Occupational exposure to methyl methacrylate monomer induces generalised neuropathy in a dental technician

Sadoh, D; Sharief, Mohammed; Howard, Robin S.

doi:10.1038/sj.bdj.4800117

Cited by 37 publications

(8 citation statements)

References 8 publications

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“…Silzbach et al were the first to report pneumoconiosis in a dental technician (Silzbach, 1939). Since then, investigations into the health of dental technicians have increased (Becklake, 1992;De et al, 1986;Rom et al, 1984;Sherson et al, 1988;Choudat et al, 1993;Selden et al, 1995;Birgitta et al, 2006;Sadoh et al, 1999;Yoshida et al, 1991;Kimura et al, 2003;Kihara et al, 1995;Ishitake et al, 1993;Mori, 1995).…”

Section: Introductionmentioning

confidence: 93%

Effects of occupational environmental controls and work management on chromosomal damage in dental technicians in Japan

Ishikawa

Shindo

et al. 2013

International Journal of Hygiene and Environmental Health

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Section: Introductionmentioning

confidence: 93%

Effects of occupational environmental controls and work management on chromosomal damage in dental technicians in Japan

Ishikawa

Shindo

et al. 2013

International Journal of Hygiene and Environmental Health

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“…Based on theoretically similar CNS accessibilities, systemic exposure to methyl acrylate, ethyl methacrylate, or other weak type-2 alkene electrophiles (Table 1) should also cause selective neurotoxicity. Indeed, the results of both human (Sadoh et al 1999; Seppalainen and Rajaniemi 1984) and animal (Abou-Donia et al 2000) studies suggest that exposure to these chemicals can produce ACR-like neurotoxicity. Clearly, relative softness (σ) and electrophilicity (ω) determine not only the toxicodynamic character of ACR and other type-2 alkenes (i.e., amino acid targets and mechanisms of toxicity), but also tissue distribution and corresponding toxic manifestations.…”

Section: Molecular Mechanism Of Acr Synaptotoxicitymentioning

confidence: 99%

Molecular Mechanism of Acrylamide Neurotoxicity: Lessons Learned from Organic Chemistry

LoPachin

Gavin

2012

Environ Health Perspect

168

127

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Background: Acrylamide (ACR) produces cumulative neurotoxicity in exposed humans and laboratory animals through a direct inhibitory effect on presynaptic function.Objectives: In this review, we delineate how knowledge of chemistry provided an unprecedented understanding of the ACR neurotoxic mechanism. We also show how application of the hard and soft, acids and bases (HSAB) theory led to the recognition that the α,β-unsaturated carbonyl structure of ACR is a soft electrophile that preferentially forms covalent bonds with soft nucleophiles.Methods: In vivo proteomic and in chemico studies demonstrated that ACR formed covalent adducts with highly nucleophilic cysteine thiolate groups located within active sites of presynaptic proteins. Additional research showed that resulting protein inactivation disrupted nerve terminal processes and impaired neurotransmission.Discussion: ACR is a type-2 alkene, a chemical class that includes structurally related electrophilic environmental pollutants (e.g., acrolein) and endogenous mediators of cellular oxidative stress (e.g., 4-hydroxy-2-nonenal). Members of this chemical family produce toxicity via a common molecular mechanism. Although individual environmental concentrations might not be toxicologically relevant, exposure to an ambient mixture of type-2 alkene pollutants could pose a significant risk to human health. Furthermore, environmentally derived type-2 alkenes might act synergistically with endogenously generated unsaturated aldehydes to amplify cellular damage and thereby accelerate human disease/injury processes that involve oxidative stress.Conclusions: These possibilities have substantial implications for environmental risk assessment and were realized through an understanding of ACR adduct chemistry. The approach delineated here can be broadly applied because many toxicants of different chemical classes are electrophiles that produce toxicity by interacting with cellular proteins.

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“…For example dental resins (primarily acrylics) and rubber products cause adverse reactions mainly in dental staff. Hand and fingertip reactions such as dry, cracking and flaking skin, itching, irritation, and swelling have been reported [4] as well as generalized neuropathy after 14 years exposure to methacrylates [6]. Reactions to many types of prosthodontic materials can be severe, career-threatening, and even life threatening in rare instances [7].…”

Section: Introductionmentioning

confidence: 99%

Biocompatibility of Resin-based Dental Materials

2009

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Oral and mucosal adverse reactions to resin-based dental materials have been reported. Numerous studies have examined the biocompatibility of restorative dental materials and their components, and a wide range of test systems for the evaluation of the biological effects of these materials have been developed. This article reviews the biological aspects of resin-based dental materials and discusses the conventional as well as the new techniques used for biocompatibility assessment of dental materials.

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Occupational exposure to methyl methacrylate monomer induces generalised neuropathy in a dental technician

Cited by 37 publications

References 8 publications

Effects of occupational environmental controls and work management on chromosomal damage in dental technicians in Japan

Effects of occupational environmental controls and work management on chromosomal damage in dental technicians in Japan

Molecular Mechanism of Acrylamide Neurotoxicity: Lessons Learned from Organic Chemistry

Biocompatibility of Resin-based Dental Materials

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