United Kingdom, Germany, Netherlands, Sweden, Italy, Greece
Country specific noise exposure models: both aircraft and road traffic noise
Home BP readings with hypertension defined as 140/90 mmHg OR self-reported physician diagnosis of hypertension OR use of antihypertensive medication
Significant exposure-response relationship between night-time aircraft noise, average daily road traffic noise exposure, and risk of hypertension
Night-time aircraft noise: OR 1.14 (95% CI: 1.01–1.29) of hypertension with 10 dB(A) increase in exposure; average road traffic noise: OR 1.097 (95% CI: 1.00–1.20) of hypertension with 10 dB(A) increase in exposure
Significant relationship between exposure to residential road traffic noise and hypertension; association stronger among women and among those who have lived at the address for >10 years; exposure-response relationship suggested
The odds ratio for hypertension was 1.38 for every 5 dB(A) increase in noise exposure
Nordic prediction model for road traffic noise and railway noise
Incident hypertension over 5 years identified by questionnaire; baseline association between measured blood pressure and residential exposure to road traffic noise
Exposure-response relationship between road traffic noise and systolic blood pressure levels; effect size statistically significant only in males; no association between road traffic noise levels and diastolic BP; there was a borderline statistically significant relationship between railway noise and incident hypertension cases
Cross section: increase of 0.59 mmHg in systolic BP (95% CI: 0.13–1.05) per 10 dB(A) increase in road traffic noise levels; prospective: 8% higher risk of hypertension with exposure to railway noise above 60 dB(A) (95% CI: −2%–19%)
Self-reported physician diagnosis, use of antihypertensive medications, measured blood pressure ≥140/90
Stronger significant estimates of the noise effect were found in subjects with long residence time and with respect to the exposure of the living room during daytime, no association with respect to exposure of the bedroom during night-time
OR for developing hypertension while living at the residence was 1.11 interval (95% CI: 1.00–1.23) per noise level increment of 10 dB(A); effect size stronger with resident time >10 years (OR: 1.20; 95% CI: 1.05–1.37); OR for development of hypertension was 1.24 (95% CI: 1.08–1.41) in those living with exposure of the living room during daytime
Traffic load (millions of vehicle kilometers per year) within 500 m around residential address; subpopulation had additional assessment using Nordic prediction method
Self-reported physician diagnosis of hypertension
No significant association noted between traffic load and hypertension
OR for diagnosis of HTN with exposure to ≥65 dB(A) with <50 dB(A) as reference was 0.96 (95% CI 0.59–1.59)
2 samples (1) City of Groningen sample (2) Sample from observational study: Prevention of Renal and Vascular End-Stage Disease (PREVEND)
Road traffic noise exposure of the subjects was calculated at the most exposed facade of the dwelling with standard method
Groningen subjects were defined as having hypertension when they reported using medication for elevated blood pressure
Adjusted ORs summarizing noise exposure and hypertension were not significant; significant findings in subjects who were between 45 and 55 years old; associations seemed to be stronger at higher noise levels
In the Groningen sample, adjusted OR for having hypertension in subjects between 45 and 55 years old was 1.19 (95% CI: 1.02–1.40) per 10 dB increase in noise level (Lden) PREVEND cohort OR 1.39 (1.08–1.77)
SONBASE national data repository on railway and traffic noise linked to residential addresses
Measured at rest by study staff
Positive association of railway noise with SBP and DBP; effect size stronger among subjects with reported physician-diagnosed hypertension, DM, or CVD; traffic noise was not impressive except for people with DM
For a 10 dB(A) increase in railway noise during the night 0.84 mmHg increase in SBP (95% CI: 0.22–1.46) and during the day 0.60 mmHg increase (0.07–1.13)
GIS and validated model to assess road and railway traffic noise
Self-report of physician diagnosis or taking antihypertensive medications
Association between road traffic and hypertension noted along with an exposure-response relationship; there were no clear associations in women or for railway noise
OR for hypertension was 1.9 (95% CI: 1.1 to 3.5) in the highest noise category for road traffic noise; OR for hypertension was higher in men—3.8 (95% CI: 1.6 to 9.0)
Incidence cases of hypertension defined by self-report of physician diagnosis or use of medications or BP measured at ≥140/90 mmHg
Long-term aircraft noise exposure increases risk for hypertension
For subjects exposed to energy-averaged levels above 50 dB(A) the adjusted relative risk for hypertension was 1.19 (95% CI: 1.03–1.37); maximum aircraft noise levels presented similar results, with a relative risk of 1.20 (1.03–1.40) for those exposed above 70 dB(A)
Measured systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg or current use of antihypertensive therapy
Long-term exposure to PM2.5 is associated with increased blood pressure; more impressive findings with traffic noise proximity
An IQR increase in PM2.5 (2.4 μg/m3) was associated with estimated increases in mean systolic and diastolic BP of 1.4 mmHg CI 95%: 0.5–2.3 and 0.9 mmHg (CI 95% CI: 0.4–1.4), respectively
North America: Multiethnic Study of Atherosclerosis (MESA)
PM2.5 using 24-hour integrated samplers with 5 retrospective exposure phases recorded
Resting seated BP
Stronger effect sizes from longer exposures (1-2 months) of ambient PM2.5 exposure compared with shorter (≤1 week) exposures; systolic blood pressure was only significantly affected (diastolic was not); effects stronger in the presence of higher traffic exposure
10 μg/m3 increase in PM2.5 prior 30-day mean was associated with 2.8 mmHg SBP (95% CI: 1.38 to 4.22) Note that this is a relatively short exposure study
1-year averaged criteria air pollutants measured by local monitoring stations (PM2.5, PM10, nitrogen dioxide (NO(2)), and ozone (O3))
Measured blood pressure
PM2.5 retained the strongest association with blood pressure (both systolic and diastolic) among the four air pollutants
For an IQR increase in PM2.5 (20.42 μg/m3), there were 32.4 mmHg (95% CI: 22.4–42.5) and 29.3 mmHg (95% CI: 19.2–39.3) increases in systolic and diastolic blood pressure, respectively, (controlling for ozone), and 31.1 mmHg (95% CI: 21.1 to 41.2) and 30.0 mmHg (95% CI 18.0 to 41.9) increases in systolic and diastolic blood pressure, respectively, (controlling for NO(2))
Local monitoring stations: three-year average concentration PM10, sulfur dioxide (SO2), nitrogen dioxides (NO2), and ozone (O3)
Measured blood pressure
Note that these are findings for more coarse particles, comparing apples and oranges; it addresses exposures to a mixture including not only PM2.5
Odds ratio for hypertension increased by 1.12 (CI 95%: 1.08–1.16) per 19 μg/m3 increase in PM10; the estimated increases in mean systolic and diastolic blood pressure were 0.87 mmHg (95% CI, 0.48–1.27) and 0.32 mmHg (95% CI, 0.08–0.56) per 19 μg/m3 increase in PM10
Participants’ residential addresses with land use regression models (nitrogen oxides) and interpolation from monitoring station measurements (PM2.5)
Incident case of hypertension as self-report of physician-diagnosed hypertension during follow-up and concurrent use of antihypertensive medications
Exposure to ambient fine particulate pollution increased risk; association did not quite reach statistical significance and got weaker when controlling for nitrogen containing air pollutants
Over 10-year follow-up incidence rate ratio for hypertension for a 10 μg/m3 increase in PM2.5 was 1.48 (95% CI, 0.95–2.31)
PM2.5 data from the US Environmental Protection Agency
Self-reported physician diagnosis of hypertension or use of medications
Odds ratio for prevalent hypertension was higher with higher levels of PM2.5 in Whites and not Blacks
Amongst Whites, a 10 μg/m3 increase in PM2.5 exposure was associated with a small elevated risk of hypertension (adjusted odds ratio (OR) 1.05, 95% confidence interval (CI) 1.04–1.17); OR in Blacks was 0.90 (95% CI: 0.79–1.03)
Sørensen, 2012 [64] (cross-sectional and prospective)
57,053
Denmark
Dispersion model to calculate residential long-term nitrogen oxide
Self-reported incident hypertension was assessed by questionnaire
Nitrogen oxide (a measure of traffic air pollution that correlates well with fine particles and is easier to measure) was inversely associated with systolic and diastolic BP and the prevalence of self-reported hypertension, and there was no association with the risk of incident self-reported hypertension during approximately 5 years of follow-up
There were 0.53 mmHg and 0.50 mmHg decrease in systolic BP with nitrogen oxide exposure during 1- and 5-year periods preceding enrollment, respectively; the OR of self-reported hypertension with long-term exposure was 0.96 (95% CI: 0.91, 1.00)
Monitoring stations by Taiwan Environmental Protection Agency
Measured BP
PM10 was associated with elevated systolic BP, triglyceride, apolipoprotein B, hemoglobin A1c, and reduced high-density lipoprotein cholesterol; elevated ozone was associated with increased diastolic BP
Increase of 0.47 mmHg; (95% CI, −0.09 to 1.02) with each interquartile range (34 μg/m3) PM10
Increase in black soot was associated with increase in systolic and diastolic BP
An IQR increase in 1-year average black soot exposure (0.32 μg/m3) was associated with a 2.64 mmHg increase in systolic blood pressure (95% CI 1.47 to 3.80) and a 2.41 mmHg increase in diastolic blood pressure (95% CI 1.77 to 3.05)
Arousal responsiveness increased with sound levels; awakenings (>10 s) were produced more frequently by freight train (compared to automotive/passenger)
Increase in noise level had main effect on the percentage of awakenings (, ), and microarousals (, ); there were increase in sleep fragmentation () and a shorter arousal onset latency (, ), with increasing noise level
Traffic noise events were recorded with class 1 sound level meters in bedrooms of residents living close to a road, a railway track, or an airport
Polysomnography, actigraphs, self-report
Subjective sleep assessment and recuperation were affected; indicators for sleep continuity were pronounced significantly except for awakening frequency
There were difficulty falling asleep (+89, ), increased sleep disturbance (+126, ), lighter sleep (+121, ), and less recuperative sleep (+111, ) in triple compared to single night exposure to noise; slow-wave sleep latency was 5.2 min longer in triple than single exposure night; REM latency was 9.0 min longer with the same exposure; time spent in REM was shorter in the triple than single or double exposure nights
Noise (45–80 dB(A)) was recorded with class 1 sound level meters (NC-10, Cortex Industries) in the vicinity of Dusseldorf Airport with closed or tilted windows
Polysomnography
Aircraft noise was associated with signs of sleep fragmentation (increased stage 1 and number of awakenings)
Slow-wave sleep was significantly reduced by 5.3 min, and total sleep time increased on average by 2.5 min
Subjectively evaluated sleep quality decreased gradually with increasing noise levels; SWS latency prolongation, total sleep time reduction, and decrease of SWS during first sleep cycle were significant
The SWS latency and waketime after sleep onset were increased; total sleep time (TST) and sleep efficiency were decreased; In relation to sleep period time (SPT), the amount of time awake and in stage S1 (S0 and 1) was increased (+13 min), but REM-sleep and SWS were decreased (−11.7 min)
Air pollution associated with increases in respiratory disturbance index and decrease in sleep efficiency
In the summer period, for every interquartile increase in short-term PM10 levels, there were 12.9% increase (95% CI: 2.77, 24.09) in RDI, 19.4% increase (95% CI: 3.67, 37.5) in percentage of sleep time at <90% oxygen saturation, and 1.20% decrease (95% CI: −2.40, −0.004) in sleep efficiency
Increased sleep duration with annual BC in Blacks with no observation in Whites and Hispanics; sleep duration decreased in men and those with low socioeconomic status (SES) per IQR increase in BC but not in women and those with medium or high SES
OR for short sleep in men is 1.7 per IQR increase in BC (95% CI: 1.1, 2.6) and 1.6 (95% CI: 1.1, 2.3) for low socioeconomic status; OR for short sleep in Hispanics is 1.4 (95% CI: 1.1, 1.8); Blacks experienced increased sleep duration with increasing BC ( per IQR; 95% CI: 0.12, 0.57)
PM10 and disorder of initiation and maintaining sleep were significantly associated () and sleep hyperhidrosis was 0.045; PM10 and global sleep disturbance were marginally associated ()
