Mobile phone use and brain tumour risk - COSMOS, a prospective cohort study.

BACKGROUND: Each new generation of mobile phone technology has triggered discussions about potential carcinogenicity from exposure to radiofrequency electromagnetic fields (RF-EMF). Available evidence has been insufficient to conclude about long-term and heavy mobile phone use, limited by differential recall and selection bias, or crude exposure assessment. The Cohort Study on Mobile Phones and Health (COSMOS) was specifically designed to overcome these shortcomings. METHODS: We recruited participants in Denmark, Finland, the Netherlands, Sweden, and the UK 2007-2012. The baseline questionnaire assessed lifetime history of mobile phone use. Participants were followed through population-based cancer registers to identify glioma, meningioma, and acoustic neuroma cases during follow-up. Non-differential exposure misclassification was reduced by adjusting estimates of mobile phone call-time through regression calibration methods based on self-reported data and objective operator-recorded information at baseline. Hazard ratios (HR) and 95% confidence intervals (CI) for glioma, meningioma, and acoustic neuroma in relation to lifetime history of mobile phone use were estimated with Cox regression models with attained age as the underlying time-scale, adjusted for country, sex, educational level, and marital status. RESULTS: 264,574 participants accrued 1,836,479 person-years. During a median follow-up of 7.12 years, 149 glioma, 89 meningioma, and 29 incident cases of acoustic neuroma were diagnosed. The adjusted HR per 100 regression-calibrated cumulative hours of mobile phone call-time was 1.00 (95 % CI 0.98-1.02) for glioma, 1.01 (95 % CI 0.96-1.06) for meningioma, and 1.02 (95 % CI 0.99-1.06) for acoustic neuroma. For glioma, the HR for ≥ 1908 regression-calibrated cumulative hours (90th percentile cut-point) was 1.07 (95 % CI 0.62-1.86). Over 15 years of mobile phone use was not associated with an increased tumour risk; for glioma the HR was 0.97 (95 % CI 0.62-1.52). CONCLUSIONS: Our findings suggest that the cumulative amount of mobile phone use is not associated with the risk of developing glioma, meningioma, or acoustic neuroma.

Long-term residential exposure to air pollution and risk of testicular cancer in Denmark: A population-based case-control study.

BACKGROUND: The incidence rate risk of testicular cancer has increased over the last four decades, and most significant increase has been among Caucasian men in Nordic countries. Second-generation immigrant studies indicate a significant role of environmental exposure in testicular cancer. METHODS: We conducted a nationwide register-based case-control study, including 6,390 testicular cancer cases registered in the Danish Cancer Registry between 1989 and 2014. Up to four age-matched controls for each case (n=18,997) were randomly selected from Civil Registration System. Ambient air pollution levels were estimated at addresses of cases and controls with a state-of-the-art air pollution modeling system. RESULTS: We mostly found ORs close to 1.00 and with 95% confidence intervals (CI) spanning 1.00. Exposure during the year preceding birth was associated with ORs for NO2 of 0.87 (95%CI: 0.77-0.97) per 10 µg/m3 and for organic carbon of 0.84 (95%CI: 0.72-0.98) per 1 µg/m3. Exposure during the first 10 years of life was associated with ORs for organic carbon of 0.79 (95%CI: 0.67-0.93) per 1 µg/m3, for O3 of 1.20 (95%CI: 1.07-1.34) per 10 µg/m3 and for secondary inorganic aerosols of 1.07 (95%CI: 1.00-1.15) per 1 µg/m3. CONCLUSIONS: Early-life exposure to NO2 and OC was associated with lower risk for testicular cancer whereas early-life exposure to O3 and SIA was associated with higher risk. IMPACT: We report both positive and negative associations between ambient air pollutants and risk of testicular, dependent on pollutant, exposure time window and age at diagnosis. This is the first study to investigate such associations.

Components of particulate matter air-pollution and brain tumors.

BACKGROUND: Air pollution is an established carcinogen. Evidence for an association with brain tumors is, however, inconclusive. We investigated if individual particulate matter constituents were associated with brain tumor risk. METHODS: From comprehensive national registers, we identified all (n = 12 928) brain tumor cases, diagnosed in Denmark in the period 1989-2014, and selected 22 961 controls, matched on age, sex and year of birth. We established address histories and estimated 10-year mean residential outdoor concentrations of particulate matter < 2.5 µm, primarily emitted black carbon (BC) and organic carbon (OC), and combined carbon (OC/BC), as well as secondary inorganic and organic PM air pollutants from a detailed dispersion model. We used conditional logistic regression to calculate odds ratios (OR) per inter quartile range (IQR) exposure. We adjusted for income, marital and employment status as well as area-level socio-demographic characteristics. RESULTS: Total tumors of the brain were associated with OC/BC (OR: 1.053, 95%CI: 1.005-1.103, per IQR). The data suggested strongest associations for malignant tumors with ORs per IQR for OC/BC, BC and OC of 1.063 (95% CI: 1.007-1.123), 1.036 (95% CI: 1.006-1.067) and 1.030 (95%CI: 0.979-1.085), respectively. The results did not indicate adverse effects of other PM components. CONCLUSIONS: This large, population based study showed associations between primary emitted carbonaceous particles and risk for malignant brain tumors. As the first of its kind, this study needs replication.

Traffic-related air pollution and risk for leukaemia of an adult population.

Air pollution causes lung cancer, but associations with other cancers have not been established. We investigated whether long-term exposure to traffic-related air pollution is associated with the risk of the general population for leukaemia. We identified 1,967 people in whom leukaemia was diagnosed in 1992-2010 from a nation-wide cancer registry and selected 3,381 control people at random, matched on sex and year of birth, from the entire Danish population. Residential addresses since 1971 were traced in a population registry, and outdoor concentrations of NOx and NO2 , as indicators of traffic-related air pollution, were calculated at each address in a dispersion model. We used conditional logistic regression to estimate the risk for leukaemia after adjustment for income, educational level, cohabitation status and co-morbidity. In linear analyses, we found odds ratios for acute myeloid leukaemia of 1.20 (95% confidence interval: 1.04-1.38) per 20 µg/m(3) increase in NOx and 1.31 (1.02-1.68) per 10 µg/m(3) increase in NO2 , calculated as time-weighted average exposure at all addresses since 1971. We found no association with chronic myeloid or lymphocytic leukaemia. This study indicates an association between long-term exposure to traffic-related air pollution and acute myeloid leukaemia in the general population, but not for other subtypes of leukaemia.

Residential exposure to traffic noise and risk for non-hodgkin lymphoma among adults.

Exposure to traffic noise may result in stress and sleep disturbances, which have been associated with impairment of the immune system. People with weakened immune systems are known to have a higher risk for non-Hodgkin lymphoma (NHL). We aimed to determine whether traffic noise was associated with risk for NHL in a nationwide case-control study. We identified 2753 cases aged 30-84 years with a primary diagnosis of NHL in Denmark between 1992 and 2010. For each case we selected two random population controls, matched on sex and year of birth. Road traffic and railway noise were calculated, and airport noise was estimated for all present and historical residential addresses of cases and controls from 1987 to 2010. Associations between traffic noise and risk for NHL were estimated using conditional logistic regression, adjusted for disposable income, education, cohabiting status and comorbidity. We found that a 5-year time-weighted mean of road traffic noise above 65 dB was associated with an 18% higher risk for NHL (95% confidence interval (CI) 1.01-1.37) when compared to road traffic noise below 55 dB, whereas for exposure between 55 and 65 dB no association was found (odds ratio: 0.98; 95% CI: 0.88-1.08). In analyzes of NHL subtypes, we found no association between road traffic noise and risk for T-cell lymphoma, whereas increased risks for B-cell lymphoma and unspecified lymphomas were observed at exposures above 65 dB. In conclusion, our nationwide study may indicate that high exposure to traffic noise is associated with higher NHL risk.

Mobile phones and multiple sclerosis--a nationwide cohort study in Denmark.

We investigated the risk of, prognosis of and symptoms of multiple sclerosis (MS) among all Danish residents who owned a mobile phone subscription before 1996. Using the Danish Multiple Sclerosis Registry and Civil Registration System, study subjects were followed up for MS through 2004. Poisson models were used to calculate incidence rate ratios (IRR, age range: 18-64 years) and mortality rate ratios (MRR, age range: 18+) and to compare presenting symptoms among subscribers and all non-subscribers. A total of 405 971 subscription holders accrued four million years of follow up, with men accounting for 86% of the observation time. Among subscription holding men, the IRR of MS was close to unity, overall as well as 13+ years after first subscription (IRR 1.02, 95% CI: 0.48-2.16). Among women, the IRR was 3.43 (95% CI: 0.86-13.72) 13+ years after first subscription, however, based on only two cases. Presenting symptoms of MS differed between subscribers and non-subscribers (p = 0.03), with slightly increased risk of diplopia in both genders (IRR: 1.38, 95% CI: 1.02-1.86), an increased risk of fatigue among women (IRR: 3.02, 95% CI: 1.45-6.28), and of optic neuritis among men (IRR: 1.38, 95% CI: 1.03-1.86). Overall the MRR was close to one (MRR: 0.91, 95%CI 0.70-1.19) among MS-patients with a subscription and although we observed some increased MRR estimates among women, these were based on small numbers. In conclusion, we found little evidence for a pronounced association between mobile phone use and risk of MS or mortality rate among MS patients. Symptoms of MS differed between subscribers and nonsubscribers for symptoms previously suggested to be associated with mobile phone use. This deserves further attention, as does the increased long-term risk of MS among female subscribers, although small numbers and lack of consistency between genders prevent causal interpretation.