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Risk populations

Many of the accidents considered in the investigation could occur without causing any significant public casualties. However, if the conditions at the time of the accident were sufficiently unfavorable, the number of deaths among the public could range from tens up to thousands (Table 11.4-1). Table 11.4-1 is the summarized population risk assessed by the study team. It is in frequency per 10,(XX) years of an accident at the indicated facility that causes casualties exceeding the indicated limit. Reference should be made to Canvey (1978) for details. [Pg.438]

A risk estimate indicates Uie likelihood of occurrence of the different types of health or enviroinnental effects in exposed populations. Risk assessment should include both liuimn health and environmental evaluations (i.c., impacts on ecosystems). Ecological impacts include actual or potential effects on plants and animals (other than domesticated species). The number produced from the risk characleriznlion, representing the probability of adi crse... [Pg.294]

There me two major types of risk ina. imuin individual risk and population risk. Maximum risk is defined e.xacUy as it implies, Uiat is the ma.ximum risk to an individual person. Tliis person is considered to have a 70-year lifetime of exposure to a process or a chemical. Population risk is Uie risk to a population. It is expressed as a certain number of deaths per Uiousand or per million people. For example, a fatal annual risk of 2 x 10 refers to 2 deatlis per year for every million individuals. These risks are based on very conser ative assumptions, llich may yield too high a risk. [Pg.295]

Other ground water Laek of information individual risks eonsidered less tluui 10" , with rough estimate of total population risk at <1... [Pg.411]

Compare individual hazard risk with population risk. [Pg.436]

Population Risk (PR) - Tliis is a risk to a population, expressed as a given number of deatlis per tliousand or per million people. [Pg.515]

Risk characterization estimates tlie healtli risk associated with tlie process under investigation. The result of tliis cliaracterization is a number tliat represents tlie probability of adverse healtli effects from tliat process or from a substance released in tliat process. Tlie major types of risk include Individual Risk, Maximum Individual Risk (MIR), Population Risk (PR), Societal Risk, and Risk Indices. [Pg.535]

Green, R.E., Taggart, M.A., and Das, D. et al. (2006). Collapse of Asian vulture populations Risk of mortality from residues of the veterinary drug diclofenac in carcasses of treated cattle. Journal of Applied Ecology 43, 949-956. [Pg.349]

It is possible to infer cross population risk if the detailed dose delivered to target cells in bronchial epithelium is calculated for the various population groups since it is the dose which confers the risk. [Pg.420]

Mohrenweiser, H.W. and I.M. Jones, "Variation in DNA Repair is a Factor in Cancer Susceptibility A Paradigm for the Promises and Perils of Individual and Population Risk Estimation " Mutat. Res., 400, 15-24 (1998). [Pg.56]

Of course individual people can, for causes under their personal control, also benefit from the results of epidemiology studies even though epidemiology results apply to populations, individuals at least have an increased chance of benefiting by avoiding the substances or factors identified as causes of disease, especially when, as in the case of smoking, the population risk from the causative agent is unusually... [Pg.165]

On the basis of the foregoing discussion, it appears that, if traditional criteria for hazard evaluation are applied to the toxicologic data on experimental animals, there is little room for complacency r arding current ambient concentrations of ozone. Functional, biochemical, and structural effects in both pulmonary and extrapulmonary sterns have been reported by numerous investigators at or near concentrations that are at least occasionally achieved in some polluted urban centers. Unfortunately, there are no adequate methods for extrapolating data to obtain reliable quantitative estimates of population risk at environmental concentrations near the standard, and there is no assurance that the risk is zero. [Pg.376]

In carrying out the exposure assessment the risk reduction/control measures that are already in place should be taken into account. Consideration should be given to the possibility that, for one or more of the defined populations, risk reduction/control measures which are required or appropriate in one use scenario may not be required or appropriate in another (i.e., there might be subpopulations legitimately using different patterns of control, which could lead to different exposure levels). [Pg.323]

Coombs NJ, Taylor R, Wilcken N, Boyages J. HRT and breast cancer impact on population risk and incidence. Eur J Cancer 2005 41(12) 1775-81. [Pg.777]

In 1976, a final report from the International Register of Lithium Babies contained information on 225 infants exposed to lithium in the first trimester. Cardiovascular anomalies occurred in 18 (8%) of the newborns, of which 6 (2.7%) had Ebstein s anomaly (Weinstein, 1976). A comprehensive review of this report and the multiple studies that have been conducted since (Cohen et ah, 1994) revealed that the risk of congenital defects after in utero exposure to lithium is less than previously anticipated. Currently, the risk for Ebstein s anomaly after first-trimester exposure to lithium is estimated to be 1 in 1000 (0.1%) (Altshuler et ah, 1996), or 10-20 times greater than the general population risk of 1 in 20,000 (Weinstein, 1976). Thus, the absolute risk for Ebstein s anomaly is small. [Pg.644]

Insurance markets work well when damages occur at a known population rate, individuals can do little to alter their own damage risks, individuals have little knowledge about how their own damage risks deviate from the mean population risk, and real interest rates and property rights are stable. [Pg.65]

Clewell, H. J., and M. E. Andersen. Use of physiologically based pharmacokinetic modeling to investigate individual versus population risk. Toxicol. 111(1-3) 315-329, 1996. [Pg.437]

It is challenging to extrapolate general surveillance data, particularly with limited health-effects data, to individual risk estimates without the genetic, external-exposure, lifestyle, and other data that a clinician could use to adjust population risk estimates for individual cases. As a result, previous comments about communication difficulties with respect to health implications apply far more to surveillance studies than they do to the interaction of a personal or occupational physician with an individual patient or worker on whom the physician also has extensive nonbiomarker information. For example, clinicians might in rare cases determine that BEIs are appropriate comparison values for a specific patient s biomarker concentrations. [Pg.251]

The greater ease of clinical communication about biomarkers and health than of other biomonitoring communication comes with several caveats. First, not all clinical communication involves people who were study subjects for example, announcement of local (if not national) surveillance results might prompt members of the wider population to visit their doctors for consultation. The experience of environmental-risk assessors in communicating the distinction between population risks (the usual focus of risk estimates) and individual risks does not augur well for either professionals ability to communicate the difference well or constituents ability to comprehend. Second, some people subject to biomonitoring (including those... [Pg.251]

Schmidt-Nowara WW, Coultas DB, Wiggins C, Skipper BE, Samet JM. Snoring in a Hispanic-American population risk factors and association with hypertension and other morbidity. Arch Intern Med 1990 150(3) 597-601. [Pg.225]

Fig. 3.13. Summary of EPA regulatory decisions prior to 1985 on whether to regulate carcinogenic hazardous materials (Travis et al., 1987) lower-right region comprising high population risks is excluded based on assumed United States population. Fig. 3.13. Summary of EPA regulatory decisions prior to 1985 on whether to regulate carcinogenic hazardous materials (Travis et al., 1987) lower-right region comprising high population risks is excluded based on assumed United States population.
Crow, J.F. The evaluation of chemical mutagenicity data in relation to population risk Impact of various types of genetic damage and risk assessment. Environ. Health Perspect. 6 1-5, 1973. [Pg.259]

Ruffle B, Burmaster DE, Anderson PD, Gordon HD (1994) Lognormal distributions for fish consumption by the general US population. Risk Analysis, 14(44) 395 104. [Pg.93]

Currently (2004) The R. Samuel McLaughlin Centre for Population Risk Assessment, University of Ottawa, Ontario, Canada... [Pg.1]


See other pages where Risk populations is mentioned: [Pg.26]    [Pg.234]    [Pg.72]    [Pg.93]    [Pg.14]    [Pg.337]    [Pg.315]    [Pg.701]    [Pg.53]    [Pg.85]    [Pg.30]    [Pg.99]    [Pg.292]    [Pg.154]    [Pg.373]    [Pg.103]    [Pg.144]    [Pg.234]    [Pg.37]   
See also in sourсe #XX -- [ Pg.427 ]




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