In situ degradation of metal-alloy implants is undesirable for two reasons: the degradation process may decrease the structural integrity of the implant, and the release of degradation products may elicit an adverse biological reaction in the host Degradation may result from electrochemical dissolution phenomena, wear, or a synergistic combination of the two Electrochemical processes may include generalized corrosion, uniformly affecting the entire surface of the implant, and localized corrosion, affecting either regions of the device that are shielded from the tissue fluids (crevice corrosion) or seemingly random sites on the surface (pitting corrosion) Electrochemical and mechanical processes (for example, stress corrosion cracking, corrosion fatigue, and fretting corrosion) may interact, causing premature structural failure and accelerated release of metal particles and ions

The clinical importance of degradation of metal implants is evidenced by particulate corrosion and wear products in tissue surrounding the implant, which may ultimately result in a cascade of events leading to periprosthetic bone loss Furthermore, many authors have reported increased concentrations of local and systemic trace metal in association with metal implants1,4,5,9-11,14,18,25,26,28,29,47,49-55,58,71,72,75-77,87,90,108-110 There also is a low but finite prevalence of corrosion-related fracture of the implant

This review focuses on electrochemical corrosion phenomena in alloys used for orthopaedic implants A summary of basic electrochemistry is followed by a discussion of retrieval studies of the response of the implant to the host environment and the response of local tissue to implant corrosion products The systemic implications of the release of metal particles also are presented Finally, future directions in biomaterials research and development …

/pdf/corrosion-of-metal-orthopaedic-implants-2h3sv09cdv.pdf

Corrosion of metal orthopaedic implants.

Application of chitosan and its derivatives as adsorbents for dye removal from water and wastewater: a review.

The plasticizer di(2-ethylhexyl) phthalate (DEHP), to which humans are extensively exposed, was found to be hepatocarcinogenic in rats and mice. DEHP is potentially set free from objects made of synthetic materials (e.g., those used in medicine). Chronically, the greatest amounts are transferred to persons undergoing hemodialysis (up to 3.1 mg/kg b.w. per day) who would thus be considered the individuals most endangered by tumorigenesis. Although toxicokinetics seem to play a certain unclear role in the course of DEHP-related toxicity, toxicodynamic factors appear more decisive. DEHP is a representative of "peroxisome proliferators" (PP), a distinct group of substances that, in rodents, do not only induce peroxisomes but also specific enzymes in other organelles, organ growth, and DNA synthesis. The cluster of the characteristic effects of PP is generally, although perhaps not quite appropriately summarized as "peroxisome proliferation," and is strongest in the liver. The lowest observed effect level (LOEL) and the no observed effect level (NOEL) of peroxisome proliferation in the rat, as determined by the induction of specific enzymes (peroxisomal beta-oxidation, carnitine-acetyl-transferase, cytochrome P-452), DNA synthesis, and hepatomegaly, may be assumed as 50 and 25 mg/kg b.w. per day, respectively. DEHP and other carcinogenic PP are neither genotoxic nor tumor initiators, but they appear to be tumor promoters, also implicating a threshold level for the carcinogenic effect. Although a causal relationship between a particular effect of peroxisome proliferation and hepatocarcinogenesis is as yet unknown, peroxisome proliferation as a whole phenomenon appears to be associated with the potential of tumor induction, as shown by comparison of the relative strength of individual PP and by comparison of species and organ specificities. Likewise, LOEL and NOEL of rodent carcinogenesis, that is, 300 and 50 to 100 mg/kg b.w. per day, respectively, are above but not too far from the corresponding values for the investigated parameters of peroxisome proliferation. Thus, with respect to dose alone, worst-case exposure in hemodialysis patients is at least 16-fold below the LOEL of any characterized PP-specific effect of DEHP and approximately 100-fold below that of DEHP-related tumorigenesis. Also, primates are less responsive to PP than rats with respect to the investigated biochemical and morphological parameters. If this lower primate responsiveness is extrapolated to estimate carcinogenicity in humans, we might thus arrive at an even larger safety margin than when based on exposure alone. Doses of PP hypolipidemics that had clearly induced several indicators of peroxisome proliferation in rats did not cause any clear-cut enhancements in the peroxisomes of patients, even though most of these hypolipidemics were considerably stronger PP than DEHP. Thus, an actual threat to humans by DEHP seems rather unlikely. Accordingly, hepatocarcinogenesis was neither enhanced in workers exposed to DEHP nor in patients treated with hypolipidemics.

Hepatocarcinogenic Potential of Di(2-Ethylhexyl)phthalate in Rodents and its Implications on Human Risk

In various biological systems, 1,2-epoxides are able to cause biological effects with genetic mechanisms: point mutations, deletions, chromosomal aberrations, gene conversion, crossing-over, cancer and virus (prophage) induction. Dose—response curves are linear, or should be interpreted to have a linear component that predominates at low doses or concentrations. In forward mutation systems the effectiveness is related to the dose in the target cells and to the chemical reactivity. By applying experimentally determined correction factors for difunctionality (in the case of diepoxides or monoepoxides with a reactive substituent such as a carbonyl group), genetic risks may be estimated by a unitary approach, valid for epoxides in general, if not for all alkylating agents. The use of this approach, to calculate type-II errors in negative carcinogenicity tests, indicates that no data presently available support a conclusion that certain epoxides are non-mutagenic or non-carcinogenic, i.e. are less effective than expected from reactivity data. Determination of the rad-equivalence of genetic risks, i.e. the use of corresponding risks from a unit dose of ionizing radiation as a standard, indicates that the risks associated with Threshold Limit Values for epoxides in work environments in Western countries are 1–2 orders of magnitude higher than permissible risks for radiological workers.

Genetic toxicity of some important epoxides

The Scientific Panel on Food Additives, Flavourings, Processing Aids and Materials in Contact with Food (the Panel) is asked to advise the Commission on the implications for human health of chemically defined flavouring substances used in or on foodstuffs in the Member States. In particular, the Scientific Panel is asked to evaluate the 47 flavouring substances in this Flavouring Group Evaluation 6, Revision 1 (FGE.06Rev1), using the procedure as referred to in the Commission Regulation EC No 1565/2000. These 47 flavouring substances belong to chemical groups 1 and 4 of Annex I of the Commission Regulation (EC) No 1565/2000.

Opinion of the Scientific Panel on Food Additives, Flavourings, Processing Aids and Materials in contact with Food (AFC) on a request from the Commission, Flavouring Group Evaluation 22: Ring-substituted phenolic substances from chemical groups 21 and 25: Question No EFSA-Q-2003-165

A toxicological investigation of some acute, short-term, and chronic effects of administering di-2-ethylhexyl phthalate (DEHP) and other phthalate esters.

Toxicity Profile of Epichlorohydrin

A series of systemic toxicity tests for various types of compounds are presented with illustrative data and discussed in regard to their relevance as potential screening tests for dental compounds and products. In developing and marketing a new dental material, it is important not only to ensure safety for the patient but also for the dentist, dental assistant, and laboratory worker who routinely handles and uses the product. Data are presented on a number of commercially available dental products as well as various chemical entities, which were tested by one or more of the methods described.

M. Malik

Papers

A toxicological investigation of some acute, short-term, and chronic effects of administering di-2-ethylhexyl phthalate (DEHP) and other phthalate esters.

Toxicity Profile of Epichlorohydrin

Development of a toxicity evaluation program for dental materials and products. II. Screening for systemic toxicity