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Exposure chemical, fatal

Measures of Response for Substances Causing Deterministic Responses. For purposes of health protection in routine exposure situations, incidence has been the primary measure of deterministic response for both radionuclides and hazardous chemicals. Fatalities also are of concern for substances that cause deterministic responses, but only at doses substantially above the thresholds for nonfatal responses. Given that the objective of standards for health protection is to prevent the occurrence of deterministic responses, incidence is not modified by any subjective factors that take into account, for example, the relative severity of different nonfatal responses with respect to a diminished quality of life. Judgments about the importance of deterministic responses are applied only in deciding which responses are sufficiently adverse to warrant consideration in setting protection standards. [Pg.259]

In some cases, hypersensitivity is an induced response to exposure to a substance. After one or more doses of a chemical, a subject may develop an extreme reaction to it. This occurs with penicillin, for example, in cases where people develop such a severe allergic response to Ihe antibiotic that exposure is fatal if countermeasures are not taken. [Pg.735]

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 ... [Pg.2277]

The chemical process industry is vast and varied. The value of chemicals and chemical products in 1993 was 0.5 trillion for the Ll.S," involving 67,000 chemical engineers, 98,000 chemists. There were 5.5 non-fatal occupational injuries per 100 employees in 1995 involving chemical and allied products, and 4.8 per 100 workers in petroleum and coal products, There were 101 fatalities due to exposure to caustic, noxious or allergenic substances and 208 deaths from fires and explosions in 1995. [Pg.262]

There me two major types of risk ina. imuin individual risk and population risk. Maximum risk is defined e.xacUy as it implies, Uiat is the ma.ximum risk to an individual person. Tliis person is considered to have a 70-year lifetime of exposure to a process or a chemical. Population risk is Uie risk to a population. It is expressed as a certain number of deaths per Uiousand or per million people. For example, a fatal annual risk of 2 x 10 refers to 2 deatlis per year for every million individuals. These risks are based on very conser ative assumptions, llich may yield too high a risk. [Pg.295]

The reader should note tliat since many risk assessments have been conducted on the basis of fatal effects, there are also uncertainties on precisely what constitutes a fatal dose of thennal radiation, blast effect, or a toxic chemical. Where it is desired to estimate injuries as well as fatalities, tlie consequence calculation can be repeated using lower intensities of exposure leading to injury rather titan dcatli. In addition, if the adverse healtli effect (e.g. associated with a chemical release) is delayed, the cause may not be obvious. Tliis applies to both chronic and acute emissions and exposures. [Pg.525]

The most important potential complication of phenol-based peels is cardiotoxicity. Phenol is directly toxic to myocardium. Studies in rats have shown a decrease in myocardial contraction and in electrical activity following systemic exposure to phenol [i6]. Since fatal doses ranged widely in these studies, it seems that individual sensitivity of myocardium to this chemical exists. In humans neither sex/age nor previous cardiac history/blood phenol levels are accurate predictors for cardiac arrhythmia susceptibility [17]. [Pg.85]

When organizations focus on the root causes of worker injuries, it is helpful to analyze the manner in which workplace fatalities occur (see Figure 1-4). Although the emphasis of this book is the prevention of chemical-related accidents, the data in Figure 1-4 show that safety programs need to include training to prevent injuries resulting from transportation, assaults, mechanical and chemical exposures, and fires and explosions. [Pg.12]

Dermal (skin) contact with sulfur mustard agents causes erythema and lesions (blistering), while contact with vapor may result in first and second degree burns contact with liquid typically produces second and third degree chemical burns. Any burn area covering 25 percent or more of the body surface area may be fatal. Respiratory contact is a dose-related factor in the sense that inflammatory reactions in the upper and lower airway begin to develop several hours after exposure and progress over several days. [Pg.242]

In retrospect, I was stunned by my failure to act appropriately in the moment. Bart of the reason was because I had lost sight of the fact that chemical reactions can be fatal, and because Carolyn s reaction was, for the most part, invisible. I also did not understand how dependent she was on her attendants in these kinds of situations. However, another major factor was that I d been exposed to the smell of fragrances, dryer sheets and cleaning products that morning in the bed and breakfast where I was staying. My exposure had been brief and I thought I was recovered, but in fact my thinking and reactions were still considerably dulled. This was a wake-up call. [Pg.128]

Chemotherapy used to treat cancer is toxic by almost anyone s standards. How would it affect someone like Peggy, who experiences life-threatening reactions to even low-level chemical exposures There are no answers. Peggy believes chemotherapy or surgery could be fatal for her, because her lungs burn and airways can close even from exposure to fragrances and other ordinary products. She has chosen to treat her cancer with a non-chemical, non-invasive alternative program, and her trust in God. [Pg.158]

Carmichael WW, Azevedo SFMO, An JS, Molica RJR, Jochimsen EM, Lau S, Rinehart KL, Shaw GR, Eaglesham GK (2001) Human fatalities from cyanobacteria chemical and biological evidence for cyanotoxins. Environ Health Persp 109 663-668 Codd GA, Bell SG, Kaya K, Ward CJ, Beattie KA, Metcalf JS (1999) Cyanobacterial toxins, exposure routes and human health. Eur J Phycol 34 405 115 Cronin G, Hay M (1996) Induction of seaweed chemical defenses by amphipod grazing. Ecology 77 2287-2301... [Pg.116]


See other pages where Exposure chemical, fatal is mentioned: [Pg.52]    [Pg.782]    [Pg.123]    [Pg.88]    [Pg.468]    [Pg.72]    [Pg.875]    [Pg.53]    [Pg.69]    [Pg.240]    [Pg.246]    [Pg.351]    [Pg.352]    [Pg.397]    [Pg.398]    [Pg.240]    [Pg.248]    [Pg.252]    [Pg.287]    [Pg.332]    [Pg.341]    [Pg.68]    [Pg.347]    [Pg.1193]    [Pg.63]    [Pg.163]    [Pg.234]    [Pg.241]    [Pg.258]    [Pg.270]    [Pg.278]    [Pg.165]    [Pg.71]    [Pg.85]   


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