The study tests the hypothesis that conditional probability judgments can be influenced by causal links between the target event and the evidence even when the statistical relations among variables are held constant. Three experiments varied the causal structure relating three variables and found that (a) the target event was perceived as more probable when it was linked to evidence by a causal chain than when both variables shared a common cause; (b) predictive chains in which evidence is a cause of (...) the hypothesis gave rise to higher judgments than diagnostic chains in which evidence is an effect of the hypothesis; and (c) direct chains gave rise to higher judgments than indirect chains. A Bayesian learning model was applied to our data but failed to explain them. An explanation-based hypothesis stating that statistical information will affect judgments only to the extent that it changes beliefs about causal structure is consistent with the results. (shrink)

The authors challenge the reigning “causal power framework” as an explanation for whether a particular outcome was actually caused by a specific potential cause. They test a new measure of causal attribution in two experiments by embedding the measure within the Structure Induction model of Singular Causation (SISC, Stephan & Waldmann, 2016).

Currently, two frameworks of causal reasoning compete: Whereas dependency theories focus on dependencies between causes and effects, dispositional theories model causation as an interaction between agents and patients endowed with intrinsic dispositions. One important finding providing a bridge between these two frameworks is that failures of causes to generate their effects tend to be differentially attributed to agents and patients regardless of their location on either the cause or the effect side. To model different types of error attribution, we augmented (...) a causal Bayes net model with separate error sources for causes and effects. In several experiments, we tested this new model using the size of Markov violations as the empirical indicator of differential assumptions about the sources of error. As predicted by the model, the size of Markov violations was influenced by the location of the agents and was moderated by the causal structure and the type of causal variables. (shrink)

Many theories of actual causation implicitly endorse the claim that if c is an actual cause of e, then either c causes e directly or every intermediary by which c indirectly causes e is itself both an actual cause of e and also an actual effect of c. We think this compositionality constraint is plausible. However, as we show, it is not always satisfied by the causal attributions ordinary people make. We conclude by considering what philosophers working on causation should (...) do when the deliverances of their theories diverge from what ordinary people say. (shrink)

Moral philosophers and psychologists often assume that people judge morally lucky and morally unlucky agents differently, an assumption that stands at the heart of the Puzzle of Moral Luck. We examine whether the asymmetry is found for reflective intuitions regarding wrongness, blame, permissibility, and punishment judg- ments, whether people’s concrete, case-based judgments align with their explicit, abstract principles regarding moral luck, and what psychological mechanisms might drive the effect. Our experiments produce three findings: First, in within-subjects experiments favorable to reflective (...) deliberation, the vast majority of people judge a lucky and an unlucky agent as equally blameworthy, and their actions as equally wrong and permissible. The philosophical Puzzle of Moral Luck, and the challenge to the very possibility of systematic ethics it is frequently taken to engender, thus simply do not arise. Second, punishment judgments are significantly more outcome- dependent than wrongness, blame, and permissibility judgments. While this constitutes evidence in favor of current Dual Process Theories of moral judgment, the latter need to be qualified: punishment and blame judgments do not seem to be driven by the same process, as is commonly argued in the literature. Third, in between-subjects experiments, outcome has an effect on all four types of moral judgments. This effect is mediated by negligence ascriptions and can ultimately be explained as due to differing probability ascriptions across cases. (shrink)

Knowledge of mechanisms is critical for causal reasoning. We contrasted two possible organizations of causal knowledge—an interconnected causal network, where events are causally connected without any boundaries delineating discrete mechanisms; or a set of disparate mechanisms—causal islands—such that events in different mechanisms are not thought to be related even when they belong to the same causal chain. To distinguish these possibilities, we tested whether people make transitive judgments about causal chains by inferring, given A causes B and B causes C, (...) that A causes C. Specifically, causal chains schematized as one chunk or mechanism in semantic memory led to transitive causal judgments. On the other hand, chains schematized as multiple chunks led to intransitive judgments despite strong intermediate links. Normative accounts of causal intransitivity could not explain these intransitive judgments. (shrink)

In moral dilemmas performing an action often leads to both a good primary and a bad secondary effect. In such cases, how do people judge whether the bad secondary effect was brought about intentionally, and how do they assess the moral value of the act leading to the secondary effect? Various theories have been proposed that either focus on the causal role or on the moral valence of the secondary effect as the primary determinants of intentionality and morality assessments. We (...) present experiments which show that these theories have neglected a further important factor, the primary effect. A new theory is proposed that is based on the key assumption that people’s judgments of intentionality and morality depend on the strength of assumed reasons the agent has for the primary and secondary effects. (shrink)