Evidence From Humans
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The relationship between genetic damage from polycyclic aromatic hydrocarbons in breast tissue and breast cancer
Rundle, A., Tang, D., Hibshoosh, H., Estabrook, A., Schnabel, F., Cao, W., Grumet, S., Perera, F. P. Carcinogenesis. 2000. 21:7, 1281-9.
Topic area
Environmental pollutant - PAH
Study design
Hospital based case-control
Funding agency
DOD Other: Noreen T. Holland Foundation
Study Participants
Menopausal Status
The menopausal status of women included in this study is listed here.
Pre menopausal
Post menopausal
Number of Controls
Controls: 105
Participant selection: Inclusion and exclusion criteria
Criteria used to select participants in the study.
Breast surgery patients > 35 and < 75 years of age with first breast cancer compared with benign breast disease without atypia. Patients with prior cancer (other than basal skin cancer), current pregnancy, recent bone fracture, or recent breastfeeding were excluded.
Comment about participation selection
Controls at slightly higher risk for breast cancer than a general population. Controls had higher than expected family history of breast cancer (perhaps because women with family history are screened more frequently). This could bias results toward the null.
Exposure Investigated
Exposures investigated
PAH-DNA adducts in breast tissue (tumor and nontumor tissue for cases), immunohistochemical assay reported in optical density (OD) units.
Exposure assessment comment
Strength: Scoring found to be reliable across technicians
Statistical Analysis
Breast cancer outcome investigated
Primary breast cancer, Invasive ductal or lobular cancer
Ethnic groups with separate analysis
If this study provided a separate analysis by ethnic or racial group, the groups are listed here.
Caucasian, non-Caucasian
Confounders considered
Other breast cancer risk factors, such as family history, age at first birth, and hormone replacement therapy use, that were taken into account in the study.
Reproductive risk factors, active and passive smoking, diet, environmental and occupational exposures, diet, vitamin consumption
Genetic characterization included
If the study analyzed relationships between environmental factors and inherited genetic variations, this field will be marked “Yes.” “No”, if not.
Description of major analysis
Natural-log transformed; Student's t-test, ANOVA, regression.
Strength of associations reported
Arithmetic mean adduct levels were significantly higher in tumor than non-tumor tissues and somewhat higher in non-tumor tissue from cases than controls. Distribution is right-skewed. Adduct levels in tumor and nontumor tissue from cases were correlated: r = 0.56, p <0.001.
Multivariate (controlled for breast cancer risk factors and PAH exposures from diet and tobacco smoke) OR for tumor tissue compared with controls = 4.43 (95% CI 1.09-18.01) for each increasing OD unit; 27% of cases (tumor tissue) compared with 13% of controls had elevated adduct levels (dichotomous variable defined as above the control mean plus one standard deviation ). For these samples, OR = 2.40 (95%CI 1.18-4.92, n = 205).
Comparing non-tumor case tissue and controls, OR = 1.97 (95% CI 0.94-4.17, n = 195).
Controls with a family history had nonsignificantly higher adduct levels than controls with no family history. ORs were similar when restricted to women with no family history.
Active smoking did not predict adduct levels. Charred meat consumption negatively predicts adduct levels in cases, not controls; current ETS exposure negatively predicted adduct levels in controls.
Results Comments
Authors suggest possibility that PAH is related to progression rather than initiation of disease. PAH exposure sources other than diet and smoking appear to be important.
Author address
Division of Environmental Health Sciences, Joseph L. Mailman School of Public Health, 60 Haven Ave, New York, NY 10032, USA.
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