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516 results on '"Vineis, P."'

1. Lifestyle changes in middle age and risk of cancer: evidence from the European Prospective Investigation into Cancer and Nutrition

Author

Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Hoff, G, Heath, A, Cross, A, Vineis, P, Dossus, L, Johansson, M, Freisling, H, Matta, K, Huybrechts, I, Chen, S, B. Borch, K, Sandanger, T, H. Nost, T, Dahm, C, Antoniussen, C, Tin Tin, S, Fournier, A, Marques, C, Artaud, F, Sanchez, M, Guevara, M, Santiuste, C, Agudo, A, Bajracharya, R, Katzke, V, Ricceri, F, Agnoli, C, Bergmann, M, Schulze, M, Panico, S, Masala, G, Tjonneland, A, Olsen, A, Stocks, T, Manjer, J, Aizpurua-Atxega, A, Weiderpass, E, Riboli, E, Gunter, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Hoff G., Heath A. K., Cross A. J., Vineis P., Dossus L., Johansson M., Freisling H., Matta K., Huybrechts I., Chen S. L. F., B. Borch K., Sandanger T. M., H. Nost T., Dahm C. C., Antoniussen C. S., Tin Tin S., Fournier A., Marques C., Artaud F., Sanchez M. -J., Guevara M., Santiuste C., Agudo A., Bajracharya R., Katzke V., Ricceri F., Agnoli C., Bergmann M. M., Schulze M. B., Panico S., Masala G., Tjonneland A., Olsen A., Stocks T., Manjer J., Aizpurua-Atxega A., Weiderpass E., Riboli E., Gunter M. J., Ferrari P., Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Hoff, G, Heath, A, Cross, A, Vineis, P, Dossus, L, Johansson, M, Freisling, H, Matta, K, Huybrechts, I, Chen, S, B. Borch, K, Sandanger, T, H. Nost, T, Dahm, C, Antoniussen, C, Tin Tin, S, Fournier, A, Marques, C, Artaud, F, Sanchez, M, Guevara, M, Santiuste, C, Agudo, A, Bajracharya, R, Katzke, V, Ricceri, F, Agnoli, C, Bergmann, M, Schulze, M, Panico, S, Masala, G, Tjonneland, A, Olsen, A, Stocks, T, Manjer, J, Aizpurua-Atxega, A, Weiderpass, E, Riboli, E, Gunter, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Hoff G., Heath A. K., Cross A. J., Vineis P., Dossus L., Johansson M., Freisling H., Matta K., Huybrechts I., Chen S. L. F., B. Borch K., Sandanger T. M., H. Nost T., Dahm C. C., Antoniussen C. S., Tin Tin S., Fournier A., Marques C., Artaud F., Sanchez M. -J., Guevara M., Santiuste C., Agudo A., Bajracharya R., Katzke V., Ricceri F., Agnoli C., Bergmann M. M., Schulze M. B., Panico S., Masala G., Tjonneland A., Olsen A., Stocks T., Manjer J., Aizpurua-Atxega A., Weiderpass E., Riboli E., Gunter M. J., and Ferrari P.

Abstract

In this study, we aimed to provide novel evidence on the impact of changing lifestyle habits on cancer risk. In the EPIC cohort, 295,865 middle-aged participants returned a lifestyle questionnaire at baseline and during follow-up. At both timepoints, we calculated a healthy lifestyle index (HLI) score based on cigarette smoking, alcohol consumption, body mass index and physical activity. HLI ranged from 0 (most unfavourable) to 16 (most favourable). We estimated the association between HLI change and risk of lifestyle-related cancers—including cancer of the breast, lung, colorectum, stomach, liver, cervix, oesophagus, bladder, and others—using Cox regression models. We reported hazard ratios (HR) with 95% confidence intervals (CI). Median time between the two questionnaires was 5.7 years, median age at follow-up questionnaire was 59 years. After the follow-up questionnaire, we observed 14,933 lifestyle-related cancers over a median follow-up of 7.8 years. Each unit increase in the HLI score was associated with 4% lower risk of lifestyle-related cancers (HR 0.96; 95%CI 0.95–0.97). Among participants in the top HLI third at baseline (HLI > 11), those in the bottom third at follow-up (HLI ≤ 9) had 21% higher risk of lifestyle-related cancers (HR 1.21; 95%CI 1.07–1.37) than those remaining in the top third. Among participants in the bottom HLI third at baseline, those in the top third at follow-up had 25% lower risk of lifestyle-related cancers (HR 0.75; 95%CI 0.65–0.86) than those remaining in the bottom third. These results indicate that lifestyle changes in middle age may have a significant impact on cancer risk.

Published
2024

2. Meta-analysis of diagnostic performance of serological tests for SARS-CoV-2 antibodies up to 25 April 2020 and public health implications

Author

Caini, S, Bellerba, F, Corso, F, Díaz-Basabe, A, Natoli, G, Paget, J, Facciotti, F, De Angelis, S, Raimondi, S, Palli, D, Mazzarella, L, Pelicci, P, Vineis, P, Gandini, S, Caini S, Bellerba F, Corso F, Díaz-Basabe A, Natoli G, Paget J, Facciotti F, De Angelis SP, Raimondi S, Palli D, Mazzarella L, Pelicci PG, Vineis P, Gandini S, Caini, S, Bellerba, F, Corso, F, Díaz-Basabe, A, Natoli, G, Paget, J, Facciotti, F, De Angelis, S, Raimondi, S, Palli, D, Mazzarella, L, Pelicci, P, Vineis, P, Gandini, S, Caini S, Bellerba F, Corso F, Díaz-Basabe A, Natoli G, Paget J, Facciotti F, De Angelis SP, Raimondi S, Palli D, Mazzarella L, Pelicci PG, Vineis P, and Gandini S

Abstract

We reviewed the diagnostic accuracy of SARS-CoV-2 serological tests. Random-effects models yielded a summary sensitivity of 82% for IgM, and 85% for IgG and total antibodies. For specificity, the pooled estimate were 98% for IgM and 99% for IgG and total antibodies. In populations with ≤ 5% of seroconverted individuals, unless the assays have perfect (i.e. 100%) specificity, the positive predictive value would be ≤ 88%. Serological tests should be used for prevalence surveys only in hard-hit areas.

Published
2020

3. Lifestyle factors and risk of multimorbidity of cancer and cardiometabolic diseases: A multinational cohort study

Author

Freisling, H, Viallon, V, Lennon, H, Bagnardi, V, Ricci, C, Butterworth, A, Sweeting, M, Muller, D, Romieu, I, Bazelle, P, Kvaskoff, M, Arveux, P, Severi, G, Bamia, C, Kuhn, T, Kaaks, R, Bergmann, M, Boeing, H, Tjonneland, A, Olsen, A, Overvad, K, Dahm, C, Menendez, V, Agudo, A, Sanchez, M, Amiano, P, Santiuste, C, Gurrea, A, Tong, T, Schmidt, J, Tzoulaki, I, Tsilidis, K, Ward, H, Palli, D, Agnoli, C, Tumino, R, Ricceri, F, Panico, S, Picavet, H, Bakker, M, Monninkhof, E, Nilsson, P, Manjer, J, Rolandsson, O, Thysell, E, Weiderpass, E, Jenab, M, Riboli, E, Vineis, P, Danesh, J, Wareham, N, Gunter, M, Ferrari, P, Freisling H., Viallon V., Lennon H., Bagnardi V., Ricci C., Butterworth A. S., Sweeting M., Muller D., Romieu I., Bazelle P., Kvaskoff M., Arveux P., Severi G., Bamia C., Kuhn T., Kaaks R., Bergmann M., Boeing H., Tjonneland A., Olsen A., Overvad K., Dahm C. C., Menendez V., Agudo A., Sanchez M. -J., Amiano P., Santiuste C., Gurrea A. B., Tong T. Y. N., Schmidt J. A., Tzoulaki I., Tsilidis K. K., Ward H., Palli D., Agnoli C., Tumino R., Ricceri F., Panico S., Picavet H. S. J., Bakker M., Monninkhof E., Nilsson P., Manjer J., Rolandsson O., Thysell E., Weiderpass E., Jenab M., Riboli E., Vineis P., Danesh J., Wareham N. J., Gunter M. J., Ferrari P., Freisling, H, Viallon, V, Lennon, H, Bagnardi, V, Ricci, C, Butterworth, A, Sweeting, M, Muller, D, Romieu, I, Bazelle, P, Kvaskoff, M, Arveux, P, Severi, G, Bamia, C, Kuhn, T, Kaaks, R, Bergmann, M, Boeing, H, Tjonneland, A, Olsen, A, Overvad, K, Dahm, C, Menendez, V, Agudo, A, Sanchez, M, Amiano, P, Santiuste, C, Gurrea, A, Tong, T, Schmidt, J, Tzoulaki, I, Tsilidis, K, Ward, H, Palli, D, Agnoli, C, Tumino, R, Ricceri, F, Panico, S, Picavet, H, Bakker, M, Monninkhof, E, Nilsson, P, Manjer, J, Rolandsson, O, Thysell, E, Weiderpass, E, Jenab, M, Riboli, E, Vineis, P, Danesh, J, Wareham, N, Gunter, M, Ferrari, P, Freisling H., Viallon V., Lennon H., Bagnardi V., Ricci C., Butterworth A. S., Sweeting M., Muller D., Romieu I., Bazelle P., Kvaskoff M., Arveux P., Severi G., Bamia C., Kuhn T., Kaaks R., Bergmann M., Boeing H., Tjonneland A., Olsen A., Overvad K., Dahm C. C., Menendez V., Agudo A., Sanchez M. -J., Amiano P., Santiuste C., Gurrea A. B., Tong T. Y. N., Schmidt J. A., Tzoulaki I., Tsilidis K. K., Ward H., Palli D., Agnoli C., Tumino R., Ricceri F., Panico S., Picavet H. S. J., Bakker M., Monninkhof E., Nilsson P., Manjer J., Rolandsson O., Thysell E., Weiderpass E., Jenab M., Riboli E., Vineis P., Danesh J., Wareham N. J., Gunter M. J., and Ferrari P.

Abstract

Background: Although lifestyle factors have been studied in relation to individual non-communicable diseases (NCDs), their association with development of a subsequent NCD, defined as multimorbidity, has been scarcely investigated. The aim of this study was to investigate associations between five lifestyle factors and incident multimorbidity of cancer and cardiometabolic diseases. Methods: In this prospective cohort study, 291,778 participants (64% women) from seven European countries, mostly aged 43 to 58 years and free of cancer, cardiovascular disease (CVD), and type 2 diabetes (T2D) at recruitment, were included. Incident multimorbidity of cancer and cardiometabolic diseases was defined as developing subsequently two diseases including first cancer at any site, CVD, and T2D in an individual. Multi-state modelling based on Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (95% CI) of developing cancer, CVD, or T2D, and subsequent transitions to multimorbidity, in relation to body mass index (BMI), smoking status, alcohol intake, physical activity, adherence to the Mediterranean diet, and their combination as a healthy lifestyle index (HLI) score. Cumulative incidence functions (CIFs) were estimated to compute 10-year absolute risks for transitions from healthy to cancer at any site, CVD (both fatal and non-fatal), or T2D, and to subsequent multimorbidity after each of the three NCDs. Results: During a median follow-up of 11 years, 1910 men and 1334 women developed multimorbidity of cancer and cardiometabolic diseases. A higher HLI, reflecting healthy lifestyles, was strongly inversely associated with multimorbidity, with hazard ratios per 3-unit increment of 0.75 (95% CI, 0.71 to 0.81), 0.84 (0.79 to 0.90), and 0.82 (0.77 to 0.88) after cancer, CVD, and T2D, respectively. After T2D, the 10-year absolute risks of multimorbidity were 40% and 25% for men and women, respectively, with unhealthy lifestyle, and 30% and 18% for men and

Published
2020

4. Association of neighbourhood disadvantage and individual socioeconomic position with all-cause mortality: a longitudinal multicohort analysis.

Author

Ribeiro, AI, Fraga, S, Severo, M, Kelly-Irving, M, Delpierre, C, Stringhini, S, Kivimaki, M, Joost, S, Guessous, I, Severi, G, Giles, G, Sacerdote, C, Vineis, P, Barros, H, LIFEPATH Consortium, Ribeiro, AI, Fraga, S, Severo, M, Kelly-Irving, M, Delpierre, C, Stringhini, S, Kivimaki, M, Joost, S, Guessous, I, Severi, G, Giles, G, Sacerdote, C, Vineis, P, Barros, H, and LIFEPATH Consortium

Abstract

BACKGROUND: Few studies have examined the interactions between individual socioeconomic position and neighbourhood deprivation and the findings so far are heterogeneous. Using a large sample of diverse cohorts, we investigated the interaction effect of neighbourhood socioeconomic deprivation and individual socioeconomic position, assessed using education, on mortality. METHODS: We did a longitudinal multicohort analysis that included six cohort studies participating in the European LIFEPATH consortium: the CoLaus (Lausanne, Switzerland), E3N (France), EPIC-Turin (Turin, Italy), EPIPorto (Porto, Portugal), Melbourne Collaborative Cohort Study (Melbourne, VIC, Australia), and Whitehall II (London, UK) cohorts. All participants with data on mortality, educational attainment, and neighbourhood deprivation were included in the present study. The data sources were the databases of each cohort study. Poisson regression was used to estimate the mortality rates and associations (relative risk, 95% CIs) with neighbourhood deprivation (Q1 being least deprived to Q5 being the most deprived). Baseline educational attainment was used as an indicator of individual socioeconomic position. Estimates were combined using pooled analysis and the relative excess risk due to the interaction was computed to identify additive interactions. FINDINGS: The cohorts comprised a total population of 168 801 individuals. The recruitment dates were 2003-06 for CoLaus, 1989-91 for E3N, 1992-98 for EPIC-Turin, 1999-2003 for EPIPorto, 1990-94 for MCCS, and 1991-94 for Whitehall II. We use baseline data only and mortality data obtained using record linkage. Age-adjusted mortality rates were higher among participants residing in more deprived neighbourhoods than those in the least deprived neighbourhoods (Q1 least deprived neighbourhoods, 369·7 per 100 000 person-years [95% CI 356·4-383·2] vs Q5-most deprived neighbourhoods 445·7 per 100 000 person-years [430·2-461·7]), but the magnitude of the associat

Published
2022

5. Metabolic Signatures of Healthy Lifestyle Patterns and Colorectal Cancer Risk in a European Cohort.

Author

Rothwell, JA, Murphy, N, Bešević, J, Kliemann, N, Jenab, M, Ferrari, P, Achaintre, D, Gicquiau, A, Vozar, B, Scalbert, A, Huybrechts, I, Freisling, H, Prehn, C, Adamski, J, Cross, AJ, Pala, VM, Boutron-Ruault, M-C, Dahm, CC, Overvad, K, Gram, IT, Sandanger, TM, Skeie, G, Jakszyn, P, Tsilidis, KK, Aleksandrova, K, Schulze, MB, Hughes, DJ, van Guelpen, B, Bodén, S, Sánchez, M-J, Schmidt, JA, Katzke, V, Kühn, T, Colorado-Yohar, S, Tumino, R, Bueno-de-Mesquita, B, Vineis, P, Masala, G, Panico, S, Eriksen, AK, Tjønneland, A, Aune, D, Weiderpass, E, Severi, G, Chajès, V, Gunter, MJ, Rothwell, JA, Murphy, N, Bešević, J, Kliemann, N, Jenab, M, Ferrari, P, Achaintre, D, Gicquiau, A, Vozar, B, Scalbert, A, Huybrechts, I, Freisling, H, Prehn, C, Adamski, J, Cross, AJ, Pala, VM, Boutron-Ruault, M-C, Dahm, CC, Overvad, K, Gram, IT, Sandanger, TM, Skeie, G, Jakszyn, P, Tsilidis, KK, Aleksandrova, K, Schulze, MB, Hughes, DJ, van Guelpen, B, Bodén, S, Sánchez, M-J, Schmidt, JA, Katzke, V, Kühn, T, Colorado-Yohar, S, Tumino, R, Bueno-de-Mesquita, B, Vineis, P, Masala, G, Panico, S, Eriksen, AK, Tjønneland, A, Aune, D, Weiderpass, E, Severi, G, Chajès, V, and Gunter, MJ

Abstract

BACKGROUND & AIMS: Colorectal cancer risk can be lowered by adherence to the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) guidelines. We derived metabolic signatures of adherence to these guidelines and tested their associations with colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition cohort. METHODS: Scores reflecting adherence to the WCRF/AICR recommendations (scale, 1-5) were calculated from participant data on weight maintenance, physical activity, diet, and alcohol among a discovery set of 5738 cancer-free European Prospective Investigation into Cancer and Nutrition participants with metabolomics data. Partial least-squares regression was used to derive fatty acid and endogenous metabolite signatures of the WCRF/AICR score in this group. In an independent set of 1608 colorectal cancer cases and matched controls, odds ratios (ORs) and 95% CIs were calculated for colorectal cancer risk per unit increase in WCRF/AICR score and per the corresponding change in metabolic signatures using multivariable conditional logistic regression. RESULTS: Higher WCRF/AICR scores were characterized by metabolic signatures of increased odd-chain fatty acids, serine, glycine, and specific phosphatidylcholines. Signatures were inversely associated more strongly with colorectal cancer risk (fatty acids: OR, 0.51 per unit increase; 95% CI, 0.29-0.90; endogenous metabolites: OR, 0.62 per unit change; 95% CI, 0.50-0.78) than the WCRF/AICR score (OR, 0.93 per unit change; 95% CI, 0.86-1.00) overall. Signature associations were stronger in male compared with female participants. CONCLUSIONS: Metabolite profiles reflecting adherence to WCRF/AICR guidelines and additional lifestyle or biological risk factors were associated with colorectal cancer. Measuring a specific panel of metabolites representative of a healthy or unhealthy lifestyle may identify strata of the population at higher risk of colorectal cancer.

Published
2022

6. Association between work characteristics and epigenetic age acceleration:cross-sectional results from UK – understanding society study

Author

Freni-Sterrantino, A. (Anna), Fiorito, G. (Giovanni), d’Errico, A. (Angelo), Virtanen, M. (Marianna), Ala-Mursula, L. (Leena), Järvelin, M.-R. (Marjo-Riitta), Vineis, P. (Paolo), Robinson, O. (Oliver), Freni-Sterrantino, A. (Anna), Fiorito, G. (Giovanni), d’Errico, A. (Angelo), Virtanen, M. (Marianna), Ala-Mursula, L. (Leena), Järvelin, M.-R. (Marjo-Riitta), Vineis, P. (Paolo), and Robinson, O. (Oliver)

Abstract

Occupation-related stress and work characteristics are possible determinants of social inequalities in epigenetic aging but have been little investigated. Here, we investigate the association of several work characteristics with epigenetic age acceleration (AA) biomarkers. The study population included employed and unemployed men and women (n = 631) from the UK Understanding Society study. We evaluated the association of employment and work characteristics related to job type, job stability; job schedule; autonomy and influence at work; occupational physical activity; and feelings regarding the job with four epigenetic age acceleration biomarkers (Hannum, Horvath, PhenoAge, GrimAge) and pace of aging (DunedinPoAm, DunedinPACE). We fitted linear regression models, unadjusted and adjusted for established risk factors, and found the following associations for unemployment (years of acceleration): HorvathAA (1.51, 95% CI 0.08, 2.95), GrimAgeAA (1.53, 95% CI 0.16, 2.90) and 3.21 years for PhenoAA (95% CI 0.89, 5.33). Job insecurity increased PhenoAA (1.83, 95% CI 0.003, 3.67), while working at night was associated with an increase of 2.12 years in GrimAgeAA (95% CI 0.69, 3.55). We found effects of unemployment to be stronger in men and effects of night shift work to be stronger in women. These results provide evidence of associations between unemployment with accelerated ageing and suggest that insecure employment and night work may also increase age acceleration. Our findings have implications for policies relating to current changes in working conditions and highlight the utility of biological age biomarkers in studies in younger populations without long-term health information.

Published
2022

7. Methylation-based markers of aging and lifestyle-related factors and risk of breast cancer: a pooled analysis of four prospective studies

Author

Dugue, P-A, Bodelon, C, Chung, FF, Brewer, HR, Ambatipudi, S, Sampson, JN, Cuenin, C, Chajes, V, Romieu, I, Fiorito, G, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Vineis, P, Polidoro, S, Baglietto, L, English, D, Severi, G, Giles, GG, Milne, RL, Herceg, Z, Garcia-Closas, M, Flanagan, JM, Southey, MC, Dugue, P-A, Bodelon, C, Chung, FF, Brewer, HR, Ambatipudi, S, Sampson, JN, Cuenin, C, Chajes, V, Romieu, I, Fiorito, G, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Vineis, P, Polidoro, S, Baglietto, L, English, D, Severi, G, Giles, GG, Milne, RL, Herceg, Z, Garcia-Closas, M, Flanagan, JM, and Southey, MC

Abstract

BACKGROUND: DNA methylation in blood may reflect adverse exposures accumulated over the lifetime and could therefore provide potential improvements in the prediction of cancer risk. A substantial body of research has shown associations between epigenetic aging and risk of disease, including cancer. Here we aimed to study epigenetic measures of aging and lifestyle-related factors in association with risk of breast cancer. METHODS: Using data from four prospective case-control studies nested in three cohorts of European ancestry participants, including a total of 1,655 breast cancer cases, we calculated three methylation-based measures of lifestyle factors (body mass index [BMI], tobacco smoking and alcohol consumption) and seven measures of epigenetic aging (Horvath-based, Hannum-based, PhenoAge and GrimAge). All measures were regression-adjusted for their respective risk factors and expressed per standard deviation (SD). Odds ratios (OR) and 95% confidence intervals (CI) were calculated using conditional or unconditional logistic regression and pooled using fixed-effects meta-analysis. Subgroup analyses were conducted by age at blood draw, time from blood sample to diagnosis, oestrogen receptor-positivity status and tumour stage. RESULTS: None of the measures of epigenetic aging were associated with risk of breast cancer in the pooled analysis: Horvath 'age acceleration' (AA): OR per SD = 1.02, 95%CI: 0.95-1.10; AA-Hannum: OR = 1.03, 95%CI:0.95-1.12; PhenoAge: OR = 1.01, 95%CI: 0.94-1.09 and GrimAge: OR = 1.03, 95%CI: 0.94-1.12, in models adjusting for white blood cell proportions, body mass index, smoking and alcohol consumption. The BMI-adjusted predictor of BMI was associated with breast cancer risk, OR per SD = 1.09, 95%CI: 1.01-1.17. The results for the alcohol and smoking methylation-based predictors were consistent with a null association. Risk did not appear to substantially vary by age at blood draw, time to diagnosis or tumour characteristics. CONCLUSION

Published
2022

8. Epigenetic mechanisms of lung carcinogenesis involve differentially methylated CpG sites beyond those associated with smoking

Author

Petrovic, D, Bodinier, B, Dagnino, S, Whitaker, M, Karimi, M, Campanella, G, Haugdahl Nost, T, Polidoro, S, Palli, D, Krogh, V, Tumino, R, Sacerdote, C, Panico, S, Lund, E, Dugue, P-A, Giles, GG, Severi, G, Southey, M, Vineis, P, Stringhini, S, Bochud, M, Sandanger, TM, Vermeulen, RCH, Guida, F, Chadeau-Hyam, M, Petrovic, D, Bodinier, B, Dagnino, S, Whitaker, M, Karimi, M, Campanella, G, Haugdahl Nost, T, Polidoro, S, Palli, D, Krogh, V, Tumino, R, Sacerdote, C, Panico, S, Lund, E, Dugue, P-A, Giles, GG, Severi, G, Southey, M, Vineis, P, Stringhini, S, Bochud, M, Sandanger, TM, Vermeulen, RCH, Guida, F, and Chadeau-Hyam, M

Abstract

Smoking-related epigenetic changes have been linked to lung cancer, but the contribution of epigenetic alterations unrelated to smoking remains unclear. We sought for a sparse set of CpG sites predicting lung cancer and explored the role of smoking in these associations. We analysed CpGs in relation to lung cancer in participants from two nested case-control studies, using (LASSO)-penalised regression. We accounted for the effects of smoking using known smoking-related CpGs, and through conditional-independence network. We identified 29 CpGs (8 smoking-related, 21 smoking-unrelated) associated with lung cancer. Models additionally adjusted for Comprehensive Smoking Index-(CSI) selected 1 smoking-related and 49 smoking-unrelated CpGs. Selected CpGs yielded excellent discriminatory performances, outperforming information provided by CSI only. Of the 8 selected smoking-related CpGs, two captured lung cancer-relevant effects of smoking that were missed by CSI. Further, the 50 CpGs identified in the CSI-adjusted model complementarily explained lung cancer risk. These markers may provide further insight into lung cancer carcinogenesis and help improving early identification of high-risk patients.

Published
2022

9. DNA methylation signature of chronic low-grade inflammation and its role in cardio-respiratory diseases

Author

Wielscher, M. (Matthias), Mandaviya, P. R. (Pooja R.), Kuehnel, B. (Brigitte), Joehanes, R. (Roby), Mustafa, R. (Rima), Robinson, O. (Oliver), Zhang, Y. (Yan), Bodinier, B. (Barbara), Walton, E. (Esther), Mishra, P. P. (Pashupati P.), Schlosser, P. (Pascal), Wilson, R. (Rory), Tsai, P.-C. (Pei-Chien), Palaniswamy, S. (Saranya), Marioni, R. E. (Riccardo E.), Fiorito, G. (Giovanni), Cugliari, G. (Giovanni), Karhunen, V. (Ville), Ghanbari, M. (Mohsen), Psaty, B. M. (Bruce M.), Loh, M. (Marie), Bis, J. C. (Joshua C.), Lehne, B. (Benjamin), Sotoodehnia, N. (Nona), Deary, I. J. (Ian J.), Chadeau-Hyam, M. (Marc), Brody, J. A. (Jennifer A.), Cardona, A. (Alexia), Selvin, E. (Elizabeth), Smith, A. K. (Alicia K.), Miller, A. H. (Andrew H.), Torres, M. A. (Mylin A.), Marouli, E. (Eirini), Gao, X. (Xin), van Meurs, J. B. (Joyce B. J.), Graf-Schindler, J. (Johanna), Rathmann, W. (Wolfgang), Koenig, W. (Wolfgang), Peters, A. (Annette), Weninger, W. (Wolfgang), Farlik, M. (Matthias), Zhang, T. (Tao), Chen, W. (Wei), Xia, Y. (Yujing), Teumer, A. (Alexander), Nauck, M. (Matthias), Grabe, H. J. (Hans J.), Doerr, M. (Macus), Lehtimaki, T. (Terho), Guan, W. (Weihua), Milani, L. (Lili), Tanaka, T. (Toshiko), Fisher, K. (Krista), Waite, L. L. (Lindsay L.), Kasela, S. (Silva), Vineis, P. (Paolo), Verweij, N. (Niek), van der Harst, P. (Pim), Iacoviello, L. (Licia), Sacerdote, C. (Carlotta), Panico, S. (Salvatore), Krogh, V. (Vittorio), Tumino, R. (Rosario), Tzala, E. (Evangelia), Matullo, G. (Giuseppe), Hurme, M. A. (Mikko A.), Raitakari, O. T. (Olli T.), Colicino, E. (Elena), Baccarelli, A. A. (Andrea A.), Kahonen, M. (Mika), Herzig, K.-H. (Karl-Heinz), Li, S. (Shengxu), BIOS consortium, Conneely, K. N. (Karen N.), Kooner, J. S. (Jaspal S.), Kottgen, A. (Anna), Heijmans, B. T. (Bastiaan T.), Deloukas, P. (Panos), Relton, C. (Caroline), Ong, K. K. (Ken K.), Bell, J. T. (Jordana T.), Boerwinkle, E. (Eric), Elliott, P. (Paul), Brenner, H. (Hermann), Beekman, M. (Marian), Levy, D. (Daniel), Waldenberger, M. (Melanie), Chambers, J. C. (John C.), Dehghan, A. (Abbas), Järvelin, M.-R. (Marjo-Riitta), Wielscher, M. (Matthias), Mandaviya, P. R. (Pooja R.), Kuehnel, B. (Brigitte), Joehanes, R. (Roby), Mustafa, R. (Rima), Robinson, O. (Oliver), Zhang, Y. (Yan), Bodinier, B. (Barbara), Walton, E. (Esther), Mishra, P. P. (Pashupati P.), Schlosser, P. (Pascal), Wilson, R. (Rory), Tsai, P.-C. (Pei-Chien), Palaniswamy, S. (Saranya), Marioni, R. E. (Riccardo E.), Fiorito, G. (Giovanni), Cugliari, G. (Giovanni), Karhunen, V. (Ville), Ghanbari, M. (Mohsen), Psaty, B. M. (Bruce M.), Loh, M. (Marie), Bis, J. C. (Joshua C.), Lehne, B. (Benjamin), Sotoodehnia, N. (Nona), Deary, I. J. (Ian J.), Chadeau-Hyam, M. (Marc), Brody, J. A. (Jennifer A.), Cardona, A. (Alexia), Selvin, E. (Elizabeth), Smith, A. K. (Alicia K.), Miller, A. H. (Andrew H.), Torres, M. A. (Mylin A.), Marouli, E. (Eirini), Gao, X. (Xin), van Meurs, J. B. (Joyce B. J.), Graf-Schindler, J. (Johanna), Rathmann, W. (Wolfgang), Koenig, W. (Wolfgang), Peters, A. (Annette), Weninger, W. (Wolfgang), Farlik, M. (Matthias), Zhang, T. (Tao), Chen, W. (Wei), Xia, Y. (Yujing), Teumer, A. (Alexander), Nauck, M. (Matthias), Grabe, H. J. (Hans J.), Doerr, M. (Macus), Lehtimaki, T. (Terho), Guan, W. (Weihua), Milani, L. (Lili), Tanaka, T. (Toshiko), Fisher, K. (Krista), Waite, L. L. (Lindsay L.), Kasela, S. (Silva), Vineis, P. (Paolo), Verweij, N. (Niek), van der Harst, P. (Pim), Iacoviello, L. (Licia), Sacerdote, C. (Carlotta), Panico, S. (Salvatore), Krogh, V. (Vittorio), Tumino, R. (Rosario), Tzala, E. (Evangelia), Matullo, G. (Giuseppe), Hurme, M. A. (Mikko A.), Raitakari, O. T. (Olli T.), Colicino, E. (Elena), Baccarelli, A. A. (Andrea A.), Kahonen, M. (Mika), Herzig, K.-H. (Karl-Heinz), Li, S. (Shengxu), BIOS consortium, Conneely, K. N. (Karen N.), Kooner, J. S. (Jaspal S.), Kottgen, A. (Anna), Heijmans, B. T. (Bastiaan T.), Deloukas, P. (Panos), Relton, C. (Caroline), Ong, K. K. (Ken K.), Bell, J. T. (Jordana T.), Boerwinkle, E. (Eric), Elliott, P. (Paul), Brenner, H. (Hermann), Beekman, M. (Marian), Levy, D. (Daniel), Waldenberger, M. (Melanie), Chambers, J. C. (John C.), Dehghan, A. (Abbas), and Järvelin, M.-R. (Marjo-Riitta)

Abstract

We performed a multi-ethnic Epigenome Wide Association study on 22,774 individuals to describe the DNA methylation signature of chronic low-grade inflammation as measured by C-Reactive protein (CRP). We find 1,511 independent differentially methylated loci associated with CRP. These CpG sites show correlation structures across chromosomes, and are primarily situated in euchromatin, depleted in CpG islands. These genomic loci are predominantly situated in transcription factor binding sites and genomic enhancer regions. Mendelian randomization analysis suggests altered CpG methylation is a consequence of increased blood CRP levels. Mediation analysis reveals obesity and smoking as important underlying driving factors for changed CpG methylation. Finally, we find that an activated CpG signature significantly increases the risk for cardiometabolic diseases and COPD.

Published
2022

10. Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging.

Author

McCartney D.L., Min J.L., Richmond R.C., Lu A.T., Sobczyk M.K., Davies G., Broer L., Guo X., Jeong A., Jung J., Kasela S., Katrinli S., Kuo P.-L., Matias-Garcia P.R., Mishra P.P., Nygaard M., Palviainen T., Patki A., Raffield L.M., Ratliff S.M., Richardson T.G., Robinson O., Soerensen M., Sun D., Tsai P.-C., van der Zee M.D., Walker R.M., Wang X., Wang Y., Xia R., Xu Z., Yao J., Zhao W., Correa A., Boerwinkle E., Dugue P.-A., Durda P., Elliott H.R., Gieger C., de Geus E.J.C., Harris S.E., Hemani G., Imboden M., Kahonen M., Kardia S.L.R., Kresovich J.K., Li S., Lunetta K.L., Mangino M., Mason D., McIntosh A.M., Mengel-From J., Moore A.Z., Murabito J.M., Ollikainen M., Pankow J.S., Pedersen N.L., Peters A., Polidoro S., Porteous D.J., Raitakari O., Rich S.S., Sandler D.P., Sillanpaa E., Smith A.K., Southey M.C., Strauch K., Tiwari H., Tanaka T., Tillin T., Uitterlinden A.G., Van Den Berg D.J., van Dongen J., Wilson J.G., Wright J., Yet I., Arnett D., Bandinelli S., Bell J.T., Binder A.M., Boomsma D.I., Chen W., Christensen K., Conneely K.N., Elliott P., Ferrucci L., Fornage M., Hagg S., Hayward C., Irvin M., Kaprio J., Lawlor D.A., Lehtimaki T., Lohoff F.W., Milani L., Milne R.L., Probst-Hensch N., Reiner A.P., Ritz B., Rotter J.I., Smith J.A., Taylor J.A., van Meurs J.B.J., Vineis P., Waldenberger M., Deary I.J., Relton C.L., Horvath S., Marioni R.E., McCartney D.L., Min J.L., Richmond R.C., Lu A.T., Sobczyk M.K., Davies G., Broer L., Guo X., Jeong A., Jung J., Kasela S., Katrinli S., Kuo P.-L., Matias-Garcia P.R., Mishra P.P., Nygaard M., Palviainen T., Patki A., Raffield L.M., Ratliff S.M., Richardson T.G., Robinson O., Soerensen M., Sun D., Tsai P.-C., van der Zee M.D., Walker R.M., Wang X., Wang Y., Xia R., Xu Z., Yao J., Zhao W., Correa A., Boerwinkle E., Dugue P.-A., Durda P., Elliott H.R., Gieger C., de Geus E.J.C., Harris S.E., Hemani G., Imboden M., Kahonen M., Kardia S.L.R., Kresovich J.K., Li S., Lunetta K.L., Mangino M., Mason D., McIntosh A.M., Mengel-From J., Moore A.Z., Murabito J.M., Ollikainen M., Pankow J.S., Pedersen N.L., Peters A., Polidoro S., Porteous D.J., Raitakari O., Rich S.S., Sandler D.P., Sillanpaa E., Smith A.K., Southey M.C., Strauch K., Tiwari H., Tanaka T., Tillin T., Uitterlinden A.G., Van Den Berg D.J., van Dongen J., Wilson J.G., Wright J., Yet I., Arnett D., Bandinelli S., Bell J.T., Binder A.M., Boomsma D.I., Chen W., Christensen K., Conneely K.N., Elliott P., Ferrucci L., Fornage M., Hagg S., Hayward C., Irvin M., Kaprio J., Lawlor D.A., Lehtimaki T., Lohoff F.W., Milani L., Milne R.L., Probst-Hensch N., Reiner A.P., Ritz B., Rotter J.I., Smith J.A., Taylor J.A., van Meurs J.B.J., Vineis P., Waldenberger M., Deary I.J., Relton C.L., Horvath S., and Marioni R.E.

Abstract

Background: Biological aging estimators derived from DNA methylation data are heritable and correlate with morbidity and mortality. Consequently, identification of genetic and environmental contributors to the variation in these measures in populations has become a major goal in the field. Result(s): Leveraging DNA methylation and SNP data from more than 40,000 individuals, we identify 137 genome-wide significant loci, of which 113 are novel, from genome-wide association study (GWAS) meta-analyses of four epigenetic clocks and epigenetic surrogate markers for granulocyte proportions and plasminogen activator inhibitor 1 levels, respectively. We find evidence for shared genetic loci associated with the Horvath clock and expression of transcripts encoding genes linked to lipid metabolism and immune function. Notably, these loci are independent of those reported to regulate DNA methylation levels at constituent clock CpGs. A polygenic score for GrimAge acceleration showed strong associations with adiposity-related traits, educational attainment, parental longevity, and C-reactive protein levels. Conclusion(s): This study illuminates the genetic architecture underlying epigenetic aging and its shared genetic contributions with lifestyle factors and longevity.Copyright © 2021, The Author(s).

Published
2021

11. Association of markers of inflammation, the kynurenine pathway and B vitamins with age and mortality, and a signature of inflammaging.

Author

Dugue P.-A., Hodge A.M., Ulvik A., Ueland P.M., Midttun O., Rinaldi S., Macinnis R.J., Li S.X., Meyer K., Navionis A.-S., Flicker L., Severi G., English D.R., Vineis P., Tell G.S., Southey M.C., Milne R.L., Giles G.G., Dugue P.-A., Hodge A.M., Ulvik A., Ueland P.M., Midttun O., Rinaldi S., Macinnis R.J., Li S.X., Meyer K., Navionis A.-S., Flicker L., Severi G., English D.R., Vineis P., Tell G.S., Southey M.C., Milne R.L., and Giles G.G.

Abstract

BACKGROUND: Inflammation is a key feature of aging. We aimed to i) investigate the association of 34 blood markers potentially involved in inflammatory processes with age and mortality, ii) develop a signature of 'inflammaging'. METHOD(S): Thirty-four blood markers relating to inflammation, B vitamin status and the kynurenine pathway were measured in 976 participants in the Melbourne Collaborative Cohort Study at baseline (median age=59 years) and follow-up (median age=70 years). Associations with age and mortality were assessed using linear and Cox regression, respectively. A parsimonious signature of inflammaging was developed and its association with mortality was compared with two marker scores calculated across all markers associated with age and mortality, respectively. RESULT(S): The majority of markers (30/34) were associated with age, with stronger associations observed for neopterin, cystatin C, IL-6, TNF-alpha, several markers of the kynurenine pathway and derived indices KTR (kynurenine/tryptophan ratio), PAr index (ratio of 4-pyridoxic acid and the sum of pyridoxal 5'-phosphate and pyridoxal), and HK:XA (3-hydroxykynurenine/xanthurenic acid ratio). Many markers (17/34) showed an association with mortality, in particular IL-6, neopterin, CRP, quinolinic acid, PAr index, and KTR. The inflammaging signature included ten markers and was strongly associated of mortality (HR per SD=1.40, 95%CI:1.24-1.57, P=2x10 -8), similar to scores based on all age-associated (HR=1.38, 95%CI:1.23-1.55, P=4x10 -8) and mortality-associated markers (HR=1.43, 95%CI:1.28-1.60, P=1x10 -10), respectively. Strong evidence of replication of the inflammaging signature association with mortality was found in the Hordaland Health Study. CONCLUSION(S): Our study highlights the key role of the kynurenine pathway and vitamin B6 catabolism in aging, along with other well-established inflammation-related markers. A signature of inflammaging based on ten markers was strongly associated with

Published
2021

12. Inflammation-Related Marker Profiling of Dietary Patterns and All-cause Mortality in the Melbourne Collaborative Cohort Study.

Author

Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., Dugue P.-A., Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., and Dugue P.-A.

Abstract

BACKGROUND: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. OBJECTIVE(S): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. METHOD(S): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). RESULT(S): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. CONCLUSION(S): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

Published
2021

13. Inflammation-related marker profiling of dietary patterns and all-cause mortality in the melbourne collaborative cohort study.

Author

Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., Dugue P.-A., Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., and Dugue P.-A.

Abstract

Background: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. Objective(s): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. Method(s): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). Result(s): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. Conclusion(s): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

Published
2021

14. Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., Berndt, S.I., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., and Berndt, S.I.

Published
2021

15. Short-term personal and outdoor exposure to ultrafine and fine particulate air pollution in association with blood pressure and lung function in healthy adults

Author

LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Hoek, G., Tsai, M.-Y., Probst-Hensch, N., Imboden, M., Jeong, A., Naccarati, A., Tarallo, S., Raffaele, D., Nieuwenhuijsen, M., Vlaanderen, J., Gulliver, J., Amaral, A.F.S., Vineis, P., Vermeulen, R., LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Hoek, G., Tsai, M.-Y., Probst-Hensch, N., Imboden, M., Jeong, A., Naccarati, A., Tarallo, S., Raffaele, D., Nieuwenhuijsen, M., Vlaanderen, J., Gulliver, J., Amaral, A.F.S., Vineis, P., and Vermeulen, R.

Published
2021

16. Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging.

Author

McCartney D.L., Min J.L., Richmond R.C., Lu A.T., Sobczyk M.K., Davies G., Broer L., Guo X., Jeong A., Jung J., Kasela S., Katrinli S., Kuo P.-L., Matias-Garcia P.R., Mishra P.P., Nygaard M., Palviainen T., Patki A., Raffield L.M., Ratliff S.M., Richardson T.G., Robinson O., Soerensen M., Sun D., Tsai P.-C., van der Zee M.D., Walker R.M., Wang X., Wang Y., Xia R., Xu Z., Yao J., Zhao W., Correa A., Boerwinkle E., Dugue P.-A., Durda P., Elliott H.R., Gieger C., de Geus E.J.C., Harris S.E., Hemani G., Imboden M., Kahonen M., Kardia S.L.R., Kresovich J.K., Li S., Lunetta K.L., Mangino M., Mason D., McIntosh A.M., Mengel-From J., Moore A.Z., Murabito J.M., Ollikainen M., Pankow J.S., Pedersen N.L., Peters A., Polidoro S., Porteous D.J., Raitakari O., Rich S.S., Sandler D.P., Sillanpaa E., Smith A.K., Southey M.C., Strauch K., Tiwari H., Tanaka T., Tillin T., Uitterlinden A.G., Van Den Berg D.J., van Dongen J., Wilson J.G., Wright J., Yet I., Arnett D., Bandinelli S., Bell J.T., Binder A.M., Boomsma D.I., Chen W., Christensen K., Conneely K.N., Elliott P., Ferrucci L., Fornage M., Hagg S., Hayward C., Irvin M., Kaprio J., Lawlor D.A., Lehtimaki T., Lohoff F.W., Milani L., Milne R.L., Probst-Hensch N., Reiner A.P., Ritz B., Rotter J.I., Smith J.A., Taylor J.A., van Meurs J.B.J., Vineis P., Waldenberger M., Deary I.J., Relton C.L., Horvath S., Marioni R.E., McCartney D.L., Min J.L., Richmond R.C., Lu A.T., Sobczyk M.K., Davies G., Broer L., Guo X., Jeong A., Jung J., Kasela S., Katrinli S., Kuo P.-L., Matias-Garcia P.R., Mishra P.P., Nygaard M., Palviainen T., Patki A., Raffield L.M., Ratliff S.M., Richardson T.G., Robinson O., Soerensen M., Sun D., Tsai P.-C., van der Zee M.D., Walker R.M., Wang X., Wang Y., Xia R., Xu Z., Yao J., Zhao W., Correa A., Boerwinkle E., Dugue P.-A., Durda P., Elliott H.R., Gieger C., de Geus E.J.C., Harris S.E., Hemani G., Imboden M., Kahonen M., Kardia S.L.R., Kresovich J.K., Li S., Lunetta K.L., Mangino M., Mason D., McIntosh A.M., Mengel-From J., Moore A.Z., Murabito J.M., Ollikainen M., Pankow J.S., Pedersen N.L., Peters A., Polidoro S., Porteous D.J., Raitakari O., Rich S.S., Sandler D.P., Sillanpaa E., Smith A.K., Southey M.C., Strauch K., Tiwari H., Tanaka T., Tillin T., Uitterlinden A.G., Van Den Berg D.J., van Dongen J., Wilson J.G., Wright J., Yet I., Arnett D., Bandinelli S., Bell J.T., Binder A.M., Boomsma D.I., Chen W., Christensen K., Conneely K.N., Elliott P., Ferrucci L., Fornage M., Hagg S., Hayward C., Irvin M., Kaprio J., Lawlor D.A., Lehtimaki T., Lohoff F.W., Milani L., Milne R.L., Probst-Hensch N., Reiner A.P., Ritz B., Rotter J.I., Smith J.A., Taylor J.A., van Meurs J.B.J., Vineis P., Waldenberger M., Deary I.J., Relton C.L., Horvath S., and Marioni R.E.

Abstract

Background: Biological aging estimators derived from DNA methylation data are heritable and correlate with morbidity and mortality. Consequently, identification of genetic and environmental contributors to the variation in these measures in populations has become a major goal in the field. Result(s): Leveraging DNA methylation and SNP data from more than 40,000 individuals, we identify 137 genome-wide significant loci, of which 113 are novel, from genome-wide association study (GWAS) meta-analyses of four epigenetic clocks and epigenetic surrogate markers for granulocyte proportions and plasminogen activator inhibitor 1 levels, respectively. We find evidence for shared genetic loci associated with the Horvath clock and expression of transcripts encoding genes linked to lipid metabolism and immune function. Notably, these loci are independent of those reported to regulate DNA methylation levels at constituent clock CpGs. A polygenic score for GrimAge acceleration showed strong associations with adiposity-related traits, educational attainment, parental longevity, and C-reactive protein levels. Conclusion(s): This study illuminates the genetic architecture underlying epigenetic aging and its shared genetic contributions with lifestyle factors and longevity.Copyright © 2021, The Author(s).

Published
2021

17. Association of markers of inflammation, the kynurenine pathway and B vitamins with age and mortality, and a signature of inflammaging.

Author

Dugue P.-A., Hodge A.M., Ulvik A., Ueland P.M., Midttun O., Rinaldi S., Macinnis R.J., Li S.X., Meyer K., Navionis A.-S., Flicker L., Severi G., English D.R., Vineis P., Tell G.S., Southey M.C., Milne R.L., Giles G.G., Dugue P.-A., Hodge A.M., Ulvik A., Ueland P.M., Midttun O., Rinaldi S., Macinnis R.J., Li S.X., Meyer K., Navionis A.-S., Flicker L., Severi G., English D.R., Vineis P., Tell G.S., Southey M.C., Milne R.L., and Giles G.G.

Abstract

BACKGROUND: Inflammation is a key feature of aging. We aimed to i) investigate the association of 34 blood markers potentially involved in inflammatory processes with age and mortality, ii) develop a signature of 'inflammaging'. METHOD(S): Thirty-four blood markers relating to inflammation, B vitamin status and the kynurenine pathway were measured in 976 participants in the Melbourne Collaborative Cohort Study at baseline (median age=59 years) and follow-up (median age=70 years). Associations with age and mortality were assessed using linear and Cox regression, respectively. A parsimonious signature of inflammaging was developed and its association with mortality was compared with two marker scores calculated across all markers associated with age and mortality, respectively. RESULT(S): The majority of markers (30/34) were associated with age, with stronger associations observed for neopterin, cystatin C, IL-6, TNF-alpha, several markers of the kynurenine pathway and derived indices KTR (kynurenine/tryptophan ratio), PAr index (ratio of 4-pyridoxic acid and the sum of pyridoxal 5'-phosphate and pyridoxal), and HK:XA (3-hydroxykynurenine/xanthurenic acid ratio). Many markers (17/34) showed an association with mortality, in particular IL-6, neopterin, CRP, quinolinic acid, PAr index, and KTR. The inflammaging signature included ten markers and was strongly associated of mortality (HR per SD=1.40, 95%CI:1.24-1.57, P=2x10 -8), similar to scores based on all age-associated (HR=1.38, 95%CI:1.23-1.55, P=4x10 -8) and mortality-associated markers (HR=1.43, 95%CI:1.28-1.60, P=1x10 -10), respectively. Strong evidence of replication of the inflammaging signature association with mortality was found in the Hordaland Health Study. CONCLUSION(S): Our study highlights the key role of the kynurenine pathway and vitamin B6 catabolism in aging, along with other well-established inflammation-related markers. A signature of inflammaging based on ten markers was strongly associated with

Published
2021

18. Inflammation-Related Marker Profiling of Dietary Patterns and All-cause Mortality in the Melbourne Collaborative Cohort Study.

Author

Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., Dugue P.-A., Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., and Dugue P.-A.

Abstract

BACKGROUND: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. OBJECTIVE(S): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. METHOD(S): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). RESULT(S): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. CONCLUSION(S): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

Published
2021

19. Inflammation-related marker profiling of dietary patterns and all-cause mortality in the melbourne collaborative cohort study.

Author

Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., Dugue P.-A., Li S.X., Hodge A.M., MacInnis R.J., Bassett J.K., Ueland P.M., Midttun O., Ulvik A., Rinaldi S., Meyer K., Navionis A.-S., Shivappa N., Hebert J.R., Flicker L., Severi G., Jayasekara H., English D.R., Vineis P., Southey M.C., Milne R.L., Giles G.G., and Dugue P.-A.

Abstract

Background: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. Objective(s): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. Method(s): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). Result(s): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. Conclusion(s): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

Published
2021

20. Stochastic epigenetic mutations are associated with risk of breast cancer, lung cancer, and mature b-cell neoplasms.

Author

Gagliardi A., Dugue P.-A., Nost T.H., Southey M.C., Buchanan D.D., Schmidt D.F., Makalic E., Hodge A.M., English D.R., Doo N.W., Hopper J.L., Severi G., Baglietto L., Naccarati A., Tarallo S., Pace L., Krogh V., Palli D., Panico S., Sacerdote C., Tumino R., Lund E., Giles G.G., Pardini B., Sandanger T.M., Milne R.L., Vineis P., Polidoro S., Fiorito G., Gagliardi A., Dugue P.-A., Nost T.H., Southey M.C., Buchanan D.D., Schmidt D.F., Makalic E., Hodge A.M., English D.R., Doo N.W., Hopper J.L., Severi G., Baglietto L., Naccarati A., Tarallo S., Pace L., Krogh V., Palli D., Panico S., Sacerdote C., Tumino R., Lund E., Giles G.G., Pardini B., Sandanger T.M., Milne R.L., Vineis P., Polidoro S., and Fiorito G.

Abstract

Background: Age-related epigenetic dysregulations are associated with several diseases, including cancer. The number of stochastic epigenetic mutations (SEM) has been suggested as a biomarker of life-course accumulation of exposure-related DNA damage; however, the predictive role of SEMs in cancer has seldom been investigated. Method(s): A SEM, at a given CpG site, was defined as an extreme outlier of DNA methylation value distribution across individuals. We investigated the association of the total number of SEMs with the risk of eight cancers in 4,497 case-control pairs nested in three prospective cohorts. Furthermore, we investigated whether SEMs were randomly distributed across the genome or enriched in functional genomic regions. Result(s): In the three-study meta-analysis, the estimated ORs per one-unit increase in log(SEM) from logistic regression models adjusted for age and cancer risk factors were 1.25; 95% confidence interval (CI), 1.11-1.41 for breast cancer, and 1.23; 95% CI, 1.07-1.42 for lung cancer. In the Melbourne Collaborative Cohort Study, the OR for mature B-cell neoplasm was 1.46; 95% CI, 1.25-1.71. Enrichment analyses indicated that SEMs frequently occur in silenced genomic regions and in transcription factor binding sites regulated by EZH2 and SUZ12 (P < 0.0001 and P 1/4 0.0005, respectively): two components of the polycomb repressive complex 2 (PCR2). Finally, we showed that PCR2-specific SEMs are generally more stable over time compared with SEMs occurring in the whole genome. Conclusion(s): The number of SEMs is associated with a higher risk of different cancers in prediagnostic blood samples. Impact: We identified a candidate biomarker for cancer early detection, and we described a carcinogenesis mechanism involving PCR2 complex proteins worthy of further investigations. The authors are very thankful to Dr. Akram Ghantous (IARC, Lyon, France) for the methylation analyses of PEM-Turin study, produced within the Exposomics EC FP7 grant (gran

Published
2021

21. Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging

Author

McCartney, DL, Min, JL, Richmond, RC, Lu, AT, Sobczyk, MK, Davies, G, Broer, L, Guo, X, Jeong, A, Jung, J, Kasela, S, Katrinli, S, Kuo, P-L, Matias-Garcia, PR, Mishra, PP, Nygaard, M, Palviainen, T, Patki, A, Raffield, LM, Ratliff, SM, Richardson, TG, Robinson, O, Soerensen, M, Sun, D, Tsai, P-C, van der Zee, MD, Walker, RM, Wang, X, Wang, Y, Xia, R, Xu, Z, Yao, J, Zhao, W, Correa, A, Boerwinkle, E, Dugue, P-A, Durda, P, Elliott, HR, Gieger, C, de Geus, EJC, Harris, SE, Hemani, G, Imboden, M, Kahonen, M, Kardia, SLR, Kresovich, JK, Li, S, Lunetta, KL, Mangino, M, Mason, D, McIntosh, AM, Mengel-From, J, Moore, AZ, Murabito, JM, Ollikainen, M, Pankow, JS, Pedersen, NL, Peters, A, Polidoro, S, Porteous, DJ, Raitakari, O, Rich, SS, Sandler, DP, Sillanpaa, E, Smith, AK, Southey, MC, Strauch, K, Tiwari, H, Tanaka, T, Tillin, T, Uitterlinden, AG, van den Berg, DJ, van Dongen, J, Wilson, JG, Wright, J, Yet, I, Arnett, D, Bandinelli, S, Bell, JT, Binder, AM, Boomsma, DI, Chen, W, Christensen, K, Conneely, KN, Elliott, P, Ferrucci, L, Fornage, M, Hagg, S, Hayward, C, Irvin, M, Kaprio, J, Lawlor, DA, Lehtimaki, T, Lohoff, FW, Milani, L, Milne, RL, Probst-Hensch, N, Reiner, AP, Ritz, B, Rotter, JI, Smith, JA, Taylor, JA, van Meurs, JBJ, Vineis, P, Waldenberger, M, Deary, IJ, Relton, CL, Horvath, S, Marioni, RE, McCartney, DL, Min, JL, Richmond, RC, Lu, AT, Sobczyk, MK, Davies, G, Broer, L, Guo, X, Jeong, A, Jung, J, Kasela, S, Katrinli, S, Kuo, P-L, Matias-Garcia, PR, Mishra, PP, Nygaard, M, Palviainen, T, Patki, A, Raffield, LM, Ratliff, SM, Richardson, TG, Robinson, O, Soerensen, M, Sun, D, Tsai, P-C, van der Zee, MD, Walker, RM, Wang, X, Wang, Y, Xia, R, Xu, Z, Yao, J, Zhao, W, Correa, A, Boerwinkle, E, Dugue, P-A, Durda, P, Elliott, HR, Gieger, C, de Geus, EJC, Harris, SE, Hemani, G, Imboden, M, Kahonen, M, Kardia, SLR, Kresovich, JK, Li, S, Lunetta, KL, Mangino, M, Mason, D, McIntosh, AM, Mengel-From, J, Moore, AZ, Murabito, JM, Ollikainen, M, Pankow, JS, Pedersen, NL, Peters, A, Polidoro, S, Porteous, DJ, Raitakari, O, Rich, SS, Sandler, DP, Sillanpaa, E, Smith, AK, Southey, MC, Strauch, K, Tiwari, H, Tanaka, T, Tillin, T, Uitterlinden, AG, van den Berg, DJ, van Dongen, J, Wilson, JG, Wright, J, Yet, I, Arnett, D, Bandinelli, S, Bell, JT, Binder, AM, Boomsma, DI, Chen, W, Christensen, K, Conneely, KN, Elliott, P, Ferrucci, L, Fornage, M, Hagg, S, Hayward, C, Irvin, M, Kaprio, J, Lawlor, DA, Lehtimaki, T, Lohoff, FW, Milani, L, Milne, RL, Probst-Hensch, N, Reiner, AP, Ritz, B, Rotter, JI, Smith, JA, Taylor, JA, van Meurs, JBJ, Vineis, P, Waldenberger, M, Deary, IJ, Relton, CL, Horvath, S, and Marioni, RE

Abstract

BACKGROUND: Biological aging estimators derived from DNA methylation data are heritable and correlate with morbidity and mortality. Consequently, identification of genetic and environmental contributors to the variation in these measures in populations has become a major goal in the field. RESULTS: Leveraging DNA methylation and SNP data from more than 40,000 individuals, we identify 137 genome-wide significant loci, of which 113 are novel, from genome-wide association study (GWAS) meta-analyses of four epigenetic clocks and epigenetic surrogate markers for granulocyte proportions and plasminogen activator inhibitor 1 levels, respectively. We find evidence for shared genetic loci associated with the Horvath clock and expression of transcripts encoding genes linked to lipid metabolism and immune function. Notably, these loci are independent of those reported to regulate DNA methylation levels at constituent clock CpGs. A polygenic score for GrimAge acceleration showed strong associations with adiposity-related traits, educational attainment, parental longevity, and C-reactive protein levels. CONCLUSION: This study illuminates the genetic architecture underlying epigenetic aging and its shared genetic contributions with lifestyle factors and longevity.

Published
2021

22. Co-benefits from sustainable dietary shifts for population and environmental health: an assessment from a large European cohort study

Author

Laine, JE, Huybrechts, I, Gunter, MJ, Ferrari, P, Weiderpass, E, Tsilidis, K, Aune, D, Schulze, MB, Bergmann, M, Temme, EHM, Boer, JMA, Agnoli, C, Ericson, U, Stubbendorff, A, Ibsen, DB, Dahm, CC, Deschasaux, M, Touvier, M, Kesse-Guyot, E, Perez, M-JS, Barranco, MR, Tong, TYN, Papier, K, Knuppel, A, Boutron-Ruault, M-C, Mancini, F, Severi, G, Srour, B, Kuhn, T, Masala, G, Agudo, A, Skeie, G, Rylander, C, Sandanger, TM, Riboli, E, Vineis, P, Laine, JE, Huybrechts, I, Gunter, MJ, Ferrari, P, Weiderpass, E, Tsilidis, K, Aune, D, Schulze, MB, Bergmann, M, Temme, EHM, Boer, JMA, Agnoli, C, Ericson, U, Stubbendorff, A, Ibsen, DB, Dahm, CC, Deschasaux, M, Touvier, M, Kesse-Guyot, E, Perez, M-JS, Barranco, MR, Tong, TYN, Papier, K, Knuppel, A, Boutron-Ruault, M-C, Mancini, F, Severi, G, Srour, B, Kuhn, T, Masala, G, Agudo, A, Skeie, G, Rylander, C, Sandanger, TM, Riboli, E, and Vineis, P

Abstract

BACKGROUND: Unhealthy diets, the rise of non-communicable diseases, and the declining health of the planet are highly intertwined, where food production and consumption are major drivers of increases in greenhouse gas emissions, substantial land use, and adverse health such as cancer and mortality. To assess the potential co-benefits from shifting to more sustainable diets, we aimed to investigate the associations of dietary greenhouse gas emissions and land use with all-cause and cause-specific mortality and cancer incidence rates. METHODS: Using data from 443 991 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, a multicentre prospective cohort, we estimated associations between dietary contributions to greenhouse gas emissions and land use and all-cause and cause-specific mortality and incident cancers using Cox proportional hazards regression models. The main exposures were modelled as quartiles. Co-benefits, encompassing the potential effects of alternative diets on all-cause mortality and cancer and potential reductions in greenhouse gas emissions and land use, were estimated with counterfactual attributable fraction intervention models, simulating potential effects of dietary shifts based on the EAT-Lancet reference diet. FINDINGS: In the pooled analysis, there was an association between levels of dietary greenhouse gas emissions and all-cause mortality (adjusted hazard ratio [HR] 1·13 [95% CI 1·10-1·16]) and between land use and all-cause mortality (1·18 [1·15-1·21]) when comparing the fourth quartile to the first quartile. Similar associations were observed for cause-specific mortality. Associations were also observed between all-cause cancer incidence rates and greenhouse gas emissions, when comparing the fourth quartile to the first quartile (adjusted HR 1·11 [95% CI 1·09-1·14]) and between all-cause cancer incidence rates and land use (1·13 [1·10-1·15]); however, estimates differed by cancer type. Through coun

Published
2021

23. Short-term personal and outdoor exposure to ultrafine and fine particulate air pollution in association with blood pressure and lung function in healthy adults

Author

LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Hoek, G., Tsai, M.-Y., Probst-Hensch, N., Imboden, M., Jeong, A., Naccarati, A., Tarallo, S., Raffaele, D., Nieuwenhuijsen, M., Vlaanderen, J., Gulliver, J., Amaral, A.F.S., Vineis, P., Vermeulen, R., LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Hoek, G., Tsai, M.-Y., Probst-Hensch, N., Imboden, M., Jeong, A., Naccarati, A., Tarallo, S., Raffaele, D., Nieuwenhuijsen, M., Vlaanderen, J., Gulliver, J., Amaral, A.F.S., Vineis, P., and Vermeulen, R.

Published
2021

24. Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., Berndt, S.I., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., and Berndt, S.I.

Published
2021

25. Metabolic profiles of socio-economic position:a multi-cohort analysis

Author

Robinson, O. (Oliver), Carter, A. R. (Alice R.), Ala-Korpela, M. (Mika), Casas, J. P. (Juan P.), Chaturvedi, N. (Nishi), Engmann, J. (Jorgen), Howe, L. D. (Laura D.), Hughes, A. D. (Alun D.), Järvelin, M.-R. (Marjo-Riitta), Kähönen, M. (Mika), Karhunen, V. (Ville), Kuh, D. (Diana), Shah, T. (Tina), Ben-Shlomo, Y. (Yoav), Sofat, R. (Reecha), Lau, C. E. (Chung-Ho E.), Lehtimäki, T. (Terho), Menon, U. (Usha), Raitakari, O. (Olli), Ryan, A. (Andy), Providencia, R. (Rui), Smith, S. (Stephanie), Taylor, J. (Julie), Tillin, T. (Therese), Viikari, J. (Jorma), Wong, A. (Andrew), Hingorani, A. D. (Aroon D.), Kivimäki, M. (Mika), Vineis, P. (Paolo), Robinson, O. (Oliver), Carter, A. R. (Alice R.), Ala-Korpela, M. (Mika), Casas, J. P. (Juan P.), Chaturvedi, N. (Nishi), Engmann, J. (Jorgen), Howe, L. D. (Laura D.), Hughes, A. D. (Alun D.), Järvelin, M.-R. (Marjo-Riitta), Kähönen, M. (Mika), Karhunen, V. (Ville), Kuh, D. (Diana), Shah, T. (Tina), Ben-Shlomo, Y. (Yoav), Sofat, R. (Reecha), Lau, C. E. (Chung-Ho E.), Lehtimäki, T. (Terho), Menon, U. (Usha), Raitakari, O. (Olli), Ryan, A. (Andy), Providencia, R. (Rui), Smith, S. (Stephanie), Taylor, J. (Julie), Tillin, T. (Therese), Viikari, J. (Jorma), Wong, A. (Andrew), Hingorani, A. D. (Aroon D.), Kivimäki, M. (Mika), and Vineis, P. (Paolo)

Abstract

Background: Low socio-economic position (SEP) is a risk factor for multiple health outcomes, but its molecular imprints in the body remain unclear. Methods: We examined SEP as a determinant of serum nuclear magnetic resonance metabolic profiles in ∼30 000 adults and 4000 children across 10 UK and Finnish cohort studies. Results: In risk-factor-adjusted analysis of 233 metabolic measures, low educational attainment was associated with 37 measures including higher levels of triglycerides in small high-density lipoproteins (HDL) and lower levels of docosahexaenoic acid (DHA), omega-3 fatty acids, apolipoprotein A1, large and very large HDL particles (including levels of their respective lipid constituents) and cholesterol measures across different density lipoproteins. Among adults whose father worked in manual occupations, associations with apolipoprotein A1, large and very large HDL particles and HDL-2 cholesterol remained after adjustment for SEP in later life. Among manual workers, levels of glutamine were higher compared with non-manual workers. All three indicators of low SEP were associated with lower DHA, omega-3 fatty acids and HDL diameter. At all ages, children of manual workers had lower levels of DHA as a proportion of total fatty acids. Conclusions: Our work indicates that social and economic factors have a measurable impact on human physiology. Lower SEP was independently associated with a generally unfavourable metabolic profile, consistent across ages and cohorts. The metabolites we found to be associated with SEP, including DHA, are known to predict cardiovascular disease and cognitive decline in later life and may contribute to health inequalities.

Published
2021

26. Short-term personal and outdoor exposure to ultrafine and fine particulate air pollution in association with blood pressure and lung function in healthy adults

Author

LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Hoek, G., Tsai, M.-Y., Probst-Hensch, N., Imboden, M., Jeong, A., Naccarati, A., Tarallo, S., Raffaele, D., Nieuwenhuijsen, M., Vlaanderen, J., Gulliver, J., Amaral, A.F.S., Vineis, P., Vermeulen, R., LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Hoek, G., Tsai, M.-Y., Probst-Hensch, N., Imboden, M., Jeong, A., Naccarati, A., Tarallo, S., Raffaele, D., Nieuwenhuijsen, M., Vlaanderen, J., Gulliver, J., Amaral, A.F.S., Vineis, P., and Vermeulen, R.

Published
2021

27. Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., Berndt, S.I., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., and Berndt, S.I.

Published
2021

28. Trihalomethanes in drinking water and bladder cancer burden in the European Union

Author

Evlampidou, I. (Iro), Font-Ribera, L. (Laia), Rojas-Rueda, D. (David), Gracia-Lavedan, E. (Esther), Costet, N. (Nathalie), Pearce, N. (Neil), Vineis, P. (Paolo), Jaakkola, J. J. (Jouni J. K.), Delloye, F. (Francis), Makris, K. C. (Konstantinos C.), Stephanou, E. G. (Euripides G.), Kargaki, S. (Sophia), Kozisek, F. (Frantisek), Sigsgaard, T. (Torben), Hansen, B. (Birgitte), Schullehner, J. (Jörg), Nahkur, R. (Ramon), Galey, C. (Catherine), Zwiener, C. (Christian), Vargha, M. (Marta), Righi, E. (Elena), Aggazzotti, G. (Gabriella), Kalnina, G. (Gunda), Grazuleviciene, R. (Regina), Polanska, K. (Kinga), Gubkova, D. (Dasa), Bitenc, K. (Katarina), Goslan, E. H. (Emma H.), Kogevinas, M. (Manolis), Villanueva, C. M. (Cristina M.), Evlampidou, I. (Iro), Font-Ribera, L. (Laia), Rojas-Rueda, D. (David), Gracia-Lavedan, E. (Esther), Costet, N. (Nathalie), Pearce, N. (Neil), Vineis, P. (Paolo), Jaakkola, J. J. (Jouni J. K.), Delloye, F. (Francis), Makris, K. C. (Konstantinos C.), Stephanou, E. G. (Euripides G.), Kargaki, S. (Sophia), Kozisek, F. (Frantisek), Sigsgaard, T. (Torben), Hansen, B. (Birgitte), Schullehner, J. (Jörg), Nahkur, R. (Ramon), Galey, C. (Catherine), Zwiener, C. (Christian), Vargha, M. (Marta), Righi, E. (Elena), Aggazzotti, G. (Gabriella), Kalnina, G. (Gunda), Grazuleviciene, R. (Regina), Polanska, K. (Kinga), Gubkova, D. (Dasa), Bitenc, K. (Katarina), Goslan, E. H. (Emma H.), Kogevinas, M. (Manolis), and Villanueva, C. M. (Cristina M.)

Abstract

Background: Trihalomethanes (THMs) are widespread disinfection by-products (DBPs) in drinking water, and long-term exposure has been consistently associated with increased bladder cancer risk. Objective: We assessed THM levels in drinking water in the European Union as a marker of DBP exposure and estimated the attributable burden of bladder cancer. Methods: We collected recent annual mean THM levels in municipal drinking water in 28 European countries (EU28) from routine monitoring records. We estimated a linear exposure–response function for average residential THM levels and bladder cancer by pooling data from studies included in the largest international pooled analysis published to date in order to estimate odds ratios (ORs) for bladder cancer associated with the mean THM level in each country (relative to no exposure), population-attributable fraction (PAF), and number of attributable bladder cancer cases in different scenarios using incidence rates and population from the Global Burden of Disease study of 2016. Results: We obtained 2005–2018 THM data from EU26, covering 75% of the population. Data coverage and accuracy were heterogeneous among countries. The estimated population-weighted mean THM level was 11.7μg/L [standard deviation (SD) of 11.2]. The estimated bladder cancer PAF was 4.9% [95% confidence interval (CI): 2.5, 7.1] overall (range: 0–23%), accounting for 6,561 (95% CI: 3,389, 9,537) bladder cancer cases per year. Denmark and the Netherlands had the lowest PAF (0.0% each), while Cyprus (23.2%), Malta (17.9%), and Ireland (17.2%) had the highest among EU26. In the scenario where no country would exceed the current EU mean, 2,868 (95% CI: 1,522, 4,060; 43%) annual attributable bladder cancer cases could potentially be avoided. Discussion: Efforts have been made to reduce THM levels in the European Union. However, assuming a causal association, current levels in certain countries still could lead to a considerable burden of bladder cancer

Published
2020

29. Special Report: The Biology of Inequalities in Health: The Lifepath Consortium

Author

Vineis, P. (Paolo), Avendano-Pabon, M. (Mauricio), Barros, H. (Henrique), Bartley, M. (Mel), Carmeli, C. (Cristian), Carra, L. (Luca), Chadeau-Hyam, M. (Marc), Costa, G. (Giuseppe), Delpierre, C. (Cyrille), D'Errico, A. (Angelo), Fraga, S. (Silvia), Giles, G. (Graham), Goldberg, M. (Marcel), Kelly-Irving, M. (Michelle), Kivimaki, M. (Mika), Lepage, B. (Benoit), Lang, T. (Thierry), Layte, R. (Richard), MacGuire, F. (Frances), Mackenbach, J.P. (Johan), Marmot, M. (Michael), McCrory, C. (Cathal), Milne, R.L. (Roger), Muennig, P. (Peter), Nusselder, W.J. (Wilma), Petrovic, D. (Dusan), Polidoro, S. (Silvia), Ricceri, F. (Fulvio), Robinson, O. (Oliver), Stringhini, S. (Silvia), Zins, M. (Marie), Vineis, P. (Paolo), Avendano-Pabon, M. (Mauricio), Barros, H. (Henrique), Bartley, M. (Mel), Carmeli, C. (Cristian), Carra, L. (Luca), Chadeau-Hyam, M. (Marc), Costa, G. (Giuseppe), Delpierre, C. (Cyrille), D'Errico, A. (Angelo), Fraga, S. (Silvia), Giles, G. (Graham), Goldberg, M. (Marcel), Kelly-Irving, M. (Michelle), Kivimaki, M. (Mika), Lepage, B. (Benoit), Lang, T. (Thierry), Layte, R. (Richard), MacGuire, F. (Frances), Mackenbach, J.P. (Johan), Marmot, M. (Michael), McCrory, C. (Cathal), Milne, R.L. (Roger), Muennig, P. (Peter), Nusselder, W.J. (Wilma), Petrovic, D. (Dusan), Polidoro, S. (Silvia), Ricceri, F. (Fulvio), Robinson, O. (Oliver), Stringhini, S. (Silvia), and Zins, M. (Marie)

Abstract

Funded by the European Commission Horizon 2020 programme, the Lifepath research consortium aimed to investigate the effects of socioeconomic inequalities on the biology of healthy aging. The main research questions included the impact of inequalities on health, the role of behavioral and other risk factors, the underlying biological mechanisms, the efficacy of selected policies, and the general implications of our findings for theories and policies. The project adopted a life-course and comparative approach, considering lifetime effects from childhood and adulthood, and pooled data on up to 1.7 million participants of longitudinal cohort studies from Europe, USA, and Australia. These data showed that socioeconomic circumstances predicted mortality and functional decline as strongly as established risk factors currently targeted by global prevention programmes. Analyses also lo

Published
2020
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30. Epigenome-wide meta-analysis of blood DNA methylation in newborns and children identifies numerous loci related to gestational age

Author

Merid, S.K. (Simon Kebede), Novoloaca, A. (Alexei), Sharp, G.C. (Gemma C.), Küpers, A.M. (Marlijn), Kho, A.T. (Alvin T.), Roy, R. (Ritu), Gao, L. (Lu), Annesi-Maesano, I. (Isabella), Jain, P. (Pooja), Plusquin, M. (Michelle), Kogevinas, M. (Manolis), Allard, C. (Catherine), Vehmeijer, F.O.L. (Florianne O.L.), Kazmi, N. (Nabila), Salas, L.A. (Lucas A.), Rezwan, F.I. (Faisal I.), Zhang, H. (Hongmei), Sebert, S. (Sylvain), Czamara, D. (Darina), Rifas-Shiman, S.L. (Sheryl), Melton, P.E. (Phillip E.), Lawlor, D.A. (Debbie A.), Pershagen, G. (Göran), Breton, C. (Carrie), Huen, K. (Karen), Baïz, N. (Nour), Gagliardi, L. (Luigi), Nawrot, T.S. (Tim S.), Corpeleijn, E. (Eva), Perron, P. (Patrice), Duijts, L. (Liesbeth), Nohr, C. (Christian), Bustamante, M. (Mariona), Ewart, S. (Susan), Karmaus, W. (Wilfried), Zhao, S. (Shanshan), Page, C.M. (Christian M.), Herceg, Z. (Zdenko), Jarvelin, M.-R. (Marjo-Riitta), Lahti, J. (Jari), Baccarelli, A.A. (Andrea), Anderson, D. (Denise), Kachroo, P. (Priyadarshini), Relton, C.L. (Caroline), Bergström, A. (Anna), Eskenazi, B. (B.), Soomro, M.H. (Munawar Hussain), Vineis, P. (Paolo), Snieder, H. (Harold), Bouchard, L. (Luigi), Jaddoe, V.W.V. (Vincent), Sørensen, T.I.A. (Thorkild), Vrijheid, M. (Martine), Arshad, S.H. (Syed), Holloway, J.W. (John W.), Håberg, S.E. (Siri E), Magnus, P. (Per), Dwyer, T. (Terence), Binder, E.B. (Elisabeth), Demeo, D.L. (Dawn), Vonk, J.M. (Judith), Newnham, J.P. (John), Tantisira, K.G. (Kelan G.), Kull, C.A. (Christian), Wiemels, J. (Joseph), Heude, B. (Barbara), Sunyer, J. (Jordi), Nystad, W. (Wenche), Munthe-Kaas, M.C. (Monica Cheng), Räikkönen, K. (Katri), Oken, E. (Emily), Huang, R.-C. (Rae-Chi), Weiss, S.T. (Scott T.), Antó, J.M. (Josep Maria), Bousquet, J. (Jean), Kumar, A. (Ashish), Söderhäll, C. (Cilla), Almqvist, C. (Catarina), Cardenas, A. (Andres), Gruzieva, O. (Olena), Xu, C.-J. (Cheng-Jian), Reese, S.E. (Sarah E.), Kere, J. (Juha), Brodin, P. (Petter), Solomon, O. (Olivia), Wielscher, M. (Matthias), Holland, N. (Nina), Ghantous, A. (Akram), Hivert, M.-F. (Marie-France), Felix, J.F. (Janine), Koppelman, G.H. (Gerard), London, S.J. (Stephanie J.), Melén, E. (Erik), Merid, S.K. (Simon Kebede), Novoloaca, A. (Alexei), Sharp, G.C. (Gemma C.), Küpers, A.M. (Marlijn), Kho, A.T. (Alvin T.), Roy, R. (Ritu), Gao, L. (Lu), Annesi-Maesano, I. (Isabella), Jain, P. (Pooja), Plusquin, M. (Michelle), Kogevinas, M. (Manolis), Allard, C. (Catherine), Vehmeijer, F.O.L. (Florianne O.L.), Kazmi, N. (Nabila), Salas, L.A. (Lucas A.), Rezwan, F.I. (Faisal I.), Zhang, H. (Hongmei), Sebert, S. (Sylvain), Czamara, D. (Darina), Rifas-Shiman, S.L. (Sheryl), Melton, P.E. (Phillip E.), Lawlor, D.A. (Debbie A.), Pershagen, G. (Göran), Breton, C. (Carrie), Huen, K. (Karen), Baïz, N. (Nour), Gagliardi, L. (Luigi), Nawrot, T.S. (Tim S.), Corpeleijn, E. (Eva), Perron, P. (Patrice), Duijts, L. (Liesbeth), Nohr, C. (Christian), Bustamante, M. (Mariona), Ewart, S. (Susan), Karmaus, W. (Wilfried), Zhao, S. (Shanshan), Page, C.M. (Christian M.), Herceg, Z. (Zdenko), Jarvelin, M.-R. (Marjo-Riitta), Lahti, J. (Jari), Baccarelli, A.A. (Andrea), Anderson, D. (Denise), Kachroo, P. (Priyadarshini), Relton, C.L. (Caroline), Bergström, A. (Anna), Eskenazi, B. (B.), Soomro, M.H. (Munawar Hussain), Vineis, P. (Paolo), Snieder, H. (Harold), Bouchard, L. (Luigi), Jaddoe, V.W.V. (Vincent), Sørensen, T.I.A. (Thorkild), Vrijheid, M. (Martine), Arshad, S.H. (Syed), Holloway, J.W. (John W.), Håberg, S.E. (Siri E), Magnus, P. (Per), Dwyer, T. (Terence), Binder, E.B. (Elisabeth), Demeo, D.L. (Dawn), Vonk, J.M. (Judith), Newnham, J.P. (John), Tantisira, K.G. (Kelan G.), Kull, C.A. (Christian), Wiemels, J. (Joseph), Heude, B. (Barbara), Sunyer, J. (Jordi), Nystad, W. (Wenche), Munthe-Kaas, M.C. (Monica Cheng), Räikkönen, K. (Katri), Oken, E. (Emily), Huang, R.-C. (Rae-Chi), Weiss, S.T. (Scott T.), Antó, J.M. (Josep Maria), Bousquet, J. (Jean), Kumar, A. (Ashish), Söderhäll, C. (Cilla), Almqvist, C. (Catarina), Cardenas, A. (Andres), Gruzieva, O. (Olena), Xu, C.-J. (Cheng-Jian), Reese, S.E. (Sarah E.), Kere, J. (Juha), Brodin, P. (Petter), Solomon, O. (Olivia), Wielscher, M. (Matthias), Holland, N. (Nina), Ghantous, A. (Akram), Hivert, M.-F. (Marie-France), Felix, J.F. (Janine), Koppelman, G.H. (Gerard), London, S.J. (Stephanie J.), and Melén, E. (Erik)

Abstract

BACKGROUND: Preterm birth and shorter duration of pregnancy are associated with increased morbidity in neonatal and later life. As the epigenome is known to have an important role during fetal development, we investigated associations between gestational age and blood DNA methylation in children. METHODS: We performed meta-analysis of Illumina's HumanMethylation450-array associations between gestational age and cord blood DNA methylation in 3648 newborns from 17 cohorts without common pregnancy complications, induced delivery or caesarean section. We also explored associations of gestational age with DNA methylation measured at 4-18 years in additional pediatric cohorts. Follow-up analyses of DNA methylation and gene expression correlations were performed in cord blood. DNA methylation profiles were also explored in tissues relevant for gestational age health effects: fetal brain and lung. RESULTS: We identified 8899 CpGs in cord blood that were associated with gestational age (range 27-42 weeks), at Bonferroni significance, P < 1.06 × 10- 7, of which 3343 were novel. These were annotated to 4966 genes. After restricting findings to at least three significant adjacent CpGs, we identified 1276 CpGs annotated to 325 genes. Results were generally consistent when analyses were restricted to term births. Cord blood findings tended not to persist into childhood and adolescence. Pathway analyses identified enrichment for biological processes critical to embryonic development. Follow-up of identified genes showed correlations between gestational age and DNA methylation levels in fetal brain and lung tissue, as well as correlation with expression levels. CONCLUSIONS: We identified numerous CpGs differentially methylated in relation to gestational age at birth that appear to reflect fetal developmental processes across tissues. These findings may contribute to understanding mechanisms linking gestational age to health effects.

Published
2020
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31. microRNA expression profiles and personal monitoring of exposure to particulate matter

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, LS IRAS EEPI GRA (Gezh.risico-analyse), dIRAS RA-I&I RA, Mancini, F.R., Laine, J.E., Tarallo, S., Vlaanderen, J., Vermeulen, R., van Nunen, E., Hoek, G., Probst-Hensch, N., Imboden, M., Jeong, A., Gulliver, J., Chadeau-Hyam, M., Nieuwenhuijsen, M., de Kok, T.M., Piepers, J., Krauskopf, J., Kleinjans, J.C.S., Vineis, P., Naccarati, A., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, LS IRAS EEPI GRA (Gezh.risico-analyse), dIRAS RA-I&I RA, Mancini, F.R., Laine, J.E., Tarallo, S., Vlaanderen, J., Vermeulen, R., van Nunen, E., Hoek, G., Probst-Hensch, N., Imboden, M., Jeong, A., Gulliver, J., Chadeau-Hyam, M., Nieuwenhuijsen, M., de Kok, T.M., Piepers, J., Krauskopf, J., Kleinjans, J.C.S., Vineis, P., and Naccarati, A.

Published
2020

32. Agnostic Cys34-albumin adductomics and DNA methylation: Implication of N-acetylcysteine in lung carcinogenesis years before diagnosis

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Dagnino, S., Bodinier, B., Grigoryan, H., Rappaport, S.M., Karimi, M., Guida, F., Polidoro, S., Edmands, W.B., Naccarati, A., Fiorito, G., Sacerdote, C., Krogh, V., Vermeulen, R., Vineis, P., Chadeau-Hyam, M., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Dagnino, S., Bodinier, B., Grigoryan, H., Rappaport, S.M., Karimi, M., Guida, F., Polidoro, S., Edmands, W.B., Naccarati, A., Fiorito, G., Sacerdote, C., Krogh, V., Vermeulen, R., Vineis, P., and Chadeau-Hyam, M.

Published
2020

33. A multi-omics approach to investigate the inflammatory response to life course socioeconomic position

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Castagné, R., Kelly-Irving, M., Krogh, V., Palli, D., Panico, S., Sacerdote, C., Tumino, R., Hebels, D.G.A.J., Kleinjans, J.C.S., De Kok, T.M.C.M., Georgiadis, P., Kyrtopoulos, S.A., Vermeulen, R., Stringhini, S., Vineis, P., Chadeau-Hyam, M., Delpierre, C., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Castagné, R., Kelly-Irving, M., Krogh, V., Palli, D., Panico, S., Sacerdote, C., Tumino, R., Hebels, D.G.A.J., Kleinjans, J.C.S., De Kok, T.M.C.M., Georgiadis, P., Kyrtopoulos, S.A., Vermeulen, R., Stringhini, S., Vineis, P., Chadeau-Hyam, M., and Delpierre, C.

Published
2020

34. Prenatal Exposure to Multiple Air Pollutants, Mediating Molecular Mechanisms, and Shifts in Birthweight

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Laine, J.E., Bodinier, B., Robinson, O., Plusquin, M., Scalbert, A., Keski-Rahkonen, P., Robinot, N., Vermeulen, R., Pizzi, C., Asta, F., Nawrot, T., Gulliver, J., Chatzi, L., Kogevinas, M., Nieuwenhuijsen, M., Sunyer, J., Vrijheid, M., Chadeau-Hyam, M., Vineis, P., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Laine, J.E., Bodinier, B., Robinson, O., Plusquin, M., Scalbert, A., Keski-Rahkonen, P., Robinot, N., Vermeulen, R., Pizzi, C., Asta, F., Nawrot, T., Gulliver, J., Chatzi, L., Kogevinas, M., Nieuwenhuijsen, M., Sunyer, J., Vrijheid, M., Chadeau-Hyam, M., and Vineis, P.

Published
2020

35. Associations between modeled residential outdoor and measured personal exposure to ultrafine particles in four European study areas

Author

LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Vermeulen, R., Tsai, M.-Y., Probst-Hensch, N., Ineichen, A., Imboden, M., Naccarati, A., Tarallo, S., Raffaele, D., Ranzi, A., Nieuwenhuijsen, M., Jarvis, D., Amaral, A.F., Vlaanderen, J., Meliefste, K., Brunekreef, B., Vineis, P., Gulliver, J., Hoek, G., LS IRAS EEPI GRA (Gezh.risico-analyse), IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, dIRAS RA-I&I RA, van Nunen, E., Vermeulen, R., Tsai, M.-Y., Probst-Hensch, N., Ineichen, A., Imboden, M., Naccarati, A., Tarallo, S., Raffaele, D., Ranzi, A., Nieuwenhuijsen, M., Jarvis, D., Amaral, A.F., Vlaanderen, J., Meliefste, K., Brunekreef, B., Vineis, P., Gulliver, J., and Hoek, G.

Published
2020

36. Education, biological ageing, all-cause and cause-specific mortality and morbidity: UK biobank cohort study

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Afd. Theologie, Chadeau-Hyam, M., Bodinier, B., Vermeulen, R., Karimi, M., Zuber, V., Castagné, R., Elliott, J., Muller, D., Petrovic, D., Whitaker, M., Stringhini, S., Tzoulaki, I., Kivimäki, M., Vineis, P., Elliott, P., Kelly-Irving, M., Delpierre, C., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Afd. Theologie, Chadeau-Hyam, M., Bodinier, B., Vermeulen, R., Karimi, M., Zuber, V., Castagné, R., Elliott, J., Muller, D., Petrovic, D., Whitaker, M., Stringhini, S., Tzoulaki, I., Kivimäki, M., Vineis, P., Elliott, P., Kelly-Irving, M., and Delpierre, C.

Published
2020

37. A multi-omic analysis of birthweight in newborn cord blood reveals new underlying mechanisms related to cholesterol metabolism

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Alfano, R., Chadeau-Hyam, M., Ghantous, A., Keski-Rahkonen, P., Chatzi, L., Perez, A.E., Herceg, Z., Kogevinas, M., de Kok, T.M., Nawrot, T.S., Novoloaca, A., Patel, C.J., Pizzi, C., Robinot, N., Rusconi, F., Scalbert, A., Sunyer, J., Vermeulen, R., Vrijheid, M., Vineis, P., Robinson, O., Plusquin, M., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Alfano, R., Chadeau-Hyam, M., Ghantous, A., Keski-Rahkonen, P., Chatzi, L., Perez, A.E., Herceg, Z., Kogevinas, M., de Kok, T.M., Nawrot, T.S., Novoloaca, A., Patel, C.J., Pizzi, C., Robinot, N., Rusconi, F., Scalbert, A., Sunyer, J., Vermeulen, R., Vrijheid, M., Vineis, P., Robinson, O., and Plusquin, M.

Published
2020

38. Special Report: The Biology of Inequalities in Health: The Lifepath Consortium

Author

Vineis, P, Avendano-Pabon, M, Barros, H, Bartley, M, Carmeli, C, Carra, L, Chadeau-Hyam, M, Costa, G, Delpierre, C, D'Errico, A, Fraga, S, Giles, G, Goldberg, M, Kelly-Irving, M, Kivimaki, M, Lepage, B, Lang, T, Layte, R, MacGuire, F, Mackenbach, JP, Marmot, M, McCrory, C, Milne, RL, Muennig, P, Nusselder, W, Petrovic, D, Polidoro, S, Ricceri, F, Robinson, O, Stringhini, S, Zins, M, Vineis, P, Avendano-Pabon, M, Barros, H, Bartley, M, Carmeli, C, Carra, L, Chadeau-Hyam, M, Costa, G, Delpierre, C, D'Errico, A, Fraga, S, Giles, G, Goldberg, M, Kelly-Irving, M, Kivimaki, M, Lepage, B, Lang, T, Layte, R, MacGuire, F, Mackenbach, JP, Marmot, M, McCrory, C, Milne, RL, Muennig, P, Nusselder, W, Petrovic, D, Polidoro, S, Ricceri, F, Robinson, O, Stringhini, S, and Zins, M

Abstract

Funded by the European Commission Horizon 2020 programme, the Lifepath research consortium aimed to investigate the effects of socioeconomic inequalities on the biology of healthy aging. The main research questions included the impact of inequalities on health, the role of behavioral and other risk factors, the underlying biological mechanisms, the efficacy of selected policies, and the general implications of our findings for theories and policies. The project adopted a life-course and comparative approach, considering lifetime effects from childhood and adulthood, and pooled data on up to 1.7 million participants of longitudinal cohort studies from Europe, USA, and Australia. These data showed that socioeconomic circumstances predicted mortality and functional decline as strongly as established risk factors currently targeted by global prevention programmes. Analyses also looked at socioeconomically patterned biological markers, allostatic load, and DNA methylation using richly phenotyped cohorts, unraveling their association with aging processes across the life-course. Lifepath studies suggest that socioeconomic circumstances are embedded in our biology from the outset-i.e., disadvantage influences biological systems from molecules to organs. Our findings have important implications for policy, suggesting that (a) intervening on unfavorable socioeconomic conditions is complementary and as important as targeting well-known risk factors, such as tobacco and alcohol consumption, low fruit and vegetable intake, obesity and a sedentary lifestyle, and that (b) effects of preventive interventions in early life integrate interventions in adulthood. The report has an executive summary that refers to the different sections of the main paper.

Published
2020

39. Epigenome-wide meta-analysis of blood DNA methylation in newborns and children identifies numerous loci related to gestational age

Author

Merid, SK, Novoloaca, A, Sharp, GC, Kupers, LK, Kho, AT, Roy, R, Gao, L, Annesi-Maesano, I, Jain, P, Plusquin, M, Kogevinas, M, Allard, C, Vehmeijer, FO, Kazmi, N, Salas, LA, Rezwan, FI, Zhang, H, Sebert, S, Czamara, D, Rifas-Shiman, SL, Melton, PE, Lawlor, DA, Pershagen, G, Breton, CV, Huen, K, Baiz, N, Gagliardi, L, Nawrot, TS, Corpeleijn, E, Perron, P, Duijts, L, Nohr, EA, Bustamante, M, Ewart, SL, Karmaus, W, Zhao, S, Page, CM, Herceg, Z, Jarvelin, M-R, Lahti, J, Baccarelli, AA, Anderson, D, Kachroo, P, Relton, CL, Bergstrom, A, Eskenazi, B, Soomro, MH, Vineis, P, Snieder, H, Bouchard, L, Jaddoe, VW, Sorensen, TIA, Vrijheid, M, Arshad, SH, Holloway, JW, Haberg, SE, Magnus, P, Dwyer, T, Binder, EB, DeMeo, DL, Vonk, JM, Newnham, J, Tantisira, KG, Kull, I, Wiemels, JL, Heude, B, Sunyer, J, Nystad, W, Munthe-Kaas, MC, Raikkonen, K, Oken, E, Huang, R-C, Weiss, ST, Anto, JM, Bousquet, J, Kumar, A, Soderhall, C, Almqvist, C, Cardenas, A, Gruzieva, O, Xu, C-J, Reese, SE, Kere, J, Brodin, P, Solomon, O, Wielscher, M, Holland, N, Ghantous, A, Hivert, M-F, Felix, JF, Koppelman, GH, London, SJ, Melen, E, Merid, SK, Novoloaca, A, Sharp, GC, Kupers, LK, Kho, AT, Roy, R, Gao, L, Annesi-Maesano, I, Jain, P, Plusquin, M, Kogevinas, M, Allard, C, Vehmeijer, FO, Kazmi, N, Salas, LA, Rezwan, FI, Zhang, H, Sebert, S, Czamara, D, Rifas-Shiman, SL, Melton, PE, Lawlor, DA, Pershagen, G, Breton, CV, Huen, K, Baiz, N, Gagliardi, L, Nawrot, TS, Corpeleijn, E, Perron, P, Duijts, L, Nohr, EA, Bustamante, M, Ewart, SL, Karmaus, W, Zhao, S, Page, CM, Herceg, Z, Jarvelin, M-R, Lahti, J, Baccarelli, AA, Anderson, D, Kachroo, P, Relton, CL, Bergstrom, A, Eskenazi, B, Soomro, MH, Vineis, P, Snieder, H, Bouchard, L, Jaddoe, VW, Sorensen, TIA, Vrijheid, M, Arshad, SH, Holloway, JW, Haberg, SE, Magnus, P, Dwyer, T, Binder, EB, DeMeo, DL, Vonk, JM, Newnham, J, Tantisira, KG, Kull, I, Wiemels, JL, Heude, B, Sunyer, J, Nystad, W, Munthe-Kaas, MC, Raikkonen, K, Oken, E, Huang, R-C, Weiss, ST, Anto, JM, Bousquet, J, Kumar, A, Soderhall, C, Almqvist, C, Cardenas, A, Gruzieva, O, Xu, C-J, Reese, SE, Kere, J, Brodin, P, Solomon, O, Wielscher, M, Holland, N, Ghantous, A, Hivert, M-F, Felix, JF, Koppelman, GH, London, SJ, and Melen, E

Abstract

BACKGROUND: Preterm birth and shorter duration of pregnancy are associated with increased morbidity in neonatal and later life. As the epigenome is known to have an important role during fetal development, we investigated associations between gestational age and blood DNA methylation in children. METHODS: We performed meta-analysis of Illumina's HumanMethylation450-array associations between gestational age and cord blood DNA methylation in 3648 newborns from 17 cohorts without common pregnancy complications, induced delivery or caesarean section. We also explored associations of gestational age with DNA methylation measured at 4-18 years in additional pediatric cohorts. Follow-up analyses of DNA methylation and gene expression correlations were performed in cord blood. DNA methylation profiles were also explored in tissues relevant for gestational age health effects: fetal brain and lung. RESULTS: We identified 8899 CpGs in cord blood that were associated with gestational age (range 27-42 weeks), at Bonferroni significance, P < 1.06 × 10- 7, of which 3343 were novel. These were annotated to 4966 genes. After restricting findings to at least three significant adjacent CpGs, we identified 1276 CpGs annotated to 325 genes. Results were generally consistent when analyses were restricted to term births. Cord blood findings tended not to persist into childhood and adolescence. Pathway analyses identified enrichment for biological processes critical to embryonic development. Follow-up of identified genes showed correlations between gestational age and DNA methylation levels in fetal brain and lung tissue, as well as correlation with expression levels. CONCLUSIONS: We identified numerous CpGs differentially methylated in relation to gestational age at birth that appear to reflect fetal developmental processes across tissues. These findings may contribute to understanding mechanisms linking gestational age to health effects.

Published
2020

40. Reducing socio-economic inequalities in all-cause mortality: a counterfactual mediation approach

Author

Laine, JE, Baltar, VT, Stringhini, S, Gandini, M, Chadeau-Hyam, M, Kivimaki, M, Severi, G, Perduca, V, Hodge, AM, Dugue, P-A, Giles, GG, Milne, RL, Barros, H, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Goldberg, M, Zins, M, Delpierre, C, Alenius, H, Vineis, P, Laine, JE, Baltar, VT, Stringhini, S, Gandini, M, Chadeau-Hyam, M, Kivimaki, M, Severi, G, Perduca, V, Hodge, AM, Dugue, P-A, Giles, GG, Milne, RL, Barros, H, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Goldberg, M, Zins, M, Delpierre, C, Alenius, H, and Vineis, P

Abstract

BACKGROUND: Socio-economic inequalities in mortality are well established, yet the contribution of intermediate risk factors that may underlie these relationships remains unclear. We evaluated the role of multiple modifiable intermediate risk factors underlying socio-economic-associated mortality and quantified the potential impact of reducing early all-cause mortality by hypothetically altering socio-economic risk factors. METHODS: Data were from seven cohort studies participating in the LIFEPATH Consortium (total n = 179 090). Using both socio-economic position (SEP) (based on occupation) and education, we estimated the natural direct effect on all-cause mortality and the natural indirect effect via the joint mediating role of smoking, alcohol intake, dietary patterns, physical activity, body mass index, hypertension, diabetes and coronary artery disease. Hazard ratios (HRs) were estimated, using counterfactual natural effect models under different hypothetical actions of either lower or higher SEP or education. RESULTS: Lower SEP and education were associated with an increase in all-cause mortality within an average follow-up time of 17.5 years. Mortality was reduced via modelled hypothetical actions of increasing SEP or education. Through higher education, the HR was 0.85 [95% confidence interval (CI) 0.84, 0.86] for women and 0.71 (95% CI 0.70, 0.74) for men, compared with lower education. In addition, 34% and 38% of the effect was jointly mediated for women and men, respectively. The benefits from altering SEP were slightly more modest. CONCLUSIONS: These observational findings support policies to reduce mortality both through improving socio-economic circumstances and increasing education, and by altering intermediaries, such as lifestyle behaviours and morbidities.

Published
2020

42. Lifestyle factors and risk of multimorbidity of cancer and cardiometabolic diseases: a multinational cohort study

Author

Freisling, H, Viallon, V, Lennon, H, Bagnardi, V, Ricci, C, Butterworth, AS, Sweeting, M, Muller, D, Romieu, I, Bazelle, P, Kvaskoff, M, Arveux, P, Severi, G, Bamia, C, Kuehn, T, Kaaks, R, Bergmann, M, Boeing, H, Tjonneland, A, Olsen, A, Overvad, K, Dahm, CC, Menendez, V, Agudo, A, Sanchez, M-J, Amiano, P, Santiuste, C, Gurrea, AB, Tong, TYN, Schmidt, JA, Tzoulaki, I, Tsilidis, KK, Ward, H, Palli, D, Agnoli, C, Tumino, R, Ricceri, F, Panico, S, Picavet, HSJ, Bakker, M, Monninkhof, E, Nilsson, P, Manjer, J, Rolandsson, O, Thysell, E, Weiderpass, E, Jenab, M, Riboli, E, Vineis, P, Danesh, J, Wareham, NJ, Gunter, MJ, Ferrari, P, Freisling, H, Viallon, V, Lennon, H, Bagnardi, V, Ricci, C, Butterworth, AS, Sweeting, M, Muller, D, Romieu, I, Bazelle, P, Kvaskoff, M, Arveux, P, Severi, G, Bamia, C, Kuehn, T, Kaaks, R, Bergmann, M, Boeing, H, Tjonneland, A, Olsen, A, Overvad, K, Dahm, CC, Menendez, V, Agudo, A, Sanchez, M-J, Amiano, P, Santiuste, C, Gurrea, AB, Tong, TYN, Schmidt, JA, Tzoulaki, I, Tsilidis, KK, Ward, H, Palli, D, Agnoli, C, Tumino, R, Ricceri, F, Panico, S, Picavet, HSJ, Bakker, M, Monninkhof, E, Nilsson, P, Manjer, J, Rolandsson, O, Thysell, E, Weiderpass, E, Jenab, M, Riboli, E, Vineis, P, Danesh, J, Wareham, NJ, Gunter, MJ, and Ferrari, P

Abstract

BACKGROUND: Although lifestyle factors have been studied in relation to individual non-communicable diseases (NCDs), their association with development of a subsequent NCD, defined as multimorbidity, has been scarcely investigated. The aim of this study was to investigate associations between five lifestyle factors and incident multimorbidity of cancer and cardiometabolic diseases. METHODS: In this prospective cohort study, 291,778 participants (64% women) from seven European countries, mostly aged 43 to 58 years and free of cancer, cardiovascular disease (CVD), and type 2 diabetes (T2D) at recruitment, were included. Incident multimorbidity of cancer and cardiometabolic diseases was defined as developing subsequently two diseases including first cancer at any site, CVD, and T2D in an individual. Multi-state modelling based on Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (95% CI) of developing cancer, CVD, or T2D, and subsequent transitions to multimorbidity, in relation to body mass index (BMI), smoking status, alcohol intake, physical activity, adherence to the Mediterranean diet, and their combination as a healthy lifestyle index (HLI) score. Cumulative incidence functions (CIFs) were estimated to compute 10-year absolute risks for transitions from healthy to cancer at any site, CVD (both fatal and non-fatal), or T2D, and to subsequent multimorbidity after each of the three NCDs. RESULTS: During a median follow-up of 11 years, 1910 men and 1334 women developed multimorbidity of cancer and cardiometabolic diseases. A higher HLI, reflecting healthy lifestyles, was strongly inversely associated with multimorbidity, with hazard ratios per 3-unit increment of 0.75 (95% CI, 0.71 to 0.81), 0.84 (0.79 to 0.90), and 0.82 (0.77 to 0.88) after cancer, CVD, and T2D, respectively. After T2D, the 10-year absolute risks of multimorbidity were 40% and 25% for men and women, respectively, with unhealthy lifestyle, and 30% and 18% for men and

Published
2020

43. Corrigendum to: Reducing socio-economic inequalities in all-cause mortality: a counterfactual mediation approach.

Author

Laine, JE, Baltar, VT, Stringhini, S, Gandini, M, Chadeau-Hyam, M, Kivimaki, M, Severi, G, Perduca, V, Hodge, AM, Dugué, P-A, Giles, GG, Milne, RL, Barros, H, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Goldberg, M, Zins, M, Delpierre, C, LIFEPATH Consortium, Vineis, P, Laine, JE, Baltar, VT, Stringhini, S, Gandini, M, Chadeau-Hyam, M, Kivimaki, M, Severi, G, Perduca, V, Hodge, AM, Dugué, P-A, Giles, GG, Milne, RL, Barros, H, Sacerdote, C, Krogh, V, Panico, S, Tumino, R, Goldberg, M, Zins, M, Delpierre, C, LIFEPATH Consortium, and Vineis, P

Published
2020

44. The impact of lifecourse socio-economic position and individual social mobility on breast cancer risk.

Author

Berger, E, Maitre, N, Romana Mancini, F, Baglietto, L, Perduca, V, Colineaux, H, Sieri, S, Panico, S, Sacerdote, C, Tumino, R, Vineis, P, Boutron-Ruault, M-C, Severi, G, Castagné, R, Delpierre, C, Berger, E, Maitre, N, Romana Mancini, F, Baglietto, L, Perduca, V, Colineaux, H, Sieri, S, Panico, S, Sacerdote, C, Tumino, R, Vineis, P, Boutron-Ruault, M-C, Severi, G, Castagné, R, and Delpierre, C

Abstract

BACKGROUND: Women with an advantaged socioeconomic position (SEP) have a higher risk of developing breast cancer (BC). The reasons for this association do not seem to be limited to reproductive factors and remain to be understood. We aimed to investigate the impact of lifecourse SEP from childhood and social mobility on the risk of BC considering a broad set of potential mediators. METHODS: We used a discovery-replication strategy in two European prospective cohorts, E3N (N = 83,436) and EPIC-Italy (N = 20,530). In E3N, 7877 women were diagnosed with BC during a median 24.4 years of follow-up, while in EPIC-Italy, 893 BC cases were diagnosed within 15.1 years. Hazard ratios (HR) were estimated using Cox proportional hazard models on imputed data. RESULTS: In E3N, women with higher education had a higher risk of BC (HR [95%CI] = 1.21 [1.12, 1.30]). This association was attenuated by adjusting for reproductive factors, in particular age at first childbirth (HR[95%CI] = 1.13 [1.04, 1.22]). Health behaviours, anthropometric variables, and BC screening had a weaker effect on the association. Women who remained in a stable advantaged SEP had a higher risk of BC (HR [95%CI] = 1.24 [1.07; 1.43]) attenuated after adjustment for potential mediators (HR [95%CI] = 1.13 [0.98; 1.31]). These results were replicated in EPIC-Italy. CONCLUSIONS: These results confirm the important role of reproductive factors in the social gradient in BC risk, which does not appear to be fully explained by the large set of potential mediators, including cancer screening, suggesting that further research is needed to identify additional mechanisms.

Published
2020

45. Agnostic Cys34-albumin adductomics and DNA methylation: Implication of N-acetylcysteine in lung carcinogenesis years before diagnosis

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Dagnino, S., Bodinier, B., Grigoryan, H., Rappaport, S.M., Karimi, M., Guida, F., Polidoro, S., Edmands, W.B., Naccarati, A., Fiorito, G., Sacerdote, C., Krogh, V., Vermeulen, R., Vineis, P., Chadeau-Hyam, M., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Dagnino, S., Bodinier, B., Grigoryan, H., Rappaport, S.M., Karimi, M., Guida, F., Polidoro, S., Edmands, W.B., Naccarati, A., Fiorito, G., Sacerdote, C., Krogh, V., Vermeulen, R., Vineis, P., and Chadeau-Hyam, M.

Published
2020

46. Education, biological ageing, all-cause and cause-specific mortality and morbidity: UK biobank cohort study

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Afd. Theologie, Chadeau-Hyam, M., Bodinier, B., Vermeulen, R., Karimi, M., Zuber, V., Castagné, R., Elliott, J., Muller, D., Petrovic, D., Whitaker, M., Stringhini, S., Tzoulaki, I., Kivimäki, M., Vineis, P., Elliott, P., Kelly-Irving, M., Delpierre, C., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Afd. Theologie, Chadeau-Hyam, M., Bodinier, B., Vermeulen, R., Karimi, M., Zuber, V., Castagné, R., Elliott, J., Muller, D., Petrovic, D., Whitaker, M., Stringhini, S., Tzoulaki, I., Kivimäki, M., Vineis, P., Elliott, P., Kelly-Irving, M., and Delpierre, C.

Published
2020

47. Prenatal Exposure to Multiple Air Pollutants, Mediating Molecular Mechanisms, and Shifts in Birthweight

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Laine, J.E., Bodinier, B., Robinson, O., Plusquin, M., Scalbert, A., Keski-Rahkonen, P., Robinot, N., Vermeulen, R., Pizzi, C., Asta, F., Nawrot, T., Gulliver, J., Chatzi, L., Kogevinas, M., Nieuwenhuijsen, M., Sunyer, J., Vrijheid, M., Chadeau-Hyam, M., Vineis, P., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Laine, J.E., Bodinier, B., Robinson, O., Plusquin, M., Scalbert, A., Keski-Rahkonen, P., Robinot, N., Vermeulen, R., Pizzi, C., Asta, F., Nawrot, T., Gulliver, J., Chatzi, L., Kogevinas, M., Nieuwenhuijsen, M., Sunyer, J., Vrijheid, M., Chadeau-Hyam, M., and Vineis, P.

Published
2020

48. A multi-omics approach to investigate the inflammatory response to life course socioeconomic position

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Castagné, R., Kelly-Irving, M., Krogh, V., Palli, D., Panico, S., Sacerdote, C., Tumino, R., Hebels, D.G.A.J., Kleinjans, J.C.S., De Kok, T.M.C.M., Georgiadis, P., Kyrtopoulos, S.A., Vermeulen, R., Stringhini, S., Vineis, P., Chadeau-Hyam, M., Delpierre, C., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Castagné, R., Kelly-Irving, M., Krogh, V., Palli, D., Panico, S., Sacerdote, C., Tumino, R., Hebels, D.G.A.J., Kleinjans, J.C.S., De Kok, T.M.C.M., Georgiadis, P., Kyrtopoulos, S.A., Vermeulen, R., Stringhini, S., Vineis, P., Chadeau-Hyam, M., and Delpierre, C.

Published
2020

49. microRNA expression profiles and personal monitoring of exposure to particulate matter

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, LS IRAS EEPI GRA (Gezh.risico-analyse), dIRAS RA-I&I RA, Mancini, F.R., Laine, J.E., Tarallo, S., Vlaanderen, J., Vermeulen, R., van Nunen, E., Hoek, G., Probst-Hensch, N., Imboden, M., Jeong, A., Gulliver, J., Chadeau-Hyam, M., Nieuwenhuijsen, M., de Kok, T.M., Piepers, J., Krauskopf, J., Kleinjans, J.C.S., Vineis, P., Naccarati, A., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, LS IRAS EEPI GRA (Gezh.risico-analyse), dIRAS RA-I&I RA, Mancini, F.R., Laine, J.E., Tarallo, S., Vlaanderen, J., Vermeulen, R., van Nunen, E., Hoek, G., Probst-Hensch, N., Imboden, M., Jeong, A., Gulliver, J., Chadeau-Hyam, M., Nieuwenhuijsen, M., de Kok, T.M., Piepers, J., Krauskopf, J., Kleinjans, J.C.S., Vineis, P., and Naccarati, A.

Published
2020

50. A multi-omic analysis of birthweight in newborn cord blood reveals new underlying mechanisms related to cholesterol metabolism

Author

IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Alfano, R., Chadeau-Hyam, M., Ghantous, A., Keski-Rahkonen, P., Chatzi, L., Perez, A.E., Herceg, Z., Kogevinas, M., de Kok, T.M., Nawrot, T.S., Novoloaca, A., Patel, C.J., Pizzi, C., Robinot, N., Rusconi, F., Scalbert, A., Sunyer, J., Vermeulen, R., Vrijheid, M., Vineis, P., Robinson, O., Plusquin, M., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Alfano, R., Chadeau-Hyam, M., Ghantous, A., Keski-Rahkonen, P., Chatzi, L., Perez, A.E., Herceg, Z., Kogevinas, M., de Kok, T.M., Nawrot, T.S., Novoloaca, A., Patel, C.J., Pizzi, C., Robinot, N., Rusconi, F., Scalbert, A., Sunyer, J., Vermeulen, R., Vrijheid, M., Vineis, P., Robinson, O., and Plusquin, M.

Published
2020

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