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Estimated human intake

Vanadium. Vanadium is essential in rats and chicks (85,156). Estimated human intake is less than 4 mg/d. In animals, deficiency results in impaired growth, reproduction, and Hpid metaboHsm (157), and altered thyroid peroxidase activities (112). The levels of coen2yme A and coen2yme Q q in rats are reduced and monoamine oxidase activity is increased when rats are given excess vanadium (157). Vanadium may play a role in the regulation of (NaK)—ATPase, phosphoryl transferases, adenylate cyclase, and protein kinases (112). [Pg.388]

The Margin of Exposure (MOE) in the context of the assessment of compounds that are both genotoxic and carcinogenic, as defined in EFSA (2005), is different from the OECD/IPCS definition given above The Margin of Exposure (MOE) is the ratio between a defined point on the dose-response curve (reference point) for the adverse effect of the compound in the animal carcinogenicity study and the estimated human intake of the compound. ... [Pg.312]

The MOEs are calculated by dividing the reference point on the dose-response curve (e.g., BMDLio or T25) by the estimated human intakes (BMDLio or T25/intake). [Pg.313]

Exposure Levels in Environmental Media. Volumes of data exist on levels of 1,1,1-trichloroethane in environmental media, with the exception of levels in soil samples. Continued monitoring of environmental media is warranted. Blind monitoring at this stage, however, might be replaced with methods that allow both the continued determination of the environmental burden of 1,1.1-trichloroethane and correlation with human burden, like that performed in the TEAM studies. These and other studies have estimated human intake of 1,1,1-trichloroethane from environmental media. For members of the general population near hazardous waste sites, total exposure to... [Pg.166]

In summary, the estimated concentrations are not necessarily consistent with the measured concentrations, and therefore, it is not reliable to estimate human intakes of SCCPs via food based on the results of the model estimation. Also, it is assumed that the high concentrations in fat are probably from exposure sources overseas however, it is not possible to estimate those concentrations by the model. Therefore, for risk characterization in this assessment, it is considered relevant to estimate human intakes directly using the analytical results by the market basket survey as actual intakes of the Japanese. [Pg.182]

The Committee previously concluded that the NOEL of 750 mg/kg bw per day for inflammatory responses in the gastrointestinal tract greatly exceeded the estimated human intake of carrageenan or processed Eucheuma seaweed of 30-50 mg/person per day from their use as food additives and therefore allocated a group ADI not specified . The new information available to the Committee did not alterthis conclusion. The group ADI not specified for the sum of carrageenan and processed Eucheuma seaweed was maintained for food additive uses in foods other than infant formula. [Pg.82]

Exposure. The exposure of humans and animals to mercury from the general environment occurs mainly by inhalation and ingestion of terrestrial and aquatic food chain items. Pish generally rank the highest (10—300 ng/g) in food chain concentrations of mercury. Swordfish and pike may frequently exceed 1 p.g/g (27). Most of the mercury in fish is methyl mercury [593-74-8]. Worldwide, the estimated average intake of total dietary mercury is 5—10 p-g/d in Europe, Russia, and Canada, 20 pg/d in the United States, and 40—80 pg/d in Japan (27). [Pg.108]

An attempt to estimate human daily impact of N nitroso compounds is shown in Table I. The apparent intake from food of preformed nitrosamines is comparatively low, at least in these surveys of a Western diet in England (3). The Intake directly to the respiratory tract from smoking could be somewhat larger. However, if the blood levels reported are confirmed as correct, then inputs of up to 700 meg per day of at least N nitrosodimethylamine (NDMA) may be calculated, based on pharmacokinetic considerations of data obtained in animals and extrapolated to man. It should be emphasized that no information is available at present on nitrosamide intake or in vivo formation, largely because of analytical limitations. [Pg.196]

Daily consumption of various fruits, vegetables, and derived juices contributes to human intake of carotenoids. The estimation of carotenoid intakes has been made possible throngh publication of the qnalitative and qnantitative carotenoid contents of commonly consnmed foods. Average intake estimates in the United States are around 6.5 mg/day. In seven conntries in Enrope, the average total carotenoid intake based on the snm of the five carotenoids was approximately 14 mg/day. When dietary source of carotenoids were analyzed, carrots appeared as the major sonrces of p-carotene in all conntries except Spain, where spinach was the main contribntor. [Pg.128]

Generation of data on the nutrient content of agricultural products and foods forms the basis for estimating nutrient intakes of populations via dietary surveys, nutritional labelling for consumer protection, nutrition education for consumer food choice, home and institution menu planning and food purchase, and for research in nutrient requirements and metabolism, toxicant chemical composition is used to assess effects of farm management practices, crop culture, and food processing on chemical content and implications for human health. [Pg.210]

EUSES. As in the case of USEtox model, the present model provides outputs such as human intake fraction of a certain substance for different exposure pathways. In the present case study, estimation of the human intake doses for Guiyu was calculated. These results were compared with the incidence and severity of the effects (dose-response assessment). [Pg.360]

Human intake of total mercury from the diet normally ranges between 7 and 16 pg daily (Schumacher et al. 1994 Richardson et al. 1995). Fish consumption accounts for much of this exposure in the form of methylmercury 27% of the intake, and 40% of the absorbed dose. Intake of inorganic mercury arises primarily from foods other than fish, and is estimated at 1.8 pg daily with 0.18 pg absorbed daily (Richardson etal. 1995). In certain areas of India, blood mercury concentrations of people who ate fish were three to four times higher than non-fish eaters (Srinivasen and Mahajan 1989). In some countries, mercury in dental amalgams accounts for 2.8 pg daily, equivalent to as much as 36% of the total mercury intake and 42% of the absorbed dose (USPHS... [Pg.367]

Exposure Levels in Environmental Media. 1,2-Dibromoethane has been detected in ambient air, groundwater, soils, and foodstuffs (Brodzinsky and Singh 1983 EPA 1983 Ewing et al. 1977 Daft 1989 Page 1981 Pellizzari et al. 1978 Singh et al. 1981 Williams et al. 1988). However, the monitoring data for these media are not current. Estimates of human intake have been made on the basis of these older data. Additional information is needed on the current levels of... [Pg.99]

Exposure Levels in Environmental Media. All humans are exposed to at least low levels of chloroform via inhalation of contaminated air, and most humans are exposed by drinking contaminated water. Estimates from intake via inhalation and ingestion of drinking water, based on limited data, are available (see Section 5.5). Exposure from foods cannot be estimated, due to the lack of data. Current information on exposure to chloroform from water, air, and foods, especially for workers or people who live near manufacturing and use facilities, water and waste water-treatment plants, municipal and industrial... [Pg.219]

Hutchins et al. 1980 Oliveira and Sitar 1985 Ram et al. 1985 Sawhney and Kozlowski 1984 Stuermer et al. 1982 Weber and Matsumota 1987) only (sources of groundwater contamination include hazardous waste sites). Data describing the exposure levels in air and surface water are lacking. It is not clear whether monitoring studies were not performed, or were not found. Quantified levels of cresols in food are also lacking. Estimates of human intake are not available. [Pg.130]

No information was found in the available literature on estimates of human intake of HDI Irom the various environmental media. Because the potential for significant widespread environmental contamination is expected to be very low, such estimates would appear to be needed primarily for populations living or working near potential emission sources of HDI. [Pg.149]

Polybrominated Biphenyls. Only limited data on the levels of PBBs in ambient air are available (DeCarlo 1979). Data are available on the levels of PBBs in effluent water from manufacturing plants, in river water, stream sediment, and soil in the vicinity of the plants, in sludge of a waste treatment plant, and in groundwater of a landfill site (Hesse and Powers 1978 Shah 1978). No data on the level of PBBs in drinking water from the contaminated sites were located. No estimate on the human intake of PBBs from any of the various environmental media was located in the literature. [Pg.381]

An important outcome of the JECFA evaluation is the establishment of an ADI for a food additive. The ADI is based on the available toxicological data and the no adverse effect level in the relevant species. JECFA defines the ADI as an estimate of the amount of a food additive, expressed on a body weight basis, that can be ingested daily over a lifetime without appreciable health risk (8). JECFA utilizes animal data to determine the ADI based on the highest no-observed-adverse-effect level (NOAEL), and a safety factor is applied to the NOAEL to provide a margin of safety when extrapolating animal data to humans. JECFA typically uses safety factors of 50, 100, or 200 in the determination of an ADI. The NOAEL is divided by the safety factor to calculate the ADI. The food additive is considered safe for its intended use if the human exposure does not exceed the ADI on a chronic basis. This type of information may potentially be used to help assess the safety of a pharmaceutical excipient that is also used as a food additive, based on a comparison of the ADI to the estimated daily intake of the excipient. [Pg.72]


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