Toxic mold and mycotoxins in neurotoxicity cases: Stachybotrys, Fusarium, Trichoderma, Aspergillus, Penicillium, Cladosporium, Alternaria, Trichothecenes

Presented is the argument that psychologists and neuropsychologists have no scientific basis for rendering opinions about causation given the current state of the literature. The critical question is whether in a residence or office inhalation of mold spores or mold metabolites, including mycotoxins, causes neuropsychological impairment or mental and emotional disorders. There has not been sufficient research to support such conclusions. Nonetheless, in the context of litigation, speculative opinions are rendered in lieu of scientifically well-founded conclusions. Resources for recognizing and coping with pseudoscientific arguments are suggested.     

Avoiding Type II error in assessing lead toxicity plaintiffs

This article discusses statistical parallels between excessive conservatism and insufficient conservatism in rendering forensic opinions. The elements of a tort are reviewed and their relation to psychological and psychiatric opinions is also discussed, as are psychometric and clinical approaches to assessment of impairment and causation in individual lead poisoned children. It is argued that assessments in lead poisoning cases consisting solely of cranial nerve examinations result in considerable Type II Error. Sources of Type II Error in research using analysis of covariance techniques to study the toxic effects of lead include variance stealing, use of excessive numbers of covariates, lack of attention to interactions, and use of covariates that are actually substitute measures of lead ingestion. When experts cite nonsignificant findings of studies of low-level lead exposure, it inappropriately negates lead effects in more severely lead poisoned plaintiffs. In true experimental studies where there is no ambiguity regarding causation, the destructive effects of lead are quite clear. © 1998 John Wiley & Sons, Ltd.     

Forensic neuropsychiatric evaluation of a personal injury case

Civil litigation involving the forensic neuropsychiatric evaluation of a personal injury case requires an assessment of damages and causation. The expert witness is obliged to integrate data from three critical sources of information: the review of records; the results of neuropsychological testing; and the findings from the clinical examination. In civil litigation involving a personal injury claim, the expert witness can be expected to address causation and prognosis of any neuropsychiatric damages. We discuss the undertaking of a forensic neuropsychiatric evaluation, psychiatric disorders often encountered in personal injury litigation, provide case vignettes and describe a number of special types of forensic neuropsychiatric evaluations, for example, Workers' Compensation, VA Disability and Social Security Disability.     

Chances, Individuals and Toxic Torts

We currently live in a world of silent risks caused by invisible agents acting through mechanisms poorly understood. It is not surprising that the resulting harms have led to litigation. Playing a visible role in all these cases is the 'causation problem'; plaintiffs face sometimes insurmountable hurdles in providing evidence for causation. However, the fact that mechanisms are hidden does not mean that one cannot have reliable evidence and information about them.
In this paper I argue that the law has taken an ill-founded, skeptical stance towards statistical evidence for causation in toxic tort cases, making the task of plaintiffs unjustly difficult. I address two frequently cited skeptical claims about statistical evidence and argue that they are unfounded as applied in tort law. I conclude that the skeptical stance results from a failure to distinguish physical chances from epistemic probabilities, and that such a distinction is necessary if plaintiffs are to have a chance of prevailing.     

Psycholegal standards and the role of psychological assessment in personal injury litigation

Conceptual and procedural aspects of the forensic practitioner's role in personal injury litigation are identified relative to the provision of evaluative, consultative, and court-related services. A model is presented for comprehensive clinical and psychodiagnostic assessment consistent with concepts of legal relevance and probative value. The model facilitates rendering psycholegal formulations and opinions regarding compensatory damages when retained to examine mental and emotional elements entered as causes of action in tort. The differential contribution of state and trait level conditions, and of proximate, pre-existing, and coexisting factors to the causal nexus of impairment is considered in this context toward establishing preincident baseline functioning and making pre-post comparisons. Approaches toward delineating the range and severity of impairments that are related to the instant event, and separating these from nonproximate factors and from the dynamics of primary and secondary gain, are considered.     

EVIDENTIARY STANDARDS IN EMPLOYMENT DISCRIMINATION: A VIEW TOWARD THE FUTURE

This article reviews recent changes in evidentiary standards in employment discrimination litigation as they relate to disparate impact theory. Precedents established in Watson v. Fort Worth Bank and Wards Cove Packing Co. v. Atonio , altering the employee's and the employer's responsibilities in discrimination cases are analyzed. In reaction to these and other Supreme Court rulings, Congress introduced a civil rights bill which was eventually signed into law after numerous compromises. The debate surrounding the development of the 1991 Civil Rights Act and the legislation itself are reviewed. With respect to disparate impact, the Act addresses the criteria for establishing a prima facie case (causation), burden of proof standards, and a definition of business necessity. However, a close reading of the Act and a review of recent disparate impact cases suggest the causation and business necessity issues are not fully resolved. Potential implications for managing personnel decision systems in this new environment are discussed.     

Agent causation as a solution to the problem of action

My primary aim is to defend a nonreductive solution to the problem of action. I argue that when you are performing an overt bodily action, you are playing an irreducible causal role in bringing about, sustaining, and controlling the movements of your body, a causal role best understood as an instance of agent causation. Thus, the solution that I defend employs a notion of agent causation, though emphatically not in defence of an account of free will, as most theories of agent causation are. Rather, I argue that the notion of agent causation introduced here best explains how it is that you are making your body move during an action, thereby providing a satisfactory solution to the problem of action.     

Decision‐making in civil litigation: Effects of attorney credibility,evidence strength,and juror cognitive processing

The current study examined the relationship between juror cognitive processing (measured by need for cognition [NFC]), attorney credibility, evidence strength, and civil litigation verdicts (liability, likelihood of causation, and compensatory damages). Participants (N = 446) viewed a videotaped mock civil trial in which the credibility of the attorneys and the strength of the plaintiff's evidence were manipulated. Plaintiff attorney credibility, defense attorney credibility, and strength of evidence interacted with one another for liability verdicts. In the strong evidence condition, the likelihood of a liable verdict was higher for a credible plaintiff attorney than a non‐credible plaintiff attorney when facing a non‐credible defense attorney. In the ambiguous evidence condition, the likelihood of a liable verdict was higher for a credible plaintiff attorney than a non‐credible plaintiff attorney when facing a credible defense attorney. Plaintiff attorney credibility, however, was found to be more influential on jurors’ decision‐making than case evidence for likelihood of causation and compensatory damage award decisions. Participants’ NFC also interacted with plaintiff attorney credibility. High NFC jurors were more influenced by a credible plaintiff attorney than low NFC jurors. Although these findings are counter to common findings in the NFC literature, they conform to a body of literature that supports the notion that jurors view attorney credibility as a piece of case evidence and not a peripheral cue as is often assumed. Thus, the findings indicate that attorneys do matter to the outcomes of cases. Policy and practice implications for attorneys and the courts are discussed.     

Evidence and the Assessment of Causal Relations in the Health Sciences

This contribution claims that the two fundamental notions of causation at work in the health sciences are manipulative and mechanistic, and investigates what kinds of evidence matter for the assessment of causal relations. This article is a development of our 2007 article, ‘Plurality of Causality’, where we argue for a pluralistic account of causation with an eye to econometrics and a single medical example. The present contribution has a wider focus, and considers the notion of evidence within a whole range of disciplines belonging to the health sciences. Section 1 addresses the relations between kinds of evidence and causal accounts, and it is shown how different notions of causation can be employed in various medical cases. Section 2 calls attention to issues crucial for any adequate epistemological theory of causation, such as the distinctions between types and tokens, observational and experimental regimes, explanation and prediction. Lastly, the notion of context is articulated, highlighted in its role in the assessment of causal links. All these issues are tackled in the framework of what we label a ‘bottom–up’ epistemology.     

Negative causation in causal and mechanistic explanation

Instances of negative causation—preventions, omissions, and the like—have long created philosophical worries. In this paper, I argue that concerns about negative causation can be addressed in the context of causal explanation generally, and mechanistic explanation specifically. The gravest concern about negative causation is that it exacerbates the problem of causal promiscuity—that is, the problem that arises when a particular account of causation identifies too many causes for a particular effect. In the explanatory context, the problem of promiscuity can be solved by characterizing the phenomenon to be explained as a contrast between two or more events or non-events. This contrastive strategy also can solve other problems that negative causation presents for the leading accounts of mechanistic explanation. Along the way, I argue that to be effective, accounts of causal explanation must incorporate negative causation. I also develop a taxonomy of negative causation and incorporate each variety of negative causation into the leading accounts of mechanistic explanation.     

Emerging from the causal drain

For over 20 years, Jaegwon Kim’s Causal Exclusion Argument has stood as the major hurdle for non-reductive physicalism. If successful, Kim’s argument would show that the high-level properties posited by non-reductive physicalists must either be identical with lower-level physical properties, or else must be causally inert. The most prominent objection to the Causal Exclusion Argument—the so-called Overdetermination Objection—points out that there are some notions of causation that are left untouched by the argument. If causation is simply counterfactual dependence, for example, then the Causal Exclusion Argument fails. Thus, much of the existing debate turns on the issue of which account of causation is appropriate. In this paper, however, I take a bolder approach and argue that Kim’s preferred version of the Causal Exclusion Argument fails no matter what account one gives of causation. Any notion of causation that is strong enough to support the premises of the argument is too strong to play the role required in the logic of the argument. I also consider a second version of the Causal Exclusion Argument, and suggest that although it may avoid the problems of the first version, it begs the question against a particular form of non-reductive physicalism, namely emergentism.     

Causal Reasoning and Clinical Practice: Challenges from Molecular Biology

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 (at least) 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.

     

The case for regularity in mechanistic causal explanation

How regular do mechanisms need to be, in order to count as mechanisms? This paper addresses two arguments for dropping the requirement of regularity from the definition of a mechanism, one motivated by examples from the sciences and the other motivated by metaphysical considerations regarding causation. I defend a broadened regularity requirement on mechanisms that takes the form of a taxonomy of kinds of regularity that mechanisms may exhibit. This taxonomy allows precise explication of the degree and location of regular operation within a mechanism, and highlights the role that various kinds of regularity play in scientific explanation. I defend this regularity requirement in terms of regularity??s role in individuating mechanisms against a background of other causal processes, and by prioritizing mechanisms?? ability to serve as a model of scientific explanation, rather than as a metaphysical account of causation. It is because mechanisms are regular, in the expanded sense described here, that they are capable of supporting the kinds of generalizations that figure prominently in scientific explanations.     

Causation in Personal Injury Law: The Case for a Probabilistic Approach

This paper makes the case for a wider acceptance of a probabilistic approach to causation in negligence. This acceptance would help to remove much of the incoherence which has come to afflict the English law of personal injury law. This incoherence can also be found in other common law jurisdictions (notably those of the United States, Canada and Australia). Concentrating upon recent UK case law, the argument opposes the contention that ‘naked statistics’ can play no role in establishing causation. The argument is controversial but it can be reduced to three unremarkable grounds: (1) With its acceptance (albeit in certain carefully prescribed circumstances) of liability for a negligently increased risk which has eventuated, the common law has already embraced a probabilistic conception of causation; (2) The English common law already employs a probabilistic (frequentist) approach to identifying coincidences; and (3) With the ‘balance of probabilities’ as the standard of proof in civil cases, the common law has long had a probabilistic (epistemic) concept at its core. Probabilistic approaches (at both the type and token level) are shown to be consistent with laypersons’ understanding of the concepts such as risk, chance, odds and likelihood. Moreover, a wider acceptance of a probabilistic perspective on causation would entail no major challenge to the fundamental aims of tort, viz. deterrence and corrective justice.     

Causes,Counterfactuals, and Non-Locality

In order to motivate the thesis that there is no single concept of causation that can do justice to all of our core intuitions concerning that concept, Ned Hall has argued that there is a conflict between a counterfactual criterion of causation and the condition of causal locality. In this paper I critically examine Hall's argument within the context of a more general discussion of the role of locality constraints in a causal conception of the world. I present two strategies that defenders of counterfactual accounts of causation can pursue to respond to Hall's challenge—including the adoption of a counterfactual condition that is sufficient for causal action-at-a-distance in place of Hall's ‘process’ condition—and conclude that Hall's argument against counterfactual accounts of causation is unsuccessful.     

Testpsychologische Ansätze der Beschwerdenvalidierung

The presence of cognitive impairment has been documented for a large number of diseases, conditions and mental disorders. Due to their impact on functioning in professional life and in everyday activities, there appears to be an increasing demand of qualified neuropsychological examinations in civil forensic contexts. While neuropsychological testing is the method of choice for determining the presence and the profile of cognitive impairment, it is easy to underperform in such tests. The authenticity of test results has to be thoroughly checked using modern approaches of symptom validity assessment. Without adequate validity checks, forensic psychological examinations are incomplete.     

Grounding in the image of causation

Grounding is often glossed as metaphysical causation, yet no current theory of grounding looks remotely like a plausible treatment of causation. I propose to take the analogy between grounding and causation seriously, by providing an account of grounding in the image of causation, on the template of structural equation models for causation.     

Dispositions,Causes, Persistence As Is,and General Relativity

I argue that, on a dispositionalist account of causation and indeed on any other view of causation according to which causation is a real relation, general relativity (GR) does not give causal principles a role in explaining phenomena. In doing so, I bring out a surprisingly substantial constraint on adequate views about the explanations and ontology of GR, namely the requirement that such views show how GR can explain motion that is free of disturbing influences.     

A longitudinal examination of stress generation in depressive and anxiety disorders

The current study compared two competing theories of the stress generation model of depression (stress causation vs. stress continuation) using interview-based measures of episodic life stress, as well as interpersonal and noninterpersonal chronic life stress. We also expanded on past research by examining anxiety disorders as well as depressive disorders. In addition, we examined the role of neuroticism and extraversion in these relationships. Participants were 627 adolescents enrolled in a two-site, longitudinal study of risk factors for depressive and anxiety disorders. Baseline and follow-up assessments were approximately one year apart. Results supported the stress causation theory for episodic stress generation for anxiety disorders, with neuroticism partially accounting for this relationship. The stress causation theory was also supported for depression, but only for more moderate to severe stressors; neuroticism partially accounted for this relationship as well. Finally, we found evidence for interpersonal and noninterpersonal chronic life stress continuation in both depressive and anxiety disorders. The present findings have implications regarding the specificity of the stress generation model to depressive disorders, as well as variables involved in the stress generation process.