Naturally occurring radionuclides in drinking water: An exercise in risk benefit analysis.

The scientific background information describing the occurrence, measurement, health effects, treatment technology, risk assessment and economic consequences of the presence of naturally occurring radionuclides in drinking water are described for 60,000 public drinking water supplies. The relevant data for the occurrence of radium, uranium and radon in drinking water supplies are discussed and analysed. Radon is of importance because it is released in the process of taking showers and baths and in washing dishes and clothes. Its progeny is then inhaled, leading to the risk of lung cancer. Radium and uranium can both cause bone cancer. The range of average occurrence of natural radioactivity in drinking water is as follows:(226)Ra, 0.3 to 0.8 pCi L(-1);(228)Ra, 0.4 to 1.0 pCi L(-1); uranium, 0.3 to 2.0 pCi L(-1) and(222)Rn, 500 to 600 pCi L(-1). The estimated lifetime risks due to the mean groundwater concentrations of naturally occurring radionuclides are:(226)Ra and(228Ra), 1.0 10(-5); uranium, 2.0 × 10(-6) and radon, 4.0 × 10(-4). The cost to reduce total radium levels to 5.0 pCi L(-1) is about $9 million. An equivalent expenditure would be required to reduce radon levels to about 4,000 pCi L(-1), or uranium levels to about 100 pCi L(-1). The problem of maximizing the total mortality and the reduction per unit dollar outlay per unit dollar cost for the uranium/radon case is examined.

A general guideline for management of risk from carcinogens.

A simple relationship is formulated that helps to discriminate between acceptable and unacceptable individual lifetime risks (RL) to populations that are exposed to chemical carcinogens. The relationship is an empirical one and is developed using objective risk data as well as subjective risk levels that have found substantial acceptance among those concerned with carcinogenic risk assessment issues. The expression sets acceptable levels of lifetime carcinogenic risk and is a function of the total population exposed to the carcinogen. Its use in risk assessment and risk management provides guidance in distinguishing those carcinogens that should be regulated because of the health hazard they pose from those whose regulation may not be needed.

Mutagenic studies with acrylonitrile.

The mutagenicity of acrylonitrile (vinyl cyanide, propenenitrile) has been demonstrated in the Ames Salmonella typhimurium/liver microsome assay system. Acrylonitrile, in the presence of a mouse liver homogenate produced mutations in the TA 1535, TA 1538 and TA 1978 strains. Exposure of the bacteria was achieved by spotting the acrylonitrile on a "lawn" of salmonella, by shaking a reaction mixture consisting of bacteria, liver homogenate and acrylonitrile, and by exposing the homogenate and bacteria to an atmosphere containing the acrylonitrile. Mutagenesis by this latter method was observed at exposures as low as 57 ppm, less than three times the TLV of 20 ppm that is designated in the United States.

Vinyl chloride dependent mutagensis: effects of liver extracts and free radicals.

The mutagenic effects of vinyl chloride (VC) on Salmonella typhimurium strain TA1530 are enhanced by mouse or rat liver extracts. The extracts prepared from mice pretreated either with vinyl chloride or the microsomal enzyme inducer, Aroclor 1254, did not produce any greater stimulation of VC-dependent mutagenesis than extracts from untreated animals. These same extracts, however, differed markedly in their capacity to stimulate the mutagenicity of dimethylnitrosamine (DMN), a compound which is converted to a mutagen by an NADPH dependent microsomal mixed function oxidase. The order of activity of the extracts with DMN was Aroclor pretreated is greater than untreated is greater than VC pretreated. Furthermore, the stimulatory effect of the liver extracts on VC mediated mutagenesis did not require NADPH and was still evident in liver extracts in which the microsomal mixed function oxidase system had been heat inactivated. The mutagenic activity of VC also was found to be stimulated by riboflavin in the presence of light suggesting that free radicals may be involved in VC dependent mutagenesis.