Risk Paradigm Research Articles

The Relations among Organizational and Distribution Forms and Capital and Asset Risk Structures in the Life Insurance Industry

AbstractThis article is the first step toward integrating in a single framework two previously separate lines of research on major structural decisions of life insurers. The literature has previously studied the relation between capital structure and asset risk on the one hand, and the relation between organizational form and distribution system on the other hand, without integrating them. Using life insurer data for 1993–1999, we model the four key insurer decisions of capital structure, asset risk, organizational form, and distribution system as endogenous choices in a single interrelated set of simultaneous equations. The model assesses the nature of the interactions among these decisions. The model also assesses the impact of insurers' fundamental business strategy (treated as predetermined) on these choices. The business‐strategy hypothesis views other key decisions as jointly determined and driven by the fundamental business strategy, once the latter is set in motion. Confirming previous studies, we find a positive relation between capital ratios and asset risk. We also find an association in the simultaneous context between stock ownership and brokerage distribution, which was not found in prior studies. Stock ownership is related to greater financial and asset risk taking, whereas brokerage distribution is associated with lower risk taking. These and other results are interpreted in light of several theories, including transaction‐cost economics (TCE), agency theory, and regulatory and bankruptcy cost avoidance. Deriving from these theories, the finite risk paradigm emerges as the most comprehensive interpretation of the results, as opposed to the risk‐subsidy hypothesis of the impact of guarantee funds. We also find support for the notion that the business strategy drives the capital and distribution decisions, as predicted by TCE.

Lessons from case studies of metals: investigating exposure, bioavailability, and risk

Since metals are widely distributed in environmental matrices, humans are exposed to them by either anthropogenic activities or inadvertently by necessity. Selected metals: arsenic, mercury, iron, tin, lead and chromium were chosen on the basis of their economic and public health importance to illustrate the diversity of exposure pathways and differences in factors governing bioavailability. Bioavailability is central to the toxicity of metals and this is discussed from the health risk paradigm standpoint of risk assessment and risk management and the impacts of including or excluding bioavailability in such assessment. The lessons from the case studies of arsenic, mercury, tin and chromium provide a unified concept of methods that can be used in investigating and controlling outbreaks due to metal poisoning in other similar situations.

Scenario–model–parameter: a new method of cumulative risk uncertainty analysis

The recently developed concepts of aggregate risk and cumulative risk rectify two limitations associated with the classical risk assessment paradigm established in the early 1980s. Aggregate exposure denotes the amount of one pollutant available at the biological exchange boundaries from multiple routes of exposure. Cumulative risk assessment is defined as an assessment of risk from the accumulation of a common toxic effect from all routes of exposure to multiple chemicals sharing a common mechanism of toxicity. Thus, cumulative risk constitutes an improvement over the classical risk paradigm, which treats exposures from multiple routes as independent events associated with each specific route. Risk assessors formulate complex models and identify many realistic scenarios of exposure that enable them to estimate risks from exposures to multiple pollutants and multiple routes. The increase in complexity of the risk assessment process is likely to increase risk uncertainty. Despite evidence that scenario and model uncertainty contribute to the overall uncertainty of cumulative risk estimates, present uncertainty analysis of risk estimates accounts only for parameter uncertainty and excludes model and scenario uncertainties. This paper provides a synopsis of the risk assessment evolution and associated uncertainty analysis methods. This evolution leads to the concept of the scenario–model–parameter (SMP) cumulative risk uncertainty analysis method. The SMP uncertainty analysis is a multiple step procedure that assesses uncertainty associated with the use of judiciously selected scenarios and models of exposure and risk. Ultimately, the SMP uncertainty analysis method compares risk uncertainty estimates determined using all three sources of uncertainty with conventional risk uncertainty estimates obtained using only the parameter source. An example of applying the SMP uncertainty analysis to cumulative risk estimates from exposures to two pesticides indicates that inclusion of scenario and model sources increases uncertainty of risk estimates relative to those estimated using only the parameter source. Changes in uncertainty magnitude may affect decisions made by risk managers.

Pandora's Poison: Chlorine, Health, and a New Environmental Strategy

Review: Pandora's Poison: Chlorine, Health, and a New Environmental Strategy By Joe Thornton Reviewed by Dale Stirling Intertox, Inc., USA Joe Thornton. Pandora's Poison: Chlorine, Health, and a New Environmental Strategy. Cambridge, MA: MIT Press, 2000. 599 pp. ISBN 0-262-20124-0. Organochlorines are an abundant presence in our lives. The introduction of chlorine chemistry in the 20th century has tremendously impacted how we live and work. At the same time, the ubiquitous nature of organochlorines has affected human health, wildlife, and the environment. In this wide- ranging book, the author takes the chlorine industry to task as well as traditional science for not managing the threats posed by organochlorines to our health and the environment. The book consists of three parts and eleven chapters ending with several appendices, notes, references, and an index. In Part One, The Problem: A Global Health Hazard, the author focuses on the failure of the risk paradigm, which includes risk assessment, toxicology, epidemiology, and other scientific and engineering tools, to manage organochlorines. Chapter One, Organochlorines Around the World, focuses on the pervasiveness of organochlorines in our lives. Thornton notes that even though the current regulatory environment is based on the concept that toxic chemicals tend to stay local, evidence shows that pollutants do not stay where we put them (p. 23). He demonstrates this by describing the resistance of organochlorines to degradation and their corresponding persistence in air, water, and soil and their bioaccumulation in human and animal tissue and foods. The author singles out some well-known organochlorines including various PCBs and some dioxins and furans. Chapter Two, First Class Poisons: The Toxicology of Organochlorines, first reviews the effect of organochlorines on animal and human health. That is followed by a discussion on why some organochlorines are more toxic than others. The largest portion of this chapter reviews why organochlorines are toxic. The issue of threshold limit values for organochlorines is briefly examined as are chemical mixtures, genetic mutations, endocrine disruption, and neurotoxicity. Moving away from science, the author discusses the impact of political interests on how threshold values are set. He also illustrates a key problem in organochlorine regulation-data is not available on the more than 11,000 organochlorines in commerce as well as their byproducts. Chapter Three, The Damage Done: Health Impacts in People and Wildlife, examines how organochlorines have caused large-scale damage to human and

Overview of EPA Superfund human health research program

AbstractThis paper presents major research needs for the Superfund program, and provides an overview of the EPA Office of Research and Development's (ORDs) current human health research program designed to fill some of those data gaps. Research is presented in terms of the risk paradigm and covers exposure, effects, and assessment activities directly funded by Superfund, as well as research not funded by Superfund but directly applicable to Superfund research needs. Research on risk management is not covered. Current research activities conducted by the Superfund program office are also included to provide a full picture of Superfund human health research activities being conducted by EPA.

Predictors of Home Care Readiness for Managed Care: A Multivariate Analysis

ABSTRACT As home care agencies change from cost-based reimbursement to the managed care risk paradigm, many lack experience with organizational resources and functions needed to successfully operate in the managed care environment. This survey assessed the level of “readiness” for managed care reported by 162 randomly selected home care agencies in three mid-western states. Managed care readiness was measured by a 32-item mailed questionnaire addressing clinical, financial, operational, and informational systems within each agency. Higher levels of readiness were significantly related to the perception of being ready, proprietary auspices, and moderate agency size in a multivariate regression model. Agencies with these characteristics appear to be well positioned as home care moves into the managed care environment.

Management of chemical exposure: the limitations of a risk-based approach

Risk assessment and risk-based management approaches are becoming incorporated into a wide range of disciplines as frameworks for use in critical decision-making pathways. During its rapid expansion, many of the assumptions, subjective judgements and irreducible uncertainties inherent within the risk paradigm are becoming increasingly overlooked. This paper provides a critical review of the processes underpinning risk assessment and management, which in turn place fundamental limitations on the utility of risk as a decision-making tool, drawing illustrative examples from the field of hazardous chemical regulations. It is argued that the risk paradigm cannot provide adequately for environmental protection and that uncertainty and indeterminacy implicit in natural systems can only be addressed through implementation of a precautionary approach. In this regard, it is essential that the Precautionary Principle be recognised not as an additional tool in a suite of risk management options but as an overarching paradigm for environmental protection.

Neuropsychological assessment of young people at high genetic risk for developing schizophrenia compared with controls: preliminary findings of the Edinburgh High Risk Study (EHRS).

Finding risk indicators for schizophrenia among groups of individuals at high genetic risk for the disorder, has been the driving force of the high risk paradigm. The current study describes the preliminary results of a neuropsychological assessment battery conducted on the first 50% of subjects from the Edinburgh High Risk Study. One hundred and four high risk subjects and 33 normal controls, age and sex matched, were given a neuropsychological assessment battery. The areas of function assessed and reported here include intellectual function, executive function, perceptual motor speed, mental control/ encoding, verbal ability and language, learning and memory measures, and handedness. The high risk subjects performed significantly more poorly than the control subjects in the following domains of neuropsychological function: intellectual function, executive function, mental control/encoding and learning, and memory. Controlling for IQ, high risk subjects made significantly more errors on the Hayling Sentence Completion Test (HSCT), took longer to complete section A of the HSCT, had lower scores on the delayed recall condition of the visual reproductions subtest of the Wechsler Memory Scale-Revised, and had significantly poorer Rivermead Behavioural Memory Test (RBMT) standardized scores. The presence of significant group by IQ interactions for the RBMT and time to complete section A of the HSCT suggested that differences among the groups were more marked in the lower IQ range. Performance on the HSCT was found to be related to the degree of family history of schizophrenia. High risk subjects performed more poorly than controls on all tests of intellectual function and on aspects of executive function and memory.

Precursores conductuales infantiles de los trastornos del espectro esquizofrénico : esquizofrenia y trastorno esquizotípico de la personalidad

Given the wide and growing appearance of studies on biobehavioural markers of schizophrenia spectrum disorders, we have pursued to synthesise the data focusing on the possible differences in such markers as precursors of development towards schizotypal disorder and schizophrenia. Following a conceptual setting of high-risk studies we first outline classic and recent works about psychobiological markers from the genetic risk paradigm for schizophrenia and, secondly, we present findings coming from studies that have used other than genetic markers and have focused on the analysis of the soft conditions of the spectrum (i.e., schizotypy and schizotypal personality disorder). Lastly, limitations and theoretical and applied implications of these studies are discussed

Paradigms for ecological risk assessment.

Ecological risk assessment developed from the convergence of human health risk assessment, ecology, and ecotoxicology to provide data for environmental management and decision making. There has been an emphasis on using the health risk paradigm. However, ecological systems are much more complex than the single-species, single-lifetime approach used in human health risk assessment; hence several modifications are necessary, as ecological risk assessment evolves for particular uses. The advancement of ecological risk assessment is particularly timely, given competing considerations for cleanup of a variety of hazardous-waste sites, including the huge Department of Defense and Department of Energy sites, as well as the 1000+ Superfund sites. Sufficient resources are not available to clean up all sites completely, much less at the same time. Some sites pose no current identifiable risk to human receptors, but may be unusable for human habitation. Where human receptors are not the targets, ecological risk assessment can be used not only to evaluate the risks to ecosystems, but to help determine the degree of cleanup required to restore degraded environments to functioning ecosystems that provide valuable ecological services, and to rank sites for possible cleanup.

The Chesapeake Bay Program: An Example of Ecological Risk Assessment

Ecological risk assessment grew from earlier efforts of federal agencies to protect human health from chemical releases. Over the past several years, the U.S. Environmental Protection Agency (U.S. EPA) adapted the human health paradigm for use in protecting ecological end-points, including ecosystems such as the Chesapeake Bay. The Bay restoration effort may be seen as an ecological risk assessment in the sense that the program participants followed the paradigm developed by U.S. EPA. This analysis of the program and risk assessment process provides an additional perspective on the success and efficacy of the Bay restoration efforts. Early efforts to determine the problems in the Bay system targeted hypoxia, habitat deterioration and natural resource degradation for corrective actions. Additional monitoring and data gathering refined and focused program efforts on hypoxia caused by nutrient enrichment. Thus far, the ecological risk paradigm has been effectively applied to the Bay clean-up in a general sense. Recent research demonstrates that detailed application of a narrow risk approach will likely fail to include important biological effects or processes

The NAS Risk Paradigm as a Medium for Communication

Many journalists, public interest groups and other recipients of risk assessment information are familiar with the National Academy of Sciences risk assessment paradigm. From time to time, paradigm concepts appear in news features or community group discussions on environmental issues. With knowledge of the paradigm common to scientists, journalists, and other interested parties, the paradigm is a potentially important medium for communication between risk scientists, journalists, and the public. Specifically, the paradigm offers widely‐accepted organizing principles for presenting risk information, a common language for addressing a variety of issues and concepts, and a flexible analytical system that accommodates the diversity of scientific information and policy perspectives that characterize the risk assessment process. In addition, the paradigm outlines important relationships and distinctions between risk assessment and risk management. Informed and creative use of these features of the paradigm can guide and simplify interviews between journalists or community groups and their expert sources, clarify presentation of risk information, and promote collaboration between risk scientists, journalists, and others to assure complete, objective and fair comment on risk issues of interest to the public.

Familial resemblance for psychoactive substance use disorders: behavioral profile of high risk boys.

Familial transmission plays an etiologically important role in psychoactive substance use disorders (PSUD). The delineation of the risk status of families is central to implementation of the "high risk paradigm" in studying liability characteristics for PSUD. We have utilized a latent variable approach to characterizing familial resemblance for PSUD which incorporates elements of both the affected parent design, as well as a genetic epidemiologic indicator of familial aggregation of disease. Family resemblance scores were computed for 175 families in which fathers either met diagnostic criteria for PSUD or did not. We then compared the problem behavior profiles of 10-12 year-old boys grouped by familial resemblance for PSUD, and by paternal PSUD only. Boys grouped by paternal PSUD only had higher problem behavior scores than controls across all scales except for somatic complaints. Boys from families that have significant PSUD familial resemblance were characterized by higher scores on measures of externalizing conduct and socialization problems. Thus, the familial resemblance approach was more specific for the externalizing problem behaviors that have been described in longitudinal studies of childhood risk factors for later substance abuse.

Efficacy of Perceived Risk as a Correlate of Reported Donation Behavior: An Empirical Analysis

Various environmental trends suggest a challenging future for nonprofit organizations’ quests for fund-raising and volunteer recruitment. Previous research indicates that the perceived risk paradigm may be a valuable framework for examining donation behavior. The evidence generated in this study shows that risk perception has little bearing on money and time donation behaviors. Results also suggest that while perceived risk does not predict donation behavior well, it improves prediction when used in conjunction with demographic variables.

Potential biological markers in individuals at high risk for developing alcoholism.

N THE PAST two decades a plethora of scientific I evidence has been accumulated to support the notion that alcoholism is a familial disorder with the presence of genetic factors. It is now well established that sons of alcoholic fathers are approximately four times more likely to develop alcoholism compared to the male offspring of nonalcoholics.’ Indeed, the evidence supporting the contribution of genetic factors in alcoholism is sufficiently compelling to warrant a search for markers of the genetic influence. It should be noted that the antecedent factors or predisposition toward alcoholism might well be assessed with the use of various strategies. It may be possible to study genetic factors by comparing abstinent alcoholics to control subjects or by comparing abstinent alcoholics with a positive family history to abstinent alcoholics with a negative family history of alcoholism. While this particular strategy may yield interesting findings, the interpretation of the data may be confounded by significant differences in drinking history, differential age of onset of alcohol abuse, as well as numerous other clinical variables such as number and severity of withdrawal episodes, alcohol-related medical complications, etc. A strategy typically used in the study of genetically determined disorders is the use of large family pedigrees. This powerful approach enables the investigator to study large families with alcoholism, and compare them to control families where alcoholism is absent. This particular strategy is most compelling if one studies genetically determined diseases such as Huntington’s disease where the phenotypic expression is easily characterized and specific phenotypic markers are readily available. This ap proach is indeed most powerful to examine the pattern of inheritance. However this method is most difficult to implement without the availability of valid and reliable biological or behavioral markers. In the last few years investigators concerned with the potential role of genetic factors in alcoholism have used the high risk paradigm. Comparing the sons of alcoholic fathers and nonalcoholic fathers is a useful approach for examining potential biologid or behavioral factors associated with a predisposition for alcoholism. This particular strategy has been utilized in biological as well as behavioral investigations, and has already yielded promising data fiom various studies. EEG

Personality traits related to monoamine oxidase activity in platelets

Platelet monoamine oxidase (MAO) activity and intellectual level were examined in a large series of 1,129 18-year-old boys, selected from the general population. Personality traits were determined by means of selected subscales from several personality inventories such as the Zuckerman Sensation Seeking Scale, the Eysenck Personality Inventory, and the Karolinska Hospital Personality Inventory. Information was also gathered concerning alcohol consumption habits, signs of alcohol dependence, and use and abuse of tobacco, cannabis, glue, opiates, and amphetamine. Low MAO subjects were found to be more sensation seeking and to have higher scores on impulsivity and monotony avoidance. They also had higher use of tobacco and alcohol, showed more signs of possible alcohol dependence, and showed more drug abuse. When low MAO subjects were subdivided according to intellectual level, low MAO subjects with high intellectual level were found to have higher psychological functioning as judged by a psychologist after a clinical interview. Low MAO subjects with low intellectual level were found to have more use and abuse of alcohol and drugs, i.e., less accepted forms of sensation seeking, and they had a significantly lower level of psychological functioning. This subgroup seems to be the real “high risk” group that according to the high risk paradigm could be expected to show more alcohol abuse and higher tendencies to suicidal behavior.

Platelet aggregation and chlorpromazine therapy.

British Journal of Clinical PharmacologyVolume 6, Issue 6 p. 538-540 Free Access Platelet aggregation and chlorpromazine therapy. DJ Boullin, DJ BoullinSearch for more papers by this authorJM Know, JM KnowSearch for more papers by this authorJR Peters, JR PetersSearch for more papers by this authorMW Orr, MW OrrSearch for more papers by this authorMG Gelder, MG GelderSearch for more papers by this authorDG Grahame-Smith, DG Grahame-SmithSearch for more papers by this author DJ Boullin, DJ BoullinSearch for more papers by this authorJM Know, JM KnowSearch for more papers by this authorJR Peters, JR PetersSearch for more papers by this authorMW Orr, MW OrrSearch for more papers by this authorMG Gelder, MG GelderSearch for more papers by this authorDG Grahame-Smith, DG Grahame-SmithSearch for more papers by this author First published: December 1978 https://doi.org/10.1111/j.1365-2125.1978.tb00881.xCitations: 20AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References Ball, S.E., Boullin, D.J. & Glenton, P.A.M. (1977). Interactions between noradrenaline and 5-hydroxytryptamine involving platelet aggregation. J. Physiol., 272, 98– 99P. Benedict, C.R. & Grahame-Smith, D.G. (1978). Plasma noradrenaline and adrenaline concentrations and dopamine-β-hydroxylase activity in patients with shock due to septicaemia, trauma and haemorrhage. Quart. J. Med., New Series 47, 185, 1– 20. Boullin, D.J. & Glenton, P.A.M. (1978) Characterisation of receptors mediating 5-hydroxytryptamine and catecholamine-induced platelet aggregation, assessed by the actions of α and β blockers, butyrophenones, 5-HT antagonists and chlorpromazine. Br. J. Pharmac., 62, 537– 542. Boullin, D.J. & Grimes, R.P.J. (1976). Increased platelet aggregation in patients receiving chlorpromazine: responses to 5-hydroxytryptamine, dopamine and N-dimethyldopamine. Br. J. clin. Pharmac., 3, 649– 654. Boullin, D.J., Orr, M.W. & Peters, J.R. (1978). The platelet as a model for investigating the clinical efficacy of centrally acting drugs: relations between platelet aggregation and clinical condition in patients treated with chlorpromazine. In Platelets: A Multidisciplinary Approach, eds G.S. Gaetano & S. Garattini, New York: Raven Press, (in press). Boullin, D.J., Woods, H.F., Grimes, R.P.J., Grahame-Smith, D.G., Wiles, D., Gelder, M.G. & Kolakowska, T. (1975). Increased platelet aggregation responses to 5-hydroxytryptamine in patients taking chlorpromazine. Br. J. clin. Pharmac., 2, 29– 35. Buchsbaum, M.S., Coursey, R.D. & Murphy, D.L. (1976). The biochemical high risk paradigm: behavioural and familial correlates of low platelet monoamine oxidase activity. Science, 194, 339– 341. Mills, D.C.B. & Roberts, G.C.K.(1967). Membrane active drugs and the aggregation of human blood platelets. Nature, 213, 35– 38. Orr, M.W. & Boullin, D.J. (1976). The relationship between changes in 5-HT induced platelet aggregation and clinical state in patients treated with fluphenazine. Br. J. clin. Pharmac., 3, 925– 928. Pletscher, A. (1978). Platelets as models for monoaminergic neurones. In Essays in Neurochemistry and Neuropharmacology, M.B.H. Youdim, W. Lovenberg, D.F. Sharman and J.R. Lagnado eds, pp. 49– 101. Chichester: Wiley. Citing Literature Volume6, Issue6December 1978Pages 538-540 ReferencesRelatedInformation