OCCUPATIONAL SETTING

Exposure to wood dust occurs in many industries, including logging and sawmill operations, furniture manufacturing, paper manufacturing, construction of residential and commercial buildings, and especially carpentry and cabinet making. Workers are exposed when wood is sawed, chipped, routed, or sanded.

Wood may also contain biological or chemical contaminants. Biological contaminants include molds and fungi, which often grow on the bark of wood. Exogenous chemicals include those used in treating the wood. Common wood preservatives are arsenic, chromium, copper, creosote, and pentachlorophenol. Wood also contains many endogenous chemicals that are responsible for its biological actions.

EXPOSURE (ROUTE)

Wood dust exposure occurs through inhalation. In general, the finer particles of wood dust are more biologically active due to their greater surface area and their ability to penetrate and adhere to the respiratory mucosa. Furniture manufacturing and cabinet making are operations that produce the finer particles. Contact with skin or mucous membranes may also have health consequences.

PATHOBIOLOGY

Wood dust is composed of wood particles generated by the processing or handling of wood. Hardwoods, such as maple, oak, and cherry, come from deciduous trees with broad leaves. Softwoods come from evergreen trees such as pine, spruce, and fir. The terms are somewhat misleading in that some of the hardwoods may be soft and some of the softwoods may be relatively hard.

Health effects of wood dust may be classified primarily as irritation, sensitization, and cancer. In the case of irritation, these effects can involve the skin, eyes, or respiratory tract. Allergic manifestations can involve skin or respiratory tract, and cancer associated with wood dust exposure involves the sinonasal tract.

Skin irritation caused by wood dust is often mechanical. Splinters or tiny particles of wood can get under the skin and cause irritation or infection. Soaps and chemicals can add to the irritation. Particles may lodge between the folds of skin, and sweat and rubbing can result in inflammation. Good personal hygiene practices and protection of exposed areas can obviate this type of problem.

Some woods, mostly foreign and exotic species, contain chemicals that are irritants. These can cause dermatitis, resulting in redness and blistering. Eyes may also become irritated. Teak, mansonia, and radiata pine have been reported to cause such reactions.

Allergic contact dermatitis can result from some species, again mostly from foreign woods such as teak and African mahogany. However, some of the North American woods, such as Douglas fir, western red cedar, poplar, airborne pine dust due to colophony,¹ and rosewood, may cause allergic contact dermatitis.² Specific chemicals used in glues and resin binders, such as urea or phenol–formaldehyde, potassium dichromate, ethylene glycol, and propylene glycol, can also be responsible for allergic contact dermatitis.

Wood dust is a particulate that causes irritation of the eyes and the upper and lower respiratory tracts. As with all particulates, the magnitude of the effect depends on the size of the particulate and the amount of exposure. Some woods with strong chemicals are more irritating, and most wood is more irritating than inert dust. For example, wood dust has been found to be almost four times as irritating as plastic dust in the same concentration.³

Clinical epidemiologic studies of woodworkers have found frequent symptoms and physical findings of nasal irritation. Symptoms often consist of continued colds, nosebleeds, sneezing, and sinus inflammation. Unfortunately, most of the studies lack adequate controls and dose–response information. In one study, the employees in a dusty furniture plant, including office workers, had decreases in 1-second forced expiratory volume (FEV1) and forced vital capacity (FVC) during the workshift.⁴ A large Vermont study that also measured pulmonary function found an inverse association between pulmonary flow (FEV1/FVC ratio) and indexes of wood dust exposure.⁵ Similarly, a study of sawmill workers in Canada exposed to pine and spruce showed lower average values for FEV1 and FEV1/FVC(%).⁶ A recent study in India showed that carpenters had lower peak expiratory flow rates compared with controls.⁷ Mucociliary clearance in the nose has also been measured in woodworkers. Andersen et al. found a higher percentage of individuals with mucostasis among workers exposed to higher wood dust levels.⁸ Mucociliary clearance is important in cleansing the nasal passages. Individuals with impaired mucous flow may be more susceptible to infection and other problems.

Western red cedar is well known for its potential to cause asthma. Workers in British Columbia, Canada, have been studied extensively.^9–20 Plicatic acid, an extract of western red cedar, was shown to be the cause of bronchial asthma.²⁰ Other domestic species capable of causing asthma include oak, ash, redwood, mahogany, eastern white cedar, and spruce.^21–24 A number of foreign exotic species are capable of causing allergic asthma. In a case report, Kespohl et al. determined that the allergens in spruce wood were peroxidases.²⁵

Microorganisms on wood bark can cause Type III allergic reactions, or extrinsic allergic alveolitis.^26–28 Maple bark disease, sequoiosis, and suberosis are caused by the inhalation of fungal spores associated with maple, redwood, and cork, respectively.

Wood dust may also cause other lung diseases. High levels of small dust particles that penetrate into the bronchial tubes or smaller airways may produce irritation and bronchitis. Whether they produce irreversible changes is not known. Most reports of serious or permanent lung disease associated with wood dust exposure, until recently, have been anecdotal. However, later studies showed lower pulmonary function in wood mill workers,²⁹ higher prevalence of respiratory impairment,³⁰ and significant cross-shift declines of pulmonary function in wood dust-exposed workers.³¹

An English otolaryngologist was the first to note an unusually high incidence of nasal cancer in the chair making and furniture industry of High Wycombe, Buckinghamshire.³² This finding was confirmed by Acheson et al.,^{33, 34} who found an incidence of nasal adenocarcinoma from 1956 to 1965 of 0.7 cases per 1000 per year, an incidence approximately 1000 times greater than that seen in the general population. Dust depositions were noted on the nasal mucosa of furniture workers at the anterior part of the nasal septum and at the anterior ends of the middle turbinates.³⁵ A biopsy of these areas revealed squamous metaplasia. Excesses of nasal adenocarcinoma have also been described in France, Australia, Finland, Italy, Holland, Denmark, and Belgium.^36–44 An early study in Canada showed no excess of nasal cancer in woodworkers; however, few furniture workers were involved in the study.⁴⁵ A 1967 Canadian study showed an odds ratio of 2.5 for occupations involving exposure to wood dust when compared to the general population.⁴⁶ A more recent study in five Nordic countries that followed 2.8 million incident cancer cases in 15 million people through 2005 observed a standardized incidence ratio (SIR) for nasal cancer of 1.84 (95% CI 1.66–2.04) in male and 1.88 (0.90–3.46) in female woodworkers. For nasal adenocarcinoma, the SIR in males was 5.50 (4.60–6.56).⁴⁷

In the United States, a case-control study published in 1977 showed an approximate fourfold increase of nasal cancer in furniture workers in North Carolina.⁴⁸ Also, a Connecticut study showed an odds ratio of 4.0 for nasal cancer among persons exposed to wood dust.⁴⁹ In a follow-up study, Brinton et al. found an overall relative risk of nasal cancer among furniture workers of 0.74 in men and 0.91 in women; however, the relative risk of the rarer adenocarcinoma in male furniture workers was 5.68.⁵⁰ These excesses of adenocarcinoma, a very rare disease, are far lower than those noted in the United Kingdom and other countries. A review of nasal cancer in furniture manufacturing and woodworking in North Carolina suggested that there was some excess of nasal cancer in the industry prior to World War II, but it found little or no evidence of continuing excess risk,⁵¹ while another review of US woodworkers confirmed this disparity between the United States and the United Kingdom.⁵² Another pooled reanalysis observed excesses of nasal cancer only among workers in British furniture manufacturers as compared with those in the United States.⁵³ Likewise, in the United Kingdom, Acheson postulated that the factor in furniture manufacturing that gave rise to the nasal adenocarcinomas was present only between 1920 and 1940, since cases did not occur among workers who entered the industry after World War II.⁵⁴

It is unlikely that exogenous chemicals were responsible for the excess nasal cancer, since they were not widely used prior to World War II. It may well be that differences in processing, including the use of tools that create more heat, or dust, or different particle sizes, account for the increased disease of the earlier years.⁵¹

It is less clear whether there is an association between wood dust exposure and lung cancer as studies have produced conflicting results.⁵⁵

Beach and teak (hardwoods) and pine and spruce (softwoods) dusts have been shown to effect expression of cytokines and chemokines in an in vitro murine macrophage cell line.⁵⁶ They were all shown to induce TNF-α and inhibit IL-1β expression. Similarly, they induced the expression of CCL2, CCL3, CCL4, and CXCL2/3 chemokines and inhibited CCL24 expression. In a human epithelial cell line, wood dusts from beech, oak, teak, birch, pine, spruce, and medium-density fiberboard (MDF) dusts all induced a cytokine response with increased expression of cellular IL-6 and IL-8 mRNA.⁵⁷ There was also evidence of genotoxicity with an increase in DNA strand breaks after incubation with beech, teak, pine, and MDF dusts. No difference in genotoxicity was seen between hardwoods and softwoods in this study. Genotoxicity of beech and other woods has also been demonstrated in other in vitro models.^58–60 In respiratory epithelial cells, dusts from birch, oak, and pine were cytotoxic and stimulated the production of reactive oxygen species, and also caspace-3, one of the components of the apoptotic cascade.⁶¹

In 1995, the International Agency for Research on Cancer (IARC) classified wood dust: “Group I, carcinogenic to humans”.⁶² A 2009 review reaffirmed the classification (IARC 2011).⁶³

DIAGNOSIS

A clinical diagnosis of allergy or asthma can be made based on a careful medical and occupational history along with a physical examination. A detailed respiratory and dermatologic history will reveal symptoms of allergic disorders. Respiratory symptoms may include rhinitis, conjunctivitis, sneezing spells, nasal congestion, cough, shortness of breath, and wheezing.

Documenting the occurrence of these symptoms as temporally associated with exposure to wood dust and the resolution of symptoms while away from work is critical to the diagnosis. Objective evidence of temporality may be obtained by doing a physical examination or peak flow measurements prior to exposure and again at the end of the workshift. The finding of objective evidence of bronchoconstriction, such as wheezes or a decrement in FEV1 and FVC, supports the diagnosis of occupational asthma. However, asthma due to allergenic wood dust may be delayed, occurring during evening or night after the work shift.

To evaluate suspected contact dermatitis, a patch test can be done with the sawdust of the wood itself or, in some cases, with an extract of woods such as teak. Patch testing can also be performed with exogenous chemicals if they are suspected of being the causative agent.

TREATMENT

Avoidance of exposure to wood dust should be the goal of treatment of allergy. Sensitized workers who have rhinitis should be counseled on their risk of developing asthma and the risk of eventual intolerance of exposure.

Symptomatic care may include antihistamines and/or nasal topical corticosteroids for upper tract symptoms. Treatment of wood dust asthma is the same as for other types of asthma, which, in addition to avoidance of exposure, includes short-term inhaled bronchodilators for acute attacks. For chronic wood dust asthma, standard treatments for asthma include inhaled corticosteroids alone or combined with long-acting bronchodilators. Oral medications include leukotriene modifiers, such as montelukast, and theophylline.

Skin disease can be treated with topical or, in severe cases, systemic corticosteroids. Work practices and controls should be modified to prevent further exposure.

MEDICAL SURVEILLANCE

Respiratory history may be used to document early symptoms of allergy. If nasal symptoms are detected early and further exposure is eliminated, subsequent progression to asthma may be prevented. Pre-placement, periodic, and possibly cross-shift pulmonary function testing may be useful, depending upon the type and quantity of wood dust, and any indicators of employee health problems related to their exposure.

PREVENTION

Containment of wood dust should be the cornerstone of allergy and irritation prevention measures. Efforts should be made to limit airborne dust through engineering controls such as ventilation systems. Personal protective equipment, including skin coverings and respirators, should be considered where significant exposure cannot be engineered out. The concentration of airborne dust is dependent on the activities in the contaminated areas.

Dust exposure evaluation should be made in accordance with good industrial hygiene practices, which will include personal inspection of the work site and use of a dust monitor for screening purposes. Personal sampling for both total and respirable dust should be done when the result indicates potential overexposure or if employee(s) complaints have been received. The American Conference of Governmental Industrial Hygienists (ACGIH) standard for western red cedar is 0.5 mg/m³ (which is labeled as a sensitizer).⁶⁴ For all other wood dusts, the occupational exposure level (OEL) is 1 mg/m³. The National Institute for Occupational Safety and Health (NIOSH) has set the recommended exposure limit for wood dust at 1 mg/m³.

Until January 19, 1989, the Occupational Safety and Health Administration (OSHA) regulated wood dust as a nuisance dust with a permissible exposure level (PEL) of 15 mg/m³. After that date, OSHA adopted the PEL standard, which at that time regulated wood dust at 5 mg/m³ for hardwood and softwood; for western red cedar, the PEL was 2.5 mg/m³. On July 7, 1992, the US Court of Appeals vacated the PEL standard. As a result, OSHA regulates wood dust as a nuisance dust for total dust at 15 mg/m³ and respirable dust at 5 mg/m³.⁶⁵ However, the use of lower exposure levels is prudent to reduce the risk of illness. The ACGIH recommendations are followed in many locations outside the United States.

Though this chapter has dealt with health issues pertaining to wood dust exposure, it should be noted that excess accumulation of wood dust in a workplace is a risk of fire and explosion. Therefore, work surfaces, machinery, floors, and rafters should be regularly cleaned of accumulations, and ambient air levels kept low. A Guide to Combustible Dust can be obtained from the North Carolina Department of Labor.⁶⁶

References

1. 1. Watsky KL. Airborne allergic contact dermatitis from pine dust. Am J Contact Dermat 1997; 8:118–20.
2. 2. Weber LE. Dermatitis veneata due to native woods. AMA Arch Dermatol Syphilol 1953; 67:388–94.
3. 3. Andersen I. Effects of airborne substances on nasal function in human volunteers. In: Carrow CS, ed. Toxicology of the nasal passages. Washington, DC: Hemisphere, 1986, 143–54.
4. 4. Zuhair YS, Whitaker CJ, Cinkotai EF. Ventilatory function in workers exposed to tea and wood dust. Br J Ind Med 1981; 38:339–45.
5. 5. Whitehead LW, Asbikaga T, Vacek P. Pulmonary function status of workers exposed to hardwood or pine dust. Ann Ind Hyg Assoc 1981; 42:1780–6.
6. 6. Hessel, PA, Herbert FA, Melenka, LS, et al. Lung health in sawmill workers exposed to pine and spruce. Chest 1995; 108(3), 642–6.
7. 7. Mohan M, Aprajita, Panwar NK. Effect of wood dust on respiratory health status of carpenters. J Clin Diagn Res 2013; 7(8): 1589–91.
8. 8. Andersen HC, Solgaard J, Andersen I. Nasal cancer and nasal mucus transport rates in woodworkers. Acta Otolayngol 1976; 82:263–5.
9. 9. Brooks SM, Edwards JJ, Edwards FE. An epidemiologic study of workers exposed to western red cedar and other wood dusts. Chest 1981; 80(suppl 1):30–2.
10. 10. Chan-Yeung M. Maximal expiratory flow and airway resistance during induced bronchoconstriction in patients with asthma due to western red cedar (Thuja plicata). Am Rev Respir Dis 1973; 108:1103–10.
11. 11. Chan-Yeung M. Fate of occupational asthma. A follow-up study of patients with occupational asthma due to western red cedar (Thuja plicata). Am Rev Respir Dis 1977; 116:1023–9.
12. 12. Chan-Yeung M. Immunologic and nonimmunologic mechanisms in asthma due to western red cedar (Thuja plicata). J Allergy Clin Immunol 1982; 70:32–7.
13. 13. Chan-Yeung M, Abboud R. Occupational asthma due to California redwood (Sequoia sempervirens) dusts. Am Rev Respir Dis 1976; 114:1027–31.
14. 14. Chan-Yeung J, Ashley MJ, Corey P, et al. A respiratory survey of cedar mill workers. I. Prevalence of symptoms and pulmonary function abnormalities. J Occup Med 1978; 20:323–7.
15. 15. Chan-Yeung M, Barton GM, MacLean L, et al. Bronchial reactions to western red cedar (Thuja plicata). Can Med Assoc J 1961; 105:56–8.
16. 16. Chan-Yeung M, Barton GM, MacLean L, et al. Occupational asthma and rhinitis due to western red cedar (Thuja plicata). Am Rev Respir Dis 1973; 108:1094–102.
17. 17. Chan-Yeung M, Lam S, Koener S. Clinical features and natural history of occupational asthma due to western red cedar (Thuja plicata). Am J Med 1982; 72:411–5.
18. 18. Chan-Yeung M, Veda S, Kus J, et al. Symptoms, pulmonary function, and bronchial hyperreactivity in western red cedar workers compared with those in office workers. Am Rev Respir Dis 1984; 130:1038–41.
19. 19. Vedal S, Chan-Yeung M, Enarson D, et al. Symptoms and pulmonary function in western red cedar workers related to duration of employment and dust exposure. Arch Environ Health 1986; 41:179–83.
20. 20. Chan-Yeung M, Gicias PC, Henson PM. Activation of complement by plicatic acid, the chemical responsible for asthma due to western red cedar (Thuja plicata). J Allergy Clin Immunol 1980; 65:333–7.
21. 21. Malo JL, Cartier A, Desjardins A, et al. Occupational asthma caused by oak wood dust. Chest 1995; 108:856–8.
22. 22. Fernandez-Rivas M, Perez-Carral C, Senent CJ. Occupational asthma and rhinitis caused by ash (Fraxinus excelsior) wood dust. Allergy 1997; 52:196–9.
23. 23. Malo JL, Cartier A, L’Archeveque J, et al. Prevalence of occupational asthma among workers exposed to eastern white cedar. Am J Respir Crit Care Med 1994; 150:1697–701.
24. 24. Wittczak T, Dudek W, Walusiak-Skorupa J, et al. Occupational asthma due to spruce wood. Occup Med 2012; 62:301–4.
25. 25. Kespohl, S., Kotschy-Lang, N., Tomm, J. M., et al. Occupational IgE-mediated softwood allergy: characterization of the causative allergen. Int Arch Allergy Immunol 2012; 157:202–8.
26. 26. Rask-Andersen A, Land CJ, Enlund K, et al. Inhalation fever and respiratory symptoms in the trimming department of Swedish sawmills. Am J Ind Med 1994; 25:65–7.
27. 27. Dahlqvist M, Johard U, Alexandersson R, et al. Lung function and precipitating antibodies in low exposed wood trimmers in Sweden. Am J Ind Med 1992; 21:549–9.
28. 28. Dahlqvist M, Ulfvarson U. Acute effects on forced expiratory volume in one second and longitudinal change in pulmonary function among wood trimmers. Am J Ind Med 1994; 25:551–8.
29. 29. Rastogi SK, Gupta BN, Husain T, et al. Respiratory health effects from occupational exposure to wood dust in sawmills. Am Ind Hyg Assoc J 1989; 50:574–8.
30. 30. Liou SH, Cheng SY, Lai FM, et al. Respiratory symptoms and pulmonary function in mill workers exposed to wood dust. Am J Ind Med 1996; 30:293–9.
31. 31. Mandryk J, Alwis KU, Hocking AD. Work related symptoms and dose–response relationships for personal exposures and pulmonary function among woodworkers. Am J Ind Med 1999; 35:481–90.
32. 32. Macbeth R. Malignant disease of the paranasal sinuses. J Laryngol Otol 1965; 79:592–612.
33. 33. Acheson ED, Hadfleld EH, Macbeth RG. Carcinoma of the nasal cavity and accessory sinuses in wood workers. Lancet 1967; 1:311–2.
34. 34. Acheson ED, Cowdell RH, Hadfield F, et al. Nasal cancer in woodworkers in the furniture industry. Br Med J 1968; 2:587–96.
35. 35. Hadfield EH. A study of adenocarcinoma of the paranasal sinuses in woodworkers in the furniture industry. Ann R Coll Surg Engl 1970; 46:301–19.
36. 36. Cignoux M, Bernard P. Malignant ethmoid bone tumors in woodworkers. J Med Lyon 1969; 25:92–3.
37. 37. Ironside P, Matthews J. Adenocarcinoma of the nose and paranasal sinuses in woodworkers in the state of Victoria, Australia. Cancer 1975; 36:1115–21.
38. 38. Klintenberg C, Olofsson J, Hellquist H, et al. Adenocarcinoma of the ethmoid sinuses: a review of 28 cases with special reference to wood dust exposure. Cancer 1984; 54:482–8.
39. 39. Cecchi F, Buiatti E, Kriebel D, et al. Adenocarcinoma of the nose and paranasal sinuses in shoemakers and woodworkers in the province of Florence, Italy (1963–77). Br J Ind Med 1980; 37:222–5.
40. 40. Battista G, Cavallucci F, Comba P, et al. A case-referent study on nasal cancer and exposure to wood dust in the province of Sienna Italy. Scand J Work Environ Health 1983; 9(1):25–9.
41. 41. Debois JM. Tumors of the nasal cavity in woodworkers. Tjidschr Diergeneeskd 1969; 25:92–3.
42. 42. Mosbech J, Acheson ED. Nasal cancer in furniture makers in Denmark. Dan Med Bull 1970; 18:34–5.
43. 43. Van den Oever R. Occupational exposure to dust and sinonasal cancer. An analysis of 386 cases reported to the NCCSF Cancer Registry. Acta Otorhinolaryngol Belg 1996; 50:19–24.
44. 44. Demers PA, Kogevinas M, Boffetta P, et al. Wood dust and sinonasal cancer: pooled reanalysis of twelve case–control studies. Am J Ind Med 1995; 28:151–66.
45. 45. Ball MJ. Nasal cancer and occupation. Lancet 1967; 2:1089–90.
46. 46. Elwood JM. Wood exposure and smoking: association with cancer of the nasal cavity and paranasal sinuses in British Columbia. Can Med Assoc J 1981; 124:1573–7.
47. 47. Pukkala E, Martinsen, JI, Lynge E, et al. Occupation and cancer – follow-up of 15 million people in five Nordic countries. Acta Oncol, 2009; 48: 646–790.
48. 48. Brinton LA, Blot WJ, Stone BJ. A death certificate analysis of nasal cancer among furniture workers in North Carolina. Cancer Res 1977; 37:3473–4.
49. 49. Roush GC, Meigs JW, Kelly J. Sinonasal cancer and occupation: a case control study. Am J Epidemiol 1980; 111:183–93.
50. 50. Brinton LA, Blot WJ, Becker JA. A case–control study of cancers of the nasal cavity and paranasal sinuses. Am J Epidemiol 1984; 119:896–906.
51. 51. Imbus HR, Dyson WE. A review of nasal cancer in furniture manufacturing and woodworking in North Carolina, the United States, and other countries. J Occup Med 1987; 29:734–40.
52. 52. Blot WJ, Chow WH, McLaughlin JK. Wood dust and nasal cancer risk. A review of the evidence from North America. J Occup Environ Med 1997; 39:148–56.
53. 53. Demers PA, Boffetta P, Kogevinas M, et al. Pooled reanalysis of cancer mortality among five cohorts of workers in wood-related industries. Scand J Work Environ Health 1995; 21:179–90.
54. 54. Acheson ED. Nasal cancer in the furniture and boot and shoe manufacturing industries. Prez´ı Med 1976; 5:295–315.
55. 55. Vallieres E, Pintos J, Parent M-E, Siematycki J. Occupational exposure to wood dust and risk of lung cancer in two population-based case–control studies in Montreal, Canada. Environ Health 2015; 14:1.
56. 56. Määttä J, Luukkonen R, Husgafvel-Pursiainen K, et al. Comparison of hardwood and softwood dust-induced expression of cytokines and chemokines in mouse macrophage RAW 264.7 cells. Toxicology 2006; 218:13–21.
57. 57. Bornholdt J, Saber AT, Sharma AK, et al. Inflammatory response and genotoxicity of seven wood dusts in the human epithelial cell line A549. Mutat Res/Genet Toxicol Environ Mutagen 2007; 632:78–88.
58. 58. Nelson E, Zhou Z, Carmichael PL, et al. Genotoxic effects of subacute treatments with wood dust extracts on the nasal epithelium of rats: assessment by the micronucleus and 32P-postlabelling. Arch Toxicol 1993; 67:586–9.
59. 59. Mohtashamipur E, Norpoth K, Ernst H, et al. The mouse-skin carcinogenicity of a mutagenic fraction from beech wood dusts. Carcinogenisis 1989; 10:483–7.
60. 60. Mohtashamipur E, Norpoth K, Hallerberg B. A fraction of beech wood mutagenic in the Salmonella/mammalian microsome assay. Int Arch Occup Environ Health 1986; 58:227–34.
61. 61. Pylkkänen L, Stockmann-Juvala H, Alenius H, et al. Wood dusts induce the production of reactive oxygen species and caspase-3 activity in human bronchial epithelial cells. Toxicology 2009; 262:265–70.
62. 62. IARC Working Group. Wood dust and formaldehyde. In: IARC Monographs on the evaluation of carcinogenic risks to humans, Vol. 62. Lyon: World Health Organization, 1995.
63. 63. IARC. Monograph Volume 100: A review of human carcinogens—Part C: metals, arsenic, dusts, and fibres. Lyon: World Health Organization, 2012. Available at: http://monographs.iarc.fr/ENG/Monographs/vol100C/mono100C.pdf (accessed on June 21, 2016).
64. 64. American Conference of Governmental Industrial Hygienists. 2014 TLVs and BEIs. Cincinnati, OH, 2014.
65. 65. Compliance and Enforcement Activities Affected by the PELs Decision. Available at: https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=INTERPRETATIONS&p_id=21220 (accessed on June 21, 2016).
66. 66. Occupational Safety and Health Division, 2012. A Guide to Combustible Dust, NC Department of Labor, Raleigh, NC.