alcohol consumption and the risk of mucinous and nonmucinous epithelial ovarian cancer

ORIGINAL RESEARCH

Alcohol Consumption and the Risk of Mucinous andNonmucinous Epithelial Ovarian Cancer

Francesmary Modugno, PhD, MPH, Roberta B. Ness, MD, MPH, and Glenn O. Allen, MPH

OBJECTIVE: To examine alcohol consumption as a riskfactor for epithelial ovarian cancer according to tumorhistology.

METHODS: We examined total alcohol consumption andconsumption of beer, wine, and spirits as risk factors formucinous and nonmucinous tumors in a population-based, case–control study comparing 761 incident cases ofepithelial ovarian cancer with 1352 community controlsfrequency-matched to cases by age and three-digit tele-phone exchange. Multivariable, unconditional logistic re-gression was used to calculate odds ratios (ORs) and 95%confidence intervals (CIs) for mucinous and nonmucinoustumors associated with alcohol consumption. Adjustmentswere made for age, parity, oral contraceptive use, educa-tion, tubal ligation, smoking, and family history of ovariancancer.

RESULTS: Overall, no association between total alcoholconsumption and ovarian cancer was found. However,current heavy alcohol consumption (24 g or more per day)was associated with mucinous (OR 1.93; 95% CI 1.02, 3.65)but not nonmucinous tumors (OR 0.88; 95% CI 0.57, 1.37).The association between heavy current consumption andmucinous tumors was strongest for spirits (OR 8.83; 95%CI 2.89, 27.01) and apparent for beer (OR 2.53; 95% CI0.86, 7.42). For nonmucinous tumors, no such associationswere found for either spirits (OR 1.53; 95% CI 0.58, 4.00) orbeer (OR 0.92; 95% CI 0.39, 2.14).

CONCLUSIONS: Current heavy consumption of alcoholmight be a risk factor for mucinous but not nonmucinousepithelial ovarian cancer. This supports the hypothesis of adistinct etiology for mucinous tumors. (Obstet Gynecol2003;102:1336–43. © 2003 by The American College ofObstetricians and Gynecologists.)

Because alcohol intake can affect steroid hormone levelsin women1–3 and because steroid hormones are believed

to be involved in the etiology of ovarian cancer,4–7 it ispossible that alcohol might play a role in ovarian cancerdevelopment. However, previous studies have foundeither no association between alcohol and ovarian can-cer8–14 or a slight, but often nonsignificant, increasedassociation.15–18 Many of these studies have small sam-ple sizes, and few have standardized alcohol exposureaccording to ethanol content. Both these methodologicissues could potentially obscure any true association.Moreover, only one small previous study11 has exam-ined the association between alcohol and ovarian canceraccording to histologic subtype.

There is mounting evidence that risk factors for ovar-ian cancer might vary by histology.19–22 Recently, datafrom the Cancer and Steroid Hormone Study19 showedan association between cigarette smoking and an in-creased risk of mucinous epithelial ovarian canceronly. We confirmed these findings in a large, popula-tion-based case– control study of ovarian cancer in theDelaware Valley.20 In particular, we found that ciga-rette smoking is a risk factor for mucinous epithelialovarian tumors (odds ratio [OR] 1.9; 95% confidenceinterval [CI] 1.3, 2.9) but not nonmucinous tumors(OR 1.0; 95% CI 0.8, 1.0). The relationship betweenmucinous tumors and smoking was even stronger forcurrent smokers (OR 2.7; 95% CI 1.7, 4.3). Further-more, the ORs for smokers with mucinous tumorsincreased with increasing pack-years of smoking (OR1.0, 1.9, and 2.7 for less than 5, 5–24, and 25 or morepack-years, respectively; P for trend � .01). Similarresults have subsequently been reported in an Austra-lian population.21

The association of cigarette smoking with mucinoustumors only and the fact that mucinous tumors arehistologically similar to colon tumors,23 which have beenassociated with both cigarette smoking24–26 and alco-hol,27–35 suggest a possible link between alcohol con-sumption and mucinous epithelial ovarian cancer. Wetherefore used data from a large, population-based, case–control study of epithelial ovarian cancer to examine theassociation between lifetime alcohol intake (standardized

From the Department of Epidemiology, Graduate School of Public Health,University of Pittsburgh, Pittsburgh, Pennsylvania.

Supported in part by the National Cancer Institute grants R01CA61095, R25CA57703-06A1, and K07-CA80668-01A1.

The authors thank the participants and other researchers involved in the Study ofHealth and Reproduction Project.

1336 VOL. 102, NO. 6, DECEMBER 2003 0029-7844/03/$30.00© 2003 by The American College of Obstetricians and Gynecologists. Published by Elsevier. doi:10.1016/S0029-7844(03)00949-9

to grams of ethanol) and the development of mucinousand nonmucinous epithelial ovarian tumors.

MATERIALS AND METHODS

This analysis is based on the Study of Health and Repro-duction Project, a case–control study of contraceptiveand reproductive risk factors for epithelial ovarian can-cer. Details of this study have been described else-where.36,37 Briefly, cases were women aged 20–69 yearsdiagnosed with incident epithelial ovarian cancer withinthe 9 months before interview. Between May 1994 andJuly 1998, 873 eligible women were identified at 39hospitals around the Delaware Valley. Fourteen physi-cians did not consent to their patients’ participation, and92 women refused to participate. Thus, 767 completedcase interviews (88% of potentially eligible, incidentcases) were eligible for the analyses presented in thisarticle. For all cases, the diagnosis of epithelial ovariancancer was confirmed by pathology.

Controls aged 65 years or younger were ascertainedby random-digit dialing and frequency-matched to casesby 5-year age groups and three-digit telephone ex-changes. Of the 14,551 telephone numbers screened forthis purpose, we identified 1637 households with a po-tentially eligible control, of whom 1215 (74%) completedinterviews. Controls aged 65–69 years were ascertainedthrough Health Care Financing Administration lists. Ofthe 263 potentially eligible participants identified, 152(58%) were interviewed. Therefore, of the 1900 screenedand potentially eligible controls, 1367 (72%) were eligi-ble for our analyses.

Institutional review board approval was obtained fromall hospitals from which subjects were recruited, and studysubjects gave informed consent for participation.

Trained interviewers conducted a standardized, 1.5-hour, in-person interview of cases and controls. Inter-view data detailed information on a subject’s medicalhistory, general demographic and anthropometric data,

Table 1. Selected Characteristics of Women With Epithelial Ovarian Cancer and Controls, Delaware Valley, 1993–1998

Controls(n � 1352)

All cases(n � 761)

Nonmucinous cases(n � 649)

Mucinous cases(n � 112)

Age (y)20–29 59 (4.4) 34 (4.5) 24 (3.7) 10 (8.9)30–39 201 (14.9) 83 (10.9) 59 (9.1) 24 (21.4)40–49 420 (31.1) 190 (25.0) 166 (25.6) 24 (21.4)50–59 383 (28.3) 245 (32.2) 214 (33.0) 31 (27.7)60–69 289 (21.4) 209 (27.5) 186 (28.7) 23 (20.5)

RaceWhite 1098 (81.2) 663 (87.1) 565 (87.1) 98 (87.5)Other 254 (18.8) 98 (12.9) 84 (12.9) 14 (12.5)

Education level�High school 127 (9.4) 81 (10.6) 71 (10.9) 10 (8.9)High school 487 (36.0) 282 (37.1) 238 (36.7) 44 (39.3)�High school 738 (54.6) 398 (52.3) 340 (52.4) 58 (51.8)

Live births0 173 (12.8) 236 (31.0) 198 (30.5) 38 (33.9)1 192 (14.2) 108 (14.2) 88 (13.6) 20 (17.9)2 437 (32.3) 195 (25.6) 166 (25.6) 29 (25.9)3� 550 (40.7) 222 (29.2) 197 (30.4) 25 (22.3)

OC useNever 503 (37.2) 400 (52.6) 293 (45.1) 44 (39.3)Ever 849 (62.8) 361 (47.4) 356 (54.9) 68 (60.7)

Tubal ligationNever 908 (67.2) 632 (83.0) 537 (82.7) 95 (84.8)Ever 444 (32.8) 129 (17.0) 112 (17.3) 17 (15.2)

Family history of ovarian cancerNo 1331 (98.4) 730 (95.9) 622 (95.8) 108 (96.4)Yes 21 (1.6) 31 (4.1) 27 (4.2) 4 (3.6)

Smoking statusNever 615 (45.5) 341 (44.8) 304 (46.8) 37 (33.0)Ever 737 (54.5) 420 (55.2) 345 (53.2) 85 (67.0)

Current 309 (22.9) 178 (23.4) 135 (20.8) 43 (38.4)Former 428 (31.7) 242 (31.8) 210 (32.4) 32 (28.6)

OC � oral contraceptive.Data are presented as n (%).

1337VOL. 102, NO. 6, DECEMBER 2003 Modugno et al Alcohol and Epithelial Ovarian Cancer

gynecologic and obstetric history, and lifestyle factors,such as cigarette smoking and alcohol consumption.Questions relating to alcohol consumption included ageat first weekly use for beer, wine and/or spirits; averagenumber of 12-oz beers, 4-oz glasses of wine, and/or 1.5-ozshots of hard liquor consumed per week; and age at lastweekly consumption of the three types of alcoholic bev-erages. Data on each type of alcoholic beverage wasrecorded separately.

Of the 767 case and 1367 control women eligible forthe analyses presented here, a total of 21 women wereexcluded because of missing or incomplete data on alco-hol consumption (six cases, 15 controls). Hence, ouranalyses include a total of 761 cases and 1352 controls.

An alcoholic beverage was defined as either a 12-ozcan of beer, a 4-oz glass of wine, or a 1.5-oz shot of hardliquor (spirits). Never drinking was defined as neverhaving consumed any alcohol on a weekly basis for atleast 6 months. For women who reported any weeklyalcohol consumption for at least 6 months, current drink-ing was defined as consuming beer, wine, or spiritswithin 9 months of interview. Former drinking wasdefined as quitting consumption of all types of alcoholmore than 9 months before interview.

To standardize ethanol exposure across the differenttypes of alcoholic beverages, the volume of ethanol inbeer, wine, and liquor was computed according to theaverage percent alcohol in each type: beer 4.8%, wine

12%, and liquor 40%. Thus, 12 oz of beer, 4 oz of wine,and 1.5 oz of hard liquor were estimated to contain0.576, 0.48, and 0.60 oz of ethanol, respectively. Theamount of ethanol consumed per day for each type ofalcoholic beverage was calculated as follows: (number ofdrinks/week � ounces of ethanol/drink)/7.

Total ethanol consumed per day was taken to be thesum of the daily ethanol consumed from each type ofalcoholic beverage. Ethanol consumption was convertedfrom ounces to grams by multiplying by a factor of28.35. Heavy alcohol consumption was defined as in-gesting greater than 24 g of ethanol per day (or theequivalent of approximately two alcoholic beverages perday).

Cases were divided into mucinous and nonmucinousovarian cancer according to the histologic subtype oftheir tumors, as determined from pathology reports.Because matching between cases and controls was basedon frequencies for only two broad criteria (age within5-year intervals and three-digit telephone exchange), wedid not preserve the “match” in the analyses. Because thematching was frequency based, we used multivariableunconditional logistic regression methods to calculatethe OR and 95% CI for mucinous and nonmucinousovarian cancer associated with alcohol consumption.Adjustments were made for age, number of live births,ever having used oral contraceptives, history of tuballigation, family history of ovarian cancer, ever having

Table 2. Multivariable Adjusted Odds Ratios for Ethanol Consumption by Histologic Subtype

Controls(n � 1352)

n (%)

Nonmucinous cases (n � 649)

n (%) Crude OR (95% CI) Adj* OR (95% CI)

Ethanol consumptionNever 788 (58.3) 375 (57.8)Ever 564 (41.7) 274 (42.2) 1.02 (0.85, 1.23) 1.03 (0.84, 1.26)

Current 311 (23.0) 146 (22.5) 0.99 (0.78, 1.24) 0.96 (0.75, 1.23)Former 253 (18.7) 128 (19.7) 1.06 (0.83, 1.36) 1.12 (0.86, 1.46)

Ethanol consumption (g/d)Never 788 (58.3) 375 (57.8)Current

�24 232 (17.2) 109 (16.8) 0.99 (0.76, 1.28) 0.98 (0.75, 1.30)�24 79 (5.8) 37 (5.7) 0.98 (0.65, 1.48) 0.88 (0.57, 1.37)

Former�24 180 (13.3) 89 (13.7) 1.04 (0.78, 1.38) 1.06 (0.78, 1.43)�24 73 (5.4) 39 (6.0) 1.12 (0.75, 1.69) 1.29 (0.83, 2.00)

Ever�24 412 (30.5) 198 (30.5) 1.01 (0.82, 1.25) 1.02 (0.81, 1.27)�24 152 (11.2) 76 (11.7) 1.05 (0.78, 1.42) 1.06 (0.77, 1.47)

OR � odds ratio; CI � confidence interval; Adj � adjusted.* Adjusted for ever-use of oral contraceptive, ever had tubal ligation, family history of ovarian cancer, race (white/other), and cigarette smoking

as dichotomous variables (yes/no); education level as a trichotomous variable (�high school (HS), HS, �HS); and number of live births and ageas continuous variables.

† P � .02.‡ P � .04.

1338 Modugno et al Alcohol and Epithelial Ovarian Cancer OBSTETRICS & GYNECOLOGY

smoked cigarettes, race (white or other), and educationlevel (less than high school, high school graduate, morethan high school). These variables were either shown todiffer between cases and controls in univariate analysesor are known to be associated with ovarian cancer risk.All P values were calculated as two-sided statistics andconsidered significant at P � .05.

RESULTS

Among the 761 cases, 112 (14.7%) were classified asmucinous tumors and 649 (85.3%) were classified asnonmucinous tumors. This histologic distribution is con-sistent with other studies.22,38,39 Table 1 shows the de-mographic and risk factor data for controls, for all cases,and for cases according to mucinous or nonmucinoussubtype. The two case groups were similar except for ageand cigarette use. Consistent with other studies,19,21,22

women who developed mucinous tumors were youngerand more likely to smoke (67% versus 53.2% ever-smokers among women with mucinous versus nonmu-cinous tumors, respectively). Compared with controls,both mucinous and nonmucinous cases were less likelyto have borne children, to have used oral contraception,or to have had a tubal ligation. In addition, nonmucinouscases were somewhat older than controls and were morelikely to report a family history of the disease. Notably,there were no differences in education level between the

two case groups or between either case group and thecontrols, which suggests similar socioeconomic levels.

As shown in Table 2, compared with controls, womenwho developed mucinous epithelial ovarian tumors weremore likely to be heavy drinkers and, in particular, to becurrent heavy drinkers (adjusted OR 1.93; 95% CI 1.02,3.65; P � .04). In contrast, the ORs for alcohol use werenot elevated in women who developed nonmucinoustumors.

Interestingly, as shown in Table 3, the associationbetween heavy alcohol consumption and mucinous tu-mors was strongest for spirits (adjusted OR 2.69; 95% CI1.18, 6.11; P � .001) and apparent for beer (adjusted OR1.76; 95% CI 0.78, 3.97). Moreover, the increase in riskof mucinous tumors associated with current heavydrinking was strong for spirits (adjusted OR 8.83; 95%CI 2.89, 27.01; P � .001) and evident for beer (adjustedOR 2.93; 95% CI 0.86, 7.42). For nonmucinous tumors,no such association with heavy drinking was found foreither spirits. Nor was there any association with currentheavy drinking for spirits. Note that because of smallnumbers in some cells, the data for wine were too sparseto interpret.

DISCUSSION

In this study, we investigated the association of alcoholconsumption with mucinous and nonmucinous epithe-lial ovarian cancer. Our data suggest that heavy alcoholconsumption is associated with mucinous ovarian tu-mors but not nonmucinous tumors. The association isstronger for current heavy drinkers and might varyaccording to type of alcohol consumed. In particular,heavy consumption of spirits was more strongly associ-ated with the risk of mucinous tumors than was heavyconsumption of beer or wine. Recent initiation of alcoholconsumption might also be a risk factor for mucinoustumor development, and again, type of alcoholic bever-age might modify this risk. These results provide clini-cians with additional data that can be used when coun-seling women regarding the risks associated withexcessive alcohol consumption. Moreover, because cer-tain drinking patterns might be associated with an in-creased risk of ovarian cancer, greater surveillance forthe disease among women currently engaging in thesebehaviors might be indicated.

Most8–14 but not all15–18 previous studies have failedto find an association between epithelial ovarian cancerand alcohol. Several limitations, including small samplesizes, failure to control for cigarette smoking and otherpotential confounders, inclusion of data on recent alco-hol consumption only, and lack of a standardized defini-tion of an alcoholic beverage, could potentially mask any

Mucinous cases(n � 112)

n (%) Crude OR (95% CI) Adj* OR (95% CI)

62 (55.4)50 (44.6) 1.13 (0.76, 1.66) 0.92 (0.61, 1.40)29 (25.9) 1.19 (0.75, 1.88) 0.97 (0.60, 1.57)21 (18.8) 1.06 (0.63, 1.27) 0.87 (0.51, 1.49)

62 (55.4)

13 (11.6) 0.71 (0.39, 1.32) 0.61 (0.32, 1.15)16 (14.3) 2.57† (1.42, 4.67) 1.93‡ (1.02, 3.65)

17 (15.2) 1.2 (0.69, 2.10) 0.97 (0.54, 1.74)4 (3.6) 0.70 (0.25, 1.97) 0.64 (0.22, 1.85)

30 (26.8) 0.93 (0.59, 1.45) 0.77 (0.48, 1.23)20 (17.9) 1.67 (0.98, 2.85) 1.36 (0.77, 2.41)


true association between alcohol and ovarian cancer,thereby explaining these null findings. However, herewe presented results from one of the largest ovariancancer case–control studies ever conducted. Our analy-ses included data on lifetime alcohol consumption,which was obtained using standardized definitions of thevarious alcoholic beverages. We further controlled forknown ovarian cancer risk factors and other potentialconfounders, such as cigarette smoking, in our analyses.Nonetheless, we, too, did not find any overall associationbetween alcohol consumption and ovarian cancer risk.

However, because ovarian cancer is a heterogeneousdisease, it is likely that the different histologic subtypesmight be associated with different risk factors. To date,only one study has investigated this possibility. Kuper etal11 compared cigarette and alcohol use between 549 inci-dent ovarian cancer cases and 516 healthy controls. Ingeneral, no case–control differences in tobacco and alcoholuse were found; however, among women with mucinoustumors, there was a modest trend (P � .06) for increasingrisk associated with increasing alcohol consumption.

The association between mucinous tumors and alco-hol is biologically plausible. Mucinous tumors consist ofmucin-producing epithelial cells similar to intestinal epi-thelial cells,23 and alcohol has been associated with colo-rectal cancers.27–35 Moreover, alcohol intake is associ-

ated with elevated postmenopausal hormone levels,including androstenedione,3 which might play a role inovarian cancer risk. In particular, a prospective study40

of ovarian cancer found significantly higher levels ofandrostenedione in the serum of postmenopausal casescompared with controls. Alcohol has also been shown toincrease testosterone and reduce progestin levels inwomen taking oral contraceptives,1,2 as well as those notusing oral contraceptives.1,2,41 High-dose progestin oralcontraceptive formulations might be more protectiveagainst ovarian cancer than low-dose formulations,42

and elevated androgen levels have been hypothesized toincrease ovarian cancer risk.7

Our findings that the risk of mucinous tumors mightvary according to type of alcoholic beverage should beinterpreted cautiously. Differences in risk associatedwith types of alcoholic beverages have been observed incardiovascular disease and cancer,43–46 although it is notknown whether these findings are due to differences inthe alcoholic beverages themselves47–49 or to differencesin lifestyle factors among those who choose to drinkcertain types of alcoholic beverages.50 In the resultsreported here, we standardized type and quantity of eachalcoholic beverage to grams of ethanol, and all ouranalyses were based on total grams of ethanol con-sumed, not number of alcoholic drinks. Thus, if ethanol

Table 3. Multivariable Adjusted Odds Ratios for Alcohol Consumption by Type of Alcoholic Beverage and HistologicSubtype

Spirits Beer

Controlsn (%)

Nonmucinous cases Mucinous cases

Controlsn (%)

Nonmucinous cases

n (%)Adj* OR(95% CI) n (%)

Adj* OR(95% CI) n (%)

Adj* OR(95% CI)

Drinking statusNever drinker 788 (74.9) 375 (75.0) 62 (68.1) 788 (74.2) 375 (75.9)Ever 264 (25.1) 125 (25.0) 0.96 (0.73, 1.25) 29 (31.9) 1.18 (0.72, 1.93) 274 (25.8) 119 (24.1) 0.95 (0.73, 1.26)Current 106 (10.1) 45 (9.0) 0.80 (0.54, 1.19) 14 (15.4) 1.43 (0.75, 2.72) 108 (10.2) 47 (95) 0.99 (0.67, 1.46)Former 158 (15.0) 80 (16.0) 1.07 (0.77, 1.48) 15 (16.5) 1.00 (0.53, 1.88) 166 (15.6) 72 (14.6) 0.93 (0.67, 1.30)

Total consumption(g/d)

Never drinker 788 (74.9) 375 (75.0) 62 (68.1) 788 (74.2) 375 (75.9)Current

�24 94 (8.9) 36 (7.2) 0.72 (0.47, 1.10) 8 (8.8) 0.86 (0.39, 1.90) 88 (8.3) 38 (7.7) 1.01 (0.66, 1.55)�24 12 (1.1) 9 (1.8) 1.53 (0.58, 4.00) 6 (6.6) 8.83† (2.89, 27.01) 20 (1.9) 9 (1.8) 0.92 (0.39, 2.14)

Former�24 118 (11.2) 58 (11.6) 0.98 (0.68, 1.41) 12 (13.2) 0.99 (0.50, 1.96) 137 (12.9) 57 (11.5) 0.88 (0.61, 1.25)�24 40 (3.8) 22 (4.4) 1.42 (0.79, 2.57) 3 (3.3) 1.07 (0.30, 3.79) 29 (2.7) 15 (3.0) 1.24 (0.63, 2.45)

Ever�24 212 (20.2) 94 (18.8) 0.86 (0.64, 1.16) 20 (22.0) 0.94 (0.53, 1.64) 225 (21.2) 95 (19.2) 0.92 (0.69, 1.24)�24 52 (4.9) 31 (6.2) 1.45 (0.87, 2.42) 9 (9.9) 2.69‡ (1.18, 6.11) 49 (4.6) 24 (4.9) 1.10 (0.64, 1.89)

Abbreviations as in Table 2.* Adjusted for ever use of oral contraceptive, ever had tubal ligation, family history of ovarian cancer, race (white/other), and cigarette smoking

as dichotomous variables (yes/no); education level as a trichotomous variable (�high school (HS), HS, �HS); and number of live births and ageas continuous variables.

† P � .001.‡ P � .001.


alone is the factor associated with mucinous ovariantumors, it is unlikely that number of drinks accounts forthe potential observed differences in risk between spirit,wine, and beer consumption. However, it is possible thatdifferent agents within the various types of alcoholicbeverages (eg, antioxidants in wine)47 might modify therisk of mucinous tumors associated with ethanol. Con-versely, the different types of alcoholic beverages mightnot be the true risk factors but instead might be markersfor other lifestyle factors,50 which might be the real riskfactors. Moreover, although our data did reach statisticalsignificance, especially for spirits, the number of subjectsin each cell was small. Replication of the findings pre-sented here in larger studies is needed before any con-clusions can be made regarding the type of alcoholicbeverage and ovarian cancer risk.

The major strengths of this study are that it is one ofthe largest population-based studies of epithelial ovariancancer ever conducted, and study data were collectedthrough a standardized, structured interview adminis-tered by trained personnel.

The major limitation of this study is the possibility oferror in the histologic classification because pathologydata on cases came from pathologists at 39 hospitals.However, the overall distribution of histologic types inour study was consistent with other studies.22,38,39 Thus,

our classifications are likely to be reasonably accurate.Moreover, the possibility of misclassifying a mucinoustumor as a nonmucinous tumor or vice versa is small.51

Even if the histologic classification of some tumors wereincorrect, the misclassification would be nondifferentialwith respect to alcohol. This would bias our resultstoward the null, thereby weakening any true associa-tions.

Another limitation is the possibility for selection biasamong controls. Data from US population-based sam-ples suggest that current drinking is positively associatedwith increasing education and income.52–55 However,among current drinkers, heavy drinking (as defined by avariety of metrics, including quantity and frequency ofdrinking) is inversely related to both education andincome.52 Thus, it is possible that heavy drinkers areunderrepresented in our control group due to the com-bined effects of higher study participation rates amongwomen with higher levels of education and the loweralcohol consumption amounts among current drinkerswithin this group of women. However, the similarities inage and education level between cases and controlssuggest that differences in socioeconomic status betweenthe two groups are unlikely. In addition, there is littleevidence that differences in socioeconomic status ac-count for differences in ovarian cancer histology.19,21,22

Wine

Mucinous cases

Controlsn (%)

Nonmucinous cases Mucinous cases

n (%)Adj* OR(95% CI) n (%)

Adj* OR(95% CI) n (%)

Adj* OR(95% CI)

62 (68.1) 788 (73.1) 375 (71.4) 62 (78.5)29 (31.9) 1.03 (0.63, 1.71) 290 (26.9) 150 (28.6) 1.05 (0.81, 1.36) 17 (21.5) 0.64 (0.35, 1.15)14 (15.4) 1.33 (0.70, 2.55) 178 (16.5) 91 (17.3) 0.98 (0.73, 1.33) 11 (13.9) 0.65 (0.32, 1.31)15 (16.5) 0.85 (0.45, 1.59) 112 (10.4) 59 (11.3) 1.17 (0.81, 1.69) 6 (7.6) 0.61 (0.25, 1.49)

62 (68.1) 788 (73.1) 375 (71.4) 62 (78.5)

9 (9.9) 1.06 (0.49, 2.28) 165 (15.3) 82 (15.6) 0.99 (0.72, 1.36) 9 (11.4) 0.59 (0.28, 1.24)5 (5.5) 2.53 (0.86, 7.42) 13 (1.2) 9 (1.7) 0.92 (0.38, 2.23) 2 (2.5) Insufficient data




We cannot eliminate the possibility of recall bias,which can occur in any case–control study. However,interviewers were trained to standardize interview ques-tions and participants were not aware of the study hy-potheses, thereby reducing recall bias. Finally we did notinclude some potential confounders, such as dietary fatintake, in our analyses.

In conclusion, the data presented here support the hy-pothesis that mucinous tumors might be etiologically dis-tinct from nonmucinous tumors. The data further indicatethat mucinous epithelial ovarian tumors share risk factorswith mucinous tumors at other body sites, including alco-hol. Additional studies of risk factors for epithelial ovariancancer by histologic type are warranted.

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Address reprint requests to: Francesmary Modugno, PhD,MPH, University of Pittsburgh, Graduate School of PublicHealth, Department of Epidemiology, 516A Parran Hall, 130DeSoto Street, Pittsburgh, PA 15261; E-mail: [email protected].

Received March 20, 2003. Received in revised form July 8, 2003.Accepted August 1, 2003.


alcohol consumption and the risk of mucinous and nonmucinous epithelial ovarian cancer

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