Deborah Mayo

Although both philosophers and scientists are interested in how to obtain reliable knowledge in the face of error, there is a gap between their perspectives that has been an obstacle to progress. By means of a series of exchanges between the editors and leaders from the philosophy of science, statistics and economics, this volume offers a cumulative introduction connecting problems of traditional philosophy of science to problems of inference in statistical and empirical modelling practice. Philosophers of science and scientific practitioners are challenged to reevaluate the assumptions of their own theories - philosophical or methodological. Practitioners may better appreciate the foundational issues around which their questions revolve and thereby become better 'applied philosophers'. Conversely, new avenues emerge for finally solving recalcitrant philosophical problems of induction, explanation and theory testing.

In empirical modeling, an important desiderata for deeming theoretical entities and processes as real is that they can be reproducible in a statistical sense. Current day crises regarding replicability in science intertwines with the question of how statistical methods link data to statistical and substantive theories and models. Different answers to this question have important methodological consequences for inference, which are intertwined with a contrast between the ontological commitments of the two types of models. The key to untangling them is the realization that behind every substantive model there is a statistical model that pertains exclusively to the probabilistic assumptions imposed on the data. It is not that the methodology determines whether to be a realist about entities and processes in a substantive field. It is rather that the substantive and statistical models refer to different entities and processes, and therefore call for different criteria of adequacy.

I argue that although the judgments required to reach statistical risk assessments may reflect policy values, it does not follow that the task of evaluating whether a given risk assessment is warranted by the evidence need also be imbued with policy values. What has led many to conclude otherwise, I claim, stems from misuses of the statistical testing methods involved. I set out rules for interpreting what specific test results do and do not say about the extent of a given risk. By providing a more objective understanding of the evidence, such rules help in adjudicating conflicting risk assessments. To illustrate, I consider the risk assessment conflict at the EPA concerning the carcinogenicity of formaldehyde.

We argue that a responsible analysis of today's evidence-based risk assessments and risk debates in biology demands a critical or metascientific scrutiny of the uncertainties, assumptions, and threats of error along the manifold steps in risk analysis. Without an accompanying methodological critique, neither sensitivity to social and ethical values, nor conceptual clarification alone, suffices. In this view, restricting the invitation for philosophical involvement to those wearing a "bioethicist" label precludes the vitally important role philosophers of science may be able to play as bioevidentialists. The goal of this paper is to give a brief and partial sketch of how a metascientific scrutiny of risk evidence might work.

The key problem in the controversy over group selection is that of defining a criterion of group selection that identifies a distinct causal process that is irreducible to the causal process of individual selection. We aim to clarify this problem and to formulate an adequate model of irreducible group selection. We distinguish two types of group selection models, labeling them type I and type II models. Type I models are invoked to explain differences among groups in their respective rates of production of contained individuals. Type II models are invoked to explain differences among groups in their respective rates of production of distinct new groups. Taking Elliott Sober's model as an exemplar, we argue that although type I models have some biological importance--they force biologists to consider the role of group properties in influencing the fitness of organisms--they fail to identify a distinct group-level causal selection process. Type II models if properly framed, however, do identify a group-level causal selection process that is not reducible to individual selection. We propose such a type II model and apply it to some of the major candidates for group selection