Atrazine dietary exposure

In 2006, after a comprehensive science review of chlorotriazines, the USEPA determined there is reasonable certainty that no harm will result to the general US population, infants, children, or other major identifiable subgroups of consumers, from the use of simazine, atrazine, and propazine (USEPA, 2006a, b). The review shows that the chlorotriazines are not likely to cause cancer in humans and that dietary exposure is extremely low, with wide margins... 

Table 27.3 Estimated dietary exposure to atrazine and corresponding chloro-metabolite residues (Tier I versus Tier III)a...

The most recent USEPA dietary assessment for atrazine used 1.8mg/kg (chronic NOAEL from a 6-month rat study) with a 1000-fold safety factor (cRfD = 0.0018mg/kg/day). This analysis also confirmed that potential dietary exposure for all exposed population subgroups was less than 1% of the cRfD (USEPA, 2003). 

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... 

A recent review by the USEPA of atrazine (USEPA, 2006) concluded that dietary exposure to atrazine and its chlorinated metabolites is low. The extremely low frequency and magnitude of detectable triazine residues in monitoring surveys of more than 250000 commodity samples confirm that human exposure to triazines through the diet is minimal. 

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). 

The distributions of the LADDs for atrazine or simazine contain only very small values for water, diet, and the combination of water and dietary exposures. Therefore, the corresponding MOEs are quite large, even when the water and dietary pathways are combined (Figures 31.11 and 31.12). 

Table 31.1 MOE assessment for herbicide handlers using flowable or WDG formulations of atrazine or simazine, and including drinking water and dietary exposures to atrazine and simazine combined3...

Bray, L. (1996a). Revised Dietary Exposure Assessment for Atrazine. Submitted to USEPA. 

No allowable daily intake of atrazine in the human diet has been established, although 0.0375 mg/kg BW daily has been proposed -equivalent to 2.25 mg daily for a 60-kg adult, or 1.5 mg/kg diet, based on 1.5 kg food daily. In humans, the theoretical maximum residue contribution (TRMC) - a worst case estimate of dietary exposure - is 0.77 mg daily, assuming 1.5 kg of food eaten daily this is equivalent to 0.51 mg/kg diet, or 0.013 mg/kg BW daily for a 60-kg person. Another TRMC calculation is based on 0.233 mg daily per 1.5 kg diet, equivalent to 0.156 mg/kg diet, or 0.0039 mg/kg... 

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. 

Figure 31.11 Distributions of the MOEs for atrazine from drinking water ingestion, dietary consumption, and both exposure pathways combined.

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. 

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). 

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. 

Unlike the drinking water and occupational exposure pathways, the dietary pathway could conceivably involve exposure to the chloro-metabolites of atrazine. Hence, the atrazine chloro-metabolites have been combined with atrazine in Figure 8.4. Atrazine chloro-metabolites have been assumed to have the same toxicity as atrazine in calculating the MOEs in this figure. 

Figure 8.4 Distributions of the margins of exposure in the USA for atrazine plus its chloro-metabolites from dietary consumption...

Figure 8.13 Distributions of the margins of exposure for atrazine herbicide handlers involved in corn production in the USA from their use of flowable formulations or water-dispersible granules and from their herbicide handling combined with both drinking water ingestion and dietary consumption FFs, flowable formulations WDGs, water-dispersible granules W, drinking water ingestion D, dietary consumption HH, herbicide handler...

Figure 8.15 Distributions of the margins of exposure in the USA for atrazine and simazine combined from drinking water ingestion (W), dietary consumption (D) and both exposure pathways combined (W - - D)...

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. 

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