Thirty years after Lewis's paper, this book brings together some of the most important recent work connecting—or, in some cases, disputing the connection ...

In this paper I offer an 'integrating account' of singular causation, where the term 'integrating' refers to the following program for analysing causation. There are two intuitions about causation, both of which face serious counterexamples when used as the basis for an analysis of causation. The 'process' intuition, which says that causes and effects are linked by concrete processes, runs into trouble with cases of 'misconnections', where an event which serves to prevent another fails to do so on a particular (...) occasion and yet the two events are linked by causal processes. The chance raising intuition, according to which causes raise the chance of their effects, easily accounts for misconnections but faces the problem of chance lowering causes, a problem easily accounted for by the process approach. The integrating program attempts to provide an analysis of singular causation by synthesising the two insights, so as to solve both problems. In this paper I show that extant versions of the integrating program due to Eells, Lewis, and Menzies fail to account for the chance-lowering counterexample. I offer a new diagnosis of the chance lowering case, and use that as a basis for an integrating account of causation which does solve both cases. In doing so, I accept various assumptions of the integrating program, in particular that there are no other problems with these two approaches. As an example of the process account, I focus on the recent CQ theory of Wesley Salmon (1997). (shrink)

Cause and Chance is a collection of specially written papers by world-class metaphysicians. Its focus is the problems facing the "reductionist" approach to causation: the attempt to cover all types of causation, deterministic and indeterministic, with one basic theory.

Mellor's subject is singular causation between facts, expressed ‘E because C’. His central requirement for causation is that the chance that E if C be greater than the chance that E if C: chc(E)>chc(E). The book is as much about chance as it is about causation. I show that his way of distinguishing chc (E) from the traditional notion of conditional chance leaves than him with a problem about the existence of chQ(P) when Q is false (Section 3); and also (...) that any notion of chance which conforms to the standard calculus has wider application than the causal instances to which Mellor's notion is restricted (Section 8). Other topics discussed may be gleaned from the headings below. 1 Review of D.H. Mellor [1995]: The Facss of Causation, London, Routledge, International Library of Philosophy. (shrink)

In this important first book in the series Cambridge Studies in Probability, Induction and Decision Theory, Ellery Eells explores and refines current ...

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 (1964) and Duncan (1975) can provide, when an additional assumption is added, adequate qualitative measures of one variable 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)

I argue that the orthodox account of probabilistic causation, on which probabilistic causes determine the probability of their effects, is inconsistent with certain ontological assumptions implicit in scientific practice. In particular, scientists recognize the possibility that properties of populations can cause the behavior of members of the populations. Such emergent population‐level causation is metaphysically impossible on the orthodoxy.

I argue that the orthodox account of probabilistic causation, on which probabilistic causes determine the probability of their effects, is inconsistent with certain ontological assumptions implicit in scientific practice. In particular, scientists recognize the possibility that properties of populations can cause the behavior of members of the populations. Such emergent population level causation is metaphysically impossible on the orthodoxy.

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)

“Probabilistic Causation” designates a group of theories that aim to characterize the relationship between cause and effect using the tools of probability theory. The central idea behind these theories is that causes change the probabilities of their effects. This article traces developments in probabilistic causation, including recent developments in causal modeling. A variety of issues within, and objections to, probabilistic theories of causation will also be discussed.

Wesley Salmon provided three classic criteria of adequacy for satisfactory interpretations of probability. A fourth criterion is suggested here. A distinction is drawn between frequency‐driven probability models and theory‐driven probability models and it is argued that single case accounts of chance are superior to frequency accounts at least for the latter. Finally it is suggested that theories of chance should be required only to be contingently true, a position which is a natural extension of Salmon's ontic account of probabilistic causality (...) and his own later views on propensities. (shrink)

A probabilistic theory of causation is a theory which holds that the central feature of causation is that causes (usually) raise the probability of their effects. In this dissertation, I defend Hans Reichenbach's original (1953) version of the probabilistic theory of causation, which analyses causal relations in terms of a three place statistical betweenness relation. Unlike most discussions of this theory, I hold that the statistical relation should be taken as a sufficient, but not as necessary, condition for causal betweenness. (...) With this difference in interpretation, Reichenbach's theory is shown to be immune to all of the criticisms which have been raised against it in the last.. (shrink)

The Facts of Causation grapples with one of philosophy's most enduring issues. Causation is central to all of our lives. What we see and hear causes us to believe certain facts about the world. We need that information to know how to act and how to cause the effects we desire. D. H. Mellor, a leading scholar in the philosophy of science and metaphysics, offers a comprehensive theory of causation. Many questions (...) about causation remain unsettled. In science, the indeterminism of modern physics and genetics have made such questions considerably harder for philosophers to answer. While progress has been made, a complete account of the nature and cosequences of causation is long overdue. This major study provides that account. (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.

We provide a formally rigorous framework for integrating singular causation, as understood by Nuel Belnap's theory of causae causantes, and objective single case probabilities. The central notion is that of a causal probability space whose sample space consists of causal alternatives. Such a probability space is generally not isomorphic to a product space. We give a causally motivated statement of the Markov condition and an analysis of the concept of screening-off. Causal dependencies and probabilities 1.1 Background: causation in branching space-times (...) 1.2 What are probabilities defined for? Basic transitions 2.1 Basics of basic transitions 2.2 Sets of basic transitions Causal probability theory 3.1 Some simple cases 3.2 General causal probabilities 3.3 Application: probability of suprema of a chain. (shrink)

Counter factual theories of Causation have had problems with cases of probabilistic causation and preemption. I put forward a counterfactual theory that seems to deal with these problematic cases and also has the virtue of providing an account of the alleged asymmetry between hasteners and delayers: the former usually being counted as causes, the latter not. I go on to consider a new type of problem case that has not received so much attention in the literature, those I dub catalysts (...) and anti-catalysts, and show how my account needs to be adjusted to deliver the right verdicts in these cases. The net result is a particular conception of a cause that I try to spell out in the closing section of the paper. In that section, I also briefly discuss causal asymmetry and the purpose behind providing a counterfactual theory of causation. (shrink)

A probabilistic and counterfactual theory of causality is developed within the framework of branching time. The theory combines ideas developed by James Fetzer, Donald Nute, Patrick Suppes, Ming Xu, John Pollock, David Lewis and Mellor among others.

Probabilistic accounts of causality have long had trouble with ‘spurious’ evidential correlations. Such correlations are also central to the case for causal decision theory—the argument that evidential decision theory is inadequate to cope with certain sorts of decision problem. However, there are now several strong defences of the evidential theory. Here I present what I regard as the best defence, and apply it to the probabilistic approach to causality. I argue that provided a probabilistic theory appeals to the notions of (...) agency and effective strategy, it can avoid the problem of spurious causes. I show that such an appeal has other advantages; and argue that it is not illegitimate, even for a causal realist. (shrink)

In a recent article, Paul Noordhof (1999) has put forward an intriguing account of causation intended to work under the assumption of indeterminism. I am going to present four problems for the account, three which challenge the necessity of the conditions he specifies, and one which challenges their joint-sufficiency.

This is an excellent anthology. The contributors are first-rate, the contributions are state-of-the-art, and the content is highly unified. The introduction further connects the essays and succinctly articulates the main themes. What results will be of interest to anyone interested in the contemporary discussion of causation.

The leading regularity, counterfactual, and agential accounts of causation converge on the idea that causation is probability-raising. While the necessity of probability-raising for causation remains in dispute, the sufficiency of probability-raising for causation is generally assumed, at least in the direct (no intermediaries involved) and precisely described case. I offer a class of counterexamples: overlappings.

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 a recent article in this journal, Federica Russo and Jon Williamson argue that an analysis of causality in terms of probabilistic relationships does not do justice to the use of mechanistic evidence to support causal claims. I will present Ronald Giere's theory of probabilistic causation, and show that it can account for the use of mechanistic evidence (both in the health sciences—on which Russo and Williamson focus—and elsewhere). I also review some other probabilistic theories of causation (of Suppes, Eells, (...) and Humphreys) and show that they cannot account for the use of mechanistic evidence. I argue that these theories are also inferior to Giere's theory in other respects. (shrink)