Song-I Yang1, Seung-Hwa Lee2, So-Yeon Lee3, Hwan-Cheol Kim4, Hyo-Bin Kim5, Jeong-Hyun Kim6, Hyeyeun Lim2, Min Jee Park3, Hyun-Ju Cho7, Jisun Yoon8, Sungsu Jung9, Hyeon-Jong Yang10, Kangmo Ahn11, Kyung Won Kim12, Youn Ho Shin13, Dong In Suh14, Hye-Sung Won15, Mi-Young Lee15, Soo Hyun Kim16, Suk-Joo Choi17, Ja-Young Kwon18, Jong Kwan Jun19, Soo-Jong Hong20. 1. Department of Pediatrics, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Republic of Korea. 2. Asan Institute for Life Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. 3. Department of Pediatrics, Childhood Asthma Atopy Center, Environmental Health Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. 4. Department of Occupational and Environmental Medicine, Inha University School of Medicine, Incheon, Republic of Korea. 5. Department of Pediatrics, Inje University Sanggye Paik Hospital, Inje University College of Medicine, Seoul, Republic of Korea. 6. Department of Medicine, University of Ulsan College of Medicine, Seoul, Republic of Korea. 7. Department of Pediatrics, International St. Mary's Hospital, Catholic Kwandong University College of Medicine, Incheon, Republic of Korea. 8. Department of Pediatrics, Mediplex Sejong Hospital, Incheon, Republic of Korea. 9. Department of Pediatrics, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea. 10. Department of Pediatrics, Soonchunhyang University School of Medicine, Seoul, Republic of Korea. 11. Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 12. Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea. 13. Department of Pediatrics, CHA Gangnam Medical Center, CHA University School of Medicine, Seoul, Republic of Korea. 14. Department of Pediatrics, Seoul National University College of Medicine, Seoul, Republic of Korea. 15. Department of Obstetrics and Gynecology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. 16. Department of Obstetrics and Gynecology, CHA Gangnam Medical Center, CHA University School of Medicine, Seoul, Republic of Korea. 17. Department of Obstetrics and Gynecology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 18. Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Republic of Korea. 19. Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Republic of Korea. 20. Department of Pediatrics, Childhood Asthma Atopy Center, Environmental Health Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. Electronic address: sjhong@amc.seoul.kr.
Abstract
BACKGROUND: The effects of prenatal particulate matter with an aerodynamic diameter ranging from 0.1 μm to 2.5 μm (PM2.5) and vitamin D on atopic dermatitis (AD) phenotypes have not been evaluated. DNA methylation and cord blood (CB) vitamin D could represent a plausible link between prenatal PM2.5 exposure and AD in an offspring. OBJECTIVE: To determine the critical windows of prenatal PM2.5 exposure on the AD phenotypes, if vitamin D modulated these effects, and if placental DNA methylation mediated these effects on AD in offspring. METHODS: Mother-child pairs were enrolled from the birth cohort of the Cohort for Childhood Origin of Asthma and allergic diseases (COCOA) study. PM2.5 was estimated by land-use regression models, and CB vitamin D was measured by chemiluminescence immunoassay. AD was identified by the parental report of a physician's diagnosis. We defined the following 4 AD phenotypes according to onset age (by the age of 2 years) and persistence (by the age of 3 years): early-onset transient and persistent, late onset, and never. Logistic regression analysis and Bayesian distributed lag interaction model were used. DNA methylation microarray was analyzed using an Infinium Human Methylation EPIC BeadChip (Illumina, San Diego, California) in placenta. RESULTS: PM2.5 exposure during the first trimester of pregnancy, especially during 6 to 7 weeks of gestation, was associated with early-onset persistent AD. This effect increased in children with low CB vitamin D, especially in those with PM2.5 exposure during 3 to 7 weeks of gestation. AHRR (cg16371648), DPP10 (cg19211931), and HLADRB1 (cg10632894) were hypomethylated in children with AD with high PM2.5 and low CB vitamin D. CONCLUSION: Higher PM2.5 during the first trimester of pregnancy and low CB vitamin D affected early-onset persistent AD, and the most sensitive window was 6 to 7 weeks of gestation. Placental DNA methylation mediated this effect.
BACKGROUND: The effects of prenatal particulate matter with an aerodynamic diameter ranging from 0.1 μm to 2.5 μm (PM2.5) and vitamin D on atopic dermatitis (AD) phenotypes have not been evaluated. DNA methylation and cord blood (CB) vitamin D could represent a plausible link between prenatal PM2.5 exposure and AD in an offspring. OBJECTIVE: To determine the critical windows of prenatal PM2.5 exposure on the AD phenotypes, if vitamin D modulated these effects, and if placental DNA methylation mediated these effects on AD in offspring. METHODS: Mother-child pairs were enrolled from the birth cohort of the Cohort for Childhood Origin of Asthma and allergic diseases (COCOA) study. PM2.5 was estimated by land-use regression models, and CB vitamin D was measured by chemiluminescence immunoassay. AD was identified by the parental report of a physician's diagnosis. We defined the following 4 AD phenotypes according to onset age (by the age of 2 years) and persistence (by the age of 3 years): early-onset transient and persistent, late onset, and never. Logistic regression analysis and Bayesian distributed lag interaction model were used. DNA methylation microarray was analyzed using an Infinium Human Methylation EPIC BeadChip (Illumina, San Diego, California) in placenta. RESULTS: PM2.5 exposure during the first trimester of pregnancy, especially during 6 to 7 weeks of gestation, was associated with early-onset persistent AD. This effect increased in children with low CB vitamin D, especially in those with PM2.5 exposure during 3 to 7 weeks of gestation. AHRR (cg16371648), DPP10 (cg19211931), and HLADRB1 (cg10632894) were hypomethylated in children with AD with high PM2.5 and low CB vitamin D. CONCLUSION: Higher PM2.5 during the first trimester of pregnancy and low CB vitamin D affected early-onset persistent AD, and the most sensitive window was 6 to 7 weeks of gestation. Placental DNA methylation mediated this effect.
Authors: A L Bosma; A Ascott; R Iskandar; K Farquhar; J Matthewman; M W Langendam; A Mulick; K Abuabara; H C Williams; P I Spuls; S M Langan; M A Middelkamp-Hup Journal: J Eur Acad Dermatol Venereol Date: 2022-02-25 Impact factor: 9.228