Study of the relation between the modulations of allergic response and the sick house syndrome caused by indoor air pollutants

2003 Fiscal Year Final Research Report Summary

• Project/Area Number: 13470078
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Hygiene
• Research Institution: Asahikawa Medical College
• Principal Investigator: YOSHIDA Takahiko Asahikawa Medical College, Professor, 医学部, 教授 (90200998)
• Co-Investigator(Kenkyū-buntansha): NAKAGI Yoshihiko Asahikawa Medical College, Assistant, 医学部, 助手 (90322908) ; ITOH Toshihiro Asahikawa Medical College, Assistant Professor, 医学部, 講師 (20271760)
• Project Period (FY): 2001 – 2003
• Keywords: Sick house syndrome / sick building syndrome / formaldehyde / humoral immune response / immediate type allergy / enterobacteria / cytokine response in liver

Research Abstract

It is well known that the immunological mechanism concerns in developing the sick building (house) syndrome (SBS,SHS), since allergy relating symptoms are frequently observed in the SBS patients. At the standing point of those findings, we exposed gaseous formaldehyde (HCHO) which is the major indoor air pollutant to cause SBS to mice (B6C3F1,female) and evaluated the health effects of HCHO by observing the modulations of the immune response and the experimentally induced allergic reactions. And we also surveyed the health effects which are reported in the SBS patients in the experimentally gaseous HCHO exposed mice without any immunological treatment. Furthermore we investigated the health effects of HCHO exposure via alimentary tract. Mice were exposed to HCHO by giving of HCHO treated animal diet pellets or HCHO added drinking water. For control group, intact diet and pure drinking water were given. Exposure of 500ppb gaseous HCHO enhanced the antibody forming response against sheep red blood cells and the lymphocyte proliferating response by mitogen stimuli. Enhancive modulations of immediate type allergic reaction were observed in both phases of sensitization and induction of symptoms. Aneuploid DNA in peripheral lymphocyte which is one of characteristic sign observed in some case of SBS patients was detected in gaseous HCHO exposed mice. Induction of prolactin mRNA in hippocampus and olfactory bulb was obvious in HCHO exposed mice. Ingestion of HCHO treated diet dramatically reduced the number of bacteria in alimentary tract dose dependency, whereas same quantity of HCHO via drinking water did weakly. Suppression of cytokine response in liver induced by i.p.of lipopolysaccharide, that phenomenon is observed in the mice with reduced number of alimentary tract bacteria, also observed in HCHO treated diet fed mice. The results indicate that both routes of HCHO exposure, inhalation or per oral, induce the modulation of immune response and allergic reactions as well as characteristic phenomena to SBS cases. It may suggest that immune function play some significant role in the development of SBS.