discusses its basis, and identifies appropriate applications. The paper also identifies assumptions built into the methodology and qualitatively addresses methodological uncertainties, the direction in which these uncertainties could bias analyses, and their relative importance. The methodology draws from several sources, including risk assessment formulations developed by the U.S. EPA's Office of Radiation Programs, the EPA's Integrated Environmental Management Project (Denver), the International Commission on Radiological Protection, and the National Institute for Occupational Safety and Health. When constructed as a spreadsheet program, the methodology easily facilitates analyses and sensitivity studies (the paper includes several sensitivity study options). The methodology will be most helpful to those who need to make decisions concerning radon testing, public education, and exposure prevention and mitigation programs.
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PMID:Screening radon risks: a methodology for policymakers. 177 Dec 67

Regulation of indoor Rn is explored in the context of cost-effectiveness of regulatory action. Evaluation of cost (i.e., mitigation expenses) and benefits (i.e., savings associated with medical expenses and lost productivity related to lung cancer) at various action levels indicate that regulatory programs would be economically inefficient and unreasonable if standards were established at or below the current EPA action guide (150 Bq m-3 or less). For the approximately 95% of U.S. homes with Rn levels near or below 150 Bq m-3, government programs should continue to focus on public information and consumer protection. For the small number of homes with high Rn levels, government programs should focus on identifying high risk homes and encouraging homeowners to reduce Rn levels. Because of the potential for substantial risk reduction, such efforts would be cost-effective in these homes.
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PMID:Regulatory control of indoor Rn. 195 38

The contribution of radon daughter exposure to excess lung cancer in underground miners is universally accepted. These miners received exposures from tens to thousands of WLM in a relatively few years. Although the miners were also exposed to other noxious agents in mines, the appearance of the excess lung cancer mortality in several types of mines and the increase with increasing exposure provide convincing evidence of the role of radon as the carcinogen. It is conceivable that exposures to radon at an average concentration of one to two pCi/liter, the levels for a majority of homes, might not produce excess lung cancers. This would require that a lifetime exposure at low concentrations produce a different response from that of a few years at higher levels for the miners. This is unlikely but not impossible. The current environmental epidemiology is of varying quality. The better studies may give some answers in a few years. These studies are more likely to establish an upper limit of risk than to provide an exposure-response model. Present risk estimates cannot be used accurately in estimating the overall lung cancer risk to the US population, since there are no good data on average exposure and exposure distribution. For example, the number of homes above the EPA guideline of four pCi/liter may range from two million to 10 million. An estimate of the actual radon exposure in the US may be forthcoming from a planned EPA survey, but these data will not be available for a few years. In the conservative tradition of radiation protection, indoor radon exposures in homes are estimated to produce a number of excess lung cancers in the population. One estimate by the NCRP is about 10,000 deaths per year in the US, for an average annual estimated exposure of 0.2 WLM (about one pCi/liter). The National Academy of Sciences (BEIR IV) estimates 13,000 deaths for the same exposure, and the EPA's estimate is 5,000 to 20,000.
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PMID:Potential lung cancer risk from indoor radon exposure. 213 21

Important issues in the carcinogenic risk assessment of chromium compounds are whether both trivalent and hexavalent chromium compounds are carcinogenic, the role of solubility in the carcinogenic response, and the carcinogenicity of ingested chromium. Hexavalent chromium compounds are carcinogenic to animals via several routes of exposure, while trivalent chromium compounds, although they demonstrate evidence of genotoxicity, have not been shown in animal studies to be carcinogenic. Workers in chromate production plants, where the risk of lung cancer is elevated, are exposed to both trivalent and hexavalent chromium compounds. A cancer unit risk estimate for Wistar rats exposed to a hexavalent chromium aerosol (sodium dichromate) is less than the risk estimate for workers in chromate production. If this difference is biologically real, a possible explanation may be that trivalent compounds also have a carcinogenic effect. For hexavalent chromium compounds, it is contended that only sparingly soluble hexavalent chromium compounds are carcinogenic. Recent evidence, however, indicates that highly soluble hexavalent chromium compounds are also carcinogenic. Animal ingestion studies have not found trivalent chromium compounds to be carcinogenic by ingestion; hexavalent compounds have not been studied. Research by EPA to address the issue of valence state and solubility with respect to carcinogenicity is currently being conducted.
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PMID:Evaluation of issues relating to the carcinogen risk assessment of chromium. 269 Mar 40

A project for increasing public awareness of radon as an environmental hazard was carried out in south central Wisconsin and northwest Illinois using local medical resources. In Wisconsin counties, measured radon levels were equal to or greater than those obtained by a 1986-87 EPA survey. More than 30% of the buildings surveyed exceeded 4 pCi/L, and 10% exceeded 10 pCi/L. Results in Illinois were similar to those from contiguous areas of Wisconsin. In view of the known link between radon-222 exposure and lung cancer, we urge that similar projects be performed by other medical communities across the state and nation.
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PMID:Community radon awareness and detection: a model program. 275 Jan 78

Indoor radon has been judged to be the most serious environmental carcinogen which the EPA must address for the general public. The optimal strategy for dealing with this problem depends on the magnitude of the risk, how the risk is distributed within the population, as well as the effectiveness and costs of mitigation measures. Based on current exposure and risk estimates, radon exposure in single-family houses may be a causal factor in roughly 20,000 lung cancer fatalities per year. Most of these projected fatalities are attributable to exposures in houses with average or moderately elevated radon levels (below 10 pCi/L). Hence to appreciably reduce radon-induced lung cancers, remediation efforts must include houses not highly elevated in radon. From either an individual risk or a cost-benefit standpoint, reduction of a few pCi/L per home appears to be justified. The optimal strategy for dealing with the indoor radon problem depends on the magnitude of the risk per unit exposure, the distribution of exposures in houses, and the effectiveness and costs of mitigation. EPA's current views with respect to these factors and the associated uncertainties are discussed.
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PMID:EPA's perspective on risks from residential radon exposure. 276 11

The proportion of lung cancer deaths attributable to Rn among residents of single-family homes in the U.S. (approximately 70% of the housing stock) is estimated using the log-normal distribution of Rn concentrations proposed by Nero et al. (1986) and the risk model developed by the National Academy of Sciences' BEIR IV Committee. The risk model, together with the exposure distribution, predicts that approximately 14% of lung cancer deaths among such residents (about 13,300 deaths per year, or 10% of all U.S. lung cancer deaths) may be due to indoor Rn exposure. The 95% confidence interval is 7%-25%, or approximately 6600 to 24,000 lung cancer deaths. These estimated attributable risks due to Rn are similar for males and females and for smokers and nonsmokers, but higher baseline risks of lung cancer result in much larger absolute numbers of Rn-attributable cancers among males (approximately 9000) and among smokers (approximately 11,000). Because of the apparent skewness of the exposure distribution, most of the contribution to the attributable risks arises from exposure rates below 148 Bq m-3 (4 pCi L-1), i.e., below the EPA "action level." As a result, if all exposure rates that exceed 148 Bq m-3 (approximately 8% of homes) were eliminated, the models predict that the total annual lung cancer burden in the U.S. would drop by 4-5%, or by about 3800 lung cancer deaths, in contrast to a maximum reduction of 14% if all indoor Rn exposure above the 1st percentile were eliminated.
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PMID:Estimating Rn-induced lung cancer in the United States. 277 48

Radon has always been a component of ground and air and it has been present in increased concentrations from the moment humans first sought shelter inside dwellings. Recent improvements in the energy efficiency of dwellings have led to increased concentrations of radon and to increased risks of lung cancer. To quantify the magnitude of this risk, well-designed epidemiological studies, including surveys of representative dwellings, are needed, and several are being implemented. In the meantime, the EPA and other agencies have offered guidance on monitoring procedures and remedial measures appropriate for the problem on indoor radon. Recent disclosures of relatively high concentrations of radon and radon decay products in homes in several parts of the country have increased public concern about the problem. More information and education are needed about the health risks of radon, the desirability of implementing monitoring procedures for radon, and about remediation measures when detected levels are above average. Educational resources are needed in communities to address local issues when they arise. These resources should include knowledgeable individuals who can work with state and county health officials to put public concerns into perspective within the local context. Physicians, other health professionals, and medical scientists have the knowledge and credentials to be these individuals. To provide health professionals with knowledge and skills to communicate with the public about the health risks of radon, the American Medical Association has prepared an authoritative report and initiated a series of regional seminars on the origin and health risks of radon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Origin and health risks of indoor radon. 327 84


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