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Health Risks Due to Coffee Dust

Marcus Oldenburg, MD; Cordula Bittner, MD; and Xaver Baur, MD

Objective: This study assessed current health risks due to occupational exposure to coffee dust.
Methods: We performed a cross-sectional study in a coffee haulage company (n � 24), a coffee silo
(n � 19), and a decaffeinating company (n � 17). Cross-shift and cross-week case histories of
these employees as well as lung function values were recorded. During the handling of green
coffee, measurements of airborne dust were conducted.
Results: The employees in these workplaces were mainly affected by erythematous and rhino-
conjunctival symptoms. They occurred especially in subjects exposed to a high dust load (> 10 mg
of inhalable dust per cubic meter of air; n � 28) [Pearson �2 test, p � 0.020 and p � 0.023]. IgE
antibodies to green coffee and castor beans were detected in 3 workers and 10 workers,
respectively. The majority of them (two employees and six employees, respectively) had shown
respiratory symptoms during the past 12 months. The preshift lung function values were below
average but were not dependent on the level of the inhalable coffee dust exposure. Employees
with a coffee dust load > 10 mg/m3 of air showed higher unspecific bronchial responsiveness
more frequently than those with lower exposures.
Conclusion: During the transshipment (especially during unloading) of green coffee, a high and
clinically relevant exposure to irritative and sensitizing dust occurs. Therefore, efforts to reduce
these dust exposures are generally recommended. (CHEST 2009; 136:536 –544)

Abbreviations: CI � confidence interval; FEV1/FVC% � FEV1/FVC percentage; kUA � kilounits; OR � odds ratio;
PD20 � applied dose of methacholine inducing a 20% drop in FEV1; PM � particulate matter

C offee is a favorite beverage of millions of people.Only the two coffee species Arabica and Robusta
are of economic importance. Coffee cherries are
harvested up to twice a year and collected in jute
bags. After emptying the bags, the cores, the so-
called green coffee beans, are removed from the
pulp of the coffee cherries. These beans are shipped
worldwide, mainly in big bags inside 20-ton contain-

ers. During the transport and refinement of the
green coffee in ports, exposures to irritative and
sensitizing dust occur.1

A high frequency of asthmatic diseases among
workers of a green coffee processing factory was
already observed in the 1950s.1 It was also described
that roasted coffee may be implicated in occupa-
tional asthma due to heat-resistant allergens.2 In
addition to coffee, castor beans were also regarded
as a cause of asthma.3 Castor beans have a wide
variety of uses. Among others, they are used in
lamps, in laxatives, and as a fertilizer. In the
countries of origin, the plantations of castor and
coffee beans frequently border each other, and the
harvested beans are transported by the same ship.
Castor beans are thought to be an accidental
contaminant of green coffee beans because some
coffee bags may have been used previously for the
transportation of castor beans or stored in conta-
minated ship containers.3– 6

Nowadays, green coffee stored in big containers is
imported by ships and transported by trucks of

Manuscript received August 11, 2008; revision accepted February
19, 2009.
Affiliations: From the Institute for Occupational and Maritime
Medicine (Drs. Oldenburg, Bittner, and Baur), University of
Hamburg, Hamburg, Germany; and the Hamburg State Depart-
ment for Social Affairs, Family, Health and Consumer Protection
(Drs. Oldenburg, Bittner, and Bauer), Hamburg, Germany.
© 2009 American College of Chest Physicians. Reproduction
of this article is prohibited without written permission from the
American College of Chest Physicians (www.chestjournal.org/site/
misc/reprints.xhtml).
Correspondence to: Marcus Oldenburg, MD, Department of
Maritime Medicine, Institute for Occupational and Maritime
Medicine (ZfAM), University of Hamburg, Hamburg State De-
partment for Social Affairs, Family, Health and Consumer
Protection, Germany, Seewartenstrasse 10, D-20459 Hamburg,
Germany; e-mail: marcus.oldenburg@bsg.hamburg.de
DOI: 10.1378/chest.08-1965

CHEST Original Research
COFFEE DUST EXPOSURE

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specialized haulage companies to coffee-processing
factories (eg, coffee silos or decaffeinating compa-
nies). The drivers of the haulage companies unload
the coffee at tilting stations. In coffee silos, the
coffee is roughly purged and placed in the silos for
interim storage on call. In decaffeinating companies,
the green coffee is impacted by steam after a rough
cleaning and decaffeinated by chemical treatment.
Afterward, the coffee is dried and polished. The aim
of our study was to determine whether the exposure
to coffee dust during loading and processing under
the presently improved hygienic conditions (eg, use
of effective exhaust systems during discharge) still
represents a health hazard to employees.

Materials and Methods

We performed an occupational medical cross-sectional study in
a haulage company mainly dealing with the transport of coffee, in
a coffee silo, and in a decaffeinating company. Willing partici-
pants were 24, 19, and 17 exclusively male subjects (82.8%,
100%, and 100%, respectively). All employees of the three
investigated companies were personally informed about the study
by the management and the company physician. Furthermore, a
separate meeting was held to explain the objective of our
investigation. The participation in this study was absolutely
voluntary. All participants gave their informed consent, and the
authors received institutional review board approval for the
study.

We performed three investigations in each of the three
companies: at the beginning of the shift on Monday morning, at
the end of that shift, and on the following Friday noon. Each time
the focus was on exposure-related symptoms, and a spirometry,
including measurements of bronchial responsiveness by means of
methacholine testing, was conducted. Preceding the investigation
on Monday morning was a period of at least 1.5 days without
exposure to coffee dust (median, 65.6 h [range, 38 to 744 h]).

Inhalative Dust Exposure During the Handling of Green Coffee

To assess the airborne level of alveolar or inhalable dust
(particles with an aerodynamic diameter [particulate matter
(PM)] �2.5 �m [PM2.5] and 10 �m [PM10]) during the handling
of coffee, air measurements were performed using the sampling
system of the Institute for Occupational Health and Safety, St.
Augustin, Germany (Project-No. BIA 1061).7 Dust measure-
ments were conducted with a glass fiber filter, type MN 85/90, by
maintaining an airflow rate of 0.6 m3/h or 0.21 m3/h for the
inhalable or alveolar dust fraction (according to EN 481), respec-
tively.8 During five different working shifts, 12 personal and
stationary gravimetric air measurements of the alveolar or inhal-
able coffee dust were conducted over several hours.

The measurements were task related and therefore not
completely identical with the prescribed procedure in order to
obtain the shift-related mean value. In Germany, the general
threshold limit value of dust is 3 mg/m3 for the alveolar
fraction and 10 mg/m3 for the inhalable fraction. If these limits
are maintained, no increased health risk is expected in the case
of nonsensitizing agents (Technical Regulation for Hazardous
Goods 900).

The employees at the tilting stations were presumably highly
exposed to coffee dust. To evaluate the health effects of green

coffee, these workers (all employees of the haulage company and
four employees of the coffee silo; n � 28) were allotted to the
“higher dust-exposed group” (� 10 mg of inhalable dust per
cubic meter of air) and the remaining ones to the “lower
dust-exposed group” (� 10 mg/m3; n � 32).

Measurements of the Airborne Exposure to Germs

Air measurements of germs were performed in the decaffein-
ating company to roughly assess the level of germs during the
handling of organic raw coffee. Sedimentation plates were in-
stalled in several company areas for 30 min and agar specifically
incubated. To determine the total number of germs and the mold
concentration, Caso and DG-18 agars were used.

Furthermore, the impaction method RCS Plus using the serial
devices of the Biotest Company (St. Georgen, Germany) were
applied for the quantitative determination of airborne germ
concentrations. To measure the total germ count and the mold
concentration, the TC-18 and DG-18 bands were applied with
airflows of 100 L and 200 L, respectively. The colonies of bacteria
and molds were counted, and the number of colony forming units
were determined.

Questionnaire

The standardized interview included questions of demographic
data as well as airway and skin symptoms. The questions regard-
ing symptoms were mostly identical to those of the German
National Health Interview and Examination Survey 1997/98
(BGS 98).9 Moreover, specific occupational parameters were
recorded. In addition to the preshift questionnaire, we used a
postshift and a postweek questionnaire focusing the subjects’
complaints in the course of time (see Online Data Supplement).

Asthma was defined in patients with current asthma medica-
tion use and asthma attacks during the past 12 months. Further-
more, work-exacerbated asthma was defined in cases of chest
tightness, wheezing, cough, and shortness of breath during the
exposure to coffee dust. Chronic bronchitis was diagnosed if
coughing and phlegm occurred for a minimum of 3 months per
year and for not less than 2 successive years.10

Serologic Parameters

The blood of 59 coffee workers was sampled for IgE determi-
nation. Total IgE and specific IgE to green coffee beans (com-
prising Coffea arabica, Coffea canephora/robusta, and Coffea
liberica) and to castor beans were measured by fluorescent
enzyme immunoassay (UniCAP; Phadia; Freiburg, Germany). To
investigate immunologic cross-reactivity between coffee and cas-
tor beans, 100 �L of the castor bean IgE-positive serum were
incubated with 50 �L of green coffee solution (4 mg Robusta
coffee protein per milliliter) overnight at 4°C. UniCAP sub-
sequently measured the IgE binding to castor bean allergens.
Specific IgE levels above the threshold of 0.35 kilounits (kUA)
per liter of serum (CAP class 1)11 were interpreted as
sensitization according to the recommendation of the manu-
facturer.

Lung Function Analysis

During the three investigations just described, lung function
measurements were conducted in a sitting position by using a
nose clip. Lung function measurements with a portable spirom-
eter (MasterScope 4.5; Jaeger; Wuerzburg, Germany) were
performed by a trained technician in the company offices. Forced
expiratory spirograms were performed for the whole study

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population (n � 60) according to the recommendations of the
American Thoracic Society.12,13 For assessment, the reference
values by Brändli et al14,15 were used. They assumed14 an
obstructive ventilation pattern when FEV1/FVC percentage
(FEV1/FVC%) was lower than the limit for normal.

A methacholine challenge using the Pari Provocation Test (Pari
Company; Starnberg, Germany) with spirometric measurements
was conducted during each investigation.16 The applied dose of
methacholine inducing a 20% drop in FEV1 (PD20) was calcu-
lated by linear interpolation or extrapolation up to 2,000 �g of
methacholine.16 Bronchial hyperresponsiveness was diagnosed
when PD20 was � 300 �g of methacholine (inhaled cumulative
dose).17 Acute cross-shift changes in pulmonary function (� lung
function parameter) were expressed for each subject as a per-
centage of the value before exposure.16

Statistical Analysis

Data were analyzed using statistical software (SPSS for
Windows, version 13.0; SPSS GmbH Software; Munich, Ger-
many). Continuous data were expressed as mean � SD and in
case of nonnormal distribution as median (minimum to max-
imum). For the nonparametric group of metric/ordinal values,
the Mann-Whitney test and the Kruskal-Wallis test were per-
formed. The Pearson �2 test determined the frequency differ-
ences between the two groups. The provided p values were two
sided, and an � value of � 0.05 was regarded as statistically
significant.

To analyze exposure-response relationships between exposure
and obstructive ventilation patterns, the logistic regression with
or without adjusting for the potential confounding variable
smoking status (nonsmoker, former smoker, and smoker) was
conducted. Adjusted odds ratios (ORs) and 95% confidence
intervals (CIs) were estimated.

Results

Dust Exposure During the Handling of Coffee

Haulage Company: We performed dust measure-
ments in the ambient air of three representative
tilting stations and found a high inhalable coffee dust

concentration during unloading (� 10 mg inhalable
dust per cubic millimeter of air) [Table 1].

Coffee Silo: The inhalative dust load during dis-
charge was equal to the exposure of truck drivers at
tilting stations. High dust concentrations occurred
during the operation of silo systems. The cleaning
staff performed activities in different locations. The
duration was similar to that in the two other working
areas studied. Therefore, the average dust load
during coffee unloading and system operation in the
silo was calculated to estimate the exposure of these
employees (Table 1).

Decaffeinating Company: The inhalative exposure
during coffee discharge mostly performed by chain
trough conveyors was distinctly lower than that of
truck drivers and silo workers at the tilting stations.
In the working area of system operators, foremen,
and cleaning personnel, only low dust concentrations
were measurable on account of the shielded con-
veyor systems (Table 1).

The measured concentrations of germs and molds
ranged from 114 to 1,279 cfu/m3 and from 108 to 325
cfu/m3, respectively. Measurements of the total
number of bacteria in the atmosphere exclusively
showed Gram-positive normal germs occurring in
the environment (especially Bacillus spp). Measure-
ments of molds revealed Cladosporium spp, As-
pergillus niger, and Penicillium spp. The total mold
concentrations in reference areas were distinctly
higher than on system tracks exposed to coffee dust.

Demographic Data and Clinical Symptoms

The demographic data on employees of the haul-
age company, silo, and decaffeinating company were

Table 1—Measuring Results of Personal Coffee Dust Concentrations in the Air During Different Activities in
Investigated Companies

Variables

Dust Concentration, mg/m3 Employees

Alveolar Inhalable
Haulage Company

(n � 24)
Coffee Silo

(n � 19)
Decaffeinating Company

(n � 17)

Coffee discharge
At tilting station 1.38 11.65 (10.1–15.7) 24 4 3*
By chain trough conveyors 3.80 (2.6–4.0)

System operation
Coffee silo 0.85 (0.3–1.35) 7.05 (3.7–10.3) 7
Decaffeinating company 1.60 (1.3–1.9) 7

Activities in several areas (cleaning
staff, foremen)

Coffee silo 1.12† 9.35† 8
Decaffeinating company 0.70 (� 0.2–1.1) 7

Data are presented as the median (minimum-maximum) or No.
*Twenty percent of the coffee discharge at tilting stations and 80% by chain trough conveyors.
†Mean value of dust concentrations during coffee discharge and system operation in silo.

538 Original Research

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not significantly different (Table 2). On the basis of
these anamnestic data, we placed the employees
according to the exposure median in categories with
current and cumulative exposure to low and high
dust levels (Table 2). Compared to employees with
lower dust exposure, an increase of symptoms, lung
functional impairments, or allergologic findings was
not observed in employees with anamnestically
higher current or cumulative dust exposure.

The total group reported that Arabica coffee trig-
gers symptoms twice as often as Robusta coffee (18
times vs 9 times). In particular, the coffee of Brazil-

ian origin was reported to elicit complaints. The
participants exhibited mainly erythematous and rhi-
noconjunctival symptoms during the past 12 months
(Fig 1). Employees with currently higher dust expo-
sure (� 10 mg/m3) complained more frequently than
those with currently lower dust exposure about ery-
thematous (42.9% vs 15.6%, respectively; Pearson �2

test, p � 0.020), conjunctival (53.6% vs 25.0%, respec-
tively; p � 0.023), and sneezing (35.7% vs 25.0%, respec-
tively; p � 0.366) symptoms during the past 12 months.

According to the questionnaire, symptoms of the
lower airways in the sense of asthmatic complaints

Table 2—Demographic Data and Level of Anamnestically Recorded Coffee Dust Exposure in the Investigated
Companies

Variables
Haulage Company

(n � 24)
Coffee Silo
(n � 19)
Decaffeinating Company

(n � 17) p Value*

Participation rate, % 82.8 100 100
Age, yr 40.4 (7.7) 39.6 (10.5) 44.5 (10.3) 0.202
Smoking status, No. (% of company)

Nonsmokers 2 (8.3) 7 (36.8) 2 (11.8)
Former smokers 6 (25.0) 4 (21.1) 6 (35.3)
Smokers 16 (66.7) 8 (42.1) 9 (52.9)

Pack-years, No. 28.4 (17.0) 17.6 (9.1) 21.9 (11.3) 0.116
Period without coffee exposure before Monday

morning examination, h
77 (58–727) 63 (38–233) 66 (63–744) � 0.001†

Coffee dust exposure (according to anamnestical
data)

Current, h/d 3 (1–8) 6 (0.5–8) 5 (0–8) 0.086
Cumulative, yr 10.7 (0.5–32) 11.8 (0.5–35) 17.3 (4–34) 0.074

Data are presented as mean (SD) or median (minimum-maximum) unless otherwise indicated.
*Kruskal-Wallis test.
†Indicates significant findings.

Figure 1. Prevalence (%) of symptoms during the past 12 mo among employees with coffee dust
exposure � 10 mg/m3 and � 10 mg/m3 inhalable dust (n � 32 and n � 28, respectively); work-related
symptoms are shown as hatched columns.

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occurred more rarely, however. Because none of the
investigated employees took any antiasthmatic med-
ication or had suffered from an asthma attack during
the past 12 months, no participant was regarded as
having asthma. Thus, based on our questionnaire,
there was no evidence for preemployment asthma in
the study sample. During the period of exposure to
coffee dust, work-exacerbated asthma (increase in
chest tightness, wheezing, cough, and shortness of
breath) developed in two subjects. Both subjects had
a currently higher exposure to inhalable coffee dust.
Furthermore, these two subjects showed IgE anti-
bodies to green coffee and castor beans but no
obstructive ventilation pattern; one employee exhib-
ited bronchial hyperresponsiveness.

The diagnostic criteria of chronic bronchitis were
fulfilled in three employees. All of them were non-
smokers and had a currently lower coffee dust
exposure. These three subjects had no obstructive
ventilation pattern (risk group 0 according to the
Global Initiative for Chronic Obstructive Lung Dis-
ease criteria of COPD).18 Work-related erythema
and conjunctivitis during the past 12 months were
more often observed in employees exposed to � 10
mg/m3 than to � 10 mg/m3 (erythematous symptoms,
22.2% vs 9.4%, respectively [p � 0.172]; conjunctivitis,
42.9% vs 12.5%, respectively [p � 0.008]).

Postshift and postweek increases of work-related
symptoms were mainly found in workers with a coffee
dust exposure � 10 mg/m3 (erythematous symptoms,
21.4% vs 0%, respectively [p � 0.006]; conjunctivitis,
25.0% vs 6.3%, respectively [p � 0.090]; sneezing,
17.9% vs 15.6%, respectively [p � 0.631]; chest tight-
ness, 14.8% vs 3.1%, respectively [p � 0.140]; wheez-
ing, 7.1% vs 0%, respectively [p � 0.165]; cough,
17.9% vs 9.4%, respectively [p � 0.335]). The same
exposure-dependent increase of work-related symp-
toms was observed in the postweek examination.

Lung Function Parameters

Due to the respiratory complaints of five employ-
ees, their methacholine challenge testing was not
possible at the end of the week. The lung function
comparison of the smoker group (n � 33) with that of the
total group (n � 60) did not reveal noticeable differences.
Therefore, we evaluated the lung function findings inde-
pendent of the employees’ smoking status.

With regard to lung function parameters of the
total group, the average percentage deviations from
reference mean values by Brändli et al14 of FVC,
FEV1, and FEV1/FVC% were 94.5%, 93.6%, and
96.0%, respectively, indicating slight lung function
impairments. Seven employees showed an obstruc-
tive ventilation pattern (FEV1/FVC � FEV1/FVC%
lower limit of normal) before the Monday shift (two

workers and five workers with a dust exposure � 10
mg/m3 and � 10 mg/m3); three were smokers, and
four were former smokers. The pack-year history of
these seven people did not differ from those of the
other smokers/former smokers (showing normal lung
function) of the total group (mean, 25.6 pack-years vs
23.5 pack-years; Mann-Whitney test, p � 0.841). No
significant association between obstructive lung func-
tion impairment and dust exposure level (� 10 mg/m3

vs � 10 mg/m3 air) was found. Among the seven
employees with obstructive ventilation patterns, five were
assigned to risk group 1 and two to risk group 2
according to the Global Initiative for Chronic
Obstructive Lung Disease criteria of COPD.18

On Monday before the shift, lung function was
independent of the exposure level of inhalable coffee
dust (Table 3). Results of the preshift methacholine
challenge on Monday showed that workers with
coffee dust exposure � 10 mg/m3 had bronchial
hyperresponsiveness significantly more often (25.0%
vs 6.3%). Postshift and postweek measurements also
revealed bronchial hyperresponsiveness more fre-
quently in workers with higher work-related dust
concentrations. Therefore, in the three investigations
we calculated a significantly lower effective PD20 for
employees with a dust concentration � 10 mg/m3.
Based on the anamnestic data about the period of
coffee dust exposure (in years), no association be-
tween cumulative dust exposure and lung function
impairment was found (Fig 2).

The prevalence of postweek bronchial hyperre-
sponsiveness (n � 10) was associated with dust ex-
posure level (OR, 5.47; 95% CI, 1.04 to 28.74). After
adjusting for smoking status (nonsmoker, former
smoker, and smoker), this relationship remained
significant (OR, 5.31; 95% CI, 1.01 to 28.01), and the
smoking status did not reach statistical significance
(OR, 1.33; 95% CI, 0.42 to 4.26). Thus, no major
effect of smoking on bronchial hyperresponsiveness
in employees was observed in this study.

In the total group (n � 60), the cross-shift course
of lung function values revealed an average change in
FEV1, FEV1/FVC%, and FVC of 0.8%, 2.2%,
and
0.7%, respectively. The lung function com-
parison before the shift with that at the end of the
week showed a slightly stronger lung function im-
pairment in the postweek measurement ( 2.5%,
2.1%, and 0.4%, respectively).

In the course of the week, the subjects with
preshift bronchial hyperresponsiveness demon-
strated work-related symptoms significantly more often
than the rest of the group (chest tightness, 22.2% vs
6.0%, respectively [p � 0.014]; wheezing, 12.5% vs
4.2%, respectively [p � 0.05]; cough, 44.4% vs 7.8%,
respectively [p � 0.003]; erythematous symptoms,
37.5% vs 4.2%, respectively [p � 0.002]; conjunctivitis,

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25.0% vs 20.8%, respectively [p � 0.05]; sneezing,
50.0% vs 16.7%, respectively [p � 0.033]). The seven
subjects with obstructive ventilation patterns did not
notice work-related airway symptoms. This may be due
to a good adaptation to their lung function limitation.

Allergologic Findings

IgE antibodies to green coffee and castor beans
were detectable in three workers and six workers

with an inhalable coffee dust exposure � 10 mg/m3

(Table 4). The three employees with IgE antibodies
to coffee beans also demonstrated IgE antibodies to
castor beans. Also, four subjects with a coffee dust
load � 10 mg/m3 revealed IgE antibodies to castor
beans. Elevated total IgE (� 100 kUA/L) occurred
20 times in the total group independent of the level
of the subjects’ average coffee dust load.

Two workers and six workers with IgE antibodies
to green coffee and castor beans, respectively, had
respiratory symptoms during the past 12 months. In
total, no association between specific/total IgE and
work-related symptoms during the past 12 months was
found. UniCAP inhibition assays with coffee extracts
did not suppress the IgE binding to castor beans.

Discussion

This study shows that high exposures to inhalable
dust (� 10 mg/m3) occur during the handling of
green coffee. We observed great differences be-
tween the haulage company, coffee silo, and decaf-
feinating company. Concentrations of the alveolar

Figure 2. Baseline lung function of all employees independent
of the number of years of cumulative coffee dust exposure.

Table 3—Lung Function Findings of Examined Employees (n � 60) Depending on Inhalable Coffee Dust Exposure

Variables

Coffee Dust Exposure (Inhalable Fraction)

p Value� 10 mg/m3 (n � 32) � 10 mg/m3 (n � 28)

Preshift measurement (Monday)
FEV1, L 3.9 (0.7) 4.0 (0.6) 0.876*
FEV1/FVC% 75.5 (6.7) 75.8 (6.0) 0.801*
FVC, L 4.9 (0.7) 5.3 (0.8) 0.073*
FEV1, % predicted 95.4 (13.4) 91.4 (10.8) 0.110*
FEV1/FVC%, % predicted 96.2 (7.3) 95.9 (7.8) 0.988*
FVC, % predicted 93.9 (8.8) 95.2 (12.8) 0.778*
Positive BHR, No. (% of exposure

group)
2 (6.3) 7 (25.0) 0.042†‡

PD20, mg 2 (0–2) 1.5 (0–2) 0.013*†
Postshift measurement (Monday)

Positive BHR, No. (% of exposure
group)

4 (12.5) 7 (25.0) 0.212‡

PD20, mg 2 (0.1–2) 1.2 (0–2) 0.029*†
Postweek measurement (Friday)§

Positive BHR, No. (% of exposure
group)

2 (7.1) 8 (29.6) 0.031†‡

PD20, mg 2 (0–2) 2 (0–2) 0.020*†
Postshift vs preshift findings, %

�FEV1 1.4 ( 15.7–18.1) 1.1 ( 11.9–37.6) 0.133*
�FEV1/FVC% 2.1 ( 17.4–9.1) 2.8 ( 21.3–18.7) 0.859*
�FVC 1.9 ( 10.3–27.5) 0.3 ( 25.1–59.1) 0.830*

Postweek§ vs preshift findings, %
�FEV1 3.9 ( 100.0–18.9) 1.4 ( 11.9–41.0) 0.033*†
�FEV1/FVC% 3.5 ( 100.0–18.4) 0 ( 14.0–19.2) 0.039*†
�FVC 2.1 ( 100.0–10.0) 2.2 ( 22.1–38.5) 0.218*

Data are presented as mean (SD) or median (minimum-maximum). BHR � bronchial hyperresponsiveness.
*Mann-Whitney test.
†Indicates significant findings.
‡Pearson �2 test.
§Five employees did not undergo bronchial hyperresponsiveness test due to respiratory complaints.

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dust fraction � 3 mg/m3 were not detectable, how-
ever. High exposures to inhalable dust were espe-
cially found during the discharge of green coffee at
tilting stations. The containers with green coffee
were unloaded without protective equipment in a
relatively short period of time (30 to 45 min). The
alternative coffee discharge via chain trough con-
veyor required more time (45 to 60 min) but resulted
in a distinctly lower dust load due to the uniform and
optimal velocity. The described transshipment of
green coffee represents the current standard. An
optimization of the coffee unloading process, such as
the use of chain trough conveyors, is generally
recommended. Engineering controls and personal
respiratory equipment might be effective preventive
measures. So far, they have not been realized,
however.

The microbial ambient air measurements during
the handling of coffee did not reveal an extraordinary
concentration of bacteria or molds. Therefore, a
noticeable influence on lung function caused by
microorganism is unlikely.

Green coffee elicits sensitizing as well as irritative
effects. According to the literature, coffee dust ex-
posures primarily result in asthmatic symptoms and
rhinoconjunctival complaints.19 –25 The subjects of
our study with an exposure � 10 mg/m3 air showed
significantly more frequent erythematous and rhino-
conjunctival symptoms in the first examination as
well as in the cross-shift and cross-week course.
Considering our measurements of higher concentra-
tions of the inhalable dust fraction in some investi-
gated areas, these coffee workers are generally at a
higher risk for irritant-induced symptoms of differ-
ent organs such as erythema and conjunctivitis.

The predominance of upper airway symptoms in
this study could be due to the high exposure to
inhalable but not to the alveolar dust fraction. Our

questionnaire revealed manifest symptoms of the
lower airways during coffee dust exposure in only
two subjects. Both had a currently higher exposure
to inhalable coffee dust and IgE antibodies to green
coffee and castor beans. One employee showed
bronchial hyperresponsiveness consistent with the
beginning of work-exacerbated allergic asthma. In
addition, one-third of the examined employees of
both subgroups (� 10 mg/m3 and � 10 mg/m3) had
increased total IgE levels, indicating an immunologic
stimulation.

Our study group reported work-related symptoms
to occur twice as often by Arabica than by Robusta
coffee. This indicates that the Arabica species, re-
garded as a high-grade and pure coffee, constitutes a
higher health hazard than the qualitatively lower
Robusta coffee. To our knowledge, this study de-
scribes work-related symptoms due to different cof-
fee species for the first time.

Lung function parameters of examined workers
were, on the average, below reference mean values.
Jones et al26 had already described lower mean FEV1
values in men exposed to green coffee dust. This is
surprising because the working population is ex-
pected to have supranormal values. In this study,
however, no long-term effect of coffee dust exposure
on lung function was observed. All three investiga-
tions showed bronchial hyperresponsiveness to be
significantly related to the dust exposure level; this
relationship remained significant after adjusting for
smoking status. Thus a major effect of smoking on
the employees’ bronchial hyperresponsiveness is un-
likely.

The reason why the spirometry improved slightly
in the high exposure group at the end of the week
cannot be explained definitively. This may indicate a
work-organizational effect because in contrast to the
employees with coffee dust exposure � 10 mg/m3,

Table 4 —Allergologic Findings of Examined Employees (n � 59) Depending on Fraction of Inhalable Coffee
Dust Exposure*

Variables

Coffee Dust � 10 mg/m3 (n � 32) Coffee Dust � 10 mg/m3 (n � 27)

Exposure Group, No. (%) Respiratory Symptoms, No.† Exposure Group No. (%) Respiratory Symptoms, No.†

Total IgE
� 100 kUA/L 21 (65.6) 9 18 (66.7) 8
� 100 kUA/L 11 (34.4) 5 9 (33.3) 5

Specific IgE
Green coffee beans

CAP class � 1 32 (100) 14 24 (88.9) 11
CAP class � 1 0 0 3 (11.1) 2

Castor beans
CAP class � 1 28 (87.5) 11 21 (77.8) 10
CAP class � 1 4 (12.5) 3 6 (22.2) 3

*One subject rejected blood sampling.
†Sneezing, chest tightness, wheezing, and/or shortness of breath during the past 12 mo.

542 Original Research

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those workers with high exposure (especially the
truck drivers unloading the coffee at the tilting
stations) had shorter assignments in these coffee dust
areas on Friday and thereby the opportunity to
compensate for their overtime worked.

Due to respiratory complaints, the methacholine
challenge test with five subjects could not be per-
formed on Friday. This indicates that the dust load
had impaired their lung function so that the risk of
bronchial hyperresponsiveness on Friday might have
been underestimated. Zuskin et al27 showed that the
inhalation of green coffee extracts can lead to an
obstructive ventilation pattern in healthy subjects.

According to several, mostly older studies, the
frequency of sensitization to green coffee beans is
between 20% and 25% in coffee workers.4,5,27,28
Osterman et al6 found a level � 50%. In our study,
however, specific IgE antibodies to green coffee
beans were only detectable in three workers (5%).
All of them were exposed to � 10 mg/m3. In recent
years, coffee producers have started using new bur-
lap or plastic bags and/or specific containers that
considerably reduce the risk of castor bean contam-
ination of green coffee beans.20 Furthermore, the
use of dust exhaust systems during the coffee un-
loading process in some of the investigated tilting
stations improved the hygiene. This may explain the
relatively low prevalence of sensitization to coffee
dust in our study in comparison with former inves-
tigations.

Our examination showed 10 subjects (17%) had
IgE antibodies to castor beans. Four of them had a
low coffee dust exposure (� 10 mg/m3). Inhibition
test results of antibody-allergen reactions indicate
that the identified castor bean sensitization cannot
be explained by a cross-reactivity with coffee. The
causative source of the castor bean allergens in
imported green coffee has not yet been finally
explained (castor beans were never transported or
handled by the examined employees).6

A limitation of this study is its relatively small
sample size, so it cannot be excluded that some
findings might be accidental. The participation rate
of the coffee dust exposed workers, however, was
extraordinarily high and constituted a representative
sample of each coffee company. Furthermore, in
spite of the low number of examined employees, we
observed statistically significant differences between
workers with currently higher and lower coffee dust
exposure. These differences not only covered bron-
chial hyperresponsiveness but were consistently
also true of work-exacerbated clinical symptoms
among bronchial hyperresponsive subjects. Thus, the
exposure-related bronchial hyperresponsiveness was
associated with a higher frequency of work-related
respiratory symptoms.

In summary, our results demonstrate a signifi-
cantly higher prevalence of erythematous and con-
junctival symptoms as well as bronchial hyperrespon-
siveness among employees with a higher coffee dust
exposure than in those with a lower one (� 10
mg/m3 vs � 10 mg/m3).

In addition to the known sensitizing potential,
irritative effects of green coffee dust appear to be
important pathogenetically. Thus, coffee bean dust
still represents a health hazard to employees, so the
improvement of hygienic conditions (ie, further op-
timization of exhaust systems) is recommended.

Acknowledgment

Author contributions: Dr. Oldenburg was responsible for the
study design, the statistical analysis as well as for the on-spot
investigation. Dr. Bittner was engaged in the allergological
investigations, including their interpretations. Dr. Baur was
responsible for the study design and the interpretation of the
employees’ lung function.
Financial/nonfinancial disclosures: The authors have no sig-
nificant conflicts of interest with any companies/organizations
whose products or services may be discussed in this article.
Other contributions: The authors wish to thank the volunteers
and the management of the investigated coffee subcontracting
firms and the haulage company. We also thank L. Barbinova, D.
Johannsen, E. Nern, and B. Poschadel for the performed medical
examinations (lung function and blood sampling). The authors
also express their gratitude to the Pari Company in Starnberg,
Germany, for making three Pari Provocation Test II(R) available
for our cross-shift survey.

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256

Review

Tea, Coffee and Prostate Cance

r

Andy H

.

Lee, Michelle L. Fraser and Colin W. Binns

School of Public Health, Curtin University of Technology, Perth, WA, Australia

Worldwide, prostate cancer has the second highest incidence of all cancers in males with incidence
and mortality being much higher in affluent developed countries. Risk and progression of the disease
may be linked to both genetic and environmental factors, especially dietary factors. Tea and coffee
are two of the most popular beverages in the world and have been investigated for possible effects on
health outcomes, including cancer. However, very little dietary advice for their consumption exists.
The evidence for a relationship between coffee or tea consumption and prostate cancer is reviewed in
this paper. While current evidence indicates that coffee is a safe beverage, its consumption probably
has no relationship with prostate cancer. Tea, especially green tea, has shown some potential in the
prevention of prostate cancer. While evidence from epidemiologic studies is currently inconclusive,
strong evidence has emerged from animal and in vitro studies. We also consider what level of evi-
dence is required to make recommendations for preventive measures to the public. Although evidence
on the relationship between coffee, tea and prostate cancer is not complete, we consider it strong
enough to recommend tea as a healthier alternative to coffee.

Keywords: Coffee / Dietary guidelines / Epidemiologic studies / Prostate cancer / Tea /

Received: April 30, 2008; revised: June 2, 2008; accepted: June 5, 2008

1 Introduction

Worldwide, prostate cancer has the second highest inci-
dence of all cancers in males [1] and in many developed
countries, it is the most common neoplasm in men beyond
middle age [2]. Prostate cancer incidence and mortality
varies widely between geographic regions, with overall
rates in high-income countries such as Australia and USA
being nearly six times higher than in middle to low-income
countries such as China, Japan, and African countries [1,
2]. However, the reported incidence in countries such as
China is increasing rapidly [3]. This variation in incidence
suggests that risk and progression of the disease may be
linked to both genetic and environmental factors, especially
dietary factors. Discovering possible chemopreventive diet-
ary factors is important in the case of prostate cancer due to
the aging populations of most Western nations. Prostate
cancer is also an ideal candidate disease for chemopreven-

tion because relative survival after diagnosis is high [4] due
to its long latency and typical detection in older men who
usually have a slower rate of progression [2].

Tea and coffee are two popular beverages that have been
investigated for possible effects on health outcomes, includ-
ing cancer. Coffee was once suspected of increasing the risk
of various cancers [5] whereas tea, especially green tea has
shown promise in the prevention of cancers including gas-
trointestinal tract [6 – 8], skin [9, 10], breast [11 – 13], pan-
creas, esophagus, and lung [14]. Epidemiological studies
on tea and prostate cancer have generated inconsistent
results [15], however a recent Chinese case-control study
reported a significant dose response relationship between
green tea consumption and prostate cancer risk [16].

Despite coffee and tea being two of the most commonly
consumed beverages all over the world [17], very little diet-
ary advice for their consumption exists. Recently, several
reviews have addressed the potential relationship between
tea and prostate cancer prevention [18 – 20]. Although they
have concluded that tea or tea compounds show promise in
prostate cancer prevention, little effort has been made to
translate these findings into public health guidelines. This
paper therefore, considers whether evidence is currently
strong enough to make any dietary recommendations on tea
or coffee and prostate cancer prevention by presenting the
epidemiologic evidence as well as mechanistic evidence
from in vitro and animal model studies.

Correspondence: Professor Colin W. Binns, School of Public Health,
Curtin University of Technology, GPO Box U 1987, Perth, WA 6845,
Australia
E-mail: c.binns@curtin.edu.au
Fax: +61-8-92662958

Abbreviations: CI, confidence interval; EGCG, ( – )epigallocatechin-
3-gallate; GTC, green tea catechin; OR, odds ratio; RCT, randomized
controlled trial; RR, relative risk

i 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.mnf-journal.com

DOI 10.1002/mnfr.200800218 Mol. Nutr. Food Res. 2009, 53, 256 – 265

Mol. Nutr. Food Res. 2009, 53, 256 –

265

2 Materials and methods

Published articles were located by searching the PubMed,
CINAHL, and ProQuest databases with the keywords “tea”
and “prostate cancer” and “coffee” and “prostate cancer”
without any restriction on publication date. The corre-
sponding reference lists were also searched for relevant
articles. The National Health and Medical Research Coun-
cil’s Levels of Evidence for Clinical Practice Guidelines
were used to divide and evaluate existing evidence for both
coffee and tea [21]. The level of evidence refers to the study
design used to minimize bias with the highest level involv-
ing a systematic review of randomized controlled trials
(RCTs), followed by at least one properly designed RCT,
then pseudo- RCTs, then observational studies. Also con-
sidered is evidence quality – methods used to minimize
bias in the study design and conduct, evidence relevance –
extent to which findings can be applied in other settings,
and strength of evidence – magnitude and reliability of the
treatment effect [21]. In addition, animal model and in vitro
studies have been included to establish biological plausibil-
ity of the observed effects.

3 Results

3.1 Coffee and tea: Patterns of consumption

Tea and coffee are two of the world’s most popular bever-
ages and both are consumed in most countries [17]. World-
wide, tea consumption is second only to water and approxi-
mately three cups of tea are drunk for every cup of coffee
[17]. However, coffee is the preferred drink throughout the
majority of Europe and the Americas with 71.5% of coffee
consumption taking place in developed countries [17]. Tea
consumption dominates in the developing world with
76.6% of consumption taking place in these countries [17].
Tea is also the more popular beverage in liters in Australia
[22] and Britain [17]. Of the total tea produced and con-
sumed, 78% is black, 20% green, and less than 2% oolong
[23]. Black tea is primarily consumed in Western countries
while green tea is mainly consumed in China, Japan, India,
and a few countries in North Africa and the Middle East
[23].

3.2 The composition of tea and coffee

Coffee is produced by infusing ground, roasted coffee
beans, the most popular forms being Coffea arabica and C.
canephoria var. robusta [17]. The three most common kinds
of tea are green, black, and oolong tea and these are all
derived from the Camellia sinensis plant [24]. Green tea
leaves are steamed when harvested to prevent fermentation
whereas black tea is fermented as leaves wither then are
rolled and crushed. Oolong tea is partially fermented and
considered to be about half as fermented as black tea [24].

Coffee and tea are both complex substances consisting of
many compounds. Coffee is reported to contain more than a
thousand different chemicals, several of which have been
shown to have physiological effects [5]. The stimulatory
effects of caffeine [25] and antioxidant activity of chloro-
genic acid and caffeic acid have been extensively
researched [26] and other micronutrients including magne-
sium, potassium, niacin, and vitamin E have also been sus-
pected of health effects [5].

Green, oolong, and black teas all contain potentially can-
cer preventive compounds, however the different manufac-
turing process changes the profile of these compounds con-
siderably [24]. Polyphenols are the most researched compo-
nent of tea. Most of the polyphenolic content of green tea is
flavanols, know as catechins, including (–)-epicatechin,
(–)-epicatechin-3-gallate, (–)epigallocatechin, and (–)epi-
gallocatechin-3-gallate (EGCG) [24]. In black and oolong
tea, the fermentation process results in oxidation of simple
polyphenols to complex theaflavins and thearubigins and
reduces the catechin content of black tea to approximately a
third of that of green tea [24].

3.3 Coffee and prostate cancer: Epidemiologic
evidence

Coffee has been studied extensively for relationships with
various cancers. Early case-control studies indicated a pos-
sible positive relationship between coffee consumption and
several cancers [27, 28]. It is possible however, that the
association between coffee drinking and other unhealthy
behaviors such as smoking and lack of exercise generated
these observations as subsequent studies have produced lit-
tle evidence of any significant relationship with cancer [5].

The possible relationship between coffee and prostate
cancer has been investigated in epidemiologic studies since
the 1980s. We identified seven case-control [29 – 35] and
four cohort studies [36 – 39] reporting on coffee consump-
tion and prostate cancer risk and two cohort studies examin-
ing prostate cancer mortality [40, 41]; see Table 1. Results
of these studies were very inconsistent. Overall, no relation-
ship has emerged with almost all studies reporting no asso-
ciation or nonsignificant positive and nonsignificant
inverse associations with prostate cancer. No dose-response
relationship emerged from any of these studies and only
one reported statistically significant results [29]. However,
this hospital-based case-control study conducted in Taiwan,
only quantified coffee consumption as “yes” or “no” and
the number of coffee consumers in the sample was very low
consisting of 31 cases (13.1%) and 36 controls (7.5%) [29].
It is also possible that consumption of coffee in this Taiwa-
nese study was associated with other aspects of a Western
diet that may increase cancer risk. Although many of the
other studies quantified coffee consumption in more detail
and were all conducted in North American and European
populations where coffee drinking is more common, coffee

257

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A. H. Lee et al. Mol. Nutr. Food Res. 2009, 53, 256 – 265

was rarely the main focus of the dietary questionnaire.
Hence, exposure misclassification including cup size and
caffeine variation of particular coffees [42] as well as con-
founding may have affected the results of these studies.

3.4 Coffee and prostate cancer: In vitro and animal
evidence

A vast amount of research in animals and in vitro cell cul-
tures has also generated inconsistent findings about the role
of coffee and its components in cancer. Coffee contains
large number of compounds, some of which have been
identified as having potentially chemopreventive effects
including caffeine [43], chlorogenic and caffeic acids [44]
and the diterpenes cafestol and kahweol [45], and others,
having potentially carcinogenic effects also including caf-
feine and methylglyoxal [46].

Some early evidence from molecular, cellular, and animal
studies indicated that coffee could inhibit relevant DNA

repair mechanisms, modify the apoptotic response and per-
turb cell cycle checkpoint integrity [47, 48]. One study
reported an association between coffee drinking and muta-
tions in the K-ras gene in exocrine pancreatic cancer [49].
However, the majority of research has reported a wide range
of chemopreventive effects [45, 46]. Recent in vitro and in
vivo studies in rats have also shown that coffee can suppress
proliferation and invasion, possibly by inducing cell cycle
arrest, apoptosis and the invasion by scavenging ROS, and
can ameliorate abnormal lipoprotein profiles [50].

It is possible that coffee may possess both mutagenic and
antimutagenic potential. In the past there has been concern
that coffee consumption may increase the risk of bladder
and pancreatic cancer, however, two recent reviews have
concluded that it is unlikely to have any substantial effect
on risk [1, 51]. For all other cancers, the World Cancer
Research Fund reported that evidence is too limited to draw
a conclusion [1]. In light of all the evidence, coffee prob-
ably has no relationship with the risk of prostate cancer.

258

i 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.mnf-journal.com

Table 1. Summary of epidemiologic studies of coffee and prostate cancer

Country Study design Sample size Coffee consumption level Results: Adjusted OR,
RR (95% CI) or p for
trend

Reference

Taiwan Case-control (hospital-
based

)

237 cases, 481 controls Coffee drinking versus non-
drinking

OR: 1.88 (1.07 – 3.30) [29]

Canada Case-control (popula-
tion-based)

399 cases, 476 popula-
tion controls, 621 cancer
controls

A119 drink years versus a57
drink yearsa)

OR: 1.1 (0.6 – 2.0) for
population controls

[30]

Greece Case-control (hospital-
based)

320 cases, 246 controls F3 cups/day versus none p for trend: 0.27 [31]

Canada Case-control (popula-
tion-based)

1623 cases, 1623
controls

a1 cup/day versus none
1 – 3 cups/day versus none
F4 cups/day versus none

OR: 0.8 (0.6 – 1.1)
OR: 1.0 (0.7 – 1.3)
OR: 1.1 (0.8 – 1.5)

[32]

Canada Case-control (popula-
tion-based)

617 cases 637 controls 0 – 500 g/day versus none
>500 g/day versus none

OR: 0.84 (0.58 – 1.22)
OR: 0.97 (0.65 – 1.44)

[33]

Sweden Case-control (popula-
tion-based)

406 cases, 1218 controls 1 – 2 cups/day versus none
3 – 5 cups/day versus none
6 – 9 cups/day versus none

OR: 1.77 (0.65 – 5.09)
OR: 1.99 (0.78 – 5.46)
OR: 1.91 (0.73 – 5.30)

[34]

USA (Utah) Case-control (popula-
tion-based)

326 cases, 685 controls 1 – 20 cups/week versus none
A20 cups/week versus none

OR: 0.99 (0.68 – 1.47)
OR: 1.09 (0.75 – 1.60)

[35]

Canada Cohort (retrospective) 3400 (145 developed
prostate cance

r)

A250 mL/day versus none RR: 1.4 (0.84 – 2.32) [36]

USA (Hawaii) Cohort 20 316 (198 developed
prostate cancer)

A2.5 cups/day versus none RR: 1.1 (0.7 – 1.7) [37]

USA (Hawaii) Cohort 7999 (174 developed
prostate cancer)

2 – 4 cups/week versus f 1
cup/week F5 cup/week versus
f1 cup/week

RR: 0.96 (0.39 – 2.37)
RR: 0.92 (0.59 – 1.44)

[38]

USA (Hawaii) Cohort 7355 men, 108 prostate
cancer

Not stated Not stated, no signifi-
cant relationship ob-
served

[39]

USA

Cohort (examined
mortality)

17 633 men, 149 died of
prostate cancer

3 – 4 cups/day versus
<3 cups/day F5 cups/day versus <3 cups/day

RR: 0.8 (0.6 – 1.2)

RR: 1.0 (0.6 – 1.6)

[40]

USA
(California)

Cohort (examined
mortality)

21 295 seventh day
adventists, 113000 non
adventists

Not stated Not stated, nonstatisti-
cally significant inverse
association

[41]

a) Drink years: average number of drinks daily multiplied by duration of drinking in years.

Mol. Nutr. Food Res. 2009, 53, 256 – 265 259

i 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.mnf-journal.com

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A. H. Lee et al. Mol. Nutr. Food Res. 2009, 53, 256 – 265

3.5 Tea and prostate cancer: Epidemiologic
evidence

Table 2 summarizes epidemiologic studies of tea and pros-
tate cancer from the literature. A hospital-based case-control
study in China, where green tea is predominantly consumed
provides promising evidence for a role of tea in prostate can-
cer prevention [16]. A total of 130 cases and 274 hospital
inpatients without any malignant disease were interviewed
in detail about the type, duration, quantity, and frequency of
tea consumption. Compared to nontea drinkers, the odds
ratio (OR) was 0.28 (95% confidence interval (CI): 0.17 –
0.47) for those drinking green tea, 0.12 (95% CI: 0.06 – 0.26)
for drinking tea longer than 40 years, 0.09 (95% CI: 0.04 –
0.21) for consuming more than 1.5 kg of tea leaves per year,
and 0.27 (95% CI: 0.15 – 0.48) for drinking more than three
cups (1 L) daily. According to the US Food and Drug Admin-
istration, this study received high methodological quality
ratings [52]. Another hospital-based case control study of
140 cases and 140 controls in Japan reported an OR for
drinking two to ten cups of green tea daily ranging from 0.67
to 0.99 [53], but did not attain statistical significance, prob-
ably due to the small sample size [52].

A slight reduction in prostate cancer risk was also
reported by a larger Canadian case-control study involving
617 cases and 637 population controls [33]. An OR of 0.70
(95% CI: 0.50 – 0.99) was reported with consumption of
more than 500 g (approximately two cups) of tea per day
[33]. Another case-control study conducted in Montreal,
Canada [30] reported an increased risk and two conducted
in Canada [32] and Utah, USA [35] reported no association
between tea consumption and prostate cancer, although
alternative explanations for the observed effects could not
be ruled out [30].

Cohort studies have reported inconsistent results, how-
ever a recent prospective cohort study in Japan reported a
significant dose-dependant relationship between green tea
consumption and reduced risk of advanced prostate cancer
but no association with localized prostate cancer [54].
These findings suggest the effects of green tea may vary
according to prostate cancer stage and are supported by ear-
lier results of small clinical trials and animal model studies
[55 – 57]. In the cohort study, the multivariate relative risk
(RR) for advanced prostate cancer for consumption of five
or more cups/day versus less than one cup was 0.52 (95%
CI: 0.28 – 0.96) [54]. Another Japanese cohort study of
19 561 men (110 cases) reported a slight but nonsignificant
decrease in risk [58]. The hazard ratio for consumption of
five cups of green tea/day versus a 1/day was 0.85 (95% CI:
0.50 – 1.43). Another cohort of 7999 men of Japanese
ancestry living in Hawaii showed a borderline significant
increase in risk for green tea consumption, OR = 1.47 (95%
CI: 0.99 – 2.19), but no association for black tea [38]. How-
ever, an earlier cohort study involving 7833 Hawaii men of
Japanese ancestry observed a weak albeit significant

inverse association between black tea intake and prostate
cancer incidence, with RR being 0.6 for consuming more
than one cup daily versus almost never [59]. Three subse-
quent cohort studies conducted in the UK [60], Italy [61],
and Canada [36] where black tea is predominantly con-
sumed [23], found little association between tea consump-
tion and prostate cancer incidence.

The epidemiologic evidence to date is limited in several
aspects. Of the three studies reporting positive results [16,
53, 54] two were relatively small case-control study designs
that are open to bias due to their retrospective design [52]. In
addition, the majority of studies lacked comprehensive
assessment of tea intake. For example, only six specified the
type of tea consumed as green [16, 38, 53, 54, 58] or black
[38, 53, 59]. Although green tea has produced more promis-
ing results, only a small number of studies (5) specifically
examined its consumption. Also, many studies did not com-
prehensively assess level of tea intake, for example, one clas-
sified consumption only as “never” or “ever” [38]. In addi-
tion, few studies considered duration of tea drinking or the
preparation method in their assessment. Various methodo-
logical issues including the failure to control for potential
confounding factors also could have affected the findings.

The possibly more promising results for green than black
tea could be the result of several factors. The higher cate-
chin content and antioxidant activity of green tea is one pos-
sibility. Also, tea intake was considerably higher in the Chi-
nese study [16] and prospective study in Japan [54] than
any others, suggesting low consumption might explain the
lack of significance elsewhere. In addition, confounding
factors including Asian-style diets such as the consumption
of soy products and certain vegetables, low fat and alcohol
intake, as well as the small numbers of studies published
may contribute.

3.6 Tea and prostate cancer: Clinical trials

A recent double blind placebo controlled study examined the
effect of green tea catechins (GTCs) on high-risk men with
high-grade prostate intraepithelial neoplasia [55]. Of the 30
men treated daily with GTC capsules, only one tumor was
diagnosed after 1 year as opposed to nine tumors diagnosed
in the 30 placebos. Despite the small sample, this study pro-
vides the first evidence that GTC may possess potent in vivo
chemopreventive activity in men prone to prostate cancer.
Another small clinical trial reported minimal clinical activ-
ity of green tea extract capsules in 15 men already diagnosed
with hormone refractory prostate cancer [56].

3.7 Animal model studies on tea and prostate
cancer

Consistent evidence has emerged from animal models for a
protective effect of tea and its components against prostate

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Mol. Nutr. Food Res. 2009, 53, 256 – 265

cancer. Studies in the transgenic adenocarcinoma of the
mouse prostate model have reported reduction in the devel-
opment of prostate cancer with feeding of GTCs [57].
Apoptosis and significant inhibition of tumor development
and metastasis was also reported with oral infusion of green
tea polyphenols at a human dose equivalent to six cups of
green tea per day [62] and with oral feeding of 0.1% GTC
[63]. Injecting EGCG has also been shown to inhibit pros-
tate cancer growth in nude mice [63]. In addition, black tea
extract has recently showed a significant protective effect
against testosterone induced oxidative injury in Wistar rat
prostate [64]. Significant inhibition in growth of implanted
prostate tumors in athymic nude mice and reduction in pros-
tate specific antigen was also recently reported with treat-
ment of water extract of black tea, theaflavins as well as
green tea polyphenols [65].

3.8 In vitro cell culture studies on tea and prostate
cancer

In vitro cell culture studies have consistently revealed bio-
logically plausible mechanisms by which tea polyphenols
and EGCG may affect the development or progression of
prostate and other cancers. These components can inhibit
cell growth and induce apoptosis through various pathways
and can affect multiple cellular events [66].

3.8.1 Antioxidant properties of green tea
Androgens induce oxidative stress, making them key fac-
tors in prostate cancer development [64]. Catechins, espe-
cially EGCG, are antioxidants or highly effective scav-
engers of oxidizing molecules including singlet oxygen and
various free radicals that many contribute to DNA damage
and tumor promotion [67].

3.8.2 Modulation of cyclin kinase inhibitor
One pathway by which cell growth is inhibited and apopto-
sis induced is through the modulation of cyclin kinase
inhibitor. Cyclins are over expressed in prostate cancer and
EGCG has been shown to upregulate cyclin-dependent kin-
ase inhibitors such as p21WAFI/CIPI [68 – 71], p27KIPI, p16INK4A,
and p15INK4B and down modulate cyclin D1, cyclin E, cdk2,
cdk4, and cdk6 [72].

3.8.3 Effects on proteasome activity
EGCG has also been reported to be a proteasome inhibitor,
capable of inducing growth arrest in tumor cells by inhibit-
ing the system that allows cell – cycle progression and pro-
tects tumor cells against apoptosis [73].

3.8.4 Alteration of gene expression
Analysis of gene expression found that 25 genes in LNCaP
cells, belonging to different regulatory pathways responded
to treatment by EGCG [74]. It induced 16 growth inhibitory
genes and repressed nine genes most of which belong to the

G-protein signaling network. The most prominent suppres-
sion was of the PKC-agene [74]. Green tea polyphenols can
also cause significant inhibition of insulin-like growth fac-
tor in mice [62], while EGCG may influence the tumor sup-
pressor gene p53 [70, 71].

3.8.5 Influence on enzymes
EGCG has been shown to inhibit transcription factors
including p53 and NF-jB. This leads to the activation of
p21WAFI and Bax, changing the ratio of Bax to Bcl-2 and
activating capases, enzymes that favor apoptosis [71]. Other
enzymes also targeted by green tea polyphenols or EGCG
include 5a-reductases [75], fatty acid synthase [76], cyclo-
oxygenase-2 [72], urokinase-like plasminogen activator
[68], ornithine decarboxylase [77], nitric-oxide synthase
[78], mitogen-activated protein kinase [79], and matrix
metalloproteinase [80]. A recent study suggests that activa-
tion of ERK1/2 (a member of the mitogen-activated protein
kinase family) is partially responsible for the antiprolifera-
tive effects of EGCG [81].

4 Discussion

Despite coffee and tea being two of the most commonly
consumed beverages in the world [17], very little dietary
advice on their consumption exists. In the case of coffee,
this review of epidemiologic, animal and in vitro evidence
indicates that coffee consumption probably has no relation-
ship with the risk of prostate cancer. A recent review from
the World Cancer Research Fund/American Institute for
Cancer Research also stated the level of evidence for effects
of coffee on prostate cancer as “limited- no conclusion” [1].
Research to date agrees that coffee consumption is safe for
healthy adults [25] but probably has no preventive effects
on chronic diseases including cancers [5] and cardiovascu-
lar disease [82 – 84].Tea is also a safe beverage but tea and
its components, especially green tea have shown promise in
the prevention of prostate cancer in animal and in vitro stud-
ies, in some epidemiological studies and a small clinical
trial. Evidence also exists for a possible preventive role of
tea for other cancers [85 – 87] and cardiovascular disease
[88 – 90].Current evidence for a role of tea in prostate can-
cer prevention however, is definitely not conclusive and fur-
ther studies are warranted [1, 91]. The inverse relationships
reported by the Japanese prospective study [54] and Chi-
nese case-control study [16] are promising but have not
been replicated. Case-control studies, in particular are sub-
ject to bias due to their retrospective design [52]. Consistent
results have also been reported in animal and in vitro studies
but these effects are not always reproducible in humans.
Also, different types and brands of tea vary greatly in terms
of their polyphenol profiles and content [92] and animal
and in vitro studies often use very high concentrations of tea
compounds that may not reflect the actual levels found in

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A. H. Lee et al. Mol. Nutr. Food Res. 2009, 53, 256 – 265

the human body after ingestion [93]. The oral bioavailabil-
ity of GTCs is low and the effective concentration levels
determined in in vitro studies are many fold more than the
resulting systemic levels in humans meaning in vitro effects
should be interpreted with caution [19, 94].

The National Health and Medical Research Council’s
hierarchy of evidence describes a meta-analysis or pooled
analysis of data from a number of RCTs as the gold standard
for clinical practice guidelines [21]. However, the bulk of
evidence on tea and prostate cancer comes from epidemio-
logical as well as animal and in vitro studies, meaning the
level of evidence cannot rise above level III. Kroke et al.
[95] acknowledge that reaching this gold standard is usually
unrealistic when making recommendations for preventive
rather than therapeutic measures. Using RCTs to evaluate
the effect of lifetime tea drinking on the prostate cancer risk
would be difficult and expensive. It would be difficult to
use controls due to the impracticality of blinding and ran-
domizing them and the long latency of prostate cancer.
Prostate cancer is usually diagnosed in men aged over 65
[1]. However, these factors also make this cancer an ideal
candidate for chemoprevention. Considering this, future
research should utilize a variety of observational study
designs and strengthen current evidence through shorter-
term RCTs that examine the effects of tea consumption on
prostate cancer development in men with premalignant
lesions.It is clear that current evidence is not nearly strong
enough to make recommendations when standards for ther-
apeutic substances are considered. However, if nutritionists
are asked to recommend either tea or coffee as the healthier
option, we believe evidence is sufficient to recommend tea
over coffee. World trends indicate that consumption is mov-
ing away from tea toward coffee. This is the case, for exam-
ple, in Australia [22]; see Table 3. In addition, the aging
population of many developed countries means the inci-
dence of prostate cancer and other chronic diseases is likely
to increase. Therefore, waiting decades for more complete
evidence to emerge before making any dietary guidelines
on tea and coffee could result in unnecessary morbidity and
mortality. Tea is both a safe and popular beverage, its pro-
posed health effects are biologically plausible and recom-
mending its consumption is not inconsistent with any pre-
vious public health advice. These factors make it suitable to
create dietary guidelines recommending the consumption
of tea as a healthier choice than coffee [96].

Evidence on the dosage of tea required for effect, the
efficacy of absorption in the human body and the different

chemopreventive effects of green, black, and oolong teas is
required before any specific and quantifiable dietary guide-
lines regarding tea consumption and prevention of prostate
and other cancers can be made.

The authors have declared no conflict of interest.

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