Development of California Public Health Goals (PHGs) for chemicals in drinking water.

As part of a program for evaluation of environmental contaminants in drinking water, risk assessments are being conducted to develop Public Health Goals (PHGs) for chemicals in drinking water, based solely on public health considerations. California's Safe Drinking Water Act of 1996 mandated the development of PHGs for over 80 chemicals by 31 December 1999. The law allowed these levels to be set higher or lower than federal maximum contaminant levels (MCLs), including a level of zero if data are insufficient to determine a specific level. The estimated safe levels and toxicological rationale for the first 26 of these chemicals are described here. The chemicals include alachlor, antimony, benzo[a]pyrene, chlordane, copper, cyanide, dalapon, 1,2-dichlorobenzene, 1,4-dichlorobenzene, 2,4-D, diethylhexylphthalate, dinoseb, endothall, ethylbenzene, fluoride, glyphosate, lead, nitrate, nitrite, oxamyl, pentachlorophenol, picloram, trichlorofluoromethane, trichlorotrifluoroethane, uranium and xylene(s). These risk assessments are to be considered by the State of California in revising and developing state MCLs for chemicals in drinking water (which must not exceed federal MCLs). The estimates are also notable for incorporation or consideration of newer guidelines and principles for risk assessment extrapolations.

Ploidy dependence of induced mutation frequency in transformed Syrian hamster cells.

The ploidy dependence of the induced frequency of a phenotype can be used to determine the dominant or recessive nature of a somatic mutation to a given trait. To demonstrate this we induced mutations in diploid and spontaneously occurring tetraploid clones of Syrian hamster embryo cells by treatment with EMS (1.2 mg/ml, 4 h). Mutagenized cells were assayed for the recessive mutation to 6-thioguanine resistance (5 micrograms/ml) and the dominant mutation to ouabain resistance (1.2 mM). The frequency of induction of the dominant mutation was equal in the diploid and tetraploid clones (2.3 x 10(-4)). The frequency of induction of the recessive mutation was greatly reduced in the tetraploid clone relative to the diploid clone (1.8 x 10(-4) vs. 1.2 x 10(-3)). 6TGr mutant subclones from the tetraploid clone remain nearly tetraploid, or even increase in ploidy, but show a reduction in the number of X chromosomes from two to one, or in some cases none (based on chromosome morphology). The principle of ploidy dependence is now being used to study the induction of phenotypes related to neoplastic transformation.