Smoke Inhalation and Glutathione

The respiratory tract is a major interface with the oxygen laden environment. The respiratory tract is rich in glutathione which protects lungs from oxidative stress. Irritant exposure seen in the lungs of individuals who smoke can result in a combination of problems. Most of these problems occur when there is inadequate glutathione to compensate for the excess of irritants and resulting oxidant stress in the lung.(1)

Chronic smokers raise their defenses by increasing glutathione in the lung epithelial lining fluid. Acute smoke exposure lowers the levels of glutathione.(1)

While the exposure to smoke from wood fires is for a limited period, when the exposure is heavier than normal it  will have a varying effect on each individual depending on their genetic ability to respond to the irritants and the resulting oxidative stress. Oxidative stress is considered to play a main role in the pathogenesis of inflammatory lung disease and can lead to chronic obstructive pulmonary disease (COPD).(2)

In smokers, oxidative stress may result from the irritation of the components of the particulates in smoke, and from the oxidants released by inflammatory cells that are recruited as a result of the smoke induced injury (3).

The cells of the lung, called epithelium, is normally restored by a repair process that occurs after low level cigarette smoke condensate, but can be overwhelmed by high doses resulting in cell toxicity (2).  Chronic exposure to irritants such as cigarette smoke at a repeated, sub-lethal basis results in epithelial cell proliferation that is a key feature of changes observed in smoking-induced lung disease(2).

The studies relating to the effects of inhalation of wood smoke were performed primarily in animals. Sheep exposed to cool western pine bark smoke showed evidence of oxidative stress at 48 hours after the exposure (4).  After this exposure, there was an elevation of oxidative stress markers (TBARS) that were over 65% higher than controls.  In the lung fluid, a TBARS elevation was also found. The lung TBAR elevation corresponded to the degree of smoke inhalation with the highest oxidative stress (4 times normal) occurring with the highest level of smoke inhalation. Smoke exposure also caused a direct injury to the lining membrane of the trachea.

Hardwood smoke (HWS) inhalation was studied in male and female rats.(5) These results reflect the changes seen in lung lavage fluid (Bronchial alveolar lavage fluid (BALF). HWS decreased glutathione in the BALF of female rats. In male rats exposed to HWS, the response at low exposure showed increases in glutathione.  For males, the pattern is similar to that seen in smokers, who show an elevation of glutathione.(5)

1. Rahman I, MacNee W. Lung glutathione and oxidative stress: implications in cigarette smoke-induced airway disease. The American journal of physiology. 1999;277(6 Pt 1):L1067-88. Cited in PubMed; 10600876.
2. Luppi F, Aarbiou J, van Wetering S, Rahman I, de Boer WI, Rabe KF, et al. Effects of cigarette smoke condensate on proliferation and wound closure of bronchial epithelial cells in vitro: role of glutathione. Respiratory research. 2005;6:140. Cited in PubMed; 16309548.
3. MacNee W, Rahman I. Is oxidative stress central to the pathogenesis of chronic obstructive pulmonary disease? Trends in molecular medicine. 2001;7(2):55-62. Cited in PubMed; 11286755.
4. Park MS, Cancio LC, Jordan BS, Brinkley WW, Rivera VR, Dubick MA. Assessment of oxidative stress in lungs from sheep after inhalation of wood smoke. Toxicology. 2004;195(2-3):97-112. Cited in PubMed; 14751667.
5. Seagrave J, McDonald JD, Reed MD, Seilkop SK, Mauderly JL. Responses to subchronic inhalation of low concentrations of diesel exhaust and hardwood smoke measured in rat bronchoalveolar lavage fluid. Inhalation toxicology. 2005;17(12):657-70. Cited in PubMed; 16087572.