Introduction

PAH exposure through air, water, soil, and food sources occurs on a regular basis for most people. Routes of exposure include ingestion, inhalation, and dermal contact in both occupational and non-occupational settings. Some exposures may involve more than one route simultaneously, affecting the total absorbed dose (such as dermal and inhalation exposures from contaminated air). All non-workplace sources of exposure such as diet, smoking, and burning of coal and wood should be taken into consideration.

Air

PAH concentrations in air can vary from less than 5 to 200,000 nanograms/cubic meter (ng/m³) [Cherng et al. 1996; Georgiadis and Kyrtopoulos 1999].

Although environmental air levels are lower than those associated with specific occupational exposures, they are of public health concern when spread over large urban populations [Zmirou et al. 2000].

The background levels of seventeen of the Agency for Toxic Substances and Disease Registry’s toxicological profile priority PAHs in ambient air are reported to be 0.02–1.2 nanograms/m³ in rural areas and 0.15–19.3 ng/m³ in urban areas [ATSDR 1995].

Cigarette smoking and environmental tobacco smoke are other sources of air exposure. Smoking one cigarette can yield an intake of 20–40 ng of benzo (a) pyrene [Phillips 1996; O’Neill et al. 1997]. Smoking one pack of unfiltered cigarettes per day yields 0.7 µg/day benzo(a)pyrene exposure. Smoking a pack of filtered cigarettes per day yields 0.4 µg/day [Sullivan and Krieger 2001].

Environmental tobacco smoke contains a variety of PAHs, such as benzo(a)pyrene, and more than 40 known or suspected human carcinogens. Side-stream smoke (smoke emitted from a burning cigarette between puffs) contains PAHs and other cytotoxic substances in quantities much higher than those found in mainstream smoke (exhaled smoke of smoker) [Jinot and Bayard 1996; Nelson 2001].

Water

PAHs can leach from soil into water. Water contamination also occurs from industrial effluents and accidental spills during oil shipment at sea. Concentrations of benzo(a)pyrene in drinking water are generally lower than those in untreated water and about 100-fold lower than the U.S. Environmental Protection Agency’s (EPA) drinking water standard. (EPA’s maximum contaminant level [MCL] for benzo(a)pyrene in drinking water is 0.2 parts per billion [ppb].)

Soil

Soil contains measurable amounts of PAHs, primarily from airborne fallout. Documented levels of PAHs in soil near oil refineries have been as high as 200,000 micrograms per kilogram (µg/kg) of dried soil. Levels in soil samples obtained near cities and areas with heavy traffic were typically less than 2,000 µg/kg [IARC 1973].

Foodstuffs

In non-occupational settings, up to 70% of PAH exposure for a non-smoking person can be associated with diet [Skupinska et al. 2004]. PAH concentrations in foodstuffs vary. Charring meat or barbecuing food over a charcoal, wood, or other type of fire greatly increases the concentration of PAHs. For example, the PAH level for charring meat can be as high as 10–20 µg/kg [Phillips 1999]. Charbroiled and smoked meats and fish contain more PAHs than do uncooked products, with up to 2.0 µg/kg of benzo(a)pyrene detected in smoked fish. Tea, roasted peanuts, coffee, refined vegetable oil, cereals, spinach, and many other foodstuffs contain PAHs. Some crops, such as wheat, rye, and lentils, may synthesize PAHs or absorb them via water, air, or soil [Grimmer 1968; Menzie et al. 1992; Shabad and Cohan 1972; IARC 1973].

Other Sources of Exposure

PAHs are found in prescription and nonprescription coal tar products used to treat dermatologic disorders such as psoriasis and dandruff [Van Schooten 1996].

PAHs and their metabolites are excreted in breast milk, and they readily cross the placenta.

Anthracene laxative use has been associated with melanosis of the colon and rectum [Badiali et al. 1985].

Background Exposures

In the Third National Report on Human Exposure to Environmental Chemicals [CDC 2005], urinary levels of hydroxylated metabolites of PAHs were measured in a subsample of the National Health and Nutrition Examination Survey (NHANES) among participants aged 6 years and older during 1999–2002. Participants were selected within the specified age range to be a representative sample of the U.S. population. Measurements of the 22 metabolites reflect exposure to PAHs that occurred a few days prior to the urine samples being taken.

Pyrene is commonly found in PAH mixtures, and its urinary metabolite, 1-hydroxypyrene, has been used as an indicator of exposure to PAH chemicals [Becher and Bjorseth 1983; Granella and Clonfero 1993; Popp 1997; Santella et al.1993, CDC 2005]. The American Conference of Governmental Industrial Hygienists recommends measurement of 1-hydroxypyrene in the end-of-shift, end-of-work-week urine samples as a biological exposure index (BEI) for assessment of exposure to mixtures containing PAHs [ACGIH 2005; Heikkila et al. 1995].

The geometric mean of urine concentrations (in nanograms/grams creatinine) of 1-hydroxypyrene for the U.S. population aged 6 years and older for survey years 1999–2000 was 74.2, and in survey years 2001–2002 it was 46.4 [CDC 2005]. The geometric mean levels of 1-hydroxypyrene in a NHANES 2001–2002 subsample is similar to that of other general populations residing in an urban setting [Goen et al. 1995; Chuang et al. 1999; Heudorf and Angerer 2001; Roggi et al. 1997; Yang et al. 2003]. Higher levels have been noted for residents of industrialized urban areas than in rural or suburban settings [Adonis et al. 2003; Kanoh et al. 1993; Kuo et al. 2004]. Many-fold higher levels can be found in workers from certain occupations [Jacob and Seidel 2002], including aluminum smelting [Alexandrie et al. 2000]; diesel engine mechanics [Adonis et al. 2003; Kuusimaki et al. 2004]; taxi, bus, and truck drivers [Chuang et al. 2003; Hansen et al. 2004; Kuusimaki et al. 2004]; painters [Lee et al. 2003], boilermakers [Mukherjee et al. 2004]; toll booth operators [Tsai et al. 2004]; traffic police [Merlo et al. 1998] and coke oven plant workers [Lu et al. 2002; Serdar et al. 2003; Siwinska et al. 2004]. Tobacco smoking leads to higher levels in smokers [Chuang et al. 2003; Adonis et al. 2003; Heudorf and Angerer 2001b] as well as in the non-smoking children of smokers [Tsai et al. 2003]. Coal stove exposure or consumption of broiled, fried, or grilled meat contribute to higher levels of 1-hydroxypyrene [Siwinska et al. 1999; Scheepers et al. 2002; Yang et al. 2003; [CDC 2005].

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