Air Pollution & Asthma

1. Air Pollution & Asthma Prepared by: Maya Beidoun, Justine del Rosario, Stacy Mangal, Emily Tian PHM142 Fall 2013 Coordinator: Dr. Jeffrey Henderson Instructor: Dr. David Hampson

2. Asthma: What is it? • A chronic respiratory disorder • Sensitive and inflamed airways • Airways overreact to certain air pollutants • Bronchial tube tightens  less airflow to lungs • Increased mucous production  narrows airways • Shortness of breath, chest tightness, coughing, wheezing

3. Simple Statistics on Asthma Affects ~ 3 mill. people in Canada; increasing Prevalence in urban areas > rural areas Due to combination of genetic predisposition factors + environmental exposure to airway irritants Air pollution: nitric oxides, ozone, particulate matter

4. Nitric Oxide • Atmospheric pollutant • Cigarette smoke • Vehicles • Dual effects in asthma pathology • Quantity • Type of enzyme • Location of release • Endogenous NO vs. NO produced by iNOS

5. Dual Effects of NO in Asthma Pathology H. C Prado et al. “Nitric Oxide in Asthma Physiopathology” ISRN Allergy. vol 328, no. 4, pp. 302-315.

6. Ozone • In the troposphere, sunlight reacts with: • Ozone precursors (ie. NOx, such as NO2) • Volatile organic compounds(VOC)s • Increased ozone production NO2 + Sun UV  NO + O O2 + O  O3 "Ozone Layer." Government of Canada, Environment Canada. N.p., n.d. Web. 28 Oct. 2013. <http://www.ec.gc.ca/ozone/default.asp?lang=En&n=DB5CBDE6-1>.

7. Ozone-Induced Cytokine Response • Acts on the respiratory epithelia in healthy and asthmatic individuals • Elevated cytokine expression in asthmatic individuals • IL-5  eosinophil recruitment • GM-CSF (granulocyte macrophage- colony stimulating factor) • Elevated levels of neutrophil chemoattractants: • ENA-78, IL-8, GRO-α • Overall, causes inflammation and constriction of the airway

8. Particulate Matter The Engineering Toolbox. (2008) Retrieved from http://www.engineeringtoolbox.com/particle-sizes-d_934.html • Sources  Industrial processes, wood combustion & fossil fuels, construction, wild fires, windblown dust, etc. • Sulfur and nitrogen oxide are contributors Composition  bioaerosol components, metals, organic molecules, and elemental carbon

9. Particulate Matter • Increased PM  increased emergency room visits and medication use by asthmatics • Promotes sensitization leading to: • Allergic inflammation & airway hyper-responsiveness • Samples with transition metals are the most capable of exacerbating asthma • Promotes ROS formation  epithelial injury  airflow limitations/asthma symptoms • Increased peroxidation products in lungs, blood, and urine of asthmatic subjects

10. Summary People with asthma have very sensitive and inflamed airways, which tend to overreact by constricting and/or overproduce mucous when certain substances in the air are inhaled Symptoms: shortness of breath, chest tightness, coughing, and wheezing Endogenous NO produced by constitutive isoforms has beneficial effects ie. Vasodilation and bronchodilation NO produced via iNOS has adverse effects ie. é oxidative stress, é smooth muscle contraction, é mucous production Many asthma medications are iNOSinhibitors Ozone production is elevated by the presence of ozone precursors and volatile organic compounds (VOCs) Ozone causes respiratory epithelia to release high levels of cytokines (IL-5, GM-CSF) and neutrophil chemoattractants (ENA-78, IL-8, GRO-α) Particulate matter (PM) sources  anthropogenic (burning fossil fuels & wood) and natural (windblown dust and wild fires) PM samples with high concentrations of transition metals are the most capable of exacerbating existing asthma and sensitization. Transition metals lead to generation of ROS, which promote allergic reactions, inflammation, and tissue damage leading to an amplification of symptoms

11. References Asthma Society of Canada. “Asthma Facts and Statistics.” <www.asthma.ca/corp/newsroom/pdf/asthmastats.pdf> Bayram, H., Sapsford, R., Abdelaziz, M., Khair, O. & . (2002). Effect of ozone and nitrogen dioxide on the permeability of bronchial epithelial cell cultures of non‐asthmatic and asthmatic subjects. Clinical & Experimental Allergy, 32(9), 1285-1292. Bosson, J., Stenfors, N., Bucht, A., Helleday, R., Pourazar, J., Holgate, S. T., et al. (2003). Ozone‐induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects. Clinical & Experimental Allergy, 33(6), 777-782. H. C Prado et al. “Nitric Oxide in Asthma Physiopathology” ISRN Allergy. vol 328, no. 4, pp. 302-315, 2011. F.L. M. Ricciardolo, P. J. Sterk, B. Gaston, and G. Folkerts, “Nitric oxide in health and disease of the respiratory system,” Physiological Reviews, vol. 84, no. 3, pp. 731–765, 2004. U. Flodin, and P. Jonsson. “Non-sensitizing air pollution at workplaces and adult onset asthma.” Int Arch Occup Environ Health. vol. 77, no. 1, pp. 17-22, 2003. Gavett, S.H., Koren, H.S. (2001). The Role of Particulate Matter in Exacervation of Atopic Asthma. Int Arch Allergy Immunolo., 124, 109-112. MinqiHao, N. et al. (2003). Particulate air pollutants and asthma: A paradigm for the role of oxidative stress in PM-induced adverse health effects. Clinical Immunology, 109, 250-265. San Joaquin Valley Air Pollution Control District. (2006-2012). Particulate Matter (PM) Sources. Retrieved from http://www.valleyair.org/air_quality_plans/AQ_plans_PM_sources.htm. Y. Jie et al. “Urban vs. rural factors that affect adult asthma.” Rev. Environ ContamToxicol. vol 226, pp. 33-63, 2013.