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Distribution human exposure estimation

The Toxic Substances Control Act (TSCA) was enacted in 1976 to identify and control toxic chemical ha2ards to human health and the environment. One of the main provisions of TSCA was to estabUsh and maintain an inventory of all chemicals in commerce in the United States for the purpose of regulating any of the chemicals that might pose an unreasonable risk to human health or the environment. An initial inventory of chemicals was estabhshed by requiring companies to report to the United States Environmental Protection Agency (USEPA) all substances that were imported, manufactured, processed, distributed, or disposed of in the United States. Over 50,000 chemical substances were reported. PoUowing this initial inventory, introduction of all new chemical substances requires a Premanufacturing Notification (PMN) process. To be included in the PMN are the identity of the new chemical, the estimated first year and maximum production volume, manufacture and process information, a description of proposed use, potential release to the environment, possible human exposure to the new substance, and any health or environmental test data available at the time of submission. In the 10 years that TSCA has been in effect, the USEPA has received over 10,000 PMNs and up to 10% of the submissions each year are for dyes (382)... [Pg.388]

Risk assessment pertains to characterization of the probability of adverse health effects occurring as a result of human exposure. Recent trends in risk assessment have encouraged the use of realistic exposure scenarios, the totality of available data, and the uncertainty in the data, as well as their quality, in arriving at a best estimate of the risk to exposed populations. The use of "worst case" and even other single point values is an extremely conservative approach and does not offer realistic characterization of risk. Even the use of arithmetic mean values obtained under maximum use conditions may be considered to be conservative and not descriptive of the range of exposures experienced by workers. Use of the entirety of data is more scientific and statistically defensible and would provide a distribution of plausible values. [Pg.36]

Another case of multimedia fate modeling may be exemplified by human inhalation exposure estimates for PCB spills. The spill size is estimated considering both spread and soil infiltration. Volatilization calculations were carried out to get transfer rates into the air compartment. Finally, plume calculations using local meteorological statistics produced ambient concentration patterns which can be subsequently folded together with population distributions to obtain exposures. [Pg.94]

Due to the second criterion, time-to-tumor models were eliminated from consideration. These models require more detailed experimental data than is generally available. Moreover, it is difficult and unproductive to interpret the distribution of time-to-tumor in the context of human exposures. In most cases, the time-to-tumor variable would be integrated over a human lifetime, thus reducing the model to a purely dose-dependent one. Therefore we restrict our attention to quantal response models that estimate lifetime risks. [Pg.303]

Regulatory agencies also attempt to develop more realistic estimates, but this is difficult, and a scientific consensus on just what exposure pattern should be presumed desirable for risk assessment is not available, except for a few circumstances (food additives, human drugs, and a few others). Much attention is now focused on methods to develop information on the full distribution of exposures in a population, but this can be technically difficult to achieve. [Pg.230]

Cumulative distributions of the logarithms of NOELs were plotted separately for each of the stmcmral classes. The 5th percentile NOEL was estimated for each stmctural class and this was in mrn converted to a human exposure threshold by applying the conventional default safety factor of 100 (Section 5.2.1). The stmcmre-based, tiered TTC values established were 1800 p,g/person/ day (Class I), 540 pg/person/day (Class II), and 90 pg/person/day (Class III). Endpoints covered include systemic toxicity except mutagenicity and carcinogenicity. Later work increased the number of chemicals in the database from 613 to 900 without altering the cumulative distributions of NOELs (Barlow 2005). [Pg.198]

Quantitative estimation of human exposure, environmental release/emissions rates and environmental distribution. This may be achieved through modelling or by field monitoring. [Pg.117]

Absorption, Distribution, Metaboiism, and Excretion. There is relatively little quantitative information on the systemic absorption of inhaled carbon tetrachloride in animals and humans, with estimates ranging from 30% to 60% (Lehmann and Schmidt-Kehl 1936 McCollister et al. 1951). In order to confirm the dose absorbed during inhalation exposures to carbon tetrachloride, it would be useful to determine the systemic uptake of carbon tetrachloride in additional animal experiments, with special attention to concentration- and time-dependency of absorption. It may be useful to conduct short-term studies of the relative absorption, disposition, and toxicity of inhaled versus ingested carbon tetrachloride. Such studies can yield information pertinent to route-to-route extrapolation and may be more economical than conducting a 2-year inhalation cancer bioassay of carbon tetrachloride. [Pg.101]

Radium is a naturally-occurring metal and is almost ubiquitous at low concentrations in air, water, soil, rocks, and food. The median concentrations of radium-226 and radium-228 in drinking water are generally low, but there are geographic areas where higher concentrations of radium are known to occur. The utilization of coal and uranium has resulted in re-distributing radium in the environment, but the overall effects appear to be small. Estimated levels of average human exposure to radium of nonoccupational populations are presented in Table 5-1. [Pg.58]

Probabilistic techniques (including Monte Carlo methods) were used to incorporate the variation in individual human exposures and resulting intakes. The frequency distributions of individual intakes and MOEs in a population were estimated from the number of individuals in each of the population s component subpopulations and their corresponding intake distributions. [Pg.477]

Accurate exposure and biological monitoring data are crucial to the evaluation of residential exposure and risk estimates since the potential health risks associated with a pesticide depend on the amount of exposure to the pesticide, its toxicity and the susceptibility of the exposed population. Prediction of whether adverse health effects will occur in humans can be made by comparing the exposure estimate to the No Observed Adverse Effect Level (NOAEL) derived from the animal toxicity data. Uncertainty arises from the input data used in an assessment, e.g. variability in time-activity patterns, contact with exposure media, bioavailability, exposure duration, frequency of product use and differences in the route of exposure in humans from that in the animal studies (since absorption, distribution, metabolism and elimination kinetics may differ substantially by exposure route). [Pg.137]

Fushimi A, Hasegawa S, Takahashi K et al (2008) Atmospheric fate of nuclei-mode particles estimated from the number concentrations and chemical composition of particles measured at roadside and background sites. Atmos Environ 42 949-959 Gehin E, Ramalho O, Kirchner S (2008) Size distribution and emission rate measurements of fine and ultrafine particle from indoor human activities. Atmos Environ 42 8341-8352 Graham S, McCurdy T (2004) Developing meaningful cohorts for human exposure models. J Expo Anal Environ Epidemiol 14 23 3... [Pg.496]

Chlordane is readily absorbed by warm-blooded animals through skin, diet, and inhalation. It is quickly distributed in the body and tends to concentrate in liver and fat (WHO 1984). Up to 75% of a single oral dose of chlordane administered to rats and mice was absorbed in the gut, and up to 76% of an aerosol dose was absorbed in the respiratory tract (Nomeir and Hajjar 1987). Rabbits absorbed 33% in the gut following oral administration (USEPA 1988). Chlordane residues in mammals were usually not measurable 4 to 8 weeks after cessation of exposure (Ingle 1965). Chlordane persistence in human serum and whole body was estimated at 88 days and 21 days, respectively this compares to a Tb 1/2 of about 23 days in rats fed chlordane for 56 days (USEPA 1980). [Pg.831]


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