sewage, and atmospheric circulation and subsequent deposition of particulate air pollution. soil and river sediment near industrial sites such as creosote manufacturing facilities can be highly contaminated with pahs. oil spills, creosote, coal mining dust, and other fossil fuel sources can also distribute pahs in the environment. two- and three-ringed pahs can disperse widely while dissolved in water or as gases in the atmosphere, while pahs with higher molecular weights can disperse locally or regionally adhered to particulate matter that is suspended in air or water until the particles land or settle out of the water column. pahs have a strong affinity for organic carbon, and thus highly organic sediments in rivers, lakes, and the ocean can be a substantial sink for pahs. algae and some invertebrates such as protozoans, mollusks, and many polychaetes have limited ability to metabolize pahs and bioaccumulate disproportionate concentrations of pahs in their tissues; however, pah metabolism can vary substantially across invertebrate species. most vertebrates metabolize and excrete pahs relatively rapidly. tissue concentrations of pahs do not increase (biomagnify) from the lowest to highest levels of food chains. pahs transform slowly to a wide range of degradation products. biological degradation by microbes is a dominant form of pah transformation in the environment. soil-consuming invertebrates such as earthworms speed pah degradation, either through direct metabolism or by improving the conditions for microbial transformations. abiotic degradation in the atmosphere and the top layers of surface waters can produce nitrogenated, halogenated, hydroxylated, and oxygenated pahs; some of these compounds can be more toxic, water-soluble, and mobile than their parent pahs. urban soils the british geological survey reported the amount and distribution of pah compounds including parent and alkylated forms in urban soils at 76 locations in greater london. the study showed that parent (16 pah) content ranged from 4 to 67 mg/kg (dry soil weight) and an average pah concentration of 18 mg/kg (dry soil weight) whereas the total pah content (33 pah) ranged from 6 to 88 mg/kg and fluoranthene and pyrene were generally the most abundant pahs. benzopyrene (bap), the most toxic of the parent pahs, is widely considered a key marker pah for environmental assessments; the normal background concentration of bap in the london urban sites was 6.9 mg/kg (dry soil weight). london soils contained more stable four- to six-ringed pahs which were indicative of combustion and pyrolytic sources, such as coal and oil burning and traffic-sourced particulates. however, the overall distribution also suggested that the pahs in london soils had undergone weathering and been modified by a variety of pre-and post-depositional processes such as volatilization and microbial biodegradation. peatlands managed burning of moorland vegetation in the uk has been shown to generate pahs which become incorporated into the peat surface. burning of moorland vegetation such as heather initially generates high amounts of two- and three-ringed pahs relative to four- to six-ringed pahs in surface sediments, however, this pattern is reversed as the lower molecular weight pahs are attenuated by biotic decay and photodegradation. evaluation of the pah distributions using statistical methods such as principal component analyses (pca) enabled the study to link the source (burnt moorland) to pathway (suspended stream sediment) to the depositional sink (reservoir bed). rivers, estuarine and coastal sediments concentrations of pahs in river and estuarine sediments vary according to a variety of factors including proximity to municipal and industrial discharge points, wind direction and distance from major urban roadways, as well as tidal regime which controls the diluting effect of generally cleaner marine sediments relative to freshwater discharge. consequently, the concentrations of pollutants in estuaries tends to decrease at the river mouth. understanding of sediment hosted pahs in estuaries is important for the protection of commercial fisheries (such as mussels) and general environmental habitat conservation because pahs can impact the health of suspension and sediment feeding organism. river-estuary surface sediments in the uk tend to have a lower pah content than sediments buried 10–60 cm from the surface reflecting lower present day industrial activity combined with improvement in environmental legislation of pah. typical pah concentrations in uk estuaries range from about 19 to 16,163 µg/kg (dry sediment weight) in the river clyde and 626 to 3,766 µg/kg in the river mersey. in general estuarine sediments with a higher natural total organic carbon content (toc) tend to accumulate pahs due to high sorption capacity of organic matter. a similar correspondence between pahs and toc has also been observed in the sediments of tropical mangroves located on the coast of southern china. human health cancer is a primary human health risk of exposure to pahs. exposure to pahs has also been linked with cardiovascular disease and poor fetal development. cancer pahs have been linked to skin, lung, bladder, liver, and stomach cancers in well-established animal model studies. specific compounds classified by various agencies as possible or probable human carcinogens are identified in the section "regulation and oversight" below. history an 18th-century drawing of chimney sweeps. historically, pahs contributed substantially to our understanding of adverse health effects from exposures to environmental contaminants, including chemical carcinogenesis. in 1775, percivall pott, a surgeon at st. bartholomew's hospital in london, observed that scrotal cancer was unusually common in chimney sweepers and proposed the cause as occupational exposure to soot. a century later, richard von volkmann reported increased skin cancers in workers of the coal tar industry of germany, and by the early 1900s increased rates of cancer from exposure to soot and coal tar was widely accepted. in 1915, yamigawa and ichicawa were the first to experimentally produce cancers, specifically of the skin, by topically applying coal tar to rabbit ears. in 1922, ernest kennaway determined that the carcinogenic component of coal tar mixtures was an organic compound consisting of only carbon and hydrogen. this component was later linked to a characteristic fluorescent pattern that was similar but not identical to benzanthracene, a pah that was subsequently demonstrated to cause tumors. cook, hewett and hieger then linked the specific spectroscopic fluorescent profile of benzopyrene to that of the carcinogenic component of coal tar, the first time that a specific compound from an environmental mixture (coal tar) was demonstrated to be carcinogenic. in the 1930s and later, epidemiologists from japan, the uk, and the us, including richard doll and various others, reported greater rates of death from lung cancer following occupational exposure to pah-rich environments among workers in coke ovens and coal carbonization and gasification processes. mechanisms of carcinogenesis an adduct formed between a dna strand and an epoxide derived from a benzopyrene molecule (center); such adducts may interfere with normal dna replication. the structure of a pah influences whether and how the individual compound is carcinogenic. some carcinogenic pahs are genotoxic and induce mutations that initiate cancer; others are not genotoxic and instead affect cancer promotion or progression. pahs that affect cancer initiation are typically first chemically modified by enzymes into metabolites that react with dna, leading to mutations. when the dna sequence is altered in genes that regulate cell replication, cancer can result. mutagenic pahs, such as benzopyrene, usually have four or more aromatic rings as well as a "bay region", a structural pocket that increases reactivity of the molecule to the metabolizing enzymes. mutagenic metabolites of pahs include diol epoxides, quinones, and radical pah cations. these metabolites can bind to dna at specific sites, forming bulky complexes called dna adducts that can be stable or unstable. stable adducts may lead to dna replication errors, while unstable adducts react with the dna strand, removing a purine base (either adenine or guanine). such mutations, if they are not repaired, can transform genes encoding for normal cell signaling proteins into cancer-causing oncogenes. quinones can also repeatedly generate reactive oxygen species that may independently damage dna. enzymes in the cytochrome family (cyp1a1, cyp1a2, cyp1b1) metabolize pahs to diol epoxides. pah exposure can increase production of the cytochrome enzymes, allowing the enzymes to convert pahs into mutagenic diol epoxides at greater rates. in this pathway, pah molecules bind to the aryl hydrocarbon receptor (ahr) and activate it as a transcription factor that increases production of the cytochrome enzymes. the activity of these enzymes may at times conversely protect against pah toxicity, which is not yet well understood. low molecular weight pahs, with two to four aromatic hydrocarbon rings, are more potent as co-carcinogens during the promotional stage of cancer. in this stage, an initiated cell (a cell that has retained a carcinogenic mutation in a key gene related to cell replication) is removed from growth-suppressing signals from its neighboring cells and begins to clonally replicate. low-molecular-weight pahs that have bay or bay-like regions can dysregulate gap junction channels, interfering with intercellular communication, and also affect mitogen-activated protein kinases that activate transcription factors involved in cell proliferation. closure of gap junction protein channels is a normal precursor to cell division. excessive closure of these channels after exposure to pahs results in removing a cell from the normal growth-regulating signals imposed by its local community of cells, thus allowing initiated cancerous cells to replicate. these pahs do not need to be enzymatically metabolized first. low molecular weight pahs are prevalent in the environment, thus posing a significant risk to human health at the promotional phases of cancer. cardiovascular disease adult exposure to pahs has been linked to cardiovascular disease. pahs are among the complex suite of contaminants in tobacco smoke and particulate air pollution and may contribute to cardiovascular disease resulting from such exposures. in laboratory experiments, animals exposed to certain pahs have shown increased development of plaques (atherogenesis) within arteries. potential mechanisms for the pathogenesis and development of atherosclerotic plaques may be similar to the mechanisms involved in the carcinogenic and mutagenic properties of pahs. a leading hypothesis is that pahs may activate the cytochrome enzyme cyp1b1 in vascular smooth muscle cells. this enzyme then metabolically processes the pahs to quinone metabolites that bind to dna in reactive adducts that remove purine bases. the resulting mutations may contribute to unregulated growth of vascular smooth muscle cells or to their migration to the inside of the artery, which are steps in plaque formation. these quinone metabolites also generate reactive oxygen species that may alter the activity of genes that affect plaque formation. oxidative stress following pah exposure could also result in cardiovascular disease by causing inflammation, which has been recognized as an important factor in the development of atherosclerosis and cardiovascular disease. biomarkers of exposure to pahs in humans have been associated with inflammatory biomarkers that are recognized as important predictors of cardiovascular disease, suggesting that oxidative stress resulting from exposure to pahs may be a mechanism of cardiovascular disease in humans. developmental impacts multiple epidemiological studies of people living in europe, the united states, and china have linked in utero exposure to pahs, through air pollution or parental occupational exposure, with poor fetal growth, reduced immune function, and poorer neurological development, including lower iq. regulation and oversight some governmental bodies, including the european union as well as niosh and the united states environmental protection agency (epa), regulate concentrations of pahs in air, water, and soil. the european commission has restricted concentrations of 8 carcinogenic pahs in consumer products that contact the skin or mouth. priority polycyclic aromatic hydrocarbons identified by the us epa, the us agency for toxic substances and disease registry (atsdr), and the european food safety authority (efsa) due to their carcinogenicity or genotoxicity and/or ability to be monitored are the following: compoundagency epa mcl in water acenaphtheneepa, atsdr acenaphthyleneepa, atsdr anthraceneepa, atsdr benzanthraceneepa, atsdr, efsa 0.0001 benzofluorantheneepa, atsdr, efsa 0.0002 benzofluorantheneatsdr, efsa benzofluorantheneepa, atsdr, efsa 0.0002 benzofluoreneefsa benzoperyleneepa, atsdr, efsa benzopyreneepa, atsdr, efsa 0.0002 benzopyreneatsdr chryseneepa, atsdr, efsa 0.0002 coroneneatsdr compoundagency epa mcl in water cyclopentapyreneefsa dibenzanthraceneepa, atsdr, efsa 0.0003 dibenzopyreneefsa dibenzopyreneefsa dibenzopyreneefsa dibenzopyreneefsa fluorantheneepa, atsdr fluoreneepa, atsdr indenopyreneepa, atsdr, efsa 0.0004 5-methylchryseneefsa naphthaleneepa phenanthreneepa, atsdr pyreneepa, atsdr a considered probable or possible human carcinogens by the us epa, the european union, and/or the international agency for research on cancer (iarc). detection and optical properties a spectral database exists for tracking polycyclic aromatic hydrocarbons (pahs) in the universe. detection of pahs in materials is often done using gas chromatography-mass spectrometry or liquid chromatography with ultraviolet-visible or fluorescence spectroscopic methods or by using rapid test pah indicator strips. structures of pahs have been analyzed using infrared