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Originally Published 18 October 2021
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Blood Pressure and Arterial Stiffness in Association With Aircraft Noise Exposure:Long-Term Observation and Potential Effect of COVID-19 Lockdown

Wiktoria Wojciechowska https://orcid.org/0000-0003-3075-3508, Andrzej Januszewicz, Tomasz Drożdż, Marta Rojek, Justyna Bączalska https://orcid.org/0000-0001-5999-0203, Michał Terlecki https://orcid.org/0000-0002-1762-8043, Karol Kurasz, … Show All … , Agnieszka Olszanecka https://orcid.org/0000-0001-7020-9641, Mikołaj Smólski, Aleksander Prejbisz, Piotr Dobrowolski https://orcid.org/0000-0002-8919-1661, Tomasz Grodzicki, Tomasz Hryniewiecki, Reinhold Kreutz https://orcid.org/0000-0002-4818-211X [email protected], and Marek Rajzer https://orcid.org/0000-0001-7074-7263 [email protected]Author Info & Affiliations
Hypertension
Volume 79, Number 2
https://doi.org/10.1161/HYPERTENSIONAHA.121.17704
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VIEW EDITORIAL:Reduced Aircraft Noise Pollution During COVID-19 Lockdown Is Beneficial to Public Cardiovascular Health: a Perspective on the Reduction of Transportation-Associated Pollution

Abstract

In a cross-sectional analysis of a case-control study in 2015, we revealed the association between increased arterial stiffness (pulse wave velocity) and aircraft noise exposure. In June 2020, we evaluated the long-term effects, and the impact of a sudden decline in noise exposure during the coronavirus disease 2019 (COVID-19) lockdown, on blood pressure and pulse wave velocity, comparing 74 participants exposed to long-term day-evening-night aircraft noise level >60 dB and 75 unexposed individuals. During the 5-year follow-up, the prevalence of hypertension increased in the exposed (42% versus 59%, P=0.048) but not in the unexposed group. The decline in noise exposure since April 2020 was accompanied with a significant decrease of noise annoyance, 24-hour systolic (121.2 versus 117.9 mm Hg; P=0.034) and diastolic (75.1 versus 72.0 mm Hg; P=0.003) blood pressure, and pulse wave velocity (10.2 versus 8.8 m/s; P=0.001) in the exposed group. Less profound decreases of these parameters were noticed in the unexposed group. Significant between group differences were observed for declines in office and night-time diastolic blood pressure and pulse wave velocity. Importantly, the difference in the reduction of pulse wave velocity between exposed and unexposed participants remained significant after adjustment for covariates (−1.49 versus −0.35 m/s; P=0.017). The observed difference in insomnia prevalence between exposed and unexposed individuals at baseline was no more significant at follow-up. Thus, long-term aircraft noise exposure may increase the prevalence of hypertension and accelerate arterial stiffening. However, even short-term noise reduction, as experienced during the COVID-19 lockdown, may reverse those unfavorable effects.

Graphical Abstract

According to the newest European Environment Agency Report published in 2020, over 4 million European Union citizens are exposed to aircraft noise on a level exceeding 55 dB LDEN (long-term day-evening-night noise level).1 LDEN values above 55 dB are associated with adverse health effects and are also higher than the upper limit recommended by the current World Health Organization guidelines2 for the European region for all types of environmental noise. Arterial hypertension is well recognized as one of the negative health consequences of environmental noise.3–7 Stress reaction to environmental noise is considered to be a primary causal link to hypertension development.8–10 Nocturnal noise exposure is yet more relevant for cardiovascular disorders, including hypertension, than exposure during daytime.11 Noise annoyance, along with the noise exposure level, has been shown to increase the risk of hypertension and cardiovascular disorders.12,13 Aircraft noise is perceived as the most annoying and sleep-disturbing among all transportation noise sources.14 In a meta-analysis performed by Babisch and van Kamp,12 each increase in the aircraft noise level LDEN by 10 dB increased the relative risk of arterial hypertension by 13%.12 Conversely, however, we cannot assume that a corresponding reduction of 10 dB in aircraft noise exposure can also reduce the risk of hypertension. This is based entirely on the fact that studies addressing this question have not yet been conducted. Accordingly, the potential impact of a reduction in aircraft noise exposure on arterial stiffness in people previously exposed to increased aircraft noise is also unknown.
See Editorial, pp 335–337
In a previous cross-sectional case-control study in 2015, we revealed an increase in blood pressure (BP) and arterial stiffness as determined by carotid-femoral pulse wave velocity (PWV) in individuals exposed to increased aircraft noise levels.15 The aim of this study was to evaluate the long-term effects of aircraft noise exposure after 5 years and the potential impact of an unexpected sudden decline in aircraft noise exposure. The latter resulted from the substantial decrease in aircraft traffic since the beginning of the coronavirus disease 2019 (COVID-19) pandemic.

Methods

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Study Population

We previously conducted in 2015 a population-based case-control study, to compare BP, arterial stiffness, and cardiac organ damage in a group of individuals exposed to aircraft noise (N=101), with control subjects unexposed to increased aircraft noise (N=100).15 Individuals living in 2 suburban areas of Krakow, Poland, were examined to obtain an equal number of participants exposed and unexposed to aircraft noise.15 The 2 study areas were selected based on the acoustic maps, in which we identified an area with high aircraft noise exposure (exceeding 60 dB) near the Krakow John Paul II airport and an area with low exposure (below 55 dB) of LDEN.16,17 These cutoff levels were consistent with the European environmental guidelines for evaluating the health effects of noise.17
Data on aircraft noise exposure during follow-up were obtained from the obligatorily collected noise-monitoring data for Krakow airport, provided by the Chief Inspectorate of Environmental Protection. The detailed study protocol was previously reported.15 Inclusion criteria were age between 40 and 65 years, which was considered optimal for assessing hypertension-mediated organ damage, and time of residence in the given area (minimum of 3 years). The exclusion criteria were coronary artery disease, stroke, heart failure, chronic kidney disease, respiratory disease, liver disease, and deafness or serious hearing loss. All participants from the original investigation in 2015 were invited for a follow-up evaluation in June 2020, for assessment by the same study protocol. Finally, 74 participants in exposed and 75 in the unexposed group were available for re-evaluation in 2020 (dropout causes are described in Figure S1 in the Data Supplement). The study was conducted according to the Helsinki declaration for Investigation of Human Subjects. The Jagiellonian University Ethics Committee approved the study protocol. All participants submitted a written informed consent.

BP Measurement

The study was conducted in an outpatient clinic of the University Hospital in Krakow during one visit. Office and 24-hour ambulatory BP measurements (ABPM) were performed during the baseline visit and follow-up visit, as previously reported, using OMRON M5-I and SpaceLabs 90207 devices. ABPM measurements were taken every 15 minutes during the day (06:00–22:00 hours) and every 20 minutes during the night (22:00–06:00 hours). Hypertension was defined based on a prior diagnosis, or use of antihypertensive treatment, or elevated office systolic BP (SBP) or diastolic BP (DBP) values ≥140 or ≥90 mm Hg or elevated 24-hour SBP ≥130 or DBP ≥80 mm Hg during ABPM.

PWV Measurements

We assessed carotid-femoral PWV using a SphygmoCor device (AtCor Medical Pty Ltd, West Ryde, New South Wales, Australia) running software Version 7.1 at baseline and Version XCEL at follow-up. The measurements were performed in agreement with the expert consensus document on the measurement of aortic stiffness in daily practice using PWV.18

Echocardiographic Measurements

Echocardiographic measurements were obtained by 2 examiners using the Vivid 7 and Vivid 9 ultrasound devices (General Electric Healthcare, Milwaukee, WI), at baseline and at follow-up, respectively. The examination protocol was in agreement with European Society of Cardiology recommendations.19 Relevant functional and structural parameters of the left ventricle and left atrium were determined as reported previously.15

Other Measurements

We used a standardized questionnaire to obtain information on the medical history, including concomitant diseases, smoking and drinking habits, and use of medications.
Additionally, we evaluated the subjective noise annoyance and sleep quality. Noise annoyance was evaluated using a 3-point scale from 0 to 2, where 0 indicated lack of annoyance and 2 indicated maximal annoyance. The sleep quality assessment included the following self-reported parameters: difficulties with falling asleep, awakening during the night and fatigue during the day as described by Thorpy.20 In participants with presence of all of the above-mentioned parameters, insomnia was defined according to the classification of sleep disorders.20 Additionally, the presence of snoring and diagnosed sleep apnea, and the duration of overnight sleep, were obtained in the questionnaire.
To explore the potential influence of COVID-19 lockdown on studied parameters, we introduced additional items into the questionnaire by asking about lifestyle changes caused by the lockdown in the opinion of the participants (analyzed parameters listed in Table S1).

Statistical Methods

For database management and statistical analysis, we used SAS software, Version 9.2 (SAS Institute, Cary, NC). For comparison of means and proportions, we applied a t test for paired observations and the χ2-statistic, respectively, or Wilcoxon Signed Rank test, for nonparametric data. For independent group comparison, a 2-sample t test or Wilcoxon Rank-sum test for parametric and nonparametric types of test were used. The differences between groups exposed and unexposed to aircraft noise in BP changes were assessed using ANOVA for repeated measurements in a PROC GLM procedure with adjustment for age, gender, changes in body mass index (BMI), and antihypertensive treatment in one model; an additional model was used with the same covariates in which baseline BP values were also implemented. The analysis of differences between exposed and unexposed to aircraft noise groups in PWV decrease were adjusted for age, gender, changes in BMI, 24-hour SBP and DBP, antihypertensive treatment, and baseline PWV. To explore the potential influence of a lockdown on BP values, we assessed the cross-sectional association between BP and age among participants without antihypertensive treatment at baseline. Based on obtained parameter estimates (PE; PE) and time of follow-up (5.5 years), the expected BP of each subject (without antihypertensive treatment at the follow-up observation) was calculated as baseline DBP+5.5×PE. We tested the null hypothesis of no differences between the regression slopes of expected and measured values at the follow-up visit BP on age, using multivariable ANOVA in the PROC GLM procedure of the SAS package. In all analyses, statistical significance was a P value of 0.05 or less on 2-sided tests.

Results

During the follow-up period between 2015 and March 2020, the exposure to aircraft noise remained constant in the exposed group. In contrast, a marked decrease in the average aircraft noise level occurred in April 2020, resulting in a reduction from 61.7 to 47 dB during the day and from 55.4 to 43.4 dB during the night, as compared with April 2019 (detailed data are summarized in Figure S2). Thus, starting from April 2020, the formerly exposed group was exposed to aircraft noise levels similar to the control group. In the latter, the environmental noise exposure conditions did not change in the corresponding residential area and remained below <55 dB throughout the entire follow-up period between 2015 and 2020 (mean of 5.5 years).

Characteristics of Participants

Table 1 shows the characteristics of participants for both the exposed (N=75) and unexposed (N=74) groups at baseline and at the follow-up visit. The data for the overall cohort (N=100 and N=101, respectively) at the baseline visit are also shown for comparison.
Table 1. Characteristics of Participants by Study Phase and Noise Exposure Area
ParametersAll participants at baselineParticipants with follow-up
   Unexposed Exposed 
UnexposedExposedP valueBaselineFollow-upP value*BaselineFollow-upP value*
Number of participants100101 7575 7474 
Age, y53.6 (8.5)53.4 (8.1)0.9153.4 (8.2)58.6 (8.3)NA53.3 (7.2)58.4 (7.1)NA
Female, n (%)71 (71)65 (64.4)0.3952 (69.3)  50 (67.6)  
Body mass index, kg/m227.7 (4.7)27.2 (4.3)0.4128.2 (4.9)28.7 (4.4)0.0627.0 (4.4)28.2 (6.0)0.01
Current smoking10 (10)14 (13.9)0.534 (5.3)5 (6.7)0.735 (6.7)6 (8.1)0.62
Alcohol intake23 (23)31 (30.7)0.2817 (22.7)18 (24)0.8421 (28.4)23 (31)0.85
Regular physical activity, times a week3 (0.4)3.8 (0.42)0.612.7 (0.53)3.19 (0.42)0.392.7 (0.5)3.8 (0.42)0.80
Hypercholesterolemia28 (28)34 (33.7)0.4724 (32)32 (43)0.1125 (33.9)30 (40.5)0.49
Hypertension50 (50)53 (52.5)0.8330 (40)37 (49)0.3231 (42)44 (59)0.048
Diabetes8 (8)8 (7.9)0.995 (6.7)10 (13.3)0.275 (6.7)5 (6.7)1.0
Antihypertensive medication use, n (%)42 (42)39 (38.6)0.7327 (36.0)34 (45.6)0.3223 (31.1)36 (48.6)0.039
Number of antihypertensive drugs1.9 (1.5)2.1 (0.9)0.392.03 (0.8)2.0 (0.8)0.482.0 (0.8)1.9 (0.9)0.36
Time of residence in the selected area, y34.8 (19.9)35.7 (17.3)0.7435.7 (18.0)37.3 (20.4)0.1036.6 (16.9)38.8 (16.3)0.62
Time spent at home within 24 h17 (5.0)16.3 (4.8)0.3117.5 (5.0)16.4 (5.7)0.6216.3 (4.9)16.4 (6.3)0.87
Aircraft noise annoyance0.01 (0.01)1.37 (0.06)<0.0010.016 (0.02)0.063 (0.03)0.371.36 (0.8)†1.06 (0.09)‡0.006
Values are mean (SD), numbers of subjects (%), aircraft noise annoyance and regular physical activity as mean (SE). One alcohol dose (50 mL vodka/cognac/liqueur or 150 mL wine or 250 mL beer) per week. Regular physical activity means 40 minutes once a week. P value denotes significance of between group differences for all participants at baseline. NA - not applicable.
*
P value: significance of changes from baseline to follow-up within unexposed or exposed group in participants with follow-up.
†
P<0.05 for differences between unexposed and exposed participants at baseline.
‡
P<0.05 for differences between unexposed and exposed participants at follow-up visit.
During follow-up, a significant increase in BMI, the prevalence of hypertension and the percentage of patients treated with antihypertensive medications was observed in the group exposed to aircraft noise (Table 1).
The incidence of arterial hypertension in the exposed group tended to be higher. The average number of drugs used by the patient and the particular drug class use did not change significantly during follow-up. The exposed participants at follow-up visit reported significantly lower noise annoyance (P=0.006) in comparison to the baseline visit, but still had higher levels than the unexposed group (P=0.001, Table 1). During follow-up, no significant changes were revealed in the unexposed group in comparison to the baseline visit (Table 1).

Sleep Characteristics

Table 2 summarizes the results obtained with the sleep quality questionnaire. The average sleep duration in both groups was similar, with about 7 hours both at baseline and during follow-up. Difficulties in falling asleep were more prevalent in the group exposed to aircraft noise compared with the control group at baseline (P=0.02). A significant increase in difficulty falling asleep at the follow-up visit was observed in both studied groups (Table 2). At baseline, >40% of the subjects in the exposed group reported awakenings at night, compared with only 24% in the unexposed group. Of note, this difference between groups in awakening during the night was no longer significant at the follow-up visit during the lockdown period. Similarly, the significantly higher prevalence of reported fatigue during the day observed in the exposed group at baseline was not maintained at the follow-up visit (Table 2).
Table 2. Sleep Quality Parameters and Insomnia in Subjects Exposed or Unexposed to Aircraft Noise and Changes During 5-Years of Follow-Up
ParametersUnexposed, N=75 Exposed, N=74 
BaselineFollow-upP valueBaselineFollow-upP value
Difficulty falling asleep9 (12.0)18 (24.0)0.03820 (27.0)*27 (36.5)†0.008
Awakening during the night18 (24.0)30 (40.0)0.0632 (43.2)*44 (59.4)0.11
Fatigue during the day11 (14.7)37 (49.3)0.6132 (43.2)*42 (56.7)0.66
Insomnia5 (6.7)16 (21.3)0.0412 (16.2)*18 (24.3)0.21
Snoring20 (26.7)36 (48.0)0.00926 (35.1)31 (41.9)0.026
Sleep apnea2 (2.7)3 (4.0)0.993 (4.0)5 (6.8)0.9
Average sleep duration, h7.0 (0.8)7.0 (1.0)0.887.0 (0.8)7.1 (1.2)0.43
Values are expressed as number (%), total score categories mean (SE), average sleep duration mean (SD). P value denotes significance of changes from baseline to follow-up in unexposed or exposed group in participants with follow-up.
*
P<0.05 for differences between unexposed and exposed participants at baseline.
†
P<0.05 for differences between unexposed and exposed participants at follow-up visit.
The prevalence of insomnia was higher at baseline in the exposed group compared with participants unexposed to aircraft noise, but this difference disappeared at the follow-up visit because the unexposed participants experienced a significant increase in insomnia frequency (P=0.04; Table 2).

Lockdown Lifestyle Changes

Self-reported lifestyle parameters and working habits during the COVID-19 lockdown period did not change significantly as compared with the period before the lockdown in 2020, in either group (Table S1).

BP Phenotypes and Changes During Follow-Up

The baseline and follow-up BP measurements are shown in Table 3. During the baseline visit, participants in the exposed group had higher office and night-time DBP, as well as higher central SBP and DBP, compared with the unexposed group. At follow-up, significant group differences in BP phenotypes were only detected for central SBP. At the follow-up visit, a substantial drop in BP was observed in participants from both groups. In the unexposed group, 24-hour SBP, daytime SBP, and daytime DBP were lower at follow-up visit than during the initial measurements (P≤0.013). In participants exposed to aircraft noise, a significant decrease of DBP was observed for all measurement methods (P≤0.022), while a decrease of SBP was significant in averaged 24-hour values and during daytime measurements (P≤0.034; Table 3).
Table 3. Office, Central and Ambulatory Blood Pressure in Subjects Exposed or Unexposed to Aircraft Noise and Changes During 5-Years of Follow-Up
mm HgUnexposed, N=75 Exposed, N=74 
BaselineFollow-upP valueΔBaselineFollow-upP valueΔ
Office BP
 Systolic pressure138.0 (15.8)136.4 (16.8)0.43−1.6142.3 (18.5)140.5 (18.4)0.44−1.8
 Diastolic pressure80.1 (8.0)80.1 (9.7)0.970.087.5 (11.6)*82.2 (8.1)0.001−5.3‡
 Pulse pressure58.0 (11.9)56.3 (12.5)0.28−1.754.8 (12.4)58.2 (15.3)0.0233.4‡
Central BP
 Systolic pressure124.1 (15.5)122.7 (18.8)0.55−1.4130.4 (17.5)*128.7 (15.7)†0.46−1.7
 Diastolic pressure79.9 (8.0)81.1 (9.9)0.321.286.8 (11.4)*83.2 (8.4)0.022−3.6‡
 Pulse pressure44.1 (11.4)43.2 (11.5)0.49−0.943.6 (12.2)45.5 (12.2)0.191.9
ABPM 24-hour
 Systolic pressure120.9 (9.5)117.5 (10.4)0.011−3.4121.2 (14.6)117.9 (12.1)0.034−3.3
 Diastolic pressure72.8 (6.4)71.7 (7.4)0.14−1.175.1 (8.9)72.0 (7.6)0.003−3.1
 Pulse pressure48.1 (6.5)45.8 (7.8)0.01−2.346.1 (10.0)45.8 (9.5)0.81−0.3
ABPM daytime
 Systolic pressure127.1 (10.3)121.9 (11.0)0.012−5.2126.9 (15.2)122.3 (12.6)0.008−4.6
 Diastolic pressure78.9 (9.3)75.7 (7.8)0.013−3.279.3 (8.9)75.9 (8.6)0.002−3.4
 Pulse pressure48.3 (9.9)46.3 (7.8)0.12−1.447.6 (10.1)46.4 (9.5)0.17−1.2
ABPM night-time
 Systolic pressure107.9 (9.3)107.6 (11.3)0.61−0.3110.4 (15.8)108.1 (12.7)0.23−2.3
 Diastolic pressure62.7 (6.5)63.2 (6.9)0.720.566.2 (9.9)*63.8 (6.9)0.014−2.4‡
 Pulse pressure45.1 (7.2)44.5 (8.1)0.34−0.644.2 (10.2)44.3 (10.5)0.430.1
Values are mean (SD). P value denotes significance of changes from baseline to follow-up within unexposed or exposed group in participants with follow-up; and Δ, changes of BP parameters calculated as follow-up BP minus baseline BP. ABPM indicates ambulatory blood pressure measurement; and BP, blood pressure.
*
P<0.05 for differences between unexposed and exposed participants at baseline.
†
P<0.05 for differences between unexposed and exposed participants at follow-up.
‡
P<0.05 for differences between the unexposed and exposed groups in BP phenotypes changes (Δ) during follow-up.
Unadjusted comparison of changes in BP parameters from baseline to follow-up are summarized in Table 3. The magnitude of the DBP decreases at follow-up visit in office, central and night-time values, as compared with the baseline, was significantly greater in the exposed group also after adjustment for age, gender, BMI, and antihypertensive treatment (Figure S3). Introduction of baseline BP values in the adjusted analysis ameliorated this difference resulting in no significant group differences. There was no significant relationship between BP changes and the decline in noise annoyance. The heart rate decreased in the comparison between baseline and follow-up in both groups during office BP measurements (unexposed group: 71.4 versus 66.8 beats per minute, P=0.001; exposed group: 71.5 versus 66.1 beats per minute, P=0.001). However, ABPM heart rates were comparable (unexposed group: 62.8 versus 62.2 beats per minute, P=0.66; exposed group 63.7 versus 62.7 beats per minute, P=0.16).

Explorative Analysis of Differences Between Expected and Measured BP in Untreated Participants

From regression modeling of BP phenotypes with age at baseline, the presumable yearly increase of BP in untreated participants was obtained, and the estimated BP values at 5.5 years follow-up were calculated. The latter were compared with the actually measured BP values. This analysis revealed that, in the exposed participants without antihypertensive treatment at follow-up (n=38), the observed office DBP was significantly lower than the expected DBP (DBP [least squares means]: expected 87.6 mm Hg, observed 82.7 mm Hg; P=0.048). In contrast, in untreated participants of the unexposed group (n=41), there was no difference between the expected and observed DBP values (DBP [least squares means]: expected 78.7 mm Hg, observed 77.8 mm Hg; P=0.61, Figure S4). No differences were detected for other BP phenotypes.

Pulse Wave Velocity

Table 4 shows the mean values of PWV in studied groups at baseline and follow-up visits with changes observed in PWV during follow-up. At baseline, PWV was significantly higher in the exposed group as compared with the unexposed group (Table 4), with a mean value exceeding the normal range of PWV; that is, 10 m/s. At the follow-up visit, PWV was similar with 8.8 m/s in both groups due to a significant decrease in the exposed group. The differences in the reduction of PWV remained significant after adjustment for age, gender, changes in BMI, averaged 24-hour SBP and DBP, antihypertensive treatment, and baseline PWV (estimate: −1.49 versus −0.35 m/s; P=0.017).
Table 4. Pulse Wave Velocity and Echocardiographic Parameters in Subjects Exposed or Unexposed to Aircraft Noise and Changes During 5-Years of Follow-Up
ParametersUnexposed, N=75 Exposed, N=74 
BaselineFollow-upP valueΔBaselineFollow-upP valueΔ
PWV, m/s9.3 (1.5)8.8 (1.8)0.002−0.510.2 (1.8)*8.8 (1.7)0.001−1.4‡
Echocardiographic parameters
LVMI, g/m2100.9 (22.5)98.7 (23.9)0.09−2.2104.9 (24.6)100.4 (22.2)0.36−4.5
RWT, mm0.41 (0.07)0.42 (0.06)0.120.010.40 (0.06)0.43 (0.06)0.090.03
LAVI, mL/m224.7 (7.3)31.9 (6.5)0.0017.225.6 (7.5)31.7 (5.2)0.0016.1
E′, cm/s9.1 (3.4)9.2 (2.9)0.850.18.7 (3.0)9.1 (2.8)0.200.4
E/E′8.6 (2.6)8.4 (2.8)0.88−0.28.6 (2.9)8.3 (2.6)0.33−0.3
E/A1.07 (0.3)1.19 (0.31)0.0560.121.06 (0.35)1.00 (0.32)0.032−0.06
Values are mean (SD). A indicates late diastolic mitral peak flow velocity; E, early diastolic mitral peak flow velocity; E/A, ratio of E to A; E/E′, ratio of E to E′; E′, early diastolic mitral annulus mean (of septal and lateral) velocity; LAVI, left atrial volume index; LVMI, left ventricle mass index; PWV, carotid–femoral pulse wave velocity; and RWT, relative wall thickness. Δ denotes changes in PWV and echocardiographic parameters calculated as follow-up values minus baseline values; and P value, significance of changes from baseline to follow-up within unexposed or exposed group in participants with follow-up.
*
P<0.05 for differences between unexposed and exposed participants at baseline.
†
P<0.05 for differences between the unexposed and exposed groups for changes (Δ) in PWV and echocardiographic parameters during follow-up.
The univariate linear regression analyses between PWV and age among untreated participants are shown in Figure. Of interest, in the group with exposure to aircraft noise at baseline no significant association was detected (PE=0.01 m/s/y; P=0.71), while in the unexposed group a strong, association was found (PE=0.13 m/s/y; P<0.001). At the follow-up visit, the significant association between PWV and age became evident (PE=0.15 m/s/y; P<0.001) in the exposed group and was comparable to the unexposed group (PE=0.12 m/s/y; P=0.003). However, the mean PWV in untreated participants remained still higher in the exposed than in the unexposed group (8.5±1.69 m/s versus 7.8±1.51 m/s; P=0.03, Figure).
Figure. Unadjusted associations of pulse wave velocity (PWV) with age at baseline, and follow-up in untreated unexposed (Nbaseline=48; Nfollow-up=41) and exposed (Nbaseline =51; Nfollow-up=38) participants.

Echocardiographic Parameters

Table 4 summarizes the data obtained by echocardiographic assessment. There were no between group differences in left ventricular mass index at baseline and follow-up visit.
In the exposed group, a significant, albeit small, decrease in the ratio of early and late diastolic mitral peak velocity (E/A) was observed at the follow-up visit. The average values of left atrium volume index at follow-up were significantly higher as compared with the baseline in both groups. Moreover, the magnitude of changes in the examined parameters over time did not differ between groups.

Discussion

Transportation noise, particularly aircraft noise, is increasingly recognized as an important risk factor for arterial hypertension, cardiovascular organ damage, stroke, and coronary artery disease.21,22 An increase in arterial stiffness, as reflected by an elevated PWV after adjustments for other covariates in subjects exposed to aircraft noise was an important finding in the baseline cross-sectional analysis of our case-control study conducted in 2015.15 In the current follow-up analysis, we investigated whether a short-term reduction in aircraft noise exposure caused by the COVID-19 lockdown may have beneficial effects on the increases in BP and arterial stiffness, as previously reported.23 First of all, we demonstrated that long-term exposure for 5 years to increased (>60 dB) aircraft noise levels does indeed increase the prevalence of hypertension in our cohort. However, at the time of re-examination during the follow-up visit, participants in the exposed group had been unloaded from increased aircraft noise for about 4 months due to the significant air traffic reduction due to COVID-19. Instead of progression in arterial stiffness, that is, a further increase in PWV, as a result of aging and the 5 years aircraft noise exposure,24 we detected a normalization of the elevated at baseline PWV. In addition, the formerly seen decoupling of the association between age and PWV at baseline was also restored at the follow-up visit in untreated participants of the exposed group, in parallel with the normalization of PWV. Along with the reduction in aircraft noise in the exposed group a significant reduction in aircraft-noise-induced annoyance was observed in the participants, which provides a possible mechanistic link.23 Hence, the study by Van Gerven et al25 assessed the relation between age and self-reported annoyance from environmental noise (including aircraft noise). The results revealed an inverted U-shaped pattern, where the largest number of highly annoyed individuals was found in the middle-aged segment of the sample (peaking at around 45 years).25 These results can be extrapolated to our group (mean age of 53 years) and explain the high annoyance level and subsequently higher PWV in this group observed at baseline. Consequently, the aircraft noise decrease and decline in annoyance at follow-up may, at least in part, explain the PWV reduction and the restoration of the positive physiological26 correlation between PWV and age.27
Increased PWV as a consequence of aortic stiffening is associated mainly with older age and elevated BP.27,28 Carotid-femoral PWV as an index of arterial stiffening is a BP-dependent parameter,26 so changes in PWV should be considered with the changes in BP observed at the follow-up visit. Lower BP values were detected in the exposed group but also in the unexposed group at the follow-up visit. In particular, the magnitude of the decrease in office, central, and ABPM night-time DBP were significantly more pronounced in the group exposed to aircraft noise in comparison to the unexposed group, even after accounting for age, gender, and antihypertensive treatment. Acute hemodynamic changes result in substantial changes in PWV.29 Thus, lower BP in the exposed group may have contributed to the detected lower PWV at the follow-up visit. Taken together, both the reduction in aircraft noise–induced annoyance and the drop in BP are likely to be responsible for the decrease in PWV and may share a common pathogenic background. On the contrary, the effect size of mechanisms, for example, as mediated by endothelial dysfunction and neurohumoral activation, on BP and PWV could be different. Earlier, Schmidt et al9,10 showed that aircraft noise exposure dose-dependently impairs endothelial function and increases adrenaline release, which might have a greater impact on PWV as compared with BP. In addition, Osborne et al30 showed that noise exposure is related to cardiovascular diseases by a mechanism that begins with increased stress-associated limbic activity and includes arterial inflammation which has been also associated with a higher risk of major adverse cardiovascular events. Activation of amygdala, which is responsible for emotional stress and fear, is also responsible for the anger/annoyance reactions.30 Neurobiological resilience defined as lower amygdalar activity despite stress exposure including transportation noise may protect against major adverse cardiac events.31
Available human data are consistent with animal experiments demonstrating an increased release of stress hormones (catecholamines and cortisol), endothelial dysfunction, and oxidative stress in aircraft noise-exposed mice.32 Of note, a recent experimental study in mice indicated that aircraft noise exposure during the sleep phase but not awake phase caused increased BP, endothelial dysfunction, increased markers of vascular/systemic oxidative stress, and inflammation.33 Mechanistically, this was linked to increased cerebral oxidative stress and downregulation of neuronal nitric oxide synthase in response to noise exposure.33
Previous studies showed positive associations between aircraft noise, BP, and arterial hypertension.5,6,12,34–37 The authors concluded that environmental night-time noise is more likely to cause cardiovascular disease than daytime noise. This is emphasized by the World Health Organization night-time noise guidelines.38
The meaningful effect of night-time aircraft noise on arterial hypertension was observed in the cross-sectional multicenter HYENA (hypertension and exposure to noise near airports) study37 and in the prospective observation of the subset of individuals from that study.21 In a longitudinal observation of 420 participants, higher aircraft noise exposure during the night significantly associated with the incidence of hypertension.21
The above-described data showed a similarity to results obtained in our study; that is, night-time DBP at baseline was significantly higher in participants exposed to noise as compared with unexposed participants. At follow-up in the group of previously exposed participants, DBP decreased substantially mainly due to higher baseline BP values and became similar to DBP in the unexposed group. This could be a consequence of the aircraft noise decline during the COVID-19 lockdown. It appears possible that in participants previously prehypertensive, the development of sustained hypertension and subsequent introduction of antihypertensive treatment could have in fact influence on drop in BP compared with baseline in these individuals. However, our sensitivity analysis in untreated participants showed also a similar tendency towards lower BP levels at follow-up (Table S2 and Figure S4).
Besides the BP reduction in the group previously exposed to aircraft noise, we found (in unadjusted analysis) an increase in the prevalence of arterial hypertension during follow-up. This is in agreement with previous reports showing the long-lasting effect of aircraft noise exposure on hypertension prevalence.5,36,37
Among the echocardiographic parameters assessed in our study, left atrium volume index showed a gradual increase during follow-up, while no changes in left ventricular mass index were observed. This lack of progression in left ventricular mass index could be related to overall normal or only slightly elevated BP on both visits in studied groups. The increase in left atrium volume index might be explained by aging.39 This notion is supported by a recent study showing a significant correlation of the left atrium size with age (r=0.48, P<0.0001).39 Moreover, as a potential result of the increased prevalence of hypertension during the 5-year follow-up in the exposed group, the significant decrease of E/A ratio could be noted as an indicator for early LV diastolic dysfunction.
At baseline, participants exposed to aircraft noise had a higher prevalence of insomnia as compared with the unexposed group. At the follow-up visit, the prevalence of insomnia became equal in both groups. This may be partially explained by the observed significant increase of insomnia in the unexposed group as a potential adverse effect of the COVID-19 lockdown.40
In this regard, our results are in agreement with work by Voitsidis et al,41 who described increased prevalence of insomnia in a large Greek population as a result of the COVID-19 pandemic. Therefore, this effect should be expected in both groups of our study. However, in the exposed group the increase in the prevalence of insomnia was not significant, which may be attributable, at least in part, to the observed reduction in aircraft noise exposure.
A few limitations of our study should be taken into consideration. First, we presented data pertaining to a relatively small group of individuals exposed to aircraft noise; however, their BP and cardiovascular parameters were carefully phenotyped. Another shortcoming of our study is the lack of a follow-up investigation with maintained aircraft noise exposure in the exposed group that preceded the current investigation as closely as possible. However, due to the unforeseen lockdown caused by the COVID-19 pandemic this was not feasible. Looking into the future, it remains to be seen when and whether a future follow-up study with similar aircraft noise exposure levels in the exposed group will be conducted by us, since the return to the previous normal air traffic intensity in the post-COVID-19 area appears to be questionable.40
In conclusion, long-term aircraft noise exposure increases the prevalence of arterial hypertension. The unprecedented situation with an aircraft noise decline due to the COVID-19 lockdown indirectly confirmed this observation by reversing unfavorable changes of BP and arterial stiffness. Our study supports the importance of noise mitigation strategies for cardiovascular health.

Perspectives

In this study, we investigated whether the significant noise reduction caused by the COVID-19 lockdown could reverse an unfavorable long-term aircraft noise effect on BP and arterial stiffness. In summary, we revealed that long-lasting exposure to aircraft noise is associated with higher prevalence of arterial hypertension, while during a short-term reduction in noise exposure due to the COVID-19 lockdown a significant decline in PWV was observed. Moreover, the natural relation of PWV with age previously blunted by the noise influence was restored. Our findings emphasize the importance of noise pollution on BP and arterial stiffening. Whether the noise reduction due to COVID-19 will have an effect on arterial hypertension epidemiology or not remains uncertain, and needs future research. The consecutive waves of the COVID-19 pandemic continue to cause a considerable increase in morbidity and mortality, having a profound effect on numerous aspects of society health and environment worldwide. Thus, the cumulative effect of the COVID-19 pandemic on arterial hypertension is rather unpredictable, and the consequences of the overall traffic and particularly the decrease in aircraft noise are contributing to this complex scenario. Nevertheless, the potential reversal of aircraft noise–induced health side effects during the lockdown could stimulate the discussion with authorities to put more emphasis on the implementation of World Health Organization noise limits. In addition, the same applies to the inclusion of corresponding recommendations into cardiovascular prevention programs.

Acknowledgments

We are sincerely grateful to Mrs Elzbieta Zietara and her team for the organizational support and technical assistance with the measurements of arterial stiffness and ambulatory blood pressure. We gratefully acknowledge assistance of Władysław Palmowski, Edward Pasteczko, and Paweł Ciećko.

Novelty and Significance

VIEW EDITORIAL:Reduced Aircraft Noise Pollution During COVID-19 Lockdown Is Beneficial to Public Cardiovascular Health: a Perspective on the Reduction of Transportation-Associated Pollution

What is New?

•
The blood pressure and arterial stiffness decline was documented as a consequence of aircraft noise reduction during the coronavirus disease 2019 (COVID-19) lockdown.

What is Relevant?

•
Although long-term aircraft noise exposure increases arterial hypertension prevalence and arterial stiffness, even short-term aircraft noise reduction may substantially reduce blood pressure and improve arterial compliance.

Summary

These findings confirm the relationship between aircraft noise exposure and development of arterial hypertension, as well as the potential reversal effect of environmental noise limitations in this regard.

Footnote

Nonstandard Abbreviations and Acronyms

ABPM
ambulatory BP measurement
BMI
body mass index
BP
blood pressure
COVID-19
coronavirus disease 2019
DBP
diastolic BP
PE
parameter estimate
PWV
pulse wave velocity
SBP
systolic BP

Supplemental Material

File (hyp_hype-2021-17704_supp2.pdf)
File (hyp_hype-2021-17704_supp3.pdf)

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Published In

Go to Hypertension
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Hypertension
Volume 79 • Number 2 • February 2022
Pages: 325 - 334
PubMed: 34657440

Copyright

© 2021 American Heart Association, Inc.

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History

Received: 14 May 2021
Accepted: 12 September 2021
Published online: 18 October 2021
Published in print: February 2022

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Keywords

  1. aircraft
  2. arterial
  3. arterial stiffness
  4. COVID-19
  5. hypertension

Subjects

  1. Hypertension
  2. Risk Factors

Authors

Affiliations

Wiktoria Wojciechowska* https://orcid.org/0000-0003-3075-3508
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Andrzej Januszewicz*
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Tomasz Drożdż
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Marta Rojek
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Justyna Bączalska https://orcid.org/0000-0001-5999-0203
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Michał Terlecki https://orcid.org/0000-0002-1762-8043
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Karol Kurasz
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Agnieszka Olszanecka https://orcid.org/0000-0001-7020-9641
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Mikołaj Smólski
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Aleksander Prejbisz
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Piotr Dobrowolski https://orcid.org/0000-0002-8919-1661
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Tomasz Grodzicki
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Tomasz Hryniewiecki
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Reinhold Kreutz https://orcid.org/0000-0002-4818-211X [email protected]
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Marek Rajzer https://orcid.org/0000-0001-7074-7263 [email protected]
From the Jagiellonian University Medical College, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Kraków, Poland (W.W., T.D., M. Rojek, J.B., M.T., A.O., M.R.); Department of Hypertension, National Institute of Cardiology, Warsaw, Poland (A.J., M.S., A.P., P.D.); Medical Faculty, Dresden University of Technology, Germany (M. Rojek); Chief Inspectorate Of Environmental Protection (K.K.); Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland (T.G.); Department of Valvular Heart Diseases, National Institute of Cardiology (T.H.); and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Klinische Pharmakologie und Toxikologie, Germany (R.K.).
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Notes

*
W. Wojciechowska and A. Januszewicz contributed equally.
The Data Supplement is available with this article at Supplemental Material.
For Sources of Funding and Disclosures, see page 333.
Correspondence to: Marek Rajzer, 1st Department of Cardiology, Interventional Electrocardiology and Arterial Hypertension, Jagiellonian University Medical College, Jakubowskiego St. 2, 30-688 Kraków, Poland, Email [email protected]
Reinhold Kreutz, Institute of Clinical Pharmacology and Toxicology, Charitéplatz 1, 10117 Berlin, Germany, Email [email protected]

Disclosures

None.

Sources of Funding

The research was supported by Jagiellonian University Medical College (grant number N41/DBS/000134).

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Blood Pressure and Arterial Stiffness in Association With Aircraft Noise Exposure:Long-Term Observation and Potential Effect of COVID-19 Lockdown
Hypertension
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