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Air Quality Criteria for Lead Volume II of II - (NEPIS)(EPA) - US ...

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AX5-90<br />

Table AX5-6.8. Genotoxic/Carcinogenic Effects <strong>of</strong> <strong>Lead</strong>—Genotoxicity Animal Cell Cultures Mutagenicity<br />

Compound Assay and Duration Cell Type Co-exposure Effects Reference<br />

Pb acetate Cytotoxicity (1–25 µM <strong>for</strong> 24 h)<br />

Mutagenesis—HPRT (0.5–5 µM <strong>for</strong> 44 h)<br />

Pb acetate<br />

—insoluble<br />

precipitate at high<br />

dose.<br />

Cytotoxicity (0.5–2000 µM <strong>for</strong> 5 days)<br />

Mutagenesis—gpt (0.5–1700 µM <strong>for</strong> 5 days)<br />

Pb chloride Cytotoxicity (0.1–1 µM <strong>for</strong> 1 h)<br />

Mutagenicity—gpt assay<br />

(0.1–1 µM <strong>for</strong> 1 h)<br />

Pb chloride Cytotoxicity (0.1–1 µM <strong>for</strong> 1 h)<br />

Mutagenicity—gpt assay<br />

(0.1–1 µM <strong>for</strong> 1 h)<br />

Pb chloride Mutagenicity—gpt assay<br />

(0.1–1 µM <strong>for</strong> 1 h)<br />

PCR/Southern to analyze mutants <strong>for</strong><br />

sequence<br />

Pb chromate Cytotoxicity (10–100 µM <strong>for</strong> 24 h)<br />

HGPRT assay (10–100 µM <strong>for</strong> 24 h)<br />

Pb chromate Mutagenicity as Sodium/potassium ATPase<br />

(ouabain resistance) or 6-thioguanine<br />

resistance (25–100 µM <strong>for</strong> 5 h)<br />

V79 in AMEM + 10%<br />

FBS<br />

G12–CHV79 cells<br />

with 1 copy gpt gene<br />

in Ham’s F12 + 5%<br />

FBS<br />

AS52-CHO-gpt, lack<br />

hprt in HBSS<br />

followed by Ham’s<br />

F12 + 5% FBS<br />

AS52-CHO-gpt, lack<br />

hprt in HBSS<br />

followed by Ham’s<br />

F12 + 5% FBS<br />

AS52-CHO-gpt, lack<br />

hprt in HBSS<br />

followed by Ham’s<br />

F12 + 5% FBS<br />

V79 CHL–HPRT low<br />

clone in MEM + 10%<br />

FCS<br />

C3H10T1/2 cells in<br />

EMEM + 10% FBS<br />

None<br />

See also<br />

Table AX5-6.16<br />

See also Table<br />

AX5-6.17<br />

LC50 = 3 µM<br />

Pb acetate alone was not mutagenic.<br />

LC50 = 1700 µM<br />

Pb acetate was mutagenic, but only at toxic<br />

concentration (1700 µM) where precipitate <strong>for</strong>med<br />

not at lower concentrations (500 or 1000 µM).<br />

There were no statistical analyses <strong>of</strong> these data.<br />

None LC74 = 1 µM (maximum concentration tested)<br />

Allopurinol (50 µM)<br />

to inhibit xanthine<br />

oxidase<br />

Pb chloride induced a dose-dependent increase in<br />

the number <strong>of</strong> 6 thioguanine resistant mutants.<br />

Did not adjust and compare as previous studies.<br />

LC74 = 1 µM. Allopurinol had no effect on<br />

cytotoxicity.<br />

Pb chloride was mutagenic (0.8 and 1 µM).<br />

Allopurinol reduced mutagenesis.<br />

None Pb chloride (0.1–0.4 µM) caused mostly point<br />

mutations. Higher concentrations (0.5–1 µM)<br />

caused more deletions.<br />

There were no statistical analyses <strong>of</strong> these data.<br />

Usually examined fewer mutations than control.<br />

NTA Mutagenesis was assessed with HGPRT assay. Pb<br />

chromate was not mutagenic.<br />

Co-exposure to NTA caused Pb chromate to<br />

become mutagenic through increased solubilization.<br />

This mutagenic effect was completely attributed to<br />

the Cr(VI) ions.<br />

Hartwig et al.<br />

(1990)<br />

Roy and Rossman<br />

(1992)<br />

Ariza et al. (1996)<br />

Ariza et al. (1998)<br />

Ariza and Williams<br />

(1999)<br />

Celotti et al. (1987)<br />

None Pb chromate was not mutagenic. Patierno et al.<br />

(1988) and Patierno<br />

and Landolph<br />

(1989) (both papers<br />

present the same<br />

data)

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