Polycyclic aromatic hydrocarbon

Most are produced by the incomplete combustion of organic matter— by engine exhaust fumes, tobacco, incinerators, in roasted meats and cereals,[1] or when biomass burns at lower temperatures as in forest fires.

[29] A year-long sampling campaign in Athens, Greece found a third (31%) of PAH urban air pollution to be caused by wood-burning, like diesel and oil (33%) and gasoline (29%).

[30][29] Substantially higher outdoor air, soil, and water concentrations of PAHs have been measured in Asia, Africa, and Latin America than in Europe, Australia, the U.S., and Canada.

[35] The rare minerals idrialite, curtisite, and carpathite consist almost entirely of PAHs that originated from such sediments, that were extracted, processed, separated, and deposited by very hot fluids.

[35] 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.

[51][55] 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.

[59] Exposure also occurs through drinking alcohol aged in charred barrels, flavored with peat smoke, or made with roasted grains.

[35] People can also be occupationally exposed during work that involves fossil fuels or their derivatives, wood-burning, carbon electrodes, or exposure to diesel exhaust.

[35][62][63] PAHs typically disperse from urban and suburban non-point sources through road runoff, sewage, and atmospheric circulation and subsequent deposition of particulate air pollution.

[65][69][70] 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.

[71] 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.

[73] 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).

[73] 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.

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

[81] 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.

In 1915, Yamigawa and Ichicawa were the first to experimentally produce cancers, specifically of the skin, by topically applying coal tar to rabbit ears.

[82] 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 benz[a]anthracene, a PAH that was subsequently demonstrated to cause tumors.

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.

[84][85] PAHs that affect cancer initiation are typically first chemically modified by enzymes into metabolites that react with DNA, leading to mutations.

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.

[90] 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.

[91] 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.

Low molecular weight PAHs are prevalent in the environment, thus posing a significant risk to human health at the promotional phases of cancer.

[92] 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.

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.

[98][99][100][101] 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.

[114] PAHs, subjected to interstellar medium (ISM) conditions, are transformed, through hydrogenation, oxygenation, and hydroxylation, to more complex organic compounds—"a step along the path toward amino acids and nucleotides, the raw materials of proteins and DNA, respectively".