Effect of pollutants in rhinitis

  • David B. Peden


Allergic rhinitis is a very common disease worldwide and is influenced by both genetic and environmental factors. Exposure to environmental allergens is the most significant environmental factor in development and exacerbation of allergic rhinitis. However, air pollutants that are not allergens may affect allergic inflammation in the nasal airway. The nasal airway possesses a number of defense mechanisms to deal with environmental irritants. This article examines the effect of ozone and particulate air pollution on TH2-type inflammation in the airway and how nasal defenses protect the upper and lower airway from adverse effects of pollutants.

References and Recommended Reading

  1. 1.
    Togias A: Unique mechanistic features of allergic rhinitis. J Allergy Clin Immunol 2000, 105:S599-S604.PubMedCrossRefGoogle Scholar
  2. 2.
    Health effects of outdoor air pollution: Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society. Am J Respir Crit Care Med 1996, 153:3–50.Google Scholar
  3. 3.
    Nathan RA, Meltzer EO, Seiner JC, Storms W: Prevalence of allergic rhinitis in the United States. J Allergy Clin Immunol 1997, 99:S808-S814.CrossRefGoogle Scholar
  4. 4.
    Weiss KB, Sullivan SD: The health economics of asthma and rhinitis: I: assessing the economic impact. J Allergy Clin Immunol 2001, 107:3–8.PubMedCrossRefGoogle Scholar
  5. 5.
    Weiss ST: Environmental risk factors in childhood asthma. Clin Exp Allergy 1998, 28(suppl 5):29–34.PubMedCrossRefGoogle Scholar
  6. 6.
    Holgate ST: Genetic and environmental interaction in allergy and asthma. J Allergy Clin Immunol 1999, 104:1139–1146.PubMedCrossRefGoogle Scholar
  7. 7.
    Peden DB: Controlled exposures of asthmatics to air pollutants. In Air Pollution and Health. Edited by Holgate S, Koren H, Samet J. London: Academic Press; 1999:865–880. This is a review of the effect of air pollutants on airway inflammation as demonstrated by human challenge studies. Included is discussion of inflammatory effects of ozone, diesel exhaust, and other pollutants in the upper and lower airway.Google Scholar
  8. 8.
    Durham SR: Mechanisms of mucosal inflammation in the nose and lungs. Clin Exp Allergy 1998, 28(suppl 2):11–16.PubMedGoogle Scholar
  9. 9.
    Lippmann M, Maynard RL: Air quality guidelines and standards. In Air Pollution and Health. Edited by Holgate ST, Samet JM, Koren HS, Maynard RL. San Diego: Academic Press; 1999:983–1017.Google Scholar
  10. 10.
    National ambient air quality standard for ozone final rule. Washington DC: US Congress; 1997. [Fed Reg 62:38856-38896.]Google Scholar
  11. 11.
    Graham DE, Koren HS: Biomarkers of inflammation in ozone-exposed humans: comparison of the nasal and bronchoalveolar lavage. Am Rev Respir Dis 1990, 142:152–156.PubMedGoogle Scholar
  12. 12.
    Koren HS, Hatch GE, Graham DE: Nasal lavage as a tool in assessing acute inflammation in response to inhaled pollutants. Toxicology 1990, 60:15–25.PubMedCrossRefGoogle Scholar
  13. 13.
    Bascom R, Naclerio RM, Fitzgerald TK, et al.: Effect of ozone inhalation on the response to nasal challenge with antigen of allergic subjects. Am Rev Respir Dis 1990, 142:594–601.PubMedGoogle Scholar
  14. 14.
    Peden DB, Setzer RW Jr, Devlin RB: Ozone exposure has both a priming effect on allergen-induced responses and an intrinsic inflammatory action in the airways of perennially allergic asthmatics. Am J Respir Criti Care Med 1995,151:1336–1345.Google Scholar
  15. 15.
    Michelson PH, Dailey L, Devlin RB, Peden DB: Ozone effects on the immediate phase response to allergen in the nasal airways of allergic asthmatics. Otolaryngol Head Neck Surg 1999, 120:225–232.PubMedCrossRefGoogle Scholar
  16. 16.
    McBride DE, Koenig JQ, Luchtel DL, et al.: Inflammatory effects of ozone in the upper airways of subjects with asthma. Am J Respir Crit Care Med 1994, 149:1192–1197.PubMedGoogle Scholar
  17. 17.
    Kopp MV, Ulmer C, Ihorst G, et al.: Upper airway inflammation in children exposed to ambient ozone and potential signs of adaptation. Eur Respir J 1999, 14:854–861. This paper demonstrates that ozone induces nasal inflammation in children in "real-life" settings associated with natural exposure to ozone, not in experimental challenge.PubMedCrossRefGoogle Scholar
  18. 18.
    Calderon-Garciduenas L, Rodriguez-Alcaraz A, Garcia R, et al.: Nasal inflammatory responses in children exposed to a polluted urban atmosphere. J Toxicol Environ Health 1995, 45:427–437.PubMedCrossRefGoogle Scholar
  19. 19.
    Calderon-Garciduenas L, Delgado R, Calderon-Garciduenas A, et al.: Malignant neoplasms of the nasal cavity and paranasal sinuses: a series of 256 patients in Mexico City and Monterrey: is air pollution the missing link? Otolaryngol Head Neck Surg 2000, 122:499–508.PubMedCrossRefGoogle Scholar
  20. 20.
    Calderon-Garciduenas L, Wen-Wang L, Zhang YJ, et al.: 8- hydroxy-2′-deoxyguanosine, a major mutagenic oxidative DNA lesion, and DNA strand breaks in nasal respiratory epithelium of children exposed to urban pollution. Environ Health Perspect 1999, 107:469–474.PubMedCrossRefGoogle Scholar
  21. 21.
    Wang Z, Larsson K, Palmberg L, et al.: Inhalation of swine dust induces cytokine release in the upper and lower airways. Eur Respir J 1997, 10:381–387.PubMedCrossRefGoogle Scholar
  22. 22.
    Teeuw KB, Vandenbroucke-Grauls CM, Verhoef J: Airborne gram-negative bacteria and endotoxin in sick building syndrome: a study in Dutch governmental office buildings. Arch Intern Med 1994, 154:2339–2345.PubMedCrossRefGoogle Scholar
  23. 23.
    Bonner JC, Rice AB, Lindroos PM, et al.: Induction of the lung myofibroblast PDGF receptor system by urban ambient particles from Mexico City. Am J Respir Cell Mol Biol 1998, 19:672–680. This article identifies endotoxin as a component of ambient air particles.PubMedGoogle Scholar
  24. 24.
    Michel O, Kips J, Duchateau J, et al.: Severity of asthma is related to endotoxin in house dust. Am J Respir Crit Care Med 1996, 154:1641–1646.PubMedGoogle Scholar
  25. 25.
    Martin TR: Recognition of bacterial endotoxin in the lungs. Am J Respir Cell Mol Biol 2000, 23:128–132.PubMedGoogle Scholar
  26. 26.
    Dubin W, Martin TR, Swoveland P, et al.: Asthma and endotoxin: lipopolysaccharide-binding protein and soluble CD14 in bronchoalveolar compartment. Am J Physiol 1996, 270:L736-L744.PubMedGoogle Scholar
  27. 27.
    Virchow JC, Julius P, Mattys H, et al.: CD14 expression and soluble CD14 after segmental allergen provocation in atopic asthma. Eur Respir J 1998, 11:317–323. This is an important demonstration of the ability of allergen exposure to upregulate response to endotoxin, a stimulus that does not activate inflammation via IgE.PubMedCrossRefGoogle Scholar
  28. 28.
    Peden DB, Tucker K, Murphy P, et al.: Eosinophil influx to the nasal airway after local, low-level LPS challenge in humans. J Allergy Clin Immunol 1999, 104:388–394.PubMedCrossRefGoogle Scholar
  29. 29.
    Eldridge MW, Peden DB: Allergen provocation augments endotoxin-induced nasal inflammation in subjects with atopic asthma. J Allergy Clin Immunol 2000, 105:475–481. This report describes the ability of allergen-induced inflammation to enhance response to endotoxin, which is found in particles, suggesting that nasal atopy may be a risk factor in enhancing response to a pollutant.PubMedCrossRefGoogle Scholar
  30. 30.
    Diaz-Sanchez D, Dotson AR, Takenaka H, Saxon A: Diesel exhaust particles induce local IgE production in vivo and alter the pattern of IgE messenger RNA isoforms. J Clin Invest 1994, 94:1417–1425.PubMedCrossRefGoogle Scholar
  31. 31.
    Diaz-Sanchez D, Tsien A, Fleming J, Saxon A: Combined diesel exhaust particulate and ragweed allergen challenge markedly enhances human in vivo nasal ragweed-specific IgE and skews cytokine production to a T helper cell 2-type pattern. J Immunol 1997, 158:2406–2413.PubMedGoogle Scholar
  32. 32.
    Fujieda S, Diaz-Sanchez D, Saxon A: Combined nasal challenge with diesel exhaust particles and allergen induces in vivo IgE isotype switching. Am J Respir Cell Mol Biol 1998, 19:507–512.PubMedGoogle Scholar
  33. 33.
    Wang M, Saxon A, Diaz-Sanchez D: Early IL-4 production driving Th2 differentiation in a human in vivo allergic model is mast cell derived. Clin Immunol 1999, 90:47–54.PubMedCrossRefGoogle Scholar
  34. 34.
    Diaz-Sanchez D, Penichet-Garcia M, Saxon A: Diesel exhaust particles directly induce activated mast cells to degranulate and increase histamine levels and symptom severity. J Allergy Clin Immunol 2000, 106:1140–1146. This report demonstrates that DEPs can directly augment mast cell degranulation in vivo. This has not been observed in humans with other agents.PubMedCrossRefGoogle Scholar
  35. 35.
    Diaz-Sanchez D, Tsien A, Fleming J, Saxon A: Effect of topical fluticasone propionate on the mucosal allergic response induced by ragweed allergen and diesel exhaust particle challenge. Clin Immunol 1999, 90:313–322.PubMedCrossRefGoogle Scholar
  36. 36.
    Diaz-Sanchez D, Garcia MP, Wang M, et al.: Nasal challenge with diesel exhaust particles can induce sensitization to a neoallergen in the human mucosa. J Allergy Clin Immunol 1999, 104:1183–1188. This report demonstrates more directly that DEPs promote an IgEtype response to a neoantigen, suggesting that DEPs contribute to development of allergy not only simple exacerbation of allergic inflammation.PubMedCrossRefGoogle Scholar
  37. 37.
    Diaz-Sanchez D: The role of diesel exhaust particles and their associated polyaromatic hydrocarbons in the induction of allergic airway disease. Allergy 1999, 52(suppl 38):52–56. This review discusses the effect of specific compounds found in diesel exhaust that impact IgE switch mechanisms.Google Scholar
  38. 38.
    Peden D, Hohman R, Brown ME, et al.: Uric acid is a major antioxidant in human nasal airway secretions. Proc Natl Acad Sci U S A 1990, 87:7638–7642.PubMedCrossRefGoogle Scholar
  39. 39.
    Peden DB, Swiersz M, Ohkubo K, et al.: Nasal secretion of the ozone scavenger uric acid. Am Rev Respir Dis 1993, 148:455–461.PubMedGoogle Scholar
  40. 40.
    Linn WS, Shamoo DA, Spier CE, et al.: Respiratory effects of 0.75 ppm sulfur dioxide in exercising asthmatics: influence of upper-respiratory defenses. Environ Res 1983, 30:340–348.PubMedCrossRefGoogle Scholar
  41. 41.
    Mudway IS, Blomberg A, Frew AJ, et al.: Antioxidant consumption and repletion kinetics in nasal lavage fluid following exposure of healthy human volunteers to ozone. Eur Respir J 1999, 13:1429–1438.PubMedCrossRefGoogle Scholar
  42. 42.
    Ohashi Y, Nakai Y, Kihara S, et al.: Ciliary activity in patients with nasal allergies. Arch Otorhinolaryngol 1985, 242:141–147.PubMedCrossRefGoogle Scholar
  43. 43.
    Harkema JR, Morgan KT, Gross EA, et al.: Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies: part VII: effects on the nasal mucociliary apparatus. Res Rep Health Eff Inst 1994, 65:3–34.Google Scholar
  44. 44.
    Cho HY, Hotchkiss JA, Bennett CB, Harkema JR: Neutrophildependent and neutrophil-independent alterations in the nasal epithelium of ozone-exposed rats. Am J Respir Crit Care Med 2000, 162:629–636.PubMedGoogle Scholar
  45. 45.
    Wang JH, Devalia JL, Duddle JM, et al.: Effect of six-hour exposure to nitrogen dioxide on early-phase nasal response to allergen challenge in patients with a history of seasonal allergic rhinitis. J Allergy Clin Immunol 1995, 96:669–676.PubMedCrossRefGoogle Scholar
  46. 46.
    Corren J: The relationship between allergic rhinitis and bronchial asthma. Curr Opin Pulm Med 1999, 5:35–37.PubMedCrossRefGoogle Scholar

Copyright information

© Current Science Inc 2001

Authors and Affiliations

  • David B. Peden
    • 1
  1. 1.Center for Environmental Medicine & Lung BiologyUniversity of North Carolina at Chapel HillChapel HillUSA

Personalised recommendations