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ORIGINAL ARTICLE
Year : 2014  |  Volume : 58  |  Issue : 2  |  Page : 84-91  

Association between transportation noise and cardiovascular disease: A meta-analysis of cross-sectional studies among adult populations from 1980 to 2010


Professor, Department of Environmental Science, Banwarilal Bhalotia College, Asansol, Burdwan, West Bengal, India

Date of Web Publication12-May-2014

Correspondence Address:
Dr. Dibyendu Banerjee
79-Rabindranagar, Asansol, Burdwan - 713 304, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-557X.132279

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   Abstract 

Background: It is hypothesized that exposure to transportation noise is associated with an increased risk of cardiovascular disease among adult population. The present study further explores this association in the light of new findings. The objective of this study was to perform a meta-analysis of studies reported during the last 3 decades on the association of transportation noise exposure with cardiovascular disease endpoints among adult population in cross-sectional studies. Materials and Methods: Relative risks were pooled from 12 studies by using an inverse-variance weighted fixed-effects model. The cardiovascular health outcomes included ischemic heart disease, myocardial infraction, angina pectoris, electrocardiogram-ischemia and cardiovascular medication. Results: The pooled risk estimate (95% confidence interval) of 1.04 (0.96-1.12), shows a positive but nonsignificant association. The sensitivity analysis, conducted by excluding studies one by one, resulted in a positive and significant risk estimate. Contrary to the earlier meta-analysis, this study observed heterogeneity among subgroups and produced significant positive results to show that there exists an association between air traffic noise exposure and cardiovascular disease. It was also observed that the risk of cardiovascular disease due to exposure to transportation noise has increase to significant levels over the last 30 years. Conclusion: It can be concluded that though the association between transportation noise exposure and cardiovascular disease is evident, but not at a significant level. This study although provides evidence that air traffic noise is a serious cause of concern.

Keywords: Cardiovascular diseases, Cross-sectional study, Meta-analysis, Myocardial ischemia, Transportation noise


How to cite this article:
Banerjee D. Association between transportation noise and cardiovascular disease: A meta-analysis of cross-sectional studies among adult populations from 1980 to 2010. Indian J Public Health 2014;58:84-91

How to cite this URL:
Banerjee D. Association between transportation noise and cardiovascular disease: A meta-analysis of cross-sectional studies among adult populations from 1980 to 2010. Indian J Public Health [serial online] 2014 [cited 2019 Nov 11];58:84-91. Available from: http://www.ijph.in/text.asp?2014/58/2/84/132279


   Introduction Top


Cardiovascular disease is reported to cause more than a quarter of death among adults and is one of the major causes for loss of disability adjusted life years worldwide. The important cardiovascular disorders are arterial hypertension (raised blood pressure), coronary heart disease and cerebrovascular disease. Ischemic heart disease (IHD) or myocardial ischemia is characterized by interruption of blood supply to a part of the heart, resulting in necrosis of heart cells (myocardial infraction [MI]) and chest pain due to reduced supply of oxygen in the heart (angina pectoris [AP]). The conventional risk factors of coronary heart disease, including blood cholesterol, hypertension, smoking, obesity, physical inactivity, diabetes, etc., accounts for about 50% of the incidence. [1] Among other potential and emerging risk issues, environmental factors including noise exposure is considered to be linked to cardiovascular disease through a stress model, where it has been postulated that acute noise exposure activate the autonomic and endocrine systems, triggering temporary changes in blood pressure, heart rate, and vasoconstriction. If exposure continuous to chronic levels than hypertension and IHD are predicted. [2] There is evidence that chronic noise exposure is associated with increased risk of cardiovascular disease, including IHD. [3],[4],[5],[6] Country-wise reviews of studies investigating the potential association between noise exposure and cardiovascular effect have been put forward to support the evidence. [7],[8],[9],[10],[11],[12] The outputs of these studies are suggestive that there exists a positive association between the noise exposure and cardiovascular disease, although the evidence is not substantive.

Although several review studies have been conducted on the theme of noise exposure and cardiovascular disease, meta-analysis has been limited. The present study further synthesizes the results from the most recent evidences. The major objective of this meta-analysis study was to examine whether exposure to transportation noise increases the risk of IHD among the adult population by synthesizing results from cross-sectional studies. The study further aimed to explore the sources of heterogeneity, if any, among the studies considered.


   Materials and Methods Top


Study design and extraction

The meta-analysis was conducted following the preferred reporting items for systematic reviews and meta-analyses statement guidelines. [13] Studies reporting association between transportation noise exposure and cardiovascular disease were searched in electronic databases, including Medline, Scopus, Google Scholar and Cochrane. The last search was run on February 11, 2012. The reference lists of the identified studies and three meta-analyses were also searched [3],[6] screened. The steps included the initial identification of the records, followed by screening to remove duplicates and then evaluation of the title and abstracts to prepare a list for eligibility assessment. In the eligibility assessment, the identified papers were studied in details in relation to eligibility criteria and were either marked as "included" and "excluded." Included studies were further explored to analyze whether they could be used for meta-analysis. For the entire procedure all the lists were recorded separately in structured spread-sheets and included information such as title, abstract, journal reference, author, year of publication, PubMed ID, etc., for each article.

Eligibility criteria

Cross-sectional studies, published between 1980 and 2010 were included for data extraction. Adult populations, both male and female were considered. The exposure criteria included all transportation noise sources, either measured or calculated and includes comparison of reference group with one or higher noise exposed groups, measured objectively. No restrictions were used on the type of noise measure as a broad variety of indexes are applicable. All outcomes considered were defined as per ICD-10: Version: 2010: Codes 120-125. [14] For this study health outcomes included were IHD, MI, AP, electrocardiogram-ischemia (ECG-I) and/or using cardiovascular medication as indicated by self-reporting, diagnosis by physicians and/or laboratory measurements.

Exclusion criteria

The present study was limited to adults as because it has been reported that findings from children are difficult to interpret in relation to possible health outcomes that may occur in later life and also cardiovascular diseases in them are rare. [3] Cohort, ecological, and case control studies were excluded since they are less useful in determining prevalence and in identifying associations where the outcome is rare. The comparing of effect estimate across the different study designs may induce error. Studies before 1980 were excluded because, the present meta-analysis aimed to explore the more recent decades. Studies that did not quantify health outcomes were excluded. Hypertension as an outcome was not used in this study.

Statistical analysis

All analysis was conducted in STATA-9 (StataCorp., Station College, TX, USA). For this study effect size was extracted from the included studies. Effect estimates comparing the most distant noise groups were used for the meta-analysis. Studies that reported more than one exposure or those that considered more than one outcome were treated as separate studies, under the same author. The studies and their effect estimates were reported in the form of forest plots. For heterogeneity assessment, which indicates the variations in study outcome between the studies, the I2 statistics and χ2 test were taken into account. The I² statistic describes the percentage of variation across studies that are due to heterogeneity (>25% low, 25-50% moderate, >50% high) rather than by chance. [15]

Summary estimate and publication bias

It is recognized that effect of noise on the outcome varies to some extent with the type of source; consequently summary estimates were obtained and reported for each outcome of interest, separately for air and road traffic noise exposure. To study possible publication bias in the present meta-analysis, both graphical (funnel plot) and statistical analysis (Begg's adjusted rank correlation test and Egger's regression asymmetry test) was conducted. A symmetrical funnel is resulted in the absence of publication bias, whereas a skewed asymmetrical funnel indicates the existence of possible publication bias.

Sensitivity and subgroup analysis

Additional analysis such as sensitivity and subgroup analysis help to understand whether the results of the meta-analysis are robust. While sensitivity analyses are used to explore the degree to which the main findings of a systematic review are affected by changes in its methods or in the data used from individual studies, subgroup analyses deal with whether the summary effects vary in relation to specific characteristics of the included studies or their participants. [13] Sensitivity analysis conducted by excluding studies one at a time, to see if the resultant new summary results change significantly (P < 0.05) and how each study influenced the summary estimate of the outcome effect size. To explore variability in the association between different noise exposure and potential cardiovascular diseases, subgroup analysis were performed using: gender (male, female and both), age (>16, 20-65, 40-70 years), number of participants (<1000, 1000-1999, 2000-3000, >3000), publication period (1980s, 1990s, and 2000s), noise sources and outcomes.


   Results Top


Study selection

The search of electronic databases provided a total of 644 citations. After screening for unrelated titles and duplicates 176 remained. Of these, 150 studies that did not meet the study criteria were rejected after reviewing the abstracts. Two additional studies were discarded because full text was not available. The full text of the remaining 24 citations was examined in more detail. Among them 10 studies did not meet the inclusion criteria. Although, 14 studies were screened, a total of 12 studies were included in the final meta-analysis. The design and selecting strategy is depicted in [Figure 1].
Figure 1: Flow diagram for selection of pooled and meta-analysis studies of association between transportation noise and ischemic heart disease among adult population

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Study characteristics

[Table 1] shows the characteristics of the studies used for data extraction. All studies were cross-sectional and published between 1980 and 2010. The studies reported association between transportation noise and various cardiovascular diseases.
Table 1: Characteristics of included studies used for meta-analysis data extraction

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Participants

Five studies involved only male participants; whereas the remaining included both male and female subjects. The age of the subjects varied between 16 and 90 years. For nine studies the number of participants varied between 417 and 2874 while two studies had 11,601 and 11,812 subjects respectively. One very large study was reported from Cologne-Bonn, Germany. [16]

Exposure

The exposure used in all studies involved noise from transposition sources. No studies reported association between rail noise and outcome of interest. Seven studies reported road traffic exposure, three air traffic and two studies described both. Reported noise level from for air traffic varied between 38 and 75 dB(A), whereas it was 41-80 dB(A) for road traffic.

Outcomes

The health endpoints selected as outcome of interest for this meta-analysis included IHD, AP, MI, ECG-I and use of cardiovascular medicine (MC) as indicator of heart disease. Two studies reported IHD, AP, MI and ECG-I. One study reported IHD only; whereas three studies described both MI and AP as outcome. MI and MC as sole outcome were reported by five and one studies respectively.

Individual studies and synthesis of results

The effect estimate (95% confidence interval [CI]) of individual studies is shown as forest plot [Figure 2]. Of the 14 included studies, two were excluded for subsequent analysis. One of the studies was excluded from meta-analysis as it reported multiple noise exposure sources. After the preliminary meta-analysis run, another study [17] was excluded since it was observed that more than 60% weight was attributed to this study and could influence the results of the analysis. Of the 12 studies finally used in the meta-analysis, nine showed a positive association between exposure to traffic noise and cardiovascular disease. The effect measure varied between 1.05 and 1.30 in these nine studies. The lower and upper 95% CI varied between 0.20-1.06 and 1.60-3.56 respectively. Positive and significant association between noise exposure and IHD was reported in one study only. [18] The pooled risk estimate (95% CI) of the association between traffic noise exposure (all sources) and cardiovascular disease was 1.04 (0.96-1.12). Heterogeneity was absent in all the 12 studies (I2 = 0.0%, P = 0.546). The forest plot of summary estimates of each of the outcome, grouped by source of noise (air or road) is given as [Figure 3]. The pooled risk estimate (95% CI) for air traffic noise exposure was 1.00 (0.91-1.09) and for road traffic noise exposure was 1.03 (0.97-1.09). Heterogeneity was nearly absent, when air traffic was source of noise exposure (I2 = 0.30%, P = 0.448), whereas for road traffic it was intermediate (I2 = 25.2%, P = 0.237). For studies involving air traffic noise, MI and AP were positively, but not significantly associated with exposure; whereas for road traffic, IHD, MC usage and AP were positively related to noise exposure.
Figure 2: Forest plot showing results of main meta-analysis for studies of association between transportation noise and ischemic heart disease among adult population and reported between 1980 and 2010. CI is confidence interval. The dashed vertical line corresponds to no effect of noise exposure. I2 is measure of heterogeneity across the studies

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Figure 3: Summary estimates for association between air and road traffic noise exposure, and different types of cardiovascular health outcomes. The data were extracted from 12 studies published between 1980 and 2010. CI is confidence interval. The dashed vertical line corresponds to no effect of noise exposure. I2 is measure of heterogeneity across the studies

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Sensitivity and subgroup analysis

It was observed that the results of meta-analysis, after removal of individual studies were not significantly affected. The overall (pooled) meta-analysis result from the sensitivity analysis though returned a positive and significant association between traffic noise exposure and cardiovascular disease. The risk estimate varied between 1.04 (1.01-1.06) and with no heterogeneity. The result of the subgroup analysis is presented in [Figure 4]. The subgroup analysis helps in identification of diversity and heterogeneity among the different studies. The results of the subgroup analysis resulted in an overall positive and significant pooled estimate of RR (95% CI) of 1.06 (1.02-1.11) with low heterogeneity (I2 = 24.9%). Subgroup wise significant positive results were obtained for studies reporting age group >16 years (estimate: 1.29; 1.05-1.53), number of subjects (estimate: 1.29; 1.06-1.52), >3000, period of publication between 1999 and 2010 (estimate: 1.28; 1.06-1.52), air traffic noise exposure (estimate: 1.29; 1.06-1.52) and MC intake (estimate: 1.30; 1.03-1.57). The subgroup analysis provides evidence of heterogeneity among the studies involved at different levels, the important being the exposure subgroup.
Figure 4: Subgroup analysis for the association between transportation noise and ischemic heart disease among adult population. CI is confidence interval. The dotted vertical line corresponds to no effect of noise exposure on health outcome. I2 is measure of heterogeneity across the studies

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Publication bias

[Figure 5] shows the funnel plot for visualizing publication bias amongst the 12 studies used for meta-analysis. Based on the heterogeneity data of I2 and statistically insignificant tests of Egger's (P = 0.668) and Begg's test ( P = 0.732), it may be said conservatively that there were no evidence of publication bias among the included studies.
Figure 5: Funnel plot of the results of studies investigating the association between transportation noise exposure and the risk of ischemic heart disease

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   Discussion Top


Main results

The findings provide some evidence to support the hypothesis that cardiovascular disease may be associated with transportation noise exposure among adults. The results of the main meta-analysis using the 12 studies yield positive estimates. The additional studies (sensitivity and subgroup) yielded positive and significant estimates showing association between exposure and health end point. Subgroup analysis showed heterogeneity and that air traffic noise was significantly and positive associated with cardiovascular outcomes. The results of the main analysis is comparable with previous reviews that there is evidence to support the fact that cardiovascular diseases maybe linked with exposure to air and road traffic noise. Studies by Belojevic and Saric-Tanaskovic [19] and Lercher [20] reported strong association between road noise exposure and MI (in male) and AP (in male and female) respectively. Diverging from earlier studies, this study observed heterogeneity among subgroups and produced significant positive results to show that there exists an association between air traffic noise exposure and cardiovascular disease. It was also observed that the risk has increased over the years, with more significant results being reported by studies from the last decade.

Limitations

The present study on traffic noise exposure and cardiovascular effects, excluding hypertension, was conducted using best practice in meta-analysis with sound methodology and procedures by stratified analysis of the included studies using subgroup, sensitivity and publication bias analysis using established statistical tools. Heterogeneity was address among the main studies and subgroups. Inclusion and exclusion criteria were well-defined and only one effect size measure of association was used for comparing the studies. This study incorporated results from a wide span of time period, including the most recent research reported. The low heterogeneity and no publication bias also reassure that systematic and random errors are very low. Some limitations however are to be considered when interpreting the results of this meta-analysis. The searches yielded only a few studies that were included based on the criteria set and objectives of the study. Although gender wise subgroup differences were desired, but only one study reported separate estimate for female. The included studies were of cross-sectional design only, which may have resulted in bias of the overall estimate, since a number of case-control and cohort studies, reporting significant results were excluded. Occupational exposure studies were not included. The effect size in epidemiology studies are influenced by confounders and effect modifiers; and all of the included studies performed adjustments for various potential confounders, varying from two to more than ten, but most of them did not include cardiovascular risk factors. Adjustments were mostly limited to demographic variables. These might have influenced the individual risk estimates and in turn the results of this meta-analysis. The presence of pre-existing disease condition and family history of cardiovascular disease in the studies is also a limitation, since these factors may moderate the cause-effect link. Overall outcome level limitations could be assumed as the meta-analysis reported here combined results of effect estimate data across various studies. No analysis was conducted to estimate the risk quantitatively, which may limit the application of further statistical analysis. Furthermore, there was a major difference in participant population, with the highest number being 25 times the lowest sample size.

Biological plausibility

It is a well-known fact that stress can induce ischemia heart disease. Stress can be caused by a wide variety of exposures and situations, including noise. [21],[22],[23],[24] Chronic noise exposure may affect the hypothalamic-pituitary-adrenal (HPA) axis, linked to the reticular arousal system through the auditory apparatus. The former being a significant part of the neuro-endocrine system controlling reactions to stress. [3] In the event of acute stress due to perceived noise, the pituitary gland releases Adrenocorticotropic hormone in the blood stream, this then triggers the release of cortisol (stress hormone) from the adrenal gland along with catecholamine (noradrenalin). Acute stress related to noise exposure activates both sympathetic and the endocrine system, possibly leading to fluctuations in blood pressure, heart and level of the cortisol. Chronic stress, dysfunctions this HPA axis and may lead to hyper secretion of cortisol and elevate its level in the blood stream, that may eventually cause cardiovascular damage along with other diseases. Passchier-Vermeer [25] also proposed a secondary stress behavior mechanism; where noise exposed individuals elevate the risk of cardiovascular disease by increasing in smoking, alcohol intake, and medicine use. Annoyance and sleep disturbance are also indicators of such pathophysiological reactions that may lead to cardiovascular risk. [26] The manifestation of cardiovascular disease although will occur in susceptible groups in the population and vary across gender, age groups, socio-economic conditions and pre-existing of other diseases. Along with IHD prolonged noise stress may also lead to changes in blood lipids, plasma volume, blood viscosity, blood glucose, blood clotting, increased vascular hypertrophy, insulin resistance, and dyslipidemia. Changes in renal circulation, favoring blood plasma elevation through elevated sodium resorption are also possible. Overall it can be said that the plausibility of a biological pathway between noise exposure and cardiovascular effects hold true although the mechanism is complex.

Based on the results of this meta-analysis, it may be conservatively concluded that:

  • Overall, the pooled meta-analysis results do not reveal a statistically significant association between exposure to traffic noise and IHD, although the relationship is positive.
  • The risk estimate (95% CI) have increased over the three decades from 0.97 (0.37-1.67) in 1980s to 1.28 (1.05-1.62) in 2010s. This provides support to the fact that the risk of cardiovascular disease due to transportation noise exposure has increased.
  • Aircraft noise is positively and significantly associated to prevalence of IHD cases, compared with road traffic. Pooled subgroup effect estimate yielded a positive association.


It can be concluded that the results of this meta-analysis are consistent to the notion that mild risk of cardiovascular disease may be more pronounced among the transportation noise exposed population. This study reports a positive association, but it is limited to cross-sectional studies. Additional research using more adjustments for important cardiovascular risk factors is needed to provide support to the underlying relationship between traffic noise exposure and cardiovascular disease.[29]

 
   References Top

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1]


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