Persistent organic pollutant

Persistent organic pollutants(POPs) areorganic compoundsthat are resistant to degradation throughchemical,biological,andphotolyticprocesses.[1]They are toxic and adversely affect human health and the environment around the world.[1]Because they can be transportedby windand water, most POPs generated in one country can and do affect people and wildlife far from where they are used and released.

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 theStockholm Convention on Persistent Organic Pollutantsin 2001.

Most POPs arepesticidesorinsecticides,and some are alsosolvents,pharmaceuticals,and industrial chemicals.[1]Although some POPs arise naturally (e.g. from volcanoes), most are man-made.[2]The "dirty dozen" POPs identified by the Stockholm Convention includealdrin,chlordane,dieldrin,endrin,heptachlor,HCB,mirex,toxaphene,PCBs,DDT,dioxins,andpolychlorinated dibenzofurans.However, there have since been many new POPs added (e.g.PFOS).

Consequences of persistence

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POPs typically are halogenated organic compounds (see lists below) and as such exhibit highlipid solubility.For this reason, theybioaccumulateinfatty tissues.[3][4][5][6]Halogenatedcompounds also exhibit greatstabilityreflecting the nonreactivity of C-Cl bonds towardhydrolysisandphotolytic degradation.The stability and lipophilicity of organic compounds often correlates with their halogen content, thus polyhalogenated organic compounds are of particular concern.[1]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.[7]Compounds that make up POPs are also classed asPBTs(persistent, bioaccumulative and toxic) or TOMPs (toxic organic micro pollutants).[8]

Long-range transport

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POPs enter thegasphase under certain environmental temperatures andvolatilizefromsoils,vegetation,andbodies of waterinto theatmosphere,resisting breakdown reactions in the air, to travel long distances before being re-deposited.[9]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 asAntarctica,and theArctic Circle.[10]POPs can be present as vapors in the atmosphere or bound to the surface of solidparticles(aerosols). A determining factor for the long-range transport is the fraction of a POP that is adsorbed on aerosols. In adsorbed form it is – as opposed to the gas phase – protected from photo-oxidation, i.e. directphotolysisas well as oxidation byOH radicalsor ozone.[11][12]

POPs have low solubility in water but are easily captured by solid particles, and are soluble in organic fluids (oils,fats,andliquid fuels). POPs are not easily degraded in the environment due to their stability and lowdecompositionrates. 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.[1][13][14]

Bioaccumulation

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Bioaccumulationof POPs is typically associated with the compounds high lipid solubility and ability to accumulate in thefatty tissuesof living organisms including human tissues for long periods of time.[13][15]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 animalsgastrointestinal tractto concentrate ingested chemicals, along with poorlymetabolizedandhydrophobicnature of POPs, makes such compounds highly susceptible to bioaccumulation.[16]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.[9][17]This increase in concentration is called biomagnification, which is where organisms higher up in the food chain have a greater accumulation of POPs.[18]Bioaccumulation and long-range transport are the reason why POPs can accumulate in organisms like whales, even in remote areas like Antarctica.[19]

Stockholm Convention on Persistent Organic Pollutants

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State parties to the Stockholm Convention on Persistent Organic Pollutants

The Stockholm Convention was adopted and put into practice by theUnited 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 2024, there are 185 countries plus the European Union have ratified the Stockholm Convention.[20]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. The initial meeting in 2001 made a preliminary list, termed the "dirty dozen", of chemicals that are classified as POPs.[21]As of 2024, theUnited Stateshas 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.[20]

Compounds on the Stockholm Convention list

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In May 1995, the UNEP Governing Council investigated POPs.[22]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][21][23]

  1. Aldrin,an insecticide used in soils to killtermites,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 reportedhalf-lifeof one year. Chlordane has been postulated to affect the human immune system and is classified as a possible humancarcinogen.Chlordane air pollution is believed the primary route of human 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 toParkinson's disease,breast cancer,and classified as immunotoxic, neurotoxic, withendocrine disruptingcapacity. 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 aneurotoxin.Human exposure results primarily through food.
  5. Heptachlor,apesticideprimarily used to kill soil insects and termites, along with cotton insects, grasshoppers, other crop pests, and malaria-carrying mosquitoes. Heptachlor, even at very low doses has been associated with the decline of several wild bird populations –Canada geeseandAmerican 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 1945–59 to treat seeds because it can killfungion food crops. HCB-treated seed grain consumption is associated with photosensitive skin lesions,colic,debilitation, and ametabolic disordercalled 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 aflame retardantin 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 andcrustaceanspecies, 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 asheat exchange fluids,inelectrical transformers,andcapacitors,and as additives in paint, carbonless copy paper, and plastics. Persistence varies with degree ofhalogenation,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 andmucous membranesand swelling of the eyelids, along with fatigue, nausea, and vomiting. Effects aretransgenerational,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 biologistRachel CarsonpublishedSilent 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 including increased risk of cancer and diabetes, reduced reproductive success, and neurological disease.
  11. Dioxinsare 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, andhazardous 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. Dioxins were present inAgent Orange,which was used by the United States in chemical warfare against Vietnam and caused devastating multi-generational effects in both Vietnamese and American civilians.
  12. Polychlorinated dibenzofuransare by-products of high-temperature processes, such as incompletecombustionafterwaste incinerationor in automobiles, pesticide production, andpolychlorinated biphenylproduction. 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

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Since 2001, this list has been expanded to include somepolycyclic aromatic hydrocarbons(PAHs),brominated flame retardants,and other compounds. Additions to the initial 2001 Stockholm Convention list are the following POPs:[24][21]

  • Chlordecone,a synthetic chlorinated organic compound, is primarily used as an agricultural pesticide, related to DDT and Mirex. Chlordecone is toxic to aquatic organisms, and classified as a possible human carcinogen. Many countries have banned chlordecone sale and use, or intend to destroy stockpiles.
  • α-Hexachlorocyclohexane(α-HCH) andβ-Hexachlorocyclohexane(β-HCH) are insecticides as well as by-products in the production oflindane.α-HCH and β-HCH are highly persistent in the water of colder regions. α-HCH and β-HCH have been linked toParkinson'sandAlzheimer's disease.[citation needed]
  • Hexabromodiphenyl ether(hexaBDE) andheptabromodiphenyl ether(heptaBDE) are main components of commercialoctabromodiphenyl ether(octaBDE). Commercial octaBDE is highly persistent in the environment, whose only degradation pathway is through debromination and the production ofbromodiphenyl ethers,which themselves can be toxic.
  • Lindane(γ-hexachlorocyclohexane), a pesticide used as a broad spectrum insecticide for seed, soil, leaf, tree and wood treatment, and againstectoparasitesin animals and humans (head lice and scabies). Lindane undergoes rapidbiomagnificationand isimmunotoxic,neurotoxic,carcinogenic,linked to liver and kidney damage as well as adverse reproductive and developmental effects in various laboratory animals. Production of lindane unintentionally produces two other POPs α-HCH and β-HCH.[25]
  • Pentachlorobenzene(PeCB), is a pesticide and unintentional byproduct. PeCB has also been used in PCB products, dyestuff carriers, as a fungicide, a flame retardant, and a chemical intermediate. This compound is moderately toxic to humans, whilst being highly toxic to aquatic organisms.
  • Tetrabromodiphenyl ether(tetraBDE) and pentabromodiphenyl ether (pentaBDE) are industrial chemicals and the main components of commercial pentabromodiphenyl ether (pentaBDE). This pair of molecules have been detected in humans in all regions of the world.
  • Perfluorooctanesulfonic acid(PFOS) and related compounds are extremely persistent and readilybiomagnify.
  • Endosulfansare a group of chlorinated insecticides used to control pests on crops such coffee, cotton, rice and sorghum and soybeans, tsetse flies, ectoparasites of cattle. They are used as awood preservative.Global use and manufacturing of endosulfan has been banned under the Stockholm convention in 2011, although many countries had previously banned or introduced phase-outs of the chemical when the ban was announced. Toxic to humans and aquatic and terrestrial organisms, linked to congenital physical disorders, mental retardation, and death. Endosulfans' negative health effects are primarily liked to its endocrine disrupting capacity acting as anantiandrogen.
  • Hexabromocyclododecane(HBCD) is abrominated flame retardantprimarily used inthermal insulationin the building industry. HBCD is persistent, toxic andecotoxic,withbioaccumulativeand long-range transport properties.

Health effects

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POP exposure may cause developmental defects, chronic illnesses, and death. Some are carcinogens perIARC,possibly includingbreast cancer.[1]Many POPs are capable ofendocrine disruptionwithin thereproductive system,thecentral nervous system,or theimmune system.[26]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.[15]

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 ahuman health risk assessmentwhich takes into account the pollutants'bioavailabilityand theirdose-response relationships.[27]

Endocrine disruption

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The majority of POPs are known to disrupt normal functioning of the endocrine system. Low level exposure to POPs during criticaldevelopmentalperiods of fetus, newborn and child can have a lasting effect throughout their lifespan. A 2002 study[28]summarizes 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 arein utero,in ovo,and during reproductive periods. In humans, the critical development timeframe is duringfetal development.[28]

Reproductive system

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The same study in 2002[28]with evidence of a link from POPs toendocrine disruptionalso linked low dose exposure of POPs toreproductive healtheffects. The study stated that POP exposure can lead to negative health effects especially in themale reproductive system,such as decreasedspermquality and quantity, altered sex ratio and earlypubertyonset. For females exposed to POPs, alteredreproductive tissuesandpregnancyoutcomes as well asendometriosishave been reported.[2]

Gestational weight gain and newborn head circumference

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A Greek study from 2014 investigated the link between maternal weight gain during pregnancy, theirPCB-exposure level and PCB level in their newborn infants, theirbirth weight,gestational age,and head circumference. The lower the birth weight and head circumference of the infants was, the higher POP levels duringprenatal developmenthad been, but only if mothers had either excessive or inadequate weight gain during pregnancy. No correlation between POP exposure and gestational age was found.[29] A 2013case-control studyconducted 2009 in Indian mothers and their offspring showed prenatal exposure of two types oforganochlorine pesticides(HCH,DDTandDDE) impaired the growth of thefetus,reduced the birth weight, length, head circumference and chest circumference.[30][31]

Health effects of PFAS

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Effects of exposure to PFASs on human health[32][33][34]

Additive and synergistic effects

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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 beadditive.[35]Mixtures of POPs can in principle producesynergistic 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.[7]

In urban areas and indoor environments

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Traditionally it was thought that human exposure to POPs occurred primarily throughfood,howeverindoor pollutionpatterns that characterize certain POPs have challenged this notion. Recent studies of indoordustandairhave implicated indoor environments as a major sources for human exposure via inhalation and ingestion.[36]Furthermore, significant indoor POP pollution must be a major route of human POP exposure, considering the modern trend in spending larger proportions of life indoors. Several studies have shown that indoor (air and dust) POP levels to exceed outdoor (air and soil) POP concentrations.[35]

In rainwater

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In 2022, levels of at least four perfluoroalkyl acids (PFAAs) inrainwater worldwide greatly exceeded the EPA's lifetimedrinking waterhealth advisories as well as comparable Danish, Dutch, andEuropean Unionsafety standards, leading to the conclusion that "the global spread of these four PFAAs in the atmosphere has led to theplanetary boundaryfor chemical pollution being exceeded ".[37]

It had been thought that PFAAs would eventually end up in the oceans, where they would be diluted over decades, but a field study published in 2021 by researchers atStockholm Universityfound that they are often transferred from water to air when waves reach land, are a significant source ofair pollution,and eventually get into rain. The researchers concluded that pollution may impact large areas.[38][39][40]

In 2024, a worldwide study of 45,000 groundwater samples found that 31% of samples contained levels of PFAS that were harmful to human health; these samples were taken from areas not near any obvious source of contamination.[41]

Soil is also contaminated and the chemicals have been found in remote areas such asAntarctica.[42]Soil contaminationcan result in higher levels of PFAs found in foods such as white rice, coffee, and animals reared on contaminated ground.[43][44][45]

Control and removal in the environment

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Current studies aimed at minimizing POPs in the environment are investigating their behavior inphotocatalytic oxidation reactions.[46]POPs that are found in humans and inaquatic environmentsthe most are the main subjects of these experiments.Aromaticandaliphaticdegradation products have been identified in these reactions.Photochemical degradationis negligible compared to photocatalytic degradation.[2]A method of removal of POPs from marine environments that has been explored is adsorption. It occurs when an absorbable solute comes into contact with a solid with a porous surface structure. This technique was investigated by Mohamed Nageeb Rashed of Aswan University, Egypt.[47]Current efforts are more focused on banning the use and production of POPs worldwide rather than removal of POPs.[15]

See also

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References

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