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Xia, X., Jönsson, L., Tazzeo, C., Qiu, C., Rizzuto, D., Laukka, E. J., . . . Vetrano, D. L. (2024). Associations of Orthostatic Hypotension and Frailty With Dementia and Mortality in Older Adults: A Population-Based Cohort Study. The journals of gerontology. Series A, Biological sciences and medical sciences, 79(4), Article ID glae010.
Open this publication in new window or tab >>Associations of Orthostatic Hypotension and Frailty With Dementia and Mortality in Older Adults: A Population-Based Cohort Study
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2024 (English)In: The journals of gerontology. Series A, Biological sciences and medical sciences, ISSN 1079-5006, E-ISSN 1758-535X, Vol. 79, no 4, article id glae010Article in journal (Refereed) Published
Abstract [en]

Background

This study aimed to assess the associations of orthostatic hypotension (OH), in the presence or absence of frailty, with dementia and mortality in older adults.

Methods

We conducted a 15-year population-based cohort study including 2 703 baseline dementia-free individuals from the Swedish National Study on Aging and Care in Kungsholmen. At baseline, OH was defined as a decline in systolic/diastolic blood pressure ≥20/10 mm Hg 1 minute after standing up from a supine position. Frailty status was defined following Fried's frailty phenotype. Dementia was diagnosed following the Diagnostic and Statistical Manual of Mental Disorders-fourth edition criteria. Multistate flexible parametric survival models were used to estimate associations of OH and frailty with dementia and mortality.

Results

Robust people with OH (adjusted hazard ratio [HR] = 2.28; 95% confidence interval [CI] = 1.47-3.54) and frail people without OH (HR = 1.98; 95% CI = 1.40-2.82) or with OH (HR = 2.73; 95% CI = 1.82-4.10) had a higher dementia risk than OH-free and robust people. Moreover, frail people, independently of the presence of OH, had higher mortality rate than OH-free and robust people. In individuals who developed dementia during the follow-up period, neither OH nor frailty was significantly associated with mortality.

Conclusions

Older adults with OH, whether robust or frail, may have a higher dementia risk than those without OH. Older adults with OH, when having frailty, may have a higher mortality rate than those without OH. The concurrent assessments of OH and frailty may provide prognostic values in terms of dementia and mortality risk in older adults.

Keywords
Cognitive aging, Epidemiology, Public health
National Category
Geriatrics Gerontology, specialising in Medical and Health Sciences
Identifiers
urn:nbn:se:su:diva-228140 (URN)10.1093/gerona/glae010 (DOI)001180129100001 ()38195215 (PubMedID)
Available from: 2024-04-10 Created: 2024-04-10 Last updated: 2024-04-10Bibliographically approved
Wu, J., Grande, G., Pyko, A., Laukka, E. J., Pershagen, G., Ögren, M., . . . Rizzuto, D. (2024). Long-term exposure to transportation noise in relation to global cognitive decline and cognitive impairment: Results from a Swedish longitudinal cohort. Environment International, 185, Article ID 108572.
Open this publication in new window or tab >>Long-term exposure to transportation noise in relation to global cognitive decline and cognitive impairment: Results from a Swedish longitudinal cohort
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2024 (English)In: Environment International, ISSN 0160-4120, E-ISSN 1873-6750, Vol. 185, article id 108572Article in journal (Refereed) Published
Abstract [en]

Background and aims: Transportation noise is an environmental exposure with mounting evidence of adverse health effects. Besides the increased risk of cardiovascular and metabolic diseases, recent studies suggest that long-term noise exposure might accelerate cognitive decline in older age. We examined the association between transportation noise and cognitive function in a cohort of older adults.

Methods: The present study is based on 2594 dementia-free participants aged 60 + years from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). Global cognition score and CIND (cognitive impairment, no dementia) were assessed with a comprehensive neuropsychological battery at baseline and up to 16 years. Residential transportation noise resulting from road traffic, railway, and aircraft were estimated at the most exposed façade and the time-weighted average exposure was assessed. Linear mixed-effect models were used to assess the effect of long-term traffic noise exposure on the rate of change in global cognition score. Hazard ratios (HRs) and 95 % confidence intervals (CIs) of CIND by transportation noise exposure were obtained with Cox proportional hazard models.

Results: Global cognition score decreased at an average rate of −0.041 (95 %CI −0.043, −0.039) per year. Aircraft noise was associated with a 0.007 (per 10 dB Lden; 95 %CI −0.012, −0.001) faster annual rate of decline. Global cognition score seems to be not affected by road traffic and railway noise. During the follow-up, 422 (21 %) participants developed CIND. A 10-dB Lden difference in exposure to aircraft and railway noise was associated with a 16 % (HR 1.16, 95 %CI 0.91, 1.49) and 26 % (HR 1.26, 95 %CI 1.01, 1.56) increased hazard of CIND in the multi-pollutant model, respectively. No association was found for road traffic (HR 1.00, 95 %CI 0.83, 1.21).

Conclusions: Transportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results.

Keywords
Transportation noise, Global cognitive decline, Cognitive impairment
National Category
Occupational Health and Environmental Health Gerontology, specialising in Medical and Health Sciences
Identifiers
urn:nbn:se:su:diva-229035 (URN)10.1016/j.envint.2024.108572 (DOI)001204459200001 ()38479058 (PubMedID)2-s2.0-85187543882 (Scopus ID)
Available from: 2024-05-13 Created: 2024-05-13 Last updated: 2024-05-13Bibliographically approved
Thiesmeier, R., Abbadi, A., Rizzuto, D., Calderón-Larrañaga, A., Hofer, S. M. & Orsini, N. (2024). Multiple imputation of systematically missing data on gait speed in the Swedish National Study on Aging and Care. Aging, 16(4), 3056-3067
Open this publication in new window or tab >>Multiple imputation of systematically missing data on gait speed in the Swedish National Study on Aging and Care
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2024 (English)In: Aging, E-ISSN 1945-4589, Vol. 16, no 4, p. 3056-3067Article in journal (Refereed) Published
Abstract [en]

Background: There is insufficient investigation of multiple imputation for systematically missing discrete variables in individual participant data meta-analysis (IPDMA) with a small number of included studies. Therefore, this study aims to evaluate the performance of three multiple imputation strategies - fully conditional specification (FCS), multivariate normal (MVN), conditional quantile imputation (CQI) - on systematically missing data on gait speed in the Swedish National Study on Aging and Care (SNAC).

Methods: In total, 1 000 IPDMA were simulated with four prospective cohort studies based on the characteristics of the SNAC. The three multiple imputation strategies were analysed with a two-stage common-effect multivariable logistic model targeting the effect of three levels of gait speed (100% missing in one study) on 5-years mortality with common odds ratios set to OR1 = 0.55 (0.8-1.2 vs ≤0.8 m/s), and OR2 = 0.29 (>1.2 vs ≤0.8 m/s).

Results: The average combined estimate for the mortality odds ratio OR1 (relative bias %) were 0.58 (8.2%), 0.58 (7.5%), and 0.55 (0.7%) for the FCS, MVN, and CQI, respectively. The average combined estimate for the mortality odds ratio OR2 (relative bias %) were 0.30 (2.5%), 0.33 (10.0%), and 0.29 (0.9%) for the FCS, MVN, and CQI respectively.

Conclusions: In our simulations of an IPDMA based on the SNAC where gait speed data was systematically missing in one study, all three imputation methods performed relatively well. The smallest bias was found for the CQI approach.

Keywords
simulation, systematically missing values, individual participant data, meta-analysis, gait speed
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:su:diva-228176 (URN)10.18632/aging.205552 (DOI)001179364200022 ()38358907 (PubMedID)
Available from: 2024-04-15 Created: 2024-04-15 Last updated: 2024-07-04Bibliographically approved
Wu, J., Grande, G., Triolo, F., Pyko, A., Sjöberg, L., Ljungman, P., . . . Rizzuto, D. (2023). Air pollution, social engagement, and depression in older adults: Results from a Swedish population-based cohort study. Environmental Pollution, 336, Article ID 122394.
Open this publication in new window or tab >>Air pollution, social engagement, and depression in older adults: Results from a Swedish population-based cohort study
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2023 (English)In: Environmental Pollution, ISSN 0269-7491, E-ISSN 1873-6424, Vol. 336, article id 122394Article in journal (Refereed) Published
Abstract [en]

Although emerging research has investigated the relationship between outdoor air pollution and depression risk in older adults, the results remain inconclusive. We aimed to determine the relationship between long-term exposure to ambient air pollution and depression among older adults and explore whether active social engagement may modify this association. At baseline (2001–2004), 2812 depression-free older adults from Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) were included. SNAC-K is a longitudinal population-based cohort in Stockholm, Sweden. Incident depression cases occurred during 2004–2013 were ascertained using the Diagnostic and Statistical Manual of Mental Disorders 4th Edition. Air pollution [particulate matter (PM) and nitrogen oxides (NOx)] at the residency were estimated using dispersion models. Social engagement was measured as active participation in social activities (at least twice/week) or inactive (less than twice/week) in the last 12 months. The hazard ratios (HR) and 95% confidence intervals of depression from air pollution exposure of 3-year moving average before diagnosis (1-μg/m3 difference in PM2.5 and PM10, and 10-μg/m3 difference in NOx) were obtained from Cox models considering greenspace and noise. A product term of air pollutant and social activity was added to test the multiplicative interaction and attributable proportion due to interaction was calculated for assessing additive interaction. We identified 137 (4.9%) incident depression cases. Participants exposed to higher concentrations of PM2.5, NOx, and PM10 had 53% (HR:1.53 [1.22, 1.93]), 26% (HR:1.26 [1.01, 1.58]), and 7% (HR:1.07 [0.98, 1.18]) increased hazard of depression, respectively. These associations were largely attenuated in people with active social engagement (HR for PM2.5: 1.04 [0.70, 1.55]; HR for PM10: 0.98 [0.81, 1.18]; and HR for NOx: 1.09 [0.71, 1.66]). Our findings suggest long-term exposure to air pollution may be a risk factor for depression among older adults. An active social engagement might however decrease this risk.

Keywords
Late-life depression, Air pollution, Particulate matter, Nitrogen Dioxide, Social engagement, Population-based study
National Category
Occupational Health and Environmental Health Gerontology, specialising in Medical and Health Sciences
Identifiers
urn:nbn:se:su:diva-223280 (URN)10.1016/j.envpol.2023.122394 (DOI)001072432600001 ()37597733 (PubMedID)2-s2.0-85169784916 (Scopus ID)
Available from: 2023-10-24 Created: 2023-10-24 Last updated: 2023-10-24Bibliographically approved
Imahori, Y., Vetrano, D. L., Ljungman, P., Laukka, E. J., Wu, J., Grande, G., . . . Qiu, C. (2023). Association of ischemic heart disease with long-term risk of cognitive decline and dementia: A cohort study. Alzheimer's & Dementia: Journal of the Alzheimer's Association, 19(12), 5541-5549
Open this publication in new window or tab >>Association of ischemic heart disease with long-term risk of cognitive decline and dementia: A cohort study
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2023 (English)In: Alzheimer's & Dementia: Journal of the Alzheimer's Association, ISSN 1552-5260, E-ISSN 1552-5279, Vol. 19, no 12, p. 5541-5549Article in journal (Refereed) Published
Abstract [en]

INTRODUCTION: The independent and joint effect of ischemic heart disease (IHD) and coexisting atrial fibrillation (AF) and heart failure (HF) on dementia risk is largely unknown.

METHODS: This population-based cohort study included 2568 dementia-free participants (age ≥60 years) in SNAC-K, who were regularly examined from 2001–2004 through 2013–2016. Dementia was diagnosed following the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) criteria. Global cognitive function was assessed using a global cognitive composite z-score derived from five cognitive domains. Data were analyzed using Cox, Fine-Gray, and linear mixed-effects models.

RESULTS: Overall, IHD at baseline was associated with multivariable-adjusted hazard ratio (HR) of 1.39 (95% confidence interval = 1.06−1.82) for dementia and multivariable-adjusted β-coefficient of −0.02 (−0.03 to −0.01) for annual changes in global cognitive z-score, independent of AF, HF, and cerebrovascular disease. Coexisting AF or HF did not add further risk to dementia and cognitive decline.

DISCUSSION: IHD is independently associated with dementia and cognitive decline in older adults, whereas coexisting AF/HF is not associated with an increased risk.

Keywords
cognitive decline, cohort study, dementia, heart disease, ischemic heart disease
National Category
Gerontology, specialising in Medical and Health Sciences Neurosciences Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:su:diva-220471 (URN)10.1002/alz.13114 (DOI)000997624100001 ()37249150 (PubMedID)2-s2.0-85161336197 (Scopus ID)
Available from: 2023-08-29 Created: 2023-08-29 Last updated: 2024-01-11Bibliographically approved
Guo, J., Dove, A., Shang, Y., Marseglia, A., Johnell, K., Rizzuto, D. & Xu, W. (2023). Associations Between Mid- to Late-Life Body Mass Index and Chronic Disease-Free Survival: A Nationwide Twin Study . The journals of gerontology. Series A, Biological sciences and medical sciences
Open this publication in new window or tab >>Associations Between Mid- to Late-Life Body Mass Index and Chronic Disease-Free Survival: A Nationwide Twin Study 
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2023 (English)In: The journals of gerontology. Series A, Biological sciences and medical sciences, ISSN 1079-5006, E-ISSN 1758-535XArticle in journal (Refereed) Epub ahead of print
Abstract [en]

Background: Some studies have linked late-life overweight to a reduced mortality risk compared to normal body mass index (BMI). However, the impact of late-life overweight and its combination with mid-life BMI status on healthy survival remains unclear. We aimed to investigate whether and to what extent mid- and/or late-life overweight are associated with chronic disease-free survival.

Methods: Within the Swedish Twin Registry, 11 597 chronic disease-free twins aged 60−79 years at baseline were followed up for 18 years. BMI (kg/m2) was recorded at baseline and 25−35 years before baseline (ie, midlife) and divided as underweight (<20), normal (≥20−25), overweight (≥25−30), and obese (≥30). Incident chronic diseases (cardiovascular diseases, type 2 diabetes, and cancer) and deaths were ascertained via registries. Chronic disease-free survival was defined as years lived until the occurrence of any chronic diseases or death. Data were analyzed using multistate survival analysis.

Results: Of all participants, 5 640 (48.6%) were overweight/obese at baseline. During the follow-up, 8 772 (75.6%) participants developed at least 1 chronic disease or died. Compared to normal BMI, late-life overweight and obesity were associated with 1.1 (95% CI, 0.3, 2.0) and 2.6 (1.6, 3.5) years shorter chronic disease-free survival. Compared to normal BMI through mid- to late life, consistent overweight/obesity and overweight/obesity only in mid-life led to 2.2 (1.0, 3.4) and 2.6 (0.7, 4.4) years shorter disease-free survival, respectively.

Conclusions: Late-life overweight and obesity may shorten disease-free survival. Further research is needed to determine whether preventing overweight/obesity from mid- to late life might favor longer and healthier survival.

Keywords
Cancer, Cardiovascular disease, Diabetes, Obesity, Overweight
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:su:diva-217311 (URN)10.1093/gerona/glad111 (DOI)000985156500001 ()37096341 (PubMedID)
Available from: 2023-05-24 Created: 2023-05-24 Last updated: 2023-08-16
Thacher, J. D., Oudin, A., Flanagan, E., Mattisson, K., Albin, M., Roswall, N., . . . Sorensen, M. (2023). Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts. Environment International, 178, Article ID 108108.
Open this publication in new window or tab >>Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts
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2023 (English)In: Environment International, ISSN 0160-4120, E-ISSN 1873-6750, Vol. 178, article id 108108Article in journal (Refereed) Published
Abstract [en]

Background: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence. Methods: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution. Results: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th-95th percentile) 5-year residential road traffic noise was 54.8 (40.0-67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2-65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99-1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96-1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM2.5 and attenuated when adjusted for NO2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99-1.18) for road traffic and 1.19 (0.95-1.49) for railway noise. Conclusions: We found weak associations between road and railway noise and breast cancer risk. More high -quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made.

Keywords
Noise, Traffic noise, Railway noise, Aircraft noise, Air pollution, Traffic, Breast cancer, Estrogen receptor
National Category
Earth and Related Environmental Sciences
Identifiers
urn:nbn:se:su:diva-221328 (URN)10.1016/j.envint.2023.108108 (DOI)001048475600001 ()37490787 (PubMedID)2-s2.0-85165505340 (Scopus ID)
Available from: 2023-09-19 Created: 2023-09-19 Last updated: 2023-09-19Bibliographically approved
Cole-Hunter, T., Zhang, J., So, R., Samoli, E., Liu, S., Chen, J., . . . Andersen, Z. J. (2023). Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort: An ELAPSE study. Environment International, 171, Article ID 107667.
Open this publication in new window or tab >>Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort: An ELAPSE study
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2023 (English)In: Environment International, ISSN 0160-4120, E-ISSN 1873-6750, Vol. 171, article id 107667Article in journal (Refereed) Published
Abstract [en]

Background: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson’s Disease (PD) remains limited.

Objective: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts.

Methods: Within the project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders.

Results: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01–1.55), NO2 (1.13; 0.95–1.34 per 10 µg/m3), and BC (1.12; 0.94–1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58–0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95–1.62) or BC (1.28; 0.96–1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5.

Conclusion: Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality.

Keywords
Air pollution, Adults, Parkinson's Disease, Long-term exposure, Low-level exposure, Pooled-cohort study
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:su:diva-215993 (URN)10.1016/j.envint.2022.107667 (DOI)000920450700006 ()36516478 (PubMedID)2-s2.0-85143661053 (Scopus ID)
Available from: 2023-04-03 Created: 2023-04-03 Last updated: 2023-04-03Bibliographically approved
Roswall, N., Thacher, J. D., Ögren, M., Pyko, A., Åkesson, A., Oudin, A., . . . Sørensen, M. (2023). Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts. Environmental Research, 224, Article ID 115454.
Open this publication in new window or tab >>Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts
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2023 (English)In: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 224, article id 115454Article in journal (Refereed) Published
Abstract [en]

Background

Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this.

Objectives

The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons.

Methods

We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data.

Results

During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99–1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98–1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure.

Discussion

A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.

Keywords
Road traffic noise, Railway noise, Colon cancer, Proximal, Distal, Pooled cohort study
National Category
Cancer and Oncology Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:su:diva-216442 (URN)10.1016/j.envres.2023.115454 (DOI)000951077000001 ()36764429 (PubMedID)2-s2.0-85148731232 (Scopus ID)
Available from: 2023-05-05 Created: 2023-05-05 Last updated: 2023-05-05Bibliographically approved
Pyko, A., Roswall, N., Ögren, M., Oudin, A., Rosengren, A., Eriksson, C., . . . Pershagen, G. (2023). Long-Term Exposure to Transportation Noise and Ischemic Heart Disease: A Pooled Analysis of Nine Scandinavian Cohorts. Journal of Environmental Health Perspectives, 131(1), Article ID 017003.
Open this publication in new window or tab >>Long-Term Exposure to Transportation Noise and Ischemic Heart Disease: A Pooled Analysis of Nine Scandinavian Cohorts
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2023 (English)In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 131, no 1, article id 017003Article in journal (Refereed) Published
Abstract [en]

Background: Transportation noise may induce cardiovascular disease, but the public health implications are unclear.

Objectives: The study aimed to assess exposure–response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes.

Methods: Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted long-term exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors.

Results: A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB Lden for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB Lden for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure–response relations. A threshold at around 55 dB Lden was suggested in the exposure–response relation for road traffic noise and IHD.

Discussion: Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. https://doi.org/10.1289/EHP10745

National Category
Occupational Health and Environmental Health Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:su:diva-227299 (URN)10.1289/EHP10745 (DOI)001124408100015 ()36607286 (PubMedID)2-s2.0-85145955612 (Scopus ID)
Available from: 2024-03-20 Created: 2024-03-20 Last updated: 2024-03-20Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-6199-9629

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