Exposure to indoor background radiation and urinary concentrations of 8-hydroxydeoxyguanosine, a marker of oxidative DNA damage. (1/218)

We investigated whether exposure to indoor [gamma]-radiation and radon might be associated with enough free radical formation to increase urinary concentrations of 8-hydroxydeoxyguanosine (8-OHdG), a sensitive marker of DNA damage, due to a hydroxyl radical attack at the C8 of guanine. Indoor radon and [gamma]-radiation levels were measured in 32 dwellings for 6 months by solid-state nuclear track detectors and thermoluminescent dosimeters, respectively. Urine samples for 8-OHdG determinations were obtained from 63 healthy adult subjects living in the measured dwellings. An overall tendency toward increasing levels of 8-OHdG with increasing levels of radon and [gamma]-radiation was seen in the females, presumably due to their estimated longer occupancy in the dwellings measured. Different models were considered for females, with the steepest slopes obtained for [gamma]-radiation with a coefficient of 0.500 (log nmol/l of 8-OHdG for each unit increase of [gamma]-radiation on a log scale) (p<0.01), and increasing to 0.632 (p = 0.035), but with larger variance, when radon was included in the model. In conclusion, there seems to be an effect of indoor radioactivity on the urinary excretion of 8-OHdG for females, who are estimated to have a higher occupancy in the dwellings measured than for males, for whom occupational and other agents may also influence 8-OHdG excretion. ree radicals; [gamma]-radiation; radon.  (+info)

Radon and lung cancer: a cost-effectiveness analysis. (2/218)

OBJECTIVES: This study examined the cost-effectiveness of general and targeted strategies for residential radon testing and mitigation in the United States. METHODS: A decision-tree model was used to perform a cost-effectiveness analysis of preventing radon-associated deaths from lung cancer. RESULTS: For a radon threshold of 4 pCi/L, the estimated costs to prevent 1 lung cancer death are about $3 million (154 lung cancer deaths prevented), or $480,000 per life-year saved, based on universal radon screening and mitigation, and about $2 million (104 lung cancer deaths prevented), or $330,000 per life-year saved, if testing and mitigation are confined to geographic areas at high risk for radon exposure. For mitigation undertaken after a single screening test and after a second confirmatory test, the estimated costs are about $920,000 and $520,000, respectively, to prevent a lung cancer death with universal screening and $130,000 and $80,000 per life-year for high risk screening. The numbers of preventable lung cancer deaths are 811 and 527 for universal and targeted approaches, respectively. CONCLUSIONS: These data suggest possible alternatives to current recommendations.  (+info)

p53 Mutations in lung cancer associated with residential radon exposure. (3/218)

Unusual mutation patterns in lung tumors among underground miners have been indicated, suggesting radon-specific alterations in the genome, but the data are not consistent. To investigate the association between residential radon exposure and p53 mutations in lung tumors, we performed a study on cases from a nation-wide population-based investigation in Sweden. Our study included 83 nonsmoking lung cancer cases and 250 smoking lung cancer cases, diagnosed 1980-1984, with a time-weighted average radon exposure over 140 Bq/m3 or up to 50 Bq/m3. Radon was measured in dwellings occupied by the study subjects at some time since 1947. Information on smoking habits and other risk factors was obtained from questionnaires. After exclusions because of the initiation of treatment or insufficient material, the p53-status of 243 tumors was determined using PCR-single-stranded conformation polymorphism analysis and sequencing determination of exons 5-8. The overall mutation prevalence was 23.9%. An increased mutation prevalence was suggested among those with high exposure to residential radon [odds ratio (OR), 1.4; 95% CI, 0.7-2.6], especially among nonsmokers (OR, 3.2; 95% CI, 0.7-15.5), but no specific mutational pattern was indicated. Furthermore, the mutation prevalence seemed to be higher among smoking lung cancer cases than among nonsmoking cases (OR, 2.1; 95% CI, 0.9-5.0), and particularly among those smoking less than 10 cigarettes per day. It may be concluded that residential exposure to radon seems to contribute to a higher mutation prevalence of the p53 gene in lung tumors.  (+info)

A healthy home environment? (4/218)

Over the past seven years, the U.S. Environmental Protection Agency has consistently ranked indoor air pollution among the top five risks to public health. One of the most dangerous indoor air pollutants is carbon monoxide (CO). CO can be lethal, but perhaps more important, many people suffer ill health from chronic, often undetected exposure to low levels of this gas, resulting in fatigue, headache, dizziness, nausea, and vomiting. Another dangerous pollutant is volatile organic compounds (VOCs), which come from sources including building products, cleaning agents, and paints. One VOC, formaldehyde, can act as an irritant to the conjunctiva and upper and lower respiratory tract. Formaldehyde is also known to cause nasal cancer in test animals.  (+info)

Residential radon exposure and risk of lung cancer in Missouri. (5/218)

OBJECTIVES: This study investigated residential radon exposure and lung cancer risk, using both standard radon dosimetry and a new radon monitoring technology that, evidence suggests, is a better measure of cumulative radon exposure. METHODS: Missouri women (aged 30 to 84 years) newly diagnosed with primary lung cancer during the period January 1, 1993, to January 31, 1994, were invited to participate in this population-based case-control study. Both indoor air radon detectors and CR-39 alpha-particle detectors (surface monitors) were used. RESULTS: When surface monitors were used, a significant trend in lung cancer odds ratios was observed for 20-year time-weighted-average radon concentrations. CONCLUSIONS: When surface monitors were used, but not when standard radon dosimetry was used, a significant lung cancer risk was found for radon concentrations at and above the action level for mitigation of houses currently used in the United States (148 Bqm-3). The risk was below the action level used in Canada (750 Bqm-3) and many European countries (200-400 Bqm-3).  (+info)

Radon testing in households with a residential smoker--United States, 1993-1994. (6/218)

Epidemiologic investigations of underground miners and studies of alpha particle carcinogenesis among laboratory animals suggest that exposure to the radioactive decay products (progeny) of radon is an important risk factor for lung cancer. Persons who smoke cigarettes and are exposed to these radon progeny have a substantially greater risk for developing malignancy than nonsmokers. Residential radon concentrations above the U.S. Environmental Protection Agency's (EPA) action level of 4 pCi/L are the primary sources of exposure among the general population. EPA and the Public Health Service promote home testing for radon, especially in households with a person who smokes. However, it is unknown whether households that contain smokers are more likely than those without smokers to test for radon. To characterize radon testing practices of households that contain a person who smokes within the dwelling (i.e., residential smoker), CDC analyzed survey data from the National Health Interview Survey (NHIS). This report summarizes the results of this analysis, which indicates that households with a residential smoker are significantly less likely to test for radon than those without smokers.  (+info)

Intercomparison of retrospective radon detectors. (7/218)

We performed both a laboratory and a field intercomparison of two novel glass-based retrospective radon detectors previously used in major radon case-control studies performed in Missouri and Iowa. The new detectors estimate retrospective residential radon exposure from the accumulation of a long-lived radon decay product, (210)Pb, in glass. The detectors use track registration material in direct contact with glass surfaces to measure the alpha-emission of a (210)Pb-decay product, (210)Po. The detector's track density generation rate (tracks per square centimeter per hour) is proportional to the surface alpha-activity. In the absence of other strong sources of alpha-emission in the glass, the implanted surface alpha-activity should be proportional to the accumulated (210)Po, and hence to the cumulative radon gas exposure. The goals of the intercomparison were to a) perform collocated measurements using two different glass-based retrospective radon detectors in a controlled laboratory environment to compare their relative response to implanted polonium in the absence of environmental variation, b) perform collocated measurements using two different retrospective radon progeny detectors in a variety of residential settings to compare their detection of glass-implanted polonium activities, and c) examine the correlation between track density rates and contemporary radon gas concentrations. The laboratory results suggested that the materials and methods used by the studies produced similar track densities in detectors exposed to the same implanted (210)Po activity. The field phase of the intercomparison found excellent agreement between the track density rates for the two types of retrospective detectors. The correlation between the track density rates and direct contemporary radon concentration measurements was relatively high, considering that no adjustments were performed to account for either the residential depositional environment or glass surface type. Preliminary comparisons of the models used to translate track rate densities to average long-term radon concentrations differ between the two studies. Further calibration of the retrospective detectors' models for interpretation of track rate density may allow the pooling of studies that use glass-based retrospective radon detectors to determine historic residential radon exposures.  (+info)

Indoor residential radon exposure and risk of childhood acute myeloid leukaemia. (8/218)

Exposure to radon has been identified as a risk factor for lung cancer in uranium miners, but evidence of adverse health effects due to indoor radon exposure is inconsistent. Ecological studies have suggested a correlation between indoor radon levels and leukaemia incidence. We evaluated the risk associated with indoor residential radon exposure within a larger interview-based case-control study of risk factors for childhood acute myeloid leukaemia (AML). A total of 173 cases and 254 controls met the eligibility criteria, and information was collected through telephone interviews with parents and analysis of alpha-track radon detectors placed in the home for a period of 1 year. No association was observed between radon exposure and risk of AML, with adjusted odds ratios of 1.2 (95% confidence interval (CI) 0.7-1.8) for 37-100 Bq m(-3) and 1.1 (95% CI 0.6-2.0) for > 100 Bq m(-3) compared with < 37 Bq m(-3). Although there was an inverse association between radon level and AML risk among children < 2 years at diagnosis, among children > or = 2 years, AML risk was increased among those with higher radon exposure. The observed association after age 2 is most likely due to chance. Overall, there was no association between residential radon and risk of childhood AML.  (+info)