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1.
Environ Res ; 252(Pt 3): 118942, 2024 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-38649012

RESUMO

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 (NO2), black carbon (BC), ozone (O3), particulate matter ≤2.5 µm (PM2.5) and several elemental constituents of PM2.5. 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 PM2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03-1.66) per 5 µg/m3, BC (1.26 (1.03-1.53) per 0.5 × 10- 5/m), NO2 (1.13 (0.93-1.38) per 10 µg/m3) and inverse for O3 (0.71 (0.54-0.93) per 10 µg/m3). 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Exposição Ambiental , Insuficiência Renal Crônica , Humanos , Insuficiência Renal Crônica/mortalidade , Insuficiência Renal Crônica/epidemiologia , Insuficiência Renal Crônica/induzido quimicamente , Masculino , Feminino , Europa (Continente)/epidemiologia , Pessoa de Meia-Idade , Idoso , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/efeitos adversos , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Material Particulado/análise , Material Particulado/efeitos adversos , Adulto
2.
Int J Cancer ; 154(11): 1900-1910, 2024 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-38339851

RESUMO

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 (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone in the warm season (O3w) 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 PM2.5, NO2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 µg/m3 increase in PM2.5, 1.19 (1.08-1.30) per 10 µg/m3 increase in NO2, 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/m3 increase in O3w. We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM2.5, NO2 and BC increased incidence of UADT cancer was observed.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Gástricas , Humanos , Material Particulado/efeitos adversos , Material Particulado/análise , Dióxido de Nitrogênio/efeitos adversos , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia , Incidência , Exposição Ambiental/efeitos adversos , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise
3.
Environ Pollut ; 343: 123097, 2024 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-38065336

RESUMO

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 (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) at residences. We also estimated concentrations of PM2.5 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/m3 NO2, 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 PM2.5 (HR = 1.16; 95% CI: 1.02-1.34) and potassium content of PM2.5, 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Ambientais , Leucemia , Linfoma , Adulto , Feminino , Humanos , Masculino , Dióxido de Nitrogênio/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Material Particulado/análise , Poluentes Ambientais/análise , Leucemia/induzido quimicamente , Leucemia/epidemiologia , Linfoma/induzido quimicamente , Linfoma/epidemiologia , Potássio/análise , Poluentes Atmosféricos/análise
4.
Sci Total Environ ; 912: 168789, 2024 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-37996018

RESUMO

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 PM2.5 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 NO2, 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Gástricas , Humanos , Material Particulado/análise , Neoplasias Gástricas/induzido quimicamente , Neoplasias Gástricas/epidemiologia , Incidência , Exposição Ambiental/análise , Poluição do Ar/análise , Poluentes Atmosféricos/análise
5.
Environ Res ; 239(Pt 1): 117230, 2023 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-37806476

RESUMO

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 (NO2), fine particles (PM2.5), black carbon (BC), and ozone (O3) 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 NO2, 1.04 (0.82, 1.33) per 5 µg/m³ PM2.5, 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 O3. CONCLUSIONS: We did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Mieloma Múltiplo , Humanos , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Mieloma Múltiplo/induzido quimicamente , Mieloma Múltiplo/epidemiologia , Dióxido de Nitrogênio/toxicidade , Dióxido de Nitrogênio/análise , Material Particulado/análise
6.
Br J Cancer ; 129(4): 656-664, 2023 09.
Artigo em Inglês | MEDLINE | ID: mdl-37420001

RESUMO

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 (NO2), fine particles (PM2.5), black carbon (BC), ozone (O3) and eight elemental components of PM2.5 (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 NO2, 1.17 (0.96, 1.41) per 5 µg/m³ PM2.5, 1.10 (0.97, 1.25) per 0.5 10-5m-1 BC, and 0.99 (0.84, 1.17) per 10 µg/m³ O3. CONCLUSIONS: We observed indications of an association between exposure to NO2, PM2.5, and BC and tumours of the CNS. The PM elements were not consistently associated with CNS tumour incidence.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Encefálicas , Ozônio , Humanos , Material Particulado/efeitos adversos , Dióxido de Nitrogênio , Exposição Ambiental/efeitos adversos , Poluição do Ar/efeitos adversos , Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Poluentes Atmosféricos/efeitos adversos
7.
Environ Pollut ; 328: 121642, 2023 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-37061017

RESUMO

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 (PM2.5 and NO2). 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.


Assuntos
Doenças Cardiovasculares , Neoplasias , Ruído dos Transportes , Humanos , Estudos de Coortes , Ruído dos Transportes/efeitos adversos , Fatores de Risco , Doenças Cardiovasculares/epidemiologia , Neoplasias/epidemiologia , Dinamarca/epidemiologia , Exposição Ambiental
8.
Environ Res ; 220: 115179, 2023 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-36584852

RESUMO

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 (PM2.5), ultrafine particles (UFP), elemental carbon (EC) and nitrogen dioxide (NO2) 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 ß-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/cm3. 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 PM2.5, UFP, EC and NO2 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doenças Cardiovasculares , Humanos , Adulto , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Dióxido de Nitrogênio/toxicidade , Dióxido de Nitrogênio/análise , Pressão Sanguínea , Doenças Cardiovasculares/induzido quimicamente , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Material Particulado/toxicidade , Material Particulado/análise , Lipídeos , Exposição Ambiental
9.
Cancer Epidemiol Biomarkers Prev ; 32(1): 105-113, 2023 01 09.
Artigo em Inglês | MEDLINE | ID: mdl-36215200

RESUMO

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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias da Mama , Ozônio , Pessoa de Meia-Idade , Humanos , Feminino , Material Particulado/efeitos adversos , Dióxido de Nitrogênio , Incidência , Neoplasias da Mama/induzido quimicamente , Neoplasias da Mama/epidemiologia , Poluição do Ar/efeitos adversos , Poluentes Atmosféricos/efeitos adversos , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise
10.
Environ Res ; 217: 114795, 2023 01 15.
Artigo em Inglês | MEDLINE | ID: mdl-36402187

RESUMO

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 (PM2.5). 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 PM2.5 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 PM2.5. 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.


Assuntos
Diabetes Mellitus Tipo 2 , Exposição Ambiental , Ruído dos Transportes , Humanos , Estudos de Coortes , Dinamarca/epidemiologia , Diabetes Mellitus Tipo 2/epidemiologia , Exposição Ambiental/efeitos adversos , Ruído dos Transportes/efeitos adversos
11.
Environ Res ; 216(Pt 3): 114740, 2023 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-36356668

RESUMO

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 (PM2.5), elemental carbon (EC) and nitrogen dioxide (NO2) 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/m3 higher PM2.5 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/m3) and NO2 (per 10 µg/m3) 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 PM2.5 changed only little, whereas ORs for EC or NO2 approached the null. In an analysis of persons below 55 years, PM2.5 was associated with an OR of 1.32 (95% CI: 1.09-1.60) per 10 µg/m3 increase. CONCLUSION: We found evidence of an association between the investigated air pollutants and breast cancer, especially PM2.5. 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias da Mama , Feminino , Humanos , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Neoplasias da Mama/induzido quimicamente , Neoplasias da Mama/epidemiologia , Carbono/análise , Estudos de Casos e Controles , Dinamarca/epidemiologia , Exposição Ambiental/análise , Dióxido de Nitrogênio/análise , Material Particulado/análise
12.
Environ Res ; 215(Pt 2): 114385, 2022 12.
Artigo em Inglês | MEDLINE | ID: mdl-36154858

RESUMO

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 (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight elemental components of PM2.5 (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 NO2, PM2.5, BC and O3 were 24.1 µg/m3 (12.8-39.2), 15.3 µg/m3 (8.6-19.2), 1.6 10-5 m-1 (0.7-2.1), and 87.0 µg/m3 (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 NO2, 1.04 (95% CI: 0.88, 1.21) per 5 µg/m³ PM2.5, 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 O3. We did not find associations between any of the elemental components of PM2.5 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Renais , Ozônio , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Carbono/análise , Carcinógenos/análise , Cobre/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Ferro/análise , Rim , Neoplasias Renais/induzido quimicamente , Neoplasias Renais/epidemiologia , Níquel , Dióxido de Nitrogênio/análise , Dióxido de Nitrogênio/toxicidade , Ozônio/análise , Material Particulado/análise , Material Particulado/toxicidade , Potássio/análise , Silício , Fuligem/análise , Enxofre/análise , Vanádio , Emissões de Veículos/análise , Zinco/análise
13.
Occup Environ Med ; 2022 Apr 21.
Artigo em Inglês | MEDLINE | ID: mdl-35450950

RESUMO

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 (LAeq8h): <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.

14.
Environ Res ; 212(Pt A): 113180, 2022 09.
Artigo em Inglês | MEDLINE | ID: mdl-35395236

RESUMO

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 (Lden max) and least (Lden 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 Lden 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.


Assuntos
Neoplasias , Ruído dos Transportes , Estudos de Casos e Controles , Criança , Estudos de Coortes , Dinamarca/epidemiologia , Exposição Ambiental , Humanos , Neoplasias/epidemiologia , Neoplasias/etiologia , Ruído dos Transportes/efeitos adversos
15.
Artigo em Inglês | MEDLINE | ID: mdl-35191985

RESUMO

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.

16.
Br J Cancer ; 126(10): 1499-1507, 2022 06.
Artigo em Inglês | MEDLINE | ID: mdl-35173304

RESUMO

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 (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 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 PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93-1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99-1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00-1.16 per 10 ng/m3). CONCLUSIONS: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias da Bexiga Urinária , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Incidência , Masculino , Dióxido de Nitrogênio , Material Particulado/efeitos adversos , Doenças Raras , Neoplasias da Bexiga Urinária/epidemiologia , Neoplasias da Bexiga Urinária/etiologia , Zinco
17.
Cancer Causes Control ; 32(12): 1447-1455, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34467460

RESUMO

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 (Lden) at the most and least exposed facades of all addresses as well as air pollution (PM2.5). 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.


Assuntos
Neoplasias do Colo , Ruído dos Transportes , Estudos de Coortes , Dinamarca/epidemiologia , Exposição Ambiental/efeitos adversos , Humanos , Ruído dos Transportes/efeitos adversos
18.
Cancer Causes Control ; 32(9): 935-942, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34050843

RESUMO

PURPOSE: The etiology of Hodgkin lymphoma (HL) is obscure. Research on air pollution and risk of HL provides inconsistent results. We aimed to investigate the association between long-term residential exposure to air pollution and risk of adult Hodgkin lymphoma in Denmark. METHODS: We performed a nationwide register-based case-control study, including all (n = 2,681) Hodgkin lymphoma cases registered in the nationwide Danish Cancer Registry between 1989 and 2014. We randomly selected 8,853 age- and sex-matched controls from the entire Danish population using the Civil Registration System, and identified 20-year residential address history for all cases and controls. We modeled outdoor air pollution concentrations at all these addresses using the high-resolution multiscale air pollution model system DEHM/UBM/AirGIS. We used conditional logistic regression to estimate odds ratios adjusted for individual and neighborhood level sociodemographic variables. RESULTS: There was no association between 1, 5, 10, and 20 years' time-weighted average exposure to fine particles (PM2.5), O3, SO2, NO2, or the PM2.5 constituents OC, NH4, NO3, and SO4 and risk of Hodgkin lymphoma. CONCLUSION: Residential exposure to ambient air pollution does not seem to increase the risk of developing Hodgkin lymphoma.


Assuntos
Poluição do Ar , Doença de Hodgkin , Adulto , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Estudos de Casos e Controles , Dinamarca/epidemiologia , Exposição Ambiental/efeitos adversos , Doença de Hodgkin/epidemiologia , Doença de Hodgkin/etiologia , Humanos , Material Particulado
19.
Cancer Epidemiol ; 73: 101947, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-33979714

RESUMO

BACKGROUND: The aetiology for most solid tumours in childhood is largely unknown. The lack of evidence concerns also the relationship between socioeconomic position (SEP) and risk of childhood solid tumours other than in the central nervous system (CNS). We sought to access the association between individual and neighbourhood SEP measures and risk of childhood non-CNS solid tumours in Denmark and to evaluate whether associations varied by measure of SEP, time point of SEP assessment (during pregnancy versus before diagnosis) and tumour type. METHODS: We conducted a nationwide case-control study based on Danish registry data. We identified all children born in 1980-2013 and diagnosed with a non-CNS solid tumour at ages 0-19 years (N = 1961) from the Danish Cancer Registry and sampled four individually matched controls per case using the Population Registry. We fitted conditional logistic regression models to estimate associations with register-based individual-level and neighbourhood-level SEP measures. RESULTS: We observed a tendency of increased odd ratios (OR) in association with medium and high maternal income for most tumour types (e.g. OR for the highest income quintile and malignant bone tumours = 2.11; 95 % CI: 1.01, 4.38) and for parental education in association with higher education for some tumour types. For malignant epithelial neoplasms, higher parental education and income level were overall associated with an increased risk, e.g. OR = 1.63 (95 % CI: 1.00, 2.65) for the fourth group of maternal income during pregnancy. We found no risk pattern for neighbourhood SEP. CONCLUSION: This large register-study with minimal risk of bias found a tendency of slightly to moderately increased risks for most childhood non-CNS solid tumours in association with higher maternal income and parental education. Future research examining the underlying mechanisms of these socioeconomic differences in non-CNS solid tumours as well as other childhood cancer types are warranted.


Assuntos
Neoplasias do Sistema Nervoso Central , Adolescente , Adulto , Estudos de Casos e Controles , Neoplasias do Sistema Nervoso Central/epidemiologia , Criança , Pré-Escolar , Dinamarca/epidemiologia , Feminino , Humanos , Lactente , Recém-Nascido , Gravidez , Sistema de Registros , Características de Residência/estatística & dados numéricos , Fatores de Risco , Fatores Socioeconômicos , Adulto Jovem
20.
Environ Res ; 195: 110739, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33460635

RESUMO

OBJECTIVE: Previous studies have suggested that transportation noise may increase risk for breast cancer, but existing literature is scarce and inconclusive. We aimed to investigate associations between road traffic and railway noise and risk for breast cancer across the entire Danish female population. METHODS: For all 2.8 million residential addresses across Denmark, we modelled road and railway noise at the most and least exposed façades for the period 1990-2017. We calculated 10-year time-weighted mean noise exposure for 1.8 million women aged >35 years, of whom 66,006 developed breast cancer during follow-up from 2000 to 2017. We analysed data using Cox proportional hazards models with noise exposure included as 10-year running means and adjusted for a number of individual and area-level socioeconomic co-variates and air pollution with fine particles estimated for all addresses. RESULTS: For exposures at the least exposed façade, we found that a 10 dB increase in 10-year time-weighted noise was associated with incidence rate ratios (IRRs) and 95% confidence intervals (CI) for breast cancer of 1.032 (1.019-1.046) for road noise and 1.023 (0.993-1.053) for railway noise. For exposures at the most exposed façade, the IRRs (95% CIs) were 1.012 (1.002-1.022) for road noise and 1.020 (1.001-1.039) for railway noise. Associations were strongest among women with human epidermal growth factor receptor 2 negative breast cancer. CONCLUSIONS: Road traffic and railway noise were associated with higher risk for breast cancer, especially noise at the least exposed façade, which is a proxy for noise exposure during sleep.


Assuntos
Neoplasias da Mama , Ruído dos Transportes , Adulto , Neoplasias da Mama/epidemiologia , Neoplasias da Mama/etiologia , Estudos de Coortes , Dinamarca/epidemiologia , Exposição Ambiental , Feminino , Humanos , Ruído dos Transportes/efeitos adversos
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