As air infiltrates through unintentional openings in building envelopes, pollutants may interact with adjacent surfaces. Such interactions can alter human exposure to air pollutants of outdoor origin. We present modeling explorations of the proportion of particles and reactive gases (e.g., ozone) that penetrate building envelopes as air enters through cracks and wall cavities. Calculations were performed for idealized rectangular cracks, assuming regular geometry, smooth inner crack surface and steady airflow. Particles of 0.1-1.0 [im diameter are predicted to have the highest penetration efficiency, nearly unity for crack heights of 0.25 mm or larger, assuming a pressure difference of 4 Pa or greater and a flow path length of 3 cm or less. Supermicron and ultrafine particles are significantly removed by means of gravitational settling and Brownian diffusion, respectively. In addition to crack geometry, ozone penetration depends on its reactivity with crack surfaces, as parameterized by the reaction probability. For reaction probabilities less than ~ 10" 5

Particle penetration into buildings influences human exposure to particles of ambient origin. In this study, we present the results of laboratory experiments measuring particle penetration through surrogates of cracks in building envelopes. Rectangular slots were prepared, with crack heights of 0.25 and 1 mm and flow-path lengths of 4-10 cm, using common building materials: aluminum, brick, concrete, plywood, redwood lumber, pine lumber, and strand board. Air was drawn through a slot from a well-mixed chamber by applying a pressure difference (∆P) of 4 or 10 Pa. Nonvolatile, electrically neutralized particles were generated and introduced into the chamber. The particle penetration factor was determined, for particle sizes 0.02-7 µm, as the ratio of the particle concentration downstream of the slot to that in the chamber. Particle size and crack height were the two main factors that governed fractional particle penetration. Consistent with prior modeling results, the penetration factor was nearly unity for particles of diameter 0.1-1.0 µm at ≥0.25 mm crack height and ∆P of ≥4 Pa. Particle penetration diminished for larger and smaller particles and for cracks with significant surface roughness and irregular geometry.

Photolysis of heptanal is investigated from an experimental and theoretical point of view. Photoexcited heptanal is believed to undergo rapid intersystem crossing to the triplet manifold and from there undergoes internal H-abstraction to form biradical intermediates. The favored gamma-H abstraction pathway can cyclize or cleave to 1-pentene and hydroxyethene, which tautomerizes to acetaldehyde. Yields of 1-pentene and acetaldehyde were measured at 62 +/- 7% and 63 +/- 7%, respectively, relative to photolyzed heptanal. Additionally, small quantities of hexanal and hexanol were observed. On the basis of combined experimental and theoretical evidence, the remaining heptanal photolysis proceeds to form an estimated 10% HCO + hexyl radical and 30% cyclic alcohols, particularly 2-propyl cyclobutanol and 2-ethyl cyclopentanol.

Astragaloside IV, the active component of Astragalus membranaceus, exhibits diverse biological roles including the antitumor activity. In this study, we evaluated the chemosensitive role of astragaloside IV in non-small cell lung cancer cells. Cell Counting Kit-8 analysis was performed to determine cell viability. Real-time polymerase chain reaction and western blot were used to measure the messenger RNA and protein expression. Results showed that astragaloside IV treatment could suppress the proliferation of non-small cell lung cancer cells. In addition, combined treatment with astragaloside IV remarkably enhanced the chemosensitivity to gefitinib in three non-small cell lung cancer cell lines including NCI-H1299, HCC827, and A549. Furthermore, compared with gefitinib-treated cells, the messenger RNA expression of SIRT6 was obviously increased in non-small cell lung cancer cells treated with gefitinib combined with astragaloside IV. In addition, downregulation of SIRT6 was accomplished using small interference RNA technology. As a result, SIRT6 inhibition abolished the sensitization role of astragaloside IV in non-small cell lung cancer cells. Taken together, these data demonstrated that astragaloside IV sensitized tumor cells to gefitinib via regulation of SIRT6, suggesting that astragaloside IV may serve as potential therapeutic approach for lung cancer.

No abstract