Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter

Traboulsi, Hussein; Guerrina, Necola; Iu, Matthew; Maysinger, Dušica; Ariya, Parisa A.; Baglole, Carolyn J.

doi:10.3390/ijms18020243

Cited by 141 publications

(105 citation statements)

References 132 publications

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“…We think it is unlikely that our null findings were based on lack of toxicity of UFP as there is convincing evidence that UFP can drive inflammation [32, 33]. Therefore, we suspect that there are limitations to our study design that undermined our ability to see benefits from reducing PM in homes.…”

Section: Discussionmentioning

confidence: 95%

Lessons from in-home air filtration intervention trials to reduce urban ultrafine particle number concentrations

Brugge

Simon

Hudda

et al. 2017

Building and Environment

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Background Exposure to airborne ultrafine particle (UFP; <100 nm in aerodynamic diameter) is an emerging public health problem. Nevertheless, the benefit of using high efficiency particulate arrestance (HEPA) filtration to reduce UFP concentrations in homes is not yet clear. Methods We conducted a randomized crossover study of HEPA filtration without a washout period in 23 homes of low-income Puerto Ricans in Boston and Chelsea, MA (USA). Most participants were female, older adults who were overweight or obese. Particle number concentrations (PNC, a proxy for UFP) were measured indoors and outdoors at each home continuously for six weeks. Homes received both HEPA filtration and sham filtration for three weeks each in random order. Results Median PNC under HEPA filtration was 50–85% lower compared to sham filtration in most homes, but we found no benefit in terms of reduced inflammation; associations between hsCRP, IL-6, or TNFRII in blood samples and indoor PNC were inverse and not statistically significant. Conclusions Limitations to our study design likely contributed to our findings. Limitations included carry-over effects, a population that may have been relatively unresponsive to UFP, reduction in PNC even during sham filtration that limited differences between HEPA and sham filtration, window opening by participants, and lack of fine-grained (room-specific) participant time-activity information. Our approach was similar to other recent HEPA intervention studies of particulate matter exposure and cardiovascular risk, suggesting that there is a need for better study designs.

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Section: Discussionmentioning

confidence: 95%

Lessons from in-home air filtration intervention trials to reduce urban ultrafine particle number concentrations

Brugge

Simon

Hudda

et al. 2017

Building and Environment

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“…PM exposure has been shown to be a major risk factor for acute and chronic diseases including cardiovascular disease, liver fibrosis, various gastrointestinal diseases, and chronic respiratory disease, such as asthma and chronic obstructive pulmonary disease (COPD), along with lung cancer [4-8]. The sources of PM are complex and include transportation (e.g., vehicle exhaust), factory emissions (e.g., industries and coal-fired power plants), combustion (e.g., biomass and cigarette smoke) and agriculture (e.g., fertilizer and animal waste), and natural sources (e.g., volcanoes, forest fires and dust storms) [5]. Regardless of the origin, PM is a widespread air pollutant containing various toxins such as carbonaceous cores, polycyclic aromatic hydrocarbons (PAHs), quinones, metals, endotoxins, and many others [9].…”

Section: Introductionmentioning

confidence: 99%

Necroptosis Contributes to Urban Particulate Matter-Induced Airway Epithelial Injury

Luo

et al. 2018

Cell Physiol Biochem

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Background/Aims: Necroptosis, a form of programmed necrosis, is involved in the pathologic process of several kinds of pulmonary diseases. However, the role of necroptosis in particulate matter (PM)–induced pulmonary injury remains unclear. The objective of this study is to investigate the involvement of necroptosis in the pathogenesis of PM-induced toxic effects in pulmonary inflammation and mucus hyperproduction, both in vitro and in vivo. Methods: PM was administered into human bronchial epithelial (HBE) cells or mouse airways, and the inflammatory response and mucus production were assessed. The mRNA expressions of IL6, IL8 and MUC5AC in HBE cells and Cxcl1, Cxcl2, and Gm-csf in the lung tissues were detected by quantitative real-time RT-PCR. The secreted protein levels of IL6 and IL8 in culture supernatants and Cxcl1, Cxcl2, and Gm-csf in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). We used Western blot to measure the protein expressions of necroptosis-related proteins (RIPK1, RIPK3, and Phospho-MLKL), NF-κB (P65 and PP65), AP-1 (P-c-Jun and P-c-Fos) and MUC5AC. Cell necrosis and mitochondrial ROS were detected using flow cytometry. In addition, pathological changes and scoring of lung tissue samples were monitored using hemoxylin and eosin (H&E), periodic acid-schiff (PAS) and immunohistochemistry staining. Results: Our study showed that PM exposure induced RIP and MLKL-dependent necroptosis in HBE cells and in mouse lungs. Managing the necroptosis inhibitor Necrostatin-1 (Nec-1) and GSK’872, specific molecule inhibitors of necroptosis, markedly reduced PM-induced inflammatory cytokines, e.g., IL6 and IL8, and MUC5AC in HBE cells. Similarly, administering Nec-1 significantly reduced airway inflammation and mucus hyperproduction in PM-exposed mice. Mechanistically, we found PM–induced necroptosis was mediated by mitochondrial reactive oxygen species-dependent early growth response gene 1, which ultimately promoted inflammation and mucin expression through nuclear factor κB and activator protein-1 pathways, respectively. Conclusions: Our results demonstrate that necroptosis is involved in the pathogenesis of PM–induced pulmonary inflammation and mucus hyperproduction, and suggests that it may be a novel target for treatment of airway disorders or disease exacerbations with airborne particulate pollution.

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“…Another opportunity is around reducing the toxicants generated from burning fuel . This releases tons of particulate matter in the atmosphere.…”

Section: Operationalizing Epigenetics In a Healthcare Systemmentioning

confidence: 99%

RW‐2018—Research Workshop: The Effect of Nutrition on Epigenetic Status, Growth, and Health

Skinner

Lumey

Fleming

et al. 2019

J Parenter Enteral Nutr

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The goal of the 2018 American Society for Parenteral and Enteral Nutrition (ASPEN) Research Workshop was to explore the influence of nutrition and dietary exposure to xenobiotics on the epigenome during critical periods in development and how these exposures influence both disease incidence and severity transgenerationally. A growing compendium of research indicates that the incidence and severity of common and costly human diseases may be influenced by dietary exposures and deficiencies that modify the epigenome. The greatest periods of vulnerability to these exposures are the periconception period and early childhood. Xenobiotics in the food chain, protein malnutrition, and methyl donor deficiencies could have a profound bearing on the risk of developing heart disease, diabetes, obesity, hypertension, and mental illness over multiple generations. The financial impact and the life burden of these diseases are enormous. These and other aspects of nutrition, epigenetics, and health are explored in this research workshop.

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Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter

Cited by 141 publications

References 132 publications

Lessons from in-home air filtration intervention trials to reduce urban ultrafine particle number concentrations

Lessons from in-home air filtration intervention trials to reduce urban ultrafine particle number concentrations

Necroptosis Contributes to Urban Particulate Matter-Induced Airway Epithelial Injury

RW‐2018—Research Workshop: The Effect of Nutrition on Epigenetic Status, Growth, and Health

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