The association between tea consumption and bladder cancer risk based on the Bladder Cancer Epidemiology and Nutritional Determinants (BLEND) international consortium

Yan-Xi Zhang; Richard Albers; Ya-Ting Chen; Gunnar Steineck; Eliane Kellen; Kenneth C Johnson; Chih-Ming Lu; Hermann Pohlabeln; Carlo La Vecchia; Stefano Porru; Angela Carta; Jerry Polesel; Cristina Bosetti; Xuejuan Jiang; Li Tang; James Marshall; Margaret R Karagas; Zuo-Feng Zhang; Jack A Taylor; Maurice P A Zeegers; Anke Wesselius; Evan Yi-Wen Yu

doi:10.1080/01635581.2025.2488063

. Author manuscript; available in PMC: 2026 Apr 8.

Published in final edited form as: Nutr Cancer. 2025 Apr 8;77(6):687–698. doi: 10.1080/01635581.2025.2488063

The association between tea consumption and bladder cancer risk based on the Bladder Cancer Epidemiology and Nutritional Determinants (BLEND) international consortium

Yan-Xi Zhang ^1,², Richard Albers ³, Ya-Ting Chen ^1,², Gunnar Steineck ⁴, Eliane Kellen ⁵, Kenneth C Johnson ⁶, Chih-Ming Lu ⁷, Hermann Pohlabeln ⁸, Carlo La Vecchia ⁹, Stefano Porru ^10,¹¹, Angela Carta ^11,¹², Jerry Polesel ¹³, Cristina Bosetti ¹⁴, Xuejuan Jiang ¹⁵, Li Tang ¹⁶, James Marshall ¹⁶, Margaret R Karagas ¹⁷, Zuo-Feng Zhang ¹⁸, Jack A Taylor ¹⁹, Maurice P A Zeegers ³, Anke Wesselius ³, Evan Yi-Wen Yu ^1,^2,^3,^*

¹Key Laboratory of Environmental Medicine and Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing, China

²Department of Epidemiology & Biostatistics, School of Public Health, Southeast University, Nanjing, China

³Department of Epidemiology, CAPHRI Care and Public Health Research Institute, School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands

⁴Department of Oncology and Pathology, Division of Clinical Cancer Epidemiology, Karolinska Hospital, Stockholm, Sweden

⁵Leuven University Centre for Cancer Prevention (LUCK), Leuven, Belgium

⁶Department of Epidemiology and Community Medicine, University of Ottawa, Ottawa, ON, Canada

⁷Department of Urology, Buddhist Dalin Tzu Chi General Hospital, Dalin Township 62247, Chiayi County, Taiwan

⁸Leibniz Institute for Prevention Research and Epidemiology-BIPS, Bremen, Germany

⁹Department of Clinical Medicine and Community Health, University of Milan, Milan, Italy

¹⁰Department of Diagnostics and Public Health, Section of Occupational Health, University of Verona, Verona, Italy

¹¹University Research Center ‘Integrated Models for Prevention and Protection in Environmental and Occupational Health’ MISTRAL, University of Verona, Milano Bicocca and Brescia, Italy

¹²Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy

¹³Unit of Cancer Epidemiology, Centro di Riferimento Oncologico di Aviano (CRO) IRCCS, Aviano, Italy

¹⁴Department of Medical Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy

¹⁵Department of Preventive Medicine, University of Southern California, Los Angeles, CA, USA

¹⁶Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, NY, USA

¹⁷Department of Epidemiology, Geisel School of Medicine at Dartmouth, Hanover, NH, USA

¹⁸Departments of Epidemiology, UCLA Center for Environmental Genomics, Fielding School of Public Health, University of California, Los Angeles (UCLA), Los Angeles, CA, USA

¹⁹Epidemiology Branch, and Epigenetic and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA

Author Contribution

The work reported in the paper has been performed by the authors, unless clearly specified in the text. Conceived and designed the study: YXZ and RA; supervision: MPZ, AW and EYWY; conducted data analyses and interpretation and drafted the manuscript: YXZ and RA; data curation: YXZ and RA; Critical revision of the manuscript: YTC, GS, EK, KC.J, CMingL, HP, CLV, SP, AC, JP, CB, XJ, LT, JM, MRK, ZFZ, JAT, MPAZ, AW, EYWY. All authors read and approved the final manuscript.

Correspondence to: Evan Yi-Wen Yu, Mail address: Universiteitssingel 40 (Room C5.570), 6229 ER, Maastricht, the Netherlands.; evan.yu@maastrichtuniversity.nl

PMCID: PMC12433241 NIHMSID: NIHMS2107012 PMID: 40200560

Abstract

Objectives

Evidence regarding the association between tea consumption and bladder cancer (BC) risk is inconsistent. This study aimed to increase our knowledge of the association by using international data from the Bladder Cancer Epidemiology and Nutritional Determinants Consortium.

Methods

Individual data on 2,347 cases and 6,871 controls from 15 case-control studies with information on black, green, herbal, or general tea was pooled. The association was estimated using multilevel multivariable logistic regression analysis adjusted for multiple (non-)dietary factors.

Results

Association between tea consumption and BC risk was observed (odds ratio, OR = 0.72, 95% confidence interval, 95% CI = 0.65-0.80) compared to non-tea drinkers. Stratified analyses based on gender and smoking status yielded similar results. Stratified analysis showed no significant association between black or green tea consumption and BC risk across models, while herbal tea consumption was linked to a reduced BC risk (OR = 0.59, 95% CI = 0.36-0.96). As daily tea consumption increased within a suitable range (<5.67 cups/day), BC risk decreased.

Conclusions

Camellia sinensis tea showed no association with BC risk, while herbal tea was inversely linked to BC incidence. Despite some significant findings in the selected strata, further studies are required to clarify the underlying mechanisms.

Keywords: Bladder cancer, Tea consumption, BLEND consortium, Case-control studies, Dose-response relationship

Introduction

Worldwide, there are 165,000 annual deaths of bladder cancer (BC) and around 430,000 new cases per year, making this neoplasm the 9th most common cancer type ^1,2. Owing to its high rate of recurrence, BC is reported to be the most expensive of all cancers in terms of lifetime treatment ³. In Europe, 3% of all cancer-related costs are caused by BC ⁴. The most well-established risk factors for BC are smoking, occupational exposure to carcinogens, and Schistosoma haematobium infection ^5–8. For patients presenting with hematuria symptoms, urine cytology, urine tumor marker tests, and imaging tests (e.g., ultrasound, CT urography) are performed first. If the result of any one of these tests is positive or abnormal, further cystoscopy and biopsy (if necessary) are required to clarify the diagnosis. Studies have shown that cessation of smoking and the presence of cardiovascular disease are independent protective factors for bladder cancer (BC)⁹. Due to the use of antiplatelet/antithrombotic medications, patients with cardiovascular disease typically have a higher risk of hematuria. Consequently, they often require additional diagnostic evaluations such as ultrasound, cystoscopy, or CT, which may increase the detection rate of benign pseudocancerous lesions.

Since the bladder is an excretion organ, and thereby the bladder is exposed to carcinogens in fluid via the urine, the role of fluid consumption could also be important in the occurrence of BC ⁸. Tea is the second most common beverage worldwide (after water). Among teas, black and green tea are the most favored types ¹⁰ and originate from the same plant (Camellia sinensis). Black tea leaves are completely fermented, and green tea leaves are unfermented ^11,12. Anticancer properties are associated with the polyphenol compounds of black tea, especially theaflavins and thearubigins ^12–14 and green tea, mainly epigallocatechin-3-gallate (EGCG) ^12,14–17. Polyphenols inhibit apoptosis and cancer cell proliferation and exhibit antioxidant characteristics. The amount of anticancer polyphenols was higher in green tea than in black tea ¹². In addition, herbal tea, which is rich in phytochemicals and has antimicrobial potential, may be beneficial for soothing moods and preventing colds and other chronic diseases ¹⁸.

Consistent evidence posits that green tea consumption has a favorable effect on various cancer types in humans ¹⁹, such as gastric ²⁰ and breast cancer ²¹. In vitro and in vivo studies have also demonstrated an inverse relationship between green tea consumption and the risk of BC ¹⁵, whereas research on the relationship between black or herbal tea and BC is lacking. The exact molecular processes of tea polyphenols are still being investigated. However, epidemiological evidence regarding tea consumption and BC, is unclear. While three meta-analyses concluded that there was no significant association between general tea consumption and black or green tea consumption individually and BC ^22–24, one meta-analysis showed a significant inverse association between BC risk and both black and green tea ²⁵. These conflicting or inconsistent results might be due to the lack of detailed information on tea consumption and adjustment for influential or important confounding factors ¹⁵. We hypothesized that the inverse association between tea consumption and BC risk could be clarified by addressing the limitations of previous research.

The current study aimed to increase our knowledge of the effects of black, green, herbal, and general tea consumption in general and BC risk by bringing together world data on this topic.

Methods

Study design

Data were obtained from the bladder cancer, epidemiology and nutritional determinants study (BLEND), an international nutritional consortium currently involving 19 case-control studies and 16 cohort studies, aimed to investigate the association between diet and BC²⁶. In the present study, case-control studies from BLEND were included if they provided data on tea consumption and covariates of interest. Out of the 19 case-control studies in BLEND, 15 studies met the inclusion criteria. Fifteen case-control studies with a total of 2,347 BC cases and 6,871 controls, originated from seven countries on three continents: Belgium ²⁷, Canada ²⁸, China ^29,30, Germany ³¹, Italy ^32–34, Sweden ³⁵, and the USA ^36–41 (Supplementary Table 1). Each study was approved by their local ethic committee ²⁶.

Data collection and coding

Details of the methodology of the BLEND consortium have been described elsewhere ²⁶. All the studies collected dietary data by (food frequency) questionnaires or interviews. Except for three studies ^41–43, data on dietary intake were collected at least one year before enrolment. For harmonization purposes, the BLEND consortium used the Eurocode 2 food coding system developed by the European Union ⁴⁴. The weekly, monthly, or yearly intake was converted to daily milliliters (ml) or grams (g). This resulted in an aggregated dataset with a unified tea consumption across the included studies. In the present study, tea consumption includes tea derived from the leaves of the plant Camellia sinensis, such as black tea and green tea, as well as herbal tea, a common drink widely consumed in many countries. Additionally, the BLEND consortium collected data on study characteristics (design, method of dietary assessment, geographical region), participant demographics (age, gender, and ethnicity), and smoking status (current, former, never). Smoking was defined as 0 (never smokers), 1 [current light smokers (i.e., smoking less than 20 pack-years)], 2 [current heavy smokers (i.e., smoking more than 20 pack-years)], 3 [current smokers (no information on pack-years)], 4 [former light smokers (i.e., smoking less than 20 pack-years)]; 5 [former heavy smokers (i.e., smoking more than 20 pack-years)]; and 6 [former smokers (no information on pack-years)].

All studies identified BC cases through cancer (surveillance) registries or hospital records, including data on BC subtypes: non-muscle-invasive BC (NMIBC) and muscle-invasive BC (MIBC).

NMIBC consists of carcinoma in situ (CIS), non-invasive papillary carcinoma (Ta), and invasive carcinoma in different layers of the bladder (T1). MIBC involves tumors in the muscle (T2), tumors that spread in and around the kidney or ureter (T3), and tumors that grow into the surrounding organs (T4).

Statistical Analysis

Black, green, herbal, and (combined) tea (i.e., black, green, herbal and unspecified tea) consumption was divided into three groups defined by tertiles based on the distribution of the pooled data from 15 case-control studies. To estimate the effect of tea consumption on BC risk, multilevel multivariable adjusted logistic regression analysis was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs). Multicollinearity between the covariates was checked when needed, using a variance inflation factor ⁴⁵. No consumption was used as the reference group and associations were assessed using three models: model (A) adjusted for study center, model (B) adjusted for study center, age (years), gender (male and female), and smoking, model (C) additionally adjusted for alcohol (ml/day, continuous), fruit juice (ml/day, continuous), soft drink (ml/day, continuous), milk (ml/day, continuous), vegetable (g/day, continuous), and fruit intake (g/day, continuous).

The interaction was tested for smoking status (if applicable, smoking pack-years) and gender using the Wald chi-squared test. P-interaction <0.05 was considered statistically significant. Regarding the different etiologies of BC subtypes (i.e., NMIBC and MIBC), stratification was performed on BC subtypes. Tests for trends were assessed by assigning medians to each consumption category as a continuous variable. Only subjects with complete data on the outcome, gender, age, smoking, and tea intake were included in the analysis. The main covariates with missing data were coffee, alcohol, and fruits. Multiple imputation by chained equations (MICE) was used for the imputation of missing values ^46,47 and was checked by visual trace plots ⁴⁷. Missing values were imputed for each study individually and subsequently combined into one data set.

A restricted cubic spline (RCS) with five knots at the 5th, 35th, 50th, 65th, and 95th percentiles was used to flexibly model and visualize the association of BC risk between tea consumption. One dose was 150 ml/day (i.e., the average European teacup size). The RCS model used the logarithm of the OR and the CI of each corresponding dose/teacup(s), ranging from one (150 ml) to ten (1,500 ml) daily consumption, adjusted for model (C). No consumption was used as the reference category for each dose. Accordingly, the increment BC risk of 1 cup/day and the non-linearity of the curve were analyzed.

Analyses were performed using R (version 4.3.0) utilizing the RStudio IDE tool (version 2023.03.01). A two-sided p-value <0.05 was considered statistically significant.

Results

Baseline characteristics

This study included 2,347 cases and 6,871 controls, of which 3,524 (38.2%) were female and 5,694 (61.8%) were male. The mean age was 61.4 years for cases and 58.4 years for controls. Most participants were Caucasian (42.4%). The mean tea consumption was higher among the cases (323.0 ml/day) than among the controls (209.7 ml/day). Compared to the controls, patients were less likely to be never smokers (40.5% vs 22.2%). A more detailed overview of the baseline characteristics is provided in Table 1.

Table 1.

Baseline characteristic: cases and controls with information on tea consumption and bladder cancer

	Cases			Controls

	Both genders	Females	Males	Both genders	Females	Males
Total (%)	2347(25.46)	545(23.22)	1802(76.78)	6871(74.54)	2979(43.36)	3892(56.64)
Black tea, ml/day mean (SD)	267.63(417.10)	236.83(373.24)	274.31(427.47)	262.18(419.32)	114.88(249.83)	302.46(446.69)
No (%)	222(49.22)	37(41.11)	185(51.25)	232(50.33)	62(62.63)	170(46.96)
Low (%) <129 ml/day	85(18.85)	23(25.56)	62(17.17)	90(19.52)	22(22.22)	68(18.78)
Medium (%) >160 - <900 ml/day	112(24.83)	25(27.78)	87(24.10)	101(21.91)	14(14.14)	87(24.03)
High (%) >1125 ml/day	32(7.1)	5(5.56)	27(7.48)	38(8.24)	1(1.01)	37(10.22)
Green tea, ml/day mean (SD)	337.62(474.25)	204.56(354.22)	369.55(493.86)	338.31(490.77)	241.57(461.79)	364.77(495.73)
No (%)	134(28.82)	32(35.56)	102(27.20)	132(28.63)	41(41.41)	91(25.14)
Low <129 ml/day (%)	133(28.60)	30(33.33)	103(27.47)	138(29.93)	29(29.29)	109(30.11)
Medium >150 - <600 ml/day (%)	96(20.65)	16(17.78)	80(21.33)	84(18.22)	15(15.15)	69(19.06)
High >675 ml/day (%)	102(21.94)	12(13.33)	90(24.00)	107(23.21)	14(14.14)	93(25.69)
Herbal tea, ml/day mean (SD)	28.62(61.69)	26.36(58.64)	29.02(62.36)	38.89(70.72)	49.3(78.54)	31.93(64.18)
No (%)	165(73.99)	24(70.59)	141(74.60)	259(57.68)	88(48.89)	171(63.57)
Low <113 ml/day (%)	28(12.56)	7(20.59)	21(11.11)	109(24.28)	49(27.22)	60(22.30)
Medium >118 - <300 ml/day (%)	8(3.59)	0(0.00)	8(4.23)	24(5.35)	14(7.78)	10(3.72)
High >310 ml/day (%)	22(9.87)	3(8.82)	19(10.05)	57(12.69)	29(16.11)	28(10.41)
Tea, ml/day mean (SD)	322.99(684.02)	255.11(503.65)	343.52(728.71)	209.70(443.41)	172.85(284.25)	237.91(532.42)
No (%)	1104(47.04)	214(39.27)	890(49.39)	2451(35.67)	860(28.87)	1591(40.88)
Low <120 ml/day (%)	448(19.09)	142(26.06)	306(16.98)	2162(31.47)	1083(36.35)	1079(27.72)
Medium >120 - <300 ml/day (%)	328(13.98)	92(16.88)	236(13.10)	1342(19.53)	697(23.40)	645(16.57)
High >305 ml/day (%)	467(19.90)	97(17.80)	370(20.53)	916(13.33)	339(11.38)	577(14.83)
Coffee ml/day mean (SD)	447.09(599.94)	453.02(495.81)	445.19(629.75)	450.83(491.43)	456.08(464.35)	446.46(512.93)
Juice ml/day mean (SD)	57.91(105.29)	65.99(98.73)	54.89(107.52)	73.01(118.99)	81.39(129.14)	65.62(108.73)
Soft drink ml/day mean (SD)	23.65(110.10)	17.14(71.27)	24.95(116.32)	29.40(124.20)	23.21(91.78)	31.95(135.26)
Milk ml/day mean (SD)	301.47(431.17)	361.42(456.66)	283.20(421.53)	428.74(568.25)	459.25(590.41)	405.39(549.63)
Alcohol ml/day mean (SD)	124.86(284.00)	52.42(144.46)	151.54(316.33)	127.81(270.65)	66.58(174.45)	180.54(322.70)
Vegetable g/day mean (SD)	145.09(121.46)	119.41(104.42)	153.34(125.37)	119.42(112.24)	110.37(109.50)	127.06(113.96)
Subtypes BC
NMIBC (%)	178(7.58)	31(5.69)	147(8.16)	-	-	-
MIBC (%)	174(7.41)	35(6.42)	139(7.71)	-	-	-
Neither (%)	1995(85.00)	479(87.89)	1516(84.13)	-	-	-
Smoking status
Current (%)	897(38.21)	161(29.54)	736(40.84)	1519(22.11)	506(16.99)	1013(26.03)
Former (%)	930(39.63)	116(21.28)	814(45.17)	2568(37.37)	784(26.32)	1784(45.84)
Never (%)	520(22.16)	268(49.17)	252(13.98)	2784(40.52)	1689(56.70)	1095(28.13)
Age; mean (SD)	63.40(10.19)	62.06(11.17)	63.80(9.84)	58.40(13.13)	57.08(12.39)	59.41(13.58)
Ethnic groups
Black (%)	16(0.68)	1(0.18)	15(0.83)	98(1.43)	47(1.58)	51(1.31)
Caucasian (%)	996(42.44)	304(55.78)	692(38.40)	4433(64.51)	2200(73.85)	2233(57.37)
Chinese (%)	470(20.03)	91(16.70)	379(21.03)	585(8.51)	148(4.97)	437(11.23)
Any other ethnic group(%)	45(1.91)	10(1.83)	35(1.94)	162(2.36)	37(1.24)	125(3.21)

Open in a new tab

SD, standard deviation; ml, milliliter; g, gram

Association between tea and BC risk

A statistically significant association between tea consumption and BC risk was observed in the total population (OR = 0.72, 95% CI = 0.65-0.80) and those stratified by gender and smoking status. (Table 2). Additionally, the results showed that the OR of BC was lower in the low (OR = 0.61, 95% CI = 0.53-0.70) and medium (OR = 0.64, 95% CI = 0.55-0.74) tea intake groups. The association between black or green tea consumption and BC risk in the overall population was statistically non-significant in each adjusted model (Supplementary Table 2). However, herbal tea consumption was associated with a low BC risk (OR = 0.59, 95% CI = 0.36-0.96).

Table 2.

Odds ratios and 95% confidence intervals for the association between bladder cancer and tea consumption by gender and smoking status

Population	Adjustments	Cases/controls	Never	Ever	Low (OR, 95%CIs)	Medium (OR, 95%CIs)	High (OR, 95%CIs)
Overall	Model C	2347/6871	Reference	0.72(0.65 to 0.80)	0.61(0.53 to 0.70)	0.64(0.55 to 0.74)	0.99(0.86 to 1.15)
Females	Model C	545/2979	Reference	0.65(0.53 to 0.80)	0.58(0.46 to 0.75)	0.54(0.41 to 0.71)	0.99(0.74 to 1.31)
Males	Model C	1802/3892	Reference	0.76(0.67 to 0.86)	0.63(0.53 to 0.74)	0.69(0.58 to 0.83)	1.01(0.85 to 1.20)
Current smokers	Model C	897/1519	Reference	0.90(0.75 to 1.09)	0.70(0.54 to 0.91)	0.71(0.53 to 0.94)	1.36(1.06 to 1.75)
Former smokers	Model C	930/2568	Reference	0.68(0.57 to 0.80)	0.66(0.53 to 0.81)	0.69(0.55 to 0.86)	0.70(0.54 to 0.90)
Never smokers	Model C	520/2784	Reference	0.66(0.54 to 0.82)	0.51(0.39 to 0.66)	0.52(0.38 to 0.69)	1.17(0.89 to 1.53)

Open in a new tab

Model C: adjusted for study center, age, gender, smoking, alcohol, coffee, juice, soft drink, milk, fruit.

Tertiles tea: low (≤120 ml/day), medium (>120 - ≤300 ml/day), high (>305ml/day).

Bold numbers indicate statistically significant results.

Stratification by gender and smoking status

Tea consumption was a protective factor for BC in both male and female subgroups. The OR based on overall tea intake was slightly lower for females (OR = 0.65, 95% CI = 0.53-0.80) than for males (OR = 0.76, 95% CI = 0.67-0.86). Among the types of tea consumed by women, herbal teas were significantly associated with a lower risk of BC (OR = 0.24, 95% CI = 0.06-0.70). (Supplementary Table 2).

When stratified by smoking status, a similar association for tea consumption was noted among former smokers (OR = 0.68, 95% CI = 0.57-0.80) and never-smokers (OR = 0.66, 95% CI = 0.54-0.82). For people with a history of smoking, low and medium tea consumption was associated with a lower risk of BC.

Stratification by BC subtypes

Stratified results for BC stage groups (i.e., NMIBC and MIBC) showed that tea consumption was positively associated with overall NMIBC risk (OR = 2.36, 95% CI = 1.63-3.42) and MIBC risk (OR = 2.19, 95% CI = 1.39-3.47). While medium tea consumption was inversely associated with lower NMIBC risk (OR = 0.66, 95% CI = 0.52-0.85) and lower MIBC risk (OR = 0.75, 95% CI = 0.70-0.80), high tea consumption was associated with higher NMIBC risk (OR = 5.34, 95% CI = 3.90-7.31) and higher MIBC risk (OR = 5.27, 95% CI = 3.87-7.17).

Based on these results, it appears to be a contrary to the previous conclusion that higher tea consumption is associated with a lower BC risk. Therefore, we performed a stratified analysis of patients without information on NMIBC or MIBC, and the results showed that tea consumption may lower the risk for all other cases (OR = 0.60, 95%CI = 0.54-0.67) (Table 3).

Table 3.

Odds ratios and 95% confidence intervals for the association between bladder cancer and tea consumption by bladder cancer subtypes

Population	Adjustments	Cases/controls	Never	Ever	Low (OR, 95%CIs)	Medium (OR, 95%CIs)	High (OR, 95%CIs)
NIMBC
Overall	Model C	178/6871	Reference	2.36(1.63 to 3.42)	0.88(0.57 to 1.36)	0.66(0.52 to 0.85)	5.34(3.90 to 7.31)
Females	Model C	31/2979	Reference	1.38(0.63 to 3.01)	0.86(0.36 to 2.08)	0.41(0.28 to 0.61)	3.85(1.82 to 8.12)
Males	Model C	147/3892	Reference	2.63(1.73 to 4.01)	0.88(0.53 to 1.45)	0.79(0.58 to 1.09)	5.39(3.81 to 7.63)
Current smokers	Model C	77/1519	Reference	4.28(2.28 to 8.05)	1.56(0.88 to 2.76)	2.15(1.30 to 3.57)	9.18(5.92 to 14.22)
Former smokers	Model C	38/2568	Reference	1.60(0.73 to 3.54)	0.02(0.02 to 0.02)	0.15(0.14 to 0.16)	4.73(2.20 to 10.16)
Never smokers	Model C	63/2784	Reference	1.44(0.82 to 2.52)	0.75(0.36 to 1.60)	0.21(0.18 to 0.25)	3.84(2.18 to 6.77)
MIBC
Overall	Model C	174/6871	Reference	2.19(1.39 to 3.47)	0.93(0.80 to 1.09)	0.75(0.70 to 0.80)	5.27(3.87 to 7.17)
Females	Model C	35/2979	Reference	1.84(0.73 to 4.67)	0.74(0.54 to 1.01)	0.23(0.22 to 0.25)	3.38(1.72 to 6.64)
Males	Model C	139/3892	Reference	2.89(1.69 to 4.97)	1.25(0.78 to 2.01)	1.16(0.77 to 1.77)	6.53(4.54 to 9.41)
Current smokers	Model C	73/1519	Reference	3.71(1.66 to 8.31)	2.10(1.52 to 2.88)	0.40(0.39 to 0.41)	9.15(5.76 to 14.53)
Former smokers	Model C	30/2568	Reference	-	-	-	-
Never smokers	Model C	71/2784	Reference	1.30(0.72 to 2.36)	0.49(0.20 to 1.18)	0.37(0.12 to 1.15)	3.45(1.82 to 6.53)
NEITHER NIMBC NOR MIBC
Overall	Model C	1995/6871	Reference	0.60(0.54 to 0.67)	0.60(0.52 to 0.69)	0.64(0.55 to 0.74)	0.56(0.47 to 0.66)
Females	Model C	479/2979	Reference	0.59(0.48 to 0.73)	0.58(0.45 to 0.75)	0.56(0.42 to 0.74)	0.67(0.48 to 0.93)
Males	Model C	1516/3892	Reference	0.62(0.54 to 0.70)	0.62(0.52 to 0.74)	0.68(0.56 to 0.82)	0.54(0.44 to 0.66)
Current smokers	Model C	747/1519	Reference	0.66(0.54 to 0.81)	0.60(0.46 to 0.79)	0.65(0.48 to 0.87)	0.75(0.56 to 0.99)
Former smokers	Model C	862/2568	Reference	0.55(0.47 to 0.65)	0.58(0.47 to 0.71)	0.61(0.49 to 0.77)	0.42(0.32 to 0.56)
Never smokers	Model C	386/2784	Reference	0.53(0.42 to 0.67)	0.49(0.36 to 0.65)	0.54(0.40 to 0.74)	0.61(0.43 to 0.86)

Open in a new tab

NMIBC: non-muscle-invasive bladder cancer; MIBC: muscle-invasive bladder cancer; NEITHER NIMBC NOR MIBC:bladder cancer patients with missing bladder cancer staging information

Model C: adjusted for study center, age, gender, smoking, alcohol, coffee, fruit juice, soft drink, milk, fruit

Tertiles tea: low (≤120 ml/day), medium (>120 - ≤300 ml/day), high (>300ml/day)

Bold numbers indicate statistically significant results.

Dose-response analysis

The dose-response analysis revealed a significantly lower risk of BC with low and medium tea consumption in the overall population, females, males, current smokers, and never smokers (Figure 1.A–D, F).

Odds ratios are indicated by solid lines and 95% CIs by shaded areas. Reference point is 0 for tea consumption, with knots placed at 5th, 27.5th, 50th, 72.5th, and 95th centiles of tea consumption. All models were adjusted for model C with adjustments of study center, age, gender, smoking, alcohol, coffee, juice, soft drink, milk and fruit.

In the overall population, a significantly lower risk of BC with increased tea consumption was observed until around 1.56 cups of tea. However, the trend showed a slight increase afterward, with a significantly increased risk over around 5.67 cups/day. This nonlinear trend is also reflected in females, males, current smokers, and never smokers.

Discussion

This study showed a significant association between tea consumption within the appropriate limits and a reduced risk of BC. Additionally, a statistically significantly lower BC risk was found among females, males, former smokers, and never-smokers through stratification by gender and smoking status. Green and black tea consumption was not associated with BC risk. However, females and former smokers also showed an association between herbal tea consumption and BC risk.

In the present study, green tea consumption was unrelated to BC risk. This is in line with three previously conducted observational studies, which also, showed no association between green tea consumption and BC risk ^48,49. In contrast, another study found a higher BC risk for females who consumed five to nine cups of green tea daily ⁵⁰. Moreover, one study identified an inverse association between green tea consumption and BC risk, if participants consumed 14 cups daily or more ⁵¹. Wang et al ⁵¹also identified distinct genetic variants of UDP-glucuronosyltransferases (metabolic enzymes) that are associated with BC risk. It has been suggested that these genetic variants may modulate the activation and degradation of nutrients differently, including tea. Therefore, the inconsistent effects of green tea consumption on BC risk could be a consequence of specific genes. Other reasons that could explain the discrepancies between the different studies are as follows: i) In vitro studies suggest that a high concentration of the green tea polyphenol EGCG is needed to affect the correct disease-related cellular processes. Owing to the low bioavailability (i.e., the amount of EGCG appearing in the blood and tissue or systemic circulation after drinking green tea) and low pharmacokinetic properties of EGCG (i.e., the activity of EGCG in the body over a period of time) a high or moderate concentration is mostly not achieved in animals or humans. However, the most appropriate dose is not known yet ^52,53. Nonetheless, very high doses of green tea (e.g., >10 cups per day) might have a protective effect on BC, since very high green tea consumption decreased the risk of other cancer types in previous studies ^54–57. ii) Different pH conditions in the stomach and intestinal tract, digestive enzymes, administration conditions or nutritional environment can influence the bioavailability of EGCG and cause inconsistent results between studies ^52,53. The exact processes involved are still under investigation. iii) The amount of green tea leaves in the cup can differ between subjects as well as the frequency of renewing the same tea in a pot ⁵⁸, the type of green tea or its environmental factors ¹².

Overall, black tea consumption was not associated with BC risk. Seven observational studies reached the same conclusion and showed no association between black tea consumption and the risk of BC ^{48–50,59–62}, whereas one study found that black tea lowered the BC risk ⁵¹. Although the anticancer properties of black tea are known, green tea (polyphenols) has been more extensively studied than black tea (polyphenols). The reason might be the higher amounts of anticancer polyphenols and especially the antioxidant properties of green tea compared to black tea ¹². Besides the lesser anticancer characteristics of black tea ¹², its low bioavailability ⁶³ could be an additional factor that explains the null effect between black tea consumption and BC in most of the studies. Additionally, our subgroup analysis indicated a higher risk for females who consumed a medium amount of black tea. These findings are not related to previous studies or the literature. More research on this topic is needed.

Herbal tea consumption was associated with a lower risk of BC in our analyses. Herbal tea is made by infusing water from various plants other than the caffeine-containing tea plant (Camellia sinensis)⁶⁴. These herbal teas are typically made from plant parts such as rhizomes (licorice), stems (cinnamon), leaves (peppermint), and inflorescences (chamomile) through infusion or decoction. Unlike the Camellia sinensis containing methylxanthines like caffeine, these plant-based preparations exhibit unique phytochemical profiles rich in secondary metabolites, including polyphenols, terpenoids, and volatile aromatic compounds¹⁸. Herbal infusions provided a better medium for water-soluble phytochemicals and probably became more efficient ⁶⁵. As a form of traditional medicines, herbal medicines are beneficial in some areas of clinical and preventative health ¹⁸. Current research on the most commonly mentioned herbal teas is related to phytochemistry, pharmacology, food science, and nutrition. For example, honeysuckle tea has traditionally been used to treat certain infectious diseases, and its crude aqueous extract has been shown to have anti-inflammatory effects on A549 cells⁶⁶. In addition, some studies have suggested that due to the presence of different phenolics in the aqueous tea extracts, these herbs may have the potential to act as natural anticancer agents and have high antioxidant activity^64,67. While this study provides novel observational evidence for the association between herbal tea consumption and BC risk, several important limitations warrant caution in interpretation. The heterogeneous nature of herbal tea compositions precludes drawing definitive conclusions about specific bioactive components. Our analysis treated herbal tea as a unified exposure category, which inherently obscures the pharmacological contributions of individual herbs, such as chrysanthemum, that may differentially influence BC. We explicitly clarify that the observed associations do not establish causality and remain susceptible to residual confounding from unmeasured lifestyle factors. The current findings should thus be interpreted as hypothesis-generating evidence, which requires mechanistic validation. Particular emphasis should be placed on isolating individual herbal constituents through experimental models that permit causal inference. Therefore, future studies should specify herbal tea types more precisely in dietary questionnaires. This will enable deeper investigations into their biological mechanisms and clarify their potential for clinical therapy and health prevention.

Our results overall showed that tea derived from Camellia sinensis had no significant association with BC risk, whereas herbal tea consumption was inversely associated with BC incidence. The findings of nine studies concur with our study, which demonstrate no statistically significant association between Camellia sinensis-derived tea consumption and BC risk^59,68–75.Furthermore, one study suggested that herbal tea consumption may have protective effects against BC⁵¹.

Stratification by smoking status and gender showed similar findings to the total population in which tea consumption was associated with lower BC risk. This result is not in line with previous studies that have shown different associations between different smoking statuses. Contrary results were demonstrated by Woolcott et al. ⁷³, who observed no association between either never smokers or smokers and the risk of BC, and by Clavel and Cordier et al. ⁷⁶, who found a lower BC risk with higher tea consumption in current smoking females, but not in males. However, an additional study reported a lower BC risk among current smoking males who drink 3-4 cups of green tea per day. No association was found between tea consumption, BC risk, and never or former smokers ⁷⁷. The most recent study described variation in BC recurrence based on green tea consumption and smoking status. More than five cups per day significantly lowered the risk of BC recurrence in never smokers, but not in ever smokers. In addition, the study observed significantly lower human antigen R (RNA-binding protein) expression in never smokers than in ever smokers. It is hypothesized that high green tea consumption down-regulates human antigen R in never smokers, which regulates various cancer-related molecules. The exact underlying mechanisms cannot be explained yet ⁷⁸.

Our dose-response analysis also observed that tea consumption within the appropriate range lowered the risk of BC. This aligns with a meta-analysis that identified a lower BC risk in Western countries. Since the majority of our population was derived from Western countries as well, these findings support ours ²³. In contrast, another meta-analysis reported no association between tea consumption and the risk of BC ⁷⁹. However, the explanation for these results remains unclear. Hence, further studies on the dose-response relationships between tea consumption and BC risk are warranted.

Among the strengths of the BLEND study is its large sample size, allowing it to perform detailed analyses with sufficient statistical power to detect smaller effects, the study also has some limitations. First, this study analyzed three common and well-documented tea types in the BLEND database, including black tea, green tea, and herbal tea. However, data on tea consumption were available for only 14.5% of cases and 11.7% of controls which may introduce selection bias. The limited data on specific tea types prevented a more detailed analysis. Further research with larger sample sizes and more comprehensive information on tea types is required. Second, it is often suggested that case-control studies are limited in showing causal relation owing to the potential recall bias of case-control studies. This might have led to the lower reliability of the results compared to those of the cohort studies. These biases decrease the internal validity of the investigation and should be carefully addressed and reduced in the study design. However, although this issue has been addressed and analyzed for its consequences in many epidemiological and methodological papers ^80–83, no clear answer on the magnitude of the effect of this specific type of bias could be drawn. Thirdly, information on other potential risk factors was limited, such as socioeconomic status, physical activity, body mass index, (work-related) exposure to carcinogens and sources of arsenic (e.g., drinking water or pesticides). Fourthly, although the status of smoking was taken into account in our analysis, the adjustment for smoking might still be imperfect due to differences in smoking practices (e.g., depth of inhalation or amount of inhalation), or differences in types of smoke exposure. The intensity and duration of smoking exhibit distinct pathogenic effects on BC. Notably, emerging evidence demonstrates that under equivalent cumulative pack-year exposure, prolonged low-intensity smoking confers a greater oncogenic risk than transient high-intensity consumption⁸⁴. This observation critically undermines the validity of using pack-years as a standalone risk quantification metric. To address this methodological limitation, future research protocols must incorporate more granular smoking exposure data to account for potential confounding factors. In addition, since smoking is perceived as a socially undesirable behavior, the use of self-reported questionnaires for smoking status, duration, and intensity might have led to the underreporting of the actual smoking habits. Finally, the present study sample consisted mostly of Caucasians, which may limit the generalizability of our results to other racial/ethnic populations or geographic regions.

Furthermore, with the current rapid development and widespread application of artificial intelligence (AI) in the medical field, AI subsets represented by machine learning (ML) and deep learning (DL) technologies have been extensively studied in areas such as risk factors, diagnosis, prognosis assessment, and outcome prediction for BC^85–87. Future studies are expected to leverage AI to automatically gather extensive global datasets and advanced algorithms, thereby facilitating a deeper understanding of the association between tea intake levels and bladder cancer risk⁸⁸.

Conclusion

This study showed a significantly lower risk of BC with tea consumption. Stratified analyses based on gender and smoking status yielded similar results. Further stratified analyses of tea types revealed that tea consumption derived from Camellia sinensis had no significant association with BC risk, whereas herbal tea consumption was inversely associated with BC incidence. Further studies are required to clarify the mechanisms underlying for these findings.

Supplementary Material

Supplementary materials

NIHMS2107012-supplement-Supplementary_materials.docx^{(44.1KB, docx)}

Acknowledgments

We gratefully acknowledge all principal investigators for their willingness to participate in this jointed project.

Funding

MPAZ was supported by the World Cancer Research Fund International (WCRF 2012/590), and European Commission (FP7-PEOPLE-618308). EYWY was supported by the National Natural Science Foundation of China (82204033), Natural Science Foundation of Jiangsu Province (BK20220826), The Scientific Research Project for Health Commission of Anhui Province (AHWJ2023A20172; AHWJ2023BAa20055), Fundamental Research Funds for the Central Universities of China (2242022R10062/3225002202A1), Medical Foundation of Southeast University (4060692202/021), and Zhishan Young Scholar Award at the Southeast University (2242023R40031), JP was partially supported by Italian Ministry of Health-Ricerca corrente (no grant number provided), the Italian Association for Cancer Research (AIRC) Foundation for supporting data collection of Italian studies. The funder had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the article; and decision to submit the article for publication.

Authors’ Disclosures

Z.-F. Zhang reports grants from NIH during the conduct of the study. No disclosures were reported by the other authors.

Footnotes

Conflict of interest

All the authors declare that they have no conflicts of interest.

The authors declare no potential conflicts of interest

Ethical Approval

Each participating study has been approved by the local ethic committee.

Data Availability

The data that support the findings of this study are available on reasonable request pending approval from the corresponding author. The data are not publicly available owing to their containing information that could compromise the privacy of research participants.

References

1.Cumberbatch MGK, Noon AP. Epidemiology, aetiology and screening of bladder cancer. Transl Androl Urol. Feb 2019;8(1):5–11. doi: 10.21037/tau.2018.09.11 [DOI] [PMC free article] [PubMed] [Google Scholar]
2.Antoni S, Ferlay J, Soerjomataram I, Znaor A, Jemal A, Bray F. Bladder Cancer Incidence and Mortality: A Global Overview and Recent Trends. Eur Urol. Jan 2017;71(1):96–108. doi: 10.1016/j.eururo.2016.06.010 [DOI] [PubMed] [Google Scholar]
3.Mossanen M, Gore JL. The burden of bladder cancer care: direct and indirect costs. Curr Opin Urol. Sep 2014;24(5):487–91. doi: 10.1097/mou.0000000000000078 [DOI] [PubMed] [Google Scholar]
4.Leal J, Luengo-Fernandez R, Sullivan R, Witjes JA. Economic Burden of Bladder Cancer Across the European Union. Eur Urol. Mar 2016;69(3):438–47. doi: 10.1016/j.eururo.2015.10.024 [DOI] [PubMed] [Google Scholar]
5.Salehiniya H, Mohammadian-Hafshejani A, Borujeni NN, et al. Essentials of bladder cancer worldwide: incidence, mortality rate and risk factors. Biomedical Research and Therapy. 2017;4(9)doi: 10.15419/bmrat.v4i9.371 [DOI] [Google Scholar]
6.Cumberbatch MGK, Jubber I, Black PC, et al. Epidemiology of Bladder Cancer: A Systematic Review and Contemporary Update of Risk Factors in 2018. Eur Urol. Dec 2018;74(6):784–795. doi: 10.1016/j.eururo.2018.09.001 [DOI] [PubMed] [Google Scholar]
7.Wong MCS, Fung FDH, Leung C, Cheung WWL, Goggins WB, Ng CF. The global epidemiology of bladder cancer: a joinpoint regression analysis of its incidence and mortality trends and projection. Sci Rep. Jan 18 2018;8(1):1129. doi: 10.1038/s41598-018-19199-z [DOI] [PMC free article] [PubMed] [Google Scholar]
8.Kwan ML, Garren B, Nielsen ME, Tang L. Lifestyle and nutritional modifiable factors in the prevention and treatment of bladder cancer. Urol Oncol. Jun 2019;37(6):380–386. doi: 10.1016/j.urolonc.2018.03.019 [DOI] [PMC free article] [PubMed] [Google Scholar]
9.Barone B, Finati M, Cinelli F, et al. Bladder Cancer and Risk Factors: Data from a Multi-Institutional Long-Term Analysis on Cardiovascular Disease and Cancer Incidence. J Pers Med. Mar 13 2023;13(3)doi: 10.3390/jpm13030512 [DOI] [PMC free article] [PubMed] [Google Scholar]
10.Vieux F, Maillot M, Rehm CD, Drewnowski A. Tea Consumption Patterns in Relation to Diet Quality among Children and Adults in the United States: Analyses of NHANES 2011-2016 Data. Nutrients. Nov 3 2019;11(11)doi: 10.3390/nu11112635 [DOI] [PMC free article] [PubMed] [Google Scholar]
11.Prasanth MI, Sivamaruthi BS, Chaiyasut C, Tencomnao T. A Review of the Role of Green Tea (Camellia sinensis) in Antiphotoaging, Stress Resistance, Neuroprotection, and Autophagy. Nutrients. Feb 23 2019;11(2)doi: 10.3390/nu11020474 [DOI] [PMC free article] [PubMed] [Google Scholar]
12.Musial C, Kuban-Jankowska A, Gorska-Ponikowska M. Beneficial Properties of Green Tea Catechins. Int J Mol Sci. Mar 4 2020;21(5)doi: 10.3390/ijms21051744 [DOI] [PMC free article] [PubMed] [Google Scholar]
13.O’Neill EJ, Termini D, Albano A, Tsiani E. Anti-Cancer Properties of Theaflavins. Molecules. Feb 13 2021;26(4)doi: 10.3390/molecules26040987 [DOI] [PMC free article] [PubMed] [Google Scholar]
14.Beltz LA, Bayer DK, Moss AL, Simet IM. Mechanisms of cancer prevention by green and black tea polyphenols. Anticancer Agents Med Chem. Sep 2006;6(5):389–406. doi: 10.2174/187152006778226468 [DOI] [PubMed] [Google Scholar]
15.Miyata Y, Matsuo T, Araki K, et al. Anticancer Effects of Green Tea and the Underlying Molecular Mechanisms in Bladder Cancer. Medicines (Basel). Aug 10 2018;5(3)doi: 10.3390/medicines5030087 [DOI] [PMC free article] [PubMed] [Google Scholar]
16.Miyata Y, Shida Y, Hakariya T, Sakai H. Anti-Cancer Effects of Green Tea Polyphenols Against Prostate Cancer. Molecules. Jan 7 2019;24(1)doi: 10.3390/molecules24010193 [DOI] [PMC free article] [PubMed] [Google Scholar]
17.Zhao J, Blayney A, Liu X, et al. EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction. Nat Commun. Feb 12 2021;12(1):986. doi: 10.1038/s41467-021-21258-5 [DOI] [PMC free article] [PubMed] [Google Scholar]
18.Poswal FS, Russell G, Mackonochie M, MacLennan E, Adukwu EC, Rolfe V. Herbal Teas and their Health Benefits: A Scoping Review. Plant Foods Hum Nutr. Sep 2019;74(3):266–276. doi: 10.1007/s11130-019-00750-w [DOI] [PubMed] [Google Scholar]
19.Khan N, Mukhtar H. Tea Polyphenols in Promotion of Human Health. Nutrients. Dec 25 2018;11(1)doi: 10.3390/nu11010039 [DOI] [PMC free article] [PubMed] [Google Scholar]
20.Huang Y, Chen H, Zhou L, et al. Association between green tea intake and risk of gastric cancer: a systematic review and dose-response meta-analysis of observational studies. Public Health Nutr. Dec 2017;20(17):3183–3192. doi: 10.1017/s1368980017002208 [DOI] [PMC free article] [PubMed] [Google Scholar]
21.Gianfredi V, Nucci D, Abalsamo A, et al. Green Tea Consumption and Risk of Breast Cancer and Recurrence-A Systematic Review and Meta-Analysis of Observational Studies. Nutrients. Dec 3 2018;10(12)doi: 10.3390/nu10121886 [DOI] [PMC free article] [PubMed] [Google Scholar]
22.Wu S, Li F, Huang X, et al. The association of tea consumption with bladder cancer risk: a meta-analysis. Asia Pac J Clin Nutr. 2013;22(1):128–37. doi: 10.6133/apjcn.2013.22.1.15 [DOI] [PubMed] [Google Scholar]
23.Zhang YF, Xu Q, Lu J, et al. Tea consumption and the incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Eur J Cancer Prev. Jul 2015;24(4):353–62. doi: 10.1097/cej.0000000000000094 [DOI] [PubMed] [Google Scholar]
24.Qin J, Xie B, Mao Q, Kong D, Lin Y, Zheng X. Tea consumption and risk of bladder cancer: a meta-analysis. World J Surg Oncol. Aug 25 2012;10:172. doi: 10.1186/1477-7819-10-172 [DOI] [PMC free article] [PubMed] [Google Scholar]
25.Bai Y, Yuan H, Li J, Tang Y, Pu C, Han P. Relationship between bladder cancer and total fluid intake: a meta-analysis of epidemiological evidence. World J Surg Oncol. Jul 17 2014;12:223. doi: 10.1186/1477-7819-12-223 [DOI] [PMC free article] [PubMed] [Google Scholar]
26.Goossens ME, Isa F, Brinkman M, et al. International pooled study on diet and bladder cancer: the bladder cancer, epidemiology and nutritional determinants (BLEND) study: design and baseline characteristics. Arch Public Health. 2016;74:30. doi: 10.1186/s13690-016-0140-1 [DOI] [PMC free article] [PubMed] [Google Scholar]
27.Kellen E, Zeegers M, Paulussen A, Van Dongen M, Buntinx F. Fruit consumption reduces the effect of smoking on bladder cancer risk. The Belgian case control study on bladder cancer. Int J Cancer. May 15 2006;118(10):2572–8. doi: 10.1002/ijc.21714 [DOI] [PubMed] [Google Scholar]
28.Gaertner RR, Trpeski L, Johnson KC. A case-control study of occupational risk factors for bladder cancer in Canada. Cancer Causes Control. Dec 2004;15(10):1007–19. doi: 10.1007/s10552-004-1448-7 [DOI] [PubMed] [Google Scholar]
29.Hemelt M, Hu Z, Zhong Z, et al. Fluid intake and the risk of bladder cancer: results from the South and East China case-control study on bladder cancer. Int J Cancer. Aug 1 2010;127(3):638–45. doi: 10.1002/ijc.25084 [DOI] [PubMed] [Google Scholar]
30.Lu CM, Lan SJ, Lee YH, Huang JK, Huang CH, Hsieh CC. Tea consumption: fluid intake and bladder cancer risk in Southern Taiwan. Urology. Nov 1999;54(5):823–8. doi: 10.1016/s0090-4295(99)00281-2 [DOI] [PubMed] [Google Scholar]
31.Pohlabeln H, Jöckel KH, Bolm-Audorff U. Non-occupational risk factors for cancer of the lower urinary tract in Germany. Eur J Epidemiol. May 1999;15(5):411–9. doi: 10.1023/a:1007595809278 [DOI] [PubMed] [Google Scholar]
32.D’Avanzo B, La Vecchia C, Negri E, Decarli A, Benichou J. Attributable risks for bladder cancer in northern Italy. Ann Epidemiol. Nov 1995;5(6):427–31. doi: 10.1016/1047-2797(95)00057-7 [DOI] [PubMed] [Google Scholar]
33.Shen M, Hung RJ, Brennan P, et al. Polymorphisms of the DNA repair genes XRCC1, XRCC3, XPD, interaction with environmental exposures, and bladder cancer risk in a case-control study in northern Italy. Cancer Epidemiol Biomarkers Prev. Nov 2003;12(11 Pt 1):1234–40. [PubMed] [Google Scholar]
34.Polesel J, Bosetti C, di Maso M, et al. Duration and intensity of tobacco smoking and the risk of papillary and non-papillary transitional cell carcinoma of the bladder. Cancer Causes Control. Sep 2014;25(9):1151–8. doi: 10.1007/s10552-014-0416-0 [DOI] [PubMed] [Google Scholar]
35.Steineck G, Hagman U, Gerhardsson M, Norell SE. Vitamin A supplements, fried foods, fat and urothelial cancer. A case-referent study in Stockholm in 1985-87. Int J Cancer. Jun 15 1990;45(6):1006–11. doi: 10.1002/ijc.2910450604 [DOI] [PubMed] [Google Scholar]
36.Jiang X, Castelao JE, Groshen S, et al. Alcohol consumption and risk of bladder cancer in Los Angeles County. Int J Cancer. Aug 15 2007;121(4):839–45. doi: 10.1002/ijc.22743 [DOI] [PubMed] [Google Scholar]
37.Tang L, Zirpoli GR, Guru K, et al. Consumption of raw cruciferous vegetables is inversely associated with bladder cancer risk. Cancer Epidemiol Biomarkers Prev. Apr 2008;17(4):938–44. doi: 10.1158/1055-9965.Epi-07-2502 [DOI] [PubMed] [Google Scholar]
38.Mettlin C, Graham S. Dietary risk factors in human bladder cancer. Am J Epidemiol. Sep 1979;110(3):255–63. doi: 10.1093/oxfordjournals.aje.a112810 [DOI] [PubMed] [Google Scholar]
39.Brinkman MT, Karagas MR, Zens MS, Schned A, Reulen RC, Zeegers MP. Minerals and vitamins and the risk of bladder cancer: results from the New Hampshire Study. Cancer Causes Control. Apr 2010;21(4):609–19. doi: 10.1007/s10552-009-9490-0 [DOI] [PMC free article] [PubMed] [Google Scholar]
40.Cao W, Cai L, Rao JY, et al. Tobacco smoking, GSTP1 polymorphism, and bladder carcinoma. Cancer. Dec 1 2005;104(11):2400–8. doi: 10.1002/cncr.21446 [DOI] [PubMed] [Google Scholar]
41.Taylor JA, Umbach DM, Stephens E, et al. The role of N-acetylation polymorphisms in smoking-associated bladder cancer: evidence of a gene-gene-exposure three-way interaction. Cancer Res. Aug 15 1998;58(16):3603–10. [PubMed] [Google Scholar]
42.Porru S, Pavanello S, Carta A, et al. Complex relationships between occupation, environment, DNA adducts, genetic polymorphisms and bladder cancer in a case-control study using a structural equation modeling. PLoS One. 2014;9(4):e94566. doi: 10.1371/journal.pone.0094566 [DOI] [PMC free article] [PubMed] [Google Scholar]
43.Randi G, Pelucchi C, Negri E, et al. Family history of urogenital cancers in patients with bladder, renal cell and prostate cancers. Int J Cancer. Dec 15 2007;121(12):2748–52. doi: 10.1002/ijc.23037 [DOI] [PubMed] [Google Scholar]
44.Unwin I MA, Ireland J. Eurocode 2: European Food information Resource. http://archives.foodcomp.info/eurofir/Downloads/Documents/Deliverables2006/Eurocode2%20Position%20Paper%20D167.pdf.
45.Tabachnick BG, Fidell LS. Using multivariate statistics (5th ed.). Pearson/Allyn & Bacon; 2007. [Google Scholar]
46.Azur MJ, Stuart EA, Frangakis C, Leaf PJ. Multiple imputation by chained equations: what is it and how does it work? Int J Methods Psychiatr Res. Mar 2011;20(1):40–9. doi: 10.1002/mpr.329 [DOI] [PMC free article] [PubMed] [Google Scholar]
47.STATA. mi impute chained — Impute missing values using chained equations https://www.stata.com/manuals/mimiimputechained.pdf.
48.Chyou PH, Nomura AM, Stemmermann GN. A prospective study of diet, smoking, and lower urinary tract cancer. Ann Epidemiol. May 1993;3(3):211–6. doi: 10.1016/1047-2797(93)90021-u [DOI] [PubMed] [Google Scholar]
49.Nagano J, Kono S, Preston DL, et al. Bladder-cancer incidence in relation to vegetable and fruit consumption: a prospective study of atomic-bomb survivors. Int J Cancer. Apr 1 2000;86(1):132–8. doi: 10.1002/(sici)1097-0215(20000401)86.1<132::aid-ijc21>3.0.co;2-m [DOI] [PubMed] [Google Scholar]
50.Wakai K, Hirose K, Takezaki T, et al. Foods and beverages in relation to urothelial cancer: case-control study in Japan. Int J Urol. Jan 2004;11(1):11–9. doi: 10.1111/j.1442-2042.2004.00740.x [DOI] [PubMed] [Google Scholar]
51.Wang J, Wu X, Kamat A, Barton Grossman H, Dinney CP, Lin J. Fluid intake, genetic variants of UDP-glucuronosyltransferases, and bladder cancer risk. Br J Cancer. Jun 11 2013;108(11):2372–80. doi: 10.1038/bjc.2013.190 [DOI] [PMC free article] [PubMed] [Google Scholar]
52.Cai ZY, Li XM, Liang JP, et al. Bioavailability of Tea Catechins and Its Improvement. Molecules. Sep 13 2018;23(9)doi: 10.3390/molecules23092346 [DOI] [PMC free article] [PubMed] [Google Scholar]
53.Andreu-Fernández V, Almeida Toledano L, Pizarro N, et al. Bioavailability of Epigallocatechin Gallate Administered With Different Nutritional Strategies in Healthy Volunteers. Antioxidants (Basel). May 19 2020;9(5)doi: 10.3390/antiox9050440 [DOI] [PMC free article] [PubMed] [Google Scholar]
54.Imai K, Suga K, Nakachi K. Cancer-preventive effects of drinking green tea among a Japanese population. Prev Med. Nov-Dec 1997;26(6):769–75. doi: 10.1006/pmed.1997.0242 [DOI] [PubMed] [Google Scholar]
55.Nakachi K, Matsuyama S, Miyake S, Suganuma M, Imai K. Preventive effects of drinking green tea on cancer and cardiovascular disease: epidemiological evidence for multiple targeting prevention. Biofactors. 2000;13(1–4):49–54. doi: 10.1002/biof.5520130109 [DOI] [PubMed] [Google Scholar]
56.Kono S, Ikeda M, Tokudome S, Kuratsune M. A case-control study of gastric cancer and diet in northern Kyushu, Japan. Jpn J Cancer Res. Oct 1988;79(10):1067–74. doi: 10.1111/j.1349-7006.1988.tb01528.x [DOI] [PMC free article] [PubMed] [Google Scholar]
57.Inoue M, Tajima K, Hirose K, et al. Tea and coffee consumption and the risk of digestive tract cancers: data from a comparative case-referent study in Japan. Cancer Causes Control. Mar 1998;9(2):209–16. doi: 10.1023/a:1008890529261 [DOI] [PubMed] [Google Scholar]
58.Nagano J, Kono S, Preston DL, Mabuchi K. A prospective study of green tea consumption and cancer incidence, Hiroshima and Nagasaki (Japan). Cancer Causes Control. Aug 2001;12(6):501–8. doi: 10.1023/a:1011297326696 [DOI] [PubMed] [Google Scholar]
59.Wilkens LR, Kadir MM, Kolonel LN, Nomura AM, Hankin JH. Risk factors for lower urinary tract cancer: the role of total fluid consumption, nitrites and nitrosamines, and selected foods. Cancer Epidemiol Biomarkers Prev. Mar 1996;5(3):161–6. [PubMed] [Google Scholar]
60.Kunze E, Chang-Claude J, Frentzel-Beyme R. Life style and occupational risk factors for bladder cancer in Germany. A case-control study. Cancer. Apr 1 1992;69(7):1776–90. doi: 10.1002/1097-0142(19920401)69:7<1776::aid-cncr2820690721>3.0.co;2-p [DOI] [PubMed] [Google Scholar]
61.Nomura AM, Kolonel LN, Hankin JH, Yoshizawa CN. Dietary factors in cancer of the lower urinary tract. Int J Cancer. May 10 1991;48(2):199–205. doi: 10.1002/ijc.2910480208 [DOI] [PubMed] [Google Scholar]
62.Heilbrun LK, Nomura A, Stemmermann GN. Black tea consumption and cancer risk: a prospective study. Br J Cancer. Oct 1986;54(4):677–83. doi: 10.1038/bjc.1986.226 [DOI] [PMC free article] [PubMed] [Google Scholar]
63.Liu Z, Bruins ME, Ni L, Vincken JP. Green and Black Tea Phenolics: Bioavailability, Transformation by Colonic Microbiota, and Modulation of Colonic Microbiota. J Agric Food Chem. Aug 15 2018;66(32):8469–8477. doi: 10.1021/acs.jafc.8b02233 [DOI] [PubMed] [Google Scholar]
64.Liu Y, Ahmed S, Long C. Ethnobotanical survey of cooling herbal drinks from southern China. J Ethnobiol Ethnomed. Dec 19 2013;9:82. doi: 10.1186/1746-4269-9-82 [DOI] [PMC free article] [PubMed] [Google Scholar]
65.Periche A, Koutsidis G, Escriche I. Composition of antioxidants and amino acids in Stevia leaf infusions. Plant Foods Hum Nutr. Mar 2014;69(1):1–7. doi: 10.1007/s11130-013-0398-1 [DOI] [PubMed] [Google Scholar]
66.Xu Y, Oliverson BG, Simmons DL. Trifunctional inhibition of COX-2 by extracts of Lonicera japonica: direct inhibition, transcriptional and post-transcriptional down regulation. J Ethnopharmacol. May 22 2007;111(3):667–70. doi: 10.1016/j.jep.2007.01.017 [DOI] [PubMed] [Google Scholar]
67.Elansary HO, Mahmoud EA. Egyptian herbal tea infusions’ antioxidants and their antiproliferative and cytotoxic activities against cancer cells. Nat Prod Res. 2015;29(5):474–9. doi: 10.1080/14786419.2014.951354 [DOI] [PubMed] [Google Scholar]
68.Risch HA, Burch JD, Miller AB, Hill GB, Steele R, Howe GR. Dietary factors and the incidence of cancer of the urinary bladder. Am J Epidemiol. Jun 1988;127(6):1179–91. doi: 10.1093/oxfordjournals.aje.a114911 [DOI] [PubMed] [Google Scholar]
69.La Vecchia C, Negri E, Franceschi S, D’Avanzo B, Boyle P. Tea consumption and cancer risk. Nutrition and Cancer. 1992/January/01 1992;17(1):27–31. doi: 10.1080/01635589209514170 [DOI] [PubMed] [Google Scholar]
70.Michaud DS, Spiegelman D, Clinton SK, et al. Fluid intake and the risk of bladder cancer in men. N Engl J Med. May 6 1999;340(18):1390–7. doi: 10.1056/nejm199905063401803 [DOI] [PubMed] [Google Scholar]
71.Bianchi GD, Cerhan JR, Parker AS, et al. Tea consumption and risk of bladder and kidney cancers in a population-based case-control study. Am J Epidemiol. Feb 15 2000;151(4):377–83. doi: 10.1093/oxfordjournals.aje.a010217 [DOI] [PubMed] [Google Scholar]
72.Geoffroy-Perez B, Cordier S. Fluid consumption and the risk of bladder cancer: results of a multicenter case-control study. Int J Cancer. Sep 2001;93(6):880–7. doi: 10.1002/ijc.1411 [DOI] [PubMed] [Google Scholar]
73.Woolcott CG, King WD, Marrett LD. Coffee and tea consumption and cancers of the bladder, colon and rectum. Eur J Cancer Prev. Apr 2002;11(2):137–45. doi: 10.1097/00008469-200204000-00005 [DOI] [PubMed] [Google Scholar]
74.Ros MM, Bas Bueno-de-Mesquita HB, Büchner FL, et al. Fluid intake and the risk of urothelial cell carcinomas in the European Prospective Investigation into Cancer and Nutrition (EPIC). Int J Cancer. Jun 1 2011;128(11):2695–708. doi: 10.1002/ijc.25592 [DOI] [PubMed] [Google Scholar]
75.Bruemmer B, White E, Vaughan TL, Cheney CL. Fluid intake and the incidence of bladder cancer among middle-aged men and women in a three-county area of western Washington. Nutr Cancer. 1997;29(2):163–8. doi: 10.1080/01635589709514619 [DOI] [PubMed] [Google Scholar]
76.Clavel J, Cordier S. Coffee consumption and bladder cancer risk. Int J Cancer. Jan 21 1991;47(2):207–12. doi: 10.1002/ijc.2910470208 [DOI] [PubMed] [Google Scholar]
77.Kurahashi N, Inoue M, Iwasaki M, Sasazuki S, Tsugane S. Coffee, green tea, and caffeine consumption and subsequent risk of bladder cancer in relation to smoking status: a prospective study in Japan. Cancer Sci. Feb 2009;100(2):294–91. doi: 10.1111/j.1349-7006.2008.01027.x [DOI] [PMC free article] [PubMed] [Google Scholar]
78.Yasuda T, Miyata Y, Nakamura Y, et al. High Consumption of Green Tea Suppresses Urinary Tract Recurrence of Urothelial Cancer via Down-regulation of Human Antigen-R Expression in Never Smokers. In Vivo. Jul-Aug 2018;32(4):721–729. doi: 10.21873/invivo.11300 [DOI] [PMC free article] [PubMed] [Google Scholar]
79.Weng H, Zeng XT, Li S, Kwong JS, Liu TZ, Wang XH. Tea Consumption and Risk of Bladder Cancer: A Dose-Response Meta-Analysis. Front Physiol. 2016;7:693. doi: 10.3389/fphys.2016.00693 [DOI] [PMC free article] [PubMed] [Google Scholar]
80.BARRY D Differential recall bias and spurious associations in case/control studies. Statistics in medicine. 1996;15(23):2603–2616. [DOI] [PubMed] [Google Scholar]
81.Barry D, Livingstone V. The investigation and correction of recall bias for an ordinal response in a case-control study. Statistics in medicine. 2006;25(6):965–975. [DOI] [PubMed] [Google Scholar]
82.Chouinard E, Walter S. Recall bias in case-control studies: an empirical analysis and theoretical framework. Journal of clinical epidemiology. 1995;48(2):245–254. [DOI] [PubMed] [Google Scholar]
83.Gefeller O Invited commentary: recall bias in melanoma—much ado about almost nothing? American journal of epidemiology. 2009;169(3):267–270. [DOI] [PubMed] [Google Scholar]
84.van Osch FHM, Vlaanderen J, Jochems SHJ, et al. Modeling the Complex Exposure History of Smoking in Predicting Bladder Cancer: A Pooled Analysis of 15 Case-Control Studies. Epidemiology. May 2019;30(3):458–465. doi: 10.1097/ede.0000000000000964 [DOI] [PMC free article] [PubMed] [Google Scholar]
85.Borhani S, Borhani R, Kajdacsy-Balla A. Artificial intelligence: A promising frontier in bladder cancer diagnosis and outcome prediction. Crit Rev Oncol Hematol. Mar 2022;171:103601. doi: 10.1016/j.critrevonc.2022.103601 [DOI] [PubMed] [Google Scholar]
86.Eun SJ, Kim J, Kim KH. Applications of artificial intelligence in urological setting: a hopeful path to improved care. J Exerc Rehabil. Oct 2021;17(5):308–312. doi: 10.12965/jer.2142596.298 [DOI] [PMC free article] [PubMed] [Google Scholar]
87.Zhanghuang C, Zhang Z, Wang J, et al. Surveillance of prognostic risk factors in patients with SCCB using artificial intelligence: a retrospective study. Sci Rep. May 30 2023;13(1):8727. doi: 10.1038/s41598-023-35761-w [DOI] [PMC free article] [PubMed] [Google Scholar]
88.Ferro M, Falagario UG, Barone B, et al. Artificial Intelligence in the Advanced Diagnosis of Bladder Cancer-Comprehensive Literature Review and Future Advancement. Diagnostics (Basel). Jul 7 2023;13(13)doi: 10.3390/diagnostics13132308 [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary materials

NIHMS2107012-supplement-Supplementary_materials.docx^{(44.1KB, docx)}

Data Availability Statement

[R1] 1.Cumberbatch MGK, Noon AP. Epidemiology, aetiology and screening of bladder cancer. Transl Androl Urol. Feb 2019;8(1):5–11. doi: 10.21037/tau.2018.09.11 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R2] 2.Antoni S, Ferlay J, Soerjomataram I, Znaor A, Jemal A, Bray F. Bladder Cancer Incidence and Mortality: A Global Overview and Recent Trends. Eur Urol. Jan 2017;71(1):96–108. doi: 10.1016/j.eururo.2016.06.010 [DOI] [PubMed] [Google Scholar]

[R3] 3.Mossanen M, Gore JL. The burden of bladder cancer care: direct and indirect costs. Curr Opin Urol. Sep 2014;24(5):487–91. doi: 10.1097/mou.0000000000000078 [DOI] [PubMed] [Google Scholar]

[R4] 4.Leal J, Luengo-Fernandez R, Sullivan R, Witjes JA. Economic Burden of Bladder Cancer Across the European Union. Eur Urol. Mar 2016;69(3):438–47. doi: 10.1016/j.eururo.2015.10.024 [DOI] [PubMed] [Google Scholar]

[R5] 5.Salehiniya H, Mohammadian-Hafshejani A, Borujeni NN, et al. Essentials of bladder cancer worldwide: incidence, mortality rate and risk factors. Biomedical Research and Therapy. 2017;4(9)doi: 10.15419/bmrat.v4i9.371 [DOI] [Google Scholar]

[R6] 6.Cumberbatch MGK, Jubber I, Black PC, et al. Epidemiology of Bladder Cancer: A Systematic Review and Contemporary Update of Risk Factors in 2018. Eur Urol. Dec 2018;74(6):784–795. doi: 10.1016/j.eururo.2018.09.001 [DOI] [PubMed] [Google Scholar]

[R7] 7.Wong MCS, Fung FDH, Leung C, Cheung WWL, Goggins WB, Ng CF. The global epidemiology of bladder cancer: a joinpoint regression analysis of its incidence and mortality trends and projection. Sci Rep. Jan 18 2018;8(1):1129. doi: 10.1038/s41598-018-19199-z [DOI] [PMC free article] [PubMed] [Google Scholar]

[R8] 8.Kwan ML, Garren B, Nielsen ME, Tang L. Lifestyle and nutritional modifiable factors in the prevention and treatment of bladder cancer. Urol Oncol. Jun 2019;37(6):380–386. doi: 10.1016/j.urolonc.2018.03.019 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R9] 9.Barone B, Finati M, Cinelli F, et al. Bladder Cancer and Risk Factors: Data from a Multi-Institutional Long-Term Analysis on Cardiovascular Disease and Cancer Incidence. J Pers Med. Mar 13 2023;13(3)doi: 10.3390/jpm13030512 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R10] 10.Vieux F, Maillot M, Rehm CD, Drewnowski A. Tea Consumption Patterns in Relation to Diet Quality among Children and Adults in the United States: Analyses of NHANES 2011-2016 Data. Nutrients. Nov 3 2019;11(11)doi: 10.3390/nu11112635 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R11] 11.Prasanth MI, Sivamaruthi BS, Chaiyasut C, Tencomnao T. A Review of the Role of Green Tea (Camellia sinensis) in Antiphotoaging, Stress Resistance, Neuroprotection, and Autophagy. Nutrients. Feb 23 2019;11(2)doi: 10.3390/nu11020474 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R12] 12.Musial C, Kuban-Jankowska A, Gorska-Ponikowska M. Beneficial Properties of Green Tea Catechins. Int J Mol Sci. Mar 4 2020;21(5)doi: 10.3390/ijms21051744 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R13] 13.O’Neill EJ, Termini D, Albano A, Tsiani E. Anti-Cancer Properties of Theaflavins. Molecules. Feb 13 2021;26(4)doi: 10.3390/molecules26040987 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R14] 14.Beltz LA, Bayer DK, Moss AL, Simet IM. Mechanisms of cancer prevention by green and black tea polyphenols. Anticancer Agents Med Chem. Sep 2006;6(5):389–406. doi: 10.2174/187152006778226468 [DOI] [PubMed] [Google Scholar]

[R15] 15.Miyata Y, Matsuo T, Araki K, et al. Anticancer Effects of Green Tea and the Underlying Molecular Mechanisms in Bladder Cancer. Medicines (Basel). Aug 10 2018;5(3)doi: 10.3390/medicines5030087 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R16] 16.Miyata Y, Shida Y, Hakariya T, Sakai H. Anti-Cancer Effects of Green Tea Polyphenols Against Prostate Cancer. Molecules. Jan 7 2019;24(1)doi: 10.3390/molecules24010193 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R17] 17.Zhao J, Blayney A, Liu X, et al. EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction. Nat Commun. Feb 12 2021;12(1):986. doi: 10.1038/s41467-021-21258-5 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R18] 18.Poswal FS, Russell G, Mackonochie M, MacLennan E, Adukwu EC, Rolfe V. Herbal Teas and their Health Benefits: A Scoping Review. Plant Foods Hum Nutr. Sep 2019;74(3):266–276. doi: 10.1007/s11130-019-00750-w [DOI] [PubMed] [Google Scholar]

[R19] 19.Khan N, Mukhtar H. Tea Polyphenols in Promotion of Human Health. Nutrients. Dec 25 2018;11(1)doi: 10.3390/nu11010039 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R20] 20.Huang Y, Chen H, Zhou L, et al. Association between green tea intake and risk of gastric cancer: a systematic review and dose-response meta-analysis of observational studies. Public Health Nutr. Dec 2017;20(17):3183–3192. doi: 10.1017/s1368980017002208 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R21] 21.Gianfredi V, Nucci D, Abalsamo A, et al. Green Tea Consumption and Risk of Breast Cancer and Recurrence-A Systematic Review and Meta-Analysis of Observational Studies. Nutrients. Dec 3 2018;10(12)doi: 10.3390/nu10121886 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R22] 22.Wu S, Li F, Huang X, et al. The association of tea consumption with bladder cancer risk: a meta-analysis. Asia Pac J Clin Nutr. 2013;22(1):128–37. doi: 10.6133/apjcn.2013.22.1.15 [DOI] [PubMed] [Google Scholar]

[R23] 23.Zhang YF, Xu Q, Lu J, et al. Tea consumption and the incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Eur J Cancer Prev. Jul 2015;24(4):353–62. doi: 10.1097/cej.0000000000000094 [DOI] [PubMed] [Google Scholar]

[R24] 24.Qin J, Xie B, Mao Q, Kong D, Lin Y, Zheng X. Tea consumption and risk of bladder cancer: a meta-analysis. World J Surg Oncol. Aug 25 2012;10:172. doi: 10.1186/1477-7819-10-172 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R25] 25.Bai Y, Yuan H, Li J, Tang Y, Pu C, Han P. Relationship between bladder cancer and total fluid intake: a meta-analysis of epidemiological evidence. World J Surg Oncol. Jul 17 2014;12:223. doi: 10.1186/1477-7819-12-223 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R26] 26.Goossens ME, Isa F, Brinkman M, et al. International pooled study on diet and bladder cancer: the bladder cancer, epidemiology and nutritional determinants (BLEND) study: design and baseline characteristics. Arch Public Health. 2016;74:30. doi: 10.1186/s13690-016-0140-1 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R27] 27.Kellen E, Zeegers M, Paulussen A, Van Dongen M, Buntinx F. Fruit consumption reduces the effect of smoking on bladder cancer risk. The Belgian case control study on bladder cancer. Int J Cancer. May 15 2006;118(10):2572–8. doi: 10.1002/ijc.21714 [DOI] [PubMed] [Google Scholar]

[R28] 28.Gaertner RR, Trpeski L, Johnson KC. A case-control study of occupational risk factors for bladder cancer in Canada. Cancer Causes Control. Dec 2004;15(10):1007–19. doi: 10.1007/s10552-004-1448-7 [DOI] [PubMed] [Google Scholar]

[R29] 29.Hemelt M, Hu Z, Zhong Z, et al. Fluid intake and the risk of bladder cancer: results from the South and East China case-control study on bladder cancer. Int J Cancer. Aug 1 2010;127(3):638–45. doi: 10.1002/ijc.25084 [DOI] [PubMed] [Google Scholar]

[R30] 30.Lu CM, Lan SJ, Lee YH, Huang JK, Huang CH, Hsieh CC. Tea consumption: fluid intake and bladder cancer risk in Southern Taiwan. Urology. Nov 1999;54(5):823–8. doi: 10.1016/s0090-4295(99)00281-2 [DOI] [PubMed] [Google Scholar]

[R31] 31.Pohlabeln H, Jöckel KH, Bolm-Audorff U. Non-occupational risk factors for cancer of the lower urinary tract in Germany. Eur J Epidemiol. May 1999;15(5):411–9. doi: 10.1023/a:1007595809278 [DOI] [PubMed] [Google Scholar]

[R32] 32.D’Avanzo B, La Vecchia C, Negri E, Decarli A, Benichou J. Attributable risks for bladder cancer in northern Italy. Ann Epidemiol. Nov 1995;5(6):427–31. doi: 10.1016/1047-2797(95)00057-7 [DOI] [PubMed] [Google Scholar]

[R33] 33.Shen M, Hung RJ, Brennan P, et al. Polymorphisms of the DNA repair genes XRCC1, XRCC3, XPD, interaction with environmental exposures, and bladder cancer risk in a case-control study in northern Italy. Cancer Epidemiol Biomarkers Prev. Nov 2003;12(11 Pt 1):1234–40. [PubMed] [Google Scholar]

[R34] 34.Polesel J, Bosetti C, di Maso M, et al. Duration and intensity of tobacco smoking and the risk of papillary and non-papillary transitional cell carcinoma of the bladder. Cancer Causes Control. Sep 2014;25(9):1151–8. doi: 10.1007/s10552-014-0416-0 [DOI] [PubMed] [Google Scholar]

[R35] 35.Steineck G, Hagman U, Gerhardsson M, Norell SE. Vitamin A supplements, fried foods, fat and urothelial cancer. A case-referent study in Stockholm in 1985-87. Int J Cancer. Jun 15 1990;45(6):1006–11. doi: 10.1002/ijc.2910450604 [DOI] [PubMed] [Google Scholar]

[R36] 36.Jiang X, Castelao JE, Groshen S, et al. Alcohol consumption and risk of bladder cancer in Los Angeles County. Int J Cancer. Aug 15 2007;121(4):839–45. doi: 10.1002/ijc.22743 [DOI] [PubMed] [Google Scholar]

[R37] 37.Tang L, Zirpoli GR, Guru K, et al. Consumption of raw cruciferous vegetables is inversely associated with bladder cancer risk. Cancer Epidemiol Biomarkers Prev. Apr 2008;17(4):938–44. doi: 10.1158/1055-9965.Epi-07-2502 [DOI] [PubMed] [Google Scholar]

[R38] 38.Mettlin C, Graham S. Dietary risk factors in human bladder cancer. Am J Epidemiol. Sep 1979;110(3):255–63. doi: 10.1093/oxfordjournals.aje.a112810 [DOI] [PubMed] [Google Scholar]

[R39] 39.Brinkman MT, Karagas MR, Zens MS, Schned A, Reulen RC, Zeegers MP. Minerals and vitamins and the risk of bladder cancer: results from the New Hampshire Study. Cancer Causes Control. Apr 2010;21(4):609–19. doi: 10.1007/s10552-009-9490-0 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R40] 40.Cao W, Cai L, Rao JY, et al. Tobacco smoking, GSTP1 polymorphism, and bladder carcinoma. Cancer. Dec 1 2005;104(11):2400–8. doi: 10.1002/cncr.21446 [DOI] [PubMed] [Google Scholar]

[R41] 41.Taylor JA, Umbach DM, Stephens E, et al. The role of N-acetylation polymorphisms in smoking-associated bladder cancer: evidence of a gene-gene-exposure three-way interaction. Cancer Res. Aug 15 1998;58(16):3603–10. [PubMed] [Google Scholar]

[R42] 42.Porru S, Pavanello S, Carta A, et al. Complex relationships between occupation, environment, DNA adducts, genetic polymorphisms and bladder cancer in a case-control study using a structural equation modeling. PLoS One. 2014;9(4):e94566. doi: 10.1371/journal.pone.0094566 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R43] 43.Randi G, Pelucchi C, Negri E, et al. Family history of urogenital cancers in patients with bladder, renal cell and prostate cancers. Int J Cancer. Dec 15 2007;121(12):2748–52. doi: 10.1002/ijc.23037 [DOI] [PubMed] [Google Scholar]

[R44] 44.Unwin I MA, Ireland J. Eurocode 2: European Food information Resource. http://archives.foodcomp.info/eurofir/Downloads/Documents/Deliverables2006/Eurocode2%20Position%20Paper%20D167.pdf.

[R45] 45.Tabachnick BG, Fidell LS. Using multivariate statistics (5th ed.). Pearson/Allyn & Bacon; 2007. [Google Scholar]

[R46] 46.Azur MJ, Stuart EA, Frangakis C, Leaf PJ. Multiple imputation by chained equations: what is it and how does it work? Int J Methods Psychiatr Res. Mar 2011;20(1):40–9. doi: 10.1002/mpr.329 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R47] 47.STATA. mi impute chained — Impute missing values using chained equations https://www.stata.com/manuals/mimiimputechained.pdf.

[R48] 48.Chyou PH, Nomura AM, Stemmermann GN. A prospective study of diet, smoking, and lower urinary tract cancer. Ann Epidemiol. May 1993;3(3):211–6. doi: 10.1016/1047-2797(93)90021-u [DOI] [PubMed] [Google Scholar]

[R49] 49.Nagano J, Kono S, Preston DL, et al. Bladder-cancer incidence in relation to vegetable and fruit consumption: a prospective study of atomic-bomb survivors. Int J Cancer. Apr 1 2000;86(1):132–8. doi: 10.1002/(sici)1097-0215(20000401)86.1<132::aid-ijc21>3.0.co;2-m [DOI] [PubMed] [Google Scholar]

[R50] 50.Wakai K, Hirose K, Takezaki T, et al. Foods and beverages in relation to urothelial cancer: case-control study in Japan. Int J Urol. Jan 2004;11(1):11–9. doi: 10.1111/j.1442-2042.2004.00740.x [DOI] [PubMed] [Google Scholar]

[R51] 51.Wang J, Wu X, Kamat A, Barton Grossman H, Dinney CP, Lin J. Fluid intake, genetic variants of UDP-glucuronosyltransferases, and bladder cancer risk. Br J Cancer. Jun 11 2013;108(11):2372–80. doi: 10.1038/bjc.2013.190 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R52] 52.Cai ZY, Li XM, Liang JP, et al. Bioavailability of Tea Catechins and Its Improvement. Molecules. Sep 13 2018;23(9)doi: 10.3390/molecules23092346 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R53] 53.Andreu-Fernández V, Almeida Toledano L, Pizarro N, et al. Bioavailability of Epigallocatechin Gallate Administered With Different Nutritional Strategies in Healthy Volunteers. Antioxidants (Basel). May 19 2020;9(5)doi: 10.3390/antiox9050440 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R54] 54.Imai K, Suga K, Nakachi K. Cancer-preventive effects of drinking green tea among a Japanese population. Prev Med. Nov-Dec 1997;26(6):769–75. doi: 10.1006/pmed.1997.0242 [DOI] [PubMed] [Google Scholar]

[R55] 55.Nakachi K, Matsuyama S, Miyake S, Suganuma M, Imai K. Preventive effects of drinking green tea on cancer and cardiovascular disease: epidemiological evidence for multiple targeting prevention. Biofactors. 2000;13(1–4):49–54. doi: 10.1002/biof.5520130109 [DOI] [PubMed] [Google Scholar]

[R56] 56.Kono S, Ikeda M, Tokudome S, Kuratsune M. A case-control study of gastric cancer and diet in northern Kyushu, Japan. Jpn J Cancer Res. Oct 1988;79(10):1067–74. doi: 10.1111/j.1349-7006.1988.tb01528.x [DOI] [PMC free article] [PubMed] [Google Scholar]

[R57] 57.Inoue M, Tajima K, Hirose K, et al. Tea and coffee consumption and the risk of digestive tract cancers: data from a comparative case-referent study in Japan. Cancer Causes Control. Mar 1998;9(2):209–16. doi: 10.1023/a:1008890529261 [DOI] [PubMed] [Google Scholar]

[R58] 58.Nagano J, Kono S, Preston DL, Mabuchi K. A prospective study of green tea consumption and cancer incidence, Hiroshima and Nagasaki (Japan). Cancer Causes Control. Aug 2001;12(6):501–8. doi: 10.1023/a:1011297326696 [DOI] [PubMed] [Google Scholar]

[R59] 59.Wilkens LR, Kadir MM, Kolonel LN, Nomura AM, Hankin JH. Risk factors for lower urinary tract cancer: the role of total fluid consumption, nitrites and nitrosamines, and selected foods. Cancer Epidemiol Biomarkers Prev. Mar 1996;5(3):161–6. [PubMed] [Google Scholar]

[R60] 60.Kunze E, Chang-Claude J, Frentzel-Beyme R. Life style and occupational risk factors for bladder cancer in Germany. A case-control study. Cancer. Apr 1 1992;69(7):1776–90. doi: 10.1002/1097-0142(19920401)69:7<1776::aid-cncr2820690721>3.0.co;2-p [DOI] [PubMed] [Google Scholar]

[R61] 61.Nomura AM, Kolonel LN, Hankin JH, Yoshizawa CN. Dietary factors in cancer of the lower urinary tract. Int J Cancer. May 10 1991;48(2):199–205. doi: 10.1002/ijc.2910480208 [DOI] [PubMed] [Google Scholar]

[R62] 62.Heilbrun LK, Nomura A, Stemmermann GN. Black tea consumption and cancer risk: a prospective study. Br J Cancer. Oct 1986;54(4):677–83. doi: 10.1038/bjc.1986.226 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R63] 63.Liu Z, Bruins ME, Ni L, Vincken JP. Green and Black Tea Phenolics: Bioavailability, Transformation by Colonic Microbiota, and Modulation of Colonic Microbiota. J Agric Food Chem. Aug 15 2018;66(32):8469–8477. doi: 10.1021/acs.jafc.8b02233 [DOI] [PubMed] [Google Scholar]

[R64] 64.Liu Y, Ahmed S, Long C. Ethnobotanical survey of cooling herbal drinks from southern China. J Ethnobiol Ethnomed. Dec 19 2013;9:82. doi: 10.1186/1746-4269-9-82 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R65] 65.Periche A, Koutsidis G, Escriche I. Composition of antioxidants and amino acids in Stevia leaf infusions. Plant Foods Hum Nutr. Mar 2014;69(1):1–7. doi: 10.1007/s11130-013-0398-1 [DOI] [PubMed] [Google Scholar]

[R66] 66.Xu Y, Oliverson BG, Simmons DL. Trifunctional inhibition of COX-2 by extracts of Lonicera japonica: direct inhibition, transcriptional and post-transcriptional down regulation. J Ethnopharmacol. May 22 2007;111(3):667–70. doi: 10.1016/j.jep.2007.01.017 [DOI] [PubMed] [Google Scholar]

[R67] 67.Elansary HO, Mahmoud EA. Egyptian herbal tea infusions’ antioxidants and their antiproliferative and cytotoxic activities against cancer cells. Nat Prod Res. 2015;29(5):474–9. doi: 10.1080/14786419.2014.951354 [DOI] [PubMed] [Google Scholar]

[R68] 68.Risch HA, Burch JD, Miller AB, Hill GB, Steele R, Howe GR. Dietary factors and the incidence of cancer of the urinary bladder. Am J Epidemiol. Jun 1988;127(6):1179–91. doi: 10.1093/oxfordjournals.aje.a114911 [DOI] [PubMed] [Google Scholar]

[R69] 69.La Vecchia C, Negri E, Franceschi S, D’Avanzo B, Boyle P. Tea consumption and cancer risk. Nutrition and Cancer. 1992/January/01 1992;17(1):27–31. doi: 10.1080/01635589209514170 [DOI] [PubMed] [Google Scholar]

[R70] 70.Michaud DS, Spiegelman D, Clinton SK, et al. Fluid intake and the risk of bladder cancer in men. N Engl J Med. May 6 1999;340(18):1390–7. doi: 10.1056/nejm199905063401803 [DOI] [PubMed] [Google Scholar]

[R71] 71.Bianchi GD, Cerhan JR, Parker AS, et al. Tea consumption and risk of bladder and kidney cancers in a population-based case-control study. Am J Epidemiol. Feb 15 2000;151(4):377–83. doi: 10.1093/oxfordjournals.aje.a010217 [DOI] [PubMed] [Google Scholar]

[R72] 72.Geoffroy-Perez B, Cordier S. Fluid consumption and the risk of bladder cancer: results of a multicenter case-control study. Int J Cancer. Sep 2001;93(6):880–7. doi: 10.1002/ijc.1411 [DOI] [PubMed] [Google Scholar]

[R73] 73.Woolcott CG, King WD, Marrett LD. Coffee and tea consumption and cancers of the bladder, colon and rectum. Eur J Cancer Prev. Apr 2002;11(2):137–45. doi: 10.1097/00008469-200204000-00005 [DOI] [PubMed] [Google Scholar]

[R74] 74.Ros MM, Bas Bueno-de-Mesquita HB, Büchner FL, et al. Fluid intake and the risk of urothelial cell carcinomas in the European Prospective Investigation into Cancer and Nutrition (EPIC). Int J Cancer. Jun 1 2011;128(11):2695–708. doi: 10.1002/ijc.25592 [DOI] [PubMed] [Google Scholar]

[R75] 75.Bruemmer B, White E, Vaughan TL, Cheney CL. Fluid intake and the incidence of bladder cancer among middle-aged men and women in a three-county area of western Washington. Nutr Cancer. 1997;29(2):163–8. doi: 10.1080/01635589709514619 [DOI] [PubMed] [Google Scholar]

[R76] 76.Clavel J, Cordier S. Coffee consumption and bladder cancer risk. Int J Cancer. Jan 21 1991;47(2):207–12. doi: 10.1002/ijc.2910470208 [DOI] [PubMed] [Google Scholar]

[R77] 77.Kurahashi N, Inoue M, Iwasaki M, Sasazuki S, Tsugane S. Coffee, green tea, and caffeine consumption and subsequent risk of bladder cancer in relation to smoking status: a prospective study in Japan. Cancer Sci. Feb 2009;100(2):294–91. doi: 10.1111/j.1349-7006.2008.01027.x [DOI] [PMC free article] [PubMed] [Google Scholar]

[R78] 78.Yasuda T, Miyata Y, Nakamura Y, et al. High Consumption of Green Tea Suppresses Urinary Tract Recurrence of Urothelial Cancer via Down-regulation of Human Antigen-R Expression in Never Smokers. In Vivo. Jul-Aug 2018;32(4):721–729. doi: 10.21873/invivo.11300 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R79] 79.Weng H, Zeng XT, Li S, Kwong JS, Liu TZ, Wang XH. Tea Consumption and Risk of Bladder Cancer: A Dose-Response Meta-Analysis. Front Physiol. 2016;7:693. doi: 10.3389/fphys.2016.00693 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R80] 80.BARRY D Differential recall bias and spurious associations in case/control studies. Statistics in medicine. 1996;15(23):2603–2616. [DOI] [PubMed] [Google Scholar]

[R81] 81.Barry D, Livingstone V. The investigation and correction of recall bias for an ordinal response in a case-control study. Statistics in medicine. 2006;25(6):965–975. [DOI] [PubMed] [Google Scholar]

[R82] 82.Chouinard E, Walter S. Recall bias in case-control studies: an empirical analysis and theoretical framework. Journal of clinical epidemiology. 1995;48(2):245–254. [DOI] [PubMed] [Google Scholar]

[R83] 83.Gefeller O Invited commentary: recall bias in melanoma—much ado about almost nothing? American journal of epidemiology. 2009;169(3):267–270. [DOI] [PubMed] [Google Scholar]

[R84] 84.van Osch FHM, Vlaanderen J, Jochems SHJ, et al. Modeling the Complex Exposure History of Smoking in Predicting Bladder Cancer: A Pooled Analysis of 15 Case-Control Studies. Epidemiology. May 2019;30(3):458–465. doi: 10.1097/ede.0000000000000964 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R85] 85.Borhani S, Borhani R, Kajdacsy-Balla A. Artificial intelligence: A promising frontier in bladder cancer diagnosis and outcome prediction. Crit Rev Oncol Hematol. Mar 2022;171:103601. doi: 10.1016/j.critrevonc.2022.103601 [DOI] [PubMed] [Google Scholar]

[R86] 86.Eun SJ, Kim J, Kim KH. Applications of artificial intelligence in urological setting: a hopeful path to improved care. J Exerc Rehabil. Oct 2021;17(5):308–312. doi: 10.12965/jer.2142596.298 [DOI] [PMC free article] [PubMed] [Google Scholar]

[R87] 87.Zhanghuang C, Zhang Z, Wang J, et al. Surveillance of prognostic risk factors in patients with SCCB using artificial intelligence: a retrospective study. Sci Rep. May 30 2023;13(1):8727. doi: 10.1038/s41598-023-35761-w [DOI] [PMC free article] [PubMed] [Google Scholar]

[R88] 88.Ferro M, Falagario UG, Barone B, et al. Artificial Intelligence in the Advanced Diagnosis of Bladder Cancer-Comprehensive Literature Review and Future Advancement. Diagnostics (Basel). Jul 7 2023;13(13)doi: 10.3390/diagnostics13132308 [DOI] [PMC free article] [PubMed] [Google Scholar]

PERMALINK

The association between tea consumption and bladder cancer risk based on the Bladder Cancer Epidemiology and Nutritional Determinants (BLEND) international consortium

Yan-Xi Zhang

Richard Albers

Ya-Ting Chen

Gunnar Steineck

Eliane Kellen

Kenneth C Johnson

Chih-Ming Lu

Hermann Pohlabeln

Carlo La Vecchia

Stefano Porru

Angela Carta

Jerry Polesel

Cristina Bosetti

Xuejuan Jiang

Li Tang

James Marshall

Margaret R Karagas

Zuo-Feng Zhang

Jack A Taylor

Maurice P A Zeegers

Anke Wesselius

Evan Yi-Wen Yu

Abstract

Objectives

Methods

Results

Conclusions

Introduction

Methods

Study design

Data collection and coding

Statistical Analysis

Results

Baseline characteristics

Table 1.

Association between tea and BC risk

Table 2.

Stratification by gender and smoking status

Stratification by BC subtypes

Table 3.

Dose-response analysis

Figure 1. Association of tea consumption and bladder cancer risk.

Discussion

Conclusion

Supplementary Material

Acknowledgments

Funding

Authors’ Disclosures

Footnotes

Data Availability

References

Associated Data

Supplementary Materials

Data Availability Statement

ACTIONS

PERMALINK

RESOURCES

Similar articles

Cited by other articles

Links to NCBI Databases