Antibody response to long-term and high-dose mould-exposed sawmill workers.

Exposure to moulds is thought to cause adverse health effects ranging from vague subjective symptoms to allergy and respiratory diseases. Until now, most studies have been emphasizing low levels of exposure. In Norwegian sawmills during the 1980s, extensively high spore counts up to 10(7) spores/m3 air were reported. By using serum samples obtained from sawmill workers during that period, in addition to control sera, we studied the antibody response of all classes and IgG subclasses to Rhizopus microsporus at different levels of exposure. Antigen specificity was further studied by Western blotting. Exposure to R. microsporus was accompanied by R. microsporus-specific antibody production against a wide range of antigenic components most likely of both protein and carbohydrate nature. Increasing levels of mould-specific IgG1, IgG2, IgG4 and IgA antibodies were associated with increased exposure, while the highest levels of exposure were associated with a somewhat reduced level of mould-specific IgE antibodies. In conclusion, the present study strongly suggests that high mould exposure can induce a strong IgG and IgA response in a dose-dependent manner.

The adjuvant effect of particles-importance of genetic background and pre-sensitisation.

BACKGROUND: We have previously reported that simple and well-characterised particles, such as polystyrene particles (PSP), have an IgE adjuvant effect in mice. The purpose of this study was to explore the importance of genetic background concerning the adjuvant effect of PSP in different strains of mice. METHODS: Inbred NIH/Ola, BALB/c and C3H/HeJ mice were given two intraperitoneal injections with either PSP plus OVA or OVA alone, and then an intraperitoneal challenge with OVA alone. NIH/Ola mice were also pre-sensitised to develop a weak or strong IgE response to OVA, and then given an intraperitoneal challenge with PSP plus OVA or OVA alone. Serum levels of total and allergen-specific IgE and IgG2a were measured. RESULTS: PSP had a specific IgE and IgG2a adjuvant effect in NIH/Ola mice but not in C3H/HeJ and BALB/c mice. Weakly pre-sensitised NIH/Ola mice showed the same response pattern as the naive NIH/Ola mice. In contrast, strongly pre-sensitised mice showed an antibody response pattern similar to that of high-responder BALB/c mice. CONCLUSIONS: Our results indicate that the allergen responder status, either genetic or induced, is of importance for the adjuvant effect from particles. The IgE and IgG2a adjuvant effect may depend on the genetically determined susceptibility of an individual to be influenced by exposure to the adjuvant. Therefore, the allergy-enhancing effect from particle pollution may differ between individuals.