Polycyclic Aromatic Hydrocarbons (PAHs)*

Polycyclic Aromatic Hydrocarbons (PAHs)*

Polycyclic Aromatic Hydrocarbons (PAHs) 513 not transported in water but adsorb onto soil and sediments. Leaching is negligible. Bioaccumulation is n...

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Polycyclic Aromatic Hydrocarbons (PAHs) 513

not transported in water but adsorb onto soil and sediments. Leaching is negligible. Bioaccumulation is not considered a concern.

Ecotoxicology Little information is available concerning the ecotoxicity of this class of chemicals.

Further Reading Hodgson E and Goldstein JA (2001) Metabolism of toxicants: Phase I reactions and pharmacogenetics. In: Hodgson E and Smart R (eds.) Introduction to Biochemical Toxicology, 2nd edn., pp. 67–113. New York: Wiley. Kitchen KT (1999) Carcinogenicity. New York: Dekker.

Relevant Website http://www.cdc.gov – National Institute of Occupational Safety and Health.

See also: Carcinogenesis; Oil, Crude.

Polycyclic Aromatic Hydrocarbons (PAHs)





Shayne C Gad and Samantha E Gad


& 2005 Elsevier Inc. All rights reserved. This article is a revision of the previous print edition article by Shayne C Gad and Jayne E Ash, volume 2, p. 577, & 1998, Elsevier Inc.

PAHS are readily absorbed via the gastrointestinal tract and then metabolically transformed to more reactive forms. These toxicants are typically converted into more reactive metabolites through phase I biotransformations, and then converted into more readily excretable conjugates via phase II processes.

CHEMICAL ABSTRACTS SERVICE REGISTRY NUMBERS: CAS 129-00-0 (Pyrene); CAS 153-78-6 (Fluoren2-amine) CHEMICAL FORMULA: C16H10 (for pyrene); C13H9NH2 (for fluoren-2-amine) OTHER COMPOUNDS: Benzo[a]pyrene; 3-Methylcholanthrene CHEMICAL STRUCTURES:

Mechanism of Toxicity Pyrene increases photosensitivity and suppresses the immune system. P450 metabolism of a number of PAHs leads to carcinogenic and mutagenic potential. PAHs have different toxicity profiles; some are more toxic than others. However, the mechanism of toxicity often relies on adduct formation with macromolecules following biotransformation.


Acute and Short-Term Toxicity (or Exposure) Animal

Uses Pyrene is used in biochemical research. Polycyclic aromatic hydrocarbons (PAHs) occur naturally in coal tar, fossil fuel combustion, forest fires, and open flame grilled meats. PAHs are found in cigarette smoke and in diesel emissions, when asphalt surfacing and tar roofing, and also in aluminum and coke plants. Pyrene was used in the 1930s as an insecticide.

In animals, pyrene is a mild dermal irritant and primary irritant. The oral LD50 is 2.7 g kg  1 in rats and 800 mg kg  1 in mice. Human

Photosensitization of skin and eyes can be caused by dermal exposure and inhalation causing skin effects including erythema and lesions.

Chronic Toxicity (or Exposure) Animal

Exposure Routes and Pathways Dermal contact, ingestion, and inhalation are possible exposure routes.

Several PAHs have been shown to cause reproductive and developmental effects in rodents. Genotoxic properties have been found in vitro and in vivo.

514 Polycyclic Aromatic Hydrocarbons (PAHs) Human

Toxic dermal effects are increased by exposure to ultraviolet light. Lesions on sun exposed skin may progress to skin cancer. Respiratory effects include cough, chronic bronchitis, and naematuria. Workers exposed to high airborne concentrations of some PAHs have shown increased rates of cancer and is therefore considered a probable carcinogen. Pyrene produces a carcinogenic effect from exposure to skin as well as a presence in bloodstream. It also produces immunodepression. Benzo[a]pyrene is found in relatively high levels in the environment and is a probable mutagen and teratogen; it has caused severe and long lasting hyperplasia and metaplasia as precancerous lesions.

Clinical Management The victim should be removed from exposure. Exposed skin and eyes should be thoroughly flushed with tepid water. Supportive therapy should be provided.

Environmental Fate The PAHs are produced by the incomplete combustion of fossil fuels, wood, and other organic material. These compounds are largely adsorbed onto smoke particles/aerosols and are a major component of industrial air pollution. Partitioning between water and air, between water and sediment, and between water and biota are the most important of the distribution processes. Even though most of these toxicants are released into the atmosphere, considerable amounts are found in water. These toxicants can enter the aquatic environment in many ways but mostly through large oil spills. Their affinity for organic matter in sediment, soil, and biota is high, and these compounds therefore accumulate in organisms in water and sediments. In Daphnia, accumulation of PAHs from water is correlated with their octanol–water partition coefficient. In organisms that actively metabolize these chemicals, absorbed concentrations are not correlated with the partition coefficient. Biomagnification is not observed with these toxicants. PAHs undergo photodegradation, microbial degradation, and metabolism in higher organisms. Hydrolysis plays essentially no role in their degradation. These chemicals are photooxidized in air and water in the presence of radicals; for example, OH, NO3, and O3. The reaction of two- to four-ring structures with NO3 leads to nitro-derivatives, which are known mutagens. PAHs exhibit toxic properties at low concentrations and several have been listed as priority

pollutants to be monitored in industrial effluents, natural waters, soils, and sediments. They enter soil systems and natural waters via wastewater effluents from coke and petroleum refining industries, accidental spills and leakages, rainwater runoff from highways and roadways, or from intentional disposal in the past. Low aqueous solubilities of PAHs and high octanol–water partition coefficients (KOW) often result in their accumulation in soils and sediments to levels several orders of magnitude above aqueous concentrations. PAHs can be potent carcinogens, and their presence in groundwater, streams, soil, and sediments may constitute a chronic human health hazard. There has been tremendous interest in understanding the fate and transport of PAHs in subsurface environments that are largely microaerobic or anaerobic. Little is known about anaerobic biotransformation of these contaminants, particularly in the context of soil and ground water contamination. Aerobic transformation of PAHs associated with soil and groundwater often leads to rapid depletion of dissolved oxygen and this eventually decreases the redox potential (Eh). Such decrease in the redox potential can result in favorable growth environments for denitrifying, sulfate-reducing, or even methanogenic (Eh o  0.3 V) microbial populations. Nearly 10–15% of the bacterial population in soil, water, and sediments consists of anaerobic organisms. Anaerobic transformations may, therefore, play a significant role in oxygen-depleted natural habitats.

Ecotoxicology Marine organisms adsorb and accumulate PAHs from water. Concentrations up to 7 mg kg  1 have been noted in organisms living near industrial effluents, and average levels in aquatic animals at contaminated sites were 10–500 mg kg  1. Average levels of these toxicants in aquatic organisms at sites with unspecified sources of PAH were 1–100 mg kg  1, but high concentrations (up to 1 mg kg  1) were found in some species, for example, lobsters in Canada. Concentrations of PAHs in insects ranged from 0.7 to 5.5 mg kg  1. In heavily contaminated locations, concentrations of benzo[a]pyrene in earthworm feces may reach 2 mg kg  1.

Exposure Standards and Guidelines The Occupational Safety and Health Administration permissible exposure limit for benzo[a]pyrene is 0.2 mg m  3. See also: Absorption; Benz[a]anthracene; Carcinogenesis; Methylcholanthrene, 3-; Respiratory Tract.

Polyethylene Glycol


Further Reading

Relevant Websites

Ballantyne B, Marrs T, and Syversen T (eds.) (1999) General and Applied Toxicology, 2nd edn. Oxford: Macmillan. Bostrom CE, Gerde P, Hanberg A, et al. (2002) Cancer risk assessment, indicators, and guidelines for polycyclic aromatic hydrocarbons in the ambient air. Environmental Health Perspectives 110(Suppl. 3): 451–488. Klaassen CD (2001) Casarett and Doulls Toxicology, 6th edn. New York: Mcgraw-Hill.

http://www.atsdr.cdc.gov – Agency for Toxic Substances and Disease Registry. Toxicological Profile for Polycyclic Aromatic Hydrocarbons (PAHs). http://www.inchem.org – Selected Non-Heterocyclic Polycyclic Aromatic Hydrocarbons (Environmental Health Criteria 202 from the International Programme on Chemical Safety.

Polyethylene Glycol Hon-Wing Leung & 2005 Elsevier Inc. All rights reserved.





CHEMICAL ABSTRACTS SERVICE REGISTRY NUMBER: CAS 25322-68-3 SYNONYMS: a-Hydro-o-hydroxypoly-(oxy-1,2ethanediyl); Macrogol; PEG; Carbowax; Jeffox; Nycolin; Pluracol E; Poly-G; Polyglycol E; Solbase; Polyox CHEMICAL/PHARMACEUTICAL/OTHER CLASS: A distribution of liquid and solid polymers of varying molecular weights (from 200 to several million) corresponding to an average number of oxyethylene groups CHEMICAL STRUCTURE: HðOCH2 2CH2 Þn OH Where n ¼ average number of oxyethylene groups

Uses Polyethylene glycols are widely used in food, cosmetics, and topical pharmaceuticals (e.g., ointments and suppository base).

circulation for a longer period than low-molecularweight polyethylene glycols. Polyethylene glycols are not appreciably metabolized. Ethylene glycol is not known to be a metabolite. The distribution of the higher members of polyethylene glycols within the body is extracellular, whereas the lower-molecular-weight members of the series diffuse intracellularly to a considerable extent. Polyethylene glycols tend to accumulate in the muscle, skin, bone, and the liver to a higher extent than the other organs, irrespective of the molecular weight. Liquid polyethylene glycols are rapidly excreted in the urine, while the higher-molecular-weight members are mainly eliminated in the feces.

Mechanism of Toxicity Many years of human experience in the workplace and in the use of consumer products containing polyethylene glycols have not shown any adverse health effects, except for administering high doses to sensitive or unhealthy persons. Nephrotoxicity associated with the topical treatment of burn patients with polyethylene glycols may reflect the compromised function of the patients’ kidneys rather than the direct toxic effects of polyethylene glycols.

Exposure Routes and Pathways

Acute and Short-Term Toxicity (or Exposure)

Ingestion and skin contact are the most common routes of both accidental and intentional exposures.



Polyethylene glycols have a very low level of acute toxicity to animals. They do not produce appreciable irritation to the rabbit skin and are only mildly irritating to the rabbit eyes.

The absorption of orally administered polyethylene glycols is dependent on their molecular size. While 50–65% of liquid polyethylene glycols (molecular weight up to 600) are absorbed, only from 0% to 2% of solid polyethylene glycols (molecular weight more than 1000) are absorbed. High-molecular-weight polyethylene glycols are retained in the blood


There have not been any reports of acute toxic or irritative effects in humans exposed to polyethylene glycols. The lowest-molecular-weight members (200– 300) have been observed to produce at most only a