Oral contraceptive use and breast cancer risk: current status.
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Breast Neoplasms↗
Biomedical subjects
James R Cerhan
Publications and source records attributed to James R Cerhan.
Antibodies to JC and BK viruses among persons with non-Hodgkin lymphoma.
Two related polyomaviruses, JC virus (JCV) and BK virus (BKV), commonly cause lifelong infections in humans, with periodic reactivation manifesting as viral shedding in urine. Because JCV can infect lymphocytes and cause chromosomal damage, it is a plausible candidate to cause non-Hodgkin lymphoma (NHL). To test this hypothesis, we measured IgG antibodies to JCV and BKV capsids using a virus-like particle enzyme immunoassay in 3 separate groups of subjects. First, in a U.S. population-based case-control study of NHL (724 cases, 622 controls), we found lower JCV antibody levels in cases than controls (median optical density = 0.12 vs. 0.21, p < 0.0001); likewise, JCV seroprevalence was lower in cases (49% vs. 59%, adjusted odds ratio [OR] = 0.70, 95% confidence interval [CI] = 0.56-0.87). In contrast, BKV antibody levels did not differ between groups. Second, we found that JCV and BKV antibody levels changed little over time among 24 NHL patients receiving chemotherapy. Third, we evaluated 126 homosexual men, of whom 46 were shedding JCV and 14 were shedding BKV in urine. Antibody levels were much higher in shedders than non-shedders (JCV: median optical density = 0.67 vs. 0.07, p < 0.0001; BKV: 0.87 vs. 0.40, p = 0.003), indicating that these antibodies are a marker for viral replication. Because no deficit of BKV antibody was seen in NHL cases, and because antibody levels did not change materially with chemotherapy, we suggest that the lower levels of JCV antibody observed in NHL patients may not be due entirely to a disease or treatment effect. Additional research is needed to determine whether JCV replication is decreased in individuals with NHL and whether these findings are consistent with an etiologic role for JCV in NHL.
Adult↗
Alcohol intake in adolescence and mammographic density.
Adolescent exposures may be important in the development of breast cancer later in life. We examined the association of adolescent alcohol consumption and adult mammographic density, a strong risk factor for breast cancer. Women within the Minnesota Breast Cancer Family Cohort with detailed mammogram and risk factor information (n = 1,893) formed our sample. Breast cancer cases were excluded. Adolescent alcohol consumption (before age 18) was solicited through a mailed questionnaire. Percent density (PD) was estimated using the computer-assisted thresholding program, Cumulus. Statistical analyses were performed using linear mixed effect models. Women who reported ever drinking alcohol before age 18 (n = 390; 21%) had a higher unadjusted PD than women who never drank during adolescence (mu(unadj) = 26.5% vs. 22.2%), but this difference disappeared with adjustment for risk factors for mammographic density (mu(adj) = 21.0% vs. 21.2%, p = 0.94). Adult PD was not associated with age at initiation, amount of alcohol consumed at one sitting or frequency of alcohol use before age 18. The lack of differences was seen across strata of menopausal status. There was suggestion of higher PD among heavy and more frequent drinkers (24.0%, 95% CI 21.1-26.8%) compared to lighter (21.3%, 95% CI 20.3-22.3%) and never drinkers (21.4%, 95% CI 20.9-21.9%) and also among regular adolescent drinkers who were daily or weekly adult drinkers (25.0%, 95% CI 23.0-27.0%) compared to less regular drinkers in these 2 time periods (23.0-23.4%). However, these associations were not statistically significant (p = 0.27 and p = 0.22, respectively). In summary, there was no evidence that adolescent alcohol use was associated with large and persistent effects on adult PD.
Adolescent↗
Persistent organochlorine chemicals in plasma and risk of non-Hodgkin's lymphoma.
Polychlorinated biphenyls (PCB) have been suspected as possible contributors to increasing non-Hodgkin's lymphoma incidence during the latter half of the 20th century based on their toxicologic properties and provocative epidemiologic reports. We investigated PCBs and other organochlorines and risk of non-Hodgkin's lymphoma in a population-based case-control study in the United States. Congeners of PCBs (including coplanar congeners), dioxins, furans and pesticides or pesticide metabolites were measured in plasma of 100 untreated cases and 100 control subjects. We used a multiple imputation procedure to fill in missing values of levels determined to be below the detection limits. Risks of non-Hodgkin's lymphoma associated with each analyte were estimated using conditional logistic regression for the continuous measure, exposure quartiles, trend across quartile categories, and exposures above the 95th percentile. Certain PCB congeners were associated with increased risk of non-Hodgkin's lymphoma, including coplanar PCBs 156, 180, and 194, with odds ratios for the highest versus lowest quartile ranging from 2.7 to 3.5, and significant trends. Each of the furan congeners was associated with risk of non-Hodgkin's lymphoma, as were total furans, with 3.5-fold increased risk for the highest versus lowest quartile and a significant trend across quartiles (P = 0.006). The toxic equivalency quotient (TEQ), a summed metric that weights congeners by their dioxin-like potency, was associated with non-Hodgkin's lymphoma, with 35% increased risk per 10 TEQ pg/g lipid (95% confidence interval, 1.02-1.79). Our results add to existing literature, which suggests that exposure to organochlorines contributes to non-Hodgkin's lymphoma risk; these risks were most apparent for certain PCBs and furans.
Adult↗
Immune-related conditions and immune-modulating medications as risk factors for non-Hodgkin's lymphoma: a case-control study.
In immunosuppressed or autoimmune disease states, disordered immune responses may lead to non-Hodgkin's lymphoma (NHL). In a US population-based case-control study of NHL (1998-2000), the authors collected personal histories of immune-related conditions and use of immune-modulating therapies as well as family histories of autoimmune conditions. The study included 1,321 NHL cases and 1,057 controls; only half received some questionnaire components. NHL was associated with Sjögren's syndrome (odds ratio (OR) = 13, 95% confidence interval (CI): 1.7, 100) and lupus (OR = 4.2, 95% CI: 1.2, 15). Two specific NHL subtypes were strongly associated with Sjögren's syndrome: salivary gland (OR = 290, 95% CI: 33, 2600) and marginal zone (OR = 75, 95% CI: 9.1, 610). NHL was less convincingly associated with receipt of an organ transplant (OR = 2.0, 95% CI: 0.4, 11). Other autoimmune conditions were too rare to evaluate or not associated with NHL. Corticosteroid use was unrelated to NHL (OR = 1.0, 95% CI: 0.8, 1.2), but methotrexate use was marginally associated (OR = 2.3, 95% CI: 0.7, 7.5). Family history of dermatomyositis was associated with NHL (7 cases vs. 0 controls, OR = infinite; two-sided p = 0.02), but dermatomyositis was absent in cases themselves. Family history of remaining conditions was unrelated to NHL. Results suggest that disordered immunity in some immune-related conditions can lead to NHL.
Adult↗
Meat and meat-mutagen intake and risk of non-Hodgkin lymphoma: results from a NCI-SEER case-control study.
Non-Hodgkin Lymphoma (NHL) incidence has risen dramatically over past decades, but the reasons for most of this increase are not known. Meat cooked well-done using high-temperature cooking techniques produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (B[a]P). This study was conducted as a population-based case-control study in Iowa, Detroit, Seattle and Los Angeles and was designed to determine whether meat, meat-cooking methods, HCAs or PAHs from meat were associated with NHL risk. This study consisted of 458 NHL cases, diagnosed between 1998 and 2000, and 383 controls. Participants completed a 117-item food frequency questionnaire (FFQ), with graphical aids to assess the meat-cooking method and doneness level, which was linked to a HCA and B[a]P database. Logistic regression, comparing the fourth to the first quartile, found no association between red meat or processed meat intake and risk for NHL [odds ratio (OR) and 95% confidence interval (CI): 1.10 (0.67-1.81) and 1.18 (0.74-1.89), respectively]. A marginally significant elevated risk for NHL was associated with broiled meat [OR and 95% CI: 1.32 (0.99-1.77); P trend = 0.09], comparing those who consumed broiled meat with those who did not. The degree to which meat was cooked was not associated with the risk for NHL, although one of the HCAs, DiMeIQx (2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline), was associated with an inverse risk. Fat intake was associated with a significantly elevated risk for NHL [OR and 95% CI: 1.60 (1.05-2.45); P trend = 0.12]; in contrast, animal protein was inversely associated with risk for NHL [OR and 95% CI: 0.39 (0.22-0.70); P trend = 0.004]. Overall, our study suggests that consumption of meat, whether or not it is well-done, does not increase the risk of NHL. Furthermore, neither HCAs nor B[a]P from meat increase the risk of NHL.
Adult↗
Associations of dietary protein with disease and mortality in a prospective study of postmenopausal women.
Some weight loss diets promote protein intake; however, the association of protein with disease is unclear. In 1986, 29,017 postmenopausal Iowa women without cancer, coronary heart disease (CHD), or diabetes were followed prospectively for 15 years for cancer incidence and mortality from CHD, cancer, and all causes. Mailed questionnaires assessed dietary, lifestyle, and medical information. Nutrient density models estimated risk ratios from a simulated substitution of total and type of dietary protein for carbohydrate and of vegetable for animal protein. The authors identified 4,843 new cancers, 739 CHD deaths, 1,676 cancer deaths, and 3,978 total deaths. Among women in the highest intake quintile, CHD mortality decreased by 30% from an isoenergetic substitution of vegetable protein for carbohydrate (95% confidence interval (CI): 0.49, 0.99) and of vegetable for animal protein (95% CI: 0.51, 0.98), following multivariable adjustment. Although no association was observed with any outcome when animal protein was substituted for carbohydrate, CHD mortality was associated with red meats (risk ratio = 1.44, 95% CI: 1.06, 1.94) and dairy products (risk ratio = 1.41, 95% CI: 1.07, 1.86) when substituted for servings per 1,000 kcal (4.2 MJ) of carbohydrate foods. Long-term adherence to high-protein diets, without discrimination toward protein source, may have potentially adverse health consequences.
Aged↗
Hormone replacement therapy is not associated with an increased risk of leukemia (United States).
OBJECTIVE: Recent studies have reported an increased risk of certain cancers associated with hormone replacement therapy (HRT), possibly due to stimulation of estrogen receptors. Since estrogen receptors are expressed on certain hematopoietic cells, it is possible that HRT use may also increase the risk of leukemia. METHODS: A cohort of 37,172 post-menopausal Iowa women ages 55-69 years with no history of prior cancer was linked annually to the population-based state cancer registry through 2001. In addition to other self-reported cancer risk factors, participants were asked about current and former use of HRT in 1986 and on four subsequent follow-up questionnaires. A total of 201 cases of leukemia were identified over 16 years of follow-up including 74 acute myeloid leukemias (AMLs) and 87 chronic lymphocytic leukemias (CLLs). RESULTS: Compared to never users of HRT at study baseline, current [multivariate relative risk (RR), 1.09; 95% confidence interval (CI) 0.70-1.71)] and former users (RR=0.82, 95% CI=0.59-1.15) were at no increased risk of developing leukemia. For AML, current users also had no increased risk (RR=0.83, 95% CI=0.37-1.84) and there was a suggestion that former users had a slightly decreased risk (RR=0.66, 95% CI=0.37-1.17). For CLL, all RRs were around unity. CONCLUSION: We conclude that HRT is unlikely to be an appreciable risk factor for leukemia.
Age Factors↗
Anthropometrics, physical activity, related medical conditions, and the risk of non-hodgkin lymphoma.
BACKGROUND: Recent reports suggest that obesity, or conditions associated with obesity, might be risk factors for non-Hodgkin lymphoma (NHL), a cancer with dramatically increasing incidence in western countries over the last several decades. Physical inactivity increases the risk of obesity and of type 2 diabetes, but there are few data on the association of physical activity with risk of NHL. METHODS: We evaluated these factors in a population-based case-control study conducted in Detroit, Iowa, Los Angeles, and Seattle from 1998 to 2000. Incident HIV-negative NHL cases aged 20-74 years were rapidly reported in each area (n = 1321). Controls were identified through random digit dialing and Medicare files, and were frequency matched to cases on sex, age, race, and study site (n = 1057). Risk factor data were collected by in-person interviews and self-administered questionnaires. Unconditional logistic regression was used to estimate the odds ratio (OR) and 95% confidence intervals (CI), adjusted for age, sex, race and study center. RESULTS: High body mass index (OR = 1.73 for 35+ versus <25 kg/m2; 95% CI 1.15-2.59) and history of gallstones (OR = 1.95, 95% CI 1.11-3.40) were positively associated with diffuse NHL, but were not associated with follicular or all NHL combined. Height was positively associated with risk of all NHL combined (OR = 1.38 for >70 versus <65 inches; 95% CI 0.98-1.94), and positive associations were apparent for both diffuse and follicular NHL. Non-occupational physical activity was inversely associated with risk of all NHL combined (ORs with increasing level: 1, 0.75, 0.71, 0.55, 0.68; p-trend = 0.04) and for diffuse and follicular NHL. We observed no association of total energy intake, type 2 diabetes, or hypertension with risk of NHL. In a multivariable model to predict risk of diffuse NHL, BMI (OR = 2.15 for 35+ versus <25 kg/m2; 95% CI 1.09-4.25) and height (OR = 1.63 for 71+ versus <65 inches; 95% CI 0.75-3.57) were positively associated with risk while physical activity was weakly and inversely associated risk (ORs with increasing level: 1, 0.76, 0.72, 0.78, 0.82; p-trend = 0.9). CONCLUSION: BMI and history of gallstones were positively associated with risk of diffuse NHL, supporting a role for obesity in this NHL subtype. Height was positively associated with NHL risk across subtypes, and suggests a role for early life nutrition in NHL risk. Non-occupational physical activity was only weakly and inversely associated with NHL risk after adjustment for obesity, height and alcohol use.
Adult↗
Alcohol consumption and risk of non-Hodgkin lymphoma: a pooled analysis.
BACKGROUND: Previous epidemiological studies of the relation between alcohol consumption and risk of non-Hodgkin lymphoma (NHL) have been inconsistent, probably because of small sample sizes of individual studies that result from stratification by NHL subtype and type of alcoholic beverage. We aimed to assess the role of alcohol consumption in NHL with sufficient sample size to analyse by both type of alcoholic beverage and disease subtype. METHODS: We obtained original data from nine case-control studies from the USA, UK, Sweden, and Italy in the International Lymphoma Epidemiology Consortium (InterLymph), yielding a pooled study population of 15 175 individuals (6492 cases and 8683 controls). We derived odds ratios (OR) and 95% CI from unconditional logistic regression models, controlling for study centre and other confounding factors. Heterogeneity between studies was assessed by comparison of results from joint fixed-effects logistic regression and two-stage random-effects logistic regression, and by calculation of Wald chi(2) statistics. FINDINGS: People who drank alcohol had a lower risk of NHL than did non-drinkers (OR 0.83 [95% CI 0.76-0.89]). Compared with non-drinkers, risk estimates were lower for current drinkers than for former drinkers (0.73 [0.64-0.84] vs 0.95 [0.80-1.14]), but risk did not decrease with increasing alcohol consumption. The protective effect of alcohol did not vary by beverage type, but did change with NHL subtype. The lowest risk estimates were recorded for Burkitt's lymphoma (0.51 [0.33-0.77]). INTERPRETATION: People who drink alcoholic beverages might have a lower risk of NHL than those who do not, and this risk might vary by NHL subtype. Further study designs are needed to determine whether confounding lifestyle factors or immunomodulatory effects of alcohol explain this association.
Adolescent↗
Organochlorines in carpet dust and non-Hodgkin lymphoma.
BACKGROUND: The incidence of non-Hodgkin lymphoma (NHL) has risen over the past several decades. Reasons for this increase are largely unexplained. METHODS: In this population-based case-control study, we examined NHL risk and exposure to organochlorine compounds using concentrations in carpet dust as an exposure indicator. We identified NHL cases, uninfected with HIV, diagnosed between 1998 and 2000 among women and men ages 20-74 years in Iowa, Los Angeles County, and the Detroit and Seattle metropolitan areas. Controls were selected using random-digit-dialing or Medicare files. Organochlorine concentrations were measured in vacuum bag dust from 603 white cases and 443 white controls who had owned most of their carpets for at least 5 years. RESULTS: NHL risk was elevated if any of the polychlorinated biphenyl (PCB) congeners (PCBs 105, 138, 153, 170, or 180) was detected (odds ratio = 1.5; 95% confidence interval = 1.2-2.0). Risk was elevated in the top tertile of PCB 180 (1.7; 1.1-2.6) and in the top 2 tertiles of total PCBs (middle tertile, 1.6 [1.1-2.4]; top tertile 1.5 [1.0-2.2]). There was a positive trend in risk with increasing PCB 180 levels (P trend = 0.03). NHL risk was elevated if dichlorodiphenyldichloroethylene (DDE) was detected (1.3; 1.0-1.7), but only among men. A positive, but not monotonic, dose-response relationship was observed for DDE (P trend = 0.02). CONCLUSIONS: Our findings suggest an increased risk of NHL associated with exposure to PCBs, with evidence of greater effects for PCB 180. There is also some evidence of an association with DDE.
Adult↗
Anthropometric characteristics and risk of multiple myeloma.
BACKGROUND: Few studies have examined obesity and risk for multiple myeloma, and the results are inconsistent. Laboratory evidence suggests mechanisms through which obesity could influence carcinogenesis of this hematopoietic malignancy. METHODS: We examined the association between anthropometric characteristics and incident multiple myeloma in a prospective, population-based sample of 37,083 postmenopausal women. In 1986, the women completed a mailed questionnaire that included self-report of height and weight, and friend measurement of waist and hip circumferences. During 16 years of follow up, 95 cases of multiple myeloma were identified through linkage to the Iowa Cancer Registry. RESULTS: In an age-adjusted model, women in the highest category of several anthropometric measurements compared with the lowest category were at increased risk of developing multiple myeloma. For body mass index (kg/m), the rate ratio (95% confidence interval) was 1.5 (0.92-2.6); for weight, 1.9 (1.1-3.4); for waist circumference, 2.0 (1.1-3.5); and for hip circumference, 1.8 (1.0-3.0). CONCLUSION: Greater adiposity may increase the risk of multiple myeloma.
Aged↗
The association of alcohol consumption with coronary heart disease mortality and cancer incidence varies by smoking history.
OBJECTIVE: To evaluate the effect of alcohol on coronary heart disease (CHD), cancer incidence, and cancer mortality by smoking history. DESIGN/SETTING: A prospective, general community cohort was established with a baseline mailed questionnaire completed in 1986. PARTICIPANTS: A population-based sample of 41,836 Iowa women aged 55-69 years. MEASUREMENTS: Mortality (total, cancer, and CHD) and cancer incidence outcomes were collected through 1999. Relative hazard rates (HR) were calculated using Cox regression analyses. MAIN RESULTS: Among never smokers, alcohol consumption (> or =14 g/day vs none) was inversely associated with age-adjusted CHD mortality (HR, 0.40; 95% confidence interval [CI], 0.19 to 0.84) and total mortality (HR, 0.71; 95% CI, 0.55 to 0.92). Among former smokers, alcohol consumption was also inversely associated with CHD mortality (HR, 0.45; 95% CI, 0.23 to 0.88) and total mortality (HR, 0.78; 95% CI, 0.62 to 0.97), but was positively associated with cancer incidence (HR, 1.25; 95% CI, 1.03 to 1.51). Among current smokers, alcohol consumption was not associated with CHD mortality (HR, 1.05; 95% CI, 0.73 to 1.50) or total mortality (HR, 1.07; 95% CI, 0.92 to 1.25), but was positively associated with cancer incidence (HR, 1.30; 95% CI, 1.10 to 1.54). CONCLUSIONS: Health behavior counseling regarding alcohol consumption for cardioprotection should include a discussion of the lack of a decreased risk of CHD mortality for current smokers and the increased cancer risk among former and current smokers.
Aged↗
Association of gain and loss of weight before and after menopause with risk of postmenopausal breast cancer in the Iowa women's health study.
Obesity and adult weight gain are well-established risk factors for postmenopausal breast cancer. Although there are a few studies demonstrating the contribution of adult weight gain to breast cancer risk, whether weight gain during a critical time period is specifically associated with risk, or whether subsequent weight loss among women who have gained weight will reduce the excess risk, is not firmly established. We investigated the association of changes in weight (loss or gain in excess of 5% of body weight) using two risk factor models: (a) age 18 to 30 years and age 30 years to menopause and (b) age 30 years to menopause and after the menopause to the baseline study in 1986 on risk of postmenopausal breast cancer in a prospective cohort of 33,660 postmenopausal women in Iowa. Over 15 years of follow-up, 1,987 cases of breast cancer occurred. Data were analyzed using proportional hazards regression models adjusted for established breast cancer risk factors. The most frequently observed pattern of body weight over time was a consistent increase; these women were observed to have the highest rates of breast cancer and served as the reference category for all comparisons. The lowest-risk groups were (a) women who maintained or lost weight from age 18 to 30 years and then lost weight from age 30 years to menopause [risk ratio (RR), 0.36; 95% confidence interval (95% CI), 0.22-0.60] and (b) women who maintained or lost weight from age 30 years to menopause and then lost weight after the menopause (RR, 0.48; 95% CI, 0.22-0.65). Women who gained weight from age 30 years to menopause but then lost weight after the menopause experienced risk reductions (RR, 0.77; 95% CI, 0.64-0.92) although perhaps slightly smaller in magnitude than women who maintained their weight in both time intervals (RR, 0.63; 95% CI, 0.55-0.73). Women who gained weight from age 18 to 30 years and then lost weight from age 30 years to menopause had comparable risk reductions (RR, 0.61; 95% CI, 0.46-0.8) with women who maintained their weight in both time intervals (RR, 0.73; 95% CI, 0.64-0.84). Women who gained weight during the period from age 30 years to menopause but who had stable weight after menopause had rates similar to the reference group. These data suggest prevention of weight gain between age 18 years and menopause or weight loss and maintenance during these years reduces risk of postmenopausal breast cancer.
Adolescent↗
Antibody responses to simian virus 40 T antigen: a case-control study of non-Hodgkin lymphoma.
A possible role for SV40, a macaque polyomavirus, in non-Hodgkin lymphoma (NHL) in humans was raised recently by the reported detection of SV40 DNA in tumor tissue. Animals with SV40-induced tumors frequently produce high-level antibodies against T antigen, the SV40 oncoprotein. In this study, we assessed whether SV40 T antibody measured in humans supported a relationship between SV40 and NHL. Subjects were sampled from a U.S. population-based case-control study of NHL, according to presence of antibodies against capsids of SV40 and BK, a related human polyomavirus (n = 85 cases, n = 95 controls). T antibody was measured by enzyme immunoassay. We also evaluated serum specimens from SV40-infected and SV40-uninfected macaques (n = 19 and n = 8, respectively), SV40-uninfected hamsters (n = 5), and hamsters with SV40-induced tumors (n = 10). Hamsters with SV40-induced tumors all produced robust SV40 T antibody [median absorbance, 0.99), whereas SV40-uninfected hamsters and macaques had much lower levels (median absorbance, 0.05 and 0.04, respectively). NHL cases, controls, and SV40-infected macaques resembled these latter two groups, generally showing only low-level T antibody (median absorbance, 0.03, 0.04, and 0.04, respectively). Overall, only five cases (6%) and five controls (5%) had T antibody responses classified as seropositive (odds ratio, 1.2; 95% confidence interval, 0.3-4.6). Interestingly, all 10 humans with T antibody responses also showed antibody responses to BK capsid. We found no association between the presence of T antibody and NHL, arguing against SV40 as a cause of NHL. Infrequent and low-level T antibody responses among humans could represent cross-reactivity to BK virus T antigen.
Adult↗
Cigarette smoking and risk of non-Hodgkin lymphoma: a pooled analysis from the International Lymphoma Epidemiology Consortium (interlymph).
BACKGROUND: The International Lymphoma Epidemiology Consortium (InterLymph) provides an opportunity to analyze the relationship between cigarette smoking and non-Hodgkin lymphoma with sufficient statistical power to consider non-Hodgkin lymphoma subtype. The results from previous studies of this relationship have been inconsistent, likely due to the small sample sizes that arose from stratification by disease subtype. To clarify the role of cigarette smoking in the etiology of non-Hodgkin lymphoma, we conducted a pooled analysis of original patient data from nine case-control studies of non-Hodgkin lymphoma conducted in the United States, Europe, and Australia. METHODS: Original data were obtained from each study and uniformly coded. Risk estimates from fixed-effects and two-stage random-effects models were compared to determine the impact of interstudy heterogeneity. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived from unconditional logistic regression models, controlling for study center, age, sex, and race. RESULTS: In our pooled study population of 6,594 cases and 8,892 controls, smoking was associated with slightly increased risk estimates (OR, 1.07; 95% CI, 1.00-1.15). Stratification by non-Hodgkin lymphoma subtype revealed that the most consistent association between cigarette smoking and non-Hodgkin lymphoma was observed among follicular lymphomas (n = 1452). Compared with nonsmokers, current smokers had a higher OR for follicular lymphoma (1.31; 95% CI, 1.12-1.52) than former smokers (1.06; 95% CI, 0.93-1.22). Current heavy smoking (> or = 36 pack-years) was associated with a 45% increased OR for follicular lymphoma (1.45; 95% CI, 1.15-1.82) compared with nonsmokers. CONCLUSIONS: Cigarette smoking may increase the risk of developing follicular lymphoma but does not seem to affect risk of the other non-Hodgkin lymphoma subtypes we examined. Future research is needed to determine the biological mechanism responsible for our subtype-specific results.
Adult↗
Residential herbicide use and risk of non-Hodgkin lymphoma.
CONTEXT: Environmental exposure to herbicides has been hypothesized to contribute to the long-term increase in non-Hodgkin lymphoma (NHL). OBJECTIVE: To estimate the effects of residential herbicide exposure on NHL risk. DESIGN: Population-based case-control study. SETTING: Iowa and metropolitan Detroit, Los Angeles, and Seattle, 1998 to 2000. PARTICIPANTS: NHL patients ages 20 to 74 years and unaffected residents identified by random digit dialing and Medicare eligibility files. MAIN OUTCOME MEASURES: Computer-assisted personal interviews (1,321 cases, 1,057 controls) elicited data on herbicide use at each home occupied since 1970. Levels of 2,4-dichlorophenoxy-acetic acid and dicamba were measured in dust taken from used vacuum cleaner bags in the current home (679 cases, 510 controls who had owned at least half of their carpets for > or = 5 years). RESULTS: Herbicide use on the lawn or garden was similar among cases and controls (adjusted relative risk, 1.02; 95% confidence interval, 0.84-1.23). Estimated risk did not increase with greater duration, frequency, or total number of applications of herbicides to the lawn, the garden, or to both combined. Risk was not elevated for respondents who applied the herbicides themselves and not for those exposed during the 1970s, 1980s, or 1990s. We detected 2,4-dichlorophenoxy-acetic acid equally often in homes of cases and controls (78%). We found dicamba in homes of 15% of cases and 20% of controls. We also found no elevation in risk among the respondents who had the highest dust levels and highest self-reported exposures. We found no consistent patterns for specific histologies. CONCLUSIONS: We found no detectable excess associated with residential exposures. Residential herbicide exposures are unlikely to explain the long-term increase in NHL.
Adult↗
Prenatal and perinatal correlates of adult mammographic breast density.
BACKGROUND: Adult mammographic percent density is one of the strongest known risk factors for breast cancer. In utero exposure to high levels of endogenous estrogens (or other pregnancy hormones) has been hypothesized to increase breast cancer risk in later life. We examined the hypothesis that those factors associated with higher levels of estrogen during pregnancy or shortly after birth are associated with higher mammographic breast density in adulthood. METHODS: We analyzed data on 1,893 women from 360 families in the Minnesota Breast Cancer Family Study who had screening mammograms, risk factor data, over age 40, and no history of breast cancer. Prenatal and perinatal risk factor data were ascertained using a mailed questionnaire. Mammographic percent density and dense area were estimated from the mediolateral oblique view using Cumulus, a computer-assisted thresholding program. Linear mixed effects models incorporating familial correlation were used to assess the association of risk factors with percent density, adjusting for age, weight, and other breast cancer risk factors, all at time of mammography. RESULTS: The mean age at mammography was 60.4 years (range, 40-91 years), and 76% were postmenopausal. Among postmenopausal women, there was a positive association of birthweight with percent density (P trend <0.01), with an adjusted mean percent density of 17.1% for <2.95 kg versus 21.0% for > or = 3.75 kg. There were suggestive positive associations with gestational age (mean percent density of 16.7% for preterm birth, 20.2% for term birth, and 23.0% for late birth; P trend = 0.07), maternal eclampsia/preeclampsia (mean percent density of 19.9% for no and 14.6% for yes; P = 0.16), and being breast-fed as an infant (mean percent density of 18.2% for never and 20.0% for ever; P = 0.08). There was no association of percent density with maternal age, birth order, maternal use of alcohol or cigarettes, or neonatal jaundice. Except for being breast-fed, these associations showed similar but attenuated trends among premenopausal women, although none were statistically significant. The results for dense area paralleled the percent density results. The associations of gestational age and being breast-fed as an infant with percent density attenuated when included in the same model as birthweight. CONCLUSIONS: Birthweight was positively associated with mammographic breast density and dense area among postmenopausal women and more weakly among premenopausal women, suggesting that it may be a marker of this early life exposure. These results offer some support to the hypothesis that pregnancy estrogens or other pregnancy changes may play a role in breast cancer etiology, and suggest that these factors may act in part through long-term effects on breast density.
Adult↗