Aircraft noise and cardiovascular disease near Heathrow airport in London: small area studyBMJ 2013; 347 doi: https://doi.org/10.1136/bmj.f5432 (Published 08 October 2013) Cite this as: BMJ 2013;347:f5432
All rapid responses
Kolstad and colleagues cite largely negative results of a large Danish study of occupational noise exposure, hypertension (based on registry data)  and stroke  to question whether results of our study on aircraft noise and cardiovascular disease may reflect confounding rather than causal associations. Occupational studies are subject to the ‘healthy worker’ bias – for example, those prone to ill-health related to noise exposure are more likely to leave or never start working in occupations with high noise exposures; while adjustment was made for early leavers in the study some residual bias may remain. Further, the widespread use of hearing protection devices in noisy occupations is likely to influence this relationship, which the authors were not able to adjust for. A meta-analysis of 15 occupational studies published 1991-2007 (i.e. some relating to exposures prior to widespread use of hearing protection devices) showed associations between high occupational noise exposure and hypertension and ECG abnormalities , which this later study did not.
Findings for cortisol in long-term exposure studies are more mixed. Kolstad and colleagues did not find an association with morning salivary cortisol in their occupational study . However, the Hypertension and Exposure to Environmental Noise around Airports (HYENA) population-based study found salivary cortisol was raised in women but not men in association with 24 hour average aircraft noise exposure .
Published research into potential health effects of environmental noise exposure is expanding. For example, a recently published long-term prospective cohort study with careful consideration of confounders including smoking found long-term exposure to fine particulate air pollution (PM10) and night-time traffic noise were both independently associated with subclinical atherosclerosis . A recently published experimental field study of short-term effects of aircraft noise exposure at night  found noise was associated with increases in plasma adrenaline (but not cortisol), decreases in pulse transit time (a measure of arterial stiffness) and a dose-dependent effect on endothelial dysfunction.
Ongoing evaluation of evidence from a range of studies in different settings with different designs including occupational, cohort and experimental such as these is needed to help clarify the possible relationship between noise exposure and cardiovascular disease.
 Stokholm ZA, Bonde JP, Christensen KL, Hansen AM, Kolstad HA. Occupational noise exposure and the risk of hypertension. Epidemiology 2013; 24(1):135-42.
 Stokholm ZA, Bonde JP, Christensen KL, Hansen AM, Kolstad HA. Occupational noise exposure and the risk of stroke. Stroke 2013; 44(11):3214-6.
 Tomei G, Fioravanti M, Cerratti D, Sancini A, Tomao E, Rosati MV et al. Occupational exposure to noise and the cardiovascular system: A meta-analysis. Sci total environ 2010; 408(4):681-689
 Stokholm ZA, Hansen ÅM, Grynderup MB, Bonde JP, Christensen KL, Frederiksen TW, et al. Recent and long-term occupational noise exposure and salivary cortisol level. Psychoneuroendocrinology 2014; 1;39(0):21-32
 Selander, J, Bluhm, G, Theorell, T, Pershagen, G, Babisch, W, Seiffert, I et al. Saliva cortisol and exposure to aircraft noise in six European countries. Environ health persp, 2009; 117(11), 1713–1717.
 Kälsch H, Hennig F, Moebus S, Möhlenkamp S, Dragano N, Jakobs H et al. Are air pollution and traffic noise independently associated with atherosclerosis: the Heinz Nixdorf Recall Study. Eur Heart J 2013; Nov [Epub ahead of print]
 Schmidt FP, Basner M, Kröger G, Weck S, Schnorbus B, Muttray A, Sariyar M, Binder H, Gori T, Warnholtz A, Münzel T. Effect of nighttime aircraft noise exposure on endothelial function and stress hormone release in healthy adults. Eur Heart J 2013;34(45):3508-14
Competing interests: The authors declare: financial support for the submitted work through the funding of the UK Small Area Health Statistics Unit by Public Health England as part of the MRC-PHE Centre for Environment and Health, funded also by the UK Medical Research Council; financial support from the European Network for Noise and Health (ENNAH), EU FP7 grant No 226442; PE acknowledges support from the National Institute for Health Research (NIHR) Biomedical Research Centre based at Imperial College Healthcare NHS Trust and Imperial College London; PE is an NIHR Senior Investigator; ALH declares consultancy fees from AECOM as part of a Defra report on health effects of environmental noise; ALH declares a Greenpeace membership but has not received any money from the organisation nor been involved in campaigns; nor other relationships or activities that could appear to have influenced the submitted work.
Hansell et al respond to my suggestion of shift work as a confounder by saying "We think this is an unlikely explanation ─ stroke and coronary heart disease are most common in older individuals who are less likely to be in the workforce."
Although their statement is of course true, 1/3 of strokes are thought to occur in those under 65 and although I have no data but personal experience of them as patients there are quite a few people above the age of 65 who continue to work at Heathrow. I therefore do not think shift work as a confounder can be that easily dismissed.
Competing interests: I live on the flight path
Studies addressing health risks from occupational noise exposure may contribute to the interpretation of Hansell and colleagues’ findings of increasing risk of stroke, coronary heart disease, and cardiovascular disease with higher levels of aircraft noise at the residence. Recently, we did a follow-up of 100,000 blue-collar industrial workers and although we had sufficient power, we observed no increasing risk of stroke or hypertension by increasing noise exposure level above 80 dB(A) on normal working days.[2, 3] Contrary to the study by Hansell and colleagues, these analyses included information on long-term noise exposure and showed no trend by cumulative exposure. Such information is crucial because the extra-auditive effects of noise are not expected to be due to transient but long-term exposure. The occupational noise levels were furthermore orders of magnitude higher than the community aircraft noise levels. Therefore these analyses were more likely to detect cardiovascular effects unless it is hypothesized that leisure time exposure is crucial, for example through disruption of sleep.
Residual confounding is a probable key to understanding the findings of Hansell et al. In our study population, occupational noise exposure levels were strongly related to socioeconomic status, age, sex, income, smoking, and BMI, all being well-documented risk factors for cardiovascular disease. Interestingly, the level of occupational noise was also strongly associated with the level of noise during leisure time as recorded by personal 24-hour dosimeters. Hansell and colleagues had no access to individual level but only small area level information on a limited set of potential confounders. Adjusting for these reduced risk estimates considerably but we question if this, as the authors adequately discuss, eliminated residual confounding.
A final comment; if Hansell and colleagues’ observations represent casual effects, what is then the mechanism? They suggest, among other possibilities, increase in stress hormone levels. Activation of the hypothalamic-pituitary-adrenal axis and release of cortisol are considered major components of the stress response in humans. However, we observed no effect of recent or long-term occupational noise exposure level on salivary cortisol concentration in 500 noise-exposed workers; a finding that should also apply to community aircraft noise unless the effect on cortisol is not merely a question of noise exposure level.
In our opinion, it is thus still unsolved if noise exposure may cause stroke or hypertension. The annoying effect by increasing levels of noise from aircraft, train, and road traffic is, on the other hand, documented beyond any doubt and deserves policy response.
1. Hansell AL, Blangiardo M, Fortunato L, Floud S, de Hoogh K, Fecht D, et al. Aircraft noise and cardiovascular disease near Heathrow airport in London: small area study. BMJ 2013; Oct 8;347:f5432.
2. Stokholm ZA, Bonde JP, Christensen KL, Hansen AM, Kolstad HA. Occupational noise exposure and the risk of hypertension. Epidemiology 2013; Jan;24(1):135-42.
3. Stokholm ZA, Bonde JP, Christensen KL, Hansen AM, Kolstad HA. Occupational noise exposure and the risk of stroke. Stroke 2013; Nov;44(11):3214-6.
4. Basner M, Babisch W, Davis A, Brink M, Clark C, Janssen S, et al. Auditory and non-auditory effects of noise on health. Lancet 2013; Oct 29;.
5. Stokholm ZA, Hansen ÅM, Grynderup MB, Bonde JP, Christensen KL, Frederiksen TW, et al. Recent and long-term occupational noise exposure and salivary cortisol level. Psychoneuroendocrinology 2014; 1;39(0):21-32.
6. Kirschbaum C, Hellhammer DH. Noise and Stress - Salivary Cortisol as a Non-Invasive Measure of Allostatic Load. Noise Health 1999;1(4):57-66.
7. Miedema HM, Oudshoorn CG. Annoyance from transportation noise: relationships with exposure metrics DNL and DENL and their confidence intervals. Environ Health Perspect 2001; Apr;109(4):409-16.
Competing interests: No competing interests
In our recently published paper looking at aircraft noise and cardiovascular disease near Heathrow airport in London  we stated “As well as the possibility of causal associations, alternative explanations such as residual confounding ...should be considered.” Responses by Corbin, Moore, and Coebergh put forward candidates for these possible confounders.
Corbin suggests ultrafine particulate air pollution (PM0.1) from aircraft could be a potential explanation for our findings. While ultra-fine particles have been found to rise near the runway during take-off , we are unaware of data to suggest elevated levels from aircraft in well mixed air up to tens of kilometres away from the airport. PM0.1 is not a regulated pollutant in the UK, so we do not have readily available data to investigate this.
Moore questions the choice of confounders. Information on age, sex area-level ethnicity and lung cancer (as proxy for smoking) were adjusted for in our analyses, but information on e.g., hypertension, cholesterol, family history are not currently available within routine datasets at small-area scale. Also, care would be required in adjustment for hypertension if raised blood pressure lies on the causal pathway between aircraft noise and cardiovascular disease.
Coebergh raises the possibility that our findings reflect occupational hazards related to Heathrow. We think this is an unlikely explanation ─ stroke and coronary heart disease are most common in older individuals who are less likely to be in the work-force.
As we conclude in our paper “Further work to understand better the possible health effects of aircraft noise is needed”, which these rapid responses support.
 Hansell AL, Blangiardo M, Fortunato L, Floud S, de Hoogh K, Fecht D et al. Aircraft noise and cardiovascular disease near Heathrow airport in London: small area study. BMJ 2013;347:f5432
 Corbin, JC. [electronic response to Hansell AL, et al Aircraft noise and cardiovascular disease near Heathrow airport in London: small area study] BMJ 2013 http://www.bmj.com/content/347/bmj.f5432?tab=responses (accessed 07/11/13).
 Moore N. [electronic response to Hansell AL, et al Aircraft noise and cardiovascular disease near Heathrow airport in London: small area study] BMJ 2013 http://www.bmj.com/content/347/bmj.f5432?tab=responses (accessed 07/11/13).
 Coebergh, J. [electronic response to Hansell AL, et al Aircraft noise and cardiovascular disease near Heathrow airport in London: small area study] BMJ 2013 http://www.bmj.com/content/347/bmj.f5432?tab=responses (accessed 07/11/13).
 Zhu Y, Fanning E, Yu RC, Zhang Q, Froines JR. Aircraft emissions and local air quality impacts from takeoff activities at a large International Airport. Atmospheric Environment 2011;45:6526-6533
Competing interests: (As declared in our publication "Aircraft noise and cardiovascular disease near Heathrow airport in London: small area study") Financial support was provided through the funding of the UK Small Area Health Statistics Unit by Public Health England as part of the MRC-PHE Centre for Environment and Health, funded also by the UK Medical Research Council; financial support from the European Network for Noise and Health (ENNAH), EU FP7 grant No 226442; PE acknowledges support from the National Institute for Health Research (NIHR) Biomedical Research Centre based at Imperial College Healthcare NHS Trust and Imperial College London; PE is an NIHR Senior Investigator; ALH declares consultancy fees from AECOM as part of a Defra report on health effects of environmental noise; ALH declares a Greenpeace membership but has not received any money from the organisation nor been involved in campaigns; nor other relationships or activities that could appear to have influenced the submitted work.
Hansell and colleagues’ findings plus the numerous Letters to Editor that followed highlighted the impact of sleep disturbance on risks of cardiovascular diseases and their mortality. For instance, the relative risks for hospital admission for stroke, coronary heart disease (CHD) and cardiovascular disease (CVD) as reported by Hansell et al. was 1.29 (CI: 1.14 , 1.46), 1.12 (1.04, 1.20) and 1.09 (1.04, 1.14) respectively in the context of exposure to night time aircraft noise. The relative risks for mortality from the corresponding three conditions due to the same exposure was 1.23 (1.02, 1.49), 1.11 (0.99, 1.24) and 1.14 (1.03, 1.26) respectively. As such, the data suggested higher relative risks due to night time noise exposure for stroke, CHD and CVD in terms of hospital admissions and mortality.
Hansell et al’s research suggested possible mechanisms from the chronic exposure to night time noises leading to increased activation of the neuroendocrine system, subsequently resulting in heart rate and blood pressure increases. It will be interesting to know about the incidence and prevalence of insomnia in the boroughs and districts exposed to aircraft noise on a long-term basis, especially when it is known that noises which disrupt sleep is a common cause of insomnia. A Finnish study of night-time exposure to outdoor traffic explored the association of exposure to outside traffic noise of >55 dB with any insomnia symptom ≥ 2 nights per week. For the total study population, exposure to outside traffic noise was associated with any insomnia symptom at an odds ratio (OR) of 1.32 (1.05, 1.65). For subjects with anxiety traits, the OR is 1.61 (1.07 – 2.42). 
There has been a study which evaluated patients from Pennsylvania by Vgontzas and colleagues which explored the amount of sleep with risk of hypertension. They found that the highest risk of hypertension was in insomniac patients with <5 hours of sleep with an OR of 5.1 (2.2, 11.8). The second highest risk was in insomniacs who slept 5 – 6 hours with an OR of 3.5 (1.6, 7.9).  This led subsequently to the conclusion that insomnia with short sleep duration is associated with an increased risk for hypertension.
Another study evaluated the association of insomnia and short sleep duration with atherosclerosis in a vulnerable population – the elderly aged ≥ 65 years. Atherosclerosis was determined using ultrasonic measurement of carotid intima-media thickness (IMT). In patients with ≤ 5 hours of sleep, their IMT was 1.3 ± 0.5 vs 0.9 ± 0.3 mm (P = 0.009) in those who have > 7 hours of sleep. IMT was also determined to be larger in the insomniac group in comparison with the non-insomniac group at 1.3 ± 0.5 vs 1.1 ± 0.4 mm (P = 0.03). Furthermore, IMT was significantly correlated with systolic blood pressure (SBP), diastolic blood pressure (DBP) and total sleep time (TST) at SBP: r = 0.49, P < 0.0001; DBP: r = 0.33, P = 0.0021; TST: r = -0.28, P = 0.010 respectively. 
There is also evidence from a population-based study in Pennsylvania that insomnia with short sleep duration is associated with higher risk for type 2 diabetes. Vgontzas and colleagues found that the highest risk of diabetes was in insomniacs with ≤ 5 hours of sleeping duration at OR = 2.95 (1.2 – 7.0). Even in insomniacs who slept 5 – 6 hours, the risk of diabetes is OR = 2.07 (0.68 – 6.4).  It goes without saying that diabetes itself is a risk for stroke and cardiovascular events.
Since, the earlier mentioned studies described the association of insomnia with hypertension, type 2 diabetes and in the elderly population, CHD, the question is whether insomnia is associated with cardiovascular events – acute myocardial infarction (AMI), and cerebrovascular events – stroke. Hsu and colleagues found during an average follow-up period of 4 years that the insomniac group had higher incidence of AMI at 1.63 vs 0.76%, P ≤ 0.001, and a higher incidence of stroke at 11.18 vs 6.47%, P ≤ 0.001. They also performed a Cox proportional hazard regression model analysis and found that insomnia was associated with increased risk of developing future AMI at Hazard Ratio (HR) = 2.30, 1.90 – 2.79, P < 0.0001 and stroke, HR = 1.99, 1.86 – 2.14, P < 0.001, even after adjusting for age, gender and co-morbidities.
Hence, given the association of insomnia with cardiovascular risks and events, there is an increasing need to develop research capabilities and guidelines on the prevention and management of cardiovascular diseases in population chronically exposed to loud noises. Preventive approaches can include wearing ear plugs or requiring builders of homes to use soundproof materials in areas where there is significant exposure to loud sounds. With regards to preventive and management approaches at the primary care level, sleep hygiene can be explored which allows the clinician to elicit the patient’s quality and duration of sleep, including establishing whether or not the latter has insomnia. There is also the opportunity to perform cardiovascular screening, identifying whether the patient is at risk of a cardiovascular event based on blood pressure, blood glucose levels and other risk factors.
1.Halonen JI, Vahtera J, Stansfeld S, Yli-Tuomi T, Salo P, Pentti J, Kivimäki M, Lanki T. Associations between nighttime traffic noise and sleep: the Finnish public sector study. Environ Health Perspect. 2012 Oct;120(10):1391-6
2. Vgontzas AN, Liao D, Bixler EO, Chrousos GP, Vela-Bueno A. Insomnia with objective short sleep duration is associated with a high risk for hypertension. Sleep. 2009 Apr;32(4):491-7
3. Nakazaki C, Noda A, Koike Y, Yamada S, Murohara T, Ozaki N. Association of insomnia and short sleep duration with atherosclerosis risk in the elderly. Am J Hypertens. 2012 Nov;25(11):1149-55.
4.Vgontzas AN, Liao D, Pejovic S, Calhoun S, Karataraki M, Bixler EO. Insomnia with objective short sleep duration is associated with type 2 diabetes: A population-based study. Diabetes Care. 2009 Nov;32(11):1980-5.
5. Hsu C, Huang C, Huang P, Chiang C & Leu H. Abstract 15883: Insomnia and Risk of Cardiovascular Disease. Circulation.2012; 126: A15883
Competing interests: No competing interests
Upon reading this article, we would like to expand upon the point made by Dr Jan Coebergh about the ‘shift-work’ at Heathrow acting as a confounding variable for this research from a more personal view. Both of the primary respondent’s parents work in Heathrow airport.
“My mother works part-time in the terminal and my father full-time (before the addition of over-time hours) as an engineer. We also live under a flight path leading to Heathrow. As I progress further through my medical degree I am becoming increasingly aware of the dangers of shift work upon an individual’s health - for the purpose of this response I will focus on my father as an example.
My father left school at the age of sixteen, became an engineer apprentice and has worked at Heathrow ever since (coming up to 37 years). Throughout my life I have been aware of the long hours, often including ‘double shifts’ (16 hours) and ‘overtime’ that my father and his colleagues work to allow the airport to run through the night. While over-time and ‘double shifts’ are optional, my understanding of it is that these shifts are highly sort after by the employees and contribute to a significant amount of time spent at work.”
This has various implications for workers’ health. Sleeping patterns are difficult to establish, there is an irregular pattern to the shifts with little time between to adjust to new work patterns and the jump from ‘earlies’ to ‘lates’ occurring on a weekly basis. Factors which have a negative impact on establishing a regular sleeping pattern and limit the amount of sleep include living under a flight path. Lack of sleep has been associated with cardiovascular risk factors [1-4] and associated with all-cause mortality , with one study already mentioned by Dr Jan Coebergh attributing shift-work to cardiovascular events . As well as sleeping patterns, other health-behaviours, such as healthy eating and exercise also become a challenge. Further challenges include poorly established meal time breaks, working through meal-times and irregularity of shift work creating difficulty in partaking in regular recreational activities as many of these are aimed at 9-5 workers. Both of these factors should also be considered as cofounding variables when considering shift workers as a cohort as both have an impact on risk of cardiovascular disease [7,8].
Arguably, engineering at the airport is similar in many ways to working in a hospital. Engineers must be alert and in control at all times for the safety of thousands of passengers a day and are held accountable and responsible for their actions, often needing to attend courses with exams to keep the standard of work high. This creates a high stress environment, and anecdotal evidence suggests many ground staff need time off to allow them to cope (a pattern that might be assumed to be universal among all classes of airport staff given the highly stressful environment!). Uncontrollable factors such as weather can account for the airport grinding to a halt, resulting in managing thousands of stranded and very unhappy passengers. Stress, while the relationship is not well understood, is also linked to cardiovascular disease .
While we have used a very particular example, this highlights the importance of accounting for such confounding variables in this study. Many of the workers at Heathrow live within the boroughs and districts described in the study and will have lifestyle factors specific to them as a cohort of individuals as discussed above.
1. Sabanayagam C, Shanka A. Sleep duration and cardiovascular disease: results from the National Health Survey. Sleep. 2010;33:1037–1042. [PMC free article] [PubMed]
2. Ikehara S, Iso H, Date C, et al. Association of sleep duration with mortality from cardiovascular disease and other causes for Japanese men and women: the JACC study. Sleep. 2009;32:295–301.[PMC free article] [PubMed]
3. Amagai Y, Ishikawa S, Gotoh T, Kayaba K, Nakamura Y, Kajii E. Sleep duration and incidence of cardiovascular events in a Japanese population: the Jichi Medical School cohort study. J Epidemiol.2010;20:106–110. [PubMed]
4. Ayas NT, White DP, Manson JE, et al. A prospective study of sleep duration and coronary heart disease in women. Arch Inter Med. 2003;163:205–209
5. F Cappuccio, L D’Elia, P Strazzullo, M Miller (2010) Sleep Duration and All-Cause Mortality: A Systematic Review and Meta-Analysis of Prospective Studies American Academy of Sleep Medicine v.33 Issue: 05
6. M Vyas, A Garg, A Iansavichus, J Costella, A Donner, L Laugsand, I Janszky, M Mrkobrada, G Parraga, D Hackam (2012) Shift work and vascular events: systematic review and meta-analysis BMJ 345:e4800
7. Kromhout D. (2001) Diet and cardiovascular disease J Nutr Health Aging. 5(3):144-9
8. P. Thomas et al (2003) Exercise and Physical Activity in the prevention and treatment of atherosclerotic cardiovascular disease American Heart Association 107: 3109-3116 available online : http://circ.ahajournals.org/content/107/24/3109.short last accessed 19/10/2013
9. A Steptoe and M Kivimäki (2012) Stress and Cardiovascular disease Nature Reviews Cardiology 9, 360-370
Competing interests: No competing interests
Please could the authors explain the process for selecting confounders in this article?
In the acute clinical setting we estimate cardiovascular risk by accounting for age, sex, smoking, diabetes, blood pressure, hypercholesterolemia and family history.
I could find no explanation in the article as to why smoking, ethnicity and deprivation (in addition to age and sex) were picked out as confounders over other well defined associations.
In particular, the authors have gone to the effort of working back from lung cancer to create a proxy marker for smoking prevalence. Despite this, there is no evidence of an attempt to include hypertension as a confounding factor. In the discussion, hypertension is postulated as being the missing link in causality between noise and coronary heart disease. This is supported by multiple human studies demonstrating a transient rise in blood pressure with noise, and animal models exhibiting a chronic association between the two. It seems a shame that the opportunity to confirm (or refute) this theory of causality has been missed by negating to including hypertension in the calculation.
The effect of classical risk factors on cardiovascular disease is substantial, and a disparity in the prevalence of any of these factors could account for the results seen here. Until these confounders have been considered, the results of this well powered study demonstrate correlation only.
But who knows? Perhaps one day ‘Miles from Heathrow’ (MFH) will be considered alongside pack years of smoking as a risk factor for cardiovascular disease in the acute clinical clerking.
Competing interests: No competing interests
[Note: formatted PDF attachment at end]
Hansell et al. carefully considered the association of aircraft noise with the risk of stroke, coronary heart disease and cardiovascular disease. The authors statistically controlled for a number of confounding variables; particulate matter pollution was represented by “PM10.” I wish to express the concern that variations in PM10 are unlikely to correlate with variations in particulate pollution from aircraft, such that the aircraft-noise conclusions may remain confounded by the well-known detrimental effects of engine exhaust on health.
PM has traditionally been divided into PM10, PM2.5 (fine) and PM0.1 (ultrafine) fractions. Each subscript refers in microns to the largest particle diameter allowed in each fraction. Because PM is traditionally reported as mass concentrations, the largest-allowed particles tend to dominate each category. Since different sizes of particles are typically formed and lost via physically different pathways, PM10 and PM2.5 typically follow very different temporal patterns in the UK. Freshly-emitted aircraft particles are found in the PM0.1 fraction, and are not large enough to dominate even PM2.5. While these particles will not be well-represented by PM2.5 nor by PM10, PM10 is an especially poor proxy for aircraft pollution.
The exceptionally small size of aircraft-exhaust particles would allow them to penetrate deep into the lungs and translocate into the blood. They contain significant amounts of polyaromatic hydrocarbons (PAHs)[5, 6] and have an exceptionally high surface-area-to-mass ratio, which may enhance their toxicity. The PM0.1 fraction has been associated with increased risks of stroke, coronary heart disease and cardiovascular disease. In the atmosphere, aircraft PM0.1 will coagulate within hours to become PM2.5 and persist in the atmosphere for days. A difference in health effects between fresh and older aircraft emissions is therefore to be expected on the timescales used by the Hansell et al. study, where noise was averaged over 8 or 16 hours for day- or night-time periods. This possibility, and the possibility of aircraft PM0.1 transport to the surface, has not been considered.
PM0.1 and gaseous-pollutant databases are not always available, and when they exist may reflect nearby vehicular traffic more strongly than regional aircraft activity. The data on aircraft height and engine power used to estimate noise by Hansell et al. might possibly represent the best-available proxy for aircraft PM0.1 pollution. The distinction between noise and PM0.1 is significant for policymakers: noise will disperse immediately, but PM0.1 may have diluted effects over a longer period and wider area.
1. Hansell, A.L., et al., Aircraft noise and cardiovascular disease near Heathrow airport in London: small area study. BMJ, 2013. 347.
2. Heal, M.R., P. Kumar, and R.M. Harrison, Particles, air quality, policy and health. Chemical Society Reviews, 2012. 41(19): p. 6606-6630.
3. Liu, Y.-J. and R.M. Harrison, Properties of coarse particles in the atmosphere of the United Kingdom. Atmospheric Environment, 2011. 45(19): p. 3267-3276.
4. Westerdahl, D., et al., The Los Angeles International Airport as a source of ultrafine particles and other pollutants to nearby communities. Atmospheric Environment, 2008. 42(13): p. 3143-3155.
5. Rogers, F., et al., Real-time measurements of jet aircraft engine exhaust. Journal of the Air & Waste Management Association, 2005. 55(5): p. 583-593.
6. Lighty, J.S., J.M. Veranth, and A.F. Sarofim, Combustion aerosols: factors governing their size and composition and implications to human health. Journal of the Air & Waste Management Association, 2000. 50(9): p. 1565-1618.
7. Brook, R.D., et al., Particulate matter air pollution and cardiovascular disease an update to the scientific statement from the American heart association. Circulation, 2010. 121(21): p. 2331-2378.
8. Seinfeld, J.H. and S.N. Pandis, Atmospheric chemistry and physics: from air pollution to climate change. 2012: John Wiley & Sons.
9. Hsu, H.-H., et al., The relationship between aviation activities and ultrafine particulate matter concentrations near a mid-sized airport. Atmospheric Environment, 2012. 50: p. 328-337.
Competing interests: No competing interests
I've come on to the website because I live in West Putney, under the flight path to Heathrow and, like my neighbours, am driven crazy by aircraft noise. Interestingly, the Heathrow expansionists' noise contours seem not to include us, even though we are badly affected. The same is true of Hammersmith/Fulham where I have experienced noise as a patient in Charing Cross Hospital. I recall one weekend in August 2011 when I was marooned in Riverside ward, unablet to get discharged. Woken by aircraft noise, I dragged myself out of bed, hauling the drain with me, to check the time on the ward clock: 04.50. This is no way to live. Many object to being woken early. I think I find the noise most dementing at the end of the day, about 10.30 pm when I would like to get to sleep.
If I go to the website www.qrisk.org and type in the medical details requested, I get a less good outcome than if I type in the same details for other postcodes, for instance the much less affluent area of Plymouth where I grew up. And, if estate agents are to be believed, this part of Putney is affluent and highly desirable! So it is not just the lower socio-economic groups or ethnic communities who are adversely affected. I now regret coming here, but 32 years ago aircraft noise was not the detriment to quality of life it is now.
"Compensation" in the form of help with installing double glazing is pointless. My windows are uPVC double glazed, but the noise is still audible. And if you open a window in the summer..... Conversation outside the house is wearying or impossible. Walking around the streets is equally unpleasant.
I read about the study last week in the Austrian newspaper Kurier when I was visiting my old pen friend in Vienna. She lives in the far west of the city; the airport is far to the east. It is so blissfully quiet there.
I wonder if it is possible to quantify the cost to UK plc of the negative health impact of aircraft noise, in terms of heart attacks, strokes and children's impaired learning. Thank you for conducting the research. It is a relief to know my neighbours and I are not fanticising when we complain about the noise.
Competing interests: No competing interests
Indeed, the possibility of residual confounding is suggested and correlation is not causation. I would like to suggest a confounder. As a doctor in the vicinity of Heathrow I frequently am struck by the amount and irregularity of the hours of its many employees, many of whom presumably live under the flight path. It is known that shift work is associated with vascular events (see e.g. BMJ 2012;345:e4800) and perhaps this is one residual confounder. It could of course also be possible that the flight noise disturbs their sleep even further!
If the effect of noise and cardiovascular events is immediate, a big if, then perhaps the variation in flight paths (personal experience, approximately 7 days a month affected) or case control with the 6 days of silence during the Ash Cloud in 2010 can be studied. A move of the airport to Boris Island would help to study this phenomenon as well of course!
Dr Jan Coebergh
Competing interests: I live under a flight path of Heathrow