Introduction.– Impact of exposure to environmental allergens during early life on allergic sensitization and disease development is controversial. Here, we investigated whether airborne allergen from Dermatophagoides pteronyssinus (Der p) house dust mite (HDM), a major cause of allergic asthma, is found in human colostrum and milk samples and set up a mouse model to assess its impact on allergic outcome in offspring. Methods.– Der p 1was quantified in human milk (1 and 6 months postpartum samples from Australia, n = 71 and n = 161, respectively) and colostrum from Brasil (n = 76), France (n = 97) and Australia (n = 34) by ELISA. A basophil degranulation assay was used to confirm immunogenicity of ELISA-detected Der p. Balb/c mice were fostered by mothers exposed intra-nasally to Der p extract before pregnancy and during lactation. Progeny response to Der p was measured at 6 weeks and included assessment of allergic sensitization, airway inflammation and lungs function. Results.– Der p 1 was present in 58% Brazilian, 70% French, and 78% Australian colostrum. Median [Der p 1] was similar between countries (96 pg/mL; IQR 50.2–201.6 pg/mL). In mature milk, Der p1 was found in 52% of 1-month and 6-month samples. Median [Der p 1] in milk was 65.9 pg/mL; IQR 41.5–172 pg/mL) and was significantly lower than in colostrum (P = 0.0001). Der p 1-containing milks were able to induce degranulation of human anti-Der p IgE coated basophils. Mice breastfed by Der p-exposed mothers had 5-fold increased levels of Der p specific IgE and IgG1 compared to mice breastfed by naïve mothers and their allergic airway inflammation and lung function was not affected. Conclusion.– This study demonstrates that early life exposure to ubiquitous respiratory allergens can take place through breastfeeding. An animal model mimicking the human situation shows early life exposure to Der p through milk primes the immune system rather than protect it as we reported with OVA. These data highlight that antigen administration to the neonate through the oral route may contribute to child allergic sensitization and have important implications for the design of studies assessing early oral antigen exposure for allergic disease prevention.