Mechanisms of ultrafine particle-induced respiratory health effects

Leikauf, George D.; Kim, Sang Heon; Jang, An Soo

doi:10.1038/s12276-020-0394-0

Cited by 209 publications

(129 citation statements)

References 89 publications

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“…Oxidative stress is thought to be a key underlying mechanism driving in ammation following PM exposure (3,43,48). We demonstrated a mild transient systemic in ammation, in terms of increased neutrophil counts, that was similar following all exposures over the observation period.…”

Section: Discussionmentioning

confidence: 52%

“…From our results, it is not possible to draw any conclusions regarding the composition of the different particle size modes. Though, still the subject of debate, it has been proposed that PM in the ultra ne range may be a major contributor to the adverse health effects following inhalation, due to greater surface area relative to mass of PM and higher deposition in the alveoli (42,43). In relation to health effects, particle size remains a complex issue, which is yet to be resolved and it remains speculative to suggest to what extent the shift in particle size in uenced any endpoints in the current studies.…”

Section: Discussionmentioning

confidence: 99%

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Acute Cardiovascular Effects of Controlled Exposure to Dilute Petrodiesel and Biodiesel Exhaust in Healthy Volunteers: A Crossover Study

Unosson

Kabele

Boman

et al. 2020

Preprint

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Background Air pollution derived from combustion is associated with considerable cardiorespiratory morbidity and mortality in addition to environmental effects. Replacing petrodiesel with biodiesel may have ecological benefits, but impacts on human health remain unquantified. Objectives To compare acute cardiovascular effects of blended and pure biodiesel exhaust exposure against known adverse effects of petrodiesel exhaust (PDE) exposure in human subjects. Methods In two randomized controlled double-blind crossover studies, healthy volunteers were exposed to PDE or biodiesel exhaust for one hour. In study one, 16 subjects were exposed, on separate occasions, to PDE and 30% rapeseed methyl ester biodiesel blend (RME30) exhaust, aiming at PM 10 300 µg/m 3 . In study two, 19 male subjects were separately exposed to PDE and exhaust from a 100% RME fuel (RME100) using similar engine load and exhaust dilution. Generated exhaust was analyzed for physicochemical composition and reactive potential. Following exposure, vascular endothelial function was assessed using forearm venous occlusion plethysmography and ex vivo thrombus formation was assessed using a Badimon chamber technique. Results In study 1, PDE and RME30 exposures were at comparable PM levels (314 ±27 µg/m 3 ; (PM 10 ± SD ) and 309 ±30 µg/m 3 respectively), whereas in study 2, the PDE exposure concentrations remained similar (310 ±34 µg/m 3 ) , but RME100 levels were lower in PM (165 ±16 µg/m 3 ) and PAHs, but higher in particle number concentration. Compared to PDE, PM from RME had less oxidative potential. Forearm infusion of the vasodilators acetylcholine, bradykinin, sodium nitroprusside and verapamil resulted in dose-dependent increases in blood flow after all exposures. V asodilatation to vasoactive infusions and ex vivo thrombus formation were similar following exposure to exhaust from petrodiesel and the two biodiesel formulations (RME30 and RME100). Conclusions Cardiovascular impairment did not differ following controlled exposure to biodiesel exhaust as compared to PDE, despite differences in PM composition and particle reactivity. We suggest that the potential adverse health effects of biodiesel fuel emissions should be taken into account when evaluating future fuel policies.

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Acute Cardiovascular Effects of Controlled Exposure to Dilute Petrodiesel and Biodiesel Exhaust in Healthy Volunteers: A Crossover Study

Unosson

Kabele

Boman

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…In our study too, long-term exposure to PM 2.5 was associated with high systemic inflammation markers (CRP and LDH) and low FEV 1 % and D LCO among study populations. PM 2.5 and UFP induced inflammation at the alveolar epithelium level [26,27]. D LCO measurement is based on exchanged oxygen from the lungs into the blood at the level of the alveolar membrane and vascular endothelium.…”

Section: Discussionmentioning

confidence: 99%

Cigarette-related cadmium and environmental pollution exposure are reflected in airway ultrafine particle content

Klein

Adir²,

Fireman

et al. 2020

ERJ Open Res

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IntroductionParticulate matter (PM) and cigarette-related cadmium exposure increases inflammation and smokers' susceptibility to developing lung diseases. The majority of inhaled metals are attached to the surface of ultrafine particles (UFPs). A low inhaled UFP content in exhaled breath condensate (EBC) reflects a high inflammatory status of airways.MethodsEBC was collected from 58 COPD patients and 40 healthy smokers and nonsmokers. Participants underwent spirometry, diffusion capacity, EBC and blood sampling. Environmental pollution data were collected from monitoring stations. UFPs were measured in EBC and serum, and cadmium content was quantified.ResultsSubjects with low UFP concentrations in EBC (<0.18×108·mL−1) had been exposed to higher long-term PM2.5 levels versus subjects with high UFP concentrations in EBC (>0.18×108·mL−1) (21.9 µg·m−3versus 17.4 µg·m−3, p≤0.001). Long-term PM2.5 exposure levels correlated negatively with UFP concentrations in EBC and positively with UFP concentrations in serum (r=−0.54, p≤0.001 and r=0.23, p=0.04, respectively). Healthy smokers had higher cadmium levels in EBC versus healthy nonsmokers and COPD patients (25.2 ppm versus 23.7 ppm and 23.3 ppm, p=0.02 and p=0.002, respectively). Subjects with low UFP concentrations in EBC also had low cadmium levels in EBC versus subjects with high UFP levels (22.8 ppm versus 24.2 ppm, p=0.004)ConclusionsLow UFP concentration in EBC is an indicator of high-level PM exposure. High cadmium levels in EBC among smokers and the association between cadmium and UFP content in EBC among COPD patients indicate cadmium lung toxicity.

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“…Fine and ultra ne PMs have been reported to induce lung diseases through generation of ROS and oxidative stress as well as activation of innate and adaptive immunity, leading to cell barrier and tissue damage (22,23). Several known promoters of in ammatory response, such as nuclear factor-κB (NF-κB), activation protein-1 (AP-1), nuclear factor erythroid 2 related factor 2 (Nrf2), and CREB-binding proteins (CBPs), are activated by oxidative stress (24)(25)(26).…”

Section: Discussionmentioning

confidence: 99%

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

Jheng¹,

Putri²,

Chuang³

et al. 2020

Preprint

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Background: Exposure to particulate matter (PM) pollution has direct impacts on the respiratory organs, yet the molecular alterations underlying PM-induced pulmonary injury remain unclear. In this study, we investigated the effect of PM on lung tissues of SD rats with whole-body exposure to traffic-related PM1 (< 1 mm in aerodynamic diameter) pollutants and compared it with rats exposed to high-efficiency particulate air-filtered gaseous pollutants and clean air control for 3 and 6 months. Lung function and histological examinations as well as quantitative proteomics analysis and functional validation were performed. Results: The rats in 6-month PM1-exposed group showed significant decline in lung function by decreased forced expiratory flow and forced expiratory volume, but the histological analysis revealed an earlier lung damage evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2,673 proteins which highlighted dysregulations on proteins involved in oxidative stress, cellular metabolisms, calcium signaling, inflammatory responses, and actin dynamics. The presence of fine particles specifically enhanced the oxidative stress and inflammatory reactions under sub-chronic exposure of traffic-related PM1 and suppressed the glucose metabolism and actin cytoskeleton signaling which might lead to repair failure and thus lung function decline after chronic exposure of traffic-related PM1. A detailed pathogenic mechanism was proposed to depict the temporal and dynamic molecular regulations associated with PM1-induced lung injury.Conclusion: Our study explored the earlier lung injury prior to lung function decline and proposed potential molecular features for traffic-related PM1-induced lung injury.

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Mechanisms of ultrafine particle-induced respiratory health effects

Cited by 209 publications

References 89 publications

Acute Cardiovascular Effects of Controlled Exposure to Dilute Petrodiesel and Biodiesel Exhaust in Healthy Volunteers: A Crossover Study

Acute Cardiovascular Effects of Controlled Exposure to Dilute Petrodiesel and Biodiesel Exhaust in Healthy Volunteers: A Crossover Study

Cigarette-related cadmium and environmental pollution exposure are reflected in airway ultrafine particle content

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

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