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Compared to other environmental issues, only a limited number of epidemiological studies is available on the relationship between traffic noise and cardiovascular diseases. The available literature provides no epidemiological evidence of a relationship between noise exposure and mean blood pressure readings in adults. However, noise-related increases in blood pressure are consistently seen in children. As far as hypertension as a clinical outcome is concerned, there is little evidence that exposure to high traffic noise levels is associated with an increased risk. With regard to ischaemic heart disease there is some evidence in the literature of an increased risk in subjects who live in noisy areas with outdoor noise levels of greater than 65-70 dBA. Keywords: Traffic noise, Noise annoyance, Cardiovascular effects, Hypertension, Ischaemic heart disease, Epidemiology
How to cite this article:
Babisch W. Traffic noise and cardiovascular disease : Epidemiological review and synthesis. Noise Health 2000;2:9-32 |
Biological model and hypothesis
Non-auditory health effects of noise have been studied in humans for a couple of decades using laboratory and empirical methods (reviews: Rehm, 1983; Borg, 1985; Kjellberg, 1990; v Dijk, 1990; Passchier-Vermeer, 1993; Schwarze & Thompson, 1993; Berglund & Lindvall, 1995; Lercher et al., 1998). Biological reaction models have been derived which are based on the general stress concept (Ising et al., 1980; Passchier-Vermeer, 1993; Lercher, 1996; Babisch, 1998; Gezondheidsraad, 1999).
Test persons who are exposed to high noise levels have shown decreases of electrical skin resistance, skin temperature and blood flow in peripheral blood vessels (due to vasoconstriction), and increases in blood pressure and heart rate, indicating an arousal of the sympathetic branch of the autonomous nervous system (Lehmann & Tamm, 1956; Anticaglia & Cohen, 1970; Andren, 1982). Elevated levels of stress hormones (epinephrine, norepinephrine and cortisol) have been found in blood or urine samples of noise exposed subjects, indicating an arousal of the endocrine system (Ortiz et al., 1974; Maninen O. & Aro S., 1979; Cavatorta et al., 1987). In contrast to the acute noise effects observed at high - namely occupational - noise levels, physiological effects of relatively low environmental noise levels primarily occur when the sound level disturbs cognitive functions, causes emotional reactions, or interferes with activities of the individual such as mental tasks, relaxation or sleep (Mosskov & Ettema, 1977; Frankenhauser & Lundberg, 1977; Ising & Gunther, 1983; Di Nisi et al., 1990; Eiff, 1992; Eiff, 1993; de Jong, 1993; Maschke et al., 1993; Berglund & Lindvall, 1995).
According to the general stress model, the activation of the sympathetic and the endocrine systems (stress indicators) is associated with changes in physiological functions and the metabolism of the organism, including blood pressure, cardiac output, blood lipids (cholesterol, triglycerides, free fatty acids, phosphatides) and carbohydrates (glucose), electrolytes (magnesium, calcium), blood clotting factors (thrombocyte aggregation, blood viscosity, leukocyte count) and others (Selye, 1955; Friedman & Rosenman, 1974; Henry & Stephens, 1977; Atkinson & Milsum, 1983; Cohen et al., 1995; Lundberg, 1999).
Since many of these factors are known to be classical cardiovascular risk factors, the hypothesis has emerged that chronic noise exposure causes permanent changes in these risk factors (due to dysregulation) and thus increases the risk of cardiovascular disease - in particular hypertension and ischaemic heart disease (Cantrell, 1979; Hattis & Richardson, 1980). However, the epidemiological evidence of the long-term effects of environmental noise on health is still inconclusive or limited (Suter, 1992; Berglund & Lindvall, 1995; Porter et al., 1998).
The effects of environmental noise cannot be extrapolated from results of occupational noise studies because noise effects are source-specific and dependent on the individual's activities. For example, it may very well be that a truck driver reacts little to the sound of his engine, but shows a greater effect if disturbed by traffic noise at home although the exposure level is much lower. The two noise environments cannot be merged into one sound energy related dose-response model. Meta-analytic approaches comprising work noise and traffic noise studies as done recently (Duncan et al., 1993), appear to be questionable from this point of view. Epidemiological studies are needed to answer the question of the possible pathophysiology of traffic noise exposure.
Traffic noise studies
From social surveys it is known that annoyance due to traffic noise is a major source of discomfort in the home environment (Schultz, 1978; Fidell et al., 1991; Berglund & Lindvall, 1995). [Table 1 in pdf] shows an overview of epidemiological traffic noise studies where cardiovascular effects were studied as statistical endpoints (outcome). The studies with their characteristics are given in chronological order. The data provided are: references (location, country, first author, year of publication); the type of the study (SU = survey, EC = ecological study, PM = proportional morbidity study, CS = cross-sectional study, GP = general population follow-up study, CC = case-control, CO = cohort study; p = prospective, r = retrospective, t = repeated); the subjects under study (sample size, gender, age range); and the exposure, outcome and control variables considered. The numbers given in the column listing control variables indicate how statistical control of factors other than noise was primarily carried out (0 = no control, 1 = group comparison, 2 = stratification, 3 = model adjustment, 4 = matching). The purpose of this coding is simply informative and does not imply a ranking of the studies in terms of internal or external validity. Nevertheless, studies of the categories 0 or 1 do not fulfil modern criteria of adequate treatment of confounding in the analyses.
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 nonsignificant results remain unpublished. This quantitative review corresponds with an earlier review where the results were presented in a graphical manner (Babisch, 1998). However, two new studies have been added (Bluhm et al., 1998; Morell et al., 1998).
Relative risks set out in the tables, estimated as risk or odds ratios (model-adjusted) of the prevalence or incidence, were either obtained from the cited publication or 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. For one study a proportional mortality ratio had to be calculated due to lack of information (Schulze et al., 1983). If not
explicitly given in the publication, test-based 95%-confidence intervals (Hennekens & Buring, 1987) were estimated on the basis of the available information, where possible.
In most of the following tables the results are grouped according to 5 dBA-categories of the daytime (6-22 h) outdoor average A-weighted sound pressure level. Other noise level indicators used in the various studies were converted for this purpose on the basis of approximate formulas (Passchier-Vermeer, 1993). With regard to noise level assessment, it should be noted that doubling/halving of road traffic volume results in a 3 dBA higher/lower average sound pressure level. In urban settings, nighttime average noise levels (22-6 h) from road traffic tend to be approx. 7-10 dBA lower than daytime average noise levels, relatively independent (no freeways) of the traffic volume of the street (Utley, 1985; Ullrich, 1998). 24h noise levels of road traffic are usually 1 to 3 dBA lower than daytime noise levels (Rylander et al., 1986). Therefore, in epidemiological studies in which the relative effects of road traffic noise is studied, the sound emission during the daytime can as well be viewed as an approximate relative measure of the overall sound emission including the night. 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, as pointed out earlier. Type of road (e. g. busy street, side street etc.), disturbances or annoyance were rated by the study subjects on given scales. In the related following tables the results of these studies were grouped into four ordinal categories: 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", "major trunk road" or "affected", depending on the items in the questionnaires.
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:
In an early study with schoolchildren, from schools in Halle, exposed to different levels of road traffic noise (Karsdorf & Klappach, 1968) blood pressure readings of more than 10 mmHg higher were found in the group with the highest exposure. Blood pressure was probably measured under acute noise conditions in the classrooms. A dose-response 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 city of Bratislava pre-school children attending Kindergartens in different road traffic noise exposed districts were examined (Regecova & Kellerova, 1995). Blood pressure measurements were taken in the Kindergartens. Children from homes and/or Kindergartens exposed to much traffic noise (70 dBA) showed systolic and diastolic blood pressure readings 2 to 5 mmHg higher than those from less exposed areas (60 dBA). This was significant. A dose response relationship was found.
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 (Cohen et al., 1980; Cohen et al., 1981) support this finding. In this study blood pressure differences of 2 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 systolic and diastolic. However, the results may be confounded by incomplete control of ethnicity (Morell et al., 1998). The blood pressure measurements were taken under quiet noise conditions in the schools. The longitudinal approach of analysis of a study which was repeated a year later (Cohen et al., 1981) failed to show a relationship between noise exposure of the schools and change in blood pressure probably due to selective migration of the schoolchildren.
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 (Leq, 24hr = 68 dBA) as compared to unexposed (Leq, 24hr = 59 dBA). This was borderline significant. No noise effect was found with regard to diastolic blood pressure (Evans et al., 1995). 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 a unaffected control area (Evans et al., 1998; Hygge et al., 1998). In the noise-impacted communities the 24-hr average sound pressure level (Leq) was 53 dBA before the opening as compared to 62 dBA after the start of operation of the airport. In the control area the before and after noise levels were 53 dBA and 55 dBA, respectively. Children from the noisy area showed a 2 to 3 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 wellmatched 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 school children living in the vicinity of the Sydney airport revealed nonsignificant regression coefficients for the relationship with aircraft noise (range: 15 to 45 ANEI (Australian Noise Energy Index)) of r = -0.01 and r = +0.01, respectively (Morell et al., 1998). This corresponds to mean blood pressure differences of -0.3 mmHg and +0.3 mmHg respectively, across the whole noise range. The elapsed time since a reduction of noise exposure due to the opening of a new runway was significantly negative related with diastolic blood pressure. This was interpreted as responses to changes in aircraft noise level are reversible over time.
Summary
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 not be relevant to permanent health damage. Although there is evidence during childhood (Gillman et al., 1992), adolescence (Yong et al., 1993) and adulthood (Tate et al., 1985) that 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 on blood pressure development.
Adults
In the Munich aircraft noise study around the old Munich airport (Eiff et al., 1974; Rohrmann, 1974) 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 similar relationship was found in the Caerphilly study (Babisch et al., 1988, Babisch & Gallacher, 1990a) with a mean systolic blood pressure difference of 2 mmHg between subjects of the extreme groups of road traffic noise exposure (66-70 dBA versus 51-55 dBA). However, the twin study carried out in Speedwell (Babisch & Gallacher, 1990a; Babisch et al., 1993a) revealed an inverse relationship - the subjects in the highest noise category showing the lowest blood pressure readings. In a subsample, an effect modifying impact of work noise exposure on systolic blood pressure was demonstrated (Babisch et al., 1990b). A Dutch cross-sectional study (Altena, 1989; Pulles et al., 1990) looked at the association between road and military aircraft noise and blood pressure. 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 nonsignificant 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 (due to curvi-linear association across categories). Subjects with prevalent hypertension due to renal disease ("secondary hypertension") or chronic diseases which can cause hypertension or influence IHD, such as diabetes melitis, 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 problem of overcontrolling. This applies also to the clinical blood pressure measurements of the Bonn road traffic noise study (Eiff et al., 1981), which refers to normotensive subjects. No blood pressure differences were found between subjects from the high noise and the low noise area.
Another Dutch study on road traffic noise carried out in Amsterdam (Knipschild et al., 1984) revealed a trend towards lower blood pressure readings in subjects exposed to higher traffic noise levels, as did an Austrian cross-sectional study carried out in five villages in the state of Tyrol (Lercher, 1992; Lercher & Kofler, 1993), both across noise level categories and annoyance categories. These negative findings were significant in some cases. In the extreme group comparison, the clinical data of the Luebeck blood pressure study (Hense et al., 1989; Herbold et al., 1989) showed an increase only of up to 2 mmHg (diastolic) in readings in male subjects exposed to higher road traffic noise levels, but not in females. Across noise level categories a curvi-linear association was found. With regard to the subjective description of the type of road, given by the subjects in a questionnaire, the noise effect proved to be only slightly more pronounced. An attempt to conduct a prospective study (Eiff et al., 1987; Otten et al., 1990) failed due to a high and probably selective migration rate amongst the young subjects under study, particularly in the noisy areas. The effects of military low flying aircraft noise were studied in two regions in Germany (Schulte & Otten, 1992). Neither in the 150 m nor in the 75 m limit altitude areas for aircraft operation were found higher mean blood pressure readings for the adult population as compared to subjects from control areas. It can be argued whether it is the noise or fear from aircrafts which is the relevant stressor.
Conclusion
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. But in studies on noise exposed children, higher blood pressure readings are seen to be in agreement with each other. The public health impact of traffic noise on children's development regarding blood pressure needs further clarification. In longitudinal studies problems arose from migration of subjects, which had a considerable impact on cohort size, and selfselection. 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. In principle, hypotension - a fall in blood pressure - can also be a stress reaction, which makes it more reasonable to look at manifest hypertension as a clinical outcome rather than at mean blood pressure readings (Ising, 1983; Winkleby et al., 1988). In conclusion, there is no epidemiological evidence of an increase in mean blood pressure readings in traffic noise exposed adult subjects.
Hypertension
[Table - 3] gives the results of epidemiological traffic noise studies on the relationship between noise level and prevalence of hypertension. In fact, one study (Schulze et al., 1983) refers to the incidence of hypertension. Hypertension in these studies was either defined by WHO (World Health Organization, 1978) or similar criteria based on measurements of systolic and diastolic blood pressure, or was defined by antihypertensive treatment, information on which was obtained from a clinical interview or a social survey questionnaire. All studies except one which refers to aircraft noise (Knipschild, 1977a) deal with road traffic noise. The subjects studied were the adult male and female population, sometimes restricted to certain age ranges.
An early and often cited study is not considered (Karagodina et al., 1969) in the table because no detailed information is given in the reference. 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 far away. In children, higher rates of blood pressure abnormalities and autonomic vascular changes were found. Two studies which refer to military low-flying aircraft noise (Schulte & Otten, 1992) are not considered in the table because single event noise levels rather than average sound pressure levels are only given. The study carried out in Northern Germany suffers from a very low response rate (6%) with regard to clinically examined prevalence of hypertension. Non-significant prevalence ratios of 1.0 and 0.9 were found in males and females, respectively, from exposed areas as compared to less exposed. The other study carried out in Southern Germany (response rate 49%) revealed non-significant prevalence ratios less than 1.0 in exposed subjects.
With regard to air and road traffic noise, again, the picture is quite heterogeneous. Some of the earlier studies carried out in Amsterdam, (Knipschild, 1977a), Bonn (Eiff & Neus, 1980; Eiff et al., 1981; Neus et al., 1983), Erfurt (Schulze et al., 1983) suggest an increased risk at noise levels above 60-70 dBA with significant relative risks of between 1.5 and 2.4 for subjects who live in areas where traffic noise levels are higher. The Amsterdam study and the Bonn study are cross-sectional studies in which response rates of approx. 42 % and 60 % of the subjects identified in the source populations were obtained. The Erfurt study is difficult to conceptualise. It appears to be a retrospective cohort study (see Hennekens & Buring, 1987) 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 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. The reference provides no error terms. The study carried out in Doetinchem (Knipschild & Salle, 1979), and later studies from Amsterdam (Knipschild et al., 1984), Luebeck (Hense et al., 1989), Berlin (Babisch et al., 1992), Tyrol (Lercher, 1992) which may be of higher validity as far as statistical control of possible confounding is concerned, do not support the noise hypothesis, showing relative risks of between 0.5 and 1.0 for the group comparisons with regard to objective noise measurements. The response rates obtained in these studies were approx. 74 %, 70 %, 75 %, 64 % and 62 %, respectively.
In the cross-sectional part of a before-after study carried out in a village near Erfurt (Wolke et al., 1990), a significant relative risk of 2.4 was found for the period prevalence of hypertension. The prevalence ratios were probably calculated as proportional morbidity ratios. The selection criteria of exposed and unexposed subjects are not quite clear from the publication. Unfortunately, little information was given about the assessment of possible confounding factors. The longitudinal approach of the study was concerned with the health benefit of a 10 dBA 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 high traffic noise levels than that of the control subjects, which suggests that primary essential hypertension due to stress (catecholamine) - induced vasoconstrictive and cardiac mechanisms may have been more prevalent in the exposed group than in the control group.
[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 (Knipschild et al., 1984) and Tyrol (Lercher, 1992; Lercher & Kofler, 1995) give no indication of an increased risk of hypertension in subjects more annoyed/disturbed by traffic noise as compared to less annoyed/disturbed. Based on prevalence of hypertension as reported on a selfadministered 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 (Wiens, 1995; Babisch et al., 1992). 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 (Muller et al., 1994; Bellach et al., 1995). Although designed as a general population follow-up study (see Rothman, 1986) on the incidence of various diseases in a pre-defined disease-free cohort, disturbance due to traffic noise and incidence of disease were assessed at the same time by questionnaire. With regard to traffic noise this study must be viewed as crosssectional. The response rate was approx. 79 %. A relative risk of 0.9 (males: 1.2, females: 0.9) was found with regard to global annoyance ("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 (Herbold et al, 1989; Hense et al., 1989), 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.
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 (Bluhm et al., 1998). Medical diagnosis of hypertension was assessed with a self-administered questionnaire. The 24 hour average sound pressure levels the a road traffic exposed group ranged from 50 to 65 dBA and those for train noise from 55 to 65 dBA. Noise levels for the unexposed reference group were below 50 dBA (personal communication). Response rates of approx. 76 % were achieved. After adjustment for confounding factors, a significant relative risk of 1.8 was found in the road traffic noise exposed group. The effect was only seen in women (relative risk of 3.3) but not in males (relative risk 1.0). A possible explanation could be that women spend more time at home. Regarding train noise, the opposite association was found. The subjects in the exposed area were at lower risk of hypertension than those in the control area. The relative risk of
0.8 was not significant. In contradiction to this, the prevalence of annoyance and sleep disturbance due to noise was highest in the railway noise exposed group as compared to the other groups.
Conclusion
With regard to hypertension, the relative risks found in four significantly positive studies range between 1.5 and 3.3 for subjects who live in areas with a daytime average sound pressure level in the range of 60-70 dBA or more. One study shows a significantly negative association. Across all studies no consistent pattern of the relationship between traffic noise level and prevalence of hypertension can be seen. Doseresponse relationships which may support a causal interpretation of findings were rarely studied. When subjective ratings of noise or disturbances due to traffic noise are considered as exposure instead of the noise level, the pattern is also inconsistent. The relative risks found here range from 0.8 to 2.3. These studies, however, are of lower validity due to methodological reasons. Since housewives are probably more exposed to noise at home than their husbands when they are out at work, the effects of noise may lead to a greater tendency towards hypertension in females than in males. However, improper control of use of contraceptives (Eiff, 1993) may act conservatively on the results. In conclusion, there is little epidemiological evidence of an increased risk of hypertension in traffic noise exposed subjects.
Ischaemic heart disease
[Table - 5],[Table - 6],[Table 7] refer to the risk of ischaemic heart disease (IHD). In cross-sectional studies IHD prevalence was assessed by clinical symptoms of angina pectoris, myocardial infarction or ECG abnormalities as defined by WHO criteria (Rose & Blackburn, 1968). In longitudinal studies IHD incidence was assessed by clinical myocardial infarction as obtained from hospital records, ECG measurements or clinical interview.
[Table - 5] gives the results of epidemiological traffic noise studies on the relationship between noise level and prevalence of IHD. The studies carried out in Amsterdam (Knipschild, 1977a; Knipschild, 1977b) and partly the Dutch study carried out around the cities of Groningen, Twenthe, Leeuwarden and Amsterdam (Altena, 1989; Pulles et al., 1990) refer to aircraft noise, all other studies to road traffic noise.
A lot of information came from the Amsterdam aircraft noise studies. Significant prevalence ratios of between 1.0 and 1.9 were calculated - depending on the IHD endpoints looked at - in subjects who lived in noise exposed areas of more than approx. 60 dBA outdoor noise level (Knipschild, 1977a; Knipschild, 1977b). The response rate of the "community cardiovascular survey" (Knipschild, 1977a) was approx. 42 %. The "general practice survey" (Knipschild, 1977b) can be considered as an ecological study on contact rates for specific diseases with general practitioners; aggregated data of populations - not individuals - have been analysed statistically. Multiple consultations were allowed. The study provides information on prevalence of cardiovascular disease which must be viewed as a combination of hypertension and ischaemic heart disease. The results from the "drug survey" (Knipschild & Oudsdoorn, 1977) where the annual data of the pharmacies about the purchase of cardiovascular drugs were analysed (repeated crosssectional survey), showed an increase in drug consumption over time in the exposed areas but not in the less exposed. Furthermore a relationship with changes in night-flight regulations was found.
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 four Dutch towns (Altena, 1989) regarding to road traffic noise. With regard to air traffic noise, prevalence ratios greater than 1.0 were found for noise level categories greater than approx. 55 dBA. However, no dose response relationship was found across the categories, and the relative risk to 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 can be a matter of concern regarding selection bias in the study because high blood pressure is a major risk factor for IHD.
The non-significant results of the cross-sectional road traffic noise studies carried out in Doetinchem (Knipschild & Salle, 1979), Bonn (Eiff & Neus, 1980; Eiff et al., 1981), Caerphilly (Babisch et al., 1993b), Speedwell (Babisch et al., 1993b) and Berlin (Babisch et al., 1994) with response rates of approx. 74 %, 60 %, 89 %, 92 %, and 64 %, consistently suggest an IHD risk of 1.1-1.4 higher for outdoor noise levels of greater than 65-70 dBA. The result of the Bonn study was not controlled for confounding factors because IHD was not the major interest. Another study carried out in Tyrol (Lercher, 1992), revealed a significant relative risk of 2.1 with regard to angina pectoris, for subjects from areas of more than 60 dBA while a nonsignificant relationship - relative risk 0.8 - was found with regard to myocardial infarction. The response rate here was approx. 62 %.
[Table - 6] gives the results of epidemiological traffic noise studies, on 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 (Schulze et al., 1983). Some methodological issues concerning the validity of the results were raised earlier. No confidence intervals can be calculated from the data given. The other studies are prospective ones. In the Berlin hospital-based and population-based (Babisch et al., 1992; Babisch et al., 1994) casecontrol studies, non-significant relative risks of 1.1-2.1 were observed for outdoor noise levels of more than 70 dBA, following a dose-response relationship. Response rates for cases/controls were approx. 90/90 % and 90/64 %, respectively. In the 10-year follow-up studies in Caerphilly and Speedwell (Babisch et al., 1995; Babisch et al., 1999) with response rates of approx. 89 % and 92 %, no noise effects were detected with regard to the (address-related) outdoor traffic noise level. 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 66-70 dBA category. 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.
[Table 7] gives results of studies on the relationship between subjective ratings of traffic noise exposure and prevalence or incidence of ischaemic heart diseases. The cross-sectional studies from Tyrol (Lercher, 1992; Lercher & Kofler, 1995), Berlin (Babisch et al., 1992; Wiens, 1995) and the noise related analyses carried out as part of a general population follow-up study of a random German population sample (Miller et al., 1994; Bellach et al., 1995), revealed relative risks of between 0.8 and 1.9 in subjects greatly annoyed/disturbed ("affected") by traffic noise in comparison with subjects who were less annoyed/disturbed. Relative risks greater than 1 were found in particular with regard to angina pectoris. Response rates were approx. 62 %, 64% and 79 % in these studies. The prospective studies carried out in Caerphilly and Speedwell (Babisch et al., 1995) with response rates of approx. 90 % revealed pooled relative IHD risks 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. This was significant in the case of some forms of disturbance on the item list. As pointed out earlier, there is some concern about the subjective assessment of exposure in terms of recall bias.
Conclusion
With regard to ischaemic heart disease, there is not much indication of an increased IHD risk for subjects who live in areas with a daytime average sound pressure level of less than 60 dBA across the studies. For higher noise categories increases in IHD risk are relatively consistently found amongst the studies. Statistical significance was rarely achieved. Some studies permit reflections on dose-response relationships. These mostly prospective studies suggest an increase in IHD risk at noise levels above 65-70 dBA, the relative risks ranging from 1.1 to 1.5 when the higher exposure categories are grouped together. Noise effects were larger when mediating factors like years in residence, room orientation and window opening habits were considered in the analyses. This accounts for induction period and improves exposure assessment. The results appear as consistent when subjective responses of disturbances and annoyance are considered as exposure with relative risks ranging from 0.8 to 2.7. However, these findings may be of lower validity due to methodological issues. In conclusion, there is some epidemiological evidence of an increased risk of ischaemic heart disease in traffic noise exposed subjects.
General conclusion
As compared to other environmental issues, only a limited number of epidemiological studies is available on the relationship between traffic noise and cardiovascular diseases. Whilst nearly all studies regarding blood pressure are crosssectional, there are some longitudinal studies which have considered ischaemic heart disease. With the exception of a few studies, the results of the environmental noise studies are not statistically significant. This means that the confidence intervals include a relative risk of 1. Lack of statistical power is one reason, but also misclassification of individual exposure plays a role, diluting the true effect if there is one. The magnitude of the estimates of effect tends to be small, which makes the results susceptible to unknown and residual confounding - a common problem in environmental epidemiology. Nevertheless, the study results can be interpreted with regard to their consistency: The available literature provides no epidemiological evidence of a relationship between noise exposure and mean blood pressure readings in adults. However, in children noise-related higher blood pressure readings have been measured repeatedly. The public health impact of these findings needs further clarification. As far as hypertension is concerned as the clinical outcome, there is little epidemiological evidence that exposure to high traffic noise levels is associated with an increased risk. With regard to ischaemic heart disease there is some epidemiological evidence in the literature of an increased risk in subjects who live in noisy areas with outdoor noise levels of more than 65-70 dBA. The terms "no" < "little" < "some" are used in order to rank the scientific evidence in contrast to the terms "limited" and "sufficient" evidence which are used for decision (policy) making. For example, "some" scientific evidence may be "sufficient" for precautionary action (Horton, 1998). Given the large proportion of the population - approx. 10-20 % (WHO European Centre for Environment and Health, 1995) - that is exposed to considerable traffic noise levels at home, even small relative risks may be of public health relevance (Neus et al., 1994). This points to the need for more adequate studies in this field of noise research. These studies should consider mediating factors like room orientation, window opening habits and residence time, in order to reduce exposure misclassification and to account for longer induction periods (Eiff & Neus, 1980; Lercher & Kofler, 1993; Bluhm et al., 1999; Babisch et al., 1999). Some epidemiological investigations suggest a closer relationship between outcome variables and sleep-related variables of noise exposure rather than with daytime exposure (Bellach et al., 1995, Babisch et al., 1996). Other noise exposures - e. g. work noise - and coping strategies of the individual may act as effect modifiers (interaction) on the relationship between traffic noise and health outcome (Babisch et al., 1990b; Evans & Lepore, 1997; Lercher & Kofler, 1993; Lercher, 1996; Lercher & Kofler, 1996; Babisch et al., 1996).[110]
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Wolfgang Babisch
Federal Environmental Agency, Dept. of Environment and Health, P.O. Box 330022, D-14191 Berlin
Germany
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 12689458 
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