The Critical Noncarcinogenic effect of acrylamide is classified as “Degenerative Nerve
Changes”. This means that chronic ingestion of acrylamide resulted in an observable damaging of the central and peripheral nervous system, thus classifying it as a neurotoxin. This conclusion was determined after the results of two separate chronic (2year) drinking water studies performed on lab rats. (Friedman et al., 1995, 224307; Johnson et
14
al., 1986, 061340). The doseresponse data for acrylamide was determined from the combined data of each of these two separate experiments. The RfD however, is based solely on the latter.
In this experiment, a group of rats was divided up and given drinking water with acrylamide concentrations of 0, 0.01, 0.1, 0.5, …show more content…
4.2 Toxicity Information for Carcinogenic Effects
Acrylamide has an Oral Cancer Slope Factor of 5 (mg/kgday)
1
(Johnson et al., 1986,
061340). Acrylamide’s carcinogenicity has been characterized as “B2” or “likely to be carcinogenic to humans” based off of four separate experimental observations. (U.S.
EPA, 2005, 086237)
The first observation is that chronic exposure of acrylamide to F344 rats resulted in a statistically significant increase in thyroid, scrotal, and mammary cancers in two bioassays. The second is that dermal contact and oral ingestion of acrylamide in
SwissICR
mice resulted in skin tumors. Thirdly, injections of acrylamide into A/J mice resulted in cancer of the lung, and brain. Lastly, acrylamide is an observed genotoxin,
15
capable of interfering with the genetic data in most cells, which always increases cancer risk. The mechanisms by which acrylamide causes specific types of cancer is not yet understood, it is only known that it is a common mammalian mutagen, and therefore a probable risk to humans. However, no studies have been done that have …show more content…
Several studies have attempted to correlate acrylamide consumption to a number of different cancer risks after a number of different exposures (smoking, dietary, dermal).
However, none of the studies used entirely trustworthy data, and either made assumptions about the population that disqualified the research (such as assuming dietary trends based on geography), or had too small a population to be statistically significant.
4.3 Uncertainties Related to Toxicity Information
Two separate 2year bioassays (Friedman et al., 1995, 224307; Johnson et al., 1986,
061340) corroborate the presence of thyroid, skin, lung, and CNSrelated cancers as a result of acrylamide exposure. These experiments were performed on the same species of mouse however, which limits the amount of confidence one can have in how acrylamide may specifically react with other organisms. There is also a large lack of proper human testing to support acrylamide’s human carcinogenicity.
4.4 Summary of Toxicity Information
Acrylamide is a scientifically tested and observed neurotoxin which causes the degradation of the myelin sheaths in both general and specific areas of the nervous system. It directly damages the axon terminals of brain’s neurons, but most heavily
Changes”. This means that chronic ingestion of acrylamide resulted in an observable damaging of the central and peripheral nervous system, thus classifying it as a neurotoxin. This conclusion was determined after the results of two separate chronic (2year) drinking water studies performed on lab rats. (Friedman et al., 1995, 224307; Johnson et
14
al., 1986, 061340). The doseresponse data for acrylamide was determined from the combined data of each of these two separate experiments. The RfD however, is based solely on the latter.
In this experiment, a group of rats was divided up and given drinking water with acrylamide concentrations of 0, 0.01, 0.1, 0.5, …show more content…
4.2 Toxicity Information for Carcinogenic Effects
Acrylamide has an Oral Cancer Slope Factor of 5 (mg/kgday)
1
(Johnson et al., 1986,
061340). Acrylamide’s carcinogenicity has been characterized as “B2” or “likely to be carcinogenic to humans” based off of four separate experimental observations. (U.S.
EPA, 2005, 086237)
The first observation is that chronic exposure of acrylamide to F344 rats resulted in a statistically significant increase in thyroid, scrotal, and mammary cancers in two bioassays. The second is that dermal contact and oral ingestion of acrylamide in
SwissICR
mice resulted in skin tumors. Thirdly, injections of acrylamide into A/J mice resulted in cancer of the lung, and brain. Lastly, acrylamide is an observed genotoxin,
15
capable of interfering with the genetic data in most cells, which always increases cancer risk. The mechanisms by which acrylamide causes specific types of cancer is not yet understood, it is only known that it is a common mammalian mutagen, and therefore a probable risk to humans. However, no studies have been done that have …show more content…
Several studies have attempted to correlate acrylamide consumption to a number of different cancer risks after a number of different exposures (smoking, dietary, dermal).
However, none of the studies used entirely trustworthy data, and either made assumptions about the population that disqualified the research (such as assuming dietary trends based on geography), or had too small a population to be statistically significant.
4.3 Uncertainties Related to Toxicity Information
Two separate 2year bioassays (Friedman et al., 1995, 224307; Johnson et al., 1986,
061340) corroborate the presence of thyroid, skin, lung, and CNSrelated cancers as a result of acrylamide exposure. These experiments were performed on the same species of mouse however, which limits the amount of confidence one can have in how acrylamide may specifically react with other organisms. There is also a large lack of proper human testing to support acrylamide’s human carcinogenicity.
4.4 Summary of Toxicity Information
Acrylamide is a scientifically tested and observed neurotoxin which causes the degradation of the myelin sheaths in both general and specific areas of the nervous system. It directly damages the axon terminals of brain’s neurons, but most heavily