Outdoor Air Pollution and Arterial Hypertension

Air pollution is a major environmental risk factor. There is accumulating evidence that air pollution could induce elevated blood pressure and potentiate hypertension. Acute elevations in the outdoor air pollution levels can trigger immediate or shortly delayed increases in arterial blood pressure. Moreover, few studies suggest that short-term increases in the levels of particulate and gaseous pollutants could lead to an acute onset of hypertension. Prolonged exposure to outdoor air pollution is associated with elevated blood pressure. Furthermore, some longitudinal studies have linked long-term exposure to air pollution with the incidence of hypertension. Various components of air pollution, such as inhalable particulate matter (PM2.5, PM10), nitrogen oxides, sulfur dioxide, and ozone, have shown associations with blood pressure in some studies. The hypothesized underlying mechanisms include inflammatory reactions and oxidative stress in lungs and in systemic circulation, imbalance of autonomous nervous system, and pathologic changes in vascular endothelium. In addition to “traditional” susceptible groups such as elderly individuals or patients with chronic diseases, children and pregnant women could be especially susceptible to the adverse effects of air pollution. The interplay of air pollution with the related environmental exposures, such as traffic noise and climate change, should be investigated further

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

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)

We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts.; 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.; Long-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension

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

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

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)

Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific

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 >= 140 mmHg, or diastolic BP >= 90 mmHg, 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 1 km(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 1 mu g/m(3) of exposure concentration. Results: PM2.5ALL was highly correlated with PM25IND. (Spearman's rho = 0.92) and moderately with PM2.5TRA (rho = 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, 0.801) and diastolic (0.25 [0.04, 0.461] BP. Higher, but less precise estimates were found for PM2.5IND (systolic: 0.55 [-0.05, 1.14]; diastolic: 0.35 [0.03, 0.671) and PM2.5TRA (systolic: 0.88 [-1.55, 3.31]; diastolic: 0.41 [-0.91, 1.731). 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. (C) 2016 Published by Elsevier GmbH