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Year : 2006  |  Volume : 8  |  Issue : 30  |  Page : 1--29

Transportation noise and cardiovascular risk: Updated Review and synthesis of epidemiological studies indicate that the evidence has increased

Wolfgang Babisch 
 Federal Environmental Agency, Berlin, Germany

Correspondence Address:
Wolfgang Babisch
Department of Environmental Hygiene, Federal Environmental Agency, P.O. Box 33 00 22, 14191 Berlin
Germany

Abstract

The review provides an overview of epidemiological studies that were carried out in the field of community noise and cardiovascular risk. The studies and their characteristics are listed in the tables. Risk estimates derived from the individual studies are given for 5 dB(A) categories of the average A-weighted sound pressure level during the day. The noise sources considered in the studies are road and aircraft noise. The health endpoints are mean blood pressure, hypertension and ischaemic heart disease, including myocardial infarction. Study subjects are children and adults. The evidence of an association between transportation noise and cardiovascular risk has increased since the previous review published in Noise and Health in the year 2000.



How to cite this article:
Babisch W. Transportation noise and cardiovascular risk: Updated Review and synthesis of epidemiological studies indicate that the evidence has increased.Noise Health 2006;8:1-29


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Babisch W. Transportation noise and cardiovascular risk: Updated Review and synthesis of epidemiological studies indicate that the evidence has increased. Noise Health [serial online] 2006 [cited 2021 Dec 3 ];8:1-29
Available from: https://www.noiseandhealth.org/text.asp?2006/8/30/1/32464


Full Text

 Introduction



In section 1, chapter 6 of the Agenda 21 of the global action plan of the United Nations' conference held in Rio de Janeiro in 1992 (UN, 1993), five health-related target areas were addressed. [1] Three of these could be directly applied to community noise. These are: the reduction of health risks related to the environment, the health problems in cities and the protection of sensitive groups. [2] Furthermore, it was stated explicitly in the protocol, that "Nationally determined action programmes, with international assistance, support and coordination, where necessary, in this area should include: Develop criteria for maximum permitted safe noise exposure levels and promote noise assessment and control as part of environmental health programmes". Transportation noise was addressed as a major factor of concern in this respect in the green paper of the European commission on future noise policy and at the 3 rd European ministerial conference held in London in 1999. [3],[4] The issue of action plans to reduce harmful effects of noise exposure is addressed in the European directive relating to the assessment and management of environmental noise. [5] However, the criteria for a quantitative risk assessment are not yet established.

It is a common experience that noise is unpleasant and affects the quality of life. It disturbs and interferes with activities of the individual including concentration, communication, relaxation and sleep. [6],[7],[8] Besides the psychosocial effects of community noise, there is concern about the impact of noise on public health, particularly regarding cardiovascular outcomes. [9],[10],[11],[12] Non-auditory health effects of noise have been studied in humans for a couple of decades using laboratory and empirical methods. Biological reaction models have been derived, which are based on the general stress concept. [13],[14],[15],[16]

Amongst other non-auditory health endpoints, short-term changes in circulation including blood pressure, heart rate, cardiac output and vasoconstriction as well as stress hormones (epinephrine, norepinephrine and corticosteroids) have been studied in experimental settings for many years. [17],[18] However, not all biologically notifiable effects are of clinical relevance. Classical biological risk factors have been shown to be elevated in subjects that were exposed to high levels of traffic noise. [19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34] From this, the hypothesis emerged that persistent noise stress increases the risk of cardiovascular disorders including high blood pressure (hypertension) and ischaemic heart disease:

Sound/noise is a psychosocial stressor that activates the sympathetic and endocrine system.Acute noise effects do not only occur at high sound levels in occupational settings, but also at relatively low environmental sound levels when, more importantly, certain activities such as concentration, relaxation or sleep are disturbed.

The questions that need to be answered are:

Do these changes observed in the laboratory habituate or do they persist under chronic noise exposure? If they habituate, what are the physiological costs? If they persist, what are the long-term health effects?

Epidemiological research provides the possibility of an integral risk estimation based directly on empirical data gained under genuine conditions of exposure, taking into account any factors which may amplify or attenuate the noise effects. Determination of such effect modifications and identification of the groups at risk is an important assignment of future noise effects research. [35] Exposure-effect relationships derived from epidemiological data offer a reliable basis for the determination of environmental standards. [36],[37],[38],[39],[40] It can be used for the derivation of "no/lowest observed adverse effect levels (NOAEL/LOAEL)", [41] which are important determinants in public health policy.

Decision-making and risk management rely on a quantitative risk assessment. Since many of the stress indicators and risk factors that have been investigated in relation to noise, impose a higher risk of cardiovascular diseases for noise exposed subjects, the focus in noise epidemiology is on cardiovascular health, including mean blood pressure, hypertension and ischaemic heart diseases. Furthermore, its relevance for public health comes from the high prevalence of cardiovascular diseases in developed and industrialized countries. Ischemic heart diseases (IHD) are one of the major causes of premature death in modern societies. [42],[43] The biological plausibility of the association derives from the numerous noise experiments that have been carried out in the laboratory.

 Previous reviews



Classical, systematic and quantitative reviews have been published in the past, summarizing the results of studies that were carried out up to the end of the last century. The obstacles of such reviews were discussed in the respective literature. [44] Expert groups have assessed the evidence of the relationship between community noise and cardiovascular disease outcomes. [10],[17],[45],[46],[47],[48],[49],[50],[51] Included was a classical review and synthesis report by Babisch [45] and a systematic review (meta-analysis) by V. Kempen et al . [52] The status of evidence of the relationship between transportation noise and cardiovascular health as concluded in the literature was summarized as follows. [53],[54]

Biochemical effects: limited evidence

Hypertension: inadequate or limited or sufficient evidence

IHD: limited or sufficient evidence

The highest degree of evidence was for the association between community noise and ischaemic heart disease. Regarding hypertension the ratings were extremely heterogeneous.

New studies have appeared in the meantime, which are included in the present updated review. [31],[55],[56],[57],[58],[59],[60],[61],[62],[63],[64],[65] Others are on their way or have not yet been finalized or fully published, e.g. the pan-European projects "Hyena" [66] and "Ranch". [67],[68],[69],[70]

 Epidemiological studies



Sixty-one epidemiological studies were recognized as having either objectively or subjectively assessed the relationship between transportation noise and cardiovascular endpoints. The identification of studies was based on the author's expert-knowledge of the topic and the respective literature. All data presented in the following tables were obtained from the quoted literature, with the review laying no claim to completeness. In particular, full technical reports containing further information may not have been considered. In general, the scientific community is confronted with the problem of publication bias, which means that often studies with non-significant results remain unpublished. If not given in the references, adjusted estimates for the relative risk (odds ratio, risk ratio, proportional morbidity ratio) set out in the tables were recalculated for the purpose of this review on the basis of the data provided there in, with the least traffic noise exposed group of subjects as the reference group. If not explicitly given in the publication, test-based 95%-confidence intervals [71] were estimated on the basis of the available information, if possible (software: Epi 6, Episheet, Depid).

[Table 1-in pdf], lists epidemiological noise studies where cardiovascular effects were studied in relation to community noise levels, mainly road traffic noise and aircraft noise. Only one study refers to railway noise. The studies with their characteristics are given in chronological order and numbered (# number) for reference in the text and other tables. In the table, the location (town and country where the study was carried out), the reference (first author and year of publication), the type of the study, the study subjects, sample size, exposure, outcome and control variables (covariates) are given. A classification of the statistical control of covariates in the analyses is given (0 = no control, 1 = group comparison, 2 = stratification/standardisation, 3 = model adjustment, 4 = matching). Also, an indication is given as to whether exposure and outcome were assessed on a subjective or objective basis ("S", "O").

In most of the Tables the results are grouped according to 5 dB(A)-categories for the daytime (L day : 6-22 h) outdoor average A-weighted sound pressure level, which was considered in most studies. Information on night-time exposure (L night : 22-6 hr or 23-7 hr) was seldom available. Newer studies used non-weighted or weighted averages of the 24 h exposure (L eq , L dn , L den ) (Directive 2002/49/EC, 2002). Some aircraft noise studies used national calculation methods (e.g., Dutch Kosten units). Sound levels were converted on the basis of best guess approximations to L day . [64],[72],[73],[74] It should be noted in this context that doubling/halving of road traffic volume results in a 3 dB(A) higher/lower average sound pressure level. In urban settings, night-time average noise levels (22-6 h) for road traffic tend to be approx. 7-10 dB(A) lower than daytime average noise levels, relatively independent (no freeways) of the traffic volume of the street. [60],[75],[76] 24h noise levels of road traffic are usually 1 to 3 dB(A) lower than daytime noise levels. [77] Such empirical factors are considered in calculations of weighted averages. According to the European directive on the assessment and management of environmental noise, penalties of 5 dB(A) and 10 dB(A) are considered for the evening period and the night period, respectively, for the calculation of the weighted noise indicator L den (Directive 2002/49/EC, 2002). Therefore, in epidemiological studies in which the relative effects of road traffic noise are studied, the sound emission during the daytime can as well be viewed as an approximate indicator of the sound exposure during the night (approx. 10 dB(A) lower), if no freeways are considered and where the day/night difference is less. Not all studies allow dose-response reflections because some of them considered very broad exposure categories.

Besides objective noise measurements, subjective measurements of exposure have been used in some epidemiological noise studies, which is in accordance with the noise-stress model. Type of road (e.g., busy street, side street etc.), disturbances and annoyance were rated by the study subjects from given scales. In the related following Tables the results of these studies were grouped into four ordinal categories, depending on the items in the questionnaires: 1 = "never", "not at all", "dead end street" or "not affected"; 2 = "seldom", "a little" or "side street"; 3 = "sometimes", "moderate" or "busy road"; 4 = "often + always", "much + very much", "strongly", "major trunk road" or "affected".

Mean blood pressure

[Table 2] lists the major findings of epidemiological traffic noise studies in which mean blood pressure was considered as the outcome. It indicates mean systolic and diastolic blood pressure differences as obtained from extreme group comparisons of noise exposure. The effects in children and in adults are discussed separately.

 Children



Aircraft noise

Very crude data regarding more blood pressure abnormalities in children living in the vicinity of Russian airports were reported in the late Sixties [#03]. No detailed information is available in the international literature.

The results from a cross-sectional study on schoolchildren from schools and homes around Los Angeles airport exposed to different levels of air traffic noise support this finding [#10]. In this study blood pressure differences of 3 to 7 mmHg were found between the groups, depending on the years enrolled in school. A decreasing trend was found with increasing years of enrolment; the overall difference between the groups was 3 mmHg for systolic and diastolic pressure. However, the results may be confounded by incomplete control of ethnicity. [78] The blood pressure measurements were taken under quiet conditions in the schools. The longitudinal approach of analysis (1 yr follow-up) failed to show a relationship between noise exposure at the schools and change in blood pressure of the schoolchildren probably due to selective migration of the children's families [#11].

A cross-sectional study carried out around the old Munich airport revealed 2 mmHg higher systolic blood pressure readings in schoolchildren from noise exposed areas (L eq , 24hr = 68 dB(A) as compared to unexposed (L eq , 24hr = 59 dBA) [#36]. This difference was borderline significant. No noise effect was found with regard to diastolic blood pressure. In a longitudinal approach, blood pressure readings were analysed in schoolchildren before and after the opening of the new Munich airport in a noise-impacted and an unaffected control area [#39]. In the noise-impacted communities the 24-hr average sound pressure level (L eq ) was 53 dB(A) before the opening as compared to 62 dB(A) after the start of operation of the airport. In the control area the before and after noise levels were 53 dB(A) and 55 dB(A), respectively. Children from the noisy area showed a 2 to 4 mmHg higher increase in blood pressure readings than their counterparts from the quiet areas. However, 18 months after the opening, no difference in blood pressure readings was found between the well-matched children from the both areas. The higher change in blood pressure was due to lower values at the beginning of the follow-up.

The cross-sectional comparison of systolic and diastolic blood pressure readings in primary schoolchildren living in the vicinity of the Sydney airport revealed non-significant regression coefficients for the relationship with aircraft noise (range: 15 to 45 ANEI (Australian Noise Energy Index) at school of r = -0.017 (systolic) and r = -0.043 (diastolic) [#40]. This corresponds to mean blood pressure differences of -1 mmHg across the whole noise range. The aircraft noise level at home was also not associated with the blood pressure (r = -0.010 and r = +0.010), nor was the road/rail traffic noise level at school. The longitudinal results regarding the change of blood pressure over time did not show an association with the noise level [#41]. The elapsed time since a reduction of noise exposure due to the opening of a new runway, however, was significantly negative correlated with diastolic blood pressure [#40]. This was interpreted as responses to changes in aircraft noise level being reversible over time.

Studies were carried out in Germany, regarding noise from low-flying military aircrafts. At that time particular areas were identified for pilot training. A pre-study revealed higher readings in children of up to 9 mmHg in systolic blood pressure, particularly, in extreme low-flying areas (75 m) where sound levels were raised to L max = 125 dB(A) [#21]. The effect was found in girls, but not in boys. However, these findings were not confirmed in the main study [#22] and another area [#20], where mock attack areas were largely excluded. It is reasonable to assume that the combination of noise and fear was the driving force. Other studies on low-altitude jet noise also did not show higher blood pressure readings in children [#26].

A very speculative interpretation was given with respect to a study that compared the blood pressure of deaf-mute children and children with normal hearing [#31]. The deaf-mute group had lower blood pressure readings, which was discussed with respect to the perception of the acoustic environment. However, the effect diminished with increasing age of the children.

Road traffic noise

In an early study with schoolchildren, from schools in the German town of Halle, exposed to different levels of road traffic noise, blood pressure readings were more than 10 mmHg higher in the group with the highest exposure [#01]. Blood pressure was probably measured under acute noise conditions in the classrooms. A exposure-effect relationship was found. Confounding factors such as social class were not assessed, but children with clinical manifestations of blood pressure related diseases were excluded from the analysis.

In the Tyrol study, children from 7 villages exposed to road traffic noise from transit routes were compared with children from 6 control villages with low traffic [#29]. Slightly lower, non-significant, mean blood pressure readings were found in the exposed group. Another study carried out years later in the same region in the Inn Valley revealed only a marginal and borderline significant higher systolic blood pressure in children, who were exposed to high noise levels (L dn > 60 dB(A)) from road and railway noise, compared to less exposed children [#53].

In the city of Bratislava pre-school children attending kindergartens in different road traffic noise exposed districts were examined [#37]. Blood pressure measurements were taken in the kindergartens. Children from homes and/or kindergartens exposed to more traffic noise (70 dB(A)) showed systolic and diastolic blood pressure readings 2 to 5 mmHg higher than those from less exposed areas (60 dB(A)). This was statistically significant. Noise at the kindergartens had a higher impact on the blood pressure than the noise at home. A dose response relationship was found.

 Discussion



The findings in children are difficult to interpret with regard to possible health risks in their later life. The effect may be of a temporary nature and may not be relevant to permanent health damage. There is evidence during childhood, [79] adolescence [80] and adulthood [81] that the blood pressure level at an early age is an important predictor of the blood pressure level at a later age. Studies over the full age range are missing (tracking). Growth and body weight are important factors for blood pressure development. The impact of body size was not adequately considered in some of the studies. A crude hint regarding reversible effects on blood pressure came from one study. [82] Results of the Munich intervention study on the effects of a reduction of aircraft noise have only been reported regarding cognitive performance but not with respect to change of blood pressure. [83] It was concluded from the available data on the length of exposure that children do not seem to adapt to high levels of road traffic noise but to some extent to aircraft noise. [10],[84] However, the data base appears to be too poor to draw final conclusions. Aircraft noise studies focussed on the exposure at school, while road traffic noise studies mostly considered the noise exposure at home. Different mechanisms (disturbed learning/concentration vs. disturbed relaxation/sleep) may be involved.

The conclusions given by Evans and Lepore seem still to hold true: [85] "We know essentially nothing about the long-term consequences of early noise exposure on developing cardiovascular systems. The degree of blood pressure elevations is small. The clinical significance of such changes in childhood blood pressure is difficult to determine. The ranges of blood pressure among noise-exposed children are within the normal levels and do not suggest hypertension. The extent of BP elevations found from chronic exposure are probably not significant for children during their youth, but could portend elevations later in life that might be health damaging."

 Adults



Aircraft noise

In the Munich aircraft noise study around the old Munich airport [#04], men and women from the noisiest areas had the highest blood pressure readings with a mean difference of approx. 3 mmHg (diastolic) as compared to the least exposed group. There, a "u"-shaped association was found across noise categories. A Japanese study compared the blood pressure of females that lived in different aircraft noise zones of Fukuoka airport with a control group. In the cross-sectional part of the study, a 4 mmHg higher systolic blood pressure was found in the higher exposed group (L dn ≥ 70 dB(A)) compared to the reference group (L dn Road traffic noise

A Dutch cross-sectional study looked at the association between road and military aircraft noise and blood pressure [#17]. No clear blood pressure pattern was observed. While there was a significant positive trend of an increase in systolic blood pressure of 0.12 mmHg per noise category (6 categories) for aircraft noise after adjustment for covariates, a non-significant inverse trend of -0.03 mmHg per category was found with regard to road traffic noise. The diastolic blood pressure showed similar but non-significant trends across noise categories. When the two highest and the two lowest aircraft noise categories were combined (>50 KE versus 40 KE, KE = Dutch aircraft noise measure), mean group differences in systolic and diastolic blood pressure of 5 mmHg and 2 mmHg, respectively, were found for this extreme group comparison (due to curvi-linear association across categories). Subjects with prevalent hypertension due to renal disease or chronic diseases which can cause hypertension or influence IHD, such as diabetes mellitus, congenital heart disease, heart valve disease, were not included in the sample subjected to medical examinations. Furthermore, participants who were receiving medication or dietary treatment for hypertension were excluded from the statistical analyses, which suggests the possibility of over-controlling. This applies also to the clinical blood pressure measurements of the Bonn road traffic noise study, which refers to normotensive subjects [#09]. No remarkable blood pressure differences were found between subjects from the high noise (L day > 65 dB(A)) and the low noise area (L day [33],[34]

A Dutch study on road traffic noise carried out in Amsterdam revealed a trend towards lower blood pressure readings in subjects exposed to higher traffic noise levels [#14], as did an Austrian cross-sectional study carried out in five villages in the state of Tyrol [#30]. This was both across noise level categories and annoyance categories. These negative findings were significant. A later study carried out in the same region did not show an association with mean blood pressure readings with any of the various noise level indicators that were considered [#52]. However, distance to the highway and distance to the rail track (in the valley) were meaningful predictors of the blood pressure (higher readings in subjects that lived closer to the traffic artery). When the results were stratified with respect to annoyance ratings, only in the "not at all" annoyed, was there a tendency towards higher readings for subjects exposed to higher noise levels. In the extreme group comparison, the clinical data of the Luebeck blood pressure study showed an increase of 2 mmHg (diastolic) in readings in male subjects exposed to high road traffic noise levels (>65 dB(A)), but not in females [#15]. Across noise level categories a non-linear association was found. Significantly higher systolic and diastolic blood pressure readings were found for men in the intermediate noise category 61-65 dB(A) (+4/+2 mm Hg). When the subjective description of the type of road was used to classify exposure (given by the subjects in a questionnaire), the noise effect proved to be more pronounced.

 Discussion



Regarding mean blood pressure, no consistent findings in the relationship between traffic noise level and mean systolic or diastolic blood pressure can be seen in adults across the studies. In longitudinal studies, problems arose from migration of subjects, which had a considerable impact on sample size. The latter problem also applies to cross-sectional studies in general. Sensitive subjects may tend to move out of the polluted areas, which dilutes the effect of interest. Medication due to high blood pressure may affect the blood pressure readings. However, the exclusion of subjects with hypertension or hypertension treatment, dilutes the true effect on blood pressure differences, if the hypothesis (noise causes high blood pressure) is true. In principle, hypotension - a fall in blood pressure - can also be a stress reaction. All this makes it more reasonable to look at manifest hypertension (defined by a cut off criterion) as a clinical outcome rather than at mean blood pressure readings. [86],[87] To date, there is no evidence from epidemiological data, that community noise increases mean blood pressure readings in the adult population. However, this does not discard the noise hypothesis as such. Studies suffered from insufficient power, narrow exposure range or other difficulties in the study design.

 Hypertension



[Table 3] shows the results of epidemiological traffic noise studies for the relationship between community noise level and the prevalence or incidence of hypertension. Hypertension in these studies was either defined by WHO criteria [88] or similar criteria based on measurements of systolic and diastolic blood pressure or from information which was obtained from a clinical interview or a social survey questionnaire about doctor diagnosed hypertension. Most studies refer to road traffic noise. However, in recent years some new aircraft noise studies have been put into the database. The subjects studied were the adult male and female population, sometimes restricted to certain age groups.

Aircraft noise

An early and often cited study is not considered in [Table 3] because no detailed information regarding study design was given in the reference [#02]. There it is reported that adult subjects who lived near to an airport showed 2-4 times higher prevalence rates of cardiovascular (hypertension, hypotension, etc.) and other diseases, than those subjects who lived further away. In children, higher rates of blood pressure abnormalities and autonomic vascular changes were found [#02].

The well-known cross-sectional study carried out in the vicinity of the Amsterdam airport in the Seventies (response rate 42%) suggests relative risks of 1.5 (clinical interview) and 1.7 (blood pressure measurement), respectively, for noise levels of KE > 40 (Dutch "Kosten units") compared with subjects who lived in areas where the noise levels were lower [#05]. The data were analysed dichotomously, because the noise data showed a clustered pattern (due to the selection of communities). However, the study was re-analysed using a continuous logistic regression approach, resulting in a relative risk for hypertension of 1.26 (95% CI: 1.14-1.39) per 5 dB(A) increase in noise level, within the measurement range from approx. L Aeq , 7-19h = 55-72 dB(A). [52],[89]

The analyses of health registration data with respect to the spatial distribution of the hospital admissions due to cardiovascular diseases (amongst which was hypertension), from 62 municipalities around Schiphol airport did not show a specific pattern of clustering in areas close to the airport [#48]. However, high blood pressure is not a particular reason for hospital admission. It is mostly treated by local general practitioners. A feasibility study was carried out around the Paris Roissy airport using the approach of a practice-based survey [#45]. The diagnoses of 7 doctors' practices from high and low aircraft noise exposed areas were analysed with respect to their patient's contacts over a week. No higher blood pressure was found in subjects exposed to high aircraft noise compared with less exposed subjects. However, subjects could have gone to other doctors outside the study area and vice versa. This problem of an unknown population at risk in practice-based epidemiology (e.g., sentinel practice systems) has been previously discussed in the literature. [90]

The clinical examination of inhabitants (no response rate given) around a military air base on the island of Okinawa revealed a significantly higher prevalence (RR = 1.4) of hypertension in the group exposed to L dn  70 dB(A) [#49]. A study (postal questionnaire survey) carried out in Sweden around Stockholm's airport (response rate > 70%) showed a exposure-effect relationship with an increasing risk of hypertension starting at rather low ambient noise levels around FBN = 55 dB(A) (the Swedish weighted noise calculation method). For subjects exposed to noise levels >55 dB(A), a relative risk of 1.6 was found, which was significant [#50]. The preliminary results of another study carried out around this airport also give some first indications of a higher risk for aircraft noise exposed subjects (FBM > 55 dB(A)) of 1.6 [#60]. In the road traffic noise study carried out in the Berlin district of Spandau (response rate > 80%), aircraft noise was also assessed [#58]. The exposure assignment was based on old prognostic noise contours, which implies that there would be a problem of exposure misclassification. A steady increase in risk was found with increasing noise exposure. In the highest noise zone (according to the German Aircraft noise Act) of L eq (4) = 67-75 dB(A) the period prevalence (during the past 2 years) was 1.5. However, due to the small number of exposed subjects in the sample the confidence intervals were large. Since the subjects were taken from an ongoing health surveillance survey where subjects have voluntarily assigned themselves, the sample is then a highly selected one. Participating subjects could have a particular interest in a regular (free) clinical health check (subjects with health problems or health-aware subjects).

A telephone survey in Northern Germany [#23], as well as the clinical examinations [#24, #25] carried out on adults in different communities of military low-altitude flight zones in Germany, did not reveal any differences in the prevalence of high blood pressure (response rate 56%). The studies are not considered in [Table 3]A because single event noise levels rather than average sound pressure levels were given. The clinical examinations carried out in Muensterland [#24] suffer from a very low response rate (6%). Non-significant prevalence ratios of 1.0 and 0.9 for clinically examined prevalence of hypertension were found in males and females respectively, for exposed areas compared to less exposed. The subjects were recruited from those participating in the telephone survey [#23]. The objective prevalence of hypertension was higher than the subjective prevalence of hypertension. The other study carried out in Franken (response rate 49%) revealed non-significant prevalence ratios of less than 1.0 in exposed subjects [#25].

Road traffic noise

The German road traffic noise study (response rate 60%) carried out in Bonn [#09] suggested a relative risk for hypertension of 1.5 for subjects who lived in areas where the traffic noise level exceeded L day = 65 dB(A)). This finding was significant.

The study carried out in Erfurt [#12] is difficult to interpret. It appears to be a retrospective cohort study where disease frequencies in differently exposed groups (contact rates of patients with two medical centres) during the same period of time (1 year) were collected on an individual basis, but the data were analysed in terms of a proportional morbidity ratio. This means that the significantly higher risk of hypertension treatment in the exposed group may either be due to a higher incidence of hypertension (nominator) or to a lower incidence of treatment for other diseases (denominator) in the exposed group. A significant relative risk of 2.4 was found for subjects exposed to L day = 75 dB(AI) compared to subjects that lived in a street where the noise level was L day = 67 dB(AI). Even the control group was highly noise exposed.

The study carried out in Doetinchem [#08] and later studies carried out in the eighties and early Nineties in Amsterdam [#14], Luebeck [#15], Berlin [#34] and Tyrol [#30] may be of higher validity as far as statistical control of possible confounding is concerned. They do not support the noise hypothesis, showing relative risks of between 0.5 and 1.0 for the group comparisons with regard to the road traffic noise level. The response rates obtained in these studies were approx. 74%, 70%, 75%, 64% and 62%, respectively. Also the results of another study that was carried out in the Inn Valley, with respect to road and railway noise (response rate: 51%) did not fall in the hypothesised direction [#52]. In the cross-sectional part of a before-after study carried out in a village near Erfurt [#18], a significant relative risk of 2.4 was found for the period prevalence of hypertension in subjects that lived in a street where the noise level exceeded L day = 75 dB(AI). The prevalence ratios were probably calculated as proportional morbidity ratios. The selection criteria of exposed and unexposed subjects are not clear and the possible impact of confounding factors remains unclear. The longitudinal approach of the study was concerned with the health benefit of a 10 dB(A) reduction in noise level in the exposed streets. Five years after this intervention, the recovery rate of patients with hypertension was markedly higher in the area previously subject to higher traffic noise levels than that of the control subjects [#19]. This suggests that primary essential hypertension due to stress-induced vasoconstrictive and cardiac mechanisms may have been more prevalent in the exposed group than in the control group before the intervention.

The picture changes a little, when new studies from more recent years are considered. While a Japanese study carried out in Tokyo also showed a negative finding (no association) with respect to prevalence of hypertension as assessed in a questionnaire survey [#38], two Swedish and one German study revealed significant results pointing in the direction of a higher risk in higher exposed subjects. As with the Swedish aircraft noise studies, higher risks were found at relatively low road traffic noise levels, L eq,24hr > 50 dB(A). Using geographical information about distances of houses from main roads and railway lines, the association between noise from road traffic and railway traffic and the prevalence of hypertension was studied in the Swedish town of Sollentuna [#46]. Medical diagnosis of hypertension was assessed with a self-administered questionnaire. The noise levels in the road traffic noise exposed group ranged from Leq,24hr 40 to 65 dB(A) and those for train noise from L eq,24hr 55 to 65 dBA. Response rates of approx. 76% were achieved. After adjustment for confounding factors, a significant relative risk of 1.8 for the total group was found in the road traffic noise exposed group when comparing groups exposed to L eq,24hr >50 dB(A) with L eq,24hr day night day >65 dB(A)) and 1.9 (L night >55 dB(A)) depending on whether the exposure during the day of the living room or during the night of the bedroom was considered. The latter was significant. When subjects were analysed separately, for those who used to sleep with an open bedroom window, the relative risk was greater. However, due to a small sample size, this risk estimate cannot be interpreted in absolute terms (large confidence interval).

Annoyance (subjective ratings)

[Table 4] shows the results of studies on the relationship between subjective ratings of traffic noise exposure and prevalence of hypertension. The cross-sectional studies from Amsterdam [#14] and Tyrol [#39] gave no indication of an increased risk of hypertension in subjects more annoyed/disturbed by traffic noise as compared to those less annoyed/disturbed. Based on prevalence of hypertension as reported on a self-administered questionnaire, a significant relative risk of 1.3 was found in subjects disturbed by heavy road traffic noise, in a cross-sectional study carried out in Berlin [#34]. Since exposure and disease were assessed on a subjective basis, these results are susceptible to recall bias due to over-reporting. This reservation is true for all cross-sectional studies where exposure and disease are assessed subjectively and applies also to the prospective study carried out on a random sample of the German population [#35]. Although designed as a general population follow-up study on the incidence of various diseases in a pre-defined disease-free cohort, disturbance due to noise at home (presumable mainly traffic noise) and incidence of disease were assessed at the same time by questionnaire (during follow-up). With regard to noise at home, the study, therefore, must be viewed as cross-sectional (response rate approx. 79%). A relative risk of 0.9 (males: 1.2, females: 0.9) was found with regard to global disturbances ("affected" by traffic noise). However, a relative risk of hypertension of 2.3 was found with regard to reported sleep disturbances, which was significant.

In the Luebeck study [#15], a borderline significant relative risk of 1.3 was found in male subjects who described the street in which they lived as busy, as compared to those who described their residential streets as quiet. A exposure-effect relationship was found in the cross-sectional study carried out in Pancevo, Serbia (response rates 77% and 92% in non-exposed and exposed areas, respectively). Across annoyance categories a steady increase in risk of self-reported hypertension was found [#54]. The estimate of the relative risk of 1.8 for the highly annoyed subjects was significant. In the Spandau Health Survey no significantly higher risks were found in subjects that where annoyed by the noise [#58]. However, the relative risks of 1.2 (road traffic noise) and 1.3 (aircraft noise) were slightly higher for the annoyance/disturbance during the night than the annoyance during the day (relative risks 1.0 and 1.2).

Results from the LARES study, which is a questionnaire survey that was carried out in 8 European cities using identical methods, showed in noise annoyed subjects a higher morbidity with respect to various self-reported health outcomes (as diagnosed by a doctor) than in not annoyed subjects [#62]. Amongst these was hypertension, which was significantly more prevalent in subjects strongly annoyed by general traffic noise (relative risk 1.6) and general neighbourhood noise (relative risk 1.7). Sleep disturbed subjects showed a similar relative risk of 1.5. The effects were not found in the elderly population (60 years and older).

 Discussion



With regard to the association between community noise and hypertension, the picture is heterogeneous. With respect to aircraft noise and hypertension, studies consistently show higher risks in higher exposed areas. The evidence has improved since the previous review. [45] The relative risks found in four studies showing significantly positive associations range between 1.4 and 2.1 for subjects who live in high exposed areas, with approximate daytime average sound pressure level in the range of 60-70 dB(A) or more. Swedish studies found a relative risk of 1.6 at even lower levels (>55 dB(A)).

With respect to road traffic noise, the picture remains unclear. New studies, more likely than older studies, tend to suggest a higher risk of hypertension in subjects exposed to high levels of road traffic noise, showing relative risks between 1.5 and 3.0. However, the earlier studies cannot be neglected in the overall judgement process. Across all studies no consistent pattern of the relationship between community noise and prevalence of hypertension can be seen. Exposure-effect relationships were considered in new studies. Subjective ratings of noise or disturbances due to traffic noise seem to consistently show a positive association with prevalence of hypertension. The relative risks found here range from 0.8 to 2.3. These studies, however, are of lower validity due principally to methodological issues regarding over-reporting. [91]

 IHD



[Table 5] gives the results of cross-sectional epidemiological traffic noise studies on the relationship between noise level and prevalence of IHD; [Table 6] gives the results of case-control and cohort studies on the association between noise level and incidence of IHD. In cross-sectional studies, IHD prevalence was assessed by clinical symptoms of angina pectoris, myocardial infarction (MI), electrocardiogram (ECG) abnormalities as defined by WHO criteria [92] or from self-reported questionnaires regarding doctor-diagnosed heart attack. In longitudinal studies, IHD incidence was assessed by clinical myocardial infarction as obtained from hospital records, ECG measurements or clinical interviews. The majority of studies refer to road traffic noise.

Aircraft noise

The calculation of standardized morbidity ratios (SMR) in an ecological study of 62 municipalities around Amsterdam's airport Schiphol, using aggregated data from the health registries recording the hospital admissions due to cardiovascular diseases (myocardial infarction, hypertension, ischaemic heart diseases and cerebrovascular diseases), did not show any apparent clustering in areas close to the airport [#48].

A lot of information came from the Amsterdam aircraft noise studies that were carried out in the 1980's [#05, #06]. Significant prevalence ratios of between 1.0 and 1.9 were calculated - depending on which IHD endpoint was looked at. The subjects lived in areas exposed to more than approx. 60 dB(A) outdoor noise level. The response rate of the "community cardiovascular survey" [#05] was approx. 42%. The "general practice survey" [#06] can be considered as an ecological study on contact rates for specific diseases, with general practitioners. Aggregated data of populations, not individuals, were analysed statistically. Multiple consultations were not excluded. The study provides information on the prevalence of cardiovascular disease, which must be viewed as a combination of hypertension and ischaemic heart diseases.

In the study carried out in the four Dutch cities of Groningen, Twenthe, Leeuwarden and Amsterdam [#17], regarding aircraft traffic noise, prevalence ratios greater than 1.0 were found for noise level categories greater than approx. 55 dB(A). However, no dose response relationship was found across the categories and the relative risk for subjects in the highest noise category was 0.9. The response rate of approx. 43% refers to the subjects that participated in a previous psychological questionnaire survey (response rate there approx. 32%). Subjects that were identified in the questionnaire screening phase as being treated for hypertension were not included in the statistical analysis. This could be a matter of concern regarding selection bias in the study because high blood pressure is a major risk factor for IHD.

The Spandau health survey (response rate > 80%), which was primarily conducted with respect to road traffic noise, was also analysed with respect to aircraft noise [#58]. In the noise zone (according to the German Aircraft noise Act) of L eq (4) > 62 dB(A) the period prevalence (during the past 2 years) with respect to self-reported doctor's diagnosed angina pectoris was 1.6 and was not significant. However, with respect to the prevalence of myocardial infarction, a lower risk was found in the exposed group (relative risk = 0.4). The preliminary results of an ongoing study around the Stockholm airport showed the opposite [#60]: a higher risk of MI (relative risk = 2.6) in subjects exposed to FBM > 55 dB(A) (the Swedish calculation method of aircraft noise) and a lower risk for angina pectoris (relative risk = 0.9).

Road traffic noise

The non-significant results of the cross-sectional road traffic noise studies carried out in Bonn [#09], Caerphilly [#27], Speedwell [#28] and Berlin [#33], with response rates of approx. 60%, 89%, 92% and 64%, consistently suggest relative IHD risks between 1.1 and 1.4 for outdoor noise levels of L day >65 to 70 dB(A). The result of the Bonn study was not controlled for confounding factors because IHD was not the major interest. A very high significant relative risk of 4.9 was found in a study carried out in Tokyo, with respect to subjectively reported heart disease [#38]. However, the confidence intervals were also large due to the small sample size (response rate probably 93%). L 24hr 65 dB(A) was identified as a critical noise level above which the prevalence of ill health increased markedly. The Spandau health survey also revealed relatively high relative risks greater than 3 for road traffic noise levels L day >60 dB(A) und L night >50 dB(A), which were not significant [#58]. Again, the confidence intervals were large due to small numbers, which makes it difficult to interpret the data with respect to a exposure-effect relationship.

A study carried out in Tyrol [#30], revealed a significant relative risk of 2.1 with regard to angina pectoris, for subjects from areas of more than 60 dB(A), while a non-significant relationship - relative risk 0.8 - was found with regard to myocardial infarction. The response rate here was approx. 62%. The results of a Dutch study carried out in Doetinchem (response rate 74%) were also inconclusive and non-significant: a very small increase in risk at noise levels L day > 65 dB(A) when clinical signs of ECG abnormalities were considered (relative risk 1.1), but a lower relative risk of 0.7 when angina pectoris was considered [#08]. No noise level related increase in IHD risk, as defined by the clinical interview and the ECG, was found in the study carried out in the four Dutch cities of Groningen, Twenthe, Leeuwarden and Amsterdam [#17] regarding road traffic noise.

[Table 6]A gives the results of epidemiological traffic noise studies, about the relationship between noise level and incidence of IHD. All these studies are concerned with road traffic noise. A high and significant proportional morbidity ratio of 4.4 was derived from the retrospective study carried out in Erfurt for subjects exposed to L day 75 dB(AI) compared to subjects that lived in a street where the noise level was L day 67 dB(AI) [#12]. Some methodological issues concerning the validity of the results were raised earlier. The other studies are prospective ones. In the Berlin hospital- and population-based case-control studies (pre- and main study), non-significant relative risks of 1.2-1.3 were observed for men where the outdoor noise levels were higher than 70 dB(A) for L day , suggesting a threshold at about 70 dB(A) [#32, #33]. Response rates for cases/controls were approx. 90%/90% and 90%/64%, respectively. The risk increased in the main study, when only subjects were considered that had lived for at least 15 years in their residence. While the pre-study suffers from small numbers, the main study refers to a large sample size. In the 10-year follow-up cohort studies in Caerphilly and Speedwell (response rates > 90%), no noise effects were detected with regard to the (address-related) outdoor traffic noise level [#42, #43]. However, the 6-year follow-up analyses of the pooled reconstructed cohort (first follow-up survivors plus newly recruited subjects, response rate approx. 90%), in which exposure assessment accounted for residence time, room orientation and window opening habits, revealed non-significant relative risks of between 1.2 and 1.6 for subjects in the highest L day 66-70 dBA category compared to the lowest (51-55 dB(A)) [#44]. Furthermore, only in this highest noise category was a positive relationship between IHD risk and years in residence found, showing relative risks of between 1.01 and 1.02 per year.

A similar approach for a hospital-based case-control study was carried out 10 years later in the "NaRoMI"-study [#61]. Males and females from the entire city of Berlin (including former Eastern political part) were considered (response rate: 86%). No higher risk was found in traffic noise exposed women. However, the earlier findings in men were confirmed [#33]. A exposure-effect relationship was found over the range from L day 70 dB(A)) and increased to 1.8 when subjects were considered that had lived at least for 10 years at their residence.

Indirect support for the noise hypothesis comes from a large cohort study, which was originally not designed as a noise study, but for studying the effects of air pollution. The study considered all-cause mortality and specific mortality, including cardiopulmonary causes over a follow-up period of 8 years [#55]. After adjustment for confounders, the association between air pollutants decreased and was not significant while the association between living near a major road (within 50 m of a major urban road or within 100 m of a freeway) and all cause mortality increased and was significant. When indicator variables of air pollution and distance to major road were treated simultaneously in the model, the effect estimates for the single pollutant models decreased substantially, while distance to major road showed a strong and significant association (relative risk = 1.95 (1.09-3.51)). The authors concluded that unmeasured confounders were to some extent responsible for the association. It appears to be reasonable that road traffic noise could be an "unknown" confounder. This interpretation is further supported by the fact that non-cardiopulmonary death and death due to lung cancer were not associated with any of the air pollution variables in the study.

The approach of a time-series study is often applied in air pollution epidemiology to investigate the acute effects of changes in air pollutants. In a time-series study carried out in Madrid [#51], significantly higher rates of emergency admissions to a major hospital were found for all causes, circulatory and to a lesser extent for respiratory causes on days with higher background noise levels after controlling for the effect air pollutants. The variation of noise levels was small (L 10 -L 90  4 dB(A)) as one would expect from experience in noise measurement. An increase of 1 dB(A) was approximately equivalent to an increase of 25 µg/m 3 of air pollutants for the relative risk. The findings are difficult to interpret. Although acute and temporary autonomic responses to noise were frequently found in laboratory studies, the long-term and severe effects of chronic noise exposure - according to the noise hypothesis - are related to the development of cardiovascular disorders in the long run. Residual confounding can be an explanation for these acute effects associated with changes in noise.

Annoyance (subjective ratings)

[Table 7] gives results of studies on the relationship between subjective ratings of road traffic noise exposure and prevalence or incidence of ischaemic heart diseases. The cross-sectional studies from Tyrol [#30], Berlin [#34], Pancevo [#54] and the noise related analyses carried out as part of a general population follow-up study of two random German population samples [#35], revealed relative risks of between 0.8 and 1.9 in subjects highly annoyed/disturbed or subjectively "affected" by traffic noise, in comparison with subjects who were less annoyed/disturbed/affected. Response rates were approx. 62%, 64%, 79% and 86%, respectively, in these studies (#35: of those who participated in a previous survey). The significant effect in the Pancevo study was only found for men (relative risk: 1.7) not for women.

The results of the LARES study carried out in 9 European cities, showed in noise annoyed subjects higher risks of heart attack than in non-annoyed subjects [#62]. The relative risks for strongly annoyed of 1.4 (general traffic noise) and 2.0 (general neighbourhood noise) were not significant. In the Spandau Health Survey the numbers were too small for a reliable analysis of data [#58]. However, there was a tendency that relative risks of angina pectoris for highly annoyed subjects were higher with respect to the annoyance during the day than the night. This applies to annoyance due to road traffic noise as well as aircraft noise.

The prospective studies carried out in Caerphilly and Speedwell [#42, #43, #44] revealed pooled relative risks of IHD of between 1.0 and 1.4 only in subjects of the highest annoyance/disturbance category considered. A strong effect-modifying impact of pre-existing diseases on the relationship was found in the Caerphilly and Speedwell study. Relative risks were higher in healthy subjects, ranging from 1.7 to 2.7, but not in subjects with prevalent chronic diseases. This was discussed with respect to recall bias. The new case-control study carried out in Berlin ("NaRoMI"-study) revealed a significant relative risk (odds ratio) of 1.10 per category on a 5-point noise annoyance scale, with respect to annoyance due to road traffic noise during the night in males [#61]. This corresponds with a calculated risk of 1.3 for highly annoyed subjects. In females no such association was found. However, annoyance due to aircraft noise during the night was significantly associated with a higher MI risk in females (relative risk 2.1), which was not found in males. Annoyance due to noise during the day was not associated with MI risk.

 Discussion



With regard to IHD, the evidence of an association between community noise and IHD risk has increased since a previous review. [45] There is not much indication of a higher IHD risk for subjects who live in areas with a daytime average sound pressure level of less than 60 dB(A) across the studies. For higher noise categories, a higher IHD risk was relatively consistently found amongst the studies. Statistical significance was rarely achieved. Some studies permit reflections on exposure-effect relationships. These mostly prospective studies suggest an increase in IHD risk for noise levels above 65-70 dB(A), the relative risks ranging from 1.1 to 1.5 when the higher exposure categories were grouped together. Noise effects were larger when mediating factors like residence time, room orientation and window opening habits were considered in the analyses. This accounts for long induction periods [93,94] and improves exposure assessment. The results appear as consistent when subjective responses of disturbances and annoyance are considered, showing relative risks ranging from 0.8 to 2.7 in highly annoyed/disturbed/affected subjects. However, these findings may be of lower validity due to methodological issues.

 Medication and Drug Consumption



[Table 8] gives the results of studies on the relationship between drug consumption and community noise. Medication was primarily investigated with respect to aircraft noise. A significant prevalence ratio for cardiovascular medication of 1.4 was found in the sample of the Amsterdam airport [#05]. The results of the "drug survey", where the annual data of the pharmacies regarding the purchase of cardio-vascular drugs were analysed (repeated cross-sectional survey) supported this finding. An increase in drug purchase with time was found in the exposed areas and not in the less exposed. This refers to the purchase of cardiovascular and antihypertensive drugs, as well as the purchase of hypnotics, sedatives and antacids. Furthermore a dependency with changes in night-flight regulations was found (decrease after reduction of night-flights). A large recent study around Amsterdam airport found only a slightly higher risk of self-reported medication with cardiovascular drugs, including antihypertensive drugs, (relative risk 1.2) in aircraft noise exposed subjects where the noise level Lden exceeded 50 dB(A) [#59]. Exposure-effect relationships across noise levels (Lden = Residence time

Support for any noise effect relationship may come from subgroup analyses that are in line with the noise hypothesis. This refers to effect modification with respect to residence time, window opening behaviour and other determinants that affect the noise exposure and cumulative noise dose.

In the Amsterdam aircraft noise studies, a steady increase in the purchase of cardiovascular and antihypertensive drugs at local pharmacies was found over the period of 8 years in a community newly exposed to aircraft noise. No such increase was found in a control community that was not exposed to aircraft noise. Positive associations between the prevalence of cardiovascular diseases and residence time in exposed areas (but not in unexposed) were also found in the road traffic noise studies carried out in Bonn with respect to hypertension [#09] and in Caerphilly and Speedwell with respect to the ischaemic heart disease [#44].

When the analyses of the road traffic noise studies carried out in Berlin, Caerphilly and Speedwell were restricted to subjects who had not moved within a retrospective period of 10 to 15 years, the effect estimates turned out to be larger than for the total samples of each study [#33, #44, #61]. This is illustrated in [Figure 1],[Figure 2],[Figure 3]. Similarly, when only subjects with long residence time were considered, a larger noise effect was found in the study in Sollentuna with respect to hypertension [#47]. No such an effect was found in the Luebeck study [#15].

The cross-sectional data of the study carried out in Los Angeles on children regarding mean blood pressure, indicated some habituation to aircraft noise [#10]. The longer the children were enrolled in the school, the smaller was the difference in blood pressure between exposed and non-exposed children. However, the follow-up study suggested that this may also be an effect of attrition [#11]. The longer the families experienced the noise, the more likely that they moved away from the exposed areas (selection bias). In general, effects on children due to noise exposure at school and effects on adults due to noise exposure at home reflect different kinds of disturbances (e.g., speech intelligibility vs. sleep). In contradiction to this, blood pressure differences between children exposed and not-exposed to road traffic noise increased with school-grade [#01].

Intervention studies were conducted with respect to changes in blood pressure and changes in air traffic operation (e.g., opening/closing of airports or runways). In the Munich study, a larger increase in blood pressure was found in children from a noisy area [#39]. Other Studies suggested reversible effects on blood pressure when the exposure was lowered [#40, #19].

 Room Orientation and Window Opening



In the Tyrol study, significantly lower blood pressure readings were found in subjects who kept the windows closed throughout the night [#30]. When the subjects lived close to the highway (within a distance of approx. 500 m), the prevalence of hypertension was higher in subjects whose bedroom was facing the main road than in those, whose bedroom was not facing the main road. The orientation of rooms and window opening was also found to be an effect modifier of the association between road traffic noise and ischaemic heart disease in the Caerphilly and Speedwell studies [#44]. The relative risk with respect to the noise level was slightly higher in subjects with rooms facing the street and subjects keeping the windows usually open when spending time in the room [Figure 1]. A much greater relative risk of hypertension was found in subjects who slept with open bedroom windows in the Spandau health survey [#58].

 Other Modifiers



Hearing impairment was found to be an effect modifier on the association between aircraft noise and hypertension [#50]. Amongst the exposed subjects, a higher risk associated with the noise was only found in subjects without hearing loss.

 Risk Groups



Age and gender

Most epidemiological noise studies looked at cardiovascular effects of community noise in men. This may simply be due to the fact that the prevalence of cardiovascular diseases in middle-aged subjects is higher in men than in women. [68] Statistical power is an important issue for the design of a study. Furthermore, in noise experiments, physiological reactions controlled by the autonomic nervous system were less pronounced in females than in males. [96],[97] Improper control for possible differential effects of the intake of sex hormones including contraceptives, which may protect or promote adverse (noise-) stress effects, [98] may act conservatively on the results. [99],[100],[101]

In the studies carried out in Luebeck [#15], Pancevo [#54], Berlin [#61], Stockholm [#50], a German population sample [#35], Bonn (when considering residence time) [#09] and in Amsterdam (when considering angina pectoris) [#05], higher prevalences of hypertension, ischaemic heart diseases and the use of cardiovascular drugs, were found in noise exposed men rather than in women. The opposite was found in the studies carried out in Bonn (when considering sound level) [#09], Sollentuna [#47] and in Amsterdam (heart trouble] [#05].

In the studies carried out in the Soviet Union, it was reported that noise effects on the cardiovascular system were more pronounced in young and middle-aged subjects [#02]. Similar results were found in Swedish noise studies [#47, #60] and the "LARES" study [#62]. The opposite (larger effects in elderly subjects) was reported from the Amsterdam study [#05] and the Stockholm study [#50].

Children

The available database on cardiovascular effects of noise in children is poor. No data is available that refers, in particular, to noise and sleep. The quantitative impact of transportation noise on the cardiovascular system is still a matter of research. A quantitative health risk assessment for children cannot be made at the moment.

Based on the available information from noise studies, it must be concluded that children do not appear to be a particular risk group with respect to cardiovascular outcomes, especially blood pressure. This does not mean that the literature does not suggest higher blood pressure readings in children. It only means, that the effect in children does not appear to be different than that in adults. However, children may be longer exposed to noise throughout their lifetime than the adults that have already been studied. No long-term follow-up studies are known that focus on noise exposure. Most studies on children considered noise in schools rather than noise at home, which implies different mechanisms about how noise could contribute to a rise in blood pressure (raised effort in learning/speech perception vs. disturbed relaxation/sleep).

Health impaired subjects

The prospective part of the Caerphilly and Speedwell studies gave a small hint that health status could be a modifying factor. In subjects with prevalent chronic diseases, road traffic noise was associated with a slightly larger increase in the incidence (new cases) of ischaemic heart diseases than in subjects without prevalent diseases - when the objective noise level was considered. [91] Surprisingly, when annoyance and disturbances due to traffic noise were considered for exposure, the opposite was found. Noise effects were only seen in subjects without prevalent diseases. This was discussed with respect to reporting bias.

Evidence

The evidence for a causal relationship between community or transportation noise and cardiovascular risk, appears to have increased throughout the recent years due to new studies that complement the data base. Compared with earlier conclusions this refers, in particular, to hypertension and ischaemic heart diseases. According to the author's judgement, the current evidence can be concluded as follows.

Biochemical effects: limited evidence

Hypertension: limited or sufficient evidence

IHD: sufficient evidence

Regarding biochemical effects, the evidence has not changed compared with earlier ratings. The reason for this is not that contradictory study results were found, but that no new data is available. With regard to hypertension and ischaemic heart disease, new studies with improved control for confounding factors, point in the direction of a positive association between community noise and CVD endpoints in adults. The evidence appears to have increased by one category on the scale. The quality of IHD studies tends to be better than those of cross-sectional BP studies because for the IHD studies, observational studies (case-control, cohort) are also available. With respect to blood pressure in children, no clear picture can be seen. This may be due to the fact that the acute and chronic effects were not clearly distinguishable in some studies. This corresponds with the fact that some studies considered the exposure at school and others the exposure at home. New studies focusing on chronic effects in children should consider the exposure of the child's bedroom[153].

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