Site Title Goes Here

Shortcut Navigation:

ACT FOR CHANGE

Take Action on Legislation

Tell Congress to stop playing politics with our health!

TAKE ACTION

STRONG VOICES

Janet Gray, Ph.D.
Janet Gray, Ph.D.

As author of our 2008 and 2010 State of the Evidence reports, Dr. Gray drives the science behind all our work.

LEARN MORE >
Printer Friendly

Polycyclic Aromatic Hydrocarbons (PAHs)

CATEGORY*: IARC probable carcinogen, NTP reasonably anticipated carcinogen, Endocrine disruptor

FOUND IN: Products of combustion in cigarette smoke, diesel exhaust, grilled meats, and coal and coke-burners

THE GIST: PAHs are products of combustion—and enter the body from coal and coke burners, diesel-fueled engines, grilled meats and cigarettes. PAHs are toxic to aquatic life, contribute to global warming and are suspected human carcinogens. Multiple studies have linked breast cancer incidence with PAH exposure. Studies show that exposure to these chemicals at critical periods of breast cancer development can influence later cancer risk.

State of the Evidence on Polycyclic Aromatic Hydrocarbons

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous byproducts of combustion, which enter the body from sources as varied as coal and coke burners, diesel-fueled engines, grilled meats and cigarettes. PAH residues are often associated with suspended particulate matter in the air, so inhalation is a major means of PAH exposure (Bonner, 2005).

TIPS FOR PREVENTION

Bike, walk, take public transportation, or drive an electric or hybrid-electric vehicle. You will lower your carbon footprint and protect public health at the same time.

More tips for protecting yourself and the environment >

In the Silent Spring Institute study of environmental contaminants in house dust, three PAHs (pyrene, benz[a]anthracene and benz[a]pyrene) were found in more than three-quarters of the homes tested (Rudel, 2003). Although they are still found extensively in suspended particulate matter, federally imposed standards on vehicular emissions have led to a statistically significant decrease in PAH release by vehicles compared to their highest levels in the 1970s (Beyea, 2008).

Like many other environmental chemicals that are associated with breast cancer risk, PAHs are lipophilic (fat-seeking) and are stored in the fat tissue of the breast. PAHs have been shown to increase risk for breast cancer through a variety of mechanisms. The most common PAHs are weakly estrogenic (estrogen-mimicking), because they interact with the cellular estrogen receptor (Pliskova, 2005). However, the major receptor-directed pathway is different, with PAHs also associating with a protein called the aryl hydrocarbon receptor (AhR), initiating a series of cell changes that lead to altered cell signaling and ultimately to increases in DNA mutations (Kemp, 2006; Santodonato, 1997). Although it is currently unclear what the naturally occurring ligand (substance that binds) for the AhR is, evidence suggests that the AhR system is important in regulating responses to cellular stress that can lead to disruption of normal cell functioning (Kung, 2009). At least some of the effects of PAHs are mediated through complex interactions between the AhR-regulated and estrogen-receptor-regulated pathways (Ohura, 2009; Swedenborg, 2010). PAHs can also be directly genotoxic, meaning that the chemicals themselves or their breakdown products can directly interact with genes and cause damage to DNA (Ralston, 1997).

Several epidemiological studies have implicated PAH exposure in increased risk for breast cancer. One of the studies from the Long Island Breast Cancer Study Project found a 50 percent greater risk of breast cancer in women with the highest level of PAH-DNA adducts. PAH-DNA adducts are indicators of problems in DNA repair in cells, one of the early hallmarks of tumor development (Gammon, 2002). In an earlier report, researchers explored the presence of PAH-DNA adducts in breast tissue samples taken from women diagnosed with cancer as compared with those diagnosed with benign breast disease. Cancerous samples were twice as likely to have PAH-DNA adducts as were benign samples (Rundle, 2000). Follow-up work indicates that those women who had higher levels of PAH-DNA adducts may not necessarily have had higher exposures to PAHs, but instead were more sensitive to the exposures to PAHs because they had particular genetic profiles that encouraged the deficits in DNA repair (Gammon, 2008). Other studies support the existence of different genetic profiles in women who have increased numbers of PAH-DNA adducts, including polymorphisms in genes involved in cell metabolism, tumor-suppressor mechanisms and DNA repair (Gammon, 2008; Mahadevan, 2005). Differences were not found in the profiles of genes whose products are involved in the activation and deactivation of the PAHs themselves (McCarty, 2009).

A population-based case-control study found that exposures to PAHs were associated with specific mutations of the p53 tumor suppressor gene in breast tumor samples. These data suggest that very specific p53 mutations, as well as possibly other DNA-repair and replication pathways, may be involved in the development of PAH-related breast cancer (Mordukhovich, 2010).

Occupational exposure studies have looked at workers exposed regularly to gasoline fumes and vehicular exhaust, major sources of PAHs (as well as of benzene). These occupational exposures are associated with an increased risk of breast cancer for pre-menopausal women (Petralia, 1999) and also for men. PAHs may increase the risk of breast cancer specifically in men carrying a BRCA1 or BRCA2 mutation (Palli, 2004). 

A case-control study in western New York indicated that very early life exposure (around the time of birth) to high levels of total suspended particulates, a proxy measure for PAH levels, is associated with increased risk of breast cancer in post-menopausal women (Bonner, 2005). An extension of this study, examining PAH exposures at critical times in women’s reproductive histories, demonstrated a relationship between particulate exposures around the time of the first menstrual period and incidence of pre-menopausal breast cancer, and a relationship between exposure level at the time a woman first gives birth and her risk of post-menopausal breast cancer (Nie, 2007). The results are complex, but all contribute to our understanding that exposures to environmental toxicants at critical periods of breast development can influence later cancer risk.

The studies above all looked at breast cancer incidence. Two reports examined the relationship between PAH exposures and mortality. Using an ecological model exploring the association between suspended fine particulate matters in several municipalities in Taiwan, researchers found that women living in areas with high levels of particulate matter in the air had an increased probability of dying from breast cancer, as compared to those living in cleaner areas (Hung, 2012). Another report examined PAH-DNA adduct levels and mortality among women who had been diagnosed with breast cancer. In an extension of the Long Island study described above, researchers found no overall relationship between survivorship and PAH-DNA adduct levels. Looking more closely at groups of women who had undergone different types of treatments, however, revealed a twofold increase in deaths from breast cancer among women with high PAH-DNA adduct levels who had received radiation treatment. However, there was an increased survival rate for women with adducts who had received hormone therapy as part of the treatment for their breast cancers (Sagiv, 2009).

*For chemicals that have been shown to be carcinogens, we provide classifications from two authoritative bodies: the International Agency for Research on Cancer (IARC, an international body) and the National Toxicology Program (NTP, a division of the U.S. Department of Health and Human Services). We have categorized endocrine-disrupting compounds where the body of peer-reviewed research indicates a strong foundation for doing so.