Causality proving

Remarkably enough, Brush immediately adds to this claim the admission that in many cases it is difficult to prove a causal relation [between the success of the predictions and the frequency with which the periodic law is mentioned] since the authors do not mention the prediction ibid.). Two points should be made ... 

SIC are not performed all the time as some clinicians don t have access to these specialized centers or none are available. For some sensitizers, a challenge test is not needed since other information is available and sufficient to prove OA. For example, if an allergen has been identified in the workplace and the worker is sensitized to the allergen and has asthma symptoms at work that resolve or improve away from work then the causal relationship can be ascertained and diagnosis of OA be reported. 

Other, often made distinction in types of research, are between exploration, description, explanation, and testing, van der Zwaan (Zwaan van der, 1990). Exploration is conducted when theoretical knowledge in literature lacks information on which variables are important. Description types of research aim at the relevance of the variables. Explanation types of research aim at identifying the causal links between variables and phenomena. Finally, testing types of research aim at proving the hypotheses derived from the causal links. The research project discussed in this thesis is mainly explorative in nature. The emphasis is to design concepts and a protocol, which increases the understanding of the problem of how and why accidents continue to occur in companies in the chemical process industry. In this way a contribution to the solution of the problem will be made and consequently this research can be typified as applied positivistic exploratory research. 

This diversity of mental retardation, in both cause and phenotype, carries important implications for consideration of the biochemistry of consciousness. On the one hand, because this is an investigation of multiple causalities—including, for example, inborn errors of metabolism, each of which has its own unique biochemical profile (Cook Leventhal, 1996), it may not prove possible to identify specific neurotransmitter abnormalities which are common to mental retardation as such. On the other hand common themes concerning key neurotransmitters may be identified from studies of mental retardation. Altered neurotransmitter functioning associated with the severity of mental retardation is open to different interpretations, either reflecting fundamentally impaired development of cerebral structure or a more general impairment of central transmitter activity and functioning. 

One way to circumvent such (unjustified) labeling is to try to prove a causal relationship between the maternal effects and those in offspring, thus trying to show that the latter ones are unspecific secondary consequences of the former ones. So for the sound interpretation of study results it is important to find a good balance between maternal and fetal effects. For example, if a 10% reduction in maternal net weight gain is accompanied by a comparable reduction in fetal weight, then this puts the fetal effects in the correct perspective and would not lead the experimenter to conclude that the compound is a (specific) developmental toxicant. On the other hand if in the same situation the number of fetal anomalies (in particular malformations) is increased, then this could most unlikely be explained as a consequence of maternal toxicity. 

At the other extreme are effects such as endocrine disruption, carcinogenicity, chronic toxicity and ozone depletion, which are not apparent to those who deal with the chemical. Causal relationships between specific chemicals and their effects are generally difficult to prove, perhaps because they occur remote from the site of use of the chemical, either in time or space, or because they are caused by very low concentrations, or perhaps only when other substances are also present. A much greater proportion of those who suffer from these effects than the first sort will not have had any dealings with the chemical as a chemical substance, so will be unaware of their exposure to it. 

In the case of addiction, we know a great deal about the neurobiological substrate of the core cases. Some of the borderline cases are likely to prove very different. Yet there are some causal mechanisms common to chemical and behavioral addictions, notably those that are linked to the axvareness of being addicted. These mechanisms generate secondary features of phenomena that are linked by analogy rather than by common causal mechanisms. 

This association does not prove a causal relation. The authors of the second report pointed to previous observations of myotonia both in sarcoidosis and during the administration of various drugs. 

For a number of reasons, including the difficulties inherent in proving a direct causal relationship between fatigue and adverse medical events and the lack of systems for reporting various types of adverse events and errors, few studies to date have examined the specific contribution of sleep deprivation to actual medical errors. Several recent studies, in attempting to unravel this relationship, have employed a number of different methodologies to assess prevalence, type, and risk factors for medical errors. For example, in one recent study of anesthetic... 

MDMA and MDA abuse has been associated with panic disorder, depression and chronic paranoid psychosis. As these conditions may also occur independently of these drugs, it is difficult to prove causality but it seems reasonable to conclude that some individuals are more vulnerable to such psychiatric disorders which are exacerbated by these drugs. In... 

Before ecological significance can be assigned to an interaction, a series of steps should be followed—in the manner Koch s postulates are followed to prove a causal relationship between a microbe and a disease. The first step involves considerable observation—a correlation must be documented. For example, negative association between two species... 

A number of studies, including several large prospective studies, such as the Framingham Study (Anderson et al, 1987), the Multiple Risk Intervention Trial (Stamler et al, 1986) and the Lipid Research Clinics Program (Pekkanen et al., 1990), as well as the Seven Countries Study (Verschuren et al, 1995) showed a positive correlation between levels of plasma cholesterol and mortality from CHD. However, epidemiological associations cannot prove causality and elevated cholesterol levels could be either a cause, a correlate or a consequence of CHD. 

Finally, summarising the burden of proof in TSCA, it basically always rests on the EPA. Not even if the concept is divided into the burden of persuasion and the burden of proving a causal link (see further in Ashford 2007) does any component fall on chemical companies. 

Although a causal relation between this violent incident and donepezil cannot be proved, the temporal relation was suggestive. 

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