The relationship between noise pollution and cardiovascular diseases: an umbrella review on meta-analyses

Abstract

Cardiovascular disease (CVD) is a global health concern, with established risk factors like smoking, hypertension (HTN), diabetes, and dyslipidemia. Emerging evidence suggests that environmental noise resulting from urbanization and industrialization may contribute to CVD. A comprehensive assessment of existing research is needed to understand the role of environmental noise in cardiovascular health. Following PRISMA guidelines, we conducted a comprehensive literature search across PubMed, Scopus, and Web of Science from inception to 8 May 2025, identifying relevant meta-analyses with specific inclusion and exclusion criteria. Data extraction encompassed study characteristics, exposure-outcome details, and effect estimates. Methodological quality was assessed using the GRADE framework. In our umbrella review of 20 studies, we found that noise pollution is associated with an increased risk of HTN (RR 1.81, 95% CI: 1.51–2.18), atrial fibrillation (RR 1.05, 95% CI: 1.02–1.09), coronary heart disease (RR 1.08, 95% CI: 1.04–1.13), and ischemic heart disease (RR 1.06, 95% CI: 1.03–1.09) per 10-decibel (dB) increase in noise exposure. The exposure-response relationship indicated effects at lower noise levels (50 dB). However, noise exposure did not significantly impact myocardial infarctions (RR 1.02, 95% CI: 1.00–1.05), ischemic heart disease mortality (RR 1.03, 95% CI: 0.99–1.08), or cardiovascular mortality (RR 1.01, 95% CI: 0.98–1.05). We also observed an elevated risk of stroke (RR 1.04, 95% CI: 1.00–1.08) and stroke mortality (RR 1.05, 95% CI: 0.97–1.14). Blood pressure dysregulations (RR 2.55, 95% CI: 1.94–3.36) and ECG abnormalities (RR 2.27, 95% CI: 1.96–2.62) were substantially higher in individuals exposed to noise. Our umbrella review strongly suggests noise exposure as a significant potential risk factor for CVD. The substantial evidence and consistent effect sizes found in our analysis underscore the crucial importance of recognizing noise pollution as a substantial contributor to CVD. With urbanization and industrialization driving increased noise levels, understanding this link is of paramount importance for public health and future research.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12872-025-04864-9.

Introduction

Cardiovascular disease (CVD) is a broad category encompassing a range of interconnected pathologies, typically including coronary heart disease (CHD), cerebrovascular disease, peripheral arterial disease, rheumatic and congenital heart conditions, and venous thromboembolism. On a global scale, CVD is responsible for 31% of all deaths, with a significant portion attributed to CHD and cerebrovascular accidents [1]. CVD accounts for around 34% of all deaths in England, compared to approximately 40% in the European Union [2]. As the prevalence of CVD risk factors rises in formerly low-risk locations, it is anticipated that the incidence of CVD will increase globally [3]. Currently, emerging nations account for 80% of CVD-related fatalities [4].

Over the mid-20th century and beyond, a substantial body of research has been dedicated to unraveling the causes and risk factors associated with CVD due to its widespread prevalence worldwide. These investigations have identified specific contributing factors such as smoking, hypertension (HTN), diabetes, and dyslipidemia as key elements in the risk profile for CVD [5, 6]. Studies have shown that a combination of medication, surgery, and lifestyle modifications can effectively treat CVD [6]. These lifestyle changes include giving up smoking, cutting back on salt, keeping a healthy body weight, adopting a healthy diet, and getting regular exercise [7].

Despite significant advancements in the understanding and management of CVD risk factors, there exists a growing body of evidence suggesting that environmental factors, particularly noise pollution, may contribute to the development and progression of CVD [8, 9]. There is significant biological evidence suggesting that noise impacts human health [10]. In recent decades, the process of urbanization and industrialization has resulted in a significant, exponential rise in noise levels, affecting both urban and suburban areas [11, 12]. The rise in noise pollution, defined as harmful sounds disrupting daily life, has been linked to various health issues. These include sleep disturbances, heightened stress levels, and the development of cardiovascular disorders [9, 13, 14]. There’s growing concern that prolonged exposure to environmental noise, whether stemming from sources like traffic, industrial operations, or others, may play a crucial role in the development of CVD [15]. As an illustrative case, a case-control study conducted by Zhou and colleagues revealed that exposure to occupational noise may represent a potential risk factor for HTN among workers in the automobile industry [16]. Moreover, exposure to different types of noise, like road traffic, aircraft, and railways, could significantly increase the risk of atrial fibrillation (AF) [17].

In light of the emerging evidence regarding the potential link between noise pollution and cardiovascular disease, the need for a comprehensive evaluation of existing research is evident. This umbrella review is essential in light of the emerging evidence linking noise pollution and cardiovascular disease. Our primary aim is to comprehensively assess the existing research to understand how environmental noise impacts cardiovascular health.

Methods

Reporting

We conducted the current umbrella review under the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) [18] (Fig. 1).

Fig. 1.

PRISMA flow chart of study selection

Data sources

We conducted a comprehensive literature search across multiple databases, including PubMed, Scopus, and Web of Science (WOS) from the inception to 8 May 2025. These databases were selected to ensure the retrieval of a wide range of relevant meta-analyses.

Search strategy

A systematic search strategy was developed to identify eligible meta-analyses. The strategy included a combination of relevant keywords and Medical Subject Headings (MeSH) terms. The following key search terms were utilized: “Cardiovascular Diseases”, “Noise”, “Systematic review”, and “Meta-analysis”. The search strategy used in the PubMed, ISI, and Scopus databases is provided in the Supplementary Material file 1.

Study design

This umbrella review employs a systematic approach to synthesize and evaluate the existing meta-analyses that investigate the relationship between noise exposure and the risk of CVD.

Inclusion and exclusion criteria

The researchers utilized EndNote software (version 20) to import articles, automatically eliminating duplicates from the dataset. Two independent researchers selected relevant studies based on predefined inclusion criteria. Whenever uncertainties arose, they engaged in discussions to ensure mutual understanding. Upon refining their search strategy and eliminating repeated entries, they carefully analyzed the titles, abstracts, and full texts to identify and exclude unrelated studies. The inclusion and exclusion criteria are detailed below.

Inclusion criteria:

• Published in peer-reviewed journals.

• Investigated the relationship between noise exposure and CVD.

• Studies that examined both environmental and occupational noise exposure.

• Included quantitative data and effect estimates (for example, odds ratios and hazard ratios).

• Utilized a meta-analytic approach to synthesize primary studies.

• Used with an adult population.

The exclusion criteria were as follows:

• Non-systematic literature reviews or narrative reviews.

• Studies not published in English.

• Studies with insufficient data or unclear methodologies.

Data extraction and synthesis

Data extraction from the included meta-analyses encompassed the following aspects:

Author(s) and publication year, characteristics of the primary studies (for example, study design, sample size), exposure and outcome measures, effect estimates (for example, risk ratios, confidence intervals), and methodological quality assessment. Also, a systematic approach was applied to evaluate the quality of the included meta-analyses, using established tools or criteria relevant to the field.

Quality assessment

The quality of the included meta-analyses in this umbrella review was systematically evaluated using the GRADE (Grading of Recommendations, Assessment, Development, and Evaluation) framework. This comprehensive assessment considered factors such as study design, risk of bias, precision, consistency, directness, and publication bias. The quality of evidence for each review was graded as “high,” “moderate,” “low,” or “very low” based on these criteria. For more details, you can refer to the supplementary materials.

Statistical analysis

In the analysis section of our umbrella review, we employed the odds ratio (OR) and risk ratio (RR) as the effect size measures for synthesizing the findings from the included meta-analyses. Additionally, we calculated and reported I² statistics, which measure the degree of heterogeneity among the included studies. To address overlap, primary studies across meta-analyses were cross-checked, and sensitivity analyses excluded redundant entries. Heterogeneity sources (noise type, region) were analyzed post hoc. We also used the AMSTAR checklist 2 to assess the quality of the included studies. This AMSTAR 2 includes 16 questions regarding the quality of systematic reviews and meta-analyses. For more details, you can refer to the supplementary materials. The final quality is reported as “High”, “Moderate”, “Low”, and Critically Low”. All analyses were performed using CMA version 3 statistical software.

Results and discussion

Aim and trend

The current umbrella review was conducted to provide an update regarding the impact of noise exposure and potential risk for CVD by accumulating meta-analyses.

Study selection process

We presented the basis of our search steps in Fig. 1 according to the guidelines of PRISMA. After an initial search in global databases such as PubMed, Scopus, and Web of Science in 119 records, followed by the removal of duplicates, a total of 90 articles were identified for careful screening. Through title and abstract screening, 44 articles were selected for full-text assessment. Ultimately, 22 articles that met our inclusion criteria were chosen for inclusion in our umbrella review.

The main characteristics of the included studies

We illustrate the main characteristics of our studies in Table 1. From the included studies, eight studies evaluated the effect of noise on the risk of HTN [19–26], four studies assessed noise exposure effect on the risk of ischemic heart diseases (IHD) [21, 27–29], three studies assessed dysregulation of blood pressure [28, 30, 31], three studies evaluated stroke as an outcome of noise exposure [21, 32, 33], three assessed myocardial infarctions as their main result of noise exposure [33–35], two studies assessed the effect of noise exposure on risk of ECG abnormalities [20, 30], two studies assessed the effect of noise exposure on risk of CHD [36, 37], two studies assessed AF as a risk factor [33, 38], two studies assessed CVD as their result [33, 39], and Cardiovascular mortality, IHD mortality, and Stroke mortality were evaluated in two studies [38, 40]. From the included studies, nine were from China [22, 23, 25, 30, 32–34, 36, 38], three were from Germany [19, 26, 37], two from Iran [31, 35], two from the UK [39, 40], and each country of Brazil, Bulgaria, Italy, Sweden, Switzerland, and Netherlands had one study [20, 21, 24, 27–29, 40]. Additionally, fourteen studies reported their main results in risk ratio (RR) [21, 24–28, 32–36, 38–40] and eight studies reported their results in odds ratio (OR) [19, 20, 22, 23, 29–31, 37].

Table 1.

The main characteristics of the included studies

First author, Year of publication	Aim of study	Searching databases	Date of search	The number of total included studies	Number of total participants	Effect size	Main outcomes	Quality assessment
Brown, 2025 [39]	Noise and CVD	MEDLINE, The Cochrane Library, Web of Science, and Embase	Up to 20th October 2024	28	-	RR	1.03 [95% CI: 1.02–1.05	Low
Pyko, 2023[29]	Nosie and IHD	-	-	9	132,801	OR	1.03 (95% CI 1.00, 1.05)	Low
Fu, 2023 [33]	Noise and HF9, AF, CVD, Stroke, and MI	PubMed, Embase, and Web of Science	Articles published before April 4, 2022	23	-	RR	2% (RR 1.020, 95% CI 1.006–1.035) for CVD, 3.4% (1.034, 1.026–1.043) for stroke, 5% (1.050, 1.006–1.096) for heart failure, 1.1% (1.011, 1.002–1.021) for AF, 1% (1.010, 1.003–1.017) for MI, and 2.3% (1.023, 1.016–1.030) for HF	Low
Song, 2022[38]	Noise and AF3	Embase, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), SinoMed (CBM), Wanfang Data Knowledge Service Platform, China Science and Technology Journal VIP Database	January 5, 2022	5	3,866,986	RR	(1.05; 95% CI: 1.02–1.09)	Low
Liu, 2022[34]	Noise and MI1	PubMed, Embase, and Web of Science	December 19, 2021	20	13,764,940	RR2	(1.18, 95% CI: 1.12 − 1.24)	Moderate
Fu, 2022[32]	Noise and stroke	PubMed, Embase, Web of Science, and Scopus	June 26, 2022	21	16,075,204	RR	(1.03, 95%CI:1.00–1.07)	Moderate
Rabiei, 2021[31]	Noise and BP7	Medline/PubMed, Embase, Scopus, ISI/web of knowledge, and Google Scholar	2020 (March to May)	139	-	OR	(1.28, 95% CI: 1.15–1.42)	Very low
Teixeira, 2021[21]	Noise and IHD8, Stroke, and HTN	PubMed/Medline, Embase, Web of Science, Scopus, Lilacs + grey literature	April 2019 and January 2020	14	534,688	RR	(1.29, 95% CI 1.15–1.43) for IHD, (1.11, 95% CI 0.88–1.39) for Stroke, and (1.07, 95% CI 0.90–1.28) for HTN	Low
Chen, 2021[25]	Noise and HTN	PubMed and Embase	October 2019	11	224,829	RR	(1.18; 95% CI: 1.06 to 1.32).	Moderate
Cai, 2020[40]	Noise and cardiovascular mortality	PubMed, Scopus, Web of Science, and EMBASE	January 01, 2000, and October 05, 2020	13	-	RR	1.01 (95% CI: 0.98, 1.05)	Moderate
Khosravipour, 2020[35]	Noise and MI	Scopus, Web of Science, Embase, and PubMed	November 29, 2019	13	1,626,910	RR	1.02 (95%CI: 1.00, 1.05)	High
Bolm-Audorff, 2020[26]	Noise and HTN6	Medline, Embase, Scopus, Web of Science	May 19, 2019	24	-	RR	1.81 (95% CI 1.51–2.18)	High
Yang, 2018[30]	Noise and BP, and ECG abnormalities	PubMed, Embase, Chinese SciencePeriodical Database, Chinese Science and Technology JournalDatabase, and Chinese Journal Full–text Database	2000 to 2017	11	7839	OR	2.55 (95% CI: 1.94–3.36) for BP and 2.27 (I2 = 22%, 95% CI: 1.96–2.62) for ECG abnormalities	Moderate
Dzhambov, 2018[24]	Noise and HTN	MEDLINE (PubMed) and EMBASE (ScienceDirect)	August 5, 2017	14	-	RR	1.01 (95% CI: 0.98, 1.05)	Low
Fu, 2017[23]	Noise and risk of HTN	PubMed and Embase	December 2016	32	264 678	OR	1.62 (95% CI: 1.40–1.88)	Low
Miao, 2016[36]	Noise exposure and CHD	PubMed and Web of Knowledge	October 2015	8	23,749	RR	(1.21, 95% CI = 1.05–1.40)	Very low
Huang, 2015[22]	Noise and HTN	PubMed, Embase, Web of Science, the Cochrane Library, and the Chinese Biomedical Literature	PubMed, Embase, the Cochrane Library, Web of Science, and the Chinese Biomedical Literature Database	5	16,784	OR	1.63 (95% CI, 1.14–2.33)	Moderate
Vienneau, 2015[27]	Noise and IHD	PubMed and EMBASE	for the 20-year period prior to January 2014	10	-	RR	1.06 (95% CI 1.03–1.09)	Low
Babisch, 2014[37]	Noise and CHD4	PubMed and Scopus	2013	14	-	OR5	1.08 (95% CI: 1.04,1.13)	Very low
Van Kempen, 2012[19]	Noise and HTN	PubMed	until 2010	24	-	OR	1.03 (95% CI:1.01–1.05)	Very low
Tomei, 2010[20]	Noise and HTN and ECG abnormalities	PubMed Embase Scopus BioMed Central Toxline NIOSHTIC-2	from 1950 to May 2008	15	18,658	OR	2.51 (95% CI: 2.00 to 3.26) for HTN and 2.47 (95% CI: 1.71 to 3.58) for ECG abnormalities.	Low
Van Kempen, 2002[28]	Noise, BP, and IHD	MEDLINE, EMBASE, BIOSIS, and SCISEARCH	between 1970 and 1999	43	-	RR	1.14 (95% CI 1.01–1.29)	Low

1 = Myocardial infarction / 2 = Risk ratio / 3 = Atrial fibrillation / 4 = coronary heart disease / 5 = Odd ratio / 6 = Hypertension / 7 = Blood pressure / 8 = ischemic heart disease

Result of quality assessment

We showed the main result of our quality assessment conducted by the GRADE approach in Table S1. According to the result of the quality assessment, two studies were high quality [26, 35], six studies were moderate [22, 25, 30, 32, 34, 40], ten were low [20, 21, 23, 24, 27–29, 33, 38, 39], and four studies were very low quality [19, 31, 36, 37]. Based on the result of quality assessment, studies discussing the potential effect of noise on the risk of HTN and myocardial infarction had higher quality compared to other outcomes [26, 35]. In Table S2, we presented the quality assessment based on the AMSTAR-2 framework. This assessment found that seven studies were of moderate quality [22, 25, 27, 32–34, 39], nine were low quality [20, 21, 23, 24, 28–30, 38, 40], four were critically low [19, 31, 36, 37], and two were classified as high quality [26, 35].

Main results

Risk of HTN

Through a systematic search and meticulous screening process, we evaluated eight studies to assess the relationship between noise exposure and the risk of HTN [19–26]. Using the GRADE approach to assess the quality of the studies, we determined that the study by Bolm-Audorff in 2020 exhibited the highest level of quality among the selected studies [26]. According to their findings, it was observed that the risk of HTN could significantly increase in individuals exposed to noise levels of 80 decibels (dB) or higher, with a calculated risk ratio (RR) of 1.81 (95% CI: 1.51–2.18).

Risk of AF

In our analysis, two of the included studies examined the impact of noise exposure on the risk of AF. According to Song et al., their findings revealed a statistically significant association between noise exposure and the risk of AF, with an RR of 1.05 and a 95% CI of 1.02–1.09 [38].

Risk of CHD

Our analysis included two studies that examined the impact of noise exposure on the risk of CHD. Babisch’s study yielded a significant pooled estimate of the RR, with a value of 1.08 (95% CI: 1.04–1.13) for each increase in the weighted day-night noise level [37]. Similarly, Miao et al. also identified a significant association between noise exposure and the risk of CHD, reporting an RR of 1.21 (95% CI: 1.05–1.40) [36].

Risk of MI

In our analysis, three studies investigated the risk of MI among individuals exposed to noise [33–35]. Following the GRADE quality assessment, Khosravipour’s study was identified as a higher-quality article. Their findings suggested that noise exposure may lead to a minimal, non-significant increase in the risk of MI, with an RR of 1.02 (95% CI: 1.00, 1.05) [35].

Risk of IHD

Four studies in total were included in our analysis to assess the impact of noise exposure on the risk of IHD [21, 27–29]. Following the quality assessment conducted using the GRADE approach, Vienneau et al. ‘s study was identified as the higher quality article among the four studies [27]. Their main result revealed a pooled RR of 1.06 (95% CI: 1.03–1.09) for IHD per each 10-decibel (dB) increase in noise exposure. Notably, the linear exposure-response relationship began to show an effect at noise levels as low as 50 dB.

Risk of stroke

In our analysis, three studies were dedicated to assessing the impact of noise exposure on the risk of stroke [21, 32, 33]. After employing the GRADE approach, Fu et al.‘s study was identified as higher quality research [32]. Their findings indicated a noteworthy association between noise exposure and the risk of stroke. Specifically, they discovered that the risk of stroke incidence increased by up to 4% for every 10 dB increment in noise exposure.

Risk of stroke mortality

We had only one study that focused on the impact of noise exposure on the risk of stroke mortality [40]. According to Cai et al.‘s findings, the pooled RR for mortality from stroke increased by 1.05 (95% CI: 0.97, 1.14) for every 10 dB increase in noise exposure.

Risk of IHD mortality

In our analysis, we identified a single study that specifically examined the impact of noise exposure on the risk of IHD mortality (Cai et al.) [40]. According to their findings, the pooled RR for mortality from IHD increased by 1.03 (95% CI: 0.99, 1.08) for every 10 dB increase in noise exposure.

Risk of cardiovascular mortality

During our investigation, we were able to locate just one study (Cai et al.) that looked explicitly at how noise exposure affected the risk of death from cardiovascular diseases [40]. Their results showed that for every 10dB increase in noise exposure, the pooled RR for death from cardiovascular diseases increased by 1.01 (95% CI: 0.98, 1.05).

Risk of BP

Based on our results, we included three articles in our analysis that examined the effect of noise exposure on the risk of BP dysregulations [28, 30, 31]. Following the application of the GRADE approach for quality assessment, Yang et al.‘s study was determined to be a higher-quality article. Their main result indicated that the risk of developing high BP for individuals exposed to noise is 2.55 times higher than for the control group (95% CI: 1.94–3.36) [30].

Risk of ECG abnormalities

In our analysis, we considered two studies that explored the effect of noise exposure on the risk of ECG abnormalities [20, 30]. Following the application of the GRADE approach, Yang et al.‘s study was chosen as the higher-quality article [30]. Their main result revealed that the risk of developing ECG abnormalities is 2.27 times higher among individuals exposed to noise compared to the control groups (95% CI: 1.96–2.62).

In Fig. 2, we summarize the total effect of noise exposure on the risk of cardiovascular diseases based on the type of reported data (OR or RR).

Fig. 2.

Result of included studies. A: Assessing the effect of noise exposure on the risk of cardiovascular diseases by reporting an odds ratio (OR). B: assessed the effect of noise exposure on the risk of cardiovascular diseases by reporting risk ratio (RR)

Our findings suggest a compelling association between noise pollution and increased HTN, AF, CHD, and IHD risk. The exposure-response relationship revealed a significant impact of noise exposure at levels as low as 50 dB. In a 2013 case-control study by Zhou et al., they examined the impact of occupational noise exposure on HTN among 1527 automobile company workers. The study found a significant association between occupational noise exposure and HTN, indicating that noise-exposed workers had a higher risk of HTN. The relationship between noise exposure and HTN was also found to be nonlinear [16]. Moreover, in a recent cross-sectional study at an aircraft manufacturing enterprise, researchers examined the connection between chronic occupational noise exposure and HTN. Among 4746 participants, primarily middle-aged men, a significant association was found. High occupational noise exposure (≥ 85 dBA) was linked to a greater risk of HTN, especially in younger participants [41].

Thacher and colleagues conducted a comprehensive study investigating the effects of road, railway, and aircraft noise on the risk of IHD and its subtypes. This large-scale cohort study included over 2.5 million individuals aged 50 and older in Denmark, with a follow-up period spanning 12 years. The findings revealed a significant association between road traffic noise at the most exposed façade and an increased risk of both IHD and myocardial infarction. Notably, the exposure-response relationships observed were nearly linear, underscoring the dose-dependent nature of the risk [42].

Recent studies have highlighted the significant health risks posed by transportation noise, particularly in developing nations. A cross-sectional study in Srinagar, India, found that residents exposed to road traffic noise levels above 60 dB(A) faced 2.24 times higher odds of IHD. Notably, males showed a 16% higher prevalence of the disease than females [43]. Similarly, another study demonstrated that every 5 dB(A) increase in road traffic noise was associated with a 2.25 times higher risk of CAD. Subgroup analysis revealed that older individuals, those with higher stress levels, poor sleep quality, or noise sensitivity were particularly vulnerable [44]. Both studies emphasize the importance of integrating noise mitigation strategies into public health policies, with a focus on noise mapping, urban mobility optimization, and stricter regulations to curb noise pollution’s adverse health impacts.

Researchers also looked at the relationship between AF, a heart condition, and long-term exposure to air pollution and road traffic noise in a study comprising 23,528 female participants from the Danish Nurse Cohort. In comparison to nurses exposed to lower noise levels (below 48 dB), the results showed that nurses exposed to greater levels of road traffic noise (above 58 dB) had an 18% increased risk of AF [45].

Despite the strong evidence for the link between noise pollution and several cardiovascular outcomes, our analysis did not find a significant impact on myocardial infarctions, IHD mortality, or cardiovascular mortality. This suggests that noise pollution’s effects may be more pronounced for certain cardiovascular conditions. A study conducted around São Paulo’s airport in Brazil from 2011 to 2016 investigated the link between aircraft noise and cardiovascular mortality. Among areas exposed to high noise levels (> 65 dB), there was a slight increase in the relative risk for cardiovascular mortality [46]. While our study did not find a significant association between noise exposure and cardiovascular mortality, it is essential to acknowledge that our findings may diverge from certain prior research. Several factors could contribute to these discrepancies, including variations in the study populations, differences in noise exposure levels, and variations in data collection and analysis methods. Additionally, the complexity of the relationship between noise pollution and CVD warrants further investigation, as individual susceptibility and other confounding variables may play crucial roles in shaping the outcomes of such studies.

In addition, the observed elevated risk of stroke and stroke mortality in individuals exposed to noise highlights the need for further investigation into the mechanisms through which noise pollution may contribute to cerebrovascular health issues.

Seidler et al. assessed the potential impact of noise exposure on the risk of stroke in a case-control study. This study investigated the stroke risks associated with aircraft, road traffic, and railway noise exposure among over a million individuals aged 40 and older living near Frankfurt Airport. The research identified a 7% increased stroke risk for those exposed to nighttime aircraft noise levels exceeding 50 dB, even with lower continuous noise exposure. For road and railway traffic noise, a positive linear exposure-risk relationship was observed, with a 10 dB increase leading to a 1.7% and 1.8% increased stroke risk, respectively [47]. The study highlights the potential link between traffic noise and an increased risk of stroke, emphasizing the importance of nighttime maximum noise levels in influencing stroke risk, even with low continuous noise exposure.

To justify the different results between the articles, several aspects could be discussed. Recognizing that individuals may vary in their susceptibility to the effects of noise pollution is crucial. Some people may be more resilient to noise-related stress, while others may be particularly vulnerable. Factors such as genetics, pre-existing health conditions, and socioeconomic status can all play a role in determining an individual’s response to noise pollution [48–51]. Emerging evidence elucidates physiological pathways linking chronic noise exposure to cardiovascular pathology. Experimental and epidemiological studies suggest that noise activates the sympathetic nervous system, leading to increased catecholamine release, elevated heart rate, and vasoconstriction, which may precipitate hypertension and arrhythmias. Concurrently, chronic noise exposure induces endothelial dysfunction through reduced nitric oxide bioavailability and increased oxidative stress, fostering pro-inflammatory states and atherosclerosis. Oxidative stress, driven by noise-induced overproduction of reactive oxygen species, further exacerbates vascular damage and contributes to ischemic heart disease [46]. Sleep disruption caused by noise fragments restorative sleep stages, dysregulates circadian rhythms, and activates hypothalamic-pituitary-adrenal axis signaling, amplifying metabolic and cardiovascular risk [14, 51]. These mechanisms align with recent WHO guidelines, which recognize environmental noise as a modifiable risk factor for cardiovascular morbidity, emphasizing the need for policy interventions to mitigate exposure [4, 14].

Future studies should consider these individual differences and explore whether certain subpopulations are at higher risk, allowing for more targeted interventions and public health strategies.

In addition to physiological mechanisms, psychosocial factors related to noise exposure should also be explored [52, 53]. Chronic noise pollution can lead to increased stress, sleep disturbances, and reduced overall quality of life, all of which can contribute to CVD risk [13, 54]. Chronic noise exposure is a persistent environmental stressor that activates the sympathetic nervous system and endocrine signaling pathways. According to the established noise reaction model, even chronic low levels of noise can trigger non-auditory effects, including disturbances of activity, sleep, and communication, which subsequently generate emotional responses such as annoyance and psychological stress [55]. This chronic stress activation presents profound implications for cardiovascular health through multiple pathophysiological mechanisms. Persistent activation of stress responses leads to dysregulation of the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal-medullary system, resulting in elevated levels of stress hormones, including cortisol, adrenaline, and noradrenaline [56]. These neurohormonal changes have direct consequences on cardiovascular function, promoting vasoconstriction, increased cardiac output, and heightened blood pressure variability [57]. Research into the psychological and emotional responses to noise exposure and their impact on cardiovascular health could provide valuable insights into this multifaceted issue.

Public health recommendations

• Routine Blood Pressure Monitoring.

• Integrate Noise Exposure into CVD Risk Stratification.

• Awareness Campaigns.

• Policy Interventions for Noise Mitigation.

Limitation

1. Variability in Study Quality and Reporting: The quality and reporting standards of the included meta-analyses varied significantly. While some studies employed robust methodologies and provided comprehensive reporting, others had limitations in design or incomplete reporting of key details. This variability affects the consistency and reliability of the data analyzed.

2. Ecological vs. Individual-Level Exposure Assessment: Noise exposure levels were often assessed at the ecological level, using average noise levels in residential areas or communities. However, individual-level exposure data were limited in many of the included studies. This ecological approach may not fully capture individual variations in exposure, potentially leading to the misclassification of noise exposure levels for certain individuals.

3. Temporal Trends in Noise Pollution: Noise exposure levels in urban areas have changed over time due to technological advancements and policy measures. Unfortunately, the current review does not account for potential temporal trends in noise pollution and their impact on cardiovascular health.

4. Overlap of Studies Across Meta-Analyses: Some studies were included in more than one meta-analysis, resulting in overlapping studies. This overlap presents a challenge for fully correcting for redundancy in our analysis, as noted in the context of the CCA method [58].

Clinical responses for high-risk populations

Individuals residing in high-noise environments, such as near airports, highways, or industrial zones, face elevated cardiovascular risks. To mitigate these risks, the following clinical strategies are proposed:

1. Targeted Screening Programs:

   • Routine Blood Pressure Monitoring: Annual or biannual blood pressure screenings for individuals in areas with sustained noise levels ≥ 50 dB (e.g., near major roads or airports). This aligns with the observed exposure-response relationship for hypertension starting at 50 dB.
   • Cardiovascular Function Assessments: Electrocardiograms (ECGs) and stress tests for populations with long-term noise exposure (> 5 years) to detect early signs of arrhythmias or ischemic heart disease.

2. Stress Management Interventions:

   • Cognitive-behavioral therapy (CBT) or mindfulness-based programs to reduce noise-induced psychological stress, which exacerbates sympathetic activation and hypertension.
   • Partnerships with occupational health services to provide noise-exposed workers (e.g., aviation staff, drivers) with access to stress-reduction resources.

3. Community-Healthcare Collaboration:

   • Urban planners and healthcare providers should collaborate to map noise hotspots and prioritize these areas for CVD prevention initiatives.
   • Mobile health units could offer on-site screenings in high-risk neighborhoods.

Conclusion

Our umbrella review highlights the substantial impact of noise pollution on cardiovascular health. Noise exposure is associated with an increased risk of HTN, AF, CHD, and IHD. These effects can be observed at noise levels as low as 50 dB. While noise exposure does not significantly affect myocardial infarctions or cardiovascular mortality, it elevates the risk of stroke and stroke mortality. Blood pressure dysregulations and ECG abnormalities are more prevalent in individuals exposed to noise. Recognizing noise pollution as a major contributor to cardiovascular diseases is vital, given the growing urbanization and industrialization. Public health interventions and further research are crucial to address this issue and protect cardiovascular well-being.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Abbreviations

AF

Atrial Fibrillation

BP

Blood Pressure

CHD

Coronary Heart Disease

CVD

Cardiovascular Disease

db

Decibel

ECG

Electrocardiogram

GRADE

Grading of Recommendations, Assessment, Development, and Evaluation

HTN

Hypertension

IHD

Ischemic Heart Diseases

MESH

Medical Subject Headings

MI

Myocardial Infarction

OR

Odds Ratio

PRISMA

Preferred Reporting Items for Systematic Reviews and Meta-Analyses

RR

Risk Ratio

WOS

Web of Science

Author contributions

ST and SST designed and conceptualized the study. ST and SST also revised the manuscript. GB contributed to performing the statistical analyses and interpreting data; SRG and MP contributed to the data collection and were responsible for the interpretation of the results. GB contributed to writing and revising the manuscript. All authors read and approved the final version of the manuscript; and agreed to be responsible for all aspects of the study including the accuracy of the work done.

Funding

No funding.

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.