Exposure to higher particulate matter with an aerodynamic diameter less than 2.55 μm (PM2.5) early in pregnancy increases the probability for AD in infancy, especially in boys with higher maternal anxiety, according to a study published in Clinical and Translational Allergy. Therefore, avoiding PM2.5 exposure and maternal anxiety from the first trimester may prevent infant AD, the study authors noted. They found that higher PM2.5 during the first trimester of pregnancy, higher prenatal maternal anxiety, and male gender were associated with AD at age 1 (adjusted ORs [aORs], 1.86, 1.58, and 1.54, respectively). Furthermore, higher PM2.5 during the first trimester and higher maternal anxiety during pregnancy showed an additive effect on the risk of AD (aOR, 3.13). Among boys exposed to higher maternal anxiety during pregnancy, gestational weeks 5-8 were the critical period of PM2.5 exposure for the development of AD.
Racial Differences & Endotypes Among Children With AD
Black and White children with AD have distinct allergic trajectories defined by different longitudinal endotypes, according to a study published in the Journal of Allergy and Clinical Immunology. Investigators sought to define the atopic march in Black and White children and explore mechanisms for racial differences. Utilizing the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohort (n = 601), they assessed longitudinal sensitization, food allergy (FA), allergic rhinitis (AR), risk of asthma development, transepidermal water loss (TEWL), skin filaggrin (FLG) expression, exposures, and genetic heritability to define AD progression endotypes in Black and White children. They found that White MPAACH children were more likely to be sensitized to aero and food allergens and were more than three times likely to develop FA and/ or AR without asthma risk. In contrast, Black children were more than six times as likely to proceed to high asthma risk without FA, sensitization, or AR. White children had higher lesional and non-lesional TEWL and decreased non-lesional keratinocyte FLG expression. Black children had increased genetic heritability for asthma risk and higher rates of exposure to secondhand smoke and traffic-related air pollution.
