Toxicology Issues - Report Example

Name: Tutor: Title: Toxicology Course: Date: Forensic Testing The use of performance-enhancing substances in the Australian sport setting Drug use in sports, and the procedures of drug testing that have been established as a result, have become a key focus at both amateur and professional levels in the present years (Quinn, 2011). A lot of episodes of illicit use of drugs within sports setting have brought so much attention to this matter, involving both recreational and performance-enhancing drugs. In Australia for instance, the percentage of athletes who have been involved in the illicit performance-enhancing use substances has increased significantly in modern years. The civil governments, International Olympic Community (IOC) and the medical fraternity in Australia regard drugs that enhance performance as dangerous to the athletes’ health, the Games’ integrity and the spectators who adore the athletes. Performance-enhancing drugs can result to lasting adverse effects on health making the performance benefits that are short-term less appealing (Quinn, 2011). Side effects have the scope from minor problems to fatality. Additionally, medical communities have established that performance-enhancing substances can be very addictive psychologically. The illicit performance-enhancing substances include anabolic steroids, amphetamines, caffeine, erythropoietin (EPO), and ephedrine among others. Amphetamines are generally stimulant drugs of the central nervous system (CNS) that enhance self confidence, alertness, decrease appetite, and create an increased energy feeling (Quinn, 2011). Amphetamines like Dexedrine, benzodrine and adderall have a great addiction potential and Australian sports organizations have banned these substances. Anabolic steroids are testosterone male hormone found in the synthetic versions. Any use of these drugs with non-medical intention is illegal and banned in Australian sports organization due to their serious health issues. However, a number of athletes still use them illegally so as to enhance their sports performance. Caffeine is not generally harmful but in high doses, it is banned in sports organization because it improves alertness and enhances endurance. Forensic testing and detection procedures for Amphetamine Drug detection plays a significant role in sports society. They are likely to be analyzed to establish their origins. For instance, in Australia, a Forensic testing and detection procedures can be done for recreational substances like Amphetamine. Forensic testing can entail drug analysis. The detection procedure for recreational drugs like Amphetamine includes taking samples like hair. Analysis of hair offers a unique benefit over other samples like blood and urine because of the fact that a lot of drugs are integrated into the shaft of hair via ingestion and stay in the hair always (American Association for Clinical Chemistry, 2012). Thus, provides the widest window of drug detection. On the other hand, the value of quantitative and qualitative hair evaluation is further weakened due to the ethnicity differences and color of hair in the uptake of particular drugs. These matters are specifically appropriate in enforcement of law, where bias of race could possibly affect the natural justice process in Australia. In the forensic context, hair analysis has been used reliably to establish compliance with regimes of therapeutic drugs or to check the truthfulness of a witness testimonial that an illegal substance has not been used (Lewis, 2001). Hair analysis for recreational substances like Amphetamine is an increasingly universal method of evaluation in misuse of substances, specifically in legal proceedings which is a common practice in sports setting in Australia. Toxic gases and vapours The formation and potential health effects of low level atmospheric ozone Ozone has similar chemical structure (O3) regardless of where it occurs; at the ground level or miles over the earth. At the level of the ground, ozone formation takes place when there is a reaction of specific compounds in direct sunlight presence (Bakker, 2009). VOCs + NOx + Sunlight = Ozone. Volatile organic compounds (VOCs) are broadly used as basic ingredients in products of the household including; wax, disinfectants, cosmetic, varnishes, and paints. Even though some VOCs are considered safe to use and have little effects on health, other VOCs are considered highly toxic. Additionally, VOCs are also found in natural forms since some trees produce VOCs in substantial amounts. Nitrogen oxide gases (NOx) is the generic form of a group of extremely reactive gases, all containing oxygen and nitrogen in amounts that vary (Bakker, 2009). The fundamental sources of NOx are electric utilities, motor vehicles, and other commercial, residential and industrial sources that involve fuel burning. When high levels of NOx and VOCs are present in air, a reaction occurs. A reaction in sunlight presence causes low level atmospheric ozone formation. Other factors for low level ozone formation include low wind speeds, cloud cover, and wind direction. Low level atmospheric ozone has potential effects on health. Since it is close to the level of ground, it causes headaches, coughing, eye and throat irritation, impaired function of the nose, lung and eye. Children and asthmatics are greatly at risk. The probability of experiencing unpleasant health issues from ozone levels that are elevated increases in an event of an outdoor activity or heavy exercise (Bakker, 2009). Low level atmospheric ozone can as well damage plants, trees, and decrease visibility. The pathophysiology of carbon monoxide intoxication Initially, the pathophysiology of poisoning due to Carbon monoxide (CO) was considered to be exclusively as a result of the cellular hypoxia brought about by oxyhemoglobin replacement by CO-Hgb and causing a relative anemia (Kao & Nanagas, 2004). CO greatly binds to hemoglobin with an affinity of 200 times above that of oxygen thus causing a leftward change in the dissociation curve of oxygen-hemoglobin, reducing delivery of oxygen to the tissues and finally causing tissue hypoxia (Kao & Nanagas, 2004). CO also binds to several proteins that are heme-containing apart from hemoglobin, including myoglobin, guanylyl cyclase, and cytochromes. CO binds to myoglobin hence reducing availability of oxygen in the heart leading to cardiac dysfunction and arrhythmias and may also contribute to rhabdomyolysis and direct toxicity of skeletal muscle (Kao & Nanagas, 2004). In an animal setting of poisoning by CO, CO causes stimulation of guanylyl cyclase, which triggers guanylyl cyclase, which enhances cyclic guanosine monophosphate leading to cerebral vasodilation, associated with consciousness loss. According to Kao & Nanagas (2004) levels of carboxyhemoglobin are significant for ascertaining exposure to CO but are not able to be used to determine poisoning severity, predict prognosis, or establish a certain plan of treatment. The key treatment for intoxication of CO is oxygen therapy. Particulates and fibres, tobacco smoke The carcinogenic effects of asbestos fibres on the human body Asbestos is basically not regarded as acutely toxic, as few spontaneous effects are noted subsequent to exposure. High degree inhalation of asbestos exposure that is short-term has been linked with mesothelioma, cancer of the lung and pleural disorders like pleural plaques (Bull, 2007). Effects like these may be identified after a latency period of nearly thirty years. Epidemiology researches have revealed that chronic inhalation of every kind of asbestos fibre is connected with pleural anomalies, asbestosis, lung cancer and mesothelioma (Bull, 2007). Parenchymal asbestosis is acknowledged as the element of great occupational exposure while disorders of the pleural, lung cancer and mesothelioma are mostly associated with lasting to low levels. Even though asbestosis is not malignant, its occurrence enhances the possibility of lung cancer, particularly in smokers. Mesothelioma, an uncommon peritoneum or pleural malignant tumour, is mainly induced by amphibiole asbestos and to some extent by chrysotile. Cancer of the lung may be as a result of chronic inhalation of amosite, anthophyllite, chrysotile, and mixed fibres that have tremolite, crocidolite and actinolite or anthophyllite with tremolite, although it is not known if various fibres vary in the effectiveness (Bull, 2007). For mesothelioma, latency duration of almost thirty years may take place between the first exposure and disease onset. Unlike mesothelioma, lung cancer incidence is linked with smoking since smoking and asbestos act synergistically to impose their carcinogenic effect. Health and legal aspects of the case against James Hardie Industries Ltd, as relating to asbestos product manufacture in Australia Companies within the group of James Hardie were chief participants in manufacturing asbestos products during 1920s, whichwere extensively used in Australia during most part of the past century, specifically in insulation materials and building products (Hargovan, 2009). The company had been accountable for seventy per cent of Australian consumption of asbestos. Asbestos is harmful to health and its fibres can cause lung cancer, mesothelioma and asbestosis, all of which are fatal. Manifestation of these diseases may not be spontaneous. Due to the health injuries caused by asbestos exposure, it is legally important that James Hardie Industries compensated their workers for these harmful exposures. It is very important that directors consult with its members about any intended course of action so that misunderstanding and misconceptions do not come up. This is seen in the case where James Hardie’s director did not consult with the organization about the financial state of the company in order to approve the compensation foundation for future asbestos claims and this is why the company got itself in a legal case. The Australian Securities and Investments Commission (ASIC) claimed that a draft announcement regarding the Compensation Foundation formation was endorsed by the panel (Hargovan, 2009). The public also received this announcement. It claimed that the announcement of the draft asserted that the Foundation would possibly begin operations with significant resources and there would be enough funds to fulfill every Asbestos Claims in the future. ASIC claimed that those reports were not correct and that they were misleading. This is why the case of James Hardie demonstrates that courts are ready to find managers accountable for violating the duty of diligence and care if they do not examine the financial state of their organization or a specific decision or action course which the organization is about to execute (Hargovan, 2009). The directors at James Hardie should have examined the matter on which their decision was made to form the Foundation and their postulation that it had enough resources to cover Asbestos Claims in future. The case thus reminds directors to be very careful in public disclosures process; the information being disclosed must be correct. Bibliography Hargovan, A, 2009, Australian Securities and Investments, Commission v MacDonald (No 11), Corporate Governance Lessons From James Hardie, Melbourne University Law Review, Vol. 33, pp 985-995. Bull, S, 2007, Asbestos, Toxicological overview, Retrieved on 21, September 2012, from http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1202487029823 Kao, L & Nanagas, K, 2004, Carbon monoxide poisoning, Emergency Medicine Clinics of North America, Vol. 22, pp 985-1018. American Association for Clinical Chemistry, 2012, The World of Forensic Laboratory Testing, Retrieved on 21 September, 2012, from https://labtestsonline.org/understanding/features/forensics/start/2 Lewis, J, 2001, Drug Detection and its Role in Law Enforcement, Australian Institute of Criminology, Retrieved on 21 September, 2012, from http://faculty.ksu.edu.sa/18856/454/Drug%20Detection%20and%20its%20Role%20in%20Law%20Enforcement.pdf Quinn, E, 2011, Performance Enhancing Drugs in Sports, Retrieved on 21 September, 2012, from http://sportsmedicine.about.com/od/performanceenhancingdrugs/a/ErgogenicAids.htm Bakker, S. H, 2009, Ozone depletion, chemistry, and impacts, Hauppauge, N.Y., Nova Science Publishers. Read More