The association of residential mold exposure and adenotonsillar hypertrophy in children living in damp environments.

BACKGROUND: There are many consequences of mold exposure related to respiratory system health of children This retrospective cohort study aims to find the association between adenoid hypertrophy and mold exposure in children living in damp environments. METHODS: Children with history of recurrent respiratory tract infections were enrolled in the study between June 2012 and June 2013 and were followed up for adenoid hypertrophy from June 2013 to June 2016. One hundred and forty two children were residents of moldy houses and 242 were living in normal houses. Skin prick test results for 60 common allergens, vitamin D levels, IgE levels, age, presence of comorbidities such as urticaria, atopic dermatitis, allergic conjunctivitis, allergic rhinitis, asthma, frequency of upper respiratory tract infections and lower respiratory tract infections, were evaluated in both groups. RESULTS: A total of 384 children (mean age ± standard deviation = 53.37 ± 36 months; 198 males and 186 females) were included. The children were classified into 2 groups (1)Children living normal houses (n = 242) (2); Children living in damp houses (n = 142) according to mold exposure. Children with adenoid hypertrophy (p < 0,001) and higher IgE levels (p < 0,001) were more common in mold exposed group. Lower respiratory tract infections were more common in children with mold exposure (p < 0,05). Bivariate correlation analysis showed no significant association between IgE levels and adenoid hypertrophy. Multiple linear regression analysis was performed to evaluate IgE levels, vitamin D levels, and presence of adenoid as independent variables; age as dependent variable among two groups and was found statistically significant (p < 0,001). Dermatophagoid sensitive group living in damp houses had a significant increase in adenoid hypertrophy (p = 0,01). Housedustmite sensitive children with recurrent lower respiratory tract infection and upper respiratory tract infection were mainly residents of damp houses (p < 0,001). Allergic comorbidities were significantly more in damp environment group (p < 0,001), but there was no significant increase in any of the subgroups. CONCLUSIONS: Children with mold exposure had significantly increased adenoid hypertrophy regardless of their atopic nature, however, they may have become more sensitized due to other environmental triggers and genetic factors. In damp environments, sensitization to dermatophagoids, was significantly increased in children with adenoid hypertrophy. During the period of infancy, when children were mostly vitamin D supplemented, they were not sensitized and had normal adenoids. As children with recurrent respiratory tract infections grow, they tend to have lower vitamin D levels, become more atopic and tend to have adenoid hypertrophy.