Risk assessment epidemiology

Dodson, R.F. and Hammar, S.P., Asbestos Risk Assessment, Epidemiology, and Health Effects, Taylor Francis Group, Boca Raton, FL, 2006. 

Grandjean, P., White, R. E, and Weihe, P. (1996). Neurobehavioral epidemiology Application in risk assessment. Enniron. Health Perspect. 104(2), 397- 00. 

Klasson-Wehler, E., Kuroki, H., and Athanasiadou, M. et al. (1992). Selective retention of hydroxylated PCBs in blood. In Organohalogen Compounds Vol 10 Toxicology, Epidemiology, Risk Assessment, and Management, Helsinki Finnish Institute of Occupational Health 121-122. 

There is a growing need to better characterize the health risk related to occupational and environmental exposure to pesticides. Risk characterization is a basic step in the assessment and management of the health risks related to chemicals (Tordoir and Maroni, 1994). Evaluation of exposure, which may be performed through environmental and biological monitoring, is a fundamental component of risk assessment. Biomarkers are useful tools that may be used in risk assessment to confirm exposure or to quantify it by estimating the internal dose. Besides their use in risk assessment, biomarkers also represent a fundamental tool to improve the effectiveness of medical and epidemiological surveillance. 

Ellett, W. H. and N. S. Nelson, Epidemiology and risk assessment Testing models for radon-induced lung cancer, in Indoor Air and Human Health (R. B. Gammage and S. V. Kaye, eds) pp. 79-107, Lewis Publishers, Inc., Chelsea, Michigan (1985). 

While profound immunosuppression can lead to an increased incidence of infectious or neoplastic diseases, interpreting data from experimental immunotoxicology studies or epidemiological studies for quantitative risk assessment purposes can be problematic. This is because inadvertent exposures to immunotoxic agents may often be expressed as a mild-to-moderate change, reflected, for example, by a 15 to 25% decrement in an immune parameter compared to control values. To help address the clinical consequences of mild-to-moderate immunosuppression, we examined available experimental, clinical and epidemiological studies that examined the association between suppression of immune function and infectious disease, independent of the etiology of suppression. 

Exposures in the population of interest will generally reveal that incurred dose is only a small fraction, and sometimes a very tiny fraction, of that at which toxic responses has been or can be directly measured, in either epidemiology or animal studies. Occupational populations (Table 8.1, Scenario C) may be exposed at doses close to those for which data are available, but general population exposures are usually much smaller. Thus, to estimate risk it will be necessary to incorporate some form of extrapolation from the available dose-response data to estimate toxic response (risk) in the range of doses expected to be incurred by the population that is the subject of the risk assessment. 

Most scientists would hold that these unknowns and uncertainties in the regulatory risk-assessment model would tend to favor risk overestimation rather than underestimation or accurate prediction. While this view seems correct, it must be admitted that there is no epidemiological method available to test the hypothesis of an extra lifetime cancer risk of about 10 per 1000 000 from methylene chloride in drinking water. The same conclusion holds for most environmental carcinogens. It is also the case that more uncertainties attend the risk assessment process than we have indicated above. 

Two of the more interesting uses of pharmacokinetic data in risk assessment involve the neurotoxic agents lead and methylmercury (Chapter 4). In the case of lead, epidemiological studies have typically involved the development of quantitative relationships between levels of lead in the blood and adverse health effects. Other measures of lead in the body have also been used. Levels in blood are now very easy to measure, and they do carry the strong advantage that they integrate cumulative exposures from many possible sources (water, food, paint, soil, air, consumer products). Current public health targets for lead are expressed as blood concentrations, typically in pg/dL (Chapter 4). 

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