Publications
1358 results found
Vineis P, Avendano-Pabon M, Barros H, et al., 2020, Special report: the biology of inequalities in health: the lifepath consortium, Frontiers in Public Health, Vol: 8, Pages: 1-37, ISSN: 2296-2565
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.
Martens DS, Janssen BG, Bijnens EM, et al., 2020, Association of Parental Socioeconomic Status and Newborn Telomere Length, JAMA NETWORK OPEN, Vol: 3, ISSN: 2574-3805
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- Citations: 28
Cox B, Luyten LJ, Dockx Y, et al., 2020, Association between maternal prepregnancy body mass index and anthropometric parameters, blood pressure, and retinal microvasculature in children age 4 to 6 years., JAMA Network Open, Vol: 3, Pages: 1-12, ISSN: 2574-3805
Importance: Maternal prepregnancy body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) has previously been associated with offspring cardiometabolic risk factors, such as fat mass, glucose and insulin levels, and blood pressure, but these associations appear to be largely mediated by offspring BMI. To our knowledge, no studies have assessed alterations in the retinal microvasculature in association with maternal prepregnancy BMI. Objective: To investigate the association between maternal prepregnancy BMI and anthropometric parameters, blood pressure, and retinal vessel parameters in children age 4 to 6 years. Design, Setting, and Participants: Participants included mother-child pairs of the population-based Environmental Influence on Early Aging (ENVIRONAGE) birth cohort study (Flanders, Belgium) who were recruited at birth from February 2010 to June 2014 and followed-up at age 4 to 6 years between October 2014 and July 2018. Data were analyzed from February 2019 to April 2019. Exposures: Maternal prepregnancy BMI based on height and weight measurements at the first antenatal visit (weeks 7-9 of gestation). Main Outcomes and Measures: Children's anthropometric, blood pressure, and retinal microcirculation measurements at age 4 to 6 years. Retinal vessel diameters and the tortuosity index, a measure for the curvature of the retinal vasculature, were obtained by fundus image analysis. Results: This study included 240 mothers and children with a mean (SD) age of 29. 9 (4.2) years and 54.8 (4.7) months, respectively. Of these, 114 children (47.5%) were boys. Maternal prepregnancy BMI was positively associated with the child's birth weight, BMI, waist circumference, blood pressure, and retinal vessel tortuosity. A 1-point increase in maternal prepregnancy BMI was associated with a 0.26-mm Hg (95% CI, 0.08-0.44) higher mean arterial pressure for their children, with similar estimates for systolic and diastolic blood pressure.
VINEIS P, 2020, Forum: COVID-19 - The immune capital, Quaderni Storici, Vol: 55, Pages: 259-269, ISSN: 0301-6307
van Nunen E, Vermeulen R, Tsai M-Y, et al., 2020, Associations between modeled residential outdoor and measured personal exposure to ultrafine particles in four European study areas, Atmospheric Environment, Vol: 226, ISSN: 1352-2310
Land use regression (LUR) models for Ultrafine Particles (UFP) have been developed to assess health effects of long-term average UFP exposure in epidemiological studies. Associations between LUR modeled residential outdoor and measured long-term personal exposure to UFP have never been evaluated, adding uncertainty in interpretation of epidemiological studies of UFP. Our aim was to assess how predictions of recently developed LUR models for UFP compared to measured average personal UFP exposure in four European areas.Personal UFP exposure was measured in 154 adults from Basel (Switzerland), Amsterdam and Utrecht (the Netherlands), Norwich (United Kingdom), and Turin (Italy). Subjects performed three 24-h exposure measurements by carrying a real-time monitor measuring particles between 10 and 300 nm (MiniDisc). Subjects reported whereabouts and indoor sources of UFP in questionnaires. In Basel and the Netherlands contemporaneously residential outdoor UFP concentrations were monitored. Area-specific LUR models were applied to model residential outdoor UFP concentrations. Associations between modeled and measured UFP concentrations were assessed with linear regression.LUR model predictions were significantly associated with median but not mean personal UFP exposures, likely because of the high impact of indoor peaks on mean personal exposures. Regression slopes (±se) combined for the four areas were 0.12 ± 0.04 for median and −0.06 ± 0.17 for mean personal exposure. The LUR model explained variance of the median personal exposure less than variance of residential outdoor measurements. Associations did not change when personal exposure was calculated for the time spent at home or when presence of indoor sources was incorporated in the regression models. Regression slopes for measured residential outdoor versus personal exposure were smaller for UFP (0.16 ± 0.04) than for simultaneously measured PM2.5 and soot (0.32 ± 0.10 and 0.4
Laine J, Baltar VT, Stringini S, et al., 2020, Reducing socioeconomic inequalities in all-cause mortality: a counterfactual mediation approach, International Journal of Epidemiology, Vol: 49, Pages: 497-510, ISSN: 0300-5771
Background: Socioeconomicinequalities inmortality arewell 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 underlyingsocioeconomicassociated-mortality and quantifiedthe potentialimpact of reducing early all-cause mortality by hypothetically altering socioeconomic risk factors. Methods: Data were fromsevencohort studies participating in the LIFEPATH consortium (total n=179,090). Using bothsocioeconomic position (SEP) (based on occupation) and education, we estimated thenaturaldirect effect on all-cause mortality, and thenatural indirect effect via the joint mediatingrole of smoking, alcohol intake, dietary patterns, physical activity, body mass index,hypertension, diabetes, and coronary artery disease.Hazard ratios(HR)were estimated, using counterfactual natural effect modelsunder different hypothetical actions of either lower or higher SEP or education. Results: Lower SEP and educationwereassociated with anincreaseinall-cause mortalitywithin an average follow up time of 17.5 years.Mortality wasreducedviamodelled hypothetical actions of increasing SEP oreducation. Through higher educationtheHR was0.85(95% confidence interval (CI) 0.84, 0.86) for women and 0.71(95% CI 0.70, 0.74)for men,compared to lower education. In addition, 34% and 38% of the effect was jointlymediatedfor womenand men, respectively. The benefits from alteringSEP were slightly more modest.Conclusions: Theseobservational findings supportpoliciesto reducemortalityboththrough improving socioeconomic circumstances and increasing education,andby altering intermediaries, such as lifestyle behaviours and morbidities.
Vineis P, 2020, THE IMMUNE CAPITAL, QUADERNI STORICI, Vol: 55, Pages: 259-269, ISSN: 0301-6307
Laine JE, Baltar VT, Stringhini S, et al., 2020, Reducing socio-economic inequalities in all-cause mortality: a counterfactual mediation approach (vol 49, pg 497, 2020), INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, Vol: 49, Pages: 707-707, ISSN: 0300-5771
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- Citations: 4
Merid SK, Novoloaca A, Sharp GC, et al., 2020, Epigenome-wide meta-analysis of blood DNA methylation in newborns and children identifies numerous loci related to gestational age, Genome Medicine: medicine in the post-genomic era, Vol: 12, Pages: 1-17, ISSN: 1756-994X
BackgroundPreterm 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.MethodsWe 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.ResultsWe 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.ConclusionsWe 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 a
Vineis P, Demetriou CA, Probst-Hensch N, 2020, Long-term effects of air pollution: an exposome meet-in-the-middle approach, International Journal of Public Health, Vol: 65, Pages: 125-127, ISSN: 0303-8408
McCrory C, Fiorito G, McLoughlin S, et al., 2020, Epigenetic Clocks and Allostatic Load Reveal Potential Sex-Specific Drivers of Biological Aging, JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES, Vol: 75, Pages: 495-503, ISSN: 1079-5006
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- Citations: 29
Tarallo S, Ferrero G, Gallo G, et al., 2020, Altered Fecal Small RNA Profiles in Colorectal Cancer Reflect Gut Microbiome Composition in Stool Samples (vol 4, e00289-19, 2019), MSYSTEMS, Vol: 5, ISSN: 2379-5077
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- Citations: 2
Parodi S, Seniori Costantini A, Crosignani P, et al., 2020, Childhood infectious diseases and risk of non‐Hodgkin's lymphoma according to the WHO classification: A reanalysis of the Italian multicenter case–control study, International Journal of Cancer, Vol: 146, Pages: 977-986, ISSN: 0020-7136
Since 1960, incidence of non-Hodgkin's lymphoma (NHL) has been increasing in most industrialized countries, but causes of this trend remain unclear. A role of the decreased exposure to infectious agents during childhood has been proposed. Our study evaluates the association between common childhood infectious diseases and the risk of NHL and its major subtypes by a reanalysis of the Italian multicenter case-control study. After exclusion of next-of-kin interviews, 1,193 cases, diagnosed between 1990 and 1993, and 1,708 population-based controls were included in the analyses. OR estimates were obtained by logistic regression, adjusting for gender, age, residence area, education, smoking habit and exposure to radiations, pesticides and aromatic hydrocarbons. Among B-cell lymphomas (n = 1,102) an inverse association was observed for rubella (OR = 0.80, 95% CI: 0.65-0.99), pertussis (OR = 0.74, 95% CI: 0.62-0.88) and any infection (OR = 0.75, 95% CI: 0.61-0.93). A negative trend by number of infections was observed, which was more evident among mature B-cell lymphoma (OR = 0.66 for three infections or more, 95% CI: 0.48-0.90). Our results indicate a potential protective role of common childhood infections in the etiology of B-cell NHL.
Vineis P, Delpierre C, Castagne R, et al., 2020, Health inequalities: Embodied evidence across biological layers, Social Science and Medicine, Vol: 246, Pages: 1-7, ISSN: 0277-9536
RationaleSocioeconomic disparities have been documented in major non-communicable diseases and in their risk factors, such as obesity, hypertension, diabetes, smoking, physical inactivity, unhealthful diet and heavy drinking. However, a key research question has remained unanswered: is there a separate biological embodiment of socio-economic conditions underlying health disparities, additional and independent of those risk factors? As lifelong socioeconomic circumstances cannot be randomised, one way forward is the examination of different biological layers of evidence, including molecular changes.MethodIn this methodological paper we report the association of socio-economic disadvantage with (a) long-term health outcomes, before and after taking risk factors into account; (b) biological intermediaries that increase susceptibility to disease, such as childhood obesity; (c) intermediate circulating biomarkers and omic measurements (transcriptomics, DNA methylation, inflammatory proteins, allostatic load); and (d) immunity. In our Lifepath consortium, these analyses have been performed in several cohort studies, countries and contexts, and at different stages of the life course in up to 1.7 million subjects. The main goal is to test the assumption that each layer (death, functional outcomes, DNA, RNA, proteins, infections) is characterized by different types of bias and confounding, and that consistency across layers reinforces causality assessment.ResultsThe findings show consistent associations of social disparities with unfavourable health outcomes spanning inflammatory biomarkers, DNA or RNA-based markers, infection, indicators of physical functioning and mortality. Although each of these associations has a different set of confounders, a dose-response relationship is nevertheless consistently observed, thus showing the power of our multi-layered approach.ConclusionsThis new evidence supports biological embodiment of social disadvantage, in addition to the impact
Vaccarella S, Weiderpass E, Vineis P, 2020, Present and future of health inequalities: Rationale for investing in the <i>biological capital</i>, ECLINICALMEDICINE, Vol: 19
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- Citations: 2
Heath A, Muller D, van den Brandt P, et al., 2020, Nutrient-wide association study of 92 foods and nutrients and breast cancer risk, Breast Cancer Research, Vol: 22, ISSN: 1465-542X
Background: Several dietary factors have been reported to be associated with risk of breast cancer, but to date unequivocal evidence only exists for alcohol consumption. We sought to systematically assess the association between intake of 92 foods and nutrients and breast cancer risk using a nutrient-wide association study. Methods: Using data from 272,098 women participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, we assessed dietary intake of 92 foods and nutrients estimated by dietary questionnaires. Cox regression was used to quantify the association between each food/nutrient and risk of breast cancer. A false discovery rate (FDR) of 0.05 was used to select the set of foods and nutrients to be replicated in the independent Netherlands Cohort Study (NLCS). Results: Six foods and nutrients were identified as associated with risk of breast cancer in the EPIC study (10,979 cases). Higher intake of alcohol overall was associated with a higher risk of breast cancer (hazard ratio (HR) for a 1 SD increment in intake = 1.05, 95% CI 1.03–1.07), as was beer/cider intake and wine intake (HRs per 1 SD increment = 1.05, 95% CI 1.03–1.06 and 1.04, 95% CI 1.02–1.06, respectively), whereas higher intakes of fibre, apple/pear, and carbohydrates were associated with a lower risk of breast cancer (HRs per 1 SD increment = 0.96, 95% CI 0.94–0.98; 0.96, 95% CI 0.94–0.99; and 0.96, 95% CI 0.95–0.98, respectively). When evaluated in the NLCS (2368 cases), estimates for each of these foods and nutrients were similar in magnitude and direction, with the exception of beer/cider intake, which was not associated with risk in the NLCS Conclusions: Our findings confirm a positive association of alcohol consumption andsuggest an inverse association of dietary fibre and possibly fruit intake with breast cancer risk.
Freisling H, Viallon V, Lennon H, et al., 2020, Lifestyle factors and risk of multimorbidity of cancer and cardiometabolic diseases: a multinational cohort study, BMC Medicine, Vol: 18, Pages: 5-5, ISSN: 1741-7015
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
Kachuri L, Johansson M, Rashkin SR, et al., 2020, Immune-mediated genetic pathways resulting in pulmonary function impairment increase lung cancer susceptibility, Nature Communications, Vol: 11, ISSN: 2041-1723
Impaired lung function is often caused by cigarette smoking, making it challenging to disentangle its role in lung cancer susceptibility. Investigation of the shared genetic basis of these phenotypes in the UK Biobank and International Lung Cancer Consortium (29,266 cases, 56,450 controls) shows that lung cancer is genetically correlated with reduced forced expiratory volume in one second (FEV1: rg = 0.098, p = 2.3 × 10-8) and the ratio of FEV1 to forced vital capacity (FEV1/FVC: rg = 0.137, p = 2.0 × 10-12). Mendelian randomization analyses demonstrate that reduced FEV1 increases squamous cell carcinoma risk (odds ratio (OR) = 1.51, 95% confidence intervals: 1.21-1.88), while reduced FEV1/FVC increases the risk of adenocarcinoma (OR = 1.17, 1.01-1.35) and lung cancer in never smokers (OR = 1.56, 1.05-2.30). These findings support a causal role of pulmonary impairment in lung cancer etiology. Integrative analyses reveal that pulmonary function instruments, including 73 novel variants, influence lung tissue gene expression and implicate immune-related pathways in mediating the observed effects on lung carcinogenesis.
Ponzi E, Vineis P, Chung K, et al., 2020, Accounting for measurement error to assess the effect of air pollution on omics signals, PLoS One, Vol: 15, Pages: 1-16, ISSN: 1932-6203
Studies on the effects of air pollution and more generally environmental exposures onhealth require measurements of pollutants, which are affected by measurement error.This is a cause of bias in the estimation of parameters relevant to the study and canlead to inaccurate conclusions when evaluating associations among pollutants, diseaserisk and biomarkers. Although the presence of measurement error in such studies hasbeen recognized as a potential problem, it is rarely considered in applications andpractical solutions are still lacking. In this work, we formulate Bayesian measurementerror models and apply them to study the link between air pollution and omic signals.The data we use stem from the “Oxford Street II Study”, a randomized crossover trialin which 60 volunteers walked for two hours in a traffic-free area (Hyde Park) and in abusy shopping street (Oxford Street) of London. Metabolomic measurements were madein each individual as well as air pollution measurements, in order to investigate theassociation between short-term exposure to traffic related air pollution and perturbationof metabolic pathways. We implemented error-corrected models in a classical frameworkand used the flexibility of Bayesian hierarchical models to account for dependenciesamong omic signals, as well as among different pollutants. Models were implementedusing traditional Markov Chain Monte Carlo (MCMC) simulative methods as well asintegrated Laplace approximation. The inclusion of a classical measurement error termresulted in variable estimates of the association between omic signals and traffic relatedair pollution measurements, where the direction of the bias was not predictable a priori.The models were successful in including and accounting for different correlationstructures, both among omic signals and among different pollutant exposures. Ingeneral, more associations were identified when the correlation among omics and amongpollutants were modeled, and their number
Carmeli C, Steen J, Petrovic D, et al., 2020, Mechanisms of life-course socioeconomic inequalities in adult systemic inflammation: Findings from two cohort studies, Social Science and Medicine, Vol: 245, ISSN: 0277-9536
Disadvantaged socioeconomic conditions in childhood heighten systemic inflammatory levels in adulthood; however, life-course mechanisms underlying this association are largely unknown. In the present observational study, we investigated the roles of adulthood socioeconomic and lifestyle factors in mediating this association. Participants were from two prospective Swiss population-based cohorts (N = 5,152, mean age 60 years). We estimated the total effect of paternal occupational position on adult heightened systemic inflammatory levels (C-reactive protein>3 mg/L), and the indirect effects via adulthood socioeconomic positions (SEPs: education and occupational position), financial hardship, and lifestyle factors (body mass index, smoking status, physical inactivity, and alcohol consumption). We estimated odds ratio (OR) and proportion mediated using counterfactual-based mediation models. Individuals whose father had a low occupational position had an OR of 1.51 [95% confidence interval (CI): 1.25, 1.84] for heightened inflammation compared to their more advantaged counterparts. This was jointly mediated (33 [95% CI: 14, 69]%) by adulthood SEPs, whereby the pathway through education followed by occupational position mediated 30 [95% CI: 11, 64]%, while the pathway via occupational position only mediated 3 [95% CI: 4, 13]%. Individuals with the lowest life-course SEPs had an OR of 2.27 [95% CI: 1.71, 2.98] for heightened inflammation compared to having the highest life-course SEPs. This was jointly mediated (63 [95% CI: 44, 97]%) by financial hardship and lifestyle factors. Our study supports a cumulative effect of life-course SEPs on adult heightened systemic inflammation along the pathway paternal occupational position -> education -> adult occupational position. Financial hardship and lifestyle factors in adulthood mediate half of that effect.
Vineis P, Bisceglia L, Forastiere F, et al., 2020, Covid-19: how to get prepared for Autumn, EPIDEMIOLOGIA & PREVENZIONE, Vol: 44, Pages: 202-204, ISSN: 1120-9763
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- Citations: 2
Forastiere F, Micheli A, Salmaso S, et al., 2020, Epidemiology and Covid-19 in Italy. Accessing and sharing data to foster collaboration, EPIDEMIOLOGIA & PREVENZIONE, Vol: 44, Pages: 112-113, ISSN: 1120-9763
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Demetriou C, Vineis P, 2020, Biomarkers and omics of health effects associated with traffic-related air pollution, Traffic-Related Air Pollution, Pages: 281-309, ISBN: 9780128181225
Environmental causes feature among the top global health risks, and several prospective studies demonstrate generally consistent results, indicating that long-term exposure to air pollution is associated with lung cancer incidence and mortality. Biomarkers can enhance research on the health effects of air pollution by improving exposure assessment, increasing the understanding of mechanisms, and enabling the investigation of individual susceptibility. The development of high-resolution and high-throughput technologies interrogating -omics has yielded an unprecedented perspective in air pollution science and it can be used to interrogate the exposome, which comprises biologically active chemicals in response to external environmental stimuli and the internal chemical environment. Thus, the exposome approach to air pollution looks like a promising avenue to make sense of the multitude of signals emerging from -omic investigations and to strengthen causal inferences on the health effects of air pollution.
Demetriou CA, Kakkoura MG, Hadjisavvas A, et al., 2020, The Mediterranean diet and breast cancer risk, The Mediterranean Diet: An Evidence-Based Approach, Pages: 381-391, ISBN: 9780128186497
There is ample evidence that the Mediterranean diet reduces breast cancer risk, despite the fact that evidence across studies and populations has not been consistent. The protective effect of the Mediterranean diet is in line with the fact that some of its key components, such as fruit, vegetables, folate, and olive oil, have also been shown to have beneficial effects with regard to breast carcinogenesis.
Evlampidou I, Font-Ribera L, Rojas-Rueda D, et al., 2020, Trihalomethanes in Drinking Water and Bladder Cancer Burden in the European Union, ENVIRONMENTAL HEALTH PERSPECTIVES, Vol: 128, ISSN: 0091-6765
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- Citations: 71
Preston GW, Dagnino S, Ponzi E, et al., 2020, Relationships between airborne pollutants, serum albumin adducts and short-term health outcomes in an experimental crossover study, Chemosphere, Vol: 239, ISSN: 1879-1298
Exposure to air pollution can have both short-term and long-term effects on health. However, the relationships between specific pollutants and their effects can be obscured by characteristics of both the pollution and the exposed population. One way of elucidating the relationships is to link exposures and internal changes at the level of the individual. To this end, we combined personal exposure monitoring (59 individuals, Oxford Street II crossover study) with mass-spectrometry-based analyses of putative serum albumin adducts (fixed-step selected reaction monitoring). We attempted to infer adducts' identities using data from another, higher-resolution mass spectrometry method, and were able to detect a semi-synthetic standard with both methods. A generalised least squares regression method was used to test for associations between amounts of adducts and pollution measures (ambient concentrations of nitrogen dioxide and particulate matter), and between amounts of adducts and short-term health outcomes (measures of lung health and arterial stiffness). Amounts of some putative adducts (e.g., one with a positive mass shift of approximately 143Da) were associated with exposure to pollution (11 associations), and amounts of other adducts were associated with health outcomes (eight associations). Adducts did not appear to provide a link between exposures and short-term health outcomes.
Grigoryan H, Schiffman C, Gunter MJ, et al., 2019, Cys34 Adductomics Links Colorectal Cancer with the Gut Microbiota and Redox Biology, CANCER RESEARCH, Vol: 79, Pages: 6024-6031, ISSN: 0008-5472
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- Citations: 19
Ursin G, Malila N, Chang-Claude J, et al., 2019, Sharing data safely while preserving privacy, LANCET, Vol: 394, Pages: 1902-1902, ISSN: 0140-6736
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- Citations: 5
Ursin G, Stenbeck M, Chang-Claude J, et al., 2019, Data must be shared-also with researchers outside of Europe, LANCET, Vol: 394, Pages: 1902-1903, ISSN: 0140-6736
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- Citations: 7
Ghesquieres H, Drouet Y, Zala M, et al., 2019, Individualized Prediction of Follicular Lymphoma Risk Using a Combination of Blood t(14;18) Frequency Years before Diagnosis and a Polygenic Risk Score (PRS) of 9 SNPs Associated with Follicular Lymphoma Susceptibility, 61st Annual Meeting and Exposition of the American-Society-of-Hematology (ASH), Publisher: AMER SOC HEMATOLOGY, ISSN: 0006-4971
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