Association of long-term exposure to air pollution with arterial blood pressure and hypertension

Bluthochdruck ist der wichtigste Risikofaktor für Mortalität und Morbidität weltweit. Daher besitzen Faktoren, die den Blutdruck erhöhen und auf große Teile der Bevölkerung einwirken, eine hohe Relevanz bei der Erforschung von kardiovaskulären Erkrankungen. Es gibt erste Hinweise darauf, dass Luftverschmutzung ein solcher Faktor ist. Der Zusammenhang zwischen Luftverschmutzung und kardiovaskulärer Morbidität und Mortalität ist in den letzten zwei Jahrzehnten eingehend untersucht und nachgewiesen worden. Einige Studien haben gezeigt, dass eine kurzfristige Erhöhung der Konzentration der Luftschadstoffe zu einer akuten Steigerung des Blutdrucks führen kann. Es wird vermutet, dass Langzeitexpositionen gegenüber Luftverschmutzung stärkere Auswirkungen auf den Blutdruck haben könnten. Außerdem könnte chronisch erhöhter Blutdruck als Teil des pathologischen Wirkungspfads verstanden werden, wie Luftverschmutzung zu Herz-Kreislauf Erkrankungen und Mortalität führen könnte. Bislang ist die Evidenz für den Zusammenhang zwischen langfristiger Belastung gegenüber Luftverschmutzung und arteriellem Blutdruck nicht ausreichend. Es ist außerdem nicht klar, welche Partikel, Gase und andere Komponenten der Luftverschmutzung für eine Erhöhung des Blutdrucks verantwortlich sein könnten. Auch der biologische Wirkungspfad der Luftverschmutzung auf den Blutdruck ist noch nicht etabliert beschrieben worden. Ziel dieser Studie war es, sowohl die Assoziation zwischen der langfristigen Luftschadstoffexposition und dem arteriellen Blutdruck, als auch mögliche zugrundeliegende Wirkungspfade, zu untersuchen. Die Forschungsfragen wurden mithilfe zweier methodischer Ansätze beantwortet: (1) Auswertung von Daten einer großen bevölkerungsbasierten Kohortenstudie und (2) Messung und statistische Auswertung von Daten aus einem Tierexperiment. Für den ersten methodischen Ansatz wurden Daten aus der Heinz Nixdorf Recall Studie, einer prospektiven Kohorte im Ruhrgebiet, ausgewertet. Langzeitkonzentrationen verschiedener Komponenten der Luftverschmutzung aus urbanem Hintergrund wurden mit einem Dispersions- und Chemie-Transport Modell geschätzt und den Wohnadressen der Studienteilnehmer zugewiesen. Blutdruckmessungen, Laboruntersuchungen, anthropometrische Messungen sowie Befragungen zum Lebensstil, zur Bildung, zu Vorerkrankungen und anderen Risikofaktoren wurden von geschulten Mitarbeitern anhand standardisierter Vorgaben durchgeführt und erfasst. Außerdem wurden Informationen über Verkehrslärm und der sozioökonomische Status der Nachbarschaft erhoben. Der Zusammenhang zwischen Langzeitbelastung gegenüber Luftschadstoffen mit dem gemessenen Blutdruck und einer Hypertonie wurden mit multiplen Regressionsmodellen analysiert, welche für relevante Kovariablen und die Einnahme von antihypertensiven Medikationen adjustiert wurden. Multi-Pollutant Modelle (Einbeziehung mehrerer Luftverschmutzungskomponenten) wurden berechnet, um die verantwortlichen Komponenten für eine Blutdrucksteigerung zu identifizieren. Die Analysen wurden sowohl im Querschnitt (Blutdruck, Prävalenz der Hypertonie) als auch im Längsschnitt (Inzidenz einer Hypertonie) durchgeführt. Die Analysen zeigten eine positive Assoziation zwischen der langfristigen Exposition gegenüber Feinstaub aus dem städtischen Hintergrund und einer Erhöhung des Blutdrucks. Dieser Zusammenhang war unabhängig von Expositionen gegenüber gasförmigen Luftschadstoffen (mit der Ausnahme von Ammoniak). Die Assoziation war linear, ohne Schwellenwert. Verkehrslärm, der sozioökonomische Status der Nachbarschaft und andere relevante Störfaktoren hatten auf diesen Befund keinen Einfluss. Zusätzlich weisen die Ergebnisse auf einen positiven Zusammenhang von langfristigen Ammoniak-Expositionen am Wohnort und Blutdruckwerten hin, welcher in weiteren Studien Bestätigung finden sollten. Assoziationen mit arterieller Hypertonie wurden nicht beobachtet. Im experimentellen Tierversuch wurde die 13-wöchige Exposition gegenüber Dieselabgasen und Stickstoffoxiden untersucht. Die Expression von Genen, die auf dem Wirkungspfad zwischen Luftverschmutzung und höheren Blutdruckwerten beteiligt sein können, wurde mithilfe quantitativer Echtzeit-Polymerase-Kettenreaktion in Mäuselungen gemessen. Die Exposition gegenüber Dieselabgasen und Stickoxide wirkte sich auf die Aktivität von fünf Genen aus: CYP1A1, NQO1, iCAM, iNOS und TNF. Die Produkte dieser Gene sind in den Fremdstoffmetabolismus, in Entzündungsprozesse, oxidativen Stress und Gefäßtonus-Regelung eingebunden. Zusammenfassend lässt sich festhalten, dass sich positive Assoziationen zwischen der langfristigen Exposition gegenüber Luftverschmutzung mit erhöhtem Blutdruck in einer bevölkerungsbasierten Kohorte zeigten. Erkenntnisse des experimentellen Teils dieser Studie deuten drauf hin, dass verkehrsbezogene Luftverschmutzungspartikel zu Entzündungen, oxidativem Stress und Gefäßreaktionen führen können, was wiederum den Bluthochdruck beeinflussen könnte. Blutdruck ist einer der wichtigsten modifizierbaren Risikofaktoren für Morbidität und Mortalität weltweit. Die Zahl der Hypertoniker in der Bevölkerung steigt stetig an. Eine relativ geringe Erhöhung des Blutdrucks aufgrund der Einwirkung von Luftverschmutzung könnte, auf Bevölkerungsebene, zu einer wesentlich höheren Belastung der Bevölkerung führen. Die Ergebnisse dieser Studie liefern Hinweise dafür, dass weitere Maßnahmen zur Verringerung der Luftverschmutzung zu erheblichen gesundheitlichen Vorteilen für die Bevölkerung führen könnten.High blood pressure is a major determinant for mortality and disability in the developed world. Therefore, factors which increase blood pressure and which affect large populations have a high priority in cardiovascular health research. One of such factors may be ambient air pollution. The link between air pollution and cardiovascular morbidity and mortality has been established in the last two decades. There are studies showing that short-term elevations in air pollution can lead to increased blood pressure within hours or days. It has been suggested that long-term exposure to air pollution would have an even stronger effect on blood pressure. Moreover, chronically elevated blood pressure could be a part of the pathophysiologic mechanism on how exposure to air pollution can lead to cardiac events and mortality. So far, only few studies have investigated the effect of long-term exposure to air pollution on blood pressure, with mixed results. Multiple questions remain unanswered yet. Which pollutant (or pollutants) in the air pollution mixture could be responsible for blood pressure elevation? Is the association of air pollution with blood pressure confounded by the influence of concurrent residential exposures, such as road traffic noise and neighborhood deprivation? Finally, it is not clear through which biologic pathways air pollution could chronically increase blood pressure and lead to hypertension. It is likely that inflammation and oxidative stress, triggered by inhaled pollutants, play a central role in this process. Oxidative damage, autonomic nervous system imbalance, and vascular endothelial dysfunction could be some of the mechanisms involved in chronic blood pressure elevation following long-term air pollution exposure. The aim of this study was to investigate the effect of long-term air pollution and its specific components on blood pressure and hypertension and to investigate possible underlying pathophysiologic mechanisms. In the research part of this study, I applied two methodologies: (1) observational, including statistical analyses of the data from a prospective cohort study, and (2) experimental, using a controlled-exposure animal study. I conducted the observational part of this study using a population-based cohort, the Heinz Nixdorf Recall Study in the highly urbanized Ruhr area of Germany. Long-term concentra-tions of urban background air pollution (particulate and gaseous pollutants) at participants’ residences were modeled with dispersion and chemistry transport model. Related residential exposures (road traffic noise, area-level socio-economic status) were also assessed. Blood pressure was measured at baseline and after five years of follow-up with a standardized procedure. Information on cardiovascular risk factors, co-morbidities, lifestyle and socio-economic factors was collected. Cross-sectional and longitudinal multiple regression analyses were performed, taking into account relevant confounders, and the intake of blood pressure lowering medication. I also employed multi-pollutant models to identify the responsible compounds. I found a positive association of long-term exposure to fine particulate matter with blood pressure. This association was independent of gaseous pollutants (except ammonia), traffic noise, other co-exposures, and relevant confounders. The association of air pollution with blood pressure was linear and without a threshold. I also found a positive association of long-term ammonia exposure at residence with blood pressure, which should be confirmed in further studies. I observed no associations with prevalent or incident hypertension. In the experimental part of this study, I measured and compared gene expression in mice lungs after controlled 13-week exposure to diesel engine exhaust and nitrogen oxides. I found changes in the activity of the following genes: CYP1A1, NQO1, iCAM, iNOS, and TNFα. These genes are involved in xenobiotic metabolism, inflammation, oxidative stress and vascular tone regulation. In summary, I found a positive association of long-term exposure to air pollution with elevated blood pressure in a population-based cohort. This association is likely attributable to fine particulate matter and independent from co-exposure to most gases in the air pollution mixture, to road traffic noise, to residential deprivation, or from relevant confounders. My findings from the experimental part of this study provide supportive evidence that traffic-related air pollution can induce inflammation, oxidative stress and vascular reactions, which might favor hypertension in the long run

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

The effect of exposure to radiofrequency electromagnetic fields on cognitive performance in human experimental studies: A protocol for a systematic review

Background The World Health Organization (WHO) is currently assessing the potential health effects of exposure to radiofrequency electromagnetic fields (RF-EMFs) in the general and working population. Related to one such health effect, there is a concern that RF-EMFs may affect cognitive performance in humans. The systematic review (SR) aims to identify, summarize and synthesize the evidence base related to this question. Here, we present the protocol for the planned SR. Objectives The main objective is to present a protocol for a SR which will evaluate the associations between short-term exposure to RF-EMFs and cognitive performance in human experimental studies. Data sources We will search the following databases: PubMed, Embase, Web of Science, Scopus, and the EMF-Portal. The reference lists of included studies and retrieved review articles will be manually searched. Study eligibility and criteria We will include randomized human experimental studies that assess the effects of RF-EMFs on cognitive performance compared to no exposure or lower exposure. We will include peer-reviewed articles of any publication date in any language that report primary data. Data extraction and analysis Data will be extracted according to a pre-defined set of forms developed and piloted by the review author team. To assess the risk of bias, we will apply the Rating Tool for Human and Animal Studies developed by NTP/OHAT, supplemented with additional questions relevant for cross-over studies. Where sufficiently similar studies are identified (e.g. the heterogeneity concerning population, exposure and outcome is low and the studies can be combined), we will conduct random-effects meta-analysis; otherwise, we will conduct a narrative synthesis. Assessment of certainty of evidence The certainty of evidence for each identified outcome will be assessed according to Grading of Recommendations Assessment, Development, and Evaluation (GRADE). Performing the review according to this protocol will allow the identification of possible effects of RF-EMFs on cognitive performance in humans. The protocol has been registered in PROSPERO, an open-source protocol registration system, to foster transparency