Metabolic Syndrome Among Asian Indians in the United States.

INTRODUCTION: Metabolic syndrome (MetS), a clustering of cardiometabolic risk factors of type 2 diabetes and cardiovascular disease, disproportionately affects Asian Indians (AIs). We examined prevalence of MetS using 3 ethnicity-specific MetS criteria among immigrant AIs in the United States. We also examined associations between MetS and health promotion behaviors. OBJECTIVE: To present MetS prevalence estimates by the 3 ethnicity-specific criteria and investigate differences in health promotion behaviors among AIs with and without MetS to highlight the critical need for lifestyle modification strategies for this population. DESIGN: We analyzed data from a national cross-sectional study of 1037 AIs in the United States (2004-2006). We used the consensus criteria, International Diabetes Federation criteria, and modified criteria to estimate MetS prevalence. The Health Promotion Lifestyle Profile II scale measured health promotion behaviors. Bioclinical data (fasting blood glucose, triglyceride levels) were collected. Directed acyclic graphs and Likelihood Ratio Test assisted with model selection. Multiple imputation inference incorporated uncertainty due to missing data and made use of all available data. Adjusted multivariable logistic regression analysis tested for associations. RESULTS: Out of all participants, 40.3% met the consensus criteria, 34.8% met the International Diabetes Federation criteria, and 52.5% met the modified criteria. We found no statistically significant associations between engagement in health promotion measures and the prevalence of MetS and its criteria. CONCLUSION: Our study confirmed the high prevalence of MetS in the immigrant AI population in the United States. Our results showed that AIs with MetS did not exhibit an increased level of engagement in health promotion behaviors. We recommend continued refining of criteria for diagnosis and culturally suitable, age-appropriate strategies to increase engagement in healthier lifestyles among this high-risk population.

Thyroid cancer incidence attributable to overdiagnosis in the United States 1981-2011.

Papillary thyroid cancer incidence has increased in the United States from 1978 through 2011 for both men and women of all ages and races. Overdiagnosis is partially responsible for this trend, although its magnitude is uncertain. This study examines papillary thyroid cancer incidence according to stage at diagnosis and estimates the proportion of newly diagnosed tumors that are attributable to overdiagnosis. We analyzed stage specific trends in papillary thyroid cancer incidence, 1981-2011, using the Surveillance, Epidemiology and End Results national cancer registries. Yearly changes in early and late-stage thyroid cancer incidence were calculated. We estimate that the proportion of incident papillary thyroid cancers attributable to overdiagnosis in 2011 was 5.5 and 45.5% in men ages 20-49 and 50+ and 41.1 and 60.1% in women ages 20-49 and 50+, respectively. Overdiagnosis has resulted in an additional 82,000 incident papillary thyroid cancers that likely would never have caused any clinical symptoms. The detection of early-stage papillary thyroid cancer outpaced that of late-stage disease from 1981 through 2011, in part due to overdiagnosis. Further studies into the prevention, risk stratification and optimal treatment of papillary thyroid cancer are warranted in response to these trends.

Analgesic use in relation to sex hormone and prolactin concentrations in premenopausal women.

PURPOSE: Common analgesics (aspirin, non-aspirin NSAIDs, and acetaminophen) may be associated with hormone-related cancers, possibly via effects on sex hormone and prolactin concentrations. METHODS: Between 1996 and 1999, 29,611 participants in the Nurses' Health Study II (NHSII) provided blood samples; 18,521 provided samples timed in the early follicular and mid-luteal phases of the menstrual cycle, the remainder provided untimed samples. We assessed the cross-sectional relationship between analgesic use and plasma sex hormone and prolactin concentrations among 2,034 premenopausal women, 32-54 years old, who served as controls in nested case-control studies, or participated in a within-person hormone reproducibility study in the NHSII; this included 1,700 timed and 334 untimed samples. Estrogens and progesterone were measured in timed samples; androgens and prolactin were measured in timed and untimed samples. RESULTS: In multivariable models, non-aspirin NSAIDs were positively associated with follicular free estradiol [13.5 % higher, use ≥4 days/week vs. nonusers (p = 0.04; p trend = 0.11)]; results for follicular total estradiol were similar (13.2 % higher, p = 0.06; p trend = 0.11). Acetaminophen use was inversely associated with prolactin (11.8 % lower, use 2 days/week vs. nonusers, p = 0.01, p trend = 0.04). Acetaminophen was also inversely associated with free testosterone (7.1 % lower, use 2 days/week vs. nonusers, p = 0.04; p trend = 0.04). No other associations were observed with the other hormones, or with aspirin use. CONCLUSIONS: There were no clear patterns between analgesic use and sex hormones in premenopausal women. Acetaminophen use may be modestly associated with prolactin and free testosterone. Our results do not support that analgesic use influences cancer risk through alterations in premenopausal circulating sex hormones or prolactin.

ABO blood group and breast cancer incidence and survival.

ABO blood type has been associated with risk and survival for several malignancies; however, data for an association with breast cancer are inconsistent. Our study population consisted of Nurses' Health Study participants with self-reported serologic blood type and/or ABO genotype. Using Cox proportional hazards regression, we examined the association between serologic blood type and incident breast cancer among 67,697 women, including 3,107 cases. In addition, we examined the association with ABO genotype in a nested case-control study of 1,138 invasive breast cancer cases and 1,090 matched controls. Finally, we evaluated the association between serologic blood type and survival among 2,036 participants with breast cancer. No clear association was seen between serologic blood type or ABO genotype and risk of total breast cancer, invasive breast cancer or breast cancer subtypes. Compared to women with blood type O, the age-adjusted incidence rate ratios for serologic blood type and total breast cancer were 1.06 (95% CI, 0.98-1.15) for type A, 1.06 (95% CI, 0.93-1.22) for AB and 1.08 (95% CI, 0.96-1.20) for B. In genetic analyses, odds ratios for invasive breast cancer were 1.05 (95% CI, 0.87-1.27) for A/O, 1.21 (95% CI, 0.86-1.69) for A/A, 0.84 (95% CI, 0.56-1.26) for A/B, 0.84 (95% CI, 0.63-1.13) for B/O and 1.17 (95% CI, 0.35-3.86) for B/B, compared to O/O. No significant association was noted between blood type and overall or breast cancer-specific mortality. Our results suggest no association between ABO blood group and breast cancer risk or survival.

ABO blood group and risk of epithelial ovarian cancer within the Ovarian Cancer Association Consortium.

PURPOSE: Previous studies have examined the association between ABO blood group and ovarian cancer risk, with inconclusive results. METHODS: In eight studies participating in the Ovarian Cancer Association Consortium, we determined ABO blood groups and diplotypes by genotyping 3 SNPs in the ABO locus. Odds ratios and 95 % confidence intervals were calculated in each study using logistic regression; individual study results were combined using random effects meta-analysis. RESULTS: Compared to blood group O, the A blood group was associated with a modestly increased ovarian cancer risk: (OR: 1.09; 95 % CI: 1.01-1.18; p = 0.03). In diplotype analysis, the AO, but not the AA diplotype, was associated with increased risk (AO: OR: 1.11; 95 % CI: 1.01-1.22; p = 0.03; AA: OR: 1.03; 95 % CI: 0.87-1.21; p = 0.76). Neither AB nor the B blood groups were associated with risk. Results were similar across ovarian cancer histologic subtypes. CONCLUSION: Consistent with most previous reports, the A blood type was associated modestly with increased ovarian cancer risk in this large analysis of multiple studies of ovarian cancer. Future studies investigating potential biologic mechanisms are warranted.

Associations of commonly used medications with urinary incontinence in a community based sample.

PURPOSE: We examined the association between the use of medications and the prevalence of urinary incontinence in gender specific analyses of a community based, representative sample. MATERIALS AND METHODS: A population based epidemiological study was conducted of 5,503 men and women 30 to 79 years old residing in Boston, Massachusetts (baseline data collected from 2002 to 2005). Urological symptoms were ascertained in a 2-hour, in person interview. Urinary incontinence was defined as urine leakage occurring weekly or more often during the last year. Medications used in the last month were considered current use. Associations of 20+ medications and prevalent urinary incontinence were examined using multivariate logistic regression (ORs and 95% CIs) with adjustments for known urinary incontinence risk factors. RESULTS: The prevalence of urinary incontinence in the analysis sample was 9.0% in women and 4.6% in men. For women the prevalence was highest among users of certain antihistamines (28.4%) and angiotensin II receptor blockers (22.9%). For men the prevalence was highest among angiotensin II receptor blocker (22.2%) and loop diuretic (19.1%) users. After final multivariate adjustment there were significant positive associations for certain antihistamines, beta receptor agonists, angiotensin II receptor blockers and estrogens with urinary incontinence in women (all ORs greater than 1.7), and a borderline significant association for anticonvulsants (OR 1.75; 95% CI 1.00, 3.07). Among men only anticonvulsants were associated with urinary incontinence after final adjustments (OR 2.50; 95% CI 1.24, 5.03), although angiotensin II receptor blockers showed an adjusted association of borderline significance (OR 2.21; 95% CI 0.96, 5.10). CONCLUSIONS: Although a cross-sectional analysis cannot determine causality, our analysis suggests certain medications should be further examined in longitudinal analyses of risk to determine their influence on urological symptoms.

Non steroidal anti-inflammatory drug use and levels of oestrogens and androgens in men.

OBJECTIVE: Studies suggest that regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) may lower oestrogen levels in women. However, no large, population-based studies have assessed NSAID/hormone associations in men. Our objective was to examine the association between use of prescription and over-the-counter NSAIDs, and levels of oestrogens and androgens in men. DESIGN: The Boston Area Community Health Survey, an observational survey with initial data collection in 2002-2005. PATIENTS: A total of 1766 men who provided a blood sample and data on recent analgesic use. MEASUREMENTS: Adjusted geometric mean levels of androgens, oestrogens, SHBG, LH and FSH for each category of NSAID use and the per cent difference in hormone levels for users vs nonusers. RESULTS: There was no significant association between prescription/over-the-counter NSAID use and any hormone examined after adjustment for potential confounders. For example, geometric mean testosterone levels were 13·8, 13·6 and 14·2 nM in nonusers, prescription users and over-the-counter NSAID users, respectively; the corresponding levels for estradiol were 80·3, 70·4 and 79·9 pM. In stratified analyses, however, prescription NSAID use was associated with lower testosterone, estradiol and estrone levels in obese men and lower testosterone and dehydroepiandrosterone sulphate levels in inactive men. CONCLUSIONS: While overall these data do not provide strong support for an association between NSAID use and hormone levels in men, prescription NSAIDs may decrease levels of certain oestrogens and androgens in obese and inactive men.

ABO blood group and incidence of epithelial ovarian cancer.

Previous studies have observed an association between ABO blood group and risk of certain malignancies, including ovarian cancer; however, no prospective studies of the association with ovarian cancer risk are available. Using data from 49,153 women in the Nurses' Health Study, we examined the association between ABO blood group and incidence of epithelial ovarian cancer. Study participants reported their blood type and Rh factor in 1996, and 234 women were diagnosed with incident ovarian cancer during 10 years of follow-up. We used Cox proportional hazards regression to model the incidence rate ratios (RR) and 95% confidence intervals (CI) of ovarian cancer for each blood group category. Compared to women with blood group O, women with blood group AB or B had a nonsignificant 38% increase in ovarian cancer incidence (95% CI = 0.88-2.16 for blood group AB and 0.96-1.99 for blood group B), whereas blood group A was not associated with risk (RR = 0.95, 95% CI = 0.70-1.30). Combining blood groups AB and B, we observed a statistically significant positive association with presence versus absence of the B antigen overall (RR = 1.41, 95% CI = 1.06-1.88) and for the serous invasive subtype (RR = 1.53, 95% CI = 1.08-2.17). In this large, prospective cohort of women, presence of the B antigen was positively associated with ovarian cancer incidence, whereas blood group A was not associated with risk. Additional studies are needed to confirm this association and to explore the mechanisms through which blood group may influence ovarian cancer risk.

Nonsteroidal antiinflammatory drug use and lower urinary tract symptoms: results from the Boston area community health survey.

There is evidence for a role of inflammation in the etiology of lower urinary tract symptoms (LUTS), raising the possibility that use of nonsteroidal antiinflammatory drugs (NSAIDs) may inhibit the development or progression of LUTS. The authors examined the association between use of prescription and over-the-counter NSAIDs and LUTS among 1,974 men and 2,661 women in the Boston Area Community Health Survey (2002-2005). Multivariable-adjusted logistic regression was used to estimate odds ratios and 95% confidence intervals for LUTS, voiding symptoms, storage symptoms, and nocturia. There was no clear association between use of prescription or over-the-counter NSAIDs (compared with no NSAID use) and overall LUTS, voiding symptoms, or nocturia in men or women. However, over-the-counter NSAID use was positively associated with storage symptoms in women (odds ratio = 1.37, 95% confidence interval: 1.03, 1.83), and there was a positive association between over-the-counter NSAID use and overall LUTS among women with a history of arthritis (odds ratio = 2.09, 95% confidence interval: 1.20, 3.64). These results do not provide strong support for an association between NSAIDs and LUTS. However, the associations between over-the-counter NSAID use and certain urologic symptoms, particularly among women with arthritis, and the potential mechanisms involved should be evaluated in future studies.

Risk factors for ductal and lobular breast cancer: results from the nurses' health study.

INTRODUCTION: Ductal and lobular carcinomas are the two most common types of invasive breast cancer. Whether well-established risk factors are differentially associated with risk on the basis of histologic subtype is not clear. We prospectively investigated the association between a number of hormonal and nonhormonal exposures and risk defined by histologic subtype among 4,655 ductal and 659 lobular cases of postmenopausal breast cancer from the Nurses' Health Study. METHODS: Multivariate Cox proportional hazards regression stratified by histologic subtype and time period was used to examine the association between risk factors and the incidence of ductal and lobular subtypes. For each exposure, we calculated the P value for heterogeneity using a likelihood ratio test comparing models with separate estimates for the two subtypes versus a single estimate across subtypes. RESULTS: The associations with age at menarche (P-heterogeneity (het) = 0.03), age at first birth (P-het < 0.001) and postmenopausal hormone use (P-het < 0.001) were more strongly associated with lobular cancers. The associations with age, nulliparity, parity, age at menopause, type of menopause, alcohol intake, adult body mass index (BMI), BMI at age 18, family history of breast cancer and personal history of benign breast disease did not vary by subtype (P-het ≥ 0.08). Results were similar when we restricted the analyses to estrogen receptor-positive and progesterone receptor-positive tumors. CONCLUSIONS: These data indicate that breast cancer is a heterogeneous disease, and the differential association with a number of risk factors is suggestive of etiologically distinct tumors. Epidemiological analyses should continue to take into account a modifying role of histology.

Risk factors for epithelial ovarian cancer by histologic subtype.

Previous epidemiologic studies suggest that the major histologic subtypes of epithelial ovarian cancer may have different risk factor profiles; however, no known prospective study has systematically examined differences in risk by subtype. The authors used Cox proportional hazards regression, stratified by histologic subtype and time period, to examine the association between ovarian cancer risk factors and incidence of serous invasive, endometrioid, and mucinous ovarian cancers in the US Nurses' Health Study (1976-2006) and Nurses' Health Study II (1989-2005). For each exposure, they calculated P-heterogeneity using a likelihood ratio test comparing models with separate estimates for the 3 subtypes versus a single estimate across subtypes. Analysis included 221,866 women and 721 cases with the histologies of interest (496 serous invasive, 139 endometrioid, 86 mucinous). In analyses of reproductive/hormonal exposures, the associations with age, duration of breastfeeding, age at natural menopause, and duration of estrogen use differed significantly by subtype (all P-heterogeneity < or =0.05). The associations with several nonreproductive exposures also appeared to vary by subtype, but only the association with smoking differed significantly (P-heterogeneity = 0.03). Results suggest that associations with several ovarian cancer risk factors vary by subtype, and these differences are consistent with known similarities between each major histologic subtype and its normal tissue counterpart.

MTHFR polymorphisms in relation to ovarian cancer risk.

OBJECTIVE: Folate has been hypothesized to influence carcinogenesis due to its dual role in DNA methylation, which regulates gene expression, and synthesis of purine and thymidylate, which is vital for DNA repair. Thus, we examined ovarian cancer risk in relation to two functional polymorphisms (C677T and A1298C) in the MTHFR gene. METHODS: We genotyped the C677T (rs1801133) and A1298C (rs1801131) MTHFR polymorphisms in 1642 cases and 2068 controls from three studies, the New England Case Control Study (NEC), Nurses' Health Study (NHS), and Mayo Clinic Ovarian Cancer Case Control Study (MAY). RESULTS: Overall, we observed no association between either SNP and ovarian cancer risk (pooled C677T p(trend)=0.59 and A1298C p(trend)=0.58). Significant associations (C677T p(trend)=0.001, A1298C p(trend)=0.02) between these MTHFR SNPs and serous ovarian cancer risk were observed in the NEC study, but were not replicated in the NHS and MAY studies. CONCLUSIONS: MTHFR SNPs C677T and A1298C are not associated with ovarian cancer risk. Our results highlight the need for validation of genetic findings.

Common genetic variation in IGF1, IGFBP1 and IGFBP3 and ovarian cancer risk.

Insulin-like growth factor (IGF) 1 and its binding proteins foster cellular proliferation and inhibit apoptosis. In vitro studies show that IGF1 increases ovarian cell growth and invasive potential, suggesting a role for the IGF1 pathway in ovarian cancer etiology. We evaluated genetic variation in the IGF1, IGFBP1 and IGFBP3 genes in relation to ovarian cancer risk by genotyping 29 haplotype-tagging single nucleotide polymorphisms in 1173 cases and 1201 controls from the New England Case-Control (NECC) study and 296 cases and 854 controls from the Nurses' Health Study (NHS). The association of haplotypes and single nucleotide polymorphisms (SNPs) with ovarian cancer was estimated using unconditional (NECC) and conditional (NHS) logistic regression. Additionally, we evaluated the association of SNPs with IGF1, IGF-binding protein (IGFBP) 3 and IGFBP2 plasma levels (n = 380 NHS controls). Our data suggest a decreased risk for women carrying haplotype 2C of the IGF1 gene [odds ratios (ORs) = 0.82, 95% confidence intervals (CIs) = 0.69-0.98] and an increased risk for women carrying haplotype 1D (OR = 1.41, 95% CI = 1.03-1.94) or 2D (OR = 1.20, 95% CI = 1.01-1.41) in the binding proteins. When evaluated individually, three SNPs in the IGFBPs (rs10228265, rs4988515 and rs2270628) were associated with increased ovarian cancer risk, and several IGF1 (rs11111285, rs1996656 and rs1019731) and IGFBP3 (rs2270628, rs2854746 and rs2854744) SNPs were significantly associated with IGF1, IGFBP3 and IGFBP2 plasma levels. Some haplotypes and SNPs in the IGF pathway genes may be associated with ovarian cancer risk; however, these results need to be confirmed. Of particular interest was the IGFBP3 SNP rs2270628, which was associated with both increased IGF1 plasma levels and higher ovarian cancer risk.

Flavonoid intake and ovarian cancer risk in a population-based case-control study.

Several recent studies have evaluated the association between dietary flavonoid intake and ovarian cancer risk, and all reported significant or suggestive inverse associations with certain flavonoids or flavonoid subclasses; however, most of these studies were small to moderate in size. We, therefore, examined this association in a large, population-based case-control study. We calculated intake of 5 common dietary flavonoids (myricetin, kaempferol, quercetin, luteolin, and apigenin), as well as total intake of these flavonoids, for 1,141 cases and 1,183 frequency-matched controls. We used unconditional logistic regression to estimate the relative risk (RR) of ovarian cancer for each quintile of flavonoid intake when compared with the lowest quintile. We did not observe an association between total flavonoid intake and ovarian cancer risk. The multivariable-adjusted RR for the highest versus lowest quintile of total flavonoid intake was 1.06 (95% confidence interval [CI] = 0.78-1.45). In analyses of each individual flavonoid, only intake of apigenin was associated with a borderline significant decrease in risk (RR, highest vs. lowest quintile = 0.79, 95% CI = 0.59-1.06; p-trend = 0.26), and this association was significant after adjustment for intake of the other 4 individual flavonoids (comparable RR = 0.72, 95% CI = 0.53-0.98; p-trend = 0.09). These results provide limited support for an association between flavonoid intake and ovarian cancer risk. However, given the findings of previous studies and the biologic plausibility of this association, additional studies are warranted.

Breast cancer susceptibility alleles and ovarian cancer risk in 2 study populations.

Recent genome-wide scans identified several novel breast cancer risk alleles, including variants of the FGFR2, MAP3K1 and LSP1 genes, and a study of associations between these alleles and characteristics of breast cancer patients reported a borderline significant correlation between the number of FGFR2 minor alleles and family history of breast/ovarian cancer. Given these results and similarities in the etiology of breast and ovarian cancer, we examined the association between 7 novel breast cancer susceptibility alleles and epithelial ovarian cancer risk in 2 large study populations. Our analysis included 1,173 cases and 1,201 controls from a New England-based Case-Control study and 210 cases and 603 controls from the prospective Nurses' Health Study. We used logistic regression to estimate the odds ratio (OR) for individuals heterozygous or homozygous for the minor allele at each locus, compared to individuals with the wild-type genotype. We examined the associations separately in each population and, after testing for heterogeneity in the results, pooled the estimates using a random effects model. There was no clear association between these polymorphisms and ovarian cancer risk in either population. The pooled per allele OR for FGFR2 was 1.06 (95% confidence interval (CI)=0.95-1.18) for rs1219648 and 1.04 (95% CI=0.93-1.15) for rs2981582. We had more than 80% power to detect a log-additive OR of 1.16-1.18 per allele at the alpha=0.05 level in the pooled analysis. Our results do not provide strong support for an association between these breast cancer susceptibility alleles and epithelial ovarian cancer risk.

Validation of tissue microarray technology in ovarian cancer: results from the Nurses' Health Study.

BACKGROUND: Tissue microarrays (TMAs) allow high-throughput evaluation of protein expression from archived tissue samples. We identified characteristics specific to ovarian cancer that may influence TMA interpretation. METHODS: TMAs were constructed using triplicate core samples from 174 epithelial ovarian cancers. Stains for p53, Ki-67, estrogen receptor-alpha, progesterone receptor, Her-2, WT-1, cytokeratin 7, and cytokeratin 20 were evaluated by intraclass correlation coefficients, Spearman correlation coefficients, the effect of sample age, and tumor histology on the ability to score the cores, and inter-rater reliability. RESULTS: The interclass correlation coefficient and the mean Spearman correlation coefficients among 3 cores were > or = 0.91 and 0.87, respectively. Tissue age and tumor histology were not predictive of an inability to evaluate stains, but borderline tumors had a 2 to 4-fold increase in the risk of having uninterpretable cores over invasive tumors. There was moderate to substantial concordance between the two pathologists for estrogen receptor-alpha [Cohen's Kappa (kappa), 0.79] and Ki-67 (kappa, 0.52). The prevalence of positive staining cells by histologic type was comparable with previous studies. CONCLUSION: TMA is a valid method for evaluating antigen expression in invasive ovarian cancer but should be used with caution for borderline tumors. We suggest several methods of quality control based on intercore comparisons and show that some antigens may be affected by age of the samples.

Talc use, variants of the GSTM1, GSTT1, and NAT2 genes, and risk of epithelial ovarian cancer.

Epidemiologic evidence suggests a possible association between genital use of talcum powder and risk of epithelial ovarian cancer; however, the biological basis for this association is not clear. We analyzed interactions between talc use and genes in detoxification pathways [glutathione S-transferase M1 (GSTM1), glutathione S-transferase T1 (GSTT1), and N-acetyltransferase 2 (NAT2)] to assess whether the talc/ovarian cancer association is modified by variants of genes potentially involved in the response to talc. Our analysis included 1,175 cases and 1,202 controls from a New England-based case-control study and 210 cases and 600 controls from the prospective Nurses' Health Study. We genotyped participants for the GSTM1 and GSTT1 gene deletions and three NAT2 polymorphisms. We used logistic regression to analyze the main effect of talc use, genotype, and gene-talc interactions in each population and pooled the estimates using a random-effects model. Regular talc use was associated with increased ovarian cancer risk in the combined study population (RR, 1.36; 95% CI, 1.14-1.63; P(trend) < 0.001). Independent of talc, the genes examined were not clearly associated with risk. However, the talc/ovarian cancer association varied by GSTT1 genotype and combined GSTM1/GSTT1 genotype. In the pooled analysis, the association with talc was stronger among women with the GSTT1-null genotype (P(interaction) = 0.03), particularly in combination with the GSTM1-present genotype (P(interaction) = 0.03). There was no clear evidence of an interaction with GSTM1 alone or NAT2. These results suggest that women with certain genetic variants may have a higher risk of ovarian cancer associated with genital talc use. Additional research is needed on these interactions and the underlying biological mechanisms.

A prospective study of dietary flavonoid intake and incidence of epithelial ovarian cancer.

Flavonoids are antioxidant compounds found in plants, including fruits, vegetables and tea. No prior prospective studies have examined the association between intake of flavonoids in the flavonol and flavone subclasses and ovarian cancer risk. We analyzed the association between intake of 5 common dietary flavonoids and incidence of epithelial ovarian cancer among 66,940 women in the Nurses' Health Study. We calculated each participant's intake of myricetin, kaempferol, quercetin, luteolin and apigenin from dietary data collected at multiple time points, and used Cox proportional hazards regression to model the incidence rate ratio (RR) of ovarian cancer for each quintile of intake. Our analysis included 347 cases diagnosed between 1984 and 2002, and 950,347 person-years of follow-up. There was no clear association between total intake of the 5 flavonoids examined and incidence of ovarian cancer (RR = 0.75 for the highest versus lowest quintile, 95% confidence interval [CI] = 0.51-1.09). However, there was a significant 40% decrease in ovarian cancer incidence for the highest versus lowest quintile of kaempferol intake (RR = 0.60, 95% CI = 0.42-0.87; p-trend = 0.002), and a significant 34% decrease in incidence for the highest versus lowest quintile of luteolin intake (RR = 0.66, 95% CI = 0.49-0.91; p-trend = 0.01). There was evidence of an inverse association with consumption of tea (nonherbal) and broccoli, the primary contributors to kaempferol intake in our population. These data suggest that dietary intake of certain flavonoids may reduce ovarian cancer risk, although additional prospective studies are needed to further evaluate this association. If confirmed, these results would provide an important target for ovarian cancer prevention.

Operating room nursing and lung cancer risk in a cohort of female registered nurses.

OBJECTIVES: Smoke generated during laser surgery and electrocautery contains respiratory irritants and human carcinogens. Although laboratory and animal studies have demonstrated that this smoke has inflammatory and mutagenic potential, no population-based studies of the health effects of exposure to surgical smoke have been published. We examined the association between duration of employment as an operating room nurse, a proxy measure for surgical smoke exposure, and subsequent lung cancer risk. METHODS: This study was conducted among 86 747 women in the Nurses' Health Study. Information on the duration of prior operating room employment was collected in 1984, and the women were followed for incident, confirmed lung cancer. Cox proportional hazards regression was used to model the incidence rate ratio of lung cancer for each exposure category using women with no prior operating room employment for comparison. All of the models were adjusted for age, smoking history, passive smoke exposure, fruit and vegetable consumption, and alpha carotene and lycopene intake. RESULTS: A history of operating room employment was not associated with an increased rate of lung cancer in multivariable analyses [rate ratio (RR) 0.99, 95% confidence interval (95% CI) 0.86-1.15]. In fact, nurses in the highest exposure category, > or =15 years of operating room employment, had a significantly lower rate of lung cancer than nurses with no prior operating room employment (RR 0.58, 95% CI 0.37-0.91), possibly due to confounding by overall health status or residual confounding by smoking history. CONCLUSIONS: Long-term exposure to surgical smoke, as measured by the duration of operating room employment, does not appear to increase the risk of lung cancer.