Fatal lung fibrosis

In persons professionally exposed to aluminium dust, Kahlau (1941,1942,1947/48, Koelsch 1941, 1942) and Kirch (1943, 1942/43) described several cases of fatal lung fibrosis, and Edwards (1947), therefore, firmly demanded that its use should be allowed only under the supervision of expert observers. ... 

Respiratoiy Lung disease after long-term nitrofurantoin therapy has again been described in [134, 135, 136, 137 ]. In two cases there was bronchiolitis obliterans and in two cases interstitial lung disease with pneumonitis, one with fatal lung fibrosis. There was complete or partial resolution of symptoms after treatment with glucocorticoids. 

Exposures to relatively low concentrations of silica for a prolonged period may be capable of causing hilar node fibrosis, impairing the clearance of any silica inhaled subsequently. In one case, 30 years of exposure to <0.1mg/m led to hilar node fibrosis and calcification in an exposed stonemason subsequent exposure for 5 years to about 2 mg/m led to rapid, progressive silicosis that proved fatal. Estimates of exposure tallied with postmortem measurement of lung burden, suggesting retention of all dust deposited in the lungs over his final period of work. ... 

Although paraquat can be corrosive at the point of contact, it is a systemic poison that is devastating to a number of organs. The most prominent initial symptom of poisoning is vomiting, sometimes followed by diarrhea. Within a few days, dyspnea, cyanosis, and evidence of impairment of the kidneys, liver, and heart become obvious. In fatal cases, the lungs develop pulmonary fibrosis, often with pulmonary edema and hemorrhaging. 

Toxicity. Diquat produces similar adverse effects to those of paraquat except that it does not seem to cause the progressive fibrosis in the lungs. A fatality after ingestion of about 2 g has been reported and the ingestion of about 20 to 50 ml of a 20% concentrate has caused death within 2 to 7 days. The maximum permissible atmospheric concentration is 0.5 mg/m (as the dibromide) and the maximum acceptable daily intake (as the dichloride) is 5 pg/kg. 

Cystic fibrosis—a fatal, hereditary disease characterized by a heavy mucus buildup in the lungs—is caused by a defective plasma membrane protein. In persons with cystic fibrosis this transport protein, known as the sodium-potassium pump, abnormally transports sodium ions across the membrane without carrying the chloride ions that usually accompany them. Research is currently underway to correct through genetic engineering the faulty gene that codes for the plasma membrane protein. 

Generally, titanium dioxide is considered physiologically inert by all routes however, if relatively high concentrations of titanium dioxide dusts are inhaled, toxicological actions are noted. A weak fibrosis of the lung tissue occurs but is not fatal. 

This can prove a real problem in hospitals where there are many susceptible patients suffering from cancer or cystic fibrosis. Burn victims are particularly prone to infection and this can lead to septicaemia which can be fatal. The organism is also responsible for serious lung infections. Carbenicillin represents one of the few penicillins which is effective against this organism. 

Recently, Cl" channels have been discovered. These channels have no sequence relationship to the voltage-gated Na, and Ca channels. One such channel is involved in the disease, cystic fibrosis. In this disease, regulation of the channel is defective. The altered function of the channel in epithelia causes elevated levels of sodium and chloride ions in sweat and, through unknown processes, the accumulation of mucus in the respiratory tract and failure of exocrine secretion in glands, such as the pancreas. Blockage of airways leads to chronic lung infections that, with other effects of the Cl" transport deficiency, can be fatal. 

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