The halogenated aromatic hydrocarbons are chemicals which contain one or more atoms of a halogen (chloride, fluoride, bromide, iodide) and a benzene ring.
Chlorobenzene (and derivatives such as dichlorobenzene; m-dichlorobenzene;
p-dichlorobenzene; 1,2,3-trichlorobenzene; 1,3,5-trichlorobenzene; 1,2,4-trichlorobenzene; hexachlorobenzene; 1-chloro-3-nitrobenzene; 1-bromo-4-chlorobenzene). Monochlorobenzene and dichlorobenzenes have been widely used as solvents and chemical intermediates. Dichlorobenzenes, especially the p-isomer, are employed as fumigants, insecticides and disinfectants. A mixture of trichlorobenzene isomers is applied to combat termites. 1,2,3-Trichlorobenzene and 1,3,5-trichlorobenzene were formerly used as heat transfer media, transformer fluids and solvents.
Hexachlorobenzene is a fungicide and intermediate for dyes and hexafluorobenzene. It is also the raw material for synthetic rubber, a plasticizer for polyvinyl chloride, an additive for the military’s pyrotechnic compositions, and a porosity controlling agent in the manufacture of electrodes.
Benzyl chloride serves as an intermediate in the manufacture of benzyl compounds. It is used in the manufacture of quaternary ammonium chlorides, dyes, tanning materials, and in pharmaceutical and perfume preparations. Benzoyl chloride is used in the textile and dye industries as a fastness improver for dyed fibre or fabrics.
The chloronaphthalenes in industrial use are mixtures of tri-, tetra-, penta- and hexachloronaphthalenes. Many of these compounds have been formerly used as heat transfer media, solvents, lubricant additives, dielectric fluids and electric insulating material (pentachloronaphthalene, octachloronaphthalene, trichloronaphthalene, hexachloronaphthalene and tetrachloronaphthalene). In most cases, plastics have been substituted for chlorinated naphthalenes.
DDT was extensively used for the control of insects, which are parasites or vectors of organisms causing disease in humans. Among such diseases are malaria, yellow fever, dengue, filariasis, louse-borne typhus and louse-borne relapsing fever, which are transmitted by arthropod vectors vulnerable to DDT. Although the use of DDT has been discontinued in European countries, the United States and Japan, DDT may be used by public health officials and the military for the control of vector diseases, for health quarantine, and in drugs for controlling body lice.
Hexachlorophene is a topical anti-infective agent, a detergent and an antibacterial agent for soaps, surgical scrubs, hospital equipment and cosmetics. It is used as a fungicide for vegetables and ornamentals. Benzethonium chloride is also used as a topical anti-infective in medicine as well as a germicide for cleansing food and dairy utensils, and as a controlling agent for swimming pool algae. It is also an additive in deodorants and hairdressing preparations.
Polychlorinated biphenyls (PCBs). The commercial production of technical PCBs increased in 1929, when PCBs began to be used as non-flammable oils in electrical transformers and condensers. It has been estimated that 1.4 billion pounds of PCBs were produced in the United States from the late 1920s to the mid-1970s, for example. The main properties of PCBs that accounted for their use in the production of a variety of items are: low solubility in water, miscibility with organic solvents and polymers, high dielectric constant, chemical stability (very slow breakdown), high boiling points, low vapour pressure, thermostability and flame resistance. PCBs are also bacteriostatics, fungistatics and pesticide synergists.
PCBs had been used in “closed” or “semiclosed” systems, such as electrical transformers, capacitors, heat transfer systems, fluorescent light ballasts, hydraulic fluids, lubricating oils, insulated electric wires and cables, and so on, and in “open end” applications, such as: plasticizers for plastic materials; adhesives for waterproof wall coatings; surface treatment for textiles; surface coating of wood, metal and concrete; caulking material; paints; printing inks; paper, carbonless copy paper, impregnated citrus fruit wrapping paper; cutting oils; microscopic mounting medium, microscope immersion oil; vapour suppressants; fire retardants; and in insecticide and bactericide formulations.
There are numerous hazards associated with exposure to halogenated aromatic hydrocarbons. The effects can vary considerably, depending on the type of compound. As a group, toxicity of the halogenated aromatic hydorcarbons has been associated with acute irritation of the eyes, mucous membranes and lungs, as well as gastrointestinal and neurological symptoms (nausea, headaches and central nervous system depression). Acne (chloracne) and liver dysfunction (hepatitis, jaundice, porphyria) can also occur. Reproductive disorders ( including abortions, stillbirths and low birthweight babies) have been reported, as have certain malignancies. What follows is a closer look at the particular effects associated with selected chemicals from this group.
The chlorinated toluenes as a group (benzyl chloride, benzal chloride and benzotrichloride) are classified by the International Agency for Research on Cancer (IARC) as Group 2A carcinogens. As a result of its strong irritant properties benzyl chloride concentrations of 6 to 8 mg/m3 cause a light conjunctivitis after 5 minutes of exposure. Airborne concentrations of 50 to 100 mg/m3 immediately cause weeping and twitching of the eyelids, and in concentrations of 160 mg/m3 it is unbearably irritating to the eyes and mucous membrane of the nose. The complaints of workers exposed to 10 mg/m3 and more of benzyl chloride included weakness, rapid fatigue, persistent headaches, increased irritability, feeling hot, loss of sleep and appetite, and, in some, itching of the skin. Medical examinations of workers revealed asthenia, dystonia of the autonomic nervous system (hyperhidrosis, tremors in the eyelids and fingers, unsteadiness in Romberg’s test, dermatographic changes, and so on). There may also be disturbances of liver function, such as increased bilirubin content of the blood and positive Takata-Ara and Weltmann tests, a decrease in the number of leucocytes, and a tendency to illness similar to colds and allergic rhinitis. Cases of acute poisoning have not been reported. Benzyl chloride can cause dermatitis, and if it enters the eyes, the result is intense burning, weeping and conjunctivitis.
Chlorobenzene and its derivatives can cause acute irritation of the eyes, nose and skin. At higher concentrations, headache and respiratory depression occur. Of this group, hexachlorobenzene deserves special mention. Between 1955 and 1958, a severe outbreak took place in Turkey after ingestion of wheat that had been contaminated with the fungicide hexachlorobenzene. Thousands of people developed porphyria, which began with bullous lesions progressing to ulceration, healing with pigmented scars. In children the initial lesions resembled comedones and milia. Ten per cent of those affected died. Infants who ingested breast milk contaminated with hexachlorobenzene had a 95% mortality rate. Massive discharges of porphyrins were detected in urine and faeces of the patients. Even 20 to 25 years later, between 70 and 85% of survivors had hyperpigmentation and residual scarring on their skin. Arthritis and muscle disorders have also persisted. Hexachlorobenzene is classified as a Group 2B carcinogen (possibly carcinogenic to humans) by IARC.
The toxicity of chloronaphthalenes increases with a higher degree of chlorination. Chloracne and toxic hepatitis are the primary problem caused by exposure to this substance. The higher chlorinated naphthalenes may cause severe injury to the liver, characterized by acute yellow atrophy or by subacute necrosis. Chloronaphthalenes also have a photosensitizing effect on the skin.
During manufacture and/or handling of PCBs, these compounds may penetrate into the human body following cutaneous, respiratory or digestive exposure. PCBs are very lipophilic and hence distribute readily into fat. Metabolism occurs in the liver, and the higher the chlorine content of the isomer the slower it is metabolized. Hence these compounds are very persistent, and are detectable in fatty tissue years after exposure. The highly chlorinated biphenyl isomers undergo a very slow metabolism in the animal body and are consequently excreted in very low percentages (less than 20% of 2,4,5,2',4',5'-hexachlorobiphenyl was excreted within the lifetime of rats that received a single intravenous dose of this compound).
Although PCB manufacture, distribution and use was banned in the United States in 1977, and later elsewhere, accidental exposure (such as leakages or environmental contamination) is still a concern. It is not uncommon for transformers containing PCBs to catch fire or explode, leading to widespread contamination of the environment with PCBs and toxic decomposition products. In some occupational exposures, the gas-chromatographic pattern of PCB residues differs from that of the general population. Diet, concomitant exposure to other xenobiotics and features of biochemical individuality may also influence the PCB gas-chromatogram pattern. The decrease of plasma PCB levels after withdrawal from occupational exposure was relatively fast in workers exposed for short periods and very slow in those exposed for more than 10 years and/or in those exposed to highly chlorinated PCB mixtures.
In people occupationally exposed to PCBs a broad spectrum of adverse health effects have been reported. Effects include skin and mucous membrane changes; swelling of the eyelids, burning of the eye, and excessive eye discharge. Burning sensation and oedema of the face and hands, simple erythematous eruptions with pruritus, acute eczematous contact dermatitis (vesiculo-erythematous eruptions), chloracne (an extremely refractory form of acne), hyperpigmentation of skin and mucous membranes (palpebral conjunctiva, gingiva), discolouration of fingernails and thickening of the skin can also occur. Irritation of the upper respiratory airways is frequently seen. A decrease in forced vital capacity, without radiological changes, was reported in a relatively high percentage of the workers exposed in a capacitor factory.
Digestive symptoms such as abdominal pain, anorexia, nausea, vomiting and jaundice, with rare cases of coma and death, may occur. At autopsy, acute yellow atrophy of the liver was found in lethal cases. Sporadic cases of acute yellow atrophy of the liver were reported.
Neurological symptoms such as headache, dizziness, depression, nervousness and so on, and other symptoms such as fatigue, loss of weight, loss of libido and muscle and joint pains were found in various percentages of exposed people.
PCBs are Group 2A carcinogens (probably carcinogenic to humans) according to the IARC evaluation. After the environmental disaster in Yusho, Japan, where PCBs contaminated cooking oils, an excess of malignant tumours was observed. Pathological pregnancies (toxaemia of pregnancy, abortions, stillbirths, underweight births and so on) were frequently associated with increased PCB serum levels in Yusho patients and in the general population.
PBBs (polybrominated biphenyls) are chemical analogues of PCBs with bromine rather than chlorine substituents of the biphenyl rings. Like PCBs, there are numerous isomers, although commercial PBBs are predominantly hexabrominated and have been used mainly as fire retardants. They are lipophilic, and accumulate in adipose tissue; being poorly metabolized they are excreted only slowly. Human health effects are known largely because of a 1973 episode in which about 900 kg were inadvertently mixed into livestock feed in Michigan, after which numerous farm families were exposed to dairy and meat products. Adverse health effects noted included acne, drying and darkening of skin, nausea, headache, blurred vision, dizziness, depression, unusual fatigue, nervousness, sleepiness, weakness, paresthesia, loss of balance, joint pain, back and leg pain, elevated liver enzymes SGPT and SGOT, and decreased immune function. PBB has been reported in serum and adipose tissue of PBB production workers and in breast milk, umbilical cord blood, biliary fluid, and faeces of women and infants exposed via diet.
IARC has classified PBBs as possible human carcinogens (Group 2B).
Dioxin—2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)—is not manufactured commercially but is present as an impurity in 2,4,5-trichlorophenol (TCP). Minute traces may be present in the herbicide 2,4,5-T and in the antibacterial agent hexachlorophene, which are produced from trichlorophenol.
TCDD is formed as a by-product during the synthesis of 2,4,5-trichlorophenol from 1,2,4,5-tetrachlorobenzene under alkaline conditions by the condensation of two molecules of sodium trichlorophenate. When temperature and pressure keeping the reaction in progress are observed carefully, the crude 2,4,5-trichlorophenol contains less than 1 mg/kg up to a maximum of 5 mg/kg TCDD (1 to 5 ppm). Greater amounts are formed at higher temperatures (230 to 260 °C).
The chemical structure of TCDD was identified in 1956 by Sandermann et al., who first synthetized it. The laboratory technician working on the synthesis was hospitalized with very severe chloracne.
There are 22 possible isomers of tetrachlorodibenzo-p-dioxin. TCDD is commonly used to mean 2,3,7,8-tetrachlorodibenzo-p-dioxin, without excluding the existence of the other 21 tetraisomers. TCDD can be prepared for chemical and toxicological standard by catalytic condensation of potassium 2,4,5-trichlorophenate.
TCDD is a solid substance with very low solubility in common solvents and water (0.2 ppb) and is very stable to thermal degradation. In the presence of a hydrogen donor it is rapidly degraded by light. When incorporated in the soil and aquatic systems, it is practically immobile.
The major source of TCDD formation in the environment is thermal reaction either in the chemical production of 2,4,5-trichlorophenol or in the combustion of chemicals which may contain precursors of the dioxins in general.
Occupational exposure to TCDD may occur during the production of trichlorophenol and its derivatives (2,4,5-T and hexachlorophene), during their incineration, and during the use and handling of these chemicals and their wastes and residues.
General exposure of the public may occur in relation to a herbicide spraying programme; bioaccumulation of TCDD in the food chain; inhalation of fly ashes or flue gases from municipal incinerators and industrial heating facilities, during combustion of carbon-containing material in the presence of chlorine; unearthing of chemical wastes; and contact with people wearing contaminated clothes.
TCDD is extremely toxic in experimental animals. The mechanism by which death occurs is not yet understood. Sensitivity to the toxic effect varies with the species. The lethal dose ranges from 0.5 mg/kg for the guinea-pig to over 1,000 mg/kg for the hamster by the oral route. The lethal effect is slow and ensues several days or weeks after a single dose.
Chloracne and hyperkeratosis are a distinctive feature of TCDD toxicity which is observed in rabbits, monkeys and hairless mice, as well as in the human being. TCDD has teratogenic and/or embryotoxic effects in the rodent. In the rabbit the major site of the toxic action appears to be the liver. In the monkey the first sign of toxicity is in the skin, whereas the liver remains relatively normal. Several species develop disturbance of the hepatic porphyrin metabolism. Immunosuppression, carcinogenicity, enzyme induction and mutagenicity have also been observed under experimental conditions. The half-life in the rat and guinea-pig is approximately 31 days, and the major route of excretion is the faeces.
The identification of TCDD as the toxic agent responsible for the lesions and symptoms observed in humans after exposure to trichlorophenol or 2,4,5-trichlorophenoxyacetic acid was made in 1957 by K.H. Schulz in Hamburg, who eventually determined in tests with rabbits its chloracnegenic and hepatotoxic properties. In a self-administered skin test (10 mg applied two times), he also demonstrated the effect on human skin. A human experiment was repeated by Klingmann in 1970: in humans, application of 70 mg/kg produced definite chloracne.
Toxic effects produced by TCDD in humans have been reported as a consequence of repetitive occupational exposure during the industrial production of trichlorophenol and 2,4,5-T, and of acute exposure in factories and their environment from accidents during the manufacture of the same products.
The annual world production of 2,4,5-trichlorophenol was estimated to be about 7,000 tonnes in 1979, the major part of which was used for the production of the herbicide 2,4,5-T and its salts. The herbicide is applied annually to regulate plant growth of forests, ranges and industrial, urban and aquatic sites. The general use of 2,4,5-T has been partially suspended in the United States. It is prohibited in some countries (Italy, Netherlands, Sweden); in others such as the United Kingdom, Germany, Canada, Australia and New Zealand, the herbicide is still in use. The normal application of 2,4,5-T and its salts (0.9kg/acre) would disperse no more than 90 mg TCDD on each treated acre at the highest allowed concentration of 0.1 ppm TCDD in technical 2,4,5-T. In the period since the first commercial production of 2,4,5-T (1946–1947) there have been several industrial episodes involving exposure to TCDD. This exposure usually occurred during the handling of contaminated intermediate products (i.e., trichlorophenol). On eight occasions explosions occurred during the production of sodium trichlorophenate and workers were exposed to TCDD at the time of the accident, during the clean-up or from subsequent contamination from the workshop environment. Four other episodes are mentioned in the literature, but no precise data about the humans involved are available.
About 1,000 people have been involved in these episodes. A wide variety of lesions and symptoms has been described in connection with the exposure, and a causal association has been assumed for some of them. Symptoms include:
- dermatological: chloracne, porphyria cutanea tarda, hyperpigmentation and hirsutism
- internal: liver damage (mild fibrosis, fatty changes, haemofuscin deposition and parenchymal-cell degeneration), raised serum hepatic enzyme levels, disorders of fat metabolism, disorders of carbohydrate metabolism, cardiovascular disorders, urinary tract disorders, respiratory tract disorders, pancreatic disorders
- neurological: (a) peripheral: polyneuropathies, sensory impairments (sight, hearing, smell, taste); (b) central: lassitude, weakness, impotence, loss of libido
Actually only very few cases have been exposed to TCDD on its own. In almost all cases the chemicals utilized for manufacturing TCP and its derivatives (i.e., tetrachlorobenzene, sodium or potassium hydroxide, ethylene glycol or methanol, sodium trichlorophenate, sodium monochloracetate and a few others depending upon the manufacturing procedure) participated in the contamination and might have been the cause of many of these symptoms independently from TCDD. Four clinical signs are probably related to TCDD toxicity, because the toxic effects were predicted by animal testing or they have been consistent in several episodes. These symptoms are:
- chloracne, which was present in the great majority of recorded cases
- enlarged liver and impairment of liver function, occasionally
- neuromuscular symptoms, occasionally
- deranged porphyrin metabolism in some cases.
Chloracne. Clinically chloracne is an eruption of blackheads, usually accompanied by small, pale-yellow cysts which in all but the worst cases vary from pin-head to lentil size. In severe cases there may be papules (red spots) or even pustules (pus-filled spots). The disease has a predilection for the skin of the face, especially on the malar crescent under the eyes and behind the ears in the very mild cases. With increasing severity the rest of the face and neck soon follow, whilst the outer upper arms, chest, back, abdomen, outer thighs and genitalia may be involved in varying degrees in the worst cases. The disease is otherwise symptomless and is simply a disfigurement. Its duration depends to a great extent upon its severity, and the worst cases may still have active lesions 15 and more years after the contact has ceased. In human subjects within 10 days after beginning the application there was redness of the skin and a mild increase in keratin in the sebaceous gland duct, which was followed during the second week by plugging of the infundibula. Subsequently sebaceous cells disappeared and were replaced by a keratin cyst and comedones which persisted for many weeks.
Chloracne is frequently produced by skin contact with the causative chemical, but it appears also after its ingestion or inhalation. In these cases it is almost always severe and may be accompanied by signs of systemic lesions. Chloracne in itself is harmless but is a marker indicating that the affected person has been exposed, however minimally, to a choracnegenic toxin. It is therefore the most sensitive indicator we have in the human subject of overexposure to TCDD. However, the absence of chloracne does not indicate absence of exposure.
Enlarged liver and impairment of liver functions. Increased transaminase values in serum over the borderline may be found in cases after exposure. These usually subside within a few weeks or months. However, liver function tests can stay normal even in cases exposed to TCDD concentration in the environment of 1,000 ppm and suffering from severe chloracne. Clinical signs of liver dysfunction such as abdominal disturbances, gastric pressure, loss of appetite, intolerance to certain foods, and enlarged liver have also been observed in up to 50% of cases.
Laparoscopy and biopsy of the liver showed slight fibrous changes, haemofucsin deposition, fatty changes and slight parenchymal cell degeneration in some of these cases. Liver damage caused by TCDD is not necessarily characterized by hyperbilirubinaemia.
Follow-up studies in those cases which still have acneform manifestations after 20 years and more, report that enlargement of the liver and pathological liver function tests have disappeared. In almost all experimental animals the liver damage is not sufficient to cause death.
Neuromuscular effects. Severe muscle pains aggravated by exertion, especially in the calves and thighs and in the chest area, fatigue, and weakness of the lower limbs with sensory changes have been reported to be the most disabling manifestations in some cases.
In the animals, central and peripheral nervous systems are not target organs of TCDD toxicity, and there are no animal studies to substantiate the claims of muscular weakness or impaired skeletomuscular function in humans exposed to TCDD. The effect can therefore be related to the concurrent exposure to other chemicals.
Disturbed porphyrin metabolism. TCDD exposure has been associated with disturbance of the intermediary metabolism of lipids, carbohydrates and porphyrins. In animals TCDD has produced an accumulation of uroporphyrin in the liver with increase of d-amino-laevulinic acid (ALA) and of uroporphyrin excretion in the urine. In cases of occupational exposure to TCDD an increased excretion of uroporphyrins has been observed. The abnormality is disclosed by a quantitative increase in the urinary excretion of uroporphyrins and a change in the proportion with coproporphyrin.
TCDD produces a variety of adverse health effects in animals and humans, including immunotoxicity, teratogenicity, carcinogenicity, and lethality. Acute effects in animals include death due to wasting, often accompanied by atrophy of the thymus, a gland that plays an active role in immune function in adult animals (but not adult humans). TCDD causes chloracne, a severe skin condition, in animals and humans, and alters immune function in many species. Dioxins cause birth defects and other reproductive problems in rodents, including cleft palate and deformed kidneys.
Effects reported in heavily exposed workers include chloracne and other skin conditions, porphyria cutanea tarda, elevated serum hepatic levels, disorders of fat and carbohydrate metabolism, polyneuropathies, weakness, loss of libido, and impotence.
Teratogenicity and embryotoxicity. TCDD is an extremely potent teratogen in rodents, especially mice, in which it induces cleft palate and hydronephrosis. TCDD causes reproductive toxicity such as decreased sperm production in mammals. In large doses TCDD is embryotoxic (lethal to the developing fetus) in many species. However, few studies of human reproductive outcomes are available. Limited data from the population exposed to TCDD from the 1976 Seveso accident showed no increase in birth defects, although the number of cases was too small to detect an increase in very rare malformations. Lack of historical data and possible reporting bias make it difficult to evaluate spontaneous abortion rates in this population.
Carcinogenicity. TCDD induces cancer at a number of sites in laboratory animals, including lung, oral/nasal cavities, thyroid and adrenal glands, and liver in the rat and lung, liver, subcutaneous tissue, thyroid gland, and lymphatic system in the mouse. Consequently, many studies of dioxin-exposed workers have focussed on cancer outcomes. Definitive studies have been more difficult in humans because workers are ordinarily exposed to dioxin-contaminated mixtures (such as phenoxy herbicides) rather than pure dioxin. For example, in case-control studies, herbicide-exposed agricultural and forestry workers were found to be at increased risk of soft-tissue sarcoma and non-Hodgkins lymphoma.
Many cohort studies have been carried out, but few have furnished definitive results because of the relatively small numbers of workers in any given manufacturing plant. In 1980 the International Agency for Research on Cancer (IARC) established a multinational cohort mortality study that now includes over 30,000 male and female workers in 12 countries, whose employment spans 1939 to the present. A 1997 report noted a two-fold increase in soft-tissue sarcoma, and a small but significant increase in total cancer mortality (710 deaths, SMR=1.12, 95% confidence interval=1.04-1.21). Non-Hodgkins lymphoma and lung cancer rates were also slightly elevated, especially in workers exposed to TCDD contaminated herbicides. In a nested case-control study in this cohort, a ten-fold risk of soft tissue sarcoma was associated with exposure to phenoxy herbicides.
The diagnosis of TCDD contamination is actually based on the history of logical opportunity (chronological and geographical correlation) of exposure to substances which are known to contain TCDD as a contaminant, and on the demonstration of TCDD contamination of the surroundings by chemical analysis.
The clinical features and symptoms of the toxicity are not sufficiently distinctive to permit clinical recognition. Chloracne, an indicator of TCDD exposure, is known to have been produced in the human subject by the following chemicals:
- chlornaphthalenes (CNs)
- polychlorinated biphenyls (PCBs)
- polybrominated biphenyls (PBBs)
- polychlorinated dibenzo-p-dioxins (PCDDs)
- polychlorinated dibenzofurans (PCDFs)
- 3,4,3,4-tetrachlorazobenzene (TCAB)
- 3,4,3,4-tetrachlorazoxybenzene (TCAOB).
Laboratory determination of TCDD in the human organism (blood, organs, systems, tissues and fat) has only just provided evidence of actual deposition of TCDD in the body, but the level which is liable to produce toxicity in humans is not known.
Safety and Health Measures
Safety and health measures are similar to those for solvents. In general, skin contact and vapour inhalation should be minimized. The manufacturing process should be enclosed as completely as possible. Effective ventilation should be provided together with local exhaust equipment at the main sources of exposure. Personal protective equipment should include industrial filter respirators, eye and face protection as well as hand and arm protection. Work clothes should be frequently inspected and laundered. Good personal hygiene, including a daily shower, is important for workers handling chloronaphthalenes. For some of the agents, such as benzyl chloride, periodic medical examinations should be carried out. Particular safety and health issues surrounding PCBs will be discussed below.
In the past, PCB air levels in the workrooms of plants manufacturing or using PCBs, varied generally up to 10 mg/m3 and often exceeded these levels. Because of the toxic effects observed at these levels, a TLV of 1 mg/m3 for the lower chlorinated biphenyls (42%) and of 0.5 mg/m3 for the higher chlorinated biphenyls (54%) in the working environment were adopted in the United States (US Code for Federal Regulations 1974) and in several other countries. These limits are still in effect today.
The PCB concentration in the work environment should be controlled annually in order to check the efficacy of preventive measures in keeping these concentrations at recommended levels. The surveys should be repeated within 30 days of any change in the technological process likely to increase the occupational exposure to PCBs.
If PCBs leak or are spilled, the personnel should be evacuated from the area immediately. Emergency exits should be clearly marked. Instructions with regard to emergency procedures appropriate to the specific features of the plant technology should be implemented. Only personnel trained in emergency procedures and adequately equipped should enter the area. The duties of the emergency personnel are to repair leaks, clean up spills (dry sand or earth should be spread on the leak or spill area) and fight fires.
Employees should be informed of the adverse health effects caused by occupational exposure to PCBs, as well as on the carcinogenic effects in animals exposed experimentally to PCBs and the reproductive impairment observed in mammals and humans with relatively high PCB residue levels. Pregnant women should be aware that PCBs may endanger the health of woman and foetus, due to the placental transfer of PCBs and their foetotoxicity and provided options for other work during pregnancy and lactation. Nursing by these women should be discouraged because of the high amount of PCBs excreted with milk (the quantity of PCBs transferred to the infant by milk is higher than that transferred by the placenta). A significant correlation was found between plasma levels of PCBs in mothers occupationally exposed to these compounds and the PCB milk levels. It has been observed that if these mothers nursed their babies for more than 3 months, the PCB levels in the infants exceeded that of their mothers.These compounds were subsequently retained in the childrens’ bodies for many years. Extraction and discarding of the milk may, however, help in decreasing the mothers’ PCB body burden.
Access to PCB work areas should be limited to authorized personnel. These workers should be provided with suitable protective clothing: long-sleeved overalls, boots, overshoes and bib-type aprons that cover the boot tops. Gloves are needed to reduce skin absorption during special tasks. The bare-handed handling of cold or heated PCB materials should be forbidden. (The quantity of PCBs absorbed through the intact skin may equal or exceed that absorbed by inhalation.) Clean working clothes should be provided daily (they should be periodically inspected for defects). Safety glasses with side shields should be worn for eye protection. Respirators (meeting legal requirements) should be used in areas with PCB vapours and during installation and repair of containers and emergency activities, when the air concentration of PCBs is unknown or exceeds the TLV. Ventilation will prevent accumulation of vapours. (The respirators must be cleaned after use and stored.)
The employees should wash their hands before eating, drinking, smoking and so on, and refrain from such activities in the polluted rooms. Street clothes should be stored during the work shift in separate lockers. These clothes should be put on at the end of the working day only after a shower bath. Showers, eyewash fountains and washroom facilities should be readily accessible to the workers.
Periodic clinical examination of employees (at least annually) with special emphasis upon skin disorders, liver function and reproductive history is required.
The experience of occupational exposure to TCDD, either from an accident during the production of trichlorophenol and its derivatives or originating from regular industrial operations, has shown that the injuries sustained may completely incapacitate workers for several weeks or even months. Resolution of the lesions and healing can occur, but in several cases skin and visceral lesions can linger on and reduce working capacity to 20 to 50% for more than 20 years. TCDD toxic exposures can be prevented if the chemical processes concerned are carefully controlled. By good manufacturing practice it is possible to eliminate the risk of exposure of workers and applicators handling the products or for the population at large. In case of an accident (i.e., if the process of synthesis of 2,4,5-trichlorophenol is running out of control and high levels of TCDD are present), contaminated clothing should immediately be removed, avoiding contamination of the skin or other parts of the body. Exposed parts should be washed immediately and repeatedly until medical attention is obtained. For workers engaged in the decontamination process after an accident, it is recommended that they wear complete throw-away equipment to protect the skin and prevent exposure to dust and vapours from the contaminated materials. A gas mask should be used if any procedure that may produce inhalation of airborne contaminated material cannot be avoided.
All workers should be obliged to take a shower daily following the work shift. Street clothes and shoes should never come in contact with work clothes and shoes. Experience has shown that several spouses of workers affected by chloracne developed chloracne too, although they had never been in a plant producing trichlorophenol. Some of the children had the same experience. The same rules about safety for workers in case of accident have to be borne in mind for laboratory staff working with TCDD or contaminated chemicals, and for medical staff such as nurses and assistants who treat injured workers or contaminated persons. Animal keepers or other technical personnel coming in contact with contaminated material or with instruments and glassware used for TCDD analysis must be aware of its toxicity and handle the material accordingly. Waste disposal including carcasses of experimental animals requires special incineration procedures. Glassware, benchtops, instruments and tools should be regularly monitored with wipe tests (wipe with filter paper and measure amount of TCDD). TCDD containers as well as all glassware and tools should be segregated, and the whole working area should be isolated.
For the protection of the general public and especially of those categories (applicators of herbicides, hospital staff and so on) more exposed to potential risk, the regulatory agencies throughout the world enforced in 1971 a maximum manufacturing specification of 0.1 ppm TCDD. Under constantly improving manufacturing practice, commercial grades of the products in 1980 contained 0.01 ppm of TCDD or less.
This specification is intended to prevent any exposure to and any accumulation in the human food chain of amounts which would pose a substantial risk for the individual. Furthermore, to prevent contamination of the human food chain of even the extremely low concentration of TCDD which might be present on range or pasture grasses immediately following 2,4,5-T application, grazing of dairy animals on treated areas has to be prevented for 1 to 6 weeks following application.
Halogenated aromatic hydrocarbons tables
Table 1 - Chemical information.
Table 2 - Health hazards.
Table 3 - Physical and chemical hazards.
Table 4 - Physical and chemical properties.