Proteins (CMP) involved in milk allergy are numerous and heterogeneous, with very few structural or functional common features. This heterogeneity is complicated by their genetic polymorphism, resulting in several variants for each protein. These variants are characterized by point substitutions of amino acids or by deletions of peptide fragments of varying size or by post-translational modifications such as phosphorylation or glycosylation. All of these modifications may affect allergenicity. No common molecular structure can be associated with allergenicity, although some homologous regions such as casein phospho-peptides can explain an IgE cross-reactivity. Three-dimensional structure is an important feature in CMP allergenicity but denatured and linear epitopes are also involved. Epitopes are numerous and widely spread along the CMP molecule. They may be located in hydrophobic parts of the molecule where they are inaccessible for IgE antibodies in the native conformation of the protein but become bioavailable after digestive processes. Peptides as short as ca. 12-14 amino acid residues may account for a significant part of the allergenicity of the whole molecule, which justifies the need to be careful before proposing any CMP hydrolysate for highly allergenic children.

This paper describes the medical examination of 26 residents living in Finnish houses with indoor air problems and Stachybotrys contamination. Environmental samples were obtained from patients at the Clinic for Indoor Air Health Problems where special attention was paid to the presence of possible health effects caused by moulds, especially by Stachybotrys chartarum. S. chartarum was isolated and identified in samples collected from the homes or work places of 26 patients admitted for respiratory illness. Most of the isolated S. chartarum strains showed slight toxicity when tested in a cell culture but only two were found to produce satratoxins G and H. Diverse spectra of non-specific symptoms were reported by the 26 patients and irritation of the upper airways and eyes were the most common. Lymphocytosis was found in the bronchoalveolar lavage fluid in 6 of the 10 patients who underwent bronchofibreoscopy. IgG antibodies against S. chartarum were determined in the serum of 20 patients and increased levels were found in 10 of them. The symptoms or the severity of the illnesses were not associated with the IgG level. Patients were followed-up for 1—5 years, with a few patients experiencing persistent health effects such as severe eye irritation. We conclude that some of the symptoms may be caused by Stachybotrys exposure but a causal relationship could not be shown. Lymphocytosis was found in bronchial lavage in half of the patients examined by bronchoscopy suggesting that immunoactivation in lungs may quite often occur from exposure to water-damaged microbes.