<b>Bijsluiter</b>. De hyperlink naar het originele document werkt niet meer. Daarom laat Woogle de tekst zien die in dat document stond. Deze tekst kan vreemde foutieve woorden of zinnen bevatten en de opmaak kan verdwenen of veranderd zijn. Dit komt door het zwartlakken van vertrouwelijke informatie of doordat de tekst niet digitaal beschikbaar was en dus ingescand en vervolgens via OCR weer ingelezen is. Voor het originele document, neem contact op met de Woo-contactpersoon van het bestuursorgaan.<br><br>====================================================================== Pagina 1 ======================================================================

<pre>      Cellulose
      (CAS Reg no: 9004-34-6)
      Health-based Reassessment of Administrative
      Occupational Exposure Limits
      Committee on Updating of Occupational Exposure Limits,
      a committee of the Health Council of the Netherlands
      No. 2000/15OSH/031, The Hague, 7 March 2002
031-1
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<pre>      Preferred citation:
      Health Council of the Netherlands: Committee on Updating of Occupational
      Exposure Limits. Cellulose; Health-based Reassessment of Administrative
      Occupational Exposure Limits. The Hague: Health Council of the Netherlands,
      2002; 2000/15OSH/031.
      all rights reserved
031-2
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<pre>1     Introduction
      The present document contains the assessment of the health hazard of cellulose
      by the Committee on Updating of Occupational Exposure Limits, a committee of
      the Health Council of the Netherlands. The first draft of this document was
      prepared by MA Maclaine Pont, M.Sc. (Wageningen University, Wageningen,
      the Netherlands).
          Literature was retrieved from the data bases Toxline, Medline, and Chemical
      Abstracts, covering the periods 1981 to May 2000, 1966 to May 2000, and 1937 to
      March 2000, and using the following key words: (cellulose or 9004-34-6) and
      (occupational or skin or dermal or dust or inhal*). Data considered to be critical
      were evaluated by reviewing the original publications. The final literature search
      has been carried out in May 2000.
          In July 2001, the President of the Health Council released a draft of the
      document for public review. The committee received no comments.
      Occupational exposure to cellulose is expected in various jobs related to
      extracting cellulose from its original material and in the industries using the
      cellulose for further processing. However, in none of these jobs, the workers are
      exclusively exposed to cellulose.
          In 1972, the US Food and Drug Administration declared cellulose to be
      generally recognised as safe (GRAS), based upon a review of research between
      1920 and 1972 (And92).
          Cellulose from cotton can contain small amounts of waxes, pectin's,
      hemicellulose, metal salts like ferric chloride, and chemical defoliants (arsenic,
      quaternary ammonium compounds). In the processing of fibers into yarn,
      compounds are used like starch or a starch derivative, bleaching compounds,
      anti-statics, lubricants, several dyes, carriers to facilitate the dyeing, chemical
      binders to retain the dye on the surface, etc. (Bar75).
          Cotton dust contains only 10-15% cellulose (Dom86). Paper dust and wood
      dust contain primarily compounds other than cellulose (Jäp87, Jag85).
          In the production of cellulose triacetate, the exposure is mainly to
      dichloromethane (Lan90). In the production of viscose rayon, the exposure is
      mainly to carbon disulphide (Van91).
031-3 Cellulose
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<pre>2     Identity
       name                      :       cellulose
       synonyms                  :       ß-amylose; alpha-cellulose; cupricellulose;
                                         hydroxycelllulose; pyrocellulose; sulphite
                                         cellulose
       molecular formula         :       (C6 H10 O5 )n
       structural formula        :
       CAS reg no                :       9004-34-6
      Data from How92.
      Cellulose is a natural polysaccharide with the glucose units linked as in
      cellobiose. Cellulose is widely distributed in nature. Wood, depending on its
      type, contains about 50 to 70% cellulose. Cotton and textile fibers of vegetable
      origin, such as flax, hemp, and jute, contain 65 to 95% cellulose (ACG99).
           Natural cellulose is a white substance existing in a microcrystalline form and
      as a nonfibrous form with a bulk density of 18 - 19 lb/ft 3 (288 - 305 kg/m3).
      Technical cellulose refers to that portion of the plant cell wall derived exclusively
      from glucose in its physical and chemical properties. Unbleached sulphate
      cellulose, obtained from wood, contains 3 to 5% lignin and has a brown colour.
      Unbleached sulphite cellulose also obtained from wood, also contains 3 to 5 %
      lignin and has a very light brown colour (MoDo97).
           CellulonTM fibre is a cellulose produced by a bacterial fermentation process
      employing a strain of Acetobacter acetic subsp xylinum and most closely
      resembles powdered and microcrystalline cellulose (Sch91).
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<pre>3     Physical and chemical properties
       molecular weight        :     300,000 to over 1,000,000
       melting point           :     not found
       boiling point           :     not applicable
       flash point             :     -
       vapour pressure         :     not applicable
       solubility in water     :     practically insoluble
       odour threshold         :     odourless
       log P octanol/water     :     not found
       conversion factors      :     not applicable
       (20 0C, 101.3 kPa)
      Data from ACG99, Har94.
4     Uses
      Cellulose is primarily used for the preparation of textile fibers, i.e., viscose
      (rayon), and for the production of paper and cardboard. For paper production,
      cellulose should contain at least 3% of lignin in order to maintain its strength
      (MoDo97). CellulonTM fibre is used as a thickener and suspending agent of food
      (Sch91).
           Derivatives of cellulose are used in a variety of applications:
           nitro-cellulose is used for the manufacturing of explosives, collodion, and
           lacquers.
           DEAE cellulose (diethylaminoethylcellulose) is used as ion exchange material
           in chromatography.
           cellulose acetates (partially acetylated) are used to prepare thermoplastic
           products: rubber and celluloid substitutes, photographic and cinema films,
           phonographic records, coating skins, insulating electric wires, etc.
           cellulose ethylhydroxyethylether is used as a laxative (Bud96).
5     Biotransformation and kinetics
      The committee did not find data on the (toxico)kinetics of cellulose.
031-5 Cellulose
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<pre>6     Effect and mechanism of action
      Human data
      Employment in cellulose plants was associated with a significantly increased
      incidence of gliomas, the predominant type of brain tumour among adults
      (p<0.05). The Cancer Environment Registry of Sweden was used, which links
      cancer incidence and employment data. At least 500 individuals were evaluated
      in the group of cellulose plant workers, and 45 cases were found (Standardised
      Incidence Ratio 1.6, compared with the general Swedish population). However,
      the authors explain the aetiology of the glioma as a result of exposure to acids,
      bleaches, finishing oils, and mercury compounds (McL87). There are no
      quantitative exposure data. The committee concludes that there is no proof that
      the gliomas are caused by exposure to cellulose.
           In human studies with microcrystalline cellulose, doses up to 30 g/day were
      tolerated therapeutically as a bulk laxative (Mon82).
      Animal data
      Irritation and sensitisation
      Instillation of 50 mg CellulonTM into the eyes of 6 rabbits was mildly irritating 1
      hour posttreatment. The redness subsided in all but one animal 24 hours after
      treatment. No irritation was noted in the cornea and iris (Sch91).
           A dermal patch of 500 mg CellulonTM applied for 4 hours on the shaved skin
      of 6 rabbits did not induce erythema, oedema, or other dermal effects (Sch91).
           The committee did not find data on the potential sensitising properties of
      cellulose.
      Acute toxicity
      After a single oral dose in rats, the LD 50 of CellulonTM with sucrose (1 : 1) was
      greater than 2000 mg/kg (Sch91).
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<pre>      Inhalation exposure
      A single inhalation exposure during 6 hours to respirable particles of cellulose
      had no effects in guinea pigs. The mean mass aerodynamic diameter (MMAD)
      was 2.9 - 3.0 µm, with a geometric standard deviation of 1.4 µm in both cases. The
      exposure concentration for each of the 4 animals ranged from 19.2 to 22.0 mg/m3.
      The following parameters were measured or calculated prior to exposure, after 6
      hours of exposure, and 18 hours postexposure: number of breaths per minute (f),
      tidal volume (VT) and pressure changed during each breath (∆P), VT x f and flow
      resistive work per breath during inspiration and expiration. The lungs were not
      investigated histologically. A challenge with 10 % CO2 before and after each
      exposure to cellulose did not influence the lung functions either (in all cases:
      p>0.05, compared with a control group). In a group of 4 guinea pigs exposed to
      cotton dust, all lung function parameters were affected (p<0.05) except VT x f and
      flow resistive work per breath after 6 hours of exposure. The authors concluded
      that the different results after cotton and cellulose exposure rule out the
      possibility that the respiratory reactions were caused by mechanical properties
      of the dust (Ell84). The committee considers that this study cannot be used for
      the risk assessment since the exposure duration was too short.
          Groups of male Crl:CDBR rats were exposed 'nose only' to cellulose fibres, 6
      hours/day, 5 days/week, for 2 weeks. The target concentrations were 300 and 575
      fibres/mL. The median length of the fibres was 10-13 µm. Following exposures,
      the lungs of rats were evaluated 3 and 10 days, as well as 1 and 3 months
      postexposure by bronchoalveolar lavage (BAL), and immediately after, as well as
      10 days, 1, and 3 months for biopersistence/clearance studies. The inhalation
      exposure produced lung burdens in the range of 3x107 fibres. Clearance of
      cellulose fibres was moderate to slow with mean values in the high dose group of
      2.84x107 reduced to 1.55x107 after 3 months postexposure. The cellulose fibres
      produced a mild but transient pulmonary inflammatory response, which returned
      to control levels within 10 days postexposure (War98).
          Groups of male Wistar rats were exposed 'whole body' to 0 (n=3) or 1000
      fibres of cellulose / ml (n=6), 7 hours/day, for 1, 3, 8, and 14 days of actual
      exposure over a 3-week calendar period. An additional group of 6 exposed rats
      were maintained without further inhalation exposure, for a period of 28 days
      (after 14 days of actual exposure). The respirable fibres were well characterised:
      the size distribution was determined, as well as aerodynamic diameter and
      density. The bulk of the fibres was within the respirable range for rats. The
      concentration was 73 mg/m3 (SE 1.8). Inhalation exposure induced an early
031-7 Cellulose
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<pre>      inflammatory response in rat lungs, as determined by bronchialveolar lavage,
      which peaked at day 1 following the start of inhalation and thereafter declined,
      despite a further 13 days of exposure. In vitro production of the
      pro-inflammatory cytokine tumour necrosis factor x (TNFα ) by lavaged alveolar
      macrophages was markedly depressed by the end of the exposure period,
      compared to sham-exposed controls and this effect was still present in rats that
      had been allowed to recover for 28 days beyond the end of exposure. The
      authors concluded that the cellulose material studied was less inflammogenic
      than crocidolite and that the extent of the inflammatory response within the
      lungs appeared to reduce with continued exposure over a 14-day period (Cul00).
      Intratracheal instillation
      Intratracheal administration of cellulose dust into rats caused pulmonary toxicity.
      The size of the particles was not specified. A quantity of 15 mg instilled into the
      trachea of 10 male rats (body weight: 230-260 g), induced interstitial oedema, as
      well as signs of inflammation after 1 day. After one month the developing
      bronchioalveolitis was fibrous in character. Compared with quartz-treated rats
      the inflammatory processes were less explicit and less extensive. In the lungs of
      control rats, no histological changes or lymph nodes were observed. In the
      bronchoalveolar lavage, fluid protein, lactate dehydrogenase, acid phosphatase,
      phospholipid, and cell count were enhanced after days 1 and 3 (p<0.01) (Ada97).
           Further observations on the animals were reported by Tatrai and coworkers.
      After 6 and 12 months, groups of 10 rats were investigated. A fibrosing
      alveobronchiolitis developed and with moderate progression by the end of the
      first year reached degree III according to Belt-King's system for classifying
      experimental fibrosis. Other rats were sacrificed one day, 7 days, and 2 weeks
      after a single intratracheal instillation of 15 mg cellulose and the IgG, IgA, and
      IgM levels were determined in blood and bronchoalveolar lavage (BAL). The
      IgA level was increased in BAL after 2 weeks (p<0.05). The other levels were not
      increased in serum and BAL at all time points. Secretory IgA is considered to be
      an important first line of defence against different agents and might be involved
      in the immunopathogenesis of fibrosing alveoli's (Tat96). The committee is aware
      of the severity of the bronchoalveolar effects but considers, at the same time, the
      route of administration as very burdensome.
           A single intratracheal instillation of 15 mg respirable germ-free hardwood
      dust (pine) or cellulose caused identical histological changes in the lungs of rats
      after one month: fibrosing alveobronchiolitis. The authors did not indicate
031-8 Health-based Reassessment of Administrative Occupational Exposure Limits
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<pre>      whether the severity of the effects was comparable; therefore, the two treatments
      cannot be compared. A fibre-free extract from wood dust did not cause any
      histological changes in the lung (Tat95).
          Intratracheal administration of 15 mg respirable paprika dust, free of fungi, or
      cellulose dust in rats caused alveobronchiolitis at the end of the first month and
      fibrotic changes at the end of the third month. The two treatments resulted in a
      comparable severity of the effects. A fibre-free extract from paprika dust resulted
      in no histological changes. The authors concluded that the effects caused by
      paprika dust can at least partly be ascribed to the cellulose present in the paprika
      (approximately 20%) (Tat92).
          The committee concludes that the lung effects arising after exposure to
      germ-free wood dust or paprika dust, in combination with the absence of effects
      after exposure to fibre-free extracts, indicate that mainly the fibrous nature of the
      compounds is the cause of the effects.
          Intratracheal instillation of cellulose dust into hamsters caused pulmonary
      toxicity. The MMAD of the particles was 4.8 µm. A quantity of 7.5 mg/kg bw
      (n=6) was instilled (approx. 3 mg/g lung), twice per week, for 6 weeks. Surviving
      animals (n=4) were killed 8 weeks after the last instillation. The animals had a
      decreased lung distensibility (n=4, p<0.05), normal surface-to-volume (S/V) ratio
      (n=6), and significant numbers of granulomata with patchy areas of thickened
      interalveolar septa (n=6, p<0.05). In the same study, groups of hamsters were
      exposed to cotton dust and endotoxins. Cellulose introduced the smallest
      change in lung distensibility, the largest number of granulomata and the smallest
      changes in surface density of the alveoli in the parenchyma (for all 3 compounds:
      p<0.05). The S/V ratio was decreased after exposure to cotton dust or endotoxins
      (p<0.05). The authors concluded that the accumulation of particles and toxicity
      may be due to an overload of the lung's capacity to remove insoluble foreign
      material as well as any intrinsic toxicity of cellulose. Such overload may occur
      from exposure to the level of respirable dust set by the ACGIH Nuisance Dust
      TLV (Mil90). The committee concludes that an overload of the lungs of hamsters
      with a respirable fraction of cellulose may have some effects on the alveoli.
      However, the effects are less severe than the effects of cotton dust or
      endotoxins. Further, the committee does not believe that exposure to levels at the
      TLV for nuisance dust (5 mg/m3 respirable particles) leads to an intratracheal
      concentration of 7.5 mg/kg bw. Moreover, exposure by intratracheal instillation is
      more toxic than exposure by inhalation.
      Oral administration
031-9 Cellulose
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<pre>       Anderson and co-workers reviewed the available data on long-term oral
       administration to laboratory animals, using purified cellulose. The chronic
       ingestion of purified cellulose over the entire lifespans in rats and mice does not
       result in any increase in spontaneous disease or neoplasia. Further, purified
       cellulose does not display promotional activity in the mammary gland, the colon,
       or the bladder of rats, and does not significantly alter the absorption or the
       metabolism of dietary compounds. At least two studies were considered valid by
       the authors in showing no adverse effects. However, the administered doses
       were not high: 3% and 5% of the diet. While these doses remove any
       confounding influence from caloric restriction, they are not the maximum doses
       desired to conclusively prove safety (And92).
           Six African green monkeys (Cercopithecus aethiops spp vervets) were fed a
       diet containing 9.7% cellulose fibres for 3.5 years. They were killed and their
       intestines investigated. They served as a control group for 4 monkeys receiving
       a diet containing 9.7% psyllium husk. In the cellulose-fed group, mild damage
       was observed at villous tips of the duodenum, and there was a higher degree of
       necrosis in the lamina propria (results from scanning electron microscopy). No
       other effects were found (Pau87).
           The feeding of rats with diets containing 0,5 or 10% CellulonTM for 13 weeks
       did not induce any toxic effects. The rats were compared with rats receiving diets
       with microcrystalline cellulose (positive control) and with rats receiving diets
       without cellulose (negative control). Also, the positive control group did not
       show any signs of toxicity compared with the negative control group (Sch91).
       Mutagenicity and genotoxicity
       CellulonTM fibre was negative or did not induce mutations in the:
           Ames assay, using S. typhimurium strains TA98, TA100, TA1535, TA1537
           and TA1538, with and without metabolic activation
           unscheduled DNA synthesis assay in rat hepatocytes
           chromosomal aberrations assay in Chinese hamster ovary (CHO) cells with
           and without metabolic activation
           HGPRT forward mutation assay (hypoxanthine-guanine phosphoribosyl
           transferase) in CHO cells with and without rat metabolic activation
           (all studies: Sch91).
       Reproduction toxicity
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<pre>       Anderson and co-workers reviewed the available data on reproduction toxicity of
       cellulose in laboratory animals. In 1972, the US Food and Drug Administration
       concluded that exogenous cellulose did not induce adverse reproductive effects,
       based on a 3-generation reproductive study in rats using purified cellulose at a
       30% level in the diet. Also in subsequent studies, no adverse effects were found
       in reproduction or neonate development in rats and mice (And92).
7      Existing guidelines
       The current administrative occupational exposure limit (MAC) for cellulose in the
       Netherlands is 2 mg/m3, as inhalable particles as an 8-hour TWA.
           Existing occupational exposure limits for cellulose in some European
       countries and in the USA are summarised in the annex.
8      Assessment of health hazard
       Cellulose is a rather inert material. In humans, bulk doses up to 30 g per day are
       used as a laxative (Mon82). In experimental animals, no effects have been found
       in rats and mice after lifetime dosing in the diet (And92). After 3.5 years of
       dosing via the diet, mild duodenal effects were observed in monkeys (Pau87). No
       reproduction toxicity was found after oral dosing in rats and mice (And92).
           CellulonTM, a cellulose obtained by bacterial fermentation, was not a skin and
       eye irritant in rabbits (Sch91).
           The only toxic effects induced by cellulose occurred after intratracheal
       instillation. The effects were localised in the lungs and not compound-specific,
       like an increase in protein particles, granolomas, bronchioalveolitis, or
       alveobronchiolitis. Probably, the fibrous nature of cellulose is the cause of the
       effects because fibre-free extracts from wood dust and paprika dust did not
       cause any histological changes in the lungs (Tat92, Tat95). However, the route
       of administration is not indicative for a possible target organ.
           In a study with inhalation exposure of guinea pigs, no lung effects were
       observed after 6 hours of exposure to 19 - 22 mg/m3 (Ell84). Higher
       concentrations were investigated in rats, where 575 x 106 fibers/m3, as respirable
       particles inhaled for 2 weeks, only produced transient increases in pulmonary cell
       proliferative parameters (War98) and where 1000x106 fibres/m3 (73 mg/m3),
       intermittently inhaled for 3 weeks, also induced pulmonary inflammation in rats
       (Cul00). These studies cannot be used for the hazard assessment because the
031-11 Cellulose
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<pre>       exposure periods were too short, only one concentration was tested, and
       NOAELs were not obtained.
            The committee considers the local irritant effect on lungs and trachea to be
       the critical effects.
       The committee considers the toxicological data base on cellulose too poor to
       justify recommendation of a health-based occupational exposure limit.
       The committee concludes that there is insufficient information to comment on the
       level of the present MAC-value.
       References
ACG99  American Conference of Governmental Industrial Hygienists (ACGIH). Cellulose. In: TLVs ®
       and other occupational exposure values - 1999. [CD-ROM]. Cincinnati OH, USA: ACGIH® ,
       Inc, 1999.
ACG00  American Conference of Governmental Industrial Hygienists (ACGIH). Guide to occupational
       exposure values - 2000. Cincinnati OH, USA: ACGIH® , Inc, 2000: 21.
ACG01  American Conference of Governmental Industrial Hygienists (ACGIH). 2001 TLVs ® and
       BEIs® . Threshold Limit Values for chemical substances and physical agents. Biological
       Exposure Indices. Cincinnati OH, USA: ACGIH® , Inc, 2001: 21.
Ada97  Adamis Z, Tatrai E, Honma K, et al. In vitro and in vivo assessment of the pulmonary
       toxicity of cellulose. J Appl Toxicol 1997; 17: 137-41.
And92  Anderson RL, Owens JW, Timms CW. The toxicity of purified cellulose in studies with
       laboratory animals. Cancer Lett 1992; 63: 83-92.
Arb00a Arbejdstilsynet. Grænseværdier for stoffer og materialer. Copenhagen, Denmark:
       Arbejdstilsynet, 2000; (At-vejledning C.0.1).
Arb00b Arbetarskyddstyrelsen. Hygieniska gränsvärden och åtgärder mot luftföroreningar. Solna,
       Sweden: National Board of Occupational Safety and Health, 2000; (Ordinance AFS 2000/3).
Bar75  Barker RH. Additives in fibers and fabrics. Environ Health Perspect 1975; 11: 41-5.
Bud96  Budavari S, O'Neill MJ, Smith A, et al , eds. The Merck index. An encyclopedia of chemicals,
       drugs, and biologicals. 12th ed. Whitehouse Station NJ, USA: Merck & Co, 1996: 326-7.
CEC00  Commission of the European Communities (CEC). Commission Directive 2000/39/EC of 8
       June 2000 establishing a first list of indicative occupational exposure limit values in
       implementation ofCouncil Directive 98/24/EC on the protection of the health and safety of
       workers from the risks related to chemical agents at work. Official Journal of the European
       Communities 2000; L142 (16/06/2000): 47-50.
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<pre>Cul00  Cullen RT, Searl A, Miller BG, et al. Pulmonary and intraperitoneal inflammation induced by
       cellulose fibres. J Appl Toxicol 2000; 20: 49-60.
DFG01  Deutsche Forschungsgemeinschaft (DFG): Commission for the Investigation of Health
       Hazards of Chemical Compounds in the Work Area. List of MAK and BAT values 2001.
       Maximum concentrations and biological tolerance values at the workplace. Weinheim, FRG:
       Wiley-VCH, 2001; (rep no 37).
Dom86  Domelsmith LN, Berni RJ. The chemical composition of standard cotton dust. Environ
       Health Perspect 1986; 66: 109-12.
Ell84  Ellakkani M, Alarie YC, Weyel DA, et al. Pulmonary reactions to inhaled cotton dust: an
       animal model for byssinosis. Toxicol Appl Pharmacol 1984; 74: 267-84.
Har94  Harris LR, Sarvadi DG. Synthetic polymers. In: Clayton GD, Clayton FE, eds. Toxicology.
       4th ed. New York, USA: John Wiley & Sons, Inc. 1994: 3673-4005; (Patty's Industrial
       hygiene and toxicology ; Vol II, Part E).
How92  Howard PH, Neil M, eds. Dictionary of chemical names and synonyms. Chelsea MD, USA:
       Lewis Publishers, 1992.
HSE01  Health and Safety Executive (HSE). EH40/2001. Occupational Exposure Limits 2001.
       Sudbury (Suffolk), England: HSE Books, 2001: 14.
Jäp87  Jäppinen P. A mortality study of Finnish pulp and paper workers. Br J Ind Med 1987; 44:
       580-7.
Jag85  Jagels R. Health hazards of natural and introduced chemical components of boatbuilding
       woods. Am J Ind Med 1985; 8: 241-51.
Lan90  Lanes SF, Cohen A, Rothman KJ, et al. Mortality of cellulose fiber production workers.
       Scand J Work Environ Health 1990; 16: 247-51.
McL87  McLaughlin JK, Malker HSR, Blot WJ, et al. Occupational risks for intracranial gliomas in
       Sweden. J Natl Cancer Inst 1987; 78: 253-8.
Mil90  Milton DK, Godleski JJ, Feldman HA, et al. Toxicity of intratracheally instilled cotton dust,
       cellulose and endotoxin. Am Rev Respir Dis 1990; 142: 184-92.
MoDo97 Mo och Domsjö AB. Bleaching - an important stage in the production of cellulose. Dutch.
       [Bleking - een belangrijke fase bij de produktie van cellulose.] Stockholm, Sweden, 1997.
Mon82  Montgomery RR. Polymers. In: Clayton GD, Clayton FE, ed. Toxicology. 3rd ed. New York,
       USA, John Wiley & Sons, Inc. 1982: 4209-526; (Patty's Industrial hygiene and toxicology ;
       Vol II, Part C).
Pau87  Paulini J, Mehta T, Hargis A. Intestinal structural changes in African green monkeys after
       long term psyllium or cellulose feeding. J Nutr 1987; 117: 253-66.
Sch91  Schmitt DF, Frankos VH, Westland J, et al. Toxicologic evaluation of CellulonTM fiber:
       genotoxicity, pyrogenicity, acute and subchronic toxicity. J Am Coll Toxicol 1991; 10:
       541-54.
031-13 Cellulose
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<pre>SZW01  Ministerie van Sociale Zaken en Werkgelegenheid (SZW). Nationale MAC-lijst 2001. The
       Hague, the Netherlands: Sdu, Servicecentrum Uitgevers, 2001: 20.
Tat92  Tatrai E, Ungvary G. The aetiology of experimental fibrosing alveobronchiolitis induced in
       rats by paprika dust. Br J Ind Med 1992; 49: 494-8.
Tat95  Tatrai E, Adamis Z, Bohm U, et al. Role of cellulose in wood dust-induced fibrosing
       alveo-bronchiolitis in rat. J Appl Toxicol 1995; 15: 45-8.
Tat96  Tatrai E, Brozik M, Adamis Z, et al. In vivo pulmonary toxicity of cellulose in rats. J Appl
       Toxicol 1996; 16: 129-35.
TRG00  TRGS 900. Grenzwerte in der Luft am Arbeitsplatz; Technische Regeln für Gefahrstoffe.
       BArbBl 2000; 2.
Van91  Vanhoorne M, Van den Berge L, Devreese A, et al. Survey of chemical exposures in a viscose
       rayon plant. Ann Occup Hyg 1991; 35: 619-31.
War98  Warheit, DB, Snajdr SI, Hartsky MA, et al. Two weeks inhalation study in rats with cellulose
       fibers. In: Chiyotani K, Hosoda Y, Aizawa Y, eds. Advances in the prevention of
       occupational respiratory diseases. Proceedings of the 9th International Conference on
       Occupational Respiratory Diseases, Kyoto, Japan, 13-16 October, 1997. Tokyo, Japan:
       Elsevier, 1998: 579-82.
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<pre>            Annex
Occupational exposure limits for cellulose in various countries.
country                              occupational                time-weighted type of           notea   lit refb
- organisation                       exposure limit              average       exposure limit
                                     ppm        mg/m 3
the Netherlands
- Ministry of Social Affairs and     -          2c               8h            administrative            SZW01
Employment
Germany
- AGS                                -          -                                                        TRG00
- DFG MAK-Kommission                 -          -                                                        DFG01
Great Britain
- HSE                                -          10 c             8h            OES                       HSE01
                                     -          20 c             15 min
                                     -          4d               8h            OES
Sweden                               -          -                                                        Arb00b
Denmark                              -          -                                                        Arb00a
USA
- ACGIH                              -          10               8h            TLV                       ACG01
- OSHA                               -          15 e             8h            PEL                       ACG00
                                     -          5d               8h            PEL
- NIOSH                              -          10 e             10 h          REL                       ACG00
                                                5d               10 h          REL
European Union
- SCOEL                              -          -                                                        CEC00
a
     S = skin notation, which means that skin absorption may contribute considerably to body burden; sens =
     substance can cause sensitisation
b
     Reference to the most recent official publication of occupational exposure limits
c
     (Total) inhalable dust
d
     Respirable fraction
e
     Total dust
031-15      Cellulose
</pre>

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