Risk dietary exposure

Some animal studies indicate that dietary exposure to methyl parathion causes decreased humoral and cellular responses (Shtenberg and Dzhunusova 1968 Street and Sharma 1975). A more recent, well-designed animal study that included a battery of immuno/lymphoreticular end points showed few effects at the nonneurotoxic doses tested (Crittenden et al. 1998). No adequate studies are available in humans to assess the immunotoxic potential of methyl parathion. Therefore, studies measuring specific immunologic parameters in occupationally exposed populations are needed to provide useful information. Further studies are also needed to investigate the mechanism for methyl parathion-induced immunotoxicity since this information would help to identify special populations at risk for such effects. 

LSMBSs are designed so that the types of data to be collected meet particular objectives regarding how the data will be used. For example, the number of exemplars collected in the LSMBS will depend on the use planned for the study results. Thus, if the levels of plasticizer in packaged foods will be determined to address an acute (i.e., short-term) dietary exposure and risk concern, the sample size (i.e., number of food packages to be collected) must be adequate to support the higher percentiles... 

One common objective of an LSMBS is to refine the estimates of actual exposure of consumers to ingredients or impurities in one or more products. For example, study results might be intended to determine a realistic human dietary exposure to pesticide residues in fresh fruits and vegetables. The advent of the Food Quality Protection Act of 1996 (FQPA) has produced an enhanced focus on the exposure of children to pesticides. A well-designed and implemented LSMBS would afford the opportunity to delineate better the exposure and risk to children and other population subgroups. The LSMBS would provide consumer-level data at or near the point of consumption, allowing the refined, relevant, and realistic assessments of dietary exposure. 

OPMBS data were intended to support a valid estimate of the dietary exposure of populations and sub-populations to organophosphate residues in fresh fmits and vegetables. The results of the study were presented to the EPA in a report, with appropriate summaries. All of the study results, i.e., residue levels of each compound determined in each sample of each commodity, were also provided to the EPA in a database. EPA has recently notified the task force that the OPMBS study on the frequency and magnitude of organophosphate residues in fruits and vegetables is acceptable. The EPA is expected to utilize the data in a new assessment of potential dietary risk from organophosphate residues. 

Based on the data from controlled human studies, the NOEL for plasma cholinesterase inhibition for a single dose of chlorpyrifos is between 0.1 and 0.5 mg/kg bw/day, and the more conservative 0.1 mg/kg bw/day (100 pg/kg bw/day) is used in this assessment as the acute NOEL for chlorpyrifos. The repeated dose NOEL in humans is 0.03 mg/kg bw/day (30 pg/kg bw/day), based on plasma cholinesterase activity, and this is the basis for the establishment of the reference dose of 0.003 mg/kg bw/day (3 pg/kg bw/day) used by the EPA in assessing dietary risk to chlorpyrifos. For the work described here, both NOELs are used as bases for assessing risks to persons who have the potential for non-dietary exposure to chlorpyrifos. For exposures that are infrequent or of short duration, the 100 pg/kg bw/day NOEL is assumed to be the more appropriate value, and the lower 30 pg/kg bw/day will be used in those situations in which exposure may be considered to be more frequent. ... 

In Tables 14.9 and 14.10, the last column reports the environmental impact points (EIPs) for typical applications of organic and conventional pesticides derived from the Pesticide Environmental Assessment System, or PEAS. This model produces relative rankings of risks based on defined use rates and use patterns (the formulation used to apply a pesticide, timing, target of the application, spray equipment used, etc). PEAS scores reflect an equal balancing of acute pesticide risks to farm workers, chronic risks via dietary exposure and exposures to birds, Daphnia and bees. 

Marti-Cid R, Huertas D, Nadal M et al (2010) Dietary exposure to organochlorine compounds in Tarragona Province (Catalonia, Spain) health risks. Hum Ecol Risk Assess 16 588-602... 

Heaton, S.N., S.J. Bursian, J.P. Giesy, D.E. Tillitt, J.A. Revder, P.D. Jones, D.A. Verbrugge, T.J. Kubiak, and R.J. Aulerich. 1995. Dietary exposure of mink to carp from Saginaw Bay, Michigan. 1. Effects on reproduction and survival and the potential risks to wild mink populations. Arch. Environ. Contam. Toxicol. 28 334-343. 

Fronczak, C.M. et al., In utero dietary exposures and risk of islet autoimmunity in children, Diabetes Care, 26, 3237, 2003. 

Category C (possible human carcinogen) was evidenced by a dose-related increase in the incidence of leiomyosarcomas in the urinary bladder, a significant dose-related trend for combined hepatocellular adenomas and carcinomas in males, and a significantly higher incidence of combined lung adenomas and carcinomas in females. For the purpose of risk characterization, the RfD approach should be used for quantification of human cancer risk. The chronic exposure analysis revealed <100% RfD, and it is assumed that the chronic dietary endpoint is protective for cancer dietary exposure [64]. 

This variation results in a population with much wider variation in exposure to meat than one could find in a typical sample of the general population. Adventists who chose to use little or no meat also tend to follow many other nutritional practices that are believed to promote health. Thus, wide variation in many dietary exposures, in a population which is relatively homogeneous in many other characteristics relevant to cancer risk, provides an ideal setting to test dietary hypotheses. 

It has been demonstrated that pesticides are frequently encountered in foods, although typically at levels not considered to cause concern from the regulatory community. When placed into perspective with other food safety risks, the dietary risks from exposure to pesticides are considered to be far lower than the... 

Exposure Levels in Environmental Media. Heptachlor and heptachlor epoxide have been detected in indoor and outdoor air, surface water, groundwater, soil, sediment, and food (Larsen et al. 1971 Lewis et al. 1986). Current monitoring data on levels of both compounds in outdoor and indoor air and soil are needed. Dietary intake data for the general population were located. Intake data for other media (air and water) are needed to estimate the risk of exposure of the general population. 

The characterisation of health hazards of food contaminants, the assessment of the occurrence of undesirable compounds in food and the estimation of the dietary intake are key issues in the risk assessment. In 2000, the European Commission published a White Paper on Food Safety, which underlined the importance of ensuring the highest possible standards of food safety and proposed a new approach to achieve them. Recently, PFCs have gained increased scientific and socioeconomic interest as emerging environmental contaminants due to the unique combination of persistence, toxicity and environmental prevalence. Risk assessment of the dietary exposure to PFCs, however, is hampered by the lack of sufficient data about the occurrence of these contaminants in food. 

Fort the risk characterisation of PFGS and PFGA, the currently available information is inadequate to characterise dietary exposure in the different regions in the European Union. 

TEFs were also used by the NRC Committee on Pesticides in the Diet of Infants and Children to estimate the aggregate risk to children from dietary exposure to a mixture of pesticides (NRC 1993). 

The UK Pesticide Safety Directorate (PSD) has decided to use the TEF approach for assessment of combined risk from exposure to mixtures of acetyl cholinesterase inhibitors (organophosphate (OP) compounds and carbamates) (PSD 1999). Despite clear differences in the action of carbamates and OP compounds, the index compounds selected for all acetyl cholinesterase inhibitors were either aldicarb (carbamate) or chlorpyrifos (OP). The POD for determining relative potency was predetermined as the dose level that produced 20% inhibition of red blood cell cholinesterase in a 90-day dietary study in rats. 

The Role of Dietary Exposure in the Evaluation of Risk of Metals to Aquatic Organisms. Fairmont Hot Springs, British Columbia, Canada, 27 Jul to 1 Aug 2002. Published by SETAC, 2005. 

NEWGENERIS (Newborns and genotoxic exposure risks) Using 300,000 mother-child birth cohorts and stored specimens from biobanks, study will develop and apply biomarkers of dietary exposure to genotoxic and immunotoxic chemicals and biomarkers of early effects (European Commission 2006). Researchers will analyze blood samples from biobanks in Norway, Denmark, the United Kingdom, Spain, and Greece (European Union 2006). 

The risk to health from chemicals in food can be assessed by comparing estimates of dietary exposure with recommended safe levels of exposure. For most metals and other elements, these are the Provisional Tolerable Weekly Intakes (PTWIs) and the Provisional Tolerable Daily Intakes (PTDIs) recommended by the Joint Expert Committee on Food Additives of the Food and Agricultural Organisation of the United Nations and the World Health Organisation International Programme on Chemical Safety (JECFA). The European Commission s Scientific Committee on Food has established other relevant safe levels. These are Acceptable Daily Intakes (ADIs) for chemicals added to food, and Tolerable Daily Intakes (TDIs) for chemical contaminants. The use of the term tolerable implies permissibility rather than acceptability. All the above recommendations are estimates of the amount of substance that can be ingested over a lifetime without appreciable risk, expressed on a daily or weekly basis as appropriate. 

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. 

A tiered approach is also used for calculating estimated residues in animal commodities (meat, milk, and eggs), and higher-tier calculations can have a significant impact in decreasing estimates of dietary exposure and risk. The Tier III assessment for atrazine and simazine (Tables 27.3 and 27.4) is based on calculations of the estimated theoretical residue in animal commodities, whereas the Tier I assessments use tolerance values. These theoretical residues are often referred to as secondary residues. Calculations for estimating secondary residues in animal commodities are performed by constructing livestock (beef, dairy, and poultry) diets comprised of treated feed items to obtain a... 

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