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Death fatal

Propoxyphene products in excessive doses, either alone or in combination with other CNS depressants (including alcohol), are a major cause of drug-related deaths. Fatalities within the first hour of overdosage are not uncommon. In a survey... [Pg.840]

Blindness, 16% mortality Fatal in 2 months Chronic toxicity No deaths Fatal... [Pg.310]

Human African trypanosomiasis (African sleeping sickness) around 60 million people at risk In sub-Saharan Africa, resulting annually in around 500,000 cases and 50,000 deaths. Fatal if not treated. Most drugs are old and difficult to administer. Until recently the only treatment available for the second-stage of the disease was Melarsoprol, an arsenic-based drug that kills 5 per cent of patients. [Pg.112]

Steffee CH, Davis GJ, Nicol KK. A whiff of death Fatal volatile solvent inhalation abuse. South Med J1996 89(9) 879-84. [Pg.491]

Year Total ADR reports Total deaths Fatal reaction as a percentage of total ADR reports... [Pg.430]

Wright, C. (1986). Routine deaths Fatal accidents in the oil industry. Sociological Review, 4,265-289. [Pg.54]

Death Fatal cardiac arrest following bladder catheterization for urinary retention after spinal anesthesia has been reported [42 ]. [Pg.286]

Major Industry Number of Deaths Fatal Rate... [Pg.109]

ERCP Complications Incidence (%) Deaths Fatality rate (%)... [Pg.354]

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. [Pg.318]

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. [Pg.470]

Balantidiasis in humans is manifest by chronic episodes of intermittent diarrhea and constipation, symptoms similar to those of amebiasis. The patient may also have abdominal pain, tenderness over the colon, anorexia, nausea, severe weight loss, and weakness. The disease may be fatal and, before the avakabihty of a treatment, was the cause of death in approximately 30% of infected individuals. [Pg.264]

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. [Pg.484]

If the probability of worker injury or death because of participation in a given work-related activity can be shown to be much less than the risk of injury or death associated with presently accepted activities under very similar circumstances (e.g., the same type of hazard), then you may feel more comfortable about accepting the status quo. Table 14 illustrates the types of public mortality data available for such comparisons. In the previous example, where the worker risk was calculated as 2 X 10 fatalities... [Pg.53]

Average rate of death The average number of fatalities that might be expected per (ROD) unit time from all possible incidents... [Pg.75]

Records show that more fatalities occur through victims being suffocated by smoke or poisoned by toxic gases emitted during a fire than by being burnt to death. This is particularly worrying when it is realised that many additives incorporated into a polymer to retard its flammability are often found to increase the amount of smoke emitted as the rate of flame propagation decreases. Most... [Pg.108]

Equation 1,4-7 is unsatisfactory because the risk from a large number of small accidents is the same as from a small number of large accidents if the total number of effects, say fatalities, is the same for each case. It is hypothesized that the perceived risk of a large accident is greater than the equivalent risk from many small accidents because of human nature and the emphasis of the news services on the unusual (50,OCX) traffic deaths per year is not newsworthy, but a single accident killing 50,000 is very newsworthy). [Pg.7]


See other pages where Death fatal is mentioned: [Pg.255]    [Pg.275]    [Pg.413]    [Pg.255]    [Pg.275]    [Pg.413]    [Pg.551]    [Pg.479]    [Pg.39]    [Pg.12]    [Pg.232]    [Pg.357]    [Pg.113]    [Pg.147]    [Pg.259]    [Pg.277]    [Pg.398]    [Pg.427]    [Pg.2338]    [Pg.2]    [Pg.109]    [Pg.112]    [Pg.798]    [Pg.875]    [Pg.5]    [Pg.9]    [Pg.80]    [Pg.245]    [Pg.246]    [Pg.6]    [Pg.456]    [Pg.464]    [Pg.917]   


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