We found no association of 1-year PM with prevalence of hypertension (Figure 3). Residential proximity ≤ 50 m to high heavy-duty traffic and long-term road traffic noise > 65 dB were associated with a some- what higher prevalence of hypertension: odds ratios (ORs) = 1.51 (95% CI: 0.98, 2.34) and 1.28 (95% CI: 1.04, 1.59), respectively. Discussion Our study shows a positive association of long-term exposure to urban background PM air pollution with systolic and diastolic BP. The observed relationship was indepen- dent of long-term exposure to road traffic noise and robust to the inclusion of a large number of potential confounders, including daily changes of PM, O3, and temperature. Traffic-related exposures (residential proxim- ity to high traffic and traffic noise) trended toward higher BP and an elevated prevalence of hypertension. Possible pathways through which PM could elevate BP include the elicitation of oxidative stress, systemic proinflammatory responses, and the activation of pulmonary reflexes leading to increased sympathetic tone, potentially causing arterial remodeling (Brook et al. 2009; Heagerty et al. 2010; Mills et al. 2009; Mulvany 2002). Autonomic nervous system imbalance after activation of pulmo- nary reflexes is most probably the responsible mechanism for acute effects of PM on BP, whereas systemic inflammation and vascular dysfunction involve a longer time of onset (Brook et al. 2009). A rise in intravascular pressure causes increased wall stress on the arterial wall, which then stimulates the acti- vation of the medial smooth muscles in the arterioles. If this happens repeatedly, hyper- trophic remodeling of the resistance vessels results in an increase in the medial thickness, which then leads to an increased total periph- eral resistance and a fixation of elevated BP. Similarly, an increase in blood flow may lead to vasodilatation, which increases wall stress, leading to hypertrophic remodeling as well (Heagerty et al. 2010; Mulvany 2002). In eutrophic remodeling, neurohumoral activity as affected by PM activation of, for example, pulmonary reflexes leads to vasoconstriction and increased BP, but wall stress remains nor- mal by decreasing the diameter of the vessel and increasing the wall thickness (Heagerty et al. 2010; Mulvany 2002). The estimated effects in our study popula- tion are smaller than those found in a recent study from Asia (Chuang et al. 2011), where per IQR change in PM2.5 of 20.4 μg/m 3, which is almost 10 times higher than in our study, systolic BP increased by 32.08 mmHg and diastolic BP increased by 31.29 mmHg. The higher effect size found by Chuang et al. (2011) might be explained by differences in 4 ) 2 g H m m ( PB 0 –2 8 6 ) 4 g H m (m2 P B 0 –2 –4 Environmental Health Perspectives • volume 119 | number 12 | December 2011 Long-term air pollution and blood pressure .5 )e 5 c 1 n < ree f e r ( 6 . 6 1 – 5 . 5 1 PM2.5 9 . 7 1 – 6 . 6 1 9 . 7 1 ≥ .6 )e 8 c 1 n < ree f e r ( Systolic 8 . 0 2 – 6 . 8 1 PM10 5 . 2 2 – 8 . 0 2 5 . 2 2 ≥ .5 )e 5 c 1 n < ree f e r ( 6 . 6 1 – 5 . 5 1 PM2.5 9 . 7 1 – 6 . 6 1 Quartiles of PM exposure (µg/m3) .179≥ .186< f)rreencee ..816208– ..822025– ( 5 . 2 2 ≥ PM10 Diastolic Figure 1. Estimated absolute increase in arterial BP (mmHg) (with 95% CI) by quartiles of yearly mean PM exposure (μg/m3) in participants of the Heinz Nixdorf Recall Study (n = 4,291); reference is quartile 1; adjusted for short-term PM, temperature, season, time trend, traffic proximity, sex, age, BMI, alcohol con- sumption, smoking, passive smoking, and physical activity. lae lea M em F 60 60 < ≥ .74 .47 oN seY 2 2 < ≥ oN seY oN seY rve xE tne eN rruC 10≤ 1311– 1417– 18≥ Antihyper- Coronary Age BMI tensive heart Sex (years) (kg/m2) medicaiton disease Diabetes Smoking Education (years) eod rkae itrde ed lyEm oemm eR lypom p /he neU v i t c a n Economic I activity trohN trneeC touhS sen um iem sE hcoB lüM h ing re nm tren pS r uSmm tuuA iW Area City Season Figure 2. Effect of yearly mean PM2.5 IQR (2.4 μg/m3) on systolic BP (mmHg) (with 95% CI) in subgroups, using interaction terms (n = 4,291); adjusted for short-term PM, temperature, season, time trend, traffic proximity, sex, age, BMI, alcohol consumption, smoking, passive smoking, and physical activity. PM2.5 (per 2.4 µg/m3) PM10 (per 3.9 µg/m3) General trafﬁc proximity (m) > 200 (reference) 101–200 51–100 ≤ 50 Heavy-duty trafﬁc proximity (m) > 200 (reference) 101–200 51–100 ≤ 50 24-hour mean noise (Lden) (dB) ≤ 55 (reference) > 55 ≤ 60 > 60 ≤ 65 > 65 0 OR (95% CI) 1 Figure 3. OR for hypertension (with 95% CI) by IQR increase PM2.5 and PM10 (µg/m3), by proximity to gen- eral-duty and heavy-duty traffic and by levels of road traffic noise (n = 4,291); adjusted for short-term PM, traffic proximity (or road traffic noise in the corresponding model), temperature, season, time trend, sex, age, BMI, alcohol consumption, smoking, passive smoking, and physical activity. 2 1709