Mette Sørensen

Long-Term Exposure to Road Traffic Noise and Incident Diabetes: A Cohort Study

Background: Road traffic noise at normal urban levels can lead to stress and sleep disturbances. Both excess of stress hormones and reduction in sleep quality and duration may lead to higher risk for type 2 diabetes. Objective: We investigated whether long-term exposure to residential road traffic noise is associated with an increased risk of diabetes. Methods: In the population-based Danish Diet, Cancer and Health cohort of 57,053 people 50–64 years of age at enrollment in 1993–1997, we identified 3,869 cases of incident diabetes in a national diabetes registry between enrollment and 2006. The mean follow-up time was 9.6 years. Present and historical residential addresses from 1988 through 2006 were identified using a national register, and exposure to road traffic noise was estimated for all addresses. Associations between exposure to road traffic noise and incident diabetes were analyzed in a Cox regression model. Results: A 10-dB higher level of average road traffic noise at diagnosis and during the 5 years preceding diagnosis was associated with an increased risk of incident diabetes, with incidence rate ratios (IRR) of 1.08 (95% CI: 1.02, 1.14) and 1.11 (95% CI: 1.05, 1.18), respectively, after adjusting for potential confounders including age, body mass index, waist circumference, education, air pollution (nitrogen oxides), and lifestyle characteristics. After applying a stricter definition of diabetes (2,752 cases), we found IRRs of 1.11 (95% CI: 1.03, 1.19) and 1.14 (95% CI: 1.06, 1.22) per 10-dB increase in road traffic noise at diagnosis and during the 5 years preceding diagnosis, respectively. Conclusion: Exposure to residential road traffic noise was associated with a higher risk of diabetes. This study provides further evidence that urban noise may adversely influence population health.

Diabetes incidence and long-term exposure to air pollution: a cohort study.

OBJECTIVE Animal and cross-sectional epidemiological studies suggest a link between air pollution and diabetes, whereas the limited prospective data show mixed results. We studied the association between long-term exposure to traffic-related air pollution and incidence of diabetes. RESEARCH DESIGN AND METHODS We followed 57,053 participants of the Danish Diet, Cancer, and Health cohort in the Danish National Diabetes Register between baseline (1993–1997) and 27 June 2006. We estimated the mean levels of nitrogen dioxide (NO2) at the residential addresses of the cohort participants since 1971 and modeled the association between NO2 and diabetes incidence with a Cox regression model, separately for two definitions of diabetes: all cases and a more strict definition where unconfirmed cases were excluded. RESULTS Over a mean follow-up of 9.7 years of 51,818 eligible subjects, there were 4,040 (7.8%) incident diabetes cases in total and 2,877 (5.5%) with confirmed diagnoses. Air pollution was not associated with all diabetes cases (hazard ratio 1.00 [95% CI 0.97–1.04] per interquartile range of 4.9 μg/m3 mean NO2 levels since 1971), but a borderline statistically significant association was detected with confirmed cases of diabetes (1.04 [1.00–1.08]). Among confirmed diabetes cases, effects were significantly enhanced in nonsmokers (1.12 [1.05–1.20]) and physically active people (1.10 [1.03–1.16]). CONCLUSIONS Long-term exposure to traffic-related air pollution may contribute to the development of diabetes, especially in individuals with a healthy lifestyle, nonsmokers, and physically active individuals.

Road traffic noise and stroke: a prospective cohort study

AIMS Epidemiological studies suggest that long-term exposure to road traffic noise increases the risk of cardiovascular disorders. The aim of this study was to investigate the relation between exposure to road traffic noise and risk for stroke, which has not been studied before. METHODS AND RESULTS In a population-based cohort of 57,053 people, we identified 1881 cases of first-ever stroke in a national hospital register between 1993-1997 and 2006. Exposure to road traffic noise and air pollution during the same period was estimated for all cohort members from residential address history. Associations between exposure to road traffic noise and stroke incidence were analysed in a Cox regression model with stratification for gender and calendar-year and adjustment for air pollution and other potential confounders. We found an incidence rate ratio (IRR) of 1.14 for stroke [95% confidence interval (CI): 1.03-1.25] per 10 dB higher level of road traffic noise (L(den)). There was a statistically significant interaction with age (P < 0.001), with a strong association between road traffic noise and stroke among cases over 64.5 years (IRR: 1.27; 95% CI: 1.13-1.43) and no association for those under 64.5 years (IRR: 1.02; 95% CI: 0.91-1.14). CONCLUSION Exposure to residential road traffic noise was associated with a higher risk for stroke among people older than 64.5 years of age.

Transition metals in personal samples of PM2.5 and oxidative stress in human volunteers.

Ambient particulate matter (PM) has been associated with increased risk of lung cancer. One proposed mechanism is that PM induces oxidative stress mediated by transition metals contained within this mixture. We examined the relationship between the personal exposure to water-soluble transition metals in PM2.5 and oxidative DNA damage. In 49 students from central Copenhagen, we determined PM2.5 exposure by personal sampling twice in 1 year, and measured in these PM2.5 samples the concentration of the soluble transition metals vanadium, chromium, iron, nickel, copper, and platinum. Collected lymphocytes and 24-hour urine samples were analyzed for DNA damage in terms of 7-hydro-8-oxo-2′-deoxyguanosine (8-oxodG). We found that the 8-oxodG concentration in lymphocytes was significantly associated with the vanadium and chromium concentrations with a 1.9% increase in 8-oxodG per 1 μg/L increase in the vanadium concentration and a 2.2% increase in 8-oxodG per 1 μg/L increase in the chromium concentration. We have previously reported that in this study population the personal exposure to PM2.5 was associated with an increase in 8-oxodG in lymphocytes. However, vanadium and chromium were associated with the 8-oxodG concentration in lymphocytes independently of the PM2.5 mass concentration. The four other transition metals were not associated with 8-oxodG in lymphocytes and none of the transition metals was significantly associated with 8-oxodG in urine. Our results could indicate that vanadium and chromium present in PM2.5 have an effect on oxidative DNA damage that is independent of particle mass and/or other possible toxic compounds contained within this particulate mixture.

Road traffic noise and incident myocardial infarction: a prospective cohort study

Background Both road traffic noise and ambient air pollution have been associated with risk for ischemic heart disease, but only few inconsistent studies include both exposures. Methods In a population-based cohort of 57 053 people aged 50 to 64 years at enrolment in 1993–1997, we identified 1600 cases of first-ever MI between enrolment and 2006. The mean follow-up time was 9.8 years. Exposure to road traffic noise and air pollution from 1988 to 2006 was estimated for all cohort members from residential address history. Associations between exposure to road traffic noise and incident MI were analysed in a Cox regression model with adjustment for air pollution (NOx) and other potential confounders: age, sex, education, lifestyle confounders, railway and airport noise. Results We found that residential exposure to road traffic noise (Lden) was significantly associated with MI, with an incidence rate ratio IRR of 1.12 per 10 dB for both of the two exposure windows: yearly exposure at the time of diagnosis (95% confidence interval (CI): 1.02–1.22) and 5-years time-weighted mean (95% CI: 1.02–1.23) preceding the diagnosis. Visualizing of the results using restricted cubic splines showed a linear dose-response relationship. Conclusions Exposure to long-term residential road traffic noise was associated with a higher risk for MI, in a dose-dependent manner.

Air pollution from traffic and cancer incidence: a Danish cohort study

BackgroundVehicle engine exhaust includes ultrafine particles with a large surface area and containing absorbed polycyclic aromatic hydrocarbons, transition metals and other substances. Ultrafine particles and soluble chemicals can be transported from the airways to other organs, such as the liver, kidneys, and brain. Our aim was to investigate whether air pollution from traffic is associated with risk for other cancers than lung cancer.MethodsWe followed up 54,304 participants in the Danish Diet Cancer and Health cohort for 20 selected cancers in the Danish Cancer Registry, from enrolment in 1993-1997 until 2006, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used modeled concentration of nitrogen oxides (NOx) and amount of traffic at the residence as indicators of traffic-related air pollution and used Cox models to estimate incidence rate ratios (IRRs) after adjustment for potential confounders.ResultsNOx at the residence was significantly associated with risks for cervical cancer (IRR, 2.45; 95% confidence interval [CI], 1.01;5.93, per 100 μg/m3 NOx) and brain cancer (IRR, 2.28; 95% CI, 1.25;4.19, per 100 μg/m3 NOx).ConclusionsThis hypothesis-generating study indicates that traffic-related air pollution might increase the risks for cervical and brain cancer, which should be tested in future studies.

Glutathione S‐transferase T1 null‐genotype is associated with an increased risk of lung cancer

Glutathione S‐transferases (GSTs) are involved in detoxification of carcinogens, e.g., from tobacco smoke. Therefore, polymorphisms in the GST genes have been considered as potential modifiers of individual cancer risk. In a population‐based case‐cohort study where cases and the subcohort sample were matched on duration of smoking, we investigated the occurrence of lung cancer and histological subtypes of lung cancer in relation to deletion polymorphism in both GSTM1 and GSTT1, single nucleotide polymorphisms (SNPs) in GSTP1 (Ile105Val and Ala114Val) and a 3 base pair deletion polymorphism in GSTM3. We further investigated the effects of the GST polymorphisms on lung cancer risk within subgroups of subjects defined by gender and age. The results showed a 2.4‐fold (CI = 1.31–4.41) increased risk of lung cancer in GSTT1 null‐genotype carriers but no significant effects of the polymorphisms in GSTM1, GSTM3, GSTP1‐105 or GSTP1‐114. The association was strongest in lower age groups, with a 9.6‐fold increase in risk for subjects with the GSTT1 null‐genotype in the 50–55 years age interval (CI = 3.03–30.59). Positive associations were found for GSTT1 within all major histological subtypes. Squamous cell carcinoma was the histological type most strongly associated with the GSTT1 genotype, with a 5.0‐fold (CI = 2.26–11.18) increase in risk for subjects carrying the GSTT1 null‐genotype. The effects of the GSTT1 null‐genotype seemed stronger in the presence of the GSTM1 null‐genotype or the GSTP1‐105 variant allele. These results suggest that the GSTT1 null‐genotype is associated with an increased risk of lung cancer, especially in younger individuals.

Long-term exposure to traffic-related air pollution associated with blood pressure and self-reported hypertension in a Danish cohort.

Background: Short-term exposure to air pollution has been associated with changes in blood pressure (BP) and emergency department visits for hypertension, but little is known about the effects of long-term exposure to traffic-related air pollution on BP and hypertension. Objectives: We studied whether long-term exposure to air pollution is associated with BP and hypertension. Methods: In 1993–1997, 57,053 participants 50–64 years of age were enrolled in a population-based cohort study. Systolic and diastolic BP (SBP and DBP, respectively) were measured at enrollment. Self-reported incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. We used a validated dispersion model to estimate residential long-term nitrogen oxides (NOx), a marker of traffic-related air pollution, for the 1- and 5-year periods prior to enrollment and before a diagnosis of hypertension. We conducted a cross-sectional analysis of associations between air pollution and BP at enrollment with linear regression, adjusting for traffic noise, measured short-term NOx, temperature, relative humidity, and potential lifestyle confounders (n = 44,436). We analyzed incident hypertension with Cox regression, adjusting for traffic noise and potential confounders. Results: A doubling of NOx exposure during 1- and 5-year periods preceding enrollment was associated with 0.53-mmHg decreases [95% confidence interval (CI): –0.88, –0.19 mmHg] and 0.50-mmHg decreases (95% CI: –0.84, –0.16 mmHg) in SBP, respectively. Long-term exposure also was associated with a lower prevalence of baseline self-reported hypertension (per doubling of 5-year mean NOx: odds ratio = 0.96; 95% CI: 0.91, 1.00), whereas long-term NOx exposure was not associated with incident self-reported hypertension during follow-up. Conclusions: Long-term exposure to traffic-related air pollution was associated with a slightly lower prevalence of BP at baseline, but was not associated with incident hypertension.

Traffic air pollution and mortality from cardiovascular disease and all causes: a Danish cohort study

BackgroundTraffic air pollution has been linked to cardiovascular mortality, which might be due to co-exposure to road traffic noise. Further, personal and lifestyle characteristics might modify any association.MethodsWe followed up 52 061 participants in a Danish cohort for mortality in the nationwide Register of Causes of Death, from enrollment in 1993–1997 through 2009, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used dispersion-modelled concentration of nitrogen dioxide (NO2) since 1971 as indicator of traffic air pollution and used Cox regression models to estimate mortality rate ratios (MRRs) with adjustment for potential confounders.ResultsMean levels of NO2 at the residence since 1971 were significantly associated with mortality from cardiovascular disease (MRR, 1.26; 95% confidence interval [CI], 1.06–1.51, per doubling of NO2 concentration) and all causes (MRR, 1.13; 95% CI, 1.04–1.23, per doubling of NO2 concentration) after adjustment for potential confounders. For participants who ate < 200 g of fruit and vegetables per day, the MRR was 1.45 (95% CI, 1.13–1.87) for mortality from cardiovascular disease and 1.25 (95% CI, 1.11–1.42) for mortality from all causes.ConclusionsTraffic air pollution is associated with mortality from cardiovascular diseases and all causes, after adjustment for traffic noise. The association was strongest for people with a low fruit and vegetable intake.

Exposure to road traffic and railway noise and associations with blood pressure and self-reported hypertension: a cohort study

BackgroundEpidemiological studies suggest that long-term exposure to transport noise increases the risk for cardiovascular disorders. The effect of transport noise on blood pressure and hypertension is uncertain.MethodsIn 1993-1997, 57,053 participants aged 50-64 year were enrolled in a population-based cohort study. At enrolment, systolic and diastolic blood pressure was measured. Incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. Residential long-term road traffic noise (Lden) was estimated for 1- and 5-year periods preceding enrolment and preceding diagnosis of hypertension. Residential exposure to railway noise was estimated at enrolment. We conducted a cross-sectional analysis of associations between road traffic and railway noise and blood pressure at enrolment with linear regression, adjusting for long-term air pollution, meteorology and potential lifestyle confounders (N = 44,083). Incident self-reported hypertension was analyzed with Cox regression, adjusting for long-term air pollution and potential lifestyle confounders.ResultsWe found a 0.26 mm Hg higher systolic blood pressure (95% confidence intervals (CI): -0.11; 0.63) per 10 dB(A) increase in 1-year mean road traffic noise levels, with stronger associations in men (0.59 mm Hg (CI: 0.13; 1.05) per 10 dB(A)) and older participants (0.65 mm Hg (0.08; 1.22) per 10 dB(A)). Road traffic noise was not associated with diastolic blood pressure or hypertension. Exposure to railway noise above 60 dB was associated with 8% higher risk for hypertension (95% CI: -2%; 19%, P = 0.11).ConclusionsWhile exposure to road traffic noise was associated with systolic blood pressure in subgroups, we were not able to identify associations with hypertension.