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NOPHER: Noise Pollution Health Effects Reduction Final Report: 2000-2003 Project Progress Summary Section 1: PROJECT IDENTIFICATION NOT CONFIDENTIAL Information to be provided for project identification Title of the project Noise Pollution Health Effects Reduction Acronym of the project NOPHER

Type of contract Concerted Action Total project cost (in euro) 399991 €

Contract number Duration (in months) EU contribution (in euro) QLK4-CT-1999-01287 36 Months 399991 € Commencement date Period covered by the 1 February 2000 progress report (e.g. 1 February 2000 – 31 January 2001) 1 February 2000 – 31 January 2003 PROJECT COORDINATOR Name Deepak Prasher Title Professor Address Institute of Laryngology and Otology, University College London, 330 Gray’s Inn Road, London WC1X 8EE, UK Telephone 44 20 7915 Telefax 44 20 7278 8041 E-mail address 1527 [email protected] Key words (5 maximum - Please include specific keywords that best describe the project.). Noise Pollution, Hearing Loss, Environmental Health.

World wide web address (the project’s www address ) www.ucl.ac.uk/noiseandhealth

List of participants Provide all partners’ details including their legal status in the contract i.e.,contractor, assistant contractor (to which contractor?). See List Below

2 List of participants

AUSTRIA Prof Armand Dancer Dr Peter Lercher French-German Research Institute, PDC, Universitaet Innsbruck, Institut fuer 5 Rue du Général Cassagou , PO BOX Sozialmedizin, Sonnenburgstr. 16, A- 34, F-68301 - Saint-Louis, France 6020 - Innsbruck, Austria Tel: +33-389695094 Tel: +43-512/5073580 Fax: +33-398695002 Fax: +43-512/5072718 [email protected] [email protected] Dr Jean-Luc Puel Dr Annelise Schrott-Fischer Institut National de la Santé et de la University of Innsbruck, ENT Department, Recherche, INSERM U 254, 71, rue de 35 Anichstrasse, A-6020 - Innsbruck, Navacelles, F-34090 - Montpellier, France Austria Tel: +33-04/67636131 Tel: +43-512/5043140 Fax: +33-04/67630292 Fax: +43-512/5043144 [email protected] [email protected] GERMANY CZECH REPUBLIC Dr Wolfgang Babisch Prof Josef Syka Federal Environmental Agency,Institute for Institute of Experimental Medicine Water, Soil and Air Hygiene, Corrensplatz, Academy of Sciences Department of PO BOX 33 00 22, D-14191 - Berlin, Auditory Neuroscience, Institute of Germany Experimental Medicine Academy of Sci. of Tel: 49-30/89032864 the Czech Rep., Videnska 1083, CZ- Fax: 49-30/89032301 14220 Prague 4, Czech Republic [email protected] Tel: 4202-4752230 Fax: 4202-4752787 Dr Jan Born [email protected] Medizinische Universität Luebeck, Dept. of Clinical Neuroendocrinology, Ratzeburger DENMARK alee 160, D-23538 - Luebeck, Germany Dr Soren Peter Lund Tel: +49-451/5003641 National Institute of Occupational Health, Fax: +49-451/5003640 Dept Chemical Working Environments, [email protected] Lerso Parkalle 105, DK-2100 Copenhagen, Denmark Dr Barbara Griefahn [email protected] Forschungsgesellschaft fuer Arbeitsschutz und Institut fuer Arbeitsphysiologie der FINLAND Universitaet Dortmund, Ardeystr. 67, D- Prof Jukka Starck 44139 - Dortmund, Germany Finnisch Institute of Occupational Health, Tel: +49-231/1084204 Department of Physics, Laajaniityntie 1, Fax: +49-231/1084326 FIN-01620 - Vantaa, Finland [email protected] Tel: +358-9/47471 Fax: +358-9/4747548 Prof Hartmut Ising [email protected] Federal Environmental Agency, Institute for Water, Soil and Air Hygiene, FRANCE Corrensplatz, PO BOX 33 00 22, D-14191 Dr Pierre Campo - Berlin, Germany Institut National de Recherche et de Tel: 49-30/89032864 Fax: 49- Securite (INRS), Service de Physiologie 30/89032301 Environmentale, Av. De Bourgogne, PO [email protected] box 27, F-54501 Vandoeuvre, France Tel: +03.83502001 Dr Clemens Kirschbaum Fax:+03.83502097 Institute of Experimental Psychology II, [email protected] University of Duesseldorf, Geb. 23.02, Ebene 01, Raum 44, Universitaetsstrasse 1, D-40225 Duesseldorf, Germany Tel: +49-211-811-2090

3 Fax: +49 211 811 2019 [email protected]

Dr Christian Maschke ISRAEL Robert-Koch Institute, Environmetnal Dr Joseph Attias Medicine, General Pape Strasse 62-66, Schneider Children' s Medical Center of 12101 Berlin, Germany Israel, Inst. for Clinical Neurophysiology [email protected] and Audiology, Kaplan st. 14, IL-49202 - Petach-Tigva, Israel Dr Susanne Mayr (nee Schaefer) Tel: 972-9253600 Medical University of Hannover, ENT- Fax: 972-9247515 Department Medizinische Hochschule [email protected] Hannover, Carl Neuberg str. 1, D-30625 - Hannover, Germany Dr Avi Frenkel Tel: 0511/5326565 National Institute of Occupational and Fax: 0511/5325558 Environmental Health, Occupational [email protected] Health Psychology Department, Ahuza 278, PO Box 3, IL-43100 Ra'Anana, Israel Dr Jens Oeken Tel: 972-9/7707201 ENT - Dept University of Leipzig, Liebigstr. Fax: 972-9/7712212 18, D-04103 - LEIPZIG, Germany [email protected] Tel: +341/9721816 Fax: +341/9721709 Dr Samuel Melamed [email protected] National Institute of Occupational and Environmental Health, Occupational Dr Fred Scheibe Health Psychology Department, Achuza Humboldt University of Berlin University 278, po box 3, IL-43100 Ra'Anana, Israel Hospital, Dept. of Otorhinolaryngology, D- Tel: 972-9/7707201 10117 Berlin, Germany Fax: 972-9/7712212 Tel: +49-30-28022091 [email protected] Fax: +49-30-28022604 [email protected] NORWAY Dr Hans Borchgrevink Dr Brigitte Schulte-Fortkamp National Hospital, Dept. Neurosurgery, Oldenburg University,Dept.of Physics / Pilestreet 32, NO-0027 - Oslo, Norway Acoustics, D-26111 - Oldenburg, Germany Tel: +47-22868002 Tel: +49-441/7985452 Fax: +47-22868011 Fax: +49-441/7982399 [email protected] [email protected] Dr Bo Engdahl Dr Helmut Strasser National Institute of Public Health, Dept of University of Siegen, Institute of Environmental Medicine, 4404 Torshov, Production Engineering, Work Science/ N-0407 Oslo, Norway Ergonomics Division, Paul Bonatz strasse [email protected] 9-11, D-57068 - Siegen, Germany Tel: +49-2717404406 POLAND Fax: +49-2717402740 Dr Krystyna Pawlas [email protected] Institute of Occupational Medicine and Environmental, Laboratory of Noise and GREECE Audiology, Koscielina 13, PL-41-200 Dr Miltos Tsalighopoulos Sosnowiec, Poland District General Hospital of Thessaloniki Tel: +48-32/2660885 Athens, Stilp Kiriakidi 1, EL-546 36 Fax: +48-32/2661124 Thessaloniki, Greece [email protected] Tel: +30.31-993102 Fax: +30.31-993096 Dr Mariola Sliwinska-Kowalska [email protected] Nofer Institute of Occupational Medicine, Dept of Physical Hazards, POB 199, 8, Sw. Teresy Str., 90-950 Lodz, Poland [email protected]

4 Prof Wieslaw Sulkowski Dr Ann-Christin Johnson Nofer Institute of Occupational Medicine, National Institute for Working Life, Dept for ENT Dept, Audiology Division, POB 199, Work and Health, Programme of 8, Sw. Teresy Str., 90-950 Lodz, Poland Ergonomics, Ekelundesvagen 16, Solna [email protected] S-112 79 Stockholm, Sweden [email protected] PORTUGAL Professor Oscar Dias Dr Ann-Cathrine Lindblad Servico ORL - Hospital Santa Maria / Fac. Karolinska Institutet, Technical Audiology, Medicina de Lisboa, Av. Egas Moniz, D-18203 - Danderyd, Sweden Lisbon 1649-035, Portugal Tel: +46-8/51776020 Fax: +46-8/51776267 SPAIN [email protected] Dr Isabel Lopez-Barrio Instituto de Acustica, CSIC, Serrano 144, Dr Evy Ohrstrom Madrid 28006, Spain Goteborg University, Dept of [email protected] Environmental Medicine, Medicinaregaten 16, PO BOX 414, S-40530 Gothenburg, SWEDEN Sweden Prof Stig Arlinger Tel: +46-31/7735345 Linköping University, Dept. of Technical Fax: +46-31/7734355 Audiology, Linköping University Hospital, [email protected] S- SE 58185 - Linkoping, Sweden Tel: +46-13/221427 Dr Bo Petterson Fax: +46-13/125142 National Board of Health and Welfare, [email protected] Ralambsv. 3, S-10630 - Stockholm, Sweden Dr Marie-Louise Barrenas Tel: +46-8/7833095 Fax: +46-8/7833409 Goteborg University, Sahlgrenska [email protected] University Hospital, Goteborg University, Dept. of Audiology, Gröna Straket 11, S- Prof Ilmari Pyykko 41345 Gothenburg, Sweden Karolinska Institute, Department of Ear Tel: +46-31/3421605 and Skin, Karolinska Hospital, S-17176 - [email protected] Stockholm, Sweden Tel: +46-8/7286587 Dr Barbara Canlon Fax: +48-8/303423 Karolinska Institutet, Department of [email protected] Physiology and Pharmacology, Doktorsringen 6a, S-17177 - Stockholm, THE NETHERLANDS Sweden Prof Guido Smoorenburg Tel: 08-7287200 University Medical Center Utrecht, UMC [email protected] Hearing Research Laboratories F.02.504, Heidelberglaan 100, PO box 85500, NL- Ms Wanda Geisendorf 3508 GA Utrecht, The Netherlands Konsumertverket (Swedish Consumer Tel: +31-30/2507724 Agency) Sakerhet, Rosenlundsgatan 9, S- Fax: +31-30/2541922 11887 - Stockholm, Sweden [email protected] Tel: +46-8/4290500 Fax: +46-8/4298900 UK [email protected] Dr Bernard Berry NPL Management ltd, CMAM Acoustics / Dr Kajsa-Mia Holgers National Physical Laboratory, Queens Rd, Goteborgs University, Sahlgrenska UK-TW11 0LW - Teddington, UK University Hospital , Goteborgs University, Tel: +44-181/9436694 Dept. of Audiology, Gröna Straket 11, S- Fax: +44-181/6140404 41345 Gothenburg, Sweden [email protected] Tel: +46-31/3421605 [email protected]

5 Section, 4676 Columbia Parkway MS C- 27, 45226 - Cincinnati, Ohio, USA Tel: +1 513/5338462 Prof Adrian Davis Fax: +1 13/5338510 Medical Research Council Institute of Hearing Research, MRC Institute of Hearing Research, University Park, NG7 2RD - Nottingham, UK Tel: +44-115/9223431 Fax: +44-115/9518503 [email protected]

Dr Hilary Dodson University College London Institute of Laryngology and Otology, 330 Gray's Inn Road, WC1X 8EE - LONDON, UK [email protected]

Dr Ian Flindell University of Southampton, Institute of Sound and Vibration Research (ISVR), Highfield, SO17 1BT Southampton, UK Tel: +44-1703 593423 Fax: +44-1703 593190 [email protected]

Dr Ken Hume Manchester Metropolitan University, Dept. of Biological Sciences Manchester, Chester Street, MI 5GD, Manchester, UK Tel: +44 161/2473664 [email protected]

Prof Mark Lutman University of Southampton, Institute of Sound and Vibration Research (ISVR), Highfield, SO17 1BT Southampton, UK Tel: +44-1703 593423 Fax: +44-1703 593190 [email protected]

Prof Deepak Prasher Institute of Laryngology and Otology, University College London, 330 Gray's Inn Road, London WC1X 8EE, UK [email protected]

Prof Peter Wheeler University of Salford, Dept of Acoustics and Audio Engineering Brindley bldg., M5 4WT - Salford, UK Tel: +44-161/2955769 Fax: +44-161/2955427 [email protected]

USA Dr Thais Morata National Institute for Occupational Safety and Health, Hearing Loss Prevention

6 Final Report A number of international scientific meetings, workshops have been conducted by NOPHER which have resulted in a significant number of publications from the Group (listed at the end of this report). The following provides further breakdown of the activities and achievements of each work package during the course of the NOPHER project from February 2000 to end January 2003.

Description of work and Results

WP 1: Determine health effects of chronic exposure to transportation noise

The aim of this work package was to seek to develop Europe-wide consensus on the strengths of the causal relationship between environmental noise from road, rail and aircraft and various non-auditory psychological and physiological effects such as annoyance, interference with speech communication, sleep disturbance, performance and learning in children, cardiovascular, endocrine, and immunological responses. The current state of the art has been summarised by the group and a discussion meeting was held on 6 April 2001 in order to try to reach some consensus on the various contentious issues regarding the relationship between noise in the environment and its health effects in particular the dose/response relations of annoyance and other effects. A publication resulting from the discussion meeting was circulated to all partners and has been made available both in print and on the website for the public at large. The methodological issues including quantification of noise and health effects measures was also discussed at this meeting to determine the inadequacies or otherwise of the measures currently in use to quantify noise and health effects and indicate whether associations based on these measures are valid considering the large number of possible variables present. The findings have been published for wider distribution to encourage improvements in the procedures used.

An International workshop was organised on 6th April 2001 with invited participants to examine the current evidence for specific health outcomes in relation to particular noise sources (road, rail and aircraft). The discussion centred around the following: Is it possible to reach consensus on: 1. The nature of the health effects 2. The appropriateness of the measures currently employed for noise and outcomes 3. The validity of the associations made on current measures 4. The ways in which future research may be improved The following topics were considered with the discussion being led by the researchers indicated below: Annoyance Peter Lercher/ Ian Flindell Sleep disturbance Barbara Griefahn / Evy Ohrstrom Performance and Learning Mary Haines/Steffan Hygge Cardiovascular risks Wolfgang Babisch/ Christian Maschke Endocrine Effects Clemens Kirschbaum

7 Mental Health Effects Stephen Stansfeld

A detailed report complete with the discussion has been prepared but in summary the following may be stated:

Annoyance: It was agreed that there is considerable evidence that environmental noise leads to annoyance. It is possible to produce a dose/response relationship for noise and annoyance although it is acknowledged that there are a considerable number of non-acoustical factors, which affect annoyance. The dose/response covers primarily related aircraft noise and road traffic noise to annoyance. It was also agreed that annoyance affects quality of life. In the EU, it is recognised that 22% (77 million) of the population is considered annoyed by environmental noise. It is recognised that there are a lot of data sets available relating noise to annoyance (Schultz, 1978;Kryter 1982;Fiddel 1991; Fields 1994;Miedema 1998;Miedema 2001)

There were discussions relating Ldn and Lden measures and about the various models for combining sources of noise, for example energy summation, dominance source model or annoyance equivalent levels from a reference noise source. Furthermore, it was acknowledged that annoyance dose/ response relations applied to steady state conditions but if changes at airports were taking place then there may be greater annoyance.

Annoyance is regarded as the most important adverse effect of environmental noise. Dose-response curves have been presented relating the percent of people highly annoyed increasing with the Ldn measure of noise level. From these curves, it is apparent that aircraft noise is more annoying than road traffic noise followed by rail. The individual noise annoyance can be predicted to maximal 33% by acoustic parameters but a number of effect modifiers influence the effect. Night and evening noise as well as weekend noise is more annoying when quietness is expected. The individual noise sensitivity is the most important personal parameter of influence. The other parameters of consideration are: 1. General appraisal of noise source 2. Confidence in people responsible for noise and noise abatement 3. History of noise exposure The importance of annoyance also lies in the extent to which this may lead to stress and further physiological changes consequent upon this.

Sleep disturbance: It is widely accepted that noise from aircraft, road and rail noise may disturb sleep. Numerous studies over the last 30 years in both the laboratory and in home settings have sometimes provided conflicting results with large discrepancies between studies. It has been difficult therefore to reach any firm conclusions as an understanding of the reasons for the discrepancies between studies is necessary to determine the true extent and nature of the problem. The discrepancies may be arising due to different noise exposure measures and different sleep parameters considered in various studies. The situation is further compounded by the fact that certain studies indicate habituation whereas others indicate physiological stress effects which do not habituate. In addition the next-day-effects of a lack of sleep or disturbed sleep also need to considered.

The most obvious effect of noise exposure during the night is the disturbance of sleep with possible effect on efficiency of work next day and long-term health effects.

8 Intermittent noise causes fragmentation of sleep progression or in the case of continuous noise shallow sleep. Both have the effect of shortening duration of deep sleep and rapid eye movement sleep. The alarm function of the sense of hearing may lead to awakening if the noise contains information perceived to be of relevance even if the level of noise is low. Arousal during sleep is a short-term noise induced activation. Frequent occurrence of arousals leads to a deformation of the circadian rhythms. Long-term disturbance of circadian rhythms has consequences for health impairment. These have been shown to have an impact on the neuro-endocrine regulation, which has an effect on the physical and psychological well being of an individual.

Endocrine Effects: Among the multitude of physiological systems which response to acute and chronic stress with high sensitivity, the hypothalamus-pituitary –adrenal axis (HPA) has a prominent position. Physical and psychological stress rapidly induces HPA activation, which is well characterised by discrete increases of cortisol levels. Ambulatory assessment of cortisol levels in saliva has facilitated the detection of stress responses in various populations of healthy individuals and patients. Following recent methodological advances, salivary cortisol levels are now measured in large groups of subjects in cross-sectional and longitudinal studies. Among other parameters, the repeated assessments of the early morning cortisol rise and circadian cortisol rhythm are most promising indices to be investigated in studies on the effects of environmental stressors on health.

Mental Health Effects: Studies suggest that exposure to aircraft and road traffic noise may cause symptoms such as headaches and tension but there is little direct evidence that environmental exposure is related to clinically defined psychiatric disorder measured by screening questionnaires in community studies. The analyses associating aircraft noise exposure and admissions to psychiatric hospitals have shown inconsistent results but have been largely negative. There is some evidence for higher tranquillisers and hypnotic consumption in noisy areas. Recent studies associating noise exposure and health functioning have also been negative. It may be that environmental noise exposure levels in the UK are not high enough to find effects but there is some suggestive evidence from Japanese studies that higher levels of aircraft noise exposure may be related to impairment of mental health. Many of these studies are limited by methodological problems such as poor characterisation of noise exposure, selection of biased samples of subjects, lack of measurement and adjustment for appropriate confounding factors and lack of standardised measures of mental ill-health outcomes. Further research is needed to address these methodological problems but nevertheless, current evidence suggests that the effects of environmental noise on mental health are likely to be small.

9 The group reported on the available current evidence for specific health outcomes in relation to particular noise sources. The deficiencies are highlighted.

1) Ischaemic heart disease in the adult population

A number of review articles, focused on evidence provided by the results of epidemiological environmental noise studies, have been published in the past years. The main criteria of assessment used were the guidelines of the "International Agency for Research on Cancer":

 Sufficient evidence is given if a positive relationship is observed between exposure to the agent and the health outcome (cancer), in studies in which chance, bias and confounding can be ruled out with reasonable confidence.

 Limited evidence is given if a positive association is observed between exposure to the agent and the health outcome (cancer), for which a causal interpretation is considered by a Working Group (experts) to be credible, but chance, bias or confounding could not be ruled out with reasonable confidence.

 Inadequate evidence is given if the available studies are insufficient in quality, consistency or statistical power to permit a conclusion regarding the presence or absence of a causal association.

The authors and expert groups of the reviews mentioned above, made the following statements from the evidence:

Health Council of the Netherlands, 1994 and Passchier-Vermeer & Passchier, 2000:

 “ Limited" evidence for the relationship between noise (including occupational noise) and biochemical effects .  “ Sufficient" evidence for the relationship between noise (including occupational noise) and hypertension.  “ Sufficient” evidence for a relationship between noise and ischaemic heart disease.

Institute for Environment and Health, 1997 and Porter et al., 1998:

 “Inconclusive” evidence for a causal link between noise exposure and hypertension.  “Sufficient” evidence for a causal association between noise exposure and ischaemic heart disease.

Health Council of the Netherlands, 1999:  “ Limited” evidence for the relationship between noise (including occupational noise) and biochemical effects.  “ Sufficient” evidence for an association between ambient noise and hypertension.  “ Sufficient” evidence for an association between ambient noise and ischaemic heart disease (observation threshold: Leq,6-22 h: 70 dB(A)).

10 Babisch, 2000:  “No” scientific evidence for association between transportation noise and mean blood pressure readings (exception: in children consistently higher readings were found in the exposed groups).

 “ Little” evidence regarding the association between transportation noise and hypertension.

 “ Some” evidence regarding the association between transportation noise and ischaemic heart disease. The latter was viewed as being “sufficient” for action.

Neus and Boikat, 2000:

 “ Limited” evidence regarding the association between traffic noise and ischaemic heart disease.

The various evidence ratings of a correlation between traffic noise and cardiovascular disease can be summarized as follows:

 Biochemical changes of risk factors: "Limited" evidence,  Hypertension: "Inadequate/limited" evidence,  Ischaemic heart diseases: "Limited/sufficient" evidence.

Recently, a systematic review was published which used the meta-analytic approach to assess quantitative estimation of the relationship between community noise and occupational noise on blood pressure, hypertension and ischaemic heart disease (IHD) [Kempen et al, 2002]. The authors concluded that the epidemiological evidence on noise exposure, blood pressure and ischaemic heart disease is still limited. With respect to blood pressure and hypertension, results were contradictory and for IHD only a few studies were available. Inconclusive findings may be due to limitations in exposure characterization, adjustment for important confounders, and the occurrence of publication bias.

Some new epidemiological studies are on its way focusing on IHD, high blood pressure and IHD risk factors.

Conclusion:

As pointed out in earlier statements, 65-70 dB(A) outdoor sound level during day and 55-60 dB(A) during night (LAeq) may be quality targets for environmental policy regarding cardiovascular diseases based on current knowledge from research carried out in this area.

2) Blood pressure in children Epidemiological studies carried out in adults suggest long-term health risks in chronically exposed adult populations. High blood pressure and myocardial infarction have been the primary focus of noise effects’ research. Also in noise-exposed children, cardiovascular (blood pressure) and endocrine (stress hormones) markers of enhanced physiological arousal have been studied on an epidemiological basis. The results can be summarised as follows:  Weak data-base

11  No systematic increase in mean BP readings in higher noise exposed children  The better control for confounding factors, the smaller the noise effect  BP increases in new studies are within normal physiological range  Dose-response relationship rarely studied  Acute or chronic noise effects?  Age range: 8-11 (16), no age*noise effect  No sex differences (except MLAF noise: girls)  No differences regarding the noise source (evidence and magnitude of effect)  Noise at school was the primary source of interest. Additional noise at home increased the effect.

Depending on the to study design, effects were seen at Leq > 60 dB(A) (road), Leq > 65 dB(A) (air). These figures may serve as quality targets although the evidence is weak. The statements given by Evans and Lepore, 1993 are still true: “ 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."

This is in line with other researchers, e. g. Maschke, 2000, who stated: “Children – with the exception of newborns – usually show a smaller reactivity to acute noise than adults. Children are less likely to wake up by noise. Regarding blood pressure, studies do not suggest lower limits values than for adults. Nevertheless, Maschke suggests 5 dB lower limit values for children from a preventive point of view, given the US EPA Agenda for Child Environmental Health, 2000: “Ensure that all standards set are protective of the potentially heightened risk faced by children…”

Babisch stated at the NOPHER-Meeting 2002 in Berlin: A quantitative health risk assessment for children cannot be given at the moment. The impact of body size was not adequately considered in studies.

The available database on cardiovascular effects of noise in children is poor. Based on the available data, children do not appear to be a particular risk group with respect to cardiovascular outcomes, with the exception that they may simply be longer exposed to noise throughout their lifetime than adults that have been studied, and who grew up when motorization was not as widely spread. This, too, justifies the 5 dB(A) safety margin suggested by Maschke.

Conclusions:

We do not see sufficient evidence for health effects in children exposed to community noise, however the current data base does not allow to conclude that effects may not occur in susceptible children or in a susceptible contexts (socio-cultural, environmental).

3) Stress hormones

12 In recent years, the measurement of stress hormones including epinephrine, norepinephrine and cortisol has been widely used to study the possible increase in cardiovascular risk of noise exposed subjects. Since endocrine changes manifesting in physiological disorders come first in the chain of cause-effect for perceived noise stress, noise effects in stress hormones may therefore be detected in populations after relatively short periods of noise exposure. This makes stress hormones a useful stress indicator, but regarding a risk assessment, the interpretation of endocrine noise effects is often a qualitative one rather than a quantitative one. Stress hormones can be used in noise studies to study mechanisms of physiological reactions to noise and to identify vulnerable groups.

Although not being a risk factor as such (in epidemiological terms), stress hormones like epinephrine, norepinephrine and cortisol can be viewed as reliable stress indicators. Stress hormones are easy to measure non-invasively, and appear to be an attractive outcome for epidemiological studies. They are particularly useful for investigating biological mechanisms, and play a crucial role in the metabolism of the organism, where they act as bio-messengers and neuro-transmitters in the regulation of autonomic and other physiological functions. They are part of a complicated system of positive and negative feedback mechanisms affecting: the activity of the heart, blood pressure, blood lipids, blood glucose, blood clotting and blood viscosity. All these are established biological risk factors for hypertension, arteriosclerosis or myocardial infarction, when considering the cause-effect chain, i.e.: sound - annoyance (noise) - physiological arousal (stress indicators) – changes in biological risk factors – morbidity – mortality. Long-term effects on the cardiovascular system are specifically focused in this respect.

In studies, free catecholamines have been analysed in plasma and urine using standard biochemical and electrochemical methods. Regarding corticosteroids, different procedures and derivates have been used to determine adrenal-cortical activity (total or free cortisol, hydroxycorticosteroids, ketosteroids). New studies have tended to focus on free cortisol in plasma or urine including certain metabolites such as 20-dehydro-cortisol; a few have considered saliva. However, due to strong circadian and weekly rhythms of hormone excretion, epidemiological studies may suffer from methodological problems when only certain parts of the day/night are considered for sampling. Problems may also arise from too short observation periods in experiments regarding the longer half-life time constants (cortisol: about 70 minutes) of the hormone metabolism.

Conclusions:  Stress hormones can be useful stress indicators in field and laboratory noise studies  Their clinical relevance in noise studies is not clear compared to classical risk factors

Chronic stress induced changes resulting in neuro-endocrine dysregulation means that the individual may not habituate to the nightly disturbance and suffer consequences in term of health without being aware of the cause. From the results of the studies it may be concluded that long-term environmental noise exposure lasting for years may in a number of exposed people lead to chronic dysregulation of their endocrine system.

Performance and Learning: A general finding in studies of noise on human performance is that noise levels have to be high to produce a reliable effect on performance or the task has to be complex or cognitively demanding. Repetitive and

13 simple tasks are unaffected by noise. There is insufficient data to generate any dose/response type of relationship for performance and learning. There is some evidence from studies in children living around airports that they have some reading or comprehension deficits as a result of noise exposure. In the Munich study children improved their long-term recall memory by approximately 25% when the old airport closed and at the new airport there was decline in performance of a similar extent. The scores were similar for reading tasks. The change in noise levels before and after was about 14dBA at the old airport and 9dBA at the new airport. There are no field studies on adults reading and memory effects in relation to noise exposure. Several studies have shown that performance is impaired if speech material is played back while the subjects are reading and memorising verbal material.

Cardiovascular Risks: Review of epidemiological studies of cardiovascular effects of occupational noise have been published regularly. Most studies have been concerned with arterial blood pressure. In the earlier studies it was concluded that prolonged exposure increases the risk of hypertension further studies with improved methodology were unable to shed further light on the association between high levels of noise exposure and elevated blood pressure. Most recent studies show an increased risk of ischaemic heart disease in higher traffic noise exposed subjects as compared to less exposed subjects while associations regarding hypertension were not as convincing. It was concluded that more research is needed particularly on establishing a dose-response relationship. At present day time (6-22h) Leq values of 66-70dBA were considered as threshold of adverse effects. The impact of night disturbance requires special attention. The results of epidemiological studies show weak but significant negative correlations between noise annoyance and blood pressure. Methodological issues are important in establishing any relationship between noise exposure and cardiovascular risk.

4) General In principle, the noise/stress hypothesis is well understood. Noise activates the pituitary-adrenal-cortical axis and the sympathetic-adrenal-medullary axis. Changes in stress hormones including epinephrine, norepinephrine and cortisol are frequently found in acute and chronic noise experiments. The catecholamines and steroid hormones influence the organism’s metabolism, thus increasing the risk for certain diseases. Cardiovascular disorders are especially in focus for epidemiological studies on adverse noise effects. However, not all biologically notifiable effects are of clinical relevance. The relative importance and significance of health outcomes to be assessed in epidemiological noise studies follow a hierarchical order, i.e. changes in physiological stress indicators, increase in biological risk factors, increase of the prevalence or incidence of diseases, premature death. Decision-making and risk management rely on quantitative risk assessment. Due to ethical aspects regarding the exposure in the laboratory and the fact that toxicological methods cannot be applied in noise research, epidemiological methods are the primary tool for providing the necessary information. However, the statistical evidence of findings from individual studies is often weak. Magnitude of effect, dose-response relationship, biological plausibility and consistency of findings among studies are issues of epidemiological reasoning. Similarly with other environmental issues, noise policy largely depends on considerations about cost-effectiveness, which may vary between populations. Limit or guideline values have to be set within the range between social and physical well-being, between nuisance and health. Following the precautionary principle it was estimated from epidemiological traffic noise studies that the threshold for a relevant increase of cardiovascular risk may be 65 dB(A) for the daytime outdoors average A-weighted sound pressure level. Because typical observational epidemiological research is hardly able to distinguish relative risks between 1 (zero risk) and 1.2 (20% increase in risk) there is an appreciable uncertainty left for

14 populations with more than 10-15 % of people with noise exposure above 65 dB(A). Because the burden of noise differs substantially from country to country - the proportion of people at risk is an important factor in estimating the population impact.

In contrast, the findings from social surveys consider a lower figure, i.e. 55 dB(A), as a threshold value regarding serious annoyance during the daytime. Whereas nuisance-related criteria may vary within populations, dependent on the type of area, (physical) health-related noise criteria should apply equivocally to all subjects within populations for ethical reasons. The cardiovascular risk is a key-outcome in non- auditory noise effects’ research because of the high prevalence of related diseases in our communities.

Specific studies regarding critical groups – including children, different noise-sources, day/evening/night comparisons, coping styles and other effect-modifying factors, and the role of annoyance as a mediator of effect are issues for future research in this field.

Exposure-Effect Indicators: This work package sought to develop methodological issues including quantification of noise and health effects measures. Meetings of leading exponents in the field discussed the inadequacies or otherwise of the measures currently in use to quantify noise and health effects and indicate whether associations based on these measures were valid considering the large number of possible variables present.

15 WP 2: Develop strategies for pharmacological protection against noise trauma

The area covered by this work package is rapidly changing and at the first international conference on noise induced hearing loss in July 2000 in Cambridge, UK a session was devoted to presentation of some ten research papers on the topic of protection from noise trauma. Preconditioning is an active process found in many neuronal and non-neuronal systems that create tolerance to subsequent detrimental forms of trauma or stress. Pre-conditioning is usually induced by low level, non- damaging stimuli that can result in long-term effects. This group has shown that a short-term conditioner (hours) is effective in protecting against a subsequent noise trauma of both low and high frequencies. Furthermore, preliminary results demonstrate that a sound conditioner can be presented after the traumatic stimulus. This finding significantly expands the clinical usefulness of the phenomenon of sound conditioning. The results from a pilot study performed on young adults demonstrates the feasibility of employing sound conditioning as a clinical therapy. The most widely used medical treatments of acoustic trauma (oxygenotherapy, carbogen, hyperbaric oxygen, vasoactive agents, and corticotherapy) have been tested. Results indicate that pure oxygen and carbogen seem ineffective, hyperbaric oxygen used alone is dangerous, and corticoids and combined corticoid/hyperbaric oxygen improve functional and morphological recovery. Antioxidants as N-acetylcysteinic acid (NAC) have been recently shown to protect guinea pig cochlea against noise trauma. Furthermore, antioxidants have been proposed to be useful in humans to protect the cochlea against oxidative stress. So far the human data is largely missing as the animal studies are not completed, as for example in guinea pigs protection was observed only at higher frequencies than 4 kHz. This work group aimed to create an animal model that could be used to evaluate possible cochlear damages in connection with ear surgery and to screen drugs that could protect the cochlea from surgical traumas. Reports of investigations of the clinical applicability of NAC and a combination of brain derived neurotrophic factor (BNDF) and ciliary neurotrophic factor (CNTF) in preventing hearing loss induced by vibration mimicking an injury caused by drilling of the temporal bone. As an antioxidant, NAC protect hearing in vibration and noise induced cochlea damage, whereas neurotrophins were somewhat effective. Clinically, NAC may not be useful for preventing or treating vibration and noise generated hearing loss. The BDNF and CNTF have so far no human approval and the protection rate was rather marginal. The group has been involved in research aimed at understanding the mechanisms of cochlear damage resulting from noise exposure in order to facilitate pharmacological intervention to prevent or reduce the effect of noise. Excitotoxic damage and repair of cochlear synapses after acoustic trauma has been studied as well as the immunocytochemical handling of the excitatory neurotransmitters in the cochlea. The role of GABA, catecholamines and indolamines in cochlear innervation is being investigated. The auditory efferent system uses several neuroactive substances such as GABA, actylcholine, dopamine, encephalines, dynorphins, and CGRP; their distribution pattern and physiology will help determine the receptor activity which may be useful in protection.

During the last three years a number of studies by the group and others have shown that noise induced oxidative stress due to the formation of reactive oxygen species (ROS) is responsible for the destruction of phospholipids of the cell and nucleus membranes, the DNA, increase in intracellular calcium which lead to up-regulation of cell death genes. Interventions designed to modify the formation of ROS or up- regulation of endogenous antioxidant systems of the inner ear have been developed to decrease the noise induced hearing loss (NIHL). These studies provide important

16 evidence of noise induced ROS formation in NIHL and new strategies for reduction of NIHL. It has been shown that a mild noise exposure results in increase in heat shock proteins and in glial cell line derived neurotrophic factor (GDNF) and provides protection from subsequent more intense noise exposure. GDNF applied directly to the inner ear has been shown to provide dose dependent protection from NIHL. It has been shown that both neurotrophins and antioxidants protect against NIHL.

Recent advances in our understanding of cell cycle and molecular mechanisms of lateral inhibition provide promising methodologies for protection and also possibilities of pharmacological rescue. It may be possible to enhance endogenous cell repair mechanisms following acoustic trauma in order to reduce the overall damage. Medical treatments for acoustic trauma have also been considered.

It is now evident that certain neuro-peptides, nitric oxide inhibitors, antagonists of glutamate or dopamine receptors, neuronal growth factors, hormones and free- radical scavengers may protect against hearing loss. This work group has been examining various means of protecting from noise and other oto-toxic agents.

Research shows that metabolic damage through reactive oxygen species plays a major part in the cochlear damage from over-exposure. The details and the critical steps in the pathway are beginning to be elucidated so that intervention may be undertaken to prevent permanent damage. The description of these mechanisms of action will allow the development of pharmacological intervention strategies to prevent hair cell damage. While much needs to be done, clinical trials for prevention and rescue of noise induced hearing loss may be possible within a few years.

Acoustic stress increases the production of reactive oxygen species within the inner ear, which is believed to lead to the final stage of cell death and subsequent hearing loss. Since frequency-specific physiological measurements can be made and correlated to site-specific morphological changes in the inner ear, the auditory system offers an attractive model for studying the effects of prenatal GlucoCortcoid (GC) treatment. Our working hypothesis was that prenatal exposure to excess GC increases cochlear susceptibility to noise trauma later in adult life by increasing oxidative stressed-induced hair cell death. Recent findings have shown that prenatal glucocorticoid treatment increases the susceptibility of the inner ear to acoustic trauma in adult life. Acute auditory threshold changes were not noted between the age-matched groups, but when measured at 48 h and 4 wks post-exposure, the DEX-treated rats showed little or no recovery from the trauma. In contrast, the normal rats showed a significant amount of recovery already by 48 h post-exposure and continued to show further recovery during 4 weeks. In addition, acoustic trauma resulted in a massive outer hair cell loss in the DEX-rats compared to minor loss in the normal rats. To determine if oxidative stress plays a role in the recovery phase of acoustic trauma, the spin trapping agent PBN (100 mg/kg) was administered before, during and several times after noise exposure. PBN treatment significantly reduced the physiological and morphological differences between DEX and control rats. These data support the hypothesis that alterations in the intrauterine environment may modify the developmental programme of the cochlea, inducing dysfunction later in adult life. Excessive prenatal exposure to dexamethasone decreases the potential for recovery of the cochlea to oxidative stress induced by acoustic trauma which can be counteracted by treatment with antioxidants.

Sound conditioning provides a means of reducing the effect of noise trauma. A variety of sound conditioning paradigms have been proven succesful in preventing morphological and physiological damage. Propsed mechanism include up regulation of endogenous antioxidants, the number of NMDA receptors, heat shock proteins,

17 calcium buffering systems, and neurtrophic factors. Further studies are needed to understand the protective mechanisms afforded by sound conditioning. It is conceviable that sound conditioning will benefit humans and provide a treatment for noise induced hearing loss.

The most widely used medical treatments for acoustic trauma are vasoactive agents, oxygen therapy, and corticotherapy. Results indicate that pure oxygen and carbogen are ineffective. Hyperbaric oxygen used alone is dangerous. Cortocoids and a combination of corticoids and hyperbaric oxygen improve functional and morphological recovery.

It has also been shown that magnesium has a preventive and therapeutic effect for noise trauma. Histological findings confirm protective action. It has been suggested intra-cochlear Mg plays a crucial role in the protective effects. The specfic mechanism responsible is not yet clear.

18 WP 3: Determine the effects of combined chemicals and noise exposure on hearing and balance

This group has produced a document detailing the protocol for the study of the extent of auditory and vestibular damage from exposure to solvents alone and in combination with noise. This has been circulated to all partners and is currently available on the website. The group discussed the protocol further at a specially convened meeting on 27-28th April 2001 in Nancy, France to reach a consensus on the unified minimum protocol for the study across East-West Europe to examine varying degrees of exposures encountered across European work environments. A proposal put forward by this group (NoiseChem) to examine the effects of solvents and noise in animals and workers has been approved and funded by the European Commission. The effects of simultaneous exposure to ethyl benzene and noise on hearing was examined in rats and guinea pigs. The results show a markedly higher susceptibility of rats to ethyl benzene than of guinea pigs. This difference was related to the ethyl benzene concentration found after the exposure in blood samples. Thus, the results from animal experiments should be used with utmost caution when setting exposure limits for man. In rats, both the electrophysiological and the acoustical measurements (together with the physical measurements) did not suggest any progressive interaction of the combined exposure. However, the histological findings did show progressive interaction (in line with previous literature). The histological results differed markedly from the physical results: 1) ethyl benzene produced outer hair cell damage, in particular in the outer rows, whereas there was no loss in the physical results and 2) the histological results did not show any damage at the light- microscopical level due to the noise exposure whereas the physical measurements did show noise-induced hearing loss. From a general point of view, the aromatic solvents such as styrene seem to decrease the auditory sensitivity mainly in the mid- frequency range. Outer hair cells are the primary targets within the organ of Corti, although the spiral ganglions are not spared. Loss of adaptability rather than loss of sensitivity may be the initial sign of auditory impairment following exposure to noise. The ototoxicity of environmental agents such as solvents, metals and asphyxiants and their interaction with noise are issues just beginning to be addressed internationally and the NOPHER group have played a significant role in bringing this research to the fore. Balance dysfunction from solvents has largely been neglected due, in some extent, to the difficulties of field-testing.

A number of meetings have been held over the years for this group in order to establish unified protocols and initiate field studies across Europe. The group have raised awareness of the issue of solvents affecting hearing and balance. A meeting was also held jointly with NIOSH in Cincinnati, United States on the topic of solvents and hearing. The workshop provided an excellent opportunity for European and US workers to interact and share expertise in this important area. Further collaborative work is planned. A meeting by the Group to update the European Solvents Industries Group was organised at their headquarters in Brussels. Major producers of solvents were provided with the latest information available on the interaction effects of chemicals and noise on the audio-vestibular systems. It was hoped that a greater interaction would result from such a meeting between manufacturers and researchers on this topic.

A specific session on chemicals and noise interaction effects was organised in Brescia, Italy at the 8th International Symposium on Neurobehavioral Methods and Effects in Occupational and Environmental Health again for the purpose of the Group getting together to discuss research and also to raise awareness of this topic amongst toxicologists. Significant findings by the group have been reported for both

19 animals and Humans. Organic solvents can produce permanent hearing impairment in people and laboratory animals. In rats styrene has been shown to affect auditory sensitivity mainly in the mid frequency range. Outer hair cells were shown to be the primary targets although spiral ganglions are also affected. Noise and styrene exposures have been shown to have synergistic effects on the auditory system. Toluene has been extensively studied and shows significant hearing effects in animals and Humans.

Chemicals such as toluene, styrene, xylene, trichloroethylene, lead, mercury, carbon disulphide and carbon monoxide commonly used in the manufacturing, services, transportation, and construction industries present a major risk to hearing and balance. The risk is further increased in the presence of noise in the workplace.

This synergistic effect of chemicals and noise is extremely hazardous as either of the toxic agents can co-exist within the current permissible levels but in combination pose a greater threat. Human field studies show that the relative risk for hearing loss is increased from four times with noise alone to eleven times with noise and chemicals. Hearing conservation programmes at present do not consider the effect of chemicals in the protection strategies.

Research on mixed exposures has benefited from interdisciplinary teams of investigators, evaluation of possible synergistic effects, determination of mechanisms of action, improved field methods to characterise simultaneous exposures of workers. This concerted action has combined molecular and epidemiological methods to assess worker exposures to individual agents and their health effects

There is a great need for basic and applied research to reduce noise pollution and its health effects. Prevention of noise induced hearing loss, which must be a public health priority, needs research in to the pathogenic mechanisms and pharmacological intervention as well as raising awareness of the hazards to prevent exposure. Two work groups will be engaged in research on pharmacological protection and identification of risk factors including individual susceptibility. The concerted action will create an effective network for improved communication and collaboration between institutions across Europe to facilitate and expand research.

The work in this area has during 2002 been done mostly in the NoiseChem project where the effects on hearing and balance after exposure to Noise and Chemicals is investigated.

The NoiseChem project began in the spring 2001 and since then we have participated in the development of better methods of assessment of auditory and vestibular dysfunction due to a combination of industrial chemicals and noise.

The main work has been focused towards determining the effect of exposure to solvents at levels commonly found in industry and the interaction effects of solvents and noise on workers’ hearing and balance function. In Sweden part of this study has been conducted assessing the hearing function of workers exposed to styrene and noise in the fibreglass reinforced plastics industry (FRP) in Sweden. Over 300 workers were tested using an extensive test battery for hearing function. The audiological test-battery consisted of audiometry, otoacoustic emissions, speech tests and test of the central auditory function.

The first results from the of the Swedish study showed that, even at the low concentrations of solvents found in the work environments investigated, the workers

20 in groups exposed to styrene nevertheless had a poorer pure tone threshold compared to controls or workers exposed only to noise.

The test-battery used in Sweden has been used as a base for the method development and the agreed protocol used by all the partners in NoiseChem. The aim of NoiseChem is to use similar methods in the studies of exposed working populations in different countries and thereby be able to pool the data and have a greater database for analysing the effects from chemicals on the hearing and balance function in the exposed workers.

The Swedish study will be continued in 2003 with balance assessment in co- operation with Jukka Starck (partner from Finland).

21 WP 4: Determine Specific Health Effects of Social and Community Noise on Children

This group has examined the prevalence of tinnitus in 7-year old children. In Göteborg 961 seven-year old children were individually interviewed. Audiometric screening on 20 dBHL thresholds was performed. 12 % (n=120) of the children experienced tinnitus. Only 12 of these 120 children had hearing loss defined as thresholds " 20dBHL (6 children with conductive hearing loss (CHL), 4 with sensorineural hearing loss (SNHL), 2 with mixed hearing loss (MHL). Only 2.5 % (n=24) reported that they experienced tinnitus after noise exposure and only 3 of them had hearing loss (n=1 SNHL, n=2 CHL). In the non-tinnitus group there were 406 girls and 436 boys and in the tinnitus group there were 63 girls and 56 boys. When investigating tinnitus in children it is important not only to consider hearing but also psychological and social aspects of the clinical history as hearing alone does not predict the prevalence of tinnitus.

Field and laboratory studies on reported annoyance from combined noise sources suggest at least two principles of summation. The first relates to the dominant source, and states that the summed effect of (in time) non-overlapping noise sources is equal to what can be predicted from the dominant noise source alone. The alternative is an averaging principle, stating that combined noise sources yield an outcome that is somewhere in the middle between the two single sources. These two contrasting principles were tested in a memory experiment. Combinations of aircraft noise with train or road traffic noise were employed, with one or the other as the dominant source. A total of 548 children aged 12-14 years read texts in both silence and noise (66 dBA Leq) in their ordinary classrooms and were tested for recall and recognition exactly one week later. Two of the combinations significantly impaired recall and for the two others the trends were in the same direction. There were no noise effects on recognition. No interactions between noise and learning ability on memory was indicated. Distraction, perceived effort, mood, and perceived difficulty while reading and learning did not explain the results.

The music-listening habits of young people are reported to be the origin of the very high sound level exposition correlated in some studies to hearing loss and/or tinnitus. The question remains if the young public wants high sound levels during music events. 700 young people attending a professional school received a questionnaire about their music-listening habits, their hearing impairment such as tinnitus and their satisfaction of sound level in discotheques and concerts. Their hearing capacity was measured by audiometry. 79% of the subjects attend discotheques, 52% concerts and 35% techno parties. For 53% of them the music exposure (Leq) was 87dB(A) or more. 71% said that they suffered from tinnitus following a loud music event. The audiometry detected 11% of the subjects with hearing loss. But there was no increased relative risk of hearing loss observed related to musical exposure. The sound level in discotheques, during the pop and rock concerts, and in techno parties was judged as too high by 42%, 35% and 39% of the questioned young people, respectively. Less than 3% generally found that the sound level during the music events was too low. These results show that the high sound levels in musical events are not demanded by the young public.

The discussions about the level of noise from toys has largely taken place in the Toy - standardisation group of the EC (CEN/TC 52/WG 3). The Directive 88/378/EEC gave the background when in 1990 the Commission made a report for the Council titled “The risk of damage to hearing resulting from noise emitted by toys”. A result of that report was the mandate to the standardisation body, CEN, to include noise limits

22 while revising the toy standard EN 71.It has always been difficult to find scientific evidence that noise exposure from toys actually lead to hearing loss. At the same time measurements of the sound pressure level from toys showed unexpectedly high noise levels. In 1994 the Swedish Market Court forbid the sale of novelty toys that released impulse noise of 173 dB (C-weighted impulse peak level at 2,5 cm). For the moment the toy manufacturers are proposing that the sound pressure level (L pC peak) in the toy standard should not exceed 134 dB at 50 cm for toys using percussion cups. From the consumer side it is being argued that the most that should be permitted is 125 dB Evidence has been accumulated from various research studies, consumer bodies and regulatory authorities about noisy activities, the levels of noise experienced by children and the possible health effects. It is increasingly clear that even in the category of children, there is a need to have subgroups such as babies and infants, 0-1 years; 1-5 years, 6-11 years and 11-18 years as they are subject to different types of noise exposure where they may leave the noise environment or are of such an age that they may not. Up to 5 years they are exposed to noisy toys, then loud music, discotheques, concerts and environmental noise such as traffic noise and aircraft noise at school. The effects range from hearing difficulties, tinnitus, reading skills, learning performance and memory. Analysis of the literature is planned and further meetings to consider the possibilities of dose-response relationship of noise and various effects specific to children. Furthermore the group plans to consider a Europe-wide collection of educational material available for enhancing awareness of the hazards of noise and consider possible approaches to examining the children’s own perspective of noise and its hazards. A number of actions have been suggested by the Group examining the issue of toys: . Lower the frequency of sound emitted by toys . Lower the intensity of sound from toys, particularly electronic toys . Determine age-specific safe levels of sound that any individual may be exposed to without incurring damage to hearing . Provide legislation for toy noise safety for manufacturers

Educate young children and their parents about the dangers of high intensity sound emitting toys.

This work package evaluated the risk of auditory damage from noisy toys and arcade games, personal cassette players, cinemas, sports activities and other noisy leisure- time pursuits and set up an international register of case-studies of children adversely affected by noisy toys. “Sound safe” labelling of toys was sought.

It has been shown that cognitively demanding tasks are adversely affected by environmental noise particularly in children. There are impacts of noise on attention, reading, memory and learning. The experiments with acute noise indicate that the strongest impairing noise effects are for children aged 13-14 years on the recall of memory when exposed top traffic noise and speech noise when reading text.

Recall and reading a difficult word list are most strongly affected by chronic aircraft noise. In real life chronic noise exposure at a given noise level is more potent in impairing cognitive function than acute noise. Recall is a sensitive measure of both the acute and chronic noise effects. It has been shown that reading ability is correlated with noise level and auditory discrimination. Auditory discrimination may predict reading ability.

Children aged 8-11 years in low and high noise exposure show a higher annoyance in noise exposed and their reading comprehension is some 6 months behind.

23 Annoyance is linked to noise in children. Poor reading and poor mathematics performance has been shown in exposed children although these findings were not significant after adjustment for social class. The mechanisms of the effects are thought to be attention and motivation as well as poor auditory discrimination.

It is considered that children’s perspective of noise must be studied without bias with adult views of effects. The reaction of children to noise must be evaluated on an open basis.

Leisure noise induced tinnitus poses widespread concern about the effect of loud music on young people who frequently attend concerts and discotheques including those who work in these premises where the levels can be in excess of 100dBALeq.

In many ways, children react differently to stress than adults. An infant girl reacts very different compared to a teenage boy. In order to establish a correlation between stress-related health effects of noise on children, a multidisciplinary approach is probably necessary. The following model illustrates the process of stress-mediated effect.

1. The Hypothalamic-Pituitary-Adrenal Axis

The endocrine system together with the nervous system provides most of the extra- cellular control of specialised tissues to function as integrated organs. There is, however, no sharp distinction between the endocrine and nervous systems. Chemical substances are released from the nervous system and can act as local mediators or circulating hormones, and hormones can act as neurogenic mediators within the central nervous system. In the hypothalamus and the pituitary there is a close connection between these three systems that integrates them into one control unit.

The physiology of the hypothalamic-pituitary-adrenal (HPA) axis is easiest understood from its anatomy. The hypothalamus is a wedged-shaped mass of primary grey matter and situated in the ventral diencephalon. The pituitary gland may be divided into one anterior, glandular and one posterior, neural portion called the adenohypophysis and neurohypophysis. Axons from the supraoptic and paraventricular nuclei of the hypothalamus project to the underlying neurohypophysis, where they release oxytocin and vasopressin. Releasing factors such as the corticotropin releasing factor (CRH), the luteinizing hormone releasing hormone (LHRH) and growth hormone releasing hormone (GHRH) are produced by hypothalamic neurones and reach the adenohypophysis via the hypophyseal-portal vessels to stimulate hormone production.

The hypothalamus has extensive and complex neural connection. The CRH- secreting neurones receive afferent regulatory signals from different parts of the brain. Stimulatory inputs arise from the suprachiasmatic nucleolus (the regulator of circadian rhythms) and the amygdale, while inhibitory inputs on CRH secretion arise in the hippocampus and in the locus coeruleus. The CRH-neurones are excitatory influenced by cholinergic and serotonergic (5-HT) central pathways and inhibitory effects are exerted by gamma-aminobutyric acid (GABA). Catecholamines can exert both inhibitory and excitatory effects. CRH stimulates the secretion of the Adrenocorticotropic Hormone (ACTH) from the adenohypophysis.

24 Hypothalamic-Pituitary-Adrenal axis

CRH Hypothalamus + - - Pituitary - ACTH -

- + -

Adrenal s Cortisol DHEA S

25 The HPA-axis is subjected to periodic or cyclic changes, which are influenced by the nervous system. These circadian rhythms are brought about by both an endogenous mechanism independently of the environment, and exogenous factors such as light- dark changes and the ratio between the lengths of day and night. The pattern of the ACTH and cortisol variations shows an early morning peak, declining levels during the daytime, and minimal secretory activity in the evening. Under steady-state there are about 15 distinct cortisol pulses within 24 hours. ACTH is also secreted in short, regular pulses. The secretion of GH is maximal shortly after sleep, and that of LH in sexually mature individuals is characterised by rapid amplitude pulsations and occur throughout the 24 hours.

The secretion of ACTH is stimulated by CRH upon endogenous mechanisms or exogenous factors such as stress. The ACTH stimulates the adrenal cortex to produce and release cortisol (fig 1), which in turn exerts a negative endocrine feedback regulation, mediated via mineral corticoid and glucocorticoid receptors in the hippocampus and amygdala. Feedback information allows the HHPA axis to adjust appropriately the cortisol secretion from the adrenals. In addition, the feedback actions of cortisol counter-regulates many of the neurochemical processes in the central nervous system, resulting in a paradoxical effect of both protection and degeneration of brain structures, especially in the hippocampus.

Intrinsic or extrinsic factors that tend to cause stress are defined as stressors, and include a variety of factors. There are physical stressors such as heat, cold, noise, trauma, fever and infection: psychological stressors such as social subordination, anxiety and depression. The stress response is mediated by two principal components located in the hypothalamus and the brainstem: the CRH neurones and the locus coeruleus-sympathetic (LC) system.

The central neurohormonal response pattern to stress has been greatly elucidated throughout studies in both animals and humans. It is also known that the individual differences in response pattern are a product of both the stressful stimulus as well as the capacity to habituate or adapt to the situation, so called coping. Two types of response pattern to stress are of particular relevance for human health and disease – namely, the defeat reaction and the defence (or fight-flight) reaction. The defeat reaction appears in humans as deep sorrow and despair and a ”no-way-out” behaviour. This type of reaction evokes primary the HPA axis with resulting increase in ACTH and cortisol secretion. As the reproductive and growth axis is functionally influenced at several levels by the HPA axis, prolonged activation of the HPA axis leads to inhibition of testosterone as well as suppression of GH secretion. Such effects as depressive behaviours have been demonstrated in humans. In primates other than humans, exposure to standardised, moderate psychosocial stress is followed by a diminished feedback regulation of the cortisol secretion, suppression of the reproductive axis, and depressive behaviour. Moreover, such social stress is associated with visceral obesity, insulin resistance, dyslipidemia, hypertension and coronary artery atherosclerosis. The defence or fight-flight reaction on the other hand, evokes primarily the locus coeruleus-sympathetic (LC) system, followed by increases levels of epinephrine-norepinephrine and testosterone.

As discussed above, the cortisol exerts a negative endocrine feedback regulation on the pituitary and the hippocampus. The feedback is initiated by binding of the steroid to regulatory gene elements, and the feedback suppression is mediated by glucocortoid receptors in the hippocampus. Once cortisol is bound to these receptors, the HPA axis activity is controlled. Studies in vitro, and in vivo, in cells from chronically stressed rats, have shown that the sensitivity of the HPA axis to

26 inhibition by cortisol is impaired. When the HPA axis is subjected to prolonged elevated cortisol levels as in chronic stress, the glucocortoid receptor gradually loses their function, ending up in a presumably irreversible neurodegenerative condition. Such hippocampus damage has been shown in individuals with Cushing syndrome, a condition also characterised by hypercortisolism.

Psychoneuroendocrine determinants for specific health effects of stress on children will be discussed in the view of these pathophysiological mechanisms.

27 WP 5: Determine individual sensitivity to noise damage

Some animal data indicates that ageing is linked to greater vulnerability to noise but the data is not without contradiction. In man no such data exists. We aimed to evaluate the effect of age and age-related factors in the noise-induced hearing loss (NIHL) in a large working population in which exposure data and health related factors could be carefully controlled. Information about work exposure, the use of hearing protective devices, audiogram, environmental and biological factors was collected from 406 paper mill workers exposed to noise levels of 91-94 dB(A), 100 forest workers exposed to noise levels of 96-99 dB(A), and 176 shipyard workers exposed to 95-97 dB(A). Confounding factors included smoking habits, serum cholesterol, systolic or diastolic blood pressure and use of analgesics. Subjects were classified; based on median values, into high and low risk groups. In addition, the effect of age was studied with matched pair technique. Age in combination with systolic blood pressure and use of analgesics resulted in a significant increase in NIHL. The confounding factors were a significant source of hearing loss in younger and elderly group of subjects, the serum cholesterol level being the most important. In risk analysis the confounding factors partly overruled the age-related increase of NIHL. For subjects with less than two confounding factors, occupational noise exposure determined the development of NIHL. As the number of confounding factors increased, the noise exposure was overruled by these factors in the development of hearing loss. In analysis where the subjects were matched with pairs by age, exposure, blood pressure and serum cholesterol level, the elderly subjects were more susceptible to NIHL than younger subjects. Factors independently but causally related to age, were important in the development of NIHL among workers exposed to noise levels below 98 dB(A). The inner ear in older subjects seems to be more vulnerable to noise than those in younger ones.

An active issue is the extent to which sensory cells are affected in the aging human ear. In the absence of exposure to noise, recent human and animal data suggest a normal population of sensory cells in the aging ear except in the most basal and apical regions. If confirmed, age-related hearing loss is not a sensorineural hearing loss, but a vascular, metabolic, neural disorder.

Noise exposure is the most common cause for the generation of tinnitus. This study evaluated the variability of spontaneous emissions in industrial workers exposed to noise and reporting the presence of tinnitus in comparison with those exposed to noise but without tinnitus. The assumption being that exposure to noise leads to some instability within the cochlea, which alters the spontaneous emission activity. Thus those experiencing tinnitus may show greater variability than those without tinnitus. 198 mill workers in Poland exposed to noise levels between 85-95dBA for a mean of 12+6.6 years, 104 of whom had reported the presence tinnitus and 94 without tinnitus were evaluated for otoscopy, audiometry and otoacoustic emissions. The tests were repeated between 5-10 days in most subjects to check for variability. There were significant differences in the mean age, pure tone average, transient emissions amplitude and variability between groups with and without tinnitus. There were no significant differences between sessions for these measures in either group. The likelihood ratio of tinnitus being present given that SOAE are present and variable is 1.87 and is significantly reduced for no tinnitus given that SOAE are present and stable at 0.156. This study has clearly demonstrated that the incidence of spontaneous emissions is higher in noise-exposed workers than previously observed and the stability from week to week is significantly lower in those with subjective tinnitus. In another study a risk of hearing loss was evaluated in employees of 4 Polish paint and lacquer manufactures exposed to a mixture of organic solvents, with remarkable content of xylene and toluene. The following groups of subjects were included: I - 113 workers exposed to organic solvents alone, II - 238 workers exposed to organic solvents and noise> 80 dB-A, III - 214 workers exposed only to noise > 80 dB-A and IV - 166 control subjects exposed to neither noise nor organic solvents at the workplace. The highest incidence of hearing loss was found among the workers exposed to organic solvents (48%) and organic solvents and noise (42%) if compared to noise-exposed group (26%) and control group (17%). There was a significant increase in relative risk (RR) of hearing loss in subjects exposed to solvents, in case of sole exposure and combined exposure with noise, within the wide spectrum of frequencies from 3 to 8 kHz (depending on the frequency RR ranged from 1.41 to 19.61). The respective increase in risk of hearing loss in subjects exposed only to noise was found exclusively at the frequency of 4 kHz. There was a positive correlation between cumulative life dose of organic solvents and the extent of hearing loss. These results provide further evidence for significant influence of organic solvents on hearing loss. Moreover, the damage due to solvents seems to be much more wide spread throughout the frequency range if compared to the effects of isolated exposure to noise.

The risk of auditory damage from exposure to noise depends on a number of variables, which are related to the sound, its transmission to an individual’s auditory system and its characteristics and specific response to that stimulus. It has been shown that a given noise exposure will result in only a fraction of a group of people having a hearing impairment. Therefore only broad risk criteria for auditory damage from noise exposure may be set as individual variations in vulnerability can be high. It is therefore important to determine the factors that underlie the large variation in susceptibility to noise damage so that it may be possible to identify specific individuals at risk.

A number of factors have been identified as possible determinants of individual sensitivity to noise damage. These include external ear canal characteristics, middle ear sound transmission efficiency including the stapedial reflex function, development of reactive oxygen species and availability of endogenous antioxidants, extent of efferent suppression, genetic vulnerability, the extent to which other risk factors such as smoking, hypertension, metabolic disorders etc interact with noise effects, previous hearing level, age, etc.

A number of studies from the Group have considered how sub-clinical micro- mechanical changes in the cochlea may provide an early indication of damage and the role the auditory efferent control system may play as a possible indicator of susceptibility in an individual. It is necessary to determine whether those individuals showing early effects on otoacoustic emissions and efferent suppression do in fact go on to develop hearing loss audiometrically compared to those with normal emissions and suppression.

The role of the auditory efferent system was explored in determining individual sensitivity to hearing and its vulnerability to damage.

Studies examined the contralateral sound activated suppression of otoacoustic emissions to assess the efferent system in individuals exposed to noise but having hearing within normal limits to determine any early indication of noise mediated effect. It was found that the suppression of emissions was indeed affected in some individuals prior to any change in the evoked emissions or indeed the audiometric changes observed later. It appears that the earliest indication is the change in the

29 efferent system which is responsible for the fine-tuning in the auditory system. It will be necessary to follow these individuals to observe whether those with weak or affected efferent systems show noise effects earlier than those unaffected.

Several other aspects of noise susceptibility were also studied. In experiments in one laboratory animals were exposed to the following: duration 1 hour, intensity 120 dB SPL, white noise. Young volunteers were exposed for four hours to amplified music at 97 dB SPL /A/ recorded previously in a discotheque.

In contrast to the similar values of temporary threshold shifts (TTS) obtained in different adult rats after noise exposure, great inter-individual variability was found in the enhancement of the middle latency response (MLR) in adult rats. In a sample of 30 rats exposed to noise, in only half of the animals were the MLR amplitudes significantly enhanced. Similar differences in noise susceptibility were observed when rats trained by an operant conditioning technique to recognize gaps in a continuously presented white noise were re-tested after noise exposure. Before noise exposure the average GDT in a group of 12 rats was 1.57+/-0.07 ms. In one group of animals, the TTS were relatively mild (40-50 dB) and the gap detection thresholds (GDT) were only slightly enhanced (never exceeding 8 ms). Enhanced MLR amplitudes were not seen in this group. In the second group, the TTS and GDT shifts were also relatively mild (60-70 dB resp. 8-50 ms); however, the MLR amplitudes were enhanced post-exposure. Approximately half of the animals exposed to noise showed enhanced susceptibility to noise exposure with large TTS (80-90 dB), the absence of behavioural responses to gap during the first week post- exposure, MLR amplitude enhancement and a very slow recovery of thresholds and behavioural responses during the post-exposure weeks. Even two months after noise exposure, threshold shifts were present in this group of animals and GDP did not return to pre-exposure values.

Susceptibility to noise-induced hearing loss was studied during maturation in 20 female pigmented rats (strain Long-Evans). Young rats, 3-7 weeks old, were exposed to noise and the thresholds and amplitudes of MLR recorded from electrodes implanted on the surface of the auditory cortex were analyzed before and after noise exposure. Noise exposure in young rats produced an adult-like pattern with an elevation of hearing thresholds. One-two weeks post-exposure, a recovery of MLR thresholds was observed, though full recovery only occurred in the low- frequency range. Recovery of thresholds in the high frequency range depended on the age of the animals at the time of exposure. In all animals aged less that 6-7 weeks, exposure resulted in a permanent threshold shift in the range of 4-32 kHz. Similar to adult rats, young rats exposed to noise exhibited enhanced MLR amplitudes. In several rats exposed at 3-5 weeks of age, the recovery period to normal amplitudes was substantially prolonged and lasted 4-8 weeks in comparison with 1-2 weeks in adult rats. These results demonstrate a greater susceptibility to noise exposure in rats during the first postnatal weeks.

Some aspects of susceptibility to noise in men were studied in a group of twelve audiometrically normal young volunteers ( age 18-25 years) who were exposed for 4 hours to amplified music (97 dBA) previously recorded in one of Prague‘s discotheques. The test battery for each ear included pure tone audiometry (PTA), Békésy high resolution audiometry, spontaneous otoacoustic emissions (SOAE), transient evoked otoacoustic emissions (TEOAE), distortion product otoacoustic emissions (OAE) with distortion product-growth function at 4 kHz, contralateral suppression of otoacoustic emissions (OAE) and gap-detection test. After music exposure a significant elevation of audiometric thresholds at frequencies of 1-5 kHz (up to 25 dB), a decrease of TEOAE amplitudes in the frequency range 1400 – 5700

30 Hz and a decrease of DPOAE amplitudes in the frequency range 200-3400 Hz were recorded. SOAE were present in 8 ears under control conditions; after exposure they disappeared in 6 ears, while in 2 ears they remained unchanged. The DP-growth function slope at 4000 Hz was significantly steeper after exposure. Contralateral suppression and gap detection function did not change significantly. Interestingly, subjects with larger TTS at frequencies of 2000-5000 Hz also showed a larger decline in the amplitude of TEOAE, with the best correlation between TTS and TEOAE shift at 4 kHz. Measurements of TEOAE amplitude decrease after exposure to loud sound may be used for the practical estimation of individual susceptibility to noise.

31 WP 6: Development of an environmental noise health information system

Hearing conservation programs (HCP) focus on occupational noise in work life. However, citizens in modern society are exposed additionally to a wide range of environmental noise that all should be included in the evaluation of the total noise exposure level. The exposure of the inner ear to noise is also dependent on the use of hearing protectors. Today for instance in Finland, 14% of the work force are exposed to noise levels exceeding the action level of 85 dB(A) at work. Annually almost 1000 compensated hearing loss (NIHL) cases has been recorded corresponding to 0.03 % incidence rate. Comparison between the top ten occupations posing the highest incidence for NIHL show the highest risk in occupations where workers are exposed to impulsive noise. In a recent study we have been able to show 12 dB more severe NIHL in an age- and exposure-matched groups of workers exposed to impulsive noise in comparison to steady state noise exposure group. This finding confirmed our earlier study in which we demonstrated that shipyard workers had a 10 dB higher NIHL than could be predicted by the model, whereas the observed hearing levels were very consistent for the forest workers. In many occupations the impulses are so rapid that their contribution to the energy content of noise is minimal. Thus these impulses do not increase the energy equivalent noise level. The noise exposure evaluation may be biased for several reasons. If the exposure conditions remain stable over the work period, the equivalent noise exposure level (LAeq) is relatively easy to calculate. Still in practice, the accuracy of the exposure measurement is hardly better than 5 dB. In the cases when noise exposure varies depending on the work task, the error in the evaluation of noise exposure may exceed 10 dB. Thus, theoretically in the worst case, noise exposure evaluation may vary 15 dB due to technical and environmental factors which seems to be too large even for the selection purposes of HPDs according to the EN 458 standard. Properly selected HPDs should decrease the noise levels at ear below the risk limit in industrial environments. However, according to our experience the usage rate of hearing protectors in industry is often low varying from 55% in paper mill to 90% in forestry work. HCP actions can be improved if we can improve the risk assessment and the accuracy of exposure evaluation. This facilitates proper selection of HPDs and can be used to motivate both employee and employer to complete the HCP actions. Technical controlling measures have always the priority. To meet this requirement noise controlling measures have to be a part of production. Present EU legislation emphasises to responsibility of work places in improving the work environment to meet the stated requirements. The urgent task is to develop expert programs and models for these purposes that can be applied at work places.

The individual HCP can be refined by using expert system. The expert system operates with input data, knowledge (to the data) and knowledge bases of the systems. Our inference method resembles the methodology of the nearest neighbour searching, but has essential features, which makes it appropriate to expert system inference. For instance, the metrics where distances in the space are computed are L1, i.e. a difference between a parameter value of a case and that to be matched is directly employed. This sort of City Block metrics emphasizes the importance of independent parameters unlike Euclidean distance of L2. The medical parameters used in the inference process are weighted according to choices of the medical experts in the current project. We have published several articles about our medical expert system studies during the past three years. The neural networks offer a possibility to construct a self-learning expert system. It can be applied in an area where the problem cannot be clearly defined or understood as in speech perception 32 and recognition in noise. To construct a neural network based expert system requires, however, a large amount of solved cases so that the learning and validation of the neural network based expert system can be done. This can be done only by using joint population studies in EU countries. The genetic algorithms are the newest step of decision-making in computer science. Genetic algorithms introduce the concept of artificial life instead of the artificial intelligence. Genetic algorithms simulate the act of real life - genes, cells and evolution. Genetic algorithms are program fragments that compete against each other to find the best solutions for the given problem. They search for the solution without beforehand set rules and the outcome is unpredicted. They fit to almost all decision-making where best solutions are searched with limited computer resources. Especially well genetic algorithms fit to complex problems, which are difficult to define. Such a hybrid program consisting of Neural network for screening the validity of base data and use of genetic algorithm for decision making seem to be best alternatives in expert program included in individual HCP.

Hearing conservation programmes (HCP) usually refer to a system using frequent evaluation for preservation of hearing of workers exposed to occupational noise. Individually tailored programmes are clearly of greater benefit to the worker. It is also important to maintain an evaluation of the risk factors for an individual in the information system in order to develop a predictive model of hearing and its protection. Review of available databases have been conducted and a NoiseScan programme has been developed and distributed to all members of NOPHER for use in their work. The data in NoiseScan is divided in to modules such as case history, noise exposure, risk factors, hearing measurement, inference engine and demonstration modules and the data is stored in a relational database. The exposure data are based on the evaluation of noise emission level in which level, duration, frequency content and usage rate and efficacy of hearing protectors are included. The programme predicts hearing loss with ISO 1999 and provides an individual evaluation based on pattern recognition technique by weighting combinations of different risk factors. The programme demonstrates present hearing and shows how this will change as hearing loss deteriorates overtime and demonstrates this through recorded and filtered music. As the development of hearing loss is not a linear function of the factors causing hearing loss in industry, further work is necessary to develop individual programmes. Further work is also continuing to develop an internet version of programme so that it is easily accessible and used by increased numbers for protection from noise exposure.

An European environmental noise health information system for standardised data collection was developed for improved evaluation of dose-response relationships, hearing conservation and education. This will help in gathering uniform data on noise measures and health effects and to improve the dose-response relationship. The data will allow improved decision making with regard to measures taken for hearing conservation. This will also help to develop new strategies for raising awareness of the value of hearing and produce an international inventory of educational material available for this purpose. An international network of noise specialists was created for wider distribution of expert knowledge and cross-boundary collaboration.

Activities

Development of an individual hearing conservation programme (IHCP) continued. In the NoiseChem project will add to the IHCP the effect of solvents. To evaluate more accurately the importance of risk factors we studied the noise induced hearing loss of a population with low number of risk factor i.e. Finnish air force military pilots. Their 33 hearing corresponded to 80 % percentile of the ISO 1999-1990, that corresponded the difference of 10 dB at the age of 40 when compared to a normal industrial worker population. Version 4.0 is now ready. Major changes include support for three languages, English, Swedish and Finnish. User manual is in English. The program will be distributed to all partners.

Development of hearing protection systems Activities Studies of the protection efficiency of hearing protectors (HPD) against high impulse industrial noise was conducted in Russia. The results show that efficiency is lower than predicted by standard estimation techniques. The need and use of hearing protectors was studied among five classical music orchestras in Helsinki. Finland. The results showed poor usage rates and poor motivation to use HPDs. The best choice of protectors for musician will provide an attenuation of 10-17 dB.

Determine the psycho social consequences of NIHL and their impact on rehabilitation and conservation programmes

Activities To evaluate the relation of ear related symptoms NIHL, tinnitus, pain in the ear to stress and work motivation a project has started among five Finnish orchestras. The preliminary findings indicate a strong correlation between ear symptoms and stress. A project concerning the prevalence of tinnitus has been started by national funding.

34 Deliverables and Dissemination of Research Results

Meetings

YEAR 1 1. NOPHER 2000: INTERNATIONAL CONFERENCE: Noise Induced Hearing Loss. 7-9 July 2000, Cambridge, UK.

2. INTERNATIONAL WORKSHOP: Development of an Environmental Noise Health Information System - 7th July 2000, Cambridge, UK. 3. INTERNATIONAL WORKSHOP: Effects of Combined Chemicals and Noise Exposures on Hearing and Balance - 9th July 2000, Cambridge, UK.

4. Mini-symposium 45. Interaction Effects of noise and industrial chemicals on hearing. Organised by Prasher, D. and Johnson, A-C. 26th International Congress on Occupational Health (ICOH). 27th August - 1st September 2000. Singapore.

YEAR 2 5. NOPHER 2001: INTERNATIONAL CONFERENCE: Noise Pollution and Health. 6-8 April 2001, Cambridge, UK.

6. INTERNATIONAL WORKSHOP: Current evidence for specific health outcomes in relation to particular noise sources (Road, Rail, Aircraft). 6 April 2001, Cambridge, UK 7. INTERNATIONAL WORKSHOP: Noise/chemicals Effects. 27-28 April 2001, Nancy, France.

8. INTERNATIONAL WORKSHOP: Noise/chemicals Effects. 20-21 Sept 2001, Bordeaux, France.

9. INTERNATIONAL WORKSHOP: Noise/chemicals Effects. 24 Oct 2001, Brussels, Belgium.

YEAR 3 10. INTERNATIONAL WORKSHOP: Environmental Noise Solutions, 10 July 2002, Cambridge, UK.

11. INTERNATIONAL WORKSHOP: Individual Susceptibility to Noise Damage, 19-20 July 2002, Novartis Foundation, London, UK.

12. INTERNATIONAL WORKSHOP: Noise Pollution: Health Effects on Children, 5-7 October 2002, Berlin, Germany.

13. INTERNATIONAL CONFERENCE: NOPHER 2002-Nordic Noise II, 24-27 Oct 2002, Stockholm, Sweden.

14. INTERNATIONAL WORKSHOP: NOPHER Co-ordinators Meeting, 18 January 2003, Novartis Foundation, London, UK.

35 Publications

YEAR 1 1. Prasher, D. (2000) A European Concerted Action on Noise Pollution Health Effects Reduction - NOPHER. Noise and Health, 7; 1-3.

2. Ising, H and Prasher, D. (2000). Noise as a stressor and its impact on health. Noise and Health, 7; 5-7.

3. Ising, H and Prasher, D.(eds.) Environmental Noise, Stress and Cardiovascular Risk: Special Issue of Noise and Health. 2000, Vol. 7.

4. Babisch, W., Ising, H., Gallacher, J.E.J. 2000 Association between noise annoyance and incidence of ischaemic heart disease in the Caerphilly and Speedwell studies. In: D. CASSEREAU (ed.) InterNoise 2000. Proceedings of the 29th International Congress on Noise Control Engineering. Société Francaise d'Acoustique, Institut National de recherche sur les Transports et leur Sécurité, Nice, 2065-2070.

5. Ising, H., Babisch, W. 2000 Schwerhörigkeit durch Freizeitlärm. In: BUNDESÄRZTEKAMMER (ed.) Fortschritt und Fortbildung in der Medizin, Band 24 (2000/2001). Deutscher Ärzte-Verlag, Köln, 31-39, ISSN 0170-3331.

6. Stansfeld SA, Haines MM, Burr M, Berry B, Lercher P. A review of environmental noise and mental health. Noise & Health 2000; 8, 55-58.

7. Meis M, Evans GW, Hygge S, Lercher P, Bullinger M, Schick A. Chronic and acute effects of transportation noise on task performance of school children. Proc. Internoise 2000 (Nice), 2000, CD-ROM.

8. Ann Christin Johnson; Thais Morata; Per R Nylen; Eva B. Svensson Hearing loss in workers exposed to styrene and/or noise. Description of audiologic test battery and preliminary results. Abstracts of the 23st Midwinter meeting of the Association for Research in Otolaryngolgy, St. Petersburg, Florida, USA, February, 2000.

9. Ilmari Pyykkö, Ann-Christin Johnson, Esko Toppila, Jukka Starck Noise Susceptibility and Ageing, Abstracts of the First European Conference: Noise Pollution Health Reduction, Cambridge, UK, July, 2000.

10. Ilmari Pyykkö, Jing Zou, Ann-Christin Johnson, Petri Erikson, Poul Bretlau, A difference between antioxidants and neurotrophins in protecting cochlea from vibration and noise trauma? Abstracts of the First European Conference: Noise Pollution Health Effects Reduction, Cambridge, UK, July, 2000.

11. H. Ising und C. Maschke (Hrsg.) (2000): Beeinträchtigung der Gesundheit durch Verkehrslärm – ein deutscher Beitrag. Im Auftrag des Bundesministeriums für Gesundheit, http://apug:[email protected]/

12. Toppila, E., Pyykko, I, Starck, J., Kaksonen, R., Ishizaki, H. (2000). Individual risk factors in the development of noise induced hearing loss. Noise and Health, Volume 3, 8; 59-71.

13. Prasher, D. (2000) Noise Pollution Health Effects Reduction (NOPHER): A European Commission Concerted Action Workplan. Noise and Health, 8; 79-85. 14. Starck, J., Toppila, E., Pyykko, I. Database experty program for individual hearing conservation. Session FP 77: Noise and Vibration. 26th International Congress on Occupational Health. 27th August - 1st September 2000. Singapore. Abstract Book, p436.

15. Starck, J., Toppila, E., Pyykko, I. Solvents, Noise and Other Factors in the genesis of hearing loss. Mini-symposium 45. Interaction Effects of noise and industrial chemicals on hearing. 6th International Congress on Occupational Health. 27th August - 1st September 2000. Singapore. Abstract Book, p143.

16. Prasher, D. and Morata, T. Noise and industrial chemicals: Testing for their effects on the auditory system. Mini-symposium 45. Interaction Effects of noise and industrial chemicals on hearing. 6th International Congress on Occupational Health. 27th August - 1st September 2000. Singapore. Abstract Book, p143.

17. Sulkowski, WJ., Prasher, D., Kostrzewski, P., Kowalska, S., Guzek, W. Ototoxic effects of occupatiobal exposure to a mixture of organic solvents: A field study. Mini- symposium 45. Interaction Effects of noise and industrial chemicals on hearing. 6th International Congress on Occupational Health. 27th August - 1st September 2000. Singapore. Abstract Book, p143.

18. Prasher, D. (2000) A European Commission Concerted Action on Noise Pollution Health Effects Reduction (NOPHER). Mini-symposium 45. Interaction Effects of noise and industrial chemicals on hearing. 6th International Congress on Occupational Health. 27th August - 1st September 2000. Singapore. Abstract Book, p144.

19. NOPHER 2000: INTERNATIONAL CONFERENCE: Noise Induced Hearing Loss. Abstracts Book. www.ucl.ac.uk/noiseandhealth.

20. NOPHER 2000: INTERNATIONAL CONFERENCE: Noise Induced Hearing Loss. Abstracts published in the Journal of Noise and Health, 2000: 3;9, 73-91.

21. NOPHER 2000: INTERNATIONAL CONFERENCE: Noise Induced Hearing Loss. Abstracts published in the Journal of Noise & Health, 2001; 3;10, 83-90.

22. INTERNATIONAL WORKSHOP: Development of an Environmental Noise Health Information System. Minutes of Meeting. 23. INTERNATIONAL WORKSHOP: Effects of Combined Chemicals and Noise Exposures on Hearing and Balance. Minutes of Meeting.

24. NOPHER Brochure for general circulation. www.ucl.ac.uk/noiseandhealth.

25. Suggested Guidelines for the Study of the Combined Effects of Occupational Exposure to Noise and Chemicals on Hearing. www.ucl.ac.uk/noiseandhealth.

26. NOPHER Newsletter: Journal of Noise and Health Volume 2 issue7.

27. NOPHER Newsletter: Journal of Noise and Health Volume 2 issue 8.

28. NOPHER Newsletter: Journal of Noise and Health Volume 3 issues 9.

29. NOPHER Newsletter: Journal of Noise and Health Volume 3 issues 10.

30. Pan European Noise research aims to probe health effects. Noise Management. June 2000, issue 5. www.ifi.co.uk

37 31. How solvents and noise can damage hearing. UCL Newsletter. November 2000. p15.

YEAR 2 32. Prasher, D., Ceranic, B., Sulkowski, W. and Guzek,W (2001) Objective evidence for tinnitus from spontaneous emission variability. Noise and Health 3(12); 61-73.

33. NOPHER 2001: INTERNATIONAL CONFERENCE: Noise Pollution and Health. Abstracts Book. www.ucl.ac.uk/noiseandhealth.

34. Noise Induced Hearing Loss: Basic Mechanisms, Prevention and Control (2001). Henderson, D., Prasher, D., Kopke, R., Salvi, R. and Hamernik, R. (eds.) NRN Publications, London, UK. ISBN 1 901747 01 8.

35. Starck, J., Toppila, E and Pyykkö, I. (2001) Do we have unnecessary hearing loss - can we improve the efficiency of hearing conservation programs? In: Noise Induced Hearing Loss: Basic Mechanisms, Prevention and Control. Henderson, D., Prasher, D., Kopke, R., Salvi, R. and Hamernik, R. (eds.) NRN Publications, London, UK. pp 197-202 ISBN 1 901747 01 8.

36. Morata, T.C. and Campo, P. (2001) Auditory Function after Single or Combined Exposure to Styrene: A Review. In: Noise Induced Hearing Loss: Basic Mechanisms, Prevention and Control. Henderson, D., Prasher, D., Kopke, R., Salvi, R. and Hamernik, R. (eds.) NRN Publications, London, UK. pp 293-304 ISBN 1 901747 01 8

37. Smoorenburg, G.F., Cappaert, N.L.M., Klis, S.F.L., Kulig. B.M., and Muijser, H. (2001). The effects of simultaneous exposure to ethyl benzene and noise on hearing In: Noise Induced Hearing Loss: Basic Mechanisms, Prevention and Control. Henderson, D., Prasher, D., Kopke, R., Salvi, R. and Hamernik, R. (eds.) NRN Publications, London, UK. pp 319-327 ISBN 1 901747 01 8.

38. Pyykkö, I., Starck, J., Toppila, E.and Johnson, A-C. (2001) Methodology and value of databases. In: Noise Induced Hearing Loss: Basic Mechanisms, Prevention and Control. Henderson, D., Prasher, D., Kopke, R., Salvi, R. and Hamernik, R. (eds.) NRN Publications, London, UK. pp 387- 399 ISBN 1 901747 01 8.

39. Barrenäs, M.-L. and Holgers, K.-M (2001) The use of Hearing Disability and Handicap Questionnaires in audiological practice and in research. In: Noise Induced Hearing Loss: Basic Mechanisms, Prevention and Control. Henderson, D., Prasher, D., Kopke, R., Salvi, R. and Hamernik, R. (eds.) NRN Publications, London, UK. pp 401-408 ISBN 1 901747 01 8.

40. Prasher, D., Ceranic, B., Sulkowski, W. and Guzek,W (2001) Objective evidence for tinnitus from spontaneous emission variability. In: Noise Induced Hearing Loss: Basic Mechanisms, Prevention and Control. Henderson, D., Prasher, D., Kopke, R., Salvi, R. and Hamernik, R. (eds.) NRN Publications, London, UK. pp 471-483 ISBN 1 901747 01 8.

41. Babisch W, Ising H. 2001 Noise induced stress is a risk factor in cardiovascular disease. In Rinus Boone (ed.) inter  noise 2001, Proceedings, The Hague, ISBN: 90- 806554-1-4.

42. Babisch W., Fromme H., Beyer A. and Ising H. (2001) Increased catecholamine levels in urine in subjects exposed to road traffic noise. The role of stress hormones in noise research. Environment International 26: 475-481.

38 43. Babisch W. and Ising H. (2001) Noise induced stress is a risk factor in cardiovascular disease. In Internoise 2001. Proceedings of the 2001 International Congress and Exhibition on Noise Control Engineering, The Hague. Vol. 4. Boone R., ed. Nederlands Akoestisch Genootschap, Maastricht, pp1703-1712.

44. Cappaert, N.L.M., Klis, S.F.L., Muijser, H. and Smoorenburg, G.F. (2001). Slechthorendheid door organische oplosmiddelen en lawaai, Vermijdbare gehoorschade, Pharmaceutisch Weekblad 136, 508- 511.

45. Cappaert, N.L.M., Klis, S.F.L., Muijser, H., Kulig, B.M. and Smoorenburg, G.F. (2001) Simultaneous exposure to ethyl benzene and noise: synergistic effects on outer hair cells. Hear. Res. 162, 67-79.

46. Demange, V., Chouaniere, D. Loquet, G.,Perrin, P. Johnson, AC.,Planeau, V.,Baudin,V., Toamain, T. Morata, T. Comment explorer l'ototoxicité des solvants dans le cadre d'études épidemiologiques en milieu professionnel. INRS notes scientifiques et techniques no:202. 2001.

47. Evans, G., Lercher, P., Meis, M., Ising, H., Kofler, W. (2001) Typical Community Noise Exposure and Stress in Children. J. Acoust. Soc. Am. 109 (3) 1023-1027

48. Fields JM, de Jong RG, Gjestland T, Flindell IH, Job RFS, Kurra S, Lercher P, Vallet M, Yano T, Guski R, Felscher-Suhr U, Schumer R. Standardized general- purpose noise reaction questions for community noise surveys: research and a recommendation. Journal of Sound and Vibration 2001; 242:641-679.

49. Ising H. Kruppa B. Babisch W. Gottlob D. Guski R. Maschke C. Spreng M. 2001. Kapitel VII-1 Lärm, In: Wichmann, Schlipköter, Fülgraff (eds.) Handbuch der Umweltmedizin. Erg. Lfg.7/01 Ecomed, Landsberg

50. Kaksonen R, Widen E, Cormand B, Toppila E, Starck J, Pyykkö I, Kere J. Autosomal dominant midfrequency hearing impairment. Scandinavian Audiology, Taylor and Francis Ltd. 2001 Vol 30 1;85-7.

51. Maassen M. Babisch W. Bachmann K. D. Ising H. Lehnert G. Plath P. Plinkert P. Rebentisch E. Schuschke G. Spreng M. Stange G. Struwe V. Zenner H.P. 2001 Ear Damage caused by Leisure Noise. Noise & Health 4; 13, 1-16.

52. Maschke C. Harder J.,Ising H. Hecht K. Thierfelder W. 2001 Stress hormone changes in persons under simulated night noise exposure. Noise & Health, in print.

53. Pyykkö I, Starck J, Toppila E, Aalto H, Kentala E, Hirvonen T, Honkavaara P, Isotalo E. Visual-vestibular interaction in meniere's disease and in vestibular schwannoma when studied on linearly moving platform. International society for postural and gait research. Control of posture and gait. Symposium of the international society for postural and gait research. ISPG 2001; 230-3.

54. Scheibe F, Haupt H, Ising H, Cherny L (2002): Therapeutic effect of magnesium on noise-induced hearing loss in the guinea pig. Magnes Research 15 (1) In Press.

55. Starck J, Toppila E, Pyykkö I. Esimerkki riskinarvioinnin asiantuntijaohjelmasta: Noisescan. Julkaisussa: Esitelmien lyhennelmät. V Hogisto ja R Helenius toim. Työhygienian päivät 15-16.5.2001 Turku. Raportti 16:24-32. (Example of expert program for risk assessment of NIHL, NoiseScan).

39 56. Starck J, Toppila E, Pyykkö I. How to improve the efficiency of hearing conservation program? The 2001 International Congress and Exhibition of Noise Control Engineering. The Hagua, The Netherlands, 2001 August 27-30. Abstracts, ed Rinus Boone, 2001:238.

57. Starck J, Toppila E, Pyykkö I. The role of free-time and military exposure in total life noise exposure. X2001 - Exposure assessment in epidemiology and practice. M Hagberg, B Knave, L Lillenberg, H Westberg eds. In Arbete och Hälsa, Vetenskaplig Skriftserie. National Institute for Working Life & authors 2001:10:100-2.

58. Suvorov G, Denisov E, Antipin V, Kharitonov V, Starck J, Pyykkö I, Toppila E. Effects of peak levels and number of impulses to hearing among forge hammering workers. Applied Occupational and Environmental Hygiene.2001;16(8):816-22.

59. Toppila E, Starck J, Pyykkö I. The effect of hearing protectors to exposure in cold environment. X2001 - Exposure assessment in epidemiology and practice. M Hagberg, B Knave, L Lillenberg, H Westberg eds. In Arbete och Hälsa, Vetenskaplig Skriftserie. National Institute for Working Life & authors 2001:10:97-9.

60. Zou J, Bretlau P, Pyykkö I, Starck J, Toppila E. Sensorineural hearing loss after vibration: an animal model for evaluating prevention and treatment of inner ear hearing loss. Acta Otolaryngol 200;121:143-8.

61. Morata, T.C. (2002) Suggested guidelines to studying the combined effects of occupational exposure to noise and chemicals on hearing. Noise and Health 4(14); 73- 87.

62. Morata, T.C. and Campo, P. (2002) Ototoxic effects of styrene alone or in concert with other agents: A review. Noise and Health 4(14); 15-24.

63. Prasher, D., Morata, T.C., Campo, P., Fechter, L., Johnson, A-C., Lund, S.P., Pawlas, K., Starck, J., Sliwinska-Kowalska, M. and Sulkowski, W. (2002) NoiseChem: An European Commission research project on the effects of exposure to noise and industrial chemicals on hearing and balance. Noise and Health 4(14); 41-48.

64. Schomer P, Berry B, Borchgrevink HM & al. Acoustics – Description, measurement and assessment of environmental noise. Part 1 Basic quantities and assessment procedures. Report ISO/CD2 19996-1 from ISO/TC 1/WG45. Geneva; ISO 2001.

65. Schomer P, Berry B, Borchgrevink HM & al. Acoustics – Description, measurement and assessment of environmental noise. Part 2 Determination of environmental noise levels. Report ISO/CD2 19996-2 from ISO/TC 1/WG45. Geneva; ISO 2001.

66. NOPHER Newsletter: Journal of Noise and Health Volume 3 issue 11.

67. NOPHER Newsletter: Journal of Noise and Health Volume 3 issue 12.

68. NOPHER Newsletter: Journal of Noise and Health Volume 4 issues 13.

69. NOPHER Newsletter: Journal of Noise and Health Volume 4 issues 14.

40 YEAR 3 70. Prasher D., Morata T., Campo P., Fechter L., Johnson A.C., Lund S.P., Pawlas K., Starck J., Sułkowski W., Śliwińska-Kowalska M. NoiseChem: An European Commission research project on the effects of exposure to noise and industrial chemicals on hearing and balance. Int. J. Occup. Med. Environ. Health, 2002, Vol. 15(1), 5-11.

71. Babisch W, Ising H, Gallacher JEJ. Health status as a potential effect modifier of the relationship between noise annoyance and incidence of ischaemic heart disease. Occupational & Environmental Medicine; accepted for publication.

72. Prasher D, Morata T, Campo P, Fechter L, Johnson A-C, Lund SP, Pawlas K, Starck J, Sliwinska-Kowalska M, Sulkowski W. NoiseChem: An European Commission research project on the effects of exposure to noise and industrial chemicals on hearing and balance. Noise & Health. 2002: Vol 4:14;41-8.

73. Starck J, Toppila E, Pyykkö I. Impulse noise and risk criteria Nordic Noise 2002. An International Symposium on Noise and Health 25-27 October 2002, Nobel Forum, Karolinska Institutet, Stockholm, Sweden. 2002: 8.

74. Toppila E, Forsman P, Pyykkö I, Starck J, Oksa P, Uitti J. Effect of noise and styrene to hearing: Description of the project Nordic Noise 2002. An International Symposium on Noise and Health 25-27 October 2002, Nobel Forum, Karolinska Institutet, Stockholm, Sweden. 2002:18.

75. Pyykkö I, Starck J, Toppila E, Ulfendahl M, Noise Induced hearing loss, Clinical aspects of hearing and balance, Martin Dunitz publishers. In Press.

76. Starck J, Toppila E, Pyykkö I, Do we have unnecessary hearing loss - can we improve the efficiency of hearing conservation programs, Noise induced hearing loss: mechanisms of damage and means of preventions, Whurr-publishers. In Press.

77. Pyykkö I, Starck J, Toppila E, Johnson AC: Methodology and value of databases, Noise induced hearing loss: mechanisms of damage and means of preventions, Whurr-publishers. In Press.

78. Toppila E, Pyykkö I, Starck J, Johnson AC, Juhola M: Methodology and value of databases and their use in individual hearing conservation program, Martin Dunitz publishers. In Press.

79. Starck J, Toppila E, Pyykkö I. The role of risk factors in noise-induced hearing loss and the management of sophistacated hearing conservation program, Archives of Complex Environmental Studies. In Press.

80. Scheibe F , Haupt H, Ising H , Cherny L. Therapeutic effect of parenteral magnesium on noise-induced hearing loss in the guinea pig. Magnes Res. 2002 Mar;15(1-2):27- 36.

81. Morata TC , Campo P . Ototoxic effects of styrene alone or in concert with other agents: A review. Noise and Health. 2002;4(14):15-24.

82. Morata TC, Johnson AC , Nylen P, Svensson EB, Cheng J, Krieg EF, Lindblad AC , Ernstgard L, Franks J. Audiometric findings in workers exposed to low levels of styrene and noise. J Occup Environ Med. 2002 Sep;44(9):806-14.

41 83. Cappaert NL, Klis SF, Muijser H , Kulig BM, Ravensberg LC, Smoorenburg GF . Differential susceptibility of rats and guinea pigs to the ototoxic effects of ethyl benzene. Neurotoxicol Teratol. 2002 Jul-Aug;24(4):503-10.

84. Noise Pollution and Health (2003) ed. D. Prasher. nRn Publications, London. ISBN 1 901747 02 6.

85. Stress Hormone Changes in Persons exposed to Simulated Night Noise (2003) C. Maschke, J. Harder, H. Ising, K. Hecht and W. Thierfelder. In Noise Pollution and Health (2003) ed. D. Prasher. nRn Publications, London. p103-113. ISBN 1 901747 02 6.

86. INTERNATIONAL WORKSHOP: Environmental Noise Solutions, 10 July 2002, Cambridge, UK. Abstract Book.

87. INTERNATIONAL WORKSHOP: Individual Susceptibility to Noise Damage, 19-20 July 2002, Novartis Foundation, London, UK. Abstract Book.

88. INTERNATIONAL WORKSHOP: Noise Pollution: Health Effects on Children, 5-7 October 2002, Berlin, Germany. Abstract Book.

89. INTERNATIONAL CONFERENCE: NOPHER 2002-Nordic Noise II, 24-27 Oct 2002, Stockholm, Sweden. Abstract Book.

90. INTERNATIONAL WORKSHOP: NOPHER Co-ordinators Meeting, 18 January 2003, Novartis Foundation, London, UK. Abstract Book.

91. INTERNATIONAL WORKSHOP: WHO/NOPHER Meeting: Combined Environmental Pollutants and Health, 16-18 June 2003, Bonn, Germany. Abstract Book.

92. NOPHER Newsletter: Journal of Noise and Health Volume 4 issue 15.

93. NOPHER Newsletter: Journal of Noise and Health Volume 4 issue 16.

94. NOPHER Newsletter: Journal of Noise and Health Volume 5 issues 17.

95. NOPHER Newsletter: Journal of Noise and Health Volume 5 issues 18.

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