S-metolachlor is not considered acutely toxic and therefore acute dietary exposure was not determined; however, in the October 2002 TRED EPA conducted an acute assessment of the majority of the crops included in this petition and determined acute risks to be
Syngenta Market Basket Survey (SMBS) S-metolachlor data were available for the following commodities: milk, potatoes and tomatoes. The Syngenta market basket survey was conducted from September 1999 through September 2000. Following the Agency tier ranking system, these chronic dietary assessments are considered as Tier III (utilizing field trial data) and Tier IV (utilizing SMBS and PDP data) assessments.
In fact, based on experience with metolachlor,[[Page 10614]]it is believed that metolachlor will be infrequently found in groundwater (less than 5% of the samples analyzed), and when found, it will be in the low ppb range.
Based on the available studies used by EPA to assess environmental exposure, Novartis anticipates that exposure to residues of metolachlor in drinking water will not exceed 20% of the RfD (0.02 mg/kg/day), a value upon which the Health Advisory Level of 70 parts per billion (ppb) for metolachlor is based.
The growth regulators include the following herbicide families: phenoxy acetic acids, benzoic acids, and the pyridines. Growth regulator herbicides can act at multiple sites in a plant to disrupt hormone balance and protein synthesis and thereby cause a variety of plant growth abnormalities. Growth regulator herbicides selectively kill broadleaf weeds; however, they are capable of injuring grass crops. Herbicides in this group can move in both the xylem and the phloem to areas of new plant growth. As a result, many herbicides in this group are effective on perennial and annual broadleaf weeds. Herbicide uptake is primarily through the foliage but root uptake is possible. Injury symptoms are most obvious on newly developing leaves.
Furthermore, histological investigation of endocrine organs in the chronic dog, rat and mouse studies conducted with metolachlor did not indicate that the endocrine system is targeted by metolachlor, even at maximally tolerated doses administered for a lifetime.
Although residues of metolachlor have been found in raw agricultural commodities, there is no evidence that metolachlor bioaccumulates in the environment.
Withoutthese amino acids, protein synthesis is decreased, certain metabolic reactionscease, and the plant gradually dies over a period of one to several weeks.
For purposes of assessing the potential dietary exposure to metolachlor, aggregate exposure has been estimated based on the Theoretical Maximum Residue Contribution (TMRC) from the use of metolachlor in or on raw agricultural commodities for which tolerances have been previously established (40 CFR 180.368).
Based on the tolerances proposed in forage (12 ppm) and hay (0.3 ppm), it has been determined that tolerances previously established for metolachlor in animal commodities of milk and meat, fat, kidney, liver and meat byproducts are adequate to cover secondary residues resulting from animal consumption of grass forage and hay.
In conducting this exposure assessment, it has been conservatively assumed that 100% of all raw agricultural commodities for which tolerances have been established for metolachlor will contain metolachlor residues and those residues would be at the level of the tolerance--which results in an overestimation of human exposure.
This classification is based upon the marginal tumor response observed in livers of female rats treated with a high (cytotoxic) dose of metolachlor (3,000 ppm).
Although metolachlor may be used on turf and ornamentals in a residential setting, that use represents less than 0.1 percent of the total herbicide market for residential turf and landscape uses.
Cumulative Effects The potential for cumulative effects of metolachlor and other substances that have a common mechanism of toxicity has also been considered.
An evaluation of the carcinogenic potential of metolachlor was made from two sets of carcinogenicity studies conducted with metolachlor in rats and mice.