Occupational Medicine 2016;66:10–16 doi:10.1093/occmed/kqv148
IN-DEPTH REVIEW
Systematic review of the cardiovascular effects of occupational noise M. Skogstad, H. A. Johannessen, T. Tynes, I. S. Mehlum, K.-C. Nordby and A. Lie Department of Occupational Medicine and Epidemiology, National Institute of Occupational Health, P.O. Box 8149 Dep., N-0033 Oslo, Norway. Correspondence to: M. Skogstad, National Institute of Occupational Health, P.O. Box 8149 Dep., N-0033 Oslo, Norway. Tel: +47 23195388; fax: +47 23195205; e-mail: [email protected]
Aims
To assess possible associations between occupational noise exposure and the risk for cardiovascular effects in follow-up studies published after 1999.
Methods
We performed a systematic critical literature review of original articles from key literature databases of associations between workplace noise and health. The studies were identified by search in Ovid Medline, Ovid Embase, Web of Science, Scopus and ProQuest Health and Safety Sciences Abstracts. We selected prospective studies of adequate quality with a measure of association between occupational noise exposure and cardiovascular health for the meta-analysis.
Results
Twelve papers, all prospective and mostly with high quality but with methodological shortcomings in exposure assessment, were included in the review and meta-analysis. Exposure to noise at work was consistently positively associated with hypertension [Hazard ratio (HR) = 1.68; 95% confidence interval (CI) 1.10–2.57] and CVD [relative risk (RR) = 1.34; 95% CI 1.15–1.56]. In addition, we found a trivial effect of noise exposure on CVD mortality (HR = 1.12; 95% CI 1.02–1.24).
Conclusions Occupational noise exposure is strongly associated with hypertension. For other cardiovascular effects, this meta-analysis suggests a weak association, but the evidence is limited. More longitudinal studies on the effects of occupational noise on the cardiovascular system are warranted. Key words
Cardiovascular disease; epidemiologic methods; noise.
Introduction Noise is a major problem in many workplaces and is associated with a number of health effects. Cardiovascular diseases (CVDs) have been frequently discussed in the scientific literature during the past 40 years and research has suggested that occupational noise exposure may possibly cause increased blood pressure (BP), hypertension and other CVDs. A literature review of publications published in the period 1981–89 found a correlation between occupational noise exposure and CVD in about half of the studies, and that an increasing quality of the studies yielded an increased coherence, which supported a possible causal relationship [1]. Two systematic reviews of occupational and environmental noise exposure and BP or CVD have been
published [2,3]. In a meta-analysis of 43 occupational and community-based epidemiological studies, van Kempen et al. [2] included 28 occupational studies published between 1970 and 1999. Most of the studies were cross-sectional. Based on the analysis of 14 studies on BP of occupationally exposed subjects, it was reported that noise had a small but significant effect on hypertension. For every 5 dB(A) increase in occupational noise exposure, the relative risk (RR) for hypertension was 1.14 [95% confidence interval (CI) 1.01–1.29]. A systematic review of studies on occupational noise exposure and CVD in the period 1950–May 2008 by Tomei et al. [3] included 15 studies for meta-analysis. A statistically significant increase in systolic and diastolic BP and Electrocardiography (ECG) abnormalities in highly exposed [92.2 ± 6.5 dB(A)] workers compared with medium-exposed [85.2 ± 6.7 dB(A)] and low-exposed
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Background Cross-sectional studies of occupational noise and cardiovascular effects show an association between noise and hypertension but for coronary heart disease or other cardiovascular diseases (CVDs) the evidence is not convincing.
M. SKOGSTAD ET AL.: SYSTEMATIC REVIEW OF NOISE AND CARDIOVASCULAR EFFECTS 11
[62.2 ± 28.7 dB(A)] workers were reported. The average BP in the three groups was 134.1/83.7, 128.0/81.5 and 126.8/80.1 mmHg, respectively. Most of the studies reported until 2000 have been cross-sectional studies with BP as the outcome. Methodological problems are present in a majority of the studies, such as lack of good reference groups, reverse causality and confounder control. Furthermore, other problems included inadequate exposure characterization, lack of standardization of BP measurements and publication bias [1,2]. Since certain methodological problems are inherent in cross-sectional studies, we wanted to conduct a systematic critical review with emphasis on prospective studies published after the last systematic reviews [2,3].
Methods
Results After removing duplicates, we identified 75 potentially relevant articles by electronic database searches. After reviewing the titles and abstracts, studies demonstrating non-compliance with the inclusion criteria were excluded. We identified 12 articles, all cohort studies from developed countries that met the inclusion criteria, of which 11 were eligible for meta-analysis (Table 1). A flow chart showing the study selection is presented in Figure 1. Four studies examined the effect of occupational noise exposure on BP, mostly in industrial male cohorts [8–11]. In all four studies, noise exposure was retrospectively assigned to study subjects based on objective sound level measures. Three of the studies encompassed industrial groups including from 578 to 10 872 men exposed to noise levels even reaching 100 dB(A) [8–10] and one was a population-based study including 145 190 men and women exposed to noise levels in the range 70–86 dB(A) [11]. In these studies, hypertension was defined as follows; either hypertensive drug prescription, hospital discharge diagnosis of hypertension, or a diagnosis of hypertension (systolic BP >140 mmHg or diastolic BP >90 mmHg) assessed by health personnel [10,11]. A significant association between noise exposure at levels above 85 dB(A) and hypertension was reported in all four studies. In the study by Stokholm et al., the association was significant for females only.
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Initially, we searched systematically for studies on occupational noise exposure and health outcomes. At this point, the search had no restrictions regarding language or publication type. The following databases were searched: Ovid Medline (1946–), Ovid Embase (1974–), Web of Science (1950–), Scopus (1995–) and ProQuest Health and Safety Sciences Abstracts (1981–). We developed and adapted one search strategy for each database. In the bases that are indexed by a hierarchical controlled vocabulary (Medline and Embase), we used a combination of free text terms and controlled vocabulary (MeSH and Emtree). The search strategy was developed with low specificity to the advantage of high sensitivity. The search was completed in May 2013. We included studies with exposure relevant for work situations and an estimate of association with any health outcome. All titles and abstracts from the literature search were assessed against the inclusion criteria for possible relevance. At this point, studies that were not dealing with noise relevant for work-related exposure, as well as studies in languages other than English, were excluded. References that we judged to be potentially relevant were read in full text and assessed for inclusion. Relevant original studies were assessed by at least one researcher regarding methodological quality, using a comprehensive checklist. The checklist was developed by the National Institute of Occupational Health for observational studies and based especially on the checklist of Ariens and Hoogendoorn for epidemiological studies [4,5]. From the identified studies with adequate validity, the studies with CVD, BP and hypertension as outcomes were selected. Furthermore, only studies with a prospective design published between 2000 and 2013 were included. None of these studies had been included in former reviews. Twelve papers were included in the review and meta-analysis.
Summary effect estimates were calculated by means of averaged associations across samples, weighting each observed association by the study’s sample size. Eligible studies for inclusion in the meta-analyses reported categorical exposure variables with the unexposed employees (or employees with the lowest exposure category) as reference category. When eligible, we used the most completely adjusted risk estimates from each study and their corresponding standard errors. In addition, three or more eligible studies were required for the computation of combined effects. We computed random effects models, which estimate the mean of a distribution of true effects. The random effects model is recommended when there is reason to assume that the true effect varies from one study to the next [6]. The Q statistic was computed to assess the heterogeneity of studies (P 85 dB >80 dB, >85 dB
PDM PDM
Hypertension Hypertension
1, 2 1, 3, 4
1 1
SLM
Hypertension
1, 3, 4, 5, 6, 7, 8, 9
1
1, 7, 25 1, 3, 4, 10, 11, 12, 13
1 2
1, 14
2
578 Aircraft 87.4 dB, 85.4 dB, manufacturing 73.2 dB 1288 Various >85 dB 507 000 Various 85 dB
Virkkunen, 2007 Finland Virtanen, 2002 Finland
M, 40–55 M, 25–64
Davies, 2005
Canada
M, 21–36
27 464 Paper mill
>85 dB, >90 dB, >95 dB
Fujino, 2007
Japan
M, 40–59
14 568 Various
>85 dB
3000 Industry
Gopinath, 2011 Australia M + F, 57–68 Virkkunen, 2005 Finland M, 40–56 Virkkunen, 2006 Finland M, 40–55 Lee, 2009 Korea M, 19–32
3654 Various 6005 Various 1947 Various 530 Metal workers
>85 dB
>85 dB >85 dB >85 dB
Hypertension Cardiovascular mortality PDM Myocardial infarction mortality Self-report Cerebrovascular diseases Self-report Ischaemic heart disease mortality Self-report CVD and mortality JEM CHD JEM CHD PDM BP
2 3, 6, 7, 8, 14, 15, 16, 17, 18 1, 3, 5, 8, 19, 20, 21 1, 7, 22 1, 5, 7, 19, 23 1, 5, 7, 20, 24 1, 6, 7, 8
2 2, 3 3 3
F, female; M, male; PDM, personal dosimeter; SLM, sound level meter; JEM, job exposure matrix. a LAeq, 8 h, the measurement range of the study. b 1 = age; 2 = ethnicity; 3 = socio-economic status; 4 = employment status; 5 = body mass index (or quetelet index or obesity); 6 = alcohol consumption; 7 = smoking (behaviour); 8 = LTPA (leisure-time physical activity); 9 = medical history of hypertension; 10 = period; 11 = marital status; 12 = income; 13 = working conditions; 14 = heart rate; 15 = high-serum triglycerides (TG); 16 = low-serum high-density lipoprotein cholesterol (HDL-C); 17 = low-density lipoprotein cholesterol (LDL-C); 18 = type 2 diabetes/glucosuria; 19 = systolic BP; 20 = dietary fat consumption; 21 = self-reported poor health; 22 = walking difficulties; 23 = cholesterol level; 24 = shift work. c 1 = hypertension meta-analysis; 2 = cardiovascular mortality meta-analysis; 3 = CVD meta-analysis.
Figure 1. Prisma flow diagram for the study.
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Suadicani, 2012 Denmark M, 57–69
JEM JEM
M. SKOGSTAD ET AL.: SYSTEMATIC REVIEW OF NOISE AND CARDIOVASCULAR EFFECTS 13
Study name
Outcome
in the Canadian Mortality Database [14]. This study had satisfactory exposure control and reported higher mortality rates due to coronary heart disease (CHD) as compared to those studies where noise exposure was assessed retrospectively or was not measured at all [13,15–17]. In the study of Davies et al. [14], a cohort of almost 30 000 Canadian lumber mill workers, with a mean age at entry of 30 years, were followed between 1950 and 1995, having a mean noise exposure of 92 dB(A). Here, the authors found a RR of 1.5 (95% CI 1.1–2.2) that was highest when the workers were still employed. A study of a subgroup of workers who had not used personal protection equipment were included, and the authors claimed that >1/5 of CHD deaths could have been prevented or delayed given lower noise exposure levels [14]. The meta-analysis summary risk estimate showed a trivial significant excess risk of mortality from diseases of the circulatory system due to workplace noise exposure (HR = 1.12; 95% CI 1.02–1.24) (Figure 3). The failsafe N estimate indicated a fragile effect. The Q statistics indicated no substantial heterogeneity between the included studies (I2 = 5%, P > 0.05). Three studies examined the effect of occupational noise exposure and CVD [16,18,19] (Figure 4). The studies of Virkkunen et al. [18,19] included 6005 and 1804 industrial employed men. Noise was assessed through a job exposure matrix and the CHD was reported from a national register. Workers exposed to noise above 80 dB(A) in combination with impulse noise had an increased risk of CHD that persisted into old age [18].
Statistics for each study
Hazard ratio and 95% CI
Hazard Lower Upper ratio limit limit Z-Value p-Value
Relativ e weight
Chang, 2013
Hypertension
1.930
1.153
3.230
2.503
0.012
20.75
Sbihi, 2007
Hypertension
1.500
1.112
2.023
2.659
0.008
26.05
Stockholm, 2013 Hypertension
1.116
1.059
1.176
4.111
0.000
29.80
Virkkunen, 2007
2.850
1.894
4.289
5.022
0.000
23.40
1.682
1.101
2.568
2.407
0.016
Hypertension
0.1 0.2 0.5 1
2
5 10
Figure 2. Random effects meta-analysis of the association between occupational noise exposure and hypertension.
Table 2. Meta-analysis of the effects of occupational noise exposure on hypertension, CVD and cardiovascular mortality (random effects model) Outcome
N studies
Combined effect estimates
Q
I2
NMS
27.1* 1.74 4.2
88.9 0.0 5.1
50* 10* 6*
95% CI Hypertension CVD CVD mortality
4 3 5
HR 1.68 RR 1.34 HR 1.12
1.10–2.57 1.15–1.56 1.02–1.24
NMS, number of missing studies that would bring P value to >0.05, based on the fail-safe N method. *P 80 dB(A) in combination with impulse noise. An increased risk for CHD was found and remained even after the workers had retired. Noise exposure measurements were based on data from the Finnish Institute of Occupational Health and were in the range 80–100 dB(A). The study by Gopinath et al. [16] assessed noise exposure by selfreports at baseline and CVD such as angina and stroke was self-reported and causes of death were drawn from national registers. The meta-analysis summary risk estimate for the three studies showed a significant excess risk of CVD (RR = 1.34; 95% CI 1.15–1.56). The fail-safe N estimate indicated a fairly robust estimate. The Q statistic indicated no substantial heterogeneity between the included studies (I2 = 0%, P > 0.05).
The present review and meta-analysis found that prospective studies on cardiovascular effects demonstrated a positive association with occupational noise exposure. This is the first time that not only BP/hypertension but also other CVD effects of occupational noise exposure have been shown. The studies on hypertension and BP show, in a dose–response manner, an association between noise exposure and health outcome once the noise levels exceed
Study name
Outcome
Statistics for each study Hazard ratio
Lower limit
Upper limit
Z-Value
p-Value
Relativ e w eight 12.70
Dav ies, 2005
CVD Mortality
1.300
0.997
1.695
1.938
0.053
Fujino, 2007
CVD Mortality
1.310
0.850
2.019
1.223
0.221
5.22
Gopinath, 2011
CVD Mortality
1.320
0.990
1.760
1.891
0.05 9
11.03
Suadicani, 2012
CVD Mortality
0.970
0.709
1.328
-0.190
0. 849
9.45
Virtanen, 2002
CVD Mortality
1.070
0.993
1.153
1.770
0.07 7
61.60
1.124
1.015
1.244
2.249
0.024 0.5
1
2
Figure 3. Random effects meta-analysis of the association between occupational noise exposure and cardiovascular mortality.
Figure 4. Random effects meta-analysis of the association between occupational noise exposure and CVD.
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Discussion
85 dB(A). In several of the studies of CVD as the outcome, noise exposure was self-reported or historically extrapol ated from present levels. In these studies, there were weaker associations between the exposure and outcome as compared with studies of noise exposure and hypertension. The strength of the present study compared to former reviews mostly reporting results from cross-sectional studies is the quantification of the meta-risk in follow-up studies of occupational noise exposure and cardiovascular effects. Our meta-analysis shows a robust association between noise exposure and hypertension. These studies were of good quality. All studies included in the meta-analysis showed a positive effect of noise exposure on hypertension. Nevertheless, the Q statistic indicated heterogeneity across studies. The heterogeneity may be explained by variability in exposure and outcome assessments. As for other cardiovascular outcomes, the results are less convincing. This could either be due to inadequate adjustment for social class in studies with positive findings or inadequate exposure characterization in the negative studies. Several studies included in this review have methodological shortcomings regarding exposure assessment. Some articles demonstrated satisfactory exposure assessment and have outcome measures that are reliable (e.g. systematic recording of BP). Others were based on self-report of exposure levels and extrapolations have been carried out using present noise levels,
M. SKOGSTAD ET AL.: SYSTEMATIC REVIEW OF NOISE AND CARDIOVASCULAR EFFECTS 15
other CVD and thus may be regarded as a mechanism on the pathway to other cardiovascular effects. Furthermore, noisy industrial processes may create particulate matter and particulate matter from air pollution can promote atherosclerosis and hypertension, even increasing BP by 7–30 mmHg [24]. Experimental studies support the hypothesis that noise exposure can cause heart disease. A study performed with 24 h BP monitoring revealed an increase in BP of 5.6 mmHg, and the effect was sustained a few hours after the end of the exposure [25]. A transient increase in BP among noise exposed was found in a study of 476 normotensive workers in which 238 were exposed to noise at a level above 85 dB(A). Noise exposure was quantified by means of a personal dosimeter and BP was monitored both during a normal working day and a non-working day. There was an increase of 6 mmHg in systolic BP among exposed versus controls during the time of exposure and a diastolic BP increase of 3 mmHg. There was no difference in BP between the noise exposed individuals and the control group during the non-working days. However, according to other studies, the evidence that any release of catecholamines, lipids and ECG change during prolonged exposure to noise can cause physiological stress reactions is still limited [26,27]. In addition to the adrenergic/catecholamine mechanism, a recent study encompassing 1300 workers in the airline industry supports the hypothesis that heredity plays an important role in noise-induced hypertension. In this prospective study over 20 years, angiotensin gene polymorphisms were studied and the outcome of interest was the incidence of hypertension. The workers were divided into four groups, with respect to the level of noise exposure classified into exposure categories of above 80 dB(A), 80–65 dB(A), 64–50 dB(A) and, as reference, 49–40 dB(A). The study demonstrated that noise exposed workers with a certain genetic trait (TT homozygotes) had >70% increased risk of developing hypertension compared to those with other traits (TM, MM) [28]. This study therefore suggests an interplay between heredity and environment. In conclusion, the strongest evidence of an association between occupational noise and cardiovascular effects relates to studies of BP/hypertension. Overall, several good prospective studies support such a relationship, but publication bias or residual confounding cannot be excluded. For other cardiovascular effects, the results are more uncertain, due to both the lack of adequate exposure data and lack of adjustment for other factors of importance for the outcome and possible publication bias. Good quality prospective studies are necessary before it can be concluded that occupational noise exposure may cause other cardiovascular effects. However, the findings suggest that increasing noise gives an increasing
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which have been converted into historical levels. This might lead to exposure misclassification that will most likely be non-differential and give conservative risk estimates. Furthermore, there are different definitions of hypertension, e.g. in some papers the BP is measured as a continuous variable but in other cases hypertension is defined as ‘those on medication’. Known risk factors for CVD are age, gender, tobacco smoking, lack of physical exercise, high BP, high blood fats (e.g. cholesterol) and low socio-economic status (low education, low income). Many of these risk factors are associated with noise exposure at work and a lack of information on such covariates will limit the possibility to adjust for confounding in the studies. Incomplete adjustment for these factors may lead to an overestimation of the cardiovascular effects of occupational noise exposure [20,21]. In this systematic review and meta-analysis of 12 follow-up studies, publication bias cannot be excluded. This could be the case for studies of CVD disease and CVD mortality. However, the meta-analysis of studies of BP/hypertension showed a robust combined effect estimate: the fail-safe N statistic showed a requirement of 50 studies reporting null results to reduce the overall effect to non-significant, suggesting that publication bias is not likely a threat regarding the estimated risk for noise exposure on hypertension. Over-adjustment may represent a potential problem for several of the included studies, given that the noise– CVD effect has the same pathway as the noise–stress– metabolic syndrome pathway [18]. This is in line with Chandola who found that work stress was a risk factor for the metabolic syndrome that again increases the risk of heart disease and type 2 diabetes [22]. The reason that the noise-exposed individuals may be at increased risk for cardiovascular effects is not completely known but may be explained by different risk factors. Noise is a stressor, which in addition to hearing loss gives rise to non-auditory problems [1]. This is in line with a review that states that ‘work stressors are related to elevated stress responses in terms of sympatho-adrenal and HPA-axis biomarkers and due to two main axis of stress response 1) the sympatho-adrenal axis which results in changes in adrenaline and noradrenaline followed by an increased heart rate and 2) hypothalamic-pituitary function which give changes in e.g. cortisol, prolactin and testosterone levels’ [22]. Noise exposure in experimental settings is associated with short-term changes in BP, heart rate, cardiac output and vasoconstriction along with increased levels of stress hormones (e.g. epinephrine, norepinephrine and corticosteroids). Noise activates the sympathetic and endocrine systems, which could explain a cardiovascular risk with increasing noise [23]. BP is also a risk factor for
16 OCCUPATIONAL MEDICINE
effect on the cardiovascular system and that workplace noise levels should be kept low.
Key points
•• This
is the first published systematic review and meta-analysis of prospective studies on cardiovascular effects of occupational noise exposure. •• Exposure to occupational noise is positively associated with hypertension and cardiovascular disease. •• There is a weak association between occupational noise and mortality due to cardiovascular disease.
Conflicts of interest None declared.
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References
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IN-DEPTH REVIEW
Systematic review of the cardiovascular effects of occupational noise M. Skogstad, H. A. Johannessen, T. Tynes, I. S. Mehlum, K.-C. Nordby and A. Lie Department of Occupational Medicine and Epidemiology, National Institute of Occupational Health, P.O. Box 8149 Dep., N-0033 Oslo, Norway. Correspondence to: M. Skogstad, National Institute of Occupational Health, P.O. Box 8149 Dep., N-0033 Oslo, Norway. Tel: +47 23195388; fax: +47 23195205; e-mail: [email protected]
Aims
To assess possible associations between occupational noise exposure and the risk for cardiovascular effects in follow-up studies published after 1999.
Methods
We performed a systematic critical literature review of original articles from key literature databases of associations between workplace noise and health. The studies were identified by search in Ovid Medline, Ovid Embase, Web of Science, Scopus and ProQuest Health and Safety Sciences Abstracts. We selected prospective studies of adequate quality with a measure of association between occupational noise exposure and cardiovascular health for the meta-analysis.
Results
Twelve papers, all prospective and mostly with high quality but with methodological shortcomings in exposure assessment, were included in the review and meta-analysis. Exposure to noise at work was consistently positively associated with hypertension [Hazard ratio (HR) = 1.68; 95% confidence interval (CI) 1.10–2.57] and CVD [relative risk (RR) = 1.34; 95% CI 1.15–1.56]. In addition, we found a trivial effect of noise exposure on CVD mortality (HR = 1.12; 95% CI 1.02–1.24).
Conclusions Occupational noise exposure is strongly associated with hypertension. For other cardiovascular effects, this meta-analysis suggests a weak association, but the evidence is limited. More longitudinal studies on the effects of occupational noise on the cardiovascular system are warranted. Key words
Cardiovascular disease; epidemiologic methods; noise.
Introduction Noise is a major problem in many workplaces and is associated with a number of health effects. Cardiovascular diseases (CVDs) have been frequently discussed in the scientific literature during the past 40 years and research has suggested that occupational noise exposure may possibly cause increased blood pressure (BP), hypertension and other CVDs. A literature review of publications published in the period 1981–89 found a correlation between occupational noise exposure and CVD in about half of the studies, and that an increasing quality of the studies yielded an increased coherence, which supported a possible causal relationship [1]. Two systematic reviews of occupational and environmental noise exposure and BP or CVD have been
published [2,3]. In a meta-analysis of 43 occupational and community-based epidemiological studies, van Kempen et al. [2] included 28 occupational studies published between 1970 and 1999. Most of the studies were cross-sectional. Based on the analysis of 14 studies on BP of occupationally exposed subjects, it was reported that noise had a small but significant effect on hypertension. For every 5 dB(A) increase in occupational noise exposure, the relative risk (RR) for hypertension was 1.14 [95% confidence interval (CI) 1.01–1.29]. A systematic review of studies on occupational noise exposure and CVD in the period 1950–May 2008 by Tomei et al. [3] included 15 studies for meta-analysis. A statistically significant increase in systolic and diastolic BP and Electrocardiography (ECG) abnormalities in highly exposed [92.2 ± 6.5 dB(A)] workers compared with medium-exposed [85.2 ± 6.7 dB(A)] and low-exposed
© The Author 2016. Published by Oxford University Press on behalf of the Society of Occupational Medicine. All rights reserved. For Permissions, please email: [email protected]
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Background Cross-sectional studies of occupational noise and cardiovascular effects show an association between noise and hypertension but for coronary heart disease or other cardiovascular diseases (CVDs) the evidence is not convincing.
M. SKOGSTAD ET AL.: SYSTEMATIC REVIEW OF NOISE AND CARDIOVASCULAR EFFECTS 11
[62.2 ± 28.7 dB(A)] workers were reported. The average BP in the three groups was 134.1/83.7, 128.0/81.5 and 126.8/80.1 mmHg, respectively. Most of the studies reported until 2000 have been cross-sectional studies with BP as the outcome. Methodological problems are present in a majority of the studies, such as lack of good reference groups, reverse causality and confounder control. Furthermore, other problems included inadequate exposure characterization, lack of standardization of BP measurements and publication bias [1,2]. Since certain methodological problems are inherent in cross-sectional studies, we wanted to conduct a systematic critical review with emphasis on prospective studies published after the last systematic reviews [2,3].
Methods
Results After removing duplicates, we identified 75 potentially relevant articles by electronic database searches. After reviewing the titles and abstracts, studies demonstrating non-compliance with the inclusion criteria were excluded. We identified 12 articles, all cohort studies from developed countries that met the inclusion criteria, of which 11 were eligible for meta-analysis (Table 1). A flow chart showing the study selection is presented in Figure 1. Four studies examined the effect of occupational noise exposure on BP, mostly in industrial male cohorts [8–11]. In all four studies, noise exposure was retrospectively assigned to study subjects based on objective sound level measures. Three of the studies encompassed industrial groups including from 578 to 10 872 men exposed to noise levels even reaching 100 dB(A) [8–10] and one was a population-based study including 145 190 men and women exposed to noise levels in the range 70–86 dB(A) [11]. In these studies, hypertension was defined as follows; either hypertensive drug prescription, hospital discharge diagnosis of hypertension, or a diagnosis of hypertension (systolic BP >140 mmHg or diastolic BP >90 mmHg) assessed by health personnel [10,11]. A significant association between noise exposure at levels above 85 dB(A) and hypertension was reported in all four studies. In the study by Stokholm et al., the association was significant for females only.
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Initially, we searched systematically for studies on occupational noise exposure and health outcomes. At this point, the search had no restrictions regarding language or publication type. The following databases were searched: Ovid Medline (1946–), Ovid Embase (1974–), Web of Science (1950–), Scopus (1995–) and ProQuest Health and Safety Sciences Abstracts (1981–). We developed and adapted one search strategy for each database. In the bases that are indexed by a hierarchical controlled vocabulary (Medline and Embase), we used a combination of free text terms and controlled vocabulary (MeSH and Emtree). The search strategy was developed with low specificity to the advantage of high sensitivity. The search was completed in May 2013. We included studies with exposure relevant for work situations and an estimate of association with any health outcome. All titles and abstracts from the literature search were assessed against the inclusion criteria for possible relevance. At this point, studies that were not dealing with noise relevant for work-related exposure, as well as studies in languages other than English, were excluded. References that we judged to be potentially relevant were read in full text and assessed for inclusion. Relevant original studies were assessed by at least one researcher regarding methodological quality, using a comprehensive checklist. The checklist was developed by the National Institute of Occupational Health for observational studies and based especially on the checklist of Ariens and Hoogendoorn for epidemiological studies [4,5]. From the identified studies with adequate validity, the studies with CVD, BP and hypertension as outcomes were selected. Furthermore, only studies with a prospective design published between 2000 and 2013 were included. None of these studies had been included in former reviews. Twelve papers were included in the review and meta-analysis.
Summary effect estimates were calculated by means of averaged associations across samples, weighting each observed association by the study’s sample size. Eligible studies for inclusion in the meta-analyses reported categorical exposure variables with the unexposed employees (or employees with the lowest exposure category) as reference category. When eligible, we used the most completely adjusted risk estimates from each study and their corresponding standard errors. In addition, three or more eligible studies were required for the computation of combined effects. We computed random effects models, which estimate the mean of a distribution of true effects. The random effects model is recommended when there is reason to assume that the true effect varies from one study to the next [6]. The Q statistic was computed to assess the heterogeneity of studies (P 85 dB >80 dB, >85 dB
PDM PDM
Hypertension Hypertension
1, 2 1, 3, 4
1 1
SLM
Hypertension
1, 3, 4, 5, 6, 7, 8, 9
1
1, 7, 25 1, 3, 4, 10, 11, 12, 13
1 2
1, 14
2
578 Aircraft 87.4 dB, 85.4 dB, manufacturing 73.2 dB 1288 Various >85 dB 507 000 Various 85 dB
Virkkunen, 2007 Finland Virtanen, 2002 Finland
M, 40–55 M, 25–64
Davies, 2005
Canada
M, 21–36
27 464 Paper mill
>85 dB, >90 dB, >95 dB
Fujino, 2007
Japan
M, 40–59
14 568 Various
>85 dB
3000 Industry
Gopinath, 2011 Australia M + F, 57–68 Virkkunen, 2005 Finland M, 40–56 Virkkunen, 2006 Finland M, 40–55 Lee, 2009 Korea M, 19–32
3654 Various 6005 Various 1947 Various 530 Metal workers
>85 dB
>85 dB >85 dB >85 dB
Hypertension Cardiovascular mortality PDM Myocardial infarction mortality Self-report Cerebrovascular diseases Self-report Ischaemic heart disease mortality Self-report CVD and mortality JEM CHD JEM CHD PDM BP
2 3, 6, 7, 8, 14, 15, 16, 17, 18 1, 3, 5, 8, 19, 20, 21 1, 7, 22 1, 5, 7, 19, 23 1, 5, 7, 20, 24 1, 6, 7, 8
2 2, 3 3 3
F, female; M, male; PDM, personal dosimeter; SLM, sound level meter; JEM, job exposure matrix. a LAeq, 8 h, the measurement range of the study. b 1 = age; 2 = ethnicity; 3 = socio-economic status; 4 = employment status; 5 = body mass index (or quetelet index or obesity); 6 = alcohol consumption; 7 = smoking (behaviour); 8 = LTPA (leisure-time physical activity); 9 = medical history of hypertension; 10 = period; 11 = marital status; 12 = income; 13 = working conditions; 14 = heart rate; 15 = high-serum triglycerides (TG); 16 = low-serum high-density lipoprotein cholesterol (HDL-C); 17 = low-density lipoprotein cholesterol (LDL-C); 18 = type 2 diabetes/glucosuria; 19 = systolic BP; 20 = dietary fat consumption; 21 = self-reported poor health; 22 = walking difficulties; 23 = cholesterol level; 24 = shift work. c 1 = hypertension meta-analysis; 2 = cardiovascular mortality meta-analysis; 3 = CVD meta-analysis.
Figure 1. Prisma flow diagram for the study.
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Suadicani, 2012 Denmark M, 57–69
JEM JEM
M. SKOGSTAD ET AL.: SYSTEMATIC REVIEW OF NOISE AND CARDIOVASCULAR EFFECTS 13
Study name
Outcome
in the Canadian Mortality Database [14]. This study had satisfactory exposure control and reported higher mortality rates due to coronary heart disease (CHD) as compared to those studies where noise exposure was assessed retrospectively or was not measured at all [13,15–17]. In the study of Davies et al. [14], a cohort of almost 30 000 Canadian lumber mill workers, with a mean age at entry of 30 years, were followed between 1950 and 1995, having a mean noise exposure of 92 dB(A). Here, the authors found a RR of 1.5 (95% CI 1.1–2.2) that was highest when the workers were still employed. A study of a subgroup of workers who had not used personal protection equipment were included, and the authors claimed that >1/5 of CHD deaths could have been prevented or delayed given lower noise exposure levels [14]. The meta-analysis summary risk estimate showed a trivial significant excess risk of mortality from diseases of the circulatory system due to workplace noise exposure (HR = 1.12; 95% CI 1.02–1.24) (Figure 3). The failsafe N estimate indicated a fragile effect. The Q statistics indicated no substantial heterogeneity between the included studies (I2 = 5%, P > 0.05). Three studies examined the effect of occupational noise exposure and CVD [16,18,19] (Figure 4). The studies of Virkkunen et al. [18,19] included 6005 and 1804 industrial employed men. Noise was assessed through a job exposure matrix and the CHD was reported from a national register. Workers exposed to noise above 80 dB(A) in combination with impulse noise had an increased risk of CHD that persisted into old age [18].
Statistics for each study
Hazard ratio and 95% CI
Hazard Lower Upper ratio limit limit Z-Value p-Value
Relativ e weight
Chang, 2013
Hypertension
1.930
1.153
3.230
2.503
0.012
20.75
Sbihi, 2007
Hypertension
1.500
1.112
2.023
2.659
0.008
26.05
Stockholm, 2013 Hypertension
1.116
1.059
1.176
4.111
0.000
29.80
Virkkunen, 2007
2.850
1.894
4.289
5.022
0.000
23.40
1.682
1.101
2.568
2.407
0.016
Hypertension
0.1 0.2 0.5 1
2
5 10
Figure 2. Random effects meta-analysis of the association between occupational noise exposure and hypertension.
Table 2. Meta-analysis of the effects of occupational noise exposure on hypertension, CVD and cardiovascular mortality (random effects model) Outcome
N studies
Combined effect estimates
Q
I2
NMS
27.1* 1.74 4.2
88.9 0.0 5.1
50* 10* 6*
95% CI Hypertension CVD CVD mortality
4 3 5
HR 1.68 RR 1.34 HR 1.12
1.10–2.57 1.15–1.56 1.02–1.24
NMS, number of missing studies that would bring P value to >0.05, based on the fail-safe N method. *P 80 dB(A) in combination with impulse noise. An increased risk for CHD was found and remained even after the workers had retired. Noise exposure measurements were based on data from the Finnish Institute of Occupational Health and were in the range 80–100 dB(A). The study by Gopinath et al. [16] assessed noise exposure by selfreports at baseline and CVD such as angina and stroke was self-reported and causes of death were drawn from national registers. The meta-analysis summary risk estimate for the three studies showed a significant excess risk of CVD (RR = 1.34; 95% CI 1.15–1.56). The fail-safe N estimate indicated a fairly robust estimate. The Q statistic indicated no substantial heterogeneity between the included studies (I2 = 0%, P > 0.05).
The present review and meta-analysis found that prospective studies on cardiovascular effects demonstrated a positive association with occupational noise exposure. This is the first time that not only BP/hypertension but also other CVD effects of occupational noise exposure have been shown. The studies on hypertension and BP show, in a dose–response manner, an association between noise exposure and health outcome once the noise levels exceed
Study name
Outcome
Statistics for each study Hazard ratio
Lower limit
Upper limit
Z-Value
p-Value
Relativ e w eight 12.70
Dav ies, 2005
CVD Mortality
1.300
0.997
1.695
1.938
0.053
Fujino, 2007
CVD Mortality
1.310
0.850
2.019
1.223
0.221
5.22
Gopinath, 2011
CVD Mortality
1.320
0.990
1.760
1.891
0.05 9
11.03
Suadicani, 2012
CVD Mortality
0.970
0.709
1.328
-0.190
0. 849
9.45
Virtanen, 2002
CVD Mortality
1.070
0.993
1.153
1.770
0.07 7
61.60
1.124
1.015
1.244
2.249
0.024 0.5
1
2
Figure 3. Random effects meta-analysis of the association between occupational noise exposure and cardiovascular mortality.
Figure 4. Random effects meta-analysis of the association between occupational noise exposure and CVD.
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Discussion
85 dB(A). In several of the studies of CVD as the outcome, noise exposure was self-reported or historically extrapol ated from present levels. In these studies, there were weaker associations between the exposure and outcome as compared with studies of noise exposure and hypertension. The strength of the present study compared to former reviews mostly reporting results from cross-sectional studies is the quantification of the meta-risk in follow-up studies of occupational noise exposure and cardiovascular effects. Our meta-analysis shows a robust association between noise exposure and hypertension. These studies were of good quality. All studies included in the meta-analysis showed a positive effect of noise exposure on hypertension. Nevertheless, the Q statistic indicated heterogeneity across studies. The heterogeneity may be explained by variability in exposure and outcome assessments. As for other cardiovascular outcomes, the results are less convincing. This could either be due to inadequate adjustment for social class in studies with positive findings or inadequate exposure characterization in the negative studies. Several studies included in this review have methodological shortcomings regarding exposure assessment. Some articles demonstrated satisfactory exposure assessment and have outcome measures that are reliable (e.g. systematic recording of BP). Others were based on self-report of exposure levels and extrapolations have been carried out using present noise levels,
M. SKOGSTAD ET AL.: SYSTEMATIC REVIEW OF NOISE AND CARDIOVASCULAR EFFECTS 15
other CVD and thus may be regarded as a mechanism on the pathway to other cardiovascular effects. Furthermore, noisy industrial processes may create particulate matter and particulate matter from air pollution can promote atherosclerosis and hypertension, even increasing BP by 7–30 mmHg [24]. Experimental studies support the hypothesis that noise exposure can cause heart disease. A study performed with 24 h BP monitoring revealed an increase in BP of 5.6 mmHg, and the effect was sustained a few hours after the end of the exposure [25]. A transient increase in BP among noise exposed was found in a study of 476 normotensive workers in which 238 were exposed to noise at a level above 85 dB(A). Noise exposure was quantified by means of a personal dosimeter and BP was monitored both during a normal working day and a non-working day. There was an increase of 6 mmHg in systolic BP among exposed versus controls during the time of exposure and a diastolic BP increase of 3 mmHg. There was no difference in BP between the noise exposed individuals and the control group during the non-working days. However, according to other studies, the evidence that any release of catecholamines, lipids and ECG change during prolonged exposure to noise can cause physiological stress reactions is still limited [26,27]. In addition to the adrenergic/catecholamine mechanism, a recent study encompassing 1300 workers in the airline industry supports the hypothesis that heredity plays an important role in noise-induced hypertension. In this prospective study over 20 years, angiotensin gene polymorphisms were studied and the outcome of interest was the incidence of hypertension. The workers were divided into four groups, with respect to the level of noise exposure classified into exposure categories of above 80 dB(A), 80–65 dB(A), 64–50 dB(A) and, as reference, 49–40 dB(A). The study demonstrated that noise exposed workers with a certain genetic trait (TT homozygotes) had >70% increased risk of developing hypertension compared to those with other traits (TM, MM) [28]. This study therefore suggests an interplay between heredity and environment. In conclusion, the strongest evidence of an association between occupational noise and cardiovascular effects relates to studies of BP/hypertension. Overall, several good prospective studies support such a relationship, but publication bias or residual confounding cannot be excluded. For other cardiovascular effects, the results are more uncertain, due to both the lack of adequate exposure data and lack of adjustment for other factors of importance for the outcome and possible publication bias. Good quality prospective studies are necessary before it can be concluded that occupational noise exposure may cause other cardiovascular effects. However, the findings suggest that increasing noise gives an increasing
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which have been converted into historical levels. This might lead to exposure misclassification that will most likely be non-differential and give conservative risk estimates. Furthermore, there are different definitions of hypertension, e.g. in some papers the BP is measured as a continuous variable but in other cases hypertension is defined as ‘those on medication’. Known risk factors for CVD are age, gender, tobacco smoking, lack of physical exercise, high BP, high blood fats (e.g. cholesterol) and low socio-economic status (low education, low income). Many of these risk factors are associated with noise exposure at work and a lack of information on such covariates will limit the possibility to adjust for confounding in the studies. Incomplete adjustment for these factors may lead to an overestimation of the cardiovascular effects of occupational noise exposure [20,21]. In this systematic review and meta-analysis of 12 follow-up studies, publication bias cannot be excluded. This could be the case for studies of CVD disease and CVD mortality. However, the meta-analysis of studies of BP/hypertension showed a robust combined effect estimate: the fail-safe N statistic showed a requirement of 50 studies reporting null results to reduce the overall effect to non-significant, suggesting that publication bias is not likely a threat regarding the estimated risk for noise exposure on hypertension. Over-adjustment may represent a potential problem for several of the included studies, given that the noise– CVD effect has the same pathway as the noise–stress– metabolic syndrome pathway [18]. This is in line with Chandola who found that work stress was a risk factor for the metabolic syndrome that again increases the risk of heart disease and type 2 diabetes [22]. The reason that the noise-exposed individuals may be at increased risk for cardiovascular effects is not completely known but may be explained by different risk factors. Noise is a stressor, which in addition to hearing loss gives rise to non-auditory problems [1]. This is in line with a review that states that ‘work stressors are related to elevated stress responses in terms of sympatho-adrenal and HPA-axis biomarkers and due to two main axis of stress response 1) the sympatho-adrenal axis which results in changes in adrenaline and noradrenaline followed by an increased heart rate and 2) hypothalamic-pituitary function which give changes in e.g. cortisol, prolactin and testosterone levels’ [22]. Noise exposure in experimental settings is associated with short-term changes in BP, heart rate, cardiac output and vasoconstriction along with increased levels of stress hormones (e.g. epinephrine, norepinephrine and corticosteroids). Noise activates the sympathetic and endocrine systems, which could explain a cardiovascular risk with increasing noise [23]. BP is also a risk factor for
16 OCCUPATIONAL MEDICINE
effect on the cardiovascular system and that workplace noise levels should be kept low.
Key points
•• This
is the first published systematic review and meta-analysis of prospective studies on cardiovascular effects of occupational noise exposure. •• Exposure to occupational noise is positively associated with hypertension and cardiovascular disease. •• There is a weak association between occupational noise and mortality due to cardiovascular disease.
Conflicts of interest None declared.
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