SITE INFORMATION AND CORRESPONDENCE

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Sent By,: BASELINE; 510 420 1707; Nov-9-99 16;33; Page 29129 chemical constants were obtained from L.S.EPA 1998(Smucker, 1998), Spence and Gomez(1999), or Lide (1995).° Also, if a COPCs included in the model did not have a reference concentration (mg/m'), the applicable reference dose was converted to a reference concentration by multiplying by 70 kg and dividing by an inhalation rate of 20 m'/day, Where toxicity values were nut available in,any of the sources reviewed above,a surrogate chemical approach was used to represent these chemicals. A surrogate chemical was selected of similar chemical and physical properties as the COPCs for which no toxicity information was identified. Toxicity information could not be located for the following chemicals: 4-methyl phenol,2-methyl. naphthalene,acenaphthylene,phenanthrene,benzo(g,h,i)perylene, endrin aldehyde,endrin ketone, and 2-hexanone. The following surrogates were therefore selected: 3-methylphenol' for 4- methylphenol; naphthalene fir 2-methyl naphthalene, acenaphthylene, phenanthrene, and bertzo(g,h,i)perylene; endrin for endrin aldehyde and endrin ketone; and methyl ethyl ketone for 2- hexanone. Where a surrogate chemical selected represented more than one C'OPC,the source term concentration of the surrogate was adjusted to account for the total rmass ofthe contaminants forthe. COPCs accounted for by the surrogate. ISSUES RELATED TO LEAD Recent toxicological and epidemiological studies indicate that low-level lead exposure does not appear to have a threshold below which no health effects occur; toxicity values have therefore not been developed for lead exposure. Instead, a blood lead threshold of 10 gg/dl for children has been established (DTSC, 1992), Blood lead levels for the 99"percentile for future residential site users (children and adults) were calculated using DTSC's LeadRisk Spreadsheet, Version 6.0 (DTSC, 1992). Exposure algorithms defined in the model included inhalation of Iead dust, incidental ingestion of soil and dust containing lead, ingestion of lead in drinking water and the diet, and den-nal contact with soil. The spreadsheet model was run using a concentration of lead in drinking water of 0M02 mg/L, as supplied to the downtown Stockton area,' respirable dust (50 I4gW, default parameter), and the maximum concentration of lead from soil samples collected at the site (184 rng/kg at WB-SB-7). Note that the maximtun concentration oflead was reported for a sample that was collected at 7.0 feet bgs, a depth which people on the site would not be expected to come into contact with. Also, the concentration of lead in air was assumed to be 0.01 µg/m3, based on air sampling at the Closest monitoring station in Sacramento. Although ingestion of plant material grown at the.site.is identified as a potential exposure algorithm in the spreadsheet, this pathway was assumed to be incomplete and was excluded from calculation of the blood lead concentrations since no vegetation Note that some chemical constants were not identified in these sources far COPCs included in the 7ohitson Ettinger model. Chemical constants for these COPC9 were selected based on similar molecular weight and chemical groups. '2-methyl-phenol was used as a surrogate for 4-methylphenol in the indoor air calculations. s The concentration of lead in drinking water supplied to the downtown Stockton area from surface waster sources. as sampled twice during the last three to five years,was S0.0002 mg/l,(Gamy, 1999). The detection limit of O.o(102 mgt. wsk used in the lead risk assessment spreadstseel calculations. 97349stk.pw.wpd—l 119/99 23