Noise and air pollution as risk factors for hypertension: part I – epidemiology

Abstract

Traffic noise and air pollution are two major environmental health risk factors in urbanized societies that often occur together. Despite co-occurrence in urban settings, noise and air pollution have generally been studied independently, with many studies reporting a consistent effect on blood pressure for individual exposures. In the present reviews, we will discuss the epidemiology of air pollution and noise effects on arterial hypertension and cardiovascular disease (part I) and the underlying pathophysiology (part II). Both environmental stressors have been found to cause endothelial dysfunction, oxidative stress, vascular inflammation, circadian dysfunction, and activation of the autonomic nervous system, thereby facilitating the development of hypertension. We also discuss the effects of interventions, current gaps in knowledge, and future research tasks. From a societal and policy perspective, the health effects of both air pollution and traffic noise are observed well below the current guideline recommendations. To this end, an important goal for the future is to increase the acceptance of environmental risk factors as important modifiable cardiovascular risk factors, given their substantial impact on the burden of cardiovascular disease.

Graphical Abstract

Introduction

A growing body of evidence supports that environmental stressors such as noise and air pollution are pervasive risk factors endangering the health of millions of people across the world^1,2. Given the substantial impact of these two environmental exposures on health parameters such as blood pressure, it is reasonable to hypothesize that a common pathophysiologic link ultimately may mediate their effects on cardiovascular diseases. Given that hypertension is the leading risk factor for global disability and mortality³, the relative contribution of environmental stressors to the development of arterial hypertension is, therefore, of substantial clinical interest. With the present review (part I), we will focus on noise and air pollution and their impact on cardiovascular disease with a focus primarily on the association with arterial hypertension.

The Burden of Disease Posed by Noise and Air Pollution

Environmental noise is increasing due to urban growth and increased mobility demands and is now considered the second-most significant environmental cause of ill health in Western Europe, behind fine particulate matter pollution⁴. According to the EEA report 2020, long-term exposure to environmental noise is estimated to cause 12,000 premature deaths and contribute to 48,000 new cases of ischemic heart disease per year in Europe⁵. It is also estimated that 22 million people suffer chronic high annoyance and 6.5 million people suffer chronic high sleep disturbance in Europe alone⁵. More precise global estimates are not available.

Ambient air pollution is a heterogeneous complex mixture of particulate matter (PM) and gaseous components that vary considerably by season, source, and atmospheric conditions⁶. PM originates from fossil fuel use, natural and synthetic crustal materials, and agriculture. The most common method to classify PM particles is based on size; coarse PM <10μm (PM₁₀), fine PM <2.5μm (PM_2.5), and ultrafine PM <0.01 μm (PM_0.1). The chemical constituents of PM vary substantially by source. They may include transition metal ions, endotoxins, reactive aldehydes, and organic compounds such as toxic polycyclic aromatic hydrocarbons (PAHs) that largely determine it’s toxicity^7,8. Among the gaseous pollutants, tropospheric ozone (O₃) is most closely associated with health effects, although the links between most gaseous pollutants and hypertension remain poorly investigated^6,9. Worldwide, excess air pollution attributed to CVD mortality was 4.2 million annually (Graphical abstract). In Europe (41 countries), air pollution, primarily PM_2.5, was held responsible for approximately 790,000 excess deaths per year, 40% due to ischemic heart disease and 8% to stroke¹⁰. The total excess CVD mortality due to air pollution in Europe was estimated at 377,000 (95%,CI:317,000–434,000) per year,¹⁰ whereas in North America, it was 126,000 (95%,CI:109,000–142,000), and in Asia, 3.25(95%,CI:2.53–3.85) million per year (Figure 1). Recent estimates based on alternative exposure estimates and exposure-response functions indicate that air pollution may even be responsible for as many as 8.8–12 million all-cause deaths annually^11,12.

Figure 1.

Estimated global excess mortality with cardiovascular causes attributable to air pollution in North America. Europe and Asia. ¹⁰

The WHO estimates that 97% of the world’s population resides in places where annual mean air pollution levels exceed the annual WHO guideline level of 10μg/m³, recently reduced to 5μg/m³, a level at which air pollution continues to have a significant impact on the health¹¹. Notably, the EU’s air pollution limit of 25μg/m³ exceeds that by the WHO by 5×¹³. A 2020 estimate stated that at least 113 million people (>20% of the population) in Europe are exposed to road traffic noise levels exceeding 55 dB(A) (calculated as the 24-h average sound levels, known as the day–evening–night noise level (L_den))¹. In the United States in 2013, 104 million individuals were exposed to annual environmental L_EQ(24) levels of >70dB(A). At least 146 million people were at potential risk of hypertension due to noise¹⁴, supported by a 2014 study demonstrating least 72.6 million urban US residents were exposed to annual L_EQ(24) levels of >70 dB(A) in 2010¹⁴. Considering the new recommendations of the World Health Organisation (WHO), there is a clear gap concerning the legal thresholds in the EU and USA for air pollution. In contrast, only guideline values exist for traffic noise (Tables 1 and 2).

Table 1.

WHO air quality guidelines and national air pollution legal thresholds for annual average concentrations (https://apps.who.int/iris/handle/10665/345329, https://www.epa.gov/criteria-air-pollutants/naaqs-table).

Air pollutant	WHO 2005	WHO 2021	EU threshold	US threshold
Nitrogen dioxide (•NO2)	40 μg/m3	10 μg/m3	40 μg/m3	100 μg/m3 (53 ppb)
PM2.5	10 μg/m3	5 μg/m3	25 μg/m3	12 μg/m3
PM10	20 μg/m3	15 μg/m3	40 μg/m3	(50 μg/m3) canceled in 2006

Table 2.

WHO recommended limits for noise exposure levels and national legal thresholds for average noise exposure (https://www.euro.who.int/__data/assets/pdf_file/0009/383922/noise-guidelines-exec-sum-eng.pdf).^*

Noise source	Lden	Lnight	Quality of evidence	EU / US threshold
Road noise	< 53 dB	< 45 dB	strong	No legally binding limits for ambient noise. Legal limits for LREL,8h of 85–90 dB (US) and LEX of 80–85 dB (EU) for occupational noise sources; peak (impulse) noise limits 135–140 dB.
Railway noise	< 54 dB	< 44 dB	strong
Aircraft noise	< 45 dB	< 40 dB	strong
Wind turbines	< 45 dB	-	limited
Leisure ambient noise	< 70 dB (LAeq,24h)	-	limited

^*dB, decibel; Lden, average sound pressure level over 24h adjusted for day-evening-night with a penalty of 5 dB for the evening time (7–11pm or 6–10pm) and a penalty of 10 dB for the night time (11pm-7am or 10pm-6am); Lnight, average sound pressure level for night time (11pm-7am or 10pm-6am); LAeq, average sound pressure level over 24h (A-weighted means adjusted for the human acoustic range). The recommended limits are related to the most seriously exposed face of the building. Strong quality of evidence requires fast action of policy makers, whereas limited quality of evidence requires substantial discussions among the decision makers, also considering the opinion of scientists, clinicians, and health care system representatives. LREL,8h, recommended exposure level over 8h at workplace by the US CDC-associated National Institute for Occupational Safety and Health (NIOSH). LEX, recommended exposure level over 24h or 7d at workplace by the European agency for occupational safety and health (EU-OSHA)

The elderly and those with concomitant non-communicable diseases (NCD), such as hypertension, type2 diabetes, and obesity, are especially susceptible to environmental triggers.^10,15 Low-income groups, including historically disadvantaged populations, tend to be the most vulnerable. Indeed, there is evidence indicating that noise exposure may aggravate health inequalities via an unequal distribution of exposure between different socioeconomic groups in a manner as has been suggested for air pollution.^16–18 The global economic impact of air pollution is considerable, given its effects in reducing life expectancy, increasing medical costs, and reducing productivity through lost working days¹³. The global mean overall loss of life expectancy is 2.9y in response to ambient air pollution and, importantly, 2.2y in response to tobacco smoking, mainly causing cardiovascular and pulmonary disease in the elderly population (Figure 2 A–D).¹⁹

Figure 2.

Mean global, and country-level loss of life expectancy from ambient air pollution (A) and tobacco smoking (B) of death refers to 2015.

(C) Age distribution of excess mortality from ambient air pollution. Globally, about 25% of the attributable mortality occurs at the age of <60 years: in Europe, about 11%, and in Africa, about 55%. (D) Percentage of global life expectancy loss from air pollution by different disease categories. CEV,cerebrovascular disease; COPD,chronic obstructive pulmonary disease; IHD,ischemic heart disease; LC,lung cancer; LRI,lower respiratory infections; NCD,non-communicable diseases. A-D adapted from ¹⁹ with permission. Copyright ^© 2020, Oxford University Press.

Recent epidemiological/observational evidence for adverse effects of noise pollution on hypertension

Many studies suggest that environmental noise exposure from traffic sources may be an essential risk factor for hypertension. In a meta-analysis of 26 studies conducted by a WHO expert group, a relative risk (RR) of 1.05 (95%,CI:1.02–1.08 per 10dB L_DEN) for the prevalence of hypertension in response to road traffic noise exposure was reported.²⁰ Other selected exposure-hypertension-association studies support this link with moderate to high heterogeneity amongst studies. Fu et al. analyzed exposure to the community and occupational noise (odds ratio (OR) 1.06, 95%,CI:1.04–1.08) (odds ratio (OR) 1.06, 95%,CI:1.04–1.08)²¹, and Chen et al. found a relative risk of 1.13 (95%,CI:0.99–1.28) with moderate heterogeneity.²² A meta-analysis found road traffic noise exposure significantly associated with 7% higher odds of prevalent hypertension in adults but no association for systolic and diastolic blood pressure in adults and children,²³. In contrast, Dzhambov et al. found suggestive evidence for increases in systolic and diastolic blood pressure in children exposed to road traffic noise at school/kindergarten and home, but with high overall heterogeneity among studies and evidence of publication bias.²⁴ Based on studies published from 2011–2017, a meta-analysis reported a RR of 1.018:95%,CI:0.984–1.053 for the association between road traffic noise and risk of incident hypertension in adults²⁵. Noise annoyance and psychological distress were associated with higher blood pressure in children and adolescents in the CASPIAN-V Study²⁶. Shin et al. found that road traffic noise increases the risk of incident hypertension by 2% (hazard ratio (HR):1.02,95%,CI:1.01–1.03)²⁷, while no evidence was shown in a Danish study (HR:0.999, 95%,CI:0.980–1.019) in response to road traffic noise exposure²⁸.

Cross-sectional data from seven European countries yielded a RR of 1.03, (95%,CI:1.01–1.06 per 10dB(A),L_night) concerning aircraft noise exposure and hypertension²⁹. Data from 1,244 aircraft noise-exposed adults living near major French airports demonstrated a higher hazard ratio of hypertension (HR:1.36, 95%,CI:1.02–1.82) and increased systolic and diastolic blood pressure³⁰ while a weakly positive relationship between aircraft noise and incident hypertension was found in two US cohort of women³¹ (aircraft noise dichotomized at 45dB(A), HRs were 1.04(95%,CI: 1.00–1.07) and 1.03(95%,CI:0.99–1.07), respectively) and in a US cohort of Mexican-Americans (HR:1.10,95%,CI:0.96–1.26 for 24h noise exposure per 11.6 dB increase)³². The HYENA study established a significant association between nighttime aircraft noise and hypertension prevalence but no association for daytime aircraft noise,³³ correlating to increased arterial stiffness and worsened endothelial function and blood pressure in patients with coronary artery disease following nighttime noise events³⁴. (Figure 3A,B)

Figure 3.

(A) Association between brachial-ankle pulse wave velocity (baPWV) and the number of daytime and nighttime noise events by quartiles. Adapted from ³³ with permission from the authors. (B) Odds ratios (ORs) of hypertension in relation to aircraft noise (5-dB-categories). L_Aeq,16h, and L_night were included separately in the model. Adjusted for country, age, sex, body mass index, alcohol intake, education, and exercise. The error bars denote 95% confidence intervals (CIs) for the categorical (5-dB) analysis. The blue and red lines show the ORs and corresponding 95% CIs for the continuous analyses. Adapted from⁴⁴ with permission from the authors.

Cross-sectional data from the large UK-Biobank (N=502,651) yielded associations between exposure and increases in systolic (0.77%,95%,CI:0.60–0.95) and diastolic blood pressure (0.49%,95%,CI:0.32–0.65)³⁵. Higher residential noise exposure was also associated with higher systolic and diastolic blood pressure and increased risk of apparent treatment-resistant hypertension³⁶. Increased blood pressure due to noise exposure was also observed in a pooled analysis of 44,698 subjects³⁷. Indoor nocturnal noise levels were associated with higher systolic blood pressure in a cross-sectional analysis from Hong Kong^38,39. Evidence shows that even a short-term reduction in aircraft noise exposure levels, e.g., because of a COVID-19 lockdown, can lower blood pressure⁴⁰.

Associations between noise and arterial hypertension have been inconsistent^41–44, but differences in methodologies between the studies, patient profile, and concomitant environmental exposures may partially explain these differences. The shape of the exposure-response curve between noise levels and blood pressure is currently unknown.

Recent epidemiological/observational evidence for adverse effects of air pollution on hypertension

The association between air pollution and hypertension has been reviewed and meta-analyzed extensively.^45–47 Epidemiologic studies have consistently revealed an association between air pollution exposure and risk for hypertension and increased blood pressure in various national and sub-national cohorts⁹. The risk for increased blood pressure has been noted for coarse and fine particulates, in men and women and across a sizeable dose-response curve, with no evidence of attenuation at high levels⁹. The largest body of evidence is for PM_2.5 exposure. In a cohort of American women, long-term exposure to PM_2.5 was prospectively associated with hypertension risk (HR:1.06,95%,CI:1.02–1.11)⁴⁸. Likewise, in Spanish adults, higher exposure to PM_2.5 and PM₁₀ was significantly related to an increased incidence of hypertension⁴⁹ and similar in cohorts of Chinese children and adolescents⁵⁰ and adults⁵¹. In a Chinese cohort exposed to extreme levels of air pollution, a relationship between black carbon (an anthropogenic surrogate of fossil fuel combustion) and ambulatory blood pressure was demonstrated: a 1μg increase in black carbon during the previous 10h was associated with an increase in systolic blood pressure of 0.53 mm Hg and diastolic blood pressure of 0.37mm Hg (95%,CI:0.17–0.89 and 0.10–0.65mmHg, respectively)⁵², which also caused heart rate variability suggestive of sympathetic dominance⁵². In India, higher levels of PM_2.5 exposure were associated with a greater risk of incident hypertension and increased systolic blood pressure⁵³. In the multicenter PURE study, PM_2.5 exposure in 21 countries showed an increased OR of 1.04 (95%,CI:1.01–1.07) for hypertension risk and substantial systolic and diastolic blood pressure increases⁵⁴.

Increases in short-term ambient PM_2.5 by 10μg/m³ are consistently associated with 0.5–3mm Hg elevations in systolic and diastolic blood pressure over the ensuing few days⁵⁵. In a study using hourly PM_2.5 and PM₁₀ ambient levels in 7,108 non-hypertensive subjects from seven Chinese cities, exposure to PM_2.5 was significantly associated with near-immediate elevated blood pressure, which attenuated slowly over 12h⁵⁵. An interquartile range (IQR, 33μg/m³) increase of PM_2.5 was significantly associated with cumulative increments of 0.58mmHg for SBP, 0.31mmHg for DBP over 0–12h. The exposure-response relationship curves were almost linear but flattened at very high concentrations⁵⁵. Longer-term exposures have been linked with chronic elevations in blood pressure and increased prevalence and incidence of hypertension as well^15,47. A meta-analysis from Zhao et al. on the association between long-term exposure to PM_2.5 and hypertension found a RR of 1.21 (95%,CI 1.07–1.35) for incident hypertension risk and an OR of 1.06 (95%,CI 1.03–1.09) for prevalent hypertension⁴⁵, and comparable results by Niu et al. showed that exposure to PM₁, PM_2.5, and PM₁₀ were significantly related to a higher risk of hypertension along with increases in systolic and diastolic blood pressure⁵⁶. These results were also confirmed by Qin et al., indicating that adult hypertension incidence was significantly influenced by exposure to PM_2.5 (OR:1.10,95%,CI:1.07–1.14), PM₁₀ (OR:1.04,95%,CI:1.02–1.07), and sulfur dioxide (SO₂, OR:1.21,95%,CI:1.08–1.36) with weaker associations in children⁴⁶. In contrast, associations between air pollution exposure and prevalent hypertension risk, as well as elevated blood pressure in children and adolescents, were found in a meta-analysis from Yan et al.⁵⁷ Significantly increased blood pressure among children and adolescents in response to short- and long-term exposure to PM was also demonstrated in a meta-analysis from Huang et al.⁵⁸ Altogether, a good body of evidence endorses the causal role of air pollutants in increased blood pressure and the development of hypertension across a broad range of concentrations, even in countries with relatively good air quality, such as Canada, the USA, and Western Europe. As such, these findings have implications for worldwide public health.

Evidence for effects of Air Pollution on Blood Pressure from Controlled Exposures and Intervention Studies

In controlled human studies, acute exposure to PM_2.5 and dilute diesel exhaust (ultrafine particles, UFP) results in rapid conduit or microvascular endothelial dysfunction or transient constriction of a peripheral conduit vessel that is reversible⁷. Concentrated PM_2.5 has not always been shown to induce endothelial dysfunction, underscoring the importance of pollution composition, propensity, and methods⁵⁹. In many studies, where an impact on endothelial function was discernible, blood pressure was either not measured and/or was not a pre-specified endpoint, and thus no changes were observed. Several controlled exposure studies have convincingly shown short-term increases in systolic and diastolic blood pressure (1–5mmHg in systolic blood pressure (SBP) and 1–3mmHg in diastolic blood pressure [DBP]) in response to particulate matter exposure (fine, coarse, and diesel exhaust) and have been reviewed previously^7,8,60. Gaseous co-pollutants such as ozone have limited to no effects on blood pressure. In a randomized crossover study of 87 healthy volunteers, 55–70 years of exposure to ozone for 3h (0ppb (filtered air), 70ppb ozone, and 120ppb ozone, alternating 15min of moderate exercise with 15min of rest did not have any effect on endothelial function or blood pressure⁶¹.

The impact of interventions such as N95 filters and/or indoor air filters in reducing PM_2.5 concentration has helped address causality (Supplemental table T1). Studies show that personal-level reductions in exposure to PM can decrease BP within a few days, demonstrating a cause-and-effect relationship. Randomized double-blind trials using portable air cleaners bolster support for the causal linkage between PM and high BP^62–64. One recent meta-analysis of 10 trials (n=604) demonstrated that 3.9 mm Hg significantly reduces systolic BP over 13.5 days by air cleaner usage⁶⁴. This benefit was observed in highly polluted and relatively clean environments, supporting a monotonic relationship between PM exposure and higher BP levels. In an analysis of the Systolic BP Intervention Trial (SPRINT) trial on Intensive BP-lowering, the benefits of intensive BP-lowering were more significant among patients chronically exposed to PM2.5 levels compared with those living in cleaner locations⁶⁵. These results generally suggest that future prevention trials should consider environmental factors and provide evidence of promise for personal strategies to lower air pollution as novel preventive interventions^60,66.

What needs to be done in the future?

There is a growing realization that co-exposures to noise and air pollution may represent an example of complex stressors that influence susceptibility through shared mechanisms⁶⁷. As we transition to macro-level interventions on urban infrastructure and city design to combat the threat of climate change, there we need to measure the impact of climate-specific measures that impact traffic and air pollutant co-exposure and cardiovascular events^68–70. Importantly, heart-healthy city design, including the reduction of heat island effects due to the generation of more green infrastructure and reduction of built area, is an essential concept for remodeling cities as they expanded⁶⁸. Herein, green infrastructure and built areas are suggested as essential confounders of the association between noise, air pollution, and hypertension⁶⁸, which have not been sufficiently considered in most published studies. Furthermore, it is essential to acknowledge an apparent lack of evidence from low- and middle-income countries in the case of noise and limited evidence for PM_2.5. Thus, extrapolating the evidence from western countries to other countries must be done cautiously. Developing technologies that provide combined access to personal cardiovascular health surrogates, such as blood pressure, in conjunction with data on environmental co-exposure, provides an unprecedented research opportunity⁷¹. Understanding the interaction of social and environmental factors in determining the onset and trajectory of hypertension may help provide novel solutions in addressing gaps in health inequities that chronically plague historically disadvantaged communities^17,18. The opportunity to design future studies that consider individual exposures to multiple environmental risk factors is within the scope of clinical trial design, given substantial access to big data, advances in machine learning, and artificial intelligence.

The availability of unbiased genetic data and environmental information provides additional opportunities to study gene-environment interactions. As Olden succinctly stated, “Genetics loads the gun and environment pulls the trigger”⁶⁸, nicely reflects the sentinel role omnipresent risk factors such as noise and air pollution play in manifesting underlying susceptibility, which otherwise may never manifest.