Increases in ambient air pollutants during pregnancy are linked to increases in methylation of IL4, IL10, and IFNγ.


Journal

Clinical epigenetics
ISSN: 1868-7083
Titre abrégé: Clin Epigenetics
Pays: Germany
ID NLM: 101516977

Informations de publication

Date de publication:
14 03 2022
Historique:
received: 01 11 2021
accepted: 21 02 2022
entrez: 15 3 2022
pubmed: 16 3 2022
medline: 7 5 2022
Statut: epublish

Résumé

Ambient air pollutant (AAP) exposure is associated with adverse pregnancy outcomes, such as preeclampsia, preterm labor, and low birth weight. Previous studies have shown methylation of immune genes associate with exposure to air pollutants in pregnant women, but the cell-mediated response in the context of typical pregnancy cell alterations has not been investigated. Pregnancy causes attenuation in cell-mediated immunity with alterations in the Th1/Th2/Th17/Treg environment, contributing to maternal susceptibility. We recruited women (n = 186) who were 20 weeks pregnant from Fresno, CA, an area with chronically elevated AAP levels. Associations of average pollution concentration estimates for 1 week, 1 month, 3 months, and 6 months prior to blood draw were associated with Th cell subset (Th1, Th2, Th17, and Treg) percentages and methylation of CpG sites (IL4, IL10, IFNγ, and FoxP3). Linear regression models were adjusted for weight, age, season, race, and asthma, using a Q value as the false-discovery-rate-adjusted p-value across all genes. Short-term and mid-term AAP exposures to fine particulate matter (PM Exposure to several AAPs was negatively associated with T-helper subsets involved in pro-inflammatory and anti-inflammatory responses during pregnancy. Methylation of IL4, IL10, and IFNγ genes with pollution exposure confirms previous research. These results offer insights into the detrimental effects of air pollution during pregnancy, the demand for more epigenetic studies, and mitigation strategies to decrease pollution exposure during pregnancy.

Sections du résumé

BACKGROUND
Ambient air pollutant (AAP) exposure is associated with adverse pregnancy outcomes, such as preeclampsia, preterm labor, and low birth weight. Previous studies have shown methylation of immune genes associate with exposure to air pollutants in pregnant women, but the cell-mediated response in the context of typical pregnancy cell alterations has not been investigated. Pregnancy causes attenuation in cell-mediated immunity with alterations in the Th1/Th2/Th17/Treg environment, contributing to maternal susceptibility. We recruited women (n = 186) who were 20 weeks pregnant from Fresno, CA, an area with chronically elevated AAP levels. Associations of average pollution concentration estimates for 1 week, 1 month, 3 months, and 6 months prior to blood draw were associated with Th cell subset (Th1, Th2, Th17, and Treg) percentages and methylation of CpG sites (IL4, IL10, IFNγ, and FoxP3). Linear regression models were adjusted for weight, age, season, race, and asthma, using a Q value as the false-discovery-rate-adjusted p-value across all genes.
RESULTS
Short-term and mid-term AAP exposures to fine particulate matter (PM
CONCLUSION
Exposure to several AAPs was negatively associated with T-helper subsets involved in pro-inflammatory and anti-inflammatory responses during pregnancy. Methylation of IL4, IL10, and IFNγ genes with pollution exposure confirms previous research. These results offer insights into the detrimental effects of air pollution during pregnancy, the demand for more epigenetic studies, and mitigation strategies to decrease pollution exposure during pregnancy.

Identifiants

pubmed: 35287715
doi: 10.1186/s13148-022-01254-2
pii: 10.1186/s13148-022-01254-2
pmc: PMC8919561
doi:

Substances chimiques

Air Pollutants 0
Environmental Pollutants 0
IL10 protein, human 0
Particulate Matter 0
Interleukin-10 130068-27-8
Interleukin-4 207137-56-2
Interferon-gamma 82115-62-6
Nitrogen Dioxide S7G510RUBH

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

40

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL081521
Pays : United States
Organisme : NIEHS NIH HHS
ID : P01 ES022849
Pays : United States
Organisme : NIEHS NIH HHS
ID : P20 ES018173
Pays : United States
Organisme : NIEHS NIH HHS
ID : R24 ES030888
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES032253
Pays : United States

Informations de copyright

© 2022. The Author(s).

Références

Chemosphere. 2015 Feb;120:722-8
pubmed: 25462318
PLoS One. 2011;6(8):e23130
pubmed: 21826232
PLoS Pathog. 2017 Nov 27;13(11):e1006757
pubmed: 29176767
Am J Reprod Immunol. 2010 Jun;63(6):601-10
pubmed: 20455873
J Clin Epidemiol. 2010 May;63(5):558-65
pubmed: 19959329
Arch Toxicol. 2019 Oct;93(10):2715-2740
pubmed: 31555878
Chest. 1993 Aug;104(2):600-8
pubmed: 7802735
J Immunol. 2008 Sep 15;181(6):3897-905
pubmed: 18768844
Int Arch Allergy Immunol. 2009;148(3):239-50
pubmed: 18849615
Environ Health Perspect. 2010 Oct;118(10):1497-502
pubmed: 20570778
Arch Toxicol. 2016 Feb;90(2):231-45
pubmed: 25480659
Sci Rep. 2021 Feb 18;11(1):4067
pubmed: 33603036
Annu Rev Immunol. 1999;17:701-38
pubmed: 10358772
Environ Res. 2016 Jul;148:513-526
pubmed: 27155984
Free Radic Biol Med. 2020 May 1;151:56-68
pubmed: 32007522
Am J Obstet Gynecol. 2020 Jun;222(6):521-531
pubmed: 32217113
Environ Res. 2021 Apr;195:110870
pubmed: 33587949
Environ Health Perspect. 2012 Oct;120(10):1425-31
pubmed: 22851337
Environ Health Perspect. 2010 May;118(5):640-6
pubmed: 20061214
Clin Exp Immunol. 1996 Oct;106(1):127-33
pubmed: 8870710
Environ Res. 2018 Nov;167:144-159
pubmed: 30014896
Environ Res. 2021 Jun;197:111165
pubmed: 33857458
Toxicol Lett. 2015 Jan 22;232(2):475-80
pubmed: 25481569
J Immunol. 1986 Apr 1;136(7):2348-57
pubmed: 2419430
Clin Epigenetics. 2012 Sep 25;4(1):17
pubmed: 23009259
J Allergy Clin Immunol. 2013 Feb;131(2):592-4.e1-3
pubmed: 23260754
PLoS One. 2008 Feb 20;3(2):e1612
pubmed: 18286169
Clin Exp Allergy. 2015 Jan;45(1):238-48
pubmed: 25048800
Front Immunol. 2014 May 27;5:253
pubmed: 24904596
Curr Protoc Immunol. 2009 Apr;Chapter 7:Unit7.1
pubmed: 19347849
Environ Int. 2015 Aug;81:1-7
pubmed: 25898227
Vaccine. 2003 Jul 28;21(24):3352-7
pubmed: 12850338
Environ Sci Process Impacts. 2016 Jul 13;18(7):908-17
pubmed: 27359112
Cell Mol Immunol. 2014 Nov;11(6):564-70
pubmed: 25027967
J Allergy Clin Immunol. 2010 Oct;126(4):845-852.e10
pubmed: 20920773
Front Immunol. 2017 Sep 15;8:1138
pubmed: 28966619
BMC Genomics. 2014 Feb 21;15:145
pubmed: 24555763
Environ Health Perspect. 2005 Apr;113(4):375-82
pubmed: 15811825
Environ Int. 2018 Dec;121(Pt 1):317-324
pubmed: 30241019
J Immunol. 1993 Nov 1;151(9):4562-73
pubmed: 8409418
Environ Pollut. 2018 Jun;237:18-27
pubmed: 29466771
Atmos Environ (1994). 2020 Dec 1;242:
pubmed: 32982565
Clin Epigenetics. 2018 Jan 5;10:2
pubmed: 29317916
Biochem Biophys Res Commun. 1998 Apr 28;245(3):933-8
pubmed: 9588218

Auteurs

Juan Aguilera (J)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University, 240 Pasteur, Stanford, CA, 94305, USA.

Xiaorui Han (X)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University, 240 Pasteur, Stanford, CA, 94305, USA.

Shu Cao (S)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University, 240 Pasteur, Stanford, CA, 94305, USA.

John Balmes (J)

Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA.
Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.

Fred Lurmann (F)

Sonoma Technology, Petaluma, CA, USA.

Tim Tyner (T)

University of California, San Francisco-Fresno, Fresno, CA, USA.
Central California Asthma Collaborative, Fresno, USA.

Liza Lutzker (L)

Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA.

Elizabeth Noth (E)

Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA.

S Katharine Hammond (SK)

Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA.

Vanitha Sampath (V)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University, 240 Pasteur, Stanford, CA, 94305, USA.

Trevor Burt (T)

Department of Pediatrics, Division of Neonatology and the Translating Duke Health Children's Health and Discovery Initiative, Duke University School of Medicine, 701 W Main St., Chesterfield Building, Suite 510, Durham, NC, 27701, USA.

P J Utz (PJ)

Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford University, 291 Campus Drive, Stanford, CA, 94305, USA.

Purvesh Khatri (P)

Center for Biomedical Informatics, Department of Medicine, Stanford University School of Medicine, Stanford University, 291 Campus Drive, Stanford, CA, 94305, USA.

Nima Aghaeepour (N)

Departments of Biomedical Data Sciences, Stanford University, 291 Campus Drive, Stanford, CA, 94305, USA.

Holden Maecker (H)

Institute for Immunity, Transplantation and Infection, Stanford University, 291 Campus Drive, Stanford, CA, 94305, USA.

Mary Prunicki (M)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University, 240 Pasteur, Stanford, CA, 94305, USA.

Kari Nadeau (K)

Sean N. Parker Center for Allergy and Asthma Research, Stanford University, 240 Pasteur, Stanford, CA, 94305, USA. knadeau@stanford.edu.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH