Chemicals Profile

DDT is a non-systemic contact insecticide with a broad spectrum of activity which has been used extensively in agriculture worldwide since the 1940s and 1950s. DDT was the first modern pesticide developed initially to combat mosquitoes spreading malaria, typhus, and other insect-borne human diseases, and as an agricultural insecticide. It was banned in several countries in the early 1970s because of human health and ecological considerations, and many other countries have more recently restricted or banned its use except when it is needed for the protection of human health. More than 30 years after the insecticide was banned, historic residues of DDT persist in agricultural soils, constituting the largest source of DDT contamination to the air. DDT is still present in soil and sediment because of its persistent chemical structure. 
DDT is currently listed in Annex B to the Stockholm Convention with its production and/or use restricted for disease vector control purposes in accordance with related World Health Organization (WHO) recommendations and guidelines. Countries that are party to the Convention can produce and/or use DDT for disease vector control when locally safe, effective and affordable alternatives are not available. The Conference of Parties (COP), in consultation with WHO, evaluates the continued need for DDT for disease vector control during its regular meetings.In2009 the COP endorsed the establishment of a Global Alliance for the development and deployment of products, methods and strategies as alternatives to DDT for disease vector control. In 2011, the COP invited the United Nations Environment Programme (UNEP) to lead its implementation while in2013,the COP invited the UNEP, in consultation with WHO, the DDT expert group and the Secretariat, to prepare a road map for the development of locally safe, effective, affordable and environmentally sound alternatives to DDT. 

Source of exposure

DDT’s manufacture sites. Persistent residues in soil and sediment of DDT used in the past, use of DDT as insecticide for vector control.Illegal trade in DDT, and actual or suspected use of DDT outside of the health sector have been reported.

Exposure

Current human exposure to DDT in countries where the insecticide is no longer used in agriculture or public health is expected to be through food. Depending on the soil type, DDT can still be found in soil and sediment.In countries still using DDT for indoor residual spraying (IRS),exposure is related to the use of DDT for controlling vectors and to the contact with residues in soils and sediments. In additional to general population exposure, occupational exposure can include workers involved in producing and dispensing DDT and public health workers involved in vector control.In such instances where DDT is being used illegally in the agriculture sector, there would likely be associated sources of exposure for end users and consumers.

Vulnerable groups

The most common scenario would be exposure to residues in the home following indoor spraying. Children are particularly vulnerable to the health impacts of DDT and women of childbearing age who can transfer DDT and its metabolites to the foetus in pregnancy and to the infant via lactation.In most cases, vector control operations control access to DDT and DDT-contaminated containers. In instances where systems are less secure, it would be very concerning if containers were being used for food/water storage, as this could lead to acute poisoning particularly of children.

Health effects

Ingestion of DDT can result in sign and symptoms as paraesthesia, dizziness, confusion, headache, fatigue and sore throat.Tremor is a characteristic manifestation, usually involving first the neck and head and particularly the eyelids. Ingestion of large doses of DDT can induce vomiting and/or diarrhoea due to local gastric irritation. Convulsions and unusual hearth rhythm can be induced as well as pulmonary problems. Prolonged and repeated exposure can irritate the eyes, skin, nose and throat.

The IARC’s DDT monograph, updated in July 2018, classifies the pesticide as probably carcinogenic to humans (Group 2A). Also, WHO published a risk assessment for the use of DDT in Indoor Residual Spraying, especially for occupational exposure and for exposure of residents and exposure via breast milk. Where studies have been done on residents of treated homes, Indoor Residual Spraying is the major source of the DDT in breast milk. Infants are exposed to DDT and its metabolites through breast feeding. For highly exposed mothers in controlled IRS studies, an average total DDT concentration of 12.8 mg/kg milk fat is found,while for the general population in malarial countries without specific exposure to IRS, a mean total DDT concentration is 2.8 mg/kg milk fat is reported.

Reference levels

The JMPR Meeting (FAO/WHO, 2001) derived a provisional tolerable daily intake(PTDI) of 0.01 mg/kg of body weight. This PTDI is used for the derivation of the water guideline value. Because infants and children may be exposed to greater amounts of chemicals in relation to their body weight and because of concern over the bioaccumulation of DDT, the guideline value was calculated on the basis of a 10-kg child drinking 1 litre of water per day. Moreover, because there can be significant exposure to DDT by routes other than water, a 1% allocation of the PTDI to drinking water was chosen. This leads to a guideline value for DDT and metabolites in drinking water of 1μg/litre. It should be emphasized that, as for all pesticides, the recommended guideline value for DDT in drinking-water is set at a level to protect human health; it may not be suitable for the protection of the environment or aquatic life. The benefits of DDT use in malaria and other vector control programmes outweigh any health risk from the presence of DDT in drinking-water.

Endosulfan (CAS No. 115-29-7) is an insecticide which has been used for over 50 years to effectively control several pests, e.g. chewing, sucking and boring insects, including aphids, thrips, beetles, foliar feeding caterpillars, mites, borers, cutworms, bollworms, bugs, white flies, leafhoppers, snails in rice paddies, and tsetse flies. It has been used in countries throughout the world to control pests on fruit, vegetables, tea and on non-food crops such as tobacco and cotton. In addition to its agricultural use, it is used in the control of the tsetse fly, as a wood preservative and for the control of home garden pests. It is sold as a mixture of two different forms of the same chemical (referred to as α-and β-endosulfan).
The use of endosulfan is 2017 was banned in at least 75 countries, with former uses replaced with alternative products and methods.

Source of exposure

Endosulfan currently used as a pesticide and persistent residues in soil and sediment of endosulfan used in the past. Manufacture sites.

Exposure

The main source of endosulfan exposure to the general population is dietary intake. Exposure will also occur by breathing contaminated air, drinking contaminated water or touching vegetable products sprayed with endosulfan. Farm workers are expected to be exposed to higher amounts of endosulfan compared to the general population. These exposures may occur through direct handling and application or through exposure in fields that were previously sprayed (occupational re-entry). Another source of exposure to endosulfan for the general population is the use of tobacco products. Endosulfan is absorbed across the skin and absorption is increased with oils or lotions on the skin, and through cuts.

Vulnerable groups

Endosulfan can pass though the placental barrier and this may have critical effects on physical development and cognitive functioning of the child. Endosulfan and its metabolites are commonly found in breast milk as well, which means that children born from an exposed mother are exposed after birth as well.

Health effects

Acute effects of occupational inhalation and dermal exposure to endosulfan are primarily neurotoxic: headaches, irritated eyes, nausea, vomiting, dizziness, confusion, irritability, weakness, shortness of breath and irregular heart rhythm, abdominal discomfort after meals; diarrhoea, muscle twitching and convulsions. Effects of ingestion of endosulfan include similar symptoms: nausea, vomiting, diarrhoea, headache, dizziness, agitation, convulsions, loss of consciousness and respiratory problems. Exposure to high doses of endosulfan can lead to death which occur from cardiorespiratory arrest, heart failure, pulmonary oedema, and cerebral hernia from massive cerebral oedema. Short-term high level and long-term low level exposures can both induce chronic liver and kidney damage. Several adverse reproductive outcomes linked with endosulfan have been reported, especially in boys and men. Endosulfan is classified as “fatal if inhaled”, but is not classified as carcinogenic or possibly carcinogenic.

Endosulfan is an endocrine disruptor. It is oestrogenic and antiandrogenic in human cells. It is toxic to and suppresses the immune system, as well as promoting allergic responses. It is linked to long-term neurological effects such as epilepsy, and may cause Parkinson’s disease. Birth defects have been seen in laboratory studies and in human populations exposed to endosulfan. Many studies show endosulfan to be mutagenic and genotoxic, and there is evidence of cancer in both laboratory animals and exposed human populations.

Numerous intentional and unintentional deaths have occurred from ingestion of endosulfan, and poisonings are reported for Benin, Colombia, Costa Rica, Cuba, Guatemala, India, Indonesia, Malaysia, Philippines, New Zealand, South Africa, Sri Lanka, Sudan, Turkey and USA.

Reference levels

Joint FAO/WHO Meeting on Pesticide Residues (2006) :

• ADI (acceptable daily intake) = 0.006 mg/kg body weight
• ARfD (acute reference dose) = 0.02 mg/kg body weight

According to WHO, health-based value of 20 μg/litre can be calculated on the basis of the ADI of 0.006 mg/kg of body weight, with an allocation of 10% of the ADI to drinking-water, and with the assumption that a 60-kg adult consumes 2 litres of drinking-water per day. However, endosulfan usually occurs at concentrations in drinking-water well below those at which toxic effects can be expected to occur, and it is therefore not considered necessary to derive a guideline value for endosulfan in drinking-water.

US EPA :

• Minimum Risk Level (acute, oral) = 0.005 mg/kg/day
• Minimum Risk Level (chronic, oral) = 0.002 mg/kg/day

The U.S. EPA recommends that the amount of endosulfan sulfate in lakes, rivers, and streams should not be more than 62 micrograms per liter (μg/L).

• Lead is a cumulative toxicant that affects multiple body systems and is particularly harmful to young children. 
• Lead in the body is distributed to the brain, liver, kidney and bones. It is stored in the teeth and bones, where it accumulates over time. Human exposure is usually assessed through the measurement of lead in blood.
• Lead in bone is released into blood during pregnancy and becomes a source of exposure to the developing foetus.
• There is no known level of lead exposure that is considered without harmful effects.
• Lead exposure is preventable.

Lead is released by various natural and anthropogenic sources to the atmosphere and to aquatic and terrestrial environments and there are fluxes between these compartments. Lead released into theatmosphere is deposited on land and into aquatic environments and some lead released onto soil overtime is also washed out to aquatic environments. Once emitted to air, lead is subject to atmospheric transport. It is mainly emitted to the atmosphere in particle form.

Important releases of lead: 

• releases resulting from the natural mobilization of naturally occurring lead from the Earth’s crust and mantle, such as volcanic activity and the weathering of rocks; 
• anthropogenic releases from the mobilization of lead impurities in raw materials such as fossil fuels and other extracted and treated metals; 
• anthropogenic releases of lead used in products and processes as a result of mining and processing activities, manufacturing, use, disposal, recycling and reclamation; 
• releases from incineration and installations for municipal waste, open burning and from residues containing lead; 
• mobilization of historical lead releases previously deposited in soils, sediments and wastes.
•  Emissions from aviation fuel for light aircraft 
• Probably oceans can be considered as the sources of relevance for the long-range transport of lead.

Sources of exposure

• Leaded petrol poisoning has been one of the world’s most serious environmental health problems, responsible for 90% or more of human lead exposure, but nowadays only  2 countries still use leaded petrol. Current sources of exposure include lead in paint, low temperature-fired ceramics, informal sector recycling of car batteries, mine tailings and the air, soil and dust in the vicinity of point sources (e.g., smelters)
• Dust in homes with paint containing lead pigment and driers can cause elevated blood lead levels in children
• Tap water from leaded pipes can also be an important exposure source
• Other potential sources of exposure include products containing lead, such as cosmetics, traditional medicines, toys and trinkets, contaminated spices and food colouring

Exposure

• Inhalation is an important route of exposure for people in the vicinity of point sources, including open burning of wastes containing lead products, for people living in the 2 countries that still use lead in petrol, for people living around airfields and in some occupational settings including secondary lead recovery
• Ingestion of lead in dust and soil is a major exposure pathway in children, because of their biological and behavioural characteristics
• Intake of food and beverages is usually the primary source of exposure for adults in the general population

Vulnerable groups:

• Special vulnerability of small children. Exposure of children can be magnified bytheir activities and behavioural patterns and biological characteristics
• Exposure starts in utero since lead passes through the placenta into the foetus; thus pregnant women are a population of concern
• Occupational exposure (E.g: workers in the informal recycling sector, but also workers in the formal sector where occupational health and safety standards are poor)
• Other vulnerable population groups include socially and economically disadvantaged populations and the malnourished, whose diets are deficient in proteins and calcium

There are three chemical forms of lead: metallic lead, inorganic lead compounds and organic lead compounds (containing carbon).

Health effects

The most critical effect of lead in young children is that on the developing nervous system. Subtle effects on intelligence quotient (IQ) may occur from blood lead levels at least as low as 5 µg/dl (50µg/l), and the effects gradually increase with increasing levels of lead in blood. Lead exposure has also been linked epidemiologically to attention deficit disorder and aggression. Exposure of pregnant women to high levels of lead can cause miscarriage, stillbirth, premature birth and low birth weight, as well as minor malformations.

Chronic lead exposure commonly causes haematological effects, such as anaemia, or neurological disturbances, including headache, irritability, lethargy, convulsions, muscle weakness, ataxia, tremors and paralysis. According to IARC, inorganic lead compounds are probably carcinogenic to humans, and therefore have been classified in Group 2A, while Organic lead compounds are not classifiable as to their carcinogenicity to humans, and therefore have been classified in Group 3.

Reference levels

Tolerable intake level

In a review of the latest scientific evidence, conducted in 2010, the Joint Food and Agriculture Organization of the United Nations (FAO)/WHO Expert Committee on Food Additives (JECFA) estimated that the previously established provisional tolerable weekly intake (PTWI) of 25 μg/kg body weight per week could no longer be considered health protective and withdrew it. As the dose–response analyses did not provide any indication of a threshold for the key adverse effects of lead, the Committee concluded that it was not possible to establish a new PTWI that would be health protective.

Drinking-water guideline

A provisional guideline value for lead of 0.01 milligrams per liter (mg/l) (10 μg/l) has been established by WHO (WHO, 2017). This is not a health-based guideline value but is designated on the on the basis of treatment performance and analytical achievability. The EU Directive 98/83/EC established a reference value of 0.01 milligrams per liter (mg/l) (10 μg/l). The value applies to a sample of water intended for human consumption. The EPA regulations for drinking water (also known as the Maximum Contaminant Level [or MCL]) limits lead in drinking water to 0.015 milligrams per liter (mg/L) (15 μg/l).

Lead in air

The WHO Air Quality Guidelines (WHO, 2001) established guideline values for lead as a time-weighted average of 0.5 μg/m3 (annual averaging time). The same limit has been set by the European Union. The EPA has set National Ambient Air Quality Standards 0.15 μg/m3 even though in areas designated nonattainment for the Pb standards prior to the promulgation of the 2008 standards, and for which implementation plans to attain or maintain the 2008) standards have not been submitted and approved, the previous standards (1.5 µg/m3 as a calendar quarter average) also remain in effect.

Lindane is the common name for the gamma isomer of hexachlorocyclohexane (gamma-HCH). It has been used as a broad-spectrum insecticide for seed and soil treatment, foliar applications, tree and wood treatment and against ectoparasites in both veterinary and human applications. The production of lindane has decreased rapidly in the last few years and it is now produced by 13 manufacturers worldwide only, including 7 in India and 4 in China, and is available from 42 suppliers, including 19 suppliers in the USA.

Lindane were primarily used as insecticides to treat wood, seed, and livestock but all such uses of lindane were banned under the Stockholm Convention. It is still used as a human health pharmaceutical for control of head lice and scabies, but these exemptions are coming to an end. As mentioned in the lindane monograph of IARC, major uses today are as insecticide for fruit and vegetable crops, and in baits and seed treatments for rodent control. Being banned, the access to lindane is only possible through illegal channels.

Lindane is mobile in the environment and, as a result of long-range atmospheric transport, has been deposited worldwide. It has been measured in food, air, surface water, groundwater, sediment, soil, fish, wildlife, and humans. Lindane is persistent, bioaccumulates easily in the food chain and bioconcentrates rapidly. There is evidence for toxic effects (immunotoxic, reproductive and developmental effects) in laboratory animals and aquatic organisms.

Source of exposure

Lindane has been produced and used as a broad-spectrum insecticide, which acts by contact, for both agricultural and non-agricultural purposes. A considerable amount of residues was generated during the manufacture of this insecticide. For decades, the waste isomers were generally disposed of in open landfills like fields and other disposal sites near the HCH manufacturing facilities. After disposal, degradation, volatilization, and run off of the waste isomers occurred.

Exposure

Occupational exposure occurs to people working in lindane factories or farmers still using it as a pesticide, probably obtained through illegal channels. Exposure of the general population occurs mainly through the diet because lindane can bio-accumulate in the food chain due to its high lipid solubility and can bioconcentrate rapidly in microorganisms, invertebrates, fish, birds and mammals. Exposure can occur to people living near pesticide plants and hazardous waste sites.

Vulnerable groups

Children are particularly vulnerable. Gamma-HCH has been found in human maternal adipose tissue, maternal blood, umbilical cord blood and breast milk. Lindane has also been found to pass through the placental barrier. An additional exposure route for children exists in regions where lindane is applied directly to milk and meat producing livestock for pest control. Medical use of products to treat head lice and scabies is also of concern when applied to children

It is listed under the Rotterdam and the Stockholm conventions. 

Health effects

Lindane (gamma-HCH) is the most acutely toxic HCH isomer affecting the central nervous and endocrine systems. In humans, effects from acute exposure at high concentrations to lindane may range from mild skin irritation to dizziness, headaches, diarrhea, nausea, vomiting, and even convulsions and death. Respiratory, cardiovascular, hepatic and endocrine effects have also been reported for humans, following acute or chronic lindane inhalation. Hematological alterations following chronic human occupational exposure to gamma-HCH at production facilities have also been reported. Gamma-HCH has been detected in the blood serum, adipose tissue and semen of occupationally and environmentally exposed individuals. According to IARC evaluation there is sufficient evidence in humans for the carcinogenicity of lindane. In 2015, IARC classified lindane as “Carcinogenic to humans (Group 1)”. Lindane causes non-Hodgkin lymphoma.

Human exposure to lindane, particularly in pregnant women and children, is a concern heightened by the ongoing presence of HCH isomers, including lindane, in human tissues and breast milk. Direct exposure from the use of pharmaceutical products for scabies and lice treatment should be of concern. Exposure from food sources is possibly of concern for high animal lipid content diets and subsistence diets of particular ethnic groups.

Reference levels 

WHO guidelines for lindane in drinking water 0.002mg/l (Sources 1 and 2)

• Mercury is a naturally occurring element that is found in air, water and soil. 
• Exposure to mercury –even small amounts –may cause serious health problems, and is a threat to the development of the child in utero and early in life.
• Mercury may have toxic effects on the nervous, digestive and immune systems, and on lungs, kidneys, skin and eyes.
• Mercury is considered by WHO as one of the top ten chemicals or groups of chemicals of major public health concern.
• People are mainly exposed to methylmercury, an organic compound, when they eat fish and shellfish that contain the compound.
• Methylmercury is very different to ethyl mercury. Ethyl mercury is used as a preservative in some vaccines and does not pose a health risk.

Sources of exposure

Mercury occurs naturally in the earth’s crust. It is released into the environment from volcanic activity, weathering of rocks and as a result of human activity. Human activity is the main cause of mercury releases, particularly coal-fired power stations, residential coal burning for heating and cooking, industrial processes, waste incinerators and as a result of mining for mercury, gold and other metals. The skin lightning products can be source of exposure to inorganic mercury. Once in the environment, mercury can be transformed by bacteria into methylmercury, which can bioaccumulate in fish and shellfish and can also biomagnify.

Exposure

People may be exposed to mercury in any of its forms under different circumstances. However, exposure mainly occurs through consumption of fish and shellfish and marine mammals contaminated with methylmercury and through worker inhalation of elemental mercury vapours during industrial or mining processes. Inorganic mercury compounds may be absorbed through the skin in toxicologically relevant quantities. Biological measurement of mercury, for example in hair and blood, allows exposure to be quantified and linked to possible health effects. It also permits estimates of the burden of disease (BoD). WHO is applying its BoD framework approach to better quantify the health impacts.

Vulnerable groups:

Children are especially vulnerable and may be exposed directly in particular by eating contaminated fish, shellfish and marine mammals. Methylmercury bio accumulated in fish, shellfish and marine mammals and consumed by pregnant women may lead to neurodevelopmental problems in the developing foetus. Trans placental exposure is the most dangerous, as the foetal brain is very sensitive. Riverside populations living in areas with artisanal small-scale gold mining, and relying heavily on fish consumption, have been identified as the most vulnerable population in terms of methylmercury exposure and developmental neurotoxicity.

Elemental mercury is lipid soluble and easily penetrates biological membranes, including the blood–brain barrier and the placenta. Metabolism of mercury compounds to other forms of mercury can occur within the tissues of the body.

DIFFERENT FORMS OF MERCURY

Health effects

Elemental and methylmercury are toxic to the central and peripheral nervous system. The inhalation of mercury vapour can produce harmful effects on the nervous, digestive and immune systems, lungs and kidneys, and may be fatal. Due to its greater lipid solubility, methylmercury is easily absorbed into the bloodstream via the gastrointestinal tract.Methylmercury can also cross the blood-brain barrier and accumulate in the central nervous system. The inorganic salts of mercury are corrosive to the skin, eyes and gastrointestinal tract, and may induce kidney toxicity if ingested. 

The most sensitive target for mercury is the central nervous system. Neurological and behavioural disorders may be observed after inhalation, ingestion or dermal application of different mercury compounds. Similar effects are seen after all durations of exposure but the symptoms may intensify and/or become irreversible as exposure duration and/or dose increase. 

Prominent symptoms include tremors, emotional lability,insomnia, memory loss, weakness, muscle atrophy, muscle twitching, headaches, paraesthesia and performance deficits in tests of cognitive function. Some long-term exposures to elemental mercury vapour have resulted in unsteady walking, poor concentration, tremulous speech, blurred vision, performance decrements in psychomotor skills and other signs of neurotoxicity. 

Respiratory symptoms are a prominent effect of short-term, high-level exposure to elemental mercury vapours. The most commonly reported symptoms include cough, dyspnoea, and chest tightness or burning pains in the chest. Pulmonary function may also be impaired. Long term effects include airway obstruction, airway restriction, as well as decreased vital capacity. Inorganic mercury compounds can also cause respiratory effects. 

The exposure to high concentrations of mercury vapours may resulted in increased blood pressure and palpitations.

Among the gastrointestinal effects inflammation of the oral mucosa, excessive salivation and difficulty swallowing have been reported. Short-term exposure to high levels of mercury can also produce abdominal pain, nausea, and diarrhoea. Ingestion of mercuric chloride is highly irritating to the tissues of the gastrointestinal tract. 

Inhalation and ingestion of mercury can impair the renal function leading to urinary excretion of several proteins and degeneration of renal tissues and structures.

Inhalation, oral, or dermal exposure to elemental mercury vapours or inorganic mercury can induce skin rashes, contact dermatitis, heavy perspiration and reddened and/or peeling skin on the palms of the hands and soles of the feet. The exposure to high concentrations of elemental mercury vapours can also lead to red and burning eyes and conjunctivitis. 

Health effects on young children and foetus exposed in utero are mainly neurological symptoms including mental retardation, seizures, vision and hearing loss, delayed development, language disorders and memory loss. The main health effects of mercury are summarized in the figure below. 

Reference levels

Elemental mercury

WHO indicates a tolerable concentration of 0.2 μg/m3for long term inhalation exposure to elemental mercury vapour for occupational exposure.

EU established the occupational exposure limit value of 0.02 mg/m3 as TWA (8 hours time-weighted average).

US EPA indicates the reference concentration (RfC) of 0.3 μg/m3 for elemental mercury. 

Inorganic mercury

WHO reports a PTWI (Provisional Tolerable Weekly Intake) of 4 μg/kg bw.

WHO guidelines for inorganic mercury in drinking water indicates a reference value of 0.006 mg/l.

US EPA Reference Dose(RfD) for mercuric chloride is 0.3μg/kg/day.

Methyl mercury

Several Governments and other organizations have estimated tolerable weekly intake /reference levels for methylmercury exposure that are intended to be protective against adverse effects, as shown in the table below: 

Table reported at page 34 of the WHO document Guidance for Identifying population at risk from mercury exposure.

Variations among reference levels reflect the different risk assessment assumptions, data sets, and uncertainty factors employed.

Mercury

The WHO air quality guideline for mercury is 1μg/m3 (annual average) (WHO, 2017).

The JointFAO/WHO Expert Committee on Food Additives provisional tolerable weekly intake (PTWI) for total mercury is 1.6μg/kg body weight, based on an assessment of results from various epidemiological studies involving fish-eating populations and developmental neurotoxicity.

• Dioxins are a group of chemically-related compounds that are persistent environmental pollutants (POPs). 
• Dioxins are found throughout the world in the environment and they accumulate in the food chain, mainly in the fatty tissue of animals. 
• More than 90% of human exposure is through food, mainly meat and dairy products, fish and shellfish. 
• Dioxins are omnipresent and highly toxic and all people have background exposure, which is not expected to affect human health. Higher than background exposure can cause reproductive and developmental problems, damage the immune system, interfere with hormones and also cause cancer. 

The term “dioxins and dioxin-like substances” commonly refers to polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs). The compounds often have similar toxicity profiles and common mechanisms of action and are generally considered together as a group to set guidelines. 

PCDDs and PCDFs are widely present in the environment, occurring naturally and as by-products of combustion and of various industrial processes but they have never been manufactured deliberately and have no known uses. PCBs are not natural substances but were globally manufactured and used in the past. Although PCB manufacture is prohibited under the Stockholm Convention, their release into the environment still occurs from the disposal of large-scale electrical equipment and waste. 

Sources of exposure 

Dioxins are unwanted by-products of a wide range of manufacturing processes including smelting, chlorine bleaching of paper pulp and the manufacturing of some herbicides and pesticides. Dioxins can also result from natural processes, such as volcanic eruptions and forest fires. Waste incinerators working at low to moderate temperatures (solid waste and hospital waste) are also sources of contamination, due to incomplete burning. The use of modern incineration technology destroys dioxins and furans, whereas inadequate incineration creates them. 

Exposure 

Human exposure occurs mainly through consumption of contaminated food, particularly meat, fish, and poultry, but also through air and drinking-water. Once dioxins enter the body, they are absorbed and stored in fatty tissues and have a half-life estimated to be 7 to 11 years. 

Vulnerable groups 

The developing foetus is most sensitive to dioxin exposure. New borns with rapidly developing organ systems, may also be more vulnerable to certain effects. Some people or groups of people may be exposed to higher levels of dioxins because of their diet (such as high consumers of fish in certain parts of the world) 1 or their occupation (such as workers in the pulp and paper industry, in incineration plants, and at hazardous waste sites). 

Health effects 

Short-term exposure of humans to high levels of dioxins may result in skin lesions, such as chloracne and patchy darkening of the skin, and altered liver function. Long-term exposure is linked to impairment of the immune system, the developing nervous system, the endocrine system and reproductive functions. 

WHO published in 2015 for the first time estimates of the global burden of foodborne disease associated with consumption of food that is unsafe because of chemical and parasitic contaminants. Dioxins’ effects on fertility and on thyroid function were considered in this context, and only considering these 2 endpoints shows that this exposure can contribute significantly to foodborne disease burden in some parts of the world. 

In the Monograph 107 published in 2016, IARC states that PCBs are carcinogenic to humans (Group 1). “Dioxin-like” PCBs, with a toxicity equivalency factor (TEF) according to WHO (PCB-77, PCB-81, PCB-105, PCB-114, PCB-118, PCB-123, PCB -126, PCB -169, PCB -156, PCB -157, PCB -167, PCB-189), are carcinogenic to humans (Group 1). 

Reference levels 

The TEF method (sources 1, 2) is an interim procedure for assessing the risks associated with exposures to complex mixtures of chemicals, such as PCDDs and PCDFs. The method relates the toxicity of all PCDDs and PCDFs to the most toxic form, 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). The TEF approach is especially useful for purposes requiring concise communication of the toxicological significance of complex mixture of PCDDs/PCDFs, such as in risk assessments and regulations. The toxic equivalency concept was developed during the mid-1980’s and last revised in 2005. The WHO-TEF is now widely accepted and TEF values have been published by WHO.

WHO-JEFCA 

The Joint Expert Committee on Food Additives (JECFA) of the WHO and Food and Agriculture Organisation (FAO) established a provisional tolerable monthly intake (PTMI) of 70 pg/kg body weight for dioxins and dl-PCBs in 2002. Converted to a tolerable daily basis, this equates to a dose of 2.3 pg/kg body weight per day. 

No water quality guidelines have been set by WHO for these substances because of their low water solubility. 

No air quality guideline for PCBs have been set by WHO because direct inhalation exposures constitute only a small proportion of the total exposure, in the order of 1–2% of the daily intake from food. Although this air concentration is only a minor contributor to direct human exposure, it is a major contributor to contamination of the food-chain. 

Europe 

In EU the Scientific Committee on Food (SCF) adopted in 2001 an opinion on dioxins and dioxin-like PCBs in food fixing a tolerable weekly intake (TWI) of 14 pg World Health Organisation toxic equivalent (WHO-TEQ)/kg body weight for dioxins and dioxin-like PCBs. 

US EPA 

The US Environmental Protection Agency (US EPA) published an assessment of the non-cancer endpoints for dioxins in February 2012, establishing an oral reference dose (RfD) of 0.7 pg per kg/ body weight per day(US EPA, 2012). The US EPA define the oral RfD as ‘an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime’. 

EPA has set the Maximum Contaminant Level (MCL=the highest level of a contaminant that is allowed in drinking water) for PCBs at 0.0005 mg/L.