Nutrition xxx (2013) 16

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Nutrition
journal homepage: www.nutritionjrnl.com

Applied nutritional investigation

Dietary ber intake modies the association between secondhand smoke

exposure and coronary heart disease mortality among Chinese non-smokers
in Singapore
Maggie L. Clark Ph.D. a, *, Lesley M. Butler Ph.D. b, c, Woon-Puay Koh Ph.D. d, e, Renwei Wang M.D. b,
Jian-Min Yuan M.D., Ph.D. b, c
a
Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO, USA
b
The University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA
c
Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA
d
Duke-NUS Graduate Medical School, Singapore, Singapore
e
Saw Swee Hock School of Public Health, National University of Singapore, Singapore

a r t i c l e i n f o a b s t r a c t

Article history: Objective: Secondhand smoke (SHS) exposure increases the risk for coronary heart disease (CHD)
Received 16 January 2013 by an estimated 25% to 30% via oxidative stress and inammatory mechanisms that may be
Accepted 6 April 2013 ameliorated by dietary components. The aim of this study was to evaluate the hypothesized
modifying role of nutrients with known antioxidant and/or anti-inammatory properties on the
Keywords: relationship between SHS exposure and CHD mortality.
Coronary heart disease
Methods: Detailed SHS exposure and dietary information was collected among 29,579 non-smokers
Dietary ber
in the Singapore Chinese Health Study, a prospective population-based cohort. The evaluation of
Environmental tobacco smoke pollution
Indoor air pollution whether or not dietary factors (b-cryptoxanthin, lutein, u-3 polyunsaturated fatty acids, ber,
Mortality isothiocyanates, and soy isoavones) modied the relationship between SHS exposure and CHD
Secondhand smoke mortality was conducted within multivariable Cox proportional hazards models by creating an
Singapore interaction term between the potential dietary effect modier (lowest quartile of intake versus the
second through fourth quartiles of intake) and the SHS exposure (none versus living with at least
one smoker[s]).
Results: Evidence for a main-effects association between SHS exposure and risk for CHD mortality
was not observed. In stratied analyses by levels of selected dietary nutrient intake, ber
modied the effects of SHS exposure on risk for CHD mortality (P for interaction 0.02). The
adjusted hazards ratio for SHS exposure (living with at least one smoker[s] versus living with no
smokers) and CHD mortality was 1.62 (95% condence interval, 1.002.63) for those with low-
ber intake. In contrast, among those with high-ber intake, there was no association with
SHS exposure.
Conclusion: We provide evidence that a diet high in ber may ameliorate the harmful effects of SHS
exposure on risk for CHD mortality.
2013 Elsevier Inc. All rights reserved.

Introduction
MLC designed the analytic strategy, conducted the data analyses, interpreted
the results, and wrote the manuscript. LMB directed the implementation, helped Cardiovascular disease (CVD) remains the number 1 cause of
in designing the analytic strategy, results interpretation, and writing of the
death worldwide [1]. Although most cases are due to risk factors
manuscript. WPK directed the Singapore Chinese Health Study implementation,
including quality assurance and control, and edited the manuscript. RW main- related to individual behavior and lifestyle (e.g., active tobacco
tains the Singapore Chinese Health Studys dataset, including constructing the use, unhealthy diet, and lack of physical activity), a strong
analytic data set for this analysis, assisted in designing the analytic strategy, and argument has been made to evaluate factors that are not per-
edited the manuscript. JMY directed the study implementation, including sonally modiable [2]. With only 7.4% of the worlds population
quality assurance and control, helped with results interpretation and editing of
the manuscript.
living in areas that are covered by smoke-free legislation [2],
* Corresponding author. Tel.: 970-491-2891; fax: 970-491-2940. exposure to secondhand smoke (SHS) is one of the most common
E-mail address: maggie.clark@colostate.edu (M. L. Clark). sources of indoor air pollution worldwide, with as many as 35% of
0899-9007/$ - see front matter 2013 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.nut.2013.04.003

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2 M. L. Clark et al. / Nutrition xxx (2013) 16
adults and 40% of children regularly exposed [3]. SHS exposure
increases the relative risk for coronary heart disease (CHD)
and overall CVD by an estimated 25% to 30% [4,5]. Approximately
600,000 deaths were attributable to SHS in 2004 [3]; however,
much uncertainty remains surrounding this estimate due to
the potential inuence that other risk factors (e.g., individual
lifestyle, community, and societal factors) have on the magni-
tudes of effect across various populations or population
subgroups [2,5]. Therefore, although a major priority is the
continued support of programs aimed to reduce smoking initi-
ation and increase smoking cessation; there is also a need to
identify factors that modify the effects of SHS exposure on CHD
outcomes [5].
SHS contains a complex mixture of PM2.5 (particulate matter
less than 2.5 microns in diameter) constituents that have
been implicated in CVD development [6,7] by inducing proin-
ammatory responses through the generation of oxidative stress
[810]. Diets are a source of compounds with anti-inammatory
and antioxidant properties, such as u-3 polyunsaturated fatty
acids (PUFAs) [11,12], carotenoids [13,14], and ber [1519], that
may counteract the adverse effects of SHS exposures on disease
risk. Epidemiologic evidence implicates diet as a modier of the
relationships between ambient air pollutant exposures and
adverse respiratory end points [20] and total mortality [21].
Additionally, we have demonstrated that ber consumption
modies the relationship between childhood SHS exposure
and risk for chronic respiratory symptoms among adult
non-smokers [22].
The potential modifying effect of dietary factors on the rela-
tionship between air pollutant exposures and cardiovascular
outcomes has not yet been extensively investigated [2326].
In a repeated-measures study, Baccarelli et al [23] reported that
the adverse effects of ambient PM2.5 exposures on heart rate
variability, an independent predictor of cardiovascular mortality,
were abrogated among those with higher intake of methyl
nutrients including B6, B12, and methionine. Similarly, supportive
evidence has been provided from trials where those who were
randomized to receive daily supplementation of sh oil as
a source of u-3 PUFAs had reduced effects of particulate matter
on heart rate variability or biomarkers of oxidative stress
[2426]. Although compelling, these previous studies were
limited by their small size and primary focus on subclinical
indicators of cardiovascular health. To date, there are no studies
that have investigated the possible modifying effect of diet on
the relationship between non-ambient sources of air pollution
and CVD mortality.
Air pollutant exposures are universal and often unintentional
and, in the case for SHS exposure reductions, require substantial
behavioral changes that are exceedingly difcult to implement
in individuals or populations. Recommending avoidance is not
always feasible; thus, identifying dietary factors that ameliorate
the cardiovascular-related adverse effects of air pollution will
have benecial public health consequences [27]. We hypothe-
sized that intake of specic dietary components, such as carot-
enoids (i.e., b-cryptoxanthin and lutein), u-3 PUFAs, ber,
isothiocyanates, and soy isoavones, would inuence mortality
due to SHS-associated CVD. By informing the mechanisms that
underlie the dietSHS interactions, we can provide insights into
specic diet-based prevention strategies. We present the rst
evaluation of the potential modifying role of dietary factors with
known antioxidant and/or anti-inammatory properties on the
relationship between SHS exposure and risk for CHD mortality
using data from a large prospective population-based cohort of
lifetime non-smoking Chinese adults in Singapore.
Please cite this article in press as: Clark ML, et al., Dietary ber intake modies the association between secondhand smoke exposure and...,
Nutrition (2013), http://dx.doi.org/10.1016/j.nut.2013.04.003
Materials and methods
The design of the Singapore Chinese Health Study has been described
previously [28]. Briey, the cohort was drawn from a population of men and
women of Chinese ethnicity, ages 45 to 74 y, who were permanent residents or
citizens of Singapore and resided in government-built housing estates that
housed 86% of the population during the period of participant enrollment. The
study was restricted to individuals belonging to the two major Chinese dialect
groups in Singapore: Cantonese and Hokkien. Between April 1993 and December
1998, we enrolled 63 257 individuals (85% of those eligible). Baseline question-
naires were administered by trained interviewers in the participants homes and
elicited information on demographics, diet, active smoking, and medical history.
Beginning in 1999 at follow-up 1, participants were interviewed by telephone
regarding active smoking and history of SHS exposure before and after age 18.
The average time between the baseline and follow-up interviews was 5.8 y.
To date, less than 1% of cohort members have been lost to follow-up. For this
analysis, we restricted the population to the 29 579 disease-free (CVD and
cancer), lifetime never-smokers with at least 5 y of follow-up after completing
the follow-up 1 interview.
The study protocol was reviewed and approved by the Institutional Review
Boards of the National University of Singapore and the University of Pittsburgh.
Written informed consent was obtained from all participants.
Exposure to SHS was ascertained by asking participants about the number of
smokers in their household during their childhood (dened as birth to age 18),
adult life (dened as since age 18), and currently (at the time of the follow-up
1 interview). For example, to assess current SHS exposure, the participant was
asked, Does anyone who currently lives in your home smoke at home on a daily
basis? SHS exposure during work was ascertained by asking if the participant
had ever had a job in which he or she could smell cigarette smoke on a daily basis.
To evaluate cumulative effects of exposures to SHS during different time periods
and at different locations, we also created variables based on the combination
of reporting exposures at home during childhood, since age 18, and currently, as
well as reporting exposure at work.
We used a 165-item quantitative food frequency questionnaire (FFQ),
developed for and validated in the study population [29], to assess usual diet over
the past year. Average daily intake of roughly 100 nutrient and non-nutrient
compounds was computed for each study participant based on the Singapore
Food Composition Database [29]. To adjust for energy intake, all nutrients were
expressed in weight unit per 1000 kcal or percentage of total energy.
Deaths were identied through record linkage with the Singapore Registry
of Births and Deaths. We updated mortality data through December 31, 2011.
Underlying causes of death were coded according to the International Classi-
cation of Diseases, Ninth Revision (ICD9); codes 410414, 427.5, 429.2, and
798 were used to dene CHD deaths. Of the 52 322 individuals who participated
in follow-up 1, we excluded participants with the following prevalent diseases:
cancer (n 2503), self-reported physician-diagnosed CHD (n 3591), or stroke
(n 1410). This resulted in 44 818 participants free of cancer and clinical CVD. We
further restricted the population to self-reported lifetime never-smokers (we
excluded 14 221 current smokers, or those with a history of smoking) and those
with self-reported information on SHS exposure (n 5 participants with missing
data). Additionally, we excluded the rst 5 y of follow-up from the follow-up
1 interview when the exposure to SHS was assessed because we were con-
cerned that those with undiagnosed CHD might have altered their behaviors
(potential for reverse causality) (we excluded n 1,013 with less than 5 years of
follow-up). In this restricted population (n 29 579), 311 incident CHD deaths
were identied through the end of 2011.
We dened SHS exposure using two categories: living with no smokers and
living with at least one smoker(s). We compared selected population charac-
teristics stratied by sex and SHS exposure. Cox proportional hazards regression
modeling was used to estimate the relative risk (hazard ratio [HR]) and 95%
condence interval (CI) of SHS exposure on CHD mortality. Follow-up for each
participant was calculated as time from 5 y after the date of the rst follow-up
interview to the date of CHD death or other causes of death, the date of migra-
tion out of Singapore, or December 31, 2011, whichever occurred rst. Multi-
variable models were assessed and included the following covariates: age at
follow-up interview (years), body mass index (BMI, kg/m2), education (no
formal education, primary school, and secondary school or beyond), and dialect
group (Cantonese, Hokkien). Moderate physical activity (none; 30 min to 3 h/wk;
> 3 h/wk), alcohol consumption (based on frequency and amount of beer, rice
wine, grape wine, and hard liquor consumption), and ever use of nonsteroidal
anti-inammation drugs (NSAIDs) were assessed as potential confounders;
however, these variables were not included in the nal models as inclusion did
not appreciably change the associations.
To evaluate the potential modifying effects of dietary factors (b-cryptoxanthin,
lutein, u-3 PUFAs, ber, isothiocyanates, and soy isoavones) on the relationship
between SHS exposure and CHD mortality, we created an interaction term bet-
ween the dietary variable (i.e., lowest quartile of intake versus the second through
fourth quartiles of intake) and SHS exposure (within the models described above).
 M. L. Clark et al. / Nutrition xxx (2013) 16 3

Dietary quartiles were dened based on nutrient density distributions within the
entire cohort. Statistical interaction was evaluated using the maximum likelihood
estimates; c2 P-value < 0.05 was considered statistically signicant.
Results
The average age at the follow-up 1 interview was 59.9 y (SD,
7.5) and the average length of follow-up was 5.5 y (SD, 1.3) with
a total of 161 422 person-years of follow-up. The 311 identied
CHD deaths were due almost exclusively to acute myocardial
infarction (47.3%; ICD 9 code 410.0) and chronic ischemic heart
disease (51.1%; ICD 9 code 414.9). Chronic ischemic heart disease
accounted for 58.1% of CHD deaths in men compared with 48.4%
in women.
Women represented 77% of lifetime never-smokers. Com-
pared with men, women were more likely to live with at least
one smoker(s) or have no formal education (Table 1). Self-
reported use of NSAIDs was low (1.9%). Dietary intake of
selected nutrients was similar by SHS exposure and by sex, with
the following exceptions (Table 1). b-Cryptoxanthin consump-
tion was higher among both men and women without SHS
exposure, compared with those who lived with at least one
smoker(s). Additionally, consumption of isothiocyanates and soy
isoavones was slightly higher among women compared with
men (Table 1).
Overall, currently living with one or more smoker(s) was not
associated with risk for CHD mortality, compared with living
with no smokers (Table 2). Although not statistically signicant,
the association between living with one or more smoker(s) and
risk for CHD mortality was stronger among men than women
(P-interaction 0.06). No associations were observed when
considering childhood SHS exposure, SHS exposure since 18 y
of age, or workplace SHS exposure, separately or combined
with current SHS exposure, in both men and women combined
or separately (data not presented). Therefore, SHS exposure as
referenced throughout the remainder of the study refers to
current SHS exposure as reported at the time of the follow-up
1 interview.
Dietary ber had a modifying effect on the SHSCHD risk
association (P 0.02; Table 3). Among low-ber consumers, SHS
was associated with a 62% increase in the risk for CHD mortality
(HR, 1.62; 95% CI, 1.002.63) after adjustment for age, sex, level of
education, and BMI, but no elevated risk was observed for SHS
exposure among those consuming high levels of dietary ber.
Although interpretation is limited by small samples sizes, the
same pattern of effect modication by ber intake on the rela-
tionship between SHS and CHD mortality was observed among
both men and women (P-interaction among women 0.09, P-
interaction among men 0.11; Table 3). However, the SHSCHD
association in low-ber consumers was stronger for men (HR,
3.26; 95% CI, 1.308.16) than for women (HR, 1.40; 95% CI, 0.79
2.46). The mean dietary ber intake per 1000 kcal/d among those
within the lowest quartile and among those at or above the
second quartile of ber intake was 5.4 g (SD, 0.8) and 9.4 g (SD,
2.3), respectively. Similar distributions of ber intake were
observed for men and women.
A sensitivity analysis to include the rst 5 y of follow-up
resulted in similar patterns; the modifying effects of ber on
the relationship between SHS exposure and risk for CHD
mortality were observed, although results were attenuated and
no longer statistically signicant (data not presented). There was
no evidence of dietary modication on the association between

Table 1
Characteristics of Singapore Chinese Health Study lifetime never smokers (n 29 579) by sex and exposure to SHS

Characteristic Women (n 22 776) Men (n 6803)

SHS exposure SHS exposure

None Lives with 1 smoker(s) None Lives with 1 smoker(s)

N (%) 17 156 (75.3) 5620 (24.7) 6402 (94.1) 401 (5.9)
Person-years of follow-up (total) 94 122 30 877 34 308 2115
Age at follow-up interview, y, mean (SD) 60.5 (7.7) 59.1 (6.9) 59.2 (7.1) 60.1 (7.3)
BMI, kg/m2, mean (SD) 23.1 (3.2) 23.6 (3.6) 23.4 (3.4) 23.3 (3.6)
Education, n (%)
No formal education 5545 (32.3) 2117 (37.7) 296 (4.6) 32 (8.0)
Primary 7040 (41.0) 2448 (43.6) 2537 (39.6) 205 (51.1)
Secondary 4571 (26.6) 1055 (18.8) 3569 (55.8) 164 (40.9)
Physical activity (moderate), n (%)
None 13 319 (77.6) 4702 (83.7) 4625 (72.2) 310 (77.3)
30 min3 h/wk 2480 (14.5) 586 (10.4) 1211 (18.9) 57 (14.2)
>3 h/wk 1357 (7.9) 332 (5.9) 566 (8.8) 34 (8.5)
Ever regularly taken NSAIDs, n (%) 334 (2.0) 119 (2.1) 103 (1.6) 8 (2.0)
History of diabetes, n (%) 1784 (10.4) 686 (12.2) 692 (10.8) 46 (11.5)
SHS exposures, n (%)
SHS exposure, childhood
No smokers 6625 (38.6) 1434 (25.5) 2036 (31.8) 83 (20.7)
1 smoker 10 531 (61.4) 4186 (74.5) 4366 (68.2) 318 (79.3)
SHS exposure, work
No 11 468 (66.9) 3648 (64.9) 3822 (59.7) 231 (57.6)
Yes 2823 (16.5) 1074 (19.1) 2577 (40.3) 170 (42.4)
Never worked 2865 (16.7) 898 (16.0) 3 (0.1) 0 (0)
Mean intake (SD) per 1000 kcal/d
Dietary ber, g 9.0 (2.7) 8.5 (2.5) 8.2 (2.4) 7.5 (2.1)
u-3 fatty acid, g 0.55 (0.18) 0.53 (0.16) 0.51 (0.16) 0.48 (0.13)
b-Cryptoxanthin, mg 183.9 (223.7) 159.8 (219.5) 174.6 (195.4) 152.8 (176.0)
Lutein, mg 1395.3 (703.5) 1356.0 (662.3) 1130.1 (558.5) 1062.6 (540.4)
Isothiocyanates, mmol 6.8 (4.3) 6.5 (4.0) 5.8 (3.6) 5.5 (4.1)
Soy isoavones, mg 13.0 (9.5) 12.6 (9.5) 11.4 (8.6) 11.3 (8.2)

BMI, body mass index; NSAID, nonsteroidal anti-inammatory drug; SHS, secondhand smoke

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4 M. L. Clark et al. / Nutrition xxx (2013) 16

Table 2
SHS exposure and CHD mortality among lifetime never smokers, Singapore Chinese Health Study

SHS exposure Total population (N 29 579) Women (n 22 776) Men (n 6803)

Person-years Deaths HR (95% CI)* Person-years Deaths HR (95% CI)* Person-years Deaths HR (95% CI)*
No smokers 128,430 257 1 (ref) 94,122 181 1 (ref) 34,308 76 1 (ref)
1 smoker(s) 32 992 54 1.00 (0.74, 1.35) 30,877 44 0.93 (0.67, 1.30) 2115 10 1.73 (0.97, 3.10)

BMI, body mass index; CHD, coronary heart disease; CI, condence interval; HR, hazard ratio; SHS, secondhand smoke
* Adjusted for age at follow-up, BMI, education, dialect, and sex (in analysis among total population).

SHS exposure and risk for CHD mortality by intake levels of
b-cryptoxanthin, lutein, u-3 PUFAs, isothiocyanates, or soy iso-
avones (data not presented).
Discussion
In a large, population-based cohort of Chinese adults from
Singapore, we provide the rst epidemiologic evidence for the
modifying effect of dietary ber on the relationship between SHS
exposure and risk for CHD mortality. A 62% increased risk for
CHD mortality for those living with at least one smoker as
compared with living with no smokers was observed among
those who were within the lowest quartile of ber intake. There
was no association between SHS exposure and risk for CHD
mortality among those who consumed higher levels of ber.
The mechanisms through which SHS exposure may induce
CVD are complex and likely involve multiple chemical agents and
pathways. With more than 4000 compounds identied, cigarette
smoke is one of the greatest exogenous sources of free radicals
and other oxidants, many of which are capable of generating
reactive oxygen species [16,17]. Evidence of SHS exposure on
subclinical effects in humans, such as endothelial function,
platelet activation, oxidative stress, chronic inammation, lipid
prole, and blood pressure, has been demonstrated [4,3032],
although inconsistently [33,34]. Our observed association bet-
ween SHS exposure and risk for CHD mortality among those
within the lowest quartile of ber intake is consistent with
known associations between PM2.5, a major constituent of SHS,
and CHD mortality [5].
Our data support a role for ber consumption as a modier of
the adverse effects of SHS exposures. Fiber has long been con-
sidered to protect against CVD [15,35]. The underlying mecha-
nisms through which ber acts are not entirely understood;
however, ber is a complex dietary component that may have
benecial effects on the cardiopulmonary system by reducing
blood glucose concentrations [3638], thereby reducing
inammation [16] and enhancing antioxidant processes [15].
Higher ber intake may act as a modier of the relationship
between SHS exposure and CHD mortality by creating a state of
lower inammation and oxidative stress that may protect the
lung and circulatory system against subsequent environmental
insults that could trigger the development of CVD [22,27].
We cannot rule out the possibility that high dietary intake
of ber is a marker for a healthy diet or a healthy lifestyle in
general. However, there was no evidence that other dietary
factors modied the relationship between SHS exposure and risk
for CHD mortality, adjustment for physical activity did not alter
the results, and our study population was restricted to lifetime
never-smokers, which eliminates the possibility of residual
confounding by active smoking. Our ndings reported here also
are consistent with our previous ndings in the Singapore
cohort, where the adverse effects of childhood SHS exposure on
risk for adult chronic cough were strongest among those with
less than median ber intake [22].
To our knowledge, there are no observational data that have
been used previously to evaluate the potential modifying roles
of dietary factors on the association between SHS exposure
and CVD or death. However, among 549 men living in the Boston,
Massachusetts area, increased exposure to ambient PM2.5
reduced heart rate variability only among men with lower than
median intakes of the methyl nutrients, vitamins B6 and B12, or
methionine [23]. These results support a hypothesis that an
increase in methionine cycle activity may ameliorate PM effects
on subclinical indicators of CVD risk by increasing oxidative
stress defenses [23,39]. Experimental and observational research
designed to evaluate the potential modifying role of diet on the
relationship between air pollutant exposures and CVD risk is
needed to further investigate the PM2.5 mechanisms of action
and ultimately to identify measures to prevent CVD and to
reduce the adverse effects of a largely unavoidable exposure [23].
A limitation of our study was the use of self-reported SHS
exposure and diet. Although some measurement error is
inherent in population research, we have the advantage of using
exposure data that were assessed before disease occurrence;
thereby eliminating the possibility of differential misclassica-
tion (e.g., recall bias). Active smoking was not validated by
biomarkers, but studies comparing serum cotinine data with
self-reported tobacco use suggest that there is little misclassi-
cation of non-smokers based on self-reporting in surveys of
the general population [1,2]. Additionally, dietary history was

Table 3
SHS exposure and CHD mortality among lifetime never smokers, stratied by ber intake, Singapore Chinese Health Study

Total population (N 29 579) Women (n 22 776) Men (n 6803)

Person-years Deaths HR (95% CI)* Person-years Deaths HR (95% CI)* Person-years Deaths HR (95% CI)*
Low ber (Q1)
SHS: No smokers 22 252 61 1 (ref) 14 202 41 1 (ref) 8049 20 1 (ref)
SHS: 1 smoker(s) 6598 23 1.62 (1.00, 2.63) 5969 17 1.40 (0.79, 2.46) 629 6 3.26 (1.30, 8.16)
High ber (Q2Q4)
SHS: No smokers 106 178 196 1 (ref) 79 920 140 1 (ref) 26 258 56 1 (ref)
SHS: 1 smoker(s) 26 393 31 0.77 (0.52, 1.13) 24 907 27 0.76 (0.50, 1.15) 1486 4 1.07 (0.38, 2.95)
P for interaction 0.02 0.09 0.11

CHD, coronary heart disease; CI, condence interval; HR, hazards ratio; SHS, secondhand smoke
* Adjusted for age at follow-up, BMI, education, dialect, and sex (in analysis among total population).

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 M. L. Clark et al. / Nutrition xxx (2013) 16
collected using a FFQ that was developed for and validated in our
study population [29]; this is a reliable method for evaluating
usual dietary intake in large observational studies [40]. Finally,
with respect to the generalizability of our results to non-Asian
populations, we have previously reported that established risk
factors for CHD in Western populations (e.g., history of type 2
diabetes, smoking, history of hypertension, and hypercholester-
olemia) also are associated with CHD in our data from the
Singapore cohort [41,42].
The main advantages of our study include its large number of
lifetime never-smokers and the availability of detailed dietary
information for which to examine relationships that could have
important public health connotations. By identifying ber con-
sumption as a relevant dietary component for modifying the
effects of SHS exposure, we can better understand the mecha-
nisms that underlie the relationship between SHS exposure
and CHD mortality. Our results can be used to inform interven-
tion studies and eventually identify prevention strategies aimed
at mitigating the harmful effects of SHS, as well as other PM2.5
exposures.
Conclusion
Diets high in nutrients with antioxidant and anti-
inammatory properties have long been promoted as defenses
against many chronic conditions, including CHD resulting from
the harmful effects of SHS exposure. We now provide evidence
that a diet high in ber may also ameliorate these harmful
effects.
Acknowledgments
This work was supported by the National Institutes of Health,
USA [RO1 CA55069, R35 CA53890, R01 CA80205, and R01
CA144034]. We thank Siew-Hong Low of the National University
of Singapore for supervising the eldwork of the Singapore
Chinese Health Study. We also thank the Ministry of Health in
Singapore for assistance with the identication of mortality
outcomes via database linkages. Finally, we acknowledge the
founding, long-standing principal investigator of the Singapore
Chinese Health StudydMimi C. Yu.
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