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Aim: The aim of this study was to study the association between alcohol consumption and periodontitis assessed as clinical attachment loss (CAL) and bleeding on probing (BOP) in a cross-sectional design. Material and Methods: The study included 1,521 adults aged 20-95 years, who underwent an oral examination including full-mouth registration of CAL and BOP. Alcohol was ascertained using a food-frequency questionnaire. The association between total and type-specific alcohol and periodontitis was assessed by means of multivariate logistic regression. Results: A lower odds ratio (OR) for CAL (defined as mean 3 mm) was observed in men consuming 21-34 [OR=0.51, 95% confidence interval (CI), 0.27-0.95] and 35+ drinks/week (OR=0.34, 95% CI, 0.15-0.79) compared with men drinking 1-13 drinks/week. Also, men with a weekly wine consumption of more than 14 drinks compared with men who reported no wine intake had lower OR for CAL (OR=0.24; 95% CI, 0.09-0.62). A higher OR for BOP (defined as 25%) among male abstainers was observed (OR=1.79, 95% CI, 1.03-3.12) compared with men in the light-drinking group (1-13 drinks/week). No significant association was observed for either CAL or BOP in women. Conclusions: The results indicate that higher alcohol consumption, particularly intake of wine, is inversely associated with CAL in men. Such an association is not found in women. [ABSTRACT FROM AUTHOR]

Despite the known link between air pollution and cause-specific mortality, its relation to chronic kidney disease (CKD)-associated mortality is understudied. Therefore, we investigated the association between long-term exposure to air pollution and CKD-related mortality in a large multicentre population-based European cohort. Cohort data were linked to local mortality registry data. CKD-death was defined as ICD10 codes N18-N19 or corresponding ICD9 codes. Mean annual exposure at participant's home address was determined with fine spatial resolution exposure models for nitrogen dioxide (NO 2 ), black carbon (BC), ozone (O 3 ), particulate matter ≤2.5 μm (PM 2.5 ) and several elemental constituents of PM 2.5 . Cox regression models were adjusted for age, sex, cohort, calendar year of recruitment, smoking status, marital status, employment status and neighbourhood mean income. Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were positive for PM 2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03-1.66) per 5 μg/m 3 , BC (1.26 (1.03-1.53) per 0.5 × 10 - 5 /m), NO 2 (1.13 (0.93-1.38) per 10 μg/m 3 ) and inverse for O 3 (0.71 (0.54-0.93) per 10 μg/m 3 ). Results were robust to further covariate adjustment. Exclusion of the largest sub-cohort contributing 226 cases, led to null associations. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different sources including traffic, biomass and oil burning and secondary pollutants, were associated with CKD-related mortality. In conclusion, our results suggest an association between air pollution from different sources and CKD-related mortality., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Previous studies show social inequality in tooth loss, but the underlying pathways are not well understood. The aim was to investigate the mediated proportion of sugary beverages (SBs) and diabetes and the association between educational level and tooth loss, and to investigate whether the indirect effect of SBs and diabetes varied between educational groups in relation to tooth loss., Methods: Data from 47,109 Danish men and women aged 50 years or older included in the Danish Diet, Cancer and Health Study was combined with data from Danish registers. Using natural effect models, SBs and diabetes were considered as mediators, and tooth loss was defined as having <15 teeth present., Results: In total, 10,648 participants had tooth loss. The analyses showed that 3% (95% confidence interval 2-4%) of the social inequality in tooth loss was mediated through SBs and diabetes. The mediated proportion was mainly due to differential exposure to SBs and diabetes among lower educational groups., Conclusions: The findings show that SBs and diabetes to a minor degree contribute to tooth-loss inequalities. The explanation indicates that individuals in lower educational groups have higher consumption of SBs and more often suffer from diabetes than higher educational groups., Competing Interests: Declaration of Conflicting InterestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Air pollution has been shown to significantly impact human health including cancer. Gastric and upper aerodigestive tract (UADT) cancers are common and increased risk has been associated with smoking and occupational exposures. However, the association with air pollution remains unclear. We pooled European subcohorts (N = 287,576 participants for gastric and N = 297,406 for UADT analyses) and investigated the association between residential exposure to fine particles (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC) and ozone in the warm season (O 3w ) with gastric and UADT cancer. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 5,305,133 and 5,434,843 person-years, 872 gastric and 1139 UADT incident cancer cases were observed, respectively. For gastric cancer, we found no association with PM 2.5 , NO 2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 μg/m 3 increase in PM 2.5 , 1.19 (1.08-1.30) per 10 μg/m 3 increase in NO 2 , 1.14 (1.04-1.26) per 0.5 × 10 -5  m -1 increase in BC and 0.81 (0.72-0.92) per 10 μg/m 3 increase in O 3w . We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM 2.5 , NO 2 and BC increased incidence of UADT cancer was observed., (© 2024 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

It is unclear whether cancers of the upper aerodigestive tract (UADT) and gastric cancer are related to air pollution, due to few studies with inconsistent results. The effects of particulate matter (PM) may vary across locations due to different source contributions and related PM compositions, and it is not clear which PM constituents/sources are most relevant from a consideration of overall mass concentration alone. We therefore investigated the association of UADT and gastric cancers with PM 2.5 elemental constituents and sources components indicative of different sources within a large multicentre population based epidemiological study. Cohorts with at least 10 cases per cohort led to ten and eight cohorts from five countries contributing to UADT- and gastric cancer analysis, respectively. Outcome ascertainment was based on cancer registry data or data of comparable quality. We assigned home address exposure to eight elemental constituents (Cu, Fe, K, Ni, S, Si, V and Zn) estimated from Europe-wide exposure models, and five source components identified by absolute principal component analysis (APCA). Cox regression models were run with age as time scale, stratified for sex and cohort and adjusted for relevant individual and neighbourhood level confounders. We observed 1139 UADT and 872 gastric cancer cases during a mean follow-up of 18.3 and 18.5 years, respectively. UADT cancer incidence was associated with all constituents except K in single element analyses. After adjustment for NO 2 , only Ni and V remained associated with UADT. Residual oil combustion and traffic source components were associated with UADT cancer persisting in the multiple source model. No associations were found for any of the elements or source components and gastric cancer incidence. Our results indicate an association of several PM constituents indicative of different sources with UADT but not gastric cancer incidence with the most robust evidence for traffic and residual oil combustion., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Leukemia and lymphoma are the two most common forms of hematologic malignancy, and their etiology is largely unknown. Pathophysiological mechanisms suggest a possible association with air pollution, but little empirical evidence is available. We aimed to investigate the association between long-term residential exposure to outdoor air pollution and risk of leukemia and lymphoma. We pooled data from four cohorts from three European countries as part of the "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration. We used Europe-wide land use regression models to assess annual mean concentrations of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC) and ozone (O 3 ) at residences. We also estimated concentrations of PM 2.5 elemental components: copper (Cu), iron (Fe), zinc (Zn); sulfur (S); nickel (Ni), vanadium (V), silicon (Si) and potassium (K). We applied Cox proportional hazards models to investigate the associations. Among the study population of 247,436 individuals, 760 leukemia and 1122 lymphoma cases were diagnosed during 4,656,140 person-years of follow-up. The results showed a leukemia hazard ratio (HR) of 1.13 (95% confidence intervals [CI]: 1.01-1.26) per 10 μg/m 3 NO 2 , which was robust in two-pollutant models and consistent across the four cohorts and according to smoking status. Sex-specific analyses suggested that this association was confined to the male population. Further, the results showed increased lymphoma HRs for PM 2.5 (HR = 1.16; 95% CI: 1.02-1.34) and potassium content of PM 2.5 , which were consistent in two-pollutant models and according to sex. Our results suggest that air pollution at the residence may be associated with adult leukemia and lymphoma., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Aims: The three correlated environmental exposures (air pollution, road traffic noise, and green space) have all been associated with the risk of myocardial infarction (MI). The present study aimed to analyse their independent and cumulative association with MI., Methods and Results: In a cohort of all Danes aged 50 or older in the period 2005-17, 5-year time-weighted average exposure to fine particles (PM2.5), ultrafine particles, elemental carbon, nitrogen dioxide (NO2), and road traffic noise at the most and least exposed façades of residence was estimated. Green space around residences was estimated from land use maps. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence interval (CI), and cumulative risk indices (CRIs) were calculated. All expressed per interquartile range. Models were adjusted for both individual and neighbourhood-level socio-demographic covariates. The cohort included 1 964 702 persons. During follow-up, 71 285 developed MI. In single-exposure models, all exposures were associated with an increased risk of MI. In multi-pollutant analyses, an independent association with risk of MI was observed for PM2.5 (HR: 1.026; 95% CI: 1.002-1.050), noise at most exposed façade (HR: 1.024; 95% CI: 1.012-1.035), and lack of green space within 150 m of residence (HR: 1.018; 95% CI: 1.010-1.027). All three factors contributed significantly to the CRI (1.089; 95% CI: 1.076-1.101)., Conclusion: In a nationwide cohort study, air pollution, noise, and lack of green space were all independently associated with an increased risk of MI. The air pollutant PM2.5 was closest associated with MI risk., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Air pollution is a growing concern worldwide, with significant impacts on human health. Multiple myeloma is a type of blood cancer with increasing incidence. Studies have linked air pollution exposure to various types of cancer, including leukemia and lymphoma, however, the relationship with multiple myeloma incidence has not been extensively investigated., Methods: We pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO 2 ), fine particles (PM 2.5 ), black carbon (BC), and ozone (O 3 ) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level., Results: During 4,415,817 person-years of follow-up (average 18.8 years), we observed 404 cases of multiple myeloma. The results of the fully adjusted linear analyses showed hazard ratios (95% confidence interval) of 0.99 (0.84, 1.16) per 10 μg/m³ NO 2 , 1.04 (0.82, 1.33) per 5 μg/m³ PM 2.5 , 0.99 (0.84, 1.18) per 0.5 10 -5  m -1 BCE, and 1.11 (0.87, 1.41) per 10 μg/m³ O 3 ., Conclusions: We did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Aryl-hydrocarbon receptor repressor ( AHRR ) hypomethylation in peripheral blood is tightly linked with tobacco smoking and lung cancer. Here, we investigated AHRR methylation in non-Hodgkin lymphoma (NHL), a non-smoking-associated cancer. In a case-cohort study within the population-based Danish Diet, Cancer and Health cohort, we measured AHRR (cg23576855) methylation in prediagnostic blood from 161 participants who developed NHL within 13.4 years of follow-up (median: 8.5 years), with a comparison group of 164 randomly chosen participants. We measured DNA-methylation levels using bisulfite pyrosequencing and estimated incidence rate ratios (IRR) using Cox proportional hazards models with adjustment for baseline age, sex, educational level, smoking status, body mass index, alcohol intake, physical activity, and diet score. Global DNA-methylation levels were assessed by long interspersed nucleotide element 1 (LINE-1) analysis. Overall, the IRR for AHRR hypomethylation (lowest vs. other quartiles) was 2.52 [95% confidence interval (CI), 1.24-5.15]. When stratified according to time between blood draw and diagnosis, low AHRR methylation levels were associated with a future diagnosis of NHL [IRR: 4.50 (95% CI, 1.62-12.50) at 0-<5 years, 7.04 (95% CI, 2.36-21.02) at 5-<10 years, and 0.56 (95% CI, 0.21-1.45) at ≥10 years]. There was no association between global DNA-methylation levels and risk of NHL. Our results show that AHRR hypomethylation in blood leukocytes is associated with a higher risk of NHL in a time-dependent manner, suggesting that it occurs as a response to tumor development., Significance: Our population-based study demonstrated that lower AHRR methylation levels in peripheral blood leukocytes were associated with an increased risk of NHL. This association was independent of tobacco smoking, sex, and lifestyle characteristics, but was highly dependent on time to diagnosis. These findings highlight the potential of AHRR methylation as a biomarker for NHL risk, effective up to 10 years after blood draw., (© 2023 The Authors; Published by the American Association for Cancer Research.)

Background: Risk factors for malignant tumours of the central nervous system (CNS) are largely unknown., Methods: We pooled six European cohorts (N = 302,493) and assessed the association between residential exposure to nitrogen dioxide (NO 2 ), fine particles (PM 2.5 ), black carbon (BC), ozone (O 3 ) and eight elemental components of PM 2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) and malignant intracranial CNS tumours defined according to the International Classification of Diseases ICD-9/ICD-10 codes 192.1/C70.0, 191.0-191.9/C71.0-C71.9, 192.0/C72.2-C72.5. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level., Results: During 5,497,514 person-years of follow-up (average 18.2 years), we observed 623 malignant CNS tumours. The results of the fully adjusted linear analyses showed a hazard ratio (95% confidence interval) of 1.07 (0.95, 1.21) per 10 μg/m³ NO 2 , 1.17 (0.96, 1.41) per 5 μg/m³ PM 2.5 , 1.10 (0.97, 1.25) per 0.5 10 -5 m -1 BC, and 0.99 (0.84, 1.17) per 10 μg/m³ O 3 ., Conclusions: We observed indications of an association between exposure to NO 2 , PM 2.5 , and BC and tumours of the CNS. The PM elements were not consistently associated with CNS tumour incidence., (© 2023. The Author(s), under exclusive licence to Springer Nature Limited.)

Air pollution is associated with increased risk of myocardial infarction (MI), but it is unresolved to what extent the association is modified by factors such as socioeconomic status, comorbidities, financial stress, residential green space, or road traffic noise. We formed a cohort of all (n = 1,964,702) Danes, aged 50-85 years, with 65,311 cases of MI during the followed-up period 2005-2017. For all participants we established residential five-year running average exposure to particulate matter <2.5 μm (PM 2.5 ), ultrafine particles (UFP, <0.1 μm), elemental carbon (EC) and nitrogen dioxide (NO 2 ). We evaluated risk in population strata, using Aalen additive hazards models to estimate absolute risk and Cox proportional hazards models to estimate relative risk of MI with 95% confidence intervals (CI). PM 2.5 and the other pollutant were associated with MI. Lower education and lower income were associated with higher absolute risks of MI from air pollution, whereas no clear effect modification was apparent for relative risk estimates. For example, 5 μg/m 3 higher PM 2.5 was associated with HR for MI of 1.16 (95% CI: 1.10-1.22) among those with only mandatory education and 1.13 (95% CI: 1.03-1.24) among those with long education. The corresponding rate differences per 100,000 person years were 243 (95% CI: 216-271) and 358 (95% CI: 338-379), respectively. Higher level of comorbidity was consistently across all four pollutants associated with both higher absolute and relative risk of MI. In conclusion, people with comorbid conditions or of lower SES appeared more vulnerable to long-term exposure to air pollution and more cases of MI may be prevented by focused interventions in these groups., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Ole Raaschou-Nielsen reports financial support was provided by Health Effects Institute., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Studies have indicated that transportation noise is associated with higher cardiovascular mortality, whereas evidence of noise as a risk factor for respiratory and cancer mortality is scarce and inconclusive. Also, knowledge on effects of low-level noise on mortality is very limited. We aimed to investigate associations between road and railway noise and natural-cause and cause-specific mortality in the Danish population. We estimated address-specific road and railway noise at the most (LdenMax) and least (LdenMin) exposed façades for all residential addresses in Denmark from 1990 to 2017 using high-quality exposure models. Using these data, we calculated 10-year time-weighted mean noise exposure for 2.6 million Danes aged >50 years, of whom 600,492 died from natural causes during a mean follow-up of 11.7 years. We analyzed data using Cox proportional hazards models with adjustment for individual and area-level sociodemographic variables and air pollution (PM 2.5 and NO 2 ). We found that a 10-year mean exposure to road LdenMax and road LdenMin per 10 dB were associated with hazard ratios (95% confidence intervals) of, respectively, 1.09 (1.09; 1.10) and 1.10 (1.10; 1.11) for natural-cause mortality, 1.09 (1.08; 1.10) and 1.09 (1.08; 1.10) for cardiovascular mortality, 1.13 (1.12; 1.14) and 1.17 (1.16; 1.19) for respiratory mortality and 1.03 (1.02; 1.03) and 1.06 (1.05; 1.07) for cancer mortality. For LdenMax, the associations followed linear exposure-response relationships from 35 dB to 60-<65 dB, after which the function levelled off. For LdenMin, exposure-response relationships were linear from 35 dB and up, with some levelling off at high noise levels for natural-cause and cardiovascular mortality. Railway noise did not seem associated with higher mortality in an exposure-response dependent manner. In conclusion, road traffic noise was associated with higher mortality and the increase in risk started well below the current World Health Organization guideline limit for road traffic noise of 53 dB., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: Long-term air pollution is a risk factor for stroke. Which types and sources of air pollution contribute most to stroke in populations is unknown. We investigated whether risk of stroke differed by type and source of air pollution., Methods: We selected all persons aged >50 years and living in Denmark in the period 2005-17. We estimated running 5-year mean residential air-pollution concentrations of particulate matter <2.5 µm (PM2.5), ultrafine particles (UFP), elemental carbon (EC) and nitrogen dioxide (NO2). Pollutants were modelled as total air pollution from all emission sources, as well as apportioned into contributions from non-traffic and traffic sources. Hazard ratios (HRs) and CIs were estimated by using Cox proportional hazards models, adjusting for area-level and personal demographic and socio-economic covariates. We identified all primary strokes from hospital and mortality registers., Results: The cohort numbered 2 million people and 94 256 cases of stroke. Interquartile ranges (IQR) of air pollution were associated with risk of stroke with HRs of 1.077 (95% CI: 1.061-1.094, IQR: 1.85 µg/m3) for PM2.5, 1.039 (1.026-1.052, IQR: 4248 particles/cm3) for UFP, 1.009 (1.001-1.018, IQR: 0.28 µg/m3) for EC and 1.028 (1.017-1.040, IQR: 7.15 µg/m3) for NO2. Traffic sources contributed little to the total exposure. HRs associated with air pollution from traffic were close to the null, whereas non-traffic sources tended to be associated with HRs higher than those for total air pollution, e.g. for non-traffic PM2.5, the HR was 1.091 (1.074-1.108)., Conclusions: Air pollution, including UFP, was associated with risk of stroke. The risk appeared attributable mainly to air pollution from non-traffic sources., (© The Author(s) 2023; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Objectives: Air pollution increases the risk of stroke, but the literature on identifying susceptible subgroups of populations is scarce and inconsistent. The aim of this study was to investigate if the association between air pollution and risk of stroke differed by sociodemographic factors, financial stress, comorbid conditions, and residential road traffic noise, population density and green space., Methods: We assessed long-term exposure to air pollution with ultrafine particles, PM 2.5 , elemental carbon and NO 2 for a cohort of 1,971,246 Danes aged 50-85 years. During follow-up from 2005 to 2017, we identified 83,211 incident stroke cases. We used Cox proportional hazards model (relative risk) and Aalen additive hazards models (absolute risk) to estimate associations and confidence intervals (CI) between 5-year running means of air pollution at the residence and risk of stroke in population strata., Results: All four pollutants were associated with higher risk of stroke. The association between air pollution and stroke was strongest among individuals with comorbidities, with shorter education, lower income and being retired. The results also indicated stronger associations among individuals living in less populated areas, and with low noise levels and more green space around the residence. Estimates of absolute risk seemed better suited to detect such interactions than estimates of relative risk. For example for PM 2.5 the hazard ratio for stroke was 1.28 (95%CI: 1.22-1.34) and 1.26 (95%CI: 1.16-1.37) among those with mandatory and medium/long education respectively. The corresponding rate difference estimates per 100,000 person years were 568 (95%CI: 543-594) and 423(95%CI: 390-456) CONCLUSION: The associations between air pollution and risk of stroke was stronger among individuals of lower socioeconomic status or with pre-existing comorbid conditions. Absolute risk estimates were better suited to identify such effect modification., Competing Interests: Declaration of competing interest The authors declare they have nothing to disclose., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Background: Air pollution, road traffic noise, and green space are correlated factors, associated with risk of stroke. We investigated their independent relationship with stroke in multi-exposure analyses and estimated their cumulative stroke burden., Methods: For all persons, ≥50 years of age and living in Denmark from 2005 to 2017, we established complete address histories and estimated running 5-year mean exposure to fine particles (PM 2.5 ), ultrafine particles, elemental carbon, nitrogen dioxide (NO 2 ), and road traffic noise at the most, and least exposed façade. For air pollutants, we estimated total, and non-traffic contributions. Green space around the residence was estimated from land use maps. Hazard ratios (HR) and 95% confidence limits (CL) were estimated with Cox proportional hazards models and used to calculate cumulative risk indices (CRI). We adjusted for the individual and sociodemographic covariates available in our dataset (which did not include information about individual life styles and medical conditions)., Findings: The cohort accumulated 18,344,976 years of follow-up and 94,256 cases of stroke. All exposures were associated with risk of stroke in single pollutant models. In multi-pollutant analyses, only PM 2.5 (HR: 1.058, 95% CI: 1.040-1.075) and noise at most exposed façade (HR: 1.033, 95% CI: 1.024-1.042) were independently associated with a higher risk of stroke. Both noise and air pollution contributed substantially to the CRI (1.103, 95% CI: 1.092-1.114) in the model with noise, green space, and total PM 2.5 concentrations., Interpretation: Environmental exposure to air pollution and noise were both independently associated with risk of stroke., Funding: Health Effects Institute (HEI) (Assistance Award No. R-82811201)., Competing Interests: The authors declare no conflicting interests., (© 2023 The Author(s).)

Background: Air pollution is negatively associated with cardiovascular health. Impediments to efficient regulation include lack of knowledge about which sources of air pollution contributes most to health burden and few studies on effects of the potentially more potent ultrafine particles (UFP)., Objective: The authors aimed to investigate myocardial infarction (MI) morbidity and specific types and sources of air pollution., Methods: We identified all persons living in Denmark in the period 2005-2017, age > 50 y and never diagnosed with MI. We quantified 5-y running time-weighted mean concentrations of air pollution at residencies, both total and apportioned to traffic and nontraffic sources. We evaluated particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ), < 0.1 μ m (UFP), elemental carbon (EC), and nitrogen dioxide ( NO 2 ). We used Cox proportional hazards models, with adjustment for time-varying exposures, and personal and area-level demographic and socioeconomic covariates from high-quality administrative registers., Results: In this nationwide cohort of 1,964,702 persons (with 18  million person-years of follow-up and 71,285 cases of MI), UFP and PM 2.5 were associated with increased risk of MI with hazard ratios (HRs) per interquartile range (IQR) of 1.040 [95% confidence interval (CI): 1.025, 1.055] and 1.053 (95% CI: 1.035, 1.071), respectively. HRs per IQR of UFP and PM 2.5 from nontraffic sources were similar to the total (1.034 and 1.051), whereas HRs for UFP and PM 2.5 from traffic sources were smaller (1.011 and 1.011). The HR for EC from traffic sources was 1.013 (95% CI: 1.003, 1.023). NO 2 from nontraffic sources was associated with MI ( HR = 1.048 ; 95% CI: 1.034, 1.062) but not from traffic sources. In general, nontraffic sources contributed more to total air pollution levels than national traffic sources., Conclusions: PM 2.5 and UFP from traffic and nontraffic sources were associated with increased risk of MI, with nontraffic sources being the dominant source of exposure and morbidity. https://doi.org/10.1289/EHP10556.

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 NO 2 -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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Air pollution is a well-recognized risk factor for cardiovascular disease. However, the mechanistic pathways underlying the association are not completely understood. Hence, further studies are required to shed light on potential mechanisms, through which air pollution may affect the development from subclinical to clinical cardiovascular disease., Objectives: To investigate associations between short-term exposure to air pollution and high-density lipoprotein (HDL), non-high density lipoprotein (non-HDL), systolic and diastolic blood pressure., Methods: The study was conducted among 32,851 Danes from the Diet, Cancer and Health - Next Generations cohort, who had a blood sample taken and blood pressure measured. We measured HDL and non-HDL in the blood samples. We modelled exposure to fine particulate matter (PM 2.5 ), ultrafine particles (UFP), elemental carbon (EC) and nitrogen dioxide (NO 2 ) in time-windows from 24 h up to 90 days before blood sampling. Pollutants were modelled as total air pollution from all sources, and apportioned into contributions from non-traffic and traffic sources. We analyzed data using linear and logistic regression, with adjustment for socio-economic and lifestyle factors., Results: Air pollution exposure over 24 h to 30 days was generally adversely associated with lipid profile and blood pressure, e.g. for 30-day UFP-exposure, adjusted β-estimates were: -0.025 (-0.043; -0.006) for HDL, 0.086 (0.042; 0.130) for non-HDL, 2.45 (1.70; 3.11) for systolic and 1.56 (1.07; 20.4) for diastolic blood pressure, per 10,000 particles/cm 3 . The strongest associations were found for the non-traffic components of air pollution, and among those who were overweight/obese., Discussion: In this large study of air pollution and lipid levels and blood pressure, we found that 24-h to 30-day PM 2.5 , UFP, EC and NO 2 concentrations were generally adversely associated with lipid profile and blood pressure, two important cardiovascular risk factors. The study suggests potential pathways, through which air pollution could affect the development of cardiovascular disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Exposure to air pollution has been associated with a higher risk of type 2 diabetes (T2D), but studies investigating whether deprived groups are more susceptible to the harmful effects of air pollution are inconsistent., Objectives: We aimed to investigate whether the association between air pollution and T2D differed according to sociodemographic characteristics, comorbidity, and coexposures., Methods: We estimated residential exposure to PM 2.5 , ultrafine particles (UFP), elemental carbon, and NO 2 for all persons living in Denmark in the period 2005-2017. In total, 1.8  million persons 50-80 y of age were included for main analyses of whom 113,985 developed T2D during follow-up. We conducted additional analyses on 1.3  million persons age 35-50 y. Using Cox proportional hazards model (relative risk) and Aalens additive hazard model (absolute risk), we calculated associations between 5-y time-weighted running means of air pollution and T2D in strata of sociodemographic variables, comorbidity, population density, road traffic noise, and green space proximity., Results: Air pollution was associated with T2D, especially among people age 50-80 y, with hazard ratios of 1.17 [95% confidence interval (CI): 1.13, 1.21] per 5   μ g / m 3 PM 2.5 and 1.16 (95% CI: 1.13, 1.19) per 10,000   UFP / cm 3 . In the age 50-80 y population, we found higher associations between air pollution and T2D among men in comparison with women, people with lower education vs. individuals with high education, people with medium income vs. those with low or high income, people cohabiting vs. those living alone, and people with comorbidities vs. those without comorbidities. We observed no marked changes according to occupation, population density, road noise, or surrounding greenness. In the age 35-50 y population, similar tendencies were observed, except in relation to sex and occupation, where we observed associations with air pollution only among women and blue-collar workers., Discussion: We found stronger associations between air pollution and T2D among people with existing comorbidities and weaker associations among people with high socioeconomic status in comparison with those with lower socioeconomic status. https://doi.org/10.1289/EHP11347.

Background: There is a growing body of evidence linking residential exposure to transportation noise with several nonauditory health outcomes. However, auditory outcomes, such as tinnitus, are virtually unexplored., Objectives: We aimed to investigate the association between residential transportation noise and risk of incident tinnitus., Methods: We conducted a nationwide cohort study including all residents in Denmark age ≥ 30 y , of whom 40,692 were diagnosed with tinnitus. We modeled road traffic and railway noise at the most ( L den max ) and least ( L den min ) exposed façades of all Danish addresses from 1990 until 2017. For all participants, we calculated 1-, 5-, and 10-y time-weighted mean noise exposure and retrieved detailed information on individual- and area-level socioeconomic covariates. We conducted analyses using Cox proportional hazards models., Results: We found positive associations between exposure to road traffic noise and risk of tinnitus, with hazard ratios of 1.06 [95% confidence interval (CI): 1.04, 1.08] and 1.02 (95% CI: 1.01, 1.03) per 10-dB increase in 10-y L den min and L den max , respectively. Highest risk estimates were found for women, people without a hearing loss, people with high education and income, and people who had never been in a blue-collar job. The association with road L den min followed a positive, monotonic exposure-response relationship. We found no association between railway noise and tinnitus., Discussion: To our knowledge, this is the first study to show that residential exposure to road traffic noise may increase risk of tinnitus, suggesting noise may negatively affect the auditory system. If confirmed, this finding adds to the growing evidence of road traffic noise as a harmful pollutant with a substantial health burden. https://doi.org/10.1289/EHP11248.

Background: Some studies have found transportation noise to be associated with higher diabetes risk. This includes studies based on millions of participants, relying entirely on register-based confounder adjustment, which raises concern about residual lifestyle confounding. We aimed to investigate associations between noise and type 2 diabetes (T2D), including investigation of effects of increasing confounder adjustment for register-data and lifestyle., Methods: In a cohort of 286,151 participants randomly selected across Denmark in 2010-2013 and followed up until 2017, we identified 7574 incident T2D cases. Based on residential address-history for all participants linked with exposure assessment of high spatial resolution, we calculated 10-year time-weighted mean road and railway noise at the most (LdenMax) and least (LdenMin) exposed façades and air pollution (PM 2.5 ). We used Cox models to calculate hazard ratios (HR) with increasing adjustment for individual- and area-level register-based sociodemographic covariates, self-reported lifestyle and air pollution., Results: We found that a 10 dB increase in 10-year mean road LdenMin was associated with HRs (95% CI) of 1.06 (1.02-1.10) after adjustment for age, sex and year, 1.08 (1.04-1.13) after further adjustment for register-based sociodemographic covariates, 1.07 (1.03-1.12) after further lifestyle adjustment (e.g. smoking, diet and alcohol) and 1.06 (1.02-1.11) after further PM 2.5 adjustment. For road LdenMax, the corresponding HRs were 1.07 (1.04-1.10), 1.05 (1.02-1.08), 1.04 (1.01-1.07) and 1.03 (1.00-1.06). Railway noise was associated with HRs of 1.04 (0.98-1.11) for LdenMax and 1.02 (0.92-1.12) for LdenMin after adjustment for sociodemographic and lifestyle covariates and PM 2.5 ., Conclusions: Long-term exposure to road traffic noise was associated with T2D, which together with previous literature indicates that T2D should be considered when calculating health impacts of noise. After sociodemographic adjustment, further lifestyle adjustment only changed HRs slightly, suggesting that large register-based studies with adjustment for key sociodemographic covariates can produce reliable results., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Established risk factors for breast cancer include genetic disposition, reproductive factors, hormone therapy, and lifestyle-related factors such as alcohol consumption, physical inactivity, smoking, and obesity. More recently a role of environmental exposures, including air pollution, has also been suggested. The aim of this study, was to investigate the relationship between long-term air pollution exposure and breast cancer incidence., Methods: We conducted a pooled analysis among six European cohorts (n = 199,719) on the association between long-term residential levels of ambient nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone in the warm season (O3) and breast cancer incidence in women. The selected cohorts represented the lower range of air pollutant concentrations in Europe. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level., Results: During 3,592,885 person-years of follow-up, we observed a total of 9,659 incident breast cancer cases. The results of the fully adjusted linear analyses showed a HR (95% confidence interval) of 1.03 (1.00-1.06) per 10 μg/m³ NO2, 1.06 (1.01-1.11) per 5 μg/m³ PM2.5, 1.03 (0.99-1.06) per 0.5 10-5 m-1 BC, and 0.98 (0.94-1.01) per 10 μg/m³ O3. The effect estimates were most pronounced in the group of middle-aged women (50-54 years) and among never smokers., Conclusions: The results were in support of an association between especially PM2.5 and breast cancer., Impact: The findings of this study suggest a role of exposure to NO2, PM2.5, and BC in development of breast cancer., (©2022 American Association for Cancer Research.)

Air pollution with particulate matter is an established lung carcinogen. Studies have suggested an association with breast cancer, but the evidence is inconsistent., Methods: From nationwide registers, we identified all breast cancer cases (n = 55 745) in Denmark between 2000 and 2014. We matched one control for each case on age and year of birth. We used a multi-scale dispersion model to estimate outdoor concentrations of particulate matter <2.5 μm (PM 2.5 ), elemental carbon (EC) and nitrogen dioxide (NO 2 ) as time-weighted average over all addresses up to 20 years prior to diagnosis. We calculated odds ratios (OR) and 95% confidence intervals (CI) by conditional logistic regression with adjustment for marital status, educational level, occupational status, personal income, region of origin, medication and area-level socio-economic indicators., Results: A 10 μg/m 3 higher PM 2.5 was associated with an OR for breast cancer of 1.21 (95% CI: 1.11-1.33). The corresponding ORs for EC (per 1 μg/m 3 ) and NO 2 (per 10 μg/m 3 ) were 1.03 (95% CI: 1.00-1.07) and 1.03 (95% CI: 1.01-1.06), respectively. In multi-pollutant models, the OR for PM 2.5 changed only little, whereas ORs for EC or NO 2 approached the null. In an analysis of persons below 55 years, PM 2.5 was associated with an OR of 1.32 (95% CI: 1.09-1.60) per 10 μg/m 3 increase., Conclusion: We found evidence of an association between the investigated air pollutants and breast cancer, especially PM 2.5 . There were indications that the association differed by age at diagnosis. We were not able to include all potential confounders and thus, results should be interpreted with caution., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Joergen Brandt reports financial support was provided by NordForsk., (Copyright © 2022 Elsevier Inc. All rights reserved.)

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 (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC), and ozone (O 3 ), as well as 8 PM 2.5 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 PM 2.5 (hazard ratio per 5 µg/m 3 : 1.25; 95% confidence interval: 1.01-1.55), NO 2 (1.13; 0.95-1.34 per 10 µg/m 3 ), and BC (1.12; 0.94-1.34 per 0.5 × 10 -5 m -1 ), and a negative association with O 3 (0.74; 0.58-0.94 per 10 µg/m 3 ). Associations of PM 2.5 , NO 2 , and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM 2.5 remained robust when adjusted for NO 2 (1.24; 0.95-1.62) or BC (1.28; 0.96-1.71), whereas associations with NO 2 or BC attenuated to null. O 3 associations remained negative, but no longer statistically significant in models with PM 2.5 . We detected suggestive positive associations with the potassium component of PM 2.5 ., Conclusion: Long-term exposure to PM 2.5 , at levels well below current EU air pollution limit values, may contribute to PD mortality., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Ambient fine particulate matter (PM 2.5 ) causes millions of deaths every year worldwide. Identification of the most harmful types of PM 2.5 would facilitate efficient prevention strategies., Objectives: The aim of this study was to investigate associations between components of PM 2.5 and mortality in a nation-wide Danish population., Methods: Our study base was Danes born 1921-1985 and aged 30-85 years, who were followed up for mortality from 1991 to 2015. We included 678,465 natural cause mortality cases and selected five age, sex and calendar time matched controls to each case from the study base. We retrieved the address history of the study population from Danish registries and assessed five-year average concentrations of eight PM 2.5 components using deterministic Chemistry-Transport Models air pollution models. We estimated mortality rate ratios (MRRs) by conditional logistic regression and adjusted for socio-demographical factors at individual and neighborhood level., Results: Single pollutant models showed the strongest associations between natural cause mortality and an interquartile increase in sulfate particles (SO 4 - - ) (MRR: 1.123; 95 % CI: 1.100-1.147 per 1.5 µg/m 3 ) and secondary organic aerosol (SOA) (MRR: 1.054; 95 % CI: 1.048-1.061 per 0.050 µg/m 3 ). Two-pollutant models showed robust associations between SO 4 - - and SOA and natural cause mortality. Elemental carbon and mineral dust showed robust associations with higher respiratory and lung cancer mortality., Conclusion: This nation-wide study found robust associations between natural cause mortality and SO 4 - - particles and SOA, which is in line with the results of previous studies. Elemental carbon and mineral dust showed robust associations with higher respiratory and lung cancer mortality., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Ambient air pollution is an established risk factor for premature mortality from chronic cardiovascular, respiratory and metabolic diseases, while evidence on neurodegenerative diseases and psychiatric disorders remains limited. We examined the association between long-term exposure to air pollution and mortality from dementia, psychiatric disorders, and suicide in seven European cohorts. Within the multicenter project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven European cohorts from six countries. Based on the residential addresses, annual mean levels of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC), ozone (O 3 ), and 8 PM 2.5 components were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and mortality from dementia, psychiatric disorders, and suicide. Of 271,720 participants, 900 died from dementia, 241 from psychiatric disorders, and 164 from suicide, during a mean follow-up of 19.7 years. In fully adjusted models, we observed positive associations of NO 2 (hazard ratio [HR] = 1.38; 95 % confidence interval [CI]: 1.13, 1.70 per 10 µg/m 3 ), PM 2.5 (HR = 1.29; 95 % CI: 0.98, 1.71 per 5 µg/m 3 ), and BC (HR = 1.37; 95 % CI: 1.11, 1.69 per 0.5 × 10 -5 /m) with psychiatric disorders mortality, as well as with suicide (NO 2 : HR = 1.13 [95 % CI: 0.92, 1.38]; PM 2.5 : HR = 1.19 [95 % CI: 0.76, 1.87]; BC: HR = 1.08 [95 % CI: 0.87, 1.35]), and no association with dementia mortality. We did not detect any positive associations of O 3 and 8 PM 2.5 components with any of the three mortality outcomes. Long-term exposure to NO 2 , PM 2.5 , and BC may lead to premature mortality from psychiatric disorders and suicide., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Objective: Air pollution, road traffic noise and lack of greenness coexist in urban environments and have all been associated with type 2 diabetes. We aimed to investigate how these co-exposures were associated with type 2 diabetes in a multi-exposure perspective., Methods: We estimated 5-year residential mean exposure to fine particles (PM 2.5 ), ultrafine particles (UFP), elemental carbon (EC), nitrogen dioxide (NO 2 ) and road traffic noise at the most (LdenMax) and least (LdenMin) exposed facade for all persons aged > 50 years living in Denmark in 2005 to 2017. For each air pollutant, we estimated total concentrations and traffic contributions. Based on land use maps, we estimated proportion of green and non-green space within 150 and 1000 m of all residences. In total, 1.9 million persons were included and 128,358 developed type 2 diabetes during follow-up. We performed analyses using Cox proportional hazards models, with adjustment for individual and neighborhood-level sociodemographic co-variates., Results: In single-pollutant models, all air pollutants, noise and lack of green space were associated with higher risk of diabetes. In two-, three- and four-pollutant analyses of the air pollutants, only UFP and NO 2 remained associated with higher diabetes risk in all models. LdenMax, LdenMin and the two proxies of green space remained associated with diabetes in two-pollutant models of, respectively, noise and green space. In a multi-pollutant analysis, we found hazard ratios (95 % confidence intervals) per interquartile range of 1.021 (1.005; 1.038) for UFP, 1.012 (0.996; 1.028) for NO 2 , 1.022 (1.012; 1.033) for LdenMin, 1.013 (1.004; 1.022) for LdenMax, and 1.038 (1.031; 1.044) and 1.018 (1.010; 1.025) for lack of green space within, respectively, 150 m and 1000 m, and a cumulative risk index of 1.131 (1.113; 1.149)., Conclusions: Air pollution, road traffic noise and lack of green space were independently associated with higher risk of type 2 diabetes., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Particulate matter (PM) is classified as a group 1 human carcinogen. Previous experimental studies suggest that particles in diesel exhaust induce oxidative stress, inflammation and DNA damage in kidney cells, but the evidence from population studies linking air pollution to kidney cancer is limited., Methods: We pooled six European cohorts (N = 302,493) to assess the association of residential exposure to fine particles (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC), warm season ozone (O 3 ) and eight elemental components of PM 2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) with cancer of the kidney parenchyma. The main exposure model was developed for year 2010. We defined kidney parenchyma cancer according to the International Classification of Diseases 9th and 10th Revision codes 189.0 and C64. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level., Results: The participants were followed from baseline (1985-2005) to 2011-2015. A total of 847 cases occurred during 5,497,514 person-years of follow-up (average 18.2 years). Median (5-95%) exposure levels of NO 2 , PM 2.5 , BC and O 3 were 24.1 μg/m 3 (12.8-39.2), 15.3 μg/m 3 (8.6-19.2), 1.6 10 -5  m -1 (0.7-2.1), and 87.0 μg/m 3 (70.3-97.4), respectively. The results of the fully adjusted linear analyses showed a hazard ratio (HR) of 1.03 (95% confidence interval [CI]: 0.92, 1.15) per 10 μg/m³ NO 2 , 1.04 (95% CI: 0.88, 1.21) per 5 μg/m³ PM 2.5 , 0.99 (95% CI: 0.89, 1.11) per 0.5 10 -5  m -1 BCE, and 0.88 (95% CI: 0.76, 1.02) per 10 μg/m³ O 3 . We did not find associations between any of the elemental components of PM 2.5 and cancer of the kidney parenchyma., Conclusion: We did not observe an association between long-term ambient air pollution exposure and incidence of kidney parenchyma cancer., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: The aetiology of most childhood cancers remains poorly understood. We conducted a nationwide register-based case-control study to assess the association between residential road traffic and railway noise exposure and risk of childhood cancers., Methods: We identified all cases of first cancers diagnosed in children aged 0-19 years in 1985-2013 from the Danish Cancer Registry (N = 3962) and sampled four individually matched (by sex and date of birth) controls per case (N = 14,790) using the Central Population Register. We estimated time-weighted exposure averages of residential road traffic and railway noise at the most (L den max) and least (L den min) exposed façades from birth to index-date (for additional analysis: in utero period) based on the individual address history for the respective time windows. We fitted conditional logistic regression models to estimate odds ratios (OR) and their 95% confidence intervals (CI)., Results: ORs varied by noise estimate and cancer type, with generally wide CIs mostly including 1.00. We found a tendency of higher ORs with increasing railway and road traffic noise for Hodgkin lymphoma (ORs for railway and road L den min were 1.63 (95% CI 1.00; 2.66) and 1.14 (95% CI 0.87; 1.48) per 10 dB), as well as a tendency of higher ORs with increasing railway noise for non-Hodgkin lymphoma. For embryonal CNS tumours and astrocytoma and other glioma we observed also some weak suggestions of a positive association. Analysing exposure to traffic noise in utero revealed similar patterns to those of the main analyses., Conclusions: This nationwide study with minimal risk of bias suggests no strong associations between traffic noise and risk of most childhood cancers. We found however some suggestive evidence for a positive association with Hodgkin lymphoma, non-Hodgkin lymphoma and some CNS tumours. Further research is warranted to confirm these associations in other populations and elucidate the underlying biological mechanisms., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Only few epidemiological studies have investigated whether chronic exposure to air pollution from different sources have different impacts on risk of diabetes. We aimed to investigate associations between air pollution from traffic versus non-traffic sources and risk of type 2 diabetes in the Danish population., Methods: We estimated long-term exposure to traffic and non-traffic contributions of particulate matter with a diameter <2.5 µg (PM2.5), elemental carbon (EC), ultrafine particles (UFP) and nitrogen dioxide (NO2) for all persons living in Denmark for the period 2005-17. In total, 2.6 million persons aged >35 years were included, of whom 148 020 developed type 2 diabetes during follow-up. We applied Cox proportional hazards models for analyses, using 5-year time-weighted running means of air pollution and adjustment for individual- and area-level demographic and socioeconomic covariates., Results: We found that 5-year exposure to all particle measures (PM2.5, UFP and EC) and NO2 were associated with higher type 2 diabetes risk. We observed that for UFP, EC and potentially PM2.5, the pollution originating from traffic was associated with higher risks than the non-traffic contributions, whereas for NO2 similar hazard ratios (HR) were observed. For example, in two-source models, hazard ratios (HRs) per interquartile change in traffic UFP, EC and PM2.5 were 1.025, 1.045 and 1.036, respectively, whereas for non-traffic UFP, EC and PM2.5, the HRs were 1.013, 1.018 and 1.001, respectively., Conclusions: Our finding of stronger associations with particulate matter from traffic compared with non-traffic sources implies that prevention strategies should focus on limiting traffic-related particulate matter air pollution., (© The Author(s) 2022; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Background: Transportation noise increases the risk of ischemic heart disease (IHD), but few studies have investigated subtypes of IHD, such as myocardial infarction (MI), angina pectoris, or heart failure. We aimed to study whether exposure to road, railway and aircraft noise increased risk for ischemic heart disease (IHD), IHD subtypes, and heart failure in the entire adult Danish population, investigating exposures at both maximum exposed and silent façades of each residence., Methods: We modelled road, railway, and aircraft noise at the most and least exposed façades for the period 1995-2017 for all addresses in Denmark and calculated 10-year time-weighted running means for 2.5 million individuals age ≥50 years, of whom 122,523 developed IHD and 79,358 developed heart failure during follow-up (2005-2017). Data were analyzed using Cox proportional hazards models, adjusted for individual and area-level sociodemographic covariates and air pollution., Results: We found road traffic noise at the most exposed façade (L den ) to be associated with higher risk of IHD, myocardial infarction (MI), angina pectoris, and heart failure, with hazard ratios (HRs) (95% confidence intervals (CI)) of 1.052 (1.044-1.059), 1.041 (1.032-1.051), 1.095 (1.071-1.119), and 1.039 (1.033-1.045) per 10 dB higher 10-year mean exposure, respectively. These associations followed a near-linear exposure-response relationship and were robust to adjustment for air pollution with PM 2.5 . Railway noise at the least exposed façade was associated with heart failure (HR 1.28; 95% CI: 1.004-1.053), but not the other outcomes. Exposure to aircraft noise (>45 dB) seemed associated with increased risk for MI and heart failure., Conclusions: We found road traffic noise and potentially railway and aircraft noise to increase risk of various major cardiovascular outcomes, highlighting the importance of preventive actions towards transportation noise., (Copyright © 2022 Elsevier Inc. All rights reserved.)

We assessed mortality risks associated with source-specific fine particles (PM 2.5 ) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM 2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM 2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 μg/m 3 increase) across five identified sources. On a 1 μg/m 3 basis, the residual oil-related PM 2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM 2.5 mass, suggesting that past estimates using the generic PM 2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.

Rationale: Ambient air pollution exposure has been linked to mortality from chronic cardiorespiratory diseases, while evidence on respiratory infections remains more limited. Objectives: We examined the association between long-term exposure to air pollution and pneumonia-related mortality in adults in a pool of eight European cohorts. Methods: Within the multicenter project ELAPSE (Effects of Low-Level Air Pollution: A Study in Europe), we pooled data from eight cohorts among six European countries. Annual mean residential concentrations in 2010 for fine particulate matter, nitrogen dioxide (NO 2 ), black carbon (BC), and ozone were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and pneumonia, influenza, and acute lower respiratory infections (ALRI) mortality. Measurements and Main Results: Of 325,367 participants, 712 died from pneumonia and influenza combined, 682 from pneumonia, and 695 from ALRI during a mean follow-up of 19.5 years. NO 2 and BC were associated with 10-12% increases in pneumonia and influenza combined mortality, but 95% confidence intervals included unity (hazard ratios, 1.12 [0.99-1.26] per 10 μg/m 3 for NO 2 ; 1.10 [0.97-1.24] per 0.5 10 -5 m -1 for BC). Associations with pneumonia and ALRI mortality were almost identical. We detected effect modification suggesting stronger associations with NO 2 or BC in overweight, employed, or currently smoking participants compared with normal weight, unemployed, or nonsmoking participants. Conclusions: Long-term exposure to combustion-related air pollutants NO 2 and BC may be associated with mortality from lower respiratory infections, but larger studies are needed to estimate these associations more precisely.

Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed., Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC), warm season ozone (O 3 ) and eight PM 2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders., Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM 2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93-1.27) per 5 µg/m 3 for 2010 exposure and 1.06 (95% CI: 0.99-1.14) for baseline exposure. Effect estimates for NO 2 , BC and O 3 were close to unity. A positive association was observed with PM 2.5 zinc (HR 1.08; 95% CI: 1.00-1.16 per 10 ng/m 3 )., Conclusions: We found suggestive evidence of an association between long-term PM 2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM 2.5 suggests the importance of industrial emissions., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)

Background: Exposure to outdoor air pollution is associated with adverse health effects. Previous studies have indicated higher levels of air pollution in socially deprived areas., Aim: To investigate associations between air pollution and socio-demographic variables, comorbidity, stress, and green space at the residence in Denmark., Methods: We included 2,237,346 persons living in Denmark, aged 35 years or older in 2017. We used the high resolution, multi-scale DEHM/UBM/AirGIS air pollution modelling system to calculate mean concentrations of air pollution with PM 2.5 , elemental carbon, ultrafine particles and NO 2 at residences held the preceding five years. We used nationwide registries to retrieve information about socio-demographic indicators at the individual and neighborhood levels. We used general linear regression models to analyze associations between socio-demographic indicators and air pollution at the residence., Results: Individuals with high SES (income, higher white-collar worker and high educational level) and of non-Danish origin were exposed to higher levels of air pollution than individuals of low SES and of Danish origin, respectively. We found comparable levels of air pollution according to sex, stress events and morbidity. For neighborhood level SES indicators, we found high air pollution levels in neighborhoods with low SES measured as proportion of social housing, sole providers, low income and unemployment. In contrast, we found higher air pollution levels in neighborhoods with higher educational level and a low proportion of manual labor. People living in an apartment and/or with little green space had higher air pollution levels., Conclusion: In Denmark, high levels of residential air pollution were associated with higher individual SES and non-Danish origin. For neighborhood-level indicators of SES, no consistent pattern was observed. These results highlight the need for analyzing many different socio-demographic indicators to understand the complex associations between SES and exposure to air pollution., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Epidemiological studies have linked transportation noise and cardiovascular diseases, however, atrial fibrillation (AF) has received limited attention. We aimed to investigate the association between transportation noise and AF risk., Methods: Over the period 1990-2017 we estimated road and railway noise (L den ) at the most and least exposed façades for all residential addresses across Denmark. We estimated time-weighted mean noise exposure for 3.6 million individuals age ≥35 years. Of these, 269,756 incident cases of AF were identified with a mean follow-up of 13.0 years. Analyses were conducted using Cox proportional hazards models with adjustment for individual and area-level sociodemographic covariates and long-term residential air pollution., Results: A 10 dB higher 10-year mean road traffic noise at the most and least exposed façades were associated with incidence rate ratios (IRR) and 95% confidence intervals (CI) for AF of 1.006 (1.001-1.011) and 1.013 (1.007-1.019), respectively. After further adjustment for PM 2.5 , the IRRs (CIs) were 1.000 (0.995-1.005) and 1.007 (1.000-1.013), respectively. For railway noise, the IRRs per 10 dB increase in 10-year mean exposure were 1.017 (1.007-1.026) and 1.035 (1.021-1.050) for the most and least exposed façades, respectively, and were slightly attenuated when adjusted for PM 2.5 . Aircraft noise between 55 and 60 dB and ≥60 dB were associated with IRRs of 1.055 (0.996-1.116) and 1.036 (0.931-1.154), respectively, when compared to <45 dB., Conclusion: Transportation noise seems to be associated with a small increase in AF risk, especially for exposure at the least exposed façade., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Objectives: To investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND)., Methods: We pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (L Aeq8h ): <70, 70-74, 75-79, 80-84, ≥85 dB(A). We identified residential address history and estimated 1-year average road traffic noise at baseline. Using national patient and mortality registers, we identified 7777 stroke cases with a median follow-up of 20.2 years. Analyses were conducted using Cox proportional hazards models adjusting for individual and area-level potential confounders., Results: Exposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75-79, 80-84 and ≥85 dB(A) exposure groups, compared with <70 dB(A), respectively. In subanalyses using time-varying occupational noise exposure, we observed an indication of higher stroke risk among the most exposed (≥85 dB(A)), particularly when restricting analyses to people exposed to occupational noise within the last year (HR: 1.27; 95% CI: 0.99 to 1.63)., Conclusions: We found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

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.

Background: Long-term exposure to ambient air pollution has been associated with premature mortality, but associations at concentrations lower than current annual limit values are uncertain. We analysed associations between low-level air pollution and mortality within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE)., Methods: In this multicentre longitudinal study, we analysed seven population-based cohorts of adults (age ≥30 years) within ELAPSE, from Belgium, Denmark, England, the Netherlands, Norway, Rome (Italy), and Switzerland (enrolled in 2000-11; follow-up until 2011-17). Mortality registries were used to extract the underlying cause of death for deceased individuals. Annual average concentrations of fine particulate matter (PM 2·5 ), nitrogen dioxide (NO 2 ), black carbon, and tropospheric warm-season ozone (O 3 ) from Europe-wide land use regression models at 100 m spatial resolution were assigned to baseline residential addresses. We applied cohort-specific Cox proportional hazard models with adjustment for area-level and individual-level covariates to evaluate associations with non-accidental mortality, as the main outcome, and with cardiovascular, non-malignant respiratory, and lung cancer mortality. Subset analyses of participants living at low pollutant concentrations (as per predefined values) and natural splines were used to investigate the concentration-response function. Cohort-specific effect estimates were pooled in a random-effects meta-analysis., Findings: We analysed 28 153 138 participants contributing 257 859 621 person-years of observation, during which 3 593 741 deaths from non-accidental causes occurred. We found significant positive associations between non-accidental mortality and PM 2·5 , NO 2 , and black carbon, with a hazard ratio (HR) of 1·053 (95% CI 1·021-1·085) per 5 μg/m 3 increment in PM 2·5 , 1·044 (1·019-1·069) per 10 μg/m 3 NO 2 , and 1·039 (1·018-1·059) per 0·5 × 10 -5 /m black carbon. Associations with PM 2·5 , NO 2 , and black carbon were slightly weaker for cardiovascular mortality, similar for non-malignant respiratory mortality, and stronger for lung cancer mortality. Warm-season O 3 was negatively associated with both non-accidental and cause-specific mortality. Associations were stronger at low concentrations: HRs for non-accidental mortality at concentrations lower than the WHO 2005 air quality guideline values for PM 2·5 (10 μg/m 3 ) and NO 2 (40 μg/m 3 ) were 1·078 (1·046-1·111) per 5 μg/m 3 PM 2·5 and 1·049 (1·024-1·075) per 10 μg/m 3 NO 2 . Similarly, the association between black carbon and non-accidental mortality was highest at low concentrations, with a HR of 1·061 (1·032-1·092) for exposure lower than 1·5× 10 -5 /m, and 1·081 (0·966-1·210) for exposure lower than 1·0× 10 -5 /m., Interpretation: Long-term exposure to concentrations of PM 2·5 and NO 2 lower than current annual limit values was associated with non-accidental, cardiovascular, non-malignant respiratory, and lung cancer mortality in seven large European cohorts. Continuing research on the effects of low concentrations of air pollutants is expected to further inform the process of setting air quality standards in Europe and other global regions., Funding: Health Effects Institute., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Objective: Recent studies on air pollution and disease have been based on millions of participants within a region or country, relying entirely on register-based confounder adjustment. We aimed to investigate the effects of increasing adjustment for register- and questionnaire-based covariates on the association between air pollution and cardiometabolic diseases., Methods: In a population-based cohort of 246,766 eligible participants randomly selected across Denmark in 2010 and 2013 and followed up until December 31, 2017, we identified 3,247 myocardial infarction (MI) cases, 4,166 stroke cases and 6,366 type 2 diabetes cases. Based on historical address-information, we calculated 5-year time-weighted exposure to PM 2.5 and NO 2 modelled using a validated air pollution model. We used Cox proportional hazards models to calculate hazard ratios (HR) with increasing adjustment for a number of individual- and area-level register-based covariates as well as lifestyle covariates assessed through questionnaires., Results: We found that a 5 μg/m 3 higher PM 2.5 was associated with HRs (95% CI) for MI, stroke and diabetes, of respectively, 1.18 (0.91-1.52), 1.11 (0.88-1.40) and 1.24 (1.03-1.50) in the fully adjusted models. For all three diseases, adjustment for either individual-level, area-level or lifestyle covariates, or combinations of these resulted in higher HRs compared to HRs adjusted only for age, sex and calendar-year, most marked for MI and diabetes. Further adjustment for lifestyle in models with full register-based individual- and area-level adjustment resulted in only minor changes in HRs for all three diseases., Conclusions: Our findings suggest that in studies of air pollution and cardiometabolic disease, which use an adjustment strategy with a broad range of register-based socioeconomic variables, there is no effect on risk estimates from subsequent lifestyle adjustment., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Epidemiologic studies have linked transportation noise to increased morbidity and mortality, particularly for cardiovascular outcomes. However, studies investigating metabolic outcomes such as diabetes are limited and have focused only on noise exposures estimated for the loudest residential façade., Objectives: We aimed to examine the influence of long-term residential exposure to transportation noise at the loudest and quietest residential façades and the risk for type 2 diabetes., Methods: Road traffic and railway noise exposures (Lden) at the most and least exposed façades were estimated for all dwellings in Denmark during 1990-2017. Aircraft noise was estimated in 5-dB categories. Ten-year time-weighted mean noise exposures were estimated for 3.56  million individuals ≥ 35  years of age. From 2000 to 2017, 233,912 incident cases of type 2 diabetes were identified using hospital and prescription registries, with a mean follow-up of 12.9 y. We used Cox proportional hazards models adjusting for individual- and area-level covariates and long-term residential air pollution. The population-attributable fraction (PAF) was also computed., Results: Hazard ratios (HRs) and 95% confidence intervals (CIs) for type 2 diabetes in association with 10-dB increases in 10-y mean road traffic noise at the most and least exposed façades, respectively, were 1.05 (95% CI: 1.04, 1.05) and 1.09 (95% CI: 1.08, 1.10). Following subsequent adjustment for fine particulate matter [particulate matter ≤ 2.5 μ m in aerodynamic diameter] (10-y mean), the HRs (CIs) were 1.03 (95% CI: 1.03, 1.04) and 1.08 (95% CI: 1.07, 1.09), respectively. For railway noise, the HRs per 10-dB increase in 10-y mean exposure were 1.03 (95% CI: 1.02, 1.04) and 1.02 (95% CI: 1.01, 1.04) for the most and least exposed façades, respectively. Categorical models supported a linear exposure-outcome relationship for road traffic noise and, to a lesser extent, for railway noise. Aircraft noise > 45  dB was associated with a 1-4% higher likelihood of type 2 diabetes compared with those who were unexposed. We found road traffic and railway noise associated with a PAF of 8.5% and 1.4%, respectively, of the diabetes cases., Discussion: Long-term exposure to road, railway, and possibly aircraft traffic noise was associated with an increased risk of type 2 diabetes in a nationwide cohort of Danish adults. Our findings suggest that diabetes should be included when estimating the burden of disease due to transportation noise. https://doi.org/10.1289/EHP9146.

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low-level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO 2 ), particulate matter with diameter <2.5 μm (PM 2.5 ), black carbon (BC), warm-season ozone (O 3 ), and eight elemental components of PM 2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO 2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 μg/m 3 ), PM 2.5 (1.12, 0.92-1.36 per 5 μg/m 3 ), and BC (1.15, 1.00-1.33 per 0.5 10 -5 /m) and liver cancer incidence. Associations with NO 2 and BC persisted in two-pollutant models with PM 2.5 . Most components of PM 2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM 2.5 or NO 2 . Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards., (© 2021 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

Purpose: Few studies have suggested that traffic noise is a risk factor for cancer, but evidence is inconclusive. We aimed to investigate whether road traffic and railway noise are associated with risk of colorectal cancer., Methods: We obtained address history for all 3.5 million people above 40 years of age and living in Denmark for the period 1990-2017 and estimated road traffic and railway noise (L den ) at the most and least exposed facades of all addresses as well as air pollution (PM 2.5 ). During follow-up (2000-2017), 35,881 persons developed colon cancer and 19,755 developed rectal cancer. Information on individual and area-level demographic and socioeconomic variables was collected from Danish registries. We analyzed data using Cox proportional hazards models, including traffic noise as time-varying 10-year average exposure., Results: Exposure to road traffic noise at the most exposed façade was associated with an incidence rate ratio and 95% confidence interval for proximal colon cancer of 1.018 (0.999-1.038) per 10 dB higher noise. We observed no associations for road traffic noise at the least exposed façade or for railway noise in relation to proximal colon cancer. Also, we found no association between road traffic or railway noise and risk for distal colon cancer or rectal cancer., Conclusion: Traffic noise did not seem associated with higher risk for colorectal cancer, although the suggestion of a slightly higher risk of proximal colon cancer following exposure to road traffic noise warrants further research., (© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)