Publications by authors named "Michail Katsoulis"

30 Publications

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Excess deaths in people with cardiovascular diseases during the COVID-19 pandemic.

Eur J Prev Cardiol 2021 Feb 21. Epub 2021 Feb 21.

Institute of Health Informatics, University College London, 222 Euston Road, London, UK, NW1 1DA.

Aims: Cardiovascular diseases (CVDs) increase mortality risk from coronavirus infection (COVID-19). There are also concerns that the pandemic has affected supply and demand of acute cardiovascular care. We estimated excess mortality in specific CVDs, both 'direct', through infection, and 'indirect', through changes in healthcare.

Methods And Results: We used (i) national mortality data for England and Wales to investigate trends in non-COVID-19 and CVD excess deaths; (ii) routine data from hospitals in England (n = 2), Italy (n = 1), and China (n = 5) to assess indirect pandemic effects on referral, diagnosis, and treatment services for CVD; and (iii) population-based electronic health records from 3 862 012 individuals in England to investigate pre- and post-COVID-19 mortality for people with incident and prevalent CVD. We incorporated pre-COVID-19 risk (by age, sex, and comorbidities), estimated population COVID-19 prevalence, and estimated relative risk (RR) of mortality in those with CVD and COVID-19 compared with CVD and non-infected (RR: 1.2, 1.5, 2.0, and 3.0).Mortality data suggest indirect effects on CVD will be delayed rather than contemporaneous (peak RR 1.14). CVD service activity decreased by 60-100% compared with pre-pandemic levels in eight hospitals across China, Italy, and England. In China, activity remained below pre-COVID-19 levels for 2-3 months even after easing lockdown and is still reduced in Italy and England. For total CVD (incident and prevalent), at 10% COVID-19 prevalence, we estimated direct impact of 31 205 and 62 410 excess deaths in England (RR 1.5 and 2.0, respectively), and indirect effect of 49 932 to 99 865 deaths.

Conclusion: Supply and demand for CVD services have dramatically reduced across countries with potential for substantial, but avoidable, excess mortality during and after the pandemic.
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http://dx.doi.org/10.1093/eurjpc/zwaa155DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7928969PMC
February 2021

Coffee consumption and risk of breast cancer: A Mendelian randomization study.

PLoS One 2021 19;16(1):e0236904. Epub 2021 Jan 19.

Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom.

Background: Observational studies have reported either null or weak protective associations for coffee consumption and risk of breast cancer.

Methods: We conducted a two-sample Mendelian randomization (MR) analysis to evaluate the relationship between coffee consumption and breast cancer risk using 33 single-nucleotide polymorphisms (SNPs) associated with coffee consumption from a genome-wide association (GWA) study on 212,119 female UK Biobank participants of White British ancestry. Risk estimates for breast cancer were retrieved from publicly available GWA summary statistics from the Breast Cancer Association Consortium (BCAC) on 122,977 cases (of which 69,501 were estrogen receptor (ER)-positive, 21,468 ER-negative) and 105,974 controls of European ancestry. Random-effects inverse variance weighted (IVW) MR analyses were performed along with several sensitivity analyses to assess the impact of potential MR assumption violations.

Results: One cup per day increase in genetically predicted coffee consumption in women was not associated with risk of total (IVW random-effects; odds ratio (OR): 0.91, 95% confidence intervals (CI): 0.80-1.02, P: 0.12, P for instrument heterogeneity: 7.17e-13), ER-positive (OR = 0.90, 95% CI: 0.79-1.02, P: 0.09) and ER-negative breast cancer (OR: 0.88, 95% CI: 0.75-1.03, P: 0.12). Null associations were also found in the sensitivity analyses using MR-Egger (total breast cancer; OR: 1.00, 95% CI: 0.80-1.25), weighted median (OR: 0.97, 95% CI: 0.89-1.05) and weighted mode (OR: 1.00, CI: 0.93-1.07).

Conclusions: The results of this large MR study do not support an association of genetically predicted coffee consumption on breast cancer risk, but we cannot rule out existence of a weak association.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0236904PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7815134PMC
April 2021

Estimated impact of the COVID-19 pandemic on cancer services and excess 1-year mortality in people with cancer and multimorbidity: near real-time data on cancer care, cancer deaths and a population-based cohort study.

BMJ Open 2020 11 17;10(11):e043828. Epub 2020 Nov 17.

Institute of Health Informatics, University College London, London, UK.

Objectives: To estimate the impact of the COVID-19 pandemic on cancer care services and overall (direct and indirect) excess deaths in people with cancer.

Methods: We employed near real-time weekly data on cancer care to determine the adverse effect of the pandemic on cancer services. We also used these data, together with national death registrations until June 2020 to model deaths, in excess of background (pre-COVID-19) mortality, in people with cancer. Background mortality risks for 24 cancers with and without COVID-19-relevant comorbidities were obtained from population-based primary care cohort (Clinical Practice Research Datalink) on 3 862 012 adults in England.

Results: Declines in urgent referrals (median=-70.4%) and chemotherapy attendances (median=-41.5%) to a nadir (lowest point) in the pandemic were observed. By 31 May, these declines have only partially recovered; urgent referrals (median=-44.5%) and chemotherapy attendances (median=-31.2%). There were short-term excess death registrations for cancer (without COVID-19), with peak relative risk (RR) of 1.17 at week ending on 3 April. The peak RR for all-cause deaths was 2.1 from week ending on 17 April. Based on these findings and recent literature, we modelled 40% and 80% of cancer patients being affected by the pandemic in the long-term. At 40% affected, we estimated 1-year total (direct and indirect) excess deaths in people with cancer as between 7165 and 17 910, using RRs of 1.2 and 1.5, respectively, where 78% of excess deaths occured in patients with ≥1 comorbidity.

Conclusions: Dramatic reductions were detected in the demand for, and supply of, cancer services which have not fully recovered with lockdown easing. These may contribute, over a 1-year time horizon, to substantial excess mortality among people with cancer and multimorbidity. It is urgent to understand how the recovery of general practitioner, oncology and other hospital services might best mitigate these long-term excess mortality risks.
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http://dx.doi.org/10.1136/bmjopen-2020-043828DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7674020PMC
November 2020

Clinical academic research in the time of Corona: A simulation study in England and a call for action.

PLoS One 2020 13;15(8):e0237298. Epub 2020 Aug 13.

Barts NHS Trust, London, United Kingdom.

Objectives: We aimed to model the impact of coronavirus (COVID-19) on the clinical academic response in England, and to provide recommendations for COVID-related research.

Design: A stochastic model to determine clinical academic capacity in England, incorporating the following key factors which affect the ability to conduct research in the COVID-19 climate: (i) infection growth rate and population infection rate (from UK COVID-19 statistics and WHO); (ii) strain on the healthcare system (from published model); and (iii) availability of clinical academic staff with appropriate skillsets affected by frontline clinical activity and sickness (from UK statistics).

Setting: Clinical academics in primary and secondary care in England.

Participants: Equivalent of 3200 full-time clinical academics in England.

Interventions: Four policy approaches to COVID-19 with differing population infection rates: "Italy model" (6%), "mitigation" (10%), "relaxed mitigation" (40%) and "do-nothing" (80%) scenarios. Low and high strain on the health system (no clinical academics able to do research at 10% and 5% infection rate, respectively.

Main Outcome Measures: Number of full-time clinical academics available to conduct clinical research during the pandemic in England.

Results: In the "Italy model", "mitigation", "relaxed mitigation" and "do-nothing" scenarios, from 5 March 2020 the duration (days) and peak infection rates (%) are 95(2.4%), 115(2.5%), 240(5.3%) and 240(16.7%) respectively. Near complete attrition of academia (87% reduction, <400 clinical academics) occurs 35 days after pandemic start for 11, 34, 62, 76 days respectively-with no clinical academics at all for 37 days in the "do-nothing" scenario. Restoration of normal academic workforce (80% of normal capacity) takes 11, 12, 30 and 26 weeks respectively.

Conclusions: Pandemic COVID-19 crushes the science needed at system level. National policies mitigate, but the academic community needs to adapt. We highlight six key strategies: radical prioritisation (eg 3-4 research ideas per institution), deep resourcing, non-standard leadership (repurposing of key non-frontline teams), rationalisation (profoundly simple approaches), careful site selection (eg protected sites with large academic backup) and complete suspension of academic competition with collaborative approaches.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0237298PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425844PMC
August 2020

Prevalence and outcome of dual aortic stenosis and cardiac amyloid pathology in patients referred for transcatheter aortic valve implantation.

Eur Heart J 2020 08;41(29):2759-2767

Barts Heart Centre, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK.

Aims: Cardiac amyloidosis is common in elderly patients with aortic stenosis (AS) referred for transcatheter aortic valve implantation (TAVI). We hypothesized that patients with dual aortic stenosis and cardiac amyloid pathology (AS-amyloid) would have different baseline characteristics, periprocedural and mortality outcomes.

Methods And Results: Patients aged ≥75 with severe AS referred for TAVI at two sites underwent blinded bone scintigraphy prior to intervention (Perugini Grade 0 negative, 1-3 increasingly positive). Baseline assessment included echocardiography, electrocardiogram (ECG), blood tests, 6-min walk test, and health questionnaire, with periprocedural complications and mortality follow-up. Two hundred patients were recruited (aged 85 ± 5 years, 50% male). AS-amyloid was found in 26 (13%): 8 Grade 1, 18 Grade 2. AS-amyloid patients were older (88 ± 5 vs. 85 ± 5 years, P = 0.001), with reduced quality of life (EQ-5D-5L 50 vs. 65, P = 0.04). Left ventricular wall thickness was higher (14 mm vs. 13 mm, P = 0.02), ECG voltages lower (Sokolow-Lyon 1.9 ± 0.7 vs. 2.5 ± 0.9 mV, P = 0.03) with lower voltage/mass ratio (0.017 vs. 0.025 mV/g/m2, P = 0.03). High-sensitivity troponin T and N-terminal pro-brain natriuretic peptide were higher (41 vs. 21 ng/L, P < 0.001; 3702 vs. 1254 ng/L, P = 0.001). Gender, comorbidities, 6-min walk distance, AS severity, prevalence of disproportionate hypertrophy, and post-TAVI complication rates (38% vs. 35%, P = 0.82) were the same. At a median follow-up of 19 (10-27) months, there was no mortality difference (P = 0.71). Transcatheter aortic valve implantation significantly improved outcome in the overall population (P < 0.001) and in those with AS-amyloid (P = 0.03).

Conclusions: AS-amyloid is common and differs from lone AS. Transcatheter aortic valve implantation significantly improved outcome in AS-amyloid, while periprocedural complications and mortality were similar to lone AS, suggesting that TAVI should not be denied to patients with AS-amyloid.
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http://dx.doi.org/10.1093/eurheartj/ehaa170DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7395329PMC
August 2020

The relationship between sleep duration, cognition and dementia: a Mendelian randomization study.

Int J Epidemiol 2019 06;48(3):849-860

Institute of Health Informatics, University College London, London, UK.

Background: Short and long sleep duration have been linked with poorer cognitive outcomes, but it remains unclear whether these associations are causal.

Methods: We conducted the first Mendelian randomization (MR) study with 77 single-nucleotide polymorphisms (SNPs) for sleep duration using individual-participant data from the UK Biobank cohort (N = 395 803) and summary statistics from the International Genomics of Alzheimer's Project (N cases/controls = 17 008/37 154) to investigate the potential impact of sleep duration on cognitive outcomes.

Results: Linear MR suggested that each additional hour/day of sleep was associated with 1% [95% confidence interval (CI) = 0-2%; P = 0.008] slower reaction time and 3% more errors in visual-memory test (95% CI = 0-6%; P = 0.05). There was little evidence to support associations of increased sleep duration with decline in visual memory [odds ratio (OR) per additional hour/day of sleep = 1.10 (95% CI = 0.76-1.57); P = 0.62], decline in reaction time [OR = 1.28 (95% CI = 0.49-3.35); P = 0.61], all-cause dementia [OR = 1.19 (95% CI = 0.65-2.19); P = 0.57] or Alzheimer's disease risk [OR = 0.89 (95% CI = 0.67-1.18); P = 0.41]. Non-linear MR suggested that both short and long sleep duration were associated with poorer visual memory (P for non-linearity = 3.44e-9) and reaction time (P for non-linearity = 6.66e-16).

Conclusions: Linear increase in sleep duration has a small negative effect on reaction time and visual memory, but the true association might be non-linear, with evidence of associations for both short and long sleep duration. These findings suggest that sleep duration may represent a potential causal pathway for cognition.
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http://dx.doi.org/10.1093/ije/dyz071DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6659373PMC
June 2019

Organic solvents and MS susceptibility: Interaction with MS risk HLA genes.

Neurology 2018 07 3;91(5):e455-e462. Epub 2018 Jul 3.

From the Department of Clinical Neuroscience and Institute of Environmental Medicine (A.K.H., L.A.), and Department of Clinical Neuroscience and Center for Molecular Medicine (I.K., T.O.), Karolinska Institutet, Stockholm; Mathematical Statistics (O.H.), Stockholm University, Sweden; UCL/Farr Institute of Health Informatics Research (M.K.), London, UK; and Centre for Occupational and Environmental Medicine (L.A.), Stockholm County Council, Sweden.

Objective: We hypothesize that different sources of lung irritation may contribute to elicit an immune reaction in the lungs and subsequently lead to multiple sclerosis (MS) in people with a genetic susceptibility to the disease. We aimed to investigate the influence of exposure to organic solvents on MS risk, and a potential interaction between organic solvents and MS risk human leukocyte antigen (HLA) genes.

Methods: Using a Swedish population-based case-control study (2,042 incident cases of MS and 2,947 controls), participants with different genotypes, smoking habits, and exposures to organic solvents were compared regarding occurrence of MS, by calculating odds ratios with 95% confidence intervals using logistic regression. A potential interaction between exposure to organic solvents and MS risk HLA genes was evaluated by calculating the attributable proportion due to interaction.

Results: Overall, exposure to organic solvents increased the risk of MS (odds ratio 1.5, 95% confidence interval 1.2-1.8, = 0.0004). Among both ever and never smokers, an interaction between organic solvents, carriage of HLA-DRB1*15, and absence of HLA-A*02 was observed with regard to MS risk, similar to the previously reported gene-environment interaction involving the same MS risk HLA genes and smoke exposure.

Conclusion: The mechanism linking both smoking and exposure to organic solvents to MS risk may involve lung inflammation with a proinflammatory profile. Their interaction with MS risk HLA genes argues for an action of these environmental factors on adaptive immunity, perhaps through activation of autoaggressive cells resident in the lungs subsequently attacking the CNS.
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http://dx.doi.org/10.1212/WNL.0000000000005906DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6093765PMC
July 2018

Variation in Interleukin 6 Receptor Gene Associates With Risk of Crohn's Disease and Ulcerative Colitis.

Gastroenterology 2018 08 5;155(2):303-306.e2. Epub 2018 Jul 5.

Institute of Cardiovascular Science, Faculty of Population Health Sciences, University College London, London, UK.

Interleukin 6 (IL6) is an inflammatory cytokine; signaling via its receptor (IL6R) is believed to contribute to development of inflammatory bowel diseases (IBD). The single nucleotide polymorphism rs2228145 in IL6R associates with increased levels of soluble IL6R (s-IL6R), as well as reduced IL6R signaling and risk of inflammatory disorders; its effects are similar to those of a therapeutic monoclonal antibody that blocks IL6R signaling. We used the effect of rs2228145 on s-IL6R level as an indirect marker to investigate whether reduced IL6R signaling associates with risk of ulcerative colitis (UC) or Crohn's disease (CD). In a genome-wide meta-analysis of 20,550 patients with CD, 17,647 patients with UC, and more than 40,000 individuals without IBD (controls), we found that rs2228145 (scaled to a 2-fold increase in s-IL6R) was associated with reduced risk of CD (odds ratio 0.876; 95% confidence interval 0.822-0.933; P = .00003) or UC (odds ratio 0.932; 95% confidence interval 0.875-0.996; P = .036). These findings indicate that therapeutics designed to block IL6R signaling might be effective in treatment of IBD.
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http://dx.doi.org/10.1053/j.gastro.2018.05.022DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6083435PMC
August 2018

Separate and combined associations of obesity and metabolic health with coronary heart disease: a pan-European case-cohort analysis.

Eur Heart J 2018 02;39(5):397-406

Public Health Institute of Navarra, IdiSNA, Calle de Irunlarrea, 3, 31008 Pamplona, Spain.

Aims: The hypothesis of 'metabolically healthy obesity' implies that, in the absence of metabolic dysfunction, individuals with excess adiposity are not at greater cardiovascular risk. We tested this hypothesis in a large pan-European prospective study.

Methods And Results: We conducted a case-cohort analysis in the 520 000-person European Prospective Investigation into Cancer and Nutrition study ('EPIC-CVD'). During a median follow-up of 12.2 years, we recorded 7637 incident coronary heart disease (CHD) cases. Using cut-offs recommended by guidelines, we defined obesity and overweight using body mass index (BMI), and metabolic dysfunction ('unhealthy') as ≥ 3 of elevated blood pressure, hypertriglyceridaemia, low HDL-cholesterol, hyperglycaemia, and elevated waist circumference. We calculated hazard ratios (HRs) and 95% confidence intervals (95% CI) within each country using Prentice-weighted Cox proportional hazard regressions, accounting for age, sex, centre, education, smoking, diet, and physical activity. Compared with metabolically healthy normal weight people (reference), HRs were 2.15 (95% CI: 1.79; 2.57) for unhealthy normal weight, 2.33 (1.97; 2.76) for unhealthy overweight, and 2.54 (2.21; 2.92) for unhealthy obese people. Compared with the reference group, HRs were 1.26 (1.14; 1.40) and 1.28 (1.03; 1.58) for metabolically healthy overweight and obese people, respectively. These results were robust to various sensitivity analyses.

Conclusion: Irrespective of BMI, metabolically unhealthy individuals had higher CHD risk than their healthy counterparts. Conversely, irrespective of metabolic health, overweight and obese people had higher CHD risk than lean people. These findings challenge the concept of 'metabolically healthy obesity', encouraging population-wide strategies to tackle obesity.
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http://dx.doi.org/10.1093/eurheartj/ehx448DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6198928PMC
February 2018

The interaction between smoking and HLA genes in multiple sclerosis: replication and refinement.

Eur J Epidemiol 2017 10 8;32(10):909-919. Epub 2017 Jun 8.

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Interactions between environment and genetics may contribute to multiple sclerosis (MS) development. We investigated whether the previously observed interaction between smoking and HLA genotype in the Swedish population could be replicated, refined and extended to include other populations. We used six independent case-control studies from five different countries (Sweden, Denmark, Norway, Serbia, United States). A pooled analysis was performed for replication of previous observations (7190 cases, 8876 controls). Refined detailed analyses were carried out by combining the genetically similar populations from the Nordic studies (6265 cases, 8401 controls). In both the pooled analyses and in the combined Nordic material, interactions were observed between HLA-DRB*15 and absence of HLA-A*02 and between smoking and each of the genetic risk factors. Two way interactions were observed between each combination of the three variables, invariant over categories of the third. Further, there was also a three way interaction between the risk factors. The difference in MS risk between the extremes was considerable; smokers carrying HLA-DRB1*15 and lacking HLA-A*02 had a 13-fold increased risk compared with never smokers without these genetic risk factors (OR 12.7, 95% CI 10.8-14.9). The risk of MS associated with HLA genotypes is strongly influenced by smoking status and vice versa. Since the function of HLA molecules is to present peptide antigens to T cells, the demonstrated interactions strongly suggest that smoking alters MS risk through actions on adaptive immunity.
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http://dx.doi.org/10.1007/s10654-017-0250-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5680370PMC
October 2017

Genetic variation in the ADIPOQ gene, adiponectin concentrations and risk of colorectal cancer: a Mendelian Randomization analysis using data from three large cohort studies.

Eur J Epidemiol 2017 05 26;32(5):419-430. Epub 2017 May 26.

Danish Cancer Society Research Center, Copenhagen, Denmark.

Higher levels of circulating adiponectin have been related to lower risk of colorectal cancer in several prospective cohort studies, but it remains unclear whether this association may be causal. We aimed to improve causal inference in a Mendelian Randomization meta-analysis using nested case-control studies of the European Prospective Investigation into Cancer and Nutrition (EPIC, 623 cases, 623 matched controls), the Health Professionals Follow-up Study (HPFS, 231 cases, 230 controls) and the Nurses' Health Study (NHS, 399 cases, 774 controls) with available data on pre-diagnostic adiponectin concentrations and selected single nucleotide polymorphisms in the ADIPOQ gene. We created an ADIPOQ allele score that explained approximately 3% of the interindividual variation in adiponectin concentrations. The ADIPOQ allele score was not associated with risk of colorectal cancer in logistic regression analyses (pooled OR per score-unit unit 0.97, 95% CI 0.91, 1.04). Genetically determined twofold higher adiponectin was not significantly associated with risk of colorectal cancer using the ADIPOQ allele score as instrumental variable (pooled OR 0.73, 95% CI 0.40, 1.34). In a summary instrumental variable analysis (based on previously published data) with higher statistical power, no association between genetically determined twofold higher adiponectin and risk of colorectal cancer was observed (0.99, 95% CI 0.93, 1.06 in women and 0.94, 95% CI 0.88, 1.01 in men). Thus, our study does not support a causal effect of circulating adiponectin on colorectal cancer risk. Due to the limited genetic determination of adiponectin, larger Mendelian Randomization studies are necessary to clarify whether adiponectin is causally related to lower risk of colorectal cancer.
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http://dx.doi.org/10.1007/s10654-017-0262-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5535815PMC
May 2017

Maternal height and breast cancer risk: results from a study nested within the EPIC-Greece cohort.

Eur J Epidemiol 2017 05 17;32(5):457-463. Epub 2017 Apr 17.

Hellenic Health Foundation, 13 Kaisareias and Alexandoupoleos Street, 115 27, Athens, Greece.

The positive association of adult height with breast cancer (BC) risk has been hypothesized to be partly accounted for by an association of this risk with maternal height (operating in utero to modify hormone effects). In a case-control study (271 BC patients and 791 controls) nested within the EPIC-Greece cohort, we applied mediation analysis to calculate the direct and indirect (through the woman's own height) effect of maternal height on BC risk. Per 5 cm increase in maternal height and depending on its reference value: the indirect effect odds ratio ranges from 1.02 to 1.07; the direct effect odds ratio from 1.06 to 1.11; and the total (direct and indirect effects) from 1.08 to 1.19. The effect sizes consistently increased for higher reference categories of maternal height, but did not generally reach statistical significance, possibly due to the limited sample size.
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http://dx.doi.org/10.1007/s10654-017-0245-zDOI Listing
May 2017

Rheumatoid arthritis and cancer risk[BULLET OPERATOR]results from the Greek European prospective investigation into cancer and nutrition cohort.

Eur J Cancer Prev 2018 09;27(5):502-506

Hellenic Health Foundation.

To investigate the relative risk of cancer development in rheumatoid arthritis (RA) patients in Greece after taking into consideration treatment modalities. The present analysis used data on the medical history of 26 331 participants in the Greek arm of the European Prospective Investigation into Cancer and Nutrition that were collected at enrollment and thereafter during active follow-up. A history of RA and of drug treatment for the disease, as reported at baseline examination, was linked to cases of cancer reported during follow-up. A total of 91 (9.9%) patients with RA developed a cancer compared with 1542 (6.1%) patients without RA. The overall hazard ratios of all cancers increased 25% [95% confidence interval (CI): 1-54] among participants with prevalent RA, and almost all the site-specific incident cancer sites considered had rate ratios above unity. In terms of the contribution of RA medication, the hazard ratios of patients treated with salicylates was close to unity (1.07, 95% CI: 0.69-1.65), whereas those who were not treated with salicylates had a 31% (95% CI: 3-67) increased risk for cancer incidence compared with those without RA at baseline. RA patients have excess cancer risk because of either underlying complex disease pathways or treatment agents targeting immune function. Administration of salicylates appears to reduce the risk of developing malignancies.
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http://dx.doi.org/10.1097/CEJ.0000000000000349DOI Listing
September 2018

Corticosteroids and hip fracture risk in elderly respiratory patients: EPIC-Greece cohort.

Adv Respir Med 2017 ;85(1):22-27

Introduction: In an ageing population the prevalence of osteoporosis and chronic respiratory diseases is expected to increase in the near future. Interestingly, several forms of corticosteroids, drugs implicated in osteoporosis pathogenesis, are prescribed to respiratory patients without taking into consideration their age and risk for osteoporotic fractures. The aim of this study was to investigate the risk for hip fracture of the elder individuals who are taking corticosteroids for respiratory disease, including inhalers.

Material And Methods: Data on incident hip fractures were collected through the active follow-up for all individuals participating in the Greek segment of the European Prospective Investigation into Cancer and Nutrition (EPIC-Greece) study who were 60 years or older at recruitment and reported "a doctor's diagnosis" of respiratory disease. Socio-demographic, life-style, health status data and use of corticosteroids were recorded from the baseline and follow-up questionnaires. Cox regression models were applied to estimate hazard ratios (HRs) adjusting for relevant confounders.

Results: We observed an increase in hip fracture risk with corticosteroid intake overall (HR: 1.68, 95% CI: 0.85-3.34). Increased risk persisted when we restricted our analysis to participants taking any form of corticosteroids for obstructive lung disease (HR: 1.40, 95% CI: 0.64-3.06) and to those using only inhalers (HR: 1.58, 95% CI: 0.71-3.50). However, these positive associations did not reach the nominal level of significance probably due to the small number of participants with hip fractures during follow-up.

Conclusion: Hip fracture risk should be taken into consideration when recommending corticosteroids to the elder respiratory patients, including inhalers.
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http://dx.doi.org/10.5603/ARM.2017.0005DOI Listing
October 2018

Quantification of the smoking-associated cancer risk with rate advancement periods: meta-analysis of individual participant data from cohorts of the CHANCES consortium.

BMC Med 2016 Apr 5;14:62. Epub 2016 Apr 5.

Department Epidemiology and Public Health, University College London, London, UK.

Background: Smoking is the most important individual risk factor for many cancer sites but its association with breast and prostate cancer is not entirely clear. Rate advancement periods (RAPs) may enhance communication of smoking related risk to the general population. Thus, we estimated RAPs for the association of smoking exposure (smoking status, time since smoking cessation, smoking intensity, and duration) with total and site-specific (lung, breast, colorectal, prostate, gastric, head and neck, and pancreatic) cancer incidence and mortality.

Methods: This is a meta-analysis of 19 population-based prospective cohort studies with individual participant data for 897,021 European and American adults. For each cohort we calculated hazard ratios (HRs) for the association of smoking exposure with cancer outcomes using Cox regression adjusted for a common set of the most important potential confounding variables. RAPs (in years) were calculated as the ratio of the logarithms of the HRs for a given smoking exposure variable and age. Meta-analyses were employed to summarize cohort-specific HRs and RAPs.

Results: Overall, 140,205 subjects had a first incident cancer, and 53,164 died from cancer, during an average follow-up of 12 years. Current smoking advanced the overall risk of developing and dying from cancer by eight and ten years, respectively, compared with never smokers. The greatest advancements in cancer risk and mortality were seen for lung cancer and the least for breast cancer. Smoking cessation was statistically significantly associated with delays in the risk of cancer development and mortality compared with continued smoking.

Conclusions: This investigation shows that smoking, even among older adults, considerably advances, and cessation delays, the risk of developing and dying from cancer. These findings may be helpful in more effectively communicating the harmful effects of smoking and the beneficial effect of smoking cessation.
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http://dx.doi.org/10.1186/s12916-016-0607-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4820956PMC
April 2016

Evaluation of a digital food photography atlas used as portion size measurement aid in dietary surveys in Greece.

Public Health Nutr 2016 09 26;19(13):2369-76. Epub 2016 Feb 26.

2Hellenic Health Foundation,Kaisareias 13 & Alexandroupoleos,GR-115 27 Athens,Greece.

Objective: To evaluate how well respondents perceive digital images of food portions commonly consumed in Greece.

Design: The picture series was defined on the basis of usual dietary intakes assessed in earlier large-scale studies in Greece. The evaluation included 2218 pre-weighed actual portions shown to participants, who were subsequently asked to link each portion to a food picture. Mean differences between picture numbers selected and portions actually shown were compared using the Wilcoxon paired signed-rank test. The effect of personal characteristics on participants' selections was evaluated through unpaired t tests (sex and school years) or through Tukey-Kramer pairwise comparisons (age and food groups).

Setting: Testing of participants' perception of digital food images used in the Greek national nutrition survey.

Subjects: Individuals (n 103, 61 % females) aged 12 years and over, selected on the basis of the target population of the Greek nutrition survey using convenience sampling.

Results: Individuals selected the correct or adjacent image in about 90 % of the assessments and tended to overestimate small and underestimate large quantities. Photographs of Greek traditional pies and meat-based pastry dishes led participants to perceive the amounts in the photos larger than they actually were. Adolescents were more prone to underestimating food quantities through the pictures.

Conclusions: The digital food atlas appears generally suitable to be used for the estimation of average food intakes in large-scale dietary surveys in Greece. However, individuals who consistently consume only small or only large food portions may have biased perceptions in relation to others.
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http://dx.doi.org/10.1017/S1368980016000227DOI Listing
September 2016

Eating out is different from eating at home among individuals who occasionally eat out. A cross-sectional study among middle-aged adults from eleven European countries.

Br J Nutr 2015 Jun 24;113(12):1951-64. Epub 2015 Apr 24.

WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens,75 Mikras Asias Street,Goudi, Athens11527,Greece.

Eating out has been linked to the current obesity epidemic, but the evaluation of the extent to which out of home (OH) dietary intakes are different from those at home (AH) is limited. Data collected among 8849 men and 14,277 women aged 35-64 years from the general population of eleven European countries through 24-h dietary recalls or food diaries were analysed to: (1) compare food consumption OH to those AH; (2) describe the characteristics of substantial OH eaters, defined as those who consumed 25 % or more of their total daily energy intake at OH locations. Logistic regression models were fit to identify personal characteristics associated with eating out. In both sexes, beverages, sugar, desserts, sweet and savoury bakery products were consumed more OH than AH. In some countries, men reported higher intakes of fish OH than AH. Overall, substantial OH eating was more common among men, the younger and the more educated participants, but was weakly associated with total energy intake. The substantial OH eaters reported similar dietary intakes OH and AH. Individuals who were not identified as substantial OH eaters reported consuming proportionally higher quantities of sweet and savoury bakery products, soft drinks, juices and other non-alcoholic beverages OH than AH. The OH intakes were different from the AH ones, only among individuals who reported a relatively small contribution of OH eating to their daily intakes and this may partly explain the inconsistent findings relating eating out to the current obesity epidemic.
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http://dx.doi.org/10.1017/S0007114515000963DOI Listing
June 2015

Natural-cause mortality and long-term exposure to particle components: an analysis of 19 European cohorts within the multi-center ESCAPE project.

Environ Health Perspect 2015 Jun 24;123(6):525-33. Epub 2015 Feb 24.

Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.

Background: Studies have shown associations between mortality and long-term exposure to particulate matter air pollution. Few cohort studies have estimated the effects of the elemental composition of particulate matter on mortality.

Objectives: Our aim was to study the association between natural-cause mortality and long-term exposure to elemental components of particulate matter.

Methods: Mortality and confounder data from 19 European cohort studies were used. Residential exposure to eight a priori-selected components of particulate matter (PM) was characterized following a strictly standardized protocol. Annual average concentrations of copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc within PM size fractions ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10) were estimated using land-use regression models. Cohort-specific statistical analyses of the associations between mortality and air pollution were conducted using Cox proportional hazards models using a common protocol followed by meta-analysis.

Results: The total study population consisted of 291,816 participants, of whom 25,466 died from a natural cause during follow-up (average time of follow-up, 14.3 years). Hazard ratios were positive for almost all elements and statistically significant for PM2.5 sulfur (1.14; 95% CI: 1.06, 1.23 per 200 ng/m3). In a two-pollutant model, the association with PM2.5 sulfur was robust to adjustment for PM2.5 mass, whereas the association with PM2.5 mass was reduced.

Conclusions: Long-term exposure to PM2.5 sulfur was associated with natural-cause mortality. This association was robust to adjustment for other pollutants and PM2.5.
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http://dx.doi.org/10.1289/ehp.1408095DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4455583PMC
June 2015

Cognitive impairment and cancer mortality: a biological or health care explanation?

Cancer Causes Control 2014 Nov 22;25(11):1565-70. Epub 2014 Aug 22.

Hellenic Health Foundation, 13 Kaisareias Street, 115 27, Athens, Greece,

Purpose: To examine whether the documented association of suboptimal cognitive function with total and cardiovascular (CVD) mortality also applies to cancer mortality and probe whether the explanation for this association is biomedical or health care related.

Methods: In a subsample of 733 participants of the EPIC-Greece cohort from Athens and surrounding area, we assessed cognitive function at age 65 or older in the period 2004-2006, using the Mini-Mental State Examination (MMSE). Incidence of cancer, mortality from cancer and CVD, and overall mortality were ascertained through active follow-up for a median of 4 years after MMSE assessment using Cox proportional hazards models.

Results: A total of 86 participants died during follow-up. A 2-point decrease in MMSE score was associated with increase in overall (hazard ratio (HR) 1.26, 95 % confidence interval (CI) 1.11-1.43), CVD (HR 1.26, 95 % CI 1.02-1.56), and cancer (HR 1.32, 95 % CI 1.02-1.70) mortality. In contrast, there was no noticeable difference in cancer incidence associated with a 2-point decrease in MMSE score (HR 1.07, 95 % CI 0.79-1.45).

Conclusions: Cognitive function appears to be inversely associated not only with CVD and overall, but also with cancer mortality. Although for CVD mortality there is a biomedical explanation invoking vascular mechanisms, for cancer mortality we may need to focus on socially conditioned factors, such as compromised ability to identify early signs and suboptimal compliance to treatment. Our hypothesis-generating results need to be confirmed in larger studies, as the issue is of major importance, since cognitive decline is not uncommon among the elderly.
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http://dx.doi.org/10.1007/s10552-014-0460-9DOI Listing
November 2014

Long-term exposure to traffic-related air pollution and cardiovascular health in a Greek cohort study.

Sci Total Environ 2014 Aug 6;490:934-40. Epub 2014 Jun 6.

Department of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Athens, Greece; Department of Primary Care & Public Health Sciences, Environmental Research Group, King's College London, London, UK. Electronic address:

Our objective is to evaluate the association of exposure to traffic-related air pollution with the incidence of fatal and non-fatal ischemic heart disease (IHD), stroke and total cardiovascular disease (CVD) events in a Greek cohort. We used data from the European Prospective Investigation on Nutrition and Cancer (EPIC) for 2752 subjects followed from 1997 to 2011, whose residence was in 10 municipalities of the Greater Athens area. Air pollution exposure estimation was based on a spatio-temporal land use regression model linking geo-coded residential addresses to long-term average NO2 and PM10 concentrations. We conducted Cox proportional hazards regression analysis, adjusting for potential confounders. Hazard ratios (HR) above 1 (not all statistically significant) were associated with higher PM10 exposure for all outcomes. Weaker associations were found with NO2 exposure. Specifically, the estimated HR for a CVD event associated with 10 μg/m(3) increase in long-term exposure to PM10 was 1.50 (1.05-2.16, p-value: 0.027). The relationship was more evident for subjects ≤50 years old at recruitment. Associations of PM10 and NO2 exposure with IHD events were found only among women with HRs respectively of 2.24 (0.89-5.64, p-value: 0.086) and 1.54 (1.01-2.37, p-value: 0.046) associated with 10 μg/m(3) increase in the corresponding pollutant. In conclusion, the present study suggests that long-term exposure to traffic-related air pollution has an impact on CVD and IHD morbidity, particularly among women and younger subjects.
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http://dx.doi.org/10.1016/j.scitotenv.2014.05.058DOI Listing
August 2014

Additive interaction between continuous risk factors using logistic regression.

Epidemiology 2014 May;25(3):462-4

Hellenic Health Foundation, Athens, Greece, University of Athens, WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology, and Medical Statistics, Athens, Greece, University of Athens, WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology, and Medical Statistics, Athens, Greece.

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http://dx.doi.org/10.1097/EDE.0000000000000083DOI Listing
May 2014

Long-term exposure to air pollution and cardiovascular mortality: an analysis of 22 European cohorts.

Epidemiology 2014 May;25(3):368-78

From the aInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands; bDepartment of Epidemiology, Lazio Regional Health Service, Rome, Italy; cDanish Cancer Society Research Center, Copenhagen, Denmark; dCenter for Epidemiology and Screening, Department of Public Health, University of Copenhagen, CSS, København K, Denmark; eMRC-HPA Centre for Environment and Health, Department of Epidemiology and Biostatistics, Imperial College London, St Mary's Campus, London, United Kingdom; fUniversity College London, CeLSIUS, London, United Kingdom; gDepartment of Hygiene, Epidemiology, and Medical Statistics, Medical School, University of Athens, Athens, Greece; hJulius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands; iInstitute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany; jIUF-Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany, and Medical Faculty, University of Düsseldorf, Düsseldorf, Germany; kInstitute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; lNational Institute for Public Health and the Environment, Bilthoven, The Netherlands; mCentre for Research in Environmental Epidemiology (CREAL), Barcelona, and Parc de Recerca Biomèdica de Barcelona-PRBB (office 183.05) C. Doctor Aiguader, Barcelona, Spain; nConsortium for Biomedical Research in Epidemiology and Public Health (CIBER en Epidemiología y Salud Pública-CIBERESP), Melchor Fernández Almagro 3-5, Madrid, Spain; oDivision of Occupational and Environmental Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden; pNational Institute for Health and Welfare, Kuopio, Finland; qNorwegian Institute of Public Health, Oslo, Norway; rInstitute of Health and Society, University of Oslo, Oslo, Norway; sInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; tDepartm

Background: Air pollution has been associated with cardiovascular mortality, but it remains unclear as to whether specific pollutants are related to specific cardiovascular causes of death. Within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE), we investigated the associations of long-term exposure to several air pollutants with all cardiovascular disease (CVD) mortality, as well as with specific cardiovascular causes of death.

Methods: Data from 22 European cohort studies were used. Using a standardized protocol, study area-specific air pollution exposure at the residential address was characterized as annual average concentrations of the following: nitrogen oxides (NO2 and NOx); particles with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and 10 μm to 2.5 μm (PMcoarse); PM2.5 absorbance estimated by land-use regression models; and traffic indicators. We applied cohort-specific Cox proportional hazards models using a standardized protocol. Random-effects meta-analysis was used to obtain pooled effect estimates.

Results: The total study population consisted of 367,383 participants, with 9994 deaths from CVD (including 4,992 from ischemic heart disease, 2264 from myocardial infarction, and 2484 from cerebrovascular disease). All hazard ratios were approximately 1.0, except for particle mass and cerebrovascular disease mortality; for PM2.5, the hazard ratio was 1.21 (95% confidence interval = 0.87-1.69) per 5 μg/m and for PM10, 1.22 (0.91-1.63) per 10 μg/m.

Conclusion: In a joint analysis of data from 22 European cohorts, most hazard ratios for the association of air pollutants with mortality from overall CVD and with specific CVDs were approximately 1.0, with the exception of particulate mass and cerebrovascular disease mortality for which there was suggestive evidence for an association.
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http://dx.doi.org/10.1097/EDE.0000000000000076DOI Listing
May 2014

Long-term exposure to elemental constituents of particulate matter and cardiovascular mortality in 19 European cohorts: results from the ESCAPE and TRANSPHORM projects.

Environ Int 2014 May 18;66:97-106. Epub 2014 Feb 18.

Danish Cancer Society Research Center, Copenhagen, Denmark.

Background: Associations between long-term exposure to ambient particulate matter (PM) and cardiovascular (CVD) mortality have been widely recognized. However, health effects of long-term exposure to constituents of PM on total CVD mortality have been explored in a single study only.

Aims: The aim of this study was to examine the association of PM composition with cardiovascular mortality.

Methods: We used data from 19 European ongoing cohorts within the framework of the ESCAPE (European Study of Cohorts for Air Pollution Effects) and TRANSPHORM (Transport related Air Pollution and Health impacts--Integrated Methodologies for Assessing Particulate Matter) projects. Residential annual average exposure to elemental constituents within particle matter smaller than 2.5 and 10 μm (PM2.5 and PM10) was estimated using Land Use Regression models. Eight elements representing major sources were selected a priori (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc). Cohort-specific analyses were conducted using Cox proportional hazards models with a standardized protocol. Random-effects meta-analysis was used to calculate combined effect estimates.

Results: The total population consisted of 322,291 participants, with 9545 CVD deaths. We found no statistically significant associations between any of the elemental constituents in PM2.5 or PM10 and CVD mortality in the pooled analysis. Most of the hazard ratios (HRs) were close to unity, e.g. for PM10 Fe the combined HR was 0.96 (0.84-1.09). Elevated combined HRs were found for PM2.5 Si (1.17, 95% CI: 0.93-1.47), and S in PM2.5 (1.08, 95% CI: 0.95-1.22) and PM10 (1.09, 95% CI: 0.90-1.32).

Conclusion: In a joint analysis of 19 European cohorts, we found no statistically significant association between long-term exposure to 8 elemental constituents of particles and total cardiovascular mortality.
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http://dx.doi.org/10.1016/j.envint.2014.01.026DOI Listing
May 2014

Additive influence of genetic predisposition and conventional risk factors in the incidence of coronary heart disease: a population-based study in Greece.

BMJ Open 2014 Feb 5;4(2):e004387. Epub 2014 Feb 5.

Hellenic Health Foundation, Athens, Greece.

Objectives: An additive genetic risk score (GRS) for coronary heart disease (CHD) has previously been associated with incident CHD in the population-based Greek European Prospective Investigation into Cancer and nutrition (EPIC) cohort. In this study, we explore GRS-'environment' joint actions on CHD for several conventional cardiovascular risk factors (ConvRFs), including smoking, hypertension, type-2 diabetes mellitus (T2DM), body mass index (BMI), physical activity and adherence to the Mediterranean diet.

Design: A case-control study.

Setting: The general Greek population of the EPIC study.

Participants And Outcome Measures: 477 patients with medically confirmed incident CHD and 1271 controls participated in this study. We estimated the ORs for CHD by dividing participants at higher or lower GRS and, alternatively, at higher or lower ConvRF, and calculated the relative excess risk due to interaction (RERI) as a measure of deviation from additivity.

Results: The joint presence of higher GRS and higher risk ConvRF was in all instances associated with an increased risk of CHD, compared with the joint presence of lower GRS and lower risk ConvRF. The OR (95% CI) was 1.7 (1.2 to 2.4) for smoking, 2.7 (1.9 to 3.8) for hypertension, 4.1 (2.8 to 6.1) for T2DM, 1.9 (1.4 to 2.5) for lower physical activity, 2.0 (1.3 to 3.2) for high BMI and 1.5 (1.1 to 2.1) for poor adherence to the Mediterranean diet. In all instances, RERI values were fairly small and not statistically significant, suggesting that the GRS and the ConvRFs do not have effects beyond additivity.

Conclusions: Genetic predisposition to CHD, operationalised through a multilocus GRS, and ConvRFs have essentially additive effects on CHD risk.
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http://dx.doi.org/10.1136/bmjopen-2013-004387DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918976PMC
February 2014

Effects of long-term exposure to air pollution on natural-cause mortality: an analysis of 22 European cohorts within the multicentre ESCAPE project.

Lancet 2014 Mar 9;383(9919):785-95. Epub 2013 Dec 9.

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Background: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants.

Methods: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis.

Findings: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13).

Interpretation: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value.

Funding: European Community's Seventh Framework Program (FP7/2007-2011).
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http://dx.doi.org/10.1016/S0140-6736(13)62158-3DOI Listing
March 2014

Challenges in estimating the validity of dietary acrylamide measurements.

Eur J Nutr 2013 Aug 1;52(5):1503-12. Epub 2012 Nov 1.

International Agency for Research on Cancer IARC-WHO, Lyon, France.

Background: Acrylamide is a chemical compound present in tobacco smoke and food, classified as a probable human carcinogen and a known human neurotoxin. Acrylamide is formed in foods, typically carbohydrate-rich and protein-poor plant foods, during high-temperature cooking or other thermal processing. The objectives of this study were to compare dietary estimates of acrylamide from questionnaires (DQ) and 24-h recalls (R) with levels of acrylamide adduct (AA) in haemoglobin.

Methods: In the European Prospective Investigation into Cancer and Nutrition (EPIC) study, acrylamide exposure was assessed in 510 participants from 9 European countries, randomly selected and stratified by age, sex, with equal numbers of never and current smokers. After adjusting for country, alcohol intake, smoking status, number of cigarettes and energy intake, correlation coefficients between various acrylamide measurements were computed, both at the individual and at the aggregate (centre) level.

Results: Individual level correlation coefficient between DQ and R measurements (r DQ,R) was 0.17, while r DQ,AA and r R,AA were 0.08 and 0.06, respectively. In never smokers, r DQ,R, r DQ,AA and r R,AA were 0.19, 0.09 and 0.02, respectively. The correlation coefficients between means of DQ, R and AA measurements at the centre level were larger (r > 0.4).

Conclusions: These findings suggest that estimates of total acrylamide intake based on self-reported diet correlate weakly with biomarker AA Hb levels. Possible explanations are the lack of AA levels to capture dietary acrylamide due to individual differences in the absorption and metabolism of acrylamide, and/or measurement errors in acrylamide from self-reported dietary assessments, thus limiting the possibility to validate acrylamide DQ measurements.
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http://dx.doi.org/10.1007/s00394-012-0457-7DOI Listing
August 2013

Mediterranean diet and CHD: the Greek European Prospective Investigation into Cancer and Nutrition cohort.

Br J Nutr 2012 Aug;108(4):699-709

Department of Hygiene, Epidemiology and Medical Statistics, WHO Collaborating Center for Food and Nutrition Policies, University of Athens Medical School, Athens, Greece.

Adherence to the Mediterranean diet (MD) has been reported to improve CHD prognosis and to be inversely associated with CHD mortality. The aim of the present study was to investigate the association of adherence to the MD with CHD incidence and mortality in the Greek European Prospective Investigation into Cancer and Nutrition cohort, a population with traditional Mediterranean roots. In a general population sample of 23,929 adult men and women with no CVD or cancer at enrolment, a validated FFQ was interviewer-administered, sociodemographic, physical activity and other characteristics were recorded, and arterial blood pressure and anthropometric characteristics were measured. In a median period of 10 years, 636 incident CHD cases and 240 CHD deaths were recorded. Associations of adherence to the MD, operationalised through a nine-component score (0, poor; 9, excellent), with CHD incidence and mortality were evaluated through Cox regression controlling for potentially confounding variables. A two-point increase in the MD score was associated with lower CHD mortality by 25 % (95 % CI 0.57, 0.98) among women and 19 % (95 % CI 0.67, 0.99) among men. The association of adherence to the MD with CHD incidence was again inverse, but weaker (hazard ratios 0.85 (95 % CI 0.71, 1.02) among women and 0.98 (95 % CI 0.87, 1.10) among men). With respect to score components, only meat among men (positively) and fruits and nuts among women (inversely) were associated with both the incidence of and mortality from CHD. The MD, as an integral entity, is inversely associated with CHD incidence and, particularly, mortality.
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http://dx.doi.org/10.1017/S0007114512001821DOI Listing
August 2012

The root causes of socioeconomic differentials in cancer and cardiovascular mortality in Greece.

Eur J Cancer Prev 2012 Sep;21(5):490-6

WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Athens, Greece.

Lower socioeconomic groups experience higher rates of premature mortality in comparison with the upper socioeconomic groups. We have undertaken a study in Greece to assess socioeconomic differentials in overall, cancer, and cardiovascular (CVD) mortality and to identify their possible roots, using educational attainment to indicate socioeconomic status. Among participants in the general population, the Greek European Prospective Investigation into Cancer and Nutrition cohort, 23 697 individuals with no prevalent cancer or CVD disease at enrollment and with complete information on education and established or likely mortality risk factors, were followed up for an average of 9.6 years. Age-adjusted odds ratios of the prevalence of risk factors by education and sex were calculated through logistic regression and mortality ratios were estimated through Cox regression. With respect to overall and CVD mortality, the results indicated a 50% to more than 100% difference between the extreme categories of educational attainment. No gradient was, however, observed in cancer mortality. Obesity, poor diet, hypertension, and low physical activity were more prevalent among the least educated participants, but smoking was almost as common among the more and the less educated men and strikingly more common among the higher educated women. Likely intermediates did not explain more than one-third of the excess mortality among the less educated persons. In the Greek population, strong socioeconomic gradients were observed in the overall and CVD mortality, but not in cancer mortality. Established risk factors for premature mortality explained only a fraction of the observed gradients.
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http://dx.doi.org/10.1097/CEJ.0b013e32834ef1bcDOI Listing
September 2012