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 Absorption, Distribution and Metabolism

Acrylamide Absorption

Absorption of Acrylamide has traditionally been researched using the oral and intraperitoneal modes of introduction into the body with relatively little research into inhalation exposure. Absorption is closely linked with the mode of environmental exposure to the human body. Acrylamide’s half-life in the open air is relatively short in comparison to its other modes of transportation.

Studies conducted involving oral exposures in rats have yielded results showing that Acrylamide is readily absorbed into the GI tract (32).

A comparison of oral vs. intraperitoneal exposure was conducted (33) showing that systemic absorption following oral exposure was less versus that of intraperitoneal exposure.

Oral exposure has been the primary focus of Acrylamide’s main entry into the human and thus a heavy focus of tissue research into its toxicology upon GI tract tissues has taken place. It is noted in the above-mentioned study by Miller (32) that after administration of Acrylamide, it was absorbed into the GI system.

Another tissue susceptible to Acrylamide absorption is in nervous tissue of the peripheral nervous system. High uptake levels of Acrylamide in the motor nerve terminus and optic nerve are two areas, which have been shown to result in degeneration of the distal axon terminal. Essentially, this process of dying back allows more acrylamide to enter the cell causing further intoxication (27). Earliest neuromuscular changes can be seen in the pacinian corpuscles followed by the muscle spindles and finally the motor nerve terminus.

In the optic nerve, mid diameter axons are most prone to acrylamide absorption in the optic tract allowing for neuronal degeneration in tested primates.

Acrylamide Distribution:

Distribution of acrylamide will vary upon how the chemical is introduced into the body, specifically, if it is introduced dermal, intravenous, or orally. Variation in the distribution is primarily affected by if the individual is exposed to monomeric versus Polyacrylamide prior to distribution in the body.

Past studies have shown that in rats, regardless of distribution, the final absorptive tissues were skeletal, smooth muscle and medium to large diameter axons. Axonal absorption is a prime concern in acrylamide toxicity as it can lead to proximal neuropathy and degeneration of the axon’s myelin sheath. In the above-mentioned study, 1mg/kg was introduced in dogs and pigs. Of the original dose, up to 50% was found contained in the muscle tissue.

Fetal studies have shown that acrylamide will cross the placental blood barrier in mice and rats resulting in impaired neurological fetal developments.

Acrylamide Metabolism

Acrylamide metabolism can have 2 possible pathways in route to the excretion of the compound. Pathway 1 involves utilizing the Cytochrome P450 metabolic enzyme to transform Acrylamide to an easier excrete able Gylcidamide. Pathway 2 involves the conjugation of Acrylamide to Glutathione (GST) there by forming N-acetyl-S- (3-amino-3-oxopropyl) Cysteine as the final product.

Differentiation between pathways 1 versus pathway 2 is dependant on the species absorption of Acrylamide. Area specific metabolism in rats has shown that the liver, kidney, brain, and erythrocyte GST has a significant higher affinity for binding Acrylamide with the liver being 3 times more prone to Acrylamide binding versus the other mentioned target organs. Solubility of the compound and its method of absorption is highly dependant on the GST pathway for conjugation to a water-soluble product. The conversion by GST to Gylcidamide results in the chemical creation of a radical epoxide, which can express toxicity independently from other neuropathies associated with Acrylamide.

Studies have been conduct in rats, which indicate that some species of rats may in fact inhibit GST conjugation thus allowing for increased amounts of the toxic product Gylcidamide (34).

Figure 1 depicts the 2 available pathways for Acrylamide metabolism.