Алдын: Химиялық қасиеттері мен экологиялық әсері

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| Watchedfields = changed
| verifiedrevid = 477316992
| Name = Aldrin
| ImageFile = Aldrin. svg
| ImageSize = 200px
| ImageName = Aldrin
| ImageFile1 = Aldrin from xtal 3D balls. png
| PIN = (1R,4S,4aS,5S,8R,8aR) 1,2,3,4,10,10 Hexachloro 1,4,4a,5,8,8a hexahydro 1,4:5,8 dimethanonaphthalene
| OtherNames = HHDN
| REL = Ca TWA 0.25 mg/m3 [skin]
| LCLo = 5.8 mg/m3 (rat, 4 hr) After research showed that organochlorines can be highly toxic to the ecosystem through bioaccumulation, most were banned from use. Before the ban, it was heavily used as a pesticide to treat seed and soil. Aldrin and related "cyclodiene" pesticides (a term for pesticides derived from Hexachlorocyclopentadiene) became notorious as persistent organic pollutants.

Pure aldrin takes form as a white crystalline powder. Though it is not soluble in water (0.003% solubility), aldrin dissolves very well in organic solvents, such as ketones and paraffins. Aldrin decays very slowly once released into the environment. Though it is rapidly converted to dieldrin by plants and bacteria, dieldrin maintains the same toxic effects and slow decay of aldrin. In the presence of oxidizing agents aldrin reacts with concentrated acids and phenols.

Aldrin is not formed in nature. It is named after the German chemist Kurt Alder, one of the coinventors of this kind of reaction. Aldrin is synthesized by combining hexachlorocyclopentadiene with norbornadiene in a Diels Alder reaction to give the adduct. In 1967, the composition of technical grade aldrin was reported to consist of 90.5% of hexachlorohexahydrodimethanonaphthalene (HHDN). Similarly, an isomer of aldrin, known as isodrin, is produced by reaction of hexachloronobornadiene with cyclopentadiene. Isodrin is also produced as a byproduct of aldrin synthesis, with technical grade aldrin containing about 3,5% isodrin. The estimated production volume of aldrin in the US peaked in the mid 1960s at about 18 million pounds a year and then declined.

There are multiple available forms of aldrin. One of these is the isomer isodrin, which cannot be found in nature, but needs to be synthesized like aldrin. When aldrin enters the human body or the environment it is rapidly converted to dieldrin. Degradation by ultraviolet radiation or microbes can convert dieldrin to photodieldrin and aldrin to photoaldrin. This phenomenon exerts its effect through two different mechanisms. One of the mechanisms uses the ability of aldrin to inhibit brain calcium ATPases. These ion pumps relieve the nerve terminal from calcium by actively pumping it out. However, when aldrin inhibits these pumps, the intracellular calcium levels rise. This results in an enhanced neurotransmitter release. The second mechanism makes use of aldrin's ability to block gamma aminobutyric acid (GABA) activity. GABA is a major inhibitory neurotransmitter in the central nervous system. Aldrin induces neurotoxic effects by blocking the GABAA receptor chloride channel complex. By blocking this receptor, chloride is unable to move into the synapse, which prevents hyperpolarization of neuronal synapses. Therefore, the synapses are more likely to generate action potentials.

The metabolism of oral aldrin exposure has not been studied in humans. However, animal studies are able to provide an extensive overview of the metabolism of aldrin. This data can be related to humans. Biotransformation of aldrin starts with epoxidation of aldrin by mixed function oxidases (CYP 450), which forms dieldrin. This conversion happens mainly in the liver. Tissues with low CYP 450 expression use the prostaglandin endoperoxide synthase (PES) instead. This oxidative pathway bisdioxygenises the arachidonic acid to prostaglandin G2 (PGG2). Subsequently, PGG2 is reduced to prostaglandin H2 (PGH2) by hydroperoxidase. Dieldrin can then be directly oxidized by cytochrome oxidases, which forms 9 hydroxydieldrin. An alternative for oxidation involves the opening of the epoxide ring by epoxide hydrases, which forms the product 6,7 trans dihydroxydihydroaldrin. Both products can be conjugated to form 6,7 trans dihydroxydihydroaldrin glucuronide and 9 hydroxydieldrin glucuronide, respectively. 6,7 trans dihydroxydihydroaldrin can also be oxidized to form aldrin dicarboxylic acid.

Considering the toxicokinetics of aldrin in the environment, the efficacy of the compound has been determined. In addition, the adverse effects after exposure to aldrin are demonstrated, indicating the risk regarding the compound.

The ability of aldrin, in its use for the control of termites, is examined in order to determine the maximum response when applied. In 1953 US researchers tested aldrin and dieldrin on terrains with rats known to carry chiggers, at a rate of The aldrin and dieldrin treatment demonstrated a decrease of 75 times less chiggers on rats for dieldrin treated terrains and 25 times less chiggers on the rats when treated with aldrin. The aldrin treatment indicate a high productivity, especially in comparison to other insecticide that were used, like DDT, sulfur or BHC.

Exposure of aldrin to the environment leads to the localization of the chemical compound in the air, soil, and water. These concentrations can also be found in animals, which eat contaminated plants or animals that reside in the contaminated water. This biomagnification can lead to a high concentrations in their fat. There are some reported cases of workers who developed anemia after multiple dieldrin exposures. However the main adverse effect of aldrin and dieldrin is in relationship to the central nervous system. Besides that other symptoms were also reported like headaches, nausea and vomiting, anorexia, muscle twitching and myoclonic jerking and EEG distortions. In all these cases removal of the source of exposure to aldrin/dieldrin led to a rapid recovery.

Most of the animal studies done with aldrin and dieldrin used rats. High doses of aldrin and dieldrin demonstrated neurotoxicity, but in multiple rat studies also showed a unique sensitivity of the mouse liver to dieldrin induced hepatocarcinogenicity. Furthermore, aldrin treated rats demonstrated an increased post natal mortality, in which adults showed an increased susceptibility to the compounds compared to children in rats.

Like related polychlorinated pesticides, aldrin is highly lipophilic. Its solubility in water is only 0.027 mg/L, which exacerbates its persistence in the environment. It was banned by the Stockholm Convention on Persistent Organic Pollutants. In the U. S., aldrin was cancelled in 1974. The substance is banned from use for plant protection by the EU.

Aldrin has rat of 39 to 60 mg/kg (oral in rats). For fish however, it is extremely toxic, with an LC50 of 0.006–0.01 for trout and bluegill. Further, an IDLH limit has been set at 25 mg/m3, based on acute toxicity data in humans to which subjects reacted with convulsions within 20 minutes of exposure. It is classified as an extremely hazardous substance in the United States as defined in Section 302 of the U. S. Emergency Planning and Community Right to Know Act (42 U. S. C. 11002), and is subject to strict reporting requirements by facilities which produce, store, or use it in significant quantities.