Toxicology - Chemical Effects on Humans, Animals, Plants, and the Environment - Case Study Example

Name Institution Professor Course Date Toxicology Toxicology involves studying the chemical effects on humans, animals, plants and the environment. It delves into the symptoms, treatment, cause, moderation and operation of the chemical in living organisms. Minamata poisoning tragedy in japan The coastal village of japan, Minamata, mainly relied on fish as a protein. Fish was a major source of food and employment in the town. An acetaldehyde manufacturing company was established in 1932 by Chisso cooperation. By the end of theSecond World War the production of acetaldehyde intensified. The company became a fundamental part of the community as it provided employment. The tragedy struck when mercury from the production process started to spill on the bay. The fish consequently ingested the mercury and died. Those that survived caused the poisoning of the villagers leading to an epidemic named the Minamata disease. Minamata disease is caused by the long term ingestion of shellfish and fish containing methyl mercury chloride. Methyl mercury is the worst from of mercury toxic (Newman, C. M, 2011). It occurs due to interactions between mercury and bacteria. Fish only hold a small amount of the toxic due to its low fat content. As the villagers continued to ingest the poisonous fish however, the toxin accumulated in their fat tissues. The half life of the mercury in the body increased by more than 200 days due to the fact that urination; breast feeding and excretion were the only methods of eliminating the toxin. Methyl mercury affects vital organs of the body such as the brain, liver and kidneys. It also affects fetuses in the womb making them be delivered with many anomalies. Around 1043 people were killed by Minamata disease (Newman, C. M, 2011). The death was mainly caused by the brain damage caused by mercury. Mental retardation, loss of balance, salivation and slobbering were the symptoms of disaster in this village. The government and the Chisso Corporation (which stopped the production of acetaldehyde) continue to compensate the victims of this disaster. Antimony in America Antimony is a metalloid salt chemical element. Antimony is a stable but toxic element that reacts with air to produce antimony trioxide. Antimony trioxide is one of the most commercial agents of antimony. This is because of its many industrial uses including flame retardant agent. It prevents the burning of leather, textiles, coatings and polymers. In 2008, laws allowing the use of flame retardant agents were passed. Antimony trioxide was used to manufacture items like pillows, cushions and mattresses. All these items are basic needs for people. They are used in motels, homes and dormitories. This ensures slow inhalation of the toxin into the human system. Within a few months people started complaining of being affected by the newly produced flame retardant items. The media and scientist spoke up on the slow poisoning by antimony trioxide (Newman, C. M, 2011). Employees of the mattress and pillow manufacturing companies complained of increased health problems since their contact with antimony trioxide. Headaches, skin irritation and body rash, fatigue, sore throats, bronchitis, nose bleeding and coughing were some of the complains by manufacturing employees and users of the new products. Scientist and doctors confirmed finding traces of antimony in bodies of patients. Fire men dress in gears made of antimony trioxide and often suffer antimony poisoning. The use of antimony in manufacturing day to day basic items may therefore be a mistake. The disadvantage of poisoning exceeds the benefit of flame retardant element. Skin cancer, pulmonary injury and heart arrhythmias are the major symptoms of antimony poisoning. Continuous inhalation could have led to the poisoning of a nation. Petrol sniffing in rural Australian indigenous communities Petrol sniffing occurs in the Australian rural areas of Northern Territory, Western Australia, northern parts of Queen’s land and South Australia. Young people between the ages of seven and thirty five are the main petrol sniffers. Most of the sniffers do it leisurely to obtain its short term effect (Mccoy, B. F, 2008). It is used as a form of drug or intoxicant like alcohol, cigarettes or drugs. The short term effects include: a light feeling, excitement, euphoria, dizziness and numbness. Petrol sniffing is mainly used because its effect wears out in a short period of around 30 minutes. However, some effects that persist after the wearing out of short term effects include: coughing and sneezing, hallucinations, nausea, and shortness of breath, loss of motor coordination, giddiness, indigestion, muscle weakness and slurred speech (Mccoy, B. F, 2008). Long term sniffing of petrol carries more acute effects than short term use. Petrol carries volatile effects which often dissolve into the tissue. Petrol sniffing affects the respiratory system, the circulatory system, the brain, spinal cord, bone marrow and pregnancy. Permanent brain cell damage, brain hemorrhage, seizures and depression are some of the effects on the brain. Miscarriage, birth defects, and low birth weight are risks faced by pregnant mothers. Irregularities in blood pressure and heart beat, and blood abnormalities are potential damages to the circulatory system. Increased infections due to lower white and red blood cells hence depressed immune response system. A reduction of oxygen in the lung, and lung infections could lead to unconsciousness or a coma (Mccoy, B. F, 2008). Sniffing petrol has existed in rural Australia since the end of the Second World War, and continues to affect the health of long term users. Physiological impact of acute and chronic poisoning with benzene Benzene is a sweet smelling petroleum based clear liquid. Inhalation is the main venue through which poisoning occurs. Touching is also a way to get poisoned. However the rate of dermal absorption for benzene is low. Loss of consciousness, delirium, dizziness, drowsiness, respiratory difficulty and death are the main results of acute benzene poisoning (Rom, W. N., & Markowitz, S, 2007). Due to its carcinogen tendencies, benzene has chronic poisoning. Anemia and leukemia consist of the major benzene chronic poisoning. The absorption of benzene into the body is quite high when inhaled. However the rate of absorption decreases after one hour of absorption. Better absorption is witnessed if benzene is dissolved in water. Benzene poisons the body by corrupting its most central part. Cells are an integral part of the body. Therefore benzene enters the cell and prevents it from working correctly. This is the reason it is classified under carcinogens. Carcinogens cause an abnormal growth of the cells. Invasion of the bone marrow for example prevents the production of adequate red blood cells which causes anemia. The production of white blood cells is also affected hence affecting the immune system. The extent of damage caused by benzene depends on factors like the length of inhaling, age, ingestion, and the subject’s medical condition (Rom, W. N., & Markowitz, S, 2007). The major organs affected by benzene on long term basis are blood forming organs. The reproduction system of women inhaling benzene is also affected. Shrunk ovaries and irregular menstrual period characterize this effect. The effect of benzene on fetuses however is unknown. Botulism food poisoning Botulism is caused by Clostridium botulinum bacteria. Clostridium botulinum exists in naturally in soil, water, plants and intestinal tracts of animals and fish. It is an anaerobic bacterium hence does not cause much destruction. It can exist for many days without causing any harm. The resistance to heat and chemicals is quite high for the spores formed by the bacterium (Mukherjee, A, 2006). There are conditions under which clostridium botulinum spores produce the botulinum toxin. These include: 4.5 to 49 degrees Celsius temperatures, low levels of acid and oxygen absence. The toxin is as a result of botulinum growth producing vegetative cells. Canned food stuffs provide an environment for the growth of the spore due to lack of air. Underground vegetables like potatoes and carrots carry high levels of botulism on their surfaces hence peeling reduces it (Mukherjee, A, 2006). Tightly wrapped and vacuum packaged substances have high risks of botulinfood poisoning. Food prepared through sealing in plastics and poaching also risks botulism poisoning. Storage methods that eliminate air in the package risk botulism poisoning. The functioning of neurotransmitters is disrupted by botulism toxin. This leads to paralysis of the victim within three to four days. It spreads from the top starting with face throat and chest. Infants can also get food poisoning from home canned fruits and vegetables, honey or corn syrup. Most victims of the poisoning are unable to recover fully due to side effects that persist. Dizziness, fatigue, dry mouth, weakness and inability to perform strenuous activities constitute the long term effects of botulism poisoning. Improperly home canned foods are the main risk of botulism poisoning. The poisoning rarely occurs in commercially packed food (Mukherjee, A, 2006). Organochlorides in Australia Organochlorides are a combination of carbon and chlorine. They were mainly used as pesticides in most countries including Australia especially after the Second World War. After the establishment of the national residue survey in 1961 in Australia, OCs came under scrutiny (Gerozisis, J., Hadlington, P. W., & Staunton, I, 2008). Their external application on food producing animals was banned shortly after this. OCs had a tendency to be very stable. Hence they remained in the soil longer than required. Their resistance to physical, chemical, and biological degradation allows them to remain active for years. OCS was therefore able to accumulate in soil and hence plats. Humans and animals that ingested these plants were also at risk of getting OC accumulation. The toxicity of OCs was mainly quite high in aquatic life. The accumulation in aquatic life led to poisoning of in the food chains. This is because fish eating predators like birds and humans risked accumulating higher levels of OCs in their fatty tissues. The OC residue in soil and food products caused the government to ban its use due to the potential health risk as well as environmental concerns (Gerozisis, J., Hadlington, P. W., & Staunton, I, 2008). Farmers also aided in the abolition of OC use due to the notion that products with OC residue were less acceptable in the market. Decade’s later OC residue still lingers in Australian agricultural soil. It becomes difficult to imagine the adverse effects that could have resulted in long term use of OCs. Laboratory animal studies show that Organochlorides affect immune and endocrine systems, development, and reproduction and promote cancer. The ministry of environment continues to monitor the levels of OCs in the soil and diet of Australia. References De, A. K., & Kumar De, A. (2005). Environmental studies (for B.A., B. Sc. and B.Com students). New Delhi, New Age International (P) Ltd., Publishers. http://site.ebrary.com/id/10318652. Gerozisis, J., Hadlington, P. W., & Staunton, I. (2008). Urban pest management in Australia. Sydney, N.S.W., University of New South Wales Press Ltd. Newman, C. M. (2011). Mercury pollution: A Transdisciplinary Treatment. CRC Press. Mccoy, B. F. (2008). Holding men: kanyirninpa and the health of Aboriginal men. Canberra, ACT, Aboriginal Studies Press. Rom, W. N., & Markowitz, S. (2007). Environmental and occupational medicine. Philadelphia, Wolters Kluwer/Lippincott Williams & Wilkins. Mukherjee, A. (2006). Food and beverage management. Delhi, Isha Books. Read More