Also, women are alleged by some to be more exposed to indoor environmental factors because they have a greater tendency to have clerical jobs, wherein they are exposed to unique office equipment and materials (example: blueprint machines, toner-based printers), whereas men often have jobs based outside of offices. History
In the late 1970s, it was noted that nonspecific symptoms were reported by tenants in newly constructed homes, offices, and nurseries. In media it was called "office illness". The term "sick building syndrome" was coined by the WHO in 1986, when they also estimated that 10–30% of newly built office buildings in the West had indoor air problems. Early Danish and British studies reported symptoms. Poor indoor environments attracted attention. The Swedish allergy study (SOU 1989:76) designated "sick building" as a cause of the allergy epidemic as was feared. In the 1990s, therefore, extensive research into "sick building" was carried out. Various physical and chemical factors in the buildings were examined on a broad front. The problem was highlighted increasingly in media and was described as a "ticking time bomb". Many studies were performed in individual buildings. In the 1990s "sick buildings" were contrasted against "healthy buildings". The chemical contents of building materials were highlighted. Many building material manufacturers were actively working to gain control of the chemical content and to replace criticized additives. The ventilation industry advocated above all more well-functioning ventilation. Others perceived ecological construction, natural materials, and simple techniques as a solution.
These studies suggest that the dis-regulated overproduction of interleukin 5 by blood mononuclear cells is an underlying cause of the eosinophilia found in at least some families with this disorder. Diagnosis
The diagnosis of familial eosinophilia rest upon a) familial clustering of the disorder; b) exclusion of "family acquired eosinophilia" (i.e. eosinophilia due to chronic parasite or other infestations that afflict multiple members of a family); c) lack of eosinophil-induced tissue destruction such as that which occurs in the hypereosinophilic syndrome; d) absence of signs or symptoms of other hereditary eosinophilias (e.g. hyperimmunoglobulin E syndrome, Omenn syndrome), Wiskott–Aldrich syndrome, and numerous other primary immunodeficiency syndromes); and d) lack of evidence for reactive eosinophilias (e.g. allergy-related), neoplastic eosinophilias (e.g. eosinophilic leukemia, clonal eosinophilia), or eosinophila associated with various hematological and non-hematological malignancies as outlined in causes of eosinophilia. Treatment
Since longitudinal data, including eosinophil counts obtained over a 20- to 30-year periods in some family members, show remarkable stability in the absolute eosinophil count with no evidence of disease   attributable to eosinophil-related tissue injury, therapy to lower eosinophil counts such as corticosteroids, tyrosine kinase inhibitors, and antibodies directed against interleukin 5 have in general not been used to treat familial eosinophilia. One patient with severe heart damage was treated with a corticosteroid but soon thereafter died. Familial eosinophilia unassociated with possible eosinophil-related tissue injuries may not require drug treatment, those cases with such tissue injuries, it is suggested, should be considered for such interventions. In all cases, however, regular follow-up of the disorder is strongly recommended.