Environmental pollutants as co-factors in IgE production.
While there is a general perception that 'pollutants' present in the natural environment may act in concert with genetic factors in the host to precipitate primary allergic sensitization, there is a clear need for more hard data to establish the degree to which this actually occurs in different environmental settings, and to elucidate the underlying mechanism. It is evident that animal model systems provide viable avenues for studies on mechanisms, and several laboratories are actively engaged in this work. However, questions relating to the magnitude of these environmental effects on human allergic disease present more substantial problems, which can only be addressed by large-scale epidemiological studies on well-defined populations, backed up by comprehensive environmental monitorings. At present, the best defined area of the human literature is clearly the early postnatal data, which establishes that the first 1-2 months of life are a major risk period for life-long allergic sensitization to seasonal antigens. Broadening of these studies to encompass environmental monitoring, aimed at the identification of environmental cofactors which may synergize with early allergen exposure, is therefore a logical step for the future research.
Holt
P G
PG
Clinical Immunology Unit, Princess Margaret Hospital, Perth, Western Australia.
D000485:Allergens / Q000008:administration & dosage; D000818:Animals; D015536:Down-Regulation; D004785:Environmental Pollutants / Q000009:adverse effects*; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology / Q000276:immunology; D007073:Immunoglobulin E / Q000096:biosynthesis*
D000485:Allergens; D004785:Environmental Pollutants; D007073:Immunoglobulin E