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1.
Int J Cancer ; 2020 Nov 19.
Artigo em Inglês | MEDLINE | ID: mdl-33210292

RESUMO

The aetiology of childhood leukaemia is poorly understood. Knowledge about differences in risk by socioeconomic status (SES) may enhance etiologic insights. We conducted a nationwide register-based case-control study to evaluate socioeconomic differences in the risk of childhood leukaemia in Denmark and to access whether associations varied by different measures of SES, time point of assessment, leukaemia type, and age at diagnosis. We identified all cases of leukaemia in children aged 0-19 years, born and diagnosed between 1980 and 2013 from the Danish Cancer Registry (N=1336) and sampled four individually matched controls per case (N=5330). We used conditional logistic regression models for analysis. Medium and high level of parental education was associated with a higher risk of acute myeloid leukaemia (AML) in the offspring, mainly driven by children diagnosed at ages 0-4 years (OR for high maternal education = 3.07; 95% CI: 1.44-6.55). We also observed a modestly increased risk for lymphoid leukaemia (LL) in association with higher level of parental education, but only in children diagnosed at ages 5-19 years. Higher parental income was associated with an increased risk of LL but not AML among children aged 5-19 years at diagnosis (OR for high maternal income=2.78; 95% CI: 1.32-5.89). Results for neighbourhood SES measures indicated null association. Bias or under-ascertainment of cases among families with low income or basic education is unlikely to explain the observed socioeconomic differences. Future research addressing explicitly the underlying mechanisms of our results may help to enhance etiologic insights of the disease.

3.
Environ Res ; : 110418, 2020 Nov 04.
Artigo em Inglês | MEDLINE | ID: mdl-33157111

RESUMO

BACKGROUND: Leukemia is one of the most common forms of hematologic malignancy, which can affect people of all ages. We previously showed an association between exposure to ambient particulate matter 2.5 µg (PM2.5) and risk for leukemia in adults. The aim of this study was to investigate which PM2.5 constituents were responsible for our previous observation. METHODS: This is a nationwide register-based case-control study. We identified 14,983 persons diagnosed with leukemia at age 20 or above, 1989-2014, in the Danish Cancer Registry. We selected up to four sex and age-matched controls per case at random from the entire Danish population (n = 51,613). We modelled concentrations of ambient PM2.5 and its constituents at the addresses of cases and controls for the 10-year period before index date with a state-of-the-art multiscale air pollution modeling system. We used conditional logistic regression to estimate odds ratios (ORs) adjusted for individual and neighborhood level socio-demographic variables. RESULT: The results showed higher risk for overall leukemia in association with interquartile range exposure to PM2.5 (OR = 1.09; 95% CI: 1.02, 1.17), black carbon (BC) (OR = 1.02; 95% CI: 1.00, 1.03), secondary inorganic aerosols (SIA) (OR = 1.15; 95% CI: 1.03, 1.29) and its components ammonium (NH4) (OR = 1.08; 95% CI: 1.00, 1.17) and nitrate (NO3) (OR = 1.08; 95% CI: 1.02, 1.14). In leukemia subtype analysis, statistically significant associations were found for AML with PM2.5 (OR = 1.14; 95% CI: 1.00, 1.29), BC (OR = 1.03; 95% CI: 1.00, 1.07), SIA (OR = 1.23; 95% CI: 1.01, 1.51), NH4 (OR = 1.16; 95% CI: 1.01, 1.34) and NO3 (OR = 1.12; 95% CI: 1.01, 1.24). The association between PM2.5 and leukemia persisted in two pollutants models including sum of primary emitted black and organic carbon (BC + OC), secondary organic aerosols (SOA), or sea-salt. The association between black carbon (BC) and leukemia persisted in two pollutants models including organic carbon (OC). The three pollutant model with sulfate (SO4), NH4 and NO3 showed an association with NO3 but not with SO4 or NH4. CONCLUSION: Ambient concentrations of the PM2.5 components BC, NH4 and NO3 at the residence showed associations with risk of incident leukemia in adults.

4.
Int J Hyg Environ Health ; 231: 113652, 2020 Oct 27.
Artigo em Inglês | MEDLINE | ID: mdl-33126026

RESUMO

BACKGROUND: Few studies have investigated whether road traffic noise is associated with gestational diabetes mellitus (GDM), and have yielded inconsistent findings. We aimed to investigate whether maternal exposure to residential transportation noise, before and during pregnancy, was associated with GDM in a nationwide cohort. METHODS: From the Danish population (2004-2017) we identified 629,254 pregnancies using the Danish Medical Birth Register. By linkage with the National Patient Registry, we identified 15,973 pregnancies complicated by GDM. Road traffic and railway noise (Lden) at the most and least exposed façades for all residential addresses from five years before pregnancy until birth were estimated for all. Analyses were conducted using generalized estimating equation models with adjustment for various individual and area-level sociodemographic covariates gathered from Danish registries, as well as green space and air pollution (PM2.5) estimated for all addresses. RESULTS: We found no positive associations between road traffic noise at either façade and GDM. For railway noise, a 10 dB increase in railway noise at the most and least exposed façades during the first trimester was associated with GDM, with an odds ratio (OR) of 1.06 (95% confidence interval (CI): 1.03-1.10) and 1.07 (95% CI: 1.02-1.13), respectively. We found indications of higher odds of GDM among women exposed to both high road traffic and railway noise at the least exposed facade during the first trimester (OR: 1.24; 95% CI: 1.07-1.44). CONCLUSION: In conclusion, this nationwide study suggests that railway noise but not road traffic noise might be associated with GDM.

5.
Int J Audiol ; : 1-12, 2020 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-33074773

RESUMO

OBJECTIVE: To introduce and document the recently established HESD (Hearing Examinations in Southern Denmark) database, including the necessary data preprocessing steps, and to describe the hearing loss (HL) characteristics of the study sample. DESIGN: Clinical auditory information has been collected for approximately 20 years in the state-funded clinics of the Region of Southern Denmark. We reviewed these data and conducted extensive preprocessing through data selection, integration, cleaning, transformation, and classification. HL profiling was then assessed in terms of severity, asymmetry, configuration, site of lesion, and audiogram shape. STUDY SAMPLE: The final number of complete audiograms available in the HESD database was 271,556, corresponding to detailed hearing information for 143,793 adults. RESULTS: The distribution of HL characteristics differed significantly (p < 0.001) between men and women for all categories analysed. Clear differences were observed for asymmetry and audiogram configuration. However, both men and women had higher prevalence of unilateral, moderate, and sensorineural HL. CONCLUSIONS: This work highlights the potential of the HESD database as a source of audiology-related epidemiological data. It can be used to evaluate the distribution of HL characteristics and also to investigate risk factors for HL and the associations between HL and other health outcomes.

6.
Br J Cancer ; 2020 Sep 17.
Artigo em Inglês | MEDLINE | ID: mdl-32939055

RESUMO

BACKGROUND: Few population-based epidemiological studies of adults have examined the relationship between air pollution and leukaemias. METHODS: Using Danish National Cancer Registry data and Danish DEHM-UBM-AirGIS system-modelled air pollution exposures, we examined whether particulate matter (PM2.5), black carbon (BC), nitrogen dioxide (NO2) and ozone (O3) averaged over 1, 5 or 10 years were associated with adult leukaemia in general or by subtype. In all, 14,986 adult cases diagnosed 1989-2014 and 51,624 age, sex and time-matched controls were included. Separate conditional logistic regression models, adjusted for socio-demographic factors, assessed exposure to each pollutant with leukaemias. RESULTS: Fully adjusted models showed a higher risk of leukaemia with higher 1-, 5- and 10-year-average exposures to PM2.5 prior to diagnosis (e.g. OR per 10 µg/m3 for 10-year average: 1.17, 95% CI: 1.03, 1.32), and a positive relationship with 1-year average BC. Results were driven by participants 70 years and older (OR per 10 µg/m3 for 10-year average: 1.35, 95% CI: 1.15-1.58). Null findings for younger participants. Higher 1-year average PM2.5 exposures were associated with higher risks for acute myeloid and chronic lymphoblastic leukaemia. CONCLUSION: Among older adults, higher risk for leukaemia was associated with higher residential PM2.5 concentrations averaged over 1, 5 and 10 years prior to diagnosis.

7.
Cardiovasc Res ; 2020 Jul 10.
Artigo em Inglês | MEDLINE | ID: mdl-32914847

RESUMO

AIMS: Nighttime aircraft noise exposure has been associated with increased risk of hypertension and myocardial infarction, mechanistically linked to sleep disturbance, stress and endothelial dysfunction. It is unclear, whether the most widely used metric to determine noise exposure, equivalent continuous sound level (Leq), is an adequate indicator of the cardiovascular impact induced by different noise patterns. METHODS AND RESULTS: In a randomized crossover study, we exposed 70 individuals with established cardiovascular disease or increased cardiovascular risk to two aircraft noise scenarios and one control scenario. Polygraphic recordings, echocardiography and flow-mediated dilation was determined for 3 study nights. The noise patterns consisted of 60 (Noise60) and 120 (Noise120) noise events, respectively, but with comparable Leq, corresponding to a mean value of 45 dB. Mean value of noise during control nights was 37 dB. During the control night, flow-mediated vasodilation (FMD) was 10.02±3.75%, compared to 7.27±3.21% for Noise60 nights and 7.21±3.58% for Noise120 nights (p<0.001). Sleep quality was impaired after noise exposure in both noise scenario nights (p<0.001). Serial echocardiographic assessment demonstrated an increase in the E/E' ratio, a measure of diastolic function, within the three exposure nights, with a ratio of 6.83±2.26 for the control night, 7.21±2.33 for Noise60 and 7.83±3.07 for Noise120 (p=0.043). CONCLUSIONS: Nighttime exposure to aircraft noise with similar Leq, but different number of noise events, results in a comparable worsening of vascular function. Adverse effects of nighttime aircraft noise exposure on cardiac function (diastolic dysfunction) seemed stronger the higher number of noise events. TRANSLATIONAL PERSPECTIVE: With the present field study, we tested whether 60 versus 120 simulated aircraft noise events with an equal average sound pressure level (Leq) have comparable adverse effects on endothelial and diastolic function of the heart of subjects with established cardiovascular disease or at increased cardiovascular risk. The results demonstrated that two different nighttime noise patterns with similar Leq, despite different number of noise events, results in a comparable worsening of vascular and cardiac diastolic function. These results may explain at least in part the increased incidence of coronary heart disease and heart failure being observed in response to nighttime aircraft noise.

8.
Commun Biol ; 3(1): 507, 2020 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-32917937

RESUMO

Cyanogenic glycosides form part of a binary plant defense system that, upon catabolism, detonates a toxic hydrogen cyanide bomb. In seed plants, the initial step of cyanogenic glycoside biosynthesis-the conversion of an amino acid to the corresponding aldoxime-is catalyzed by a cytochrome P450 from the CYP79 family. An evolutionary conundrum arises, as no CYP79s have been identified in ferns, despite cyanogenic glycoside occurrence in several fern species. Here, we report that a flavin-dependent monooxygenase (fern oxime synthase; FOS1), catalyzes the first step of cyanogenic glycoside biosynthesis in two fern species (Phlebodium aureum and Pteridium aquilinum), demonstrating convergent evolution of biosynthesis across the plant kingdom. The FOS1 sequence from the two species is near identical (98%), despite diversifying 140 MYA. Recombinant FOS1 was isolated as a catalytic active dimer, and in planta, catalyzes formation of an N-hydroxylated primary amino acid; a class of metabolite not previously observed in plants.

9.
Cancer Causes Control ; 31(10): 915-929, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32767157

RESUMO

PURPOSE: Differences in the risk of childhood central nervous system (CNS) tumors by socioeconomic status (SES) may enhance etiologic insights. We conducted a nationwide register-based case-control study to evaluate socioeconomic differences in the risk of childhood CNS tumors in Denmark and examined whether associations varied by different SES measures, time points of assessment, specific tumor types, and age at diagnosis. METHODS: We identified all children born between 1981 and 2013 and diagnosed with a CNS tumor at ages 0-19 years (n = 1,273) from the Danish Cancer Registry and sampled four individually matched controls per case (n = 5,086). We used conditional logistic regression models to estimate associations with individual-level and neighborhood-level socioeconomic measures. RESULTS: We observed elevated risks of ependymoma and embryonal CNS tumors in association with higher parental education (odds ratios (ORs) of 1.6-2.1 for maternal or paternal high education and ependymoma) and higher risk of all tumor types in association with higher maternal income, e.g., OR 1.93; 95% CI 1.05-3.52 for high versus low income for astrocytoma and other gliomas. Associations were often stronger in children diagnosed at ages 5-19 years. We found little evidence for an association with neighborhood SES. CONCLUSION: This large nationwide register study with minimal risk of bias showed that having parents with higher educational level and a mother with higher income was associated with a higher risk of childhood CNS tumors. Bias or under-ascertainment of cases among families with low income or basic education is unlikely to explain our findings.

10.
Environ Int ; 144: 106046, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32858469

RESUMO

BACKGROUND: Air pollution is an established carcinogen. Evidence for an association with brain tumors is, however, inconclusive. We investigated if individual particulate matter constituents were associated with brain tumor risk. METHODS: From comprehensive national registers, we identified all (n = 12 928) brain tumor cases, diagnosed in Denmark in the period 1989-2014, and selected 22 961 controls, matched on age, sex and year of birth. We established address histories and estimated 10-year mean residential outdoor concentrations of particulate matter < 2.5 µm, primarily emitted black carbon (BC) and organic carbon (OC), and combined carbon (OC/BC), as well as secondary inorganic and organic PM air pollutants from a detailed dispersion model. We used conditional logistic regression to calculate odds ratios (OR) per inter quartile range (IQR) exposure. We adjusted for income, marital and employment status as well as area-level socio-demographic characteristics. RESULTS: Total tumors of the brain were associated with OC/BC (OR: 1.053, 95%CI: 1.005-1.103, per IQR). The data suggested strongest associations for malignant tumors with ORs per IQR for OC/BC, BC and OC of 1.063 (95% CI: 1.007-1.123), 1.036 (95% CI: 1.006-1.067) and 1.030 (95%CI: 0.979-1.085), respectively. The results did not indicate adverse effects of other PM components. CONCLUSIONS: This large, population based study showed associations between primary emitted carbonaceous particles and risk for malignant brain tumors. As the first of its kind, this study needs replication.

11.
Environ Health ; 19(1): 81, 2020 07 08.
Artigo em Inglês | MEDLINE | ID: mdl-32641060

RESUMO

BACKGROUND: Inconclusive evidence has suggested a possible link between air pollution and central nervous system (CNS) tumors. We investigated a range of air pollutants in relation to types of CNS tumors. METHODS: We identified all (n = 21,057) intracranial tumors in brain, meninges and cranial nerves diagnosed in Denmark between 1989 and 2014 and matched controls on age, sex and year of birth. We established personal 10-year mean residential outdoor exposure to particulate matter < 2.5 µm (PM2.5), nitrous oxides (NOX), primary emitted black carbon (BC) and ozone. We used conditional logistic regression to calculate odds ratios (OR) linearly (per interquartile range (IQR)) and categorically. We accounted for personal income, employment, marital status, use of medication as well as socio-demographic conditions at area level. RESULTS: Malignant tumors of the intracranial CNS was associated with BC (OR: 1.034, 95%CI: 1.005-1.065 per IQR. For NOx the OR per IQR was 1.026 (95%CI: 0.998-1.056). For malignant non-glioma tumors of the brain we found associations with PM2.5 (OR: 1.267, 95%CI: 1.053-1.524 per IQR), BC (OR: 1.049, 95%CI: 0.996-1.106) and NOx (OR: 1.051, 95% CI: 0.996-1.110). CONCLUSION: Our results suggest that air pollution is associated with malignant intracranial CNS tumors and malignant non-glioma of the brain. However, additional studies are needed.

12.
Environ Res ; 188: 109762, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32535359

RESUMO

BACKGROUND: Particulate matter (PM) air pollution is a complex mixture and the various PM constituents likely affect health differently. The literature on the relationships among specific PM constituents and the risk of cancer is sparse. In this study, we aimed to evaluate the association of PM2.5 and its constituents with the incidence of non-Hodgkin lymphoma (NHL) and the two main NHL subtypes. METHODS: We undertook a nationwide register-based case-control study including 20,847 cases registered in the Danish Cancer Registry with NHL between 1989 and 2014. Among the entire Danish population, we selected 41,749 age and sex-matched controls randomly from the Civil Registration System. We assessed modelled outdoor PM concentrations at addresses of cases and controls with a state-of-the-art multi scale air pollution modelling system and used conditional logistic regression to estimate odds ratios (ORs) adjusted for individual and neighborhood level socio-demographic variables. RESULTS: The 10-year time-weighted average concentrations of PM2.5, primary carbonaceous particles (BC/OC), secondary inorganic aerosols (SIA), secondary organic aerosols (SOA) and sea salt were 17.4, 2.3, 7.8, 0.3, and 4.1 µg/m3, respectively among controls. The results showed higher risk for NHL in association with exposure to BC/OC (OR = 1.03; 95% CI: 1.00, 1.07, per interquartile range (IQR)) and SOA (OR = 1.54; 95% CI: 1.13, 2.09, per IQR). The results indicated a higher risk for follicular lymphoma in association with several PM components. Including PM2.5 (OR = 1.16; 95% CI: 0.98-1.38), BC/OC (OR = 1.05; 95% CI: 0.97-1.14), SIA (OR = 1.44; 95% CI: 0.80-1.08), SOA (OR = 4.52; 95% CI: 0.86-23.83) per IQR. CONCLUSION: This is the first study on PM constituents and the risk of NHL. The results indicated an association with primary carbonaceous and secondary organic PM. The results need replication in other settings before any firm conclusion can be reached.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Linfoma não Hodgkin , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Casos e Controles , Dinamarca/epidemiologia , Exposição Ambiental/efeitos adversos , Humanos , Linfoma não Hodgkin/induzido quimicamente , Linfoma não Hodgkin/epidemiologia , Material Particulado/análise , Material Particulado/toxicidade
13.
Environ Health Perspect ; 128(5): 57004, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32438890

RESUMO

BACKGROUND: Epidemiological research on effects of transportation noise on incident hypertension is inconsistent. OBJECTIVES: We aimed to investigate whether residential road traffic noise increases the risk for hypertension. METHODS: In a population-based cohort of 57,053 individuals 50-64 years of age at enrollment, we identified 21,241 individuals who fulfilled our case definition of filling ≥2 prescriptions and ≥180 defined daily doses of antihypertensive drugs (AHTs) within a year, during a mean follow-up time of 14.0 y. Residential addresses from 1987 to 2016 were obtained from national registers, and road traffic noise at the most exposed façade as well as the least exposed façade was modeled for all addresses. Analyses were conducted using Cox proportional hazards models. RESULTS: We found no associations between the 10-y mean exposure to road traffic noise and filled prescriptions for AHTs, with incidence rate ratios (IRRs) of 0.999 [95% confidence intervals (CI): 0.980, 1.019)] per 10-dB increase in road traffic noise at the most exposed façade and of 1.001 (95% CI: 0.977, 1.026) at the least exposed façade. Interaction analyses suggested an association with road traffic noise at the least exposed façade among subpopulations of current smokers and obese individuals. CONCLUSION: The present study does not support an association between road traffic noise and filled prescriptions for AHTs. https://doi.org/10.1289/EHP6273.

14.
Environ Res ; 187: 109633, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32442789

RESUMO

Transportation noise is a growing public health concern worldwide and epidemiological evidence has linked road traffic noise with mortality. However, incongruent effect estimates have been reported between incidence and mortality studies. Therefore, the present study aimed to investigate whether long-term exposure to residential road traffic noise at the most and least exposed façades was associated with all-cause, cardiovascular disease (CVD), ischemic heart disease (IHD), stroke, respiratory, or cancer mortality in a Danish cohort study. In a cohort of 52,758 individuals from Copenhagen and Aarhus, we estimated road traffic noise at the most and least exposed façades, as well as ambient air pollution, at all present and historical residential addresses from 1987 to 2016. Using the Danish cause of death register we identified cause-specific mortality. Analyses were conducted using Cox proportional hazards models. Ten-year time-weighted mean road traffic noise exposure at the most exposed façade was associated with an 8% higher risk for all-cause mortality per interquartile range (IQR; 10.4 dB) higher exposure level (95% CI: 1.05-1.11). Higher risks were also observed for CVD (HR = 1.13, 95% CI: 1.06-1.19) and stroke (HR = 1.11, 95% CI: 0.99-1.25) mortality. Road traffic noise at the least exposed façade (per IQR; 8.4 dB) was associated with CVD (HR = 1.09, 95% CI: 1.03-1.15), IHD (HR = 1.10, 95% CI: 1.01-1.21) and stroke (HR = 1.06, 95% CI: 0.95-1.19) mortality. Results were robust to adjustment for PM2.5 and NO2. In conclusion, this study adds to the body of evidence linking exposure to road traffic noise with higher risk of mortality.


Assuntos
Poluição do Ar , Ruído dos Transportes , Poluição do Ar/efeitos adversos , Estudos de Coortes , Dinamarca/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Ruído dos Transportes/efeitos adversos
15.
Sci Total Environ ; 726: 138577, 2020 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-32315856

RESUMO

Air pollution and noise originating from urban road traffic have been linked to the adverse health effects e.g. cardiovascular disease (CVD), although their generation and propagation mechanisms vary. We aimed to (i) develop a tool to model exposures to air pollution and noise using harmonized inputs based on similar geographical structure (ii) explore the relationship (using Spearman's rank correlation) of both pollutions at residential exposure level (iii) investigate the influence of traffic speed and Annual Average Daily Traffic (AADT) on air-noise relationship. The annual average (2005) air pollution (NOx, NO2, PM10, PM2.5) and noise levels (Lday, Leve, Lnight, Lden, LAeq,24h) are modelled at address locations in Copenhagen and Roskilde (N = 11,000 and 1500). The new AirGIS system together with the Operational Street Pollution Model (OSPM®) is used to produce air pollution estimates. Whereas, noise is estimated using Common Noise Assessment Methods in the EU (CNOSSOS-EU, hereafter CNOSSOS) with relatively coarser inputs (100 m CORINE land cover, simplified vehicle composition). In addition, noise estimates (Lday, Leve, Lnight) from CNOSSOS are also compared with noise estimates from Road Traffic Noise 1996 (RTN-96, one of the Nordic noise prediction standards). The overall air-noise correlation structure varied significantly in the range |rS| = 0.01-0.42, which was mainly affected by the background concentrations of air pollution as well as non-traffic emission sources. Moreover, neither AADT nor traffic speed showed substantial influence on the air-noise relationship. The noise levels estimated by CNOSSOS were substantially lower, and showed much lower variation than levels obtained by RTN-96. CNOSSOS, therefore, needs to be further evaluated using more detailed inputs (e.g. 10 m land cover polygons) to assess its feasibility for epidemiological noise exposure studies in Denmark. Lower to moderate air-noise correlations point towards significant potential to determine the independent health effects of air pollution and noise.

16.
Redox Biol ; 34: 101515, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32345536

RESUMO

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidative stress and inflammation in aortic, cardiac and/or cerebral tissues in single exposure models. In mice subjected to both stressors, most of these risk factors showed potentiated adverse changes. We also found that mice exposed to both noise and ATII had increased phagocytic NADPH oxidase (NOX-2)-mediated superoxide formation, immune cell infiltration (monocytes, neutrophils and T cells) in the aortic wall, astrocyte activation in the brain, enhanced cytokine signaling, and subsequent vascular and cerebral oxidative stress. Exaggerated renal stress response was also observed. In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. Mechanistically, noise potentiates neuroinflammation and cerebral oxidative stress, which may be a potential link between both risk factors. The results indicate that a combination of classical (arterial hypertension) and novel (noise exposure) risk factors may be deleterious for cardiovascular health.

17.
Int J Cancer ; 147(7): 1874-1880, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32175588

RESUMO

There is limited evidence regarding a possible association between exposure to ambient air pollutants and the risk of non-Hodgkin lymphoma (NHL). Previous epidemiological studies have relied on crude estimations for air pollution exposure and/or small numbers of NHL cases. The objective of our study was to analyze this association based on air pollution modeled at the address level and NHL cases identified from the nationwide Danish Cancer Registry. We identified 20,874 incident NHL cases diagnosed between 1989 and 2014 and randomly selected 41,749 controls matched on age and gender among the entire Danish population. We used conditional logistic regression to estimate odds ratios (ORs) and adjusted for individual and neighborhood level sociodemographic variables. There was no association between exposure to PM2.5 , BC, O3 , SO2 or NO2 and overall risk of NHL but several air pollutants were associated with higher risk of follicular lymphoma, but statistically insignificant, for example, PM2.5 (OR = 1.15 per 5 µg/m3 ; 95% CI: 0.98-1.34) and lower risk for diffuse large B-cell lymphoma (OR = 0.92 per 5 µg/m3 ; 95% CI: 0.82-1.03). In this population-based study, we did not observe any convincing evidence of a higher overall risk for NHL with higher exposure to ambient air pollutants.

18.
J Phys Chem B ; 124(15): 3065-3073, 2020 04 16.
Artigo em Inglês | MEDLINE | ID: mdl-32175746

RESUMO

High-potential iron-oxo species are intermediates in the catalytic cycles of oxygenase enzymes. They can cause heme degradation and irreversible oxidation of nearby amino acids. We have proposed that there are protective mechanisms in which hole hopping from oxidized hemes through tryptophan/tyrosine chains generates a surface-exposed amino-acid oxidant that could be rapidly disarmed by reaction with cellular reductants. In investigations of cytochrome P450BM3, we identified Trp96 as a critical residue that could play such a protective role. This Trp is cation-π paired with Arg398 in 81% of mammalian P450s. Here we report on the effect of the Trp/Arg cation-π interaction on Trp96 formal potentials as well as on electronic coupling strengths between Trp96 and the heme both for wild type cytochrome P450 and selected mutants. Mutation of Arg398 to His, which decreases the Trp96 formal potential, increases Trp-heme electronic coupling; however, surprisingly, the rate of phototriggered electron transfer from a Ru-sensitizer (through Trp96) to the P450BM3 heme was unaffected by the Arg398His mutation. We conclude that Trp96 has moved away from Arg398, suggesting that the protective mechanism for P450s with this Trp-Arg pair is conformationally gated.

19.
Sleep ; 43(8)2020 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-32083664

RESUMO

STUDY OBJECTIVES: Traffic noise has been associated with poor sleep quality and short sleep duration. This study investigates the association between nighttime road traffic noise at the least and most exposed façades of the residence and redemption of sleep medication. METHODS: In a cohort of 44,438 Danes, aged 50-64 at baseline (1993-1997), we identified all addresses from 1987 to 2015 from a national registry and calculated nighttime road traffic noise at the most and least exposed façades. Using Cox Proportional Hazard Models we investigated the association between residential traffic noise over 1, 5, and 10 years before redemption of the first sleep medication prescription in the Danish National Prescription Registry. During a median follow-up time of 18.5 years, 13,114 persons redeemed a prescription. RESULTS: We found that 10-year average nighttime exposure to road traffic noise at the most exposed façade was associated with a hazard ratio (HR) of 1.05, 95% confidence interval (CI) (1.00 to 1.10) for Ln greater than 55 as compared to not more than 45 dB, which when stratified by sex was confined to men (HR 1.16, 95% CI 1.08 to 1.25). For the least exposed façade the HR for Ln >45 vs ≤35 dB was 1.00, 95% CI (0.95 to 1.05). For the most exposed façade, the overall association was strongest in smokers and physically inactive. CONCLUSIONS: Long-term residential nighttime noise exposure at the most exposed façade may be associated with a higher likelihood of redeeming prescriptions for sleep medication, especially among men, smokers, and physically inactive.

20.
Annu Rev Public Health ; 41: 309-328, 2020 Apr 02.
Artigo em Inglês | MEDLINE | ID: mdl-31922930

RESUMO

Exposure to traffic noise is associated with stress and sleep disturbances. The World Health Organization (WHO) recently concluded that road traffic noise increases the risk for ischemic heart disease and potentially other cardiometabolic diseases, including stroke, obesity, and diabetes. The WHO report focused on whole-day noise exposure, but new epidemiological and translational field noise studies indicate that nighttime noise, in particular,is an important risk factor for cardiovascular disease (CVD) through increased levels of stress hormones and vascular oxidative stress, leading to endothelial dysfunction and subsequent development of various CVDs. Novel experimental studies found noise to be associated with oxidative stress-induced vascular and brain damage, mediated by activation of the NADPH oxidase, uncoupling of endothelial and neuronal nitric oxide synthase, and vascular/brain infiltration with inflammatory cells. Noise-induced pathophysiology was more pronounced in response to nighttime as compared with daytime noise. This review focuses on the consequences of nighttime noise.

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