There is no such thing as moral luck or everyone is profoundly mistaken about its nature and a radical rethinking of moral luck is needed. The argument to be developed is not complicated, and relies almost entirely on premises that should seem obviously correct to anyone who follows the moral luck literature. The conclusion, however, is surprising and disturbing. The classic cases of moral luck always involve an agent who lacks control over an event whose occurrence affects her praiseworthiness or (...) blameworthiness. Close examination of what it is to have control or to lack it reveals the logical space for counterexamples that do not fit the pattern constitutive of moral luck, and so unravel the whole. (shrink)

I present Aristotle’s theory of causation in a way that privileges a comparison with contemporary discussion on causation. I do so by selecting in Aristotle’s theory points that are interesting to contemporary discussion and by translating Aristotle in the contemporary philosophical terminology. I compare Aristotle’s views with Mackie’s (1993/1965) and Sosa’s (1993/1980). Mackie is a humean regularist regarding the metaphysics of causal necessity, but his theory postulates some formal aspects of the causal relation which are similar to the Aristotelian theory. (...) By introducing the notion of causal field as a third causal relatum – a sample in which the cause must be picked out as a explanation coextensive to the effect –, Mackie holds a point very similar to Aristotle, inasmuch as both defend that the causal relation is triadic and both have the extensional desideratum. Sosa (1993/1980) defends that every cause necessitates its effect, arguing against classical Humeanism, and he also proposes a causal pluralism. Both these theses are clearly Aristotelian. Aristotle comprehends that the causal relation has three relata: a subjacent C, a property of that subjacent A and a cause B that explains why such property is attributed to that subjacent. The subjacent is similar to Mackie’s notion of causal field, for in regard to it the cause must be coextensive to the property. But Aristotle also says that for each explanandum (property attributed to a subjacent of which one aims to investigate a cause) there is only one cause, which necessitates it. Sosa and Aristotle are similar because both develop a causal pluralism from a theory of causes as having intrinsic necessitation. For Aristotle, causes/explanations [aitiai] are central for attaining scientific knowledge, and its triadic structure determines the syllogistic structure of scientific demonstrations. Aristotle’s theory of causation also involves comprehending the actualisation of capacities (dispositional properties of objects) affirming that the causal relation is resultant from intrinsic properties of the objects, and the cause B is the essence of the explanandum. (shrink)

The aim of this paper is to apply inductive logic to the field that, presumably, Carnap never expected: legal causation. Legal causation is expressible in the form of singular causal statements; but it is distinguished from the customary concept of scientific causation, because it is subjective. We try to express this subjectivity within the system of inductive logic. Further, by semantic complement, we compensate a defect found in our application, to be concrete, the impossibility of two-place predicates (for causal relationship) (...) in inductive logic. (shrink)

A common objection to probabilistic theories of causation is that there are prima facie causes that lower the probability of their effects. Among the many replies to this objection, little attention has been given to Mellor's (1995) indirect strategy to deny that probability-lowering factors are bona fide causes. According to Mellor, such factors do not satisfy the evidential, explanatory, and instrumental connotations of causation. The paper argues that the evidential connotation only entails an epistemically relativized form of causal attribution, not (...) causation itself, and that there are clear cases of explanation and instrumental reasoning that must appeal to negatively relevant factors. In the end, it suggests a more liberal interpretation of causation that restores its connotations. Una objeción común a las teorías probabilísticas de la causalidad es que aparentemente existen causas que disminuyen la probabilidad de sus efectos. Entre las muchas respuestas a esta objeción, se le ha dado poca atención a la estrategia indirecta de D. H. Mellor (1995) para negar que un factor que disminuya la probabilidad de un efecto sea una causa legítima. Según Mellor, tales factores no satisfacen las connotaciones evidenciales, explicativas e instrumentales de la causalidad. El artículo argumenta que la connotación evidencial sólo implica una forma epistémicamente relativizada de atribución causal y no la causalidad misma, y que hay casos claros de explicación y razonamiento instrumental que deben apelar a factores negativamente relevantes. Se sugiere una interpretación más liberal de la causalidad que reinstaura sus connotaciones. (shrink)

Przedmowa Problematyka związana z zależnościami przyczynowymi, ich modelowaniem i odkrywa¬niem, po długiej nieobecności w filozofii i metodologii nauk, budzi współcześnie duże zainteresowanie. Wiąże się to przede wszystkim z dynamicznym rozwojem, zwłaszcza od lat 1990., technik obli¬czeniowych. Wypracowane w tym czasie sieci bayesowskie uznaje się za matematyczny język przyczynowości. Pozwalają one na daleko idącą auto¬matyzację wnioskowań, co jest także zachętą do podjęcia prób algorytmiza¬cji odkrywania przyczyn. Na potrzeby badań naukowych, które pozwalają na przeprowadzenie eksperymentu z randomizacją, standardowe metody ustalania zależności przyczynowych (...) opracowano na początku XX wieku. Zupełnie inaczej sprawa przedstawia się w przypadku badań nieeksperymentalnych, gdzie podobne rozwiązania pozostają kwestią przyszłości. Zadaniem tej książki jest podanie warunków, które powinny być spełnione przez te rozwiązania, oraz sformułowanie proceduralnego kryterium zależności przy¬czynowych jako szczegółowej realizacji tych warunków. Pociąga ono waż¬kie konsekwencje dla filozofii i metodologii nauk, które ujawnia – podany w Części II – zarys me-todolo¬gii proceduralnej. W literaturze przedmiotu brakuje w miarę wszechstronnego i systema¬tycznego omówie¬nia najnowszych filozoficznych i metodologicznych dys¬kusji na temat przy¬czynowości, co niech będzie wytłumaczeniem, dlaczego w niektórych punktach obecnej książki szczegółowo referuję trudno dos¬tępne teksty źró¬dłowe. Przymiotnik „proceduralny” używam tu w znaczeniu węższym niż Huw Price (w którego pracach właściwszy byłby termin „kryterialny”) dla podkre¬ślenia – zgodnie z łacińskim źródłosłowem procedo – że dla ustalenia przy¬czyny niezbędne jest podjęcie przez uczonych określonych interakcji z ba¬daną rzeczywistością. Zalążki zamysłu prezentowanego w tej książce przedstawiłem podczas warsztatów filozoficznych „Philosophy and Probability” w roku 2002, zor¬ganizowanych przez Instytut Filozofii Uniwersytetu w Konstancji. Wdzięczny jestem uczestnikom tych warsztatów za uwagi, a przede wszyst¬kim następującym osobom: Luc Bovens, Brandon Fitelson, Alan Hájek, Stephan Hartmann oraz Jon Williamson. Podczas międzynarodowej konferencji „Analytical Pragmatism”, zorgani¬zowanej w Lublinie w roku 2003 przez Wydział Filo¬zofii Katolickiego Uniwersytetu Lubelskiego, odniosłem swoją koncepcję do prac Nancy Cartwright. Szczególnie inspirujący okazał się komentarz Huw Price’a do mojego referatu i przeprowadzona z nim dysku¬sja. Ujęcie koncepcji metodologii proceduralnej na szerszym tle współ-czes¬nego nurtu empirystycznego w filozofii nauki przedstawiłem w roku 2004 podczas konferencji „5th Quadrennial Fellows Conference”, zorgani¬zowanej przez Instytut Filozofii Uniwersytetu Jagiellońskiego oraz Centrum Filozofii Nauki w Pittsburghu. Szczególnie pomocne w dalszych moich pra¬cach były uwagi Jamesa Bogena, Janet Kourany, Jamesa Lennoxa, Johna Nortona, Thomasa Bonka, Jana Woleńskiego i Johna Worralla, za które wyra¬żam swoją wdzięczność. Korpus książki powstał podczas mojego stażu w Centrum Filozofii Nauki w Pittsburghu, który odbyłem jako stypendysta Fundacji na Rzecz Nauki Polskiej w roku akademickim 2004-2005. Uczestniczyłem w tym czasie w życiu naukowym Centrum i w pracach badawczych zespołu z Instytutu Filozofii Uniwersytetu Carnegie-Mellon w Pittsburghu kierowanego przez Clarka Glymoura. Na jego ręce składam podziękowanie za wiele po¬mocnych uwag do moich wy¬stąpień oraz tekstów i za dyskusje przede wszystkim z nim samym i z jego najbliższymi współpracownikami: Peterem Spirtesem oraz Richardem Scheinesem, a także pozostałymi członkami tego zes¬połu, doktorantami i uczestnikami seminarium badawczego „Causality in the Social Sciences”. Za wieloletnie wsparcie, wielopłaszczyznowe inspiracje towarzyszące pi¬saniu tej książki, a także liczne pomocne uwagi do jej wcześniejszych wersji dziękuję przede wszystkim Księdzu Profesorowi Andrzejowi Bronkowi oraz Księdzu Profesorowi Józefowi Herbutowi, współprowadzącemu seminarium doktorskie w Katedrze Metodologii Nauk Katolickiego Uniwersytetu Lubel¬skiego im. Jana Pawła II, jak również pozostałym uczestnikom tego semina¬rium. Dziękuję mojej Żonie, dr Annie Kawalec za wiele wysiłku włożonego w ulepszenie redakcji – językowej i merytorycznej – obecnej książki. Książkę tę można czytać na kilka sposobów. Czytelnikom zainteresowa¬nym przede wszystkim prowadzeniem badań empirycznych polecałbym rozpoczęcie od Rozdziału 2. i kontynuację pozostałych rozdziałów Części I, a następnie Dodatków. Czytelnikom zainteresowanym problemami filozo¬fii i metodologii nauk polecałbym rozpoczęcie lektury książki od Części II i uzupełniającą lekturę Rozdziału 2., a następnie Wprowadzenia i Zakończenia. Czytelnikom mniej zainteresowanym zagadnieniami teoretycznymi pole¬całbym zapoznanie się z fascynującymi dziejami odkrycia przyczyn cholery przez Johna Snowa, które rekonstruuję w Rozdziale 1. W dalszej części nato¬miast polecałbym przejście do Wprowadzenia i Zakończenia, które w mniej specjalistyczny sposób przybliżają proponowane tu rozstrzygnięcia. Tekst książki nie był dotąd publikowany. Wyjątkiem są pewne fragmenty Rozdziału 8. oraz 9., które w zmienionej postaci ukazały się w Rocznikach Filozoficznych (Kawalec 2004). -/- Lublin, luty 2006 r. (shrink)

The development of causal modelling since the 1950s has been accompanied by a number of controversies, the most striking of which concerns the Markov condition. Reichenbach's conjunctive forks did satisfy the Markov condition, while Salmon's interactive forks did not. Subsequently some experts in the field have argued that adequate causal models should always satisfy the Markov condition, while others have claimed that non-Markovian causal models are needed in some cases. This paper argues for the second position by considering the multi-causal (...) forks, which are widespread in contemporary medicine (Section 2). A non-Markovian causal model for such forks is introduced and shown to be mathematically tractable (Sections 6, 7, and 8). The paper also gives a general discussion of the controversy about the Markov condition (Section 1), and of the related controversy about probabilistic causality (Sections 3, 4, and 5). (shrink)

Epistemologies and research methods are not free of metaphysics. This is to say that they are both, supported by (or presumed by), and support (or presume) fundamental ontologies. A discussion of the epistemological foundations of "multimethod" research in the social sciences—in as much as such research claims to unearth "causal" relations—therefore cannot avoid the ontological presuppositions or implications of such a discussion. But though there isn’t necessarily a perfect correspondence between ontology, epistemology, and methodology, they do constrain each other. As (...) such it is possible to make methodological choices that are at odds with one’s (implicit) ontology or argue from an ontology that is inconsistent one’s choice of methods.Yet lack of recognition of this fact has hampered methodological discussions in political science, especially with respect to the discussion on the merits of multimethod research. The ontology implicitly accepted in such discussions is "reductionist" and "regularist," that is, one that respectively defines causes in terms of noncausal relations and states of affair and affirms that such noncausal relations are regularities in nature. This article will argue that any attempt to fit "multimethod" research (where "multimethod" signifies some combination of inferential statistics and case studies) within this narrow ontology is destined to fail since such a metaphysics logically cannot accord case studies a necessary or sufficient role in the in the establishment of causal relations. However, there are metaphysical positions within the ambit of an empiricist philosophy of science that can accommodate multiple methods without contradiction. The article discusses two such ontologies and suggests ways in which they might allow the establishment of a coherent epistemological foundation for multimethod research, however, within a decidedly empiricist philosophy of science. (shrink)

The starting point in the development of probabilistic analyses of token causation has usually been the naïve intuition that, in some relevant sense, a cause raises the probability of its effect. But there are well-known examples both of non-probability-raising causation and of probability-raising non-causation. Sophisticated extant probabilistic analyses treat many such cases correctly, but only at the cost of excluding the possibilities of direct non-probability-raising causation, failures of causal transitivity, action-at-a-distance, prevention, and causation by absence and omission. I show that (...) an examination of the structure of these problem cases suggests a different treatment, one which avoids the costs of extant probabilistic analyses. (shrink)

Kolmogorov''s axiomatization of probability includes the familiarratio formula for conditional probability: 0).$$ " align="middle" border="0">.

Is the common cause principle merely one of a set of useful heuristics for discovering causal relations, or is it rather a piece of heavy duty metaphysics, capable of grounding the direction of causation itself? Since the principle was introduced in Reichenbach’s groundbreaking work The Direction of Time (1956), there have been a series of attempts to pursue the latter program—to take the probabilistic relationships constitutive of the principle of the common cause and use them to ground the direction of (...) causation. These attempts have not all explicitly appealed to the principle as originally formulated; it has also appeared in the guise of independence conditions, counterfactual overdetermination, and, in the causal modelling literature, as the causal markov condition. In this paper, I identify a set of difficulties for grounding the asymmetry of causation on the principle and its descendents. The first difficulty, concerning what I call the vertical placement of causation, consists of a tension between considerations that drive towards the macroscopic scale, and considerations that drive towards the microscopic scale—the worry is that these considerations cannot both be comfortably accommodated. The second difficulty consists of a novel potential counterexample to the principle based on the familiar Einstein Podolsky Rosen (EPR) correlations in quantum mechanics. (shrink)

The investigation of probabilistic causality has been plagued by a variety of misconceptions and misunderstandings. One has been the thought that the aim of the probabilistic account of causality is the reduction of causal claims to probabilistic claims. Nancy Cartwright (1979) has clearly rebutted that idea. Another ill-conceived idea continues to haunt the debate, namely the idea that contextual unanimity can do the work of objective homogeneity. It cannot. We argue that only objective homogeneity in combination with a causal interpretation (...) of Bayesian networks can provide the desired criterion of probabilistic causality. (shrink)

In this paper I wish to argue that counterfactual analyses of causation are inadequate. I believe the counterfactuals that are involved in counterfactual analyses of causation are often false, and thus the theories do not provide an adequate account of causation. This is demonstrated by the presentation of a counterexample to the counterfactual analyses of causation. I then present a unified theory of causation that is based upon probability and counterfactuals. This theory accounts for both deterministic and indeterministic causation, and (...) is not subject to many of the traditional problems facing theories of causation. (shrink)

This paper examines a promising probabilistic theory of singular causation developed by David Lewis. I argue that Lewis' theory must be made more sophisticated to deal with certain counterexamples involving pre-emption. These counterexamples appear to show that in the usual case singular causation requires an unbroken causal process to link cause with effect. I propose a new probabilistic account of singular causation, within the framework developed by Lewis, which captures this intuition.

Sober (1984) has considered the problem of determining the evidential support, in terms of likelihood, for a hypothesis that is incomplete in the sense of not providing a unique probability function over the event space in its domain. Causal hypotheses are typically like this because they do not specify the probability of their initial conditions. Sober's (1984) solution to this problem does not work, as will be shown by examining his own biological examples of common cause explanation. The proposed solution (...) will lead to the conclusion, contra Sober, that common cause hypotheses explain statistical correlations and not matchings between event tokens. (shrink)

After clarifying the probabilistic conception of causality suggested by Good (1961-2), Suppes (1970), Cartwright (1979), and Skyrms (1980), we prove a sufficient condition for transitivity of causal chains. The bearing of these considerations on the units of selection problem in evolutionary theory and on the Newcomb paradox in decision theory is then discussed.

This paper examines Wesley Salmon's "process" theory of causality, arguing in particular that there are four areas of inadequacy. These are that the theory is circular, that it is too vague at a crucial point, that statistical forks do not serve their intended purpose, and that Salmon has not adequately demonstrated that the theory avoids Hume's strictures about "hidden powers". A new theory is suggested, based on "conserved quantities", which fulfills Salmon's broad objectives, and which avoids the problems discussed.

The anti-causal prophecies of last century have been disproved. Causality is neither a ‘relic of a bygone’ nor ‘another fetish of modern science’; it still occupies a large part of the current debate in philosophy and the sciences. This investigation into causal modelling presents the rationale of causality, i.e. the notion that guides causal reasoning in causal modelling. It is argued that causal models are regimented by a rationale of variation, nor of regularity neither invariance, thus breaking down the dominant (...) Human paradigm. The notion of variation is shown to be embedded in the scheme of reasoning behind various causal models: e.g. Rubin’s model, contingency tables, and multilevel analysis. It is also shown to be latent – yet fundamental – in many philosophical accounts. Moreover, it has significant consequences for methodological issues: the warranty of the causal interpretation of causal models, the levels of causation, the characterisation of mechanisms, and the interpretation of probability. This book offers a novel philosophical and methodological approach to causal reasoning in causal modelling and provides the reader with the tools to be up to date about various issues causality rises in social science. (shrink)

The reduction of grounding to causation, or each to a more general relation of which they are species, has sometimes been justified by the impressive inferential capacity of structural equation modelling, causal Bayes nets, and interventionist causal modelling. Many criticisms of this assimilation focus on how causation is inadequate for grounding. Here, I examine the other direction: how treating grounding in the image of causation makes the resulting view worse for causation. The distinctive features of causal modelling that make this (...) connection appealing are distorted beyond use by forcing them to fit onto grounding. The very inferential strength that makes causation attractive is only possible because of a narrow construal of what counts as a causal relation; as soon as that broadens, the inferential capacity markedly diminishes. Making causation suitable for application to grounding spoils what was appealing about causation for this task in the first place. However, grounding need not appeal to causation: causal modelling does not have exclusive claim to structural equation modeling or other formal techniques of modelling structure. I offer a case in favour of a different kind of metaphysical frugality, which tend towards narrow, more restrictive construals of relations like causation or grounding, because then each relation behaves more homogenously. This more homogenous behavior delivers stronger inferential power per relation even though there may be more relations to which one is committed. (shrink)

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, (...) this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself. (shrink)

This essay furthers debate about the burgeoning science of Probabilistic Event Attribution (PEA) and its relevance to imminent climate policy decisions. It critically examines Allen Thompson and Friederike Otto’s recent arguments concerning the implications of PEA studies for how the United Nations Framework Convention on Climate Change (UNFCCC) policy framework should be revised during the 2016 ‘review and decision.’ I show that their contention that PEA studies cannot usefully inform decision-making about adaptation policies and strategies is misguided and argue that (...) the current UNFCCC treaty, the “Paris Agreement,” supersedes their proposed revision. (shrink)

In various areas of Anglo-American law, legal liability turns on causation. In torts and contracts, we are each liable only for those harms we havecausedby the actions that breach our legal duties. Such doctrines explicitly make causation an element of liability. In criminal law, sometimes the causal element for liability is equally explicit, as when a statute makes punishable any act that has “caused… abuse to the child….” More often, the causal element in criminal liability is more implicit, as when (...) criminal statutes prohibitkillings, maimings, rapings, burnings, etc. Such causally complex action verbs are correctly applied only to defendants who have caused death, caused disfigurement, caused penetration, caused fire damage, etc. (shrink)

My aim in this paper is to make a case for the singularist view from the perspective of a mechanical theory of causation, and to explain what, from this perspective, causal generalizations mean, and what role they play within the mechanical theory.

This paper outlines a theory and computer implementation of causal meanings and reasoning. The meanings depend on possibilities, and there are four weak causal relations: A causes B, A prevents B, A allows B, and A allows not‐B, and two stronger relations of cause and prevention. Thus, A causes B corresponds to three possibilities: A and B, not‐A and B, and not‐A and not‐B, with the temporal constraint that B does not precede A; and the stronger relation conveys only the (...) first and last of these possibilities. Individuals represent these relations in mental models of what is true in the various possibilities. The theory predicts a number of phenomena, and, contrary to many accounts, it implies that the meaning of causation is not probabilistic, differs from the meaning of enabling conditions, and does not depend on causal powers or mechanisms. The theory also implies that causal deductions do not depend on schemas or rules. (shrink)

In earlier work ( Cleland [2001] , [2002]), I sketched an account of the structure and justification of ‘prototypical’ historical natural science that distinguishes it from ‘classical’ experimental science. This article expands upon this work, focusing upon the close connection between explanation and justification in the historical natural sciences. I argue that confirmation and disconfirmation in these fields depends primarily upon the explanatory (versus predictive or retrodictive) success or failure of hypotheses vis-à-vis empirical evidence. The account of historical explanation that (...) I develop is a version of common cause explanation. Common cause explanation has long been vindicated by appealing to the principle of the common cause. Many philosophers of science (e.g., Sober and Tucker) find this principle problematic, however, because they believe that it is either purely methodological or strictly metaphysical. I defend a third possibility: the principle of the common cause derives its justification from a physically pervasive time asymmetry of causation (a.k.a. the asymmetry of overdetermination). I argue that explicating the principle of the common cause in terms of the asymmetry of overdetermination illuminates some otherwise puzzling features of the practices of historical natural scientists. (shrink)

The paper attempts to rationalize cooperation in the one-shot prisoners' dilemma (PD). It starts by introducing (and preliminarily investigating) a new kind of equilibrium (differing from Aumann's correlated equilibria) according to which the players' actions may be correlated (sect. 2). In PD the Pareto-optimal among these equilibria is joint cooperation. Since these equilibria seem to contradict causal preconceptions, the paper continues with a standard analysis of the causal structure of decision situations (sect. 3). The analysis then raises to a reflexive (...) point of view according to which the agent integrates his own present and future decision situations into the causal picture of his situation (sect. 4). This reflexive structure is first applied to the toxin puzzle and then to Newcomb's problem, showing a way to rationalize drinking the toxin and taking only one box with-out assuming causal mystery (sect. 5). The latter result is finally extended to a rationalization of cooperation in PD (sect. 6). (shrink)

This paper deals with Hans Reichenbach's common cause principle. It was propounded by him in, and has been developed and widely applied by Wesley Salmon, e.g. in and. Thus, it has become one of the focal points of the continuing discussion of causation. The paper addresses five questions. Section 1 asks: What does the principle say? And section 2 asks: What is its philosophical significance? The most important question, of course, is this: Is the principle true? To answer that question, (...) however, one must first consider how one might one argue about it at all. One can do so by way of examples, the subject of section 3, or more theoretically, which is the goal of section 4. Based on an explication of probabilistic causation proposed by me in,, and, section 4 shows that a variant of the principle is provable within a classical framework. The question naturally arises whether the proved variant is adequate, or too weak. This is pursued in section 5. My main conclusion will be that some version of Reichenbach's principle is provably true, and others may be. This may seem overly ambitious, but it is not. The paper does not make any progress on essential worries about the common cause principle arising in the quantum domain; it only establishes more rigorously what has been thought to be plausible at least within a classical framework. (shrink)

To clarify and illuminate the place of probability in science Ellery Eells and James H. Fetzer have brought together some of the most distinguished philosophers ...

This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this (...) second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory. (shrink)

The paper builds on the basically Humean idea that A is a cause of B iff A and B both occur, A precedes B, and A raises the metaphysical or epistemic status of B given the obtaining circumstances. It argues that in pursuit of a theory of deterministic causation this ‘status raising’ is best explicated not in regularity or counterfactual terms, but in terms of ranking functions. On this basis, it constructs a rigorous theory of deterministic causation that successfully deals (...) with cases of overdetermination and pre-emption. It finally indicates how the account's profound epistemic relativization induced by ranking theory can be undone. Introduction Variables, propositions, time Induction first Causation Redundant causation Objectivization. (shrink)

I deny that the world is fundamentally causal, deriving the skepticism on non-Humean grounds from our enduring failures to find a contingent, universal principle of causality that holds true of our science. I explain the prevalence and fertility of causal notions in science by arguing that a causal character for many sciences can be recovered, when they are restricted to appropriately hospitable domains. There they conform to loose and varying collections of causal notions that form folk sciences of causation. This (...) recovery of causation exploits the same generative power of reduction relations that allows us to recover gravity as a force from Einstein's general relativity and heat as a conserved fluid, the caloric, from modern thermal physics, when each theory is restricted to appropriate domains. Causes are real in science to the same degree as caloric and gravitational forces. (shrink)

In everyday life, people typically observe fragments of causal networks. From this knowledge, people infer how novel combinations of causes they may never have observed together might behave. I report on 4 experiments that address the question of how people intuitively integrate multiple causes to predict a continuously varying effect. Most theories of causal induction in psychology and statistics assume a bias toward linearity and additivity. In contrast, these experiments show that people are sensitive to cues biasing various integration rules. (...) Causes that refer to intensive quantities (e.g., taste) or to preferences (e.g., liking) bias people toward averaging the causal influences, whereas extensive quantities (e.g., strength of a drug) lead to a tendency to add. However, the knowledge underlying these processes is fallible and unstable. Therefore, people are easily influenced by additional task‐related context factors. These additional factors include the way data are presented, the difficulty of the inference task, and transfer from previous tasks. The results of the experiments provide evidence for causal model and related theories, which postulate that domain‐general representations of causal knowledge are influenced by abstract domain knowledge, data‐driven task factors, and processing difficulty. (shrink)

The notion of common cause closedness of a classical, Kolmogorovian probability space with respect to a causal independence relation between the random events is defined, and propositions are presented that characterize common cause closedness for specific probability spaces. It is proved in particular that no probability space with a finite number of random events can contain common causes of all the correlations it predicts; however, it is demonstrated that probability spaces even with a finite number of random events can be (...) common cause closed with respect to a causal independence relation that is stronger than logical independence. Furthermore it is shown that infinite, atomless probability spaces are always common cause closed in the strongest possible sense. Open problems concerning common cause closedness are formulated and the results are interpreted from the perspective of Reichenbach's Common Cause Principle. (shrink)

Darwinians are realists about the force of selection, but there has been surprisingly little discussion about what form this realism should take. Arguments about the units of selection in general and genic selectionism in particular reveal two realist assumptions: (1) for any selection process, there is a uniquely correct identification of the operative selective forces and the level at which each impinges; and (2) selective forces must satisfy the Pareto-style requirement of probabilistic causation. I argue that both assumptions are false; (...) we must temper realism about the force of selection and revise the way we think about probabilistic causation. (shrink)

In a recent article (Sober 1982), I criticized an account of causation proposed by Giere (1979, 1980) by describing a series of examples concerning natural selection. Collier (1983) has criticized my criticisms, saying that I misapplied Giere's proposal and misconstrued the biology. More recently, Giere (1984) has defended his theory against my criticisms. Here I argue that my criticisms still stand.

Causal inference in the empiricalsciences is based on counterfactuals. The mostcommon approach utilizes a statistical model ofpotential outcomes to estimate causal effectsof treatments. On the other hand, one leadingapproach to the study of causation inphilosophical logic has been the analysis ofcausation in terms of counterfactualconditionals. This paper discusses and connectsboth approaches to counterfactual causationfrom philosophy and statistics. Specifically, Ipresent the counterfactual account of causationin terms of Lewis's possible-world semantics,and reformulate the statistical potentialoutcome framework using counterfactualconditionals. This procedure highlights variousproperties and (...) mechanisms of the statisticalmodel. (shrink)

According to Nancy Cartwright, a causal law holds just when a certain probabilistic condition obtains in all test situations which in turn satisfy a set of background conditions. These background conditions are shown to be inconsistent and, on separate account, logically incoherent. I offer a corrective reformulation which also incorporates a strategy for problems like Hesslow's thrombosis case. I also show that Cartwright's recent argument for modifying the condition to appeal to singular causes fails.Proposed modifications of the theory's probabilistic condition (...) to handle effects with extreme probabilities (0 or 1) are found unsatisfactory. I propose a unified solution which also handles extreme causes. Undefined conditional probabilities give rise to three good, but non-equivalent, ways of formulating the theory. Various formulations appear in the literature. I give arguments to eliminate all but one candidate. Finally, I argue for a crucial new condition clause, and show how to extend the results beyond a simple probabilistic framework. (shrink)

Two kinds of causal inference rules which are widely used by social scientists are investigated. Two conceptions of causation also widely used are explicated — the INUS and probabilistic conceptions of causation. It is shown that the causal inference rules which link correlation, a kind of partial correlation, and a conception of causation areinvalid. It is concluded anew methodology is required for causal inference.

What does it mean to say that one event is a cause of another? The simplest counterfactual analyses identify causation with one of two counterfactual-dependence relations: if event c had not occurred, then event e would not have occurred; if c had not occurred, e's probability would have been lower. These analyses enjoy some success. For the first: the dart-throw caused the balloon-pop, because if the throw had not occurred, the pop would not have occurred. For the second: suppose two (...) radioactive samples, A and B, are introduced into a room containing a Geiger counter, and the counter clicks once due to an emission from an A-atom; then the introduction of A is a cause of the click; the click might have occurred without the A-introduction , but we can say at least that without the A-introduction, the probability of the click would have been lower. ;Ultimately, however, these analyses fail, for two clear reasons. Preemption: add to the dart scene that Lucy would have thrown her dart if I had refrained---then although my throw caused the pop, the pop is not dependent on my throw. Failed potential causes: the probability of the click would have been lower without the B-introduction, but the B-introduction did not actually succeed in causing of the click. ;I defend the two simple analyses against various other objections; I then try to home in on the precise nature of their genuine problems; I examine almost all the attempts to date to improve upon the simple analyses; and finally I propose two new analyses. One of my analyses is deterministic, the other is confined to worlds that are purely indeterministic. Both analyses take causation to be primarily a matter of counterfactual dependence in the circumstances: holding certain features of the world fixed, effects and their probabilities do indeed depend on their causes . ;My discussion of background issues---counterfactual semantics, objective chance, events---includes arguments for substantial simplifications of David Lewis's theory of events. (shrink)

This paper investigates the relations between causality and propensity. Aparticular version of the propensity theory of probability is introduced, and it is argued that propensities in this sense are not causes. Some conclusions regarding propensities can, however, be inferred from causal statements, but these hold only under restrictive conditions which prevent cause being defined in terms of propensity. The notion of a Bayesian propensity network is introduced, and the relations between such networks and causal networks is investigated. It is argued (...) that causal networks cannot be identified with Bayesian propensity networks, but that causal networks can be a valuable heuristic guide for the construction of Bayesian propensity networks. (shrink)

A probability space is common cause closed if it contains a Reichenbachian common cause of every correlation in it and common cause incomplete otherwise. It is shown that a probability space is common cause incomplete if and only if it contains more than one atom and that every space is common cause completable. The implications of these results for Reichenbach's Common Cause Principle are discussed, and it is argued that the principle is only falsifiable if conditions on the common cause (...) are imposed that go beyond the requirements formulated by Reichenbach in the definition of common cause. (shrink)

During the past decades several philosophers of science and social scientists have been interested in the problems of causation. Recently attention has been given to probabilistic causation in dichotomous causal systems. The paper uses the basic features of probabilistic causation to argue that the causal modeling approaches developed by such researchers as Blalock and Duncan can provide, when an additional assumption is added, adequate qualitative measures of one variableś causal influence upon another. Finally, some of the difficulties and issues involved (...) in developing adequate quantitative measures are discussed, and it is concluded that the causal modeling measures cannot provide adequate quantitative measures. (shrink)