Polycyclic aromatic hydrocarbon

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Three representations of hexabenzocoronene, a polycylic aromatic hydrocarbon. Top: standard line-angle schematic, where carbon atoms are represented by the vertices of the hexagons and hydrogen atoms are inferred. Middle: ball-and-stick model showing all carbon and hydrogen atoms. Bottom: atomic force microscopy image.

Polycyclic aromatic hydrocarbons (PAHs, also polyaromatic hydrocarbons) are hydrocarbonsorganic compounds containing only carbon and hydrogen—that are composed of multiple aromatic rings (organic rings in which the electrons are delocalized). Formally, the class is further defined as lacking further branching substituents on these ring structures. Polynuclear aromatic hydrocarbons (PNAs) are a subset of PAHs that have fused aromatic rings, that is, rings that share one or more sides.[citation needed] The simplest such chemicals are naphthalene, having two aromatic rings, and the three-ring compounds anthracene and phenanthrene.

PAHs are neutral, nonpolar molecules found in coal and in tar deposits. They are produced as well by incomplete combustion of organic matter (e.g., in engines and incinerators, when biomass burns in forest fires, etc.).

PAHs may also be abundant in the universe, and are conjectured to have formed as early as the first couple of billion years after the Big Bang, in association with formation of new stars and exoplanets. Some studies suggest that PAHs account for a significant percentage of all carbon in the universe, and PAHs are discussed as possible starting materials for abiologic syntheses of materials required by the earliest forms of life.

Nomenclature, structure, properties[edit]

Nomenclature and structure[edit]

The tricyclic species phenanthrene and anthracene represent the starting members of the PAHs.[1] Smaller molecules, such as benzene, are not PAHs, and PAHs are not generally considered to contain heteroatoms or carry substituents.[2]

PAHs with five or six-membered rings are most common. Those composed only of six-membered rings are called alternant PAHs, which include benzenoid PAHs.[3] The following are examples of PAHs that vary in the number and arrangement of their rings:

Physicochemical properties and bonding[edit]

PAHs are nonpolar and lipophilic. PAHs are insoluble in water.[4] The larger members are also poorly soluble in organic solvents as well as lipids. They are usually colorless.

Although PAHs clearly are aromatic compounds, the degree of aromaticity can be different for each ring segment. According to Clar's rule (formulated by Erich Clar in 1964)[5] for PAHs the resonance structure with the largest number of disjoint aromatic п-sextets—i.e. benzene-like moieties—is the most important for the characterization of the properties.[6]

Phenanthrene Clar rule.svg Anthracene Clar rule.svg Chrysene Clar rule.svg
Phenanthrene Anthracene Chrysene

For example, in phenanthrene one Clar structure has two sextets at the extremities,[clarification needed] while the other resonance structure has just one central sextet; therefore in this molecule the outer rings have greater aromatic character whereas the central ring is less aromatic and therefore more reactive.[citation needed] In contrast, in anthracene the resonance structures have one sextet, which can be at any of the three rings, and the aromaticity spreads out more evenly across the whole molecule.[citation needed] This difference in number of sextets is reflected[clarification needed] in the UV absorbance spectra of these two isomers; phenanthrene has a highest wavelength absorbance around 290 nm, while anthracene has highest wavelength bands around 380 nm.[citation needed] Three Clar structures with two sextets each are present in chrysene.[clarification needed][citation needed] Superposition of these structures reveals that the aromaticity in the outer rings is greater (each has a sextet in two of the three Clar structures) compared to the inner rings (each has a sextet in only one of the three).


Sources and distribution[edit]

Polycyclic aromatic hydrocarbons are primarily found in natural sources such as creosote.[7] They can result from the incomplete combustion of organic matter. PAHs can also be produced geologically when organic sediments are chemically transformed into fossil fuels such as oil and coal.[8] The dominant sources of PAHs in the environment are thus from human activity: Wood-burning and combustion of other biofuels such as dung or crop residues contribute more than half of annual global PAH emissions, particularly due to biofuel use in India and China.[9] As of 2004, industrial processes and the extraction and use of fossil fuels made up slightly more than one quarter of global PAH emissions, dominating outputs in industrial countries such as the United States.[9] Wild fires are another notable source.[9] Substantially higher outdoor air, soil, and water concentrations of PAHs have been measured in Asia, Africa, and Latin America than in Europe, Australia, and the U.S./Canada.[9]

PAHs are typically found as complex mixtures.[8][10] Lower-temperature combustion, such as tobacco smoking or wood-burning, tends to generate low molecular weight PAHs, whereas high-temperature industrial processes typically generate PAHs with higher molecular weights.[10]

In the aqueous environment[edit]

Most PAH's are insoluble in water, which limits their mobility in the environment.[11] Aqueous solubility of PAHs decreases approximately logarithmically as molecular mass increases.[12]

Two-ring PAHs, and to a lesser extent three-ring PAHs, dissolve in water, making them more available for biological uptake and degradation.[11][12][13] Further, two- to four-ring PAHs volatilize sufficiently to appear in the atmosphere predominantly in gaseous form, although the physical state of four-ring PAHs can depend on temperature.[14][15] In contrast, compounds with five or more rings have low solubility in water and low volatility; they are therefore predominantly in solid state, bound to particulate air pollution, soils, or sediments.[11] In solid state, these compounds are less accessible for biological uptake or degradation, increasing their persistence in the environment.[12][16]

Human exposure[edit]

Human exposure varies across the globe and depends on factors such as smoking rates, fuel types in cooking, and pollution controls on power plants, industrial processes, and vehicles.[8][9][17] Developed countries with stricter air and water pollution controls, cleaner sources of cooking (i.e., gas and electricity vs. coal or biofuels), and prohibitions of public smoking tend to have lower levels of PAH exposure, while developing and undeveloped countries tend to have higher levels.[8][9][17]

A wood-burning open-air cook stove. Smoke from solid fuels like wood is a large source of PAHs globally.

Burning solid fuels such as coal and biofuels in the home for cooking and heating is a dominant global source of PAH emissions that in developing countries leads to high levels of exposure to indoor particulate air pollution containing PAHs, particularly for women and children who spend more time in the home or cooking.[9][18]

In industrial countries, people who smoke tobacco products, or who are exposed to second-hand smoke, are among the most highly exposed groups; tobacco smoke contributes to 90% of indoor PAH levels in the homes of smokers.[17] For the general population in developed countries, the diet is otherwise the dominant source of PAH exposure, particularly from smoking or grilling meat or consuming PAHs deposited on plant foods, especially broad-leafed vegetables, during growth.[19] PAHs are typically at low concentrations in drinking water.[17]

Smog in Cairo, Egypt. Particulate air pollution, including smog, is a substantial avenue for human exposure to PAHs.

Emissions from vehicles such as cars and trucks can be a substantial outdoor source of PAHs in particulate air pollution.[8][9] Geographically, major roadways are thus sources of PAHs, which may distribute in the atmosphere or deposit nearby.[20] Catalytic converters are estimated to reduce PAH emissions from gasoline-fired vehicles by 25-fold.[8]

People can also be occupationally exposed during work that involves fossil fuels or their derivatives, wood burning, carbon electrodes, or exposure to diesel exhaust.[21][22] Industrial activity that can produce and distribute PAHs includes aluminum, iron, and steel manufacturing; coal gasification, tar distillation, shale oil extraction; production of coke, creosote, carbon black, and calcium carbide; road paving and asphalt manufacturing; rubber tire production; manufacturing or use of metal working fluids; and activity of coal or natural gas power stations.[8][21][22]

Environmental distribution and degradation[edit]

A worker’s glove touches a dense patch of black oil on a sandy beach.
Oil on a beach after a 2007 oil spill in Korea.

PAHs typically disperse from urban and suburban non-point sources through road run-off, sewage, and atmospheric circulation and subsequent deposition of particulate air pollution.[23] Soil and river sediment near industrial sites such as creosote manufacturing facilities can be highly contaminated with PAHs.[8] Oil spills, creosote, coal mining dust, and other fossil fuel sources can also distribute PAHs in the environment.[8][24]

Two- and three-ring 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.[8] 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.[20]

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.[23][25] Most vertebrates metabolize and excrete PAHs relatively rapidly.[23] Tissue concentrations of PAHs do not increase (biomagnify) from the lowest to highest levels of food chains.[23]

PAHs transform slowly to a wide range of degradation products. Biological degradation by microbes is a dominant form of PAH transformation in the environment.[16][26] Soil-consuming invertebrates such as earthworms speed PAH degradation, either through direct metabolism or by improving the conditions for microbial transformations.[26] 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.[23][27][28]

Minor sources[edit]

Volcanic eruptions may emit PAHs.[8] Certain PAHs such as perylene can also be generated in anaerobic sediments from existing organic material, although it remains undetermined whether abiotic or microbial processes drive their production.[29][30][31]

Human health[edit]

Cancer is a primary human health risk of exposure to PAHs.[32] Exposure to PAHs has also been linked with cardiovascular disease and poor fetal development.

Cancer[edit]

PAHs have been linked to skin, lung, bladder, liver, and stomach cancers in well-established animal model studies.[32] Specific compounds classified by various agencies as possible or probable human carcinogens are identified in the section "Regulation and Oversight" below.

Historical significance[edit]

A line drawing of an 18th-century man and boy, the man carrying long tools such as a broom.
An eighteenth century drawing of chimney sweeps.

Historically, PAHs contributed substantially to our understanding of adverse health effects from exposures to environmental contaminants, including chemical carcinogenesis.[33] 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.[34] 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.[34]

In 1922, Ernest Kennaway determined that the carcinogenic component of coal tar mixtures was an organic compound consisting of only C and H. This component was later linked to a characteristic fluorescent pattern that was similar but not identical to benz[a]anthracene, a PAH that was subsequently demonstrated to cause tumors.[34] Cook, Hewett and Hieger then linked the specific spectroscopic fluorescent profile of benzo[a]pyrene to that of the carcinogenic component of coal tar,[34] 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, England, and the U.S., 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.[35]

Mechanisms of carcinogenesis[edit]

An adduct formed between a DNA strand and an epoxide derived from a benzo[a]pyrene molecule (center); such adducts may interfere with normal DNA replication.

The structure of a PAH influences whether and how the individual compound is carcinogenic.[32][36] Some carcinogenic PAHs are genotoxic and induce mutations that initiate cancer; others are not genotoxic and instead affect cancer promotion or progression.[36][37]

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 benzo[a]pyrene, 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.[38] Mutagenic metabolites of PAHs include diol epoxides, quinones, and radical PAH cations.[38][39][40] These metabolites can bind to DNA at specific sites, forming bulky complexes called DNA adducts that can be stable or unstable.[34][41] Stable adducts may lead to DNA replication errors, while unstable adducts react with the DNA strand, removing a purine base (either adenine or guanine).[41] Such mutations, if they are not repaired, can transform genes encoding for normal cell signaling proteins into cancer-causing oncogenes.[36] Quinones can also repeatedly generate reactive oxygen species that may independently damage DNA.[38]

Enzymes in the cytochrome family (CYP1A1, CYP1A2, CYP1B1) metabolize PAHs to diol epoxides.[42] PAH exposure can increase production of the cytochrome enzymes, allowing the enzymes to convert PAHs into mutagenic diol epoxides at greater rates.[42] 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.[42]

Low molecular weight PAHs, with 2 to 4 aromatic hydrocarbon rings, are more potent as co-carcinogens during the promotional stage of cancer. In this stage, an initiated cell (i.e., 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.[43] 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.[43] 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[edit]

Adult exposure to PAHs has been linked to cardiovascular disease.[44] PAHs are among the complex suite of contaminants in cigarette smoke and particulate air pollution and may contribute to cardiovascular disease resulting from such exposures.[45]

In laboratory experiments, animals exposed to certain PAHs have shown increased development of plaques (atherogenesis) within arteries.[46] 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.[46] 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.[45][46] These quinone metabolites also generate reactive oxygen species that may alter the activity of genes that affect plaque formation.[46]

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.[47][48] 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.[49]

Developmental impacts[edit]

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.[50][51][52][53]

Regulation and oversight[edit]

Some governmental bodies, including the European Union as well as NIOSH and the Environmental Protection Agency in the US, regulate concentrations of PAHs in air, water, and soil.[54] The European Commission has restricted concentrations of 8 carcinogenic PAHs in consumer products that contact the skin or mouth.[55]

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:[56][57][58]

Compound Agency
acenaphthene EPA, ATSDR
acenaphthylene EPA, ATSDR
anthracene EPA, ATSDR
benz[a]anthracene[A] EPA, ATSDR, EFSA
benzo[b]fluoranthene[A] EPA, ATSDR, EFSA
benzo[j]fluoranthene ATSDR, EFSA
benzo[k]fluoranthene[A] EPA, ATSDR, EFSA
benzo[c]fluorene EFSA
benzo[g,h,i]perylene[A] EPA, ATSDR, EFSA
benzo[a]pyrene[A] EPA, ATSDR, EFSA
benzo[e]pyrene ATSDR
chrysene[A] EPA, ATSDR, EFSA
coronene ATSDR
Compound Agency
cyclopenta[c,d]pyrene EFSA
dibenz[a,h]anthracene[A] EPA, ATSDR, EFSA
dibenzo[a,e]pyrene EFSA
dibenzo[a,h]pyrene EFSA
dibenzo[a,i]pyrene EFSA
dibenzo[a,l]pyrene EFSA
fluoranthene EPA, ATSDR
fluorene EPA, ATSDR
indeno[1,2,3-c,d]pyrene[A] EPA, ATSDR, EFSA
5-methylchrysene EFSA
naphthalene EPA
phenanthrene EPA, ATSDR
pyrene EPA, 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).[58][59]

Detection and optical properties[edit]

A spectral database exists[60] for tracking polycyclic aromatic hydrocarbons (PAHs) in the universe.greatly upgraded database 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.

PAHs possess very characteristic UV absorbance spectra. These often possess many absorbance bands and are unique for each ring structure. Thus, for a set of isomers, each isomer has a different UV absorbance spectrum than the others. This is particularly useful in the identification of PAHs. Most PAHs are also fluorescent, emitting characteristic wavelengths of light when they are excited (when the molecules absorb light). The extended pi-electron electronic structures of PAHs lead to these spectra, as well as to certain large PAHs also exhibiting semi-conducting and other behaviors.

Origins of life[edit]

Main article: PAH world hypothesis
The Spitzer Space Telescope captures PAH spectral lines, producing this image of nebulosity in a stellar nursery.[61]

PAHs may be abundant in the universe.[62][63][64][65] They seem to have been formed as early as a couple of billion years after the Big Bang, and are associated with new stars and exoplanets.[60] More than 20% of the carbon in the universe may be associated with PAHs.[60] PAHs are considered possible starting material for the earliest forms of life.[60][64] Light emitted by the Red Rectangle nebula and found spectral signatures that suggest the presence of anthracene and pyrene.[66][67] This report was considered a controversial hypothesis that as nebulae of the same type as the Red Rectangle approach the ends of their lives, convection currents cause carbon and hydrogen in the nebulae's core to get caught in stellar winds, and radiate outward. As they cool, the atoms supposedly bond to each other in various ways and eventually form particles of a million or more atoms. Witt and his team inferred[66] that PAHs —which may have been vital in the formation of early life on Earth— in a nebula, by necessity they must originate in nebulae.[67]

Two extremely bright stars illuminate a mist of PAHs in this Spitzer image.[68]

More recently, fullerenes (or "buckyballs"), have been detected in other nebulae.[69] Fullerenes are also implicated in the origin of life; according to astronomer Letizia Stanghellini, "It's possible that buckyballs from outer space provided seeds for life on Earth."[70] In September 2012, NASA scientists reported results of analog studies in vitro that PAHs, subjected to interstellar medium (ISM) conditions, are transformed, through hydrogenation, oxygenation, and hydroxylation, to more complex organics—"a step along the path toward amino acids and nucleotides, the raw materials of proteins and DNA, respectively".[71][72] Further, as a result of these transformations, the PAHs lose their spectroscopic signature which could be one of the reasons "for the lack of PAH detection in interstellar ice grains, particularly the outer regions of cold, dense clouds or the upper molecular layers of protoplanetary disks."[71][72]

PAHs have been detected in the upper atmosphere of Titan, the largest moon of the planet Saturn.[73]

See also[edit]

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