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


Mechanism of Action

Risk Assessment and Management

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Acrylamide Policy

Introduction to Policy

Decision Makers and Stakeholders

Current Policy

Policy Recommendations



Acrylamide is poisonous by ingestion and inhalation and emits toxic acrid fumes when it decomposes. It can be absorbed through unbroken skin, mucous membranes, the lungs and the gastrointestinal tract. Those working with polyacrylamide experience the greatest threat. However, there are reports of increased levels in smokers since acrylamide is present in tobacco smoke.

MCLG: 0 mg/L
MCL: Treatment technique
HAL (child): 1 day: 1.5mg/L; 10-day: 0.3 mg/L

Short term exposure for a 10-kg (22lb.) child are:
1 liter of water/ day:
1-day exposure of 1.5 mg/day
10-day exposure to 0.3 mg/L
7-year exposure to 0.002mg/L

The following is a 1997 study of acrylamide in humans. It involved building workers using polyacrylamide to stabilize earthworks in tunnel digging. They were tested after acrylamide had seeped into an adjacent river killing fish and paralysing cattle. The control group is other building workers not using polyacrylamide and was unexpectedly high. Surprisingly there were low levels of adducts in wild animals compared to humans, which is now attributed acrylamide formation in food.

The Hemoglobin adducts in human blood samples:
Tunnel workers - 3.0 nmol/g
Smokers - 0.12 nmol/g
Control group - 0.04 nmol/g
J. Environmental Health, 2001, 27, 219-226

When acrylamide is used in drinking water systems, the combination of dose and monomer level may not exceed 0.05%dosed at 1 mg/L. EU migration limit from plastics packaging is 10µg/kg and in paper and board samples the maximum is 1.4ppm.

Acute: At levels above the MCL, the EPA found the acute effects to be damaging to the CNS and PNS as well as weakness and ataxia in legs. This diagnosis is based on a history of ingestion of only a few grams of acrylamide crystal. The diagnosis should be considered in an individual with access to acrylamide (for example a laboratory worker) who develops a CNS, cardiovascular and respiratory disturbance over a period of hours.

Chronic/Cancer: There is some evidence that acrylamide may have the potential to cause cancer from a lifetime exposure at levels above the MCL. In vitro and in vivo acrylamide causes damage to chromosome in mammalian cells even though it does not cause mutations in bacterial test systems. In a long-term carcinogenicity studies in rats tumors were noted after the rats were exposed to contaminated drinking-water. It has been concluded that acrylamide is a genotoxic carcinogen.

Acrylamide may be measured in urine sample however, it reacts in human blood with hemoglobin forming adducts to N-terminal valine creating [N-(2-carbomoylethyl)valine. Proof that acrylamide is converted to CEV in the body is concluded in various animal tests as the level of acrylamide is compatible with the measured levels of the CEV adduct. The CEV adduct levels observed in experimental animals (food tests) are similar the amount in nonsmoking humans. 25 µg/person/day is the average intake of acrylamide for humans. Acrylamide exposure is therefore monitored by mass spectrometric detection of the adduct, N-(2-carbamolyethyl)valine (CEV), to the N-termini of hemoglobin, according to the N-alkyl Edman method. The data is collected by gas chromatography/tandem mass spectrometry. The identity of the adduct was confirmed by comparing the product ion spectrum of the studied adduct with that of a verified standard and interpretation of the fragment ions.

This adduct reflects a cumulative intake ~over a 90-day period. The methodology in process by NCEH biomonitering program involves adding an internal standard to the sample. Red blood cells are then isolated from the blood. Hemoglobin derived peptides are then separated by enzymatic digestion. The final step is quantification by HPLC – MS/MS of N-terminal peptide.

Acrylamide has a biological half-life of 2 hours. In tissues, total acrylamide exhibits biphasic elimination with an initial half-life of 5 hours and a terminal half life of 8 days. As such acrylamide does not accumulate in the body although these data are from animal studies.