The First Fatality

This shook the organization to its core, as they had not had a fatality for 32 years, and when, at the site of the fatality, I approached the CEO and asked if I could be of any help, he simply replied with tears in his eyes, Tm devastated.  

---

With few exceptions, gene therapy was considered safe if not particularly effective until the death of an 18-year-old man in 1999, the first fatal outcome for a pa-... 

Coal mine gas (called Coal bed Gas) is a kind of associated gas from the coal seam in coal mine exploitation process in different forms, which is one of the main reasons of the coal mine accident. As the first fatal factor in coal mine, the gas accident not only causes a large number of casualties and huge economic losses, and imperils the safety of coal mine production seriously once it occurs. Gas concerns the major issues of environmental pollution, the greenhouse effect and the future of new energy. It can be used after recovered rapidly if the coal mine gas develops, storages and transports high-efficiently in moderate environment. Meanwhile it will be reduced that the cost, the hidden safety trouble and the gas emission pollution to the environment. Thus it is badly in need of a new type of gas utilization technology to make up for the current technical defects. Hydrate method is an optional way. 

Writers admittedly faced problems of public perception when they constructed the agency s official version of the disaster. The accident was the first fatal accident since British mines had denationalized in 1994. It was also the first disaster since British mines had introduced the American system of rock bolting, a method of roof support opposed by British labor unions who favored the traditional method of arch support. Unions had feared that the new system would reduce safety and increase the potential for disaster. The accident confirmed their fears that the motivation for the practice was strictly economic. 

Although the circulatory complications due to intravenous administration of fluorescein are well known, (SED VIII, p. 1070) the first fatalities directly attributable to it appear to have been reported only recently. 

Ingestion. Ingestion, unless prompt first aid or medical treatment is given, is rapidly fatal 1 mg of cyanide per kilogram of body weight can be fatal. Immediate and repeated adininistration of emetics and regurgitation (if the victim is conscious), followed or accompanied by the first aid and medical treatments described below should be carried out. If the victim is unconscious, stomach lavage should be performed by a physician or trained personnel. 

Calculate tlie Fatal Accident Rate (FAR) for the first kind of accident. 

Soon after production began, TEL was held responsible for a high incidence of illness and deaths among production workers at both the DuPont and Jersey Standard plants. The substance penetrated the skin to cause lead poisoning. Starting in late 1924, there were forty-five cases of lead poisoning and four fatalities at Jersey Standard s Bayway production plant. Additional deaths occurred at the DuPont Plant and at the Dayton Laboratory. This forced the suspension of the sale of TEL ill 1925 and the first half of 1926. 

During World War I. Haber was in charge of the German poison gas program. In April of 1915. the Germans used chlorine for the first time on the Western front, causing 5000 fatalities. Haber s wife. Clara, was aghast she pleaded with her husband to forsake poison gas. When he adamantly refused to do so. she committed suicide. 

Glucose/galactose malabsotption (GGM) is an intestinal monosaccharide (glucose and galactose) transport deficiency. The disorder manifests itself within the first weeks of life. The severe diarrhea and dehydration are usually fatal unless glucose and galactose are eliminated from the diet. Fiuctose and xylose are absorbed normally. Occurrence in both males and females, familial incidence, in particular in parental consanguinity, indicate autosomal recessive inheritance of... 

Fatal hereditary disorder that typically presents in the neonatal period. Clinical features include an array of hepatic, renal and neurological dysfunctions. Patients with Zellweger syndrome rarely survive the first year of life. The disease is caused by mutations in the Pex proteins leading to an defective import of peroxisomal matrix proteins and consequently to a loss of most peroxisomal metabolic pathways. 

A serious and potentially fatal adverse reaction to tolcapone ishepatic injury. Regular blood testing to monitor liver function is usually prescribed. The phys dan may order testing of serum transaminase levels at frequent intervals(eg, every 2 weeks for the first year and every 8 weeks thereafter). Treatment is discontinued if the ALT (SOFT) exceeds the upper normal limit or sgns or symptoms of liver failure develop. 

Type I Crigler-Najjar syndrome is a rare autosomal recessive disorder. It is characterized by severe congenital jaundice (serum bilirubin usually exceeds 20 mg/dL) due to mutations in the gene encoding bilirubin-UGT activity in hepatic tissues. The disease is often fatal within the first 15 months of life. Children with this condition have been treated with phototherapy, resulting in some reduction in plasma bilirubin levels. Phenobarbital has no effect on the formation of bilirubin glucuronides in patients with type I Crigler-Najjar syndrome. A liver transplant may be curative. 

The wide use of pesticides in the republic started in 1959 when 30% and 60% mercaptophos started to be used for the first time in the fight against cotton pests. In 1959-61, the number of incidents of poisoning, especially in the first group, was 23% of all incidents over the ten-year period 7% of those poisoned suffered fatalities. 

The loss of expensive catalyst from the reactor system can be fatal for any process. Physical loss involves the removal of active catalyst from the closed loop of the process. This can include the plating out of metal or oxides on the internal surfaces of the manufacturing plant, failure to recover potentially active catalyst from purge streams and the decomposition of active catalyst by the process of product recovery. The first two can be alleviated to some extent by improvements in catalyst or process design, the last is an intrinsic problem for all manufacturing operations and is the subject of this book. 

---