to viral and/or bacterial infection, or cause an immunological toxicity in the airways (Krishna et al 1995). Pollutants may also play a direct or indirect role in the pathophysiology and the development of allergic diseases (Cookson et al 1989; von Mutius et al 1994a; Hershey et al 1997; Matricardi et al 1997; Jarvis et al 1997; Bodner et al 1998; Krämer et al 1998; Shek et al 2001; Riedl and Diaz-Sanchez 2005) (Figure 2). More work is needed to identify which pollutants have an impact on human health and in which subgroups, and the mechanism for disease development. This will need to include the pathways of chemical, molecular, and cellular interactions. A more powerful epidemiological study must be performed on the basis of prospective settings in several regions, and with unique investigational criteria to assess the prevalence and severity of allergic disease. Control measures for indoor allergens Exposure of indoor allergens in our house environment is a common cause of perennial allergic rhinitis. Young children especially, spend most of their time inside the house. It is true that when a high concentration of one or more allergens is present in the house, the risk of allergenic sensitization in the early stages of life will increase consequently. In high- risk newborns, prenatal exposure to mite allergens from dust of the living room and the maternal mattress was found to be associated with total serum IgE at birth (Schonberger et al 2005). Allergic rhinitis House dust House dust is a heterogenous mixture, which varies according to region and household. It consists of various allergenic substances, consisting primarily of somatic and metabolic allergens of mites and secondarily of allergens derived from domestic animals, human skin scales, domestic insects such as cockroaches, and endotoxin of gram-negative bacteria. In addition, fungal spores or mycelia and other products of animal or vegetable origin such as feathers, wool, and natural fibers may be sources of dust allergens. Endotoxin, a component of the cell wall of gram-negative bacteria, is a potent proinflammatory agent commonly found in house dust. Exposure to endotoxin will induce an inflammation of the airways, characterized by a neutrophil invasion, irritation on the mucus membranes, and restricted airway diameter (Michel et al 1991, 2001). These effects are undoubtedly an enhancing factor for the severity of established allergic inflammation in rhinitis and asthma. It has been postulated that exposure to endotoxin at a critical time might shift the developing immune system to a predominantly Th1-type (increasing IFN-γ and IL-12 productions) responsiveness, thus protecting against asthma and allergies (Martinez and Holt 1999). Further studies are still needed to determine the duration and dose-related effectiveness of endotoxin on Th1 cell polarization in terms of allergen sensitization and the existence of allergic inflammation in allergic rhinitis or asthma patients. IgE production IL-4 production Production of mediators ie, histamine, LTC4, PGs Induce symptoms and hyperresponsiveness Figure 2 Possible effects of air pollution in allergic diseases. Therapeutics and Clinical Risk Management 2005:1(2) Enhance allergic sensitization organic compounds/substances Pollutants Decrease allergen clearance Reduce ciliary beat Production of cytokines and chemokines Proliferation and activation of inflammatory cells 119