Airborne Indoor Particles from Schools Are More Toxic than Outdoor Particles

High concentrations of particulate matter (PM10) were measured in classrooms. This study addresses the hazard of indoor particles in comparison to the better-studied outdoor particles. Samples were taken from six schools during teaching hours. Genome-wide gene expression in human BEAS-2B lung epithelial cells was analyzed and verified by quantitative PCR. Polycyclic aromatic hydrocarbons, endotoxin, and cat allergen (Fel d 1) were analyzed by standard methods. Enhancement of allergic reactivity by PM10 was confirmed in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM10-exposed human peripheral blood monocytes. Indoor PM10 induced serine protease inhibitor B2 (involved in blood coagulation) and inflammatory genes (such as CXCL6, CXCL1, IL6, IL8; all P < 0.001). Outdoor PM10 induced xenobiotic metabolizing enzymes (cytochrome P450 [CYP] 1A1, CYP1B1, TIPARP; all P < 0.001). The induction of inflammatory genes by indoor PM10 was explained by endotoxin (indoor 128.5 +/- 42.2 EU/mg versus outdoor 13.4 +/- 21.5 EU/mg; P < 0.001), the induction of CYP by outdoor polycyclic aromatic hydrocarbons (indoor 8.3 +/- 4.9 ng/mg versus outdoor 16.7 +/- 15.2 ng/mg; P < 0.01). The induction of serine protease inhibitor B2 was confirmed by a more rapid human blood coagulation (P < 0.05). Indoor PM10 only affected allergic reactivity from human primary basophils from cat-allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM10 (P < 0.001). Indoor PM10, compared with outdoor PM10, was six times higher and, on an equal weight basis, induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM10 had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM10 seem reasonable, perhaps through intensified ventilation.