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Polycyclic Aromatic Hydrocarbons Overview

General Information

Polycyclic aromatic hydrocarbons (PAHs) are a class of more than 100 chemicals generally produced during the incomplete burning of organic materials, including coal, oil, gas, wood, garbage, and tobacco. PAHs are composed of up to six benzene rings fused together such that any two adjacent benzene rings share two carbon bonds. Examples include phenanthrenes, naphthalene, and pyrene. Important PAH sources include motor vehicle exhaust, residential and industrial heating sources, coal, crude oil and natural gas processing, waste incineration, and tobacco smoke. The emitted PAHs can form or bind to particles in the air, and particle size depends in part on the source of the PAHs. The smaller or fine particulates (e.g., PM2.5 or smaller) have higher concentrations of PAHs than the larger or coarse particulates (Bostrom et al., 2002; Rehwagen et al., 2005). Ambient air PAH concentrations show seasonal variation (IPCS, 1998; Rehwagen et al., 2005). Smoking, grilling, broiling, or other high temperature processing leads to PAH formation in meat and in other foods, as well. Uncooked foods and vegetables generally contain low levels of PAHs but can be contaminated by airborne particle deposition or growth in contaminated soil. With the exception of naphthalene, the PAHs described here are not produced commercially in the U.S.

Human exposure usually occurs to PAH mixtures rather than to individual chemicals, and PAH mixture composition varies with the combustion source and temperature (ATSDR, 1995). For persons without occupational exposure, important sources of PAHs include ambient air pollution (especially motor vehicle exhaust), smoke from wood or fossil fuels, tobacco smoke, and foods. PAH exposure can occur in workplaces where petroleum products are burned or coked, such as coke production, coal gasification and gas refining, iron or steel production, roofing tar and asphalt application, waste incineration, and aluminum smelting. Coal tar ointments containing PAHs are used to treat several inflammatory skin conditions.

PAHs are lipid soluble and can be absorbed through the skin, respiratory tract, and gastrointestinal tract. PAH metabolism is complex and occurs primarily in the liver, and to a lesser extent, in other tissues. PAH elimination occurs via urine and feces, and urinary metabolites are eliminated within a few days (Ramesh et al., 2004). PAHs and their urinary hydroxylated metabolites measured in at CDC are shown in the table. The metabolic pathways and enzyme-inducing effects of specific PAHs, such as benz[a]pyrene, have been actively studied to elucidate cancer potential and causal mechanisms (Ramesh et al., 2004). Although immunologic, kidney and brain toxicity have been seen in animals after high doses were administered, it is unclear if similar effects may occur in humans. Lung, bladder, and skin cancers have been reported in occupational settings following high PAH exposures (Bosetti et al., 2007; Bostrom et al., 2002; Lloyd, 1971). Exposure to fine particulates has been associated with fetal growth retardation, respiratory disorders, and cardiovascular disease, but it is unknown whether PAHs contained within fine particulates are etiologic (ATSDR, 1995; Choi, 2006).

IARC classifies naphthalene as a possible human carcinogen. NTP determined that naphthalene is reasonably anticipated to be a human carcinogen. Many other PAHs are considered to be probable or possible human carcinogens. IARC and NTP have classified specific PAH-containing chemical mixtures (e.g., soot, coke oven emissions, coal tars and coal tar pitches) as human carcinogens. OSHA has developed criteria on the allowable levels of these chemicals in the workplace.

Information about external exposure (i.e., environmental levels) and health effects is available in reviews (Bosetti et al., 2007; Bostrom et al., 2002; Brandt and Watson 2003) and from ATSDR at


Biomonitoring Information

Measurement of urinary metabolites reflects recent exposure to PAHs. Some of the parent PAHs can produce more than one measurable urinary metabolite, as shown in the Table. The hydroxylated metabolites of PAHs are excreted in human urine both as free hydroxylated metabolites and as hydroxylated metabolites conjugated to glucuronic acid and sulfate. Urine metabolite profiles can vary depending on the PAH source(s), but also have been found to vary between individuals experiencing similar exposures within the same workplace (Grimmer et al., 1997; Jacob and Seidel 2002).

Finding a measurable amount of one or more metabolites in the urine does not imply that the levels of the PAH metabolites or the parent PAH cause an adverse health effect. Biomonitoring studies of urinary PAHs provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of PAHs than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

CAS No. 129-00-0

General Information

Pyrene has been used as a starting material for producing optical brighteners and dyes. Notable pyrene sources include domestic heating sources, particularly wood burning; gasoline fuel exhaust; coal tar and asphalt; and cigarette smoke. Pyrene is commonly found in PAH mixtures, and its urinary metabolite, 1-hydroxypyrene, has been used widely as an indicator of exposure to PAH chemicals, particularly in occupational exposure studies. IARC determined that pyrene was not classifiable as to its human carcinogenicity.

Biomonitoring Information

Urinary levels of 1-hydroxypyrene reflect recent exposure. The overall geometric mean of 1-hydroxypyrene levels in the NHANES 2003–2004 subsample was similar to that of general populations in other industrialized countries (Becker et al., 2003; Chuang et al., 1999; Goen et al., 1995; Heudorf and Angerer 2001a, 2001b; Yang et al., 2003). Higher levels have been noted in residents of industrialized and high traffic urban areas compared with rural or suburban settings, and the mean urinary 1-hydroxypyrene levels from the former group were somewhat higher than in the NHANES 2003–2004 subsample (Kanoh et al., 1993; Kuo et al., 2004; Yang et al., 2003). Variation also has been noted in the mean 1-hydroxypyrene urine levels between different industrialized countries (for example, South Korea or China, compared to the U.S.), which is attributable to such factors as ambient air pollution and residential heating and cooking sources (Huang et al., 2004; Kuo et al., 2004; Roggi et al., 1997; Siwinska et al., 1999; Yang et al., 2003). In general, smokers have about 2 to 4-fold higher urinary 1-hydroxypyrene levels than non-smokers (Goen et al., 1995; Heudorf and Angerer 2001b; Jacob et al., 1999). Environmental tobacco smoke may contribute to higher urinary 1-hydroxypyrene levels in exposed children (Chuang et al., 1999; Siwinska et al., 1999; Tsai et al., 2003).

Numerous studies of workers with occupational exposure to excessive vehicular exhaust have found increased urinary 1-hydroxypyrene levels compared to non-exposed individuals (Kuusimaki et al., 2004; Merlo et al., 1998; Tsai et al., 2004). The highest urinary levels of 1-hydroxypyrene measured in occupational studies have been found in aluminum smelter and coke oven workers exposed to heated tar and coal tar products (Alexandrie et al., 2000; Goen et al., 1995; Jacob and Seidel, 2002; Lu et al., 2002; Serdar et al., 2003). Results in these workers have ranged from about 100 to more than 1000 times greater than non-exposed levels and the geometric mean values found in the Fourth Report. Tobacco smoking also was associated with levels about double those in nonsmoking workers (Campo et al., 2006; Merlo et al., 1998; Mukherjee et al., 2004).

Finding a measurable amount of urinary 1-hydroxypyrene does not imply that the level of 1-hydroxypyrene causes an adverse health effect. Biomonitoring studies on levels of 1-hydroxypyrene provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrene than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.


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Becker K, Schulz C, Kaus S, Seiwert M, Seifert B. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Int J Hyg Environ Health 2003; 206:15-24.

Campo L, Buratti M, Fustinoni S, Cirla PE, Martinotti I, Longhi O, et al. Evaluation of exposure to PAHs in asphalt workers by environmental and biological monitoring. Ann NY Acad Sci 2006;1076:405-420.

Chuang JC, Callahan PJ, Lyu CW, Wilson NK. Polycyclic aromatic hydrocarbon exposures of children in low-income families. J Expo Anal Environ Epidemiol 1999;9(2):85-98.

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Heudorf U, Angerer J. Internal exposure to PAHs of children and adults living in homes with parquet flooring containing high levels of PAHs in the parquet glue. Int Arch Occup Environ Health 2001a;74(2):91-101.

Heudorf U, Angerer J. Urinary monohydroxylated phenanthrenes and hydroxypyrene–the effects of smoking habits and changes induced by smoking on monooxygenase-mediated metabolism. Int Arch Occup Environ Health. 2001b 74(3):177-83.

Huang W, Grainger J, Patterson DG, Turner WE, Caudill SP, Needham LL, et al. Comparison of 1-hydroxypyrene exposure in the US population with that in occupational exposure studies. Int Arch Occup Environ Health 2004;77:491-498.

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Jacob J, Seidel A. Biomonitoring of polycyclic aromatic hydrocarbons in human urine. J Chromatogr B 2002;778(1-2):31-47.

Kanoh T, Fukuda M, Onozuka H, Kinouchi T, Ohnishi Y. Urinary 1-hydroxypyrene as a marker of exposure to polycyclic aromatic hydrocarbons in environment. Environ Res 1993;62(2):230-241.

Kuo CT, Chen HW, Chen JL. Determination of 1-hydroxypyrene in children urine using column-switching liquid chromatography and fluorescence detection. J Chromatogr B 2004;805(2):187-193.

Kuusimaki L, Peltonen Y, Mutanen P, Peltonen K, Savela K. Urinary hydroxy-metabolites of naphthalene, phenanthrene and pyrene as markers of exposure to diesel exhaust. Int Arch Occup Environ Health 2004;77(1):23-30.

Lu PL, Chen ML, Mao IF. Urinary 1-hydroxypyrene levels in workers exposed to coke oven emissions at various locations in a coke oven plant. Arch Environ Health 2002;57(3):255-261.

Merlo F, Andreassen A, Weston A, Pan CF, Haugen A, Valerio F, et al. Urinary excretion of 1-hydroxypyrene as a marker for exposure to urban air levels of polycyclic aromatic hydrocarbons. Cancer Epidemiol Biomarkers Prev 1998;7(2):147-55.

Mukherjee S, Palmer LJ, Kim JY, Aeschliman DB, Houk RS, Woodin MA, et al. Smoking status and occupational exposure affects oxidative DNA injury in boilermakers exposed to metal fume and residual oil fly ash. Cancer Epidemiol Biomarkers Prev 2004;13(3):454-460.

Roggi C, Minoia C, Sciarra GF, Apostoli P, Maccarini L, Magnaghi S, et al. Urinary 1-hydroxypyrene as a marker of exposure to pyrene: an epidemiological survey on a general population group. Sci Total Environ 1997;199(3):247-254.

Serdar B, Waidyanatha S, Zheng Y, Rappaport SM. Simultaneous determination of urinary 1- and 2-naphthols, 3- and 9-phenanthrols, and 1-pyrenol in coke oven workers. Biomarkers 2003;8(2):93-109.

Siwinska E, Mielzynska D, Bubak A, Smolik E. The effect of coal stoves and environmental tobacco smoke on the level of urinary 1-hydroxypyrene. Mutat Res 1999;445(2):147-153.

Tsai HT, Wu MT, Hauser R, Rodrigues E, Ho CK, Liu CL, et al. Exposure to environmental tobacco smoke and urinary 1-hydroxypyrene levels in preschool children. Kaohsiung J Med Sci 2003;19(3):97-104.

Tsai PJ, Shih TS, Chen HL, Lee WJ, Lai CH, Liou SH. Urinary 1-hydroxypyrene as an indicator for assessing the exposures of booth attendants of a highway toll station to polycyclic aromatic hydrocarbons. Environ Sci Technol 2004;38(1):56-61.

Yang M, Kim S, Lee E, Cheong HK, Chang SS, Kang D, et al. Sources of polycyclic aromatic hydrocarbon exposure in non-occupationally exposed Koreans. Environ Mol Mutagen 2003;42(4):250-257.

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