Air Pollution and Progression of Atherosclerosis in Different Vessel Beds—Results from a Prospective Cohort Study in the Ruhr Area, Germany

Hennig, Frauke; Geisel, Marie Henrike; Kälsch, Hagen; Lucht, Sarah; Mahabadi, Amir A.; Moebus, Susanne; Erbel, Raimund; Lehmann, Nils; Jöckel, Karl‐Heinz; Scherag, André; Hoffmann, Barbara

doi:10.1289/ehp7077

Cited by 20 publications

(11 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Exposure to particulate matter in polluted air for hours to weeks triggers cardiovascular disease-related mortality and non-fatal events, in conjunction with arterial thrombotic complications [ 1 , 2 , 3 ]. Long-term exposure over years further increases the risk of cardiovascular mortality, as a result of vascular degenerative disease, caused by chronic inflammation, oxidative stress and atherosclerosis [ 1 , 4 , 5 ]. Experimental studies in animal models have reproduced the inhalation of particulate matter via intratracheal (i.t.)…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Cathepsin G Enhances Thrombogenicity of Mildly Injured Arteries via ADP-Mediated Platelet Sensitization

Hoylaerts

2022

IJMS

View full text Add to dashboard Cite

Inhalation of particulate matter in polluted air causes direct, size-restricted passage in the circulation and pronounced lung inflammation, provoking platelet activation and (non)-fatal cardiovascular complications. To determine potency and mechanism of platelet sensitization via neutrophil enzymes, we performed in vitro aggregation studies in washed human platelets and in murine and human blood, in the presence of elastase, cathepsin G and regular platelet agonists, present in damaged arteries. The impact of both enzymes on in vivo thrombogenicity was studied in the same thrombosis mouse model, previously having demonstrated that neutrophil activation enhances peripheral thrombogenicity. At 0.05 U/mL, cathepsin G activated washed human platelets via PAR1, whereas at 0.35 U/mL, aggregation occurred via PAR4. In Swiss mouse platelet-rich plasma no aggregation occurred by cathepsin G at 0.4 U/mL. In human and murine blood, aggregations by 0.05–0.1 U/mL cathepsin G were similar and not PAR-mediated, but platelet aggregation was inhibited by ADP antagonists, advocating cathepsin G-released ADP in blood as the true agonist of sustained platelet activation. In the mouse thrombosis model, cathepsin G and elastase amplified mild thrombogenicity at blood concentrations that activated platelets in vitro. This study shows that cathepsin G and elastase secreted in the circulation during mild air pollution-induced lung inflammation lyse red blood cell membrane proteins, leading to ADP-leakage into plasma, sensitizing platelets and amplifying their contribution to cardiovascular complications of ambient particle inhalation.

show abstract

Section: Introductionmentioning

confidence: 99%

Neutrophil Cathepsin G Enhances Thrombogenicity of Mildly Injured Arteries via ADP-Mediated Platelet Sensitization

Hoylaerts

2022

IJMS

View full text Add to dashboard Cite

show abstract

“…We previously proposed a method for a high-coverage and accurate estimation of daily PM 2.5 at a 1-km resolution in mainland China based on the satellite data of atmospheric aerosol optical depth (AOD) by solving the problem of high missing rate, which is usually ignored in previous studies and leads to inaccurate estimation of PM 2.5 (Chen et al 2020). The 1-km estimates of PM 2.5 which can be matched with the residential addresses are expected to be a more precise proxy for the exposure level of PM 2.5 for the subjects involved in studies on the health effect of air pollution, and the effect estimates tend to be more reliable (Hennig et al 2020;Wong et al 2015;Woo et al 2020). Several cohort studies have applied satellitederived exposure data to quantify the long-term effects of PM 2.5 on health outcomes, with the data of addresses of subjects (Danesh et al 2019;Guo et al 2018;Lin et al 2018).…”

Section: Introductionmentioning

confidence: 99%

Individual exposure to ambient PM2.5 and hospital admissions for COPD in 110 hospitals: a case-crossover study in Guangzhou, China

Jin

Han

Tian

et al. 2021

Environ Sci Pollut Res

View full text Add to dashboard Cite

Few studies have evaluated the short-term association between hospital admissions and individual exposure to ambient particulate matter (PM2.5). Particularly, no studies focused on hospital admissions for chronic obstructive pulmonary disease (COPD) at the individual level. We assessed the short-term effects of PM2.5 on hospitalization admissions for COPD in Guangzhou, China, during 2014–2015, based on satellite-derived estimates of ambient PM2.5 concentrations at a 1-km resolution near the residential address as individual-level exposure for each patient. Around 40,002 patients with COPD admitted to 110 hospitals were included in this study. A time-stratified case-crossover design with conditional logistic regression models was applied to assess the effects of PM2.5 based on a 1-km grid data of aerosol optical depth provided by the National Aeronautics and Space Administration on hospital admissions for COPD. Further, we performed stratified analyses by individual demographic characteristics and season of hospital admission. Around 10 μg/m3 increase in individual-level PM2.5 was associated with an increase of 1.6% (95% confidence interval [CI]: 0.6%, 2.7%) in hospitalization for COPD at a lag of 0–5 days. The impact of PM2.5 on hospitalization for COPD was greater significantly in males and patients admitted in summer. Our study strengthened the evidence for the adverse effect of PM2.5 based on satellite-based individual-level exposure data.

show abstract

“…On the one hand, inflammation and oxidative stress, commonly associated with air pollution exposure, are the basis of most pathways for the progression of ischemic stroke. The promotion of atherosclerosis is one long-term pathway to ischemic stroke [ 15 ], but impaired glucose control [ 16 , 17 ] and high blood pressure [ 10 ] are also promoting factors. Shorter term, increased blood coagulability and cardiac arrhythmias can lead to acute ischemic stroke events [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Long-term exposure to road traffic noise and stroke incidence: a Danish Nurse Cohort study

et al. 2021

Self Cite

View full text Add to dashboard Cite

Background Road traffic noise has been linked to increased risk of ischemic heart disease, yet evidence on stroke shows mixed results. We examine the association between long-term exposure to road traffic noise and incidence of stroke, overall and by subtype (ischemic or hemorrhagic), after adjustment for air pollution. Methods Twenty-five thousand six hundred and sixty female nurses from the Danish Nurse Cohort recruited in 1993 or 1999 were followed for stroke-related first-ever hospital contact until December 31st, 2014. Full residential address histories since 1970 were obtained and annual means of road traffic noise (Lden [dB]) and air pollutants (particulate matter with diameter < 2.5 μm and < 10 μm [PM2.5 and PM10], nitrogen dioxide [NO2], nitrogen oxides [NOx]) were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals [CI]) for the associations of one-, three-, and 23-year running means of Lden preceding stroke (all, ischemic or hemorrhagic), adjusting for stroke risk factors and air pollutants. The World Health Organization and the Danish government’s maximum exposure recommendations of 53 and 58 dB, respectively, were explored as potential Lden thresholds. Results Of 25,660 nurses, 1237 developed their first stroke (1089 ischemic, 148 hemorrhagic) during 16 years mean follow-up. For associations between a 1-year mean of Lden and overall stroke incidence, the estimated HR (95% CI) in the fully adjusted model was 1.06 (0.98–1.14) per 10 dB, which attenuated to 1.01 (0.93–1.09) and 1.00 (0.91–1.09) in models further adjusted for PM2.5 or NO2, respectively. Associations for other exposure periods or separately for ischemic or hemorrhagic stroke were similar. There was no evidence of a threshold association between Lden and stroke. Conclusions Long-term exposure to road traffic noise was suggestively positively associated with the risk of overall stroke, although not after adjusting for air pollution.

show abstract

Air Pollution and Progression of Atherosclerosis in Different Vessel Beds—Results from a Prospective Cohort Study in the Ruhr Area, Germany

Cited by 20 publications

References 51 publications

Neutrophil Cathepsin G Enhances Thrombogenicity of Mildly Injured Arteries via ADP-Mediated Platelet Sensitization

Neutrophil Cathepsin G Enhances Thrombogenicity of Mildly Injured Arteries via ADP-Mediated Platelet Sensitization

Individual exposure to ambient PM2.5 and hospital admissions for COPD in 110 hospitals: a case-crossover study in Guangzhou, China

Long-term exposure to road traffic noise and stroke incidence: a Danish Nurse Cohort study

Contact Info

Product

Resources

About