The insurers needed a defense based upon Standards of Professional Practice to meet a court decision that declared that in a modern, essentially sealed building, the HVAC systems must produce breathing air for suitable human consumption. ASHRAE (American Society of Heating, Refrigeration and Air Conditioning Engineers, currently with over 50,000 international members) undertook the task of codifying its indoor air quality (IAQ) standard. ASHRAE empirical research determined that "acceptability" was a function of outdoor (fresh air) ventilation rate and used carbon dioxide as an accurate measurement of occupant presence and activity. Building odors and contaminants would be suitably controlled by this dilution methodology. ASHRAE codified a level of 1,000 ppm of carbon dioxide and specified the use of widely available sense-and-control equipment to assure compliance. The 1989 issue of ASHRAE 62.1-1989 published the whys and wherefores and overrode the 1981 requirements that were aimed at a ventilation level of 5,000 ppm of carbon dioxide, (the OAHA workplace limit), federally set to minimize HVAC system energy consumption. This apparently ended the SBS epidemic. Over time, building materials changed with respect to emissions potential. Smoking vanished and dramatic improvements in ambient air quality, coupled with code compliant ventilation and maintenance, per ASHRAE standards have all contributed to the acceptability of the indoor air environment. See also
Aerotoxic syndrome
Havana syndrome
Healthy building
Multiple chemical sensitivity
NASA Clean Air Study
Nosocomial infection
Somatization disorder
Fan death

References
Further reading
Martín-Gil J., Yanguas M. C., San José J. F., Rey-Martínez and Martín-Gil F. J. "Outcomes of research into a sick hospital". Hospital Management International, 1997, pp. 80–82. Sterling Publications Limited.
In such conditions, heme along with globin chains can be released from further oxidization of met-hemoglobin (ferric Hb). In which, the free heme can then accelerate tissue damage by promoting peroxidative reactions and activation of inflammatory cascades. At this time, hemopexin, another plasma glycoprotein come to bind with heme with its privilege of high heme affinity, forming a complex of heme-hemopexin, which is non-toxic, and travel together to a receptor on hepatocytes and macrophages within the spleen, liver and bone marrow. (Note that the "free hemoglobin-haptoglobin" complex is taken up by hepatocytes and, to the lesser extent, macrophages.) Thereafter, these complexes will undergo the metabolic mechanisms like extravascular hemolysis.Nevertheless, if the binding capacities of haptoglobin and hemopexin are saturated, the remaining "free hemoglobin" in the plasma will be oxidized to met-hemoglobin eventually, and then further disassociates into free heme and others. At this stage, the "free heme" will bind to albumin, forming met-hemalbumin. As to the remaining unbound (met)hemoglobin is filtered into the primary urine and re-absorbed via proximal tubules of the kidney. In proximal tubules, the iron is extracted and stored as hemosiderin. (Long-term hemoglobinuria is associated with substantial deposition of hemosiderin in proximal tubule (excessive accumulation of hemosiderin in proximal tubule), Fanconi syndrome (damaged renal re-absorption capability of small molecules which give rises to hyper-aminoaciduria, glycosuria, hyperphosphaturia, and bicarbonate and dehydration), and chronic kidney failure.)