Lung alveolitis

A number of studies of the toxicity of zinc oxide/hexachloroethane smoke have been conducted (Brown et al. 1990 Karlsson et al. 1986 Marrs et al. 1983). These studies demonstrate that smoke exposure results in pulmonary inflammation and irritation. When male Porton Wistar rats were exposed to hexachloroethane/zinc oxide smoke for 60 minutes, the lungs showed pulmonary edema, alveolitis, and areas of macrophage infiltration 3 days later. At 14 days, there was interstitial fibrosis and macrophage infiltration. At 28 days, increased fibrosis and macrophage infiltration were noted. However, these same symptoms occurred when the animals inhaled zinc chloride there was no apparent synergism between the zinc chloride and residual hexachloroethane (Brown et al. 1990 Richard et al. 1989). This is consistent with the fact that smoke contains little hexachloroethane and the observation that acute exposure to 260 ppm hexachloroethane had no effects on the lungs of rats (Weeks et al. 1979). 

Continued lung injury from inhalation of particulates, whatever their source, size, or composition, produces inflammation (alveolitis, bronchitis), and perhaps eventually fibrosis, a pathological reaction that distorts the architecture of the airways (Lippman et al., 1971). Lung function is compro-... 

In guinea pigs 120mg zinc/m as zinc chloride 1 hour/day 5 days/week for up to 3 weeks was lethal focal alveolitis, consolidation, emphysema, infiltration with macrophages, and fibrosis were observed at necropsy. Mice and rats exposed to 122 mg zinc/m as zinc chloride for 1 hour/day, 5 days/week, survived 20 weeks of exposure but showed increased macrophages in lungs when euthanized 13 months after exposure. ... 

In a study of the time course of nickel-induced respiratory lesions, rats were exposed at 0, 0.22, or 0.95 mg nickel/m as nickel subsulfide 6 hours/day for up to 22 days (Benson et al. 1995b). Inflammatory lung lesions peaked at day 4 of exposure at the high concentration. Alveolitis was noted at the low concentration in all six exposed rats after 7 days of exposure (rats exposed to the low concentration were not examined at earlier time points). Following 6 months of exposure (6 hours/day, 5 days/week), alveolitis of moderate severity was observed in rats exposed to nickel oxide at 1.96 mg nickel/m and mild alveolitis was observed in rats exposed to nickel sulfate at 0.11 mg nickel/m (Benson et al. 1995a). In mice, interstitial pneumonia was observed at 0.98 mg nickel/m and 0.22 mg... 

All isocyanates are known to cause pulmonary toxicity. Isocyanates are the most common causes of occupational asthma and have led to the development of immediate or late asthma among workers. Isocyanates have caused bronchitis, rhinitis, conjunctivitis, chronic obstructive lung disease, contact sensitivity, dermatitis, allergic alveolitis, and immunologic hemorrhagic pneumonitis.29... 

Respiratory toxicity Upper respiratory system (nose, pharynx, larynx, and trachea) and the lower respiratory system (bronchi, bronchioles, and lung alveoli) Pulmonary irritation Asthma/bronchitis Emphysema Allergic alveolitis Fibrotic lung disease Lung cancer... 

CONSENSUS REPORTS lARC Cancer Review Group 2B IMEMDT 7,134,87 Human Inadequate Evidence IMEMDT 26,97,81. EPA Genetic Toxicology Program. SAFETY PROFILE A human poison by intravenous route moderately toxic to humans by intramuscular route. Poison experimentally by intravenous and intraperitoneal routes. Human systemic effects by ingestion and intramuscular routes dyspnea and fibrosing alveolitis (lung). Experimental reproductive effects. 

SAFETY PROFILE Human systemic effects by inhalation fibrosing alveolitis (growth of fibrous tissue in the lung), unspecified respirator system effects, and unspecified effects on the nose. Questionable carcinogen with experimental carcinogenic data. Long considered a nuisance dust (depending on silica content). When heated to decomposition it emits toxic fumes of SOx. See also CALCIUM SULFATE, CALCIUM COMPOUNDS, and SULFATES. 

Rom WN. 1992. Accelerated loss of lung function and alveolitis in a longitudinal study of non-smoking individuals with occupational exposure to asbestos. Am J Ind Med 21 835-844. 

Sprince NL, Oliver LC, McLoud TC, et al. 1992. T-cell alveolitis in lung lavage of asbestos-exposed subjects. Am J Ind Med 21 311-319. 

Lung. Amiodarone may cause pulmonary fibrosis. Sulphasalazine is associated with fibrosing alveolitis. 

Interstitial pulmonary disease (Ijmphocytic alveolitis and mild interstitial pulmonary fibrosis) has been reported in a 70-year-old woman with ulcerative colitis who had taken mesalazine 2.4 g/day for 3 months (42). Halving the dose of mesalazine to 1.2 g/day led to resolution of her lung disorder without relapse of ulcerative colitis. 

The commonest form of lung damage is an interstitial alveolitis, although pneumonitis and bronchiolitis obhter-ans have also been reported, as have sohtary localized fibrotic lesions, non-cardiac pulmonary edema, pleural effusions, acute respiratory failure, acute pleuritic chest pain, and adult respiratory distress syndrome (SEDA-17, 220) (SEDA-18, 201) (66-68). Amiodarone has also been reported to cause impairment of lung function, even in patients who do not develop pneumonitis (69), and preexisting impairment of lung function may constitute a contraindication to amiodarone. 

A 53-year-old Japanese man, who had taken skullcap intermittently for hemorrhoids, developed recurrent interstitial pneumonitis (17). Re-challenge, after he had stopped taking the herbal remedy and had become symptom free, resulted in a high fever and signs and symptoms of interstitial pneumonitis. Transbronchial lung biopsy showed Ijmphocytic alveolitis with eosinophilic infiltration. The symptoms subsided again after withdrawal. 

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