The objective of the study was to evaluate the role of the mould cell wall agent beta-glucan in environmentally related pulmonary disease. All published articles where beta-glucan was administered by the airways, either as intratracheal injection or as inhalation were utilised as data sources. Data reporting consisted of analysis of data reports concerning the effects of beta-glucan on the immune system on the cellular level, particularly on the aggregation of inflammatory cells or production of inflammatory cytokines. High doses of soluble and particulate beta-glucan cause an inflammatory response characterized by cytokine activation and neutrophil invasion in the lung tissue. At lower doses, closer to environmental exposure levels, the predominant effect is an influence on the response to antigens, the reactivity of eosinophils and other Th2 driven immune responses. It is concluded that, beta-glucan can induce Th1 as well asTh2 driven immune responses. The pathology of atopy/allergy, hypersensitivity pneumonitis, and toxic penumonitis might be induced by exposure to beta-glucan. Measurements of beta-glucan in different environments are useful for risk control and prevention.