33 Persistent Organic Pollutants

Dr. Anita Lakhani

epgp books

 

 

Contents

 

1.      Introduction: Definition of Persistent Organic Pollutants

2.      The Dirty Dozen

3.      The Four POPs Properties:

                Persistence,

                Bioaccumulation,

               Toxicity

               Long –Range Transport

4.      Polychlorinated Biphenyls

5.      Dioxins and Furans

6.      DDT (para-Dichloro Diphenyl Trichloro Ethane)

7.      Hexachlorobenzene

 

Introduction

(POP) – Definition

Organic substances that are persistent, bio-accumulative and possess toxic characteristics that may cause adverse effects on human health and/or environmental are called Persistent, Bio-accumulative, Toxic substances (PBTs). ‘Substance’ refers to either a single chemical species or a number of chemical species which form a specific group possessing similar properties and being emitted together into the environment or forming a mixture and marketed as a single product. Persistent Organic Pollutants (POPs) are a subclass of PBTs that are prone to long-range atmospheric transport and deposition. They include both man-made and natural compounds. The United Nations Environment Program (UNEP) has listed 12 organochlorine POPs- known as the ‘dirty dozen’, these are listed in Table 1 alongwith their characteristic features. The dirty dozen include dioxins and furans (polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans, PCDD/Fs); polychlorinated biphenyls (PCBs), hexachlorobenzene (HCB), several organochlorines used as pesticides: dichloro-diphenyl-trichloroethane (DDT) and its metabolites, chlordane, toxaphene, dieldrin, aldrin, endrin, heptachlor and mirex. There are however numerous other POPs which are also environmental contaminants and are of great concern. Some of them are both persistent and toxic, and still in widespread production and use, in both industrialized and less industrialized countries. These include polycyclic aromatic hydrocarbons (PAHs), hexachlorohexane (HCH) isomers––such as the organochlorine pesticide (OCP) lindane, organotin compounds (used as anti-fouling agents for ships), organic mercury compounds, some other pesticides–– pentachlorophenol, endosulfan and atrazine, chlorinated paraffins (used in cutting oils and lubricants), polybrominated diphenyl ethers (PBDE, used as flame retardants) and certain phthalates: dibutyl phthalate (DBP) and diethyl-hexylphthalate (DEHP), which are less persistent but are not less hazardous (mainly used as plastic softeners, especially in polyvinyl chloride (PVC)). Some of these compounds such as PCB’s may persist in the environment for periods of years and may bio-concentrate by factors of upto 70,000 fold.

 

Table 1: The Dirty Dozen

 

 

The Four POPs Properties: Persistence, Bioaccumulation, Toxicity and Long –Range Transport

Persistent Organic Pollutants distinguish themselves from other organic chemicals due to four characteristic properties: Persistence, Bioaccumulation, Toxicity and Long- Range Transport.

 

Persistence

Persistence is the property of a substance to remain in the environment by resisting chemical and biological degradation, particularly the effects of microbial processes. It is usually measured as a half-life which denotes the time (hours, days, months, or even years) necessary for half the chemical to be degraded. Half life is measured assuming first-order kinetics, where the amount degraded in a fixed period of time is a constant proportion of the amount present initially, i.e., Ct = C0 e–rt, where C0 and Ct are concentrations at times zero and t, and r is the rate constant for degradation (Figure 1). The degradation product may also possess POP characteristics. Degradation of the POPs in the atmosphere may occur through reaction with OH radicals, photolysis and reaction with ozone and nitrogen oxides. In soil, water and sediments, they degrade mainly by microbial action. The rate of degradation depends on the type of bacteria present, their concentration, induction relevant to the chemical undergoing degradation and the ambient conditions like temperature, moisture, availability of substrate. They may also degrade by photolysis, hydrolysis or by chemical reactions.

Figure 1- First Order Decay Kinetics

 

Bioaccumulation

Bioaccumulation is the phenomenon whereby a chemical reaches a greater concentration in the tissues of an organism than in the surrounding environment (water, sediment, soil, air), principally through respiratory and dietary uptake routes. The magnitude of bioaccumulation depends on the hydrophobicity of the chemical and the ability of a species to eliminate the chemical from its body by excretion and/or metabolism. Bioaccumulation is also referred to as bioconcentration, and biomagnification. The preferential accumulation of a chemical in a living organism through all routes of uptake with respect to concentrations in the organism’s exposure environment (water, sediment, soil) is expressed as Bioaccumulation Factor (BAF). If the bioaccumulation factor is based exclusively on uptake from water in laboratory studies, using species (most commonly fish) maintained in a known concentration of pollutant but fed an uncontaminated diet, it is expressed as “bioconcentration factor” (BCF) is used when the Biomagnification relates to the most highly accumulative substances (many of the POPs), where the concentration of the chemical in an organism exceeds that predicted for equilibrium of the organism with its diet, the concentration having been “magnified” in species higher up the food chain.

BCF/BAF values are reported either in relation to the whole-body weight of the test species or are related to the lipid (or fat) content of the animal, usually a fish because the POPs are concentrated in the fatty portions of tissues. BCF/BAF values are usually reported as the octanol-water partition coefficient (Kow) that reflects the preferential accumulation of a substance in an organic medium (n-octanol) compared with water.

 

Toxicity

The toxicity of a substance can be reported in a variety of ways, such as acute (short-term) or chronic (long-term) effects, lethal or effective dose levels (LD50 or ED50, the dose that will kill or affect 50% of test animals), or tissue levels associated with an adverse effect. Whereas certain toxic effects and levels may be easily detected and quantified in laboratory settings, their measurement in the natural environment is considerably more difficult. In field situations, the animal’s environment is impossible to control. This situation is similar to the difficulties experienced with human epidemiological studies. Multiple substances may combine to form a “toxic soup” from which individual chemical contributions can be difficult to disentangle. A corollary of multiple simultaneous exposures is that the cumulative toxicity risk is likely to be greater than when individual chemicals are evaluated in isolation. Furthermore, the low-level effects of interest in field situations may be subtle and difficult to measure, yet vital to species survival. For example, subtle POPs induced neurological impairment may not cause overt effects in a caged, fed, and protected animal, but may be of dire consequence in the complex and dangerous natural environment. Difficulties also occur when attempting to transpose laboratory toxicity data, generally measured as daily dose, to field situations where the metric is tissue concentration of a toxic substance and daily doses cannot be measured.

 

Long-Range Environmental Transport

POPs are semi-volatile, they can occur either in the vapor phase or adsorbed on atmospheric particles, therefore they can be transported over long distances. Consequently, at ordinary environmental temperatures, they can cycle among air, water and soil. Warm temperatures favor evaporation from Earth’s surface in tropical and subtropical regions while cool temperatures at higher latitudes favor deposition from the atmosphere onto soil and water. The tendency of POPs to condense, deposit and accumulate in higher latitudes is due to greater adsorption of these compounds on atmospheric particulate matter, slowing down of decomposition reactions, and lowering of their evaporation rates from water, all facilitated by low temperatures. Hence POPs can migrate to higher latitudes in a series of relatively short jumps sometimes referred to as “grasshopper effect.’ These compounds migrate, rest and migrate again in tune with seasonal temperature changes at mid-latitudes. Hence an “inverted” concentration gradient, with low concentrations in the tropics and high concentrations in the Polar Regions is observed. Moreover contaminant mixtures may change in composition, with more volatile constituents more prevalent at higher latitudes, also if there is a “pulse” (one time application in a season) release in the tropics, the chemical will move towards the poles with a delay in the maximum concentrations at higher latitudes when compared to areas close to sources. Thus, their property of unusual persistence coupled with their semi-volatility has resulted in the presence of these compounds at levels posing risks to both wildlife and humans in areas such as the Arctic, where they have never been used or produced. They have been detected in both industrialized and non-industrialized, in urban and rural areas, in densely populated areas as well as in sparsely populated areas. POPs have in fact been measured in every continent at sites representing every major climatic zone and geographic sector throughout the world including the remote regions such as open oceans, the deserts, the Arctic and the Antarctic.

It is the combination of persistence, bioaccumulation, toxicity, and long-range environmental transport that makes POPs problematic. All 12 prioritized POPs or their breakdown products rank high to extreme on measurements of these parameters. Low values on any of the parameters will substantially reduce trans-boundary concern, although local problems may remain. Investigations on laboratory animals and wildlife have shown that POPs may act as endocrine disruptors, reproductive and immune dysfunction and are likely to cause neurobehavioral; and developmental disorders and cancer. Humans can be exposed to POPs through the direct exposure, occupational accidents and indoor and outdoor environment. Short term exposure to high concentrations may result in illness and death while chronic exposure may be associated with adverse health and environmental effects. Recent investigations have shown that in infants and children, POPs may lead to reduced immunity with concomitant increase in infection, developmental abnormalities, neurobehavioral changes, cancer and tumor induction and promotion.

 

Persistent and volatile pollutants – including certain pesticides, industrial chemicals and heavy metals – evaporate out of the soil in warmer countries where they are still used, and travel in the atmosphere toward cooler areas, condensing out again when the temperature drops. The process, repeated in “hops”, can carry them thousands of kilometres in a matter of days.

 

Polychlorinated Biphenyls

Polychlorinated biphenyls (PCBs) are chlorinated aromatic hydrocarbons structurally similar to the dioxins. They are produced commercially by the direct chlorination of biphenyl using FeCl3 and/or iodine as the catalyst. The degree of chlorination varies depending on the reaction conditions, and ranges from 21 to 68% (w/w). The result is a mixture of different congeners, and contains many impurities, including polychlorinated dibenzofurans (PCDFs). The crude mixtures resulting from chlorination are fractionally distilled to produce commercial mixtures with desired properties. The di-, tri-, and tetra-chloro biphenyls are light oily fluids; the penta-chlorobiphenyls are heavy, viscous oils while the more highly chlorinated biphenyls are greases and waxes. The biphenyl molecule is made up of two connected rings of six C atoms each and PCB is any molecule having multiple chlorines attached to the biphenyl nucleus. Chlorine can be attached to the biphenyl nucleus at any or all of the available sites. Thus there are 209 different PCB compounds theoretically possible, varying in the number and position of the attached chlorines. The individual isomer and homologs are referred to as congeners. Of the 209 possible congeners, only about half are actually produced in the synthesis due to steric hindrance.

Commercial PCB mixtures were sold based on the percentage of chlorine by weight, with each manufacturer utilizing their own system for identifying their products. In the Aroclor series, a 4-digit code is used; biphenyls are generally indicated by 12 in the first two positions indicating 12 carbon atoms, while the last two numbers indicate the percentage of chlorine in the mixture; i.e. Aroclor 1260 is a polychlorinated biphenyl mixture containing 60% chlorine. Some other commercially available biphenyls were “Phenoclor”, “Pyralene”, “Clophen”, “Kanechlor”.

The important physical properties of PCB mixtures are that they are liquids, have low water solubility and excellent dielectric properties. The water solubility and vapour pressure decrease as the degree of substitution increases, and the lipid solubility increases with increasing chlorine substitution. PCBs are however stable to oxidation, flame resistant and relatively inert substances. Because of their non-flammability, electrical and stability properties they had a variety of industrial uses including heat transfer fluids, hydraulic fluids, solvent extenders, plasticizers, flame retardants, organic diluents and dielectric fluids.

 

It is estimated that in a 50 year period approximately 1.4 billion pounds of PCBs were produced and their extensive application has resulted in widespread contamination of soils, sediments, aquatic environment and bioaccumulation in the fat of biota. The accumulation of PCBs in organisms and the exposure of some industrial workers was initially a cause for concern. The 209 PCB congeners are divided into two main groups on the basis of their toxicity; the “dioxin-like PCBs”, a group of 12 PCBs showing similar toxicological properties to the dioxins and the non-dioxin-like PCBs, which are of lower toxicity and which are normally the predominant congeners in environment samples. The toxicity of PCBs is affected by the number and position of the chlorine atoms, as substitution in the ortho position hinders the rotation of the rings. PCBs without ortho substitution are generally referred to as coplanar and all others as non-coplanar. Coplanar PCBs that contain two para and at least two meta chlorines are the most toxic. They like dioxins and furans, bind to the Aryl hydrocarbon Receptor (AhR) and may exert dioxin-like effects in addition to Ah-Receptor independent effects which they share with non-coplanar PCBs. The AhR is a ligand activated transcription factor that is involved in the regulation of a number of genes, including those for enzymes that play a role in the metabolism of xenobiotics as well as genes involved in cell growth regulation and differentiation. It plays an important role in the allered gene expression and species- and tissue –specific toxicity resulting from exposure to specific PCBs congeners as well as PCDD and PCDF congeners. The toxic responses depend on several factors including the chlorine content, the purity of the commercial mixture, the route and duration of exposure, as well as on the dose, age, sex, species and strain of the animal. Early life stages (eggs, embryos, and larval stages), young animals and babies are more sensitive than adults; females are also more sensitive than males while hamsters and amphibians are more resistant. Humans, sea birds and aquatic mammals being at the highest trophic level of the food chain are priority targets and victims.

Dioxins and Furans

Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzo furans are two groups of planar tricyclic compounds possessing similar chemical structures and chemical properties. The dioxins comprise a group of 75 halogenated aromatic hydrocarbons (isomers) and may contain between 1 and 8 Cl atoms, while the furans consist of a group of 135 halogenated aromatic hydrocarbons. Dioxins in their purest form look like crystals or a colorless solid. In general they are colorless, odorless compounds containing H, O and Cl. Dioxins are not soluble in water but highly soluble in fat. They can bind to sediment and other organic matter in the environment and are absorbed in animal and human fatty tissue. They are not biodegradable so they are persistent and bio-accumulate in the food chain. The chemical property of each of the isomers varies with the number of Cl atoms present. The most extensively studied and the most toxic form of dioxin is 2,3,7,8-tetrachlorodi-benzo-p-dioxin abbreviated as 2,3,7,8,-TCDD.

 

Sources and Formation

Dioxins are not manufactured or produced intentionally. They are formed as unintentional by-products in a number of chemical processes and in almost every combustion process. These processes range from natural events like volcanic eruptions and forest fires to man-made processes such as manufacture of chemicals, pesticides, steel and paints, pulp and paper bleaching, exhaust emissions, production of solvents such as trichloroethene and perchloroethene. The industrial synthesis of 2,4,5-T i,e. 2,4,5-trichlorophenoxyacetic acid, a phenoxy herbicide, is traditionally, initiated with 2,4,5-trichlorophenol. 2,4,5 trichlorophenol is produced by reacting NaOH with tetrachlorobenzene. During this reaction, there occurs a side reaction, in which, two chlorophenoxy anions react with each other, with the elimination of two chloride ions, resulting in a new six-membered ring which has two O atoms located para to each other as is found in the simple molecule, 1,4-dioxin or p-dioxin. This central ring links the two chlorinated benzene rings. The side reaction is second order in chlorophenoxide, hence the rate of dioxin production increases with increase in the initial concentration of chlorophenoxide ion. The rate of this reaction also increases rapidly with increasing reaction temperature.

Chlorophenols (trichlorophenol, tetrachlorophenol and pentachlorophenol isomers) have many pesticidal uses (used as herbicide, insecticide, fungicide and molluscicide) and wood preservative and seed treatment. If wood treated with such derivative is burned, a fraction of the chlorophenols reacts to eliminate HCl and produce members of the chlorinated dioxin family. OCDD is a prevalent dioxin congener found in human fat.

Pulp and paper mills that use Cl2 in the bleaching of pulp are major sources of dioxins and furans. These compounds are formed from the reaction of chlorine with some of the organic molecules produced from the pulp. 2,3,7,8-TCDD is the abundant dioxin produced by the pulp and paper bleaching process. Moreover the bleaching of pulp produces more furans than dioxins; highest concentrations are observed for the congeners are the more toxic 2,3,7,8-TCDF and 1,2,7,8-TCDF. The paper and effluent may contain dioxins at ppt level. Most pulp and paper mills have now switched their bleaching agent from elemental Cl2 to chlorine dioxide, ClO2, for which the output of dioxin and furan is much smaller, may even be undetectable. Elemental Cl2 reacts with lignin present in the pulp by substitution with the aromatic rings and produces products that are soluble in alkali and can be washed away. During the oxidation of the lignin, two of the benzene rings couple together to form a dibenzofuran or dibenzo-p-dioxin system, which is subsequently chlorinated and ultimately detached from lignin. ClO2 destroys the aromaticity of the rings by free radical mechanism and therefore produces fewer chlorinated products. O3, H2O2 and high-pressure O2 are alternative bleaching agents that are used in totally Cl2 free paper mills.

Fires of many kinds, including forest fires and those in incinerators also release various congeners of dioxins; these are produced as minor byproducts from Cl2 and organic matter in the fuel. Dioxin production can be avoided by ensuring complete combustion by using very high flame temperatures. Different dioxins congeners are also emitted during the incineration of chlorine containing plastic and PVC. Incinerators are the largest anthropogenic source of dioxins in the environment. These are formed along with furans in the post-combustion zone, where the temperature is much lower (250-500◦C), than in the flame. The soot particles produced by the incomplete combustion of waste undergo oxidative degradation to produce dioxins. The reaction is catalyzed by trace metal ions present in the waste. Incineration produces a greater mass of furans than dioxins. The yield of some dioxins increases with the degree of chlorination whereas maximum production of furans occurs with four to six chlorines. Coal combustion generates little dioxin as it burns more completely generating less amount of soot to later decompose into dioxin and furan. Most furan found in the environment has 4-6 Cl atoms while dioxins are almost fully chlorinated. Furans with 4-6 Cl atoms however have toxicities similar to that of 2,3,7,8-TCDD whereas fully chlorinated dioxins have lower toxicities. Hence, the threat to human health by furans may exceed that from dioxins.

 

Toxicity

The toxicity of dioxins and furans depends on the extent and pattern of chlorine substitution. If the C atom bonded to central ring are designated as ‘α’ carbons and the outlying ones as ‘β’, then the most toxic dioxins are those which contain 3 or 4 β Cl atoms, while those dioxins containing α Cl atoms are less toxic. Therefore, 2,3,7,8-TCDD having 4 β chlorine and no outlying Cl is the most toxic.

Dioxin congeners that have three β Cl atoms but no or only one α Cl are appreciably toxic. Fully chlorinated dioxin, OCDD is less toxic as all α positions are occupied by chlorine. Monochloro and dichloro-dioxins are also not very toxic, even though Cl atoms are present at β positions. Both 2,3,7,8-TCDD and 2,3,7,8-TCDF have been considered as priority pollutants.

The toxicity pattern for furans is similar, but not identical to that for dioxins as the most toxic congeners have chlorine in all the β positions. However furan 2,3,4,7,8 congener with one Cl in β position and no α Cl atoms is the most toxic furan. The dioxin and furan molecules by virtue of their coplanar geometry and their size readily fit into the cavity in a specific biological receptor, the complex of the molecule and the receptor can pass through cell membranes and thereby initiate toxic action. The average residence time of dioxins and furans in human body is about 7 years.

 

Exposure and Health Effects in Humans

Dioxins are found in the air, soil and food and are mainly distributed in the environment through air. Dioxins can enter our body through breathing contaminated air, drinking contaminated water or eating contaminated food. As dioxins build up in the fatty tissues of animals, eating contaminated food is the primary source of exposure. Eating beef pork, poultry fish and dairy products can be a source of exposure. Although dioxins are mainly distributed through air, only a small percentage of exposure is from air. People working in or near municipal solid-waste incinerators, copper smelter, cement kiln or coal–fired power plants can be exposed to dioxins.

 

Toxic Equivalent Factors (TEFs) of PCDD, PCDF and PCBs

Each. congener of PCDD, PCDF and PCBs exhibits a different level of toxicity. In order to be able to sum up the toxicity of these different congeners, the concept of toxic equivalency factors (TEFs) has been introduced to facilitate risk assessment and regulatory control. The TEFs represent the toxicity of a particular congener relative to the most toxic congener, TCDD. Several TEF schemes have been proposed. The most common scheme currently used is that of WHO-TEFs developed by the WHO-ECEH (World Health Organization-European Centre for Environment and Health).

 

 

Individuals who burn their household wastes or burn wood can be exposed as well. Highly chlorinated dioxins and furans are stored in fatty tissues and are neither readily metabolized nor excreted. Their persistence is a consequence of their typical structures. There compounds usually contain H atom on adjacent pairs of C at which during biochemical reaction OH group can be readily added, and these are eliminated from the body. In contrast, those compounds with few chlorine contain one or more pairs of H atoms which tend to be excreted rather than being stored. Exposure to dioxins can result in a wide range of health effects including acute lethality, wasting syndrome, thymic and splenic atrophy, impairment of immune responses, hepatotoxicity and porphiria, chloracne and related dermal lesions, tissue-specific hypo- and hyperplastic responses, disruption of multiple endocrine pathways, carcinogenesis, teratogenicity and reproductive toxicity.

 

DDT (para-Dichloro Diphenyl Trichloro Ethane)

Rachel Carson in her book ‘Silent Spring’ has called DDT an ‘elixir of death,” because of its role in decreasing the

population of birds, particularly the bald eagle

DDT, or para-dichloro diphenyl trichloro ethane

(DDT = C14H9Cl5        =        1,1,1-trichloro-2,2-bis(p-

 

chlorophenylethane) was widely used during the Second World War to protect the troops and civilians from the spread of malaria, typhes and other vector borne diseases. It was therefore hailed as “miraculous” in 1945 by Sir Winston Churchill because of its use in the war. DDT was also widely used on a variety of agricultural crops for the

control of disease vectors. As a result of its overuse, its environmental concentration increased rapidly and its adverse effects were seen on the reproductive ability of wild birds as it indirectly got incorporated into their bodies. In the early 1970’s severe restrictions and bans in many countries was imposed on its use and production.

DDT is a substituted ethane, all the three H atoms are replaced by Cl atoms at one C atom of ethane, while 2 H atoms of the other C atom of ethane are replaced by a phenoxy (benzene) ring, each of the ring contains a Cl atom at the para position. DDT is a white crystalline solid with no apparent odor or taste. It is a man-made organochlorine consisting of a mixture of Dichloro Diphenyl Trichloro ethane isomers, made by a reaction between chlorine gas and the double benzene ring structure under optimal temperature and pressure conditions. When the two compounds are reacted, DDT is formed easily because of the high reactivity of chlorine gas. DDE and DDD are also made in the same reaction and often contaminate DDT, but are also both very toxic to living organisms.

DDT is highly insoluble in water (0.001-0.04 mg L-1) and is soluble in most organic solvents. It is semi-volatile and therefore can partition into the atmosphere. It is lipophilic and partitions readily into the fat of all living organism, and thus bio-concentrates and biomagnifies. Due to its low vapor pressure, slow rate of evaporation, less reactivity with light, chemicals and microorganisms in the environment and low solubility in water, it persists in the environment. In most of the animal species, DDT is metabolized into dichloro diphenyl dichloro ethane (DDE, C14H8Cl4, 1,1-dichloro-2,2-bis(chlorophenyl)ethylene) and 1,1 dichloro-2,2 –bis (4-chlorophenyl) or DDD (C14H10Cl4, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane) by the elimination of HCl through the removal of H atom from one C atom of ethane and Cl atom from other. DDE is also produced slowly in the environment by the degradation of DDT under alkaline conditions and by certain DDT resistant insects which detoxify DDT by this transformation. These breakdown products of DDT are also present virtually everywhere in the environment and are more persistent than the parent compound as they are almost non- degradable biologically and are very fat soluble.

Toxicity

The insecticidal properties of DDT and DDD are more due to their molecular shape than from the chemical interactions with specific species. Structurally DDT molecule contains two tetrahedral C in the ethane unit, and two flat benzene rings. In insects, DDT because of its three dimensional shape becomes widged in the nerve channel that leads out from the cell of the nerve. This channel usually transmits impulses only as needed by the sodium ions. A continuous series of Na+-initiated nerve impulse is produced, as the DDT molecules keep the channel open. As a result, the muscles of the insect twitch constantly, eventually exhausting it with convulsions that lead to death. In humans and other warm-blooded animals however, this process does not occur as DDT molecules do not exhibit any binding action in nerve channels. DDE unlike DDT and DDD has a planar C=C unit rather than a C-C linkage as in DDT and DDE. This planar C=C unit has tetrahedral groups, at each end, since DDE molecule is flat rather than propeller shaped, it does not become widged in the insect’s nerve channels, hence DDE is not an insecticide like DDT. In some birds DDE interferes with the enzyme that regulates the distribution of calcium, so contaminated birds produce eggs which have insufficient shell thickness due to lack of CaCO3 in the shell. These eggs are unable to withstand the weight of the parents during hatching.

Although DDT has not been used in most northern countries for over 20 years, it is still the best hope for controlling parasitic diseases such as malaria in many parts of the world. Expensive alternatives for preventing the transmission of malaria are not affordable in countries where this disease is most common. For these countries, DDT is still the most effective insecticide.

 

Hexachlorobenzene

Hexachlorobenzene is a chlorinated aromatic hydrocarbon with a molecular weight of 284.8 and vapour density 9.83. It is a white needle–like crystalline solid at room temperature with a melting point of 231.8°C and boiling point 325°C. It is almost insoluble in water (Water solubility- 4.7×10-6g L-1 at 25°C) but sparingly soluble in cold alcohol, CCl4 and soluble in benzene, chloroform, ether and carbon disulphide (Log Kow – 5.73). It is stable under normal temperature and pressures. It is combustible but not readily ignited. On decomposition it emits highly toxic fumes of HCl, other chlorinated compounds and CO and CO2.

Industrial synthesis of HCB is achieved through the chlorination of benzene at 150-200°C using a ferric chloride catalyst or from the distillation of residues from the production of perchloroethylene). HCB may also be synthesized by refluxing hexachlorocyclohexane (HCH) isomers with sulphuryl chloride or chlorosulphonic acid in the presence of a ferric chloride or aluminum catalyst. Hexachlorobenzene is also produced as a by-product in the production of a large number of chlorinated compounds, particularly lower chlorinated benzenes and pesticides such as tetrachloro  ethylene, trichloroethylene, CCl4, vinyl chloride, atrazine, propazine, simrazine, pentachloro phenol, chlorothalonil and pentachloronitro benzene. In addition it is produced and emitted to the atmosphere in flue gases during the combustion of municipal wastes or in waste streams from chloralkali and wood-preserving plants and several metallurgical industries. An assessment of global sources of hexachlorobenzene have shown that total current emissions could be around 0.023 Kt y-1 with values ranging between 0.012 and 0.092 Kt y-1.

Technical grade HCB is available as a wettable powder, liquid and dust and contains about 98% HCB, 1.8% pentachlorobenzene and 0.2% 1,2,4,5-tetrachlorobenzene , and it is known to contain a variety of impurities, including hepta- and octachlorodibenzofurans, octachlorodibenzo-p-dioxin and decachlorobiphenyl . Hexachlorobenzene has been primarily used as seed dressing for crops to prevent the growth of fungi (fungicide) particularly for onions, sorghum, wheat and other grains. Hexachlorobenzene was also used as a chemical intermediate in dye-manufacturing, in the synthesis of other organic chemicals and in the production of pyrotechnic compositions for military. It has also been used as a raw material for synthetic rubber, as a plasticizer for PVC, as a porosity controller in the manufacture of electrodes, and as wood preservative. Use of HCB is now uncommon.

HCB is distributed throughout the environment because it is mobile and resistant to degradation, therefore the general population may be exposed at low concentration. When released into the environment, it may be taken up by plants and animals and can bio-accumulate through the food chain. HCB has been detected in terrestrial, freshwater and marine food chains in the Great lakes and Arctic regions. Population with greater potential for exposure includes those who ingest fish caught from contaminated water bodies or who reside near former manufacturing or waste disposal sites. HCB when released to air tends to remain mainly in the vapor phase and therefore can be transported to great distance, as far as the poles from temperate regions. It is generally present at low concentration in ambient air. When HCB is released to water, it can strongly adsorb to particles and sediments and is not degraded or hydrolyzed. It has been detected only infrequently, and at very low concentration (< 0.1µg L-1) in drinking water supplies. It has also been detected in soil and sediment, particularly at high levels in agricultural soils where it had been used as a pesticide, at lower levels in urban soils and at higher levels in soils near uncontrolled hazardous waste sites. HCB has been detected in foods in dietary surveys conducted by the U.S. Food and Drug Administration. HCB has also been detected in the blood of numerous groups of people, especially in the indigenous populations of the Arctic region. It has been found in the blood and breast milk of pregnant and lactating women, and also in the placenta and cord blood; concentrations are found to be elevated in population of women who consumed contaminated fish, meals containing seal and whale.

HCB is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in experimental animals. Oral exposure to HCB caused tumors in several rodent species while liver tumors in female rats and mice and in hamsters of both sexes have been observed through dietary administration of HCB. It has also caused tumors in liver (hemangioendothalioma) and also benign thyroid gland tumors (follicular-cell adenoma). Similarly, it has shown to cause benign and malignant liver tumors, kidney tumors and blood-vessel tumor in liver on dietary exposure to rats.

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  • Greenpeace, 1999. “Down to Zero.’ http://archive.greenpeace.org/toxics/downtozero/POPs/exposure.html.

 

Websites of Interest :

Green Facts, Facts on Health and the Environment. Scientific facts on dioxins 2004 [displayed 12 November 2010]. Available from http://www.greenfacts.org/en/dioxins/index.htm http://www.hc-sc.gc.ca/sr-sr/finance/tsri-irst/proj/persist-org/index-eng.php http://www.hc-sc.gc.ca/fn-an/securit/chem-chim/environ/index-eng.php http://www.hc-sc.gc.ca/ewh-semt/contaminants/index-eng.php www.inac-ainc.gc.ca/ncp/index_e.html