53

MICHAEL I. GREENBERG

Textile Manufacturing Industry

After World War II ended in 1945, Seattle's economy changed. As shipbuilding, mining, and other warrelated industries slowed down, home building and other peacetime industries began to boom. In this 1949 photo, taken in a Seattle factory, a man uses an electrical welding machine to spot weld the corners of an aluminum window frame. (Courtesy of the Seattle History Museum.)

Occupational Description

he textile production industry is one of the oldest and most technologically complex of all industries.

The manufacture of textiles probably has its origin roughly around the year 8000 BC, when organic materials (usually consisting of various grasses and reeds) were the first substances used to make a form of yarn. Certainly cloth, carpets, and tapestries thousands of years old have been discovered in many parts of the world. Relics of such ancient fabrics have been found in many countries and are on display in museums, universities, and private collections around the world. Near the end of the 18th century, the Industrial Revolution brought the development of machines and the beginnings of mass production of textiles. Today the industry has grown to the point where production of textiles is one of the most important industries in the world, as well as in many parts of the United States. In the late 1980s, 574

nearly 750,000 Americans were estimated to be engaged in textile manufacturing, and that figure does not take into account the large number of people who probably participated in this industry clandestinely, off the books, or in an otherwise nonreportable fashion. Nevertheless, over the past two decades, much of the basic textile industry has shifted to developing countries, where the numbers of workers cannot be ascertained. The production of textiles includes all of the following processes: spinning, weaving, knitting, dyeing, and finishing of various natural and synthetic fibers. The technology used in these processes varies from the simplest looms found in cottage (home) industries to processes involving sophisticated, automated, and computerized machines in modern factories. Raw cotton bales are received and opened, and then the cotton may be blended with other fibers. The cotton then goes to the picking machines, which moves the fibers to devices called cards. During these first stages, fibers may be transported by means of air currents in a process known as blowing. Fibers of cotton are then carded. From the

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card, the fiber strands go to the drawing frame and then are moved onto a device called a roving frame. The product of this process, called roving, then goes to the spinning frame, where warp yarn and filling yarn are made. The next processes prepare the yarn for weaving. Warp yarn on the spinning frame is transferred from a bobbin to a large spool. A large number of these packages are placed on a warping machine to make a beam of yarn. For the process known as beaming, two specific types of winding machines are used, a spooler and a warper. Several beams are run together on the last machine before weaving, called a slasher. During this process, a hot solution of starch is applied to the warp yarn to reduce breakage and damage in the weaving. Yarn, especially wool, may be dyed before being woven on a loom. The term finishing refers specifically to any of the final processes, including dyeing, finishing, and inspecting the fabric.

Potentially Hazardous Exposures

Textile workers may be exposed to dusts (both natural and synthetic) generated from the textile products in various stages during the textile manufacturing process. While the spinning, weaving, and knitting operations involve only limited use of chemicals, other processes depend on chemicals. The most important chemicals used in spinning, knitting, and weaving are sizing agents such as starch, and the various polymers used as lubricants to prevent tangling of the yarn. Cotton textile workers may be exposed to mineral lubricants used in the spindles during an operation known as mule spinning, which involves twisting yarn to thicken it. Because of the adverse exposure potential, the mule spinning process was discontinued in Europe in the 1960s, and many countries have enacted legislation prohibiting the use of oils for mule spinning. In addition, other countries have limited the practice to the use of less harmful animal or vegetable oils only. Nonetheless, mule spinning may still be practiced in other parts of the world, and thus textile workers may have a continuing exposure to inhalation and skin contact with mineral lubricants as a result of mule spinning. Another potentially hazardous exposure for textile workers involves exposure to dyestuffs, products whose purpose is to add color to materials. The term dyestuffs applies to both dyes and pigments. At present, most textile dyes are synthetic products. The first synthetic dye, mauve, was discovered in 1865. The synthetic dyestuff industry developed rapidly soon after this discovery with the introduction of another very important dye, magenta. The subsequent development of water-soluble azo dyes represented a landmark in the synthetic dye industry. The most important dye structures include triphenylmethane compounds, indigoid and azo structures, azines, thiazines, anthraquinone derivatives, and phthalocyanines. A crucial technological advance occurred in the 1950s with the discovery of reactive dyes, which react directly with the fiber itself. Reactive dyes produce textiles with specific color fastness that had not been possible with the earlier water-soluble dyes.

Nearly 40,000 different colorants and dyes exist in the textile industry. These dyes involve more than 9000 different chemical structures. World production of dyestuffs was estimated to be 600,000 to 700,000 tons in 1978, of which 50% to 60% were used for textiles. In 1986, more than 107,000 tons of textile dyes were produced in the United States. One of the most commercially important dyes is the benzidine-based dye group. Because of health concerns, the production of benzidine-based dyes decreased drastically in the United States during the 1970s, but these dyes may still be widely used elsewhere in the world. Another important source of potential toxicity to textile workers involves the finishing processes. Finishing treatments are intended to enhance the properties of textiles and include crease-resistant, flame-retardant, water-repellent, antisoiling, and antimicrobial treatments. Crease resistance treatments are the most widely used process for textiles such as cotton and viscose because these fibers are the most likely to wrinkle significantly. Formaldehyde-based resins have been extensively used since the early 1950s to produce permanent press fabrics. The first such resin was urea-formaldehyde resin, which first came on the market in 1933. Melamine-formaldehyde resins are used for crease resistance treatments in the textile industry today. A new class of crease-resistant finishing agent for textiles was introduced in the United States in the late 1940s. These chemicals were the cyclic ethylene ureas, including dimethylol ethylene urea, which reacts directly with cellulose fibers. Application of finishing agents increased gradually as the popularity of permanent press garments grew during the 1950s. In 1959, dimethylol dihydroxy ethylene urea was formulated, and it is currently the most widely used crease-resistant finishing agent. This chemical is made from urea, formaldehyde, and glyoxal, and during production it releases significantly less formaldehyde than the earlier urea and melamine resins. In the 1980s, the release of formaldehyde from dimethylol dihydroxy ethylene urea was further reduced by alkylation. Other lowformaldehyde processes continue to be developed. The addition of flame retardants in the production of textiles dates back to antiquity, when seawater, clay, and vinegar in combination were used to form primitive flame retardants. Over the past 30 years, considerable effort has gone into developing effective fire-retardant textiles for use in work clothes, upholstery, space and aeronautical research, and military textiles. Currently, the most widely used flame retardants are inorganic salts and reactive phosphorus and nitrogen compounds. Although they tend to dissolve during normal laundering processes, inorganic salts are attractive agents because they are easier to apply during manufacturing. In addition, these compounds tend to be less toxic than the organic reactive flame retardants. ORGANIC SOLVENTS Aliphatic hydrocarbons are often used to clean parts and equipment in textile mills and plants. Stoddards solvent, mineral spirits, and kerosene are examples of such chemicals commonly used for this purpose. Specifically, 1,1,1-

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trichloroethane, a chlorinated hydrocarbon, is used to clean metal parts. In addition, it is often used for spot cleaning of cloth. Exposure to any of these solvents may cause defatting and resultant skin irritation, leading to pruritic dermatitis. In addition, these materials can be very potent central nervous system depressants. The chlorinated solvents also have the potential to produce hepatic and renal toxic effects. Studies involving textile workers exposed specifically to 1,1,1-trichloroethane have not detected any problems. Solvents of essentially historical importance include carbon disulfide, a known neurotoxicant widely used in the past in the production of the synthetic fiber viscose rayon, and methyl n-butyl ketone, a substance known to cause sensorimotor neuropathies in exposed workers. OTHER PROCESSES Other processes of importance used in the textile industry today include application of water repellents, antistatic agents, antisoiling agents, antimicrobial agents, antimildew agents, and softening agents (Table 531).

Clinical Toxicology
DUSTS AND BYSSINOSIS Byssinosis is a respiratory syndrome that occurs as the result of inhaling dust that is produced when cotton, flax, or hemp is handled. Byssinosis is among the most significant health problems in the entire textile industry today. The precise pathogenesis of byssinosis is unclear, but it does involve the development of clinically significant bronchoconstriction.1,4,9 This bronchoconstriction is thought to be related to endogenous histamine contained within the cotton bract itself. In addition, it is assumed that a direct release of histamine from pulmonary mast cells contributes to the development of the clinical signs and symptoms. Byssinosis was first reported in England but was not generally recognized in the United States until the late 1960s. This is when it became recognized as a major occupationally related health problem. Byssinosis has evolved to become a significant regulatory and political issue, particularly where textiles are manufactured or processed.

TABLE 531 M Chemicals Used in Textile Manufacturing

Processes

Process Water repellents Antistatic agents Antisoiling agents Antimicrobial agents Antimildew agents Softeners

Associated Chemicals Fluorocarbons, silicones, zirconium emulsions Polyethylene glycols, epoxy resins Aluminum, silicon and titanium oxides, starch, fluorocarbons, polymers Quaternary ammonium compounds, tributyltin oxide Pentachlorophenyl laurate, copper and zirconium compounds Tensides, polyethylene glycol, polysilicates

When cotton is first picked, a large quantity of torn and chopped-up leaves and stems is mixed in with the cotton fibers. Automated picking of cotton tends to produce a great deal of this sort of contamination and certainly significantly more than occurs with hand-picked cotton. It has been theorized that the bract leaf located just below the cotton boll itself may contain vasoactive chemicals. It is these chemicals that are specifically capable of inducing bronchospasm. Other theories hold that bacteria growing in the cotton dust itself can produce endotoxins during storage and that this endotoxin is responsible for producing the bronchospastic response associated with byssinosis. There does seem to be an association between the prevalence of byssinosis and measured levels of endotoxin in cotton dust and in workplace air.11,12 Clinically, byssinosis is first manifested by complaints described as chest tightness, which is sometimes associated with a continual cough, shortness of breath, and occasionally wheezing. These symptoms typically occur on the first day of the work week. Early in the development of the disease, symptoms occur only occasionally. Often the earliest symptoms occur during excessively humid weather. This early form of byssinosis is sometimes classified as grade a byssinosis. Over time, a distinct progression of symptoms is noted to occur. Following the initial stage (grade a), the next stage is grade I. This stage usually involves complaints of chest tightness on most workdays or at least on all first workdays of the week (typically Monday). Over the next several years, symptoms may progress to grade II byssinosis, characterized by symptoms on days other than Monday. In this stage, symptoms still are generally worse at the start of the week, with many workers noting some degree of improvement toward the end of the week. This progression of symptoms is extremely important to the clinician, as a tendency for symptoms to improve as the week progresses differentiates byssinosis from nonspecific airway reactivity. In nonspecific settings, symptoms do not improve and may actually worsen as the work week progresses. If ongoing exposure to the dust responsible for the problem is completely eliminated or at least significantly decreased, the symptoms of grade II byssinosis can be reversed. However, if the relevant exposure continues, symptoms can and do progress to become grade III byssinosis. The hallmark of this stage is a clinical picture of chronic bronchitis. Grade III byssinosis usually continues to worsen to the point of clinical irreversibility. At this point, the patient has developed significant chronic airway obstruction. An Occupational Safety and Health Administration (OSHA) standard addresses dust exposure for workers. Since this OSHA dust standard requires the measurement of both forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) in cotton dustexposed workers, it is crucial for the clinician to understand the clinical correlations at play. On the first day of the work week, the bronchospasm (which is typically reversible at that stage) seen with byssinosis can be demonstrated by the use of spirometry performed prior to the start of the workers shift. Spirometric parameters can then be measured again

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5 to 6 hours later to determine if there has been any diminution in FEV. Although most clinicians agree that the measurement of FEV1 is poorly sensitive, FEV1 measurements are often used to demonstrate bronchial hyperreactivity to cotton dust. A 10% decline in FEV is generally considered to be sufficient evidence that a worker is significantly reactive to cotton dust. It is important to note that OSHA considers FEV1 declines of as little as 5% to be clinically significant. In these cases, OSHA requires that such individuals be placed on a program of increased surveillance.31 Although byssinosis still represents a significant health problem in the cotton textile industry, it has been replaced in importance by chronic obstructive pulmonary disease (COPD) in cotton textile workers. Textile workers often smoke cigarettes, and some studies have shown that the adverse health effects of smoking and inhalation of cottoncontaining dust are additive. Perhaps one of the most pressing clinical questions in the industry today is whether smoking, cotton dust, or a combination is the cause of COPD in cotton textile workers. The answer to this question is not easy because of its health and compensation implications. A study reported in 1991 suggested that smokers may be more susceptible to adverse effects following lower levels of cotton dust exposure than nonsmokers.32 Perhaps the most important question for the clinician is what advice is most appropriate to give to cotton textile workers who have developed COPD. When COPD has been diagnosed in these workers, it is more than reasonable to strongly counsel them to stop smoking immediately. An organized smoking cessation program would be optimal. These workers have often been involved in the textile industry for many years. While simply changing jobs may represent the best possible solution and provide for elimination of exposure, such a change may not be an option. It may be possible to transfer afflicted individuals to areas in the textile plant or mill that do not involve exposure to cotton dust. When total elimination of exposure to cotton dust is not achievable, use of one of the several different types of respirators currently in use in the textile industry should be considered. TEXTILE-RELATED OCCUPATIONAL ASTHMA On occasion, a textile worker with a recognized (or unrecognized) history of atopy reacts to cotton dust exposure on the job with symptoms of acute or subacute asthma. This is thought to be due to pollens as well as other contaminants, which may be found in microscopic or macroscopic quantities in cotton dust. A complete allergy workup may or may not identify these antigens. The use of spirometry before and immediately after the work shift may be useful in identifying a significant drop in FEV1 during the time of exposure. The only obvious solution to this problem is total removal from exposure. Many, if not most, of these individuals leave the textile industry because of the severity of their symptoms and the clear-cut association with exposures at work. In addition, some of the commonly

encountered dyes are of low molecular weight and can induce asthma in exposed workers (see the next section). Other pulmonary conditions noted in workers in the cotton textile industry include mill fever and weavers cough. Both of these disorders may be due to inhalation of microorganisms found as contaminants in air conditioning systems in mills and processing plants. DYESTUFFS The chemicals that are the most widely used in the textile industry are the dyes that impart color to yarn or cloth (Table 532). Several adverse health effects and potential adverse effects have been defined for this group of substances. Two primary production processes are used today to dye fabrics and textiles. Continuous processes are used for large cotton materials and for carpets, as well as for fabrics that contain 100% synthetic fibers. Noncontinuous processes are generally used for all other materials. In the dyeing process, the dye molecules penetrate the pores of the swollen fibers and are retained there by chemical or physical forces. Cotton is generally dyed after the yarn has been woven or knitted into fabric; wool yarn is usually dyed before these processes are undertaken. The dyes developed for use with cotton can be divided into three main groups: (1) water-soluble dyes, (2) dyes soluble by alkaline reduction, and (3) dyes formed on the fiber. Water-soluble textile dyes are direct dyes that have an affinity for cellulose fibers. Reactive dyes react chemically with cellulose fibers. All water-soluble dyes in the textile industry are electrolytes. Dyes soluble by alkaline reduction include the vat and sulfur dyes. Dyes formed on the fiber include azo and oxidation dyes obtained from the oxidation of various amines. Polyester fabric is usually dyed with disperse dyes. These compounds contain different chemicals called chromophores and use carrier compounds. The purpose of these carrier compounds is to improve the ability of the polyester material to accept the dyes. Some of these carrier compounds include biphenyl, chlorinated benzene, naphthalene, naphthalene derivatives, and phthalimides. Wool and polyamides are normally dyed with acid dyes, metal complex dyes, or chromium dyes. Reactive dyes may, under certain circumstances, cause a form of occupational asthma. The typical history is that an
TABLE 532 M Important Classes of Textile Dyes

and Related Compounds

Class of Dye Acid dyes Basic (cationic) dyes Direct dyes Disperse dyes Reactive dyes Mordant dyes Sulfur dyes Vat dyes Optical brighteners Dye carriers

Major Use Wool, polyamides Cotton Cotton, viscose Synthetics Cotton, wool Wool Cotton Cotton, wool All fibers Polyester, wool

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employee who mixes or applies these dyes develops wheezing or symptoms of asthma relatively quickly following exposure. The symptoms are mild at first but progressively worsen. Fatal anaphylactic reactions can occur in workers who had previous wheezing on exposure. Consequently, any initial reaction on exposure must be treated cautiously, with careful clinical follow-up mandatory. The following lowmolecular-weight dyes have been reported to be associated with the development of asthma or asthma symptoms in exposed workers: anthraquinone, paraphenyl diamine (used in the fur industry), hexafix brilliant yellow, drimaren brilliant blue, and cibachrome brilliant scarlet. Today, many of the commonly used textile dyes are supplied as pastes rather than as powders. As a result, this form tends to diminish the potential for aerosolized exposure and subsequent sensitization. The azo-type, benzidine, and benzidine derivative dyes have been widely used in the textile industry, and their potential toxicity and carcinogenic properties are of great concern.15 The metabolism of these dyes has been studied extensively.16,17,18,19 Significant detoxification and metabolic activation take place in vivo, with both oxidative and reductive pathways involved in these processes. The majority of these dyes undergo reduction catalyzed by enzymes of the intestinal microorganisms or hepatic enzymes, including microsomal and soluble enzymes. Many of the azo dye substances in common use today have highly charged substituents such as sulfonates. These tend to resist enzymatic attack and are generally poorly absorbed from the intestinal tract. In addition, they provide poor access to the liver, which is the major site of the mixed-function oxidase system. The lipophilic dyes, which are often carcinogenic, readily access oxidative enzymes and are activated by mixed-function oxidase systems. Biochemical reduction of the carcinogenic dyes usually leads to diminution or complete loss of carcinogenic activity. In contrast, most of the highly charged water-soluble dyes become mutagenic only after reduction. Even then, most of the fully reduced amines require oxidative metabolic activation. An outstanding example is the potent human bladder carcinogen benzidine, which derives from the reduction of several azo dyes. Many problems regarding mutagenic and carcinogenic activation remain to be solved. At present, it is apparent that both oxidative and reductive pathways yield toxic products.

ingestion. This population had more bladder cancer than what might be expected in an unexposed population. Consequently, these compounds should be handled with great caution in the workplace. They should be regarded as carcinogenic, and the number of workers exposed to them at any given work site should be strictly limited. The dyestuffs used in the textile industry present other medical concerns. Recent reports indicate a statistically significant excess mortality attributable to pernicious anemia within the textile industry. Those individuals whose deaths were attributed to pernicious anemia within the industry were more than twice as likely to have worked in textile mills than anyone else. FLAME RETARDANTS Organic flame retardants, such as tetrakis (hydroxymethyl) phosphonium chloride and N-methylol dimethylphosphonyl propionamide, react with cellulosic fibers to form chemical bonds that are stable and maintain themselves through many launderings. The first compound of this type was introduced in the early 1950s and has given rise to a number of variants. One of the most widely used and most durable flame retardants, Pyrovatex CP, was patented in 1965 (Box 531). In the 1970s, tris(2,3-dibromopropyl) phosphate was commonly used as a flame retardant for textiles, specifically for childrens pajamas in the United States. Eventually

BOX 531 Industries in Which Formaldehyde Exposure Can Occur

G

Benzidine and Benzidine Derivatives

There are many specific dyes of concern in this category, but of special note are direct brown 95, direct black 38, and direct blue 6. The latter two dyes have also been used in hair color dyes. Workers exposed to these dyes excrete high levels of benzidine into their urine, as these compounds are actively metabolized to benzidine itself. Consequently, there exists a cancer risk for these workers. One of the most famous studies to address the issue of benzidine and related compounds carcinogenic ability looked at Japanese kimono painters and dyers who habitually pointed their brushes by passing the brushes through their pursed lips, resulting in dye exposure and presumed

Agricultural workers Anatomists Beauticians Biologists Bookbinders Botanists Chemical production workers Cosmetic formulators Crease-resistant textile finishers Disinfectant makers Disinfectors Dress goods shop personnel Electrical insulation makers Embalmers Embalming fluid makers Fireproofers Formaldehyde production workers Formaldehyde resin makers Foundry employees Fumigators

Fur processors Furniture makers Glue and adhesive makers Hide preservers Histology technicians (including necropsy and autopsy technicians) Hobbyists Ink makers Lacquerers and lacquer makers Medical personnel (including pathologists) Mirror manufacturers Paper makers Particle board makers Photographic film makers Plastics workers Plywood makers Rubber makers Taxidermists Textile mordanters and printers Textile waterproofers Varnish workers Wood preservers

From U.S. National Institute for Occupational Safety and Health.

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this chemical was discovered to have both carcinogenic and mutagenic properties. As a result, production of tris flame retardant was discontinued by the end of the 1970s. CREASE RESISTERS

Formaldehyde
Formaldehyde is a colorless gas with a very pungent and characteristic odor. It is readily soluble in water, ethyl alcohol, and diethyl ether. As a commercial product, it is most commonly formulated as a 30% to 50% solution in water to produce formalin. Formaldehyde is produced in great quantities in many countries. In 1992, approximately 12 million tons were produced worldwide. This chemical finds use in many different industries (see Box 531), including leather production, rubber and cement production, and foundry work. One of its most prolific uses is in the textile industry.2 Formaldehyde is generally used in the textile industry to attain a permanent press finish. Consequently, textile workers may become exposed to formaldehyde during the finishing of cloth. Less commonly, exposures can result during the sewing of cloth. Because of the exposure potential while large quantities of fabric are manufactured and treated with formaldehyde, time is allotted in the production process to allow for off-gassing to release formaldehyde from the material.5 Alternatively, the formaldehyde may be physically washed from the fabric. In either case, the procedures involved in removing formaldehyde from the fabric can pose a special threat of exposure to workers. Formaldehyde is a well-known cause of ocular and airway irritation. In addition, it can cause certain skin reactions, including contact dermatitis via either allergic or irritant mechanisms. Patch testing with a 1% to 2% aqueous solution of formaldehyde can help to differentiate these two common forms of contact dermatitis. Occasionally, contact with formaldehyde results in urticaria, which is thought to occur by both allergic and nonallergic mechanisms, depending on the clinical setting. The allergic type of dermatitis usually results in lesions in noncontact areas, and the nonallergic contact urticaria generally is limited to the area of skin that actually came into contact with the formaldehyde. Because the concentration of residual formaldehyde on the fabric surface is carefully controlled (generally limited to less than 300 ppm), contact dermatitis from just wearing finished fabrics is unusual.6 Upper respiratory and eye irritation can be expected when air concentrations of formaldehyde exceed 1 ppm.7 Currently, the OSHA permissible exposure limit (PEL) is 0.75 ppm, and the majority of textile manufacturers maintain operating formaldehyde levels below 0.5 ppm. Workers who are exposed to formaldehyde are required by OSHA to complete a questionnaire designed to assess whether symptoms are present that may be due to formaldehyde exposure when levels exceed 0.5 ppm.8 Certain individuals may develop specific respiratory sensitization to formaldehyde that results in rhinitis or an asthmalike picture. The symptoms of the former condition may be quite similar to those of allergic rhinitis. However,

after relatively high exposures, a pure asthma picture may emerge, including the development of IgE and IgG antibodies. In most cases of formaldehyde-related asthma, the specific causal mechanisms are not clearly or completely understood. There are no simple diagnostic laboratory tests to help the clinician in the diagnosis of formaldehydeinduced asthma. Skin tests that use dilute formaldehyde solutions have not been standardized, and inhalation challenge tests with formaldehyde can be dangerous unless they are conducted under very carefully controlled conditions.9 The best diagnostic option for the occupational clinician is a physical examination in conjunction with spirometry both prior to and immediately following the work shift. In this way, both clinical and spirometric differences can be compared before and after exposure. Following studies that demonstrated the ability of formaldehyde to produce nasal cancer in small laboratory animals, formaldehyde has been identified as an animal carcinogen. It is unclear, however, if the carcinogenic effects are due primarily to specific cytotoxic effects or if genotoxic mechanisms are at play. Of course, it is possible that both types of effects may come together to produce neoplasia. Although epidemiologic studies have not shown a consistent association between the development of cancer in humans and formaldehyde exposure, the suspicion of an association remains strong, based on animal data. SYNTHETIC FIBERS Polyester, acrylic, nylon, rayon, and polypropylene have long been considered to be essentially biologically inert. In fact, during early studies of byssinosis, workers exposed to synthetic fibers were used as controls for studies of cottonexposed workers. Preshift and postshift spirometry showed no changes due to acute exposure to synthetic workers. Furthermore, the mean FEV of synthetic fiber workers was normal, yet that of cotton workers was lower. However, a recent longitudinal study showed a surprising and unexplained result: workers in synthetic fiber mills had a greater annual decline in FEV than workers in cotton mills. This result cannot be explained by our knowledge of synthetic fibers. Additional research will be necessary both to validate the results and to explain them if validated.

Viscose Rayon
The chemical carbon disulfide (CS2) is prominent in the production process of the synthetic fiber viscose rayon.13 Specifically, CS2 is used in the conversion process of cellulose to rayon fiber and cellophane. In addition, CS2 has also been used in the vulcanization of rubber, the extraction of fats, and the manufacture of sulfur matches.14,17 During the early years of rubber manufacturing as well as the early days of rayon production, extremely high levels of CS2 resulted in severe CNS disorders, including acute mania and narcosis. Since the inception of stricter regulatory controls, however, ambient levels of CS2 have diminished, and, at present, acute exposures are rare.22 However, these changes have allowed the emergence of chronic exposure to low levels of CS2 and consequent clinical effects.

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The most common clinical effect of chronic CS2 exposure is a distal sensorimotor neuropathy. It preferentially attacks the long axons in the CNS and the peripheral nervous system. A clinically apparent encephalopathy, discernible on neuropsychiatric testing and associated with cerebral atrophy, has also been observed in textile workers following chronic exposure to low CS2 levels.22,23,24,25,26 Exposure to CS2 has been clearly shown to accelerate the rate of atherogenesis and is associated with increased levels of low-density lipoproteins and hypertension. Consequently, it is unclear if the encephalopathic effects of CS2 are due to the effect of accelerated atherogenesis or to the direct CNS toxicity of this chemical. Chronic low-level exposure to CS2 has also been reported to be associated with testicular atrophy, impotence, and a variety of poorly understood visual disorders. The metabolism of CS2 is noteworthy in that it may be excreted or exhaled unchanged or may actually undergo complex metabolic alteration.28 This metabolic alteration predominantly results in the production of dithiocarbamate and trithiocarbonate compounds.29,30 This is significant in that the isolation of 2-thiothiazolidine-4-carboxylic acid (TTCA) in the urine of workers exposed to CS2 has led to the use of it as a means to assay exposure to CS2 in the workplace, since TTCA remains in the urine for several days after exposure. ORGANIC SOLVENTS

Methyl n-butyl Ketone Toxicity

A group of workers in a fabric printing plant in Ohio reportedly developed symptoms of neurotoxicity possibly related to exposure to methyl n-butyl ketone. These workers reported symptoms consistent with sensorimotor neuropathies during a time frame that followed the substitution of methyl n-butyl ketone for methyl isobutyl ketone in a solvent mixture. Animal studies suggest that some neurotoxic effects associated with methyl n-butyl ketone exposure may be potentiated by methylethylketone (MEK). Since methyl n-butyl ketone and n-hexane are metabolized to the same potentially harmful metabolite, 2,5-hexanedione, it is possible that these chemicals may act in a synergistic fashion in certain biological systems. FLOCK WORKERS LUNG Flock workers lung (FWL) is a recently described chronic diffuse interstitial lung disease. FWL is characterized by the fact that it lacks characteristics usually found in other occupational lung diseases.4 Within the textile industry a subset of production techniques exist that are used in the so-called flocking industry. This industry produces fabric that exhibits a fleeced or woolly appearance. Flocked material may be used in making upholstery, clothing, carpets, rugs, and various novelty products, including childrens toys.3 Flock is essentially a powdered form of textile fibers manufactured using nylon, polyester, or other similar fibers. Flock takes the form of a powdered material that

consists of very short fibers that are generally less than 5 mm in length.4 This material is applied, or flocked, to adhesive-coated surfaces, imparting a soft and velvety feel. Some companies involved in this industry manufacture flock alone; others may only perform flocking. Some companies may be engaged in both processes. Some flock manufacturers may cut their flock from long nylon, rayon, or polyester cables known as tow. Many manufacturers cut tow using guillotine-type cutting devices. In this process, fibers of a specific length, known as precision-cut flock, are produced. Guillotine-cut flock may then be further processed by dying and drying before it is screened and packaged. Other flock manufacturers may cut tow using rotary cutters. The fibers are cut to a less exact length and are known as random-cut flock. The production of random-cut flock is much quicker than that using guillotine cutters since in this process, the tow is dyed, finished, cut, dried, and packaged in one continuous operation. During continued use, rotary cutter blades dull and thus cause increased friction and increasing blade temperatures. In the rotary cutting process, nylon tow may be cut uncleanly or may melt. Nylon flock produced by the rotary cutting technique may have minute, irregular edges, which may be released as airborne particles of respirable dimensions (i.e., less than 10 m).4 The presence of the minute excess edges on flock fibers has been verified by quality control inspectors. Investigators from the National Institute for Occupational Safety and Health have also identified their presence in bulk samples of flock produced by rotary cutting techniques and as respirable-sized particles in workroom air.4 Most, if not all, workers reportedly afflicted with flock workers lung have been exposed to flock produced by the rotary cutting technique.

REFERENCES
1. Beckett WS, et al: Womens respiratory health in the cotton textile industry: An analysis of respiratory symptoms in 973 non-smoking female workers. Occup Environ Med 51:14, 1994. 2. Cassitto MG, et al: Carbon disulfide and the central nervous system: A 15-year neurobehavioral surveillance of an exposed population. Environ Res 63:252, 1993. 3. Christiani DC, et al: Pulmonary function among cotton textile workers: A study of variability in symptoms reporting, across-shift drop in FEV1, and longitudinal change. Chest 105:1713, 1994. 4. Chronic interstitial lung diseases in nylon flocking industry workers Rhode island, 19921996. Morbid Mortal Weekly Rep 380:897901, 1997. 5. Chu CC, et al: Polyneuropathy induced by carbon disulphide in viscose rayon workers. Occup Environ Med 52:404, 1995. 6. Dement JM, Brown DP: Lung cancer mortality among asbestos textile workers: A review and update. Ann Occup Hyg 38:525, 1994. 7. Drexler H, et al: Carbon disulphide: I. External and internal exposure to carbon disulphide of workers in the viscose industry. Int Arch Occup Environ Health 65:359, 1994. 8. Drexler H, Goen T, Angerer J: Carbon disulphide: II. Investigations on the uptake of CS2. Int Arch Occup Environ Health 67:5, 1995. 9. Egeland GM, et al: Effects of exposure to carbon disulphide on low density lipoprotein cholesterol concentration and diastolic blood pressure. Br J Ind Med 49:287, 1992. 10. Fishwick D, et al: Respiratory symptoms and dust exposure in Lancashire cotton and man-made fiber mill operatives. Am J Respir Crit Care Med 150:441, 1994.

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11. Gibbs GW: The assessment of exposure in terms of fibres. Ann Occup Hyg 38:477, 1994. 12. Glindmeyer HW, et al: Exposure-related declines in the lung function of cotton textile workers: Relationship to current workplace standards. Am Rev Respir Dis 144:675, 1991. 13. Gold EB, Sever LE: Childhood cancers associated with parental occupational exposures. Occup Med 9:495, 1994. 14. Graham DG, et al: Pathogenetic studies of hexane and carbon disulfide neurotoxicity. Crit Rev Toxicol 25:91, 1995. 15. Howard K: Dyestuffs and bladder cancer (letter). N Z Med J 106:391, 1993. 16. Kremer AM, et al: Airway hyper-responsiveness and the prevalence of work-related symptoms in workers exposed to irritants. Am J Ind Med 26:655, 1994. 17. Krstev S, Perunicic B, Farkic B: The effects of long-term occupational exposure to carbon disulphide on serum lipids. Eur J Drug Metab Pharmacokinet 17:237, 1992. 18. Levine WG: Metabolism of azo dyes: Implication for detoxification and activation. Drug Metab Rev 23:253, 1991.

19. Morgan DL, et al: Summary of the National Toxicology Program benzidine dye initiative. Environ Health Perspect 102(Suppl 2):63, 1994. 20. Moya C, Anto JM, Taylor AJ (Collaborative Group for the Study of Toxicity in Textile Aerographic Factories): Outbreak of organising pneumonia in textile printing sprayers. Lancet 344:498, 1994. 21. Nilsson R, et al: Asthma, rhinitis, and dermatitis in workers exposed to reactive dyes. Br J Ind Med 50:65, 1993. 22. Phillips M: Detection of carbon disulfide in breath and air: A possible new risk factor for coronary artery disease. Int Arch Occup Environ Health 64:119, 1992. 23. Riihimaki V, et al: Assessment of exposure to carbon disulfide in viscose production workers from urinary 2-thiothiazolidine-4-carboxylic acid determinations. Am J Ind Med 22:85, 1992. 24. Roman E, et al: Pernicious anaemia in the textile industry. Br J Ind Med 48:348, 1991. 25. Sailstad DM, et al: Evaluation of an azo and two anthraquinone dyes for allergic potential. Fundam Appl Toxicol 23:569, 1994.

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26. Sanz P, Prat A: Toxicity in textile air-brushing in Spain (letter). Lancet 342:240, 1993. 27. Swaen GM, Braun C, Slangen JJ: Mortality of Dutch workers exposed to carbon disulfide. Int Arch Occup Environ Health 66:103, 1994. 28. Vanhoorne M, De Bacquer D, De Backer G: Epidemiological study of the cardiovascular effects of carbon disulphide. Int J Epidemiol 21:745, 1992. 29. Vanhoorne M, de Rouck A, de Bacquer D: Epidemiological study of eye irritation by hydrogen sulphide and/or carbon disulphide exposure in viscose rayon workers. Ann Occup Hyg 39:307, 1995. 30. Vanhoorne M, Vermeulen A, De Bacquer D: Epidemiological study of endocrinological effects of carbon disulfide. Arch Environ Health 48:370, 1993. 31. White NW, Cheadle H, Dyer RB: Workmens compensation and byssinosis in South Africa: A review of 32 cases. Am J Ind Med 21:295, 1992.

32. Zuskin E, et al: A ten-year follow-up study of cotton textile workers. Am Rev Respir Dis 143:301, 1991.

SUGGESTED READINGS
Claude J, et al: Life-style and occupational risk factors in cancer of the lower urinary tract. Am J Epidemiol 124:578, 1986. Malker HSR, et al: Occupational risks for bladder cancer among men in Sweden. Cancer Res 47:6763, 1987. Schoenberg JB, et al: Case-control study of bladder cancer in New Jersey: I. Occupational exposures in white males. J Natl Cancer Inst 72:973, 1984. Siemiatycki J, et al: Associations between several sites of cancer and nine organic dusts: Results from an hypothesis-generating case-control study in Montreal. 19791983. Am J Epidemiol 123:235, 1986.