Fatal levels

Figure 9.1. Injury and fatality levels for thermal radiation (Hymes 1983).

Although a great many deaths have occurred from accidental, intentional, or occupational exposures to HCN, in only a few cases are specific exposure concentrations known. In a review of human fatalities (ATSDR 1997), it was stated that exposure to airborne concentrations of HCN at 180 to 270 ppm were fatal, usually within several minutes, and a concentration of 135 ppm was fatal after 30 min. The average fatal concentration for humans was estimated at 546 ppm for 10 min. The latter data point is based on the work of McNamara (1976), who considered the resistance of man to HCN to be similar to that of the goat and monkey and four times that of the mouse. Fatal levels of HCN cause a brief period of central nervous system stimulation followed by depression, convulsions, coma with abolished deep reflexes and dilated pupils, and death. Several review sources, such as Dudley et al. (1942),... 

Kage et al. (75) applied their GC/ECD/GC/MS method to the analysis of blood levels in two casualties who died from cyanide poisoning. Blood levels of cyanide and thiocyanate in a subject who died following ingestion of sodium cyanide were 0.52 and 0.10 umol/ml respectively (= 13 and 5.6 xg/ml). Levels determined in a fatal victim of smoke inhalation were 0.28 and 0.13umol respectively (= 7.3 and 7.5 xg/ml). Fatal levels of cyanide are estimated as 0.05-0.1 umol/ml (= 1.3-2.6 xg/ml). The lower levels of thiocyanate in comparison to cyanide in the blood were attributed to the sudden death they were twice the mean levels ( 0.06 pmol/ml) found in cigarette smokers. 2-Aminothiazoline-4-carboxylic acid was detected in the urine of moderate cigarette smokers at concentrations between <0.3-1.1 xM (76). 

In type 1 diabetes, diabetic nephropathy follows a predictable course from onset of diabetes to the onset of microalbuminuria to frank nephropathy to end-stage renal disease or death. Microalbuminuria (a tiny amount of protein in the urine) develops 10-14 years after onset of diabetes. Without treatment, clinical nephropathy follows within 5 years, and severe renal impairment leading to end-stage renal failure develops approximately 5 years later. Hypertension develops in association with microalbuminuria and progresses with diabetic nephropathy, further damaging the kidneys. Once end-stage renal disease (ESRD) is reached, the toxins in the body can no longer be cleared by the kidneys and, unless treated by dialysis, can build up to fatal levels. 

Air that contains as little as 0.1 percent carbon monoxide can tie up about half of the hemoglobin binding sites, reducing the amount of O2 reaching the tissues to fatal levels. 

The toxicity of ricin is increased several 100-fold when administered parenterally (not via the gut). Fatal levels in rats given ricin hy intravenous injection have been shown to he as low as 0.3 pg/kg body weight (about 60 ng/animal), with mice being less sensitive (LDgg 2.7 pg/kg). Weight for weight, ricin is twice as poisonous as cobra venom. 

Fatal levels are reached at current levels >50 mA at 50/60 Hz if the current path is through vital organs heart, lung, or brain stem (see the electric chair. Section 10.16.3). 

Carbon monoxide was present at fatal levels in the blood of about 50 per cent of the victims. 

To prevent people from receiving an electric shock accidentally, all circuits contain protective devices. All exposed metal is earthed fuses and miniature circuit-breakers (MCBs) are designed to trip under fault conditions, and residual current devices (RCDs) are designed to trip below the fatal level as described in Chapter 4. 

The blast pressure wave reaches fatal levels in a few millionths of a second. 

Mudan (1984) summarizes the data of Eiscnbcrg ct al. (1975) for a range of burn injuries, including fatality, and of Mixter (1954) for second-degree bums (Figure 4.11). Eisenberg et al. (1975) develop a probit model to estimate fatality levels for a given thermal dose from pool and flash fires, based on nuclear explosion data. 

The use of a fixed thermal exposure criteria, restilting in a fixed injury or fatality level, without accounting for duration of exposure is a simplified approach. This allows the consequence models to be used to predict a standard thermal exposure level, without reference to the specific details of each incident in terms of duration. The fixed criteria may be based on an implicit exposure time. The LNG Federal Safety Standards (Department of Transportation, 1980) use a fixed criteria of 5 kW/m for defining limiting thermal flux levels for people. 

A certain pesticide is fatal to fish fingerlings at a level of 0.50 parts per million in water. A leaking metal can containing 5.00 kg of the pesticide was dumped into a stream with a flow of 10.0 L/s moving at 1 km/h. The container leaks pesticide at a constant rate of 5 mg/s. For what distance (in km) downstream is the water contaminated by fatal levels of the pesticide by the time the container is empty ... 

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