Exposures, fatal

Antibodies develop in 30% after initial and 70% after repeat exposure. Fatal anaphylaxis has been reported after sensitization... 

Gy, acute single exposure Fatal to 50% of trees >5 years old in 1-4 months no other deaths in 2 years 2... 

Dinitrophenols are extremely toxic to humans and are well absorbed from all routes of exposure. Fatal... 

Year Total human poison exposures Total dermal poison exposures % dermed poison exposures Fatal dermal poison exposures... 

The two most common toxic oxides of nitrogen are NO and NO2. The more toxic nitrogen dioxide causes severe irritation of the innermost parts of the lungs, resulting in pulmonary edema. In cases of severe exposures, fatal bronchiolitis fibrosa obliterans may develop approximately 3 weeks after exposure to NO2. FataUties can result from even brief periods of inhalation of air containing 200-700 ppm of NO2. 

It is very poisonous, 50 mg constituting an approximate fatal dose. Exposure to white phosphorus should not exceed 0.1 mg/ms (8-hour time-weighted average - 40-hour work week). White phosphorus should be kept under water, as it is dangerously reactive in air, and it should be handled with forceps, as contact with the skin may cause severe burns. 

Mild exposure to HF via inhalation can irritate the nose, throat, and respiratory system. The onset of symptoms may be delayed for several hours. Severe exposure via inhalation can cause nose and throat bums, lung inflammation, and pulmonary edema, and can also result in other systemic effects including hypocalcemia (depletion of body calcium levels), which if not promptly treated can be fatal. Permissible air concentrations are (42) OSHA PEL, 3 ppm (2.0 mg/m ) as E OSHA STEL, 6 ppm (5.2 mg/m ) as E and ACGIH TLV, 3 ppm (2.6 mg/m ) as E. Ingestion can cause severe mouth, throat, and stomach bums, and maybe fatal. Hypocalcemia is possible even if exposure consists of small amounts or dilute solutions of HE. 

Toxicity. Lethality is the primary ha2ard of phosphine exposure. Phosphine may be fatal if inhaled, swallowed, or absorbed through skin. AH phosphine-related effects seen at sublethal inhalation exposure concentrations are relatively small and completely reversible. The symptoms of sublethal phosphine inhalation exposure include headache, weakness, fatigue, di22iness, and tightness of the chest. Convulsions may be observed prior to death in response to high levels of phosphine inhalation. Some data are given in Table 2. 

Most of them are generally classified as poisons. Exceptions to this rule are known. A notable one is 4-dimethyl aminopyridine (DMAP) (24), which is widely used in industry as a superior acylation catalyst (27). Quaternary salts of pyridines are usually toxic, and in particular paraquat (20) exposure can have fatal consequences. Some chloropyridines, especially polychlorinated ones, should be handled with extra care because of their potential mutagenic effects. Vinylpyridines are corrosive to the skin, and can act as a sensitizer for some susceptible individuals. Niacin (27), niacinamide (26), and some pyridinecarbaldehydes can cause skin flushing. 

Techniques for handling sodium in commercial-scale appHcations have improved (5,23,98,101,102). Contamination by sodium oxide is kept at a minimum by completely welded constmction and inert gas-pressured transfers. Residual oxide is removed by cold traps or micrometallic filters. Special mechanical pumps or leak-free electromagnetic pumps and meters work well with clean Hquid sodium. Corrosion of stainless or carbon steel equipment is minimi2ed by keeping the oxide content low. The 8-h TWA PEL and ceiling TLV for sodium or sodium oxide or hydroxide smoke exposure is 2 mg/m. There is no defined AID for pure sodium, as even the smallest quantity ingested could potentially cause fatal injury. 

Tb allium, which does not occur naturaHy in normal tissue, is not essential to mammals but does accumulate in the human body. Levels as low as 0.5 mg/100 g of tissue suggest thallium intoxication. Based on industrial experience, 0.10 mg /m of thallium in air is considered safe for a 40-h work week (37). The lethal dose for humans is not definitely known, but 1 g of absorbed thallium is considered sufficient to kHl an adult and 10 mg/kg body weight has been fatal to children. In severe cases of poisoning, death does not occur earlier than 8—10 d but most frequently in 10—12 d. Tb allium excretion is slow and prolonged. For example, tb allium is present in the feces 35 d after exposure and persists in the urine for up to three months. 

Care must be exercised in handling carbon disulfide because of both health concerns and the danger of fire or explosions. Occupational exposure potentially may involve as many as 20,000 workers in the United States (136). Ingestion is rare, but a 10 mL dose can prove fatal (137). Contact usually occurs by inhalation of vapor. However, vapor and Hquid can be absorbed through intact skin and poisoning may occur by the dermal route (138). 

Inhalation of vapors of lower chloroformates result in coughing, choking, and respiratory distress, and, with some chloroformates like methyl chloroformate, inhalation can be fatal as a result of the onset of pulmonary edema, which may not appear for several hours after exposure (55). Table 5 gives the acute toxicides of some chloroformates (55—57). 

The threshold limit value—time integrated average, TLV—TWA, of chlorine dioxide is 0.1 ppm, and the threshold limit value—short-term exposure limit, STEL, is 0.3 ppm or 0.9 mg /m of air concentration (87,88). Chlorine dioxide is a severe respiratory and eye irritant. Symptoms of exposure by inhalation include eye and throat irritation, headache, nausea, nasal discharge, coughing, wheezing, bronchitis, and delayed onset of pulmonary edema. Delayed deaths occurred in animals after exposure to 150—200 ppm for less than one hour. Rats repeatedly exposed to 10 ppm died after 10 to 13 days of exposure. Exposure of a worker to 19 ppm for an unspecified time was fatal. The ingested systemic effects of low concentration chlorine dioxide solutions are similar to that of chlorite. 

Toxicity of 2-Ghloroethanol. Ethylene chlorohydrin is an irritant and is toxic to the Hver, kidneys, and central nervous system. In addition, it is rapidly absorbed through the skin (73). The vapor is not sufficiently irritating to the eyes and respiratory mucous membranes to prevent serious systemic poisoning. Contact of the Hquid in the eyes of rabbits causes moderately severe injury, but in humans corneal bums have been known to heal within 48 hours. Several human fataUties have resulted from inhalation, dermal contact, or ingestion. One fatahty was caused by exposure to an estimated 300 ppm in air for 2.25 hours. In another fatal case, autopsy revealed pulmonary edema and damage to the Hver, kidneys, and brain (73). 

Inhalation. The threshold limit value of HCN is 4.7 ppm. This is defined as the maximum average safe exposure limit for a 15-min period by the Occupational Safety and Health Administration. Exposure to 20 ppm of HCN in air causes slight warning symptoms after several hours 50 ppm causes disturbances within an hour 100 ppm is dangerous for exposures of 30 to 60 min and 300 ppm can be rapidly fatal unless prompt, effective first aid is adininistered. There is always a small concentration of cyanide (0.02 to 0.04 mg/L) in the blood, and the body has a mechanism for continuous removal of small amounts, such as from smoking, by converting it to thiocyanate, which is discharged in the urine. 

Toxicology. An excellent review of the toxicity and health assessment of ethylene oxide has been compiled (233). Ethylene oxide (EO) can be relatively toxic as both a Hquid and gas. Inhalation of ethylene oxide ia high concentrations may be fatal. Estimates of lethal ethylene oxide inhalation levels in animals depend on the duration of exposure. The reported 4-h LC q values for rats, mice, and dogs are 1460, 835, and 960 ppm, respectively (234). More recent information (235) indicates that the 1-h LC q in rats is approximately 5000 ppm. 

Risk indices are usually single-number estimates, which may be used to compare one risk with another or used in an absolute sense compared to a specific target. For risks to employees the fatal accident rate (FAR) is a commonly apphed measure. The FAR is a singlenumber index, which is the expected number of fatalities from a specific event based on 10 exposure hours. For workers in a chemical plant, the FAR could be calculated as follows ... 

Most people will tolerate greater risk from activities when the threat to life is offset in time from when the risk (and the benefit) is originally accepted. For example, people may feel worse (and usually accept less risk) about a threat of immediate harm (e.g., the blast wave from an explosion) than a threat of latent harm (e.g., an increase in the chance of getting a fatal disease following a 20-year exposure to a hazardous material, like asbestos), even though the risks may be equivalent. 

Prolonged exposure may cause pulmonary oedema Systemic symptoms may occur in 0.5 to 1 hr Rapid collapse, respiratory paralysis imminent Immediately fatal... 

Effects of given concentrations of nitrogen oxides are listed in Table 5.33 the margin between concentrations that provoke mild symptoms and those proving to be fatal is small. A person with a normal respiratory function may be affected by exposure to as low as 5 ppm diseases such as bronchitis may be aggravated by such exposures. The current 8 hr TWA OES is 3 ppm with an STEL (page 99) of 5 ppm. 

From inhalation at pressures above atmospheric, used in tunnelling or diving, or from breathing apparatus or resuscitation equipment, if the pressure is too high or exposure is prolonged. This may cause symptoms from pain to dyspnoea, disorientation and unconsciousness it may be fatal. 

Serious coughing, bronchial spasms, <30 min exposure may be fatal Serious oedema, strangulation, asphyxia Fatal almost immediately... 

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