Causality offers the first comprehensive coverage of causal analysis in many sciences, including recent advances using graphical methods. Pearl presents a unified account of the probabilistic, manipulative, counterfactual and structural approaches to causation, and devises simple mathematical tools for analyzing the relationships between causal connections, statistical associations, actions and observations. The book will open the way for including causal analysis in the standard curriculum of statistics, artificial intelligence, business, epidemiology, social science and economics.

Scientific practice involves two kinds of induction. In one, generalizations are drawn about the states of a particular system of variables. In the other, generalizations are drawn across systems in a class. We can discern two questions of correctness about both kinds of induction: what distinguishes those systems and classes of system that are ‘projectible’ in Goodman’s sense from those that are not, and what are the methods by which we are able to identify kinds that are likely to be (...) projectible? In answer to the first question, numerous theories of ‘natural kinds’ have been advanced, but none has satisfactorily addressed both questions simultaneously. I propose a shift in perspective. Both essentialist and cluster property theories have traditionally characterized kinds directly in terms of the causally salient properties their members possess. Instead, we should focus on ‘dynamical symmetries’, transformations of a system to which the causal structure of that system is indifferent. I suggest that to be a member of natural kind it is necessary and sufficient to possess a particular collection of dynamical symmetries. I show that membership in such a kind is in turn necessary and sufficient for the presence of the sort of causal structure that accounts for success in both kinds of induction, thus demonstrating that has been answered satisfactorily. More dramatically, I demonstrate that this new theory of ‘dynamical kinds’ provides an answer to with methodological implications concerning the discovery of projectible kinds. (shrink)

I examine to what extent accounts of mechanisms based on formal interventionist theories of causality can adequately represent biological mechanisms with complex dynamics. Using a differential equation model for a circadian clock mechanism as an example, I first show that there exists an iterative solution that can be interpreted as a structural causal model. Thus, in principle, it is possible to integrate causal difference-making information with dynamical information. However, the differential equation model itself lacks the right modularity properties for a (...) full integration. A formal mechanistic model will therefore have to leave out either noncausal or causal explanatory relations. (shrink)

Mechanisms are often characterized as causal structures and the interventionist account of causation is then used to characterize what it is to be a causal structure. The associated modularity constraint on causal structures has evoked criticism against using the theory as an account of mechanisms, since many mechanisms seem to violate modularity. This paper answers to this criticism by making a distinction between a causal system and a causal structure. It makes sense to ask what the modularity properties of a (...) given causal structure are, but not whether a causal system is modular tout court. The counter-examples to the interventionist account are systems in which a particular structure is modular in variables, but not in parameters. A failure of parameter-modularity does not by itself threaten the interventionist interpretation of the structure and the possibility of causally explaining with that structure, but it does mean that knowledge of the structure is not sufficient to constitutively explain system-level properties of the embedding system. (shrink)

Time series of macroscopic quantities that are aggregates of microscopic quantities, with unknown one‐many relations between macroscopic and microscopic states, are common in applied sciences, from economics to climate studies. When such time series of macroscopic quantities are claimed to be causal, the causal relations postulated are representable by a directed acyclic graph and associated probability distribution—sometimes called a dynamical Bayes net. Causal interpretations of such series imply claims that hypothetical manipulations of macroscopic variables have unambiguous effects on variables “downstream” (...) in the graph, and such macroscopic variables may be predictably produced or altered even while particular microstates are not. This paper argues that such causal time series of macroscopic aggregates of microscopic processes are the appropriate model for mental causation. (shrink)

I argue that a phenotypic trait can be an adaptation to a particular environmental condition, as against others, only if the environmental condition and the phenotype interactively cause fitness. Models of interactive environmental causes of fitness generally require that environments be individuated by explicit representation rather than by measures of environmental quality, although the latter understanding of ‘environment’ is more prominent in the philosophy of biology. Hence, talk of adaptations to some but not other environmental conditions relies on conceptions of (...) ‘environment’ importantly different from that commonly presupposed in philosophy of biology. (shrink)