Road Traffic Noise and Incidence of Primary Hypertension

Background The quality of evidence regarding the associations between road traffic noise and hypertension is low due to the limitations of cross-sectional study design, and the role of air pollution remains to be further clarified. Objectives The purpose of this study was to evaluate the associations of long-term road traffic noise exposure with incident primary hypertension; we conducted a prospective population-based analysis in UK Biobank. Methods Road traffic noise was estimated at baseline residential address using the common noise assessment method model. Incident hypertension was ascertained through linkage with medical records. Cox proportional hazard models were used to estimate hazard ratios (HRs) for association in an analytical sample size of over 240,000 participants free of hypertension at baseline, adjusting for covariates determined via directed acyclic graph. Results During a median of 8.1 years follow-up, 21,140 incident primary hypertension (International Classification of Diseases-10th Revision [ICD-10]: I10) were ascertained. The HR for a 10 dB[A] increment in mean weighted average 24-hour road traffic noise level (Lden) exposure was 1.07 (95% CI: 1.02-1.13). A dose-response relationship was found, with HR of 1.13 (95% CI: 1.03-1.25) for Lden >65 dB[A] vs ≤55 dB[A] (P for trend <0.05). The associations were all robust to adjustment for fine particles (PM2.5) and nitrogen dioxide (NO2). Furthermore, high exposure to both road traffic noise and air pollution was associated with the highest hypertension risk. Conclusions Long-term exposure to road traffic noise was associated with increased incidence of primary hypertension, and the effect estimates were stronger in presence of higher air pollution.

E levated blood pressure contributes more to cardiovascular disease (CVD) and premature death than any other known and modifiable risk factor. 1  Traffic noise has emerged as an important environmental risk factor for CVD since 2010, with road traffic noise being mostly investigated for the associated health effects. 4 Epidemiological and animal studies indicate that traffic noise can trigger annoyance and disturb sleep, thus activating autonomic system and overproducing stress hormones, with subsequent activation of the renin-angiotensinaldosterone system. 5 Chronic exposure to traffic noise may cause a number of pathophysiological adaptations, such as increase in heart rate and cardiac output and a rise in blood pressure. It could also lead to development of other cardiovascular risk factors such as hyperglycemia, hypercholesterolemia, and blood clotting factor activation. These changes would ultimately manifest as CVD. 4,[6][7][8] Despite the biological plausibility of the link be- the association between road traffic noise and hypertension prevalence, with the evidence quality of very low due to the nature of cross-sectional study design. 9 An updated meta-analysis based on 14 cohort and case-control studies published between 2011 and 2017 reported that the incidence risk of hypertension was 1.02 (95% CI: 0.98-1.05) per 10 dB increase in road traffic noise. The quality of evidence was rated as low, indicating that high quality prospective studies are needed to further strengthen this risk estimate. 10 The impact of ambient air pollution on hypertension is relatively well documented, although not all previous studies have considered both air pollution and road traffic noise contemporaneously. Given that road traffic commonly leads to both noise and air pollution, 11,12 it is important to address the potential interaction or confounding between these 2 common environmental exposures in relation to any CVD outcomes.
We recently reported in a cross-sectional analysis that long-term exposure to road traffic noise above 65 dB[A] was associated with small but statistically significant elevations in both systolic and diastolic blood pressure in the UK Biobank cohort, independent of air pollution. 13   All analyses were performed using R software (version 3.6.3), and 2-sided P value <0.05 was considered as statistically significant.

RESULTS
The mean age of the study participants at recruitment was 55.0 years, and 54.6% were female ( In the fully adjusted model (model 1), the associations between categories of road traffic noise and incident  Table 2).
The exposure-response curves between road traffic noise (L den and L night ) and incident primary hypertension were almost linear, with HRs increasing continuously with higher road traffic noise exposure ( Figure 1).
Elevated HRs of air pollution on incident primary hypertension were also observed (  (P interaction <0.05) ( Figure 2). Other personal characteristics did not seem to have significant modification effects and the detailed information is shown (Supplemental Tables 3 and 4).
Sensitivity analyses showed that the association between road traffic noise and incident primary hypertension was robust after further adjustment for central obesity status and physical activity level, or adjustment for sedentary time and sleep duration.
After excluding those who were identified with primary hypertension within 2 years during the followup period, the results remained robust (Supplemental Table 5).

DISCUSSION
In this prospective analysis of 246,477 study participants followed for a median of 8.1 years in UK Biobank, we found that higher long-term residential road traffic noise exposure was associated with an increased risk of incident primary hypertension in a dose-response relationship. Categorical analyses Values are n (%), mean AE SD, or mean AE SD (range). Participants with hypertension at baseline identified either through first occurrence medical records, or self-reported answers via verbal interview were excluded. suggested that associations were highest in participants with annual mean L den >65 dB[A] or L night >55 dB[A], and the associations were all robust to adjustment for PM 2.5 and NO 2 . In combined effects analyses, the highest incident risk was seen in those exposed to the highest level of both road traffic noise and air pollution, suggesting effects of road traffic noise on incident primary hypertension may be exacerbated in areas where air pollution level is high.
The associations of road traffic noise exposure with hypertension have been studied previously. 8 However, the quality of the evidence, as summarized in previous meta-analyses, has been rated as very low to low because many studies used cross-sectional or case-control design, which by nature limit interpretation on causality. 9,10 Since 2010, prospective study designs have increasingly been utilized; however, in a 2018 review of these studies observed that  there was a positive but no significantly pooled estimate. 10  Our study found an increasing dose-response relationship between road traffic noise and incident The results were based on adjusting for the covariates shown in the fully adjusted model. Results are presented per given exposure increment. The exposure increments corresponded to 5 mg/m 3 for PM2.5, and 10 mg/m 3 for NO2.
Lden ¼ weighted average 24-h road traffic noise level; NO2 ¼ nitrogen dioxide; PM2.5 ¼ fine particles.   The results were based on adjusting for the covariates shown in the fully adjusted model.
Furthermore, the associations with road traffic noise on a continuous scale were also robust when adjusting for air pollution. The associations between air pollution (ie, PM 2.5 ) and incident hypertension were independent of road traffic noise impacts in our study.
One important finding of our study is that road traffic noise and air pollution may have synergistic effects on the incidence of primary hypertension.
Specifically, we observed strongest associations in participants who both exposed to both high traffic noise and traffic-related air pollutants PM 2.5 or NO 2 in the combined effects (P < 0.05).
It seems plausible that high levels of exposure to air pollution renders the body more sensitive to the hazardous effects of road traffic noise and vice versa.
There are some potential mechanisms for the synergistic effects. Road traffic noise and air pollution are considered as triggers of hypertension, 35  Furthermore, the effects appear to be exacerbated in higher air pollution levels.