Polycyclic aromatic hydrocarbons (PAHs)
(endorsed 2011)
Guideline
Based on health considerations, the concentration of benzo[a]pyrene in drinking water should not exceed 0.00001 mg/L (10 ng/L). Data are inadequate to set guidelines for other PAHs, however comparative carcinogenic potency can be used to determine an approximate risk when complex mixtures of PAHs are present in drinking water.
General description
The polycyclic aromatic hydrocarbons are a large group of organic compounds with two or more fused aromatic rings. Several hundred have been identified in air, emitted from various combustion and pyrolysis sources. The principal PAHs include phenanthrene, fluoranthene, pyrene, anthracene, benzo(a)pyrene, benzofluoranthene, chrysene, anthanthrene and naphthalene.
PAHs are widespread throughout the environment. They are formed in forest fires and in the combustion of fossil fuels, and are present in emissions from coke ovens, aluminium smelters and motor vehicles. Contamination of drinking water can occur by direct atmospheric deposition and by leaching from bituminous liners in water distribution systems.
There are very few data on concentrations of PAHs in drinking water supplies. The few data that exist are mainly for benzo(a)pyrene (BaP). The typical concentration of BaP in drinking water in the United States is estimated to be 0.00000055 mg/L (0.55 ng/L).
Background levels of PAHs in drinking water range from 4 to 24 ng/L (0.0004 to 0.0024 µg/L) (ATSDR 2008). The typical level of BaP in drinking water in the United States is estimated to be 0.55 ng/L (0.00055 µg/L) (WHO 1996, WHO 1998). The median value for daily intake for PAHs from exposure via drinking water has been estimated to be 0.006 µg/day (Menzie et al. 1992). Daily intake of total PAHs has also been estimated to be 0.027 µg (Santodonato et al. 1981), while the daily intake of BaP in drinking water is estimated to range from 0.1 to 1 ng (Santodonato et al. 1981, WHO 1996). In general it is suggested that PAHs in drinking water only contribute no more than 1% of total PAH intake (WHO 1996).
Food is the major source of intake of PAHs. Highest concentrations occur in smoked foods, leafy vegetables and the burnt fat of meats. Intake from foods is extremely variable but significantly higher (by at least an order of magnitude) than from drinking water.
Typical values in Australian drinking water
PAHs have not been found in Australian drinking waters. They are included here to provide guidance in the unlikely event of contamination, and because they have been detected occasionally in drinking water supplies overseas. One potential contributor to PAHs in drinking water in Australia would be periodic intense and extensive bush fires in water storage catchments.
Treatment of drinking water
The conventional water treatment processes of coagulation, settling and filtration are capable of reducing the BaP concentration of raw waters to less than 0.000001 mg/L (1 ng/L), even if the influent concentration is high. It is likely that other PAHs would be similarly reduced. Granular activated carbon would also be effective in the removal of these compounds.
Measurement
Concentrations of a wide range of PAHs in water can be determined by the use of gas chromatography–mass spectrometry (GC-MS) combined with suitable extraction and pre-concentration procedures. Alternatively, the use of fluorescence detection combined with high performance liquid chromatography (HPLC) provides a sensitive method for PAHs in water (USEPA Draft Method 550, 1990). Typically, solvent extraction employing dichloromethane or solid phase extraction using resins or commercially available adsorption cartridges or discs are used for extraction and concentration, prior to final determination by GC-MS or HPLC.
Health considerations
Most of the toxicological literature deals specifically with BaP. Few studies are available for the other PAHs. Some PAH compounds have been found to be carcinogenic by non-oral routes, but others are known to have low potential for carcinogenicity.
BaP is absorbed principally through the gastrointestinal tract and the lungs. The rate of absorption increases with increased intake of polyunsaturated fatty acids. BaP is rapidly distributed to the organs and may be stored in mammary and adipose tissue. Metabolism occurs mainly in the liver.
The International Agency for Research on Cancer (IARC) has upgraded BaP from group 2B to group 1 (carcinogenic to humans), based on mechanistic considerations and other relevant data. This evaluation is presented in full in IARC monograph 92. In addition, dibenz[a,h]anthracene and dibenzo[a,l]pyrene have been upgraded to group 2A (probably carcinogenic to humans), with supporting evidence from other relevant data. Certain substances containing complex mixtures of PAHs are classified as known human carcinogens (Group 1) by IARC. These include: coal tar pitches, coal tars and cigarette smoke condensate.
In experiments with animals, many PAH mixtures have been associated with an increased incidence of cancer. BaP is one of the most potent carcinogenic compounds, with primary tumours having been reported in a variety of studies, using different administration techniques, in mice, rats, hamsters, guinea pigs, rabbits, ducks and monkeys. Tumours have mostly appeared only at the site of administration.
BaP is metabolically activated to a series of dihydrodiol expoxides by the mixed function oxidases, particularly cytochrome P450 1A1, in combination with epoxide hydrolase. One particular dihydrodiol epoxide (+ anti isomer) is highly mutagenic and in its ultimate carcinogenic form (a carbonium ion), will bind to nucleophilic sites on DNA to product covalent DNA adducts. If these adducts are misrepaired, they may produce mutations in tumour suppression genes and cancer-causing oncogenes, which can lead to cancer. Other carcinogenic PAHs operate in a similar manner through metabolic activation and DNA adduct formation. The sensitive determination of DNA adducts can be useful in determination of human exposure to carcinogenic.
Derivation of guideline
Data are insufficient to set guideline values for PAHs except for BaP. The use of relative potencies of other PAHs can, however, give guidance to their relative contribution to risk caused by their presence in drinking water. Relative potencies of the most commonly found PAHs are given in Table 1.
The relative carcinogenic potencies of a number PAHs have been determined and are reported in the literature. Table 1 presents those data with summarised relative potencies sourced from the World Health Organization (WHO 1998) and additional data as referenced.
Table 1: Relative carcinogenic potency of selected PAHs
Benz[a]anthracene
0.1*
Benzo[a]pyrene
1*
Benzo[b]fluoranthene
0.1*
Benzo[j]flouranthene
0.1*
Benzo[k]flouranthene
0.1*
Dibenz[a,h]anthracene
1*
Indeno[1,2,3,c,d]pyrene
0.1*
Benzo[g,h,i]perylene
0.01**
Benz[a]anthracene
0.1** and ***
Chrysene
0.01** and ***
Dibenz[a,h]anthracene
5**
Dibenz[a,e]pyrene
1***
Dibenz[a,h]pyrene
10***
Dibenz[a,i]pyrene
10***
Dibenz[a,l]pyrene
10***
* Sourced from WHO (1998)
** Sourced from Nisbet and LaGoy (1992)
*** Sourced from CA EPA (2002)
A number of points in relation to Table 1 are worth noting. PAHs with relative carcinogenic potencies of less than 0.01 (100 times less carcinogenic than BaP) are not reported due to the lower level of risk they pose in water. There are three PAHs listed in Table 1 with relative carcinogenic potencies ten times that of BaP, and these PAHs should be given attention when risk assessments of PAHs in drinking water are undertaken. Slope factors for carcinogenic risk assessment of PAHs are provided by the California Environmental Protection Agency (CA EPA 2002). Additional data on slope factors and drinking water unit risk for BaP are given in the IRIS database (USEPA 2008).
While it is recognised that a guideline is available only for BaP, this can be used in conjunction with relative potencies given in Table 1 to gain an estimate of acceptable levels when complex mixtures of PAHs are present.
On the basis of a feeding study using mice (Neal and Rigdon 1967), the excess risk of lifetime consumption of water with a BaP concentration of 0.00007 mg/L (70 ng/L) was conservatively estimated by WHO, using a linear multistage model, at one additional cancer per million people.
The guideline value has been set at the limit of determination because this is slightly less than the value derived using a risk assessment calculation, and provides an adequate degree of protection. This is consistent with the general approach adopted for genotoxic carcinogens (see Section 6.3.3).
The WHO guideline value of 0.0007 mg/L was based on an oral carcinogenicity study in mice and calculated using a 2-stage birth-death mutation model, and on carcinogenicity studies in mice following oral administration (WHO, 2004).
References
ATSDR (Agency for toxic Substances and Disease Registry) (2008). Public Health Statement for Polycyclic Aromatic Hydrocarbons (PAHs). ATSDR.
CEPA (California Environmental Protection Agency) (2002). Air toxic hotspots program risk assessment guidelines. Part II. Technical support document for describing available cancer potency factors. Available from: https://oehha.ca.gov/media/downloads/crnr/tsdnov2002.pdf
IARC (International Agency for Research on Cancer) (1987). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Overall Evaluations of Carcinogenicity. An updating of IARC monographs volumes 1 to 42. World Health Organization, IARC, Supplement 7.
IARC (2010) Monograph on the Evaluation of Carcinogenic Risks to Humans. Volume 92: Some non-heterocyclic, polycyclic aromatic hydrocarbons and some related exposures. World Health Organization, International Agency for Research on Cancer, Lyon, France
Menzie CA, Potocki BB, Santodonato J (1992). Exposure to carcinogenic PAHs in the environment. Environmental Science and Technology, 26:1278-1284.
Neal J, Rigdon RH (1967). Gastric tumors in mice fed benzo(a)pyrene: a quantitative study. Texas Reports on Biology and Medicine, 25:553–557.
Nisbet ICT, Lagoy PK (1992). Toxic equivalency factors (TEF’s) for polycyclic aromatic hydrocarbons (PAHs). Regulatory and Toxicological Pharmacology, 16:290-300.
Santodonato J, Howard P, Basu D (1981). Health and ecological assessment of polynuclear aromatic hydrocarbons. Journal of Environmental Pathology and Toxicology, 5:1-364.
USEPA (United States Environmental Protection Agency) (2008). Integrated Risk Information system (IRIS), Benzo[a]pyrene CASRN 50-32-8.
USEPA Draft Method 550 (1990). Determination of polycyclic aromatic hydrocarbons in drinking water by liquid–liquid extraction and HPLC with coupled ultraviolet and fluorescence detection. United States Environmental Protection Agency, Environmental Monitoring and Support Laboratory (EMSL), Cincinnati, Ohio.
WHO (World Health Organization) (1996). Guidelines for Drinking-Water Quality, 2nd Edition, Vol. 2 – Health criteria and other supporting information. WHO, Geneva, Switzerland.
WHO (World Health Organization) (1998). Guidelines for Drinking-Water Quality, 2nd edition, Addendum to Volume. 2 – Health criteria and other supporting information. WHO, Geneva, Switzerland.
WHO (World Health Organization) (2004) Guidelines for Drinking-Water Quality, 3rd Edition, WHO, Geneva, Switzerland.
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