Persistent organic pollutant

Persistent organic pollutants (POPs) are organic compounds that are resistant to environmental degradation through chemical, biological, and photolytic processes.[1] Because of their persistence, POPs bioaccumulate with potential significant impacts on human health and the environment. The effect of POPs on human and environmental health was discussed, with intention to eliminate or severely restrict their production, by the international community at the Stockholm Convention on Persistent Organic Pollutants in 2001.

Many POPs are currently or were in the past used as pesticides, solvents, pharmaceuticals, and industrial chemicals.[1] Although some POPs arise naturally, for example volcanoes and various biosynthetic pathways, most are man-made[2] via total synthesis.

Consequences of persistence

POPs typically are halogenated organic compounds (see lists below) and as such exhibit high lipid solubility. For this reason, they bioaccumulate in fatty tissues. Halogenated compounds also exhibit great stability reflecting the nonreactivity of C-Cl bonds toward hydrolysis and photolytic degradation. The stability and lipophilicity of organic compounds often correlates with their halogen content, thus polyhalogenated organic compounds are of particular concern. They exert their negative effects on the environment through two processes, long range transport, which allows them to travel far from their source, and bioaccumulation, which reconcentrates these chemical compounds to potentially dangerous levels.[3] Compounds that make up POPs are also classed as PBTs (Persistent, Bioaccumulative and Toxic) or TOMPs (Toxic Organic Micro Pollutants).

Long-range transport

POPs enter the gas phase under certain environmental temperatures and volatize from soils, vegetation, and bodies of water into the atmosphere, resisting breakdown reactions in the air, to travel long distances before being re-deposited.[4] This results in accumulation of POPs in areas far from where they were used or emitted, specifically environments where POPs have never been introduced such as Antarctica, and the Arctic circle.[5] POPs can be present as vapors in the atmosphere or bound to the surface of solid particles. POPs have low solubility in water but are easily captured by solid particles, and are soluble in organic fluids (oils, fats, and liquid fuels). POPs are not easily degraded in the environment due to their stability and low decomposition rates. Due to this capacity for long-range transport, POP environmental contamination is extensive, even in areas where POPs have never been used, and will remain in these environments years after restrictions implemented due to their resistance to degradation.[6][7]

Bioaccumulation

Bioaccumulation of POPs is typically associated with the compounds high lipid solubility and ability to accumulate in the fatty tissues of living organisms for long periods of time.[6][8] Persistent chemicals tend to have higher concentrations and are eliminated more slowly. Dietary accumulation or bioaccumulation is another hallmark characteristic of POPs, as POPs move up the food chain, they increase in concentration as they are processed and metabolized in certain tissues of organisms. The natural capacity for animals gastrointestinal tract concentrate ingested chemicals, along with poorly metabolized and hydrophobic nature of POPs makes such compounds highly susceptible to bioaccumulation.[9] Thus POPs not only persist in the environment, but also as they are taken in by animals they bioaccumulate, increasing their concentration and toxicity in the environment.[4][10]

Stockholm Convention on Persistent Organic Pollutants

State parties to the Stockholm Convention on Persistent Organic Pollutants

The Stockholm Convention was adopted and put into practice by the United Nations Environment Programme (UNEP) on May 22, 2001. The UNEP decided that POP regulation needed to be addressed globally for the future. The purpose statement of the agreement is "to protect human health and the environment from persistent organic pollutants." As of 2014, there are 179 countries in compliance with the Stockholm convention. The convention and its participants have recognized the potential human and environmental toxicity of POPs. They recognize that POPs have the potential for long range transport and bioaccumulation and biomagnification. The convention seeks to study and then judge whether or not a number of chemicals that have been developed with advances in technology and science can be categorized as POPs or not. The initial meeting in 2001 made a preliminary list, termed the “dirty dozen,” of chemicals that are classified as POPs. As of 2014, the United States of America has signed the Stockholm Convention but has not ratified it. There are a handful of other countries that have not ratified the convention but most countries in the world have ratified the convention.[11]

Compounds on the Stockholm Convention list

In May 1995, the United Nations Environment Programme Governing Council investigated POPs.[12] Initially the Convention recognized only twelve POPs for their adverse effects on human health and the environment, placing a global ban on these particularly harmful and toxic compounds and requiring its parties to take measures to eliminate or reduce the release of POPs in the environment. [2][13][14]

  1. Aldrin, an insecticide used in soils to kill termites, grasshoppers, Western corn rootworm, and others, is also known to kill birds, fish, and humans. Humans are primarily exposed to aldrin through dairy products and animal meats.
  2. Chlordane, an insecticide used to control termites and on a range of agricultural crops, is known to be lethal in various species of birds, including mallard ducks, bobwhite quail, and pink shrimp; it is a chemical that remains in the soil with a reported half-life of one year. Chlordane has been postulated to affect the human immune system and is classified as a possible human carcinogen. Chlordane air pollution is believed the primary route of humane exposure.
  3. Dieldrin, a pesticide used to control termites, textile pests, insect-borne diseases and insects living in agricultural soils. In soil and insects, aldrin can be oxidized, resulting in rapid conversion to dieldrin. Dieldrin’s half-life is approximately five years. Dieldrin is highly toxic to fish and other aquatic animals, particularly frogs, whose embryos can develop spinal deformities after exposure to low levels. Dieldrin has been linked to Parkinson's disease, breast cancer, and classified as immunotoxic, neurotoxic, with endocrine disrupting capacity. Dieldrin residues have been found in air, water, soil, fish, birds, and mammals. Human exposure to dieldrin primarily derives from food.
  4. Endrin, an insecticide sprayed on the leaves of crops, and used to control rodents. Animals can metabolize endrin, so fatty tissue accumulation is not an issue, however the chemical has a long half-life in soil for up to 12 years. Endrin is highly toxic to aquatic animals and humans as a neurotoxin. Human exposure results primarily through food.
  5. Heptachlor, a pesticide primarily used to kill soil insects and termites, along with cotton insects, grasshoppers, other crop pests, and malaria-carrying mosquitoes. Heptachlor, even at every low doses has been associated with the decline of several wild bird populations – Canada geese and American kestrels. In laboratory tests have shown high-dose heptachlor as lethal, with adverse behavioral changes and reduced reproductive success at low-doses, and is classified as a possible human carcinogen. Human exposure primarily results from food.
  6. Hexachlorobenzene (HCB), was first introduced in 1945–1959 to treat seeds because it can kill fungi on food crops. HCB-treated seed grain consumption is associated with photosensitive skin lesions, colic, debilitation, and a metabolic disorder called porphyria turcica, which can be lethal. Mothers who pass HCB to their infants through the placenta and breast milk had limited reproductive success including infant death. Human exposure is primarily from food.
  7. Mirex, an insecticide used against ants and termites or as a flame retardant in plastics, rubber, and electrical goods. Mirex is one of the most stable and persistent pesticides, with a half-life of up to 10 years. Mirex is toxic to several plant, fish and crustacean species, with suggested carcinogenic capacity in humans. Humans are exposed primarily through animal meat, fish, and wild game.
  8. Toxaphene, an insecticide used on cotton, cereal, grain, fruits, nuts, and vegetables, as well as for tick and mite control in livestock. Widespread toxaphene use in the US and chemical persistence, with a half-life of up to 12 years in soil, results in residual toxaphene in the environment. Toxaphene is highly toxic to fish, inducing dramatic weight loss and reduced egg viability. Human exposure primarily results from food. While human toxicity to direct toxaphene exposure is low, the compound is classified as a possible human carcinogen.
  9. Polychlorinated biphenyls (PCBs), used as heat exchange fluids, in electrical transformers, and capacitors, and as additives in paint, carbonless copy paper, and plastics. Persistence varies with degree of halogenation, an estimated half-life of 10 years. PCBs are toxic to fish at high doses, and associated with spawning failure at low doses. Human exposure occurs through food, and is associated with reproductive failure and immune suppression. Immediate effects of PCB exposure include pigmentation of nails and mucous membranes and swelling of the eyelids, along with fatigue, nausea, and vomiting. Effects are transgenerational, as the chemical can persist in a mother’s body for up to 7 years, resulting in developmental delays and behavioral problems in her children. Food contamination has led to large scale PCB exposure.
  10. Dichlorodiphenyltrichloroethane (DDT) is probably the most infamous POP. It was widely used as insecticide during WWII to protect against malaria and typhus. After the war, DDT was used as an agricultural insecticide. In 1962, the American biologist Rachel Carson published Silent Spring, describing the impact of DDT spraying on the US environment and human health. DDT’s persistence in the soil for up to 10–15 years after application has resulted in widespread and persistent DDT residues throughout the world including the arctic, even though it has been banned or severely restricted in most of the world. DDT is toxic to many organisms including birds where it is detrimental to reproduction due to eggshell thinning. DDT can be detected in foods from all over the world and food-borne DDT remains the greatest source of human exposure. Short-term acute effects of DDT on humans are limited, however long-term exposure has been associated with chronic health effects such as diabetes, carcinogenic, reduced reproductive success, and has been linked to neurological disease.
  11. Dioxins are unintentional by-products of high-temperature processes, such as incomplete combustion and pesticide production. Dioxins are typically emitted from the burning of hospital waste, municipal waste, and hazardous waste, along with automobile emissions, peat, coal, and wood. Dioxins have been associated with several adverse effects in humans, including immune and enzyme disorders, chloracne, and are classified as a possible human carcinogen. In laboratory studies of dioxin effects an increase in birth defects and stillbirths, and lethal exposure have been associated with the substances. Food, particularly from animals, is the principal source of human exposure to dioxins.
  12. Polychlorinated dibenzofurans are by-products of high-temperature processes, such as incomplete combustion after waste incineration or in automobiles, pesticide production, and polychlorinated biphenyl production. Structurally similar to dioxins, the two compounds share toxic effects. Furans persist in the environment and classified as possible human carcinogens. Human exposure to furans primarily results from food, particularly animal products.

New POPs on the Stockholm Convention list

Since 2001, this list has been expanded to include some polycyclic aromatic hydrocarbons (PAHs), brominated flame retardants, and other compounds. Additions to the initial 2001 Stockholm Convention list are as following POPs:[15][16]

Additive and synergistic effects

Evaluation of the effects of POPs on health is very challenging in the laboratory setting. For example, for organisms exposed to a mixture of POPs, the effects are assumed to be additive.[17] Mixtures of POPs can in principle produce synergistic effects. With synergistic effects, the toxicity of each compound is enhanced (or depressed) by the presence of other compounds in the mixture. When put together, the effects can far exceed the approximated additive effects of the POP compound mixture.[3]

Health effects

POP exposure may cause developmental defects, chronic illnesses, and death. Some are carcinogens per IARC, possibly including breast cancer.[1] Many POPs are capable of endocrine disruption within the reproductive system, the central nervous system, or the immune system. People and animals are exposed to POPs mostly through their diet, occupationally, or while growing in the womb.[1] For humans not exposed to POPs through accidental or occupational means, over 90% of exposure comes from animal product foods due to bioaccumulation in fat tissues and bioaccumulate through the food chain. In general, POP serum levels increase with age and tend to be higher in females than males.[8]

Studies have investigated the correlation between low level exposure of POPs and various diseases. In order to assess disease risk due to POPs in a particular location, government agencies may produce a human health risk assessment which takes into account the pollutants' bioavailability and their dose-response relationships.[18]

Endocrine disruption

The majority of POPs are known to disrupt normal functioning of the endocrine system, for example all of the dirty dozen are endocrine disruptors. Low level exposure to POPs during critical developmental periods of fetus, newborn and child can have a lasting effect throughout its lifespan. A 2002 study[19] synthesizes data on endocrine disruption and health complications from exposure to POPs during critical developmental stages in an organism’s lifespan. The study aimed to answer the question whether or not chronic, low level exposure to POPs can have a health impact on the endocrine system and development of organisms from different species. The study found that exposure of POPs during a critical developmental time frame can produce a permanent changes in the organisms path of development. Exposure of POPs during non-critical developmental time frames may not lead to detectable diseases and health complications later in their life. In wildlife, the critical development time frames are in utero, in ovo, and during reproductive periods. In humans, the critical development timeframe is during fetal development.[20]

Reproductive system

The same study in 2002[19] with evidence of a link from POPs to endocrine disruption also linked low dose exposure of POPs to reproductive health effects. The study stated that POP exposure can lead to negative health effects especially in the male reproductive system, such as decreased sperm quality and quantity, altered sex ratio and early puberty onset. For females exposed to POPs, altered reproductive tissues and pregnancy outcomes as well as endometriosis have been reported.[21]

Exposure during pregnancy

POP exposure during pregnancy is of particular concern to the developing fetus.

Transport across the placenta

A study about the transfer of POPs (14 organochlorine pesticides, 7 polychlorinated biphenyls and 14 polybrominated diphenyl ethers (PBDEs)) from Spanish mothers to their unborn fetus found that POP concentrations in serum from the mother were higher than from the umbilical cord and 50 placentas.[22] Because transfer of the POPs from mother to fetus did not correspond with passive lipid-associated diffusion, authors suggested that POPs are actively transported across the placenta.[22]

Gestational weight gain and newborn head circumference

A Greek study from 2014 investigated the link between maternal weight gain during pregnancy, their PCB-exposure level and PCB level in their newborn infants, their birth weight, gestational age, and head circumference. The birth weight and head circumference of the infants was the lower, the higher POP levels during prenatal development had been, but only if mothers had either excessive or inadequate weight gain during pregnancy. No correlation between POP exposure and gestational age was found.[23] A 2013 case-control study conducted 2009 in Indian mothers and their offspring showed prenatal exposure of two types of organochlorine pesticides (HCH, DDT and DDE) impaired the growth of the fetus, reduced the birth weight, length, head circumference and chest circumference.[24][25]

Cardiovascular disease and cancer

POPs are lipophilic environmental toxins. They are often found in lipoproteins of organisms. A study published in 2014[26] found an association between the concentration of POPs in lipoproteins and the occurrence of cardiovascular disease and various cancers in human beings. The higher the concentration of POPs found in lipoproteins, the higher the occurrence of cardiovascular disease and cancer. Highly chlorinated polychlorinated biphenyls are specifically found in high concentrations in lipoproteins. Cardiovascular disease is shown to be more associated with higher concentrations of POPs in high density lipoproteins and cancer is shown to be more associated with higher concentrations of POPs in low density lipoproteins and very low density lipoproteins.[27]

Obesity

There have been many recent studies assessing the connection between serum POP levels in individuals and instances of obesity. A study released in 2011[28] found correlations between different POPs and obesity occurrence in individuals tested. The statistically significant findings from the study show that there is actually a negative correlation between various PCB congener serum levels and obesity in individuals tested. The study also showed a positive correlation between beta-hexachlorocyclohexane and various dioxin serum levels and obesity in individuals tested. Obesity was determined using the Body Mass Index (BMI). One proposed explanation in the study is that PCBs are very lipophilic, therefore they are easily stored and captured in the fat deposits in human beings. Obese individuals have higher amounts of fat deposits in their body, and thus more PCBs could be captured in the fat deposits leading to less PCBs circulating in blood serum. The study provides evidence demonstrating that the correlation between POP serum levels and obesity occurrence is more complicated than previously expected. The same study also noted a strong positive correlation between serum POP levels and age in all individuals in the experiment.[29]

Diabetes

A study published in 2006[30] revealed a positive correlation between POP serum levels and type II diabetes in individuals, after other variables, such as age, sex, race, and socioeconomic status were adjusted for. The correlation proved stronger in younger, Mexican American, and obese individuals. Individuals exposed to low doses of POPs throughout their lifetime had a higher chance for developing diabetes than individuals exposed to high concentrations of POPs for a short amount of time.[31]

POPs in urban areas and indoor environments

Traditionally it was thought that human exposure to POPs occurred primarily through food, however indoor pollution patterns that characterize certain POPs have challenged this notion. Recent studies of indoor dust and air have implicated indoor environments as a major sources for human exposure via inhalation and ingestion.[32] Furthermore, significant indoor POP pollution must be a major route of human POP exposure, considering the modern trend in spending larger proportions of life indoor. Several studies have shown that indoor (air and dust) POP levels to exceed outdoor (air and soil) POP concentrations.[17]

Control and Removal of POPs in the Environment

Current studies aimed at minimizing POPs in the environment are investigating their behavior in photo catalytic oxidation reactions. POPs that are found in humans and in aquatic environments the most are the main subjects of these experiments. Aromatic and aliphatic degradation products have been identified in these reactions. Photochemical degradation is negligible compared to photocatalytic degradation.[33] However, proper removal techniques of POPs from the environment are still unclear, due to fear that more toxic byproducts may result from uninvestigated degradation techniques. Current efforts are more focused on banning the use and production of POPs worldwide rather than removal of POPs.[34]

See also

References

  1. 1 2 3 4 Ritter L; Solomon KR; Forget J; Stemeroff M; O'Leary C. "Persistent organic pollutants" (PDF). United Nations Environment Programme. Retrieved 2007-09-16.
  2. 1 2 El-Shahawi, M.S., Hamza, A., Bashammakhb, A.S., Al-Saggaf, W.T. (2010). An overview on the accumulation, distribution, transformations, toxicity and analytical methods for the monitoring of persistent organic pollutants. Talanta. 80, 1587–1597. doi:10.1016/j.talanta.2009.09.055.
  3. 1 2 Walker, C.H., "Organic Pollutants: An Ecotoxicological Perspective" (2001).
  4. 1 2 Kelly, B.C., Ikonomou, M.G., Blair, J.D., Morin, A.E., Gobas, F.A.P.C. (2007). Food Web-Specific Biomagnification of Persistent Organic Pollutants. Science. 317, 236–239. doi:10.1126/science.1138275.
  5. ↑ Beyer, A., Mackay, D., Matthies, M., Wania, F., Webster, E. (2000). Assessing Long-Range Transport Potential of Persistent Organic Pollutants. Environmental Sciences & Technology. 34(4), 699–703. doi:10.1021/es990207w.
  6. 1 2 Wania, F., Mackay, D. (1996). Tracking the Distribution of Persistent Organic Pollutants. Environmental Science & Technology. 30 (9), 390A–396A. doi:10.1021/es962399q.
  7. ↑ Astoviza, Malena J. (15 April 2014). "Evaluación de la distribución de contaminantes orgánicos persistentes (COPs) en aire en la zona de la cuenca del Plata mediante muestreadores pasivos artificiales" (in Spanish): 160. Retrieved 16 April 2014.
  8. 1 2 Vallack, H.W., Bakker, D.J., Brandt, I., Broström-Ludén, E., Brouwer, A., Bull, K.R., Gough, C., Guardans, R., Holoubek, I., Jansson, B., Koch, R., Kuylenstierna, J., Lecloux, A., Mackay, D., McCutcheon, P., Mocarelli, P., Taalman, R.D.F. (1998). Controlling persistent organic pollutants – what next? Environmental Toxicology and Pharmacology 6, 143–175. doi:10.1016/S1382-6689(98)00036-2.
  9. ↑ Yu, G.W.,, Laseter, J., Mylander, C. Persistent organic pollutants in serum and several different fat compartments in humans. J Environ Public Health. 2011;2011:417980. doi:10.1155/2011/417980. PMID 21647350.
  10. ↑ Lohmanna, R., Breivikb, K., Dachsd, J., Muire, D. (2007). Global fate of POPs: Current and future research directions. 150, 150–165. doi:10.1016/j.envpol.2007.06.051.
  11. ↑ "STOCKHOLM CONVENTION ON PERSISTENT ORGANIC POLLUTANTS". pp. 1–43.
  12. ↑ "The Dirty Dozen". United Nations Industrial Development Organization. Retrieved 27 March 2014.
  13. ↑ "STOCKHOLM CONVENTION ON PERSISTENT ORGANIC POLLUTANTS" (PDF). pp. 1–43. Retrieved 27 March 2014.
  14. ↑ http://chm.pops.int/
  15. ↑ Depositary notification (PDF), Secretary-General of the United Nations, 26 August 2009, retrieved 2009-12-17.
  16. ↑ https://treaties.un.org/doc/Publication/CN/2013/CN.934.2013-Eng.pdf
  17. 1 2 ed. Harrad, S., "Persistent Organic Pollutants" (2010).
  18. ↑ Szabo DT, Loccisano AE, (March 30, 2012). A. Schecter, ed. "POPs and Human Health Risk Assessment". Dioxins and Persistent Organic Pollutants (John Wiley & Sons) 3rd. doi:10.1002/9781118184141.ch19.
  19. 1 2 Damstra, T. (2002). Potential Effects of Certain Persistent Organic Pollutants and Endocrine Disrupting Chemicals on Health of Children. Clinical Toxicology. 40(4), 457–465.
  20. ↑ Damstra, T. (2002). Potential Effects of Certain Persistent Organic Pollutants and Endocrine Disrupting Chemicals on Health of Children. Clinical Toxicology. 40(4), 457–465
  21. ↑ El-Shahawi, M.S., Hamza, A., Bashammakhb, A.S., Al-Saggaf, W.T. (2010). An overview on the accumulation, distribution, transformations, toxicity and analytical methods for the monitoring of persistent organic pollutants. Talanta. 80, 1587–1597
  22. 1 2 Vizcaino, E; Grimalt JO; Fernández-Somoano A; Tardon A (2014). "Transport of persistent organic pollutants across the human placenta". Environ Int 65: 107–115. doi:10.1016/j.envint.2014.01.004. PMID 24486968.
  23. ↑ Vafeiadi, M; Vrijheid M; Fthenou E; Chalkiadaki G; Rantakokko P; Kiviranta H; Kyrtopoulos SA; Chatzi L; Kogevinas M (2014). "Persistent organic pollutants exposure during pregnancy, maternal gestational weight gain, and birth outcomes in the mother-child cohort in Crete, Greece (RHEA study)". Environ Int. 64: 116–123. doi:10.1016/j.envint.2013.12.015. PMID 24389008.
  24. ↑ Dewan, Jain V,; Gupta P; Banerjee BD. (February 2013). "Organochlorine pesticide residues in maternal blood, cord blood, placenta, and breastmilk and their relation to birth size". Chemosphere 90 (5): 1704–1710. doi:10.1016/j.chemosphere.2012.09.083. PMID 23141556.
  25. ↑ Damstra, T. (2002). Potential Effects of Certain Persistent Organic Pollutants and Endocrine Disrupting Chemicals on Health of Children. Clinical Toxicology. 40(4), 457–465. PMID 12216998.
  26. ↑ Ljunggren SA, Helmfrid I, Salihovic S, van Bavel B, Wingren G, Lindahl M, Karlsson H. Persistent organic pollutants distribution in lipoprotein fractions in relation to cardiovascular disease and cancer.
  27. ↑ Ljunggren SA, Helmfrid I, Salihovic S, van Bavel B, Wingren G, Lindahl M, Karlsson H. Persistent organic pollutants distribution in lipoprotein fractions in relation to cardiovascular disease and cancer. Environ Int. 2014;65:93–99. doi:10.1016/j.envint.2013.12.017. PMID 24472825.
  28. ↑ Dirinck, E., Jorens, P.G., Covaci, A., Geens, T., Roosens, L., Neels, H., Mertens, I., Van Gaal, L. (2011). Obesity and Persistent Organic pollutants: Possible Obesogenic Effect of Organochlorine Pesticides and Polychlorinated Biphenyls. Obesity. 19(4), 709–714.
  29. ↑ Dirinck, E., Jorens, P.G., Covaci, A., Geens, T., Roosens, L., Neels, H., Mertens, I., Van Gaal, L. (2011). Obesity and Persistent Organic pollutants: Possible Obesogenic Effect of Organochlorine Pesticides and Polychlorinated Biphenyls. Obesity. 19(4), 709–714. doi:10.1038/oby.2010.133.
  30. ↑ Lee, D.H., Lee, I.K., Song, K., Steffes, M., Toscano, W. Baker, B.A., Jacobs, D.R. (2006). A Strong Dose-Response Relation Between Serum Concentrations of Persistent Organic Pollutants and Diabetes. Diabetes Cares. 29(7), 1638–1644.
  31. ↑ Lee, D.H., Lee, I.K., Song, K., Steffes, M., Toscano, W. Baker, B.A., Jacobs, D.R. (2006). A Strong Dose-Response Relation Between Serum Concentrations of Persistent Organic Pollutants and Diabetes. Diabetes Cares. 29(7), 1638–1644. doi:10.2337/dc06-0543.
  32. ↑ Walker, C.H., "Organic Pollutants: An Ecotoxicological Perspective" (2001)
  33. ↑ El-Shahawi, M.S., Hamza, A., Bashammakhb, A.S., Al-Saggaf, W.T. (2010). An overview on the accumulation, distribution, transformations, toxicity and analytical methods for the monitoring of persistent organic pollutants. Talanta. 80, 1587–1597. doi:10.1016/j.talanta.2009.09.055
  34. ↑ Vallack, H.W., Bakker, D.J., Brandt, I., Broström-Ludén, E., Brouwer, A., Bull, K.R., Gough, C., Guardans, R., Holoubek, I., Jansson, B., Koch, R., Kuylenstierna, J., Lecloux, A., Mackay, D., McCutcheon, P., Mocarelli, P., Taalman, R.D.F. (1998). Controlling persistent organic pollutants – what next? Environmental Toxicology and Pharmacology 6, 143–175. doi:10.1016/S1382-6689(98)00036-2

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