Long-term exposure to ambient air pollution and traffic noise and incident hypertension in seven cohorts of the European study of cohorts for air pollution effects (ESCAPE).

Aims: We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts. Methods and results: We included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), >2.5, and ≤10 µm (PMcoarse), soot (PM2.5 absorbance), and nitrogen oxides at the addresses of participants with land use regression. Residential exposure to traffic noise was modelled at the facade according to the EU Directive 2002/49/EC. We assessed hypertension as (i) self-reported and (ii) measured (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg or intake of BP lowering medication (BPLM). We used Poisson regression with robust variance estimation to analyse associations of traffic-related exposures with incidence of hypertension, controlling for relevant confounders, and combined the results from individual studies with random-effects meta-analysis. Among 41 072 participants free of self-reported hypertension at baseline, 6207 (15.1%) incident cases occurred within 5-9 years of follow-up. Incidence of self-reported hypertension was positively associated with PM2.5 (relative risk (RR) 1.22 [95%-confidence interval (CI):1.08; 1.37] per 5 µg/m³) and PM2.5 absorbance (RR 1.13 [95% CI:1.02; 1.24] per 10 - 5m - 1). These estimates decreased slightly upon adjustment for road traffic noise. Road traffic noise was weakly positively associated with the incidence of self-reported hypertension. Among 10 896 participants at risk, 3549 new cases of measured hypertension occurred. We found no clear associations with measured hypertension. Conclusion: Long-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension.

Air pollution is associated with depressive symptoms in elderly women with cognitive impairment.

BACKGROUND: Studies on air pollution and depression in the elderly are limited and the results are heterogeneous. OBJECTIVES: We examined the association of ambient air pollution exposure and diagnosis and symptoms of depression in the elderly; and whether any associations were confounded or modified by cognitive decline. METHODS: We enrolled 821 elderly women from the German SALIA cohort (follow-up examination, 2007-2010). Self-reported depressive symptoms and level of cognition were evaluated using the CESD-R Scale and the CERAD-Plus test, respectively. We used two depression endpoints for analyses: self-reported doctor diagnosis of depression and frequency of depressive symptoms (CESD-R score). Long-term concentrations of particulate matter (PM) size fractions and nitrogen oxides (NOx) modeled by land-use regression were assigned to home addresses. Cross-sectional associations were assessed using adjusted logistic and linear regression models. RESULTS: Concentrations of coarse particles (PMcoarse), fine particles (PM2.5 and PM2.5 abs) and NO2 were significantly associated with diagnosis of depression (e.g. for PM2.5 OR = 1.62, 95%CI: 1.06, 2.46 and for NO2 OR = 1.54, 95% CI: 1.08, 2.19). Similarly, an increase of one interquartile range in PM10, PM2.5, NO2 and NOx was associated with depressive symptoms assessed with the CESD-R score (e.g. for PM2.5 16.2% difference in the mean; 95% CI: 5.8%, 26.5% and for NO2 14.5%; 95% CI: 4.8%, 24.2%). These associations were stronger in women with cognitive decline (e.g. Pint for PM2.5:0.022 and NO2:0.017) compared to women with normal cognition. In addition, living less than 100 m distance to major roads was significantly associated with diagnosis (OR = 1.99, 95% CI: 1.14, 3.47) and symptoms (19.7%; 95% CI: 4.3%, 35.1%) of depression. We did not observe any interaction effect of cognition on prior diagnosis of depression. CONCLUSIONS: Exposure to air pollution was associated with diagnosis of depression and depressive symptoms in elderly women. Women with impaired cognition may be at greater risk of depressive symptoms when exposed to air pollution.

Road Traffic Noise at the Residence, Annoyance, and Cognitive Function in Elderly Women.

The detrimental effects of traffic noise on cognition in children are well documented. Not much is known about the health effects in adults. We investigated the association of residential exposure to road traffic noise and annoyance due to road traffic noise with cognitive function in a cohort of 288 elderly women from the longitudinal Study on the influence of Air pollution on Lung function, Inflammation and Aging (SALIA) in Germany. Residential noise levels-weighted 24-h mean (LDEN) and nighttime noise (LNIGHT)-were modeled for the most exposed facade of dwellings and dichotomized at ≥50 dB(A). Traffic noise annoyance (day and night) was estimated by questionnaire. Cognitive function was assessed using the Consortium to Establish a Registry on Alzheimer's Disease (CERAD-Plus) Neuropsychological Assessment Battery. The modeled noise levels were associated with impaired total cognition and the constructional praxis domain, independently of air pollution. Self-reported noise annoyance was associated with better performance in semantic memory and constructional praxis domains. This finding should be interpreted with caution since we could not control for potential confounding by hearing loss. Noise levels and annoyance were associated, but their health effects seemed mutually independent.

Tropospheric ozone and skin aging: Results from two German cohort studies.

During the last two decades, it has been well established that a short-term exposure to ozone (O3) elicits an oxidative stress response in human and mouse skin, which leads to aberrant transcriptional expression of genes consistent with increased skin aging. Whether a long-term exposure to ambient O3 is associated with any skin aging traits, has remained unclear. We addressed this question in two elderly German cohorts: the SALIA study (806 women aged 66-79 years), and the BASE-II study (1207 men and women aged 60-84 years). Five-year mean residential exposure to O3 was modeled as the number of days with maximum daily 8-h mean O3 concentrations ≥120 µg/m3 per year in the wider neighborhood (5-digit postcode) of a participant's residence. Extrinsic (environmentally induced) skin aging traits - coarse wrinkles and pigment spots (lentigines) on the face - were assessed by means of SCINEXA™, a validated visual score previously shown to be well suited to measure extrinsic facial skin aging in cohort studies. We observed positive associations of O3 exceedances with coarse wrinkles in the face, but not with pigment spots. These associations were present in each cohort as well as in the combined sample of both cohorts. They were independent of chronic ultraviolet radiation exposure as the most obvious confounder, and also of co-pollutants such as particulate matter and nitrogen dioxide. Thus, long-term exposure to elevated concentrations of tropospheric O3 appears to contribute to skin aging.

Residential Road Traffic Noise and High Depressive Symptoms after Five Years of Follow-up: Results from the Heinz Nixdorf Recall Study.

BACKGROUND: Traffic noise affects a large number of people, particularly in urbanized areas. Noise causes stress and annoyance, but less is known about the relationship between noise and depression. OBJECTIVE: We investigated the association of residential road traffic noise with depressive symptoms using 5-year follow-up data from a German population-based study. METHODS: We analyzed data from 3,300 participants in the Heinz Nixdorf Recall study who were between 45 and 75 years old and were without depressive symptoms at baseline (2000-2003). Depressive symptoms were defined based on the Center for Epidemiologic Studies Depression scale (CES-D) 15-item questionnaire (total score ≥ 17) and antidepressant medication intake. Road traffic noise was modeled according to European Parliament/Council Directive 2002/49/EC. High noise exposure was defined as annual mean 24-hr noise levels > 55 A-weighted decibels [dB(A)]. Poisson regression with robust variance was used to estimate relative risks (RRs) a) adjusting for the potential confounders age, sex, socioeconomic status (SES), neighborhood-level SES, and traffic proximity; b) additionally adjusting for body mass index and smoking; and c) additionally adjusting for the potential confounders/intermediates comorbidities and insomnia. RESULTS: Overall, 35.7% of the participants were exposed to high residential road traffic noise levels. At follow-up (mean = 5.1 years after baseline), 302 participants were classified as having high depressive symptoms, corresponding to an adjusted RR of 1.29 (95% CI: 1.03, 1.62; Model 1) for exposure to > 55 versus ≤ 55 dB(A). Adjustment for potential confounders/intermediates did not substantially alter the results. Associations were stronger among those who reported insomnia at baseline (RR = 1.62; 95% CI: 1.10, 2.59 vs. RR = 1.21; 95% CI: 0.94, 1.57) and appeared to be limited to those with ≤ 13 years of education (RR = 1.43; 95% CI: 1.10, 1.85 vs. 0.92; 95% CI: 0.56, 1.53 for > 13 years). CONCLUSION: Our results suggest that exposure to residential road traffic noise increases the risk of depressive symptoms. CITATION: Orban E, McDonald K, Sutcliffe R, Hoffmann B, Fuks KB, Dragano N, Viehmann A, Erbel R, Jöckel KH, Pundt N, Moebus S. 2016. Residential road traffic noise and high depressive symptoms after five years of follow-up: results from the Heinz Nixdorf Recall Study. Environ Health Perspect 124:578-585; http://dx.doi.org/10.1289/ehp.1409400.

Association of long-term exposure to local industry- and traffic-specific particulate matter with arterial blood pressure and incident hypertension.

BACKGROUND: Long-term exposure to fine particulate matter (PM2.5) may lead to increased blood pressure (BP). The role of industry- and traffic-specific PM2.5 remains unclear. OBJECTIVE: We investigated the associations of residential long-term source-specific PM2.5 exposure with arterial BP and incident hypertension in the population-based Heinz Nixdorf Recall cohort study. METHODS: We defined hypertension as systolic BP≥140mmHg, or diastolic BP≥90mmHg, or current use of BP lowering medication. Long-term concentrations of PM2.5 from all local sources (PM2.5ALL), local industry (PM2.5IND) and traffic (PM2.5TRA) were modeled with a dispersion and chemistry transport model (EURAD-CTM) with a 1km(2) resolution. We performed a cross-sectional analysis with BP and prevalent hypertension at baseline, using linear and logistic regression, respectively, and a longitudinal analysis with incident hypertension at 5-year follow-up, using Poisson regression with robust variance estimation. We adjusted for age, sex, body mass index, lifestyle, education, and major road proximity. Change in BP (mmHg), odds ratio (OR) and relative risk (RR) for hypertension were calculated per 1µg/m(3) of exposure concentration. RESULTS: PM2.5ALL was highly correlated with PM2.5IND (Spearman's ρ=0.92) and moderately with PM2.5TRA (ρ=0.42). In adjusted cross-sectional analysis with 4539 participants, we found positive associations of PM2.5ALL with systolic (0.42 [95%-CI: 0.03, 0.80]) and diastolic (0.25 [0.04, 0.46]) BP. Higher, but less precise estimates were found for PM2.5IND (systolic: 0.55 [-0.05, 1.14]; diastolic: 0.35 [0.03, 0.67]) and PM2.5TRA (systolic: 0.88 [-1.55, 3.31]; diastolic: 0.41 [-0.91, 1.73]). We found crude positive association of PM2.5TRA with prevalence (OR 1.41 [1.10, 1.80]) and incidence of hypertension (RR 1.38 [1.03, 1.85]), attenuating after adjustment (OR 1.19 [0.90, 1.58] and RR 1.28 [0.94, 1.72]). We found no association of PM2.5ALL and PM2.5IND with hypertension. CONCLUSIONS: Long-term exposures to all-source and industry-specific PM2.5 were positively related to BP. We could not separate the effects of industry-specific PM2.5 from all-source PM2.5. Estimates with traffic-specific PM2.5 were generally higher but inconclusive.

Long-Term Air Pollution and Traffic Noise Exposures and Mild Cognitive Impairment in Older Adults: A Cross-Sectional Analysis of the Heinz Nixdorf Recall Study.

BACKGROUND: Mild cognitive impairment (MCI) describes the intermediate state between normal cognitive aging and dementia. Adverse effects of air pollution (AP) on cognitive functions have been proposed, but investigations of simultaneous exposure to noise are scarce. OBJECTIVES: We analyzed the cross-sectional associations of long-term exposure to AP and traffic noise with overall MCI and amnestic (aMCI) and nonamnestic (naMCI) MCI. METHODS: At the second examination of the population-based Heinz Nixdorf Recall study, cognitive assessment was completed in 4,086 participants who were 50-80 years old. Of these, 592 participants were diagnosed as having MCI (aMCI, n = 309; naMCI, n = 283) according to previously published criteria using five neuropsychological subtests. We assessed long-term residential concentrations for size-fractioned particulate matter (PM) and nitrogen oxides with land use regression, and for traffic noise [weighted 24-hr (LDEN) and night-time (LNIGHT) means]. Logistic regression models adjusted for individual risk factors were calculated to estimate the association of environmental exposures with MCI in single- and two-exposure models. RESULTS: Most air pollutants and traffic noise were associated with overall MCI and aMCI. For example, an interquartile range increase in PM2.5 and a 10 A-weighted decibel [dB(A)] increase in LDEN were associated with overall MCI as follows [odds ratio (95% confidence interval)]: 1.16 (1.05, 1.27) and 1.40 (1.03, 1.91), respectively, and with aMCI as follows: 1.22 (1.08, 1.38) and 1.53 (1.05, 2.24), respectively. In two-exposure models, AP and noise associations were attenuated [e.g., for aMCI, PM2.5 1.13 (0.98, 1.30) and LDEN 1.46 (1.11, 1.92)]. CONCLUSIONS: Long-term exposures to air pollution and traffic noise were positively associated with MCI, mainly with the amnestic subtype. CITATION: Tzivian L, Dlugaj M, Winkler A, Weinmayr G, Hennig F, Fuks KB, Vossoughi M, Schikowski T, Weimar C, Erbel R, Jöckel KH, Moebus S, Hoffmann B, on behalf of the Heinz Nixdorf Recall study Investigative Group. 2016. Long-term air pollution and traffic noise exposures and mild cognitive impairment in older adults: a cross-sectional analysis of the Heinz Nixdorf Recall Study. Environ Health Perspect 124:1361-1368; http://dx.doi.org/10.1289/ehp.1509824.

Air Pollution from Road Traffic and Systemic Inflammation in Adults: A Cross-Sectional Analysis in the European ESCAPE Project.

BACKGROUND: Exposure to particulate matter air pollution (PM) has been associated with cardiovascular diseases. OBJECTIVES: In this study we evaluated whether annual exposure to ambient air pollution is associated with systemic inflammation, which is hypothesized to be an intermediate step to cardiovascular disease. METHODS: Six cohorts of adults from Central and Northern Europe were used in this cross-sectional study as part of the larger ESCAPE project (European Study of Cohorts for Air Pollution Effects). Data on levels of blood markers for systemic inflammation-high-sensitivity C-reactive protein (CRP) and fibrinogen-were available for 22,561 and 17,428 persons, respectively. Land use regression models were used to estimate cohort participants' long-term exposure to various size fractions of PM, soot, and nitrogen oxides (NOx). In addition, traffic intensity on the closest street and traffic load within 100 m from home were used as indicators of traffic air pollution exposure. RESULTS: Particulate air pollution was not associated with systemic inflammation. However, cohort participants living on a busy (> 10,000 vehicles/day) road had elevated CRP values (10.2%; 95% CI: 2.4, 18.8%, compared with persons living on a quiet residential street with < 1,000 vehicles/day). Annual NOx concentration was also positively associated with levels of CRP (3.2%; 95% CI: 0.3, 6.1 per 20 µg/m3), but the effect estimate was more sensitive to model adjustments. For fibrinogen, no consistent associations were observed. CONCLUSIONS: Living close to busy traffic was associated with increased CRP concentrations, a known risk factor for cardiovascular diseases. However, it remains unclear which specific air pollutants are responsible for the association.

Air pollution and atherosclerosis: a cross-sectional analysis of four European cohort studies in the ESCAPE study.

BACKGROUND: In four European cohorts, we investigated the cross-sectional association between long-term exposure to air pollution and intima-media thickness of the common carotid artery (CIMT), a preclinical marker of atherosclerosis. METHODS: Individually assigned levels of nitrogen dioxide, nitrogen oxides, particulate matter ≤ 2.5 µm (PM2.5), absorbance of PM2.5 (PM2.5abs), PM10, PMcoarse, and two indicators of residential proximity to highly trafficked roads were obtained under a standard exposure protocol (European Study of Cohorts for Air Pollution Effects-ESCAPE study) in the Stockholm area (Sweden), the Ausburg and Ruhr area (Germany), and the Girona area (Spain). We used linear regression and meta-analyses to examine the association between long-term exposure to air pollution and CIMT. RESULTS: The meta-analysis with 9,183 individuals resulted in an estimated increase in CIMT (geometric mean) of 0.72% (95% CI: -0.65%, 2.10%) per 5-µg/m3 increase in PM2.5 and 0.42% (95% CI: -0.46%, 1.30%) per 10-5/m increase in PM2.5abs. Living in proximity to high traffic was also positively but not significantly associated with CIMT. Meta-analytic estimates for other pollutants were inconsistent. Results were similar across different adjustment sets and sensitivity analyses. In an extended meta-analysis for PM2.5 with three other previously published studies, a 0.78% (95% CI: -0.18%, 1.75%) increase in CIMT was estimated for a 5-µg/m3 contrast in PM2.5. CONCLUSIONS: Using a standardized exposure and analytical protocol in four European cohorts, we found that cross-sectional associations between CIMT and the eight ESCAPE markers of long-term residential air pollution exposure did not reach statistical significance. The additional meta-analysis of CIMT and PM2.5 across all published studies also was positive but not significant.

Arterial blood pressure and long-term exposure to traffic-related air pollution: an analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE).

BACKGROUND: Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific. OBJECTIVES: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations. METHODS: We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis. RESULTS: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated. CONCLUSIONS: In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.