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’s Primary Sites for Toxicity:

Traditionally as acrylamide is part of a wide array of compounds, which stimulates axonapathies, a primary target for neuronal damage is that of the medium to large diameter axons. Within the axonapathy reaction the myelin sheath becomes degenerated and retreats away from the cell body. (Figure 2.) On A biochemical level, the acrylamide acts as a “chemical transectant” which interferes with the axon along some point in the myelin sheath, thus biologically separating it from the remaining healthy neuron but disturbing the myelin and consequently, axon potential transmission (27).

This myelin separation can have drastic affects within middle ranged diameter axons in the human peripheral nervous system. Of particular note is the degeneration of the Pbeta Type RGC’s, which project into the paracellular layer of the Lateral Geniculate Nucleus (28). This toxic effect within the optic tract results in impaired perceptual deficits as well as deficits in detecting fast and slow visual stimuli.

Another important area of effect from acrylamide is at the distal neuromuscular junction. The earliest signs of muscle spindles becoming degenerated are seen in the dying back effect within pacinian corpuscles. Of particular susceptibility are large skeletal muscles in the leg such as the tibial nerve branches supplying the calf muscles.

Forearm muscles and the digits of the hands are some of the other potiental-affected nerves, which can be impaired by acrylamide. Axonapathies in these medium to large diameter axons can drastically reduce muscle action potiental and overall muscle strength.

Carcinogenic effects at the cellular level have been studied to predict Acrylamide’s effect upon different cell types. Two carcinogenic studies in rats have yielded results showing an increase in tumors of the hormone responsive organs including tunica vaginalis, mesothelioma, mammary gland fibroadenoma and oral papillomas (30,31). It is difficult to ascertain the value of this data as both studies found inconsistent results when compared to each other; however the overall incidence of carcinoma did increase in tissues exposed to acrylamide.
Dermal human exposure has been studied in occupational exposure situations, which have yielded findings that show impairments in the sense of vibration, weak legs, numb hands, and loss of ankle and toe reflexes (29).

Of these workers most had been handling 30% aqueous acrylamide solution for a 2-year period.


Figure 2. Normal nerve axon (far left) versus a distal axonapathy (far right) as might be seen from acrylamide toxicity. (Picture from Cassarett and Doull’s Toxicology)