DEPs have been demonstrated to increase the production of inflammatory cytokines such as interleukin 1β, interleukin 8, and granulocyte-macrophage colony-stimulating factor from cyclo-oxygenase stimulation in bronchial epithelial cells. This in turn results in decreased adhesion between cells, reduction of structural integrity, and inhibited repair. Pulmonary damage incurred from DEP exposure may resemble that caused by bacterial endotoxin. Asphyxiation from diesel exhaust is more likely to be caused by acute lung injury from soot particles, nitrogen dioxide, and sulfur dioxide than by carbon monoxide. This is different from gasoline exhaust, which contains 28 times more carbon monoxide than diesel exhaust. Nevertheless, in patients with significant acute and/or chronic diesel exhaust exposure, carbon monoxide levels should be checked. In the absence of deliberate exposure, elevated carbon monoxide levels may represent a marker for serious exposure to diesel exhaust and should be further investigated. Patients with reactive and/or obstructive airway diseases such as asthma and emphysema may have their underlying disease exacerbated as a result of exposure to diesel exhaust.[31,32,33] Visits to the emergency department for pulmonary complaints have been shown to increase during periods of severe air pollution. One possible explanation is DEPs combining with atmospheric allergenic molecules to create even more inflammatory allergens. Admission rates for pediatric asthma exacerbation have been shown to be higher in areas with greater-than-average diesel emissions. DEPs have been shown to directly induce degranulation of mast cells with subsequent histamine release. Histamine release-induced by exposure to DEPs may result in allergic conjunctivitis, rhinosinusitis, pharyngitis, laryngitis, and chronic cough. Macrophages, the first line of immunologic defense within the lung, are severely impaired from exposure to high concentrations of DEPs, resulting in an increased risk of bacterial and viral bronchitis and pneumonia. Although no relevant clinical studies have been published, primary care physicians may consider the inclusion of antihistamines in addition to β-agonists and corticosteroids for the care of patients with acute exacerbation of reactive airway disease precipitated by diesel exhaust exposure.
Many substances in diesel exhaust, such as ozone, can contribute to lung tissue destruction. Ozone is formed from nitrogen oxides, which diesel engines emit in disproportionately higher amounts compared with catalytic converter-equipped gasoline engines. Many of the hydrocarbon molecules emitted by diesel engines, such as PAH, are quite toxic to the lung. Living in areas with high DEPs accelerates pulmonary disease. Chronic exposure to DEPs is associated with an increased risk for the development of asthma. Churg et al compared postmortem lung histology of nonsmoking inhabitants of Mexico City, Mexico, with those of Vancouver, British Columbia, Canada. The lungs of the Mexico City inhabitants were significantly more diseased, with smaller airways consistent with an obstructive pattern and ultra-fine particles embedded in the airway mucosa. A similar study comparing young, recently deceased patients in Los Angeles and Miami found higher levels of pulmonary centriacinar inflammation in the Los Angeles residents. A large study of children demonstrated a significant decrease in the forced expiratory volume in 1 second (FEV1) in those patients living in areas with high concentrations of DEPs. Another pediatric study concluded a dose-dependent inverse association exists between the carbon content of airway macrophages and FEV1 for children living in urban areas with significant diesel exhaust exposure. Workers in enclosed spaces such as mines and ships are especially at risk from DEP-induced pulmonary disease. Jorgensen and Svensson reported that underground miners had productive cough and frequent respiratory infections, and Wade and Newman attributed asthma in train crews to diesel exhaust.
J Am Board Fam Med. 2008;21(1):55-62. © 2008 American Board of Family Medicine
This article was externally peer reviewed.
Cite this: The Toxicity of Diesel Exhaust: Implications for Primary Care - Medscape - Jan 01, 2008.