The hygiene hypothesis suggests that early life exposure to a non-hygienic environment that contains endotoxin reduces the risk of developing allergic diseases. The mechanisms underlying the hygiene hypothesis are unclear and may involve subtle immune system interactions that occur during maturation. Experimental objectives of this study were to use a novel animal model to test the hygiene hypothesis and to characterize early life immune system responses to a non-hygienic environment. Mice were reared in corn dust, a grain processing byproduct with a high endotoxin content and microbial products or in a low endotoxin environment. The influence of early or later life exposure to corn dust on a subsequent allergen stimulus (ovalbumin) was assessed by bronchoalveolar lavage (BAL) cell analysis, lung histology, and serum IgE measurements. The influence of the corn dust environment on the developing pulmonary immune system was assessed by BAL cell and cytokine analysis, and immunostaining of lung tissue. The corn dust environment contained significantly more endotoxin (p <0.001) and the dust exposures attenuated the cellular inflammatory response to ovalbumin in the adult mouse (p <0.01) but did not reduce serum IgE levels or alter baseline BAL fluid pro-inflammatory cytokine levels. The corn dust environment did not induce significant neutrophilia in lavage fluid but significantly increased the number of antigen presenting cells in alveolar walls early in life by~37%. In conclusion, exposure to a non-hygienic environment did not induce significant airway neutrophilia, yet altered the population of immunologically active cells in the lung and reduced subsequent allergic inflammation.