Associations of accelerometer-measured physical activity and physical activity-related cancer incidence in older women: results from the WHI OPACH Study

Background: We examined the associations between accelerometry-measured physical activity (PA) and incidence of 13 cancers among a cohort of postmenopausal women. Methods: In this prospective study, 6382 women wore ActiGraph GT3X+ accelerometers at the hip for up to 7 days during 2012–2013, and were followed over a median of 4.7 years for diagnosis of 13 invasive cancers. Calibrated intensity cut points were used to define minutes per day of total, light and moderate-to-vigorous PA. We used multivariable Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for tertiles, and one-standard deviation (SD) unit increments of PA exposures in relation to cancer incidence. We examined effect measure modification by age, race/ethnicity, body mass index and smoking history. Results: The highest (vs. lowest) tertiles of total, light and moderate-to-vigorous PA were associated with covariate-adjusted HRs of 0.72 (95% CI = 0.53–0.97), 0.81 (95% CI = 0.60–1.09) and 0.66 (95% CI = 0.48–0.91), respectively. In age-stratified analyses, HRs for total PA were lower among women <80 years (HRper one-SD = 0.75, 95% CI = 0.63–0.90) than among women ≥80 years (HRper one-SD = 0.99, 95% CI = 0.82–1.18) (PInteraction = 0.03). Race/ethnicity, BMI and smoking did not strongly modify these associations. Conclusions: Engaging in physical activity may play a beneficial role in the prevention of certain cancers in older women

Plasma levels of dichlorodiphenyldichloroethene (DDE) and dichlorodiphenyltrichloroethane (DDT) and survival following breast cancer in the Carolina Breast Cancer Study

Objectives: To examine plasma levels of dichlorodiphenyldichloroethene (DDE) and dichlorodiphenyltrichloroethane (DDT) in association with survival among women with breast cancer who participated in a population-based case-control study. Methods: Participants included 456 white and 292 black women from the Carolina Breast Cancer Study Phase I who were diagnosed with primary invasive breast cancer from 1993 to 1996, and who had available DDE/DDT and lipid measurements from blood samples obtained on average 4.1 months after diagnosis. Using the National Death Index, we identified 392 deaths (210 from breast cancer) over a median follow-up of 20.6 years. We used Cox regression to estimate covariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and breast cancer-specific 5-year mortality, and 20-year mortality conditional on 5-year survival, for lipid-standardized DDE and DDT levels. Associations stratified by race and estrogen receptor (ER) status were also examined. Results: The highest versus lowest DDE tertile and the highest vs non-detectable DDT quantile were associated with HRs of 1.95 (95% CI = 1.31–2.92) and 1.64 (95% CI = 1.10–2.44), respectively, for 20-year conditional all-cause mortality. DDE levels above versus below the median were associated with a HR of 1.69 (95% CI = 1.06–2.68) for 20-year conditional breast cancer-specific mortality among women overall, and HRs were 2.36 (95% CI = 1.03–5.42) among black women and 1.57 (95% CI = 0.86–2.89) among white women (PInteraction = 0.42), and 3.24 (95% CI = 1.38–7.58) among women with ER− tumors and 1.29 (95% CI = 0.73–2.28) among women with ER+ tumors (PInteraction = 0.03). Conclusion: Exposure to DDE/DDT may adversely impact overall and breast cancer-specific survival. DDE exposure may contribute to the racial disparities in breast cancer survival

Active smoking and survival following breast cancer among African American and non-African American women in the Carolina Breast Cancer Study

Purpose: To examine racial differences in smoking rates at the time of breast cancer diagnosis and subsequent survival among African American and non-African American women in the Carolina Breast Cancer Study (Phases I/II), a large population-based North Carolina study. Methods: We interviewed 788 African American and 1,020 Caucasian/non-African American women diagnosed with invasive breast cancer from 1993 to 2000, to assess smoking history. After a median follow-up of 13.56 years, we identified 717 deaths using the National Death Index; 427 were breast cancer-related. We used Cox regression to examine associations between self-reported measures of smoking and breast cancer-specific survival within 5 years and up to 18 years after diagnosis conditional on 5-year survival. We examined race and estrogen receptor status as potential modifiers. Results: Current (vs never) smoking was not associated with 5-year survival; however, risk of 13 year conditional breast cancer-specific mortality was elevated among women who were current smokers at diagnosis (HR 1.54, 95% CI 1.06–2.25), compared to never smokers. Although smoking rates were similar among African American (22.0%) and non-African American (22.1%) women, risk of breast cancer-specific mortality was elevated among African American (HR 1.69, 95% CI 1.00–2.85), but only weakly elevated among non-African American (HR 1.22, 95% CI 0.70–2.14) current (vs. never) smokers (PInteraction = 0.30). Risk of breast cancer-specific mortality was also elevated among current (vs never) smokers diagnosed with ER− (HR 2.58, 95% CI 1.35–4.93), but not ER+ (HR 1.11, 95% CI 0.69–1.78) tumors (PInteraction = 0.17). Conclusions: Smoking may negatively impact long-term survival following breast cancer. Racial differences in long-term survival, as related to smoking, may be driven by ER status, rather than by differences in smoking patterns

The impact of patient travel time on disparities in treatment for early stage lung cancer in California

Background Travel time to treatment facilities may impede the receipt of guideline-concordant treatment (GCT) among patients diagnosed with early-stage non-small cell lung cancer (ES-NSCLC). We investigated the relative contribution of travel time in the receipt of GCT among ES-NSCLC patients. Methods We included 22,821 ES-NSCLC patients diagnosed in California from 2006–2015. GCT was defined using the 2016 National Comprehensive Cancer Network guidelines, and delayed treatment was defined as treatment initiation >6 versus ≤6 weeks after diagnosis. Mean-centered driving and public transit times were calculated from patients’ residential block group centroid to the treatment facilities. We used logistic regression to estimate risk ratios and 95% confidence intervals (CIs) for the associations between patients’ travel time and receipt of GCT and timely treatment, overall and by race/ethnicity and neighborhood socioeconomic status (nSES). Results Overall, a 15-minute increase in travel time was associated with a decreased risk of undertreatment and delayed treatment. Compared to Whites, among Blacks, a 15-minute increase in driving time was associated with a 24% (95%CI = 8%-42%) increased risk of undertreatment, and among Filipinos, a 15-minute increase in public transit time was associated with a 27% (95%CI = 13%-42%) increased risk of delayed treatment. Compared to the highest nSES, among the lowest nSES, 15-minute increases in driving and public transit times were associated with 33% (95%CI = 16%-52%) and 27% (95%CI = 16%-39%) increases in the risk of undertreatment and delayed treatment, respectively. Conclusion The benefit of GCT observed with increased travel times may be a ‘Travel Time Paradox,’ and may vary across racial/ethnic and socioeconomic groups

Family environment, children's acculturation and mothers' dietary intake and behaviors among Latinas: An autoregressive cross-lagged study

Background: Many Latinos in the U.S. do not meet dietary recommendations for healthy eating. Family systems theory posits that the family environment affects family members' dietary behaviors. Moreover, research suggests that children's acculturation is associated with Latina mothers' dietary intake and behaviors. Purpose: This longitudinal study examined the effect of the family environment on Latina mothers’ dietary intake and behaviors. Further, we examined whether these effects differed between mothers of assimilated versus bicultural children. Methods: Secondary data were collected at three time points (baseline, and four and 10 months' post-baseline) from 162 culturally traditional and bicultural Latina mothers residing in Imperial County, California, U.S. Participants were enrolled in the delayed treatment group of a randomized controlled trial. Mothers' daily fruit, vegetable, and sugary beverages intake, percent of calories from fat, weekly away-from-home eating, and percent of weekly grocery dollars spent on fruits and vegetables were examined. The family environment was measured by family expressiveness and family interactions around food. Separate autoregressive cross-lagged models examined the effects of the family environment on dietary outcomes, adjusting for sociodemographic variables. Interactions between the family environment and children's acculturation were also tested. Results: Less positive family interactions around food at baseline predicted more frequent away-from-home eating four months later among mothers of assimilated children. More family expressiveness at four months predicted more grocery dollars spent on fruits and vegetables at ten months among mothers of bicultural children. Conclusions: Findings suggest the importance of a positive family environment on socially-bound dietary behaviors (e.g., away-from-home eating) exhibited by the mother. Family interventions aimed at improving dietary intake and associated behaviors should promote a positive family environment around food and consider the moderating role of children's acculturation

Understanding the relationship between environmental arsenic and prostate cancer aggressiveness among African-American and European-American men in North Carolina

High-level exposure to arsenic, a known carcinogen and endocrine disruptor, is associated with prostate cancer (PCa) mortality. Whether low-level exposure is associated with PCa aggressiveness remains unknown. We examined the association between urinary arsenic and PCa aggressiveness among men in North Carolina. This cross-sectional study included 463 African-American and 491 European-American men with newly diagnosed, histologically confirmed prostate adenocarcinoma. PCa aggressiveness was defined as low aggressive (Gleason score < 7, stage = cT1–cT2, and PSA < 10 ng/mL) versus intermediate/high aggressive (all other cases). Total arsenic and arsenical species (inorganic arsenic (iAsIII + iAsV), arsenobetaine, monomethyl arsenic, and dimethyl arsenic)) and specific gravity were measured in spot urine samples obtained an average of 23.7 weeks after diagnosis. Multivariable logistic regression was used to estimate the covariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for PCa aggressiveness in association with arsenic tertiles/quantiles overall and by race. The highest (vs. lowest) tertile of total arsenic was associated with PCa aggressiveness ORs of 1.77 (95% CI = 1.05–2.98) among European-American men, and 0.94 (95% CI = 0.57–1.56) among African-American men (PInteraction = 0.04). In contrast, total arsenic and arsenical species were not associated with PCa aggressiveness in unstratified models. Low-level arsenic exposure may be associated with PCa aggressiveness among European-Americans, but not among African-Americans

Plasma levels of polychlorinated biphenyls (PCBs) and breast cancer mortality: The Carolina Breast Cancer Study

Background: It is unknown whether carcinogenic and endocrine disrupting polychlorinated biphenyls (PCBs) influence mortality following breast cancer. We examined plasma levels of 17 PCB congeners in association with mortality among women with breast cancer. Methods: Participants included 456 white and 292 black women in North Carolina who were diagnosed with primary invasive breast cancer from 1993 to 1996, and who had PCB and lipid measurements from blood samples obtained an average of 4.1 months after diagnosis. Over a median follow-up of 20.6 years, there were 392 deaths (210 from breast cancer). We used Cox regression to estimate covariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and breast cancer-specific 5-year mortality, and 20-year mortality (conditional on 5-year survival) in association with tertiles and continuous ln-transformed lipid-adjusted PCB levels. Results: The highest (vs. lowest) tertiles of PCB74, PCB99, and PCB118 were associated with 5-year breast cancer-specific mortality HRs of 1.46 (95%CI = 0.86–2.47), 1.57 (95%CI = 0.90–2.73), and 1.86 (95%CI = 1.07–3.23), respectively. Additionally, one-ln unit increases in PCB74, PCB99, PCB118, and total PCBs were each associated with 33–40% increases in 5-year breast cancer-specific mortality rates. The PCBs were not, however, associated with longer-term breast cancer-specific mortality. For all-cause mortality, one-ln unit increases in PCB118, PCB146, PCB153, PCB182, PCB187, and total PCBs were associated with 20–37% increases in 20-year all-cause mortality rates among women who survived at least 5 years. Conclusion: PCBs may increase the risk of short-term breast cancer-specific mortality and long-term all-cause mortality among women with breast cancer

Grilled, Barbecued, and Smoked Meat Intake and Survival Following Breast Cancer

Background: Grilled, barbecued, and smoked meat intake, a prevalent dietary source of polycyclic aromatic hydrocarbon (PAH) carcinogens, may increase the risk of incident breast cancer. However, no studies have examined whether intake of this PAH source influences survival after breast cancer. Methods: We interviewed a population-based cohort of 1508 women diagnosed with first primary invasive or in situ breast cancer in 1996 and 1997 at baseline and again approximately five years later to assess grilled/barbecued and smoked meat intake. After a median of 17.6 years of follow-up, 597 deaths, of which 237 were breast cancer related, were identified. Multivariable Cox regression was used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality as related to prediagnosis intake, comparing high (above the median) to low intake, as well as postdiagnosis changes in intake, comparing every combination of pre-/postdiagnosis intake to low pre-/postdiagnosis intake. All statistical tests were two-sided. Results: High prediagnosis grilled/barbecued and smoked meat intake was associated with increased risk of all-cause mortality (HR = 1.23, 95% CI = 1.03 to 1.46). Other associations were noted, but estimates were not statistically significant. These include high prediagnosis smoked beef/lamb/pork intake and increased all-cause (HR = 1.17, 95% CI = 0.99 to 1.38, Ptrend = .10) and breast cancer–specific (HR = 1.23, 95% CI = 0.95 to 1.60, Ptrend = .09) mortality. Also, among women with continued high grilled/barbecued and smoked meat intake after diagnosis, all-cause mortality risk was elevated 31% (HR = 1.31, 95% CI = 0.96 to 1.78). Further, breast cancer–specific mortality was decreased among women with any pre- and postdiagnosis intake of smoked poultry/fish (HR = 0.55, 95% CI = 0.31 to 0.97). Conclusion: High intake of grilled/barbecued and smoked meat may increase mortality after breast cancer

Genetic polymorphisms of diabetes-related genes, their interaction with diabetes status, and breast cancer incidence and mortality: The Long Island Breast Cancer Study Project

To examine 143 diabetes risk single nucleotide polymorphisms (SNPs), identified from genome-wide association studies, in association with breast cancer (BC) incidence and subsequent mortality. A population-based sample of Caucasian women with first primary invasive BC (n = 817) and controls (n = 1021) were interviewed to assess diabetes status. Using the National Death Index, women with BC were followed for >18 years during which 340 deaths occurred (139 BC deaths). Genotyping was done using DNA extracted from blood samples. We used unconditional logistic regression to estimate age-adjusted odds ratios and 95% confidence intervals (CIs) for BC incidence, and Cox regression to estimate age-adjusted hazard ratios and CIs for all-cause and BC-specific mortality. Twelve SNPs were associated with BC risk in additive genotype models, at α = 0.05. The top three significant SNPs included SLC30A8-rs4876369 (P = 0.0034), HHEX-rs11187146 (P = 0.0086), and CDKN2A/CDKN2B-rs1333049 (P = 0.0094). Diabetes status modified the associations between rs4876369 and rs2241745 and BC incidence, on the multiplicative interaction scale. Six SNPs were associated with all-cause (CDKAL1-rs981042, P = 0.0032; HHEX-rs1111875, P = 0.0361; and INSR-rs919275, P = 0.0488) or BC-specific (CDKN2A/CDKN2B-rs3218020, P = 0.0225; CDKAL1-rs981042, P = 0.0246; and TCF2/HNF1B-rs3094508, P = 0.0344) mortality in additive genotype models, at α = 0.05. Genetic polymorphisms that increase the risk of developing diabetes may also increase the risk of developing and dying from BC

Postdiagnosis changes in cigarette smoking and survival following breast cancer

Background: The purpose of this study was to examine whether at-diagnosis smoking and postdiagnosis changes in smoking within five years after breast cancer were associated with long-termall-cause and breast cancer-specific mortality. Methods: A population-based cohort of 1508 women diagnosed with first primary in situ or invasive breast cancer in 1996 to 1997 were interviewed shortly after diagnosis and again approximately five years later to assess smoking history. Participants were followed for vital status through December 31, 2014. After 18+ years of follow-up, 597 deaths were identified, 237 of which were breast cancer related. Multivariable Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: Compared with never smokers, risk of all-cause mortality was elevated among the 19% of at-diagnosis smokers (HR=1.69, 95% CI=1.36 to 2.11), those who smoked 20 or more cigarettes per day (HR=1.85, 95% CI=1.42 to 2.40), women who had smoked for 30 or more years (HR=1.62, 95% CI=1.28 to 2.05), and women who had smoked 30 or more pack-years (HR=1.82, 95% CI=1.39 to 2.37). Risk of all-cause mortality was further increased among the 8% of women who were at-/postdiagnosis smokers (HR=2.30, 95% CI=1.56 to 3.39) but was attenuated among the 11% women who quit smoking after diagnosis (HR=1.83, 95% CI=1.32 to 2.52). Compared with never smokers, breast cancer-specific mortality risk was elevated 60% (HR=1.60, 95% CI=0.79 to 3.23) among at-/postdiagnosis current smokers, but the confidence interval included the null value and elevated 175% (HR=2.75, 95% CI=1.26 to 5.99) when we considered postdiagnosis cumulative pack-years. Conclusions: Smoking negatively impacts long-term survival after breast cancer. Postdiagnosis cessation of smoking may reduce the risk of all-cause mortality. Breast cancer survivors may benefit from aggressive smoking cessation programs starting as early as the time of diagnosis