Skip Navigation


European Heart Journal Advance Access originally published online on February 12, 2008
European Heart Journal 2008 29(5):658-664; doi:10.1093/eurheartj/ehn013
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrowOA All Versions of this Article:
29/5/658    most recent
ehn013v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Haralabidis, A. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Haralabidis, A. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

Acute effects of night-time noise exposure on blood pressure in populations living near airports

Alexandros S. Haralabidis1, Konstantina Dimakopoulou1, Federica Vigna-Taglianti2, Matteo Giampaolo3, Alessandro Borgini4, Marie-Louise Dudley5, Göran Pershagen6, Gösta Bluhm6, Danny Houthuijs7, Wolfgang Babisch8, Manolis Velonakis9, Klea Katsouyanni1,*, Lars Jarup for the HYENA Consortium5

1 Department of Hygiene and Epidemiology, Medical School, National and Kapodistrian University of Athens, 75, Mikras Asias Street, Athens 11527, Greece
2 Environmental Epidemiologic Unit, Regional Agency for Environmental Protection, Piedmont Region, Grugliasco, Italy
3 Regional Agency for Environmental Protection, Lombardy Region, Milan, Italy
4 Cancer Register and Environmental Epidemiology Unit, National Cancer Institute, Milan, Italy
5 Department of Epidemiology and Public Health, Imperial College London, London, UK
6 Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
7 The National Institute for Public Health and the Environment, Bilthoven, The Netherlands
8 Department of Environmental Hygiene, Federal Environmental Agency, Berlin, Germany
9 Laboratory of Prevention, Nurses School, University of Athens, Athens, Greece

Received 17 September 2007; revised 11 December 2007; accepted 7 January 2008; online publish-ahead-of-print 12 February 2008.

* Corresponding author. Tel: +30 210 746 2087, Fax: +30 210 746 2205, Email: kkatsouy{at}med.uoa.gr


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Funding
 Acknowledgements
 References
 
Aims: Within the framework of the HYENA (hypertension and exposure to noise near airports) project we investigated the effect of short-term changes of transportation or indoor noise levels on blood pressure (BP) and heart rate (HR) during night-time sleep in 140 subjects living near four major European airports.

Methods and results: Non-invasive ambulatory BP measurements at 15 min intervals were performed. Noise was measured during the night sleeping period and recorded digitally for the identification of the source of a noise event. Exposure variables included equivalent noise level over 1 and 15 min and presence/absence of event (with LAmax > 35 dB) before each BP measurement. Random effects models for repeated measurements were applied. An increase in BP (6.2 mmHg (0.63–12) for systolic and 7.4 mmHg (3.1, 12) for diastolic) was observed over 15 min intervals in which an aircraft event occurred. A non-significant increase in HR was also observed (by 5.4 b.p.m.). Less consistent effects were observed on HR. When the actual maximum noise level of an event was assessed there were no systematic differences in the effects according to the noise source.

Conclusion: Effects of noise exposure on elevated subsequent BP measurements were clearly shown. The effect size of the noise level appears to be independent of the noise source.

Key Words: Environmental noise • Blood pressure • Night-time sleep • Acute effects • Epidemiological study


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Funding
 Acknowledgements
 References
 
Noise, defined as undesirable sound, is known to be a stress stimulus that can produce acute blood pressure (BP) elevation in animals1 and in humans in laboratory or occupational settings.2

Persons exposed to high-level noise (including recorded industrial or transportation noise) in the laboratory showed BP rises during the stimulus and for seconds to minutes after its cessation.3–6 In field studies, workers exposed to high-level industrial noise and having their BP measured via ambulatory BP monitoring (ABPM) showed BP increments during exposure and for a few hours after.7,8 Although sound levels of transportation (mainly aircraft and road traffic) noise are usually lower, they may produce cardiovascular effects via the neuroendocrine system by causing emotional reactions and annoyance through interference with the individual’s mental tasks, relaxation or sleep, at cortical (conscious) or subcortical level.9–11 Indeed, systolic BP responses to moderate noise in field conditions were more consistent than those to intense noise in a laboratory on the same individuals.12 Moreover, cardiovascular responses of the same individuals have been found greater during sleep than during wakefulness.13 In a sleep laboratory, BP and heart rate (HR) increments were traced after tonal acoustic stimuli or recorded transportation noise; arousal was not needed for sound to produce cardiovascular effects.14,15 Noise disturbance during sleep is regarded as one of the most important aspects of environmental noise exposure with possible effects on health.11,13,16 However, field studies on the effects of noise on BP during sleep in real life conditions are lacking.

In the present study the effect of environmental noise on BP and HR during night-time sleep of persons living in the vicinity of four major European airports was investigated within the wider framework of the HYENA (hypertension and exposure to noise near airports) project.17


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Funding
 Acknowledgements
 References
 
Sampling
The sample for the present study was selected from the main sample of the HYENA project17 and consisted of subjects living around four European airports with night flights: Athens (Greece), Malpensa (Italy), Arlanda (Sweden) and London Heathrow (UK). The initial sample for the HYENA study17 was 6000 persons living in the vicinity of the study airports. A total of 4861 persons (2404 men and 2457 women) between 45 and 70 years old at the time of interview participated in the study. The samples were representative from the populations exposed to various levels of aircraft and traffic noise around airports based on noise contours. Participation rates differed between the countries, from circa 30% in Italy and the UK, to 56% in Greece and 78% in Sweden. More details may be found in Jarup et al.18 We selected subjects from various aircraft noise exposure categories, as assessed by the A-weighted annual equivalent noise level LAeq24h based on their residence, in order to obtain a larger variability in noise exposure situations.

The following exclusion criteria were applied: (1) antihypertensive medication, (2) diagnosis of diabetes mellitus, (3) diagnosis of obstructive sleep apnoea syndrome, (4) diagnosis of secondary hypertension, (5) working in night shift, (6) using sleeping pills and sedatives, (7) diagnosis of hearing impairment, (8) regular use of earplugs, (9) diagnosis of atrial fibrillation. Criteria 1–6 were applied as they affect the night-time BP; criteria 7 and 8 as they modify noise exposure; and criterion 9 as it hinders ABPM. Twenty-one subjects were excluded due to technical problems with the monitoring equipment. The final sample consisted of 140 subjects (Table 1). Approval for the study was granted by each centre’s Ethical Committee.


View this table:
[in this window]
[in a new window]

  		Table 1 Descriptive characteristics of the 140 study subjects

 
Measurements and data management
Continuous noise measurement with the type I ‘CESVA SC310’ noise-meter19 (time constant ‘fast’ 125 ms) as well as noise recording with an MP3 recorder connected to the noise-meter’s high-quality microphone were done during the study night in each participant’s bedroom. Each participant was followed up for one night. The noise level equivalents for every second, for every 1 min before and for every 15 min period between BP measurements were calculated as follows:



Formula

where t is the 1 min or 15 min period in seconds.

Using playback and visualization of sound recordings on a computer, the source of each event was identified and synchronized with the sound measurements with a program written for this purpose. An event was defined as present if its indoor LAmax exceeded 35 dB. Noise events were classified into four categories according to source: indoor, aircraft, road traffic, and other outdoor. Other outdoor events were very rare and thus excluded from the analysis.

Non-invasive 24 h ABPM, with HR measurements, was performed at 15 min intervals with the validated ‘Mobilograph’ device,20,21 including the study night. The 15 min frequency has been implemented before7 and was chosen as optimal for frequent measurements without excessive sleep disturbance. The three instruments (noise meter, noise recorder, and ABPM device) and the participants’ alarm clock were synchronized at 1 min precision.

Specially trained nurses installed the noise equipment, placed the ABPM device on the participants and gave them written instructions, during a home visit at least 3 h before normal sleeping time. Each participant was instructed not to engage in unusually heavy activity during the measurements’ period and filled in a sleep log indicating actual sleeping times.

Statistical analysis
Linear mixed models which included random intercept and random coefficients for the various noise indicators were applied for each centre separately in order to assess acute effects of noise on BP and HR during night-time sleep. The number of repeated measurements per subject corresponds to the number of systolic and diastolic BP measurements (mmHg), as well as HR measurements (beats per minute—b.p.m.) during the self-reported sleeping period. The A-weighted indoor noise level equivalents of 1 min (LAeq1min) and of 15 min (LAeq15min) before BP measurements were used as short-term noise exposure variables. In this type of model, where an individual serves as his own ‘control’, there is no need to adjust for individual confounding factors. In order to account for the possible confounding effect of misreporting of sleeping and waking times (potentially associated with both BP and noise levels), the above noise exposure variables were also adjusted for the sequence of BP measurements, using 2 linear terms. The first linear term denoted the sequence of the BP measurements (1,2, ... ,k) from the start to the middle of each persons sleep period and the second denoted the sequence of the BP measurements (1,2, ... ,k) from the middle to the end of each persons sleep period. Other noise exposure variables were the presence or absence of a source-specific noise event during the 15 min periods and each source-specific event’s LAmax. If more than one event were present in the 15 min interval, the higher LAmax was used. Since a noise stimulus may not have the same effect in the presence of other noise, in all models assessing the source-specific noise, we adjusted for the 10th percentile of the noise level equivalent (L90) in all the 15 min intervals. After obtaining the four centre-specific effects using random effect models, we then combined the centre-specific results using either fixed or random effects meta-analysis depending on the absence or presence of heterogeneity. All reported P-values are based on two-sided hypotheses and the significance level used was 5%.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Funding
 Acknowledgements
 References
 
Table 1 shows the descriptive characteristics of the samples. The mean number of repeated BP measurements per night was similar in all centres (range 29–32). BP and HR displayed a normal distribution (data not shown). The number of aircraft events during the night-time sleep was higher in Athens compared with the other centres. The presence of subjects with no or few night aircraft events was explained by the sampling procedure through which a number of subjects were selected from the main sub-sample of low exposure to aircraft noise. In Milan and Stockholm, the number of indoor events was much larger than aircraft or traffic events. The median equivalent noise levels (LAeq15min, LAeq1min) for all centres were comparable. Also the source-specific LAmax (aircraft, road or indoor) was similar in the four samples (Figure 1).


Figure 1
View larger version (31K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 1 Box plots of the various noise indicators measured during the study night

 
Table 2 shows the pooled effect estimates of the noise exposure indicators on BP and HR. The measured noise 1 and 15 min before each BP measurement was associated with higher systolic and diastolic BP and with higher HR. For example, a 5 dB increment in LAeq15min was associated with a 0.63 mmHg increase in diastolic BP. The magnitude of the effect on BP was somewhat lower when the LAeq1min was considered but remains statistically significant. The effect remains similar when adjustment was applied for the sequence of measurements during sleep time. An increase in BP (6.2 mmHg for systolic, 7.4 mmHg for diastolic) and HR (by 5.4 b.p.m.) was observed over 15 min intervals in which an aircraft event occurs but for HR this was not statistically significant. A similar magnitude of increase in BP was observed during time periods with traffic or indoor source event. In contrast, the effect on HR was smaller during periods with indoor events and was not observed over periods with traffic events. When the actual noise level assessed by LAmax was taken into account (adjusting for the presence of an event from a specific source and for L90), a positive association was found between noise from all the three sources and BP, which was statistically significant and similar to the effect of measured noise from all sources. The corresponding effects on HR were lower than those from all sources and reached statistical significance only for indoor source noise.


View this table:
[in this window]
[in a new window]

  		Table 2 Pooled effect estimates of various noise indicators on blood pressure (BP) and heart rate (HR) measurements. Results from fixed effects models (except where noted)

 
The estimated effects of noise exposure on BP were consistent in each sample. The estimated effects on diastolic BP of measured noise by sample are shown in Figure 2. The estimates were practically identical for the three samples, whilst for London they were higher but associated with wider confidence intervals. In Figure 3 a consistent pattern may be seen for the effects of source-specific noise in the four samples. The corresponding results for systolic BP were similar, with the exception of significant heterogeneity in the effects of indoor source noise events where the effect was highest in London and lowest in Stockholm, the only non-statistically significant effect. The effects for HR were less consistent between centres. However, the only model which displayed statistically significant heterogeneity was the one assessing the presence of aircraft events.


Figure 2
View larger version (12K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 2 Centre-specific and pooled effect estimates of a 5 dB(A) increment in the equivalent noise level of 15 min (red) and 1 min (blue) before blood pressure (BP) measurement on diastolic BP

 

Figure 3
View larger version (11K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 3 Centre-specific and pooled effect estimates on diastolic blood pressure (BP) and its 95% confidence Interval (CI) associated with an increase of 5 dB in LAmax of aircraft event (red), of road traffic event (blue) and of indoor event (black) during night-time sleep (source-specific event identified as present if indoor measured LAmax >35 dB)

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Funding
 Acknowledgements
 References
 
We studied the effect of noise on BP during sleep, a state of reduced sympathetic and increased parasympathetic autonomous nervous system (ANS) tone, leading to a decrease of BP and HR.22

We found that both systolic and diastolic BP levels as well as HR increased with higher noise levels during the preceding minutes, independently of the noise source and of the sequence of the measurement during sleep time, which indicates absence of habituation during the study night, a matter of controversy in studies on humans or on experimental animals.13,23 These results are consistent with those reported by Carter et al.15 in a laboratory where both BP and HR increased after noise stimuli. There are major differences between laboratory and real life conditions. In a laboratory, background noise is steady whilst in real life conditions the analysis has to adjust for variable noise sources. Davies et al.14 studied five subjects and found an increase in diastolic BP from 4 to 6 mmHg associated with arousal according to sleep stage. We found an increase of 6–7 mmHg in diastolic BP according to the source of the noise event, not necessarily associated with awakening.

We also found significant increases in BP and, less consistently, HR when the source of the noise was taken into account. The effects of the source-specific noise were comparable for aircraft, traffic, and indoor events and were similar to those of the total measured noise.

In our study, one common source of indoor noise was snoring. Since in some cases the study subject is expected to be the snorer too (we could not assess this information) and his BP elevation could be due to disordered breathing,24,25 the effect of indoor noise on BP that we report could be overestimated.

The effect of the measured noise level as well as the source-specific noise was weaker and less consistent on HR than on BP. This finding is in accordance with results from a sleep laboratory study15 where a noise threshold was detected for the effects on HR but not on BP and with previously reported mechanisms of BP rise following noise exposure, which refer mainly to vasoconstriction.2,26 Moreover, HR has a stronger circadian component which may mask other effects.27

The remarkable consistency of the estimated effects between the four centres strengthens the evidence for causality. The effects of noise exposure on BP per specific increase in noise levels were found similar in the four samples in spite of the fact that there were differences in the profiles of noise according to the source during the night. However, the indoor LAmax levels in the presence of an event were comparable in all the four centres.

In sleep laboratories, noise stimuli of levels comparable with those of real life produced cardiovascular responses for seconds.13,14 However, in occupational or laboratory settings, BP elevations have been found to last for minutes or even hours6–8 during wakefulness. Emotional responses such as anger or fear may magnify and prolong the effects, during night-time exposure to aircraft noise in real life conditions.9 One drawback of our study is that BP was assessed every 15 min although the noise event could have happened anytime within this interval. As expected, the distribution of noise events over the 15 min intervals between BP measurements is uniform. Only 5–11.5% of events (the range reflects different sources and samples) occurred during the minute of measurement (6.7% expected). The design of our study might have led to the ‘loss’ of the effect on BP or HR if the noise event happened to occur during the first minutes of intervals between measurements and the effect was of short duration. However, the fact that the effects of noise during the preceding 1 and 15 min were of similar magnitude indicates more prolonged effects.

In this study, the indoor LAmax threshold for characterizing an event as ‘present’ was set at 35 dB. Awakening reactions are usually observed at LAmax values over 40–45 dB in the bedroom but recently lower thresholds have been also suggested.11,28 However, according to sleep laboratory studies, haemodynamic changes can also occur at lower noise levels than the ones that cause EEG changes, although the effects are stronger when arousal coexists.13,14 Indeed, autonomic responses like BP elevation have been used as a sensitive marker of sleep disturbance.29,30 The finding that consciousness is not needed for sound to produce its cardiovascular effects is also supported by experiments in which anaesthetized animals demonstrated BP increment when exposed to intense noise31 or BP reduction when exposed to music.32,33 These outcomes are attributed to the subcortical connections of the auditory pathway with the ANS (amygdala, hippocampus, hypothalamus)10 and justify the use of relatively low noise thresholds in the research of noise effects on BP during sleep.

To assess nocturnal BP, we used ABPM, which has been validated and used extensively for this purpose.19,20 ABPM has been reported to affect sleep and night-time BP34 during the cuff’s inflation similarly to noise arousal stimuli,14 although it is also supported, by means of intra-arterial recordings, that ABPM does not attenuate night-time BP reduction.35 In any case, it can be argued that there is synergy and that the effects of noise would not be the same in the absence of ABPM during the study night. Because of this possibility, the frequency of BP measurements was kept at four per hour, although up to six measurements per hour have been used before.36 Moreover, the body position during sleep can affect the ABPM measurements.37 All measurements however in our study, irrespective of noise exposure level, were done with ABPM and there is no reason to assume that body position during sleep is related to noise exposure. The use of portable, non-invasive BP recorders that register BP continuously and correct automatically hydrostatic effects,38 can be considered in future studies investigating the effect of noise on night-time BP in real life conditions.

Within the HYENA project we found effects of long-term noise exposure on the prevalence of hypertension18 and the acute effects reported here. Absence of short-term habituation to the cardiovascular effects of noise, especially those during sleep, found here and also reported before,13,16,39 as well as evidence from studies on sleep-disorder which indicate that repeated arousals are associated with a sustained increase in daytime BP,40 support a link between acute and long-term effects of noise exposure on hypertension41,42 and cardiovascular disease,43 in line with the general stress theory.44


   Funding
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Funding
Acknowledgements
 References
 
European Commission DG Research contract number (QLK4 CT-2002-02501). Funding to pay the Open Access publication charges for this article was provided by the University of Athens Special Account for Research.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Funding
 Acknowledgements
References
 
We thank all the participants for their willingness to contribute. The HYENA study was funded by the European Commission DG Research (QLK4-CT-2002-02501) in the Fifth framework programme, Quality of life and management of living resources. We thank the members of the HYENA study team Joy Read, Yvonne Tan, Yousouf Soogun, Gabriele Wölke, Jessica Kwekkeboom, Birgitta Ohlander, Eva Thunberg, Elli Davou, Yannis Zahos, Venetia Velonaki, Ageliki Athanasopoulou, Alessandro Borgini, Maria Chiara Antoniotti, Salvatore Pisani, Giorgio Barbaglia, Matteo Giampaolo, Anders Lundin, and Jenny Selander for assistance during various parts of the study.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Funding
 Acknowledgements
 References
 

  1. Baudrie V, Laude D, Chaouloff F, Elghozi JL. Genetic influences on cardiovascular responses to an acoustic startle stimulus in rats. Clin Exp Pharmacol Physiol (2001) 28:1096–1099.[CrossRef][ISI][Medline]
  2. Andren L, Hansson L, Eggertsen R, Hedner T, Karlberg BE. Circulatory effects of noise. Acta Med Scand (1983) 213:31–35.[ISI][Medline]
  3. Andren L, Hansson L, Bjorkman M, Jonsson A. Noise as a contributory factor in the development of elevated arterial pressure. A study of the mechanisms by which noise may raise blood pressure in man. Acta Med Scand (1980) 207:493–498.[ISI][Medline]
  4. Michalak R, Ising H, Rebentisch E. Acute circulatory effects of military low-altitude flight noise. Int Arch Occup Environ Health (1990) 62:365–372.[CrossRef][ISI][Medline]
  5. Holand S, Girard A, Meyer-Bisch C, Elghozi JL. [Cardiovascular responses to a acoustic startle stimulus in man][Article in French]. Arch Mal Coeur Vaiss (1999) 92:1127–1131.[ISI][Medline]
  6. Mahmood R, Khan GJ, Alam S, Safi AJ, Salahuddin, Amin-ul-Haq. Effect of 90 decibel noise of 4000 hertz on blood pressure in young adults. J Ayub Med Coll Abbottabad (2004) 16:30–33.[Medline]
  7. Fogari R, Zoppi A, Corradi L, Marasi G, Vanasia A, Zanchetti A. Transient but not sustained blood pressure increments by occupational noise. An ambulatory blood pressure measurement study. J Hypertens (2001) 19:1021–1027.[CrossRef][ISI][Medline]
  8. Chang TY, Jain RM, Wang CS, Chan CC. Effects of occupational noise exposure on blood pressure. J Occup Environ Med (2003) 45:1289–1296.[CrossRef][ISI][Medline]
  9. Ising H, Kruppa B. Health effects caused by noise: evidence in the literature from the past 25 years. Noise Health (2004) 6:5–13.[Medline]
  10. Spreng M. Central nervous system activation by noise. Noise Health (2000) 2:49–58.[Medline]
  11. Babisch W. Noise and health. Environ Health Perspect (2005) 113:A14–A15.[ISI][Medline]
  12. Ising H, Michalak R. Stress effects of noise in a field experiment in comparison to reactions to short term noise exposure in the laboratory. Noise Health (2004) 6:1–7.[Medline]
  13. Di Nisi J, Muzet A, Ehrhart J, Libert JP. Comparison of cardiovascular responses to noise during waking and sleeping in humans. Sleep (1990) 13:108–120.[ISI][Medline]
  14. Davies RJ, Belt PJ, Roberts SJ, Ali NJ, Stradling JR. Arterial blood pressure responses to graded transient arousal from sleep in normal humans. J Appl Physiol (1993) 74:1123–1130.[Abstract/Free Full Text]
  15. Carter N, Henderson R, Lal S, Hart M, Booth S, Hunyor S. Cardiovascular and autonomic response to environmental noise during sleep in night shift workers. Sleep (2002) 25:457–464.[ISI][Medline]
  16. Carter NL. Transportation noise, sleep, and possible after-effects. Environ. Int. (1996) 22:105–116.[ISI]
  17. Jarup L, Dudley ML, Babisch W, Houthuijs D, Swart W, Pershagen G, Bluhm G, Katsouyanni K, Velonakis M, Cadum E, Vigna-Taglianti F, HYENA Consortium. Hypertension and exposure to noise near airports (HYENA): study design and noise exposure assessment. Environ Health Prespect (2005) 113:1473–1478.
  18. Jarup L, Babisch W, Houthuijs D, Pershagen G, Katsouyanni K, Cadum E, Dudley ML, Savigny P, Seiffert I, Swart W, Breugelmans O, Bluhm G, Selander J, Haralabidis A, Dimakopoulou K, Sourtzi P, Velonakis M, Vigna-Taglianti F, for the HYENA Consortium. Hypertension and exposure to noise near airports—the HYENA study. Environ Health Perspect (2008) (in press).
  19. http://datasheets.cesva.com/sc310_eng.pdf.
  20. Staessen JA, O’Brien ET, Thijs L, Fagard RH. Modern approaches to blood pressure measurement. Occup Environ Med (2000) 57:510–520.[Abstract/Free Full Text]
  21. Jones CR, Taylor K, Chowienczyk P, Poston L, Shennan AH. A validation of the Mobil O Graph (version 12) ambulatory blood pressure monitor. Blood Press Monit (2000) 5:233–238.[CrossRef][ISI][Medline]
  22. Van de Borne P, Nguyen H, Biston P, Linkowski P, Degaute JP. Effects of wake and sleep stages on the 24-h autonomic control of blood pressure and heart rate in recumbent men. Am J Physiol Heart Circ Physiol (1994) 266:H548–H554.[Abstract/Free Full Text]
  23. Blanc J, Baudrie V, Tulen J, Ponchon P, Gaudet E, Elghozi JL. Social isolation affects the pattern of cardiovascular responses to repetitive acoustic startle stimuli. Clin Exp Pharmacol Physiol (1997) 24:40–45.[CrossRef][ISI][Medline]
  24. Guilleminault C, Stoohs R, Clerk A, Simmons J, Labanowski M. From obstructive sleep apnea syndrome to upper airway resistance syndrome: consistency of daytime sleepiness. Sleep (1992) 15(Suppl. 6):S13–S16.[ISI][Medline]
  25. Portaluppi F, Cortelli P, Provini F, Plazzi G, Manfredini R, Lugaresi E. Alterations of sleep and circadian blood pressure profile. Blood Press Monit (1997) 2:301–313.[Medline]
  26. Girard A, Holand S, Laude D, Elghozi J. Antihypertensive monotherapy and cardiovascular responses to an acoustic startle stimulus. J Cardiovasc Pharmacol (2001) 37:101–107.[CrossRef][ISI][Medline]
  27. Van Dongen HP, Maislin G, Kerkhof GA. Repeated assessment of the endogenous 24-hour profile of blood pressure under constant routine. Chronobiol Int (2001) 18:85–98.[CrossRef][ISI][Medline]
  28. Basner M, Buess H, Mueller U, Plath G, Samel A. Aircraft Noise Effects on Sleep: Final Results of DLR Laboratory and Field Studies of 2240 Polysomnographically Recorded Subject Nights. (2004) 33rd International Congress and Exposition on Noise Control Engineering (Internoise 2004), 22–25. 08: Prague/Czech Republic.
  29. Ali NJ, Davies RJ, Fleetham JA, Stradling JR. Periodic movements of the legs during sleep associated with rises in systemic blood pressure. Sleep (1999) 14:163–165.
  30. Pillar G, Bar A, Shlitner A, Schnall R, Shefy J, Lavie P. Autonomic arousal index: an automated detection based on peripheral arterial tonometry. Sleep (2002) 25:541–547.
  31. Flynn AJ, Dengerink HA, Wright JW. Blood pressure in resting, anesthetized and noise-exposed guinea pigs. Hear Res (1988) 34:201–205.[CrossRef][ISI][Medline]
  32. Nakamura T, Tanida M, Niijima A, Hibino H, Shen J, Nagai K. Auditory stimulation affects renal sympathetic nerve activity and blood pressure in rats. Neurosci Lett (2007) 416:107–112.[CrossRef][ISI][Medline]
  33. Sutoo D, Akiyama K. Music improves dopaminergic neurotransmission: demonstration based on the effect of music on blood pressure regulation. Brain Res (2004) 1016:255–262.[CrossRef][ISI][Medline]
  34. Heude E, Bourgin P, Feigel P, Escourrou P. Ambulatory monitoring of blood pressure disturbs sleep and raises systolic pressure at night in patients suspected of suffering from sleep-disordered breathing. Clin Sci (Lond) (1996) 91:45–50.[Medline]
  35. Villani A, Parati G, Groppelli A, Omboni S, Di Rienzo M, Mancia G. Noninvasive automatic blood pressure monitoring does not attenuate nighttime hypotension. Evidence from 24 h intraarterial blood pressure monitoring. Am J Hypertens (1992) 5:744–747.[ISI][Medline]
  36. Schwartz GL, Turner ST, Moore JH, Sing CF. Effect of time of day on intraindividual variability in ambulatory blood pressure. Am J Hypertens (2000) 13:1203–1209.[CrossRef][ISI][Medline]
  37. Van der Steen MS, Pleijers AM, Lenders JW, Thien T. Influence of different supine body positions on blood pressure: consequences for night blood pressure/dipper-status. Blood Press Monit (2000) 18:1731–1736.
  38. Schmidt TF, Wittenhaus J, Steinmetz TF, Piccolo P, Lupsen H. Twenty-four-hour ambulatory noninvasive continuous finger blood pressure measurement with PORTAPRES: a new tool in cardiovascular research. J Cardiovasc Pharmacol (1992) 19(Suppl. 6):S117–S145.[CrossRef]
  39. Muzet A, Ehrhart J, Eschenlauer R, Lienhard JP. Habituation and age differences of cardiovascular response to noise during sleep. (1980) 5th Congress on Sleep Research: Amsterdam. Basel: Karger. 212–215. Sleep.
  40. Morrell MJ, Finn L, Kim H, Peppard PE, Badr MS, Young T. Sleep fragmentation, awake blood pressure, and sleep-disordered breathing in a population-based study. Am J Respir Crit Care med (2000) 162:2091–2096.[Abstract/Free Full Text]
  41. Rosenlund M, Berglind N, Pershagen G, Jarup L, Bluhm G. Increased prevalence of hypertension in a population exposed to aircraft noise. Occup Environ Med (2001) 58:769–773.[Abstract/Free Full Text]
  42. Eriksson C, Rosenlund M, Pershagen G, Hilding A, Ostenson CG, Bluhm G. Aircraft noise and incidence of hypertension. Epidemiology (2007) 18:716–721.[Medline]
  43. Babisch W, Beule B, Schust M, Kersten N, Ising H. Traffic noise and risk of myocardial infarction. Epidemiology (2005) 16:33–40.[CrossRef][ISI][Medline]
  44. Henry JP. Biological basis of the stress response. News Physiol Sci (1993) 8:69–73.[Abstract/Free Full Text]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?



This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrowOA All Versions of this Article:
29/5/658    most recent
ehn013v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Haralabidis, A. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Haralabidis, A. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?