Dietary exposure food consumption surveys

Cohort study data on population dietary exposure, dietary data from case-control studies and food consumption surveys... 

In the eighties and early nineties, the USEPA evaluated dietary risk with an analysis method known as the Dietary Risk Evaluation System (DRES) (USEPA, 1991), which was based on the USDA s 1977 to 1978 National Food Consumption Survey. Consequently, dietary exposure assessments became genetically referred to as DRES analyses. Currently, the USEPA is using the Dietary Exposure Evaluation Model (DEEM , Version 7.87) (Exponent, 2000), which allows exposure to be calculated from 1994 to 1996 CSFII along with the 1998 supplemental children s survey information. 

In the UK, the Ministry of Agriculture, Fisheries, and Food and the Department of Health have conducted four sets of food consumption surveys between 1983 and 1997. These surveys make up the UK s National Diet and Nutrition Survey (NDNS) program. The UK has conducted surveys for infants [15], schoolchildren [16], adults [17], and most recently, yoimg people [18]. The food consumption information from these surveys is used for the various UK dietary exposure models, including the TMDI and the NESTI calculations. Elsewhere in the EU, dietary risk assessments may be based upon national food consultation surveys, such as the German data [20], or upon the regional diets... 

The FDA and EPA recognize that the diets of infants and children may differ substantially from those of adults and that they consume more food for their size than adults. As a result, they may be exposed to proportionately more residues. The FDA and EPA address these differences by combining survey information on food consumption by nursing infants, non-nursing infants, and children with data on residues to estimate their dietary exposure. The FDA and EPA also use this process to estimate exposure for other age groups, as well as several different ethnic groups and regional populations. 

The UK Total Diet Study (TDS) relies on nationally representative information about the average food consumption by individual households researched in the UK National Food Survey (based on a survey of approximately 7000 households).2,3 Typical diets are constructed based on these data. Foodstuffs are purchased from retail outlets, then prepared and cooked in the normal manner. The individual foodstuffs are then usually combined into various groups of similar foods - for example cereals, green vegetables and fish - in the proportions eaten on average by consumers. Population dietary exposures can then be calculated using data from the TDS samples. 

These are estimates of dietary exposure to inorganic contaminants for individuals who eat average amounts of food (i.e. mean consumers) and those who eat more than average (i.e. upper range (97.5th percentile) consumers) and are based on consumption data from the UK National Adult Dietary Survey (NADS).4 They are calculated using the mean upper bound concentrations of specific contaminants in each food group and the consumption data from the NADS. Consumer exposure estimates are less suitable for following trends in exposure than population estimates as they are based on consumption data from the NADS which was carried out only once in 1986 and 1987 and is not updated... 

Dietary exposure to pesticides (or to xenobiotics in general) is determined by calculating the product of the amount of chemical in or on the food and the total quantity of food consumed. The quantity of chemical potentially consumed in foods can be estimated from data obtained from residue field trials, metabolism studies, and/or monitoring data. Information from these sources is then analyzed with one of several available models containing food consumption factors from surveys conducted by the United States Department of Agriculture (USDA). For calculation of... 

Clearly, the data for food consumption is a very important component of the dietary exposure model. There are some differences in the approaches taken in the US and in the EU, although food consumption data are not collected or treated the same way across the EU. In addition to differences in survey design and collection methods, the organization of the data can also have an impact upon the dietary risk assessment. 

Dietary exposure is calculated as the very simple product of the amount of food consumed and the magnitude of the residue on the food. Unlike the food consumption value, which often is available from only one source (a government survey), the value of the residue portion of the equation may be provided from a wide variety of sources. These values range from the tolerance or MRL value, to data obtained from residue monitoring programs. The use to which various residue data may be put is often dictated by specific science policies within a given coimtry. 

Several assessments were conducted to illushate the impact of different procedures on dietary risk assessment. In all cases, consumption data from the UK surveys were used. One of the differences between the US and the EU is the food consumption data. However, conducting assessments with both US and UK food consumption data will confound the comparisons, so the assessments will be run using only the UK food consumption data. All exposure estimates are presented as percent of the chronic Reference Dose (cRiD) of 0.005 mg/kg bw/day or the acute Reference Dose (aRfD) of 0.01 mg/kg bw/day (both toxicity values are hypothetical for illushative purposes). 

The data from the Continuing Survey of Food Intake by Individuals (CSFII) generated by the U.S. Department of Agriculture from 1989 to 1995 rely on self-administered food consumption diaries for the second and third days of its 3 days of reporting (discussed in EPA 1997). The CSFII data have been used by the U.S. EPA to estimate fish consumption in the U.S. population (Jacobs et al. 1998) and to estimate MeHg intake (EPA 1997). The National Purchase Diary conducted by the Market Research Corporation used dietary diaries over 1-month periods between 1973 and 1974 (discussed in EPA 1997). The fish-consumption portions of these diary data were used to estimate MeHg exposure in the U.S. population (Stem 1993, EPA 1997). 

AFBi dietary exposure estimates were assessed in Japan based on food consumption data from the 2005 National Health and Nutrition Survey for 2 consecutive days (17 827 individuals). Surveillance data on AFBi concentration levels were available from a retail food survey, with samples purchased in a random manner from local supermarkets and small retail shops in all parts of Japan from the summer of 2004 to the winter of 2006 (Sugita-Konishi et al., 2007). Foods analysed included peanut, peanut butter, chocolate, pistachio, spices, almond, job s tears tea and buckwheat. A probabilistic approach was used to simulate the dietary exposure distributions in each age group with three different scenarios of MLs of AFT in tree nuts (10, 15 and 20 pg/kg), following the same methodology as described previously for the EFSA opinion and assuming a lognormal distribution for occurrence data. 

Food components differ greatly in lead content, reflecting in part differences in production and distribution. Food Pb intakes differ as a function of, e.g., food consumption habits. This has required attention not only to concentrations of lead in classes of dietary components but also to quantities of these components consumed on a typical or daily basis. Various national or international surveys, for that reason, have determined and reported both levels of Pb in diet categories and population consumption patterns to permit quantification of net exposures to lead in diet. 

Children are also exposed to phthalates via dietary ejqtosure, most often through the consumption of infant formnla. A stndy analyzing phthalates in 29 diet samples, 11 baby food samples, and 11 samples of infant formnla found one or more plasticizers in all of the diet samples (0.09-0.19 mg DBP/kg 0.017-0.019 mg BBP/kg 0.11-0.18 mg DEHP/kg and 0.13-0.14 mg DEHA/kg), as well as one or more phthalates in 50% of both the baby foods and infant formnla samples. An nnqnantified and unspecified isomer of DHP was identified in baby formnlas from the UK (7 of 12 formulas), and an nnspecified DHP isomer was detected, at a level below the limit of detection of 0.01 mg/kg, in breast and commercial milk, cream, nnts, and baby food. Estimated DBP exposnre levels from food ranged from 2.3 pg/kg bw/day to 5.0 mg/kg bw/day in children 12-19 years old and 6 months to 4 years of age, respectively. Based on a 1996 survey, the MAFF estimated exposure levels of DBP for infants at 2.4 pg/kg bw/day at birth and 1.4 pg/kg bw/day at 6 months of age. In a follow-np snrvey two years later, lower exposure levels were estimated. "" In 1996, the US reported DBP levels ranging from <0.005-0.011 mg/kg approximately 10-fold lower than concentrations measured in the UK. "" Other reports of DBP in baby food, breast milk, and formula in Germany and Japan were foimd to be within the range of that reported by the MAFF. The MAFF also evaluated exposure to BBP via baby formulae. Exposure of infants and children to BBP was estimated at 0.2 pg/... 

National and International Dietary Pb Surveys A number of dietary Pb surveys have been carried out in the United States and around the world. Summaries of these surveys are presented in this section. Some surveys have simply reported descriptive statistics for lead concentrations in dietary groups and levels of Pb in individual food components within those groups, e.g., measured Pb levels in cereals as a group. Other surveys have reported Pb levels in dietary components and coupled these with consumption patterns to provide intakes of food Pb in some time frame, typically as daily total intakes. Some survey reports have mainly concerned themselves with total dietary Pb intakes. This chapter confines itself to Pb levels in foods and presents intakes and uptakes in the context of human exposures in later sections. 

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