Air pollution may contribute to the etiology of ER-positive breast cancer, supporting public health interventions to reduce exposure levels.
A recent study notes that risk factors associated with air pollution point to the key role that hormones play in the etiology of breast cancer and suggest that environmental chemicals with endocrine-disrupting properties contribute to the risk for acquiring ER-positive breast cancer.
“Air pollution, a well-established risk factor for lung cancer, has been understudied in relation to other cancers, including breast cancer,” explains Alexandra J. White, PhD, MSPH. “Since breast cancer is the most common cancer diagnosis among women in the US, a need exists for a better understanding of potentially intervenable risk factors at both the policy and individual level.”
Association Positive for ER-Positive, But Not ER-Negative Breast Cancer
For a study published in the Journal of the National Cancer Institute, Dr. White and colleagues examined whether historical levels of fine particulate matter (PM2.5), which were higher in the past than today, impacted breast cancer incidence. The team used data from a nationwide spatiotemporal model for women (N=196,906) in the National Institutes of Health–AARP Diet and Health Study, a prospective cohort covering six states (California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania) and two metropolitan areas (Atlanta and Detroit), between 1995 and 1996.
“We estimated their historic residential exposure to PM2.5 for a 5-year period approximately 10 to 15 years prior to enrollment and evaluated whether women who lived in areas of higher PM2.5 had a higher incidence of breast cancer over an average of 20 years of follow-up,” Dr. White says. She emphasizes that this link was evident for estrogen receptor (ER)–positive but not ER–negative tumors.
Dr. White and colleagues identified 15, 870 breast cancer cases, with follow-up through 2017. The study team found an 8% higher incidence of breast cancer for women living in areas with higher PM2.5 exposure when compared with women living in areas with lower levels. “This suggests that PM2.5 may modestly increase the risk for breast cancer, particularly estrogen receptor (ER)-positive tumors,” Dr. White points out. “At the individual level, this association translates to a small increase in risk. However, at the population-level this finding may be more meaningful given the fact that almost everyone is exposed to air pollution.”
Focus on Intervention Efforts for Cancer-Related Sources
Dr. White and colleagues observed a consistent increase in breast cancer incidence for PM2.5 exposure across three estimated time windows of exposure (1980-1984, 1985-1989, 1990-1994), which suggests exposure during all periods was related to breast cancer risk (Table).
“Our research, the largest study of its type to date in the US, supports that air pollution may play a role in the etiology of ER-positive breast cancer and supports public health interventions to reduce air pollutant exposure levels,” Dr. White says. “For physicians, it may be useful to discuss this with patients to help them understand how their environment may play a role in breast cancer.”
Since levels of PM2.5 varies geographically across the US due to fluctuating sources of pollution, Dr. White and colleagues conclude that future research may help identify the specific components of PM2.5 that drive relationships with breast cancer, and thus help focus any intervention efforts on sources of PM2.5 that are most relevant to cancer.
