163 8 Organometallic Compounds 8.1 BACKGROUND Metalloids such as arsenic and antimony, and metals such as mercury, lead, and tin—which occupy a similar location to metalloids in the periodic system—all tend to form stable covalent bonds with organic groups. Some authorities regard tin as a metalloid. By contrast, metals such as sodium, potassium, calcium, strontium, and barium, which belong to groups 1 and 2 of the periodic system, do not form cova- lent bonds with organic groups. The compounds used as examples here all possess covalent linkages between a metal and an organic group—most commonly an alkyl group. The elements in question are mercury, tin, lead, and arsenic, all of which are appreciably toxic in their inorganic forms as well as in their organometallic forms. The attachment of the organic group to the metal can bring fundamental changes in its chemical properties, and consequently in its environmental fate and toxic action. In particular, the attachment of alkyl or other nonpolar groups to metals increases lipophilicity and thereby enhances movement into and across biological membranes, storage in fat depots, and adsorption by the colloids of soils and sediments. Thus, the question of speciation is critical to understanding the ecotoxicology of these metals. In the rst place, organometallic compounds of mercury, tin, lead, and arsenic have been produced commercially, mainly for use as pesticides, biocides, or bacte- ricides. Additionally, methyl mercury and methyl arsenic are generated from their inorganic forms in the environment, so residues of them may be both anthropogenic and natural in origin. Most of the following account will be devoted to organomer- cury and organotin compounds, which have been extensively studied. Organolead and organoarsenic compounds have received less attention from an ecotoxicological point of view, and will be dealt with only briey. 8.2 ORGANOMERCURY COMPOUNDS 8.2.1 O RIGINS AND CHEMICAL PROPERTIES A range of organomercury compounds have been produced commercially since early in the 20th century, principally for use as antifungal agents. Most of them have the gen- eral formula R–Hg–X, where R is an organic group and X is usually an inorganic group (occasionally a polar organic group such as acetate). The organic group is nonpolar (or relatively so) and gives the molecule a lipophilic character. The most common organic groups are alkyl, phenyl, and methoxyethyl (see Environmental Health Criteria 86). © 2009 by Taylor & Francis Group, LLC 164 Organic Pollutants: An Ecotoxicological Perspective, Second Edition The solubility of organomercury compounds depends primarily on the nature of the X group; nitrates and sulfates tend to be “salt-like” and relatively water-soluble, whereas chlorides are covalent, nonpolar compounds of low water solubility. Methyl mercury compounds tend to be more volatile than other organomercury compounds. The structures of some organomercury compounds are shown in Figure 8.1, and some physical properties are given in Table 8.1 The R–Hg bond is chemically stable and is not split by water or weak acids or bases. This is a reection of the low afnity of Hg for oxygen. It can, however, be readily broken biochemically. Organomercury, like other organometallic com- pounds, has a strong afnity for SH–groups of proteins and peptides. R–Hg–X + protein-SH n R–Hg–S-protein + X − + H + This tendency to interact with –SH groups appears to be the fundamental chemi- cal reaction behind most of the adverse biochemical effects of organomercury com- pounds; it is also the basis for one mechanism of detoxication. Apart from the release of human-made organomercurial compounds, methyl mer- cury can also be generated from inorganic mercury in the environment as indicated in the following equation: Hg n Hg ++ n CH 3 Hg + n [CH 3 ] 2 Hg Thus, both elemental mercury and the mineral form cinnabar (HgS) can release Hg ++ , the mercuric ion. Bacteria can then methylate it to form sequentially CH 3 Hg + , the methyl mercuric cation, and dimethyl mercury. The latter, like elemental mercury, is volatile and tends to pass into the atmosphere when formed. The methylation of mercury can be accomplished in the environment by bacteria, notably in sediments. TABLE 8.1 Properties of Organomercury Compounds Compound Water Sol mg/L Vapor Pressure mm Hg Methyl mercuric chloride 1.4 8.5 × 10 −3 Phenylmercuric acetate 4400 — Phenylmercuric acetate Hg CH 3 HgCl Where R = C n H 2n+1 , C 6 H 5 or CH 3 OC 2 H 5 Methylmercuric chloride General formula RHgX O O CCH 3 FIGURE 8.1 Organomercury compounds. © 2009 by Taylor & Francis Group, LLC Organometallic Compounds 165 A form of vitamin B12 can produce methyl carbanion, a reactive species that is responsible for methylation of Hg ++ (see Figure 8.2, Craig 1986, and IAEA Technical Report 137). Methyl carbanion acts as a nucleophilic agent toward Hg ions. It is difcult to establish to what extent methyl mercury residues found in the environment arise from natural as opposed to human sources. There is no doubt, however, that natural generation of methyl mercury makes a signicant contribution to these residues. Samples of Tuna sh caught in the late 18th century, before the synthesis of organomercury compounds by humans, contain signicant quantities of methyl mercury. 8.2.2 METABOLISM OF ORGANOMERCURY COMPOUNDS As mentioned earlier, methyl mercury compounds can undergo further methylation to generate highly volatile dimethyl mercury. Organomercury compounds can also be converted back into inorganic forms of mercury by enzymic action. Oxidative metabolism is important here, and has been reported in both microorganisms and invertebrates. Methyl mercury is slowly degraded by alpha oxidation, whereas other alkyl forms are subject to more rapid beta oxidation. This may explain why methyl mercury is degraded more slowly than other forms and is correspondingly more persistent. Phenyl mercury is degraded relatively rapidly to inorganic mercury by vertebrates and is generally less persistent than alkyl mercury. R–Hg + n Hg ++ Another type of detoxication involves the production of cysteine conjugates, which are readily excreted. (Again, organomercury compounds show their afnity for –SH groups). Methyl mercuric cysteine is an important biliary metabolite in the rat and is degraded within the gut (presumably by microorganisms) to release inorganic mer- cury (see IAEA Report 137, 1972). The following ranges of half-lives have been reported for vertebrate species, which are presumably related to rates of biotransformation as the original lipophilic compounds show little tendency to be excreted unchanged. Alkyl mercury 15–25 days Phenyl mercury 2–5 days CH 3 OH 2 R Co N NN Methylcobalamine Methylmercuric ion N Hg + + CH 3 R Co N + Hg 2+ + H 2 O NN N FIGURE 8.2 Methylation of inorganic mercury by methylcobalamine (from Crosby 1998). © 2009 by Taylor & Francis Group, LLC 166 Organic Pollutants: An Ecotoxicological Perspective, Second Edition 8.2.3 ENVIRONMENTAL FATE OF ORGANOMERCURY As noted earlier, diverse forms of organomercury are released into the environment as a consequence of human activity. Methyl mercury presents a particular case. As a product of the chemical industry, it may be released directly into the environment, or it may be synthesized in the environment from inorganic mercury which, in turn, is released into the environment as a consequence of both natural processes (e.g., weathering of minerals) and human activity (mining, factory efuents, etc.). The environmental cycling of methyl mercury is summarized in Figure 8.3. Dimethyl mercury, being highly volatile, tends to move into the atmosphere following its generation in sediments; once there, it can be converted back into elemental mer- cury by the action of UV light. Some dimethyl mercury is taken up by sh and transformed into a methyl cysteine conjugate, which is excreted. However, the most important species of methyl mercury in aquatic and terrestrial food chains is CH 3 Hg + , which exists in various states of combination with S– groups of proteins and peptides, and with inorganic ions such as chloride. Total methyl mercury of tissues, sediments, etc., is determined by chemical analysis, but the state of combination is not usually known. Some free forms of methyl mercury, for example, CH 3 HgCl, are highly lipophilic and undergo bioaccumulation and bioconcentration with progres- sion along food chains in similar fashion to lipophilic polychlorinated compounds. In a report from the U.S. EPA (1980), sh contained between 10,000 and 100,000 times the concentration of methyl mercury present in ambient water. In a study of methyl mercury in sh from different oceans, higher levels were reported in pred- ators than in nonpredators (see Table 8.2). Taken overall, these data suggest that predators have some four- to eightfold higher levels of methyl mercury than do non- predators, and it appears that there is marked bioaccumulation with transfer from prey to predator. In a laboratory study (Borg et al. 1970), bioaccumulation of methyl mercury was studied in the goshawk (Accipiter gentilis). The details are shown in Table 8.3 below. Thus, chickens bioaccumulated methyl mercury to about twice the level in their food, whereas goshawks bioaccumulated methyl mercury to about four times the level present in the chicken upon which they were fed. The period of exposure was similar (CH 3 ) 2 Hg (CH 3 ) 2 Hg C 2 H 6 Hg Atmosphere Water Sediment Hg CH 3 Hg + HgS Hg 2+ Bacteria Bacteria FIGURE 8.3 Environmental fate of methyl mercury (adapted from Crosby 1998). © 2009 by Taylor & Francis Group, LLC Organometallic Compounds 167 in both cases. This provides further evidence for the slow elimination of methyl mer- cury by vertebrates and the relatively poor detoxifying capacity of predatory birds toward lipophilic xenobiotics compared to nonpredatory birds (see Chapters 2 and 5). In a related study with ferrets fed chicken contaminated with methyl mercury, a somewhat higher bioaccumulation factor was indicated (about sixfold), albeit over the somewhat longer exposure period of 35–58 days. This provided further evidence for strong bioaccumulation by predators. Since the widespread banning of organomercury fungicides, signicant levels of organomercury have continued to be found in certain areas—much of it, presumably, having been biosynthesized from inorganic mercury. Particular interest has come to be focused on methyl mercury pollution of the aquatic environment and on levels in sh and piscivorous birds. In North America, the common loon (Gavia immer) has been identied as a suitable indicator organism for this type of pollution (Evers et al. 2008). The half-life of methyl mercury in the blood of juvenile loons after moult- ing has been estimated to be 116 days (Fournier et al. 2002). In another study, the methyl mercury half-life in blood of another piscivorous bird, Cory’s shearwater (Calonectris diomedea), was estimated to be 40–60 days (Monteiro and Furness 2001). The ecological effects of methyl mercury on common loons will be discussed later in Section 8.2.5. Apart from CH 3 Hg + , other forms of R-Hg + have been found in the natural environ- ment, which originate from anthropogenic sources but are not known to be generated from inorganic mercury. These forms have been found in terrestrial and aquatic food chains. A major source has been fungicides, in which the R group is phenyl, alkoxy- alkyl, or higher alkyl (ethyl, propyl, etc.). These forms behave in a similar manner TABLE 8.2 Methyl Mercury Residues in Fish (mg Hg/kg wet weight) Type of Fish Atlantic Ocean Pacific Ocean Indian Ocean Mediterranean Sea Nonpredators 0.03–0.27 0.03–0.25 0.005–0.16 0.1–0.24 Predators 0.3–1.3 0.3–1.6 0.004–1.5 1.2–1.8. Source: Data from Environmental Health Criteria 101 Methylmercury. TABLE 8.3 Bioaccumulation of Methylmercury Material/Species CH 3 Hg (ppm Hg) Duration of Feeding (days) Approximate Bioaccumulation Factor Dressed grain 8 Muscle of chickens fed dressed grain 10–40 40–44 2 Chicken tissue fed to goshawks 10–13 Muscle from goshawks fed chicken tissue 40–50 30–47 4 © 2009 by Taylor & Francis Group, LLC 168 Organic Pollutants: An Ecotoxicological Perspective, Second Edition to CH 3 –Hg X and do tend to undergo biomagnication, but they are generally more easily biodegradable to inorganic mercury and tend to bioaccumulate less strongly. At one time, a major source of organomercury pollution in Western countries was fungicidal seed dressings used on cereals and other agricultural products (see IAEA Technical Report 137 1972). Another important source was organomercury antifun- gal agents used in the wood pulp and paper industry. Most of these uses were discon- tinued by the 1970s, but certain practices have continued into the 1990s, including the use of phenylmercury fungicides as seed dressings in Britain and some other countries. In the 1950s and early 1960s, Sweden and other Scandinavian countries had serious pollution problems due to the use of methyl mercury compounds as seed dressings. Deaths of seed-eating birds and raptors preying upon them were attributed to methyl mercury poisoning (Borg et al. 1969). Thus, as with dieldrin, bioaccumula- tion led to secondary poisoning. Interestingly, seed-eating rodents contained lower mercury levels than seed-eating birds. Some data for total mercury levels found in Swedish birds during the mid-1960s are shown in Figure 8.4. Most of the mercury was in the methyl form. Findings such as these led to the banning of methyl mercury seed dressings in Scandinavia. Other forms of organomercury seed dressing (e.g., phenyl mercury) were not implicated in poisoning incidents and continued to be mar- keted in many Western countries after methyl mercury compounds were banned. 8.2.4 TOXICITY OF ORGANOMERCURY COMPOUNDS The toxicity of organomercury, like that of certain other types of organometals, has been related to their strong afnity for functional –SH groups of proteins (Crosby 1998). Exposure of animals to organic mercury leads to a reduction in the num- ber of free –SH groups in their tissues. Both mercury and methyl mercury bind strongly to these groups. This is consistent with the wide range of physiological and Mercury Content in Parts per Million Non-predatory birds 1050.5 60 40 20 0 60 50 40 20 0 21 20 10522040 All samples above 20 ppm All samples above 40 ppm All samples below 0.5 ppm Percentage of Whole Sample Containing Concentration within Stated Range All samples below 2 ppm Birds of prey FIGURE 8.4 Mercury residues in the livers of Swedish birds (from Walker 1975). © 2009 by Taylor & Francis Group, LLC Organometallic Compounds 169 biochemical effects arising from mercury poisoning, for many proteins depend on free –SH groups for their normal function. A prime target for methyl and other organic forms of mercury is the nervous system, especially the central nervous system (CNS). Here lies an important distinc- tion between the toxicity of organic and inorganic mercury salts. Although inorganic forms of mercury can also bind to –SH groups, they cannot readily cross the blood– brain barrier, and so show less tendency than lipophilic organic mercury to reach the CNS and cause toxic effects there. Rather, inorganic mercury expresses its toxicity elsewhere (e.g., in the kidney and on cardiac function). Methyl mercury can cause extensive brain damage, including degeneration of small sensory neurons of the cerebral cortex. At the biochemical level, it binds to cysteine groups of acetylcholine receptors (Crosby 1998) and also inhibits Na + /K + ATP-ase (Clarkson 1987). With growing interest in the sublethal effects of methyl mercury, evidence has come to light of changes in the concentration of neurochemical receptors of the brain during the early stages of poisoning. Studies with mink dosed in captivity have shown that environmentally realistic levels of methyl mercury can cause (1) an increase in the concentration of brain muscarinic receptors for acetylcholine, and (2) a decrease in the concentration of N-methyl--aspartic acid glutamate receptors for glutamate (Basu et al. 2006, and Scheuhammer and Sandheinrich 2008). In the next section, eld studies will be discussed, which have looked for evidence of effects of this kind in wild mammals and birds. BOX 8.1 THE MINAMATA INCIDENT The neurotoxicity of organomercury was graphically illustrated in an envi- ronmental disaster at Minamata Bay in Japan during the late 1950s and early 1960s. Release of both organic and inorganic mercury from a factory led to the appearance of high levels of methyl mercury in the neighboring marine ecosystem. Levels were high enough in sh to cause lethal intoxication of local people for whom sh was the main protein source. People died as a conse- quence of brain damage caused by methyl mercury. The victims had brain Hg levels in excess of 50 ppm. In mammals, methyl mercury toxicity is mainly manifest as damage to the CNS with associated behavioral effects (Wolfe et al. 1998). Initially, animals become anorexic and lethargic and, with progression of toxicity, muscle ataxia and visual impairment are seen. Finally, convulsions occur, which lead to death. In dosing experiments with mink (Mustela vison), dietary levels of methyl mercury of 1.1 ppm fed over a period of 93 days produced subclinical neurological lesions (Wobeser et al. 1976), and this has been proposed as a lowest observed adverse effect level (LOAEL). In another study, otters (Lutra canadensis) were dosed with 2, 4, or 8 ppm methyl mercury in the diet (Connor and Nielsen 1981). Anorexia and ataxia were reported at 2 ppm in two-thirds of individuals; anorexia, ataxia, and neurologi- cal lesions at 4 ppm; and all the symptoms, leading to death at 8 ppm. The brain Hg concentrations (ppm per unit wet weight) at dose levels of 2, 4, and 8 ppm were © 2009 by Taylor & Francis Group, LLC 170 Organic Pollutants: An Ecotoxicological Perspective, Second Edition 13.3, 21, and 23.7 ppm, respectively. Thus, symptoms of neurotoxicity were observed in individuals containing brain concentrations of Hg substantially lower than those associated with lethal toxicity. Interestingly, the proportion of the total mercury accounted for as organomercury declined with time, indicating that demethylation slowly occurred in the brain. Captive goshawks dying from methyl mercury poisoning contained 30–40 ppm Hg in brain and 40–50 ppm Hg in muscle (Borg et al. 1970, see also Section 8.2.3). In this study and others (Wolfe et al. 1998), it became apparent that birds, like mam- mals, experience a range of sublethal effects before tissue levels became high enough to cause death. The rst symptoms of methyl mercury poisoning in birds are reduced food consumption and weakness of the extremities. Muscular coordination is poor, there is ataxia, and birds can neither walk nor y (See Rissanen and Mietinnen in IAEA Technical Report 137 1972). The severity of sublethal neurotoxic effects produced by methyl mercury would have reduced the likelihood of predatory birds acquiring lethal concentrations of methyl mercury when chronically exposed in the eld. More likely they would have died from starvation due to sublethal effects before they could build up lethal concentrations. Predators would lose their ability to catch prey once muscular coordination was affected. These feeding skills are not tested in laboratory trials in which birds are presented with food and they may be expected to tolerate relatively high levels of methyl mercury in tissues before losing their ability to feed. This contrasts with acute exposures in the eld where predators sometimes consumed high doses of methyl mercury in poisoned prey, and a single meal might have contained a lethal dose for the predator. More generally, impairment of ability to y would have adversely affected herbivores and omnivores in their ability to feed or escape predation. The acute toxicity of different types of organomercury compounds to mammals, expressed as mg/kg, fall into the following ranges: Methyl mercury compounds 16–32 Ethyl mercury compounds 16–28 Phenyl mercury compounds 5–70 Thus, there is not a great deal of difference between the three classes in acute toxic- ity; all are highly toxic. However, methyl mercury is more persistent than the other two types, and so has the greater potential to cause chronic toxicity. The latter point is important when considering the possibility of sublethal effects. 8.2.5 ECOLOGICAL EFFECTS OF ORGANOMERCURY COMPOUNDS Of the different forms of organomercury, methyl mercury is the one most clearly implicated in toxic effects in the eld. When methyl mercury seed dressings were used in Sweden and other Northern European countries during the 1950s and 1960s, many deaths of seed-eating birds, and of predatory birds feeding upon them, were attributed to methyl mercury poisoning. There was evidence of birds experiencing sublethal effects such as inability to y. There may well have been local declines of bird populations consequent upon these effects, but these were not clearly established © 2009 by Taylor & Francis Group, LLC Organometallic Compounds 171 at the time. Methyl mercury seed dressings were subsequently banned in Western countries, so the question is now rather an academic one. Another major incident concerning methyl mercury was the severe pollution of Minamata bay in Japan (see Box 8.1). Here sh, sh-eating and scavenging birds, and humans feeding upon sh all died from organomercury poisoning. There may have been localized declines of marine species in this area due to methyl mercury, but there is no clear evidence of this. Despite the banning of methyl mercury fungicides, methyl mercury continues to exist in some areas at levels high enough to cause adverse ecological effects. In a wide-ranging review, Wolfe et al. (1998) cite a number of studies that give evidence of sublethal effects of methyl mercury upon wild vertebrates in the time since severe restrictions were placed on the use of methyl mercury fungicides. A major reason for this is the continuing synthesis of methyl mercury in the environment from inorganic mercury, the latter originating from both natural and human sources. There has been particular concern about some aquatic habitats, for it appears that a very high per- centage of total mercury in the higher trophic levels of aquatic food chains is in the form of methyl mercury. Indeed, more than 95% of the mercury found in the tissues of sh and marine invertebrates sampled from different oceans of the world was found to be in this form (Bloom 1992, Wolfe et al. 2007). Relatively high levels have been reported in lakes of Northern America, including the Great Lakes (Meyer et al. 1998; Evers et al. 1998, 2003, and 2008), and in the Mediterranean Sea (Renzoni in Walker and Livingstone 1992, Aguilar and Borrell 1994, Aguilar et al. 1996). Apart from the question of possible direct toxic effects caused by methyl mercury, there is also the possibility that there are adverse interactive effects (potentiation) with other pollutants such as PCBs, PCDDs, PCDFs, p,pb-DDE, metals, and selenium, which reach signicant levels in aquatic organisms (Walker and Livingstone 1992, Heinz and Hoffman 1998). The common loon (Gavia immer) is one sh-eating bird inhabiting lakes of North America that has been closely studied in connection with organomercury pollution (Evers et al. 2002, 2003, and 2008). Eggs collected between 1995 and 2001 in this area contained 0.07–4.42 g/g Hg (wet weight). Although fertility was not related to the mercury content of eggs, there was an inverse relationship between Hg content and egg volume. Female loons with blood Hg concentrations of >3.0 g/g laid eggs containing >1.3 g/g and often had decreased reproductive success, laying fewer eggs than the less contaminated individuals (Evers et al. 2008). Adult common loons collected in Canada were analyzed for total and methyl mercury and for neurochemi- cal receptors (Scheuhammer et al. 2008). Most of the mercury in brain was in methyl form (>78% in all cases). A positive correlation was found between total mercury in brain and the concentration of brain muscarinic receptors. On the other hand, a negative correlation was found between total mercury and N-methyl--aspartic acid receptors. This immediately raises questions about possible neurotoxic and behav- ioral effects due to methyl mercury. Similar correlations were also reported for bald eagles in the same study. In a study conducted during the period 1998–2000 at North American sites, the relationship was studied between methyl mercury blood levels in common loons and behavioral parameters (Evers et al. 2008). Adult behaviors were divided into two © 2009 by Taylor & Francis Group, LLC 172 Organic Pollutants: An Ecotoxicological Perspective, Second Edition categories: (1) high-energy and (2) low-energy. A negative correlation was found between high-energy behaviors and total mercury concentration in the blood of adult loons. High-energy behaviors included foraging for chicks, foraging for self, swimming and ying, preening, and agonistic behaviors. There was also a strong negative correlation between mercury levels in female loons and reproductive suc- cess (Burgess and Meyer 2008, Evers et al. 2008). In a laboratory investigation, adverse effects were observed when loon chicks were dosed with levels of methyl mercury comparable to the highest levels of exposure recorded in the preceding study (Kenow et al. 2007). There was evidence of demyelination of central nervous tissue and reduced immune function when the chicks were fed sh containing 0.4 g/g of methyl mercury or more. The mink (Mustela vision) is a piscivorous mammal that also has been exposed to relatively high dietary levels of methyl mercury in North America in recent times. In a Canadian study, mink trapped in Yukon territory, Ontario, and Nova Scotia were analyzed for levels of mercury and abundance of muscarinic, cholinergic and dop- aminergic receptors in the brain (Basu et al. 2005). A correlation was found between total Hg levels and abundance of muscarinic receptors, but a negative correlation was found between total Hg and abundance of dopaminergic receptors. Thus, it was suggested that environmentally relevant concentrations of Hg (much of it in methyl form) may alter neurochemical function. The highest levels of mercury contamina- tion were found in mink from Nova Scotia that had a mean concentration of total Hg of 5.7 g/g in brain, 90% of which was methyl mercury. 8.3 ORGANOTIN COMPOUNDS 8.3.1 C HEMICAL PROPERTIES Like mercury, tin is a metal that has a tendency to form covalent bonds with organic groups. The compounds to be discussed here are tributyl derivatives of tetravalent tin. The general formula for them is [n-C 4 H 9 ] 3 Sn-X, where X is an anion. The most important of the compounds from an ecotoxicological point of view, and the one that will be used here as an example, is tributyltin oxide (TBTO). Its struc- ture is shown in Figure 8.5. TBTO is a colorless liquid of low water solubility and low polarity. Its water solu- bility varies between <1.0 and >100 mg/L, depending on the pH, temperature, and presence of other anions. These other anions determine the speciation of tributyltin in natural waters. Thus, in sea water, TBT exists largely as hydroxide, chloride, and carbonate, the structures of which are given in Figure 8.5. At pH values below 7.0, the predominant forms are the chloride and the protonated hydroxide; at pH8 they are the chloride, hydroxide, and carbonate; and at pH values above 10 they are the hydroxide and the carbonate (EHC 116). The K ow for TBTO expressed as log P ow lies between 3.19 and 3.84 for distilled water, and is about 3.54 for sea water. TBTO is adsorbed strongly to particulate matter. © 2009 by Taylor & Francis Group, LLC [...]... such as lead nitrate and lead dichloride are ionic and water soluble Covalent and lipophilic forms of lead, like lipophilic forms of organomercury and organotin, can readily cross membranous barriers such as the © 2009 by Taylor & Francis Group, LLC 1 78 Organic Pollutants: An Ecotoxicological Perspective, Second Edition blood–brain barrier Consequently, they readily enter the CNS of animals, where they... plants, and textile mills; and as molluscicides Of particular interest and importance is their incorporation into antifouling paints used on boats of many kinds ranging from small leisure craft to large oceangoing vessels Release of TBT from antifouling paints has provided a small yet highly significant source of pollution to surface waters © 2009 by Taylor & Francis Group, LLC 174 Organic Pollutants:. .. following a ban on use of TBT on small craft ( . R–Hg–X, where R is an organic group and X is usually an inorganic group (occasionally a polar organic group such as acetate). The organic group is nonpolar (or relatively so) and gives the molecule. common organic groups are alkyl, phenyl, and methoxyethyl (see Environmental Health Criteria 86 ). © 2009 by Taylor & Francis Group, LLC 164 Organic Pollutants: An Ecotoxicological Perspective, . H 2 O NN N FIGURE 8. 2 Methylation of inorganic mercury by methylcobalamine (from Crosby 19 98) . © 2009 by Taylor & Francis Group, LLC 166 Organic Pollutants: An Ecotoxicological Perspective, Second