Maternal exposure to fine particulate matter during pregnancy induces progressive senescence of hematopoietic stem cells under preferential impairment of the bone marrow microenvironment and aids development of myeloproliferative disease

Bhattarai, Govinda; Lee, Jae Bong; Kim, Min-Hye; Ham, Suhan; So, Han-Sol; Oh, Sang-Min; Sim, Hyun-Jaung; Lee, Jeong-Chae; Song, Mijung; Kook, Sung‐Ho

doi:10.1038/s41375-019-0665-8

Cited by 27 publications

(15 citation statements)

References 15 publications

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“…The mechanism of PM 2.5 action is probably a reactive oxygen species formation which increases inflammatory cytokines (TNF-α, IL-1β, and IL-6) in the cells. Inflammation may inhibit differentiation and proliferation of erythroid precursor cells and enhance an erythropoietin (Epo) resistant state ( 27 – 29 ). Another potential explanation is that inflammatory cytokines can upregulate hepcidin synthesis causing breakdown of ferroportin, thus reducing iron absorption in the gastrointestinal tract ( 30 , 31 ).…”

Section: Resultsmentioning

confidence: 99%

Particulate Matter 2.5 and Hematological Disorders From Dust to Diseases: A Systematic Review of Available Evidence

et al. 2021

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Particulate matter 2.5 (PM2.5) in the air enters the human body by diffusion into the blood. Therefore, hematological abnormalities might occur because of these toxic particles, but few studies on this issue have been reported. According to Cochrane guidance, we performed a systematic review on the relationship between exposure to PM2.5 and the risk of hematological disorders. Ten articles were included in this review. Anemia was found among children and elderly populations with 2- to 5-year PM2.5 exposure. Young children from mothers exposed to air pollution during pregnancy had a higher incidence of leukemia similar to the elderly. Supporting these data, outdoor workers also showed abnormal epigenetic modifications after exposure to very high PM2.5 levels. Adults living in high PM2.5 areas for 2 years were more likely to develop thrombocytosis. Finally, elderly populations with 7- to 8-year PM2.5 exposure showed increased risks of venous thromboembolism. In conclusion, the associations between PM2.5 and hematological aberrations among high-risk people with long-term exposure were reported.

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Section: Resultsmentioning

confidence: 99%

Particulate Matter 2.5 and Hematological Disorders From Dust to Diseases: A Systematic Review of Available Evidence

et al. 2021

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“…The ROS inhibitor, NAC, inhibits the growth of leukaemia cells and could be a potential target for intervention ( Jin et al, 2016 ). Maternal exposure to PM 2.5 causes progressive senescence of HSCs via the ROS-p38 mitogen-activated protein kinase (MAPK) pathway and the nuclear factor erythroid-2 related factor 2 (Nrf2) pathway under the exposure-induced preferential impairment of the BM microenvironment with age related phenotypes ( Bhattarai et al, 2019 ). Previous mouse studies have shown that ROS levels were increased in the BM, spleen and BM-derived CFU-GM cells of formaldehyde-exposed mice and that ROS played a role in formaldehyde-induced hematopoietic toxicity ( Wei et al, 2017 ).…”

Section: Resultsmentioning

confidence: 99%

Combined exposure to formaldehyde and PM2.5: Hematopoietic toxicity and molecular mechanism in mice

Yang²,

et al. 2020

Environment International

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PM 2.5 and formaldehyde (FA) are major outdoor and indoor air pollutants in China, respectively, and both are known to be harmful to human health and to be carcinogenic. Of all the known chronic health effects, leukaemia is one of the most serious health risks associated with these two pollutants. To explore the influence and underlying mechanisms of exposure to formaldehyde and PM 2.5 on hematopoietic toxicity, we systematically studied the toxicity induced in hematopoietic organs: bone marrow (BM); spleen; and myeloid progenitor cells (MPCs). Male Balb/c mice were exposed to: PM 2.5 (20, 160 μg/kg·d) at a dose of 40 μL per mouse or formaldehyde (0.5, 3.0 mg/m 3 ) for 8 h per day for 2 weeks or co-exposed to formaldehyde and PM 2.5 (20 μg/kg·d PM 2.5 + 0.5 mg/m 3 FA, 20 μ/kg·d PM 2.5 + 3 mg/m 3 FA, 160 μg/kg·d PM 2.5 + 0.5 mg/m 3 FA, 160 μg/kg·d PM 2.5 + 3 mg/m 3 FA) for 2 weeks. Similar toxic effects were found in the formaldehyde-only and PM 2.5 -only groups, including significant decrease of blood cells and MPCs, along with decreased expression of hematopoietic growth factors. In addition, individual exposure of formaldehyde or PM 2.5 increased oxidative stress, DNA damage and immune system disorder by destroying the balance of Th1/Th2, and Treg/Th17. DNA repair was markedly inhibited by deregulating the mammalian target of rapamycin (mTOR) pathway. Combined exposure to PM 2.5 and formaldehyde led to more severe effects. Administration of Vitamin E (VE) was shown to attenuate these effects. In conclusion, our findings suggested that PM 2.5 and formaldehyde may induce hematopoietic toxicity by reducing the expression of hematopoietic growth factors, increasing oxidative stress and DNA damage, activating the ‘immune imbalance’ pathway and suppressing the DNA-repair related mTOR pathway. The hematopoietic toxicity induced by combined exposure of PM 2.5 and formaldehyde might provide further insights into the increased incidence of hematological diseases, including human myeloid leukaemia.

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“…Aerosol particles can play an important role in air quality, climate change, and human health (Kulmala et al, 2011;Zhang et al, 2015;IPCC 2019;Bhattarai et al, 2020). These aerosol particles comprise mainly organic materials and inorganic salts which are frequently internally mixed in particles found in the atmosphere (Murphy et al, 2006;Zhang et al, 2007;Jimenez et al, 2009;Wang et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Viscosity and physical state of sucrose mixed with ammonium sulfate droplets

Jeong

Lilek

Zuend

et al. 2022

Preprint

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Abstract. Although knowledge of the physical state of aerosol particles is essential to understand atmospheric chemistry model and measurements, information on the viscosity and physical state of aerosol particles consisting of organic and inorganic salts are still rare. Herein, we quantified viscosities at 293 ± 1 K upon dehydration for the binary systems, sucrose/H2O and ammonium sulfate (AS)/H2O, and the ternary systems, sucrose/AS/H2O for organic-to-inorganic dry mass ratios (OIRs) = 4 : 1, 1 : 1, and 1 : 4. For binary systems, the viscosity of sucrose/H2O particles gradually increased from ~6 × 10−1 to > ~1 × 108 Pa‧s when the relative humidity (RH) decreased from ~83 % to ~24 %, which agrees with previous studies. The viscosity of AS/H2O particles remained in the liquid state (< 102 Pa‧s) for RH > ~50 %, and for RH ≤ ~50 %, the particles showed viscosity of > ~1 × 1012 Pa‧s, corresponding to a solid state. For ternary systems, the viscosity of organic-rich particles (OIR = 4 : 1) gradually increased from ~4 × 10−2 to ~1 × 108 Pa‧s for a RH decrease from ~80 % to ~18 %, similar to the sucrose/H2O particles. In the particles for OIR = 1 : 1, the viscosities ranged smaller than ~4 × 101 for RH > 34 %, and > ~1 × 108 Pa‧s at ~27 % RH. Compared to the organic-rich particles, in the inorganic-rich particles (OIR = 1 : 4), drastic enhancement in viscosity was observed as RH decreased; the viscosity enhanced approximately 8 orders of magnitude in RH from 43 % to 25 %. Based on viscosity data, all particles studied in this work were observed to exist as a liquid, semi-solid or solid depending on the RH. Furthermore, we compared the measured viscosities of ternary systems with OIRs of 4 : 1, 1 : 1, and 1 : 4 to the predicted viscosities using the Aerosol Inorganic–Organic Mixtures Functional groups Activity Coefficients Viscosity model (AIOMFAC-VISC) predictions with the Zdanovskii–Stokes–Robinson (ZSR)-style organic–inorganic mixing model, with excellent model–measurement agreement for all OIRs.

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Maternal exposure to fine particulate matter during pregnancy induces progressive senescence of hematopoietic stem cells under preferential impairment of the bone marrow microenvironment and aids development of myeloproliferative disease

Cited by 27 publications

References 15 publications

Particulate Matter 2.5 and Hematological Disorders From Dust to Diseases: A Systematic Review of Available Evidence

Particulate Matter 2.5 and Hematological Disorders From Dust to Diseases: A Systematic Review of Available Evidence

Combined exposure to formaldehyde and PM2.5: Hematopoietic toxicity and molecular mechanism in mice

Viscosity and physical state of sucrose mixed with ammonium sulfate droplets

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