Inhalation Exposure Core
The mission of the Inhalation Exposure Core is to provide a specialized platform for the investigation of health impacts resulting from the inhalable environment and evaluation of therapeutics for the mitigation of respiratory disease, while serving as a valuable educational resource on the science and technology comprising this platform. The Inhalation Exposure Core provides short- and long-term generation, delivery, and analysis of precisely controlled atmospheres to investigate human health effects of environmental challenges using both in vitro and in vivo laboratory animal models. In coordination with Primate Medicine Services, the Inhalation Exposure Core also provides pulmonary function testing and bronchoscopy as outcome measures for health effects as a result of exposures in nonhuman primates. Minimally invasive methods, including pulmonary transfer impedance, are used for measuring pulmonary responses to disease processes, potential therapeutics, and changes across the lifespan. With an emphasis on inhalation toxicology and animal models of chronic respiratory disease, Inhalation Exposure Core faculty and staff provide critical intellectual expertise and technical support for investigators to conduct research projects that require evaluation of biological responses to atmospheric exposures.
- Inhalation Toxicology Expertise
- Large In Vivo and In Vitro Exposure Capacity
- Aerosol Generation and Characterization
- Major Gaseous Pollutant Generation and Monitoring
- Pulmonary Function Testing and Bronchoscopy Suite
- GLP Study Capabilities
- Project, Data, and Sample Management
- Inhaled Therapeutic Trials
- Adult Allergic Asthma
- Adult Non-Allergic (Intrinsic) Asthma
- Pediatric Allergic Asthma
- Air Pollution (Ozone, PM, Wood Smoke) Inhalation
- Tobacco Smoke and E-Cigarette Vaping
- Endotoxin Inhalation
- Adult and Pediatric Influenza
Beginning in 2000, under the leadership of Dr. Charles G. Plopper (UC Davis School of Veterinary Medicine, Emeritus), an important and major effort was initiated to study the development and exacerbation of asthma by oxidant air pollutants in nonhuman primates. The asthma studies necessitated the establishment of a pulmonary function laboratory with extensive capabilities for testing nonhuman primates under the direction of a pulmonary physiologist to assess function in animals undergoing exposure. Under the leadership of Dr. Dallas Hyde (UC Davis School of Veterinary Medicine, Emeritus), funding was obtained in 2010 from the US government – American Recovery and Regeneration Act – to build a Respiratory Disease Centerincluding a new inhalation exposure facility. It was recognized that the CNPRC is the only primate center with an inhalation exposure facility and respiratory diseases unit, enhancing research with nonhuman primate models of respiratory diseases.
Herring MJ, Putney LF, St George JA, Avdalovic MV, Schelegle ES, Miller LA, Hyde DM. Early life exposure to allergen and ozone results in altered development in adolescent rhesus macaque lungs. Toxicol Appl Pharmacol. 2015 Feb 15;283(1):35-41. doi: 10.1016/j.taap.2014.12.006. Epub 2014 Dec 27. PubMed PMID:25545987.
Davis BB, Zeki AA, Bratt JM, Wang L, Filosto S, Walby WF, Kenyon NJ, Goldkorn T, Schelegle ES, Pinkerton KE. Simvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy. European Respiratory Journal 43(4):350-361, 2014. PMC Journal-in-progress.
Chan JK, Charrier JG, Kodani SD, Vogel CF, Kado SY, Anderson DS, Anastasio C, Van Winkle LS. Combustion-derived flame generated ultrafine soot generates reactive oxygen species and activates Nrf2 antioxidants differently in neonatal and adult rat lungs. Particle and Fibre Toxicology 10:34, 2013. PMCID: PMC3735485
Chun K, Miller LA, Schelegle ES, Hyde DM, Capitanio JP. Behavioral inhibition in rhesus monkeys (Macaca mulatta) is related to the airways response, but not immune measures, commonly associated with asthma. PLoS One 8(8):71575, 2013. PMCID: PMC3739724
Murphy SR, Schelegle ES, Miller LA, Hyde DM, Van Winkle LS. Ozone exposure alters serotonin and serotonin receptor expression in the developing lung. Toxicological Sciences 34(1):168-179, 2013. PMCID: PMC3693130
Chan JK, Vogel CF, Baek J, Kodani SD, Uppal RS, Bein KJ, Anderson DS, Van Winkle LS. Combustion derived ultrafine particles induce cytochrome P-450 expression in specific lung compartments in the developing neonatal and adult rat. American Journal of Physiology – Lung Cellular and Molecular Physiology 304(10):665-677, 2013. PMCID: PMC3652057
Chan JK, Kodani SD, Charrier JG, Morin D, Edwards PC, Anderson DS, Anastasio C, Van Winkle LS. Age-specific effects on rat lung glutathione and antioxidant enzymes after inhaling ultrafine soot. American Journal of Respiratory Cell and Molecular Biology 48(1):114-124, 2013. PMCID: PMC3547088
Murphy SR, Schelegle ES, Edwards PC, Miller LA, Hyde DM, Van Winkle LS. Postnatal exposure history and airways: oxidant stress responses in airway explants. American Journal of Respiratory Cell and Molecular Biology 47(6):815-823, 2012. PMCID: PMC3547096
Asgharian B, Price O, McClellan G, Corley R, Einstein DR, Jacob RE, Harkema J, Carey SA, Schelegle ES, Hyde D, Kimbell JS, Miller FJ. Development of a rhesus monkey lung geometry model and application to particle deposition in comparison to humans. Inhalation Toxicology 24(13):869-899, 2012. PMC Journal-in-progress.
Avdalovic MV, Tyler NK, Putney L, Nishio SJ, Quesenberry S, Singh PJ, Miller LA, Schelegle ES, Plopper CG, Vu T, Hyde DM. Ozone exposure during the early postnatal period alters the timing and pattern of alveolar growth and development in nonhuman primates. Anatomical Record 295(10):1707-1716, 2012. PMC Journal-in-progress.
Mitchell VL, Van Winkle LS, Gershwin LJ. Environmental tobacco smoke and progesterone alter lung inflammation and mucous metaplasia in a mouse model of allergic airway disease. Clinical Reviews in Allergy & Immunology 43(1-2):57-68, 2012. PMC Journal-in-progress.
McDonnell WF, Stewart PW, Smith MV, Kim CS, Schelegle ES. Prediction of lung function response for populations exposed to a wide range of ozone conditions. Inhalation Toxicology 24(10):619-633, 2012. PMC Journal-in-progress.
Plopper CG, Joad JP, Miller LA, Schelegle ES, Fanucchi MV, Van Winkle LS, Tyler NK, Avdalovic MV, Evans MJ, Lasley WL, Buckpitt AR, Pinkerton KE, Tarkington BK, Davis S, Nishio SJ, Gershwin LJ, Wu R, Hyde DM. Lung effects of inhaled corticosteroids in a rhesus monkey model of childhood asthma. Clinical & Experimental Allergy 42(7):1104-1118, 2012. PMCID: PMC3913647
Schelegle ES, Adams WC, Walby WF, Marion MS. Modelling of individual subject ozone exposure response kinetics. Inhalation Toxicology 24(7):401-415, 2012. PMC Journal-in-progress.
Schelegle ES, Walby WF. Vagal afferents contribute to exacerbated airway responses following ozone and allergen challenge. Respiratory Physiology & Neurobiology 181(3):277-285, 2012. PMCID: PMC3366056
Moore BD, Hyde D, Miller L, Wong E, Frelinger J, Schelegle ES. Allergen and ozone exacerbate serotonin-induced increases in airway smooth muscle contraction in a model of childhood asthma. Respiration 83(6):529-542, 2012. PMC Journal-in-progress.
Chou DL, Gerriets JE, Schelegle ES, Hyde DM, Miller LA. Increased CCL24/eotaxin-2 with postnatal ozone exposure in allergen-sensitized infant monkeys is not associated with recruitment of eosinophils to airway mucosa. Toxicology and Applied Pharmacology 257(3):309-318, 2011. PMCID: PMC3226879
Chan JK, Fanucchi MV, Anderson DS, Abid AD, Wallis DA, Kumfer BM, Kennedy IM, Van Winkle LS. Susceptibility to inhaled flame-generated ultrafine soot in neonatal and adult rat lungs. Toxicological Sciences 124(2):472-486, 2011. PMCID: PMC3216412
Abbas AR, Jackman JK, Bullens SL, Davis SM, Choy DF, Fedorowicz G, Tan M, Truong BT, Meng Gloria Y, Diehl L, Miller LA, Schelegle ES, Hyde DM, Clark HF, Modrusan Z, Arron JR, Wu LC. Lung gene expression in a rhesus allergic asthma model correlates with physiologic parameters of disease and exhibits common and distinct pathways with human asthma and a mouse asthma model. American Journal of Pathology 179(4):1667-1680, 2011. PMCID: PMC3181391
Lee D, Wallis C, Van Winkle LS, Wexler AS. Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles. Inhalation Toxicology 23(9):520-531, 2011. PMC Journal-in-progress.
Bremer AA, Stanhope KL, Graham JL, Cummings BP, Wang W, Saville BR, Havel PJ. Fructose-fed rhesus monkeys: a nonhuman primate model of insulin resistance, metabolic syndrome, and type 2 diabetes. Clinical and Translational Science 4(4):243-252, 2011. PMCID: PMC3170136
Capitanio JP, Miller LA, Schelegle ES, Mendoza SP, Mason WA, Hyde DM. Behavioral inhibition is associated with airway hyperresponsiveness but not atopy in a monkey model of asthma. Psychosomatic Medicine 73(4):288-294, 2011. PMCID: PMC3090450
Maniar-Hew K, Postlethwait EM, Fanucchi MV, Ballinger CA, Evans MJ, Harkema JR, Carey SA, McDonald R J, Bartolucci AA, and Miller LA. Postnatal episodic ozone results in persistent attenuation of pulmonary and peripheral blood responses to LPS challenge. American Journal of Physiology – Lung Cellular and Molecular Physiology 300(3):462-471, 2011. PMCID: PMC3064293
Carey SA, Ballinger CA, Plopper CG, McDonald RJ, Bartolucci AA, Postlethwait EM, Harkema JR. Persistent rhinitis and epithelial remodeling induced by cyclic ozone exposure in the nasal airways of infant monkeys. American Journal of Physiology – Lung Cellular and Molecular Physiology 300(2):242-254, 2011. PMCID: PMC3043815
Van Winkle LS, Chan JK, Anderson DS, Kumfer BM, Kennedy IM, Wexler AS, Wallis C, Abid AD, Sutherland KM, and Fanucchi MV. Age specific responses to acute inhalation of diffusion flame soot particles: cellular injury and the airway antioxidant response. Inhalation Toxicology 22 Suppl 2:70-83, 2010. PMCID: PMC3110018
Lee DC, Wallis AS, Wexler ES, Schelegle LS, Van Winkle, Plopper CG, Fanucchi MV, Kumfer B, Kennedy IM, and Chan JK. Small particles disrupt postnatal airway development. Journal of Applied Physiology 109(4):1115-1124, 2010. PMC Journal-in-progress.
Sekizawa S, Bechtold AG, Tham RC, Kott KS, Hyde DM, Joad JP, Bonham AC. House-dust mite allergen and ozone exposure decreases histamine H3 receptors in the brainstem respiratory nuclei. Toxicology and Applied Pharmacology 247(3):204-210, 2010. PMC Journal-in-progress.
Van Winkle LS, Baker GL, Chan JK, Schelegle ES, Plopper CG. Airway mast cells in a rhesus model of childhood allergic airways disease. Toxicological Sciences 116(1):313-322, 2010. PMCID: PMC2886865
Evans MJ, Fanucchi MV, Plopper CG, Hyde DM. Postnatal development of the lamina reticularis in primate airways. Anatomical Record 293(6):947-954, 2010. PMC Journal-in-progress.
Evans MJ, Fanucchi MV, Miller, LA, Carlson MA, Nishio SJ, Hyde DM. Reduction of collagen VII anchoring fibrils in the airway basement membrane zone of infant rhesus monkeys exposed to house dust mite. American Journal of Physiology – Lung Cellular and Molecular Physiology 298(4):543-547, 2010. PMCID: PMC2853345
Sekizawa S, Joad JP, Pinkerton KE, Bonham AC. Secondhand tobacco smoke exposure differentially alters nucleus tractus solitarius neurons at two different ages in developing non-human primates. Toxicology and Applied Pharmacology 242(2):199-208, 2010. PMC Journal-in-progress.
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A: Yes! If you do not see your desired service, please contact the Inhalation Exposure Facility directly and inquire about custom fabrication of exposure apparatus/systems.