•COSMOS is a multi-national prospective cohort study of mobile phone use and health.•Earlier epidemiologic studies are limited by recall bias or crude exposure assessment.•COSMOS includes over 250000 ...participants, a large proportion are long-term users.•We found no evidence of increased risk of glioma, meningioma or acoustic neuroma.•Suggests that amount of mobile phone use is not associated with brain tumour risk.
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.
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.
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).
Our findings suggest that the cumulative amount of mobile phone use is not associated with the risk of developing glioma, meningioma, or acoustic neuroma.
•A nationwide, register-based, case-control study with 12 928 brain tumor cases.•State of the art air pollution modeling for all addresses 10 years before diagnosis.•Primary emitted carbonaceous ...particles was associated with malignant brain tumors.•Results need replication.
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.
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.
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.
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.
•Above median mobile phone call-time was associated with less sleep disturbance.•Above 90th percentile mobile phone call time was associated with insomnia.•Adjustment for network suggests association ...with insomnia was not due to RF-EMF.•Other potential explanations may be related to behavior and psychological factors.
Effects of radiofrequency electromagnetic field exposure (RF-EMF) from mobile phone use on sleep quality has mainly been investigated in cross-sectional studies. The few previous prospective cohort studies found no or inconsistent associations, but had limited statistical power and short follow-up. In this large prospective cohort study, our aim was to estimate the effect of RF-EMF from mobile phone use on different sleep outcomes.
The study included Swedish (n = 21,049) and Finnish (n = 3120) participants enrolled in the Cohort Study of Mobile Phone Use and Health (COSMOS) with information about operator-recorded mobile phone use at baseline and sleep outcomes both at baseline and at the 4-year follow-up. Sleep disturbance, sleep adequacy, daytime somnolence, sleep latency, and insomnia were assessed using the Medical Outcome Study (MOS) sleep questionnaire.
Operator-recorded mobile phone use at baseline was not associated with most of the sleep outcomes. For insomnia, an odds ratio (OR) of 1.24, 95% CI 1.03–1.51 was observed in the highest decile of mobile phone call-time (>258 min/week). With weights assigned to call-time to account for the lower RF-EMF exposure from Universal Mobile Telecommunications Service (UMTS, 3G) than from Global System for Mobile Communications (GSM, 2G) the OR was 1.09 (95% CI 0.89–1.33) in the highest call-time decile.
Insomnia was slightly more common among mobile phone users in the highest call-time category, but adjustment for the considerably lower RF-EMF exposure from the UMTS than the GSM network suggests that this association is likely due to other factors associated with mobile phone use than RF-EMF. No association was observed for other sleep outcomes. In conclusion, findings from this study do not support the hypothesis that RF-EMF from mobile phone use has long-term effects on sleep quality.
AbstractObjectiveTo investigate the association between long term residential exposure to road traffic and railway noise and risk of incident dementia.DesignNationwide prospective register based ...cohort study.SettingDenmark.Participants1 938 994 adults aged ≥60 years living in Denmark between 1 January 2004 and 31 December 2017.Main outcome measuresIncident cases of all cause dementia and dementia subtypes (Alzheimer’s disease, vascular dementia, and Parkinson’s disease related dementia), identified from national hospital and prescription registries.ResultsThe study population included 103 500 participants with incident dementia, and of those, 31 219 received a diagnosis of Alzheimer’s disease, 8664 of vascular dementia, and 2192 of Parkinson’s disease related dementia. Using Cox regression models, 10 year mean exposure to road traffic and railway noise at the most (Ldenmax) and least (Ldenmin) exposed façades of buildings were associated with a higher risk of all cause dementia. These associations showed a general pattern of higher hazard ratios with higher noise exposure, but with a levelling off or even small declines in risk at higher noise levels. In subtype analyses, both road traffic noise and railway noise were associated with a higher risk of Alzheimer’s disease, with hazard ratios of 1.16 (95% confidence interval 1.11 to 1.22) for road Ldenmax ≥65 dB compared with <45 dB, 1.27 (1.22 to 1.34) for road Ldenmin ≥55 dB compared with <40 dB, 1.16 (1.10 to 1.23) for railway Ldenmax ≥60 dB compared with <40 dB, and 1.24 (1.17 to 1.30) for railway Ldenmin ≥50 dB compared with <40 dB. Road traffic, but not railway, noise was associated with an increased risk of vascular dementia. Results indicated associations between road traffic Ldenmin and Parkinson’s disease related dementia.ConclusionsThis nationwide cohort study found transportation noise to be associated with a higher risk of all cause dementia and dementia subtypes, especially Alzheimer’s disease.
Noise from wind turbines (WTs) is associated with annoyance and, potentially, sleep disturbances.
Our objective was to investigate whether long-term WT noise (WTN) exposure is associated with the ...redemption of prescriptions for sleep medication and antidepressants.
For all Danish dwellings within a radius of Formula: see text heights and for 25% of randomly selected dwellings within a radius of Formula: see text heights, we estimated nighttime outdoor and low-frequency (LF) indoor WTN, using information on WT type and simulated hourly wind. During follow-up from 1996 to 2013, 68,696 adults redeemed sleep medication and 82,373 redeemed antidepressants, from eligible populations of 583,968 and 584,891, respectively. We used Poisson regression with adjustment for individual and area-level covariates.
Five-year mean outdoor nighttime WTN of Formula: see text was associated with a hazard ratio (HR) = 1.14 95% confidence interval (CI: 0.98, 1.33) for sleep medication and HR = 1.17 (95% CI: 1.01, 1.35) for antidepressants (compared with exposure to WTN of Formula: see text). We found no overall association with indoor nighttime LF WTN. In age-stratified analyses, the association with outdoor nighttime WTN was strongest among persons Formula: see text of age, with HRs (95% CIs) for the highest exposure group (Formula: see text) of 1.68 (1.27, 2.21) for sleep medication and 1.23 (0.90, 1.69) for antidepressants. For indoor nighttime LF WTN, the HRs (95% CIs) among persons Formula: see text of age exposed to Formula: see text were 1.37 (0.81, 2.31) for sleep medication and 1.34 (0.80, 2.22) for antidepressants.
We observed high levels of outdoor WTN to be associated with redemption of sleep medication and antidepressants among the elderly, suggesting that WTN may potentially be associated with sleep and mental health. https://doi.org/10.1289/EHP3909.
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Dostopno za:
CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
Noise from wind turbines (WTs) is reported as more annoying than traffic noise at similar levels, raising concerns as to whether WT noise (WTN) increases risk for cardiovascular disease, as observed ...for traffic noise.
We aimed to investigate whether long-term exposure to WTN increases risk of myocardial infarction (MI) and stroke.
We identified all Danish dwellings within a radius 20 times the height of the closest WT and 25% of the dwellings within Formula: see text the height of the closest WT. Using data on WT type and simulated hourly wind at each WT, we estimated hourly outdoor and low frequency (LF) indoor WTN for each dwelling and derived 1-y and 5-y running nighttime averages. We used hospital and mortality registries to identify all incident cases of MI (Formula: see text) and stroke (Formula: see text) among all adults age 25-85 y (Formula: see text), who lived in one of these dwellings for Formula: see text over the period 1982-2013. We used Poisson regression to estimate incidence rate ratios (IRRs) adjusted for individual- and area-level covariates.
IRRs for MI in association with 5-y nighttime outdoor WTN Formula: see text (vs. Formula: see text) dB(A) and indoor LF WTN Formula: see text (vs. Formula: see text) dB(A) were 1.21 95% confidence interval (CI): 0.91, 1.62; 47 exposed cases and 1.29 (95% CI: 0.73, 2.28; 12 exposed cases), respectively. IRRs for intermediate categories of outdoor WTN 24-30, 30-36, and Formula: see text vs. Formula: see text were slightly above the null and of similar size: 1.08 (95% CI: 1.04, 1.12), 1.07 (95% CI: 1.00, 1.12), and 1.06 (95% CI: 0.93, 1.22), respectively. For stroke, IRRs for the second and third outdoor exposure groups were similar to those for MI, but near or below the null for higher exposures.
We did not find convincing evidence of associations between WTN and MI or stroke. https://doi.org/10.1289/EHP3340.
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Dostopno za:
CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
In the Nordic countries, the use of mobile phones increased sharply in the mid-1990s especially among middle-aged men. We investigated time trends in glioma incidence rates (IR) with the perspective ...to inform about the plausibility of brain tumour risks from mobile phone use reported in some case-control studies.
We analysed IR of glioma in Denmark, Finland, Norway, and Sweden among men aged 40–69 years, using data from national cancer registries and population statistics during 1979–2016, using log-linear joinpoint analysis. Information on regular mobile phone use and amount of call-time was obtained from major studies of mobile phones in these countries. We compared annual observed incidence with that expected under various risk scenarios to assess which of the reported effect sizes are compatible with the observed IR. The expected numbers of cases were computed accounting for an impact of other factors besides mobile phone use, such as improved cancer registration.
Based on 18,232 glioma cases, IR increased slightly but steadily with a change of 0.1% (95 %CI 0.0%; 0.3%) per year during 1979–2016 among 40–59-year-old men and for ages 60–69, by 0.6 % (95 %CI 0.4; 0.9) annually. The observed IR trends among men aged 40–59 years were incompatible with risk ratios (RR) 1.08 or higher with a 10-year lag, RR ≥ 1.2 with 15-year lag and RR ≥ 1.5 with 20-year lag. For the age group 60–69 years, corresponding effect sizes RR ≥ 1.4, ≥2 and ≥ 2.5 could be rejected for lag times 10, 15 and 20 years.
This study confirms and reinforces the conclusions that no changes in glioma incidence in the Nordic countries have occurred that are consistent with a substantial risk attributable to mobile phone use. This particularly applies to virtually all reported risk increases reported by previous case-control studies with positive findings.
•Case-cohort study included a randomly selected subcohort and 809 AMI cases.•Participants had relatively low urinary cadmium compared to prior studies.•We found little evidence that cadmium at ...relatively low-levels is associated with AMI.•Results were not materially different across strata defined by sex.•Similar results using creatinine or osmolality to account for urine dilution.
Cadmium exposure has been associated with cardiovascular disease. Cigarette smoking is a key source of cadmium exposure and thus a potential confounder in observational studies of environmental cadmium and cardiovascular disease that include tobacco smokers. We leveraged up to 20 years of follow-up in the Danish Diet, Cancer and Health cohort to test the hypothesis that cadmium exposure is associated with acute myocardial infarction (AMI) among people who never smoked. Between 1993 and 1997, 19,394 never-smoking participants (ages 50–64 years) were enrolled and provided a urine sample. From this sample, we randomly selected a subcohort of 600 males and 600 females. We identified 809 AMI cases occurring between baseline and the end of 2015 using the Danish National Patient Registry. We quantified cadmium, creatinine, and osmolality in baseline urine samples. Using an unweighted case-cohort approach, we estimated adjusted hazard ratios (aHR) for AMI in Cox proportional hazards models with age as the time axis. Participants had relatively low concentrations of urinary cadmium, as expected for never smokers (median = 0.20; 25th, 75th = 0.13, 0.32 μg cadmium/g creatinine). We did not find strong evidence to support an association between higher urinary cadmium and AMI when comparing the highest versus lowest quartile (aHR = 1.16; 95% CI: 0.86 – 1.56) and per IQR increment in cadmium concentration (aHR = 1.02; 95% CI: 0.93 – 1.12). Results were not materially different across strata defined by sex. Results were generally similar using creatinine or osmolality to account for differences in urine dilution. While cadmium exposure has been identified as a risk factor for cardiovascular disease, we did not find strong evidence that urinary cadmium at relatively low-levels is associated with AMI among people who have never smoked.
Leukemia is one of the most common forms of hematologic malignancy, which can affect people of all ages. We previously showed an association between exposure to ambient particulate matter 2.5 μg ...(PM2.5) and risk for leukemia in adults. The aim of this study was to investigate which PM2.5 constituents were responsible for our previous observation.
This is a nationwide register-based case-control study. We identified 14,983 persons diagnosed with leukemia at age 20 or above, 1989–2014, in the Danish Cancer Registry. We selected up to four sex and age-matched controls per case at random from the entire Danish population (n = 51,613). We modelled concentrations of ambient PM2.5 and its constituents at the addresses of cases and controls for the 10-year period before index date with a state-of-the-art multiscale air pollution modeling system. We used conditional logistic regression to estimate odds ratios (ORs) adjusted for individual and neighborhood level socio-demographic variables.
The results showed higher risk for overall leukemia in association with interquartile range exposure to PM2.5 (OR = 1.09; 95% CI: 1.02, 1.17), black carbon (BC) (OR = 1.02; 95% CI: 1.00, 1.03), secondary inorganic aerosols (SIA) (OR = 1.15; 95% CI: 1.03, 1.29) and its components ammonium (NH4) (OR = 1.08; 95% CI: 1.00, 1.17) and nitrate (NO3) (OR = 1.08; 95% CI: 1.02, 1.14). In leukemia subtype analysis, statistically significant associations were found for AML with PM2.5 (OR = 1.14; 95% CI: 1.00, 1.29), BC (OR = 1.03; 95% CI: 1.00, 1.07), SIA (OR = 1.23; 95% CI: 1.01, 1.51), NH4 (OR = 1.16; 95% CI: 1.01, 1.34) and NO3 (OR = 1.12; 95% CI: 1.01, 1.24). The association between PM2.5 and leukemia persisted in two pollutants models including sum of primary emitted black and organic carbon (BC + OC), secondary organic aerosols (SOA), or sea-salt. The association between black carbon (BC) and leukemia persisted in two pollutants models including organic carbon (OC). The three pollutant model with sulfate (SO4), NH4 and NO3 showed an association with NO3 but not with SO4 or NH4.
Ambient concentrations of the PM2.5 components BC, NH4 and NO3 at the residence showed associations with risk of incident leukemia in adults.
•“This is a Danish register-based case-control study utilizing all adult leukemia cases between 1989 and 2014.“.•“Validated exposure modeling system with high temporal and spatial resolution was used for exposure assessment.“.•“Particulate matter constituents were associated with increased risk of adult leukemia incidence.“.
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