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Vinyl Chloride


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.

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Polychlorinated Biphenyls (PCBs)

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

FOUND IN: Banned in U.S. in 1976, but two-thirds of insulation fluids, plastics, adhesives, paper, inks, paints and dyes manufactured before the ban are still in use

THE GIST: The EPA banned PCBs from new products in 1976, but they are still found in soil, riverbeds and dust particulates in homes because of their persistent nature, and because they remain in products manufactured prior to the ban. PCBs have been demonstrated to cause cancer, but studies have shown mixed results linking breast cancer in particular to PCBs. These chemicals also have wide-ranging effects on the immune system, reproductive system, nervous system, and endocrine system.

State of the Evidence on Polychlorinated Biphenyls (PCBs)

Although the U.S. Environmental Protection Agency banned the use of PCBs in new products in 1976, as many as two-thirds of all PCB-containing insulation fluids, plastics, adhesives, paper, inks, paints, dyes and other products manufactured before the ban remain in use today. The remaining one-third was discarded, which means that these toxic compounds eventually made their way into landfills and waste dumps (Robinson, 1990; Weber, 2012).


Like DDT, PCBs have been banned but still persist in our bodies.

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Both DDT and PCBs have been banned in the United States for more than three decades, yet both are still found in soil, riverbeds and dust particulates in homes (Ertl, 2012; Rudel, 2003; Sudharshan, 2012). PCBs are persistent and bioaccumulative, meaning that despite the 1976 ban, they still persist in the environment and in people’s bodies.

Levels of bioaccumulated PCBs were high before the chemicals were banned in the United States, but generally their presence in human tissues has decreased slowly over the past decades (Hagmar, 2006). Exposures were high, though, between childhood and young adulthood for many women who are now facing breast cancer diagnoses. The persistence of these compounds has meant that levels remain high in some locations (Hong, 2012; Donaldson, 2010). PCB levels in umbilical cord blood were correlated with the distance of mothers’ residences from a Superfund site; levels were lower after site remediation (Choi, 2006). One ongoing source of PCB exposure is commercially available floor finishes that were applied in the 1950s and 1960s and may still be around (Rudel, 2008).

The science on PCBs is complicated. There are more than 200 individual PCBs, classified in three types based on their effects on cells. One type acts like an estrogen. A second type acts like an anti-estrogen. A third type appears not to be hormonally active, but can stimulate the enzyme systems of animals and humans in a manner similar to the way certain drugs (such as phenobarbital) and other toxic chemicals do (Connor, 1997). Additionally, metabolites of PCBs can alter the expression of genes involved in hormone synthesis, indicating that these compounds may act as endocrine disruptors in ways that do not directly involve estrogen or other hormone receptors (Braathen, 2009). PCBs with relatively low chlorination levels may induce damage to DNA in isolated breast tumor cells in vitro. The presence of estrogen receptors (ER+) in the cells may actually offer protection against damage (Lin, 2009).

A comprehensive review of the epidemiological literature examining possible links between total PCB exposures and breast cancer concluded that in general populations, the findings were inconsistent across studies (Brody, 2007). A 2009 review of the literature concluded that the overall picture was that PCBs, as a class, were not associated with increased risk for breast cancer (Golden, 2009). But as was true for critiques of DDT studies, the methods used to test these relationships in most studies do not account for exposures to PCBs during earlier developmental times when mammary tissue is particularly sensitive to the toxic effects of many environmental chemicals (Verner, 2010). The results from Cohn’s work on DDT and breast cancer make clear that this is a critical methodological issue (Cohn, 2011).

Most reports have looked at total PCB levels without identifying individual types. A few studies, however, have looked at relationships between cancer status and particular PCBs. For example, a 2004 case-control study found significantly higher total blood levels of PCBs, particularly PCB 153, in women with breast cancer than in presumably healthy women. PCB 153 exhibits estrogen-like activity in animal and in vitro studies (Charlier, 2004). Another study measured several types of PCBs, along with DDE, in breast biopsy tissue. Compared with healthy women, pre-menopausal women with breast cancer had significantly higher levels of PCBs 105 and 118, while post-menopausal women with breast cancer had higher levels of PCBs 170 and 180 (Aronson, 2000). None of these four PCBs was shown to have estrogenic activity in a study using breast cancer cell (MCF-7) proliferation to test estrogen responses of compounds (Decastro, 2006).

Another report has implicated PCBs in breast cancer recurrence among women with non-metastatic breast cancer. The study found that women with the highest levels of total PCBs, as well as of PCB 118, in their fat tissues were almost three times as likely to have recurrent breast cancer as women with lower levels (Muscat, 2003). Women in rural Sweden who ate higher levels of PCB-contaminated fish had higher risk for breast cancer (Helmfrid, 2012).

Although many studies have found no link between PCBs and breast cancer (Salehi, 2008), new evidence suggests that some of these compounds may have their greatest impact on women with particular susceptibilities and that looking broadly at large samples will not tell the full story of cancer risk as influenced by PCB exposures. Thus, more study is needed to determine the effect of PCB exposure on breast cancer development in specific populations. For example, researchers evaluating data from the Nurses’ Health Study revisited the issue of PCBs and breast cancer risk and revised their conclusion concerning the link between PCBs, DDE and breast cancer. In studies of PCBs and DDE in blood, they had previously concluded that exposure to these chemicals was unlikely to explain high breast cancer rates (Laden, 2001). In 2002, new evidence regarding variations in individual susceptibility due to genetic differences prompted these researchers to call for additional studies (Laden, 2002). One study examined occupational exposures to PCBs in female electrical capacitor production workers and development of breast cancer.  The authors found no overall relationship between exposure levels (based on job types, air samples and representative blood samples) or employment duration and breast cancer incidence when all women workers were considered together. But when the data were analyzed separately for non-white women, a statistically significant relationship was found between incidence of breast cancer and the duration of employment in the capacitor factory as well as cumulative levels of exposure to PCBs (Silver, 2009).

Studies examining relationships between PCBs and breast cancer have been inconsistent, but several studies have indicated that post-menopausal women who have a particular variant (the m2 variant) of the CYP1A1 gene (Laden, 2002; Moysich, 1999; Zhang, 2004) may be more vulnerable to the adverse effects of PCBs. CYP1A1 expression induces activation of an enzyme, cytochrome P450, that is involved in the metabolism of steroid hormones. Further study of CYP1A1 variants indicated that while the m2 variant increases the relationship between PCB levels and breast cancer risk in white women, the m3 variant has a similar effect in black women (Li, 2005).

Laboratory studies of human breast cancer cells have demonstrated that various specific types of PCBs promote the proliferation of breast cancer cells in vitro by stimulating estrogen-receptor-mediated pathways (Andersson, 1999; Gierthy, 1997) and the activation of key enzymes and cellular changes that are characteristic of transformation of cells to a malignant state (Hatakeyama, 1999).

A study examining PCB levels and mortality following a diagnosis of breast cancer indicates mortality is increased in association with higher PCB levels in women with estrogen-receptor-positive cancers (Hoyer, 2001).

*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.