scholarly journals Air Pollution, Neonatal Immune Responses, and Potential Joint Effects of Maternal Depression

Author(s):  
Jill Hahn ◽  
Diane R. Gold ◽  
Brent A. Coull ◽  
Marie C. McCormick ◽  
Patricia W. Finn ◽  
...  

Prenatal maternal exposure to air pollution may cause adverse health effects in offspring, potentially through altered immune responses. Maternal psychosocial distress can also alter immune function and may increase gestational vulnerability to air pollution exposure. We investigated whether prenatal exposure to air pollution is associated with altered immune responses in cord blood mononuclear cells (CBMCs) and potential modification by maternal depression in 463 women recruited in early pregnancy (1999–2001) into the Project Viva longitudinal cohort. We estimated black carbon (BC), fine particulate matter (PM2.5), residential proximity to major roadways, and near-residence traffic density, averaged over pregnancy. Women reported depressive symptoms in mid-pregnancy (Edinburgh Postnatal Depression Scale) and depression history by questionnaire. Immune responses were assayed by concentrations of three cytokines (IL-6, IL-10, and TNF-α), in unstimulated or stimulated (phytohemagglutinin (PHA), cockroach extract (Bla g 2), house dust mite extract (Der f 1)) CBMCs. Using multivariable linear or Tobit regression analyses, we found that CBMCs production of IL-6, TNF-a, and IL-10 were all lower in mothers exposed to higher levels of PM2.5 during pregnancy. A suggestive but not statistically significant pattern of lower cord blood cytokine concentrations from ever (versus never) depressed women exposed to PM2.5, BC, or traffic was also observed and warrants further study.

2016 ◽  
Vol 5 (2) ◽  
pp. 61-74 ◽  
Author(s):  
Geetanjali Kaushik ◽  
Arvind Chel ◽  
Sangeeta Shinde ◽  
Ashish Gadekar

Almost 670 million people comprising 54.5% of our population reside in regions that do not meet the Indian NAAQS for fine particulate matter. Numerous studies have revealed a consistent correlation for particulate matter concentration with health than any other air pollutant. Aurangabad city a rapidly growing city with population of 1.5 million is home to five major industrial areas, the city is also known for its historical monuments which might also be adversely affected from air pollution. Therefore, this research aims at estimating PM10 concentrations at several locations across Aurangabad. The concentration of PM10 was highest at the Railway Station followed by Waluj (an industrial zone) and City chowk is the centre of the city which has high population, tall buildings, few open spaces which causes high congestion and does not allow the particulates to disperse. Other locations with high concentrations of PM are Mill corner, Harsul T-point, Kranti Chowk, Seven Hill, TV centre and Beed Bye pass. All these locations have narrow roads, high traffic density, poor road condition with pot holes and few crossing points which cause congestion and vehicle idling which are responsible for high pollution. Therefore, it is evident that air pollution is a serious issue in the city which may be further aggravated if it is not brought under control. Hence, strategies have to be adopted for combating the menace of air pollution.INTERNATIONAL JOURNAL OF ENVIRONMENTVolume-5, Issue-2, March-May 2016, Page :61-74


2019 ◽  
Vol 7 (3) ◽  
pp. 138-139
Author(s):  
Regina Fölster-Holst

Background: Altered regulatory immune responses to microbial stimuli and intestinal colonization of beneficial bacteria early in life may contribute to the development of allergic diseases (e.g., atopic dermatitis [AD]). However, few reports have investigated these factors simultaneously. The purpose of this study was to analyze neonatal immune responses to microbial stimuli as well as intestinal colonization of beneficial bacteria, in relation to the development of AD in a birth cohort. Methods: Pregnant women were recruited, and their infants were followed up until 7 months of age. Levels of interleukin (IL)-10 released from cord-blood mononuclear cells (CBMCs) stimulated with heat-killed gram-positive bacteria (Bifidobacterium bifidum and Lactobacillus rhamnosus GG) and Lactobacillus-derived peptidoglycan were measured. Fecal Bifidobacterium counts at 4 days and 1 month were quantified using real-time polymerase chain reaction. The development of AD was determined by means of a questionnaire at 7 months of age. Results: The levels of released IL-10 were significantly lower in infants with AD (n = 17) than in infants without AD (n = 53) for all stimuli. In infants with fecal Bifidobacterium, the incidence of AD was inversely associated with the release of IL-10 from cord blood mononuclear cells. Conclusion: Our findings suggest that impaired IL-10 production in response to microbial stimuli at birth may be associated with an increased risk of developing infantile AD, even in infants with early colonization of intestinal bifidobacteria.


2012 ◽  
Vol 123 (6) ◽  
pp. 347-360 ◽  
Author(s):  
Ming-Cheng Chang ◽  
Chien-Nan Lee ◽  
Yu-Li Chen ◽  
Ying-Cheng Chiang ◽  
Wei-Zen Sun ◽  
...  

The aim of the present study was to investigate whether CBSCs [(umbilical) cord blood stem cells] can be a new source of DCs (dendritic cells), which can generate more potent antigen-specific immune responses and anti-tumour effects. CBSCs and PBMCs (peripheral blood mononuclear cells) were collected, cultured and differentiated into DCs. Surface markers, secreting cytokines, antigen-presentation activity, antigen-specific cell-mediated immunity and cytotoxic killing effects induced by these two DC origins were evaluated and compared. CBSCs were expanded ~17-fold by ex vivo culture. The expression of surface markers in CBSC-derived DCs were higher than those in PBMC-derived DCs treated with LPS (lipopolysaccharide). The CBSC-derived DCs mainly secreted IL (interleukin)-6, IL-10 and TNF (tumour necrosis factor)-α, whereas PBMC-derived DCs mainly secreted IL-5 and IFN (interferon)-γ. The CBSC-derived DCs had better antigen-presentation abilities when stimulated with LPS or TNF-α, induced higher numbers of IFN-γ-secreting antigen-specific CD8+ T-cells, as assessed using an ELISpot (enzyme-linked immunosorbent spot) assay, and stimulated more potent antigen-specific CTL (cytotoxic T-cell) activities (P<0.01, one-way ANOVA). CBSC-derived DCs had quicker and greater ERK (extracellular-signal-regulated kinase) and Akt phosphorylation, and weaker p38 phosphorylation, than PBMC-derived DCs when stimulated with LPS. In conclusion, CBSC-derived DCs have the ability to induce stronger antigen-specific immunity and more potent anti-tumour effects and therefore could be a good source of DCs for use in DC-based cancer vaccines and immunotherapy.


Author(s):  
Mohammad Hashem Askariyeh ◽  
Madhusudhan Venugopal ◽  
Haneen Khreis ◽  
Andrew Birt ◽  
Josias Zietsman

Recent studies suggest that the transportation sector is a major contributor to fine particulate matter (PM2.5) in urban areas. A growing body of literature indicates PM2.5 exposure can lead to adverse health effects, and that PM2.5 concentrations are often elevated close to roadways. The transportation sector produces PM2.5 emissions from combustion, brake wear, tire wear, and resuspended dust. Traffic-related resuspended dust is particulate matter, previously deposited on the surface of roadways that becomes resuspended into the air by the movement of traffic. The objective of this study was to use regulatory guidelines to model the contribution of resuspended dust to near-road traffic-related PM2.5 concentrations. The U.S. Environmental Protection Agency (EPA) guidelines for quantitative hotspot analysis were used to predict traffic-related PM2.5 concentrations for a small network in Dallas, Texas. Results show that the inclusion of resuspended dust in the emission and dispersion modeling chain increases prediction of near-road PM2.5 concentrations by up to 74%. The results also suggest elevated PM2.5 concentrations near arterial roads. Our results are discussed in the context of human exposure to traffic-related air pollution.


Toxics ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 169
Author(s):  
Seyram Kaali ◽  
Darby Jack ◽  
Jones Opoku-Mensah ◽  
Tessa Bloomquist ◽  
Joseph Aanaro ◽  
...  

Background: Associations between prenatal household air pollution exposure (HAP), newborn telomere length and early childhood blood pressure are unknown. Methods: Pregnant women were randomized to liquefied petroleum gas (LPG) stove, improved biomass stove or control (traditional, open fire cook stove). HAP was measured by personal carbon monoxide (CO) (n = 97) and fine particulate matter (PM2.5) (n = 60). At birth, cord blood mononuclear cells (CBMCs) were collected for telomere length (TL) analyses. At child age four years, we measured resting blood pressure (BP) (n = 97). We employed multivariable linear regression to determine associations between prenatal HAP and cookstove arm and assessed CBMC relative to TL separately. We then examined associations between CBMC TL and resting BP. Results: Higher prenatal PM2.5 exposure was associated with reduced TL (β = −4.9% (95% CI −8.6, −0.4), p = 0.03, per 10 ug/m3 increase in PM2.5). Infants born to mothers randomized to the LPG cookstove had longer TL (β = 55.3% (95% CI 16.2, 109.6), p < 0.01)) compared with control. In all children, shorter TL was associated with higher systolic BP (SBP) (β = 0.35 mmHg (95% CI 0.001, 0.71), p = 0.05, per 10% decrease in TL). Conclusions: Increased prenatal HAP exposure is associated with shorter TL at birth. Shorter TL at birth is associated with higher age four BP, suggesting that TL at birth may be a biomarker of HAP-associated disease risk.


Atmosphere ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1086
Author(s):  
Polina Maciejczyk ◽  
Lung-Chi Chen ◽  
George Thurston

In this review, we elucidate the central role played by fossil fuel combustion in the health-related effects that have been associated with inhalation of ambient fine particulate matter (PM2.5). We especially focus on individual properties and concentrations of metals commonly found in PM air pollution, as well as their sources and their adverse health effects, based on both epidemiologic and toxicological evidence. It is known that transition metals, such as Ni, V, Fe, and Cu, are highly capable of participating in redox reactions that produce oxidative stress. Therefore, particles that are enriched, per unit mass, in these metals, such as those from fossil fuel combustion, can have greater potential to produce health effects than other ambient particulate matter. Moreover, fossil fuel combustion particles also contain varying amounts of sulfur, and the acidic nature of the resulting sulfur compounds in particulate matter (e.g., as ammonium sulfate, ammonium bisulfate, or sulfuric acid) makes transition metals in particles more bioavailable, greatly enhancing the potential of fossil fuel combustion PM2.5 to cause oxidative stress and systemic health effects in the human body. In general, there is a need to further recognize particulate matter air pollution mass as a complex source-driven mixture, in order to more effectively quantify and regulate particle air pollution exposure health risks.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4459-4459
Author(s):  
Ryo Hanajiri ◽  
Makoto Murata ◽  
Kyoko Sugimoto ◽  
Miho Murase ◽  
Haruhiko Ohashi ◽  
...  

Recent statistical analyses of the clinical outcome have revealed that the presence of donor-specific anti-HLA antibodies (DSAs) in pre-transplant recipient is correlated with increased risk for graft rejection after allogeneic hematopoietic stem cell (HSC) transplantation. However, while cytotoxic T lymphocytes (CTLs) recognizing mismatched HLA molecule of the donor have been shown to be involved in graft rejection, there has been no biological evidence in humans that graft rejection is mediated by DSAs. In the present study, we demonstrate a case of cord blood allograft rejection in which DSAs acted to mediate graft rejection. Interestingly, CTL clones specific for donor HLA molecule were also isolated, suggesting that humoral and cellular immune responses were together responsible for allograft rejection. A patient with graft rejection after HLA-mismatched cord blood transplantation was studied. The white blood cell count increased transiently, subsequently decreased to undetectable level, and finally graft rejection was diagnosed on day 34. Screening for pre-transplant anti-HLA antibodies was not routinely performed at that time. We initially presumed that DSA would be responsible for graft rejection. The patient serum on day 36 were screened for HLA antibodies and further evaluated to determine HLA specificities using a LABScreen Single Antigen Kit. An antibody against HLA-B* 54:01, which was expressed in donor cells but not in patient cells, was detected. To test the effect of the DSA against HLA-B* 54:01 on HSC engraftment, antibody-dependent cellular cytotoxicity (ADCC) activity was assessed using unrelated HLA-B* 54:01-positive bone marrow mononuclear cells (BMMNCs) pre-cultured with patient serum and pre-transplant NK cells. The patient serum clearly showed an inhibitory effect on colony formation. Complement-dependent cytotoxicity activity of the DSA could not be detected. These data suggest that the DSA impaired the cord blood engraftment through ADCC activities. We next determined if cellular immunity was also responsible for allograft rejection. Two independent CTL clones, CD4-CD8+ and CD4+CD8-, were isolated from the patient blood at the time of graft rejection by limiting dilution. Both CTL clones were of patient origin by using short tandem repeat analysis and showed cytotoxicity against donor cells but not patient cells in Cr release assay. A CTL stimulation assay using COS cells transfected with various mismatched donor HLA cDNA constructs demonstrated that CD8+ and CD4+CTL clones recognized HLA-B* 54:01 and -DRB1* 15:02 molecules, respectively, both of which were expressed in donor cells but not in patient cells. To test the effect of the CTL clones on engraftment, a colony forming assay using either HLA-B* 54:01 or -DRB1* 15:02-positive unrelated BMMNCs pre-cultured with the corresponding CTL clones was performed. Each of these CTL clones inhibited colony formation from unrelated BMMNCs sharing target HLA in a dose-dependent manner. These data suggest that the CTLs also impaired the cord blood engraftment. Furthermore, anti-HLA-B* 54:01 antibody was detected in cryopreserved pre-transplant patient serum, and in nested PCR assays specific for the HLA-B* 54:01-specific CTL clone’s uniquely rearranged T cell receptor V beta chain, PCR product was detected by amplification of cDNA from pre-transplant patient peripheral blood mononuclear cells. Thus, both HLA-B* 54:01-specific antibody and CTL clone developed in the patient prior to transplantation. The present data provide the first direct evidence showing that humoral and cellular immune responses were involved in the graft rejection. Of note is the recognition of the same mismatched HLA-B* 54:01 molecule by the DSA and CTL, suggesting that humoral and cellular immune processes acted together to mediate allograft rejection. Given the difficulty in detecting HLA-specific CTLs in pre-transplant patient blood in contrast to the easiness in screening for DSAs, the presence of DSA not only means a direct deleterious effect on donor cells but it may also reflect the presence of CTLs that causes allograft rejection. Further studies are warranted to clarify whether the present observation can be duplicated in other patients with DSA. We are conducting the study to clarify whether patients with anti-HLA antibodies have CTLs that recognize the same HLA molecules before transplantation. Disclosures: No relevant conflicts of interest to declare.


2012 ◽  
Vol 13 (3) ◽  
pp. 705-715 ◽  
Author(s):  
Marko Tainio ◽  
Katarzyna Juda-Rezler ◽  
Magdalena Reizer ◽  
Aleksander Warchałowski ◽  
Wojciech Trapp ◽  
...  

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2302-2302
Author(s):  
Nagwa S. El-Badri (Dajani) ◽  
Denis English ◽  
Amal Hakki ◽  
Sriram Mudhusoodanan ◽  
Cyndy D. Sanberg ◽  
...  

Abstract Our previous studies consistently demonstrate enhanced neural protective effects of cord blood in comparison to stem cells from adult marrow. Similarly, cord blood possesses diminished immuno-stimulatory activity, and the basis of this effect has not been defined. Since neural damage may be potentiated by immune activation of inflammatory cascades, we examined the effects of cord blood-derived MSCs (mesenchymal stem cells) on immune responses. We isolated and characterized a population of cord blood MSCs. These cells maintained their pluripotency in culture. Progeny generated in the absence of differentiation were strongly adherent, did not express CD34, CD45, CD3, CD19 antigens, and did not generate hematopoietic colonies in methylcellulose. However, cultured cord blood MSCs possessed a remarkable ability to support the proliferation as well as the differentiation of hematopoietic cells in vitro. In addition, supernatants from cultured cord blood MSCs promoted survival of peripheral blood mononuclear cells cultured under conditions designed to induce cell stress and limit protein synthesis. We examined immune modulation by cord blood MSCs after co-culture with murine splenocytes. While spleen cells from normal C57Bl/6 mice exhibited a prominent IgM response after immunization with the T-cell dependent antigen, SRBCs, this response was significantly decreased after incubation with cord blood MSCs. Consistently, cord blood MSCs mitigated the enhanced mixed lymphocyte proliferative response C57Bl/6 T-cells exhibit when exposed to lymphocytes from non-related animals. To investigate whether these immune suppressive properties could be therapeutically useful in a transplantation model for autoimmune disease, cord blood MSCs were transplanted into sublethally irradiated BXSB mouse model for systemic lupus. Thirty days after infusion, defective IgM humoral immune responses of splenocytes of these mice normalized. This normalization paralleled normalization of the disrupted lymphoid cellularity observed in the spleens of diseased animals. Our results are consistent with the hypothesis that immune regulation is involved in the therapeutic utility of MSCs.


2020 ◽  
Author(s):  
Rıdvan Karacan

<p>Today, production is carried out depending on fossil fuels. Fossil fuels pollute the air as they contain high levels of carbon. Many studies have been carried out on the economic costs of air pollution. However, in the present study, unlike the former ones, economic growth's relationship with the COVID-19 virus in addition to air pollution was examined. The COVID-19 virus, which was initially reported in Wuhan, China in December 2019 and affected the whole world, has caused many cases and deaths. Researchers have been going on studying how the virus is transmitted. Some of these studies suggest that the number of virus-related cases increases in regions with a high level of air pollution. Based on this fact, it is thought that air pollution will increase the number of COVID-19 cases in G7 Countries where industrial production is widespread. Therefore, the negative aspects of economic growth, which currently depends on fossil fuels, is tried to be revealed. The research was carried out for the period between 2000-2019. Panel cointegration test and panel causality analysis were used for the empirical analysis. Particulate matter known as PM2.5[1] was used as an indicator of air pollution. Consequently, a positive long-term relationship has been identified between PM2.5 and economic growth. This relationship also affects the number of COVID-19 cases.</p><p><br></p><p><br></p><p>[1] "Fine particulate matter (PM2.5) is an air pollutant that poses the greatest risk to health globally, affecting more people than any other pollutant (WHO, 2018). Chronic exposure to PM2.5 considerably increases the risk of respiratory and cardiovascular diseases in particular (WHO, 2018). For these reasons, population exposure to (outdoor or ambient) PM2.5 has been identified as an OECD Green Growth headline indicator" (OECD.Stat).</p>


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