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Year : 2012  |  Volume : 14  |  Issue : 61  |  Page : 287--291

Noise and cardiovascular disease: A review of the literature 2008-2011

Hugh Davies1, Irene Van Kamp2,  
1 University of British Columbia, Faculty of Medicine, School of Population and Public Health, Canada
2 National Institute for Public Health and the Environment (RIVM), Centre For Environmental Health Research, Netherlands

Correspondence Address:
Hugh Davies
UBC School of Population & Public Health 2206 East Mall, Vancouver, BC,V6T 1Z3
Canada

Abstract

The association between noise and cardiovascular disease has been studied for several decades and the weight of evidence clearly supports a causal link. Nevertheless, many questions remain, such as the magnitude and threshold level for adverse effects of noise, how noise and other cardio-toxic pollutants (such as particulate matter) may interact in disease causation, identification of vulnerable populations, of exposure modifiers (i.e., location of bedrooms) and of other effect-modifiers (i.e., gender), and how epidemiologic methodology can be improved. This review describes contributions to literature over the past 3 years in the area of noise and CVD in general, with particular focus on these questions.



How to cite this article:
Davies H, Kamp IV. Noise and cardiovascular disease: A review of the literature 2008-2011.Noise Health 2012;14:287-291


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Davies H, Kamp IV. Noise and cardiovascular disease: A review of the literature 2008-2011. Noise Health [serial online] 2012 [cited 2020 Sep 20 ];14:287-291
Available from: http://www.noiseandhealth.org/text.asp?2012/14/61/287/104895


Full Text

 Introduction



The effect of noise exposure on the cardiovascular system is the key focus of ICBEN team 3. A 2008 review [1],[2] concluded that attention should aim at the effects of combined exposures (e.g., noise and air pollution), the inconsistencies found in cardiovascular effects in children, and effects in vulnerable groups as well as gender differences. It was also concluded that exposure assessment should be improved, endpoints measured more consistently, and systematic adjustment for confounding factors should be made.

A literature review was undertaken to identify studies pertaining to the theme of the physiological effects of noise exposure. The search was limited to English language literature, peer reviewed, and published during the period January 2008-July 2011"

We searched PubMed using keywords pertaining to noise, transportation, traffic, aircraft, railway, proximity to road; and cardiovascular disease, coronary heart disease, ischemic heart disease, myocardial infarction, hypertension, and stroke. Literature was also hand-searched for additional studies.

An emphasis on road traffic exposure was observed, and a focus on coexposures to noise- and traffic-related air pollution and their health effects. Correlations between traffic-related pollutants were not as high as was expected. The findings of studies on the joint effect on health were not entirely consistent, but suggested independent cardiovascular effects of noise and air pollution. Aircraft noise exposure also received considerable attention with multiple components of the HYENA project, [3],[4],[5],[6] and one very large cohort study finding independent effects for aircraft noise on risk of myocardial infarction, after adjustment for air pollution. [7] Occupational studies were still not common during this period, but new evidence showed a fairly consistent positive association between work-noise and both hypertension and ischemic heart disease. Finally, a handful of studies were reviewed that dealt with issues such as policy, methodology, and disease mechanisms. The most relevant findings regarding physiological and cardiovascular effects in vulnerable groups are also summarized here. Papers are presented by disease category within exposure category, followed by a section on effects in vulnerable groups.

Road traffic noise

Combined exposure to noise and air pollutants is a key issue in the interpretation of studies of associations between road traffic and cardiovascular disease. [8] Confounding or effect modification is anticipated, especially in studies that use proximity to roadway as a surrogate for exposure, e.g., study of Gan et al. [9]

Several recent studies examined this basic pollutant correlation [Table 1].{Table 1}

Overall, correlations were consistently low to moderate. In addition to those shown in the table, correlations between PM2.5 and noise were quite low, perhaps because road traffic is not an important generator of this size of particulate. [9],[18] The lower than expected correlations are likely due to differences in actual source and propagation paths; traffic density; and meteorological conditions. [11],[15],[19] Correlations of modeled estimates [10],[14] were similarly low in comparisons to measured values - even though both noise and traffic coexposures (TrAP) models used similar inputs and might have been expected to generate higher correlations. This may also be due to the fact that long-range transport is more relevant for air pollution than for noise pollution.

Early findings on noise and hypertension (HT) have been called "extremely heterogeneous," possibly due to limitations in study design. [20],[21] In their study Barregard et al. [21] examined physician-diagnosed HT in a cohort of 1,953 adults. Information on potential confounders was collected by questionnaire and noise exposures were modeled. Increased prevalence and incidence of HT and use of antihypertensive drugs were found, primarily in men, especially when considering the length of residency (>10 years). In order to reduce heterogeneity Belojevic et al. [22] used measured nighttime noise data from 70 downtown streets in Belgrade to assess exposure in a cohort of 2,503 adults, who had lived in the same residence for >10 years, and who slept on the "street side" of the house. The HT prevalence was 19.2%; the adjusted prevalence odds ratio was increased in men, but not in women. Bodin et al. [23] focused on age as an interaction or effect modifier in the road traffic noise - HT relation. They used modeled exposure levels, and self-reported HT. Risk of HT was "modestly" increased at levels <60 dBA (Leq, 24 hours), and increased above 60 dBA (reference level was <45 dBA). An age effect was seen with greatest risks in the "middle aged" (40-59 years) compared to younger (18-39) or old-aged (60-80). No gender differences were noted. Chang et al.'s cross-sectional study examined road traffic noise and HT in Taiwan; 90% of subjects' exposure was above 75 dBA (Leq, 8 hours at residence). [24] A dose--response in prevalence was observed in males (four noise categories ranging from <77 to ≥83 dBA). The HYENA study provided interesting data on the effects of road traffic noise in a study around six major European airports. [3],[4],[5],[6] A significant increase in risk of HT per 10 dB increase (adjusted) for road traffic noise was found with a more pronounced dose-response relation for men. [5] The same pattern showed in hypertensive medication use, but was not significant. [3] A study on a subsample of HYENA data (N = 149) showed a nondipping effect of diastolic BP at night, which has been previously identified as independent risk factor for CVD. [4] Additional findings suggested incomplete habituation to noise while sleeping. [4] Griefahn et al. showed increased heart rate evoked by noise exposure (45-77 dBA), [25] with and without awakening as well as incomplete habituation to noise during sleep. These findings were supported in a rail-noise study. [26] showing larger cardiovascular effects of nighttime freight train exposure and among younger subjects. [27] Studies into the physiological effects of nighttime exposures show inconclusive results. [28],[29] Increased cardiovascular risk was confirmed in three studies using proximity of residence to major roads as exposure estimate; [9],[30],[31] all of these studies acknowledged the difficulty in attributing cause to specific agents but identified noise as one such potential agent, along with air pollutants.

Three recent large cohort studies looked specifically at road traffic noise and heart disease, examining also the joint effect of noise and air pollution. [9],[16],[29] Gan et al. found a 9% (95% CI 1-18%) increase in CHD mortality associated with a 10 dB(A) increase in residential noise (all sources, L DEN ). [9] Beelen et al. investigated several CVD mortality endpoints in the Netherlands Cohort Study on Diet and Cancer using modeled noise levels. [16] For the highest noise exposure category (>65 dbA L DEN ) they found increased relative risk (adjusted) for all CVD (1.25, 95% CI 1.01-1.53%) and heart failure as well as risk of ischemic heart disease and dysrhythmia were also elevated, but neither of the latter effects was statistically significant. Selander et al. [29] confirmed an increased risk for acute myocardial infarction (MI) morbidity in the Stockholm Heart Epidemiology Program. With respect to the joint effect of traffic-related air and noise pollution on CVD, the findings of these three studies were similar - each pollutant seemed to have independent effects on CVD outcomes. [14],[16],[29] Sørensen et al. examined the association between road traffic exposure and incidence of stroke in a Danish cohort of 57,053. [10] Road traffic noise (LDEN) was positively associated with incidence of stroke with a relative risk of 1.14 (95% CI 1.03-1.25) overall. In people over 64.5 years an elevated risk showed at levels of 55 and 60 dBA. Sobotova et al. [32] showed that exposure to road traffic noise was associated with elevated CVD risk factor scores such as the Framingham SCORE60 and the European Society of Cardiology's relative risk SCORE.

Aircraft noise

Babisch and van Kamp summarized the literature on aircraft noise and hypertension in 2009. [33] They concluded that there was sufficient evidence of association between aircraft noise and hypertension, but that only a "best guess" quantitative effect estimate could be made, i.e., an odds ratio of 1.13 (95% CI 1.00-1.28) per increase of the noise level by 10 dB(A). In the period between 2008 and 2011 a series of papers were published describing the HYENA study, investigating noise near airports and hypertension. [4],[5],[6],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35] It involved six major European airports and 4,861 subjects, used modeled exposure data for aircraft noise, measured blood pressure levels, and collected data on potential confounders and effect modifiers. A dose-response pattern for hypertension was found for L night but not L Aeq,16hr . Hypertensive medication use was positively associated with L night and L Aeq,16hr , but varied by country and only significant in the UK (both metrics) and the Netherlands (L night only). [3] No apparent gender effect was found. The nondipping effect seen for nighttime road traffic was not confirmed for air traffic [35] but blood pressure was increased, SBP by 6.2 mmHg, DBP by 7.4 mmHg during 15-minute measurement intervals in which there was an aircraft event. [4] Finally, Selander et al. [29] found elevated morning cortisol levels in a subset of 439 HYENA subjects, in relation to aircraft noise at night, but only in women, and especially those who were currently working.

Exposure to military aircraft noise was studied in Korea. [36] Exposed subjects lived within 5 km of either a helicopter base (L Aeq,8hr 71-72 dBA) or a fighter jet base (68-82 dBA), for a minimum of 10 years and were compared to nonexposed control group. Risk for HT (diagnosed BP >140/90, or use of antihypertensive meds) was elevated in both exposed groups but was statistically significant only for helicopters.

Eriksson et al. examined cumulative incident HT (physician diagnosed or BP >140/90) in 4,721 subjects exposed to noise from Stockholm airport, and who were followed for 8-10 years. [34] Elevated risk for HT was apparent in males only. Estimated risk increased when the analysis was restricted to nonsmokers.

Finally Huss et al. found a 50% increase in AMI mortality in those exposed L DN >60 dBA in six million subjects who were followed for 5 years. [7] PM 10 was not linked to increased risk, but residing with 100 meters of a major road increased risk approximately 18%. No link between aircraft noise exposure and stroke mortality was observed.

Occupational noise

Two cohort studies of occupational exposure and hypertension were reported in this period. [37],[38] In a cohort of 10,872 sawmill workers followed for 8 years Sbihi et al. found that cumulative occupational noise exposure was a strong predictor of risk of HT, with a relative risk of 1.32 in the highest exposed group (>115 dBA*year) compared to controls (<95 dBA*year). Thirty-eight cases were identified from physician billing and hospital discharge records, and exposure based on work history data and a job-exposure matrix. There was a significant dose-response trend but trends of duration of exposure at different thresholds were inconsistent. The authors attributed this to misclassification of exposure potentially due to the unmeasured effect of subjects wearing hearing protection. [39] Lee et al. followed 530 male metal manufacturing workers for 9 years, obtaining annual blood pressure measurements and found that systolic, but not diastolic, blood pressure increased over time in all three exposed groups, in a dose-response fashion; 1.7, 2.0 and 3.8 mmHg respectively. [37]

Chang et al. examined the role of workplace coexposure of noise exposure and organic solvents in a pair of studies. [40],[41] In the first cross-sectional, study 59 subjects exposed to either noise or solvent showed greatly increased risk of hypertension, seven- to eightfold compared to a control group, but coexposure to both pollutants did not significantly increase this risk. In the second study, 20 subjects were divided into four similar exposure groups (none, noise only, solvent only and combined) and undertook 24-hour ambulatory blood pressure monitoring. [41] Only combined-exposure showed significantly elevated blood pressure. Both studies were challenged by small numbers, cross-sectional study design, and poorly controlled confounding.

In a meta-analysis of 15 studies into noise and hypertension (18,658 subjects), heart rate and ECG abnormalities. [42] positive results were found for all hypothesized associations (systolic BP, diastolic BP, heart rate, and ECG abnormality).

A secondary data analysis of the US National Health and Nutrition Examination Survey (NHANES) by Gan et al. observed excess risk for angina pectoris, myocardial infarction, and coronary heart disease across subjects employed a broad range of industries. [14] Dose-response trends were statistically significant for angina and CHD. Risks for CHD were stronger in younger age groups, current smokers, and in men. Noise was also associated with isolated diastolic BP (DBP > 90 mmHg, SBP < 140 mmHg), but not with any other BP measures or any biomarkers.

Physiological and cardiovascular effects in vulnerable groups

Analysis on the pooled data set (heathrow, schiphol) of the ranch study indicated that aircraft noise exposure at school was related to a nonsignificant increase in blood pressure and heart rate in children. [43] road traffic noise showed an unexplained "protective" effect. Babisch and van kamp [33] concluded on an inconsistent association between aircraft noise and children's blood pressure. Likewise recent reviews concluded a tendency toward positive associations, but large methodological differences between studies and inconsistent associations of aircraft noise with systolic blood pressure in children. [44],[45] based on a study among children babisch et al. [46] concluded that road traffic noise at home could affect children's blood pressure. There is some evidence that short-term cardiovascular reactions during sleep are more pronounced in children. [25] Lepore et al. Found that quiet-school children, but not noisy-school children had significantly lower blood pressure increases, when exposed to either acute noise or non-noise stressors, indicative of a generalized habituation effect. [47] studies in serbia among schoolchildren and preschool children indicated a raised bp among children from noisy schools and quiet residences, compared to children from both quiet environments. [22],[48] there is no consistent evidence that the effect of traffic noise on cardiovascular diseases is greater in older than younger people. [48] bodin et al. Found strong evidence for an age effect in the noise bp association, with a stronger relation in the middle aged; age group-specific models could account for differences in prevalence in future studies. [23]

There is a differential, but inconclusive effect regarding gender differences in cardiovascular effects of noise. [1],[20] babisch [20] showed that people with prevalent chronic diseases run a slightly higher risk of heart diseases as a result of traffic noise than those without.

Taking physiological changes as endpoint, a study in france among 10-year-old schoolchildren showed that school noise exposure was associated with higher cortisol levels indicative of a stress reaction. [49] these finding are supported by a swedish study who found increased prevalence of reduced diurnal cortisol variability in relation with classroom l eq during school day levels between 59 and 87 dba. [50]

 Conclusion



Several of the earlier identified gaps have been addressed in recent papers. Important progress was made on "untangling" the CVD effects of traffic coexposures, noise, and air pollution (TrAP). [1] The correlations between exposures were not as high as many researchers feared, and epidemiologic studies could be successfully pursued. Four large health effects examining joint effects were consistent in suggesting that both air pollution and noise are likely independent risk factors for CVD. This is consistent with several other lines of evidence of independent effects, such as that of animal and occupational studies that are less susceptible to confounding and in line with the fact that plausible biological mechanisms exist for both exposures. [20]

With respect to effects of gender on health associations, the majority of the studies found men to be at greater risk that women for noise-related cardiovascular disease irrespective of noise source (road vs. aircraft) or outcome (HT or heart disease). Exceptions were the studies of Selander et al. (cortisol response), Bodin et al. (self-reported HT), and Sörenson et al. (stroke). [6],[10],[23],[29] Jarup et al. found men at greater risk in their main analysis, but only women at risk when the sample was restricted to those aged over 65 years. [5] Several reviews concluded on an inconsistent association between aircraft noise and children's blood pressure. Effects of road traffic are understudied in children. There is some evidence that cardiovascular response to nighttime exposure is stronger in children than adults. There is inconsistent evidence of a generalized habituation effect of children frequenting high noise schools. Other issues regarding vulnerable populations are reviewed in van Kamp and Davies in this issue. [51]

Generally speaking the methodological quality has increased compared to early efforts in this field. The problem of misclassification of exposure has been addressed by the work on TrAP/noise correlation and in the occupational arena by the work of Sbihi et al. [38],[39],[52]

With respect to future research, reviewers are consistent in their call for more prospective studies to help elucidate underlying mechanisms of disease and the study of children, where results have been inconsistent. [2],[41],[48],[53],[54]

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