Acrylamide

Characteristics

Uses

Environmental Transport

Environmental Deposition

Methods for Monitoring in the Environment

Methods for Monitoring Human Exposure

Safeguards Against Acrylamide Exposure


Harmful Effects

Dose Response

Absorption, Distribution and Metabolism

Primary Sites for Toxicity

Biomarkers

Mechanism of Action

Risk Assessment and Management

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Acrylamide Policy

Introduction to Policy

Decision Makers and Stakeholders

Current Policy

Policy Recommendations


References

Acrylamide Dose-Response

Research conducted on acrylamide toxicity and dose-response has linked exposure to the chemical to neurological disorders, reduced fertility, adverse effects on germ cells and cancer. Acrylamide does not bioaccumulate in the body. It has therefore been accepted that the toxic effects of acrylamide are due to repeated cell damage. (18)

The method most commonly used to determine the effects of low exposure over long periods of time, is to extrapolate from higher exposures over a shorter period of time. It has been generally accepted that the dose-response of exposure to acrylamide is linear (18). Although it is more reliable to look at data determined from low dose exposures for long periods of time, this requires a greater number of subjects and is much more expensive.

Research has found that testicular mesotheliomas and mammary gland fibroadenomas were the most common tumor types produced in response to acrylamide dosing (Johnson et al and the American Cyanomid Research Co and Friedman et al.). These tumors were clearly induced with a significant dose in male and female rats (Figures 1 and 2). (15)


Male Rats dosed with acrylamide showed a significant increase of thyroid adenomas, testicular mesotheliomas and atrocyomas. An increase in adrenal pheochromocytomas and focal hyperplasia was found to occur in the high dose group in the first study but not the second study. (15)


There was a significant increase in thyroid adenomas and adenocarcinomas in the high dose group. An increase in fibroadenomas in the mammary gland oral cavity tumors and uterine adenocarcinomas was found to occur increasingly with increased dose. (15)

The United States Environmental Protection Agency reviewed the study conducted by Johnson et al and produced a chart relating the administered dose in rats to human exposure (Figure 3). (19)

A subchronic drinking water study looked at 344 Fischer rats dosed with varying levels of acrylamide over a 90 day period of time (Burek et al). Additional dose groups of male rats were dosed with the same acrylamide levels and held for an additional 144 days after the final dosing. At the completion of the study both groups were examined. The left sciatic nerve was removed and inspected microscopically. Damage to the sciatic nerve was discovered to increase with the increased dosing of each group. The rats that were inspected after 144 days from the final dosing indicated repair to the damaged areas. A NOAEL of 0.2mg/kg bw/day and a LOAEL of 1mg/kg bw/day was established for nerve damage in response to acrylamide dosing. (19)

The Institute of Environmental Medicine (IMM 1998) reviewed reproductive toxicity studies with rats. It was found that exposure to acrylamide resulted in reduction in sperm counts, decreased fertility and increased premature embryonic death. Based on these studies a NOAEL for reduced fertility was determined to be 5mg/kg bw/day. A NOAEL for premature embryonic death was determined to be 2mg/kg bw/day. (15)

The Norwegian Food Control Authority produced a paper detailing the health effects of acrylamide exposure. Epidemiological data reviewed during the Norwegian study indicated that acrylamide exposure was not linked to tumor formation in humans15. The data researched did not disprove that acrylamide could cause tumor formation however15. Because acrylamide has a genotoxic mechanism of action, it is generally accepted that it is likely to be carcinogenic. (15)

A study conducted by the Harvard School of Public Health and the Karolinska Institute in Stockholm, Sweden supported the epidemiological data published by the Norwegian Food Control Authority. The Harvard and Karolinska investigation reportedly found no association between the consumption of foods high in acrylamide and the risk of three forms of cancer. The researchers found that dietary levels of acrylamide are not sufficient to increase the risk of bladder, large bowel and kidney cancer in humans. (20)

Researchers involved with the Harvard and Karolinska investigation used data acquired by the Swedish National Food Administration pertaining to acrylamide levels in food. The researchers looked at the diet of 987 cancer patients and 538 healthy individuals over a five year period of time. Those people that consumed high levels of acrylamide (300-1200 micrograms/kg bw/day) and moderate levels of acrylamide (30-299 ug/kg bw/day) were at no greater risk of cancer than those with lower intake. (20)

Although this study seems to negate the effects of acrylamide as a cancer causing agent in food, the researchers recognized that acrylamide ingestion may cause certain neurological conditions. The researchers stressed that more research still needs to be done in this area. (20)