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Atrazine dietary consumption

The doses from exposure are characterized by distributions. For each possible dose level, these distributions quantify the probability that an individual in a specified population or subpopulation will receive that dose level as a result of exposure to atrazine and simazine through drinking water ingestion, dietary consumption, herbicide handling, or a combination of these potential exposure routes. For chronic toxic endpoints, the traditional (default) dose metric summarizing a lifetime of exposure is the lifetime average daily dose (LADD). Distributions of LADDs have been determined, and the corresponding distributions of the MOEs are presented herein. [Pg.479]

Using Equation (31.2), distributional analyses of dietary exposure to atrazine and its chloro-metabolites in the United States and the four regions (Northwest, North Central, Southern, or Western) indicate that at least 95% of the estimated LADDs from dietary consumption have an MOE of at least 300000 in each of the four regions and 330000 in the United States as a whole (Figure 31.4). [Pg.485]

While the following two observations are not critical in the distributional characterization of the intake of atrazine and simazine from dietary consumption, these observations can be important in other situations. First, making the assumption that the residue concentration in an individual s food is the same every time that food is consumed (as in Equation (31.2) exaggerates the variability in the intake distribution. Without this assumption, both the low and high percentiles of the intake distribution would be closer to the median intake, and the 95% lower bound on the MOE would increase. Second, when a sum is being characterized (such as the sum of intakes in Equation (31.2), it is important to determine explicitly the probability distribution of the entire sum and not to attempt to infer the characteristics of the distribution of the sum indirectly from the distributions of its components. For example, the 95th percentile of a sum may be much smaller than the sum of the 95th percentiles of its components. [Pg.485]

Figure 31.4 Distributions of the MOEs for atrazine plus its chloro-metabolites from dietary consumption. Figure 31.4 Distributions of the MOEs for atrazine plus its chloro-metabolites from dietary consumption.
Figure 31.13 Distributions of the MOEs for atrazine herbicide handlers involved in corn production from their use of flowable formulation or WDGs and from their herbicide handling combined with both drinking water ingestion and dietary consumption. Figure 31.13 Distributions of the MOEs for atrazine herbicide handlers involved in corn production from their use of flowable formulation or WDGs and from their herbicide handling combined with both drinking water ingestion and dietary consumption.
The Monte Carlo-based distributional characterizations of the MOE indicate that neither occupational exposure nor environmental exposure to atrazine and simazine is likely to produce adverse health consequences in the US population. The MOEs are very large and suggest an ample margin of safety (Tables 31.1 and 31.2). In the distributions, the MOEs are generally well above 1000 for drinking water and dietary consumption and well above 100 for herbicide handling. [Pg.494]

Distributions of the MOE have been presented for individual exposure pathways (drinking water ingestion, dietary consumption, and herbicide handling), for the combined exposure pathways, and for atrazine and simazine both separately and combined. The MOEs have been calculated using a lower bound on the ED10 for the most sensitive effect in the most sensitive sex, strain, and species studied in chronic animal bioassays (i.e., mammary tumors in female SD rats). This mammary tumor response in the SD rat is not relevant to humans (IARC, 1999 United Kingdom, 2000 USEPA, 2003 Australia, 2004). [Pg.494]

The exposure from each of the routes of exposure (drinking water ingestion, dietary consumption and herbicide handling by workers) is described by an equation in the atrazine and simazine assessment. Some of the components of these equations have values that are variable (e.g. from individual to individual, from one year to the next, from one serving of a specific food to another serving, and from one handling of a herbicide to another handling). These variable components of the exposure equations are described by probability distributions that reflect the relative frequency of the different values for the variable. [Pg.286]

Figure 8.11 Distributions of the margins of exposure for atrazine in the USA from drinking water ingestion (W), dietary consumption (D) and both exposure pathways combined (W + D)... Figure 8.11 Distributions of the margins of exposure for atrazine in the USA from drinking water ingestion (W), dietary consumption (D) and both exposure pathways combined (W + D)...
Figure 8.16 Distributions of the margins of exposure for US herbicide handlers who apply either atrazine or simazine and who are also possibly exposed to both atrazine and simazine via the water and dietary pathways FFs, flowable formulations WDGs, water-dispersible granules W, drinking water ingestion D, dietary consumption HH, herbicide handler... Figure 8.16 Distributions of the margins of exposure for US herbicide handlers who apply either atrazine or simazine and who are also possibly exposed to both atrazine and simazine via the water and dietary pathways FFs, flowable formulations WDGs, water-dispersible granules W, drinking water ingestion D, dietary consumption HH, herbicide handler...
Distributions of the MOEs have been presented for individual exposure pathways (drinking water ingestion, dietary consumption and herbicide handling), for the combined exposure pathways, and for atrazine and simazine, both separately and combined. [Pg.306]


See other pages where Atrazine dietary consumption is mentioned: [Pg.482]    [Pg.489]    [Pg.284]    [Pg.287]    [Pg.485]    [Pg.291]   


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