Органотұтық қосылыстары: Трибутилтұтық және оның экологиялық әсері

Group of organotin compounds

Tributyltin (TBT) is an umbrella term for a class of organotin compounds which contain the |(C4H9)3Sn group, with a prominent example being tributyltin oxide. For 40 years TBT was used as a biocide in anti fouling paint, commonly known as bottom paint, applied to the hulls of oceangoing vessels. Bottom paint improves ship performance and durability as it reduces the rate of biofouling, the growth of organisms on the ship's hull. The TBT slowly leaches out into the marine environment where it is highly toxic toward nontarget organisms. TBT toxicity can lead to biomagnification or bioaccumulation within such nontarget organisms like invertebrates, vertebrates, and a variety of mammals. TBT is also an obesogen. After it led to collapse of local populations of organisms, TBT was banned.

TBT, or tributyltin, tributylstannyl or tributyl stannic hydride compounds are organotin compounds. They have three butyl groups covalently bonded to a tin(IV) atom. A general formula for these compounds is |(CH3CH2CH2CH2)3Sn\sX. The |\sX is typically a chloride |\sCl, hydroxide |\sOH, or a carboxylate |RCO2\s, where R is an organyl group. TBT is also known to be an endocrine disrupting compound, which influences biological activities such as growth, reproduction and other physiological processes. TBT compounds have a low water solubility, a property that is ideal for antifouling agents. The toxicity of TBT prevents the growth of algae, barnacles, molluscs and other organisms on ships hulls. When introduced into a marine or aquatic environment, TBT adheres to bed sediments. TBT has a low Log Kow of 3.19 – 3.84 in distilled water and 3.54 for sea water, this makes TBT moderately hydrophobic. TBT compounds have a high fat solubility and tend to absorb more readily to organic matter in soils or sediment. The bioaccumulation of TBT in organisms such as molluscs, oysters and dolphins, have extreme effects on their reproductive systems, central nervous systems and endocrine systems. However, the adsorption of TBT to sediments is reversible and depends on pH level in the body of water. TBT has a half life of one or two weeks in marine water. Studies have shown that 95% of TBT can be released from the sediments back into the aquatic environment. This absorption process can complicate quantification of TBT in an environment, since its concentration in the water is not representative of its availability. Another use of TBT is that they were used as stabilizers in compounds like polyvinyl chlorides. Toxic effects in some species occur at 1 nanogram per liter of water. Air pollution from TBT has not been noticed or considered significant enough to effect the environment. In the water, photodegradation and microorganisms can break down TBT and leach into the soil sediments. The bioaccumulation increases over time, leading to a biomagnification in organisms higher up the food chain, although the biomagnification is not that considerable in size. As TBT can remain in the environment for up to 30 years due to often bonding to suspended material and sediments, it can remain in an ecosystem for a very long time. This means that bioaccumulation readily occurs in marine environments, which can lead to very high amounts of TBT being accumulated, especially in smaller organisms at the bottom of the food chain, which in turn has various health effects.

Exposure to organotin compounds causes the development of male accessory sex organs in female prosobranch gastropods. This phenomenon has been termed imposex. TBT has been shown to affect invertebrate development. Marine snails, such as the dog whelk (Nucella lapillus), has often been used as an indicator species. In gastropods, the normal process of accessory sex organ development is retinoid dependent, as has been proven by the effect 9cisRA has on male penises. TBTs mimic the endogenous ligand of Retinoid X Receptor (9cisRA), and thus activates the signalling cascades that are retinoid acid dependent, promoting female penis growth. There have been many theories as to why molluscs are affected by TBT. For example, previous literature has stated that TBT would cause the inhibition of aromatase which would lead to an increase in testosterone and therefore, causing imposex. It was theorized that TBT disrupts endocrine system by inhibiting cytochrome P450 molecule. Among its myriad functions, P450 converts androgen, which has male hormone properties, into oestrogen, which has female hormone properties. It was theorized that the high concentration of androgen lead to the masculinization of females. Another indicator species is Chironomus riparius, a species of non biting midge, which has been used to test the effects of TBT on development and reproduction at sublethal concentrations found in marine environments. Higher concentrations of TBT were found to increase the female population and the results are interesting because unlike the masculinization of the stengoglassan gastropods, feminization was present. Studies have shown that TBT is detrimental to the immune system. Research shows that TBT reduces resistance to infection in fish which live on the seabed and are exposed to high levels of TBT. These areas tend to have silty sediment like harbours and estuaries. Otters dying of infectious causes tended to have higher levels of tissue butyltins than those dying of trauma or other causes. It was also reported by scientists that sea otters typically stay near boats and closed off marinas, which may have led to these organisms experiencing higher levels of butyltins. TBT has been shown to lead to immunosuppression in sea otters and dolphins. TBT has also been linked to hearing loss in mammalian top predators such as toothed whales. In rats, the hypothalamus pituitary adrenal (HPA) axis can be affected by TBT. In the pituitary and adrenal glands, there have been findings of morphophysiological changes within rats affected by TBT. TBT can also affect humans as well. Humans can be exposed to these compounds and potentially experience headaches, fatigue, respiratory issues, and more. Long term exposure can also lead to damage of some internal organs such as the kidneys and liver.

Bans on TBT on boats less than 25 metres long first started in the 1980s. In 1990, the Marine Environment Protection Committee adopted Resolution MEPC 46(30), which recommended that the Government eliminate the use of TBT containing antifouling paints on smaller vessels. This resolution was intended to be a temporary restriction until the International Maritime Organization could implement a ban of TBT anti fouling agents for ships. Several countries followed and in 1997, Japan banned the production of TBT based anti fouling paints. The IMO began to use an Assembly resolution in 1999 that essentially wanted the MPEC to fix the severe environmental effects of the anti fouling systems. This led to a worldwide ban on organotin compound applications on ships starting in 2003. It states that ships cannot bear organotin compounds on their hulls or external parts or surfaces, unless there is a coating that forms a barrier so that organotin compounds cannot leach out to reduce exposure by allowing recovery to occur.