Hexavalent chromium Cr(VI) is a respiratory toxicant and carcinogen, with 
solubility playing an important role in its carcinogenic potential. Zinc 
chromate, a water insoluble or 'particulate' Cr(VI) compound, has been shown to 
be carcinogenic in epidemiology studies and to induce tumors in experimental 
animals, but its genotoxicity is poorly understood. Our study shows that zinc 
chromate induced concentration-dependent increases in cytotoxicity, chromosome 
damage and DNA double strand breaks in human lung cells. In response to zinc 
chromate-induced breaks, MRE11 expression was increased and ATM and ATR were 
phosphorylated, indicating that the DNA double strand break repair system was 
initiated in the cells. In addition, our data show that zinc chromate-induced 
double strand breaks were only observed in the G2/M phase population, with no 
significant amount of double strand breaks observed in G1 and S phase cells. 
These data will aid in understanding the mechanisms of zinc chromate toxicity 
and carcinogenesis.