Prenatal PM2.5 exposure and vitamin D–associated early persistent atopic dermatitis via placental methylation

Abstract

Background: The effects of prenatal particulate matter with an aerodynamic diameter ranging from 0.1 mm to 2.5 mm (PM 2.5 ) 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 PM 2.5 exposure and AD in an offspring. Objective: To determine the critical windows of prenatal PM 2.5 exposure on the AD phenotypes, if vitamin D modulated these effects, and if placental DNA methylation mediated these effects on AD in offspring. Methods: Motherechild pairs were enrolled from the birth cohort of the Cohort for Childhood Origin of Asthma and allergic diseases (COCOA) study. PM 2.5 was estimated by land-use regression models, and CB vitamin D was measured by chemiluminescence immunoassay.

Prenatal PM2.5 affects atopic dermatitis depending on maternal anxiety and gender: COCOA study

“…In our study, co-exposure to PM Our finding that the first trimester of pregnancy was a critical period for PM 2.5 exposure associated with AD at 1 year of age was consistent with those of previous COCOA studies. 4,5 In particular, 5-8 weeks of gestation was the critical period for PM 2.5 exposure in boys with higher prenatal maternal anxiety. The development of antioxidant enzyme systems begins during the mid-to-late gestational periods, and these systems continue to mature through the early postnatal years.…”

“…1,2 Among several environmental factors, particulate matter with an aerodynamic diameter of less than 2.5 μm (PM 2.5 ) and maternal distress during pregnancy are associated with AD. [3][4][5][6][7] PM 2.5 is a mixture of tiny solid and liquid particles suspended in the air. PM 2.5 is considered especially harmful to human health because they can enter deeper into our bodies.…”

The prevalence and year lived with disability of atopic dermatitis in China: Findings from the global burden of disease study 2019

“…20,21 The high prevalence and YLD of AD in children could be explained by environment factors and prenatal exposure. 22,23 Prevention and control measures should be taken in the perinatal period, targeting the skin barrier, immune/allergy and environmental aspects. 19 AD is also a part of process called the atopic march, which is generally characterized by the progression of AD to allergic rhinitis and asthma.…”

Prenatal Air Pollution Exposure and Placental DNA Methylation Changes: Implications on Fetal Development and Future Disease Susceptibility

“…Furthermore, for every 1% increase in BID methylation, there was a decrease in head circumference (−1.396 mm, 95% CI: −2.582, −0.209) and biparietal diameter (−0.330 mm, 95% CI: −0.635, −0.026) in the second trimester [42]. In Korea, the COCOA study showed that high PM 2.5 exposure and low cord blood vitamin D levels during the first trimester were associated with decreased placental methylation of AHRR, DPP10, and HLA-DRB1, and early-onset persistent atopic dermatitis in children [43]. In the ENVIRONAGE birth cohort, PM 2.5 and black carbon exposure increased placental DNA mutation rates (determined by an increase in the DNA mutation marker, Alu) as well as increased the promoter methylation of tumor suppressor (p53) and DNA repair (APEX1, OGG1, and ERCC4) genes.…”