Frédéric Lagarde

Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies

Abstract Objective To determine the risk of lung cancer associated with exposure at home to the radioactive disintegration products of naturally occurring radon gas Design Collaborative analysis of individual data from 13 case-control studies of residential radon and lung cancer. Setting Nine European countries. Subjects 7148 cases of lung cancer and 14 208 controls. Main outcome measures Relative risks of lung cancer and radon gas concentrations in homes inhabited during the previous 5-34 years measured in becquerels (radon disintegrations per second) per cubic metre (Bq/m3) of household air. Results The mean measured radon concentration in homes of people in the control group was 97 Bq/m3, with 11% measuring > 200 and 4% measuring > 400 Bq/m3. For cases of lung cancer the mean concentration was 104 Bq/m3. The risk of lung cancer increased by 8.4% (95% confidence interval 3.0% to 15.8%) per 100 Bq/m3 increase in measured radon (P = 0.0007). This corresponds to an increase of 16% (5% to 31%) per 100 Bq/m3 increase in usual radon—that is, after correction for the dilution caused by random uncertainties in measuring radon concentrations. The dose-response relation seemed to be linear with no threshold and remained significant (P = 0.04) in analyses limited to individuals from homes with measured radon < 200 Bq/m3. The proportionate excess risk did not differ significantly with study, age, sex, or smoking. In the absence of other causes of death, the absolute risks of lung cancer by age 75 years at usual radon concentrations of 0, 100, and 400 Bq/m3 would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong non-smokers, and about 25 times greater (10%, 12%, and 16%) for cigarette smokers. Conclusions Collectively, though not separately, these studies show appreciable hazards from residential radon, particularly for smokers and recent ex-smokers, and indicate that it is responsible for about 2% of all deaths from cancer in Europe.

Residential Radon Exposure and Lung Cancer in Sweden

BACKGROUND Residential radon is the principal source of exposure to ionizing radiation in most countries. To determine the implications for the risk of lung cancer, we performed a nationwide case-control study in Sweden. METHODS The study included 586 women and 774 men 35 to 74 years of age with lung cancer that was diagnosed between 1980 and 1984. For comparison, 1380 female and 1467 male controls were studied. Radon was measured in 8992 dwellings occupied by the study subjects at some time since 1947. Information on smoking habits and other risk factors for lung cancer was obtained from questionnaires. RESULTS Radon levels followed a log-normal distribution, with geometric and arithmetic means of 1.6 and 2.9 pCi per liter (60.5 and 106.5 Bq per cubic meter), respectively. The risk of lung cancer increased in relation to both estimated cumulative and time-weighted exposure to radon. In comparison with time-weighted average radon concentrations up to 1.4 pCi per liter (50 Bq per cubic meter), the relative risk was 1.3 (95 percent confidence interval, 1.1 to 1.6) for average radon concentrations of 3.8 to 10.8 pCi per liter (140 to 400 Bq per cubic meter), and it was 1.8 (95 percent confidence interval, 1.1 to 2.9) at concentrations exceeding 10.8 pCi per liter. The estimates of risk were in the same range as those projected from data in miners. The interaction between radon exposure and smoking with regard to lung cancer exceeded additivity and was closer to a multiplicative effect. CONCLUSIONS Residential exposure to radon is an important cause of lung cancer in the general population. The risks appear consistent with earlier estimates based on data in miners.

Cadmium Exposure and Distal Forearm Fractures

The aim of this study was to analyze the relationship between low‐level cadmium exposure and distal forearm fractures. Altogether, 1021 men and women exposed to cadmium in Sweden were included. The study indicates that cadmium exposure is associated with increased risk of forearm fractures in people over the age of 50.

Residential Radon and Lung Cancer among Never-Smokers in Sweden

In this study, we attempted to reduce existing uncertainty about the relative risk of lung cancer from residential radon exposure among never-smokers. Comprehensive measurements of domestic radon were performed for 258 never-smoking lung cancer cases and 487 never-smoking controls from five Swedish case-control studies. With additional never-smokers from a previous case-control study of lung cancer and residential radon exposure in Sweden, a total of 436 never-smoking lung cancer cases diagnosed in Sweden between 1980 and 1995 and 1,649 never-smoking controls were included. The relative risks (with 95% confidence intervals in parentheses) of lung cancer in relation to categories of time-weighted average domestic radon concentration during three decades, delimited by cutpoints at 50, 80, and 140 Bq m−3, were 1.08 (0.8–1.5), 1.18 (0.9–1.6), and 1.44 (1.0–2.1), respectively, with average radon concentrations below 50 Bq m−3 used as reference category and with adjustment for other risk factors. The data suggested that among never-smokers residential radon exposure may be more harmful for those exposed to environmental tobacco smoke. Overall, an excess relative risk of 10% per 100 Bq m−3 average radon concentration was estimated, which is similar to the summary effect estimate for all subjects in the main residential radon studies to date.

Residential radon and lung cancer in Sweden: risk analysis accounting for random error in the exposure assessment.

A large epidemiologic study on residential radon exposure and lung cancer has been conducted in Sweden. An attempt is now made to quantify the impact of random error in the exposure assessment on the risk estimate for lung cancer in this study. The study included 1,360 lung cancer cases, diagnosed from 1980 to 1984, and 2,847 population controls. Radon measurements were performed in 8,992 dwellings occupied by the study subjects some time since 1947. Questionnaires provided information on smoking and other risk factors. Imprecision in the retrospective exposure assessment for radon was estimated from a Monte Carlo technique modeling Swedish conditions. Adjusted risk estimates were obtained from regression analyses based on expected values for true time-weighted average residential radon concentration (TWA), conditional on observed TWA. Without adjustment for random error in the TWA estimates, the linear excess relative risk coefficient was 0.10 per 100 Bq m(-3), but an excess relative risk of about 0.15 to 0.20 per 100 Bq m(-3) was suggested following adjustment. The potentially significant consequences of errors in the retrospective radon exposure assessment should be taken into consideration in the risk estimation as well as in comparisons of results of different studies and in future pooled analyses.

Glass-based radon-exposure assessment and lung cancer risk.

Lung cancer risk estimation in relation to residential radon exposure remains uncertain, partly as a result of imprecision in air-based retrospective radon-exposure assessment in epidemiological studies. A recently developed methodology provides estimates for past radon concentrations and involves measurement of the surface activity of a glass object that has been in a subjects dwellings through the period for exposure assessment. Such glass measurements were performed for 110 lung cancer subjects, diagnosed 1985 to 1995, and for 231 control subjects, recruited in a case–control study of residential radon and lung cancer among never-smokers in Sweden. The relative risks (with 95% confidence intervals) of lung cancer in relation to categories of surface-based average domestic radon concentration during three decades, delimited by cutpoints at 50, 80, and 140 Bq m−3, were 1.60 (0.8 to 3.4), 1.96 (0.9 to 4.2), and 2.20 (0.9 to 5.6), respectively, with average radon concentrations below 50 Bq m−3 used as reference category, and with adjustment for other risk factors. These relative risks, and the excess relative risk (ERR) of 75% (−4% to 430%) per 100 Bq m−3 obtained when using a continuous variable for surface-based average radon concentration estimates, were about twice the size of the corresponding relative risks obtained among these subjects when using air-based average radon concentration estimates. This suggests that surface-based estimates may provide a more relevant exposure proxy than air-based estimates for relating past radon exposure to lung cancer risk.

Epstein-Barr virus infection is not associated with development of allergy in children.

Background. Differences in concentrations of antibodies to Epstein-Barr virus (EBV) in atopic and nonatopic children have been observed, suggesting that EBV infection may play a role in allergic diseases. Aim. To assess the association between EBV infection and atopy in Swedish children at 4 years of age. Materials and methods. Were studied 2561 children born in 1994 through 1996 in Stockholm, Sweden. The children were enrolled in a prospective birth cohort study focusing on the relation of exposure to various environmental and life style factors during early childhood and development of atopy. Blood samples were obtained when the children were ∼4 years old, and immunoglobulin G to EBV was determined by indirect immunofluorescence. The relationship between the seroprevalence to EBV and various allergic disorders was assessed, withthe use of logistic regression analysis to account for other risk factors. Results. Totally 1347 of 2561 (52%) children were EBV-seropositive. Associations between EBV seropositivity and the occurrence of asthma [adjusted odds ratio (ORadj), 1.10; 95% confidence interval (95% CI) 0.81 to 1.49] or suspected allergic rhinitis (ORadj 0.97; 95% CI 0.76 to 1.25) were not apparent. In children whose mothers were up to 25 years old, a higher EBV seroprevalence was observed than in children of older mothers (ORadj 1.34; 95% CI 1.04 to 1.71). Also in children whose mothers smoked, the seroprevalence was higher than in children of nonsmokers (ORadj 1.29; 95% CI 1.02 to 1.63). Conclusions. The study does not support the hypothesis that EBV infection in early childhood plays an important role in the pathogenesis of allergic diseases in children.

Lifetime risk of lung cancer due to radon exposure projected to Japanese and Swedish populations

Lifetime risk projections depend greatly on both background lung cancer rates and the selection of the risk model. Since background lung cancer rates differ from subject populations and the time, etiological risk of lifetime lung cancer mortality per unit radon exposure in WLM should be estimated for each subject population and the time of interest. To answer quantitatively how much are the differences among the projected risks for different populations, the Swedish case-control-study-based risk projection model was applied to the Japanese and Swedish populations from 1962 to 1997 as subject populations because of their distinct trends of lung cancer rates. To compare the results with the reference population and authorized risk projection models, U.S. population 1997 and the two risk projection models in BEIR VI report were applied, respectively. Lifetime risk of lung cancer mortality projected for Japanese, Swedish, and U.S. populations in 1997 per radon progeny exposure were estimated to range from 1.50 (0.40-3.19) x 10(-4) WLM(-1) to 9.86 (2.62-20.9) x 10(-4) WLM(-1), which could be compared to the detriment associated with a unit effective dose. Conclusive dose conversion coefficients in this study ranged from 2.05 (0.55-4.37) to 13.5 (3.59-28.6) mSv WLM(-1), and within this range the discrepancy between dosimetric and epidemiological approaches was included.