Risk homeostatic approach

My first conclusion is that the individual benefit-cost approach is highly useful for understanding traffic safety behavior and for thinking about traffic safety policy. The framework is general enough to incorporate the technolo cal and risk homeostatic approaches as special cases. My second conclusion is that roadway users are sufficiently competent and their safety... 

The risk homeostatic approach implies that safety policy can increase traffic safety through insurance rates, traffic fines, driver education and other measures which influence the benefits and costs of safety as perceived by roadway users. For detail on such incentive systems see Gerald J. S. Wilde and Paul A. Murdoch. Incentive Systems for Accident-Free and Violation-Free Driving in the General Population. Ergonomics 25,10 (1982) 879-890. 

In Chapter 2, we compared the individual benefit-cost approach to the less general technological and risk homeostatic approaches and reviewed representative evidence on insurance, gambling, risk perception and safety belt use. We concluded the approach is useful for thinking about traffic safety policy. The evidence reviewed in this chapter led us to conclude that risk compensation exists in auto safety regulation and that policy benefits were overestimated. The evidence demonstrates that a general model such as ours must be used if formulation and evaluation of traffic safety policy is to be of high quality. 

Evaluative review of modern traffic safety policy, especially automobile safety standards, yields several results. The technological approach, the basis for the 1966 legislation, is shown to produce mistakes. Benefits are overestimated and endangerment of nonoccupants is ignored. The risk homeostatic approach, the devil s idea to some in the safety community, is shown to be a limiting case of the more general individual net benefit approach. Rationality and competency in travelers safety decisions are reviewed in a broad context. Evidence beyond the realm of behavioral... 

A variety of tumours, e.g. oat-cell limg cancer, can make vasopressin, and of course they are not subject to normal homeostatic mechanisms. SIADH also occurs in some CNS and respiratory disorders (infection). Dilutional hyponatraemia follows, i.e. low plasma sodium with an inappropriately low plasma osmolality and high urine osmolality. When the plasma sodium approaches 120 mmol/I treatment should be with fluid restriction (< 500 ml/day). Treatment is primarily of the imderlying disorder accompanied by fluid restriction. Chemotherapy to the causative tumour or infection is likely to be the most effective treatment. Demeclocycline, which inhibits the renal action of vasopressin, is useful Infusion of isotonic or hypertonic saline must be reserved for extreme emergencies, associated with stupor, and undertaken with great caution. Rapid correction of hyponatraemia must be avoided because of the risk of central pontine myelinolysis the rate of correction must not exceed 12 mmol/1 per 24 h. 

The extrapolation of animal toxicology data and combination with human exposure data aiay be used to estimate risk for those situations where exposure is likely. Methods for integrating these data as well as the assumptions for extrapolation from the animal studies are dependent upon the safety data. Risk assessment includes consideration of the type of toxicity involved and its potency, species comparisons, time considerations, dose response, kinetics of homeostatic mechanisms, and mechanisms of toxicity. When the essential components for extrapolations are well understood, more precise estimates can be made. In the absence of such understanding, more conservative approaches are appropriate. 

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