Tsunami risk communication and management: Contemporary gaps and challenges

Very large tsunamis are associated with low probabilities of occurrence. In many parts of the world, these events have usually occurred in a distant time in the past. As a result, there is low risk perception and a lack of collective memories, making tsunami risk communication both challenging and complex. Furthermore, immense challenges lie ahead as population and risk exposure continue to increase in coastal areas. Through the last decades, tsunamis have caught coastal populations off-guard, providing evidence of lack of preparedness. Recent tsunamis, such as the Indian Ocean Tsunami in 2004, 2011 Tohoku and 2018 Palu, have shaped the way tsunami risk is perceived and acted upon. Based on lessons learned from a selection of past tsunami events, this paper aims to review the existing body of knowledge and the current challenges in tsunami risk communication, and to identify the gaps in the tsunami risk management methodologies. The important lessons provided by the past events call for strengthening community resilience and improvement in risk-informed actions and policy measures. This paper shows that research efforts related to tsunami risk communication remain fragmented. The analysis of tsunami risk together with a thorough understanding of risk communication gaps and challenges is indispensable towards developing and deploying comprehensive disaster risk reduction measures. Moving from a broad and interdisciplinary perspective, the paper suggests that probabilistic hazard and risk assessments could potentially contribute towards better science communication and improved planning and implementation of risk mitigation measures

Genomic and phenotypic insights from an atlas of genetic effects on DNA methylation

Characterizing genetic influences on DNA methylation (DNAm) provides an opportunity to understand mechanisms underpinning gene regulation and disease. In the present study, we describe results of DNAm quantitative trait locus (mQTL) analyses on 32,851 participants, identifying genetic variants associated with DNAm at 420,509 DNAm sites in blood. We present a database of >270,000 independent mQTLs, of which 8.5% comprise long-range (trans) associations. Identified mQTL associations explain 15–17% of the additive genetic variance of DNAm. We show that the genetic architecture of DNAm levels is highly polygenic. Using shared genetic control between distal DNAm sites, we constructed networks, identifying 405 discrete genomic communities enriched for genomic annotations and complex traits. Shared genetic variants are associated with both DNAm levels and complex diseases, but only in a minority of cases do these associations reflect causal relationships from DNAm to trait or vice versa, indicating a more complex genotype–phenotype map than previously anticipated

Tsunami risk communication and management: Contemporary gaps and challenges

Supplementary data: The following is the Supplementary data to this article: Acrobat PDF file (2MB) available at: https://ars.els-cdn.com/content/image/1-s2.0-S2212420921007329-mmc1.pdfCopyright © 2022 The Authors. Very large tsunamis are associated with low probabilities of occurrence. In many parts of the world, these events have usually occurred in a distant time in the past. As a result, there is low risk perception and a lack of collective memories, making tsunami risk communication both challenging and complex. Furthermore, immense challenges lie ahead as population and risk exposure continue to increase in coastal areas. Through the last decades, tsunamis have caught coastal populations off-guard, providing evidence of lack of preparedness. Recent tsunamis, such as the Indian Ocean Tsunami in 2004, 2011 Tohoku and 2018 Palu, have shaped the way tsunami risk is perceived and acted upon. Based on lessons learned from a selection of past tsunami events, this paper aims to review the existing body of knowledge and the current challenges in tsunami risk communication, and to identify the gaps in the tsunami risk management methodologies. The important lessons provided by the past events call for strengthening community resilience and improvement in risk-informed actions and policy measures. This paper shows that research efforts related to tsunami risk communication remain fragmented. The analysis of tsunami risk together with a thorough understanding of risk communication gaps and challenges is indispensable towards developing and deploying comprehensive disaster risk reduction measures. Moving from a broad and interdisciplinary perspective, the paper suggests that probabilistic hazard and risk assessments could potentially contribute towards better science communication and improved planning and implementation of risk mitigation measures.COST (European Cooperation in Science and Technology); Royal Society, UK (grant number CHL\R1\180173); Severo Ochoa Centers of Excellence Program (CEX 2018-000797-S) funded by MCIN/ AEI /10.13039/501100011033; Lloyd's Tercentenary Research Foundation, the Lighthill Risk Network, and the Lloyd's Register Foundation-Data Centric Engineering Programme of the Alan Turing Institute

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

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

Associations of autozygosity with a broad range of human phenotypes

In many species, the offspring of related parents suffer reduced reproductive success, a phenomenon known as inbreeding depression. In humans, the importance of this effect has remained unclear, partly because reproduction between close relatives is both rare and frequently associated with confounding social factors. Here, using genomic inbreeding coefficients (F-ROH) for >1.4 million individuals, we show that F-ROH is significantly associated (p <0.0005) with apparently deleterious changes in 32 out of 100 traits analysed. These changes are associated with runs of homozygosity (ROH), but not with common variant homozygosity, suggesting that genetic variants associated with inbreeding depression are predominantly rare. The effect on fertility is striking: F-ROH equivalent to the offspring of first cousins is associated with a 55% decrease [95% CI 44-66%] in the odds of having children. Finally, the effects of F-ROH are confirmed within full-sibling pairs, where the variation in F-ROH is independent of all environmental confounding.Peer reviewe

Association of maternal prenatal smoking GFI1-locus and cardio-metabolic phenotypes in 18,212 adults

BackgroundDNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring's adult cardio-metabolic health.MethodsWe meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n = 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult smoking. DNA methylation levels were analysed in relation to body mass index (BMI), waist circumference (WC), fasting glucose (FG), high-density lipoprotein cholesterol (HDL—C), triglycerides (TG), diastolic, and systolic blood pressure (BP).FindingsLower DNA methylation at three out of eight GFI1-CpGs was associated with exposure to maternal prenatal smoking, whereas, all eight CpGs were associated with adult own smoking. Lower DNA methylation at cg14179389, the strongest maternal prenatal smoking locus, was associated with increased WC and BP when adjusted for sex, age, and adult smoking with Bonferroni-corrected P InterpretationEpigenetic changes at the GFI1 were linked to smoking exposure in-utero/in-adulthood and robustly associated with cardio-metabolic risk factors.</p

Association of maternal prenatal smoking GFI1-locus and cardiometabolic phenotypes in 18,212 adults

Background: DNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring's adult cardio-metabolic health. Methods: We meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n= 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult smoking. DNA methylation levels were analysed in relation to body mass index (BMI), waist circumference (WC), fasting glucose (FG), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), diastolic, and systolic blood pressure (BP). Findings: Lower DNA methylation at three out of eight GFI1-CpGs was associated with exposure to maternal prenatal smoking, whereas, all eight CpGs were associated with adult own smoking. Lower DNA methylation at cg14179389, the strongest maternal prenatal smoking locus, was associated with increased WC and BP when adjusted for sex, age, and adult smoking with Bonferroni-corrected P &lt; 0.012. In contrast, lower DNA methylation at cg09935388, the strongest adult own smoking locus, was associated with decreased BMI, WC, and BP (adjusted 1 x 10(-7) &lt; P &lt; 0.01). Similarly, lower DNA methylation at cg12876356, cg18316974, cg09662411, and cg18146737 was associated with decreased BMI and WC (5 x 10(-8) &lt; P &lt; 0.001). Lower DNA methylation at all the CpGs was consistently associated with higher TG levels. Interpretation: Epigenetic changes at the GFI1 were linked to smoking exposure in-utero/in-adulthood and robustly associated with cardio-metabolic risk factors. Fund: European Union's Horizon 2020 research and innovation programme under grant agreement no. 633595 DynaHEALTH

Genomic and phenotypic insights from an atlas of genetic effects on DNA methylation

DNA methylation quantitative trait locus (mQTL) analyses on 32,851 participants identify genetic variants associated with DNA methylation at 420,509 sites in blood, resulting in a database of >270,000 independent mQTLs.Characterizing genetic influences on DNA methylation (DNAm) provides an opportunity to understand mechanisms underpinning gene regulation and disease. In the present study, we describe results of DNAm quantitative trait locus (mQTL) analyses on 32,851 participants, identifying genetic variants associated with DNAm at 420,509 DNAm sites in blood. We present a database of >270,000 independent mQTLs, of which 8.5% comprise long-range (trans) associations. Identified mQTL associations explain 15-17% of the additive genetic variance of DNAm. We show that the genetic architecture of DNAm levels is highly polygenic. Using shared genetic control between distal DNAm sites, we constructed networks, identifying 405 discrete genomic communities enriched for genomic annotations and complex traits. Shared genetic variants are associated with both DNAm levels and complex diseases, but only in a minority of cases do these associations reflect causal relationships from DNAm to trait or vice versa, indicating a more complex genotype-phenotype map than previously anticipated.Molecular Epidemiolog

Epidemiological Surveillance of Informal Workers' Health in Two Cities in Southeastern Brazil The Experience of the TRAPP-TRAPPURA Projects

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Informal labor markets have grown in peripheral countries, accounting for more than 50% of jobs. There is anecdotal evidence of a direct relation between informal sector growth and an increase in the frequency and severity of work-related diseases and injuries. Two sister Pilot Projects were conducted in Uberaba and Campinas, Brazil to develop population-based epidemiological Surveillance of workplace injuries in the informal sector. Results for Campinas and Uberaba found cumulative yearly incidences of 5.1% and 10.4%, with incidence rates of 2.2 and 6.5 injuries per 100,000 worked hours, respectively The proportions of lost work time were 0.3% and 0.31%. Rates found were comparable to those found in the literature for both formal and inforinaljobs. These results Suggest that bad working conditions in the formal labor market are replicated in the informal market as Subcontracting and outsourcing contribute to the growth of informal jobs.1613643Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Brazilian Ministry of Health/National Health [2762/03]John E. Fogarty International Center of the National Institutes of Health [D43TW005749]Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)FAPESP [2006/00970-6]Brazilian Ministry of Health/National Health [2762/03]John E. Fogarty International Center of the National Institutes of Health [D43TW005749