469 - Association Between Placental Inflammation and Development of Childhood Asthma

Publication Number: 2457.469

Jessa B. Snower, Tulane University School of Medicine, Glencoe, IL, United States; Stephanie M.. McCarthy, Endeavor Health, Evanston, IL, United States; Alexa Freedman, Northwestern University The Feinberg School of Medicine, Chicago, IL, United States; Linda Ernst, Endeavor Health, Chicago, IL, United States; Andrew Franklin, Endeavor Health System, Evanston, IL, United States

Background: Asthma is a multifactorial disorder that may originate during fetal life. While chorioamnionitis, preterm birth, and fetal inflammatory response syndrome have been associated with development of asthma in later life, placental histopathologies and asthma risk has not been well distinguished.

Objective: This study aims to determine whether an inflammatory environment in utero, demonstrated by placental inflammation by histology, is associated with an increased risk of developing asthma.

Design/Methods: A retrospective chart review of children with available placental pathology between Jan 1, 2017 and July 1, 2024 was conducted. Asthma was identified by using ICD-10 code J45 or ICD-9 code 493. Placental histology was coded for acute inflammation, chronic inflammation, fetal vascular malperfusion, and maternal vascular malperfusion according to Amsterdam criteria. Logistic regression was used to determine the odds of an asthma diagnosis associated with varying placental pathologies including acute inflammation, chronic inflammation, fetal vascular pathology, or maternal vascular pathology.

Results: We included 9833 children, 332 of which developed asthma. Table 1 shows demographics of the cohort; those that developed asthma had a significantly increased C-section deliveries, exposure to maternal gestational diabetes, and were more likely male. Those without asthma were more likely to be White. There were no differences in overall placental pathologies with asthma (see table 2). High-grade acute inflammation had 1.3-fold increased odds [1.01, 1.7] of developing asthma after adjustment for other high-grade pathologies. However, after adjustment for gestational age there was no significant difference in high-grade acute inflammation and asthma. There was a 1.7-fold increase [CI: 1.2, 2.3] in the development of asthma with multiple high-grade pathologies present. After adjustment for gestational age, there remained 1.6-fold increased odds [1.14, 2.1] of developing asthma.

Conclusion(s): We show infants exposed to high-grade acute inflammation or multiple high-grade pathologies have an increased risk of developing asthma. We hypothesize that this may be due to fetal programing leading to an abnormal inflammatory state involved in the development of asthma. Future research is crucial for understanding children at risk of developing asthma. Additionally, understanding the inflammation patterns found from placental histology that are associated with asthma development can help determine which treatment options may be more effective.

Table 1: Demographics of Cohort
*Data displayed as number (percent) for categorical variables and mean (SD) for continuous variables. P values calculated using Chi-squared tests for categorical variables and t-tests for continuous variables.

Table 2: Placental Pathology Lesion and Childhood Asthma
*Data displayed as number (percent) and p values calculated using Chi-squared tests.