Occupational noise exposure and incident hypertension in men: a
prospective cohort study
Ta-Yuan Chang*, Bing-Fang Hwang, Chiu-Shong Liu, Ren-Yin Chen, Ven-Shing
Wang, Bo-Ying Bao, and Jim-Shoung Lai
1
Footnotes:
*
Correspondence to Dr. Ta-Yuan Chang,
China Medical University,
91 Hsueh-Shih Road, Taichung 40402, Taiwan, Republic of China
Telephone: 886-4-22053366 ext 6203 Fax: 886-4-22079225.
E-mail: tychang@mail.cmu.edu.tw
Abbreviations: BMI, body mass index; 95% CI, 95% confidence interval; dBA,
A-weighted decibel; DBP, diastolic blood pressure; HPD, hearing protective device;
LAeq, A-weighted equivalent sound level; RR, relative risk; SBP, systolic blood
pressure; SD, standard deviation; TWA, time weighted average.
Running head: Occupational Noise and Hypertension
2
Abstract
The associations between occupational noise exposure and hypertension remain
controversial because of the differences in study designs, exposure assessments, and
confounding controls. This prospective study investigated the relationship between
noise exposure and the 10-year risk of hypertension. A cohort of 578 male workers in
Taiwan was followed from 1998 to 2008. All subjects were divided into high-,
intermediate-, and low-exposure groups based on noise exposure assessment. Cox
regression models were used to estimate the relative risks of hypertension after
adjustment for potential confounders. During the 7805 person-years of follow-up, 141
hypertension cases were identified. Significant increases of 3.2 [95% confidence
interval (CI): 0.2, 6.2] mmHg in systolic blood pressure and 2.5 (0.1, 4.8) mmHg in
diastolic blood pressure between the baseline and follow-up measurements were
observed in the high-exposure group. Participants exposed to ≥ 85 A-weighted
decibels (dBA) had a 1.93-fold (1.15, 3.22) risk of hypertension compared with those
exposed to < 80 dBA. There was a significant exposure-response pattern (P = 0.016)
between the risk of hypertension and the strata of noise exposure. Prolonged exposure
to noise levels ≥ 85 dBA may increase males’ systolic and diastolic blood pressure.
This association may translate into a higher incidence of hypertension.
Key words: Blood pressure, epidemiology, hypertension, men, occupational noise,
prospective studies.
3
Chronic exposure to noise has been associated with cardiovascular disease,
including ischemic heart disease (1), myocardial infarction (2-5), coronary heart
disease (6-7), and stroke (8). This association may exist because noise exposure
activates the sympathetic and endocrine systems to affect the humoral and metabolic
state of the human organism, producing the increase in blood pressure and the
changes in other biological risk factors (such as blood lipids and glucose levels) that
promote the development of hypertension and cardiovascular diseases (9).
The existence of an association between noise exposure in occupational settings
and hypertension is still controversial. Occupational noise exposure has been
associated with a sustained elevation of blood pressure or with a higher risk of
hypertension in two retrospective cohort studies (10-11), two repeated-measure
studies (12-13), and nine cross-sectional studies (14-22). However, the results of other
studies are inconsistent with these findings (23-31). Reasons for this inconsistency
may include differences in study design, differences in exposure assessment, differing
degrees of ability to control for potential confounders, and varying degrees of the use
of hearing protective devices (HPDs) at work.
One cohort study reported a relationship between occupational noise exposure
and the incidence of hypertension (10). However, these results were limited by an
exposure bias caused by no adjustments for the use of HPDs, and the association
between noise exposure and blood pressure was not reported. In addition, important
risk factors for hypertension, such as body mass index (BMI), cigarette use, alcohol
intake, regular exercise, salt intake, and a family history of hypertension (32-33), were
not considered. The objective of this study was to investigate the relationship between
prolonged exposure to occupational noise and the 10-year incidence of hypertension
by taking these important factors into account.
4
MATERIALS AND METHODS
Study population
This study was conducted by performing a follow-up study to a cross-sectional
survey in an aircraft manufacturing plant in central Taiwan. The recruitment and
selection of study subjects have been described in detail previously (21). Briefly, 790
male production line workers were recruited in 1998 and were invited to join again at
the end of 2008. To ensure study subjects without hypertension at the baseline, 10
workers were excluded because they reported to have a diagnosis of hypertension by
doctors and using anti-hypertensive medication according to a questionnaire survey in
1998. During the 10-year period, 86 workers retired and were lost to follow-up. In
addition, 116 subjects were rejected due to the lack of follow-up results in 2008.
Therefore, the study group comprised 578 male production line workers. There were
no significant differences between the 578 participants and the 202 non-participants at
baseline in terms of employment duration, BMI, high-density lipoprotein level,
triglyceride level, cigarette use, alcohol intake, and regular exercise. The present study
was reviewed and approved by the Institutional Review Board of the School of Public
Health, China Medical University before the study commenced in 2008, and written
informed consent was obtained again from each participant.
Blood pressure measurements and definition of hypertension
The procedure for baseline blood pressure measurements in 1998 was the same
as that for the follow-up measurements in 2008. All subjects were required to fast
overnight before blood sampling and blood pressure measurements during annual
health examinations. Subjects sat for 10 min in a chair with back support before blood
pressure was measured bilaterally by a trained nurse using an automated
sphygmomanometer (Ostar Model P2, Ostar Meditech Corp., Taipei, Taiwan). The
5
mean value of the two measurements was recorded to represent the individual’s blood
pressure in the present study. Subjects were defined as hypertensive if they reported a
diagnosis of hypertension given by doctors after 1998, if the mean value of their
resting systolic blood pressure (SBP) was  140 mm Hg in 2008, or if the mean value
of their resting diastolic blood pressure (DBP) was  90 mm Hg in 2008. Height, body
weight, total cholesterol level, and triglyceride level were also measured in all
subjects at baseline and follow-up. The BMI was calculated as body weight (kg)
divided by the square of height (m2).
In addition, a self-administered questionnaire was used to collect potential
confounders in 1998 and 2008. These factors included age, educational level,
employment duration, cigarette use, alcohol intake, regular exercise, the use of
anti-hypertensive medication, and the use of HPDs. Additional information (such as
salt intake and a family history of hypertension) was only included in 2008. To avoid
the information bias, the lifestyle habits for regular users were defined specifically (21,
34). The use of HPDs included the percentage of time that the subjects wore HPDs
(i.e., never use, < 2 hours, 2-4 hours, 4-6 hours, and 6-8 hours working time) and the
type of HPDs (i.e., earplugs, earmuffs, or both). High salt-intake workers were
defined as those who reported ingesting food cooked with soybean sauce for more
than one meal per day. A subject was defined as having the family history of
hypertension if a positive answer was given to the question: “Have your parents or
grandparents been diagnosed with hypertension by a physician in the past?” (21, 34).
Follow-up
We used employment personnel records to obtain each subject’s first date of
employment at this company and assigned this date as the beginning of the follow-up
period. The end of the follow-up period was defined as either the date of diagnosis by
6
a physician or the date when the subjects who had not been diagnosed with
hypertension by a physician were given their blood pressure examinations in
December 2008. Among the 141 cases classified as hypertensive in this study, 56
cases were diagnosed with hypertension (30 cases were taking anti-hypertensive
medication), and 85 cases were identified at the annual examination in 2008.
Noise exposure assessment
The procedure for noise exposure assessment in 1998 was similar to that for the
follow-up measurements in 2008. We first identified 18 departments in this company
and divided each department into different locations based on manufacturing processes
by industrial hygienists and senior workers. After the walkthrough survey, we measured
the 15-min time-weighted average (TWA) equivalent sound level (Leq) using a sound
analyzer (TES-1358, TES Electronic Corp., Taipei, Taiwan), which was calibrated with
a sound-level calibrator (TES-1356, TES Electronic Corp., Taipei, Taiwan) before
environmental monitoring. The short-term environmental sampling was performed at
337 locations where were the possibly loudest workplaces around this company. For the
121 sites exhibiting a 15-min TWA Leq  65 dBA, further 8-h TWA measurements were
conducted during September-December 1998. All subjects were divided into one of
similar exposure groups on the basis of the similarity and frequency of tasks performed,
the agents and processes with which they worked, and the ways in which they
performed the tasks (35). Each subject was assigned a specific value of noise exposure
based on the 8-h TWA Leq measured in his workplace.
To avoid an exposure bias due to the use of HPDs at work, we calculated each
participant’s level of noise reduction according to the noise reduction rating of the
HPDs that he wore (29 dB for earplugs and 25 dB for earmuffs), the protection levels of
the HPDs (an average of 28% for earplugs and an average of 62% for earmuffs), a
7
comfort factor of 0.5 (due to the minimal percentage of comfort related to the
compliance of HPDs usage) (36), and the percentage of working time that he used the
HPDs (36-37). We used the HPD-adjusted value of the 8-h TWA Leq to classify them
into three exposure groups by selecting the median and third quartile in the distribution
of noise exposure among all subjects as cut-off points. The 578 workers were
subdivided into a high-exposure group (n = 152; noise level  85 dBA), an
intermediate-exposure group (n = 221; 80 ≤ noise level < 85 dBA), and a low-exposure
group (n = 205; noise level < 80 dBA).
Statistical analysis
We first used the Shapiro-Wilk test to determine the normality of continuous
variables. The Kruskal-Wallis test was then used to perform multiple comparisons of
continuous variables between the three groups for the non-normal distribution and a
one-way analysis of variance (ANOVA) was used for the same comparison of
continuous variables that were normally distributed. We also used the Chi-square test
to compare the difference in dichotomous variables between the three groups. For
those groups with significant differences, the Mann-Whitney test (or t test) and the
Chi-square test were used to compare the high- and intermediate-exposure groups
with the low-exposure group for continuous and dichotomous variables.
To compare individual differences in SBP and DBP between the baseline and
follow-up measurements, we used the linear mixed-effect regression models for each
exposure group (38-39). The fixed effects in the mixed model included all variables in
the final model at baseline and the use of anti-hypertension medication in 2008.
Individual subjects were used as a random effect. We used the first-order
autoregressive model for covariance structures due to the minimizing value of
Akaike’s Information Criterion in both SBP and DBP measurements (38-39).
8
To avoid the information bias in observed person-years due to the availability of
only one blood pressure measurement within the past 10 years, hypertensive cases
identified by questionnaire, blood pressure measurements, and total hypertensive
cases were used as the outcomes to perform the regression analyses. We used Cox
proportional hazard regressions and calculated relative risks (RRs) with 95%
confidence intervals (CIs) to compare the differences in incidence of hypertension
between groups while controlling for potential confounders. We used a manual
stepwise regression to build the final model because only one variable of BMI (P =
0.005) was retained in the final step using an automatic stepwise procedure. A basic
model was first examined to include age at baseline for biological plausibility and two
dummy variables of exposure categories. The basic model was then extended to
include two variables (i.e., BMI and employment duration) that were significantly
associated with the risk of hypertension in the simple Cox regression models. The
final model included all variables in the extended model and important risk factors of
hypertension reported in the previous literature (32-33, 40), including socioeconomic
status (using educational levels or job positions as surrogates), cigarette use, alcohol
intake, and regular exercise. In the sensitivity analysis, the two variables of salt intake
and family history of hypertension that had been collected only in 2008 were included
in the model. The SAS standard package for Windows version 9.2 (SAS Institute
Incorporation, Cary, North Carolina, USA) was used for the statistical analyses. The
significance level was set at 0.050 for all tests.
9
RESULTS
Table 1 summarises the demographic characteristics of 578 participants at
baseline. Significant differences were identified between the exposure groups in the
mean value of employment duration, the number of individuals with educational level
≤ 12 years, and whether individuals used HPDs at work. Workers in the high- and
intermediate-exposure groups were more likely to have an educational level ≤ 12
years and were less likely to never use HPDs at work than those in the low-exposure
group. In addition, high-exposure workers had a significantly higher mean of
employment duration and were less likely to never use HPDs at work compared with
the intermediate-exposure workers. In contrast, intermediate-workers had a
significantly lower mean of employment duration than the low-exposure workers.
Table 2 shows the measurements of occupational noise exposure for the three
groups. Significant differences were identified in the mean noise levels between the
three groups either before or after an adjustment for HPD use. The high- and
intermediate-exposure groups were exposed to significantly higher mean values of
noise compared with the low-exposure group both before and after an adjustment for
HPD use.
Table 3 shows the changes in blood pressure between the baseline and follow-up
measurements and the incidence rate of hypertension in the three groups. Although
there were no significant differences in SBP and DBP between these three groups at
baseline or follow-up, the SBP of both the high-exposure (P = 0.035) and
intermediate-exposure (P < 0.001) groups significantly increased between the baseline
and follow-up measurements in the linear mixed-effect models. In addition, the DBP
of high-exposure workers significantly increased between the baseline and follow-up
measurements (P = 0.042) after controlling for potential confounders.
10
The associations between the different groups and the risk of hypertension are
summarised in Table 4. The multiple Cox proportional hazard regression models
showed that workers exposed to 86.9 ± 2.2 dBA and those exposed to 83.0 ± 1.3 dBA
had a 1.93-fold and 1.75-fold RR of hypertension, respectively, compared with those
exposed to 71.9 ± 9.0 dBA after adjusting for potential confounders. There was a
significant dose-response relationship between the levels of noise-exposure
experienced by the three groups and the risk of hypertension using total cases as the
outcomes (adjusted RR = 1.35; 95% CI: 1.06, 1.73). The similar results were found
while using job positions (managers, engineers, administrators, and technicians)
instead of educational levels in the models. In addition, the intermediate-exposure
group had a significantly higher risk of measured hypertension than the low-exposure
group.
In the sensitivity analyses, the association between occupational noise exposure
and the risk of hypertension persisted both for the high-exposure (adjusted RR = 1.95;
95% CI: 1.16, 3.28) and intermediate-exposure (adjusted RR = 1.74; 95% CI: 1.08,
2.80) groups after adding the two variables of salt intake and family history of
hypertension to model 3. Furthermore, an increasing exposure-response trend was
found (adjusted RR = 1.37; 95% CI: 1.07, 1.75; P = 0.014) in this sensitivity analysis.
No significant differences were found between the three exposure groups with regard
to salt intake (P = 0.173) or family history of hypertension (P = 0.656).
11
DISCUSSION
We found a positive relationship between occupational noise exposure  85 dBA
at baseline and the 10-year incidence of hypertension. The findings were consistent
with the results in a retrospective study that reported a significantly higher risk of
hypertension in sawmill workers exposed to  85 dBA for more than 30 years (10).
Although their findings were limited to a misclassification of noise exposure because
of no adjustment for the use of HPDs at work, the two longitudinal studies reached
similar results to show an increased risk of hypertension following long-term chronic
occupational noise exposure. Moreover, the present study overcame the lack of
individual risk factors of hypertension in the previous study (10) to provide strong
evidence that hypertension was associated with occupational noise exposure. We
suggest that the currently regulated threshold for occupational noise exposure may
expand the prevention of noise-induced hearing loss (41) to the risk of hypertension,
which is a leading cause of cardiovascular diseases.
We also observed an exposure-response pattern between noise-exposure levels
and the risk of hypertension. Our results were concordant with the findings in a
cross-sectional study showing that increasing noise exposure from 75 to 104 dBA was
associated with an increasing prevalence of hypertension in female textile mill
workers (16). One cohort study reported a significantly increasing risk of
hypertension with cumulative noise exposure ranging from 95 dBA  year to > 115
dBA  year among male workers (10). The same exposure metrics (i.e., four
categories from < 85 dBA  year to ≥ 95 dBA  year) were applied to our analyses,
but no significant dose-response relationship (adjusted RR = 1.03; 95% CI: 0.87, 1.21)
was found in the Poisson regression. The possible reason for different exposure
conditions resulting in the same dose-response association might be that workers did
12
not change the jobs and tasks in the present and previous studies (16) but there was
turnover in another cohort (10).
In addition, the inverse-U-shaped dose-response relationship for measured
hypertension indicated a role of exposure duration in the etiology of the disease.
Although we used Cox regressions to account for varying time of exposure, the
magnitude of effect on measured hypertension and diagnosed hypertension in the
high-exposure group was similar (i.e. around 2 fold), yet the effect halved from 2.22
to 1.16 in the intermediate-exposure group. These findings may indicate a "plateau"
effect of exposure intensity that is independent of exposure duration. Therefore, when
the exposure intensity is not the highest, the exposure duration is likely the second
component of exposure that "kicks in" the dys-regulation of the nervous and hormonal
systems, leading to the disease.
The significant increases in SBP between the baseline and follow-up
measurements were also observed among workers exposed to 80-85 dBA and those
exposed to  85 dBA. These findings were consistent with the results in a cohort
study showing that male workers exposed to  85 dBA and using HPDs had a mean
increase of 3.8 mmHg in SBP over 9 years of follow-up, which is a significantly
higher increase than that observed in office workers (11). Additionally, workers
exposed to  85 dBA exhibited a significant increase in DBP between the baseline and
follow-up measurements as well as a significantly higher DBP at follow-up compared
with those exposed to < 80 dBA. These findings provided the evidence to explain the
association between occupational noise exposure above 85 dBA and the higher risk of
hypertension.
The strengths of the present study include a cohort-study design, detailed
assessments of personal exposure histories and comprehensive controls for most
13
potential confounders of hypertension. In addition, occupational noise exposure
adjusted for the use of HPDs may avoid the misclassification of study subjects and an
overestimation of noise exposure to produce the consistent results associated with
road traffic noise exposure in environmental epidemiological studies (34, 42).
The validity of noise exposure assessment was also conducted to check the
precision and accuracy of a predictive model and noise levels accounted for the use of
HPDs. While using the information of departments, processes, job positions, and
noise measurements collected in 1998 to establish a predictive model of noise levels,
the adjusted R2 was 0.93 in a multiple linear regression. By comparing with
environmental measurements at 11 locations in 2004, the bias and precision in this
model was 2.4 ± 4.9 dBA to produce an accuracy of 5.5 dBA that showed an
overestimation due to engineering controls over time. In contrast, the bias and
precision of two-stage noise measurements accounted for the use of HPDs among
study subjects was 1.5 ± 2.0 dBA to have an accuracy of 2.5 dBA. Such comparisons
indicated that assessing exposure using the worst case scenario might be inaccurate
while still being precise.
One limitation of this study is the overestimation of individual cumulative levels
in occupational noise exposure. Noise levels measured 10 years ago has obviously
been reduced in response to the requirement for the improvement of engineering
controls in the workplace. Therefore, workers assigned to the high-exposure group in
1998 might be exposed to < 85 dBA in 2008. A comparison of environmental noise
levels between the baseline and follow-up in all subjects showed that the mean value
of noise levels measured in 2008 (77.6 ± 7.6 dBA) was significantly lower than that
measured in 1998 (81.6 ± 8.5 dBA) (paired t test, P < 0.001). The overall decrease of
5.2 ± 9.3 dBA had apparent decreases in the processes of peripheral element assembly
14
(-9.7 ± 16.4 dBA) and forging and casting (-7.3 ± 7.7 dBA) that might decline the
proportion of the use of HPDs from 73.3% to 27.7% and from 85.7% to 61.9%,
respectively. Because no subjects changed their jobs or tasks, the systematic
overestimation on cumulative noise exposure was equally distributed across different
groups and the non-differential misclassification of exposure might attenuate the
estimates toward the null. However, our findings still observed the significant
relationship between occupational noise exposure and the risk of hypertension.
The other limitation is that noise exposure, blood pressure and other important
risk factors of hypertension were not measured continuously over the past 10 years.
The significantly higher risk of hypertension among the workers exposed to  85 dBA
might be because they experienced the greatest changes in lifestyle. However, this
reason seems improbable because the prevalence rates of risk factors related to
hypertension such as cigarette use (58%) and alcohol intake (63%) declined
significantly (27% and 21%, respectively, both P values < 0.001) in the high-exposure
group at the follow-up examination. In addition, blood pressure was measured twice
over the past 10 years. This is our first attempt to longitudinally observe the
occupational noise exposure and the incidence of hypertension among these workers.
The four-year period of follow-up will continue in 2012 to circumvent limitations
imposed by lifestyle changes over time and to have additional measurements of noise
exposure and blood pressure.
In summary, the present study showed that occupational exposure to noise levels
 85 dBA was associated with the development of hypertension and that there was a
dose-response relationship between noise exposure and the 10-year incidence of
hypertension. The association between occupational noise exposure ≥ 85 dBA and the
risk of hypertension might be due to the increases of SBP and DBP observed in the
15
present study. The currently regulated threshold for occupational noise exposure may
prevent the adverse health effects from noise-induced hearing loss to the development
of hypertension.
16
ACKNOWLEDGEMENTS
Author affiliations: Department of Occupational Safety and Health, College of
Public Health, China Medical University, Taichung, Taiwan, Republic of China
(Ta-Yuan Chang, Bing-Fang Hwang, Ren-Yin Chen, Ven-Shing Wang,
Jim-Shoung Lai); Institute for Risk Assessment Sciences, Utrecht University,
Utrecht, The Netherlands (Ta-Yuan Chang); Department of Family Medicine, China
Medical University Hospital, Taichung, Taiwan, Republic of China (Chiu-Shong
Liu); School of Medicine, College of Medicine, China Medical University, Taichung,
Taiwan, Republic of China (Chiu-Shong Liu); Department of Pharmacy, College
of Pharmacy, China Medical University, Taichung, Taiwan, Republic of China
(Bo-Ying Bao).
Grants and/or financial support: This study was supported by the National Science
Council, Taiwan (grant NSC 97-2221-E-039 -007 -MY3).
We thank the National Science Council, Taiwan (NSC 97-2221-E-039 -007 -MY3) for
the financial support. We thank Mr. Deng-Tsai Lai for his contributions to this study.
We also thank the graduate students who assisted with the environmental sampling at
the workplace.
Conflict of interest: none declared.
17
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Cnaan A, Laird NM, Slasor P. Using the general linear mixed model to analyse
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40. Colhoun HM, Hemingway H, Poulter NR. Socio-economic status and blood
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Daniell WE, Swan SS, McDaniel MM, et al. Noise exposure and hearing loss
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Barregard L, Bonde E, Ohrstrom E. Risk of hypertension from exposure to road
traffic noise in a population-based sample. Occup Environ Med.
2009;66(6):410-415.
22
Table 1. Baseline Characteristics of Study Participants, Taichung, Taiwan, 1998–2008.
Exposure groups
Characteristics
High (n = 152)
Mean (SD)
N
%
Intermediate (n = 221)
Low (n = 205)
Mean (SD)
Mean (SD)
N
%
N
%
Total subjects (n = 578)
Mean (SD) N
%
P-Value
Age at entry (years)
27.6 (4.6)
27.5 (5.4)
28.0 (5.6)
27.7 (5.3)
0.504a
Employment duration (years)
10.2 (5.0)c
9.0 (4.8)d
10.9 (6.0)
9.8 (5.2)
0.003a
Body mass index (kg/m2)
24.0 (3.0)
23.8 (3.1)
23.6 (2.9)
23.8 (3.0)
0.493a
HDL (mg/dl)
45.4 (6.9)
46.3 (10.6)
46.0 (8.3)
46.0 (8.9)
0.909a
LDL (mg/dl)
115.1 (30.4)
114.5 (30.3)
112.3 (28.8)
113.8 (29.8)
0.609a
Triglyceride (mg/dl)
142.2 (63.4)
143.6 (86.0)
156.7 (95.1)
147.7 (83.9)
0.347a
Education,  12 years
63
41.5 e
106
48.0e
50
24.4
219
37.9
<0.001b
Current smoking, yes
88
57.9
120
54.3
111
54.2
319
55.2
0.737b
Alcohol drinking, yes)
95
62.5
136
61.5
12
60.5
355
61.4
0.927b
Regular exercise, yes
50
32.9
71
32.1
58
4
28.3
179
31.0
0.580b
<0.001b
Use of HPDs at work
Never
39
25.7 e, f
16
7.2e
12
59.0
176
30.4
< 2 hours working time
80
52.6
35
15.8
26
1
12.7
141
24.4
2-4 hours working time
31
20.4
39
17.7
24
11.7
94
16.3
4-6 hours working time
1
0.7
59
26.7
10
4.9
70
12.1
6-8 hours working time
1
0.7
72
32.6
24
11.7
97
16.8
Abbreviations: HDL, High-density lipoprotein; HPDs, hearing protective devices; LDL, Low-density lipoprotein; SD, standard deviation.
23
a
Kruskal-Wallis test of the difference between the three groups. bChi-square test of the difference between the three groups. cMann-Whitney test
for a significant difference (P < 0.05) compared with the intermediate-exposure group. dMann-Whitney test for a significant difference (P < 0.05)
compared with the low-exposure group. eChi-square test for a significant difference (P < 0.05) compared with the low-exposure group.
f
Chi-square test for a significant difference (P < 0.05) compared with the intermediate-exposure group.
24
Table 2. Occupational Noise Exposure at Baseline in Three Study Groups, Taichung, Taiwan, 1998–2008.
Exposure groups
Noise levels (dBA) before HPDs adjustment
Noise levels (dBA) after HPDs adjustment
Mean (SD)
Range
Mean (SD)
Range
High
87.4 (2.1)b, c
86.4-92.5
86.9 (2.2)b, c
85.3-92.5
Intermediate
85.4 (1.5)b
81.5-86.4
83.0 (1.3)b
80.3-84.8
Low
73.2 (9.4)
55.3-86.4
71.9 (9.0)
53.0-79.9
P-Value
<0.001a
<0.001a
Abbreviations: dBA, A-weighted decibel; HPDs, hearing protective devices; SD, standard deviation. aKruskal-Wallis test of the difference
between the three groups. bMann-Whitney test for a significant difference (P < 0.05) compared with the low-exposure group. cMann-Whitney
test for a significant difference (P < 0.05) compared with the intermediate-exposure group.
25
Table 3. Changes in Blood Pressure and Incidence of Hypertension by Study Group, Taichung, Taiwan, 1998–2008.
SBP (mmHg)
Baseline
DBP (mmHg)
Follow-up
Baseline
Follow-up
Exposure groups Person-year
Mean
Mean (SD)
Mean
Mean (SD)
95% CI
Mean (SD)
Mean (SD)
differenceb
95% CI
differenceb
Low
2873
123.1 (12.1)
124.6 (13.9)
1.5
-1.0, 4.0
80.3 (11.2)
81.6 (8.7)
1.3
-0.6, 3.2
Intermediate
3020
122.0 (11.7)
126.8 (14.4)
4.9
2.5, 7.3
81.1 (10.8)
82.5 (8.8)
1.4
-0.3, 3.2
High
1912
122.9 (11.8)
126.1 (15.3)
3.2
0.2, 6.2
80.8 (12.9)
83.3 (8.6)
2.5
0.1, 4.8
P = 0.597a
P = 0.732a
P = 0.874a
P = 0.260a
P = 0.194a
P = 0.479a
Abbreviations: CI, confidence interval; DBP, diastolic blood pressure; HT, hypertension; SBP, systolic blood pressure; SD, standard deviation.
a
One-way analysis of variance (ANOVA) test of the difference between the three groups. bLinear mixed-effect regression models were used to
test the difference between the baseline and follow-up measurements after controlling for age at baseline, anti-hypertension medication, body
mass index, employment duration, educational level, cigarette use, alcohol intake, and regular exercise.
26
Table 4. Associations Between Different Noise Exposure Levels and Incidence of Hypertension, Taichung, Taiwan, 1998–2008.
Outcomes
Diagnosed HTa
Variables
Cases
Incidence
Model 2d
RR
ARR
ARR
95% CI
95% CI
Model 3e
95% CI
ARR
95% CI
18
6.310-3
1
80-85 dBA
19
6.310-3
1.00
0.52, 1.90
1.00
0.53, 1.91
1.26
0.59, 2.70 1.16
0.54, 2.48
≥ 85 dBA
19
9.910-3
1.64
0.86, 3.12
1.65
0.87, 3.15
2.07
0.96, 4.45 2.05
0.96, 4.40
1
1
1
0.149
0.141
0.051
0.051
1
1
1
< 80 dBA
26
9.010-3
1
80-85 dBA
40
13.210-3
1.48
0.90, 2.42
1.49
0.90, 2.43
2.24
1.24, 4.05 2.22
1.20, 4.08
≥ 85 dBA
19
9.910-3
1.19
0.66, 2.15
1.20
0.66, 2.16
1.82
0.92, 3.62 1.78
0.88, 3.59
P-Value for trend
Total HT
Model 1c
< 80 dBA
P-Value for trend
Measured HTb
Crude RR
0.452
0.438
0.101
0.136
1
1
1
< 80 dBA
44
15.310-3
1
80-85 dBA
59
19.510-3
1.28
0.87, 1.89
1.28
0.87, 1.90
1.81
1.14, 2.89 1.75
1.09, 2.81
≥ 85 dBA
38
19.910-3
1.38
0.89, 2.13
1.39
0.90, 2.15
1.96
1.18, 3.27 1.93
1.15, 3.22
P-Value for trend
0.134
0.125
0.012
0.016
Abbreviations: ARR, adjusted relative risk; CI, confidence interval; dBA, A-weighted decibel; HT, hypertension; RR, relative risk. aSubjects
27
reported that a doctor had previously diagnosed them with hypertension. bSubjects had a mean value of resting systolic blood pressure  140 mm
Hg or a mean value of resting diastolic blood pressure  90 mm Hg. cThe Cox proportional hazards regression adjusted for biological plausibility
(i.e., age at baseline) as the basic model. dThe Cox proportional hazards regression adjusted for age at baseline and significant factors in simple
Cox regression models (such as body mass index and employment duration) as the extended model. eThe Cox proportional hazards regression
adjusted for all variables in model 1, model 2, and important risk factors reported in previous literature (i.e., educational level, cigarette use,
alcohol intake, and regular exercise) as the final model.
28