Current philosophical accounts of causation suggest that the same causal assertion can have different meanings. Yet, in actual social-scientific practice, the possible meanings of some causal generalisations intended to support policy prescriptions are not always spelled out. In line with a standard referentialist approach to semantics, we propose and elaborate on four questions to systematically elucidate the meaning of causal generalisations. The analysis can be useful to a host of agents, including social scientists, policy-makers, and philosophers aiming at being socially (...) relevant. To illustrate our proposal, we analyse the complexities related to the meaning of causal generalisations in the context of a concrete case of economic research which is explicitly intended to guide public policy, namely, the OECD research on the causes of unemployment. (shrink)

Part of Allen et al.’s criticism of Hamilton’s rule makes sense only if we are interested in social adaptation rather than merely social selection. Under the assumption that we are interested in casually modeling social adaptation, I illustrate how graphical causal models of social adaptation can be useful for predicting evolution by adaptation. I then argue for two consequences of this approach given some of the recent philosophical literature. I argue Birch’s claim that the proper way to understand Hamilton’s rule (...) is as providing an organizational framework for causal models is incorrect. I provide an account of a causally adequate decomposition of evolutionary change due to social adaptation and show that my account is superior to Okasha’s. (shrink)

Indicative conditionals and tendency causal claims are closely related (e.g., Frosch and Byrne, 2012), but despite these connections, they are usually studied separately. A unifying framework could consist in their dependence on probabilistic factors such as high conditional probability and statistical relevance (e.g., Adams, 1975; Eells, 1991; Douven, 2008, 2015). This paper presents a comparative empirical study on differences between judgments on tendency causal claims and indicative conditionals, how these judgments are driven by probabilistic factors, and how these factors differ (...) in their predictive power for both causal and conditional claims. (shrink)

A cause may influence its effect via multiple paths. Paradigmatically (Hesslow [1974]), taking birth control pills both decreases one’s risk of thrombosis by preventing pregnancy and increases it by producing a blood chemical. Building on Pearl ([2001]), I explicate the notion of a path-specific effect. Roughly, a path-specific effect of C on E via path P is the degree to which a change in C would change E were they to be transmitted only via P. Facts about such effects may (...) be gleaned from the structural equations commonly used to represent the causal relationships among variables. I contrast my analysis of the Hesslow case with those given by theorists of probabilistic causality, who mistakenly link it to issues of causal heterogeneity, token-causation and indeterminism. The reason probabilistic theories misdiagnose this case is that they pay inadequate attention to the structural relationships among variables. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of the (...) counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

Direct effects in mediation analysis quantify the effect of an exposure on an outcome not mediated by a certain intermediate. When estimating direct effects through measured data, misclassification may occur in the outcomes, exposures, and mediators. In mediation analysis, any such misclassification may lead to biased estimates in the direct effects. Basing on the conditional dependence between the mismeasured variable and other variables given the true variable, misclassification mechanisms can be divided into non-differential misclassification and differential misclassification. In this article, (...) several scenarios of differential misclassification will be discussed and sensitivity analysis results on direct effects will be derived for those eligible scenarios. According to our findings, the estimated direct effects are not necessarily biased in intuitively predictable directions when the misclassification is differential. The bounds of the true effects are functions of measured effects and sensitivity parameters. An example from the 2018 NCHS data will illustrate how to conduct sensitivity analyses with our results on misclassified outcomes, gestational hypertension and eclampsia, when the exposure is Hispanic women versus non-Hispanic White women and the mediator is weights gain during pregnancy. (shrink)

Causal mediation analysis is complicated with multiple effect definitions that require different sets of assumptions for identification. This article provides a systematic explanation of such assumptions. We define five potential outcome types whose means are involved in various effect definitions. We tackle their mean/distribution’s identification, starting with the one that requires the weakest assumptions and gradually building up to the one that requires the strongest assumptions. This presentation shows clearly why an assumption is required for one estimand and not another, (...) and provides a succinct table from which an applied researcher could pick out the assumptions required for identifying the causal effects they target. Using a running example, the article illustrates the assembling and consideration of identifying assumptions for a range of causal contrasts. For several that are commonly encountered in the literature, this exercise clarifies that identification requires weaker assumptions than those often stated in the literature. This attention to the details also draws attention to the differences in the positivity assumption for different estimands, with practical implications. Clarity on the identifying assumptions of these various estimands will help researchers conduct appropriate mediation analyses and interpret the results with appropriate caution given the plausibility of the assumptions. (shrink)

Causal selection and priority are at the heart of discussions of the causal parity thesis, which says that all causes of a given effect are on a par, and that any justified priority assigned to a given cause results from causal explanatory interests. In theories of causation that provide necessary and sufficient conditions for the truth of causal claims, status as cause is an either/or issue: either a given cause satisfies the conditions or it does not. Consequently, assessments of causal (...) parity and priority require more resources, which can either be additional or part of the causal analysis itself. While adding resources in terms of a theory of causal explanation has been standard, here we develop a unified conceptual analysis that includes a range of different precise causal concepts that allows for assessments of causal priority in terms of different kinds of causal relevance. (shrink)

This paper develops axiomatic foundations for a probabilistic-interventionist theory of causal strength. Transferring methods from Bayesian confirmation theory, I proceed in three steps: I develop a framework for defining and comparing measures of causal strength; I argue that no single measure can satisfy all natural constraints; I prove two representation theorems for popular measures of causal strength: Pearl's causal effect measure and Eells' difference measure. In other words, I demonstrate these two measures can be derived from a set of plausible (...) adequacy conditions. The paper concludes by sketching future research avenues. (shrink)

Questions concerning mediated causal effects are of great interest in psychology, cognitive science, medicine, social science, public health, and many other disciplines. For instance, about 60% of recent papers published in leading journals in social psychology contain at least one mediation test (Rucker, Preacher, Tormala, & Petty, 2011). Standard parametric approaches to mediation analysis employ regression models, and either the “difference method” (Judd & Kenny, 1981), more common in epidemiology, or the “product method” (Baron & Kenny, 1986), more common in (...) the social sciences. In this article, we first discuss a known, but perhaps often unappreciated, fact that these parametric approaches are a special case of a general counterfactual framework for reasoning about causality first described by Neyman (1923) and Rubin (1924) and linked to causal graphical models by Robins (1986) and Pearl (2006). We then show a number of advantages of this framework. First, it makes the strong assumptions underlying mediation analysis explicit. Second, it avoids a number of problems present in the product and difference methods, such as biased estimates of effects in certain cases. Finally, we show the generality of this framework by proving a novel result which allows mediation analysis to be applied to longitudinal settings with unobserved confounders. (shrink)

Understanding the pathways whereby an intervention has an effect on an outcome is a common scientific goal. A rich body of literature provides various decompositions of the total intervention effect into pathway-specific effects. Interventional direct and indirect effects provide one such decomposition. Existing estimators of these effects are based on parametric models with confidence interval estimation facilitated via the nonparametric bootstrap. We provide theory that allows for more flexible, possibly machine learning-based, estimation techniques to be considered. In particular, we establish (...) weak convergence results that facilitate the construction of closed-form confidence intervals and hypothesis tests and prove multiple robustness properties of the proposed estimators. Simulations show that inference based on large-sample theory has adequate small-sample performance. Our work thus provides a means of leveraging modern statistical learning techniques in estimation of interventional mediation effects. (shrink)

We present a method for assessing the sensitivity of the true causal effect to unmeasured confounding. The method requires the analyst to set two intuitive parameters. Otherwise, the method is assumption free. The method returns an interval that contains the true causal effect and whose bounds are arbitrarily sharp, i.e., practically attainable. We show experimentally that our bounds can be tighter than those obtained by the method of Ding and VanderWeele, which, moreover, requires to set one more parameter than our (...) method. Finally, we extend our method to bound the natural direct and indirect effects when there are measured mediators and unmeasured exposure–outcome confounding. (shrink)

Recent advances in causal reasoning have given rise to a computational model that emulates the process by which humans generate, evaluate, and distinguish counterfactual sentences. Contrasted with the “possible worlds” account of counterfactuals, this “structural” model enjoys the advantages of representational economy, algorithmic simplicity, and conceptual clarity. This introduction traces the emergence of the structural model and gives a panoramic view of several applications where counterfactual reasoning has benefited problem areas in the empirical sciences.

The study of causal inference has seen recent momentum in machine learning and artificial intelligence, particularly in the domains of transfer learning, reinforcement learning, automated diagnostics, and explainability. Yet, despite its increasing application to address many of the boundaries in modern AI, causal topics remain absent in most AI curricula. This work seeks to bridge this gap by providing classroom-ready introductions that integrate into traditional topics in AI, suggests intuitive graphical tools for the application to both new and traditional lessons (...) in probabilistic and causal reasoning, and presents avenues for instructors to impress the merit of climbing the “causal hierarchy” to address problems at the levels of associational, interventional, and counterfactual inference. Finally, this study shares anecdotal instructor experiences, successes, and challenges integrating these lessons at multiple levels of education. (shrink)

Mediation analysis has been used in many disciplines to explain the mechanism or process that underlies an observed relationship between an exposure variable and an outcome variable via the inclusion of mediators. Decompositions of the total effect of an exposure variable into effects characterizing mediation pathways and interactions have gained an increasing amount of interest in the last decade. In this work, we develop decompositions for scenarios where two mediators are causally sequential or non-sequential. Current developments in this area have (...) primarily focused on either decompositions without interaction components or with interactions but assuming no causally sequential order between the mediators. We propose a new concept called natural mediated interaction effect that captures the two-way and three-way interactions for both scenarios and extends the two-way MIs in the literature. We develop a unified approach for decomposing the TE into the effects that are due to mediation only, interaction only, both mediation and interaction, neither mediation nor interaction within the counterfactual framework. Finally, we compare our proposed decomposition to an existing method in a non-sequential two-mediator scenario using simulated data, and illustrate the proposed decomposition for a sequential two-mediator scenario using a real data analysis. (shrink)

Gene–environment covariance is the phenomenon whereby genetic differences bias variation in developmental environment, and is particularly problematic for assigning genetic and environmental causation in a heritability analysis. The interpretation of these cases has differed amongst biologists and philosophers, leading some to reject the utility of heritability estimates altogether. This paper examines the factors that influence causal reasoning when G–E covariance is present, leading to interpretive disagreement between scholars. It argues that the causal intuitions elicited are influenced by concepts of agency (...) and blame-worthiness, and are intimately tied with the conceptual understanding of the phenotype under investigation. By considering a phenotype-specific approach, I provide an account as to why causal ascriptions can differ depending on the interpreter. Phenotypes like intelligence, which have been the primary focus of this debate, are more likely to spark disagreement for the interpretation of G–E covariance cases because the concept and ideas about its ‘normal development’ relatively ill-defined and are a subject of debate. I contend that philosophical disagreement about causal attributions in G–E covariance cases are in essence disagreements regarding how a phenotype should be defined and understood. This moves the debate from one of an ontological flavour concerning objective causal claims, to one concerning the conceptual, normative and semantic dependencies. (shrink)

UCLA Cognitive Systems Laboratory, Technical Report (R-321), June 2005. In Proceedings of International Joint Conference on Artificial Intelligen ce, Edinburgh, Scotland, August 2005.