FLUORANTHENE IN DRINKING WATER AND ITS EFFECTS ON HUMAN HEALTH
Report No FR0276
To review the literature on the mammalian toxicity of fluoranthene, and discuss its significance to human health in relation to the levels found in drinking water.
Fluoranthene is a polycyclic aromatic hydrocarbon (PAH) which occurs widely in the environment. Concentrations in drinking water are generally well below the European Community maximum acceptable concentration (MAC) of 200 ng/1 for the total of six specified PAHs. However, there have been occasions where fluoranthene concentrations have exceeded the MAC. This is probably due to 'pick-up' from internal coal-tar linings which were commonly applied to cast iron pipes before 1977. The significance of relatively high levels of fluoranthene in water with regard to consumers health needs to be determined, particularly as other PAHs, such as benzo(a)pyrene, are known to be carcinogenic in experimental animals.
Fluoranthene is found in many drinking waters at low concentrations usually around 10 ng/1 or less. However, in some drinking waters elevated fluoranthene levels of up to 1 µg/l can be detected due to 'pick-up' from the internal coal-tar lining on cast iron pipes. Where the concentration in drinking water is low, the major source of fluoranthene exposure for the general population is through the diet and the contribution from drinking water is minimal. However, where elevated concentrations are encountered the contribution from drinking water is substantially increased and the total daily intake can be doubled.
Fluoranthene is of low acute oral toxicity but no data are available on its chronic or reproductive toxicity. It is a potent mutagen in bacterial and many mammalian in vitro test systems, but only in the presence of metabolic activation. However, the limited evidence from short-term in vivo cytogenetic and long-term skin painting carcinogenicity studies in rodents indicate that fluoranthene is not carcinogenic. There is some evidence that fluoranthene may enhance the carcinogenicity of benzo(a)pyrene but the relevance in relation to environmental exposure and human health is unclear.
Although the available data suggest that fluoranthene is not carcinogenic in rodents, the evidence is very limited and is only based on cytogenetic and skin painting studies in rodents. Further research is therefore necessary to investigate the carcinogenicity of fluoranthene via the oral route. The chronic and reproductive toxicity of fluoranthene also needs to be established. Studies should also be undertaken to determine its dermal absorption in order to establish the hazard, if any, from bathing.
The key question regarding the health effects of fluoranthene is carcinogenicity. With regard to long-term exposure the available toxicological data are insufficient to recommend a health based guideline value. Although the available evidence suggests that it is not carcinogenic, due to the lack of oral data it is recommended that, wherever possible, concentrations should be minimised.
Conventional treatment removes fluoranthene effectively from raw waters. Consequently,,it is infrequently detected in many drinking waters or is only present at very low concentrations, often below 12 ng/1. However, there are some drinking waters where levels are consistently detected at up to 1 µg/1 and, less commonly, above this concentration. These elevated levels are due to 'pick-up' from the internal coal-tar lining on some cast iron mains. Coal-tar was commonly applied as an internal
Fluoranthene exposure may occur by a variety of routes, the diet being the major source for the general population. The relative exposure via air is small, although smoking cigarettes will substantially increase the exposure by this route. Drinking water typically accounts for less than 1% of the total daily intake. However, elevated levels of 1 æg/1 substantially increase the contribution from drinking water and in some instances may double the total daily intake. There are limited data on the kinetics of fluoranthene. However, like other PAHs, it is expected to be absorbed from the gut, distributed in body fat, and excreted via the hepatobiliary system and the faeces. Metabolism of fluoranthene is via cytochrome P-450 with oxidation or hydroxylation as a first step. The arene oxide metabolite so formed can then be further metabolised by epoxide hydrolase to a 'dihydrodiol' which is either conjugated or oxidised by cytochrome P-450 to a 'diol-epoxide'. The limited toxicological data suggest that fluoranthene is of low acute oral toxicity. There are no data on its chronic or reproductive toxicity. It has consistently been shown to be mutagenic in bacterial and many mammalian in vitro test systems, but only in the presence of metabolic activation. A number of studies have indicated the active mutagenic metabolite is the 'diol-epoxide'. However, evidence from in vivo cytogenetic and skin painting carcinogenicity studies in rodents indicate it is not carcinogenic. There is some evidence that it may be a co-carcinogen since it has been shown to enhance the carcinogenicity of benzo(a)pyrene.
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