Sudam Surasinghe, Swathi Nachiar Manivannan, Samuel V. Scarpino, Lorin Crawford, C. Brandon Ogbunugafor
{"title":"结构性因果影响(SCI)可捕捉疾病动态模型中的社会不平等力量","authors":"Sudam Surasinghe, Swathi Nachiar Manivannan, Samuel V. Scarpino, Lorin Crawford, C. Brandon Ogbunugafor","doi":"arxiv-2409.09096","DOIUrl":null,"url":null,"abstract":"Mathematical modelling has served a central role in studying how infectious\ndisease transmission manifests at the population level. These models have\ndemonstrated the importance of population-level factors like social network\nheterogeneity on structuring epidemic risk and are now routinely used in public\nhealth for decision support. One barrier to broader utility of mathematical\nmodels is that the existing canon does not readily accommodate the social\ndeterminants of health as distinct, formal drivers of transmission dynamics.\nGiven the decades of empirical support for the organizational effect of social\ndeterminants on health burden more generally and infectious disease risk more\nspecially, addressing this modelling gap is of critical importance. In this\nstudy, we build on prior efforts to integrate social forces into mathematical\nepidemiology by introducing several new metrics, principally structural causal\ninfluence (SCI). Here, SCI leverages causal analysis to provide a measure of\nthe relative vulnerability of subgroups within a susceptible population, which\nare crafted by differences in healthcare, exposure to disease, and other\ndeterminants. We develop our metrics using a general case and apply it to\nspecific one of public health importance: Hepatitis C virus in a population of\npersons who inject drugs. Our use of the SCI reveals that, under specific\nparameters in a multi-community model, the \"less vulnerable\" community may\nsustain a basic reproduction number below one when isolated, ensuring disease\nextinction. However, even minimal transmission between less and more vulnerable\ncommunities can elevate this number, leading to sustained epidemics within both\ncommunities. Summarizing, we reflect on our findings in light of conversations\nsurrounding the importance of social inequalities and how their consideration\ncan influence the study and practice of mathematical epidemiology.","PeriodicalId":501266,"journal":{"name":"arXiv - QuanBio - Quantitative Methods","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Structural causal influence (SCI) captures the forces of social inequality in models of disease dynamics\",\"authors\":\"Sudam Surasinghe, Swathi Nachiar Manivannan, Samuel V. Scarpino, Lorin Crawford, C. Brandon Ogbunugafor\",\"doi\":\"arxiv-2409.09096\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Mathematical modelling has served a central role in studying how infectious\\ndisease transmission manifests at the population level. These models have\\ndemonstrated the importance of population-level factors like social network\\nheterogeneity on structuring epidemic risk and are now routinely used in public\\nhealth for decision support. One barrier to broader utility of mathematical\\nmodels is that the existing canon does not readily accommodate the social\\ndeterminants of health as distinct, formal drivers of transmission dynamics.\\nGiven the decades of empirical support for the organizational effect of social\\ndeterminants on health burden more generally and infectious disease risk more\\nspecially, addressing this modelling gap is of critical importance. In this\\nstudy, we build on prior efforts to integrate social forces into mathematical\\nepidemiology by introducing several new metrics, principally structural causal\\ninfluence (SCI). Here, SCI leverages causal analysis to provide a measure of\\nthe relative vulnerability of subgroups within a susceptible population, which\\nare crafted by differences in healthcare, exposure to disease, and other\\ndeterminants. We develop our metrics using a general case and apply it to\\nspecific one of public health importance: Hepatitis C virus in a population of\\npersons who inject drugs. Our use of the SCI reveals that, under specific\\nparameters in a multi-community model, the \\\"less vulnerable\\\" community may\\nsustain a basic reproduction number below one when isolated, ensuring disease\\nextinction. However, even minimal transmission between less and more vulnerable\\ncommunities can elevate this number, leading to sustained epidemics within both\\ncommunities. Summarizing, we reflect on our findings in light of conversations\\nsurrounding the importance of social inequalities and how their consideration\\ncan influence the study and practice of mathematical epidemiology.\",\"PeriodicalId\":501266,\"journal\":{\"name\":\"arXiv - QuanBio - Quantitative Methods\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-09-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"arXiv - QuanBio - Quantitative Methods\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/arxiv-2409.09096\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"arXiv - QuanBio - Quantitative Methods","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/arxiv-2409.09096","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Structural causal influence (SCI) captures the forces of social inequality in models of disease dynamics
Mathematical modelling has served a central role in studying how infectious
disease transmission manifests at the population level. These models have
demonstrated the importance of population-level factors like social network
heterogeneity on structuring epidemic risk and are now routinely used in public
health for decision support. One barrier to broader utility of mathematical
models is that the existing canon does not readily accommodate the social
determinants of health as distinct, formal drivers of transmission dynamics.
Given the decades of empirical support for the organizational effect of social
determinants on health burden more generally and infectious disease risk more
specially, addressing this modelling gap is of critical importance. In this
study, we build on prior efforts to integrate social forces into mathematical
epidemiology by introducing several new metrics, principally structural causal
influence (SCI). Here, SCI leverages causal analysis to provide a measure of
the relative vulnerability of subgroups within a susceptible population, which
are crafted by differences in healthcare, exposure to disease, and other
determinants. We develop our metrics using a general case and apply it to
specific one of public health importance: Hepatitis C virus in a population of
persons who inject drugs. Our use of the SCI reveals that, under specific
parameters in a multi-community model, the "less vulnerable" community may
sustain a basic reproduction number below one when isolated, ensuring disease
extinction. However, even minimal transmission between less and more vulnerable
communities can elevate this number, leading to sustained epidemics within both
communities. Summarizing, we reflect on our findings in light of conversations
surrounding the importance of social inequalities and how their consideration
can influence the study and practice of mathematical epidemiology.