Causation , proof

Causation, i.e. proof that the drug in fact caused the injury, is often impossible, particularly where it increases the incidence of a disease that occurs naturally. 

Concern over haphazard and unrecognized transfer of preponderance of evidence or more likely than not standards from the burden of persuasion to the burden of factual proof (burden of production) involves more than idle semantics. The adverse effects of failure to undertake a deliberate, two-step probabilistic analysis include (a) undue preference for particular probabilities of causation found in one epidemiologic study, especially when meta-analysis of multiple studies is not possible or available (b) unrecognized lowering of the burden of production with concomitant stiffening of the burden (standard) of persuasion (c) inappropriate fixation on simplistic quantitative rules such as the >50% likelihood rule and (d) poorly reasoned opinions because courts fail to explain exactly how they apply the >50%, more-likely than-not rule. 

As noted in previous editions of this chapter, the law of toxic torts continues to develop. Traditional legal rules continue to be strained and stretched. The tension created by the juxtaposition of scientific uncertainty and unsettled law continues to impact toxic tort litigants. The emerging interface of genetic and environmental forces creates new challenges for the proof of causation and injury, and further complicates emerging concepts of latency between exposure and either onset or manifestation of injury. 

Gold S (1986) Note, causation in toxic torts Burdens of proof, standards of persuasion, and statistical evidence. Yale Law Journal 96 376. 

In addition, ex post social control in the form of various liability laws provide an independent basis for shaping industrial safety performance by posing the threat of liability when, for example, a company s behavior fails to meet a reqnisite standard of care and causes harm, or incurs harmful results which may lead to strict or nofault liability under a prevailing legal doctrine. Although actual liability in either case necessarily requires the occurrence of harm and proof of causation, the threat of such liability may be sufhcient to deter a company and others in its industrial sector from negligent or inferior performance of safety management functions, or cause them to reduce or eliminate hazardous aspects of their activities. ... 

The proof of the existence of the Necessary of Existence through Itself appears in Chapter 4 of the Physics and Metaphysics of the Ishdrdt (11.4.9-15). Following a discussion of causation, Avicenna introduces the concepts possible existent and necessary existent , and submits that every existent must be either possible of existence in itself, or necessary of existence in itself Ishdrdt 11.4.9). A thing that is possible in itself is predisposed as such to neither existence nor nonexistence. So if such a thing becomes existent, there must be something other than itself that tips the balance and renders its existence preponderant to its nonexistence. Therefore, the existence of a possible thing must be caused by another Ishdrdt 11.4.10). What Avicenna intends by cause here is a metaphysical efficient cause (that is, a cause of existence), as opposed to a physical efficient cause (that is, a cause of motion). As such, the cause of a possible existent must coexist with its effect ... 

For this reason, other techniques are required to provide unequivocal evidence for the effect of a food or a food component in the causation or prevention of disease. One important techniqne is epidemiology, in which factors such as serum levels, adipose tissue levels, or dietary intake of a component can be correlated with the incidence of, or death from, major diseases such as cancer and coronary heart disease. Serum and adipose tissue levels of a component such as CLA can be measured accurately however, they indicate only recent intake and may not be indicative of intake in previous years or at a time close to the initiation of the disease. Although subject to assessment error, dietary intake at various periods can overcome these difficulties. Final proof of efficacy for a component in disease prevention is provided by the randomized, double-blinded, clinical intervention study. 

The remainder of this chapter discusses the evidence for the various causal relationships between Pb exposure and toxicity and disease. As set forth in Table 21.2, adverse human health effects of lead are placed in causal context using the nine proofs-of-causality criteria first enunciated by British medical statistician Sir Austin Bradford Hill in 1965 and subsequently labeled Hill s Criteria of Causation. These criteria are relevant and of particular value in the environmental epidemiology of Pb, given the many contentious arguments over association versus cause that have been lodged against Pb s human health impacts, particularly in earlier eras of lead health research and in the evolution of Pb as a major public health factor. 

Giving judgement in favour of Biosil, it was held that Mrs Foster had to prove both the fact of the defects and their cause. The burden of proof as to causation had not been changed by EU Directive 85/374, which only replaced negligence with strict liability for defective products. On the facts Mrs Foster had not established that the implants were defechve. As to leakage, the right implant was intact when removed so the liquid left behind was probably exudates rather than silicone from the implant. 

Note Proposals were based on observations of at-risk human populations, e.g., chimney sweeps in London. Decades typically passed before definitive proof of cancer causation was provided by laboratory studies. In the past half century there have been inaeased efforts to identify carcinogenic agents proactively by means of chronic toxicity testing in rodents (Chapter 5). 

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