Inhalational injury pulmonary effects

HEALTH SYMPTOMS Inhalation (pulmonary effects, injury to liver, irritates eyes, nose and throat) contact (acne-skin rash, dermatitis, hyper-pigmentation) ingestion (gastrointestinal disturbances, yellowjaundice, dark urine, fatigue). 

There is no recognized prophylactic therapy for human PFIB exposure. Animal studies suggest that increasing pulmonary concentrations of oxygen free-radical scavengers containing thiol groups may be of value N-acetyl cysteine has been found effective.65,66 No postexposure medical or chemical therapy that effectively impedes or reverses the effects of this toxic inhalational injury is known. 

SM causes injury via four major routes (i) skin damage after absorption through the integument (ii) eye damage after exposure to mustard gas vapor (iii) broncho-pulmonary effects after inhalation and (iv) systemie toxicity after ingestion or absorption of high amounts of SM. ... 

In rats, the administration of fullerene by inhalation, as nano- and microparticles generated by aerosol, does not lead to lesions and only a little increase of protein concentration in bronchoalveolar lavage fluid was obtained (Baker et al., 2007). Recently, Sayes et al. (2007) analyzed in vivo pulmonary toxicity of C60 and C60(OH)24, after intratracheal instillation in rats. They verified only transient inflammatory and cell injury effects, 1 day postexposure, without differences from water-instilled controls. No adverse lung tissue effects were measured, and the results demonstrated little or no differences in lung toxicity effects between the C60 and fiillerols, compared to controls. 

Deaths in rats resulting from single-exposure concentration/duration combinations expected to produce 50%-90% mortality usually occurred within 24 hours. These deaths were attributed to cardiac or respiratory failure and were probably a direct effect of 1,2-dibromoethane toxicity. Deaths resulting from exposure concentration/duration combinations expected to produce 0.01%-50% mortality occurred as long as 12 days after exposure and were due to pneumonia. The authors attributed pneumonia to 1,2-dibromoethane-induced lung injury, but this lesion could also have been due to intercurrent bacterial or mycoplasmal pulmonary infection. Rats free of enzootic respiratory infections were not available in 1952. More contemporary inhalation studies of 1,2-dibromoethane using commercially produced rats (Nitschke et al. 1981 NTP 1982) did not report pneumonic lesions or pneumonia-related mortality. 

The injury caused by chlorine trifluoride is in part attributed to its hydrolysis products, including chlorine, hydrogen fluoride, and chlorine dioxide. Effects in humans have not been reported but may be expected to be very severe inhalation may cause pulmonary edema, and contact with eyes or skin may cause severe burns. 

Both anhydrous hydrogen fluoride gas and hydrofluoric acid are highly corrosive and dangerous. Skin contact by even dilute aqueous HF can be severely injurious, causing deep ulceration with delayed effect. The acid can penetrate the skin and destroy tissues. It also is damaging to eyes, nose and lungs. Inhalation can cause fluorosis and pulmonary edema. 

Toxicity and health effects Selenium causes hair and nail loss, discoloration and decay of the teeth, and CNS disturbances, including pain and anesthesia of the extremities. Inhalation of hydrogen selenide causes pulmonary edema. The dusts of selenium produce respiratory tract irritation, while the fumes of selenium dioxide produce metal fume fever. Dermal exposure and ingestion of selenium oxychloride cause skin burns, corrosive injury to the gastrointestinal tract, stupor, respiratory depression, and refractory hypotension. Ingestion of selenious acid causes corrosive injury to the gastrointestinal tract, stupor, respiratory depression, and refractory hypotension... 

Most studies of respiratory diseases reported for uranium involve noncancerous alveolar epithelium damage in type II cells. These changes are characterized by interstitial inflammahon of the alveolar epithelium leading eventually to emphysema or pulmonary fibrosis in acute exposures or to hyperplasia, hypertrophy, and transdifferentiation (metaplasia) in chronic exposures (Cooper et al. 1982 Dungworth 1989 Stokinger 1981 Wedeen 1992). However, the lack of significant pulmonary injury in most inhalation animal studies indicates that other potentially toxic contaminants such as inhalable dust particles, radium, or radon may contribute to these effects. 

---