Increases in ambient air pollutants during pregnancy are linked to increases in methylation of IL4, IL10, and IFNγ.
Air Pollutants
/ adverse effects
DNA Methylation
Environmental Exposure
/ adverse effects
Environmental Pollutants
Female
Humans
Infant, Newborn
Interferon-gamma
/ genetics
Interleukin-10
/ genetics
Interleukin-4
/ genetics
Nitrogen Dioxide
/ adverse effects
Particulate Matter
/ adverse effects
Pregnancy
Pregnancy Outcome
Air pollution
DNA methylation
IFNγ
IL10
IL4
Immunology
PM2.5
Pregnancy
Th1
Th2
Journal
Clinical epigenetics
ISSN: 1868-7083
Titre abrégé: Clin Epigenetics
Pays: Germany
ID NLM: 101516977
Informations de publication
Date de publication:
14 03 2022
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
40Subventions
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).
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