Toxic exposures and

Policymakers can read stories of real people who face this risk of marginalization due to the brutal effects of everyday toxicant exposures, and take the experience of these people into their policymaking. Famous Love Canal environmentalist Lois Gibbs says Pollution begins in the boardroom. ... 

Phillips LJ. 1992a. A comparison of human toxics exposure and environmental contamination by census division. Arch Environ Contam Toxicol 22(1) 1-5. 

From a purely pragmatic perspective, it is clear that reactive metabolites are linked with toxicity and that a circumstantial link can be made to idiosyncratic toxicides. Consequently, even though the mechanism of this toxicity is not fully understood, since assays are available to measure the potential for bioactivation in an ideal world one would not carry this liability forward. Conversely, it is not an ideal world, all drug molecules have challenges and the definition of therapeutic index (i.e., the ratio between the toxic exposure and the therapeutic exposure) is critical. Covalent binding of reactive metabolites to macromolecules is a crude measure and not a full predictor of toxicity and it is well known that toxicity can be ameliorated by a lower dose. Furthermore, the so-called definitive assays require radiolabeled drug material which is expensive and generally slow to produce. 

Nelson EDP, Shikiya D, Liu CS. 1987. Multiple air toxics exposure and risk assessment in the South Coast Air Basin. Proceedings of the APCA Annual Meeting 89 87/97.4. 

There was little Indication of cumulative toxicity. Exposures and mortality are In Table 4-32. 

Ryan, R.P. and Terry, C.E., Eds., Toxicology Desk Reference The Toxic Exposure and Medical Monitoring Index, 5th CD-ROM ed., Hemisphere Publishing Co., Washington, D.C., 1999. 

Subjects tested with anticholinesterases, anticholinergics, cholinesterase reactivators, or psychochemicals did not differ significantly from NGT or OCT subjects in their replies to questions about current health status. Almost 90% of all respondents reported no health problems related to toxic exposures, and 79% reported good to excellent health. (Subjects tested with LSD were not within the purview of this investigation, inasmuch as they had been evaluated and reported on earlier by a different group, which used other methods. 

Parameters used to measure toxicity of cultured cells can be general properties related to loss of vital functions or impairment of cell-type-specific functions. These indicators can be further classified as those occurring shortly after toxicant exposure and those requiring prolonged culture for expression. 

Rockett JC, Burczynski ME, Fornace AJ, et al. Surrogate tissue analysis Monitoring toxicant exposure and health status of inaccessible tissues through the analysis of accessible tissues and cells. Toxicol Appl Pharmacol. 2004 194(2) 189-199. 

Poisoning emergencies are a common occurrence. In 2002, The Toxic Exposure Surveillance System of the American Association of Poison Control Centers reported 2 380028 toxic exposures and 1153 resultant fatalities. Of these total exposures, 548 093 (22.2%) were managed in a healthcare facility and 72 877 were admitted to a critical care unit (3.1%). The mortality rate associated with these overdose patients was less than 1%. Thorough evaluation, adequate supportive care, and the use of a few specific antidotes have resulted in lowered morbidity and mortality if the poisoned patient arrives at the hospital in time for the healthcare team to intervene. In select cases, decreasing further toxin absorption by various decontamination procedures may be of benefit. 

Size and complexity of the dietary supplement market are only a few of a number of difficulties that public health officials face when dealing with poisoning episodes. In North America alone, at least 700 plant species have been described as being poisonous in one way or another, and plant poisonings are often difficult to differentiate from environmental intoxications caused by pesticides and industrial chemicals and from adverse reactions to synthetic drugs (Der Marderosian and Liberti, 1988). Complicating the picture is the fact that symptoms of many intoxications mimic those of medical conditions not associated with a toxic exposure, and that establishing causality may therefore be difficult (Perrotta et al., 1996). 

With the evolution and development of mankind and modem society, different man-made substances (anthropogenics or xenobiotics) have been added to the toxic panorama. Furthermore, many substances or products (e.g. metals) have been collected and concentrated for medical or industrial purposes and then redistributed in a manner that, today, is causing toxic exposure and harm to the biosphere. These processes have been accelerating during the last three centuries and millions of tons of xenobiotics have been distributed in the environment. 

Lebovits AH, Chahinian P, Holland JC Exposure to asbestos psychological responses of mesothelioma patients. Am J Ind Med 4 459 66,1983 Lees-Haley PR Malingering emotional distress on the SCL-90-R toxic exposure and cancerphobia. Psychol Rep 65 1203-1208,1989a Lees-Haley PR Malingering post-traumatic stress disorder on the MMPI. Forensic Reports 2 89-91, 1989b... 

Lees-Haley PR Malingering traumatic mental disorder on the Beck Depression Inventory cancerphobia and toxic exposure. Psychol Rep 65 623-626,1989c Lees-Haley PR Malingering mental disorder on the Impact of Event Scale (IES) toxic exposure and cancerphobia. J Trauma Stress 3 315-321, 1990 Lees-Haley PR, Brown RS Biases in perception and reporting following a perceived toxic exposure. Percept Mot Skills 75 531-544, 1992 LeQuesne PM, Axford AT, McKerrow CB, et al Neurological complications after a single severe exposure to toluene di-isocyanate. British Journal of Industrial Medicine 33 72-78, 1976... 

Landrigan PJ Toxic exposures and psychiatric disease an epidemiologic approach, in Proceedings of the Third World Congress of Biological Psychiatry, June 28 to July 3, 1981, Stockholm, Sweden. Edited by Perris C, Strawe G, Jansson B. Amsterdam, Elsevier/North-Holland Biomedical Press, 1981, pp 108-113... 

Landrigan PJ Toxic exposures and psychiatric disease—lessons from the epidemiology of cancer. Acta Psychiatr Scand Suppl 303 6-15, 1983... 

The adaptive value of hormesis is seen in numerous observations demonstrating that the prior low dose stress response in the so-called hormetic response range also acts as a form of preconditioning that elicits protection against toxicity threats from subsequent toxic exposures. In this sense, the low dose hormetic response would confer a selective advantage to organisms that experienced an initial modest toxic exposure and in situations where the modest toxic exposure was followed by the more massive one a situation that would be expected to occur in both nature and evolutionary history. It is important to emphasize that a characterization of the prior low-dose response (i.e., adaptation) tends to reveal an inverted U-shaped dose response, similar to the hormetic dose response. 

Several steps have been taken to reduce the toxic exposure and likelihood of accidents. In many applications AsHj can be replaced by tertiarybutyl arsine (TBA) as evidenced by Motorla, TI and Fuji production facilities. The cost of TBA can, however, be prohibitive and carbon incorporation in the films can be an issue for several devices. Other alternatives include on-site production of arsine and other precursors. These methods are promising, although they also are presently expensive and purity often is a concern. 

After a toxic inhalational exposure, exercise may further compromise the patient. Hypoxia is a primary factor. Oxygen supplementation is necessary at rest and especially during exercise. Exercise may aggravate the effects of toxicant exposure and should be limited or restricted if possible. 

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