805 results found
Espin-Perez A, Font-Ribera L, van Veldhoven K, et al., 2018, Blood transcriptional and microRNA responses to short-term exposure to disinfection by-products in a swimming pool, ENVIRONMENT INTERNATIONAL, Vol: 110, Pages: 42-50, ISSN: 0160-4120
Gulliver J, Morley D, Dunster C, et al., 2018, Land use regression models for the oxidative potential of fine particles (PM2.5) in five European areas., Environ Res, Vol: 160, Pages: 247-255
Oxidative potential (OP) of particulate matter (PM) is proposed as a biologically-relevant exposure metric for studies of air pollution and health. We aimed to evaluate the spatial variability of the OP of measured PM2.5 using ascorbate (AA) and (reduced) glutathione (GSH), and develop land use regression (LUR) models to explain this spatial variability. We estimated annual average values (m-3) of OPAA and OPGSH for five areas (Basel, CH; Catalonia, ES; London-Oxford, UK (no OPGSH); the Netherlands; and Turin, IT) using PM2.5 filters. OPAA and OPGSH LUR models were developed using all monitoring sites, separately for each area and combined-areas. The same variables were then used in repeated sub-sampling of monitoring sites to test sensitivity of variable selection; new variables were offered where variables were excluded (p > .1). On average, measurements of OPAA and OPGSH were moderately correlated (maximum Pearson's maximum Pearson's R = = .7) with PM2.5 and other metrics (PM2.5absorbance, NO2, Cu, Fe). HOV (hold-out validation) R2 for OPAA models was .21, .58, .45, .53, and .13 for Basel, Catalonia, London-Oxford, the Netherlands and Turin respectively. For OPGSH, the only model achieving at least moderate performance was for the Netherlands (R2 = .31). Combined models for OPAA and OPGSH were largely explained by study area with weak local predictors of intra-area contrasts; we therefore do not endorse them for use in epidemiologic studies. Given the moderate correlation of OPAA with other pollutants, the three reasonably performing LUR models for OPAA could be used independently of other pollutant metrics in epidemiological studies.
Ambatipudi S, Horvath S, Perrier F, et al., 2017, DNA methylome analysis identifies accelerated epigenetic ageing associated with postmenopausal breast cancer susceptibility, EUROPEAN JOURNAL OF CANCER, Vol: 75, Pages: 299-307, ISSN: 0959-8049
Andersen ZJ, Pedersen M, Weinmayr G, et al., 2017, Long-term Exposure to Ambient Air Pollution and Incidence of Brain Tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)., Neuro Oncol
Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent. Methods: In 12 cohorts from six European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤ 2.5, ≤ 10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. Results: Of 282,194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts had also data on nonmalignant brain tumor, where among 106,786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically non-significant association between malignant brain tumor and PM2.5 absorbance (Hazard Ratio and 95% Confidence Interval: 1.67; 0.89-3.14 per 10 -5/m 3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10 -5/m 3) and all other pollutants were lower for nonmalignant than for malignant brain tumors. Conclusion: We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.
Andersen ZJ, Stafoggia M, Weinmayr G, et al., 2017, Long-Term Exposure to Ambient Air Pollution and Incidence of Postmenopausal Breast Cancer in 15 European Cohorts within the ESCAPE Project, ENVIRONMENTAL HEALTH PERSPECTIVES, Vol: 125, ISSN: 0091-6765
Baglietto L, Ponzi E, Haycock P, et al., 2017, DNA methylation changes measured in pre-diagnostic peripheral blood samples are associated with smoking and lung cancer risk, INTERNATIONAL JOURNAL OF CANCER, Vol: 140, Pages: 50-61, ISSN: 0020-7136
Barrera-Gomez J, Agier L, Portengen L, et al., 2017, A systematic comparison of statistical methods to detect interactions in exposome-health associations, ENVIRONMENTAL HEALTH, Vol: 16, ISSN: 1476-069X
Bernatsky S, Velásquez García HA, Spinelli JJ, et al., 2017, Lupus-related single nucleotide polymorphisms and risk of diffuse large B-cell lymphoma., Lupus Sci Med, Vol: 4, ISSN: 2053-8790
Objective: Determinants of the increased risk of diffuse large B-cell lymphoma (DLBCL) in SLE are unclear. Using data from a recent lymphoma genome-wide association study (GWAS), we assessed whether certain lupus-related single nucleotide polymorphisms (SNPs) were also associated with DLBCL. Methods: GWAS data on European Caucasians from the International Lymphoma Epidemiology Consortium (InterLymph) provided a total of 3857 DLBCL cases and 7666 general-population controls. Data were pooled in a random-effects meta-analysis. Results: Among the 28 SLE-related SNPs investigated, the two most convincingly associated with risk of DLBCL included the CD40 SLE risk allele rs4810485 on chromosome 20q13 (OR per risk allele=1.09, 95% CI 1.02 to 1.16, p=0.0134), and the HLA SLE risk allele rs1270942 on chromosome 6p21.33 (OR per risk allele=1.17, 95% CI 1.01 to 1.36, p=0.0362). Of additional possible interest were rs2205960 and rs12537284. The rs2205960 SNP, related to a cytokine of the tumour necrosis factor superfamily TNFSF4, was associated with an OR per risk allele of 1.07, 95% CI 1.00 to 1.16, p=0.0549. The OR for the rs12537284 (chromosome 7q32, IRF5 gene) risk allele was 1.08, 95% CI 0.99 to 1.18, p=0.0765. Conclusions: These data suggest several plausible genetic links between DLBCL and SLE.
Boccardi M, Gallo V, Yasui Y, et al., 2017, The biomarker-based diagnosis of Alzheimer's disease. 2-lessons from oncology, NEUROBIOLOGY OF AGING, Vol: 52, Pages: 141-152, ISSN: 0197-4580
Carayol M, Leitzmann MF, Ferrari P, et al., 2017, Blood Metabolic Signatures of Body Mass Index: A Targeted Metabolomics Study in the EPIC Cohort, JOURNAL OF PROTEOME RESEARCH, Vol: 16, Pages: 3137-3146, ISSN: 1535-3893
Chatziioannou A, Georgiadis P, Hebels DG, et al., 2017, Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases, SCIENTIFIC REPORTS, Vol: 7, ISSN: 2045-2322
Dossus L, Franceschi S, Biessy C, et al., 2017, Adipokines and inflammation markers and risk of differentiated thyroid carcinoma: The EPIC study., Int J Cancer
Other than the influence of ionizing radiation and benign thyroid disease, little is known about the risk factors for differentiated thyroid cancer (TC) which is an increasing common cancer worldwide. Consistent evidence shows that body mass is positively associated with TC risk. As excess weight is a state of chronic inflammation, we investigated the relationship between concentrations of leptin, adiponectin, C-reactive protein, interleukin(IL)-6, IL-10 and TNF-α and the risk of TC. A case-control study was nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) study and included 475 first primary incident TC cases (399 women and 76 men) and 1,016 matched cancer-free cohort participants. Biomarkers were measured in serum samples using validated and highly sensitive commercially available immunoassays. Odds ratios (ORs) of TC by levels of each biomarker were estimated using conditional logistic regression models, adjusting for BMI and alcohol consumption. Adiponectin was inversely associated with TC risk among women (ORT3vs.T1 =0.69, 95%CI: 0.49-0.98, Ptrend =0.04) but not among men (ORT3vs.T1 =1.36, 95%CI: 0.67-2.76, Ptrend =0.37). Increasing levels of IL-10 were positively associated with TC risk in both genders and significantly so in women (ORT3vs.T1 =1.59, 95%CI: 1.13-2.25, Ptrend =0.01) but not in men (ORT3vs.T1 =1.78, 95%CI: 0.80-3.98, Ptrend =0.17). Leptin, CRP, IL-6 and TNF-α were not associated with TC risk in either gender. These results indicate a positive association of TC risk with IL-10 and a negative association with adiponectin that is probably restricted to women. Inflammation may play a role in TC in combination with or independently of excess weight. This article is protected by copyright. All rights reserved.
Duell EJ, Lujan-Barroso L, Sala N, et al., 2017, Plasma microRNAs as biomarkers of pancreatic cancer risk in a prospective cohort study, INTERNATIONAL JOURNAL OF CANCER, Vol: 141, Pages: 905-915, ISSN: 0020-7136
Ek WE, Tobi EW, Ahsan M, et al., 2017, Tea and coffee consumption in relation to DNA methylation in four European cohorts, HUMAN MOLECULAR GENETICS, Vol: 26, Pages: 3221-3231, ISSN: 0964-6906
Fehringer G, Brenner DR, Zhang Z-F, et al., 2017, Alcohol and lung cancer risk among never smokers: A pooled analysis from the international lung cancer consortium and the SYNERGY study, INTERNATIONAL JOURNAL OF CANCER, Vol: 140, Pages: 1976-1984, ISSN: 0020-7136
Fiorito G, Polidoro S, Dugue P-A, et al., 2017, Social adversity and epigenetic aging: a multi-cohort study on socioeconomic differences in peripheral blood DNA methylation, SCIENTIFIC REPORTS, Vol: 7, ISSN: 2045-2322
Fiorito G, Vlaanderen J, Polidoro S, et al., 2017, Oxidative stress and inflammation mediate the effect of air pollution on cardio- and cerebrovascular disease: A prospective study in nonsmokers., Environ Mol Mutagen
Air pollution is associated with a broad range of adverse health effects, including mortality and morbidity due to cardio- and cerebrovascular diseases (CCVD), but the molecular mechanisms involved are not entirely understood. This study aims to investigate the involvement of oxidative stress and inflammation in the causal chain, and to identify intermediate biomarkers that are associated retrospectively with the exposure and prospectively with the disease. We designed a case-control study on CCVD nested in a cohort of 18,982 individuals from the EPIC-Italy study. We measured air pollution, inflammatory biomarkers, and whole-genome DNA methylation in blood collected up to 17 years before the diagnosis. The study sample includes all the incident CCVD cases among former- and never-smokers, with available stored blood sample, that arose in the cohort during the follow-up. We identified enrichment of altered DNA methylation in "ROS/Glutathione/Cytotoxic granules" and "Cytokine signaling" pathways related genes, associated with both air pollution (multiple comparisons adjusted p for enrichment ranging from 0.01 to 0.03 depending on pollutant) and with CCVD risk (P = 0.04 and P = 0.03, respectively). Also, Interleukin-17 was associated with higher exposure to NO2 (P = 0.0004), NOx (P = 0.0005), and CCVD risk (OR = 1.79; CI 1.04-3.11; P = 0.04 comparing extreme tertiles). Our findings indicate that chronic exposure to air pollution can lead to oxidative stress, which in turn activates a cascade of inflammatory responses mainly involving the "Cytokine signaling" pathway, leading to increased risk of CCVD. Inflammatory proteins and DNA methylation alterations can be detected several years before CCVD diagnosis in blood samples, being promising preclinical biomarkers. Environ. Mol. Mutagen., 2017. © 2017 Wiley Periodicals, Inc.
Frisoni GB, Boccardi M, Barkhof F, et al., 2017, Strategic roadmap for an early diagnosis of Alzheimer's disease based on biomarkers, LANCET NEUROLOGY, Vol: 16, Pages: 661-676, ISSN: 1474-4422
Georgiadis P, Liampa I, Hebels DG, et al., 2017, Evolving DNA methylation and gene expression markers of B-cell chronic lymphocytic leukemia are present in pre-diagnostic blood samples more than 10 years prior to diagnosis, BMC GENOMICS, Vol: 18, ISSN: 1471-2164
Gunter MJ, Murphy N, Cross AJ, et al., 2017, Coffee Drinking and Mortality in 10 European Countries A Multinational Cohort Study, ANNALS OF INTERNAL MEDICINE, Vol: 167, Pages: 236-+, ISSN: 0003-4819
Herceg Z, Ghantous A, Wild CP, et al., 2017, Roadmap for investigating epigenome deregulation and environmental origins of cancer., Int J Cancer
The interaction between the (epi)genetic makeup of an individual and his/her environmental exposure record (exposome) is accepted as a determinant factor for a significant proportion of human malignancies. Recent evidence has highlighted the key role of epigenetic mechanisms in mediating gene-environment interactions and translating exposures into tumorigenesis. There is also growing evidence that epigenetic changes may be risk factor-specific ("fingerprints") that should prove instrumental in the discovery of new biomarkers in cancer. Here, we review the state of the science of epigenetics associated with environmental stimuli and cancer risk, highlighting key developments in the field. Critical knowledge gaps and research needs are discussed and advances in epigenomics that may help in understanding the functional relevance of epigenetic alterations. Key elements required for causality inferences linking epigenetic changes to exposure and cancer are discussed and how these alterations can be incorporated in carcinogen evaluation and in understanding mechanisms underlying epigenome deregulation by the environment.
Jay R, Brennan P, Brenner, et al., 2017, Alcohol consumption and the risk of renal cancers in the European Prospective Investigation into Cancer and Nutrition (EPIC). Wozniak MB, Brennan P, Brenner DR, Overvad K, Olsen A, Tjønneland A, Boutron-Ruault MC, Clavel-Chapelon F, Fagherazzi G, Katzke V, Kühn T, Boeing H, Bergmann MM, Steffen A, Naska A, Trichopoulou A, Trichopoulos D, Saieva C, Grioni S, Panico S, Tumino R, Vineis P, Bueno-de-Mesquita HB, Peeters PH, Hjartåker A, Weiderpass E, Arriola L, Molina-Montes E, Duell EJ, Santiuste C, Alonso de la Torre R, Barricarte Gurrea A, Stocks T, Johansson M, Ljungberg B, Wareham N, Khaw KT, Travis RC, Cross AJ, Murphy N, Riboli E, Scelo G.Int J Cancer. 2015 Oct 15;137(8):1953-66. [Epub 2015 Apr 28]. doi: 10.1002/ijc.29559., Urol Oncol, Vol: 35
Epidemiologic studies have reported that moderate alcohol consumption is inversely associated with the risk of renal cancer. However, there is no information available on the associations in renal cancer subsites. From 1992 to 2010, 477,325 men and women in the European Prospective Investigation into Cancer and Nutrition cohort were followed for incident renal cancers (n = 931). Baseline and lifetime alcohol consumption was assessed by country-specific, validated dietary questionnaires. Information on past alcohol consumption was collected by lifestyle questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from Cox proportional hazard models. In multivariate analysis, total alcohol consumption at baseline was inversely associated with renal cancer; the HR and 95% CI for the increasing categories of total alcohol consumption at recruitment vs. the light drinkers category were 0.78 (0.62-0.99), 0.82 (0.64-1.04), 0.70 (0.55-0.90), and 0.91 (0.63-1.30), respectively, (ptrend = 0.001). A similar relationship was observed for average lifetime alcohol consumption and for all renal cancer subsites combined or for renal parenchyma subsite. The trend was not observed in hypertensive individuals and not significant in smokers. In conclusion, moderate alcohol consumption was associated with a decreased risk of renal cancer.
Kelly RS, Kiviranta H, Bergdahl IA, et al., 2017, Prediagnostic plasma concentrations of organochlorines and risk of B-cell non-Hodgkin lymphoma in envirogenomarkers: a nested case-control study, ENVIRONMENTAL HEALTH, Vol: 16, ISSN: 1476-069X
Kelly-Irving M, Delpierre C, Vineis P, 2017, Beyond bad luck: induced mutations and hallmarks of cancer, LANCET ONCOLOGY, Vol: 18, Pages: 999-1000, ISSN: 1470-2045
Law PJ, Berndt SI, Speedy HE, et al., 2017, Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukaemia, NATURE COMMUNICATIONS, Vol: 8, ISSN: 2041-1723
Linner RK, Marioni RE, Rietveld CA, et al., 2017, An epigenome-wide association study meta-analysis of educational attainment, MOLECULAR PSYCHIATRY, Vol: 22, Pages: 1680-1690, ISSN: 1359-4184
McCrory C, O'Leary N, Fraga S, et al., 2017, Socioeconomic differences in children's growth trajectories from infancy to early adulthood: evidence from four European countries, JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH, Vol: 71, Pages: 981-989, ISSN: 0143-005X
Mostafavi N, Vlaanderen J, Portengen L, et al., 2017, Associations Between Genome-wide Gene Expression and Ambient Nitrogen Oxides, EPIDEMIOLOGY, Vol: 28, Pages: 320-328, ISSN: 1044-3983
Obon-Santacana M, Lujan-Barroso L, Freisling H, et al., 2017, Dietary and lifestyle determinants of acrylamide and glycidamide hemoglobin adducts in non-smoking postmenopausal women from the EPIC cohort, EUROPEAN JOURNAL OF NUTRITION, Vol: 56, Pages: 1157-1168, ISSN: 1436-6207
Pardini B, Viberti C, Naccarati A, et al., 2017, Increased micronucleus frequency in peripheral blood lymphocytes predicts the risk of bladder cancer, BRITISH JOURNAL OF CANCER, Vol: 116, Pages: 202-210, ISSN: 0007-0920
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