The Reproductive and Neural Toxicities of Acrylamide and Three Analogues in Swiss Mice, Evaluated Using the Continuous Breeding Protocol

Chapin, Robert E.; Fail, Patricia A.; George, Julia D.; Grizzle, Thomas B.

doi:10.1093/toxsci/27.1.9

Cited by 21 publications

(28 citation statements)

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“…There was no effect on postnatal survival of F 2 progency. Histologic examination of tissues from F 1 males revealed no dose-related abnormal findings, other than testicular degeneration in 1 of 10 animals in the middle and high dose groups (Chapin et al 1995).…”

Section: Acrylamidementioning

confidence: 83%

“…There was prenatal lethality at the 5 mg/kg 31 dose level, but not at the other dose levels (Union Carbide 1987). Chapin et al (1995) published the results of a National Toxicology Program (NTP) study of the reproductive and neural toxicities of acrylamide and three analogues in Swiss mice using the NTP's reproductive assessment by continuous breeding (RACB) protocol. Treatment agents were acrylamide at 3, 10, and 30 ppm; N ,N -methylene bis-acrylamide (MBA) at 10, 30, and 60 ppm; N -(hydroxymethyl)acrylamide (HMA) at 60, 180, and 360 ppm; and methacrylamide (MACR) at 24, 80, and 240 ppm.…”

Section: Acrylamidementioning

confidence: 99%

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Amended Final Report on the Safety Assessment of Polyacrylamide and Acrylamide Residues in Cosmetics1

Andersen¹

2005

Int J Toxicol

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Polyacrylamide is a polymer of controllable molecular weight formed by the polymerization of acrylamide monomers available in one of three forms: solid (powder or micro beads), aqueous solution, or inverse emulsions (in water droplets coated with surfactant and suspended in mineral oil). Residual acrylamide monomer is likely an impurity in most Polyacrylamide preparations, ranging from <1 ppm to 600 ppm. Higher levels of acrylamide monomers are present in the solid form compared to the other two forms. Polyacrylamide is reportedly used in 110 cosmetic formulations, at concentrations ranging from 0.05% to 2.8%. Residual levels of acrylamide in Polyacrylamide can range from <.01% to 0.1%, although representative levels were reported at 0.02% to 0.03%. Because of the large sizes of Polyacrylamide polymers, they do not penetrate the skin. Polyacrylamide itself is not significantly toxic. For example, an acute oral toxicity study of Polyacrylamide in rats reported that a single maximum oral dose of 4.0 g/kg body weight was tolerated. In subchronic oral toxicity studies, rats and dogs treated with Polyacrylamide at doses up to 464 mg/kg body weight showed no signs of toxicity. Several 2-year chronic oral toxicity studies in rats and dogs fed diets containing up to 5% Polyacrylamide had no significant adverse effects. Polyacrylamide was not an ocular irritant in animal tests. No compound-related lesions were noted in a three-generation reproductive study in which rats were fed 500 or 2000 ppm Polyacrylamide in their diet. Polyacrylamide was not carcinogenic in several chronic animal studies. Human cutaneous tolerance tests performed to evaluate the irritation of 5% (w/w) Polyacrylamide indicated that the compound was well tolerated. Acrylamide monomer residues do penetrate the skin. Acrylamide tested in a two-generation reproductive study at concentrations up to 5 mg/kg day(- 1) in drinking water, was associated with prenatal lethality at the highest dose, with evidence of parental toxicity. The no adverse effects level was close to the 0.5 mg/kg day(- 1) dose. Acrylamide tested in a National Toxicology Program (NTP) reproductive and neurotoxicity study at 3, 10, and 30 ppm produced no developmental or female reproductive toxicity. However, impaired fertility in males was observed, as well as minimal neurotoxic effects. Acrylamide neurotoxicity occurs in both the central and peripheral nervous systems, likely through microtubule disruption, which has been suggested as a possible mechanism for genotoxic effects of acrylamide in mammalian systems. Acrylamide was genotoxic in mammalian in vitro and in vivo assays. Acrylamide was a tumor initiator, but not an initiator/promoter, in two different mouse strains at a total dose of 300 mg/kg (6 doses over 2 weeks) resulting in increased lung adenomas and carcinomas without promotion. Acrylamide was tested in two chronic bioassays using rats. In one study, increased incidence of mammary gland tumors, glial cell tumors, thyroid gland follicular tumors, oral tissue tumors, uterine...

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Section: Acrylamidementioning

confidence: 83%

Section: Acrylamidementioning

confidence: 99%

Amended Final Report on the Safety Assessment of Polyacrylamide and Acrylamide Residues in Cosmetics1

Andersen¹

2005

Int J Toxicol

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“…Animal studies have shown that the polymeric form of acrylamide is non-toxic but the monomeric form induces neurotoxicity, reproductive toxicity, genotoxicity and carcinogenicity (Chapin et al, 1995, Dearfield et al, 1995. However, only acrylamide-induced neurotoxicity has been documented in occupationally exposed populations in humans, indicating implications in human health (Kjuus et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Acrylamide affects proliferation and differentiation of the neural progenitor cell line C17.2 and the neuroblastoma cell line SH-SY5Y

Attoff

Kertika

Lundqvist

et al. 2016

Toxicology in Vitro

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Acrylamide is a well-known neurotoxic compound and people get exposed to the compound by food consumption and environmental pollutants. Since acrylamide crosses the placenta barrier, the fetus is also being exposed resulting in a risk for developmental neurotoxicity. In this study, the neural progenitor cell line C17.2 and the neuroblastoma cell line SH-SY5Y were used to study proliferation and differentiation as alerting indicators for developmental neurotoxicity. For both cell lines, acrylamide reduced the number of viable cells by reducing proliferation and inducing cell death in undifferentiated cells. Acrylamide concentrations starting at 10fM attenuated the differentiation process in SH-SY5Y cells by sustaining cell proliferation and neurite outgrowth was reduced at concentrations from 10pM. Acrylamide significantly reduced the number of neurons starting at 1μM and altered the ratio between the different phenotypes in differentiating C17.2 cell cultures. Ten micromolar of acrylamide also reduced the expression of the neuronal and astrocyte biomarkers. Although the neurotoxic concentrations in the femtomolar range seem to be specific for the SH-SY5Y cell line, the fact that micromolar concentrations of acrylamide seem to attenuate the differentiation process in both cell lines raises the interest to further investigations on the possible developmental neurotoxicity of acrylamide.

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“…That is, the BMDs were all greater than the maximum doses used in the cancer bioassays (2-3 mg/kg) by at least a factor of about 3; and at least an order of magnitude greater than the ED 10 s estimated from the most sensitive endpoints from those studies (0.3-0.5 mg/kg). BMDs estimated for reproductive endpoints from two multigeneration studies (Chapin et al, 1995; ranged between 3 and 14 mg/kg/day (data not shown). Thus, in comparison to other toxicity tests of acrylamide, the in vivo genetic toxicity assays appear not to provide the critical dose-response estimates (i.e., benchmark dose estimates) that would drive a regulatory risk assessment of acrylamide.…”

Section: Discussionmentioning

confidence: 99%

Dose–response modeling of in vivo genotoxicity data for use in risk assessment: some approaches illustrated by an analysis of acrylamide

Allen

Zeiger²,

Lawrence

et al. 2005

Regulatory Toxicology and Pharmacology

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The Reproductive and Neural Toxicities of Acrylamide and Three Analogues in Swiss Mice, Evaluated Using the Continuous Breeding Protocol

Cited by 21 publications

References 0 publications

Amended Final Report on the Safety Assessment of Polyacrylamide and Acrylamide Residues in Cosmetics1

Amended Final Report on the Safety Assessment of Polyacrylamide and Acrylamide Residues in Cosmetics1

Acrylamide affects proliferation and differentiation of the neural progenitor cell line C17.2 and the neuroblastoma cell line SH-SY5Y

Dose–response modeling of in vivo genotoxicity data for use in risk assessment: some approaches illustrated by an analysis of acrylamide

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