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Year : 2000  |  Volume : 2  |  Issue : 7  |  Page : 65-77
Evaluation of traffic noise-related cardiovascular risk

Behörde für Arbeit, Gesundheit und Soziales, Referat Umweltbezogener Gesund-heitsschutz (G25), Hamburg, Germany

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  Abstract 

In this paper we discuss the risk of myocardial infarction induced by traffic noise within the conceptual framework for risk assessment suggested by the US National Research Council. The characterisation of cardiovascular risk is evaluated using a four-dimensional set of evaluation criteria: severity of health effect, frequency of exposures considered relevant for health, size of estimated risk, and validity of risk assessment. For quantification of risk we calculated lifetime risks using standard methods applied for quantitative cancer risk estimation. In evaluation of validity we refer to criteria that the International Agency for Research on Cancer has developed for classification of epidemiological evidence.
Compared to other adverse effects regarded in regulatory toxicology, myocardial in-farction is a severe health effect. Assuming that sound pressure levels Leq, 6-22 hr above 65 dB(A) are associated with an increased cardiovascular risk, a major portion of the German population (about 16 %) is exposed to health relevant noise levels. Estimated lifetime risk amounts to 20 :1,000 and exceeds considerably the lifetime risk induced by other environmental hazards or tolerable risk levels suggested in other contexts. A causal association between noise exposure and infarction risk, however, cannot be taken as proven scientifically, because chance, bias or con-founding cannot be ruled out with reasonable confidence. Methodological quality of the studies performed, consistency of findings, dose-response relations, coherence with a recent occupational study and biological plausibility nevertheless support a causal interpretation. Thus, an integrative evaluation of all available information may justify the conclusion that a causal interrelationship is probable.
The conclusions for regulation strongly depend on how the high risk potential is balanced against the uncertain causality assessment. This question cannot be answered by science but must be decided politically. From a public health perspective noise exposure should be reduced in order to protect human health.

Keywords: Road traffic noise, cardiovascular risk, risk assessment, risk evaluation

How to cite this article:
Neus H, Boikat U. Evaluation of traffic noise-related cardiovascular risk. Noise Health 2000;2:65-77

How to cite this URL:
Neus H, Boikat U. Evaluation of traffic noise-related cardiovascular risk. Noise Health [serial online] 2000 [cited 2020 Jun 2];2:65-77. Available from: http://www.noiseandhealth.org/text.asp?2000/2/7/65/31740

  Introduction Top


In the last few years the cardiovascular effects of noise have gained increased public interest. The present paper concentrates on the administrative risk evaluation of the available scientific information. By risk evaluation we understand a characterisation of the public health relevance of an environmental hazard. Clearly, risk evaluation is not a purely scientific task, but should be advised and guided by scientific arguments and considerations to the best possible extent. In 1983, the US National Research Council (NRC) suggested a general concept as to how scientific risk analysis (risk assessment) should be integrated in decision making processes. For the analysis of the available scientific information the NRC suggested a four-step procedure, including hazard identification, exposure assessment, dose-response assessment and risk characterisation [Figure - 1]. These suggestions of the NRC have become generally accepted as a useful conceptual framework for the regulation of chemical hazards and can be applied to other hazards such as noise exposure as well.

The results of risk assessment are summarised in risk characterisation which serves as an interface to risk management. The combination of exposure assessment and dose-response assessment allows a quantitative estimate of the likelihood that the hazard of concern will affect exposed people. As all steps of analysis are subject to data interpretation and associated with uncertainties, many assumptions, judgements and conventions play a part in risk assessment. These assumptions can be chosen in different ways, depending on specific science-policy options which involve normative and value judgements (Fischoff 1989, Ozonoff 1994). Therefore, risk characterisation should include a full discussion of the uncertainties associated with the estimates of risk.

Evaluation of risk assessment requires a multidimensional set of evaluation criteria. In a previous paper we suggested considering at least four criteria as follows (Neus et al 1995):

1. Type and severity of the health effect considered.

2. Frequency of exposures considered relevant for health.

3. Size of estimated risk in dependency on exposure.

4. Validity of risk assessment.

In the following we will discuss the risk assessment for noise-induced myocardial infarction making use of these evaluation criteria. At the same time, we will make comparisons with the risk assessment of chemical hazards.

Severity of effect

Physical or chemical hazards can lead to a variety of different health effects. The fact that an organism responds to an external stimulus per se needs not be detrimental for health and well­being, but may represent a normal physiological reaction in the sense of biological adaptation. The acute reaction of finger pulse amplitude or other vegetative functions to noise exposure is usually interpreted in this way. Thus, regulatory toxicology concentrates on so-called „adverse" health effects. Environmental standards should ensure that adverse effects will not occur.

A recent review of definitions suggested by different institutions and authors (IPCS / OECD 1996) shows that meanwhile a common understanding of the adversity of an effect has been accomplished. The World Health Organisation (WHO 1994) defines an adverse effect as follows:

Change in morphology, physiology, growth, development or life-span of an organism which results in impairment of the functional capacity or impairment of the capacity to compensate for additional stress or increase in susceptibility to the harmful effects of other environmental influences. Decisions on whether or not any effect is adverse requires expert judgement.

This definition shows that the environmental standard setting in general is adjusted to subtle effects which represent early steps in biological effect chains or can be interpreted as first signs of a pathological process. Compared with the subtle considerations typical for regulatory toxicology, myocardial infarction is a gross and severe health effect whose adversity cannot be questioned.

Frequency of exposures considered relevant for health

A statement on the frequency of health relevant exposures requires to define how exposure is measured and when it is considered to be relevant for health. In the case of noise exposures the daytime average sound pressure level Leq, 6 - 22 hr is usually chosen as an indicator of exposure. The value of 65 dB(A) is considered to be health relevant as several investigations revealed consistent increases of infarction risks beyond this level (see Babisch et al 1993, 1994, 1998). This definition does not mean, however, that below this level adverse effects can be excluded.

Firstly, in the terminology of regulatory toxicology the value of 65 dB(A) corresponds to a LOAEL (Lowest Observed Adverse Effect Level), that is the lowest dose at which an adverse effect has been observed. As measures of health protection aim to prevent adverse effects, environmental standards generally should be lower than the LOAEL. An alternative measure is the NOAEL (No Observed Adverse Effect Level), that is the highest dose at which adverse effects have not been observed. But even below the NOAEL adverse effects cannot be excluded with certainty because they might exist but have remained undetected so far. In order to obtain reasonably safe standards it is usual to start from the NOAEL and to apply additional safety or uncertainty factors (WHO 1994).

Secondly, environmental monitoring data - such as the average sound pressure level in a specified time window and at a specific location - are only approximations of the biologically effective individual real-life exposures. Individual exposures strongly depend on the time-budget and mobility of the exposed humans, but also on characteristics of indoor and outdoor sound propagation. When in epidemiological studies subjects are classified according to the average sound pressure level in the streets, individual exposures are characterised imperfectly and misclassification is likely to occur. In general "non-differential misclassification" in exposure variables results in an underestimation of the true dose-response relationship (Armstrong 1990, Checkoway et al 1991, Pershagen 1995). Under this aspect, inconsistent results below 65 dB(A) do not prove biological irrelevance of exposures below this level.

Thirdly, the average daytime sound pressure level does not reflect exposure during the night and sleep and therefore may not cover all biological effect mechanisms. There is ample evidence that noise exposure during sleep is of particular biological relevance (Maschke et al 1997). In the special case of road traffic noise there is a statistical relationship between day and night values with a level difference of about 10 dB(A). Therefore, for the purpose of risk assessment it is justified using daytime levels as an approximate indicator of noise exposure during day and night. It must be questioned, however, that by using daytime values alone, if meaningful threshold values could be derived.

Finally, physiological reactions to noise strongly depend on the behavioural context of exposure and individual coping. Impairment of recreation and sleep may even be more relevant for myocardial infarction than the physically measured sound pressure level (Babisch et al 1995). Furthermore other individual factors such as genetic predisposition may play an additional role (von Eiff et al 1982). Thus, in specific conditions or in sub-populations with a specific vulnerability of infarction, risks might arise at sound pressure levels well below 65 dB(A). It is generally agreed that individual susceptibilities must adequately be considered in regulation, for example by application of additional safety or uncertainty factors.

These arguments would indeed justify considering noise exposures below 65 dB(A) as health relevant. With reference to standard setting procedures used in regulatory toxicology (use of NOAEL and application of safety or uncertainty factors) some authors have suggested a critical level of 55 dB(A) (Miiller et al 1994). But even when choosing a level of 65 dB(A) it appears that a considerable portion of population is affected.

The Federal Environmental Agency of Germany (Umweltbundesamt, UBA) has performed systematic estimations of noise exposures in the German population for a couple of years. According to these estimations about 16 % of the German population is exposed to road traffic noise exposure over 65 dB(A). To a large extent this can be attributed to lorry traffic (UBA 1994, 1997) [Figure - 2].

In conclusion, noise exposure induced by road traffic noise in the magnitude of 65 dB(A) is a frequent environmental hazard. This distinguishes noise and other traffic-related hazards from many other environmental health problems (for example industrial emissions in the vicinity of industrial plants, chemical exposures in public buildings or soil contamination in residential areas or playgrounds) which usually affect only selected population groups.

Size of estimated risk

Measures of risk: In biometrics different measures are used for quantification of risks. Results of epidemiological studies are usually expressed as odds ratios or relative risks. Relative risks are defined as the ratio of mortality or incidence rate under defined exposure conditions relative to mortality or incidence rate under conditions free of exposure. They can be interpreted as per cent increase of risk induced by exposure. By definition, statements on absolute risk levels cannot be made unless basal rates under unexposed conditions are taken into account.

Better suited in this respect are lifetime risks. Referring to methodological developments in the United States, quantitative risk estimation for carcinogenic substances in the last few years has gained increased interest in the Federal Republic of Germany (Wahrendorf and Becher 1990, Wichmann 1990, LAI 1992, Hassauer et al 1993, Becher et al 1995, Neus et al 1995, Mekel et al 1997). We have therefore chosen lifetime risks as a reference method to compare noise-induced infarction risks with other environmental health hazards.

Lifetime risk is a hypothetical measure which is defined as the probability for premature death in consequence of an exposure presumed to be constant during a lifetime. Lifetime risks cannot be empirically observed but are estimated on the basis of experimental data on animals or epidemiological studies using standardised statistical models. These models are associated with numerous assumptions and premises which cannot be proven in a strictly scientific sense. Under this aspect quantitative risk estimations should not be interpreted as exact risk prognoses. The standardised procedures on the other hand allow for risk comparisons which can be used for priority setting.

Although primarily developed for estimation of cancer risks, the methods available for quantitative risk estimation based upon epidemiological data can also be applied to other causes of death when data or estimates on relative mortality risks are at hand. Empirical data suggest a relative risk of 1.2 for myocardial infarction when sound pressure levels exceed 65 dB(A) (Babisch et al 1993, 1994). Unfortunately, these data refer to incidence instead of mortality rates. It seems to be justified, however, to estimate relative mortality risk of noise-induced myocardial infarction from relative incidence risk as there is no reasonable hypothesis why lethality of noise-induced infarction should differ from lethality of other infarctions. Under this assumption lifetime risk induced by noise exposure over 65 dB(A) would amount to 20:1,000 (Neus et al 1994, 1995). The relative risk of 1.7 observed in the Berlin case control study beyond 75 dB(A) would correspond to a lifetime risk of 70 : 1,000.

Comparison with cancer risks: These numbers can be compared with quantitative estimations for carcinogenic air pollutants performed by a German Study Group mandated by the Conference of Ministers for Environmental Affairs (LAI 1992). The study group came to the conclusion that in Germany the total lifetime cancer risk induced by the most important carcinogenic air pollutants would amount to 0.8 : 1,000 in metropolitan areas. In urban areas lifetime risk was estimated to be 0.33 : 1,000 and in rural areas 0.15 : 1,000. The emissions from road traffic contributed strongest to the total risk. Air concentrations close to major streets could result in lifetime risks of up to 2.0 : 1,000 [Table - 1]. The most important single substance was Diesel exhaust fumes which contributed about two thirds to the total risk. Thus lorry traffic deserves special attention regarding carcinogenic air pollution.

It appears that the magnitude of lifetime risk for noise-induced myocardial infarction is considerable compared with the cancer risks induced by air pollutants. It is also definitely higher when comparing with acceptable or tolerable risk levels discussed in other contexts. For example it is about a factor of 2,000 times higher than the risk level of 1 : 100,000 suggested by the WHO (1993) with regard to drinking-water quality.

Validity

Criteria for validity: The assumption that noise exposure might be a risk factor for myocardial infarction is primarily based on epidemiological data. Epidemiological knowledge originates from observational surveys and not from randomised experimentation. Hence it is not compatible with the principle of experimental reproducibility which is the traditional paradigm of natural science. Therefore, the question under which circumstances epidemiological associations can be interpreted as causal relationships has been discussed for several decades. Despite refinement of epidemiological methods the discussion on the relevance of epidemiological findings remains controversial (Neutra and Trichopoulos 1993, Taubes 1995).

On the other hand, in contrast to experimental animal data, epidemiological data refer to the real life situation of the populations investigated. It is not necessary to extrapolate from laboratory settings to real life conditions. In particular it is also not necessary to extrapolate results obtained in animals to humans. Therefore there is increased effort to improve integration of epidemiology into risk assessment (Hertz­Picciotto 1995, Wichmann 1998). Several international conferences in the last few years have dealt with this question (Graham 1995, London Panel 1996, WHO/IPCS 1999).

In 1965, Bradford Hill suggested nine criteria (strength, consistency, specificity, temporality, biological gradient, biological plausibility, coherence, experiment and analogy) to be considered in causality assessment. These criteria should not be regarded as necessary conditions. Rather, they show the character of sufficient conditions: if they are fulfilled there is a greater likelihood for a causal relationship . If they are not complied, however, it is not possible to conclude that there is no causal interrelationship. Specificity of an effect for a specific cause for example might facilitate proof of causality - but particularly myocardial infarction is a typical example that diseases can have multiple causes. Thus, a strict application of the Hill criteria would bear a risk and lead to false-negative conclusions.

The International Agency for Research on Cancer has developed other criteria in order to decide whether epidemiological data should be regarded to reflect a causal relationship (IARC 1987). Epidemiological evidence for carcinogenicity is judged in three categories - sufficient, limited and inadequate evidence. The requirements on data quality and results are fixed as follows:

Sufficient evidence of carcinogenicity: A positive relationship has been observed between exposure to the agent and cancer in studies in which chance, bias and confounding could be ruled out with reasonable confidence.

Limited evidence of carcinogenicity: A positive association has been observed between exposure to the agent and cancer for which a causal interpretation is considered by the Working Group to be credible, but chance, bias or confounding could not be ruled out with reasonable confidence.

Inadequate evidence of carcinogenicity:

The available studies are of insufficient quality, consistency or statistical power to permit a conclusion regarding the presence or absence of a causal association.

Thus, the relevant criteria whether or not epidemiological associations are accepted as an expression of a causal relationship is that chance, bias and confounding can be ruled out with reasonable confidence. Similar criteria have recently been suggested in a draft paper by WHO/IPCS (1999), with further differentiation of „bias" into the aspects information bias, selection bias and analytic bias. In the following we will discuss the studies on traffic noise and myocardial infarction using these criteria.

Validity of infarction risk: The main problem for causality assessment is the comparably small effect sizes. For methodological reasons in epidemiological studies only lifetime risks in the order of 1 : 100 or above can be identified. Statistical verification of smaller risks would require investigation of samples which had to be unrealistically large (Flesch-Janys et al 1989). This limitation is less important for identification of strong health effects such as those caused by smoking or certain occupational exposures. On the other hand regarding effect sizes typical for environmental health problems, statistical verification is more difficult and may even be impossible. Noise effects with relative risks for myocardial infarction in the order of 1.2 and lifetime risks in the order of 2 : 100 are at the borderline on the "epidemiological detection limit".

Indeed, the results of most studies on noise­induced infarction risks are not statistically significant (see Babisch et al 1993, 1994). Thus chance cannot be ruled out. Furthermore, with small effect sizes, the probability arises that bias or confounding, not (or not sufficiently) controlled deceptively suggest causality. The smaller the effect sizes are, in particular when relative risks are below 2.0, the more difficult is the exclusion of bias or confounding (see, e.g. Hertz-Picciotto 1995, Pershagen 1995). This first conclusion, however, does not imply that the causality assumption must be rejected. Pershagen (1995) suggested that causality assessment of modestly elevated relative risks should focus less on statistical properties of the associations and more on the qualitative evidence from different sources, such as quality of studies, (internal) consistency, coherence, or knowledge regarding etiologic mechanisms. With regard to these aspects a variety of arguments supports the assumption of a causal relationship.

Quality of studies: With respect to selection and participation rate of the investigated population groups, quantification of exposure and control of confounding variables the case control and cohort studies performed by the Institute for Water, Soil and Air Hygiene (see e.g. Babisch and Ising 1992) comply with the usual quality standards and show little evidence for severe bias or confounding. An independent review has judged these studies „as of reasonable high validity in terms of exposure and disease assessment and control for possible confounding variables" (Thompson 1994).

Consistency: Despite the lack of statistical significance in individual studies, a numerical increase of infarction risk of similar size has been consistently observed in data from different populations and different study types (prevalence, case control and cohort studies) (Babisch 1998). It appears unlikely that consistent findings such as these can be explained by chance alone. Likewise, systematic bias and confounding would be a plausible alternative explanation only if the same uncontrolled bias or confounding effect prevailed in all studies and evaluations. This also appears unlikely.

Biological gradient (dose-response relationship): Several evaluations revealed dose-response relationships compatible with the assumption of a causal relationship. In the Berlin case control study the infarction risk at a sound pressure level of 75 dB(A) was higher than at lower levels. This effect was most pronounced when subjects with residence time of less than 15 years were excluded (Babisch et al 1993). Statistical evaluations of the Wales cohort studies using a stepwise refinement of individual exposure assessment, taking into account window-orientation and window-opening habits, also suggested a dose-response relationship (Babisch et al 1995, 1999). Incidentally these results show that when exposure assessment is refined, by taking into account sound propagation, noise-induced infarction risks may prove to be greater than would be expected from evaluations based on less exact exposure assessment.

Coherence: A recent occupational study (Ising et al 1997) is coherent with the assumption of a causal relationship. Depending on the subjectively perceived noise exposure at the working place, in all age-groups under study increases of infarction risks have been observed which were statistically significant and exhibited dose-response relationships. Relative risks in the highest noise category varied between 3 and 6. The interpretation of epidemiological results of this magnitude is uncritical. It should be mentioned, though, that in this particular study bias cannot be excluded because noise exposure had been judged by subjective perception and sound pressure data were not available. Results of an independent validation study, however, suggest increasing sound pressure levels with increasing subjective rating. A case control study on the relationship of myocardial infarction and objectively assessed occupational and environmental noise exposure is being carried out (Trautner et al 1998)

Biological plausibility: There are several biological mechanisms which could explain an increase of infarction risk. A first explanation would be that noise exposure increases infarction risk by influencing classical cardiovascular risk factors. Experimental research on animals, including primates (Peterson et al 1981, 1984), has shown that chronic noise exposure can elicit persistent increases of blood pressure. In humans several environmental and occupational studies revealed increases of blood pressure or an increased risk for arterial hypertension induced by noise exposure. The overall picture with respect to blood pressure or hypertension appears to be less consistent, however, than the observations on myocardial infarction (Babisch 1998). An appropriate conclusion might be that dispositional, behavioural and environmental factors moderate blood pressure responses to noise exposure, and hypertension develops only in selected vulnerable groups or under certain conditions. Although heterogeneity of study designs, populations, or exposure conditions may limit or even preclude the statistical combination of multiple studies (Blair et al 1995), the results of a meta-analysis (Duncan et al 1993) are suggestive of an increased risk for hypertension induced by noise exposure.

Influences on other risk factors such as lipid metabolism or plasma viscosity might further enhance the risk of myocardial infarction. In the Welsh studies it was shown that an increased infarction risk can be predicted from the cardiovascular risk factor profile of noise­exposed people. The effect size of these prognoses was well compatible with the actual increase of infarction risk (Babisch et al 1994). Thus, although a full understanding of the exact relationship between noise exposure and cardiovascular risk factors has not yet been achieved, an integrative interpretation of all available data is well compatible with the assumption that infarction risk is increased with noise effects. Influence of noise on the endocrine system or on the magnesium metabolism may be alternative or additional explanations.

The interpretation of the available data with respect to a judgement on causality - for example according to the IARC or some other criteria - should be left to a scientific expert group. In our opinion it is justified to talk about limited evidence. Chance, bias and confounding cannot be ruled out with reasonable confidence. Taking all results together, however, a causal interpretation can be judged as being plausible and credible.


  Discussion Top


Making use of the evaluation criteria proposed in the introduction, the results of risk characterisation can be evaluated as follows [Table - 2]: with respect to the severity of effect, frequency of health, relevant exposures and size of estimated noise-induced infarction risk should be regarded as a high priority environmental health problem. With respect to validity, scientifically a causal relationship between noise exposure and infarction risk cannot be taken as proven but can be judged to be plausible.

The question which conclusions for regulation should be drawn, strongly depends on how the high risk potential of noise is balanced against the uncertain causality assessment. This question cannot be answered by science but must be decided politically. Clearly, an integrative political evaluation must additionally include an evaluation of other adverse health effects of noise such as interference with speech and communication, disturbance of rest and sleep, or interference with performance.

The analysis of scientific knowledge on noise effects suggests that it is prudent making use of the Precautionary Principle: where there are significant risks of damage to the public health, we should be prepared to take action to diminish those risks, even when scientific knowledge is not conclusive and if the balance of likely costs and benefits justifies it (Horton 1998). This viewpoint meanwhile has been adopted by decision makers. At the Third Ministerial Conference on Environment and Health (London, June 1999) the representatives of the European Member States of the WHO and of the European Commission responsible for transport, environment and health agreed upon the Charter on Transport, Environment and Health (WHO 1999). In Chapter III of the Charter they decided to incorporate the principles and approaches of sustainable development beneficial for health and the environment into their policies with relevance for transport. These principles include, among others, the precautionary principle which is described in Annex 3 as follows:

Action to prevent, control or reduce the release of, or transport emissions harmful to health and the environment should not be postponed on the ground that scientific research has not fully proved a causal link between those emissions at which such action is aimed, on the one hand, and their potentially harmful impact on health and the environment, on the other.

The decisions of the Third Ministerial Conference show that risk assessment may provide useful support for decision making even when from a scientific point of view uncertainties remain. From a public health perspective it remains to be hoped that the Charter on Transport, Environment and Health will stimulate concrete actions resulting in the reduction of noise exposure to protect human health.[50]

 
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