don't know about the vein. you should be able to find that info on the 2nd reference below. i have heard to go to a reputable place so they do it right. here is other info for you:
most are made of stainless steel or titanium. gold is pretty compatible with humans, but they use other metals with the gold, which may not be. many people are allergic to platinum as well.
Most professional studios will only pierce with stainless steel or titanium jewelry. Some use one or the other exclusively. Piercers who use titanium exclusively will note that even stainless steel can sometimes contain too much nickel to be safe for some people to wear in a piercing. The APP (Association of Professional Piercers) recognizes surgical implant stainless steel (CrNMo 316LVM, ASTM F-138), surgical implant grades of titanium(Ti6A4V ELI, ASTM F-136), niobium (Nb), solid 14 karat or higher white or yellow gold containing no nickel, and solid platinum to be appropriate materials for an initial piercing.
Decorative jewelry bought at retail stores is often highly discouraged by piercers, as much of it contains components that can be irritating or even toxic. Even some jewelry that is claimed to be titanium is often composed of cheaper metals such as nickel and iron. Silver in any use or form is also highly discouraged due to the threat of argyria and possible carcinogenic effects of various silver compounds
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2.7.6. Titanium
It is generally accepted that pure titanium is extremely well tolerated by local tissues and induces neither toxic nor inflammatory reactions (Branemark et al. 1969, Toth et al. 1985, Linder et al. 1988, Pfeiffer et al. 1994). The normal tissue concentration of titanium in humans is 0.2 ppm. Around the titanium implants no clinical tissue toxicity has been observed even at local concentrations higher than 2000 ppm (Hildebrand et al. 1998). In optimal situations, titanium is able to osseointegrate with bone, thus forming a direct contact with bone at the light microscopy level (Branemark et al. 1969). The good bone contact may be due to the ability of titanium to form a Ca-P rich layer on its surface (Hanawa 1991). Titanium is bacteriostatic (Elagli et al. 1992) and does not significantly activate or inhibit different enzyme systems specific to toxic reactions, e.g. β - glucuronidase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase and acid phosphatase (Elagli et al. 1995). The good biocompatibility and corrosion resistance are due to the naturally forming stable titanium oxide (TiO2) film on titanium surfaces (Zitter et al. 1987, Kasemo et al. 1991).
Particles from titanium arise from the passivation layer of the implant, but they are not titanium ions, but mostly insoluble titanium oxides or suboxides, which are recognized to be biologically inert. Indeed, the passivation layer is immediately reformed after abrasion because of the high oxidizability of titanium. This behavior protects the alloy and prevents the formation of chemical compounds other than oxides (Hildebrand et al. 1998). Tissue discoloration due to titanium oxide particles is sometimes seen around pure titanium implants, but this seems to have no clinical consequences (Onodera et al. 1993, Rosenberg et al. 1993). Experiments with laboratory animals and some limited analyses of human tissues have also revealed evidence of titanium release into distant tissues (Schliephake et al. 1993, Jorgenson et al. 1997).
Wear particles produced by abrasion appear especially in the vicinity of articular prostheses and implants with certain mobility, e.g. uncemented total hip replacements. These particles may induce multiple tissue reactions, including osteolysis, degradation of normal bone structure, severe macrophagic reactions, granuloma, fibrotic capsules and chronic inflammation, which may cause destabilization and loosening of prostheses and implants (Santavirta et al. 1991, Santavirta et al. 1993, Rubash et al. 1998). Particle size and composition are of essential importance in that process. Deleterious reactions have been reported with Ti-6Al-4V based prostheses (Nasser et al. 1990, Rubash et al. 1998), but not with pure titanium implants.
In vitro, pure titanium particles have also been shown to have some effects on cells. Low concentrations may stimulate fibroblast proliferation, while high concentrations may be toxic. At high particle concentrations, titanium caused a decrease in proteolytic and collagenolytic activity in the culture medium. Titanium also elevated the lysosomal enzyme marker, hexosaminidase, except at high concentrations (Maloney et al. 1993).
J Bone Joint Surg Br. 2005 May ;87:628-31 15855362
Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.
[My paper] E Dunstan , A P Sanghrajka , S Tilley , P Unwin , G Blunn , S R Cannon , T W R Briggs
Metal-on-metal hip bearings are being implanted into younger patients. The consequence of elevated levels of potentially carcinogenic metal ions is therefore a cause for concern. We have determined the levels of cobalt (Co), chromium (Cr), titanium (Ti) and vanadium (Va) in the urine and whole blood of patients who had had metal-on-metal and metal-on-polyethylene articulations in situ for more than 30 years. We compared these with each other and with the levels for a control group of subjects.We found significantly elevated levels of whole blood Ti, Va and urinary Cr in all arthroplasty groups. The whole blood and urine levels of Co were grossly elevated, by a factor of 50 and 300 times respectively in patients with loose metal-on-metal articulations when compared with the control group. Stable metal-on-metal articulations showed much lower levels. Elevated levels of whole blood or urinary Co may be useful in identifying metal-on-metal articulations which are loose.
2.7.4. Toxicity and carcinogenicity of nickel
The chemical toxicity of metal inside the body is closely related to the concentration of released ions and wear particles, the toxicity of these elements and the toxicity of the formed compounds. Even a poisonous substance has no toxic effects in small concentrations, while nutritious substances cause adverse responses when present in excessive amounts. It is difficult to know the exact concentrations of metallic compounds released from implanted material, because there are many factors affecting them, such as implantation time and the local conditions (PH, fretting, etc.).
The high nickel content of NiTi (54 % by weight) may cause biocompatibility problems if deleterious amounts if nickel dissolve from it. The toxicity of nickel has been studied using in vitro and in vivo nickel salts, solid nickel or particulate form nickel (Putters et al. 1992, Takamura et al. 1994).
The problem with using metal salts is that the toxicity of different nickel salts vary notably. The benefit of this method is that we know the exact composition of the nickel salt, and it also permits the use of very high concentrations. The benefits and weaknesses of using nickel powder are that the particle itself may have toxic, irritating and even carcinogenic effects. This has been documented with alloys normally non-toxic, such as titanium (Zhang et al. 1998, Maloney et al. 1998). Another problem associated with reading in vitro results is that different cells have different toxic responses. The benefit of using solid nickel is that solid nickel in vitro usually correlates in situation in vivo, but we cannot be sure what kind of compounds have the effect we observe. The benefit of solid and particle material testing is that metal alloys can also be tested. Also, in vitro methods can never simulate the in vivo environment completely, and these results can only be considered suggestive.
Nickel is known to have toxic effects with cellular damage in cell cultures at high concentrations (Putters et al. 1992). It also appears to be harmful to bone in tissue cultures, but less so than cobalt or vanadium, which are also routinely used in implant alloys (Gerber et al. 1980). The toxicity of metal salts in cell cultures has shown decreasing toxicity in the order cobalt > vanadium > nickel > chromium > titanium > iron (Yamamoto et al. 1998). In vitro tests have also shown cobalt, nickel and chromium to have a potency for carcinogenicity.
Pure nickel implanted intramuscularly or inside bone has been found to cause severe local tissue irritation and necrosis (Laing et al. 1967) and to have high carcinogenic and toxic potencies. The tumors that retained nickel were malignant fibrous histiocytomas or fibrosarcomas (Takamura et al. 1994). Inhaled Ni3S2 caused adenomas and carcinomas of the lungs in rats, but nickel oxide and sulphate did not (Oller et al. 1997).
Due to the corrosion of the implants, small amounts of metal ions may also be released into distant organs. Systemic toxicity may be caused by the accumulation, processing, and subsequent reaction of the host to corrosion products (Bergman et al. 1980, Lugowski et al. 1991, Ishimatsu et al. 1995).
When high-dose nickel salts were injected into mice, accumulation and some deleterious effects were seen in the liver, kidney and spleen (Pereira et al. 1998).
We do not know what compounds form inside the body after the implantation of nickel-containing alloys. However, it is likely that NiCl and NiO compounds may form in the body environment, while the most toxic and carcinogenic compounds, e.g. Ni3S2, are not likely to occur. The underlying mechanism of the carcinogens of nickel is still unclear (Hartwig et al. 1994, Oller et al. 1997).
In vivo, Ni2+ ions may cross the cell membrane using the Mg2+ ion transport system. Since the concentration of Mg2+ inside and outside the cell is in the millimolar range, the levels of soluble nickel needed to compete with Mg2+ for its uptake must be at least in the millimolar range. Additionally, once Ni2+ is inside the cell, it binds to cytoplasmic ligands and it does not accumulate in the cell nucleus at the concentrations needed to have a genetic effect (Abbracchio et al. 1982a, Abbracchio et al. 1982b). In addition, soluble Ni2+ is rapidly cleared in vivo, which is why no direct efficient delivery of Ni2+ to the target site within the cell nucleus may occur to cause carcinogenic effects in vivo (Oller et al. 1997). Thus, carcinogenesis seems to be related to some nickel compounds rather than Ni2+ ions.
Another way in which nickel may be harmful is the effect of phagocytosed nickel compound particles. Some of the characteristics of nickel compounds that increase their ability to be endocytosed include crystalline nature, negative surface charge, 2–4 µm range particle size, and low solubility (Sunderman et al. 1987). Ni3S2 and NiO, which show otherwise low in vivo solubility may act by this mechanism (Dunnick et al. 1995). It was shown early on that endocytosis by target cells was likely to play an important role in the transforming potential of nickel compounds (Costa et al. 1980). When the nickel compound particles are endocytosed by the target cells, the endocytic vesicles are acidified by fusion with lysosomes and Ni2+ is released. Deleterious changes, such as the formation of oxygen radicals and DNA damage and the inactivation of tumor supressor genes, may occur (Klein et al. 1991a, Klein et al. 1991b).
Pathological alterations of nickel metabolism have been recognized in several human diseases. The diverse clinical manifestations of nickel toxicology include (1) acute pneumonitis from inhalation of nickel carbonyl, (2) chronic rhinitis and sinusitis from inhalation of nickel aerosols, (3) cancers of nasal cavities and lungs in nickel workers, and (4) dermatitis and other hypersensitive reactions from cutaneous and parental exposures to nickel alloys (Sunderman 1977).
2.7.5. Nickel-containing biomaterial alloys in humans
Neoplasms associated with clinical implants are very rare. They may be related more to the physical than the chemical configuration of the implant. The mechanism of tumor formation is not understood, but it appears to be related to the implant fibrous capsule (Schoen 1996). Occasional reports on humans have been published, which report the development of malignant fibrous histiocytomas and osteosarcomas at the site of a prosthetic replacement or previous internal fixation. Most of these (> 80%) have been related to the cobalt-chromium alloy, some to stainless steel or other nickel-containing alloys, and none to titanium (Rock 1998).
The low toxicity of a constituent does not exclude the possibility of deleterious effects. As local or systemic toxicity is usually dose-dependent, reactions caused by the immune response may activate at much lower thresholds (Remes et al. 1992).
Nickel is the major cause of allergic contact dermatitis (Peltonen 1979). Epidemiological studies have shown a sensitization frequency up to 20 % in young females and 10 % in the elderly (Menne 1996). Two to four percent of males are sensitized. Most cases of nickel allergy may be related to skin contact with nickel-containing metallic items. The significant biological parameter is not the nickel concentration in the alloy or the coating, but the amount released to the skin during exposure to human sweat. A threshold of 0.5 microgram/cm2/week has been established, at which only a minor part of nickel-sensitive subjects will react (Menne 1996).
When implants containing perceptible amounts of nickel, for example, stainless steel implants (nickel content 10-14 %), are clinically used inside the body, no sensitization or immune disorders commonly occur (Christensen 1990, Gawkrodger 1993). Why could it be used even in patients with nickel contact dermatitis?
Allergic contact dermatitis is a cell-mediated immune response caused by Ni2+ ions. In fact, the nickel ion itself is too small to act as an antigen. It binds with a carrier protein and acts as a hapten. The nickel-protein complex activates Langerhans’ cells in the skin, which presents an antigen to T-lymphocytes. Memory T-cells develop. When circulating in the body, these memory cells are able to start cell-mediated immune reactions upon meeting the same allergen again.
The antigenic determinants created by nickel as well as the mechanisms of recognition by specific T-cell clones have not been elucidated (Moulon et al. 1995). T-cells detect haptens as structural entities attached covalently or by complexion to self-peptides anchored in the binding grooves of major histocompatibility antigens (MHC proteins) (Weltzien et al. 1996).
Two major types of hapten-specific T-cell receptors have been identified: one reacting to hapten regardless of the chemical composition of the carrier peptide, and the other contacting hapten and peptide via two apparently independent contact sites (Martin et al. 1994). The present study suggests that the presence of specific CD8+ T-cells and a distinct pattern of cytokine release (e.g. augmented production of interleukin-10) by CD4+ T-cells may be important elements in determining whether a hapten induces allergy or a silent immune response (Cavani et al. 1998). T lymphocytes are critical effectors in the pathogenesis of contact hypersensitivity. Nickel-specific CD4+ T helper cells have been extensively characterized. The characterization of nickel-specific cytotoxic CD8+ T-cells with different requirements for nickel-specific target lysis may have important implications for the development or control of human contact hypersensitivity reactions to nickel in vivo (Moulon et al. 1998).
The intercellular adhesion molecule-1 (ICAM-1), the vascular cell adhesion molecule-1 (VCAM-1), and the endothelial leukocyte adhesion molecule-1 (ELAM-1, E-selectin) are endothelial surface molecules that play a role in leukocyte recruitment to sites of inflammation during, for instance, contact hypersensitivity. NiCl2 and, to a lesser extent, CoCl2 were found to up-regulate ICAM-1, VCAM-1, and ELAM-1 expression on cultured human umbilical vein endothelium. Both Ni2+ and Co2+ , which frequently induce simultaneous contact sensitivity, have the ability to directly up-regulate endothelial adhesion molecules. This shared property may represent an adjuvant mechanism that promotes sensitization and elicitation events in contact hypersensitivity to these haptens (Goebeler et al. 1993). It was observed recently that Ni ions can either promote or suppress the expression of the intercellular adhesion molecule 1 (ICAM-1) on endothelial cells, depending on their concentration and probably the time of exposure. ICAM-1 is known to be involved in the recruitment of inflammatory cells from the bloodstream. Ni ions could promote the expression of ICAM-1 at concentrations high enough to suppress cell metabolic activity. At lower concentrations, they suppress ICAM expression (Wataha et al. 1997).
Control of the allergic reaction also requires inhibitory systems which prevent the immune response from causing systemic damage. To control the reactions, several kinds of suppressor T-cells are generated at different levels (Barnetson et al. 1993). Unresponsiveness to oral exposure (oral tolerance) to nickel is due the action of these suppressor cells (van Hoogstraten et al. 1992, Ishii et al. 1993). This is also the presumptive explanation for why sensitization and immune disorders from metallic prostheses are very unusual, although, for example, the stainless steel used in implants contains perceptible amounts of nickel (Bjurholm et al. 1990, Gawkrodger 1993, Milavec-Puretic et al. 1998).