Investigating Contributions of Physical Inactivity and Obesity to Racial Disparities in Cancer Risk and Mortality Warrants More Consideration

Racial disparities in cancer risk and mortality are an immense public health challenge in the United States today. Despite important advances in the prevention, screening, diagnosis, and treatment of cancer, striking disparities remain (1). In fact, the incidence for many of the most common cancers, including breast, prostate, colon and rectum, bladder, pancreas, and kidney or renal pelvis, remains higher among African Americans (AAs) than any other group (1,2). Additionally, although ageadjusted cancer death rates have steadily declined, AAs have experienced the highest cancer mortality rates of all racial and ethnic groups in the United States for over 4 decades (1). Today, researchers agree that race is not simply a genetic or biological concept but rather a social and cultural construct (3). As such, factors contributing to racial disparities in cancer are complex and multifactorial and include behavioral factors (obesity, physical inactivity), social factors (education, income), clinical factors (access to screening and healthcare), cultural factors, psychological factors (mental health, stress), environmental factors (transportation and housing), and biological and genetic factors (1). Importantly, racial disparities in cancer remain even after accounting for socioeconomic status, access to care, and clinical factors (1). Thus, focused work is needed to identify the relative contributions of additional modifiable exposures that are known to vary by race and to be associated with increased cancer risk and mortality (1). In this issue of the Journal, Peres et al. (4) leveraged epidemiological data from the Ovarian Cancer in Women of African Ancestry Consortium to examine whether racial differences in the incidence of epithelial ovarian cancer (EOC) may be attributable to observed differences in the prevalence of known or suspected risk factors for EOC. To accomplish this, race-specific population attributable risks (PARs) were estimated for 10 risk factors for EOC, including body mass index; parity; tubal ligation; family history of breast or ovarian cancer; use of aspirin, oral contraceptives, or body powder applied to genitals; education; and a history of endometriosis. PARs were estimated for each exposure individually and collectively, including all factors combined, reproductive factors, and modifiable factors (body mass index and use of oral contraceptives, aspirin, and body powder). Because reported PARs represent the proportion of cases in the population that would not have otherwise occurred if the exposure(s) were absent, PARs suggest which exposures could be addressed with public health interventions (4). Two important findings emerged from this novel analysis. First, the only individual risk factor yielding statistically significantly different PARs by race was family history of breast cancer (PARAA 1⁄4 10.1% vs PARWhite 1⁄4 2.6%, false discovery rate P< .001) (4). Secondly, AA women had a statistically significantly higher PAR for modifiable exposures compared with White women (36.0% vs 13.8%, respectively, false discovery rate P1⁄4 .04) (4). The authors suggest that a higher PAR for family history among AA women may reflect a higher prevalence of BRCA mutations among AA vs White women, but some studies have failed to identify a higher prevalence of BRCA mutations among AAs in the general population (4-6). Another possibility is underuse of genetic testing and prophylactic surgery among AA women (4,7). However, additional modifiable risk factors may also be contributing to varying PARs, and further efforts designed to disentangle these associations are needed. So where does this leave us in terms of our current understanding of the contribution of family history and modifiable exposures to racial disparities in cancer risk and mortality for EOC and other cancers? Interestingly, there is a small but growing body of evidence suggesting that modifiable exposures, such as physical (in)activity and obesity, are associated with BRCA1/2 penetrance and cancer incidence among other highrisk groups of women (8-20). To this end, Peres and colleagues (4) acknowledge the omission of physical (in)activity as an important limitation of their analysis—and this may be meaningful for several reasons. Recreational physical activity is a modifiable exposure that is known to vary considerably by race and is also associated with cancer risk and mortality. Indeed, nearly 30% of AAs report being entirely inactive (ie, engaging in no regular moderate to vigorous-intensity physical activity during their leisure time), whereas only 22% of Whites report inactivity (21). Further, ED IT O R IA L