Occupational acute injuries

An acute injury arising out of, and in the comse of, employment resulting from exposure to traumatizing physical or chemical agents in the workplace. Examples include amputations, fractures, eye loss, lacerations, and traumatic deaths. The Occupational Safety and Health Administration (OSHA) states that the industries with the highest risk for occupational injuries include construction, mining, manufacturing, and wholesale. Occupational Injury and Illness Classification System (OIICS)... 

Work accident represents body injury and occupational acute poisoning that occur during the process of doing the work or service and which causes temporary inability to work for at least three days, disability or death ... 

Occupational illness Any abnormal condition or disorder, other than one resulting from an occupational injury, caused by exposure to environmental factors associated with employment. It includes acute and chronic illnesses or diseases that may be caused by inhalation, absorption, ingestion, or direct contact. 

Other factors. A number of additional factors may alter the predicted response of the patient to a drug. As discussed earlier, environmental and occupational hazards may produce certain toxins that alter drug absorption and metabolism. 9 62 Factors such as cigarette smoking and alcohol consumption have been shown to influence the metabolism of specific compounds.39,49 Drug distribution and metabolism may be altered in the obese patient,6 or in response to chronic and acute exercise.7,43 Individuals with spinal cord injuries have a decreased ability to absorb cer-... 

Toxicity Any acute exposure to vapors of 1,1,1-trichloroethane leads to irritation of the nose, throat, and eyes, and results in headaches. Exposure to high concentrations or vapors of 1,1,1-trichloroethane is known to cause damage to the CNS, leading to behavioral disorders, dizzy spells, sleepiness, and, in some cases, coma reversible injuries to the liver and kidneys also have been observed. Overexposure of 1,1,1-trichloroethane in occupational/work environments causes headache, CNS depression, irritation to eyes, dermatitis, and cardiac arrhythmias. Effects of repeated or long-term exposure to the solvent causes visual problems, loss of coordination, reduction of the tactile sensitivity of the skin, trembling, giddiness, anxiety, and slowing of the pulse rate. 

Studies of occupational exposures to sulfur mustard indicate an elevated risk of respiratory tract and skin tumors following long-term exposure to acutely toxic concentrations. Overall, several factors are important regarding the assessment of the carcinogenicity of sulfur mustard. Increased cancer incidence in humans appears to be associated only with exposures that caused severe acute effects, and occupational exposures tended to involve repeated exposures and repeated injury of the same tissues. Because the therapeutic use of the sulfur mustard analog nitrogen mustard is associated with an increased incidence of CML, the reports of CML in HD-exposed individuals appear to be relevant to the eareinogenicity of sulfur mustard. 

Environmental/ industrial exposure to heavy metals, light hydrocarbons, pesticides and sdicon-containing compounds all have heen associated with the development and/or progression of renal failure. Exposure to heavy metals, more particularly lead, cadmium and mercury has heen linked with the development of acute or chronic renal failure. The current hterature also contains a growing hody of information linking solvent exposure wifh renal injury. To what extent exposure to environmental/ occupational... 

Historically, injuries and fatalities have been reported from acute methanol overexposure via ingestion, inhalation, as well as prolonged or repeated skin contact. Inhalation toxicity can occur in occupational settings or as a result of inhalant abuse (huffing). Clinical studies of individuals acutely poisoned by methanol ingestion have identified visual disturbances and possibly blindness as the most notable toxic effects in humans. Methanol is also a CNS depressant, although less potent than ethanol, and has also been shown to produce liver damage upon overexposure. 

In studies of human occupational exposures, it appears that the respiratory tract is the primary site of injury after inhalation of selenium dust or selenium compounds, but gastrointestinal (possibly due to swallowed selenium) and cardiovascular effects, as well as irritation of the skin and eyes, also occur. Little of the available information for humans, however, relates health effects exclusively to measured concentrations of the selenium dust or compounds because of the possibility of concurrent exposures to multiple substances in the workplace. In animals, the respiratory tract is also the primary site of injury following inhalation exposure to selenium dust and hydrogen selenide. Hematological and hepatic effects have also been noted in animals. Inhalation data from laboratory animal studies are available only for acute exposures. 

Other hepatic responses that can be occupationally related include steatosis, cholestatic injury, hepatoportal sclerosis, and hepatic porphyria. The acute care provider should always consider a toxic chemical etiology in the differential diagnosis of liver disease. 

Gehring U, Heinrich J, Kramer U et al (2006) Long-term exposure to ambient air pollution and cardiopulmonary mortality in women. Epidemiology 17 545-551 Ohio AJ, Devlin RB (2001) Inflammatory lung injury after bronchial instillation of air pollution particles. Am J Respir Crit Care Med 164 704-708 Gielen MH, vanderZee SC, Vanwijnen JH et al (1997) Acute effects of summer air pollution on respiratory health of asthmatic children. Am J Respir Crit Care Med 155 2105-2108 Godleski JJ (2006) Responses of the heart to ambient particle inhalation. Clin Occup Environ Med 5 849-864... 

The hallmark of an inflammatory response in the lung is the presence of infiltrating leukocytes. This process can occur in the context of a variety of disorders, including trauma, infection, autoimmune diseases, idiopathic interstitial pneumonias, asthma, chronic bronchitis, acute respiratory distress syndrome (ARDS), exposure to environmental/occupational noxious agents, cancer, aUograft rejection, and ischemia-reperfusion injury. The course of inflammation in these disease states is defined by the delicate balance and nature of inflammatory mediators expressed in the context of lung inflammation, and the specific leukocyte populations recmited in response to lung injury. 

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