Utility gains from reductions in the modifiable burden of lung cancer attributable to residential radon in Canada.

RESEARCH QUESTION: The objective of this analysis is to estimate the modifiable burden of disease according to the annual number of lung cancer deaths prevented and the associated period gain in quality-adjusted life years (QALYs) for the 2012 populations in Canada from reductions in residential radon exposures. INTERVENTIONS: Two postulated interventions for residential radon mitigation in new construction are assessed, corresponding to a 50% reduction and an 85% reduction in radon nationally, in the provinces/territories, and in 17 census metropolitan areas in Canada. METHODS: Data were derived from two recent Canadian radon surveys conducted by the Radiation Protection Bureau, Health Canada, along with Canadian mortality and quality of life data. Analyses adopted a lifetime horizon and a discount rate of 1.5%. A period life-table analysis was conducted using age- and sex-specific all-cause and lung cancer mortality rates, adjusted for smoking, and the BEIR VI exposure-age-concentration model for radon-attributable risk of lung cancer mortality. RESULTS: A reduction in residential radon by 50% could prevent 681 lung cancer deaths, associated with a gain of 15,445 QALYs in the Canadian population at a discount rate of 1.5%; a reduction in radon by 85% could prevent 1263 lung cancer deaths, associated with a gain of 26,336 QALYs. On a per population basis, the Yukon was estimated to benefit most from radon mitigation. CONCLUSION: The magnitude of QALY gains in Canada estimated under the two radon mitigation scenarios is appreciable but varies considerably across provinces due to variability in indoor radon concentrations and smoking rates.

Residential radon and small cell lung cancer. A systematic review.

Residential radon exposure is considered the second cause of lung cancer and the first in never smokers. Nevertheless, the association between the different histological types of lung cancer and radon is not completely clear, and radon effect on small cell lung cancer is not completely understood. We aim to asses the effect of residential radon exposure on the risk of small cell lung cancer (SCLC) in general population and miners through a systematic review applying predefined inclusion and exclusion criteria. 16 studies were included. Most of them point to a relationship between indoor radon and SCLC, though some investigations show no association. When comparing the risk of SCLC due to radon exposure with NSCLC, it can be observed that an increased risk for SCLC is present. Small cell lung cancer seems to be the histological type of lung cancer most tightly related with residential radon.

Geographic variation in U.S. thyroid cancer incidence and a cluster near nuclear reactors in New Jersey, New York, and Pennsylvania.

In the United States, thyroid cancer incidence (along with liver cancer) is increasing more rapidly than any other malignancy, rising nearly threefold from 1980 to 2006. Improved diagnosis has been proposed by some as the major reason for this change, while others contend that additional factors also account for the increase. Among U.S. states, 2001-2005 age-adjusted thyroid cancer incidence rates vary from 5.4 to 12.8 per 100,000. County-specific incidence data, available for the first time, document that most U.S. counties with the highest thyroid cancer incidence are in a contiguous area of eastern Pennsylvania, New Jersey, and southern New York State. Exposures to radioactive iodine emissions from 16 nuclear power reactors within a 90-mile radius in this area indicate that these emissions are a likely etiological factor in rising thyroid cancer incidence rates.

Using tensor product splines in modeling exposure-time-response relationships: application to the Colorado Plateau Uranium Miners cohort.

An adequate depiction of exposure-time-response relationships is important in assessing public health implications of an occupational or environmental exposure. Recent advances have focused on flexible modeling of the overall shape of latency. Methods are needed to allow for varying shapes of latency under different exposure profiles. A tensor product spline model is proposed for describing exposure-response relationships for protracted time-dependent occupational exposure histories in epidemiologic studies. The methods use flexible multi-dimensional techniques to jointly model age, latency and exposure-response effects. In analyzing data from the Colorado Plateau Uranium Miners cohort, a model that allows for varying exposure-dependent latency shapes is found to be superior to models that only allowed for an overall latency curve. Specifically, the model suggests that, at low exposure levels risk increased at short latencies followed by a slow decline for longer latency periods. On the other hand, risk was higher but did not change much by latency for higher exposure levels. The proposed methodology has the advantage of allowing for latency functions that vary by exposure levels and, conversely, exposure-response relationships that are influenced by the latency structure.

Decorporation of plutonium by pulmonary administration of Ca-DTPA dry powder: a study in rat after lung contamination with different plutonium forms.

This study evaluates the decorporation efficacy of a pulmonary administration of a new Ca-DTPA (diethylenetriaminepentaacetic acid) dry powder (18 micromol kg(-1) of body mass) after pulmonary contamination of rats with different Pu compounds. After inhalation of PuO2, a delayed intratracheal administration of DTPA cannot reduce significantly the retention of Pu in the lungs but limits its transfer in liver and skeleton. After pulmonary contamination by Pu nitrate, early insufflation of the DTPA powder appears twice as more efficient than an i.v injection of DTPA (30 micromol kg(-1)) to reduce Pu retention in the lungs and is as effective as i.v. injection to limit the extrapulmonary deposit. In contrast, a delayed administration of DTPA cannot reduce the lung or extrapulmonary retention. In conclusion, the improvement of aerodynamic properties of DTPA powder leads to an increase of DTPA amount deposited in the lungs and enhances the body decorporation.

Indoor air radon.

This review concerns primarily the health effects that result from indoor air exposure to radon gas and its progeny. Radon enters homes mainly from the soil through cracks in the foundation and other holes to the geologic deposits beneath these structures. Once inside the home the gas decays (half-life 3.8 d) and the ionized atoms adsorb to dust particles and are inhaled. These particles lodge in the lung and can cause lung cancer. The introduction to this review gives some background properties of radon and its progeny that are important to understanding this public health problem as well as a discussion of the units used to describe its concentrations. The data describing the health effects of inhaled radon and its progeny come both from epidemiological and animal studies. The estimates of risk from these two data bases are consistent within a factor of two. The epidemiological studies are primarily for hard rock miners, although some data exist for environmental exposures. The most complete studies are those of the US, Canadian, and Czechoslovakian uranium miners. Although all studies have some deficiencies, those of major importance include uranium miners in Saskatchewan, Canada, Swedish iron miners, and Newfoundland fluorspar miners. These six studies provide varying degrees of detail in the form of dose-response curves. Other epidemiological studies that do not provide quantitative dose-response information, but are useful in describing the health effects, include coal, iron ore and tin miners in the UK, iron ore miners in the Grangesburg and Kiruna, Sweden, metal miners in the US, Navajo uranium miners in the US, Norwegian niobian and magnitite miners, South African gold and uranium miners, French uranium miners, zinc-lead miners in Sweden and a variety of small studies of environmental exposure. An analysis of the epidemiological studies reveals a variety of interpretation problem areas. The major and almost universal problem is in estimating exposure levels. In many cases there were no direct measurements of radon or radon progeny and the exposure levels are estimates based on irregular measurements and known levels in nearby mines. Perhaps the most important variable or complicating factor in the determination of the risk due to radon exposure is the confounding factor of exposure to cigarette smoke. The general scientific concensus is that, although the interaction could be somewhere between linear and supramultiplicative, it is likely a combination, and closer to multiplicative. A number of other complexities contribute to the uncertainty in the risk estimates, likely to a lesser degree than those of exposure measurements and cigarette smoke confounding.(ABSTRACT TRUNCATED AT 400 WORDS)

Mortality among plutonium and other radiation workers at a plutonium weapons facility.

Mortality among 5,413 white males who were employed for at least two years at a plutonium weapons facility was investigated to measure risks from exposures to low levels of plutonium and external radiation. When compared with US death rates, fewer deaths than expected were found for all causes of death, all cancers, and lung cancer. No bone cancer was observed. An excess of brain tumors was found for the cohort in general. Elevated rate ratios for all causes of death and all lymphopoietic neoplasms were found when employees with plutonium body burdens greater than or equal to 2 nCi were compared with those with body burdens less than 2 nCi, while accounting for age, calendar period, and induction time. Increased rate ratios were also found for esophageal, stomach, colon, and prostate cancers, and for lymphosarcomas and reticulum cell sarcomas. No elevated rate ratios were noted for bone and liver cancers. When employees with cumulative exposures greater than or equal to 1 rem were compared with those with exposures less than 1 rem, elevated rate ratios were found for myeloid leukemia, lymphosarcoma and reticulum cell sarcoma, liver neoplasms, and unspecified brain tumors. No overall dose-response relationships were found for plutonium or external radiation exposures. Standardized rate ratios increased, however, as plutonium body burden levels increased for all causes, all cancers, and digestive cancers at five years induction time. Standardized rate ratios also increased as external radiation exposure categories increased for all lymphopoietic cancers and unspecified brain tumors for a two-year induction period. With the exception of analyses of combined categories of death, and perhaps of lung cancer, confidence limits were wide, indicating limited precision. Nevertheless, these findings suggest that increased risks for several types of cancers cannot be ruled out at this time for individuals with plutonium body burdens of greater than or equal to 2 nCi. Plutonium-burdened individuals should continue to be studied in future years.

Health effects of airborne effluents released from the nuclear cycle.

Current trends in regulations governing radioactive release from the nuclear cycle and their relationship with population dose and population health damage evaluation are discussed. It is shown that, at least in some cases, current methods may not grant a correct population-dose evaluation. A procedure to better evaluate population doses from gaseous effluents is outlined. It leads to a very simple first approximation expression which is independent of the dispersion area. Two examples, 85Kr and 222Rn, are worked out in order to give first-order evaluations of the population-dose commitment and the related risk. Strong discrepancies between the results and current evaluations are found and discussed.