Air Pollutants & Irritants
Harmful particulates, biological materials, gaseous exhaust, as well as other environmental pollutants may enter the body via the lungs through inhalation exposure.
Artificially or naturally occurring environmental pollutants have been associated with increasing incidences of morbidity and mortality from cardiovascular and respiratory disorders. Pollutant deposition along the inhalation pathway may cause widespread effects of varying severity, including local airway inflammation to large scale structural damages. Further, introduction of the pollutants into the blood stream may result in multiple systemic effects, promoting cardiovascular or neurological diseases.
REPRODUCIBLE EXPOSURE, PRECISE DELIVERY
The inExpose has been specifically designed for consistent, precise delivery of a pollutant concentration by controlling air flow rates. This is done through automated exposure profiles, which also help to reduce user error and minimize outcome variability among subjects, study, and research groups. The inExpose operates under various configurations and protocols to ensure that the subjects receive repeatable yet consistent pollutant exposures throughout experimentation.
- Comparison of airway responses induced in a mouse model by the gas and particulate fractions of gasoline direct injection engine exhaust. Maikawa, C. L., et al. International Journal of Environmental Research and Public Health, 15(3). 2018.
- Development of a Novel Simulation Reactor for Chronic Exposure to Atmospheric Particulate Matter. Ye, J., et al. Scientific Reports, 7. 2017.
- Ferulic acid-loaded nanostructured lipid carriers: A promising nanoformulation against the ischemic neural injuries. Hassanzadeh, P., et al. Life Sciences, 193, 64–76. 2018.
DETAILED OUTCOMES TO ISOLATE POLLUTANT RESPONSE
The flexiVent captures crucial changes in mechanical properties of the conducting airways, terminal airways and parenchyma in response to environmental pollutants. The flexiVent is a comprehensive tool allowing an integrated assessment of various disease determinants (e.g. extent and pattern of induced damage) on lung function decline.
- Irritant-induced asthma to hypochlorite in mice due to impairment of the airway barrier – Van Den Broucke, S. et al. Archives of Toxicology. 92(4), pp. 1551–1561. 2018.
- Exposure to Silver Nanospheres Leads to Altered Respiratory Mechanics and Delayed Immune Response in an in Vivo Murine Model – Botelho, D. et al. Frontiers in Pharmacology. Frontiers, 9, p. 213. 2018.
- Pre- and postnatal exposure of mice to concentrated urban PM 2.5 decreases the number of alveoli and leads to altered lung function at an early stage of life – de Barros Mendes Lopes, T. et al. Environmental Pollution. 241, pp. 511–520. 2018.
- Vesicular acetylcholine transport deficiency potentiates some inflammatory responses induced by diesel exhaust particles – Santana, F. P. R. et al. Ecotoxicology and Environmental Safety. 167, pp. 494–504. 2019.
- Differential Activation of TRPA1 by Diesel Exhaust Particles: Relationships between Chemical Composition, Potency, and Lung Toxicity – Deering-Rice, C. E. et al. Chemical Research in Toxicology. 2019.
- Early life inhalation exposure to mine tailings dust affects lung development – Witten, M. L. et al. Toxicology and Applied Pharmacology. 365, pp. 124–132. 2019.
- Vesicular acetylcholine transport deficiency potentiates some inflammatory responses induced by diesel exhaust particles – Santana, F. P. R., et al. Ecotoxicology and Environmental Safety, 167, 494–504. 2019.
CONSCIOUS MEASUREMENTS, SPONTANEOUS BREATHING
The induced changes in lung parenchyma resulting from pollutants and air born irritants are likely to result in impaired breathing patterns, which can be captured repeatedly in conscious spontaneously breathing subjects using a whole body plethysmograph.
- Dobutamine “stress” test and latent cardiac susceptibility to inhaled diesel exhaust in normal and hypertensive rats. – Hazari et al. Environmental health perspectives 120.8 (2012): 1088.
- Acrolein inhalation alters arterial blood gases and triggers carotid body-mediated cardiovascular responses in hypertensive rats. – Perez et al. Inhalation toxicology 27.1 (2015): 54-63.
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