The English surgeon Percival Pott was among the first to document the association of an environmental agent with cancer.² During the late 18th century, he determined that the unusually high incidence of scrotal cancer among chimney sweeps was due to their occupational exposure to soot and tar. As a consequence, recommendations for bathing and use of protective clothing were promulgated by chimney sweepers’ guilds in parts of Europe, but not in England. Subsequent decreases in the incidence of scrotal cancer were observed in continental Europe, demonstrating the efficacy of simple prevention efforts. It was not until the present century that the active carcinogens in soot and coal tar were shown to be polycyclic aromatic hydrocarbons (PAHs).³ This finding came about through the application of coal tar and fractions thereof to the skins of test animals, in which malignant skin tumors subsequently developed. Although many PAHs were identified in coal tar, most of the carcinogenic activity was attributed to the PAH benzo[a]pyrene.

Humans are exposed to PAHs from a variety of sources that include occupation, smoking, diet, and air.⁴ PAHs are readily absorbed into the body through the skin, lungs, and gastrointestinal tract. Occupational and medicinal exposures constitute the highest levels of human PAH exposure (albeit in small groups within the population), whereas diet and smoking are the major sources of exposure to PAHs in the general population. Air concentrations of greater than 10 µg benzo[a]pyrene/m³ are characteristic of topside gas and coke work environments. Broiled, barbecued, or smoked meats and fish contain relatively high concentrations of benzo[a]pyrene (1 to 20 µg/kg).

Cutaneous occupational exposure to PAHs has been associated with increased risk of skin and scrotal cancers in chimney sweeps and in persons exposed to unrefined lubricating oils in the textile and machining industries.¹ Scrotal cancer among mule spinners in the Manchester (United Kingdom) cotton industry was attributed to the saturation of the workers’ trousers with lubricating oil. A review of all admissions for scrotal cancer to the Royal Manchester Infirmary from 1902 to 1922 indicated that 49% had worked as mule spinners, whereas 16% had worked with tar or paraffin. As the textile industry declined in the middle 20th century, an increasing proportion of scrotal cancer was associated with cutting oils used in metal machining.

An excess of lung cancer has been demonstrated among persons with substantial inhalation exposure to PAHs, including roofers and pavers, coke oven workers, certain steel and iron manufacturing workers, and aluminum production workers.⁵ In addition, several studies suggest that workers highly exposed through inhalation also might be at increased risk of cancer at sites other than skin and lung. The strongest evidence for such an association is for bladder cancer, where a dose-response relationship has been demonstrated between PAH exposure and bladder cancer risk in aluminum workers after adjustment for smoking. Other sites with suggestive increases in risk include the pancreas and upper gastrointestinal tract.

Several biochemical pathways are involved in the metabolism of PAHs and of benzo[a]pyrene in particular.³ One major pathway results in highly reactive 7,8-dihydrodiol-9,10-epoxide-benzo[a]pyrene. Experimental studies demonstrate that cultured human lung or colon tissue metabolizes benzo[a]pyrene to reactive metabolites that bind to DNA in cultured tissue. Oral administration of benzo[a]pyrene to rodents produces benzo[a]pyrene-DNA adducts in liver, stomach, colon, and intestine, and cancers of the esophagus, forestomach, intestine, lungs, and mammary gland.