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Chemical exposure index calculation

Figure 10-7 Procedure for calculating the Chemical Exposure Index (CEI). Source Dow s Chemical Exposure Index Guide (New York American Institute of Chemical Engineers, 1994). Figure 10-7 Procedure for calculating the Chemical Exposure Index (CEI). Source Dow s Chemical Exposure Index Guide (New York American Institute of Chemical Engineers, 1994).
Risk indices are usually single-number estimates, which may be used to compare one risk with another or used in an absolute sense compared to a specific target. For risks to employees the fatal accident rate (FAR) is a commonly apphed measure. The FAR is a singlenumber index, which is the expected number of fatalities from a specific event based on 10 exposure hours. For workers in a chemical plant, the FAR could be calculated as follows ... [Pg.2277]

For each clironic exposure padiway (i.e., seven years to lifetime exposure), calculate a sepmate clironic hazard index from die rados of the clironic daily intake (GDI) to die clironic reference dose (RfD) for individual chemicals as described below ... [Pg.399]

The calculations of the Inherent Safety Index (ISI) are made on the basis of the worst situation. The approach of the worst case describes the most risky situation that can appear. A low index value represents an inherently safer process. In the calculations the greatest sum of flammability, explosiveness and toxic exposure subindices is used. For inventory and process temperature and pressure the maximum expected values are used. The worst possible interaction between chemical substances or pieces of equipment and the worst process structure give the values of these subindices. [Pg.60]

In many respects, the foundations and framework of the proposed risk-based hazardous waste classification system and the recommended approaches to implementation are intended to be neutral in regard to the degree of conservatism in protecting public health. With respect to calculations of risk or dose in the numerator of the risk index, important examples include (1) the recommendation that best estimates (MLEs) of probability coefficients for stochastic responses should be used for all substances that cause stochastic responses in classifying waste, rather than upper bounds (UCLs) as normally used in risk assessments for chemicals that induce stochastic effects, and (2) the recommended approach to estimating threshold doses of substances that induce deterministic effects in humans based on lower confidence limits of benchmark doses obtained from studies in humans or animals. Similarly, NCRP believes that the allowable (negligible or acceptable) risks or doses in the denominator of the risk index should be consistent with values used in health protection of the public in other routine exposure situations. NCRP does not believe that the allowable risks or doses assumed for purposes of waste classification should include margins of safety that are not applied in other situations. [Pg.320]

The results in Table 7.8 indicate that the organ- and endpoint-specific risk indexes are about 0.7 to 0.8 in all cases, due mainly to intakes of lead. The maximum risk index for any organ or endpoint is about 0.8. Truncating this result using the INTEGER function, as indicated in Equation 6.5, gives a risk index for all deterministic hazardous chemicals in the waste of zero. This result means that the calculated dose in all organs and for all endpoints due to exposure to all deterministic substances that cause deterministic responses in the waste is less than the assumed acceptable dose of 10 times RfDs. Therefore, based only on consideration of substances that... [Pg.340]

Stochastic Risk Index for Hazardous Chemical Constituents. Calculation of the risk index for all hazardous chemicals in the waste that cause stochastic effects is performed in the same manner as in the previous examples for radioactive wastes. The calculated risk for each such substance, based on the assumed exposure scenario, is summed and then divided by the acceptable lifetime risk of 10 3 for classification as low-hazard waste (see Table 7.1). The risk for each chemical is calculated by multiplying the arithmetic mean of the concentration in the waste given in Table 7.5 by the intake rate from ingestion, inhalation, or dermal absorption per unit concentration discussed in Section 7.1.7.3 and 10 percent of the appropriate slope factor in Table 7.7 (see Section 7.1.7.1) adjusted for the exposure time. Since the slope factors assume chronic lifetime exposure, they must be reduced by a factor of 70 based on the assumption that the exposure scenario at the hazardous waste site occurs only once over an individual s lifetime. In addition, a simplifying assumption is made that whenever more than one slope factor is given for a hazardous substance in Table 7.7, the higher value was applied to the total intake rate by all routes of exposure of about 4 X 10 8 mg (kg d) 1 per ppm. This assumption should be conservative. [Pg.342]

The same procedure above may be applied for simultaneous shorler-lenn exposures to several chemicals. For drinking water exposures, 1- and 10-day Hcallli Advisories can be used as reference toxicity values. Depending on available data, a separate hazard index might also be calculated for developmental toxicants (using RfDj,s), wliich might cause adverse effects following exposures of only a few days. [Pg.400]

If the hazard index is greater than 1, i.e., if exposure exceeds the estimated threshold for a specified noncancer health effect, then the exposed population is considered to be at risk. If a risk scenario includes several pathways of exposure to a chemical of concern, a hazard index is calculated separately for each pathway, and the results are summed to find the total hazard index for that chemical. [Pg.144]

Two other approaches are used to estimate noncancer risks from toxic chemicals margin of exposure and therapeutic index. Both are less formal and more approximate than the hazard index. The margin of exposure (MOE) is the ratio of the NOAEL in an animal toxicity study to the CDI projected for a human population. Uncertainty factors are omitted from the calculation. Eor example, if the NOAEL for reproductive toxicity were, say, 1.5 mg/kg/day, and the CDI were 0.003 mg/kg/day, then the MOE would be 500. The MOE is interpreted by comparing it to a margin of safety (MOS) established by a government agency. In general, an MOE of less than 100 is considered to be cause for concern. [Pg.145]

The chronic daily intake (CDI) estimated in the analysis of exposure, the second step of the risk assessment, is used to calculate the risks of both noncancer health effects and cancer. Risk calculations are also referred to as quantitative risk assessment, a term that is somewhat misleading because the word quantitative implies a high degree of accuracy, which is clearly not the case. In the first risk scenario described in Section 8.3, future residents drink arsenic-contaminated water from the aquifer beneath a former Superfund site. Their CDI by this pathway is estimated to be 0.0I6I mg/kg/day of arsenic. The oral reference dose (RfD) for arsenic is 3 x lO"" mg/kg/day, according to the EPA s Integrated Risk Information System (IRIS) (U.S. EPA 2009). The hazard index (HI) for noncancer health effects caused by this chemical of concern by this exposure pathway is calculated using Equation (8.3) ... [Pg.147]

Risks from other pathways of exposure and/or other chemicals of concern are considered to be additive unless there is evidence that the toxicities of two or more chemicals are synergistic (i.e., enhance each other so that risk is greater than the sum of the risk from either chemical alone) or inhibitory (i.e., interfere with each other so that risk is less than the sum of the risk from either chemical alone). Very little is known about the interactions between toxic chemicals, and risks from multiple chemicals and multiple exposure pathways are usually added together to obtain an estimate of total risk. In the case of noncancer health risk, the hazard index (HI) is calculated separately for each chemical and each exposure pathway, and total risk is equal to the sum of the HI values from aU chanicals and aU pathways. In the case of cancer risk, the cancer incidence is calculated for each ch ical and each exposure pathway, and total risk is equal to the sum of the caucer incideuces from all chemicals and all pathways. Cancer risk is the probability of getting cancer (morbidity), not the probability of dying from cancer (mortality). Many people get cancer and survive. [Pg.148]


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