Acrylamide is a substance that has the molecular formula of C3H5NO. The chemical acrylamide also is designated as prop- 2- amide. Acrylamide is a crystalline odorless white substrate that is soluble in chloroform, ether, ethanol and water. Acrylamide becomes decomposed in the presence of iron salts, iron, oxidizing agents, bases and acids. Acrylamide deconstructs into ammonia, carbon monoxide and nitrous oxides (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
Acrylamide is a chemical substance that is applied in specific manufacturing processes. These manufacturing processes include the treatment of wastewater, purification of drinking water, production of paper, plastics and dyes. Acrylamide is encountered in minute amounts in products that are consumed by the general public. These products include adhesive, food packaging and residential caulking. Cigarette smoke contains acrylamide. The formation of acrylamide takes place in specific starchy foods that include the processes of elevated temperature food preparation. In the processes of roasting, frying, and baking, acrylamide is formed. Acrylamide is created from amino acids and sugars that are contained in food. The acrylamide does not originate in the food packaging (Lawley et al. 340).
There has been research on several substances in order to determine if these substances cause cancer. Research that has been performed has determined that acrylamide is a human cancer causing agent. It is important that the levels of acrylamide that are found in food be placed under stringent regulation. In the United States, a government agency that is detailed as the FDA provides regulation with regards to the amount of acrylamide that can be left as a residual that are placed into contact with food. . There are presently no regulations that are applied to the amount of Acrylamide that is normally present in food system (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7). .
The drinking water in the United States is regulated by the EPA. The EPA established a specific level of safe acrylamide exposure. The amount of acrylamide that is deemed acceptable by the EPA is the amount that is below the threshold of being considered a cancer causing agent. The amount is much less than the amount that is able to affect the nervous system (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
Research has demonstrated that the presence of acrylamide in food is a major concern. There is a need for more research on the formation of acrylamide in food and the levels of toxicity that is present. It is advisable that the members of the public continue consuming diets that are rich and balanced in vegetables and fruits. It has been determined by clinical studies that the food should not be excessively cooked. It is important to thoroughly cook food, especially meat and meat products. This cooking process must be done in order to eradicate the presence of pathogens that include viruses and bacteria. Researchers experimented with investigating the level of acrylamide that is present in a number of oven- baked and fried foods. The formation of acrylamide in food has been discovered with elevated temperature cooking processes in food that are rich in carbohydrates (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
The acrylamide compound is formed from substituting organic acid radicals in place of one or more of the h hydrogen atoms that is possessed by the ammonia ( NH3) molecule. In the event that one of the hydrogen atoms that are possessed by the ammonia molecules becomes supplanted by an acid radical, the outcome is deemed a primary amide. In the event that two of the acid radical atoms are presented to ammonia. There is a secondary amide that is acquired. In the event that all there hydrogen atoms in the ammonia molecule are supplanted by acid radicals, the result is the formation of a tertiary amide. The correlation of the three subcat5egories of the amides with regards to ammonia is demonstrated by the following relationship: NH3, NH2COCH3, NH (COCH3)2, N (COCH3)3 (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
The amides can be categorized into their aromatic and fatty categories. This categorization takes place in reference to the acid radical molecules that are derived from aromatic or fatty acids. Consequently, the amide that is derived from acetic acid is a fatty category of amide. The benz amide that originates from benzoic acid is an aromatic amide (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
The main amides are more abundant and significant that the secondary or the tertiary amides. It is demonstrated that the amides are composed of two components, one of the components is the ammonia molecule and the other is an acid radical. . There have been a variety of amides that have been created by supplanting the hydrogen of the ammonia molecule (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
Acrylamide was discovered in foods over twelve years ago by researchers in Sweden. The chemical acrylamide was encountered in foods that were rich in carbohydrate. These foods included potatoes and french fries that had been heated to a temperature that exceeded 120 ®C. The development of the acrylamide was demonstrated to be dependent on the quality of the temperature that was used in cooking the food. The acrylamide has the appearance of manifesting itself as the foods are prepared over longer periods of time (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
The researchers are not completely sure of the manner by which the acrylamide forms in the foods. Many perceive that is an outcome of the Mallard reaction. This reaction takes place in baked or fried foods. The acrylamide is a potential outcome of the reaction between the reducing sugars (i.e., glucose and fructose) when they are added to asparagine. The acrylamide formation is detailed to take place at temperatures that are superior to 120® C (European Food Safety Authority 1; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7).
Acrylamide has been detailed to exert toxic effects on the reproductive system and on the nervous system. A report that was emitted in June of 2002 that issued by the United States' Food and Drug Administration demonstrated that the indexes of acrylamide ingestion that is required in order to observe neurological alterations was more that 50,000% more elevated than the average daily intake of acrylamide by individuals. In order to review the outcomes of acrylamide on fertility, the intake must be 20,000 % more than the daily average individual intake. . Research that has been conducted on laboratory specimens has revised the potential of acrylamide being a carcinogen. (European Food Safety Authority 1; European Food Safety Authority 1509; Gilbert & Maurissen 32; Grob et al. 187; Lawley et al. 340; Mattram et al. 449; National Cancer Institute 1; Skog & Viklund 365; Zhang & Chen 7)
The mother is forty years of age, the father is forty two years of age, the grandmother is sixty five years of age, the son is thirteen and the daughter is ten. The symptoms that were manifest by the family members as a result of acute acrylamide poisoning are manifest in the following table:
There has been one case of acute toxicity of acrylamide that has been documented (Siegers et al. 990). The acute toxicity more than likely took place over an extended period of exposure. A family was detailed by their exposure to acrylamide after the acrylamide seeped in to their well water supply from a nearby plant. The family applied the water from the well for the purposes of bathing, drinking and cooking. The concentration of acrylamide that was assessed in the well water was four hundred parts per million. This is a quantity that when it was fed to the laboratory animals over a few days was assessed as the casual attribute of paralysis (Siegers et al. 990).
The family demonstrated the symptoms more than a month after the work on the sewage pipe took place. . The symptoms were manifest in three of the adults who had been more influenced by the saturation of the acrylamide than the children. The symptoms that the two children had were disturbances in the gait, hallucinations and delirium. The three adults were affected with slurred speech. The three adults were also affected by horizontal nystagmus. One of the respondents was suffering from urinary retention (Siegers et al. 990).
There were no sensory defects that were found in the respondents during the initial examination. The findings were manifest in the respondents four weeks after the initial exposure. The only mental symptom that was found by the electro encephalography examinations were tendency towards sleepiness. The blood chemistry of the respondents who received the acute exposure to the acrylamide was normal. . The three adults were able to recuperate within the span of a month (Siegers et al. 990).
The children were influenced by the acrylamide exposure. The thirteen year old sibling was influenced more by the acrylamide acute toxicity than the ten year old sibling. The symptoms that were manifest were truncal ataxia and drowsiness. The thirteen year old boy has strange behavior that disappeared after three days. The distinctions n in the children are that they may have been subjected to a diminished cumulative dosage of the acrylamide that was found in the well water (Siegers et al. 990).
There have been about fifty case studies of chromic acrylamide poisoning that have been documented. In all of the cases, excluding the documentation of the acute case involving the handling of the acrylamide while it had been in the procedure of polymerization. . Conventionally, in certain cases, dermatitis was the only manifestation. The patients detailed that their skin had been exfoliating and that there was a blue pigmentation that was taking place. The blue pigmentation of the skin was where the contact with the acrylamide was realized. This was usually manifested in the arms and the hands of the patients. (Siegers et al. 990)
The patients also documented that they had experienced extreme perspiration in the area of the palms. The disturbances in the physical imbalance usually occurred simultaneously with the skin discoloration. This was followed by the paresthias, lack of sensation and weakness that was manifested in the distal extremities. In certain cases, there was slurred speech and the incontinence of urines. This was attributed to the neurogenic bladder characteristics. There had also been weight loss (Siegers et al. 990).
There was a truncal ataxia, varying sensory deficits, absence of deep tendon reactions and on occasion, the wasting of the small muscles. As the exposure to the acrylamide was ceased, all of the patients demonstrated marked improvement. The majority needed a few months in order to return to a baseline condition. In certain cases, there was no complete recovery until the interval of twelve months. The patients who had suffered chronic acrylamide exposure were employees at factories that produced flocculates (Siegers et al. 990).
There had been an examination of the nervous systems of the patients in the period of recuperation from acrylamide poisoning. There was discovered to be a disproportionate reduction in the speed of the muscular movements and diminished sensory action potential. The histologic review of the sural nerve of the patients that were recently exposed to the acrylamide demonstrated axonal decomposition, diminished nerve density with regards to the large fibers and system s of nerve regeneration (Siegers et al. 990).
There have been a number of experiments that have reviewed the effects of chronic toxicity with regards to acrylamide in animals. The acrylamide intoxication caused the development of peripheral neuropathy. The laboratory animals demonstrated an unsteadiness in the rear legs that was accompanied by an attrition of the lower and upper deep tendon reactions. This condition progressed to gross ataxia that was followed by subsequent paralysis. The paralysis was transformed into complete paralysis. In addition, there was a bladder distention in the majority of the test animals. As the exposure to the acrylamide was ceased, the majority of the test animals demonstrated immediate improvement. This improvement often required months before its completion. There was also an anamnestic reaction that was documented. The animals become more susceptible to the subsequent repeated dosages of the acrylamide. This susceptibility infers that the recuperation was not thorough (Siegers et al. 990).
The electrophysiological examinations on the animals that were exposed to acrylamide intoxication demonstrated that no symptoms of abnormalities were present. Subsequent, there was a display of the decrease in the nerve conduction speed. In the animals that received severe chronic exposure, the nerve conduction speed was decreased by twenty five percent to fifty percent in the distal areas. . The hind limbs demonstrated that they were affected to a greater extent than the front limbs. The speed and the intensity of the reduction were more manifest in the sensory conductions than it had been in the motor conduction. The depressing of the maximal nerve conduction speed was considered to be secondary to the degeneration of the widest diameter most rapidly conducting nerve fibers. The early decomposition of the large long axons was verified by the empirical histological studies (Siegers et al. 990).
Initially, the findings in the animal histological studies were unrevealing. The early fundamental microscope examinations did not explore the peripheral nerves and discovered that there were no abnormalities with the central nervous system. The median lethal dosage of the acrylamide poisoning for an initial oral dosage was discovered to be one hundred and sixty five milligrams per kilogram in rabbits, guinea pigs and rats. The lethal dosage for monkeys and cats was determined to be one hundred and fifty milligrams per kilogram of weight in the cats and the monkeys. The monkey that received the one hundred and fifty milligram injection per kilogram of weight was found not to have the ability of standing after the first day. The test monkey did have enough strength to crawl (Siegers et al. 990).
Acrylamide is produced in plastic manufacturing processes, paper manufacturing processes and dyes. The acrylamide has been found to be present in a number of foods that had been overcooked. Notwithstanding, the dosage that is contained in the foods that were overcooked is a small proportion of the amount that had been reviewed in the acute human case, chronic human cases and the laboratory animal cases. The amounts of acrylamide would require intensification in the amounts that are found to be present in potatoes and other types of foods. The amounts encountered in foods would require an intensification of two hundred to five hundred times the dosage in order to be harmful to humans. The acute case that was reviewed was attributed to the contamination of the well water that the family used for drinking, bathing and cooking. The chronic cases were attributed to factory workers that had been exposed to the acrylamide during the polymerization process. Other than exposure to the acrylamide effluents in water and the contact of acrylamide with the skin, there have been relatively few reports of its lethal effect.
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