Pulmonary injury

The respiratory system is very sensitive to SM vapor, which can lead to persistent lung damage and pulmonary disabilities that persist from the acute to the chronic phase without interruption. Delayed respiratory injury is the major cause of morbidity following exposure to SM. Up to 43% of 34000 Iranian veterans suffer from lung lesions. Most of the patients complain of chronic cough, dyspnea and sputum production. Additional symptoms can include chest pain, gastro-oesophageal reflux pain and haemoptysis. 

Restrictive lung disease (RLD) has a high prevalence and has—beside SM injury—a myriad of eauses. It is defined as a reduction in FEV and FVC, as well as a reduction in total lung capacity (TLC 20% of its normal value). RLD may have specifie causes that can be intrinsic or extrinsic. In the case of SM-induced RLD, chronic persistent bronchitis was reported in 59% of patients with a single severe exposure. These patients are heavily disabled.  

Some studies also reported chronic bronchitis as a common late effect of pulmonary SM exposure. Pulmonary fibrosis was found in SM-exposed Iranian soldiers and can result in a severe impairment of lung function. Analysis of broncho-alveolar lavage fluid from those patients revealed that inflammatory processes are still active even decades after SM exposure. Fibrotic remodeling of the lung may also cause severe scars and narrowing of the bronchial system, which can also cause severe health effects. 

Ghanei and Harandi recommend the use of corticosteroids in all forms of SM-induced chronic lung injury. However, side effects of their continued use may limit their long-term use. Additionally, beta-agonists and anticholinergics are effective in improving lung function.  

Balali-Mood and M. Hefazi, The pharmacology, toxicology, and medical treatment of sulphur mustard poisoning, Fundam. Clin. Pharmacol, 2005,19, 297. 

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Vesicant agents, such as mustard, require no special treatment once the bums have occurred. Copious washing is quite effective when used early for Hquid contamination of the eyes, and soap and water removes the Hquid agent from the skin. Bums resulting from mustard agent are treated like any other severe bum. The pulmonary injuries are treated symptomatically antibiotics are used only if indicated for the control of infection. 

Other enzyme systems may also be directly or indirectly involved in the generation of ROS in the lung, including those of the eicosanoid pathway, the mitochondrial electron transport system, and aldehyde, glucose and xanthine oxidases (Parks and Granger, 1986). These systems may also be relevant to lung damage. For example, the oedematous pulmonary injury that results from cessation of blood flow for a period followed by reinstatement of... 

Prior M, Green F, Lopez A, et al. 1990. Capsaicin pretreatment modifies hydrogen sulphide-induced pulmonary injury in rats. Toxicol Pathol 18 279-288. 

Ziqian O-Y, Zhengping Y, Yong L. 1993. Study on pulmonary injury due to acute hydrogen sulfide inhalation and its therapeutic scheme. Journal of Medical Colleges of PLA 8 308-314. 

I Pulmonary injury i I Neoplasia- Lung Neoplasia-Heart I Neoplasia-Other I I I Neoplasia-Bane I... 

Antioxidant therapy might be promising medication for the treatment of some lung disorders. For example, lecithinized phosphatidylcholine-CuZnSOD suppressed the development of bleomycin-induced pulmonary fibrosis in mice [284] these findings could be of relevance for the treatment of bleomycin-stimulated pulmonary fibrosis in humans. Davis et al. [285] recently demonstrated that the treatment of premature infants with recombinant human CuZnSOD may reduce early pulmonary injury. 

Pendino, K J. et al., Inhibition of macrophages with gadolinium chloride abrogates ozone-induced pulmonary injury and inflammatory mediator production, Am. J. Respir. Cell Molec. Biol., 13, 125, 1995. 

Henderson, R.F. and Loery, J.S. (1983). Effect of anesthetic agents on lavage fluid parameters used as indicators of pulmonary injury. Lab. Anim. Sci. 33 60-62. 

Common treatment for inhalation exposure includes removal of the patient to fresh air and observation for respiratory distress. Pulmonary injury may occur from solvents used as carriers for organochlorine pesticides. A hydrocarbon pneumonitis may be produced if aspiration of the liquid solvent occurs. 

Zucker AR, Berger S, Wood LD. 1986. Management of kerosene-induced pulmonary injury. CritCare Med 14(4) 303-304. 

Exposure of four animal species to 10 ppm for 4 hours was fatal 5 ppm for 5 hours was not fatal but caused pulmonary edema, whereas 1 ppm produced no effects. Animals exposed to 5 ppm 1 hour daily for 5 days developed signs of pulmonary injury 1 ppm for the same time period caused no effects. 

Chan K, Kan YW. 1999. Nrf2 is essential for protection against acute pulmonary injury in mice. Proc Natl Acad Sci USA 96 12731-12376. 

Pulmonary injury Pulmonary fibrosis can be produced by bleomycin... 

Rat Inhalation 10,25,50, 5,15,30 Pulmonary injury determined by lung weight Stavert and... 

Stavert, D.M. and B.E.Lehnert. 1990. Nitric oxide and nitrogen dioxide as inducers of acute pulmonary injury when inhaled at relatively high concentrations for brief periods. Inhalation Toxicol. 2 53-67. 

Charan, N.B., C.G.Myers, S.Lakshminarayan, and T.M.Spencer. 1979. Pulmonary injuries associated with acute sulfur dioxide inhalation. Am. Rev. Respir. Dis. 119(4) 555-560. 

The vesicant properties of lewisite result from direct contact with the skin. Signs of dermal toxicity (pain, inflammation) may be experienced within a minute after exposure. Acute lethality is usually the result of pulmonary injury. Ocular exposure may result in corneal necrosis. Due to its lipophilicity, percutaneous absorption of lewisite is rapid and, at a sufficient exposure, may be associated with systemic toxicity characterized by pulmonary edema, diarrhea, agitation, weakness, hypothermia, and hypotension (lOM, 1993). The threshold for severe systemic toxicity in humans following dermal exposure to lewisite has been estimated at lOmg/kg (9.1-13.4 mg/kg) (Sollman, 1957). 

Pauluhn, J., Carsom, A., Costa, D.L., Gordon, T., Kodavanti, U., Last, J.A., Matthay, M.A., Pinkerton, K.E., Sciuto, A.M. (2007). Workshop summary phosgene-induced pulmonary toxicity revisited appraisal of early and late markers of pulmonary injury from animal models with emphasis on human significance. Inhal. Toxicol. 19 789-810. 

Sciuto, A.M., Strickland, P.T., Kennedy, T.P. et al. (1996). Intratracheal administration of DBcAMP attenuates edema formation in phosgene-induced acute pulmonary injury. J. Appl. Physiol. 80 149-57. 

Hoesel, L.M., Flierl, M.A. et al. (2008). Ability of antioxidant liposomes to prevent acute and progressive pulmonary injury. Antioxid. Redox Signal. 10 973-81. 

Diller, 1985 Ohio et al, 1991). Pulmonary injury is exacerbated by elevated levels of leukotrienes and neutrophil chemotactic agents. The neutrophils release cytokines and other reactive mediators worsening pulmonary injury (Ohio et al, 1991 Sciuto et al, 1995). Localized emphysema and partial atelectasis occur. Death is from anoxia secondary to pulmonary edema (Borak and Diller, 2001 Proctor and Hughes, 2004). 

Prognosis is directly related to the severity of pulmonary injury. Animals that survive the first 24 to 48 h still have a guarded prognosis. These animals are more susceptible to infectious agents as they have suppressed natural killer cell activity. Infections may become evident 3 to 5 days after exposure. Animals may develop chronic exercise intolerance and abnormal pulmonary function (Borak and Diller, 2001). Working dogs and equines may no longer be able to fulfill their fimctions. 

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