I '1 

HEALTH EFFECTS OF EXPOSURE TO WOOD DUST 

A SUMMARY OF THE LITERATURE 

NIOSH LIBRARY SYSTEM 

MORGANTOWN LIBRARY 

10S·; h:LLOWDALE ROAD 

MORGANTOWN, WV 26505 

U.S. Department of Health and Human Services 

Public Health Service 

Centers for Disease Control 

NTIS 

National Institute for Occupational Safety and Health 

Division of Standards Oevelopment and Technology Transfer 

June 1987 

Iloo.at 

/ 

I 
DISCLAIMER 

Mention of the name of any company or product does not constitute 

endorsement by the National Institute for Occupational Safety and Health. 

i i 
FOREWORD 

This document identifies and summarizes the literature that describes the 

potential health effects resulting from exposure to wood dust. It was 

developed by the National Institute for Occupational Safety and Health 

(NIOSH) at the request of the U.S . Department of Labor, Occupational 

Safety and Heal th Administrat ion (OSHA). This document provides a 

comprehensive synopsis of the literature related to wood dust. The 

conclusions described herein are those of the cited authors. The report 

itself does not contain NIOSH recommendations for regulating occupational 

exposure to wood dust, nor is it a itical evaluation 0 the literature . 

Such recommendations and evaluati n ere preclud y e volume of 

publ ished data and the relat i vely sh r dl ine 0 devel pment of the 

document. 

\ 

",Id " II" ..... o . . a, istant Surgeon General 

ector , National Institute for 

ccupational Safety and Health 

Centers for Disease Control 

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ABSTRACT 

This report identifies and summarizes the literature on the potential health 

effects of exposure to wood dust. This comprehensive literature review 

def i nes wood. discusses occupat i ona I exposure standards and reconmendat ions 

for wood dust. describes reports of animal and in vitro testing. and 

examines human health effects including dermatitis. allergic respiratory 

effects. IllUcosal and nonallergic respi ratory effects. and carcinogenici ty. 

Also included is a campi lation of wood dust concentration ranges reported 

for var i ous woodwork i ng ope rat ions and a br i ef discuss i on of wood dust 

control technology. The report does not contain NIOSH recommendations for 

regulating occupational exposure to wood dust. 

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CONTENTS 

Foreword .... Abst ract . . . . Tables ..... Acknowledgments 

I. In t roduc t ion . . . . . II. Animal and In Vitro Studies 

" I. Dermat i tis . . ...... . IV. Allergic Respi ratory Effects ... V. Mucosal and Nonallerg ic Respiratory Effects 

VI. Carcinogenici ty ............. . VI I. Industrial Hygiene Measurements and Controls 

Re fe rences . . . . . . . . . . . . . . . . . . . . . 

v 

iii 

iv 

vi 

vi i 

1 

9 

17 

27 

41 

49 

89 

129 
TABLES 

Number 

1 Wood dust exposure standards and recommendations 

2 Woods causing dermatitis 

3 Selected case reports of wood dermatitis 

4 Selected case reports of allergic respiratory effects 

caused by wood dus t . . . . . . . . . . . . . . 

5 Comparison of Type I and Type II I allergic responses 

6 Wood dust concentrations measured in the workplace 

in various studies ............... . 

Page 

. 3 

18 

22 

28 

34 

91 

7 Summary of total dust concentrations in sanding operations 120 

8 Summary of total dust concentrations in sawing operations 121 

9 Summary of total dust concentrations in woodworking 

operations (excluding sanding/sawing) .. . . 122 

10 Summary of general area samples for total dust collected 

in woodworking operations ... . . . . .. ..... 124 

11 Summary of respirable dust concentrations in woodworking 

operat ions . . . . . . . . . . . . . . . . . . . . . . . 125 

12 Summary of particle size data in woodworking operations 126 

13 Recommended exhaust volumes for woodworking machinery 128 

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ACKNOWLEDGMENTS 

This document was developed by the Division of Standards Development and 

Technology Transfer, National Institute for Occupational Safety and Health. 

Rodger L. Tatken was responsible for preparing the document. Contributions 

of the following Division staff are gratefully acknowledged: Howard R. Ludwig, for compilation of the industrial hygiene sampling data in 

Section VII; and Bryan D. Hardin, Ph.D., G. Kent Hatfield, Ph.D., 

Theodore J. Meinhardt, Ph.D., Richard W. Niemeier, Ph.D., John J. Whalen, 

lawrence F. Mazzuckell i, David H. Groth, M.D., and Sheldon H. Rabinovitz, 

Ph.D. (currently with the U.S. Environmental Protection Agency), for their 

critical reviews and cOllll1ents. NIOSH review of this document was provided by Stephen G. Bayer, Raymond E. Biagini, Ph.D., JeAnne R. Burg, Ph.D., 

John F. Gamble, Ph.D . , Charles McCammon, Ph.D . , Michael A. McCawley , Ph .D., 

and William J. Moorman. Carolyn A. Browning performed editorial review. 

vi i 
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I . I NTROOUCTI ON 

Th i s document i dent if i es and summar i zes the literature that descr i bes the 

potential health effects resulting from exposure to wood dust . For purposes 

of this document, wood dust is defined in its broadest sense--that is , any 

wood particles arising from the processing or hand I ing of wood. Because 

this definition is so broad, every effort has been made to describe as 

thoroughly as possible the ci rcumstances of the wood dust exposures (e.g., 

type of wood, dust concentration, and concomitant exposures) as reported by 

the authors . It shou Id be noted, however. that for much. of the literature. 

this type of information is not avai lable. 

The document contains seven sections. This introductory section briefly 

defines wood and discusses occupational exposure standards and 

recommendations for wood dust. Section II summarizes reports of animal and 

in vitro testing . Sections III - VI examine human health data and are 

arranged by effects. including : dermatitis, allergic respiratory effects, 

mucosal and nonallergic respiratory effects, and carcinogenicity . Section 

V.l1 contains a compi lation of wood dust concentration ranges reported for 

various woodworking operations and a brief discussion of wood dust control 

technology. 

Wood is a complex biological and chemical material that consists primari Iy 

of cellulose, hemicellulose, and I ignin. Cellulose is a I inear glucose 

chain that serves as wood's skeleton. Hemicellulose is a small 

po Iysacchar i de that may ass i st in ce II growth and matu ra t ion. ' L i gn i n is a 

high molecular weight polymer of phenoxy I-propane units that functions in 

holding wood cells together. Wood may contain a variety of complex organic 

compounds. including glycosides, quinones. tannins, stilbenes. terpenes, 

aldehydes, and coumarins. It is beyond the scope of this paper to provide a 

detai led discussion of the chemistry of wood. The reader is referred to any 

of numerous texts on the subject (e.g .• Esau 1965,1977; Browning 1975; 

Kollmann and Cote 1968; Sjostrom 1981; Haygreen and Bowyer 1982); reviews 

are provided in Woods and Calnan (1976), IARC (1981), and HoII iday et al. 

(1986) . 

Woods have been divided into two different classes. hardwoods and softwoods. 

each with its own cellular structure and chemical composition. For example, 

hardwoods have a lower lignin content than softwoods (Holliday et al. 

1986). Hardwoods (angiosperms) are the deciduous broad-leaved flowering 

spec i es. Softwoods (gymnosperms) are the con i ferous spec i es that do not 

normally shed their leaves in winter. 

According to Woods and Calnan (1976), the first occupational reference to 

adverse hea I th effects f rom wood was made in 1700 by Bernard i no Ramazz i n i , 

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who reported nose and eye irritation in pitsawyers and headaches in wood 

turners. In 1902, upper respiratory tract i nflanwnation was described in men 

working with sequoia wood, and throat and eye irritation was reported in 

workers who used a boxwood substitute (Woods and Calnan 1976). Three years 

later, Legge (1905) reported that "African boxwood" caused such severe 

symptoms among Lancashi re shutt lemakers that the men refused to work wi th 

it. Following these initial case reports, a substantial body of literature 

on the health effects of exposure to wood and wood dust has accumulated. 

Two comprehensive reviews of wood toxicity include Woods and Calnan (1976) 

and Hausen (1981); briefer treatments are provided in Hanslian and Kadlec 

(1966), Kadlec and Hans I ian (1983), and Jagels (1985) . 

Until recently, occupational exposure to wood dust was regulated in the U.S. 

under OSHA's inert or nuisance mineral dust standard (29 CFR- 1910.1000 

Table Z-3) at an 8-hr time-weighted average (TWA) concentration of 5 mg/m3 

air for reapirable dust and 15 mg/m3 for total duat. However, several 

OSHA citations for exceeding nuisance dust levels for grain duat exposures 

were appealed to the Occupational Safety and Health Review Commission 

(OSHRC). These cases, Bunge Corporation (OSHRC Docket Nos . 77-1622, 78-838, 

and 78-2213) and Krause Mi II ing Company (OSHRC Docket No. 78-2307), 

challenged the appl icabi Ii ty of the nuisance dust standard to soybean dust 

and corn dust, respectively. In both cases, the Review Commission held that 

the nuisance dust standard did not apply to organic dusts. In a third case 

that involved wood dust exposure (Bemis Manufacturing Company, OSHRC Docket 

No. 80-3443), the Administrative Law Judge ruled that wood dust was not an 

inert mineral dust and therefore not subject to the nuisance dust standard. 

Although this rul ing was not precedent setting, OSHA elected not to appeal 

it to the OSHRC. No other related cases have since been brought before the 

Review ConInission, and OSHA has not amended Table Z-3 (29 CFR 1910.1000) . 

Therefore, the current law, as stated by the Review Commission'S decisions, 

is that the nuisance dust standard applies to mineral dusts only and not to 

organic dusts . 

Several other countries currently regulate occupational exposure to wood 

dus t . Some coun t r i es name spec i f i c wood spec i es (e. g., "p i ne, oak, fir, and 

beech" in the German Democratic Republ ic) or a particular class of wood dust 

(e.g., "hardwood" and "softwood" in Canada and Norway; "nonallergenic" in 

the Un i ted Kingdom and the Nether lands) . Other count r i es, such as Hungary 

and Poland, regulate "dust of vegetable and animal origin," with varying 

percentages of free si I ica. Sti II others, such as Switzerland, regulate 

simply "dust." A list of wood dust exposure standards and recommendations 

is included in Table 1. 

In 1980, the American Conference of Governmental Industrial Hygienists 

(ACGIH) revised its recommended wood dust threshold I imit value (TLV®) TWA 

from 5 mg/m3 air for nonallergenic dust (ACGIH 1971) to 1 mg/m3 for 

hardwood and 5 mg/m3 for softwood (nonallergenic) dusts, with a short-term 

(15-min) exposure limit (STEL) of 10 mg/rn3 for softwood only (ACGIH 

1980). The revised recommendation does not differentiate between respirable 

·Code of Federal Regulations. See CFR in references. 

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Table 1.--Wood dust exposure standards and recommendations· 

Limi tOO (mg/m3) 

Count ry TWA STEL Corrunents 

Austral ia 

New South Wales 1 Hardwood 

5 Softwood 

Queensland 1 Hardwood 

5 Softwood 

Tasmania 1 Hardwood 

5 Softwood 

Canada 

Federal 1 Hardwood 

5 20 Softwood 

Alberta 5 10 Nonallergenic wood dust 

2.5 5 Allergenic wood dust 

British Columbia 5 10 Nonallergenic wood dust 

2.5 5 Allergenic wood dust 

1 Hardwood (guideline) 

5 10 Softwood (guideline) 

Man i toba 1 Hardwood (gu ide line) 

5 10 Softwood (gu ide line) 

New Brunswick 1 Hardwood 

5 10 Softwood 

Newfoundland 1 Hardwood 

5 10 Softwood 

Nova Scot ia 1 Hardwood 

5 10 Softwood 

Pr i nce Edward 1 Hardwood (guidel ine) 

Island 5 10 Softwood (guidel ine) 

Quebec 5 10 Nonal lergenic wood dust 

(Cont i nued) 

See footnotes at end of table. 

3 
Table 1 (Continued).--Wood dust e~posure standards and recommendations· 

Count ry 

Canada (continued) 

Saskatchewan 

Northwest 

Territories 

Yukon Terr i tory 

Denmark 

Federal Republic of 

Germany (West Germany) 

Finland 

German Democratic 

Republ ic 

(East Germany) 

Hungary 

India 

Italy 

The Nether lands 

Limi tOO (mg/m3) 

TWA STEL 

5 

1 

1 

5 

1 

5 

5 

5 

10 

10 

3 

10 

10 

1 ,000 pa r tic I es 

per cc 

15 

5 

5 

.See footnotes at end of table. 

4 

Comments 

Nonallergenic wood dust 

Hardwood 

Hardwood 

Softwood 

Hardwood (guideline) 

Softwood (guideline) 

Fine dust 

No numeric exposure limits; 

beech and oak dust are listed 

as having been "shown 

epidemiologically to be 

unequivocally carcinogenic;" all other wood dust is 

"justifiably suspected of having carcinogenic potential" (DFG 1985) 

Wood dust 

Domestic wood dust only (pine, oak, fir, beech) 

Other dusts including vegetable and animal origin 

Total dust 

Proposed standard 

Nonallergenic wood dust 

(Continued) 
, 

Table 1 (Continued).--Wood dust exposure standards and recommendations* 

Count ry 

New Zealand 

Norway 

Poland 

Sweden 

Swi tzer I and 

Un i ted Kingdom 

Un i ted States 

USSR 

Limi t** 

TWA 

1 

5 

1 

5 

2 

4 

4 

2 

20 

8 

5 

5 

1 

2 

4 

See footnotes at end of table. 

(mg/m3) 

STEL 

10 

10 

10 

5 

Comments 

Hardwood (guideline) 

Softwood (guideline) 

Hardwood (exotic) 

Softwood (Nordic) 

Natural, vegetable, and animal 

dust containing more than 10% 

free Si02 

Natural, vegetable, and animal 

dust containing less than 10% 

free Si02 

Dust from wood containing no 

impregnating substances 

Dust from wood impregnated with 

silbstances whose content cannot 

be determined 

Wood dust classified as 

carcinogenic (NSBOSH 1984) 

Total dust 

Fine dust 

Nonal lergenic wood dust 

Softwood, nonallergenic (recommendation, ACGIH 1980) 

Hardwood (recommendation, 

ACGIH 1980) 

Dust of vegetable or animal 

origin; greater than 10% free 

s i I ica 

Dust of vegetable or animal 

origin; less than 10% free silica 

(Cant i nued) 
• 

Table 1 (Continued).--Wood dust exposure standards and recommendations· 

Limi t** (mg/m3) 

Country TWA STEL 

Yugoslavia 10 

3 

COlTlllents 

Total dust of vegetable or animal 

origin, without Si02 

Respirable dust of vegetable or 

animal origin, without Si02 

·This table is adapted from IARC (1981), ILO (1980), Holliday et al. (1986), 

ACGIH (1980), DFG (1985), and NSBOSH (1984). Note that the first two 

references I ist the foreign standards shown under "Limit" as "threshold 

limit values ." It is assumed that this term is used to actually mean 

"time-weighted average," since "threshold limit value" (TLV®) is a 

registered ACGIH name that refers speci fically to an ACGIH exposure 

recommendation. A TLV® may be given as either a time-weighted average (TWA) 

or short-term exposure limit (STEL) . 

**Except as noted under Comments, all values are for standards. 

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and total dust. It is based primari lyon mucostasis and its role in the 

development of adenocarcinoma in furni ture workers because of prolonged 

retention of wood dust in the nasal cavity. 

Based on thei r own research, several authors have reconmended the adoption 

of other wood dust exposure I imi ts. Hans I ian and Kadlec (1964) proposed 

maximum allowable concentrations of 1 mg respi rable dustlm3 ai r for toxic 

and strongly allergenic woods (e.g., boxwood, cocobolo, mansonia, yew); 

5 mg/m3 for biologically active woods (e.g., pine, larch, ebony, mahogany, 

teak, cedar); and 10 mg/m3 for biologically indifferent woods or those 

with littl.e biological activity (e.g., oak, beech, maple" ash, lime, 

birch). Ruppe (1973) recomnended a concentration of 5 mg/m" for "exotic 

woods" (undefined by author) to avoid allergic respi ratory reactions. 

Brooks et al. (1981) suggested that for Western red cedar dust, a TWA below 

3 .5 mg/m3 total dust would protect workers from occupational asthma. 

Whi tehead '(1982) proposed a total wood dust concentrat ion of 2 mg/m3 for 

both hardwood and softwood dusts for effects other than extreme allergic 

hypersensitivity . He connented that in the absence of a 

concentration-response relationship for wood dust and nasal cancer, this 

lim it shou I d reduce the occu r rence 0 f mucos tas i s to backg round I eve I sand 

minimize wood dust contact with nasal sinus tissue. However, he also 

indicated that this liRlit did not include a margin of safety. Imbus and 

Dyson (1985) recomnended a TlV (assumed to mean TWA) of 5 mg/m3 for both 

hardwoods and softwoods to prevent nonallergic, nonneoplastic respi ratory 

disease, and a TlV of 2.5 mg/m3 total dust for "potentially allergic woods 

where epidemiologic studies show signi ficant incidence and prevalence of 

allergic effects such as Western red cedar and mansonia, but not to woods 

where only incidental case reports are available, such as oak and 

mahogany." Stuart et al. (1986) proposed a particle-size-selective 

threshold I imit value for wood dust, although thei r reconnendation did not 

specify quantitative dust concentrations. 

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II. ANIMAL AND IN VITRO STUDIES 

A. Animal Studies 

The literature contains relatively few reports of laboratory animal studies 

on the toxicity of wood dust per se. The earliest such study appears to be 

that of Bergman et al. (1943), who exposed rabbits for 8 hr/day, 

5 1/2 days/week for up to 30 months to red cedar and pine dusts at 

concentrations of 6 to 10 million particles per cubic foot of air. 

Sixty-five percent of the particles exceeded 25 um, and only a few (percent 

unspecified) were below 10 um. Pathological examination revealed lung 

effects rang i ng f rom I arge abscesses to bronchopneumon i a and bronch it is. 

The nasal passages and upper respi ratory tracts of all animals contained 

wood dust. 

Much of the subsequent animal research has dealt with the toxicity, in 

particular the carcinogenicity, of various chemical substances found in 

plants and woods. Morton (1968) publ ished the fi rst of a series of papers 

on the tox i c propert i es of p I ants used in fol k med i cine on the island of 

Curacao. Because esophagea I cancer had been cORlllon on Curacao (E i bergen 

1961), Morton undertook research with O'Gara et al. (1971) at the National 

Cancer Institute (NCI) on the carcinogenicity of decoctions (extracts 

prepared by boi I ing) of selected parts of plants from Curacao in mice and 

rats, using the screening method devised by D'Gara (1968). After the death 

of D'Gara in January 1971, the screening program was continued in 

cooperation with a group of investigators at Howard University and NCI 

(Kapadia et al. 1976,1978; O'Gara et al. 1974; Pradhan et al . 1974; Dunham 

et al. 1974). Leaves or leafy twigs, roots or root bark, and fruits were 

the most commonly examined parts of plants; no samples of wood were 

extracted for screening . When plants were known to contain carcinogens 

other than tannic acid (IARC 1976), such as senecio alkaloids (Harris and 

Chen 197D) and safrole (Long et al. 1963), appropriate steps to free the 

extracts of these materials were taken. The general tenor of the 

information developed by this research was that the carcinogenicities of the 

extracts were functions of their concentrations of tannin; however, tannins 

did not account for all the carcinogenic activity found. 

Gibbard and Schoental (1969) identified several aldehydes, including sinapyl 

and syringic aldehydes, in Chinese incense and in eight types of wood 

(eucalyptus, teak, beech , sandlewood, oak, coconut palm, larCh, and 

juniper). Schoental et al. (1971) and Schoental and Gibbard (1972) 

administered a sinapylaldehyde derivative, 3,4,5-trimethoxycinnamaldehyde, 

intraperi toneally and subcutaneously to small groups of rats and noted the 

development of fatty kidney tumors and nasopharyngeal cancer. Although 

these experiments were too limited in nature to permit firm conclusions, it 

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was suggested that epoxidation of the aldehyde might be responsible for the 

tumorigenic activity seen. 

The carcinogenici ty of other chemical compounds found in wood has also been 

studied. A detai led descr ipt i on of these studies is beyond the scope of 

this paper, and the reader is referred to reviews by Tinkler (1986), Sigman 

et al. (1984), Niemeier (1979), and Gamble (1979) for additional information. 

The potential of wood shavings used as animal bedding material to cause 

tumors was examined in a series of studies reported in the 1970's. Interest 

was initially raised by Heston and Vlahakis (1968), who had reported on the 

high incidence of mammary gland and liver tumors in C3H-derived mice strains 

in their National Institutes of Health (NIH) laboratory. Schoental 

(1973,1974), based on her previously described work, proposed that 

spontaneous tumors in laboratory rodents might be due to carcinogenic 

constituents, including alpha, beta-unsaturated lignin aldehydes and 

podophyllotoxin, of wood shavings used as animal bedding . 

Sabine et al. (1973) reported thei r observat ions on C3H-Avy and 

C3H-AvYfB mice bred and reared in Austral ia. Historically, those strains 

had a 90-100% spontaneous incidence of liver and mammary tumors in the U.S . 

(Heston and Vlahakis 1968, Vlahakis et al. 1970). However, Sabine et al. 

(1973) reported that colonies of both mouse strains derived from U.S. 

breeding pai rs and raised in Austral ia on North American Douglas fi r sawdust 

bedding and Australian feed had a significantly (p<O.oo1) reduced incidence 

of both type of tumors when compared to those previously raised in the U.S. 

(Heston and Vlahakis 1968, Vlahakis et al. 1970). For mammary tumors, the 

incidence in Austral ia decl ined to almost zero by the second generation. 

When C3H-Avy mice in Australia were maintained on fir sawdust bedding but 

given U.S. feed, mammary tumor incidence increased nonsignificantly from 46% 

(controls) to 50%. However, when they received both U.S. bedding material 

(Eastern red cedar> and feed, the incidence of mammary tumors increased 

significantly (p<0.025) to 76%. There was also a nonsignificant decrease in 

mean latency period unti I tumor appearance from 9 .3 montha in the controls 

to 6.4 months in the mice reared on U.S. food and bedding. However, the 

U.S . feed and bedding signi ficant Iy (p<O.oo1) increased the average weight 

of the ~dult mice . The authors cautioned that these results were 

prel iminary and did not rule out other reasons for di fferences in tumor 

incidence, such as genetic variation. However, because the addition of 

cedar bedding restored the mammary tumor incidence in Austral ian mice to 

levels near that historically seen in U.S. mice, they bel ieved that cedar 

bedding was implicated as a carcinogen. 

In response to the above report by Sabine et al. (1973), Heston (1975) 

examined the occurrence of tumors in the same two strains of mice raised in 

the U.S. The animals were fed either the Australian diet used by Sabine and 

coworkers or the same U.S. food on which the colony had formerly been 

maintained . The animals raised on the softer Austral ian feed ate more and 

grew more rapidly than those on the U.S. diet. However, no significant 

di fferences in the incidence of mammary or I iver tumors due to diet were 

seen, which agreed with the observations made by Sabine and coworkers. To 

examine the effect of bedding material, C3H-Avy mice were maintained on a 

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bedding of either three-fourths pine sawdust plus one-fourth cedar shavings, 

or on pine sawdust only, and fed the NIH open-formula diet, which was more 

nutritious than the standard U.S. diet previously used. No significant 

di fferences in the growth rate or mammary and I iver tumor incidence were 

seen. Heston (1975) commented that the animals in the Sabine et al. study 

were in poorer health and more prone to infection. They had heavy mite 

infestation and significantly lower weight gain. This may have reduced the 

incidence of tumors by shortening the life span of the animals raised in 

Austral ia. Since Heston and Vlahakis (1966) had shown that factors causing 

decreased animal growth also decreased tumor occurrence, Heston concluded 

that the reduction in tumor incidence reported by Sabine and coworkers was 

due to lower weight gain and ectoparasitic infestation. 

Sabine (1975) summarized his tumor incidence data in three susceptible 

strains of mice (C3H-Avy, C3H-AvYfB, and CBA/J) raised in Austral ia and 

compared them with reported U.S. data. He reported a significantly (p<0.05) 

increased incidence of spontaneous tumors of the I iver and manmary gland, 

and a reduced mean time to tumor appearance, in all three strains of mice 

raised on cedar shavings as opposed to those raised on Douglas fir bedding. 

The hexobarbital sleeping time decreased significantly (p<0.OO1) and hepatic 

levels of cytochrome P450 and associated liver metabol izing enzymes 

increased significantly (p unspecified) in mice reared on cedar shavings in 

comparison with those bedded on Douglas fir sawdust. These sleep time 

changes and enzyme increases were simi lar to the results reported previously 

by Ferguson (1966), Vesel I (1967), Wade et al. (1968), and Hashimoto et al. 

(1972). In a "Note Added in Proof" at the conclusion of his paper, Sabine 

(1975) discussed the previous report of Heston (1975). Sabine indicated 

that the effect of cedar wou Id have been d iff i cu I t to assess because the 

tumor incidence in Heston's noncedar 9rouP was vi rtually 100%. The number 

of hepatomas per animal was slightly higher in the males raised on cedar, 

but the difference may not have been significant. Finally, the unstated 

methods used by Heston to prevent mite infestation may have elevated hepatic 

enzyme levels. Sabine, therefore, concluded that the question of cedar 

carcinogenicity in mice remained unresolved. 

Vlahakis (1977) studied the effect of bedding material on carcinogenicity in 

C3H-AvYfB .mice. Thi rty-seven brother x sister pai r matings were made on 

bedding of mixed North American species of low-resin pine sawdust, and 22 

littermate pairs were mated and bedded on a mixture of the same pine sawdust 

and red cedar shavings. All were fed the NIH open-formula diet. Among the 

fema I e Ali ce, those on mi xed bedd ing I113ter i a I had a stat i st i ca lIy 

nonsignificant decreased incidence of mammary tumors relative to those on 

pine sawdust alone (81.8% vs. 86.5%). There was also a nonsignificantly 

higher average age at manmary tumor appearance in the former group (17.0 vs. 

16.0 months). The author concluded that these data were in agreement wi th 

his previously reported data (Heston and Vlahakis 1968, Vlahakis et al. 

1970) and that the high incidence of tumors in this strain could not be 

attributed to the cedar shavings in the bedding material. He reiterated 

Heston's (1975) argument that the reduced tumor incidence reported by Sabine 

et al. (1973) was due to lower body weight and ectoparasitic infestation . 

11 
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Two additional studies of the effects of wood bedding material have been 

reported. Jacobs and Dieter (1978) examined the incidence rate of 

spontaneous hepatomas in mice inbred for 21-25 generations from noninbred 

Ha : ICR Swiss stock. They reported no significant difference in hepatoma 

incidence in male mice raised on pine bedding (31%) versus those raised on a 

pine-cedar shaving mixture (25%), and concluded that cedar shavings did not 

contribute to the high incidence of hepatomas in these mice. 

DePass et al. (1986) compared the survival , incidence, and latency of dermal 

neoplasms caused by the carcinogen benzo(a)pyrene (NTP 1985) between male 

C3H/HeJ mice housed in polycarbonate cages I ined with hardwood chips of 

maple, bi rch, or beech and mice housed in stainless steel wi re mesh cages 

with no I ining. Type of housing had no effect on survival . However, the 

time-adjusted incidence of dermal neoplasms was significantly (p<0.OO1) 

higher in the polycarbonate group than in the stainless steel group at all 

concentrations of benzo(a)pyrene (0.25%, 0.05%, and 0.01% [w/w]). The 

authors suggested that the increase in tumor incidence in the polycarbonate 

group might be due to skin contact with urinary metabolites on the bedding 

or to the slightly lower ambient temperature at which that group was 

housed. However, they considered it unl ikely that the increase was due to 

subs tances in the wood-ch i p bedd i ng, since the ch i ps we re made f rom vi rg i n 

hardwood containing relatively low levels of tannins , phenols, and other 

aromatic resins found in higher concentrations in softwood bedding, such as 

pine shavings. 

The fibrogenici ty of several wood dusts and plant fibers was studied by 

8hattacharjee et al. (1979) and Bhattacharjee and Zaidi (1982). Groups of 

eight male guinea pigs were injected intratracheally with single saline 

suspensions containing either 75 mg of sheesham or mango wood dust or hemp 

or bagasse fibers or 20 mg of jute fiber . The animals were serially 

sacrificed up to 90 days post-injection and their lungs were examined. By 

the end of 90 days, Grade I f i bros i s was observed in the I ungs of Ihe 

animals given mango and jute, and Grade II fibrosis was seen in those given 

sheesham and hemp . 

McMichael et al. (1333) exposed male and female guinea pigs by i nhalation to 

fir bark dust (average respirable dust concentration 1,143 mg/m3 ) for 

periods of' 30 min/day, 5 days/week for 24 weeks. Terminal histopathology 

revealed moderate to severe lung changes in al I the animals, including 

increased seplal connective tissue components and lymphocyte aggregation . 

Although no pulmonary fibrosis or extensive destruct ion of the parenchymal 

tissue was seen following the 24-week exposure period, the authors concluded 

that fir bark dust may cause inflammatory changes in the lung and should be 

considered more than simply a nuisance dust. 

Wi Ihelmsson et al. (1985c,1985d) and Dreltner et al . (1985) described two 

studies in which they exposed male Syrian golden hamsters by inhalation to 

beech wood dust (diameter 5-15 um) both with and without concurrent 

subcutaneous administration of the known carcinogen diethylnitrosamine (DEN) 

(NTP 1985). In each study , the animals were divided into four groups 

(12 per group in Study I , 24 per group in Study II) . Two of the groups in 

each study were exposed to fresh beech wood dust (mean total dust 

12 
concentration 15 mg/m3 [range 10-20 mg/m3] in Study I; 30 mg/m3 [range 

25-35 mg/m3] in Study II) for 6 hr/day, 5 days/week for 36 weeks (Study I) 

or 40 weeks (Study "). One of these two groups was also given 1.5 mg 

(Study I) or 3.0 mg (Study II) of DEN once a week for the fi rst 12 weeks. 

The thi rd group in each study was given a corresponding dose of DEN only 

(positive control), and the fourth group had no exposures (negative 

control). At the conclusion of the studies, the animals were sacrificed and 

examined. 

In Study I, no nasal or lung tumors were found in any of the groups, nor was 

any metaplasia found. Four of eight hamsters exposed to both wood dust and 

DEN, three of eight positive controls, and one of seven negative controls 

had squamous cell papi I loma in the trachea. The reduced number of specimens 

was due to cannibalism. No significant differences in nonpulmonary organ 

pathology or weight gain and development were noted. In Study II, with 

greater amounts of both wood dust and DEN, all sacrificed animals exposed to 

DEN had nasal lesions ranging from hyperplasia and dysplasia to papi I lomas. 

In addition, about half of the DEN-exposed animals had nasal tumors 

(adenocarcinomas) whether they had been exposed to wood dust (11/21) or not 

(10/22). Papillomas of the larynx and trachea were also found in over half 

of this same group (11/18 and 12/19, respectively). In the group exposed to 

wood dust only, two animals, both of which died spontaneously, had nasal 

lesions. One had an unclassifiable malignant nasal tumor and the other had 

focal metaplasia with mi Id dysplasia. Animals in this group also exhibited 

mi Id inflammatory reactions in the respiratory epithelium and submucosal 

stroma that were not seen in the negative controls. Because cannibal ism 

occurred in both studies, and the affected animals generally had obstructive 

tumors in the upper ai rways, the studies had to be terminated earl ier than 

planned. Although the studies were limited in nature and the group sizes 

inadequate, the authors concluded that wood dust exposure did not increase 

the tumor incidence of DEN-treated animals, but that it did affect the 

respiratory mucosa of Syrian golden hamsters. 

B. In Vitro Studies 

Evans and Nicholls (1974) examined the effects of aqueous extracts of 

Western reij cedar on pig and human lung cell cultures. They found histamine 

release in both comparable to that of an equivalent amount of cotton dust, 

and a concentration-response relationship over a narrow range of cedar dust 

concentrations (5-10 mg/mL). The authors concluded that wood dust may 

induce the release of histamine in the lungs and upper respiratory tract, 

and that this might be a significant factor in the development of 

respiratory symptoms in exposed workers. 

As part of thei r previously described studies, Bhattacharjee et al. (1979) 

and Bhattacharjee and Zaidi (1982) examined the hemolytic activity and in 

vitro cytotoxicity of wood dusts (sheesham and mango) and fibers (hemp, 

bagasse, and jute). They reported that sheesham dust was strongly hemolytic 

to sheep erythrocytes whi Ie mango dust was only weakly hemolytic. Bagasse 

fibers were strongly hemolytic to rabbit erythrocytes, whi Ie hemp and jute 

fibers were weakly hemolytic. The uptake of erythrosin B by guinea pig 

13 
• 

alveolar macrophages exposed to sheesham and mango was significantly 

(p<O.OO5) less than the uptake by macrophages exposed to chrysoti Ie 

asbestos, indicating a significantly lesser degree of toxicity for the wood 

dusts. The uptake of erythrosin B for hemp, bagasse, and jute fibers was 

equal to or greater than that for chrysoti Ie . asbestos. The authors 

suggested that hemolytic activity may be indicative of the acute response of 

pulmonary tissues whi Ie macrophage cytotoxicity may be indicative of chronic 

effects (e.g., fibrogenicity). 

liu et al. (1985) examined the in vitro cytotoxicity of wood dusts from 

three small woodworking establishments in Hong Kong: a plywood and hardwood 

sawmill, a furniture factory where polish dust was released from belt 

sanders, and the mixing room of a factory that manufactured 

sawdust-containing mosqui to repellant. Wood species were not identi fied. 

The authors sampled for total dust, particle shape and size distributions, 

and metal concentrations (Cd, Cr, Cu, Fe, Mn, Ni, Pb, and Zn). They found 

that the percent viabi I ity of cultured female albino rat alveolar 

macrophages incubated with each of the three different dusts decreased with 

time to 57% (sawmill dust), 38% (sander dust), and 47% (mosquito repellant 

factory dust) after 24 hr. These levels were significantly (p<O.05) 

different from each other and from the control. Since the dust from the 

sanding area of the the furniture factory had the highest level of most 

metals, the authors attributed the difference in macrophage viabi lity to the 

different metal contents of the dusts. 

McGregor (1982) studied the in vitro mutagenicity of ash, oak, beech, elm, 

and mahogany. Water, water/methanol, and ethyl acetate extracts of sawdusts 

from these woods were tested using Salmonella typhimurium strains TA98 and 

TA100, with and without metabolic activation. None of the aqueous extracts 

was ~utagenic. Water/methanol extracts of beech and ash were weakly 

mutagenic (strains/activation not specified), whi Ie elm was found to be 

toxic. Of the ethyl acetate extracts, beech and ash gave a positive 

mutagenic response . The former was weakly mutagenic in strain TA98 with 

activation at low concentrations; at higher levels no mutagenic activity was 

seen, although there were no obvious signs of toxicity. The ash extract was 

weakly positive at high concentrations in strain TA100 both with and without 

activation. 

Mohtashamipur et al. (1986) also examined the mutagenicity of beech. 

Methanol extracts of beech sawdust were fractionated with si I ica gel using 

as sequential solvents n-heptane, petrolether, ethyl acetate, methylene 

chloride, and methanol. Each fraction was tested using Salmonella 

typhimurium strain TA100 with and without metabolic activation. 

Concentration-dependent mutagenic activity was observed only with activation 

from the beech dust extracts after fractionation. The mutagens were found 

to be concentrated primari Iy in the ethyl acetate phase and were toxic to 

the bacteria when tested in a histidine-rich (complete) medium. A 

nonsignificant increase in the number of revertant colonies was found with 

the methanol extract (prior to fractionation) at the nontoxic concentration 

of 2.5 grams equivalent dust per plate . Further tests showed that this 

methanol extract also inhibited the activity of known mutagens. The authors 

suggested that the weak activity exhibited by this extract could indicate 

14 
, 

the presence of some mutagens in beech that are trapped among other 

compounds that inhibit mutagenicity. 

Speci fic chemical substances found in wood have also been tested for in 

vitro mutagenicity. A description of these studies can be found in Tinkler 

(1986) and Niemeier (1979) . 

C. Summary 

There are relatively I ittle in vitro and in vivo animal data from which to 

draw firm conclusions regarding the toxicity of wood dust. Certain extracts 

of beech and ash have been shown to be weak in vi t ro mutagens. I n some 

studies, the use of cedar bedding material has been associated with an 

increased incidence of manlllary and I iver tumors in susceptible strains of 

mice, although other simi lar studies have shown no such effect . Only three 

in vivo inhalation studies were found. In the first, high concentrations of 

cedar and pine dusts caused lung abscesses and bronchopneumonia in rabb i ts 

following chronic inhalation. In the second, high concentrations of fir 

bark dust caused inflammatory changes in guinea pig lungs following 

subchronic inhalation. In the thi rd, beech wood dust was administered by 

inhalation to hamaters concurrently with a known carcinogen. At the 

concentrations used, no synergistic carcinogenic effects due to wood dust 

were seen, although there were effects to the respiratory mucosa . 

15 
, 

III. DERMATITIS 

Irritation of the skin and eyes resulting from contact with woods or their 

dusts is relatively common (Senear 1933) and may result from mechanical 

action (e .g., irritation caused by bristles and splinters), chemical 

irritation, sensitization (allergic reaction), or by a combination of 

these. Woods and Calnan (1976) have publ ished a comprehensive review of 

wood dermatitis, from which much of the following introductory discussion is 

taken; no attempt will be made to duplicate their compilation of data for 

over 300 species of trees . In most reports of contact dermatitis, hardwoods 

of tropical origin have been implicated as the responsible agents; however, 

a few softwoods and hardwoods from temperate cl imates, including pine, 

spruce, Western red cedar, yew, elm, and a I der, have a I so been cited as 

causal agents. Exotic woods, such as those found in the tropics, generally 

cause more toxic systemic effects and contain more potent sensitizers. A 

list of wood species that have been identified as causes of dermatitis is 

shown in Table 2. 

I rritant chemicals are often found in the sap or latex, or in the bark or 

cracks in the wood. Since these substances exist primari Iy in the outer 

part of the tree, loggers and those involved in initial wood processing are 

most affected. Primary irritant dermatitis caused by wood contact is 

clinically simi lar to any irritant dermatitis, consisting of erythema and 

blistering, which may be accompanied by erosions and secondary infections. 

Also, the conjunctivas are often affected (Nava 1974; Kubena et . al. 1968). 

Chemicals causing sensitization are generally found in the heartwood and, 

therefore, more often affect workers involved in secondary wood processing, 

such as sawyers, carpenters, joiners, and furniture finishers and polishers 

exposed to wood dust. The early stages of allergic dermatitis (dermatitis 

venenata) ·are redness, scal ing, and itching, ini tially resembl ing irritant 

dermat i tis . The hands and forearms, eye lids, face and neck, and gen ita I s 

are generally fi rst affected. Mi Id cases may exhibit only redness and 

irritation, which may progress to vesicular dermatitis, and, after repeated 

exposures, to chronic dermatitis. Allergic dermatitis may appear after 

several weeks to several years of contact, but in general the eruptions 

appear after a few days to a few weeks of contact. High humidity, repeated 

wetting of the skin, and sweating may increase the intensity of the reaction 

(Suskind 1967, Steiner and Schwartz 1944) . Development of tolerance to some 

woods has been reported (Schwartz 1931). 

The sensitizing agents responsible for dermatitis are believed to be 

chemicals endogenous to the woods. Among agents that have been identified 

are anthothecol from African mahogany (Morgan et al. 1968), 

(R)-3,4-dimethoxydalbergione and its quinol from Machaerium scleroxylon 

(Morgan et al. 1968), and mono- and dimethoxy-substituted quinones or 

17 
, 

Table 2.--Woods causing dermatitis* 

Botanical name 

Apocynaceae Aspidosperma spp. 

Betulaceae 

Alnus spp.*** 

Bignoniaceae 

Paratecoma peroba 

Tabebuia spp. 

Burseraceae 

Aucommea klaineana 

He rnand i aceae 

Hernandia sonora 

Lauraceae 

Nectandra rodiaei 

Phoebe po rosa 

Ocotea spp. 

Legum i nosae 

Andi ra inermis 

Brya ebenus 

Cassia slamea 

Dalbergia cearensis 

Dalbergia granadi 110 

Dalbergia latifolia 

Dalbergia melanoxylon 

See footnotes at end of table. 

Common name** 

Peroba rosa 

Alder 

Peroba de Campos. peroba branca. 

peroba amarella 

Lapacho, suayacan, ipe, mayflower 

Gaboon, okoume 

Topolite 

Anti lies greenheart 

Brazilian walnut. imbuia 

Louro. jigua. pisie 

Part ridge wood 

Cocus wood 

Tagayasan 

Kingswood. violet wood 

Costa Rica rosewood 

East Indian rosewood. Bombay 

blackwood. sissoo 

African blackwood 

18 

(Continued) 
Table 2 (Continued).--Woods causing dermatitis* 

Botanical name 

Leguminosae (continued) 

Dalbergia nigra 

Dalbergia rBtusa 

Dalbergia stevensonii 

Distemonanthus 

benthamianus 

Gossweilerodendron 

balsami ferum 

Prosopis juliflora*** 

Machaerium scleroxylon 

Mel iaceae 

Guarea thompsonii 

Khaya an tho theca 

Moraceae 

Chlorophora excelsa 

Pinaceae 

Abies spp.*** 

Juniperus virginiana*** 

Libocedrus decurrens*** 

Pinus spp.*" 

Picea spp .*** 

Pseudotsuga menziesii*** 

Thuja occidentalis*** 

See footnotes at end of table . 

Common name** 

Brazi lian rosewood . riopalisander. grenadilla 

Cocobolo 

Honduras rosewood 

Ayan. Nigerian satinwood 

Agba. tola branca 

Mesqu i te 

African mahogany 

Guarea 

African mahogany 

African iroko. kambala. 

Afr ican teak 

Fir 

Eastern red cedar 

Incense cedar 

Pine 

Spruce 

Douglas fir 

Northern whi te cedar 

19 

(Continued) 
, 

Table 2 (Continued).--Woods causing dermatitis' 

Botanical name 

Pinaceae (continued) 

Thuja plicata'" 

Tsuga spp.· .. 

Rutaceae 

Chloroxylon swietenia 

~agara f lava 

sZanthOXYTUm) flavum 

Fagara macrophylla 

Sapotaceae Bassia latifolia 

Mimusops heckeli i 

Taxaceae 

Taxus baccata 

Triplochitonaceae 

Mansonia altissima 

Ulmaceae 

Ulmus spp ... • 

Verbenaceae 

Tectona grandis 

Conrnon name" 

Western red cedar 

Hemlock 

East Indian satinwood 

West Indian satinwood 

Olon 

Moah. mahwa 

Makore. baku 

Yew 

Mansonia. African black walnut 

Elm 

Teak 

'Adapted from McCord (1958). Fregert and Hjorth (1968). and Gamble (1979). 

"There is no accepted international nomenclature. 

"'North American species. 

20 
, 

quinols from cocobolo (Schulz and Dietrichs 1962), i roko (King and Grundon 

1949,1950), teak (Vermeer et al . 1949, Schulz 1962), Rio-palisander (Schulz 

and Dietrichs 1962), and mansonia (Schulz 1962) . Additional substances are 

described in Woods and Calnan (1976) and Gamble (1979). 

The earliest modern report of wood dermatitis appears to be that of Stern 

(1891), who described two flute players who developed a contact dermatitis 

of the I ips from the mouthpieces of thei r instruments, which were made of 

cocobolo wood. Jones (1904) described dermatitis among shipyard workers who 

handled East Indian satinwood. Cash (1911) demonstrated, by patch testing, that an alkaloid isolated from satinwood by Auld (1909) produced dermatitis; 

the oi Is from satinwood produced a less dramatic reaction. Matthes and 

Schreiber (1914) extracted components from six types of wood (East Indian 

moah, teak, Australian moah, lapacho, tecoma, and greenhart) and tested them 

for skin irritation. Hoffmann (1928), Senear (1933), Bergquist and Rundberg (1941), and Woods and Calnan (1976) have summarized many simi lar reports 

involving a wide variety of wood species, most Iy foreign woods. Weber 

(1953) estimated that 1% of workers develop skin sensitization to sawdust of 

native American woods. Selected case reports of wood dermatitis are 

summarized in Table 3. . 

Another type of dermatitis associated with the wood industry but not caused 

by contact with wood or wood dust itself is "woodcutters' eczema," also 

known as "wood poisoning," "cedar poisoning ," "pine poisoning," "oak 

poisoning," "spruce poisoning," and "spruce dermatitis." This condition, 

which has been described by a number of authors (Mitchell 1965; Mitchell and 

Armitage 1965; Mitchell et al . 1969; Champion 1965,1971; Suskind 1967; 

Mitchell and Chan-Yeung 1974), is prevalent among forest workers and is 

caused by contact with epiphytes, lichens, and liverworts growin9 on bark or 

surrounding shrubs. This dermatitis occurs only during work in forest 

areas, appears within a day or two after starting work, becomes worse in wet 

weather, and subsides in 2 to 4 weeks after exposure stops. The respiratory 

system may also be affected. 

Fungi growing on bark were first suspected of causing dermatitis in 1921, 

but it was a quarter of a century before woodcutters' eczema was first 

attributed to lichens and liverworts (Gamble 1979) . One of the most common 

causes of .wood poisoning is the leafy liverwort Frullania, which thrives in 

high humidity and grows on trunks and branches of trees and shrubs, and on 

cl iffs and rocks. Sesquiterpene lactones have been identified as 

sensitizers in Frullania (Mitchell and Chan-Yeung 1974). Simi larly, usnic 

acid, a compound related to the photosensitizing furocoumarans, has been 

identified as the sensitizer in lichens (Mitchell 1965). 

Summary 

A wide variety of both domestic and foreign wood species have been 

documented in case reports and epidemiol09ical studies to cause irritant and 

allergic dermatitis . For some species, chemicals present in the wood, 

including quinones and quinols, have been isolated and shown to be the 

sens it i zing agent. Another wood-re lated dermat i t is is woodcutters' eczema, 

which is caused by lichens and liverworts that grow on bark and shrubs . 

21 
N 

N 

Reference 

Schwartz 

(1931) 

Levin 

( 1933) 

Stewar t 

(1940) 

Davidson 

(1941 ) 

Table 3.--Selected case reports of wood dermatitis 

lood types 

Brazi I ian 

walnut 

Unspecified 

ConInents 

Eleven cases of dermatitis among 100 workers of a cabinetmak ing 

plant were reported . Initial symptoms included burning and 

itching of the face and eyelids, which spread to the hands, 

forearms, neck, and other exposed portions of the body . The 

condition developed 2 days to 2 weeks after the workers be9an 

handl in9 this wood . Most of the workers recovered after several 

weeks, even with continuing exposure . The author contacted 

other firms that had bought this wood from the same supplier and 

found that g of 10 who replied had experienced dermatitis in 

their workers . Walnut sawdust patch tests on three volunteers 

were positive . 

A case of severe dermatitis of the hands and arms , with itchy 

eruptions, blisters, and swellin9, was reported in a department 

store cleaner who threw handfuls of moistened sawdust on the 

floor for sweeping. The female cleaner also reacted to the 

sawdust in patch testing, and dermatitis recurred whenever 

attempts were made to resume use of the sawdust. 

Mesquite A male patient developed facial eruptions one day after handling mesquite wood. Patch tests with mesquite sawdust were positive, and no recurrence was noted after the patient stopped using the 

wood . 

African iroko Dermatitis in more than 50 men working with moist logs in a 

woodworking shop was described . Nine had severe symptoms (some 

with'in an hour of initial contact), including irritation of 

covered skin, facial edema and eye irritation, headache, 

pharyngitis, and chest symptoms . Two of these nine had 

experienced earlier cases of dermatitis attributed to exposure 

to teak. 

(Cont inued) 

-
N 

W 

Reference 

Levin 

(1941) ; 

Leider and 

Schwartzfeld 

(1950) 

Steiner and 

Schwartz 

(1944) 

VerJneer et al . (1949) 

Weber 

(1953) 

Table 3 (Continued).--Selected case reports of wood dermatitis 

Wood types 

Cocobolo 

Tobasco 

mahogany 

Peroba 

teak 

Pop lar 

Conments 

Three cases of allergic dermatitis in women were described. Two 

had developed itching and characteristic eruptions of the hands, 

which in one had spread to the face and neck. In both cases, 

sensitizat ion was traced to a cocobolo knife handle and was 

confirmed with patch testing . The third patient was a musician 

who experienced swelling of her lips after she had been playing 

a wind instrument for 1 month . A patch test for cocobolo was 

positive, and her symptoms disappeared when she ceased playing 

the instrument. 

An outbreak of occupational dermatitis among 40 workers in a 

boatyard woodshop was described. The outbreak occurred when 

"Tabasco mahogany," principally from Brazi I and Honduras, was 

substituted for "Phi lippine mahogany," described as a trade name 

for several types of Phillipine hardwood, none of which actually belongs to the mahogany family. The peak of the outbreak 

occurred during a hot part of the summer, when 13 workers who 

wore little clothing and perspired freely were treated for 

dermatitis. Several of the workers patch tested positively 

either to the wood itself or to ether extracts. 

Four cases of occupationally related eczema were reported. 

Patch tests with this wood dust were positive in all four. The 

responsible allergen was tentatively identified as lapachonon, a 

derivative of naphthalene. 

A case of allergic dermatitis in a woodworker who had also 

suffered weight loss, lymph node enlargement, itching, chills, 

and sleeplessness was described . Patch tests were positive for 

poplar. After recovering, the patient returned to work in 

another part of the plant and symptoms did not recur . 

(Cont i nued) 

-
'" ~ 

Reference 

Bourne 

(1956) 

Mor9an and 

Wi Ikinson 

(1965); 

Mor9an et al. 

(1968) 

Table 3 (Continued).--Selected case reports of wood dermatitis 

Wood types 

Mansonia 

African 

mahogany, 

Machaer i um 

scleroxylon 

Conments 

Six cases of dermatitis among 12 sanders in a radio and 

television cabinet manufacturing plant were described. Initial 

symptoms were nasal irritation and sneezing, followed by scalp , facial, neck, and shoulder irritation, nasal sores and 

discharges, and sore throat. In response to patch tests, all 

six workers developed irritation within 8-12 hr and persisted 

for as long as 4 days. Symptoms disappeared when use of this 

wood was stopped. 

Several cases of dermatitis at three furniture factories were 

reported . Six workers from two factories were patch tested 

with dust from two species of African ~hogany (Khaya anthotheca 

and Khaya ivorensis) and with anthothecol, a constituent of 

mahogany . Five of the six were positive for ~ anthotheca and 

the sixth was positive for ~ ivorensis; two of the six were 

positive for anthothecol . At the third factory, the first 

symptoms of dermatitis occurred after ~ seleroxylon was 

substituted for Rio rosewood . Within 3 weeks, 7 out of 24 

workers had developed dermatitis. Patients who were patch 

tested with Rio rosewood had moderate reactions, whereas all of 

those tested with ~ scleroxylon had very strong reactions . Four major compounds were extracted from ~ scleroxYlon : 

dalbergin, methyl dalbergin, and (R)-3,4-dimethyloxydalbergione 

and its quinol derivative. Patch testing with these four 

compounds and the completely extracted sawdust showed that the 

activity was caused by the (R)-3,4-dimethyloxydalbergione and 

its quinol. The authors noted that these two compounds were 

very similar in structure to the sensitizing constituents of Rio 

rosewood and cocobolo wood, which are also quinones and quinols. 

(Cont inued) 

-
N 

U"I 

Reference 

Findley 

(1972) 

Bleumink et al. 

(1973) 

Burry 

(1976) 

Fowler 

(1985) 

Jable 3 (Continued).--Selected case reports of wood dermatitis 

Wood types 

East Indian 

rosewood 

Western 

red cedar 

COlIIDents 

A male patient who had developed a rash on his feet, neck, and 

trunk over a 6-week period was described. Symptoms were traced 

to rosewood sawdust vented into the air by an adjacent cutlery 

handle manufacturer. Patch tests were positive. Of twenty 

other men working in the area who were examined, only one had a 

positive patch test . 

A case of allergic dermatitis of the face. hands, and arms of a 

sawyer who had been exposed for 2 years was described. Patch 

tests showed strong delayed cutaneous reaction to cedar extracts 

as well as to two specific cha.ical cooponents of the wood, 

gaama-thujaplicin and 7-hydroxy-4-isopropyltropolone. 

Radiata pine Contact dermatitis in nine patients who worked with pine sawdust 

was described. Patch tests with the sawdust or with substances 

containing colophony (pine rosin) were positive in all nine 

patients. 

Honduras 

I113hogany 

A case of allergic contact dermatitis in a male patient who had 

been employed as a woodworker for 20 years with no previous skin 

disease was described. Six months after changing jobs from a 

well-venti lated to a very dusty work site , he developed a 

diffuse dermatitis of the hands, lower arms, and face , neck, and 

upper chest. Patch testing yielded positive results for 

Honduras mahogany dust. After leaving this job, the individual 

had no recurrence of dermatitis. 

-
, 

IV. ALLERGIC RESPIRATORY EFFECTS 

An allergic respiratory response, like allergic dermatitis, is an 

immunologically mediated reaction to environmental antigens (allergens) that 

results in symptoms on exposure to the allergen (Terr 1978) . The most 

common Iy reported a II erg i c resp i ratory effect due to exposure to wood dust 

is asthma . It may occur alone or in conjunction with dermatitis and may 

manifest itself as an i1Tl11ediate (within minutes) or delayed (within hours) 

reaction, or as a combination of the two separated by a recovery period. 

Case reports have documented asthmat ic react ions to several common Woods, 

includin9 oak, mahogany, and redwood, as well as to more exotic woods such 

as i roko, cocobolo, zebrawood, and abi ruana . These reports are summarized 

in Table 4. The only epidemiol09ic studies of wood dust-induced asthma are 

those on Western red cedar, which is discussed in detai I later in this 

section. Reports of respi ratory effects not speci fically identi fied as 

aller9ic responses are discussed in Section V. 

Some reports refer to the observed asthmatic responses of individuals 

exposed to wood dust as Type I allergic reactions, as originally defined by 

Gell and Coombs (1963). The characteristics of Type I reactions are shown 

in Table 5 . In this type of reaction, allergen-specific inmunoglobulin E 

(19E) antibodies are produced within plasma cells embedded in the mucosa. 

These antibodies diffuse into tissue fluid and attach to mast cells . The 

reaction of allergen with this cell-bound antibody triggers the release of 

histamine and other substances that produce typical allergic symptoms of 

broncho-constriction, vasodi lation, smooth muscle contraction, and increased 

bronchial and nasal secretion. 

This definition of asthma as a Type I allergic reaction is a narrow one . 

Currently, asthma is more universally defined as "reversible obstructive 

airway disease" (Farr 1987). According to Farr (1987), only a fraction of 

asthmatic attacks are precipitated solely by 19E reactions. This 

observation is reflected in the literature on wood-dust-induced asthma . For 

example, case reports have demonstrated the presence of IgE antibodies in 

the serum of individuals with asthmatic reactions to African zebrawood (Bush 

et al. 1978), Quillaja bark (Ra9huprasad et al. 1980), and African maple 

(Hinojosa et al. 1984). However, other reports have fai led to show IgE 

antibodies in persons with asthmatic reactions to Tanganyika aningre 

(Pag9iaro et al . 1981) and Central American walnut (Bush and Clayton 1983). 

A similar pattern exists regarding the presence of precipitins 

(precipitatin9 antibodies) in the serum of individuals followin9 a challenge 

with wood dusts or extracts. Precipitins have been detected after a 

challenge with extracts of oak, mahogany, and cedar (Sosman et al. 1969) and 

iroko (Pickering et al . 1972), but have not been detected following 

27 
'" Q) 

Table 4.--Selected case reports of allergic respiratory effects caused by wood dust 

Reference 

Gade 

(1921) 

Bahn 

(1928 ) 

Markin 

(1930) 

Ordman 

(1949a ,1949b) 

lood types 

Unspec i f i ed 

Pine, fi r 

Boxwood 

Kejaat, 

Congo 

hardwood, 

lestern red 

cedar 

Comnents 

Respiratory symptoms, includin9 7 cases of asthma, were reported 

in 14 of 20 sawmill workers . Asthmatic symptoms first appeared 

7 months to 4 years after the men began work at the sawmi II. 

Eosinophi lia was present in three of the asthmatic cases . 

A 33-year-old male patient who developed asthma 10 months after 

beginning work in a saWQil1 was described. Intracutaneous 

administration of aqueous wood extracts provoked strong reaction 

to pine and fir but only sl ight reaction to oak and beech . Since controls did not react to the pine and fir extracts, Bahn 

described the worker's condition as allergic and noted that the 

asthmatic attacks ceased when the patient stopped working at the 

sawmi II. 

A 34-year-old male patient who had developed asthma over a 

5-year period was described. Skin scratch tests were positive 

both for sawdust used by pat ient at work and for boxwood . Although desensitization was not successful, the patient 

developed a gradual tolerance to boxwood. 

Two cases of occupational asthma were described . The first was 

a 29-year-old male cabinetmaker who developed rhinitis and asthma 

2 months after the plant he worked in switched to using the 

listed woods. Sk in scratch and intradermal tests using 

aqueous extracts of each of the woods were positive. The second 

case ~as a 39-year-old male whose symptoms began on the first 

day he handled kejaat . He had previously worked with mahogany, 

walnut, teak, and pine with no reaction. Skin scratch test was 

negative; intradermal test was positive to an aqueous extract 

but negative to the dust itself . In both cases injections for 

desensitization were successful in alleviating the symptoms . 

(Cont i nued) 

-
N 

'" 

Table 4 (Continued).--Selected case reports of allergic respiratory effects caused by wood dust 

Reference 

80sman et a I . 

(1969) 

Greenberg 

(1972) 

Pickering et al . (1972) 

Wood types 

Oak, 

mahogany , cedar 

Cedar of 

Lebanon 

Iroko, 

Western red 

cedar 

C01II11en ts 

Asthmatic symptoms in four woodworkers aged 33-54 were reported. 

Each had been exposed to wood dust of one of the listed types for 

17-25 years ; all had experienced sneezing, running nose, cough, 

wheezing, and difficulty in breathing for 4-8 years. They 

demonstrated either immediate, delayed, or combined responses to 

inhalation of the wood dusts and their aqueous or alcohol 

extracts. Both skin scratch and intradermal tests were negative 

in all cases . Precipitating antibodies against either the 

alcohol extract of oak or the aqueous extracts of mahogany or 

cedar were found in the serum of each individual . The authors 

suggested that the responses were hypersensitivity reactions . 

Symptoms of asthma and rhinitis were described in six JOlnery- shop workers . Symptoms developed rapidly after initial exposure 

(within 2 to 96 hr) and included chest tightness, cough, 

occasional sneezing, and nasal obstruction. No gross deficits 

were found in pulmonary function tests, nor were precipitating 

antibodies found. Only one worker had a positive skin patch 

test . 

Two male patients in their mid-thirties, each of whom had 

developed asthmatic symptoms following exposure to one of the 

listed woods, were described. Bronchial challenge with either 

iroko or cedar dust provo~ed late asthmatic reaction in each. 

The man who worked with iroko had an immediate reaction to 

aqueous extracts of the wood . He also had a positive skin 

scratch test, and his serum contained anti-iroko precipitins. 

The patient exposed to cedar had no serum precipitins and gave 

no skin scratch test response . 

(Continued) 
.., 

o 

Table 4 (Continued).--Selected case reports of allergic respiratory effects caused by wood dust 

Reference 

Eaton 

(1973) 

Booth et al. 

(1976) 

lood types 

Cocobolo 

Abi ruana 

Contnents 

Ast~ and nasal irritation were reported in three workers who 

handled exotic hardwoods in a billiard cue manufacturing 

factory. One subject had a positive skin patch test and the 

other two had positive skin prick tests with aqueous extracts. 

Two patients exhibited positive response to bronchial 

provocation with wood dust, although no quantitative 

measurements were reported . No immunologic testing was done. 

Treatments for desensitization with extracts of cocobolo in one 

patient and of a cocobolo-padauk mixture in the other two 

produced a reduction in skin reactions and appeared to bring 

about clinical improvement . The author suggested that 

dalbergiones were the allergenic factor . 

Pulmonary hypersensitivity was reported in two workers, both of 

whom experienced cough, wheezing, and difficulty in breathing 

when working with this wood, and one of whom had similar 

symptoms at night . Upon bronchial challenge with an aqueous 

extract of abiruana, one worker had both immediate and late 

responses whi Ie the second worker had only an immediate 

response . Both workers had positive intradermal tests with 

abiruana dust but did not exhibit serWR precipitins against 

aqueous or alcohol extracts. Authors suggested that the 

reactions were mediated primarily by immunoglobulin E (lgE). 

(Cont inuedl 

-
w 

.... 

Table 4 (Continued) .--Selected case reports of allergic respiratory effects caused by wood dust 

Reference 

Chan-Yeung and 

Abboud 

(1976) 

doPico 

(1978) 

Bush et al. 

(1978) 

Gi rard et al. 

(1980) 

Wood types 

Cal i fornia 

redwood 

Cal i fornia 

redwood 

African 

zebrawood 

Mahogany, 

teak, okoume, 

plywood 

COIIments 

Two asthmatic male patients who developed specific immediate 

and late asthmatic reactions following bronchial challenge with 

redwood dust were described. Neither had skin reactions or 

precipitating antibodies against this wood. The authors 

suggested that low molecular weight compounds found in 

California redwood extracts, such as hydroxysugiresinol, sugiresinol, and isosequiric acid, may have been responsible for 

the respiratory symptoms. 

A male patient whose sensitivity was confirmed by a late 

asthmatic reaction to bronchial challenge of redwood sawdust 

was described. Skin prick tests were negative and precipitating 

antibodies were not found. 

Asthmatic attacks in a 26-year-old nale were reported. He 

reacted positively to intradermal testing with an aqueous extract 

of zebrawood dust, to which two atopic and two normal controls 

showed no response. In inhalation tests with this extract, both 

immediate and late bronchial responses were noted. The presence 

of IgE antibodies against the zebrawood extract was demonstrated 

by the direct radioallergosorbent (RAST) test and the RAST 

inhibition procedure. 

Asthmatic symptoms were described in four Swiss sanders. Skin 

patch testing was positive in each, and each exhibited serum 

antibodies and reduced ventilatory function to bronchial 

provocation. The authors also reported that in a survey of 96 

Swiss woodworkers (mean age 37 years, range 17-69 years; mean 

exposure duration 11.5 years), 56% had rhinitis, 17% 

conjunctivitis, 9% dermatitis, and 2% asthma. 

(Conti nued) 

-
.., 

N 

Table 4 (Continued).--Selected case reports of allergic respiratory effects caused by wood dust 

Reference Wood types 

Raghuprasad et al. Quillaja 

(1980) bark 

Innocenti and 

Angotzi 

(1980) 

Paggiaro et al . (1981 ) 

Bush and Clayton 

(1983) 

Sambe 

Tanganyika 

aningre 

Central 

Amer ican 

walnut 

Corrments 

A case of asthma and rhinitis in a 24-year-old male was 

described. Allergic react ion was confirmed by positive 

methacholine challenge and immediate reaction to bronchial 

challenge with Quillaja bark dust . Presence of IgE antibodies 

was demonstrated by RAST. 

A case of occupat ional asthma was described in a 57-year-old 

male. Patient exhibited immediate response to bronchial 

challenge . 

Three cases of occupational asthma in woodworkers were 

described . Intradermal sk in tests in each were positive . Bronchial provocation with the wood dust and aqueous extracts 

caused immediate response in two of the patients; these two also 

exhibited bronchial hyperreactivity . No serum precipitins or 

specific IgE was found in any of the patients. 

A case of asthma and rhinitis was reported in a 48-year-old male 

who exhibited immediate and late responses to bronchial 

challenge with wood dust extract . Intradermal skin testing with 

walnut wood extract was negative. Specific IgE antibodies and 

precipitins in the serum were not detected. 

(Cont i nued) 

-
(.oJ 

(.oJ 

Table 4 (Continued).--Selected case reports of allergic respiratory effects caused by wood dust 

Reference 

Hinojosa et al. 

(1984 ) 

Malo et al . (1986) 

Cartier et al. 

(1986) 

lood types ConInen t s 

African maple Two male patients who developed symptoms of sneezin9, 

rhinorrhea, nasal itching, and shortness of breath several 

months after beginning exposure to African maple wood dust were 

described. Type I hypersensitivity was demonstrated by positive 

skin test reactivity, positive IgE ant ibodies, and immediate 

bronchial provocation test response to aqueous extract . No 

precipitins to aqueous extracts were found in the patients' 

blood. 

Spruce, fir, 

pine 

Eastern 

whi te cedar 

Occupational asthma was reported in 11 male sawmi II workers aged 

21 to 57 who were exposed to spruce, fir, and pine. Duration of 

exposure and symptomatology ranged from 1.5 to 40 years and 0.5 

to 10 years, respectively . Diagnosis was confirmed by 

significant changes in serial peak expiratory flow rates as 

compared to off work and significant changes in bronchial 

responsiveness to histamine at work as compared to off work. 

Seven of the workers exhibited immediate skin reactivity to 

mixed tree pollens. Bronch ial provocation tests with sawdust 

were negative in four of the workers . 

A 39-year-old female who developed symptoms of occupational 

asthma a few weeks after starting work in a shingle- manufacturing sawmill was described . Bronchial challenge with 

eastern white cedar, Western red cedar, and plicatic acid each 

caused an isolated late asthmatic reaction. Elevated specific 

IgE levels to pl icatic 'acid were found . Cross reactivity 

between Western red cedar and Eastern white cedar was 

demonstrated. The authors estimated that the latter has half 

the plicatic acid of the former. 

-
, 

Table 5.--Comparison of Type I and Type I I I allergic responses· 

Type I 

(Allergic asthma) 

Predisposing factors: Atopy 

Region affected: Ai rways of the lungs, bronchi to terminal 

airways 

Onset of symptoms: Immediate and/or late 

Systemic reaction: None 

Serological findings: Raised IgE 

Pulmonary impairment: Increased air flow 

resistance (decrease 

in FEV,) 

Eosinophi lia: Common 

Skin tests: Immediate wheal and 

flare 

Sensitivity: 

Mechanism: 

*From Gamble ('979). 

Extreme sensitivity 

to bronchoconstrictive 

action of inhaled 

histamine and 

methacholine 

Antigen: IgE-induced 

release of pharmacologic mediators 

from mast cells 

Type II I 

(Extrinsic allergic alveolitis) 

None known 

Same as asthma (middle and 

terminal airways) plus alveolar and interstitial 

tissue 

Usually after 4-6 hr 

Usual; accompanied by fever, 

chills, anorexia, tachycardia, tachypnea 

IgE normal; IgG precipitins 

may be present 

Reduced FVC·· and FEV,**, 

reduced diffusion, decreased 

compliance 

Transient and uncommon 

Edematous reaction 4-6 hr; 

skin test not of much value 

because most antigens are 

locally irritating 

Precipitating antigen-antibody 

complex and complement produce an Arthrus skin 

reaction but pulmonary lesions of the Arthrus type 

have not been observed 

··FVC=forced vital capacity; FEV,=forced expiratory volume in one second. 

34 
• 

challenges with Cedar of lebanon (Greenberg 1972), California redwood 

(Chan-Yeung and Abboud 1976; doPico 1978), abiruana (Booth et al. 1976) , 

Tanganyika aningre (Paggiaro et al . 1981), and Central American walnut (Bush 

and Clayton 1983) . 

Since antibodies are associated with the skin, the presence of specific 

antibodies can often be demonstrated by intradermal testing with the 

suspected allergen . If specific antibodies are present, there is an 

irrmediate wheal and flare reaction characteristic of cutaneous anaphylaxis . 

Such reactions to wood dust have been demonstrated in studies of i roko 

(Pickering et al. 1972), cocobolo (Eaton 1973), abi ruana (Booth et al . 

1976), and Tanganyika aningre (Paggiaro et al. 1981), but not in studies of 

oak , mahogany, and cedar (Sosman et al . 1969) , Cal i foroia redwood 

(Chan-Yeung and Abboud 1976; doPico 1978), and Central American walnut (Bush 

and Clayton 1983) . Carosso et al . (1987) reported that the prevalence of 

skin reactions to wood dust extracts (walnut , obeche, Douglas fir and other 

Abies spp., mansonia, chestnut, framire, white poplar, and oak) was 

significantly (p<0 .OOO1) greater in a group of asthmatic woodworkers than in 

a group of healthy woodworkers. 

Some authors have suggested that the sensitizing agents are chemicals 

endogenous to the wood because bronchoconstr ict ion has been produced in 

sensitized workers by inhalation challenges with aqueous or alcohol extracts 

of various woods, including oak, mah09any, and cedar (Sosman et al. 1969); 

abiruana (Booth et al. 1976); iroko (Pickering et al. 1972); and African 

zebrawood (Bush et al. 1978). 

The most frequent Iy reported and thoroughly studied allergic reaction to 

wood is that caused by exposure to Western red cedar (WRC) , Thuja plicata. 

The chern i st ry of WRC has been e I uc i da ted by Barton and MacDona I d (1971) . 

The first recognition of WAC-induced asthma is generally credited to Ooig 

(1949). WAC was also one of the woods mentioned by Ordman (1949a) and 

Pickering et al. (1972) in their previously described reports. Other 

reports of WAC asthma have been published by Milne and Gandevia (1969), 

Gandevia and Mi Ine (1970), Gandevia (1970) , Mitchell (1970), Ishizaki et al. 

(1973), Mue et al. (1975a,1975b). Hamilton et al. (1979), Cockcroft et 

al. (1979,1984), and Blainey et al. (1981). The most systematic 

characterization of WRC asthma has been made by Chan-Yeung and colleagues 

(Chan Yeung et al. 1971; Chan-Yeung 1973; Chan-Yeung et al. 1973; Chan-Yeung 

1977; Chan-Yeung et a I. 1978; Ash I ey et a I. 1978; Chan-Yeung et a I. 1980; 

Chan-Yeung 1982; Chan-Yeung et al. 1982; Tse et al. 1982; Lam et al. 1983; 

Chan-Yeung et al. 1984; Vedal et al. 1986). 

The composite clinical picture of WAC asthma described in these studies is 

as follows: 

(a) Proportion of workers affected: 

individuals. 

approximately 5% of exposed 

(b) Interval between first exposure and symptoms: weeks to years. 

35 
, 

(c) Symptoms: the first noticeable signs and symptoms included eye and 

nasal irritation, watery nasal obstruction, excessively runny nose, 

rhinorrhea, sneezing, cough, wheeze, and chest tightness. Generally these symptoms were worse at night, with those from bronchi and 

bronchioles tending to require more exposure to WRC than those from the 

upper respiratory tract. Relief occurred over the weekend. With 

cont i nued exposu re, the signs, such as paroxysma I cough and wheez i ng, 

became progressively worse, occurring in the afternoon, and in some 

cases immediately upon exposure, as well as in the evening. If exposure 

continued, the signs and symptoms continued during weekends, so that the 

syndrome resembled chronic asthma, or asthma with bronchitis. 

(d) Pulmonary function: Airway obstruction and hyperinflation were 

variable in asymptomatic workers with WRC asthma. The bronchial 

challenge of sensitized individuals is the only method of confirming the 

d i agnos is, and in sens i t i zed i nd i v i dua Is, it resu Its in (1) a de I ayed 

asthmatic reaction (maximum reduction in forced expi ratory volume in one 

second [FEV1] and forced vital capacity [FVC] in 4-8 hr lasting 

24-48 hr); (2) an immediate asthmatic reaction (diminished FEV1 and 

FVC within minutes of exposure, but return to preexposure values within 

1 to 2 hr); or (3) a dual asthmatic reaction, a combination of the 

delayed and the immediate reactions. The delayed response was most 

frequently observed, but with continued or intensified exposure the 

early response was evoked in individuals who previously had had only the 

de I ayed response. Thus, the pattern of response was 

concentration-related, at least in the sense that signs and symptoms 

intensified with increasing length of exposure. Persistence of asthma 

after cessation of exposure remains in about one-half the individuals. 

(e) Chest radiograph: 

bronchial challenge. 

Normal in asymptomatic individuals and upon 

(f) Skin testing: No apparent relation between skin sensitivity and 

respiratory changes. 

(g) Smcking and history of atopy: There was no positive association 

between smoking status and history of asthma. Among the cases studied 

there 'were more nonsmokers and exsmokers than active smokers, and more 

individuals with no prior history of asthma than of those with such a 

history. 

(h) No precipitating IgG antibodies in the serum of sensitized 

individuals. Circulating IgE antibodies were present in about one-third 

of the individuals. 

( i) Va r i ab lei nc reases in eos i noph i I s we re seen in sens i t i zed 

individuals. 

Chan-Yeung et al. (1973) identified a low molecular weight (ca. 400 daltons) 

organic acid that makes up about 40% of th~ nonvolati Ie components of WAC as 

the causati'le agent for WRC asthma, although another study (Mue et al. 

1975a) impl icated protein found in WRC. Because Chan-Yeung et al. (1973) 

36 
, 

considered the organic acid unique to WRC, they named it plicatic acid after 

the species name. Plicatic acid has since been isolated from and identified 

as the causal agent of asthma caused by eastern white cedar (Thuja 

occidental i s) (Cart ier et al . 1986) . Chan-Yeung et al . (1980) showed that 

pi icat i c acid activates complement and generates chemotactic activity in 

pooled normal human serum . The authors proposed that the acid could 

activate complement in vivo, thereby inducing an inflammatory response in 

the lungs . Chan-Yeung (1982) and lam et al . (1983) have also suggested that 

nonspecific bronchial hyperreactivity is s i gnificant in the pathogenesis of 

WRC asthma, particularly in the characteristic late asthmatic reaction. 

Several surveys of WRC workers have been reported. NIOSH conducted a health 

hazard evaluation at a wood products facility in Washington State (Edwards 

et al. 1978). Results were subsequently reported by Brooks et al. (1981). 

Seventy-four shake mi II workers exposed to WRC, 58 planer mi II workers 

exposed primari Iy to fir, hemlock, and alder, and 22 clerical and technical 

workers not exposed to wood dust were surveyed . A medical questionnaire, 

limited physical examination, and pulmonary function testing were 

administered ; personal air sampling was also conducted. WRC-exposed workers 

exhibited a si9nificant (p<0 .OO1) decrease in FEV1 between Monday preshift 

baseline and postshift tests . The planer mi II and office worker groups did 

not exhibit a simi lar reduction . No significant relationship between 

duration of employment and FEV1 was noted in any of the three groups. 

Occupational asthma (defined as an observed decl ine in FEV1 of greater 

than 10% from the Monday preshift baseline compared to one or ~re 

subsequent tests during any of the following three days and a positive 

cl inical history suggesting asthma) was diagnosed in 10 of 73 (13.5%) WRC 

workers, 3 of 58 (5 .2%) planer mi II workers , and none of the controls . 

Chan-Yeung et al. (1978) and Ashley et al. (1978) reported on a two-part 

respiratory survey of WRC workers. In the first part of the survey 

(Chan-Yeung et al . 1978) , 405 cedar-exposed workers and 252 controls exposed 

to wood dust other than cedar (pr imar i Iy hem lock, fir, and spruce) were 

examined. A medical and occupational questionnaire was administered and 

spirometric measurements (FEV1, FVC , and maximum expiratory flow rate) 

were taken. The cedar workers had a higher prevalence of respiratory signs 

and symptoms, including cough, phlegm, wheezin9, and breathlessness , as wei I 

as more rhinitis and conjunctivitis. However, there was no difference in 

lung function between cedar workers and controls . Although quantitative 

data on smoking habits were not avai lable, a correlation between respiratory 

symptoms and cigarette smoking was shown and a synergistic effect between 

cedar dust exposure and smoking was suggested. The controls who had 

previously been exposed to WRC (65 out of 252) had higher prevalence of 

respiratory symptoms than the other controls . In the companion report, 

Ashley et al . (1978) reported that the prevalence of chest symptoms in cedar 

workers increased with duration of exposure and that the decline in 

venti latory function was greater, but in both groups smoking was a more 

significant determinant . A large number of cedar workers and controls noted 

improvement when away from work. 

In a companion report to their survey, Ashley et al . (1980) reported higher 

serum alpha1-antitrypsin (A1-AT) concentrations in the noncedar 

37 
• 

woodworkers than in the cedar workers, although dust concentrations to which 

both groups were exposed were simi lar. Differences were independent of 

smoking habits. In addition, there was a strong correlation between serum 

A1-AT levels and duration of employment in the noncedar workers . The 

authors suggested that their results might be due to either an 

industry-specific factor, the characteristics of the dust, or dust 

concentration, but they could offer no explanation of the underlying 

mechanism. 

Chan-Yeung et al. (1984) compared a group of 652 cedar mi II workers to a 

group of 440 male office workers not exposed to air contaminants. A medical 

and occupational questionnaire was administered, and spirometric 

measurements, allergy skin prick tests, and methachol ine inhalation 

challenge tests were conducted . When controlled for differences in age, 

race, and smoking, cedar workers had significantly (p<O.OO1) higher 

prevalence of chronic cough, phlegm, and dyspnea. Physician-diagnosed 

asthma was not significantly greater among the cedar workers, but 

worker-reported asthma was greater. Cedar sawmi II employment was strongly 

associated (p<0.001) with lower levels of lung function as measured by 

FEY1 and FVC. The effect of cedar exposure was consistent Iy greater than 

the effect of current smoking. Among nonatopic workers, bronchial 

hyperreactivity (defined as a PC20 [methachol ine provocation concentration 

causing a 20% decrease in FEY1] of 8 mg/mL or less) was more common in 

cedar workers than in office workers . However, no difference between cedar 

and office workers was seen in the atopic individuals. Bronchial 

hyperreactivity increased with duration of employment in cedar workers but 

not in office workers . The authors calculated that the estimated odds of 

bronchial hyperreactivity for cedar workers increased by a factor of 1.30 

for each 10 years of employment (p=0.OO6). Chan-Yeung et al. 's (1918) 

earl ier survey did not show lower levels of lung function in cedar workers 

versus those exposed to other wood dusts . The authors suggested that the 

results of thei r latest survey meant that exposure to other wood dust may 

not be harmless or that an uncontrolled factor associated wi th wood mi II 

employment may also be associated with lower levels of lung function. 

Veda I et al. (1986) evaluated the association between pulmonary function and 

dust exposure in WAC workers. Their survey of 652 WRC sawmill workers 

included Ii respi ratory and occupational questionnai re and spi rometry test. 

Each worker was assigned an exposure level based on area and personal 

sampling for total dust. Total dust concentrations ranged from undetectable 

to 6.0 mg/m3 . Of the 334 workers assigned dust levels, only 33 were 

exposed to concentrations greater than 1 mg/m3 , and of those only 13 were 

greater than 2 mg/m3 . Work-related asthma, defined as asthmatic symptoms 

that improved on days off, was seen in 52 (8%) workers and was more 

prevalent with 10 or more years of employment (estimated odds ratio 2.1). 

When height, age, race, and cigarette smoking were controlled for, levels of 

venti latory function were related to dust exposure but not to duration of 

etnployment. FEV1 and FVC were significantly (p<0.05) lower in workers 

exposed to dust concentrations of 2 mg/m3 or more, but no relationship was 

seen between FEF2~-15% or FEV1/FVC and dust concentrations. The authors 

indicated tha.t thiS association was based on only 13 workers and must 

therefore be interpreted cautiously. However, if correct, it would indicate 

38 
, 

a pattern of restriction rather than ai rflow I imitation . Exposures above 

3.0 mg/m3 were also associated with eye irritation (p=0.02) . 

Not all reactions resembl ing allergic responses that have been reported in 

woodworkers have resulted from chemicals inherently present in the wood. 

Allergy- I ike effects on the lower resp i ratory tract have also been 

attributed to the inhalation of mold and fungal spores during the processing 

of contaminated wood products. These effects include maple bark disease 

caused by inhalation of Cryptostroma corticale (Towey et al . 1932; Wenzel 

and Emanuel 1967), wood pulp worker's disease caused by Alternaria 

(Schlueter et al. 1972), sequoiosis caused by inhalation of redwood sawdust 

contaminated with Pullularia (Cohen et al. 1967), and suberosis caused by 

Penicillium freguentans, a contaminant of cork (Pimentel and Avila 1973; 

Avi la and Lacy 1974) . Simi lar reactions have been attributed to wood dust 

contaminated with Bacillus subtilis (Johnson et al. 1980) and Trichoderma 

and Scopulariopsis (Halprin ·et al . 1973). These disorders are often 

referred to as extrinsic allergic alveol itis (EAA) or as hypersensitivity 

pneumonitis because of the marked interstitial inflaJllllatory changes that 

accompany them (Kaltreider 1973). Table 5 I ists some of the characteristics 

of EAA. A review of EAA has been made by Mol ina (1984) . The allergic 

responses produced by these microorganisms resemble the reactions caused by 

the inhalation of organic dust, such as moldy hay, in farmer's lung 

disease. The allergic response in farmer's lung disease is a Type III 

reaction in which the subject develops antibodies that react with antigens 

to form il1ll1une complexes, damaging vascular endothel ial and other tissues 

either at the site of the reaction or at some remote site. Common signs and 

symptoms in acutely i II patients include malaise, sweating , chi lis, fever, 

loss of appetite, breathlessness, and a sense of tightness in the chest. 

Dyspnea and cough are the prominent si9ns in chronic cases where there is 

irreversible lung damage. 

Signs and symptoms of extrinsic allergic alveolitis were described by Howie 

et al . (1976) in a patient exposed to ramin wood dust. The 34-year-old man 

was a nonsmoker who had experienced episodes of breathlessness, coughing, 

shivering, sweating, and fatigue for 2 years after heavy exposure to ramin 

dust . He was asymptomatic on weekends and holidays. His physical 

exam i nation, chest x-rays, blood tests, and pulmonary function tests were 

normal. He showed no hypersensitivity in prick tests with common allergens 

or ramin dust. Precipi tins to sal ine extracts of fresh ramin dust were 

found in his serum. Lung function tests showed a signi ficant (p<0.OO25) 

reduction in FEY1 4-6 hr after he was exposed to ramin dust at high 

concentrations, with return to baseline values after 24 hr. The authors 

attributed the reduction in FEY1 to a true impai rment of gas flow, since 

there was no significant rise in carboxyhemoglobin levels or alterations in 

computed alveolar volumes . They concluded that ram i n dust was capable of 

producing a cl inical syndrome simi lar to that of extrinsic allergic 

a I veo lit is. 

As part of their survey of Swedish furniture workers (see also Section Y), 

Wi Ihelmsson et al. (1984,1985b) conducted a survey of nasal allergies among 

268 workers at 6 wood furniture factories in southern Sweden . Sixteen 

percent of the workers (mean exposure duration 12 years) had a history 

39 
compatible with hypersensitivity. Based on skin prick and bronchial 

provocation tests, the authors reported that 2% of the workers were allergic 

to wood dust and 3% to molds found in the workplace. The most common mold 

was Paeci lomyces spp. Although providing no quantitative data, the authors 

estimated that both these figures were higher than would be found in the 

general population. 

Alexandersson et al. (1986) reported decl ines in FVC and FEV1 averaging 

0.3-0.4 L in Swedish wood trimmers exposed to high concentrations of molds 

(105-106 colony-forming units/m3), but not in trimmers exposed to mold 

levels 10 to 100 times lower. 

A case of acute respi ratory illness attributed to inhalation of wood chip 

dust contaminated with toxins from unspecified microbial species has also 

been reported (Centers for Disease Control 1986). The illness, which 

affected 5 of 11 exposed workers at a municipal golf course, was classified 

as "organic dust toxic syndrome" (ODTS). None of the workers had positive 

reactions to a standard battery of wood chip and wood chip microbe antigens. 

Summary 

Asthmat ic react ions (reversible ai rway obstruct ion) to a variety of both 

domestic and foreign woods have been reported. Immunological findings in 

individuals with wood-dust-induced asthma vary. In some cases, a Type I 

allergic reaction was confirmed by the presence of IgE antibodies. Positive 

skin reactions and the presence of precipitating antibodies to wood dust or 

extracts have also been reported, but not universally. 

The most thoroughly studied allergic respi ratory reaction to wood is WAC 

asthma. It is estimated that 5% of the exposed population is sensitive to 

this wood. Workers exposed to lAC have exhibited an increased prevalence of 

respi ratory signs and symptoms when compared to workers exposed to no or 

other types of wood dust . These symptoms increased with exposure duration. 

Decreased venti latory function, as measured by FVC and FEV1, has been 

demonstrated in workers exposed to WAC compared to those not exposed. 

However, no di fference was seen between workers exposed to WRC and those 

exposed to other wood dusts. Only a single study relating WAC dust 

concentrations to venti latory function was found; in that study 

concentrations of 2 mg/m3 or more were associated with significantly lower 

FVC and FEV1 levels. 

Another allergic respiratory effect related to wood dust is extrinsic 

allergic alveolitis, which is a Type III allergic reaction. This reaction 

is associated not wi th pure wood dust, but rather wi th exposure to wood 

contaminated by microbial species. 

40 
V. MUCOSAL AND NONALLERGIC RESPIRATORY EFFECTS 

This section summarizes studies that have examined changes in the 

structure and function of the nasal mucosa and respiratory tract due to 

exposure to wood dust. Respi ratory effects that have been identi fied as 

a II erg i c react ions (such as asthma and hypersens i t i v i ty pneumon it is) are 

discussed in Section IV. 

Bellion et al. (1964) reported pulmonary abnormalities among carpenters, 

sawmi II workers, and woodworkers exposed to chestnut, teak, rosewood, 

mahogany, birch, and kejaat. Exposure duration ranged from 3 to 

24 years. Among 225 workers examined, 97 were found to have radiologic 

evidences of pulmonary abnormality. The most frequent finding was an 

accentuation of bronchovascular markings. In 9 of 79 workers studied in 

some detail, the most apparent radiologic change was micronodular shadows, 

resembl ing those found in mi I iary tuberculosis, scattered throughout the 

entire pulmonary field. 

Simi I ar find i ngs were reported by d' Agost i no et a I. (1965), who descr i bed 

a case of di ffuse pulmonary fibrosis secondary to pneumoconiosis in a 

woman who had worked in a sawmill for 15 years. The patient complained of 

coughing and dyspnea, with moderate expectoration, for about 3 years. 

Radiographs of her lungs contained shadows indicating that small nodules 

were disseminated throughout the lungs and that they were accompanied by 

diffuse reticulation. 

Michaels (1967) described pathological changes in the lungs of two 

deceased Canadian workers who had been exposed to wood dust for 10 and 

12 years, respectively. The cause of death in both cases was unrelated to 

the lung conditions. Both workers had developed centri lobular fibrosis 

and emphysema. Michaels discovered within the alveoli of the lungs 

microscopic basophi I ic particles, thought to be grains of wood dust that 

had caused a foreign body and histiocytic reaction. Sections of lungs 

from 21 other patients who had worked in the Ontario timber industry for 

unknown lengths of time and at unknown concentrations of wood dust were 

also examined. No particles simi lar to those found in the lungs of the 

first two cases were seen. 

As part of their research on nasal cancer among British woodworkers, 

Hadfield (1969) and Hadfield and Macbeth (1971) examined the nasal 

passages of several thousand workers in furniture factories. They 

documented various mucosal changes, including metaplasia. Because of the 

relationship of these changes to carcin0genicity, they are discussed in 

more detail in Section VI . 

41 
Ruppe (1973) examined 140 East German woodworkers (average age 36.8 years) 

exposed to exotic woods (species not named) for periods ranging from 4 to 

more than 10 years. Ruppe found an increased incidence of coughing and 

expectoration, colds and sneezing, sinusitis, nasal mucosal irritation, 

and reduced venti latory function after acetylchol ine challenge compared to 

a control group of 73 workers (average age 42.5 years) not exposed to wood 

dust. All of the above symptoms, except for the positive acetylchol ine 

challenge, were seen even among the 14 workers exposed to wood dust 

concentrations below 5 mg/m3 . However, this number of subjects was too 

small to permit statistical analysis. 

Black et al. (1974) studied nine woodworkers (average age 56 years, range 

48-66) from a single factory in High Wycombe, England. Three were 

nonsmokers; four were light-to-moderate smokers. Mucoci liary transport 

rates were measured by the movement of polystyrene spheres irreversibly 

labeled with 99mtechnetium that had been placed at the center of the 

anterior end of the middle turbinate. Transport rates in 12 controls 

(average age 48 years, range 31-69; 8 nonsmokers, 3 moderate smokers, and 

1 pipe smoker), none of whom had been exposed occupationally to wood dust, 

ranged from 1.9 to 18.5 nvn/min, with a mean of 6.8 am/min. Additional 

information on normal mucoci liary transport rates were obtained from four 

other studies cited by Black et al. (1974). In these four studies, a 

total of 126 normal subjects had exhibited a mean rate of 7.8 am/min. 

Mucociliary movement in the group of nine woodworkers was severely 

depressed. During a 3O-min observation period, three of the woodworkers 

had no discernible movement and four others had only sl ight transport of 

the labeled spheres. Only the remaining two woodworkers had sufficient 

movement to yield estimates of the transport rate; these were calculated 

to be 2.7 and 1.0 nvn/min, respectively. Only the former rate was within 

the range of values measured in the controls. This worker had been 

exposed to wood dust for the shortest time, 6 years. The investigators 

concluded that exposure to wood dust in the furni ture industry for 10 

years or more can impair mucoci liary clearance at the anterior end of the 

middle turbinate. 

Solgaard and Andersen (1975) and Andersen et al. (1976,1977) have 

described a study of 68 men (average age 41 years, range 17-66) in 8 large 

Danish factories producing wooden furniture and fixtures. Workers engaged 

in varnishing, painting, etc., and those who had had colds within the 

preceding 2 weeks were not used in the investigation. The wood dust 

exposure per iods ranged from 1 to 51 years, wi th an average of 16 years. 

A questionnaire on working conditions, symptoms, and smoking habits was 

answered by each worker. Examinations of the selected workers consisted 

of oral and nasal inspections, recording of FEV1 and FEF25-75% (forced 

expiratory flow during the middle half of the FVC), taking of a moist 

nasal swab, and determi n i ng the mucus transport rate us i ng the 

saccharine/sky blue method. A control group of 66 healthy persons (age 

range 18-47 years), 19 of whom were women, was studied by the same 

techniques as were the woodworkers. 

42 
, 

Wood dust concentrations were determined gravimetrically based on samples 

taken from the general work areas as well as from the breathing zones of 

the individual workers. For the latter, 43 of 68 measurements (63%) 

exceeded 5 mg/m3 and 19 (28%) exceeded 10 mg/m3 . For the general work 

area samples, 58% exceeded 5 mg/m3 and 23% exceeded 10 mg/m3. 

Measurement of particle size yielded a maximum in the 6-10 um range . 

During the measurements, 41 workers were engaged in sanding by hand or by 

machine and 27 in sawing, planing, or drilling. The average 

concentrations of dust for these two groups were 14.3 and 5 .2 mg/m3 , 

respectively. Teak was the primary wood used on the day of examination, 

followed by oak, chipboard, pal isander, mahogany , jakaranda, beech, and 

pine . The most frequent complaints by the workers were dryness in the 

nose, irritation of the eyes, nasal obstruction, protracted colds, and 

frequent headaches. For comparison purposes, the workers were placed into 

two groups, those exposed to wood dust concentrations below 5 mg/m3 

(Group I; 25 workers) and those exposed above 5 mg/m3 (Group II; 

43 workers) . Both groups had simi lar age distributions, length of wood 

dust exposure, and smoking habits. Middle-ear inflaJM1ation and conrnon 

colds occurred significantly (p<0.05) more often in Group II. Sinusitis, 

prolonged colds, asthma, itch i ng or bleeding nose, sneezing, and nasal 

obstruction were more prevalent, but nonsignificant, in Group II. No 

relationship was found between symptoms and the type of work performed, 

age , or length of employment . FEV1 and FEF25_75% values measured for 

the workers did not differ significantly from normal calculated control 

values , nor were there any sp i rometric differences between Groups I and II. 

The mucociliary transport rate was significantly (p<0.05) lower among the 

68 woodworkers than among the 66 controls. Among the latter, only 9 (14%) 

had times longer than 40 min (defined as mucostasis) for transport of a 

particle of saccharin from the superior surface of the inferior turbinate 

to the pharynx whereas 26 (38%) of the woodworkers had transport times 

greater than 40 min. The fraction of workers with mucostasis increased 

with increasing concentration of wood dust: 63% of those exposed to the 

highest mean wood dust concentration of 25.5 mg/m3 had mucostasis 

whereas only 11% of those exposed to the lowest mean concentration 

(2 .2 mg/m3 ) had mucos tas is . I n Groups I and II , 20% and 49%, 

respectivel.y, had mucostasis. Nine subjects who had mucostasis during the 

study were reexamined in their homes after a 48-hr weekend without 

exposure to wood dust. Six of these individuals then had normal mucus 

transport times, but three sti II had mucostasis . Inert plastic dust 

particles (25 mg/m3 ) with a size distribution simi lar to that of the 

beech dust did not change the mucoci liary transport rate. Andersen et al. 

(1977) therefore concluded that the mechanical effect of the dust was not 

the cause for the mucostatic effect of the wood dust. 

Andersen (1986) subsequent Iy reported on a controlled exposure chamber 

study in which healthy volunteers (prior wood dust exposure , if any, 

unspec if i ed) we re exposed to dus t from pine, beech, oak, mahogany, 0 r 

chipboard at a concentration of 10 mg/m3 . The size distribution ranged 

from 1.6 um to 14.9 um with a maximum of approximately 30% from 4.9 um to 

8 .0 um . No effect on mucoci I iary clearance was seen following a 5-hr 

exposure . However, based on qual i tat ive discomfort responses made by the 

43 
exposed volunteers, wood dust was reported to be almost four times more 

irritating than plastic dust at the same 10 mg/m3 exposure concentration 

for 4 hr . Referring to his earl ier nasal clearance study (Andersenet al. 

1976,1977), Andersen (1986) indicated that controlled exposure chamber 

studies of acute effects on heal thy subjects cannot always be used to 

predict chronic workplace effects . 

Werner (1979) reported the results of rhinolaryngologic examinations of 

226 workers (103 men, mean age 37.1 years; 123 women, mean age 36.7 years) 

at a furniture pressboard manufacturing plant in Leipzig. Eleven percent 

of the subjects had worked for less than 2 years and over 7S% had worked 

for more than S years. The woods used included pine, fir, beech, oak, 

ash, birch, a I de r , mahogany, manson i a, and okoume. Wood dus t 

concentrations were reported only as being below the 1979 German MAC 

values, and there was concomitant exposure to formaldehyde at 

concentrations averaging 3 to 4 times the MAC value. Chronic inflammatory 

changes in the nasal mucous membranes were seen in 143 (63.3%) workers. 

These findings were signi ficant (p value unspeci fied) when compared to a 

control group of 104 individuals (60 men, mean age 41.4 years; 44 women, 

mean age 3S.S. years) not exposed to either wood dust or formaldehyde. 

Fifteen (6%) workers had a decreased sense of smell and five (2.2X) were 

anosmic. Fifteen of the 20 cases of decreased or absent sense of smell 

were associated with chronic inflammatory changes in the nasal mucosa. 

This indicated to the author that these effects were due primari Iy to 

changes in the upper respiratory tract rather than to the nervous system. 

Cytological and histological examination demonstrated severe metaplasia in 

an unspecified number of workers. 

Chan-Yeung et al. (1980) conducted a respiratory survey that included 

medical-occupational questionnaires, limited physical examinations, 

spirometry, and chest x-rays of 1,932 workers in a pulp and paper mill in 

British Columbia, Canada. The results obtained from 1,826 white male 

workers were analyzed . The authors reported that workers exposed to wood 

dust (mean total dust concentration of o.s mg/m3 , range from less than 

0.1 to 2.7 mg/m3 ) had a slight but statistically significant (p<O.OS) 

decrease in pulmonary function values (FYC and FEY,) compared to 

controls !lfter adjustments were made for differences In age, height, 

duration of employment, smoking habits, and alcohol intake. Because the 

workers were also exposed to small amounts of the chemical wood 

preservat i ves pentach loropheno I and tet rach loropheno I (max iAlum 

concentrations 0.118 mg/m3 and 0.08 mg/m3 , respectively), the authors 

concluded that wood dust or the chemical preservatives were responsible 

for the deleterious effects seen. 

AI Zuhair et al . (1981) examined ventilatory function among 124 British 

workers exposed to wood dust. At one of two furniture factories , where 

mean total dust and mean respi rable dust concentrations ranged from 1.36 

to 8.29 mg/m3 and 0.19 to 0.44 mg/m3 , respectively, a statistically 

significant (p<O.OS) decrease in FYC and FEY1 was seen during the 

workshift. Other venti latory measurements were too variable to discern a 

pattern. At the other , less dusty furniture factory (mean total dust 

concentrations of 0 .46 to 4.16 mg/m3 ) and in an inoperational power 

44 
, 

station, no such change was observed. No concentration-response 

relationship was seen at any of the work si tes between exposure 

concentrations and changes in FVC and FEV1, although those workers 

exposed to the highest wood dust concentrations in the first factory 

tended to show the largest drop. 

Whitehead et al . (1981a) presented the results of a cross-sectional survey 

of 1,157 American woodworkers at ten companies exposed to either hardwood 

(predominantly rock maple, with some ash and oak) or softwood (white 

pine). The survey included basic spi rometric pulmonary function tests 

(FVC, FEV1, and maximal mid-expiratory flow rate [MMEFR]), pulmonary 

symptom and smoking history questionnaire, and a work history. 

Approximately 100 dust measurements were taken.. These were used to 

construct a personal relative dust exposure index by multiplying average 

departlllental dust concent rat ions times the number of years the worker 

spent in each department. Workers were grouped by indices as follows: 

low (0-2 mg-years/m3), medium (2-10 mg-years/m3), and high 

(10+ lIlQ-years/m3 ). After elimination of workers in certain departments 

where exposure to chemicals and dusts other than wood occurred, the 

results from 574 workers were analyzed. To control for age, height, and 

sex, the authors used Knudson prediction equations. For both hardwood and 

softwood dusts , the authors found that exposure to higher versus lower 

dust concentrations was associated with statistically significant (p<0.05) 

higher odds for the occurrence of low pulmonary flow rates as measured by 

FEV1/FVC and MMEFR. Concentration-response effects were demonstrated 

for softwoods but only suggested for hardwood exposures. 

Beckman et al . (1980) examined a subgroup of 238 of the 1157 pine 

furniture workers studied by Whitehead et al . (1981) . Beckman and 

coworkers determined respi ratory dysfunction (defined ei ther as decreased 

pulmonary function below the fi fth percenti Ie of normals or as chronic 

cough or phlegm from questionnaire responses). They found a correlation 

between dysfunction and sex, age, and smoking, but no effect was seen for 

years of exposure to pine wood dust. This finding contradicted Whitehead 

et al.'s (1981) conclusions for pine workers, which Goldsmith (1983) 

suggested lIIay be due to the heterogeneous definition of pulmonary 

dysfuncti~n used by Beckman and coworkers. 

Goldsmith (1983) reported the results of a pi lot study of 94 workers, 55 

of whom had been exposed to wood dust, in a North Carolina hardwood 

furniture plant . The woods used were primarily oak, maple, walnut, 

mahogany, andiroba, poplar, and fiberboard. For a workshift, Goldsmith 

measured venti latory function, both basel ine performance and changes in 

respiratory flow. All mean work area wood dust concentrations except for 

carving operations were 2.0 mg/m3 or less. Mass mean aerodynamic 

diameters ranged from 2.4 urn to 23 urn; the fraction of dust less than 10 

urn in diameter ranged from 30% to 82%, depending on the operation. After 

adjusting for age, sex, height, and smoking, Goldsmith found no 

relationships between either current or cumulative wood dust exposures and 

FEV 1 ' FVC, FEFSO, FEF75, 0 r FEV 1 IFVC . Howeve r , peak f low did 

correlate significantly (p=0.0345) with cumulative person-months of 

exposure, suggesting that inhalation of wood dust may impair large airway 

45 
, 

function. Changes in venti latory function over a workshift did not 

correlate with either job classification or mean cross-sectional 

particulate concentrations. Only a difference in FEV1 and FVC for 

finishing jobs suggested a weak correlation with finishing jobs that might 

implicate finishing fume or vapor exposure. 

Lukjan and Pregowski (1984) reported finding chronic obstructive lung 

disease (COPO) in 72 of 804 Polish woodworkers (332 men, 472 women). 

Among nonsmokers, the incidence rate (4.4%) was independent of 

formaldehyde concentration. Among smokers, the incidence rate was 3 to 4 

times higher and was also independent of formaldehyde. 

Wi Ihelmsson and Orettner (1984) examined 753 workers from 50 furniture 

factories in southern Sweden. The woods used were primari Iy hardwoods, 

including birch, beech, oak, mahogany, and teak. Wood dust concentrations 

were measured at six of the Rlants. The mean concentration was 

2.0 mg/m3 (range 0.30-5.06 mg/m3 ). The authors divided the 676 

respondents (mean age 53 years, mean exposure duration 27 years) into two 

groups, those with no or only slight exposure to wood dust (192) and those 

with moderate or heavy exposure to wood dust (484). In the group with 

sl ight exposure, 12% had perennial hypersecretion from the nose, 30% had 

perennial obstruction, and 9% had more than two cORlllon colds per year. 

The corresponding figures for the heavi Iy exposed group were 20%, 40%, and 

21%, respectively. All three di fferences between the two groups were 

stat i st i ca Ily sign if i cant (p<O .05). However, no s igni f icant di fference 

was noted in the incidence of sinusitis. 

The authors also performed the following examinations on selected 

subgroups of the woodworkers: rhi nomanomet ry, ai r-cond it ion i ng capaci ty 

of the nose, mucociliary clearance. and spirometry. Fifty workers 

underwent rh i nomanomet ry. Of these, 36 were exper i enc i ng nasa I 

discomfort. The difference between measured resistance value without 

decongestant and calculated normal value with decongestant was 

significantly (p<O.05) higher in the group with nasal problems. Also, the 

difference in nasal mucosal swelling measured before and after application 

of a decongestant indicated a nonsignificant increase in the group with 

nasal complaints. Fifty-seven workers exposed to fine wood dust underwent 

ai r-conditioning capaci ty tests. Thi rty-nine of these were experiencing 

nasal discomfort. No di fference between the two groups was seen; values 

measured were comparable to those of a normal group of subjects. There 

was also no di fference seen in nasal clearance between a group of 42 

workers with nasal discomfort and a group of 19 without. For the previous 

th ree tests, the authors made no compar i sons between wood-exposed and 

nonexposed workers. However, in the fourth test (spi romet ry), workers 

exposed to wood dust had a significantly (p<0.OO1) lower FVC than would be 

expected in a normal reference group. 

Additional reports of these Swedish furniture workers (Wi Ihelmsson and 

Lundh 1984, Wi Ihelmsson et al. 1985a) discuss changes in the workers' 

nasal epithel ium. Two other Scandinavian studies of the nasal mucosa of 

woodworkers have also been publ ished (Orettner and Stenkvist 1979; Boysen 

46 
, 

and Solberg 1982). Because of their significance to nasal cancer, these 

four studies are discussed in Section VI. 

Holness et al. (1985) examined the effects of wood dust on 50 Canadian 

cabinet makers. Fifty hospital support staff were selected as controls. 

The study protocol included work history, smoking habits, and a 

respiratory symptoms questionnaire; environmental sampling; nasal 

cytology; and pulmonary function testing. Mean total dust concentrations 

were 1.83 mg/m3 for the cabinet makers and 0.43 mg/m3 for the 

controls. The woodworkers reported more nasal and eye symptoms and more 

cough, sputum, and wheez i ng (32%) than did the cont ro I s (10%). A I though 

no significant differences were seen between nasal smears of the 

woodworkers and the controls, the former had more irritated columnar cells 

in their cytological smears. The woodworkers had a significant (p=O.OO1) 

decrease in venti latory function (FVC and FEV1) over the workshi ft. The 

workers also showed significantly (p=0.OO5) larger changes in FVC and 

FEV1 than the controls. Thi rty-one percent of the woodworkers had a 

greater than 5% decrease in FVC or FEV1 over the work shi ft as compared 

to only 13% of the controls (significant at p=O .039). Usin9 a cumulative 

dust exposure index simi lar to that of Whitehead et al. (1981), Holness et 

al. (1985) demonstrated a significant (p=O.OO8) inverse relationship 

between FEV1 and FEF75 and this index for both total and respirable 

dust. FVC showed a simi lar but nonsignificant trend. The authors 

suggested that increasing exposure to wood dust may be associated with a 

progressive deterioration in lung function. Decreases in venti latory 

function over the workshi ft were not related to measured dust 

concentrations (those with larger decreases tended to be exposed to lower 

concentrat ions). The authors suggested that this was due ei ther to the 

"healthy worker effect" (where there is a selection of workers who are not 

sensitive to the dust) or to the development of a dust tolerance by 

workers wi th higher exposure that causes them to have a less pronounced 

venti latory response. Since this was an observational rather than 

exper imenta I invest i gat ion, the authors reconrnended add it i ona I study to 

clarify this question. 

Innocenti et al. (1985) examined 13 male woodworkers (mean age 46.2 years; 8 smokers, 5 nonsmokers) from 2 Italian furniture factories where European 

chestnut 'was currently being used exclusively. The mean length of 

chestnut wood exposure was 4.8 years and of other wood dust exposure was 

21 years. Twenty-four male hospital workers (mean age 44.4 years; 

11 smokers, 13 nonsmokers) who had never been exposed to wood dust were 

used as controls. All subjects underwent rhinoscopy and an evaluation of 

their sense of smell. Trigeminal nerve impairment was not seen in any of 

the subjects; however, four workers and none of the controls were 

diagnosed with anosmia. This difference was significant (p=O.0108). There was a positive correlation between olfactory scores and previous 

exposure to wood dust, but not between olfactory scores and either age or 

previous exposure to chestnut wood dust. Two other reports of anosmia in 

workers chronically exposed to hardwood dusts were cited by Amoore (1986) 

in his review of the effects of chemical exposure on human olfaction. 

47 
, 

Sunmary 

Exposure to wood dust has been reported to cause both signi ficant and 

nonsigni ficant increases in respi ratory symptoms, including nasal dryness , 

i r rita t ion, bleed i ng, and obs t ruc t ion; cough i ng, wheez i ng, and sneez i n9 ; 

sinusitis; and prolonged colds . These increases have been seen even at 

mean total dust concentrations below 4 mg/m3 . Significantly reduced 

mucociliary transport rates have also been reported in workers chronically 

exposed to wood dust, and in one study the reduced rates were related to 

increasing dust concentrations . These effects were not seen following 

acute inhalation exposure, nor were they seen following inhalation of high 

concentrations of inert plastic spheres with a size distribution simi lar 

to that of beech dust. This implies that mucostasis results from 

long-term exposure and is not caused simply by the Ilechanical action of 

the dust, although such irritation may be a contributing factor. Nasal 

mucosa I changes have a I so been reported in woodworkers. Severa I stud i 88 

have reported decreased venti latory function, as measured by FVC and 

FEV1, among workers exposed to wood dust, although two other studies 

were negative . Two stud i es have also shown a significant decrease in 

woodworkers' lung function over the workshift, although no 

concentration-response relationship was seen. 

48 
, 

VI. CARCINOGENICITY 

This section sunvnarizes human case and epidemiologic reports on wood dust 

carcinogenicity. The section is divided into four parts, each concluded by 

a brief summary. Part A contains a discussion of preneoplastic nasal mucosa 

changes and nasal and nasopharyngeal cancer." Pulmonary cancer is discussed 

in Part B, Hodgkin's disease in Part C, and other cancers in Part D. Part A 

is further subdivided by country in which the studies were conducted, 

beginning with Great Britain, where the relationship between wood dust and 

nasal cancer was fi rst systematically examined . Studies conducted in the 

United States are discussed next, followed by those in Canada, Denmark, 

Sweden, Finland, Norway, Italy, France, East and West Germany, the 

Nether lands, Be Ig i um, Aust ria, Sw i tzer land, and Aust ral i a. Organ i zat ion by 

country was used to present the large number of studies reported in the 

literature because it allows one to follow chronologically the work of 

individual researchers in their respective countries. It also segregates differences that might result from exposure conditions unique to a 

particular country (e.g., type of wood). Parts B, C, and 0 are not divided 

into subparts, although within each, studies conducted in the United States 

are discussed first. 

The association between occupational exposure to wood dust and cancer has 

been reviewed in several references, which are cited herein. In 1981, the 

International Agency for Research on Cancer evaluated the avai lable data and 

concluded the following: 

There is sufficient evidence that nasal adenocarcinomas have been caused 

by employment in the furniture-making industry. The excess risk occurs 

mainly among those exposed to wood dust. Although adenocarcinomas 

"The term "nasal cancer" refers to ICO (1980) code 160, mal ignant neoplasm 

of the nasal cavi ties, middle ear, and accessory sinuses. "Nasopharyngeal cancer" is ICO code 147 . Included wi thin ICD code 160 are codes 160.0 

(nasal cavities); 160.1 (auditory tube, middle ear, and mastoid air cells); 

160.2 (maxillary sinus); 160.3 (ethmoidal sinus); 160.4 (frontal sinus); 

160.5 (sphenoidal sinus); 160.8 (other); and 160.9 (accessory sinus, 

unspecified). Histological classes of nasal cancer tumors include squamous cell carcinoma, adenocarcinoma, transitional cell carcinoma, 

esthesioneurocytoma, other carcinomas, melanoma, sarcoma (excluding lymphoma), lymphoma, and other mal ignant neoplasms (Redmond et al. 1982). 

For a discussion of the epidemiology of nasal and nasopharyngeal cancer, see 

Redmond et al. (1982) and Shanmugaratnam (1982), respectively. The terms 

used to describe the cancers discussed in this section are those used by the 

cited authors. 

49 
, 

predominate, an increased risk of other nasal cancers among furniture 

workers is also suggested . ... No evaluation of the risk of lung cancer 

is possible .... The epidemiological data are not sufficient to make a 

definitive assessment of the carcinogenic risks of employment as a 

carpenter or JOiner. A number of studies, however, raise the 

possibility of an increased risk of Hodgkin's disease. There is 

confl icting evidence about an association between nasal adenocarcinoma 

and work as a carpenter. The highest level of relative risk reported is 

much lower than that for cabinet-makers and other woodworkers in the 

furniture industry, and much of the evidence is anecdotal; the 

possibility that the reported cases of nasal cancer had worked in these 

industries could not be ruled out . The evidence suggesting increased 

risks of lung, bladder and stomach cancer comes from large 

population-based occupational mortality statistical studies and is 

inadequate to allow an evaluation of risks for these tumors. (IARC 1981) 

Wi lis (1982) analyzed data from 12 countries and calculated that more than 

three-fourths of the adenocarcinomas observed in areas where furniture 

making or other woodworking was a significant occupation had occurred in 

woodworkers . He concluded that machine sanding of hardwoods may entai I 

special risk and that his review of the data did not contradict the 

conclusions of IARC (1981) . 

Mohtashamipur and Norpoth (1983) reviewed data from ten countries and 

concluded that "epidemiological findings . .are in agreement that the 

woodworkers are at the most risk for [adenocarcinoma of the ethmoids and 

nasa I cav i ties] . " 

A review publ ished by the Health and Safety Executive of Great Britain 

concluded the following : 

The association between adenocarcinoma of the nasal cavity and sinuses 

and work with hard wood has been demonstrated repeatedly. In a few 

studies, exposure to soft wood dust has also been associated with a 

cancer of the nasal cavi ty, but on these occasions the tumours have 

differed histologically .... [I]t is not possible to conclude whether 

this is due to the di fferent nature of the softwood dust or to the 

presenee of added wood preservat i ves. . . . There are no dose response 

data for this condition . .. . [I]t is probable that the excesses [of 

Hodgkin's disease] observed were not artifacts. Dose data are not 

avai lable. . . .Gastro-intest inal cancer, lymphoma, leukaemia, mye loma, 

mal ignant melanoma, bladder cancer and non-melanoma skin cancer, have 

all been found to excess in various studies of woodworkers. The 

observations however, have been far from consistent and require to be 

confirmed. There are no dose data .. , (Greenber9 1986) 

A review prepared by the Ontario, Canada Ministry of Labour concluded the 

followin9 : 

Exposure to wood dusts is convincingly associated with the development 

of cancer of the nasal cavity and paranasal sinuses . The association 

has been observed in populat ions wi th exposure to ei ther hardwoods or 

50 
, 

softwoods and the offending agent(s) have not yet been identified .... 

There is no convincing evidence that exposure to wood dust increases the 

risk for any other type of cancer. No dose-response information is 

avai lable for wood dust and sino-nasal cancer. (Ministry of Labour 1986) 

A. Nasal and Nasopharyngeal Cancer 

Great Britain--

According to Catal ina (1981), the earl iest report I inking woodworking and 

cancer was publ ished in France by Moure and Portman in 1925. However, 

40 years passed before interest in the occupational significance of this 

association was rekindled by a series of reports from Great Britain. 

Macbeth (1965) cited the work of laryngologist Eame Hadfield, who had 

noticed that the frequency of nasal and sinus cancer among woodworkers in 

the Buckinghamshire furniture industry was unusually high. Of a total of 20 

cases of nasal cancer from High Wycombe, the center of the Buckinghamshi re 

furniture-making industry, 17 were males and 3 were females, but none of the 

females worked with wood. Among the males, 15/17 (88 . 2%) were woodworkers; 

however, the proportion of woodworkers in the local male population was only 

23.5%. 

Stimulated by this observation of Hadfield, Acheson et al. (1967,1968) 

reviewed the hospital and cancer registry records from Oxfordshire and those 

parts of Buckinghamshi re (including High Wycombe) and Berkshi re wi thin the 

Oxford Regional Hospital Board. This region, which is located in 

south-central England, had a population of just over 1 mi II ion (as of Apri I 

1961), of which approximately 14,000 were employed as woodworkers. The 

initial report (Acheson et al. 1967) identified 85 cases (59 males, 26 

females) of carcinoma of the nose, nasal cavities, middle ear, and accessory 

sinuses first diagnosed during the decade 1956-1965. Twenty-three of these 

cases, all males, were adenocarcinomas. Of those 23, 13 were from High 

Wycombe . When the data were analyzed by occupation, it was found that 17 of 

the 59 men were woodworkers. Thirteen of the 17 had adenocarcinomas, which 

was significant (p<0.OO1) compared to the 10 adenocarcinomas in the 

remaining 42 nonwoodworkers. The authors estimated that the crude average 

annual i'ncidence rate of nasal adenocarcinoma in all types of male 

woodworkers in High Wycombe during 1958-1965 was 0.6 per 1,000, which was 

near Iy the same as that for the usually much more corrmon carcinoma of the 

bronchus. They concluded that the most probable explanation for the 

development of these adenocarcinomas was the existence of a hazardous 

exposure in the furniture industry in High Wycombe prior to the decade 

studied. 

In the followin9 year, Acheson et al. (1968) updated their preliminary 

findings. The study population had been expanded to include two groups, 

both from the Oxford Hospi tal Region. Group 1 consisted of those patients 

diagnosed between 1956 and 1965. This was the same population described in 

the initial report. Group 2 included patients dia9nosed prior to 1956 or 

after 1965. Reevaluation of the hospital records had reduced the number of 

nasal cancer cases in Group 1 from 85 to 83 (56 males, 27 females). 

51 
, 

However, there were sti I I 23 adenocarcinomas, al I in males. Group 2 

contained 65 cases (42 males, 23 females), of which 13 (10 males, 3 females) 

were adenocarcinomas . In Group 1, the high male/female ratio for 

adenocarcinoma was signi ficantly (p<O.OO1) di fferent from the ratio for 

other tumor types. In Group 2, a simi lar di fference was noted, but it was 

not significant . The age distribution of adenocarcinoma in Group 1 was also 

significantly (p<0 .OO1) different than for other nasal cancers . Only 1 out 

of 23 adenocarcinomas occurred in patients over age 65, while half the other 

types occurred in those over 65 . Similar differences were noted in Group 2, 

although they too were not significant. In Group 1 were 17 woodworkers, 15 

of whom were in the furniture industry. Of these 17, 14 (all furniture 

workers) had adenocarc i noma. Th i s assoc i at i on between adenocarc i noma and 

working in the furniture industry was significant (p<O .OO1) . One 

nonwoodworker in the furniture industry also had adenocarcinoma . In Group 2 

were seven woodworkers, five in the furniture industry. Of these seven, 

five (three furniture workers and two other woodworkers) had 

adenocarcinoma . This was not statistically significant. Nineteen of the 

adenocarcinomas occurred wi thin Buckinghamshi re (15 were in High Wycombe 

furniture workers), whereas all other types of nasal tumor were distributed 

fairly equally among the three "shires" in the study area . The authors 

recalculated an average incidence rate of adenocarcinoma among furniture 

workers in High Wycombe for 1956-1965 of 0.7±0.2 per 1,000 per year. Among 

16 patients for whom employment information was avai lable, most had been 

exposed to the hardwoods beech , oak, and mahogany . The latency per iod 

between entry in the furniture industry and diagnosis of adenocarcinoma was 

approximately 40 years. An analysis of case histories showed that 

adenocarcinomas may develop in persons working in the furniture industry for 

only 5 years. Also, they may develop as long as 34 years after leaving the 

industry. The authors concluded that the hazard was present at least at the 

start of World War II and that it was not due to substances introduced since 

the war. On this basis, they eliminated exotic hardwoods, synthetic glues, 

stains, and varnishes as causative agents. They hypothesized that 

adenocarcinoma was caused by exposure to wood dust itself, and not to 

polish, varnish , or wood-treatment chemicals. They did not consider snuff 

use to be a significant factor . 

In a subsequent discussion of nasal cancer among workers of the boot and 

shoe indust'ry in Northamptonshi re, Acheson et al. (1970) pointed out that 8 

of 26 (30 .8%) of these patients with adenocarcinoma had used snuff. This 

compares to 3 of 11 (27 .3%) of the patients with nasal adenocarcinomas in 

the furniture-making industry of Buckinghamshi re who were known to have 

indulged in this habit. The authors reversed their earlier judgment 

(Acheson et al. 1968) and suggested that the use of snuff might contribute 

to the development of nasal cancer. 

Hadfield (1969) surrmarized the 83 cases of nasal cancer in the Group 1 

portion of the Oxford Region study and reported on a survey of 131 workers 

(128 males, 3 females) in one furniture factory who had worked in the 

industry for more than 5 years . Although no premal ignant condi tion of the 

nasal mucosa was identified, pathological changes (dry and atrophic mucosa , 

nasal polyps , chronic rhinitis , and chronic hypertrophic rhinitis) were 

52 
I 

found twice as often in the group exposed to wood dust (25173; 34%) than in 

the group rarely or never exposed (9/58; 15%). 

In the following year, Hadfield (1970) enlarged Group 1 to include nasal 

cancer cases newly diagnosed during 1966-1970. The study population now 

included 92 cases diagnosed in the Oxford Hospi tal Region from 1956 to 

1970. These included 28 cases of nasal adenocarcinoma in Buckinghamshi re, 

all men, 23 of whom were from High Wycombe. Seven additional cases of 

adenocarcinoma were found in Oxfordshire, 3 of which were women not exposed 

to wood dust. Of the 32 men with adenocarcinoma, 24 were currently employed 

as woodworkers in the furniture industry (primari Iy wood machiners, 

cabinetmakers, and chai rmakers); and 5 others had previously been simi larly 

employed. The author calculated the crude annual incidence rate of 

adenocarcinoma for men in High Wycombe to be ten times greater than for men 

in the rest of Buckinghamshire. Because only a few of the cases of 

adenocarcinoma arose among men exposed to glues, stains, and varnishes 

rather than to wood dusts per se, Hadfield concluded that the former 

materials could be excluded as major contributors to the development of the 

disease. She also stated that the Ubiquitousness of smoking among patients 

made it difficult to assess its significance . However, snuff use might have 

played a contributory role, since 3 of 17 men wi th adenocarcinoma for whom 

information was avai lable used it. In all 35 adenocarcinoma patients, the 

disease originated in the ethmoid sinuses . Thi rty-one of the 35 patients 

were 65 years or older at the time of diagnosis, and the mean latency period 

was 38 years. In concluding her report, Hadfield described the initiation 

of a survey of men employed as woodworkers in the High Wycombe furniture 

industry. 

The results of this survey were reported in the fol lowing year (Hadfield and 

Macbeth 1971). The noses of 3,100 workers in furniture factories were 

exam i ned du ring the yea r from mid-June 1969 to mid-June 1970. On I y one 

mal ignancy was found. Deposits of dust were commonly found on the nasal 

septum, particularly at the anterior ends of the middle turbinates. Smears 

taken from the middle turbinates of the noses of 55 workers and examined 

l1icroscopically were normal in 9 cases (20%) and gave evidence of squamous 

metaplasia in 35 cases (77.8%); 1 revealed the adenocarcinoma cited above. 

Ten smears were unsatisfactory and could not be used. By contrast, smears 

from 28· control personnel (office and maintenance personnel, and 

upholsterers) were normal in 20 cases (80%) and indicated squamous 

metaplasia in only 5 cases (20%) (3 smears were unsatisfactory) . A group of 

22 snuff users examined simi larly yielded mid-turbinate slllears indicating 

normal conditions in 5 (23.8%) and squamous metaplasia in 16 (76.21) 

(1 smear was unsatisfactory). The authors hypothesized that squamous 

metaplasia, by reducing mucoci I iary clearance, could allow deposition and 

retention of fine wood dust that acted as a chronic irritant. In turn, this 

irritation might lead to adenocarcinoma. 

Additional information on the nasal mucosa of furni ture workers was provided 

as part of the previously described study of mucoci I iary clearance in 

woodworkers (see Section V) by Black et al . (1974). The authors took nasal 

smears from nine furniture workers from a single factory in High Wycombe. 

Only the three nonsmokers had normal mucosa. Squamous epithelial eel Is were 

53 
, 

found in one smear and metaplastic cells were found in three other smears; 

all were from smokers or snuff users. The authors suggested that in workers 

with impaired clearance, certain mucosal regions would be subject to higher 

concentrations of soluble toxic constituents, including carcinogens. This 

might account for the relatively high incidence of squamous metaplasia in 

the nasal mucosa of woodworkers. 

To examine whether the increased risk of nasal adenocarcinoma in the 

Buckinghamshire and Oxfordshire furniture industry existed in other parts of 

the country, Acheson et al. (1972) undertook a case-control study of 

adenocarcinoma among all the cancer registry regions in England and Wales 

(except for the previously studied Oxford Region). Most registries covered 

the period 1961-1966, although some covered a longer (unspecified) span. A 

total of 145 cases and 133 controls were initially identified. Controls 

were patients with types of nasal cancer other than adenocarcinoma. They 

were matched by sex, age (within 5 years), and region and year of cancer 

registry. Occupational histories were obtained from the patient or 

relative, or from a treating physician. After the elimination of records 

for which the histological classi fication of adenocarcinoma could not be 

confirmed or for which occupational histories were not available, 107 cases 

(80 males, 27 females) and 110 controls (85 males, 25 females) remained. 

For males, the authors found a signi ficant (p<0.OO1) relationship between 

nasal adenocarcinoma and employment as a woodworker. When the woodworkers 

were further divided between those in the furniture industry and those not 

in that industry (primari Iy carpenters and joiners), the ratio of observed 

to expected cases was much greater among the furniture workers (95:1) than 

the latter (5:1). A significant (p<0.OO1) excess of nasal cancer other than 

adenocarcinomas among woodworkers was also seen, and the greater relative 

risk was again to furniture workers. Because of problems of classification 

and the small numbers involved, no statistically val id conclusions could be 

drawn regarding adenocarcinomas in females. 

Acheson (1976) sunvnar i zed the two su rveys of nasa I adenocarc i noma done in 

Great Britain during the previous decade, the Oxford Hospital Region survey 

(Acheson et al. 1967 ,1968) and the national survey (Acheson et al. 1972). 

The author pointed out that the former study had led to nasal adenocarcinoma 

being listed in 1969 as a recognized and compensable industrial disease for 

workers in the furniture industry in the United Kingdom. Combining the two 

surveys, Acheson (1976) recalculated an average latency period of 42.8 

years. He noted a decline in the number of cases of adenocarcinoma 

diagnosed since 1970, but indicated that there had been a concomitant 

decline in the number of woodworkers in the Buckinghamshire furniture 

industry. He did not consider glues or varnishes to be causative agents, 

since wood dust was the only common factor in all the cases. 

Five years later, Acheson et al. (1981) updated their national survey of the 

incidence of nasal cancer in England and Wales. A total of 1,935 cases for 

the period 1963-1967 were initially ascertained from information provided by 

the Office of Population Censuses and Surveys. Of those, 1,602 were 

verified as being mal ignant disease of the nasal cavity and accessory 

sinuses in residents aged 16 and older registered with the National Cancer 

Register of England and Wales. Occupational histories were obtained from 

54 
• 

the patient or relative, or from the hospital or death certificate. The 

average annual incidence rates per mi II ion for nasal cancer of all 

histological types were 74.0 for men and 57 .8 for women (male/female ratio 

1.4:1) . For men classified as woodworkers, there were 59 observed cases of 

nasal cancer lIersus 20.8 expected cases, for a signi ficant (p<0.01) 

standardized incidence ratio (SIR) of 284. Specific occupational SIR's (all 

significant at p<0.05) were 966 (cabinetmakers and chairmakers), 616 

(machinists), and 293 (other woodworkers). The SIR for carpenters and 

JOiners (149) was not significant. The histological tumor type was 

available for 808 (92.3%) of the men and 339 (89.9%) of the women for whom 

an occupational classification could be made. There were 97 cases of nasal 

adenocarcinoma in men and 33 in women. There was a si9nificant (p value not 

provided) excess of adenocarcinomas in male woodworkers (29 observed, 6.4 

expected) . 

In the following year, Acheson et al. (1982) updated thei r data on the 

incidence of nasal adenocarcinoma in the Buckinghamshire furniture 

industry. There were now 48 cases of nasal carcinoma registered wi th the 

Oxford Regional Cancer Register between 1945 and 1981 . The authors 

indicated that ski I led furniture makers such as wood machinists, 

cabinetmakers, and chairmakers had experienced a cumulative lifetime risk of 

hailing nasal adenocarcinoma of at least 1 in 120 during the period studied. 

In addition, using a birth cohort analysis, they reported that the incidence 

ratio for nasal adenocarcinoma increased to a maximum for the men born 

during 1900-1909, whose median year of entry into the furniture industry was 

about 1920, and declined thereafter. However, the decline in incidence of 

nasal adenocarcinoma in men was not statistically significant. The 

incidence of nasal carcinoma among ski lied woodworkers in the furni ture 

industry was more than 12 times that among other workers in the industry. 

Comparing those who had worked less than 20 years in the furniture industry 

with those who had worked 20 years or more, the authors reported a 

significantly (p<0.05) greater risk for nasal cancer in the latter group. 

Rang and Acheson (1981) and Acheson et al. (1984b) reported on a group of 

more than 5,000 men who were born before January 1, 1940, and who had worked 

prior to December 31, 1968, for any period of time in at least 1 of 9 

furniture factories in Buckinghamshire . The initial report (Rang and 

Acheson 1981) examined 5,371 men through the end of 1968. The authors found 

a hundredfold increase in nasal adenocarcinoma in furniture workers as 

compared to the local population, and a significant relationship between 

increasing incidence of both nasal cancer (al I histological types) and 

adenocarcinoma and qualitatively increasing dustiness of work within the 

cohort. The follow-up study (Acheson et al. 1984b) described 5,108 men 

(1,638 of whom had died) who had been followed to the end of 1982. There 

was a significant (p<0.05) deficiency of deaths observed from al I neoplasms 

combined (standardized mortal i ty rat io [SMA] 88). However, the nine deaths 

due to nasal adenocarcinoma were significantly (p<0.05) greater than 

expected . These nine cases were all recorded in occupations qual itatively 

classified as "lIery dusty ." The mortality patterns among skilled workers 

were also examined by presumed duration of work in and by time since entry 

into the furniture industry . In both cases there were significantly 

(p<O.05) increasing trends for nasal adenocarcinoma. 

55 
, 

Sarvesvaran and Bowen (198S) described two fatal cases of nasal 

adenocarcinoma in British woodworkers. The first was an 81-year-old man who 

had been diagnosed at age 70 as having adenocarcinoma of the ethmoid 

sinuses. The second, a 63-year-old male who had been a cabinet worker for 

20 years, was dia9nosed as having adenocarcinoma of the nasal sinuses. 

Gardner and Winter (1984) described a recently developed statistical 

technique to examine the relationship between mortality and environment. As 

an example of the method, the authors reviewed nasal cancer mortality in 

British industries. Mortality data came from the Atlas of Cancer Mortality 

l.!! England and Wales for 1968-1978, and industrial data came from the 1971 

census, which contained information on 1,366 geographic areas and 207 

industrial classifications. There were 1,S56 male deaths from all types of 

nasal cancer. The furniture and upholstery industry showed the strongest 

relationship with nasal cancer (standardized slope = 0.1164, p<0.01). 

Baxter and McDowall (1986) investigated the excess of male mortality from 

pleural mesothelioma and nasal and bladder cancer also reported in the Atlas 

of Cancer Mortality l.!! England and Wales. The authors conducted a 

case-control study of four london boroughs that had significant woodworking 

industries. Fifty-four deaths were verified for the period 1968-1978, 

inclusive, for which cancer of the nose, nasal cavities, or sinuses were 

cert i f i ed. Each was matched a9ai nst two cont ro Is. The first cont ro I was 

randomly selected from male deaths from all other cancers, and matched for 

borough of residence, year of death, and age (within S years). The second 

control was randomly selected from male deaths from all causes including 

cancer (except nasal cancer) and matched as above. In the case group, eight 

deaths were among occupations known to be associated with high wood dust 

exposure: 4 cabinetmakers, 1 wood machinist, and 3 carpenters. In the 

combined control groups, there were three French pol ishers, a woodworking 

occupation which has lower wood dust exposure than the above three 

occupations. If the control group excluded the three polishers, then there 

was a significantly (p<O.OS) increased risk for nasal cancer with 

woodworking. However, if the three polishers were included in the analysis, 

the association between nasal cancer and woodworking was not statistically 

significant (relative risk 2.S, 95% confidence interval [CI] 0.7-8.8). 

I n a comp i'l at i on of occupa tiona I morta I i ty stat i st i cs (Reg i s t rar Genera I 

1986) for men in Great Britain who died aged 16-74 in the 4 years 1979, 

1980, 1982, and 1983, there was no increase in nasal cancer deaths among all 

woodworkers and pattern makers aged 20-64. However, the increase among men 

aged 65-74 was significant (proportional mortality ratio [PUR] 267 based on 

8 cases, p<O.OS). This difference between age groups was attributed to the 

long latency period for the development of nasal cancer. An increase in 

nasal cancer deaths among cabinetmakers aged 20-64 (PMR 1,020 based on 2 

cases, p<O.OS) was also seen. Carpenters and joiners had a nonsignificantly 

increased PMR (244 based on 6 cases) for ages 65-74 . The report cautioned 

that one of its shortcomin9s was the fact that the occupation coded was the 

deceased's last occupation and might not represent the primary occupation or 

the one responsible for the risk leading to death. 

56 
, 

Uni ted States--

The fi rst report I inking wood dust exposure in the U.S . to nasal cancer was 

that of Brinton et al. (1976). They described an ecological study in which 

the cancer death rates from 1950 to 1969 among inhabitants of 132 counties 

in the United States having at least 1% of their population employed in 

furniture and wood fixture manufacturing were compared with 264 control 

counties. Counties were matched for regional location, population, nonwhite 

proportion, median fami Iy income, and level of education. The ratio of the 

age-adjusted mortal i ty rate for cancer of the nasal cavi ty and sinuses among 

white males in the furniture counties to the corresponding rate in the 

control counties was significantly (p value unspecified) greater than one. 

In the following year, Brinton et al. (1977) described a death certificate 

case-control study of nasal cancer among workers in 19 North Carol ina 

counties where at least 1% of the total population was employed in wood 

furniture and fixture manufacturing. Thirty-seven deaths attributed to 

cancer of the nasal cavity and sinuses for the period 1956-1974 were 

compared with 73 controls dying from other causes. The groups were matched 

by sex, race, county of death, age at death (within 2 years), and year of 

death. Comparison of death certificates showed that 8 of 37 people (21.6%) 

dyin9 from nasal cancer had been employed in the furniture industry, whi Ie 

only 5 of the 73 controls (6.8%) had been so employed. An additional 5 

cases (13.5%) were persons with wood-related jobs, as compared with 7 (9.6%) 

of the controls. This yielded an odds ratio of 4.4 (95% CI 1.3-15.4) for 

employment in the furniture industry as compared to 1.5 (95% CI 0.4-4.3) for 

other woodworking operations. The excess risk among furniture workers was 

seen both in those who died at or above age 65 and those who died younger. 

Among the 13 cases for which histology was recorded, 4 were adenocarcinomas 

(3 of which were furniture workers), 4 were squamous cell carcinomas, 3 were 

undifferentiated carcinomas, 1 was lymphoepithelioma, and 1 was myxosarcoma . 

Brinton et al. (1984) followed up thei r previous work wi th a case-control 

study of primary mal ignancies of the nasal cavi ty and sinuses diagnosed at 

four hospi tals in North Carol ina and Vi rginia between 1970 and 1980. For 

cases alive at the time of interview (1980-1982), two controls were selected 

and matchl!d by hospital, year of admission (within 2 years), age (within 

5 years), sex, race, and state economic area (or county) of residence . 

These controls were required to be living at the time of interview. 

Excluded were patients with malignant neoplasms of the buccal cavity and 

pharynx, esophagus, nasal cavity, middle ear, accessory sinuses, larynx, or 

secondary neoplasms; benign neoplasms of the respiratory system; mental 

disorders; acute sinusitis; chronic pharyngitis and nasopharyngitis; chronic 

sinusitis; deflected nasal septum; or nasal polyps. For cases deceased at 

the time of interview, two different controls were selected. The first was 

a hospital control matched as above, but the control was not required to be 

I iving. The second came from a I ist of deceased individuals ident i tied 

through state vital statistics offices. Matching criteria were simi lar to 

those used for I iving cases and included age (within 5 years), sex, race, 

county of residence, and year of death. A total of 193 cases, 232 hospital 

controls, and 140 death certificate controls were identified, from which 

success fu I i nte rv i ews we re comp I eted for 160 cases, 178 hosp ita I cont ro Is, 

57 
, 

and next of kin for 112 death certi ficate controls. Risks were calculated 

relative to those who never worked in each industry and adjusted for sex of 

study subjects when possible. Among occupations involving potential 

exposure to wood dust, nonsigni ficant elevations in risk for males were 

associated with lumbering (relative risk 1.45), carpentry (1.60), and 

construction (1.23). There were no females in any of these categories. 

Among furniture manufacturers, the relative risk was 0.74 in males and 0.91 

in females. Additional examination according to tumor histology showed a 

signi ficantly (p<0.05) elevated risk of adenocarcinoma for males in the 

furniture manufacturing industry (relative risk 5.68) but not in other 

industries involving wood dust exposure (lumbering, carpentry, 

construction). There was no significantly increased risk of squamous cell 

carcinoma in any wood-related industry. The authors noted that of the ten 

woodworkers who developed adenocarcinoma (four of whom were furniture 

workers), seven were first employed 20 or more years prior to the 

development of the cancer, indicating a long latency period. Cigarette and 

pipe smoking and snuff use were shown to nonsignificantly increase the risk 

of cancers of the nasal cavity and sinuses. These three tobacco habits were 

most strongly related (sti II nonsignificantly) with squamous cell tumors. 

Roush (1978) and Roush et al. (1980) reported on a case-control death 

certi ficate study of cancer of the nose and paranasal sinuses in 

Connecticut. A total of 216 verified cases of sinonasal cancer were 

compared with 662 male deaths from 1935-1975 at age 35 or older, using 

random sampling without stratification or matching of any kind. However, a 

compar i son of cases and cont ro I s revea I ed a simi I ar i ty for certa i n 

demographic characteristics, including year of death, age at death, 

percentage of foreign born, percentage in two or more different industries, 

and percentage in two or more different jobs. The authors calculated an 

odds ratio of association between sinonasal cancer and wood dust of 4.0, 

which was statistically significant (p<0.011). Carpenters, most of whom 

were in the construction trade, showed no elevated risk. Although numerical 

relative risks were not calculated, cabinet workers and other woodworkers 

were considered high risk groups. There were eight cases of sinonasal 

cancer in the occupational groups associated with wood dust exposure, two of 

which were adenocarcinoma and three of which were squamous cel I carcinoma. 

Lingeman at al. (1982) reported on 72 patients (45 men, 27 women) with 

glandular neoplasia of the sinonasal tract whose biopsies had been examined 

at the Armed Forces Institute of Pathology. Ages ranged from 7 to 90 years 

(median 58). Ten of the adult males had worked in occupations with 

potential wood dust exposure; an eleventh reported working with wood in a 

home workshop. The neoplasms of all but one of these men were 

mucin-producing adenocarcinomas. No histologic tumor type predominated 

among male and female patients who had no known exposure to wood dust. 

Viren et al. (1982), in a report prepared for the Inter-Industry Wood Dust 

Task Force, described a death certificate case-control study of nasal cancer 

deaths occurring from 1963 through 1977 in the states of North Carol ina, 

Mississippi, Washington, and Oregon. These states were selected because of 

their diverse wood-related industries and wood species. The final study 

population consisted of 332 male cases, 204 female cases, and 1,072 controls 

58 
, 

(2 per case) dying of other causes matched by sex, race, year of death, age 

of death (within two years), and county of death. Within the same sex, 

cases and controls reported simi lar cigarette smoking habits . However, the 

percentage of males who had smoked (77%) was higher than that of females 

(31%), and the males had smoked for a longer time. Solvent exposures were 

also similar in both cases and controls. Histological information about 

tumor type was not obtained. The authors calculated relative risks of 1.95 

(significant at p<0.05) for industries involvin9 lumber and wood products. 

When this category was divided into those industries where timber and 

1099in9 were clear Iy involved and those where logging was not speci fied, a 

relative risk of 3.0 (significant at p<0.01) was calculated for the former. 

Other wood-related industries had a relative risk of 1.65, which was not 

statistically significant. No association between employment in the 

furni ture industry and nasal cancer was seen. When the data were analyzed 

by occupation, only those in forestry and logging demonstrated a significant 

(p<0.01) relative risk for nasal cancer. 

Based on information provided by the North Carolina Department of Vital 

Statistics, Imbus and Dyson (1985) analyzed nasal cancer deaths in the North 

Carolina furniture industry . There were 196 cases of nasal cancer between 

1964 and 1977, of which 6 were in furniture industry workers . Extrapolating 

U.S. Census figures for the North Carolina population between 1960-1980, the 

authors calculated an average incidence rate of nasal cancer in North 

Carol ina of 0.28 per mi II ion and in the North Carol ina furni ture industry of 

0.94 per million. This excess of nasal cancer in furniture workers was 

statistically significant (p<0.05). 

To demonstrate the di fference in nasal cancer rates reported by Acheson et 

al. (1967,1968) in England versus those in North Carolina, Imbus and Dyson 

(1985) calculated that 626 and 816 nasal cancer deaths would have been seen 

in North Carol ina furni ture workers and in the rest of the North Carol ina 

population, respectively, if the Engl ish occurrence rates were used. This 

compares to the 6 and 190 cases, respectively, actually seen in North 

Carolina. The authors hypothesized a number of reasons for the much greater 

excess of nasal cancer in England versus that seen in North Carolina . These 

include: (1) exposure to higher concentrations of dust, (2) different types 

of woods processed, (3) presence of chemicals or other additives in or on 

the wood (4) partial pyrolysis caused by different manufacturing methods, 

and (5) different particle size distribution. 

In addition, from the work of Brinton et al. (1984) and statistics from 

North Carol ina, Imbus and Dyson (1985) showed a decreasin9 number of nasal 

cancer deaths amon9 furniture workers during 1956-1966 (5 deaths) and 

1966-1977 (3 deaths). According to the American Furniture Manufacturers 

Association, no cases of cancer were seen during 1974-1984. From this, the 

authors concluded that a sl ight excess of nasal cancer may have existed in 

the North Carol ina furniture industry, but that the excess appeared to 

reflect earlier manufacturin9 conditions and is currently either declining 

or nonexistent. 

Barnes (1986) described the clinical and pathol09ic features of 17 cases (9 

men, 8 women) of intest inal-type adenocarcinoma (ITAC) of the sinonasal 

59 
tract. These cases were selected from the fi les of the 

Presbyterian-University Hospital and Eye and Ear Hospital of Pittsburgh for 

the years 1952 to 1984 . The occupation of 14 of the patients were 

available; only one of those, a cabinetmaker, seemed to indicate 

occupational exposure to wood dust. Eight tumors originated in the 

maxi Ilary sinus, seven in the nasal cavity, and two in the ethmoid sinus . 

The author also summarized the clinical and pathologic features of 213 cases 

of ITAC. At least 19% of these occurred in woodworkers. Based on this 

review, Barnes comnented on the di fferences between ITAC that occurs in 

woodworkers and ITAC that occurs sporadically in the general population. 

The former occurs primari Iy in men, originates almost exclusively in the 

nasal cavity or ethmoid sinus, and has a better prognosis. 

The National Cancer Institute (NCI) is currently conducting a cohort 

mortal ity study of 36,622 workers fi rst employed between 1946 and 1962 in 

the manufacture of wood, metal, and plastic furniture and identified from 

membership records of the United Furniture Workers of America insurance fund 

(IIi Iler 1987). Prel iminary results revealed two nasal cancer deaths among 

white males in the study cohort (3.6 expected). One was a 75-year-old 

chrome furni ture worker and the other was a 46-year-old upholstered wood 

furniture worker. The authors have cautioned that the study was limited by 

its use of broad industrial classifications and single job titles, by 

incomplete work histories and lack of detai led exposure information, and by 

a lack of power to detect risks for rare causes of death such as nasal 

cancer. 

Canada--

Bal I (1967) published a death certificate analysis of nasal cancer in 

Can ad i ans du r i ng the decade 1956-1965. Occupa t ions were grouped into 10 

categories; woodworkers included the logging industry, bushworkers, 

carpenters, cabinetmakers, and timber workers. Death certificates on which 

the underlying cause of death was stated to be cancer of the nose and nasal 

cavities were matched with the nearest succeeding certificates that 

corresponded in sex, year of death, and province of habitation; ages were 

matched as closely as possible, and in 96% of the cases were wi thin 2 

years. A total of 508 cases of cancer of the nose and sinuses were 

obtained: . 340 in men and 168 in women. These numbers yielded a male/female 

ratio of 2.02. 51 ightly over 58% of these cancers involved the maxi Ilary 

sinuses; the remaining number of tumors were equally divided between the 

other sinuses and the nose and nasal cavities. There were 28 cases of nasal 

cancer among woodworkers: 16 in furniture makers and carpenters; 11 in 

lumberers, loggers, and sawyers; and 1 ina wood merchant. The 

corresponding numbers of nasal cancer cases among the controls were 14, 9, 

and 1. The author concluded that woodworkers had no significant excess of 

deaths due to nasal cancer. 

In a subsequent communication based on the same collection of data, Ball 

(1968) reported no evidence for a local ization in any Canadian province of 

an excess of deaths due to nasal cancer among woodworkers. He also 

separated furniture makers from the carpenter category in his initial 

60 
, 

analysis, and he found no difference between either category and the 

controls. 

Elwood (1981) described a retrospective case-control study of 121 men with 

cancer of the nasal cavi ty or paranasal sinuses who were seen between 1939 

and 1977 at the A. Maxwell Evans Clinic, the main cancer treatment center in 

British Columbia. Each control was the next patient (after the case 

patient) admitted to the Clinic who was in the same 5-year age group as the 

case patient and whose condition had been diagnosed within a 2-year period 

of the case patient's diagnosis. This control group contained patients with 

tumors showing no strong relation to outdoor exposure or .smoking (stomach, 

large bowel, prostate, bone, connective tissue, lymphatic, and 

hematopoietic). Information on occupation, smoking habits, and ethnic 

origin were taken from each patient's standardized medical record. 

Twenty-eight cases were in occupations involving wood exposure: 10 loggers, 

7 carpenters, 4 laborers in forest industries, 4 construction workers, 2 log 

scalers, and 1 cabinetmaker. In the first control group, 15 patients were 

in a wood-related occupation. The author calculated a significant (p<0.03) 

relative risk of 2.5 for sinonasal cancer associated with wood exposure, 

when adjusted for smoking and ethnic origin. The relative risk for smoking, 

when adjusted for wood exposure and ethnic origin, was also significant 

(4.9, p<0.0003). The unmatched estimate of risk associated with both wood 

exposure and smoking was 7.1. There were 11 adenocarcinomas, 61 squamous 

cell carcinomas, 20 anaplastic carcinomas, and 6 sarcomas among the cases. 

An increased risk with wood exposure was seen for nasal cancer of all these 

tumor types. The authors concluded that both wood exposure and smoking were 

associated with increased risk of tumors of the nasal cavities and nasal 

sinuses. Using Canadian census figures they calculated an annual incidence 

of nasal cancers of 15.7 per mi Ilion for workers exposed to wood compared to 

6.5 per mi II ion for other workers. According to these estimates, a worker 

exposed to wood annua II y f rom age 20 wou I d have a risk 0 f deve lop i ng the 

disease by age 70 of almost 1 in 1,000. 

Finkelstein (1985) described a death certificate case-control study among 

Ontario workers who had died during 1973-1983 from mal ignant neoplasia of 

the nose, nasal cavities. middle ear, and accessory sinuses. A control was 

randomly selected from deaths in the same year and matched by age and sex. 

There were eight deaths identified among men with definite wood dust 

exposure (three furniture workers and five carpenters) and three among the 

controls. The resultant odds ratio was not statistically significant, but 

the author cautioned that the sample size was too small to permit meaningful 

analysis. 

Gallagher and Threlfall (1985) conducted a proportionate mortal ity study of 

420,814 deaths in individuals aged 20 and older occurring in British 

Columbia, Canada from 1950 to 1978. The study included 12,115 deaths in 

male woodworkers (carpenters. cabinetmakers, furniture makers, sawmill 

workers, lumber graders and scalers, and woodworkers not elsewhere 

classified); 9,931 in loggers; and 85 in pulp and paper workers. No deaths 

due to sinonasal cancer were reported. 

61 
, 

Denmark--

Mosbech and Acheson (1971) reviewed the 123 Danish deaths due to mal ignant 

neoplasms of the nasal cavi ty , middle ear, and accessory sinuses during 

1956-1966. Seventy- five of these were in men and 48 in women, giving a 

male/female ratio of nearly 1.6. In eight cases, woodworking was listed as 

the occupation of either the patient (six cases) or the husband of the 

patient (two cases). One of these cases was discarded because the tumor was 

in the nasopharynx rather than in the nasal cavities . A detailed 

occupational history was obtained for the remaining seven . Four of these 

seven had nasal adenocarcinoma, and all four had worked in the furniture 

making industry. A fifth man had been a woodworker for 3 years but had 

spent most of his life as a farm worker; he died from squamous carcinoma of 

the nasal cavity. Two women in the group had had no occupational contact 

with wood dust but thei r husbands were carpenters; both women died of 

undi fferentiated carcinoma of the nasal cavity. The authors concluded that 

an increased risk of nasal adenocarcinoma had existed in the Danish 

furniture industry in recent years. An addendum to the paper mentioned that 

two other Danish woodworkers, neither of whom had worked in the furniture 

making industry, had died, in one case of squamous cell carcinoma of the 

nose and, in the other, of melanoma of the nasal septum . 

Andersen (1975) and Andersen et al. (1976, 1977) described 186 patients with 

mal ignant and semimal ignant tumors of the nose and sinuses treated at the 

ear, nose, and throat department of the Aarhus CoIrmunity Hospital during 

1965-1974. Among them were 17 patients (15 men and 2 women) with nasal 

adenocarcinoma . Twelve of these 17 (70.6%) were woodworkers: 

10 woodcutters, 1 wood turner, and 1 coach maker. The latency period from 

f i rst wood dust exposure until tumor development ranged from 28 to 57 years ; 

the duration of employment ranged from 14 to 49 years. Ten of the 12 

woodworkers with adenocarcinoma were interviewed and were found to have 

worked for years in the production of furniture, principally from beech, 

oak, or walnut. Several had also worked with mahogany, teak, and 

pal isander. When the group of adenocarcinomas was el iminated from the 

totals, the proportion of woodworkers among the pat i ents with other types of 

malignancies of nose and sinuses was only 7 . 1% . Ten of these other patients 

had a I so been emp I oyed in occupat ions in wh i ch they were exposed to wood 

dust: three carpenters, two woodcutters, and one each of wood turners, 

coopers, sawyers, lumberjacks, and brush binders . The most COllll1on tumor 

among these 10 people was squamous cell carcinoma ; there were 2 mal ignant 

melanomas and 1 each of anaplast i c carcinoma, adenocystic carcinoma, and 

papilloma. Based on this sample, Andersen (1975) calculated a yearly 

incidence rate of 0.5 cases of nasal cancer per thousand for Danish 

woodcutters, which was simi lar to that reported in England by Acheson et al. 

(1967). No Danish national rates were provided for comparison. The author 

concluded that adenocarcinoma of the nasal cavity and/or paranasal sinus in 

a person who had worked at the grinding and pol ishing of wood should be 

accepted in Denmark as an occupational disease . 

Olsen and Sabroe (1979) reported on a 6-year follow-up study of mortal ity 

among Danish carpenters, joiners, and cabinetmakers . The cohort was defined 

as al I members of the Danish Carpenter/Cabinet Makers' Trade Union on 

62 
, 

January 1, 1971 aged 20-84. It included both active and reti red workers. 

Mortal ity was determined from union and insurance company reports and the 

National Board of Health for the period January 1, 1971, to 

December 31,1976 . 01 all causes of death, only the incidence of nasal 

cancer (h is to I og i ca I tumor t ype unspec iIi ed) was above the nat i ona I average 

(SMR 467, 95% CI 253-679) . However, this statistic was based on only four 

cases, three among cabinetmakers and one among carpenters . The age-adjusted 

proportional relative risk of nasal cancer for cabinetmakers compared to 

carpenters was 2.33 (95% CI 0.32-16.65) . 

Olsen et al . (1984) described a case-control study of sinonasal cancer and 

occupational exposures. Using tI.e Danish Cancer Registry and computerized 

emp loyment his tor i es from the Nal i ona I Supp I ementa I Pens i on Fund dati ng to 

1964, 839 cases of cancer of the nasal cavity, sinuses, and nasopharynx and 

2,465 cancer (colon, rectum, prostat~, and breast) controls diagnosed during 

1970-1982 were examined. The controls were matched by sex, age (within 

5 years), and year of diagnosis (within 5 years). A statistically 

significant excess risk for nasal cancer (histological tumor type 

unspecified) among males with exposure to wood dust was found (relative risk 

2.5, 95% CI 1.7-3.7). No such association was seen for nasopharyngeal 

cancer. When a latency period of 10 or more years between fi rst exposure 

and tumor diagnosis was introduced , the relative risk of sinonasal cancer 

increased to 2.9 (95% CI 1.8-5.3). When adjusted for formaldehyde exposure, 

the relative risk associated with wood dust remained significantly (p<0.05) 

elevated whether no latency (relative risk 2 . 1) or a 10 year latency 

(relative risk 3.8) period was considered. The authors indicated that 

persons with exposures to both formaldehyde and wood dust were at a higher 

risk of developing nasal cancer than were persons with exposure to only one. 

Olsen and Asnaes (1986) further analyzed the Danish Cancer Registry data 

described in the preceding report to investigate the relationship between 

formaldehyde exposure and nasal cancer . After exclusion of cases for which 

histopathologic classification could not be confirmed, there remained for 

analysis a total of 759 (509 males, 250 females) nasal cancers, including 

466 (310 males, 156 females) cancers of the nasal cavi ty and paranasal 

sinuses and 293 (199 ma I es, 94 fema I es) cancers of the nasopharynx. The 

same 2,465 controls previously selected were used. Among men, there was no 

significant (p>0.05) association of squamous cell carcinoma of the nasal 

cavity and paranasal sinuses or of cancer of the nasopharynx with either 

wood dust or formaldehyde exposure. However, for adenocarcinoma, the 

authors calculated a significant excess risk of 16.3 (95% CI 5.2-50.9) for 

wood dust after adj ust i ng for forma Idehyde among men ever-exposed. The 

relative risk for joint wood dust-formaldehyde exposure was 39.5 (95% CI 

22.0-70 .8). When a latency period of 10 years since first exposure was 

included in the analysis, the relative risk for adenocarcinoma with wood 

dust exposure increased to 30.4 (95% CI 8.9-103 .9) and the joint risk 

increased to 44.1 (95% CI 22.2-87.8). For women, no risk estimates for any 

nasal cancers could be made because the exposure rates were too low . 

63 
Sweden--

Drettner and Stenkvist (1979) described a cytologic study of cells either 

rinsed or directly sampled by probe from the noses of woodworkers. In about 

2% of the 715 woodworkers examined by di rect sampl ing, metaplastic changes 

in'mucosal cells were observed. However, no definitively precancerous or 

cancerous cells were identified. The authors stated that the frequency of 

ethmoidal cancer in the Swedish furniture industry was approximately 4-5 

cases per year among 17,000 workers (0.26 per thousand). 

Engzell et al. (1978) used the cancer registry of the Swedish National Board 

of Health and Welfare to locate cases of nasal adenocarcinoma reported 

during the decade 1961-1971. This registry covered approximately 95% of all 

new cancer cases in Sweden. There were 46 adenocarcinoma cases (36 males, 

10 females). The occupations of the 10 women could not be determined. Of 

the 36 men, 19 (53%) had been joiners, 1 had been a bui Iding worker, 6 had 

been fitters, 3 had worked in flour mi lis, 3 had been transport workers, and 

4 had had miscellaneous occupations. The authors calculated relative risk 

ratios for adenocarcinoma of 165 for joiners and 109 for furniture workers. 

They stated that there was a con v i nc i ng assoc i at i on between adenocarc i noma 

and the joinery occupation, although no statistical analysis was provided. 

They did not consider smoking or snuff use to be a significant factor. Most 

joiners had worked with multiple species of wood, both hard and soft. The 

authors also found 212 cases of squamous cell or poorly differentiated 

carcinoma of the nose in 127 men (including 5 joiners and 8 other 

woodworkers) and 85 women. Among the men, exposure to a variety of organic 

dusts was common, but no conclusions about thei r association with nasal 

cancer could be made. Very little information about female occupations was 

avai lable. 

Engzell (1979) reported the initiation by the Nordic Council of a joint 

case-control study in Denmark, Norway, Sweden, and Finland to identify 

occupa t ions and exposu res assoc i a ted with nasa I cance r . He a I so discussed 

an enlargement of the Swedish study described in his preceding paper 

(Engzell et al. 1978). The author now had information on 44 men who had 

developed nasal adenocarcinoma. Twenty-two of these men were joiners and 

one other was a bui Iding worker. The latency period from fi rst exposure to 

wood dust to the diagnosis of nasal adenocarcinoma for 21 of the joiners 

varied from 22 to 70 years, with a mean of 44.7 years. The exposure period 

ranged from 9 to more than 30 years. One man had worked in the industry for 

on Iy 9 years 5 months and was diagnosed as hav i ng a nasa I adenocarc i noma 

39.6 years after ceasing his work as a joiner. The author noted the 

similarity between these cases and those reported in England and Denmark. 

Malker et al. (19B6) updated Engzell's (1979) occupational nasal cancer 

survey to include incidence data for 1961-1979. Among males employed in 

Sweden in 1960, 648 cases of nasal cancer were identified. Seventy-seven 

(12%) were adenocarcinomas, 306 (47%) were squamous cell carcinomas, and 265 

(41%) were other histologic types. A standardized cumulative (19-year) 

incidence ratio (SIR), adjusted for age and geographic region, was used to 

estimate cancer risk. Significantly (p<O.01) increased incidences of 

adenocarcinoma (SIR 16.7) and total nasal cancers (SIR 4.1) were found for 

64 
, 

the furniture industry . A nonsignificantly elevated adenocarcinoma SIR of 

2.2 was also observed for work in the wood industry. When the data were 

examined by trade , significantly (p<0 .01) increased SIR's were found among 

woodworkers for both adenocarcinoma (4 .7) and total nasal cancers (1.5) . 

Further categorization revealed that most of the adenocarcinoma increase was 

among furni ture makers and cabinetmakers (SIR 9 .8) and to a lesser degree 

among carpenters and joiners (SIR 2 .3) . However, the incidence of total 

nasal cancer in carpenters and joiners was not elevated (SIR 1.1). No 

increases were noted in any of the industries or trades for squamous cell 

carcinoma . 

The results of the Nordic Counci I jo i nt nasal cancer case-control study 

described above by Engzell (1979) were described in two papers by Hernberg 

et al. (1983a , 1983b). Cases of cancer of the nasal cavity and paranasal 

sinuses came from Finn i sh and Swed i sh na tiona I cance r reg i s t r i e8 and from 

Danish hospital records for 1977-1980 . One hundred and sixty-seven patients 

(110 men, 57 women) answered a standardized telephone interview, and they 

were individually matched by country , sex, and age at diagnosis (within 

3 years) with I iving patients having colon or rectal cancer. The mean age 

of the interviewed cases was 64 . 1 for males and 62 .5 for females . Eighteen 

of the cases we re adenocarc i nomas. The ana Iys i s was confounded because of 

mixed exposures to wood dust as wei I as paints, lacquers, and wood 

preservatives. Analysis of smoking habits suggested a synergistic effect, 

although the authors indicated that the numbers were too sma I I to permit any 

definite conclusion . The authors reported that exposure to hardwood dust, 

either alone or in combination with softwood dust , was mainly associated 

with nasal adenocarcinoma. This association was significant (p<0.05) for 

the mixed dusts. No such relationship was found for softwood dust alone. 

The results also suggested an association between exposure to mixed wood 

dust and increased risk of epidermoid and anaplastic carcinoma. 

Hardell et al . (1982 , 1983) reported the results of a case-control study 

designed to examine the relationship between nasal and nasopharyngeal cancer 

and exposure to phenoxy acid or chlorophenols. Cases consisted of male 

patients with nasopharyngeal cancer or cancer of the nasal cavity or 

paranasal sinuses, aged 25-85, who were reported to the Swedish Cancer 

Register in 1970-1979 and who were residents of three northern Swedish 

counties at the time of diagnosis. These counties had a heavy concentration 

of forestry work and timber, pulp, and paper production . The group of 541 

controls came from a pool of controls used in earl ier cancer studies in 

northern Sweden. The controls came from the same counties as soft tissue 

sarcoma and lymphoma cases and were considered to accurately represent the 

general population . Smoking and snuff habits were similar in both cases and 

controls. A total of 44 cases of nasal cancer, including 3 adenocarcinomas, 

and 27 cases of nasopharyngeal cancer were seen. High-grade exposure 

(defined as more than 1 month total or more than 1 week continuously) to 

chlorophenols was related to a significant (p<0 .05) sevenfold increase in 

both types of cancer. However, there was no significant association between 

either type of cancer and either phenoxyacid or low-grade chlorophenol 

exposure . Additionally, in woodworkers (sawmill workers, carpenters) not 

exposed to chlorophenols, no increased cancer risk was seen . Cabinetmakers 

65 
, 

not exposed to chlorophenols had a doubled (but statistically not 

significant) risk of nasal cancer. 

The above study by Hardell and coworkers el icited responses from researchers 

in Great Britain, Denmark, and Canada. Acheson et al. (1g84a) indicated 

that chlorophenols were unl ikely to have been used to treat hardwoods used 

in the British furniture industry. In addition, nasal adenocarcinoma 

occurred in British furniture workers who had left the industry before 

chlorophenols were introduced as a timber treatment. Acheson et al. (1984a) 

therefore concluded that chlorophenol exposure was not a likely cause of the 

occupational nasal cancers seen among British furniture workers. Olsen and 

Jensen (1984) reviewed 839 cases of cancer of the nasal cavity, sinuses, and 

nasopharynx selected from the 1972-1982 Danish Cancer Registry fi les. These 

cases were compared to 2,465 controls with cancer of the colon, rectum, 

prostate, and breast (matched by age, sex, and year of diagnosis). When 

adjusted for occupational wood dust exposure, there was no increased risk of 

sinonasal cancer among males wi th former exposure to chlorophenols. The 

authors concluded that thei r findings did not support the hypothesis that 

chlorophenols were signi ficant in the etiology of nasal cancer in wood 

workers. Gallagher and Threlfall (1984) analyzed their British Columbia 

mortality data specifically for cancer deaths in male workers with presumed 

exposu re to ch I 0 ropheno I s and phenoxy herb i c ides, inc I ud i ng farmers, 

gardners and nursery workers, sawmi II workers, pulp workers, and rai I road 

track workers. The authors reported 14 deaths due to sinonasal cancer among 

farmers, which was statistically significant (p<0.05). They also reported 

one sinonasal cancer death in sawmi I I workers and one in pulp workers. The 

latter two figures differed from those published in their complete death 

record analysis (Gallagher and Threlfall 1985), in which they reported no 

deaths from sinonasal cancer among woodworkers. However, even the single 

deaths in sawmil I and pulp workers were not statistically significant. 

Klintenberg et al. (1984) described the treatment and cl inical outcome for 

28 patients (24 men, 4 women; mean age 66 years) with adenocarcinoma of the 

ethmoid sinuses seen at the Universi ty Hospi tal in Linkoping, Sweden since 

1964. The region served by the hospital had approximately 900,000 residents 

and a large amount of furniture industries. Twenty (83%) of the men had 

been exposed to dust from hardwood for 20 to 55 years (mean, 40 years). 

Data on SWedish national rates of nasal cancer were not provided. 

In the following year, Wi Ihelmsson et al. (1985a) examined the nontumorous 

part of nasal and ethmoidal mucosa adjacent to the tumors from the 20 wood 

dust-exposed men described above by Klintenberg et al. (1984) and an 

add it i ona I two cases, both of whom had been exposed to wood dus t. Fifteen 

of the 22 cases presented papi Ilary adenocarcinomas; the remaining 7 were 

al veol ar adenocarc i nomas, of wh i ch 3 were mucous-produc i ng. In 19 cases 

cuboidal metaplasia was present, and 16 of those also showed dysplasia. A 

transitional zone with dyplastic cuboidal epithelium adjacent to the tumor 

was observed in 10 cases, and squamous metaplasia was seen in 5 cases. The 

authors proposed that nasal adenocarcinomas are preceded by metaplasia and 

dysplasia in cells having the abi I ity to produce mucous. Such cells could 

then transform into either mucous-producing epithelium or metaplastic 

squamous epithelium. The predominance of observed cuboidal metaplasia might 

66 
, 

imply that it is a precursor of ethmoidal adenocarcinoma. This hypothesis 

was further supported by the fact that in 16 cases cuboidal dysplasia was 

present, and in 10 cases dyplastic cuboidal epithelium was found contiguous 

with the tumor. Squamous dysplasia was not present in any of the cases. 

Wi Ihelmsson and lundh (1984) examined a group of 45 workers (mean age 

40 years; mean exposure time 15 years, range 1-39 years) from 5 furniture 

factories in Sweden. Wood dust concentrat ions ranged from 0.35-5.1 mg/m3 

(mean 2.0 mg/m3). A control group of 17 hospital staff (mean age 

38 years) was used. Rhinoscopy was performed in all workers and controls, 

and smears were collected from the middle turbinate in the widest nasal 

cavity. Biopsies were taken from the same area at least 5 RIll behind the 

anterior curvature of the middle turbinate . Thirty-nine (87%) of the 45 

workers had normal nasal anatomy. However, 22 (49%) of the 45 had an 

abnormal mucous lining in the middle turbinate area. There was no 

correlation between histological and rhinoscopic findings. Histological 

eKamination of the biopsies revealed significant (p<0.05) increases in the 

workers relative to the controls in the occurrence of columnar epithel ium, 

ci liated columnar epithelium, and metaplastic cuboidal epithelium. 

Nonsignificant increases in goblet cell hyperplasia, metaplastic epithelium, 

fibrotic submucosal connective tissue, and infiltration of round cells 

(lymphocytes and plasma cells) and eosinophi lic leucocytes were seen in the 

exposed workers. The authors suggested that nasal mucosa changes caused by 

wood dust exposure occurred in steps. The first was loss of cilia and 

hyperplasia of the goblet cells, followed by cuboidal cell metaplasia. 

Gerhardsson et al. (1985) presented the results of a 19-year cohort study 

among 8,141 Swedish men, aged 20-64 in 1960 and classified as furniture 

workers in the 1960 census . The reference group consisted of 1.4 million 

male blue collar workers, except those classified as furniture workers, aged 

20-64 in 1960. Fourteen cases of adenocarcinoma were aeen in furniture 

workers, 11 of the nasal cavity and 3 of the maxi Ilary sinus. Seventeen 

cases of adenocarcinoma of the nasal cavi ty were seen in the reference 

population. Of these, five were in woodworkers (other than furniture 

workers). Therefore, of the 28 cases of adenocarcinomas of the nasal cavity 

that occurred between 1961 and 1979, 16 had been classi fied as woodworkers 

in the 1960 census. The authors calculated standardized 1I0rbidity ratios 

among the 'furni ture workers of 7.1 (90% CI 4.4-10.9) for sinonasal cancer, 

44.1 (90% CI 26.6-68.9) for sinonasal adenocarcinoma, and 63.4 (90% CI 

35.5-104.9) for adenocarcinoma of the nasal cavity. The authors suggested 

that the eKcess risk of sinonasal cancer in woodworkers was confined to 

adenocarc i noma and that there had been no decrease in the inc i dence of 

sinonasal cancer in furniture workers in Sweden after 1965. 

Finland--

Tola et al. (1980) described a case-control study of 45 patients over 35 

years of age with malignant tumors of the nose and paranasal sinuses 

reported to the Finnish Cancer Registry during 1970-1973 from 

southern-southwestern Finland. This area includes most of the Finnish pulp 

and paper manufacturing, wood, and furniture industries. Controls were 

selected from among other cancer patients (excluding respiratory cancer) 

67 
living in the same geographical area. Two of the cases, one of whom was a 

joiner who had been exposed primari Iy to oak dust, had adenocarcinoma. Only 

one control, a carpenter, had wood dust exposure. Because of the small 

numbers, the authors concluded that their study was noninformative since no 

occupational group with an excess risk of developing nasal cancer was 

found. Because wood dust exposure was rare in both the cases and controls, 

they concluded that a case-control comparison for Finnish data was 

ineffective, and they emphasized that the absence of incidence should not be 

interpreted as proof of no effect. A similar inability to detect increases 

in nasal cancers among Finnish woodworkers was subsequently reported in a 

case-control study by Partanen et al. (1985). 

Norway--

Boysen and Solberg (1982) examined nasal biopsies from 103 current (mean age 

48 years, mean employment 34 years) and 10 retired (mean ase 72 years, mean 

employment 44 years) Norwegian furniture workers and 57 controls (mean age 51) to determine if precancerous lesions could be detected in the nasal 

mucosa of furniture workers. Dysplasia was found in 14 of the workers (12%) 

and in 1 of the controls (2%); squamous metaplasia was found in 45 of the 

workers (40%) and 9 of the controls (17%). The biopsies were scored 

histologically on a scale of 0 (pseudostratified columnar epithelium) to 5 

(dysplasia). The mean histological score was significantly higher (p<0.05) for workers than controls. The mean score was nonsignificantly higher for 

smokers than nonsmokers in both workers and controls. Nasal stenosis and 

mechanical processing of wood were both significantly related to the 

histological score, whi Ie age, length of exposure, and type of wood (hard or 

soft) were not. The authors suggested that dysplasia might represent a 

preneoplastic lesion leading to nasal adenocarcinoma. 

Voss et al. (1985) presented the results of a study of 70 cases of sinonasal 

cancer (40 males, mean age 66; 24 females mean age 60) treated at the 

Department of Otorhinolaryngology, National Hospital of Norway during 

1972-1976. Forty-nine of ~he cases were classified as nasopharyngeal 

carc i noma, three were adenocarc i noma, and eight were non-Hodgk i n I s 

lymphoma. Occupational histories were obtained by telephone interviews. 

Twelve (30%) of the 40 male patients had worked as woodworkers (including cabinetmakers, joiners, and carpenters), in saw and planing-mi lis, or in 

fo res try and we re cons i de red to have been exposed to wood dus t. The mean 

latency period from fi rst exposure to diagnosis was 44 years; the mean 

exposure period was 32 years. Only one of the 12, a cabinetmaker, had 

adenocarcinoma. Standard proportional morbidity ratios were significant (p<O.01) for sinonasal carcinomas for the general classification of 

woodworkers, for cabinetmakers, and for sawmi II and planing-mi II workers, 

and highly significant (p<0.OO1) for all workers exposed to wood dust. With 

the exception of one cabinetmaker, who had also processed hardwood, all 

patients exposed to wood dust had been exposed exclusively to native 

softwoods (primari Iy pine and spruce). 

68 
• 

Italy--

Cecchi et al . (1980) reported a case-control study of 69 patients (47 men, 

22 women) with primary cancer of the nasal cavity and paranasal sinuses seen 

at the Otorhinolaryngology Clinic and the Radiology Institute of the 

University of Florence from 1963 to 1967. Of the 62 cases for which biopsy 

results were avai lable and patient/relative interviews conducted, 11 were 

adenocarcinomas. Three of these were woodworkers (average age 62) with 17 

years average employment. When matched to ei ther of two control groups 

(noncancer hospital patients and nonadenocarcinoma of the nose or paranasal 

sinus cancer patients), the association with woodworking was statistically 

significant (p<O.OO1) . The authors indicated that smoking habits were not 

likely to be a source of bias. 

In the following year, Merler lit al . (1981) described an epidemiological 

survey of patients with tumors of the nasal cavity and paranasal sinuses 

seen in the Ear, Nose, and Throat Departments of five Verona provincial 

hospitals from 1969 to 1979. Of 25 patients (13 males, 12 females) with 

tumors, there were 16 carcinomas and 9 nonepithelial tumors. Among the 

carcinomas were three adenocarcinomas, all in male woodworkers . Two other 

workers with epithelial tumors (one squamous and one undifferentiated) had 

been employed in wood processing industries. 

Battista et al. (1983) described a case-control study of 36 male patients 

seen at the Ear, Nose and Throat Clinic and the Radiotherapy Unit of Siena 

and diagnosed as having cancer of the nasal cavities or paranasal sinuses 

between 1963 and 1981. The controls, who were male patients admitted to the 

Medical Clinic of Siena for all causes except nasal neoplasia, were matched 

5:1 to the patients for age (within 1 year) and time of admission (within 

3 months). Information was obtained from all 36 patients and 164 controls 

by mail and telephone questionnaires. A total of 7 carcinomas, 4 of which 

were mucinous adenocarcinoma and 1 of which was squamous cell carcinoma, 

were seen in male patients employed in the wood and furniture industries . 

The median exposure duration was 40 years. The woods used by the patients 

were primarily oak, chestnut, poplar, and fir. The odds ratio associated 

with exposure to wood dust was 5.4 (95% CI 1.7-17.2) for all carcinomas and 

89.7 (95% CI 19.8-407.3) for mucinous adenocarcinomas. 

Ghezzi et al . (1983) described the incidence of mal ignant tumors of the 

nasal cavi ty and paranasal sinuses occurring in 1976-1980 in Como and Mi Ian 

provinces, a geographic area where there is a high concentration of 

furniture industries. Information was obtained from hospital records. For 

all types of nasal cancer, the ratio of incidence rates among woodworkers to 

others was 4.42, which was simi lar to that in Siena (Battista et al. 1983). 

For adenocarcinoma, the rate rat io was 56.5, but the rei iabi I i ty of this 

value was questioned because of problems in evaluating certain census 

figures. When the data were examined using a case-control approach with the 

controls being nonadenocarcinoma nasal tumors, an odds ratio of 60 was 

calculated, which was consistent with the rate ratio estimate. 

Petronio et al. (1983) reported on a retrospective study of cancer of the 

nasal cavity and paranasal sinuses in the province of Trieste during 

69 
, 

1968-1980 . Information came from the biopsy register of the Department of 

Pathology . Twenty-one cases (10 males, 11 females) were ascertained , and 

occupational histories and smoking habits were obtained by interview for 18 

of the cases. Two cases of adenocarcinoma (one in a cabinetmaker) and seven 

cases of squamous cell tumor (one in a joiner) were seen . The authors 

calculated a nat ionwide annual incidence rate of nasal cancer of 

5 .4 x 10-6 with no sex difference, which was one of the lowest in Europe, 

and an incidence rate of 6.4 x 10-5 among woodworkers. 

Loi et al. (1986) reported on the prel iminary results of a case-control 

study of 49 male pat ients wi th nasal cancer admi tted to hospi tals in the 

vicinity of Pisa. For each, five controls were selected from among those 

hospital patients with other than nasal or respiratory cancers or 

lymphomas. They were matched on sex, age, residence, and time of hospital 

adm i ss i on. Info rma t i on on occupa tiona I exposu res and amok i ng hab its was 

obtained by a mai I questionnaire. At the time of this report, responses had 

been received from 45 cases and 139 controls . Histological information was 

available on 38 nasal tumors, indicating that 12 were adenocarcinOlllas (6 of 

which were mucinous adenocarc i nomas) and 21 were squamous cell carcinomas. 

Of the cases and controls, 76.3% and 82%, respectively, were smokers . When 

all tumor types were considered , a significant (p<0.05) relative risk of 

6.16 was found for woodworkers. Wood exposure showed a significant (p<D.05) 

relative risk of 13.83 for adenocarcinomas. However, no significant risks 

were observed for mucinous adenocarcinomas or squamous cell carcinomas. The 

authors suggested that adenocarcinomas were associated with wood dust 

exposure and squamous cell carcinomas with smoking. 

France--

Gignoux et al. (1968) reported on 52 cases of mal ignant tumors of the 

ethmoid and maxi I lary sinuses seen between 1952 and 1967. Sixteen of these 

patients were woodworkers (11 cabinetmakers, 3 carpenters , 1 sawyer, and 1 

barrel maker) . Fifteen of these 16 had adenocarcinomas . The mean age of 

the woodworkers was 58 years . All had worked with wood since the age of 16, 

indicating a latency period of over 40 years from first exposure to wood 

dust unti I recognition of nasal cancer. In the following year Gignoux and 

Bernard (1969) added one more case of nasopharyngeal cancer in a 

cabinetmaker to their series. There was now a total of 53 nasal cancers, of 

which 16 were adenocarcinomas in woodworkers. Two years later, Gignoux et 

al. (1971) wrote again about the same group of 53 patients, indicating that 

no addi t ional cases of cancers of the ethmoid had come to thei r attent ion 

durin9 the 2 years since their last report. 

Fombeur (1972) described five cases of tumors of the ethmoid and maxi Ilary 

sinuses among JOiners and cabinetmakers. Three of the patients had 

ethmoidomaxillary epitheliomas, two of which were identified as 

adenocarcinomas, the fourth had Wegener's disease, and the fi fth had a 

metaplastic nasal polyp that seemed to be undergoing malignant 

transformation in a part of its periphery. Fombeur suggested that the 

irritant effect of wood dust resulted in hyperplastic, or even metaplastic, 

lesions of the sinonasal mucosa, and that such changes preceded the 

appearance of any malignant tumor . 

70 
, 

Adenis et al . (1973) reported on 125 cases of nasal cancer from among 41,613 

French hospital records (300 per 100,000 admissions) collected through 

December 1970 . Of 115 tumors that were subjected to biopsy, 103 were . carcinomas and 12 were sarcomas . Of the former group, 21 were 

adenocarcinomas (18 of the ethmoid, 1 of the nasal fossa, and 2 of the 

sphenoid and maxi lIary sinuses). Fourteen of the 18 patients with ethmoid 

adenocarcinomas were men, 10 of whom worked with wood : 6 as cabinetmakers, 

1 as a lumberjack, 1 as a sander, 1 as a cooper, and 1 as a broom maker. 

The occupations of the 4 women with ethmoid adenocarcinomas were not known . The male patients had started work between the ages of 13 and 16 years; the 

average age at which the first symptoms of nasal cancer appeared was 

60 years, giving a latency period from the first exposure to wood dust of 

44-47 years. The authors considered adenocarcinoma of the ethmoid in 

woodworkers to be an occupational cancer . 

Leroux-Robert (1974) summarized French , Engl ish, and Dutch references and 

noted that among 450 patients with cancer of the ethmoid, 124 (27.6%) were 

woodworkers. To these he added 100 new patients with cancer of the nasal 

cavity (particularly the ethmoid), 26 of whom were male woodworkers . The 

average age of these 26 men was 60 years (range 37-75 years) and the average duration of thei r exposure to wood dust was 40 years (range 22-54 years) . The patients named oak, fir, poplar, walnut, chestnut, wild cherry, sipo, 

niangon, okoume, and iroko as the woods with which they worked. Four of the 

26 patients had never used tropical woods, 7 had used them very little, and 

6 had used them for only a few years . Leroux-Robert did not consider that 

agents added to wood or coming from the other materials used by the 

woodworker were causes of the carcinomas because they were too varied and 

too inconsistent Iy used. The author suggested that tannin present in the 

wood might be responsible for ethmoid cancers in woodworkers. He concluded 

that exotic woods should not be considered to be the only ones involved in 

the induction of nasal cancers among woodworkers, which should be classified 

as an occupational disease. 

Luboinski and Marandas (1975) observed 43 cases (41 males, 2 females) of 

adenocarcinoma among 67 cases of primary malignant epithelial tumors of the 

ethmoid seen at the Gustave Roussy Institute at Vi Ilejuif during the period 

1957-1974. Twenty-one of the 43 patients (49%) with adenocarcinomas had 

been woodworkers: 11 cabinetmakers, 8 carpenters, 1 barrel maker, and 

1 coffin maker. None of the other 24 cases of nasal cancer was among 

woodworkers. The woods used by these patients included both European woods, 

such as oak, chestnut, wi Id cherry, walnut, beech, and poplar; and exotic 

woods, 8uch as mahogany, sipo, okoume, niangon, teak, makore, African 

walnut, and bosse. Among the 21 patients identified as woodworkers, 11 were 

sti II working, 7 had reti red, and 3 had changed professions. The mean 

latency period between initial wood exposure and the appearance of cancer of 

the ethmoid in these three groups was 42, 52, and 40 years . The mean 

duration of exposure to wood was 42, 45, and 6 years, respectively. The 

authors also suggested that the frequency with which cancer of the ethmoid 

affects woodworkers justifies its inclusion as an indemnifiable occupational 

disease for workers exposed to wood dust, along wi th erythematous and 

eczematous dermatitis, conjunctivitis, and asthma . The last three 

71 
, 

cond it ions had been i ndemn if i ab I e fo r woodworke rs in France since February 1967. 

Curtes et al. (1977) described 21 adenocarcinomas among 36 primary malignant 

tumors of the ethmoid seen at the otorhinolaryngological cl inic at Rennes 

between 1964 and 1973. Thi rteen of the adenocarcinomas were in 

woodworkers. One other woodworker had a squamous cell carcinoma. All the 

woodworkers were men. Three of the fourteen no longer worked wi th wood. 

Their exposure duration was 9.6 years and latency period from first exposure 

to diagnosis was 27 years. Exposure duration for the remaining 11 averaged 46 .4 years. Woods used by the woodworkers included chestnut, oak, beech, 

fir, ash, walnut, cherry, mahogany, gaboon, citron, and iroko. The authors 

sunrnarized from the I iterature and thei r own cases a total of 557 ethmoid 

cancers, of which 157 (28.2%) were in woodworkers. These cancers included 

213 adenocarcinomas, 111 (52.1%) of which were in woodworkers. The authors 

concluded that ethmoid adenocarcinoma in woodworkers should be recognized as 

an occupational disease. 

As part of a series of articles publ ished on workers in the French wood 

industry, Petiet et al. (1981) reported on 25 ethmoid cancer patients in 

Nancy diagnosed between 1975 and 1979. Nine of the 25 (36%) were 

woodworkers (average age 58 years). Six of the nine had adenocarcinoma. 

The authors also summarized eight French studies (including their own) 

between 1972 and 1979 and reported that of 458 ethmoid cancer patients, 150 

(32.75%) were woodworkers. Of these 150, 139 (92.66%) had adenocarcinoma. 

Cabal and Teyssier (1981) described eight cases of ethmoid cancer diagnosed 

In the Loi re province between 1975 and 1980. Seven of the patients were 

woodworkers. The average length of wood dust exposure for the five cases 

for which a detai led history was provided was 39 years. Brugere et al. 

(1981) reported on 53 ethmoid adenocarcinomas (48 males, 5 females) 

diagnosed at the Curie Institute in Paris between 1961 and 1980. Of the 44 

males for which occupational history was avai lable, 35 (80%) were 

woodworkers. Marandas et al. (1981) reported that between 1961 and 1979, 

there were 112 cases of ethmoid cancer out of a total of 15,712 cancers 

diagnosed at the Gustave-Roussy Institute. Of these 112, 61 were 

adenocarcinomas, and 35 of those were in woodworkers. 

East and lest Germany--

Gulzow (1975) described a case of ethmoid adenocarcinoma in a 59-year-old patient who had worked as a carpenter for 44 years. The author considered 

the possibi I i ty that this was a case of occupationally related 

adenocarcinoma. As part of his report, Gulzow also obtained thin layer 

chromatograms from methanol extracts of wood shavings, wood powder, and wood 

tar prepared from beech and oak, two types of wood used frequently by 

carpenters. The powders from both woods yielded greater amounts of 

methanol-soluble compounds, which were attributed to the powders' greater surface area. The author proposed that cases of adenocarcinoma of the 

paranasal sinuses among woodworkers exposed to fine hardwood dusts be 

compiled to determine whether this disease should be considered an 

occupational one in German workers. 

72 
, 

Lobe and Ehrhardt (1978) published a study of malignant disease of the nose 

and paranasal sinuses among 420 patients (252 males, 168 females) admitted 

for treatment to the otorhinolaryngological clinic at the University of Jena 

in the German Democratic Republic (GDR) between 1931 and June 1, 1977. The 

occupations of 179 patients (111 males, 68 females) could be determined; 37 

(20.8%) were woodworkers. Adenocarcinomas accounted for 18 (10.1%) of the 

mal ignancies, of which 13 (72.2%) were in woodworkers. This association 

between woodworking and adenocarcinoma was signi ficant (p<0 .OO1). All of 

the affected woodworkers were over age 40. Woodworkers had 19 other 

carcinomas, 3 sarcomas, and 2 other mal ignancies of the nose and paranasal 

sinuses. The woodworkers did not di ffer from the general population in 

smok i n9 hab its. 

In a retrospective epidemiological study, Smetana and Horak (1983) examined 

127 patients with mal ignant tumors of the nose and paranasal sinuses. 

Adenocarcinomas accounted for 22.8% of the total number of mal i9nancies. 

Although only 2.14% of the total number of occupationally active patients in 

the authors' area of examination were woodworkers, 17.2% of the patients 

with adenocarcinoma and adenocystic carcinoma had been exposed to wood 

dust. Exposure duration ranged from 15 to 35 years. The correlation 

between wood dust exposure and these types of tumors was significant 

(p<0.OO1). 

In an empirical case study, Grilll1l et al. (1984) reported the results of a 

survey of hospitals with otorhinolaryngology departments in the Federal 

Republ ic of Germany and West Berl in. Occupational histories were determined 

by questionnaires to both the patient or his survivors and to his supervisor 

or colleagues at work. When possible, the workplace was also inspected. Of 

the 66 cases of adenocarcinomas identified, 40 (36 males, 4 females) 

diagnosed between 1964 and 1983 were evaluated. Twenty-two of the 36 male 

cases and none of the females were in occupations involving wood exposure. 

Simi lar proportions of woodworkers (15122; 68%) and nonwoodworkers (10/14; 

71%) were smokers. Exposure to hardwood (oak and beech) was more frequently 

mentioned. The median latency period from time of first exposure to wood 

dust until diagnosis of adenocarcinoma was 40 years. No correlation between 

increasing period of exposure or latency period with frequency of 

adenocarcinoma was seen, but the authors cautioned that the small number of 

cases arialyzed made it impossible to draw statistically significant 

conclusions. 

Thurauf and Hartung (1984) described six cases of nasal adenocarcin~ 

reported for indemnification as an occupational disease in the Federal 

Republic of Germany following exposure to wood dust. 

Gibel et al. (1985) described the results of a cross-sectional study of 

cancer of the nasal cavity and paranasal sinuses carried out in seven 

districts in the GDR and East Berl in. A total of 628 patients (404 males, 

224 females) were identified from cancer registries for the period 

1958-1979. Sixty-two (15.3%) of the men and 5 (2.2%) of the women were 

woodworkers. Amon9 men, the most frequent tumor location was the ethmoid 

sinus (35.5%); adenocarcinomas were the most frequent histological type 

(35.5%). 

73 
Ernst and Ambrosch (1986) evaluated 40 patients with nasal adenocarcinoma 

and reported that they had been exposed to oak and beech dusts. The authors 

be Ii eved that th i s proved a causa I connect i on between these types of dust 

and the disease, and recommended that worker compensation be permitted in 

individual cases fol lowing occupational exposure to oak or beech dust. 

The Netherlands--

Delemarre and Themans (1971) described 16 patients who had been treated for 

nasal adenocarcinoma at the Anthony van Leeuwenhoek Hospi tal between 1944 

and 1967. Eleven of the 16 (68.8%) were woodworkers: 6 furniture makers, 2 

carpenters, 1 wagon maker, 1 mechanical woodworker, and 1 ship's carpenter 

working in a sawmi I I. These patients were compared to a control group of 33 

patients, 3 of whom were woodworkers, treated at the hospital from 1956 to 

1968 for carcinoma of the nose of a histological type other than 

adenocarc i noma. The re I at i onsh i p between woodworker occupat i on and nasal 

adenocarcinoma was significant (p<O.OOl) . 

I n a case-cant ro I study des i gned to exami ne the re I at i onsh i p between nasa I 

cancer and wood dust (Hayes et al. 1986a) and formaldehyde (Hayes et al. 

1986b) exposure, the authors identified 116 Dutch males with histologically 

confirmed cancer of the nasal cavities or accessory sinuses newly diagnosed 

between 1978-1981. Of the 116 cases, 67 were squamous cell carcinomas, 28 

were adenocarcinomas, and 21 were other types. The control group consisted 

of age-stratified random samples of living male residents of the Netherlands 

in 1982 (223 controls) and of deceased males in the Netherlands in 1980 

(36 controls). Interviews, including smoking and alcohol consumption 

information, were completed for 91 cases and 195 controls. Exposure to wood 

dust and formaldehyde was rated subjectively by one of the authors on a 

scale from 0 (none) to 9 (highest) based on job histories. When all types 

of nasal cancer were combined, only employment in the paper and wood 

industry was associated with a significantly (p<0.05) increased risk of 

nasal cancer. This was due exclusively to the strong association with 

adenocarci noma (age-adjusted odds rat io [OR]=11.3). For wood-re lated 

occupations, there was a signi ficant risk for adenocarcinomas associated 

with ever being employed in furniture and cabinetmaking (OR=139.8) and in 

factory joinery and carpentry work (OR.16.3). No increased risk was seen 

for other' types of nasal cancer. When wood dust exposure concentrations 

were stratified as low (levels 1-2), medium (levels 3-4), or high (levels 

5-9), a significant risk of squamous cell carcinoma was associated with low 

levels of exposure only (smoking-adjusted OR=2.5). There was also a 

significantly elevated relative risk for adenocarcinoma associated with high 

levels of exposure (smoking-adjusted OR=26.0). The association between wood 

dust and adenocarcinoma was strongest for those employed in wood 

dust-related occupations between 1930 and 1941 (OR=86.0), particularly with 

first employment during that period. There were no cases of adenocarcinoma 

among those newly employed in wood-related occupations after 1941. The 

authors suggested that this might mean that the risk factors associated with 

adenocarcinoma had changed since that time. However, they also cautioned 

that the long latency period generally associated with this disease may make 

such a conclusion premature. There was also a signi ficant relationship 

between duration of employment at high exposure levels and adenocarcinoma. 

74 
The odds ratios were 10.1 for less than 10 years exposure, 38.4 for more 

than 10 years exposure, and 33.0 for more than 30 years exposure. There was 

no evidence that the relative risk of adenocarcinoma was lower among those 

whose exposure ceased in 1966. 

Belgium--

Debois (1969) reported that of 29 patients from Mechelse with tumors of the 

nasa I cav i ty and the ethmo ids i nus seen between 1958 and 1968, 16 were 

woodworkers or apprent ices and 2 others (a furni ture worker and a wood 

industry freight worker) had some contact with woods. Among these 18 

people, 15 had adenocarcinomas, 2 had epidermoid carcinomas, and 1 had an 

undifferentiated cancer. Among the 11 patients without any relation to 

woodworking, 5 had adenocarcinomas, 4 had epidermoid carcinomas, and 2 had 

undifferentiated cancers. The author suggested that further epidemiological 

study of cancer in woodworkers be conducted. 

Aust r ia--

Loffler (1972) publ ished a summary of 64 patients (34 men, 30 women) with 

mal ignant tumors of the nose or the paranasal sinuses treated from 1960 to 

1970 at the First Otorhinolaryngological Clinic of the University of 

Vienna. Thi rty-seven of these patients had carcinomas, 2 of which were 

adenocarcinomas of the ethmoid and 2 others were adenocarcinomas of the 

maxi Ilary sinus. Two of the patients with adenocarcinomas had worked as or 

with a cabinetmaker; the other 2 were women without any known connection to 

a wood-processing occupation. Loffler concluded that the cl inic did not 

have sufficient industry of that sort to furnish a statistically valid 

sample for testing the hypothesis that occupational exposure to wood dust 

resulted in the development of adenocarcinoma of the nasal mucosa. 

Swi tzer land--

Ruttner and Makek (1985) described a case series of 31 Swiss patients with 

adenocarcinoma of the nose and paranasal sinuses observed between 1953 and 

1984. Thirteen of the patients had occupational exposure to wood dust. The 

authors suggested an association of adenocarcinoma with wood dust, although 

the naturw of the carcinogen was unknown, and suggested further study. 

Vader and Minder (1987) examined the relative risk of mortality from cancer 

of the nasal cavity and paranasal sinuses among Swiss furniture workers aged 

15-79. Analyzing death certificates for the years 1979-1982 and national 

census figures for 1980, they observed 9 cases of s inonasal cancer among 

41,667 furniture workers and 59 cases among 1,813,798 male workers in the 

general population. They calculated an SMR of 6 .6 (p<0.OOO1, 95% CI 

3.0-11.6) for death due to sinonasal cancer and an odds ratio of 230 

(p value not speci fied) for death from adenocarcinoma. The authors 

concluded that sinonasal cancer in furni ture workers was one of the most 

clearly defined occupational cancers in Switzerland. 

75 
• 

Austral ia--

I ronside and Matthews (1975) discussed 19 cases of adenocarcinomas found 

among 99 cases of mal ignant tumor of the nose and paranasal sinuses at the 

Cancer Institute of Victoria. Eighteen of the cases were in men and only 

one in a woman, who was listed as a homemaker . This difference in sex 

distribution was significant (p<O.OOO1) . Information regarding most recent 

occupation was avai lable for 13 of the men. These included three 

carpenters, one timber worker, and one sawmi II proprietor. When compared to 

either the 1966 male Victorian workforce or the total number of male 

patients registered at the Cancer Institute in 1973, the occurrence of nasal 

adenocarcinoma in 5 woodworkers out of a sample of 13 patients was 

significant (p<0.OOO12). 

Sulllllary--

The association between nasal cancer and occupations involving exposure to 

wood dust has been clearly established in the literature . This relationship 

was first noted in the late 1960's in Great Britain, where the incidence of 

nasal adenocarcinoma, a rare type of nasal cancer, among woodworkers in the 

furni ture industry was found to be 10 to 20 times greater than among other 

. woodworkers and 100 times greater than the general population. The 

association has been confirmed to varying degrees in Canada, Denmark, 

Sweden, Norway, Italy, France, East and West Germany, the Netherlands, 

Belgium. Switzerland, and Australia. Negative studies and insufficient data 

have also been reported in Canada. Finland. and Austria. In the United 

States, three studies have reported an approximately fourfold increased risk 

of either nasal cancer or adenocarcinoma in furniture workers, and a fourth 

has reported a simi lar relationship between nasal cancer and wood dust 

exposure . A fifth study fa i I ed to show an inc reased risk of nasa I cancer 

among furniture workers. but did indicate such an increase among workers in 

logging and timber industries. 

As noted above. the association between nasal adenocarcinoma and wood dust 

exposure is particularly strong among furniture industry workers. although 

other woodworkers have also been shown to be at risk. Simi larly. exposure 

to hardwoods has been impl icated most often, but there are several reports 

implicating· softwoods as well. There is no conclusive evidence linking 

other histologic types of nasal cancers to wood dust exposure . There are 

also no quantitative concentration-response data. although there is some 

indication that adenocarcinoma is linked with qualitatively higher levels of 

wood dust exposure and that the risk increases wi th a latency period from 

first exposure. Studies in England and Scandinavia have also detected 

metaplasia and dysplasia in the nasal mucosa of workers exposed to wood dust. 

B. Pulmonary Cancer 

In his analysis of the 1969-1971 death records of the AFL-CID United 

Brotherhood of Carpenters and Joiners of America, Mi I ham (1974) found a 

signi ficant (p<O.05) excess of mal ignant neoplasms of the bronchus and lung 

(SMR=106 .7) and a sl ight but statistically nonsigni ficant excess for 

76 
, 

malignant neoplasms of the more inclusive respiratory system category 

(SMR=102.9). When examined by trade, furniture workers, cabinetmakers, and 

millmen, lumber, and sawmill workers showed no increase in lung cancer 

incidence . Only construction workers showed a statistically significant 

elevated lung cancer rate (SMR=118) . 

Blot and Fraumeni (1976) conducted an ecological survey of lung cancer 

mortality in industrial counties of the United States during the period 

1950-1969. These counties were defined as ones in which at least 0.1% of 

the population was employed in one or more of 18 manufacturing industries. 

No excess lung cancer mortality was seen in counties with lumber or 

furniture industries. However, lung cancer mortality among white males was 

sign if i cant Iy (p<0.05) elevated in count ies wi th paper manufactur i ng 

industries. 

Harrington et al. (1978) followed up the work of Blot and Fraumeni (1976) 

with a death certificate case-control study of the 858 white males in 12 

coastal counties of Georgia who died of primary lung cancer during 

1961-1974. Each of these decedents was matched for age at death (wi thin 

1 year), year of death (within 6 years), and county of usual residence with 

a white male who died of conditions other than lung or bladder cancer or 

chronic respiratory disease. No information on smoking habits was 

p rov i ded . The re we re 97 cases emp loyed in the wood and pape r indus try 

versus 78 in the controls. This di fference was not statistically 

significant . When examined by county, there was an excess risk associated 

with the wood and paper industry (relative risk=3.3, p<0.05) in the combined 

nine smaller counties but not in any of the three largest counties. The 

nine smaller, less populated, counties had 20.1% of the people dying of 

pulmonary cancer employed in the wood and paper industry whereas only 7.2% 

of the cont ro I popu I at ion in these count i es was emp loyed in that indus try. 

Harrington et al. (1978) stated that the risk was greatest among sawmi II, 

lumber, and forestry workers, but provided no data to support this assertion . 

Blot et al. (1982) conducted a two-part case-control study to examine the 

high lung cancer mortality along the northeast coast of Florida. The first 

part of the study was hospi tal-based and included all male residents in 

Duval County newly diagnosed with primary lung cancer at one of 13 

Jacksonvi lie hospitals during the period Apri I 10, 1978, through Apri I 9, 

1979. Two controls were matched by age (within 2 years), race, and 

hospital. The second component used Florida State mortal ity fi les for 1976 

for both cases and controls. The cases were all deaths attributed to 

primary lung cancer among male residents of four counties, matched by race, 

age, and county of residence to an equal number of randomly selected 

controls . In both parts of the study, controls excluded cases of lung 

cancer and chronic respiratory disease. Occupations were coded based on SIC 

codes. There were 181 cases and 342 controls in the first part of the study 

and 217 cases and 217 controls in the second. A total of 807 interviews 

were completed; after exclusions, the final study group included 755 

subjects (321 cases and 434 controls). When adjustments were made for 

cigarette smoking, a statistically significant risk for lung cancer was seen 

for the lumber and wood industry (RR=1.7, p<0.04) and construction (RR=1.4, 

p<0 .04). The excess risk in the former category, which included primari Iy 

77 
sawmill laborers, was primarily due to those with exposure to wood dust 

(RR=1.9) rather than those without (RR=1.2). The authors commented that the 

excess risk in this category was limited to smokers, raising the possibi lity 

of a co-carcinogenic effect. 

Mi Ine et al. (1983) conducted a death certificate case-control study of lung 

cancer in Alameda County, California between 1958 and 1962. The study group 

included 925 lung cancer deaths (826 as primary cause and 99 as si9ni ficant 

condition present at death) and 6,420 deaths from other cancers. Deaths 

occurring under the age of 18 were eliminated because they were not 

considered 'to contribute to an analysis of occupational factors. No 

info rma t i on on tobacco use was ava i I ab Ie. Occupa t i on and indus try 

information were coded by Bureau of Census Industrial and Occupational 

Classification System. Analyses were stratified on age at death and 

analyzed separately for males and females. Two overlapping control groups 

were uti lized, one consisting of all other 6,420 cancer deaths and the other 

consisting of a "reduced" group of 4,880 other cancers not known to be 

strongly associated with occupational risk factors. Combined risk estimates 

were computed as the maximum I ikel ihood estimate of the odds ratio. Males 

employed in the furniture industry had a significant (p<0.01) risk of lung 

cancer when compared to either the complete or reduced control group (OR=4.2 

and 3.6 respect i ve I y) . Those emp loyed in const ruct i on a I so had a 

significant (p<0.01) risk of lung cancer (OR=1.6). No simi lar risk was 

shown for sawmi lis, or for the combined classification lumber/furniture 

manufacturing. When stratified by occupations, there was no significant 

lung cancer risk to male carpenters or cabinetmakers/furniture finishers. 

Dubrow and Wegman (1983) identified occupations with potentially high cancer 

risk by combining the results of 12 major occupational disease survei I lance 

studies covering the years 1950-1973 conducted in the United States and 

Great Britain. The analysis was limited to white males. 

Observed-to-expected rat ios and observed numbers of deaths or cases were 

abstracted from these 12 studies, and comparison tables were constructed for 

occupational categories comparable across two or more studies. Carpenters 

and cabinetmakers were I isted as having increased risk of cancer of the 

trachea, bronchus, and lung. 

Stellman and Garfinkel (1984) analyzed data compi led from 1959 through 1972 

in the American Cancer Society's prospective epidemiologic study of more 

than 1 mi II ion people in 25 states. The analysis was I imited to only males 

alive on July 1, 1960. There were 10,322 woodworkers (carpenters/joiners, 

lumber and sawmi II workers, and furniture/cabinetmakers) and 406,798 

nonwoodworkers in the study population. Smoking habits, use of 

over-the-counter medications, and beer consumption were simi lar in both 

groups. Neither the woodworker subgroups nor the woodworkers as a whole had 

an excess combined cancer death rate when compared to the nonwoodworkers. 

However, carpenters and joiners did show a significant excess of lung cancer 

(age and smoking adjusted SMR=122, p<0.03). The authors hypothesized that 

men in this subgroup were most likely to be exposed to asbestos, which might 

have contributed to the rate. As an aside, the only nasal cancers observed 

in this study were in carpenters and joiners (2 cases). This was too small 

a number to permit meaningful statistical analysis, but was twice the number 

78 
expected in woodworkers and three times that expected based on carpenters 

and joiners only. 

Digiesi (1972) described a case of di ffuse nodular bronchiolar (alveolar 

cell) carcinoma wi th hydropneumothorax in a 40-year-old man who had been 

exposed to wood dust in an Italian woodworking factory since the age of 

8 years . The patient was not a smoker . The author hypothesized that there 

was a causal relationship between the patient's exposure to wood dust and 

the onset of bronchiolar-alveolar carcinoma. 

In the Rang and Acheson (1981) study of nasal cancer in En91 ish furniture 

workers described in part A of this section, no excess cancer risk at any 

other sites, including bronchial cancer, was found. However, there was a 

significant trend (p<0.05) of increasing bronchial cancer mortality with 

increasing dustiness of work (subjectively determined by job 

classification). When SMR's were estimated for ski lied furniture workers 

(those who could reasonably be assumed to have started working before the 

age of 20), no excess of bronchial cancer was observed . However, again 

there was a trend of increasing mortality with increasing dustiness of work, 

although it was not quite statistically significant (p=0.06) . 

Esping and Axelson (1980) described a case-control study that examined the 

occurrence of respiratory and digestive tract cancer among woodworkers in 

Sweden. The study included 95 cases (25 respi rato.ry cancera, none of which 

were nasa I cancer , and 70 of the d i ges t i ve tract , inc I ud i ng mouth) se I ected 

from the local death register in the small Swedish town of Mjolby during 

1963-1977. Only males over 50 years of age were included. These were 

matched against 370 male controls from the register in the preceding and two 

succeeding positions for each case. For woodworkers, a fourfold excess of 

respiratory cancer was found (p<0 .05). Subdividing the woodworking category 

into "furni ture makers" and "other woodworkers" suggested that the risk was 

primari Iy to the former. The authors concluded that there was excess 

mortality from respiratory cancer among woodworkers, especially furniture 

makers, that could not be explained by smoking or other confounding factors. 

In thei r study of Swedish furniture workers described in part A of this 

section, Gerhardsson et al. (1985) found no increased risk for laryngeal or 

lung cance r . 

Gallagher and Threlfall (1985), in their proportionate mortality study of 

deaths in British Columbia, Canada from 195O to 1978 , reported a 

statistically significant increase in deaths due to lung cancer among 

woodworkers and the subgroup carpenters. The PUR's were 119 (95% CI 

105-134 , p<0.OO4) and 122 (95% CI 106-140, p<O.03), respectively. Sawmill 

workers had lower lung cancer PMR's than expected but the lowered risks were 

not statistically signi ficant. Lumber grader and scalers had normal lung 

cancer risk , whi Ie loggers showed a reduced risk. The authors commented 

that this might be the result of the large number of deaths due to accidents 

to loggers , which depresses the proportion of observed deaths due to cancer . 

In a case-control study, Siemiatycki et al . (1986) reviewed 19 potential 

cancer sites among 2,180 male hospital patients aged 35-70 in Montreal , 

79 
Canada from September 1979 to June 1983 . Information regarding the 

patients' I ife-styles and work histories was obtained via interviews or 

questionnaires. The control groups consisted of individuals drawn from 

those with other cancer sites in this study . Lung cancer was excluded from 

all control series. Five hundred and twenty-five (24.1%) of the subjects 

were considered to have had any exposure to wood dust, and 345 (15.8%) had 

substantial exposure. The main occupations in which wood dust exposure was 

coded were construction (carpenters, painters, pipefitters, plumbers , etc.), 

forestry and logging, and fabricating and assembl ing wood products . The 

odds ratio for the association of lung cancer with substantial exposure to 

wood dust was of borderline significance (OR=1.3, 95% CI 1.0-1 .8), but was 

significant (p<0.05) when al I wood dust exposure (doubtful plus substantial) 

was considered. Additionally, when the substantially exposed category was 

divided into two segments (less than or equal to 15 years' exposure and 

greater than 15 years' exposure), those with the longer exposure were shown 

to have a significantly (p<0 .05) increased risk of lung cancer . Because 

this study controlled for smoking and other occupational exposures (e.g., 

asbestos), the authors claimed that their positive findings were persuasive. 

Kauppinen et al. (1986) descr i bed a Finnish case-control study that examined 

a cohort of 3,805 men born after 1904 who had worked for at least 1 year in 

the particle board, plywood, sawmi II, or formaldehyde glue industries 

between 1944 and 1965. One hundred and fifty-one primary malignant 

"respiratory" tumors were ident i fied; there were no tumors of the nose or 

sinuses. From these, 57 cases were selected for which histological or 

cytological specimens or necropsy and hospital protocols were avai lable. 

Three control subjects for each case were selected from the cohort and 

matched by birth year. The comparison of exposure was based on work 

histories and job exposure matrices. These matrices were constructed by one 

of the authors based on general and plant-specific hygiene data on 

exposures , information on venti lation, work procedures, and other relevant 

factors at the plants. At least 1 month of exposure time to wood dust was 

requ i red to be cons i dered "exposed ." Exposure concent ra t ions were 

classified as follows : low level (0 . 1-1I11g/m3), moderate level 

(1-5 mg/m3) and high level (over 5 mg/m3 ) . The estimated average wood 

dust exposure concentration was 1-2 mg/m3 and the mean duration of 

exposure was 10 years. When adjusted for smoking, the odds ratios for 

respiratory· cancer for wood dust exposure were 1.60 with no provision for a 

latency period and 1.68 with a 10-year latency period . These were not 

statistically significant at the 5% level. There was no significant 

exposure-response relationship observed for either exposure concentration to 

or cumulative amount of wood dust . However, the odds ratio for cumulative 

amount over 5 mg/m3-years was higher than that for under 5 mg/m3-years. 

SUlllllary--

Data on the association between lung cancer and occupations involving 

exposure to wood dust are conflicting, and the body of literature is 

considerably smaller than that for nasal cancer . Negative studies have been 

reported in England, Sweden, and Finland. However, several case-control and 

cohort mortal ity studies in the Un i ted States, Canada, and Sweden have 

reported increases in lung cancer among wood-exposed workers, but there is 

80 
, 

not unanimity as to which particular occupational subgroup of woodworkers is 

affected. In the United States, construction workers, sawmi II workers, 

furniture workers, and carpenters and joiners have each been singled out in 

individual studies. One explanation for increased lung cancer in 

construction workers and carpenters and joiners has been potential asbestos 

exposure to individuals in those occupational classifications. One study 

implicated smoking as a potential co-carcinogenic factor. There are no 

concentration-response data. 

C. Hodgkin's Disease 

Mi Iham (1967) and Mi I ham and Hesser (1967) publ ished a case-control study of 

1,549 white males, ages 25 years or more, who had died of Hodgkin's disease 

(malignant Iymphoreticuloadenoma) in New York State during the years 

1940-1953 and 1957-1964. Each was matched to a control who died of other 

causes by age (w i th i n 5 years), sex, race, county of res i dence, and date of 

death (within 4 weeks). Seventy of the cases were categorized as 

woodworkers, whereas only 31 controls were simi larly classified. This 

difference was statistically significant (p<0.OO1). The investigators 

concluded that thei r findings suggested that death from Hodgkin's disease 

could be associated with occupational exposure to wood dust. 

In an ecological study based on data publ ished by the U.S. Publ ic Health 

Service, Bureau of the Census, and Department of Agriculture, Spiers (1969) 

analyzed the occurrence of Hodgkin's disease among whites from 1956-1965 in 

areas of the United States with various percentages of cOlll11ercial pine 

forest land. He calculated ratios for both men and women of the number of 

deaths due to Hodgkin's disease to the number of combined deaths from 

Hodgkin's disease, lymphosarcoma, and reticulosarcoma. These ratios served 

as indices of mortality. Among males in the 37 states east of the Rocky 

Mountains, Spiers found a significant (p<0.05) relationship between this 

ratio and both the percent of employed white population in the wood, lumber, 

and furniture industries and the percent of area of commercial forest land 

covered by pine. He concluded that males in the wood industry in the 

eastern states were at special risk of developing Hodgkin's disease, 

conceivab.y depending upon the extent of exposure to pine pollen, and 

pointed out that this conclusion would be strengthened greatly if it could 

be corroborated by data from primary sources. 

In Mi Iham's (1974) study of union carpenters and joiners previously 

described in part B of this section, the overall SMA for Hodgkin's disease 

was 90, but for the over 60 age 9rouP, the SMA was 177 (p<0.05). Milham 

stated that since Hodgkin's disease shows a bimodal age incidence curve, 

this would indicate that the second mode is etiologically different from the 

first and may be occupational in origin. 

Petersen and Mi I ham (1974) examined Washington State death records for all 

males 20 years and older for the period 1950-1971. Both case-control and 

proportional mortality ratio analyses were conducted. For the former, each 

of the 707 Hodgkin's disease deaths was matched against a control selected 

randomly from al I deaths except those due to Hodgkin's disease or to 

81 
accidents and violence. A subset of 158 case-control pairs was also 

selected from the Washington death fi Ie for the period 1965-1970 for a 

separate interview study. In the main case-control study, 56 of the 707 

matched pairs included a case that had a wood-related occupation 

(carpenters, cabinetmakers, sawyers, and papermakers) when its control did 

not. Thirty-two pairs had a wood-related control when its case did not. 

This difference was statistically significant (p<0.05). In the interview 

study, 23 matched pai rs had a wood-related case and not a control and 10 

pairs had a wood-related control and not a case. This was also significant 

(p<0.05). In the age-specific proportional mortality ratio analysis, there 

were 56 deaths observed and 34.34 expected. The PMR was 163, which was 

signi ficant at the p<0.001 level. Petersen and Mi I ham concluded that thei r 

study within Washington State provided additional support for the hypothesis 

that woodworking and Hodgkin's disease mortality are associated . 

Milham (1976a, 1976b) presented an additional age and death-specific 

proportionate mortality analysis of nearly 300,000 Washington State death 

records for white males over age 20 for the period 1950-1971. Loggers, 

plywood workers, and sawmi II and other mi II workers were not found to have 

increased PUR's for Hodgkin's disease, but pulp and paper makers (12 cases 

observed) and carpenters (38 cases observed) had significantly (PiO.05) 

increased PMR's of 192 and 162, respectively. 

Mi Iham (1983) subsequently updated his Washington State study to include 

nearly 430,000 male deaths for the period 1950 to 1979 and 25,000 female 

dea ths fo r 1974-1979. Among wood-exposed occupa t ions, sign i f i can t I Y 

(p<0.01) elevated PUR's for Hodgkin's disease were noted among carpenters 

(PMR 150), mi I Iwrights (PMR 324), and paper and pulp mi II workers (PMR 194) . 

Grufferman et al. (1976) conducted an incidence survey of Hodgkin's disease 

in the Boston Standard Metropolitan Statistical Area during the period 

1959-1973. The ave rage annua I inc i dence rate of Hodgk in's disease dur i ng 

the study period was 5.1 per 100,000 for males and 3.2 per 100,000 for 

females. These figures gave a male/female ratio of 1.6. During the 3 

successive 5-year periods that comprised the study period, the average 

annual incidence rates for men were relatively constant at 4.9, 4.6, and 5.4 

per 100,000. For women, the corresponding values were 2.8, 3.4, and 3.5 per 

100,000. 'l'he percentage increase from the fi rst to the thi rd value for 

women was 2.5 times that for men. When the age-specific incidence rates for 

Hodgkin's disease were plotted, the curve for males was generally above that 

for females. Both curves reached early peaks, of about 7.0 per 100,000 for 

men, at about 23 years of age. The curves then fell gradually to minima 

that were fairly constant between ages of about 30 to 50 years. Thereafter, 

the curves rose to peaks, higher than the early ones, at 80-90 years. Of 

seven urban occupations, the two with the largest relative risks of 

Hodgkin's disease were (1) lawyers and judges and (2) woodworkers, although 

neither of these were significant at the p=O.05 level . However, the authors 

concluded that thei r findings supported those of Mi Iham and Hesser (1967) 

and Petersen and Mi Iham (1974) and suggested that woodworkers have a small 

increased risk of developing Hodgkin's disease . 

82 
Greene et al. (1978) examined death certificates in North Carolina counties 

having a signi ficant proportion of the population employed in furniture 

making and lumbering. They found 167 white male deaths from Hodgkin's 

disease. Each of these decedents was matched wi th two whi te males who had 

died of other causes by county of death, age, and year of death. Matched 

triplet analysis revealed a nonsignificant relative risk of developing 

Hodgkin's disease of 1.4 (95% CI 0.5-2.3) among occupational groups with 

wood and paper exposure. The major di fference occurred for carpentry and 

lumbering, which was significant (relative risk 4.2, 95% CI 1.4-12.5). The 

authors also reported a case of fami lial occurrence of Hodgkin's disease in 

three sibl ings and a fi rst cousin, two of whom had worked for over 12 years 

with cedar wood products immersed in pentachlorophenol. The authors 

hypothesized that the association between occupational exposure to wood and 

Hodgkin's disease may be related to the use of chemical preservatives. 

Following the paper of Mi Iham and Hesser (1967), Acheson (1967) studied the 

occurrence of Hodgkin's disease during the period 1956-1965 among residents 

served by the Oxford Regional Board. This was the same population studied 

for cancer of the nasal cavities and paranasal sinuses in furniture makers. 

High Wycombe had a crude average annual Hodgkin's disease incidence rate of 

4.0 per 100,000. The rest of Buckinghamshi re had a rate of 2.9 per 100,000 

and the remai nder of the study area in Oxfordsh ire, Northamptonsh ire, and 

Berkshi re had a rate of 2.4 per 100,000. Acheson stated that the 

differences between the incidences of Hodgkin's disease in High Wycombe and 

in other parts of the study area were not significant. Using the age distributions of all woodworkers in England and Wales as the basis, Acheson 

calculated that four woodworkers in the study area would have been expected 

to develop Hodgkin's disease during the period of the study. Since only 

three cases of the disease were observed, Acheson concluded that exposure to 

wood dust in the Oxford area did not contribute appreciably to the incidence 

of Hodgkin's disease there. 

Fonte et al. (1982) reported a case-control study of 207 males and 180 

females (mean age 47.3 years, range 10-70) admitted to the University of 

Pavia Medical CI inic in Italy from January 1972 to December 1979 with a 

diagnosis of Hodgkin's disease. The controls were 441 males and 330 females 

(mean age ~8.8 years, range 11-78) admitted to an internal medicine unit in 

Pavia from June 1977 to December 1979. Occupations were coded according to 

Italian job classification systems. The authors found a statistically signi ficant risk of Hodgkin's disease for workers classi fied in the wood 

industry (relative risk 7.2, p<0.005). 

No increased risk of Hodgkin's disease or cancers of the reticuloendothelial 

system were reported in the previously described studies by Rang and Acheson 

(1981), Acheson et al. (1984), Stellman and Garfinkel (1984), and Gallagher 

and Threlfall (1985). 

Summary--

As was the case for lung cancer, there are conflicting data regarding the 

relationship of Hodgkin's disease to occupational exposure to wood dust. 

Negative studies have been reported in England, Canada, and the United 

83 
, 

States. However, several other U.S. case-control and cohort mortality 

studies have reported increases in Hodgkin's disease among woodworkers; this 

excess occurrence seems to be concentrated among carpenters. There are no 

concentration-response data. 

D. Other Cancers 

A causal relationship between multiple myeloma and wood dust exposure was 

first suggested by Brinton et al. (1976). In Mi Iham's (1983) updated survey 

of occupational mortality in Washington State, a significantly (p<0.01) 

increased risk for multiple myeloma was seen in pulp and paper mi II workers 

(PUR 182); nonsignificant increases were seen in cabinetmakers (PUR 104). 

carpenters (PUR 118), and plywood workers (PUR 144). In an ecological study 

of Texas State economic areas, Agu et al. (1980) found a significant 

(p<0.05) posi t ive associat ion between the age-adjusted mortal i ty rate from 

multiple myeloma and percentage of population employed in carpentry, when 

control was made for race. Tollerud et al. (1985), in a 1956-1980 death 

certificate case-control study in North Carolina counties in which at least 

1% of the population was employed in furniture and fixture manufacturing, 

found a nonsigni ficant excess risk of multiple myeloma, especially among 

those who died before age 65 and among those born before 1905 . A 

significantly elevated risk was seen in furniture workers born before 1905 

who died prior to age 65. Robinson et al . (1g86a), in a mortal i ty study of 

2,283 plywood mi I I workers employed for at least 1 year between 1945 and 

1955, reported a nonsignificant excess in mortality due to lymphatic and 

hematopoietic cancer excluding leukemia (SMR 156). Within this 

classification, the subgroup multiple myeloma showed the greatest excess 

(SMR 333), but the data were too sparse to distinguish clearly among 

subgroups . 

Decoufle et al. (1977) and Bross et al . (1978) reported the resul ts of a 

detai led survey of 6,434 white males and 7,815 white females, each having 1 

of 22 different kinds of cancer, from among 25,416 patients admitted to the 

Roswell Park Memorial Institute for Cancer Research, Buffalo, New York 

between 1956 and 1965. Demog raph ie, soc i a I ( inc I ud i ng smok i ng hab its) , 

medical, .and occupational information was obtained prior to diagnosis of 

disease. Fifty-four occupational/industrial groups were studied for men and 

eighteen for women. Among males ever-employed, the authors reported a 

nonsigni ficant increased age-adjusted relative risk for stomach cancer in 

carpenters , and for testicular and kidney cancer and myeloma in lumber 

laborers, and a significant (p<0 .05) relative risk for esophageal cancer in 

lumber laborers. Among men employed for at least 5 years, simi lar increased 

relative risks were not seen in carpenters and lumber laborers. 

Budy and Rashad (1977) studied mortality rates among two groups of 

carpenters in Hawai i : 227 (Group A) who died dur ing 1949-1951, inclusive, 

before arsenate-treated wood came into wide use, and 293 (Group B) who died 

during 1970-1973, inclusive, after the use of arsenate-treated wood became 

widespread . For both groups, the highest numbers of deaths from all causes 

and from all cancers occurred during the age decade of 65-74 years . 

Carpenters were matched wi th noncarpenters on the next record in sequence 

84 
that matched the carpenter in sex, age (within 5 years), and year of death. 

Age-spec i fic death rates were computed from U.S. census data from 1950 for 

the fi rst period and from 1970 for the second period . In Group A, there 

were 60 mal ignant neoplasms among the carpenters and 30 in the controls; in 

Group B the corresponding numbers were 67 and 63 . This di fference was 

stat i stically signi ficant (p<0 .05) in Group A but not in Group B. No 

significant difference between carpenters and controls in either Group A or 

B were seen for cancer of the trachea, bronchus, and lung or for cancer of 

the lymphatic and hematopoietic tissue. The overal I relative risk for 

cancer death was 3.58 for Group A and 2.72 for Group B. For Group A 

carpenters, the mean annual death rate for ages 16 to 65+ was 1,203 per 

100,000, whereas the corresponding figure for Group B was 1,259 per 

100,000 . For comparison, the mean annual death rates in the general 

population for the same two periods of time were 559 per 100,000 and 549 per 

100,000 . This is a consistent and si9n i ficant (p<0.05) increase in total 

deaths among carpenters . The authors corrmented that the excess of cancer 

death was consistent before and during a period of substantial exposure to 

arsenate-treated wood. 

Burkart et al. (1981) described a study designed to investigate the use of 

hospital records for occupational health survei Ilance . The authors reviewed 

the records of 9612 male patients aged 18 and older discharged during 1980 

from 4 hospitals in 3 southern Oregon counties . The 3 counties had 

approximately 12,000 workers employed in the sawmi II , mi Ilwork, logging , and 

other wood products industries. Those workers represented 29% of the total 

labor force. After the el imination of inval id records and patients for whom 

occupational histories could not be obtained, a total of 7,906 discharges 

were included in the final study population . The control group consisted of 

1,245 of the discharged patients chosen to represent a wide variety of 

infrequently occurring conditions that would not al I be affected to the same 

degree by a particular exposure. No statistically significant (p<0.05) 

increased risks from any types of cancer were seen, although a 

nonsignificantly increased risk for leukemia, primari Iy in workers with 10 

or more years employment in the sawmi II industry, was noted. To furth8r 

examine this potential relationship, the authors rechecked the records for 

secondary diagnoses, since the initial analysis included only primary 

diagnoses . E I even new cases of I eukemi a we re discovered, fou r of whom had 

worked 10 ' or more years in the sawmi II industry . Combining all the leukemia 

data resulted in a significant (p<0.05) concentration-response relationship 

between years of sawmi II exposure and leukemia. The bulk of the leukemia 

cases were over age 65 . 

In their cancer morbidity study among 1,070 white male model and pattern 

makers employed as of January 1, 1970, in seven Detroit automobile plants, 

Swanson and Bel Ie (1982) reported significantly (p<0 .01) increased 

age-adjusted SMA's for all types of cancer combined (SMA 150) and for 

colorectal (SMA 286) and salivary 91and cancer (SMR 2100). Nonsignificant 

increases were observed for lymphoma (SMR 301) and melanoma (SMA 323) . In 

subsequent conmunications, Chovi I (1982) and Davies (1983) questioned some 

of the methodology of the study. The authors responded to each of the 

questions raised, reemphasized the limitations of their descriptive study, 

and reiterated their findings . 

85 
• 

Swanson at al. (1985) subsequently analyzed 316 white male modelmakers and 

patternmakers employed by one U.S. automobile manufacturer as of 

January 1. 1976. Ages of the workers ranged from 18 to 68 years. with 58.5% 

between 35 and 54 years. There were 10 incident cancers diagnosed between 

1976 and 1982. of which 4 (40%) were colon cancer (SMA 487.0. p<0 .01). The 

authors indicated that this finding was consistent with earlier studies and 

recommended cohort and case-control studies to provide more definitive 

i nformat ion . 

Kurt (1986) questioned whether the increased rate of colon cancer reported 

by Swanson et al. (1985) could be due to either acrylonitri Ie exposure from 

plastics used in modelmakin9 or the workers' sedentary lifestyle. Both 

factors had previously been reported to be associated with an increase in 

colon cancer . Swanson and Burrows (1986) replied that their study was a 

descriptive analysis for which exposure data and levels of worker activity 

were not avai lable. and that future studies should incorporate these 

potential risk factors. 

In thei r 1972-1978 proportional mortal ity study of 1.257 pattern and model 

makers. Robinson et al . (1980) reported statistically significant excess 

proportions of deaths due to both colon (PMR 167. p<0 .OO2) and brain cancer 

(PMR 211 . p<0 .03). Amon9 members of the predominantly wood shop locals. 

significant excesses of colon cancer (PMR 163. p<0.01) and leukemia 

(PMR 200. p<0 .03) were found . 

In a cohort of 3.572 pulp and paper mi II workers employed for at least one 

year between 1945 and 1955. Robinson et al. (1986b) reported statistically 

nonsignificant excesses of death due to lymphosarcoma and reticulosarcoma 

(SMR 169. 90% CI 92-287) and to stomach cancer (SMR 123. 90% CI 78-185) . 

Franco and Fonte (1983) expanded the previously described case-control study 

of Fonte et al. (1982) to include 347 males and 322 females admitted to the 

University of Pavia Medical Clinic. Italy. between January 1969 and December 

1980 and diagnosed as mal ignant lymphomas (387 cases of Hodgkin's disease 

and 282 cases of non-Hodgkin's lymphoma). Among those employed in the wood 

industry. there were 14 cases and 8 controls with malignant lymphoma. This 

difference was significant at the p<0 .001 level. 

Stellman and Garfinkel (1984). in their previously reported review of 

woodworkers enrolled in the American Cancer Society's prospective 

epidemiologic study. reported significantly increased mortality ratios for 

stomach cancer (SMA 149. p<0.01) and bladder cancer (SMA 142. p<0.05) among 

al I woodworkers. and for stomach cancer (SMR 170. p<0 .01) in carpenters and 

joiners. They also noted a significantly decreased mortality ratio for 

colorectal cancer (SMA 75. p<0.05) in al I woodworkers . 

In their analysis of British Columbia death statistics. Gallagher and 

Threlfal I (1985) and Svirchev et al. (1986) reported a significant excess of 

several types of cancer in male woodworkers. These included stomach cancer 

(PMR 144. p=0.OOO1). lymphosarcoma and reticulum cell sarcoma combined (PMR 

159. p:0 .OO6). and all types of cancer (PMR 112 . p=O .OOO7) for the general 

woodworking category; stomach cancer (PMR 155. p<0 .001) . lymphosarcoma and 

86 
, 

reticulum eel I sarcoma combined (PMR 165, p<O.05), and all cancers combined 

(PMR 114, p=O.OOO6) in carpenters; pleural cavity (PMR 6553, paO.OOO9) , 

prostate (PUR 569, p=O.OO42), and all cancers combined (PW1 194, p<O.OOO1) 

in cabinetmakers and furniture makers; and lymphosarcoma and reticulum cell 

sarcoma combined (PMR 275, p<O.05) in sawmi II workers. Siemiatycki et al. 

(1986), in their case-control study of cancer patients in Montreal, reported 

an increased odds ratio of 1.7 (95% CI 1.1-2.8) for stomach cancer and wood 

duat exposure. 

Preliminary results of the NCI cohort mortality study of members of the 

Uni ted Furniture Workers of America (Mi Iler 1987) indicated reduced overall 

cancer mortality among white males in the wood furniture and other wood 

products industries, although a slight excess (p value not provided) of bone 

cancer was found. 

Sunmary--

There are insuff i c i ent and i nconc Ius i ve data regardi ng the re lat ionsh i p 

between occupational exposure to wood dust and cancers other than nasal, 

lung, and Hodgkin's disease. Multiple myeloma, stomach and colorectal 

cancer, and Iymphosarc~ are among the cancers most often mentioned in the 

avai I ab Ie cohort mortal i ty and morb id i ty stud i as as occur ring in occupat ions 

in which wood dust exposure occurs. 

87 
VII. INDUSTRIAL HYGIENE MEASUREMENTS AND CONTROLS 

This section contains a compi lation of wood dust concentrations measured in 

the workplace (Table 6 and SUlMlary Tables 7-12) and a brief discussion of 

wood dust control technology. Operations that generate wood dust can be 

classified into three general categories: sawing, sanding, and mi Iling. 

The latter includes such operations as planing, chipping, routing, moulding, 

jointing, shaping, and boring. Descriptions of these operations are 

provided in Holl iday et al. (1986), NSC (1980), and Hjorth and Holtrop 

(1966). It should be noted that the amount of wood dust generated and the 

particle size distribution wi II vary depending on the particular operation 

(e.g., sanders, shapers, and routers have been shown to give off more dust 

than other types of woodworking machinery [Ha'l!pl 1982]) as well as on the 

type of wood (Huebener 1987) and the water content of the wood (Holliday et 

al.1986). 

The various values in Tables 7-12 are presented only to provide the reader 

with a general idea of the ranges of wood dust concentrations that have been 

encountered in the workplace. They should not be general ized for 

epidemiological analysis of health effects related to wood dust exposure 

except for cases in which effects have been documented at specific dust 

concentrations. Unless otherwise noted, sampling and analyses were done by 

the gravimetric measurement of dust collected on a fi Iter. Where data are 

missing, they were not given by the investigator. Wood type and the mention 

of local exhaust venti lation (where provided) are noted. 

Good work practices, process substitution, and properly designed engineering 

controls can be used to minimize worker exposure to wood dust. A survey of 

lumber mills and furniture manufacturing plants (Anonymous 1979) revealed 

that work practices included (1) administrative controls, such as training 

programs and labeling, and standard operating procedures (e.g., housekeeping 

and cleanup programs); (2) the use of personal protective equipment, such as 

eye and face protection (e.g., safety glasses, goggles, and face shields), 

respi rators, and protective clothing (e.g., gloves, aprons, long sleeved 

shirts, and regular trousers); and (3) proper use of woodworking machinery. 

NIOSH has publ ished general health and safety work practice guidel ines for 

sawmi lis and planing mi lis (NIOSH 1978), plywood and veneer mi lis (NIOSH 

1977) , wooden furniture manufacturing (NIOSH 1975), prefabricated wooden 

bui Iding manufacturers (NIOSH 1976b), and mi Ilwork shops (NIOSH 1976a). The 

National Safety Counci I (NSC 1970-1986; NSC 1980) and the American National 

Standards Institute (ANSI 1975) have also publ ished safety guidel ines for 

various types of woodworking machinery. 

Substitution of processes that eliminate or reduce wood dust generation has 

also been reported (Hoi I iday et al. 1986). These processes include peel ing 

89 
, 

and slicing to produce veneer sheets, high-energy water jets for cutting and 

machining, and laser cutting. The first two processes are limited in their 

application; the third is sti II experimental. 

The primary engineering control for wood dust is local exhaust venti lation 

(Hampl and Johnston 1985). In addition to reducing worker exposure to wood 

dust, ventilation also reduces potential safety hazards due to fire and 

explosion (NFPA 1980). ACGIH (1986) has made general recommendations for 

local exhaust system configurations and venti lation rates for various types 

of woodworking equipment, including band, table, swing, and rip saws; disc, 

belt, drum, and swing arm sanders; single and double planers; routers; 

jointers; molders, matchers, and sizers; and lathes. ACGIH recommended 

exhaust volumes are shown in Table 13. 

Local exhaust systems have been specifically designed for belt sanders 

(Hampl and Johnston 1985), shapers (Huebener 1987), and circular table saws 

(WCBBC 1982). The belt sander exhaust ventilation system uti lizes a narrow 

low-volume, high-velocity slot hood located between the belt surface and the 

worktable, and a jet stripper consistin9 of a series of small-diameter 

nozzles located inside a driven pulley hood opposite the operator station. 

By creatin9 high velocity air streams, the jet stripper destabilizes the 

wood-dust-containing boundary ai r layer surrounding the bel t, and the hood 

collects the dust from the turbulent air before the dust can become 

reentrained in the boundary layer. With either the slot hood or the jet 

stripper operating, reductions in breathing zone wood dust concentrations 

averaging 50% were achieved. With both parts of the venti lation system 

operating, the average reduction increased to 80%. The shaper exhaust 

system consists of a flexible hood that permits the wood to pass through but 

prevents the escape of the wood dust. Dust reductions ranging from 16:1 to 

120:1 were observed in laboratory tests. The ci rcular table saw exhaust 

system consists of a conventional exhaust hood beneath the saw table and a 

second, narrower hood covering the saw blade. 

An example of the use of area venti lation to control wood dust levels is 

provided by Bullock (1979). As part of a study examining the reci rculat ion 

of industrial exhaust air, the author evaluated the venti lation system of a 

furniture manufacturing plant. The system consisted of five large blowers 

(43,850 cubic feet per minute [cfm]) connected to a dust collection system 

of 21 modular bag fi Iter compartments. The performance of the dust 

collector, which was determined by measuring the dust concentrations in the 

inlets and return streams, exceeded 99.5% during the survey. There was 

virtually no difference in total dust concentrations before and after 

recirculation of the exhaust air. 

90 
Table 6.--Wood dust concentrations measured in the workplace in various studies 

Study description 

Kubis (1963) 

Cabinetmaking 

Czechoslovakia (Nitra) 

1 plant 

1961-1962 

Area samples/total dust 

Miscellaneous details 

E9Uip!l8l1t 

Belt sander (1961) 

Belt sander (1962) 

Wood dust concentrations 

NUlllber of TWA's, !!!S/m3 

Samples Range Mean Median 

5 3.6-65 .0 27 .9 23.0 

5 4.8-34 .2 19 .2 18 .4 

10 3.6-65.0 23.6 20 .7 

NOTE : In 1961, five sanders with local exhaust ventilation rates rang ing from 0-285 m/min were 

studied; dust concentrations were inversely proportional to ventilation rates. In 1962, hard oak 

dust concentrations were determined as Kubis varied the local exhaust ventilation rate ~ (0-372 m/min), grain size of the abrasive (30-80), dimensions of the push-lever, and the belt 

width (12-15 cm) on a single sander . Up to 95% of the dust particles were <5 um with most 2-3 um 

in size. Sampling and analysis methodologies were not provided . 

Hans I ian and Kadlec (1964) 

Furniture 

Czechoslovakia 

1 plant 

1964 

Area samples/total dust 

Ope rat ion 

Sanding (machine) 

Sanding (hand) 

Sawing 

Turning 

Bor ing 

Number of 

Samples 

TWA's, mg/mJ 

!!!!!9! Mean 

?-235 

?-220 

?-175 

?-135 

?-125 

Median 

- - -

NOTE: Timber species used were ebony, beech , monsonia , mahogany, and larch . Dust concentrations 

during a full shift in a sanding shop (2-4 belt sanders) reached on the average 40 mg/m3. Analysis by optical microscopy ind icated that 5-70% of the dust particles collected were <5 um in 

size . (Continued) 

-
'" N 

Paustovskaya et al. (1968) 

Furniture (mah09any) U.S .S.R. (Kiev) 

1 plant 

1008 

Personal samples/total dust 

pepartlllltnt 

Sanding 

Hand fin i sh i ng 

Number of 

Samples 

2 

1 

3 

TWA's I !!!9/m3 

Range Mean Median 

16.7-25.5 21 .1 21.1 

23.5 23.5 23.5 

16.7-25 .5 21 .9 23 .5 

NOTE: A total dust concentration of 18.3 mg/m3 was found 1 m from the dust-producing processes; 

concentrations of 5-6 m9/m3 were measured in remote areas of the shop . The industrial hygiene 

samplin9 was by the Chernovsty Municipal Medical-Epidemiol09ical Station Laboratory; sampling and 

analysis methodologies were not provided . 

Number of TWA's, mg/m3 

Faci lity Samples Range Mean Median 

Imbus (1978) Plant 1 (1971) 4 0.6-3 .3 1.6 1.2 

Furn i ture Plant 2 (1971) 7 0.9-8 .9 3.5 2.5 

U.S.A. (North Carol ina) Plant 3 (1971) 6 1.1-5 .3 2.5 2.4 

6 plants (1 company) Plant 4 (1971) 3 2.2-7 .9 4.4 3. 1 

1971-1973 Plant 5 (1971) 4 2.8-15.4 6.6 4.1 

Area samples/total dust Plant 6 (1973) 12 0.1-4.9 1.3 0.9 

----- ._-- .. _-- ---

36 0.1- 15.4 2.8 2.2 

NOTE: These data summarize wood dust sampling conducted by a large furniture company . The highest 

total wood dust concentration (15.4 mg/m3) was found at an automatic polisher where compressed 

air-blow off was used extensively; it was recommended that this practice be eliminated . The 

concentration of respirable dust collected at a sanding operation in Plant 6 was 0.7 mg/m3. 

(Cont i nued) 

-
'" w 

Soderqvist and Ager 

Sawmi II 

(1975) NOTE: Based on 36 personal samples, it was estimated that 80% of 689 

workers had TWA total dust exposures <2 mg/m3 , 18% to 

2.1-5.0 mg/m3, and 2% to >5.0 mg/m3. This data was part of a 

multidisciplinary survey of Swedish sawmi lis. Concentrations over 

Sweden 

1972-1973 

Otto (1973) 

Woodworking 

German Democratic Republic 

27 shops 

1973 

Area samples/total dust 

. 5 mg/m3 were measured in sawing, packaging, and trimming operations. 

The chipper controllers, cleaning personnel, and slat controllers had 

the highest wood dust exposures . [Summary detai Is from IARC 1981] 

NOTE: This is a summary of wood dust sampling conducted by the Erfurt 

District Inspectorate for Occupational Health . The following types of 

wood were being processed: mansonia, makore, obeche, limba, sapeli , afromosia, okume, and zebrano. Of the 102 total dust samples 

collected, 14% were <5 mg/m3 , 24% were from 5-9 mg/m3 , 24% were 

from 10-19 mg/m3, and 38% were >20 mg/m3. The samples were 

collected mainly during the use of belt sanders on wood veneers. 

(Cont inued) 

-
ID 

~ 

Millibar of TWA's I 1II!I/113 

Operat ion Samples ~ Mean Median 

Hounam and Wi Iliams (1974) Band sawing 

Furni ture (t.tAAD= 11. 5 um) 6 1.0-7 .3 4.3 5.3 

England (High lycOftbe) Planing (t.tAAD=9 .2 un) 9 1.8-10.9 5.0 3.1 

5 plants Routing (MMAD=10 .0 um) 6 1.8-8 .6 4.1 3.6 

1973 Spindle moulding 

Personal samples/total dust (WoIAD=10.0 um) 8 1.5-8.4 5.1 5.1 

Sanding (MMAD=8.4 um) 9 2.0-22.6 7.2 3.6 

Assembly (MMAD=7.6 um) 10 2.1-25 .5 7.5 5 .2 

Turning (t.tAAO=11 .5 um) 2 4.6-12.5 8.6 8.6 

50 1.0-25.5 5.9 4.4 

NOTE: These results are among the first to be reported for England. Chairs and other types of 

furniture were made of beech, elm , mahogany , walnut , and veneered chipboard at four of the five 

plants; cupboards or cabinets were made of veneered ch ipboard at the fifth plant. The machining 

operations at all the plants surveyed were considered to be well ventilated by local exhaust 

systems. The size distributions, including the mass median aerodynamic diameter (MMAD) , of 

airborne dust particles near these operations were measured using a 4-stage cascade centripeter to 

collect 37 samples. Most of the dust was found on the second stage of the centripeter, where dust 

of 4.15-13 .65 um was collected . Less than 25% of the mass of the dust collected was from 

particles <5 um in diameter. 

(Continued) 

-
'" 01 

Rosensteel (1974) 

Cabinets 

U.S .A. (North Carol ina) 

1 plant 

1974 

Personal samples 

Job Title 

Roundtable shaper operator : 

Total dust 

Respirable dust 

Number of 

Samples 

2 

2 

TWA's, mg/m3 

Range Mean Mad i aJ! 

8.6-8.9 

0.02-0 .4 

8.8 

0.2 

8.8 

0 .2 

NOTE: This is a NIOSH health hazard evaluation (HHE) conducted at a plant that produced television 

and stereo cabinets. The roundtable shapers inscribed a predetermined pattern in particle board. 

The local exhaust ventilation on the shapers was of only limited effectiveness and improvement was 

recommended . A 10-mm nylon cyclone was used as a preselector in the respirable dust sampling . 

Andersen et al . (1977) 

Furniture 

Denmark (Aarhus county) 

8 plants 

1974-1975 

Personal samples/total dust 

Operation 

Sanding 

Dri Iling/planing/sawing 

Number of 

Samples 

41 

27 

68 

TWA's, mg/m3 

Range Mean Median 

1.3-77.5 

14 .3 

5.2 

10 .7 

NOTE : These data are part of a study of nasal mucociliary clearance rates. Teak was the most 

frequently processed wood , followed by oak, chipboard, palisander, mahogany, jakaranda, beech, 

ramin, motinej Masonite, and pine. Of the dust samples collected, 63% were >5 mg/m3 and 28% 

were >10 mg/m. It was also determined that 33% of the mass of the dust was from particles 

<5 um, 41% was from 6-10 um, 11% was from 11-15 um, and 15% was from particles >16 um in size; 

methodology for particle sizing was not given. 

(Cont inued) 

-
<0 

en 

Number of TWA's I !!!!I/m3 

Exposure:Job Tille ~ples ~ Mean Median 

Kominsky and Anstadt (1976) Total dust: 

Wood component fabrication Saw operator 17 0.7-416 38.1 1.7 

U.S.A. (Ohio) Router/groover operator 5 1.2-48.5 12.5 1.7 

1 plant 

1975 22 0.7-4-16 32.3 1.7 

Personal samples Res!! i r ab I e dus t : 

Saw operator 13 0.07-4.4 0.7 0.4 

Router/groover operator 3 0.3-0 .8 0.5 0.4 

16 0.07-4.4 0.6 0.4 

NOTE: This is a NJOSH HHE conducted at a plant involved in the fabrication of component parts 

(e.g., book case back panels, clock faces, and television cabinets). Component parts were 

fabricated mainly from Masonite hardboard; however, particle board, fiberboard, and flake board 

were also used. Most of the boards used were comprised of redwood, oak, elm, and Douglas fir; 

secondary woods included ash, cottonwood, hickory, magnolia, birch, beech, pecan, holly, maple, 

sweet gum, sycamore, walnut, willow, and poplar. The highest dust concentrations found were for a 

multi-blade rip saw helper who had an average exposure over 4 days of 153 mg/m3 (range 

1.4-416 mg/m3) and for a router operator who had a 1-day exposure of 48.5 mg/m3; it was 

recommended that the existing local exhaust ventilation for these two operations be improved . All 

other full-shift total dust samples were <7 mg/m3. Four total dust samples of 10-18 min 

duration collected during blowdown of dust bins averaged 48.2 mg/m3 (range 11.2-118 mg/m3). A 

10-mm nylon cyclone was used as a preselector in the respirable dust sampling . The MMAD of 

particles collected using a 6-stage cascade impactor was )10 um. 

(Cont inued) 

-
" '" 

Number of TWA's, mg/m3 

~ation Samples Range Mean Median 

Levy (1976) Sawin9 2 1.1-3.4 2.2 2.2 

Woodworking Sanding 2 4.3-6 .8 5.5 5.5 

U.S.A . (New York) Sawing/sanding 2 0.9-5.0 3.0 3.0 

1 shop Sawing/sand ing/planing 2 2.3-24.2 13 .2 13.2 

1976 

Personal samples/total dust 8 0 .9-24.2 6.0 3.9 

NOTE: This is a NIOSH HHE conducted at the woodworkin9 area of an art school . No local exhaust 

venti lation was provided on any of the woodworkin9 machines . Sampling times varied from 

45-250 min in duration. A 6-hr general area sample for total dust indicated a concentration of 

2.5 mg/m3 . 

Gunter (1977a) 

Furniture 

U.S.A. (Utah) 

1 plant 

1976 

Personal samples/total dust 

Job Title 

Mi II worker 

Sander in specialty department 

Number of 

Samples 

1 

1 

2 

TWA's, mg/m3 

Range Mean 

4 

90 

4-90 

4 

90 

47 

4 

90 

47 

Median 

NOTE: This is a NIOSH technical assistance study conducted at a small plant that produced office 

furniture such as desks, tables, and file cabinets. It was recommended that engineering controls 

be uti lized to eliminate the excessive wood dust exposure to the sander in the specialty 

department. 

(Cont inued) 

-
'" 00 

Number of TWA's, mq/m3 

Exposure: Departaent Samples Range Mean Median 

Edwards et al. (1978) Total dust: 

Wood products Shake Mi II (western red cedar) 85 0.06-31.9 4.7 1.6 

U.S.A. (Washington) New Planer Mil l (fir/hemlock) 59 0.1-16.7 1.3 0.3 

1 company Old Planer Mi II (fir/hemlock) 6 0.2-54 .8 18 . 1 1.0 

1976 Bark Plant (fir/alder) 5 1.2-8.3 4.0 2.4 

Personal samples Presto-log Plant (fir/alder) 5 0.6-4.6 1.7 0.9 

Si Ivacel Plant (alder) 5 2.3-21.5 13.5 15.6 

Plywood Plant (fir/cedar) 4 0.3-1.3 0.6 0.5 

169 0.06-54.8 4.0 

Respirable dust: 

Shake mi II (western red cedar) 39 0.01-1.2 0.2 0.1 

New planer mill (fir/hemlock) 23 0.07-0.3 0.2 0.2 

Old planer mil I (fir/hemlock) 1 0.3 0.3 0.3 

Bark plant (fir/alder) 1 0.3 0 .3 0 .3 

Presto-log plant (fir/alder) 2 0.2-0.2 0.2 0.2 

Silvacel plant (fir/cedar) 2 0.5-0.6 0.5 0 .5 

-- -

68 0 .01-1 .2 0.2 

NOTE: This is a NIOSH HHE conducted at a diversified wood products company. In the Old Planer 

Mi", a chipper operator had a total dust exposure of 51.4 mg/m3 and the set-up man 

54.8 mg/m3; based on lower results obtained on similar jobs in the New Planer Mill (which has 

environmental controls) it was judged possible to also reduce these dust concentrations. In the 

Presto-log plant, sawdust was compressed into fireplace logs. In Si Ivacel production, wood chips 

were ground into fibers, passed through a dryer, and bagged; due to the high concentration of 

total dust found in this area, it was recommended that engineering controls be installed. A 10-mm 

nylon cyclone was used as a preselector in the respirable dust sampling. The following average 

particle size distribution was found in the Shake Mi l l from 4 samples collected: 39% <10 um, 23% 

from 10-20 um, and 38% >20 um in size. In seven saR~les collected in the New Planer Mi", 47% of 

the particles were <10 um, 25% were 10-20 um , and 28% were >20 um in size. Methodology for 

particle sizing was not given. 

(Continued) 

-
'" '" 

Job Title 

Gunter (1977b) Pattern maker 

lood pattern making 

U.S.A. (Colorado) 

1 shop 

1977 

Personal samples/total dust 

Number of 

Samples 

6 

TWA's, mg/ml 

Range Mean Median 

0 .6-8.0 3.1 2.4 

NOTE: This is a NIOSH HHE conducted at a plant that made wood patterns for a foundry. Local 

exhaust venti lation was avai lable at each work station in the pattern shop. 

Friar (1978) 

Furni ture 

England 

7 plants 

1978 

Total dust 

Operation 

Sanding (machine) 

Assembly 

Band sawing 

Other sawing 

Number of 

Samples 

45 

35 

13 

21 

114 

TWA's, mg/m3 

Range Mean Median 

1-75 6 

2-41 8 

2-127 18 

2-35 8 

1-127 8 

NOTE: These data summarize wood dust sampling (personal and area) conducted by the Factory 

Inspectorate of the Health and Safety Executive in a traditional furniture manufacturing area. 

Out of 114 samples collected. 48% were >5 mg/m3; belt sanding and sanding during assembly were 

the dustiest operations. Almost all the sanding machines and saws were provided with local 

exhaust ventilation. 

(Continued) 

-
.-

o 

o 

Apol (1979a) 

Sawmi II/planer mi II 

U.S.A. (South Dakota) 

1 plant 

1978 

Area samples/total dust 

Departlll8llt 

Sawmill (includes chipper) 

Planer mi II 

llullber of 

Saalples 

23 

15 

38 

TWA's, ~/m3 

Range Mean Median 

0.03-0.8 0.4 0.3 

0.2-0.5 0 .3 0 .3 

0.03-0.8 0.3 0.3 

NOTE: This is a NIOSH HHE cond l~ cted at a faci lity processing pine . Area samples were fairly 

representative of the workers' exposures to wood dust. 

Nulllber of TWA's, mg/m3 

Job Title Sall1ples Range Mean Median 

Apo I (1979b) Cabinetmaker 4 2.0-3 .0 2.4 2.3 

Cabinet shop Panel saw operator 2 0.9-1.6 1.3 1.3 

U.S.A . (Colorado) Rip saw/planer operator 3 2.5-36.1 17 .4 13 .7 

1 shop Sander/shaper/rip saw/planer 3 1.9-11.9 6.4 5.2 

1978 

Personal samples/total dust 12 0.9-36.1 6.9 2.4 

NOTE: This is a NIOSH HHE conducted at a custom cabinet shop using oak, plywood veneer, and 

particle board. A worker who operated a power rip saw most of the shift had the highest exposure 

(i .e . , 36.1 mg/m3); it was recommended that a new hood be installed under this saw. 

(Con t i nued ) 

-
.... 

o 

.... 

Weaver (1979) 

Furni ture 

U.S.A. (North Carolina) 

7 plants 

1978 

Personal samples/total dust 

Facility:Operation 

Plant 1: Rip/cutoff sawin9 #1 

Rip/cutoff sawing #2 

Boring 

Drum sanding 

Plant 2: Belt sanding 

Plant 3: Routing #1 

Routing #2 

Plant 4: Double trim sawing 

Plant 5: Routing 

Plant 6: Belt sanding 

Plant 7: Hand shaping 

Edge sanding 

Number of 

Samples 

TWA' 5, mg/m3 

Range Mean Median 

8.4-77.2 

16.1-60.1 

4.8 

2.5 

27.4-56.6 

3.1-12.3 

5.8-15.5 

6.0 

5.7 

1.6-3.6 

15.3-21.1 

2.4-20.7 

2.4-77.2 

4.8 

2.5 

6.0 

5.7 

NOTE: These data summarize wood dust sampling conducted by the North Carolina Department of 

Labor. Area samples for total dust collected near the sawing operations in Plant 1 ranged from 

1.6-5.6 mg/m3. Area samples indicated a respirable dust concentration of 2.1 mg/m3 near 

cutoff sawing in Plant 1 and 1.5 mg/m3 for a router operator at Plant 5; a 10-mm nylon cyclone 

was used as a preselector for these samples. In many instances. little or no local exhaust 

venti lation was avai lable in the facilities surveyed. 

(Continued) 

-
.... 

0 

'" 

Number of TWA's, JII!:I/m3 

Faci I ity:Area Samples Range Mean Median 

Whitehead et al. (1981b) ~wood (hardwood): 

Plywood/furniture Veneer lathe/clipper 3 0.2-0.S 0.5 O.S 

U.S.A. (Vermont) Dryer 4 0.1-0.4 0.3 

1978 Dry veneer handling 4 0.2-0.5 0.3 

12 plants Edge sawing/sanding S 0.9-2.3 1.4 

Area samples/total dust Machining S 0.7-3.2 1.9 

Assembly 2 0.3-0.S 0.5 0.5 

Plywood (hardwood) 25 0.1-3.2 1.0 

Furniture (hardwood): 

Rough mi II ing 7 0.2-2.S 0.8 

De t a i led mil ling (f i n i sh i ng ) 9 0.2-S.3 1.8 

Sanding 12 1.4-11.4 4.5 

Assembly 3 1.1-2.1 1.5 1.3 

Furniture (hardwood) 31 0.2-11.4 2.S 

Furniture (softwood): 

Rough mi II ing 5 0.2-1.1 O.S 

Detai led mi Iling (finishing) 9 0.3-4.3 1.S 

Sanding 13 0.S-14.3 3.2 

Assembly 2 2.5-3.1 2.8 2.8 

Furn i tureTsoffwoodl 29 0.2-14.3 2.2 

Furni ture (hardwood & softWO()cj) SO 0.2-14.3 2.4 

NOTE: These data are part of a study of the respiratory health of woodworkers. Fifteen samples 

collected with a S-stage cascade impactor indicated that relatively little dust on a mass basis 

was present in the smallest size ranges. 

(Cont i nued) 

-
... 

o 

w 

Chan-Yeung et al. (1980) 

Sawmi II 

Canada (British Columbia) 

1 mi II 

1979 

Personal samples/total dust 

Departll8nt 

Sawmill (including 

permanently assigned 

maintenance staff) 

Number of 

Samples 

71 

TWA's, mg/m3 

Range Mean Median 

<0 .1-2.7 0.5 

NOTE: These data are part of a respiratory health effects study at a pulp and paper mi II . 

NUilber of TWA's I mg/m3 

Department Samples Range Mean Median 

Enright (1980) Research & Safety Model Shop 10 0.2-3.4 0.9 0.4 

Wood model makin9 Wood Mi II 10 1.2-10.2 4.7 4.3 

U.S.A. (Michigan) Model Shop/Body Shop 20 0 .1-22 .4 2.4 0.8 

1 shop Hardware & Styling Studio 12 0. 1-2 .0 0.5 0 .2 

1980 Die Engineering Model Shop 15 0.2-8 .3 1.7 0.4 

Personal samples/total dust Crating and Omni-mi Iling 8 0.1-0.6 0.2 0.2 

Plastics Shop 6 0 .1-0.9 0.4 0.1 

-----

81 0.1-22.4 1.7 0.5 

NOTE: These data are a summary of wood dust sampling conducted by an automobile producer . Three 

of the workers monitored had exposures greater than 10 mg/m3, i .e . , a shaper operator in the 

Wood Mi II (10 .2 mg/m3). a model maker performing sanding by hand (11.0 mg/m3), and a model 

maker using a powered orbital sander (22 .4 mg/m3). Based on sampling with a 10-mm nylon 

cyclone, only 2-5% of the mass of the particulate in the two samples collected was respirable. 

(Continued) 

-
.... 

o 

.,.. 

Operation 

Salisbury (1981) Sanding/grinding/lathe 

Woodworking 

U.S.A. (Kentucky) 

1 shop 

1980 

Personal samples/total dust 

Nu.ber of 

Samples 

4 

TWA's, mg/m3 

~ Mean Me<! i an 

15.6-45.8 29.1 27.5 

NOTE: This is a NIOSH technical assistance study conducted to help evaluate ventilation at the art 

studios of a university. The dusts generated were from maple and pine. Typical exposures per day 

(and sampling times) were 40-67 min. Computed as 8-hr TWA's, and assuming zero exposure for the 

time not sampled, the highest exposure was 5.7 mg/m3. Most of the dust was generated by 

portable disk and belt sanders. 

Boiano (1981) 

Wood model making 

U.S.A. (Indiana) 

1 shop 

1981 

Personal samples/total dust 

Job Title 

Pattern maker 

NUllber of 

Samples 

2 

NOTE: This is a NIOSH HHE conducted at a truck wood model making shop. 

TWA'S, 1119/1113 

Range Mean Median 

0.3-0.8 0.6 0.6 

(Continued) 

-
-

o 

U"I 

AI Zuhair et al. (1981) 

Furniture 

England 

2 plants 

1981 

Personal samples/total dust 

Fac iii tv: Department 

Plant 1: 

Sawmi II 

O.t.1AD= 17 . 3 um) 

Assembly 

(IofAAD=18.0 um) 

Plant 1 

Plant 2: 

Machine Floor 

(MMAD=9.3 um) 

Cabinet Shop 

(MMAD=12.5 um) 

Plant 2 

Plants 1 and 2 

Number of 

Samples 

75 

4 

79 

43 

71 

114 

193 

TWA's, mg/m3 

Range Mean Median 

3.5 

0.7 

3.4 

1.7 

8.1 

5.7 

4.1 

NOTE: These data are part of a study of venti latory function in workers exposed to wood dust. 

Plant 1 made cabinets and cupboards from veneered chipboard; Plant 2 produced chairs, tables, and 

cabinets from limba, beech, ash, and to a lesser extent, from maho9any, oak, and ramin. Average 

concentrations of total dust determined from area samples were 1.4 mg/m3 in the Saw Mill (6 

samples) and 0.8 mg/m3 in Assembly (2 samples) in Plant 1; and 0.7 mg/m3 on the Machine Floor 

(16 samples) and 4.4 mg/m3 in the Cabinet Shop (13 samples) in Plant 2. Respirable dust 

sampling (as measured by a Hexhlet) indicated average concentrations in Plant 2 of 0.19 mg/m3 (4 

samples) and 0.44 mg/m3 (4 samples) on the Machine Floor and in the Cabinet Shop, respectively. 

MMAD's were estimated from 24 samples collected with a 7-stage 'cascade impactor. 

(Cont i nued) 

-
.... 

o 

"" 

Number of TWA's, mg/m3 

Type of Wood Processed Samples Range Mean Median 

Morey (1982) Basswood 6 0.7-2 .1 1.3 1. 1 

Sawmi II (West Virginia) Poplar 18 0.7-3 .1 1.4 1 .1 

U.S.A. Soft maple 9 0 .8- 4.9 2.2 2.2 

1 mi II Red oak 5 1.0-5 .5 3.2 2.7 

1981-1982 White oak 14 1.0-10.6 3.7 2.7 

Area samples/total dust Cher ry 3 6.4-8.1 7.2 6.9 

55 0.7-10.6 2.6 2.0 

NOTE : These data are from a NIOSH survey conducted at a small sawmi II where different species of 

hardwood (as available in the yard) were processed. Samples were collected at three locations 

(the booth where the headsaw was operated; and at two sites where workers were observed 

transiently, across from the headsaw booth and on a catwalk over the edger). Moisture content of 

the wood being processed was significantly related to the dust concentrations at the three plant 

locations monitored . 

(Con t i nued ) 

-
Hualber of TWA's, mg/.,3 

Job Title Samples ~ Mean Median 

McCammon et al. (1985) Model maker (soft/hardwood) 23 0.2-8.3 0.8 

Wood model making Model maker (softwood) 4 0.2-0.5 0 .3 

U.S .A. (Michigan) Model maker (hardwood) 12 0.2-1.3 0.6 

3 shops Sweeper 5 0.1-6.1 1.6 

1981-1982 Shaper operator 7 0.3-13.9 2.7 

Personal samples/total dust Plastic shop worker 3 0.03-0.7 0.4 0.6 

Multi-axis machine operator 4 0.2-1.0 0.5 

58 0.03-13.9 1.0 

NOTE: This is a summary of the NIOSH characterization of exposures in automotive wood model 

shops . Control of dust emissions from shapers was deemed to be very difficult . The average total 

dust concentration of 29 area samples was 0 .9 mg/m3 (range 0 .05-17 .5 mg/m3 ) . Inconsistent 

results were found (i .e . , 0. 1-180% respirable dust) when samplin9 with a 10-mm nylon cyclone . It 

was hypothesized that since wood dust can acquire a static charge it may "stick" to a nylon ... cyclone. MMAO averaged 7.7 um (range 5 .2-10 um) in samples collected in nine di fferent areas with 

!:l a 9-stage cascade impactor, with 18-61% of the dust bein9 respirable. Scanning electron 

microscopy indicated that length-to-width ratios were 2.3:1 and 1.9:1 in two air samples collected 

with a 0.5-inch stainless steel cyclone. 

Job Title 

Ellenbecker and Wegman (1983) Sander 

Woodworking 

1982 

1 shop 

Personal samples/respirable dust 

Number of 

Samples 

3 

TWA's, mg/ml 

Range Mean Median 

0.5-0.9 0.6 0.5 

NOTE : This is a NIOSH HHE conducted at a grandfather clock factory . A 10-mm nylon cyclone was used 

as a preselector in the respirable wood dust sampling. Three area samples for total dust 

collected near the woodworking operations averaged 2.0 mg/m3 (range 0.2-4 .6 mg/m3). Local 

exhaust venti lation appeared to be in good operating condition. 

(Cont inued) 

-
.... 

o 

00 

Jones and Smith (1986) 

Furniture 

England (High Wycombe) 

7 plants 

1976-1983 

Personal samples/total dust 

*Individual plant averages 

Faci IIty 

Plant 1 (1983) 

Plant 2 (1983) 

Plant 3 (1983) 

Plant 4 (1983) 

Plant 5 (1983) 

Plant 6 (1983) 

Plant 7 (1983) 

1983 Results 

CoiIpar i son by operat i on 

Machine sanding: 1976-1977 

1983 

Hand sanding: 1976-1977 

1983 

Sawing: 1976-1977 

1983 

Other cuttin9: 1976-1977 

1983 

1976-1977 Resu lts 

1983 Results 

NUllber of 

Sallples 

36 

15 

22 

9 

39 

29 

60 

210 

36 

49 

33 

42 

29 

49 

44 

70 

142 

210 

TWA's I !!!!I/m3 

~ Mean Median 

1.0-6 .2 2.6 

0 .7-4.1 2.1 

0.9-13.7 2.9 

1.4-8.8 4.6 

1.1-6.8 2.8 

0.3-18.3 2.2 

0.5-53 8.1 

0.3-53 4.3 

2.1-6 .3" 3.7 

0.7-53 5.7 

5.8-32* 16.9 

0.5-27.2 6.9 

4.7- 13.1" 7.4 

1.0-30.3 3.4 

2.0-10.8* 6.9 

0.3-8.8 2.3 

2.0-32* 8.5 

0.3-53 4.3 

NOTE : These data are a summary of wood dust sampling conducted by the Health and Safety 

Executive. Tables and chairs were produced mainly from beech, ash, and elm at six of the plants; 

sideboards, wardrobes, and loudspeaker cabinets were manufactured at three of the plants from elm, 

ash, veneered chipboard, or medium density fiberboard . Almost all woodworking machines in the 

plants surveyed in 1983 were fitted with some form of local exhaust ventilation; most of the hand 

(Continued) 

-
-

0 

\D 

sanding operations were carried out in the open with no exhaust ventilation for dust control. The 

high average dust concentration in Plant 7 (i .e., 8.1 mg/m3) reflected heavy and prolonged 

sanding. Overall, narrow belt sanders created the greatest dust concentrations (8.5 mg/m3, range 1.2-20.3 mg/m3) , followed by hand sanding (6 .9 mg/m3, range 0.5-27.2 mg/m3) and drum, 

bobbin, and brush sanders (4.4 mg/m3, range 0.5-51.4 mg/m3). The MMAD of the dust collected 

with an impactor during the machine sanding of mahogany was g urn with about 54% of the mass of the 

dust in the range 4-10 urn. A comparison between the results of the 1983 survey and an earlier one 

(1976-1977) indicated that there had been a significant decline in personal exposures to wood dust 

in the furniture plants surveyed . 

Nwnber of TWA's, mg/ml 

Equipaent Satnples Range Mean Median 

McCaw I ey (1983) Router 5 1.7-8.1 4.0 3.4 

Signs/plaques Sander (large) 8 1.0-5.6 2.9 2.6 

U.S.A. (New York) Sander (sma II) 5 1.7-4.5 2.9 2.0 

1 shop 

1983 18 1.0-8.1 3.2 2.6 

Area samples/total dust 

NOTE: These data are from a NIOSH research study that evaluated different wood dust sampling 

methods at a sign shop. Wood processed included western red cedar and laminated pressed wood . All airborne dust samples were collected using a 4-stage cascade impactor. It was determined that 

45-60% of the mass of the dust was from particles <3.5 urn, 30-35% from 3.5-20 urn, and that 5-20% 

of the dust was from particles >20 urn in size. 

(Cont inued) 

-
... 

... 

o 

Lindroos (1983) 

Woodworking 

Finland 

1 shop 

1983 

Personal samples/total dust 

Departnent:Operatlon 

Pret reatment: 

Unloading wood 

Sawing 

Other I113chines 

Pretreatment Department 

Woodworking: 

Planing 

Other machines 

Woodworking Department 

Pretreatment and Woodworking 

NU1IIber of 

Salllpies 

10 

11 

6 

27 

20 

11 

31 

58 

TWA's, IIIQ/m3 

~ Mean Ned I an 

0.5-28 .0 

0.3-2 .0 

0.4-1.0 

0.3-28.0 

0.02-1.8 

0 .2-4.7 

0.02-4.7 

0.02-28.0 

4.3 

0 .8 

0.8 

2.1 

0.4 

1.1 

0 .7 

1.4 

4.3 

0.8 

0.9 

0.3 

0 .5 

NOTE : These data are part of a study that assessed working conditions when impregnated wood was 

used to sroduce windows and doors . Concentrations of total dust determined from area samples were 

0.6 mg/m (range 0.2-1.0 mg/m3) in the Pretreatment Oepartment (g samples) and 0.3 mg/m3 

(range 0.1-0 .4 mg/m3) in the Woodworking Department (13 samples) . Seven respirable dust samples 

collected in the Pretreatment Department averaged 0 .16 mg/m3 (range 0.14-0 . 19 mg/m3 ) ; 6 

respirable dust samples collected in the Woodworking Department averaged 0.14 mg/m3 (range 

0.11-0.20 mg/m3). A cyclone was used as a preselector in the respirable dust sampling . The 

number percentage of dust particles <5 um in size in 15 samples collected in processing areas 

averaged 97 .8% (range 93.6-100 .0%). Particle sizing was done by optical microscopy at SOOX 

magnification. 

(Continued) 

-
.... 

.... 

.... 

Daniels and Anderson (1983) 

Wood model making 

U.S.A. (Michigan) 

1 shop 

1983 

Personal samples/total dust 

NUllber of 

Job Title SillWples 

Wood shop operator 3 

Model maker 4 

7 

TWA' s I mg/m3 

~ Mean 

2.0-3.3 2.6 

0.5-4.0 1.7 

0.5-4.0 2.1 

NOTE: This is a NIOSH HHE conducted at an automotive wood model shop . The majority of the 

woodworkin9 machines were equipped with local exhaust venti lation . 

Crandall and Hartle (1984) 

Boat bui Iding 

U.S.A. (Maine) 

1 plant 

1983 

Personal samples/total dust 

Job Title:Operation 

Carpenters in assembly : 

Prefab 

Main line 

NUlllber of 

Sarwples 

8 

19 

27 

TWA's I mg/m3 

Range Mean 

0.8-16 .2 4.6 

0.3-2.8 1.5 

0.3-16.2 2.4 

Median 

2.5 

1.2 

2.0 

Median 

2. 9 

1.3 

1.7 

NOTE : This is a NIOSH technical assistance study conducted in the assembly buildin9 of a fibrous 

glass-reinforced boat plant. Two area total dust samples collected in prefab were 0.4 and ·1.8 mg/m3. All large woodworking machines had local exhaust ventilation. 

(Continued) 

-
.... 

.... 

N 

Number of TWA's I !!!!I/m3 

Faci I i ty Samples Range Mean Median 

Wi Ihelmsson and Drettner (1984) Plant 1 0.3-3.0 1.4 

Furniture Plant 2 1.9-5.1 4.0 

Sweden (Smaland county) Plant 3 0.4-3.2 1.3 

5 plants Plant 4 0.8-2.8 1.7 

1984 Plant 5 0.4-3.0 1.3 

Personal samples/total dust 

28 0.3-5.1 2.0 

NOTE: These data are part of a study of the occurrence· of upper respiratory symptoms in the 

furniture industry. Most of the woodworkers were exposed to hardwood such as birch, beech, oak, 

mah09any, and teak. 

(Con t i nued ) 

-
--

w 

Kauppinen et al. (1984) 

Sawmi II/plywood 

Finland 

6 mi Ils/6 plants 

1984 

Personal and area samples/ 

total dust 

Facllity:Department 

Sawmi lis: 

Sawing Department 

Framing saws 

Edg in9 

Tr imming 

Sawing surface plates 

Stapling Department 

Finishing Department 

Sorting Department 

Planing Department 

Ripping saws 

Planing 

Packaging 

Other Operations 

Cleaning 

Control of chip makers 

Plywood Plants: 

Sawing 

Fini s.h i ng 

Other operations 

Plywood Plants 

Number of 

Samples 

6 

3 

4 

1 

3 

38 

7 

5 

5 

2 

4 

2 

80 

23 

6 

2 

31 

TWA's, mg/m3 

Range Mean Median 

0.4-3.8 

0.8-3.4 

0.1-0.7 

5.1 

0.4-2.7 

0.1-9.6 

0.9-6.3 

0.5-2.0 

0.6-0.9 

0.2-0.4 

3.1-15.0 

3.5-5.0 

0.1-15 

0.4-12 

0.8-9.5 

1.4-2.1 

0.4-9.5 

1.2 

2.1 

0.4 

5.1 

1.0 

2.3 

2.2 

1.2 

0.7 

0.3 

7.6 

4.3 

2.2 

2.5 

3.2 

1.8 

2.6 

0.8 

2.1 

0.3 

5.1 

0.8 

1.4 

0.7 

0.3 

6.2 

4.3 

1.7 

2.1 

1.8 

NOTE: This was an industrial hygiene assessment. The sawmills and plywood plants processed pine, 

spruce, and birch. Two of the plywood plants also produced particle board and strip board. The 

average concentration of total dust in the Finishing areas of the plywood plants was O.g mg/m3 

(18 samples, range 0.3-2.4 mg/m3) which reflected the exposure to which most of the workers were 

subjected. In the Finishing Departments of the sawmills, the respirable dust concentration 

averaged 26% (range 2-78%) of the mass of total dust in 16 samples collected. The average 

percentages of respirable dust in the finishing departments of the plywood plants were as 

follows: 40% in sawing operations (21 samples, range 1-90%),29% in finishing operations (6 

samples, range 8-64%), and 65% in the general workroom air (15 samples, range 16-100%). A 10-mm 

nylon cyclone was used as a preselector in the respirable dust sampling. 

(Cont inued) 

-
-

Number of TWA's I l1I!I/m3 

Operation Samples Range Mean Median 

Kauppinen and Niemela (1985) Hogging" 1975-1984 3 0.1-29 11 3.9 

Particle board production Chipping" 1965-1974 1 1.1 1.1 1 .1 

Finland 1975-1984 3 0.7-1.7 1.1 1.0 

8 plants Chip dryin9" 1965-1974 2 24-29 26.5 26.5 

1965-1984 Blending" 1965-1974 3 1.0-8.0 5.3 7.0 

Area samples/total dust 1975-1984 3 0.6-0.9 0.8 0.8 

"Short-term exposures were Forming 1965-1974 9 4.0-26 13 12 

determined. 1975-1984 4 <0.1-0.5 0.4 0.4 

Prepressing 1965-1974 2 6.0-7.0 6.5 6.5 

Hot pressin9 1965-1974 6 1.0-6.1 4.1 4.6 

1975-1984 5 <0.1-2.1 0.8 0.5 

Planing 1965-1974 1 0.6 0.6 0.6 

SaVling 1965-1974 4 10-20 14 14 

1975-1984 9 <0.1-2.3 1.1 1 .1 

Gr i ndi ng 1975-1984 2 0.6-0.8 0.7 0.7 

.... Grading 1975-1984 1 1.1 1.1 1.1 .... Packing 1975-1984 2 <0.6-0.6 0.4 0.4 .". Matching 1975-1984 1 1.2 1.2 1 . 2 

1965-1974 Results 28 0.6-29 10.0 

19·'5-1984 Resu I ts 33 <0.1-29 1.8 

Particle board ~roduced from sawdust: 

Forming machines 4 26-360 

Sawing machines 3 23-58 

Prepressing area 2 15-17 16 16 

Hot pressing area 1 13 13 13 

10 13-360 

NOTE: These data are part of an epidemiological case-control study. Wood used was a mixture of 

spruce, pine, aspen, and birch. The main reason for the decrease in exposure to wood dust over 

time was likely the improved local exhaust ventilation at the forming and sawing machines. 

(Cont i nued) 
.... 

.... 

U1 

Number of TWA's I 111!1/m3 

Depart.ant Samples Range Mean Median 

Kauppinen (1986) log barking/cutting 1975-1984 4 0.2-0.7 0.4 0.4 

Plywood Peel ing 1975-1984 2 0.2-0.3 0.3 0 .2 

Finland Veneer sorting 1965-1974 1 0.4 0.4 0.4 

19 plants Veneer sawing 1965-1974 3 0.6-3.0 1.6 1.2 

1965-1984 1975-1984 4 1.1-1.5 1.3 1.3 

Personal samples/total dust Plywood sawing 1965-1974 6 0.5-12 3.3 1.9 

1975-1984 11 0.3-19 3.7 2.8 

Plywood sanding 1965-1974 5 0.3-6.4 3.0 3. 1 

1975-1984 21 0.8-22 3.8 2.6 

Plywood sort ing 1975-1984 2 1.6-1.8 1.7 1.7 

Plywood finishing 1975-1984 18 0.3-2.4 0.7 0.8 

Chipping 1975-1984 11 0.7-7.1 2.6 2.4 

1965-1974 Results 15 0.3-12 2.7 

1975-1984 Results 73 0.2-22 2.4 

NOTE : These data are part of an epidemiological case-control study . Wood used was a mixture of 

birch, spruce, and pine. Concentrations exceeding 5 mg/m3 were occasionally measured in sanding 

and sawing at sites where the local exhaust systems were insufficient. In Plywood Sanding, higher 

concentrations were measured in samples which included the work phase of cleaning a sanding belt 

with compressed air. The concentration of dust in the general air in Plywood Sanding was about 

1 mg/m3. The respirable dust comprised 15-40% of the total dust in sanders' and sawyers' 

breathing zones. General area samples in Plywood Finishing contained about 65% respirable dust . A cyclone was used as a preselector in the respirable dust sampling . 

(Continued) 

-
... 

... 

en 

Innocenti et al. (1985) 

Furni ture 

Italy 

1985 

2 plants 

Personal samples/total dust 

*GM=geometric mean 

Faci I ity 

Plant 1 

Plant 2 

Number of 

Samples 

6 

4 

10 

TWA's, mg/m3 

Range Mean Median 

2.5-25.3 

1.9-4.4 

1.9-25 .3 

9.HGM*) 

2.5(GM) 

5 :4\(}A) 

NOTE: This was part of a preliminary investigation of anosmia in chestnut woodworkers . 

Holness et al . (1985) 

Furni ture 

Canada (Toronto) 

4 plants 

1984 

NOTE: Total and respirable personal wood dust samples were collected 

for 50 woodworkers involved in sawing, sanding. and assemblying who 

were part of a health study of respiratory effects. The average 

total dust exposure was 1.8 mg/m3. The average respirable dust 

exposure was 0.3 mg/m3; a 10-mm nylon cyclone was used as a 

preselector. 

(Cont i nued) 

-
.... 

.... 

..... 

Sass-Kortsak et al. (1986) 

Cabinetmaking 

Canada (Ontario) 

4 plants 

1984 

Personal samples 

Salllple Type: Job category 

Total Oust: 

Sawing 

Sanding 

Assembly 

Laminating/Gluing 

Miscellaneous 

Total Dust 

Respi rable Dust : 

Sawing 

Sanding 

Assell1bly 

Laminat ing 

III i sce I I aneous 

Resp irable Dust 

Samp I e Type: Wood Type 

Total Dust: 

Softwood 

Hardwood 

Respirable Dust 

Softwood 

Hardwood 

NWlber of 

Sallples 

12 

7 

19 

3 

7 

48 

12 

7 

18 

3 

7 

47 

18 

14 

18 

14 

TWA's, mg/ml 

~ Mean Median 

1.7 

2.9 

1.9 

1.1 

1.2 

1.8 

0.1 

0 .6 

0 .3 

0.3 

0 .3 

0.3 

2.2 

0 .3 

2.0 

0.3 

NOTE : Softwoods processed included cedar, poplar, fir, pine, spruce , chipboard, particle board, 

and fir plywood; hardwoods included birch , cherry, oak, and walnut. Personal total dust exposures 

were significantly higher (p=O .OO3) than those that would have been estimated from 12 area wood 

dust samples collected. All table saws and stationary sanders were equipped with local exhaust 

ventilation in 3 of the 4 plants; the mean total dust exposure (3.8 mg/m3) in the 4th plant 

(without local exhaust ventil~tion) was significantly higher than the other three. 

(Con t i nued) 

-
..... 

..... 

0> 

Holl iday et al. (1986) 

Various industries 

Canada 

23 plants 

1985 

Personal samples/total dust 

• S=so ftwood 

H=hardwood 

PS=particle board 

GM=geometric mean, mg/m3 

Industry:Product 

Primary Industries: 

Sawmi II (S') 

Floor ing (S/H*) 

Veneer/plywood (H) 

Reconstituted board (H) 

Primary Industries 

Secondary Industries: 

Mi liwork (S) 

!.Ii liwork (S/H) 

Prefabricated bui Idings (S) 

Misc. wood products (S/H) 

Secondary Industries 

Tertiary Industries: 

Kitchen cabinets (H) 

Kitchen cabinets (PS*) 

Household furniture (S/PB) 

Household furniture (H) 

Household furniture (PS) 

Office furniture (H) 

Office furniture (PB) 

Pattern naking (H) 

Tertiary Industries 

A I I Indus t r i es 

HUJDber of 

Samples 

18 

7 

7 

S 

37 

15 

S 

8 

23 

Sl 

12 

5 

5 

11 

6 

7 

9 

S 

60 

148 

-

TWA I S I mg/m3 

Range Mean Median 

0.3-4.1 

0.3-1.7 

0. 1-2.6 

1.S-S.1 

O.l-S.l 1.4 (GM*=O.7) 

0.3-6.S 

0.3-1S.2 

0.4-2.S 

0.4-1S.0 

0.3-1S.2 2.2 (GM=0.9) 

0.3-S.1 

0.7-3 .7 

1.7-15.6 

0.3-5.2 

0.5-6.8 

0.5-1. 7 

0.4-S.6 

1.0-2.6 

0.3-15.6 2.4 (GM=1.6) 

0.1-1S.6 2.0 (GM=l.1) 

(Cont i nued) 
..... 

..... 

\D 

Holliday et al. (1986) 

(continued) 

NUlllber of 

Operations in All Industries: Sa!ples 

Planing 

Sanding 

Sawing/cutting 

Misc. operations in Primary Industries 

Shaping/routing 

Misc. operations not covered elsewhere 

Sawing/cutting in Primary Industries 

96 

TWA's I mg/m3 

~ Mean Median 

0.1-15.6 

3.3 «(),I=2.6) 

2.3 «(),I=1.4) 

2.2 (GA=1.2) 

1.9 (GA=1.3) 

1.9 (GA=l.1) 

1.6 (GM=1.0) 

1.2 (GM=O.7) 

2.2 

NOTE: These data are part of a background overview of the occupational health aspects of wood dust 

exposure in Ontario industry. Median total dust concentrations in the general workplace air 

determined fron area s~les were as follows: 0.3 mg/mJ in the Primary Industries (10 samples), 

0.8 mg/m3 in the Secondary Industries (12 samples), 1.2 mg/m3 in the Tertiary Industries (28 

samples), and 0.6 mg/m3 overall. Particle sizing by optical microscopy indicated that for the 

19 samples sized, particles in the 1-5 urn range were the most numerous across all operations; for 

sawing, sanding, and planing/routing/shaping, the average fractions of particles in this size 

range were roughly 62, 61, and 65%, respectively. 

Veda I et al. (1986) 

Sawmi II 

Canada (British Columbia) 

1 mi II 

1982-1985 

NOTE: These data are part of a 3-year longitudinal health study of 

workers in a western red cedar sawmill . Exposures were assigned for 

334 workers from 46 personal and 32 area total wood dust samples 

collected that ranged from undetectable to 6.0 mg/m3 . The average 

total dust exposure of the workers was 0.5 mg/m3; the median exposure 

was 0.2 mg/m3. It was determined that 10% of the workers were 

exposed to more than 1.0 mg/m3 of total wood dust and that 3.9% were 

exposed to more than 2.0 mg/~3. 

-
-

Table 7.--Summary of total dust concentrations in sanding operations 

Reference Description Number of TWA 's, mg/m3 

Samples Range Mean 

Kubis (1963) Belt sanding 10 3.6-65.0 23.6 

Hans I ian and Kadlec (1964) Be I t sand i ng 40 

Paustovskaya (1968) Sanding 2 16.7-25.5 21.1 

Imbus (1978) Sanding 17 0.2-15.4 3.7 

Ot to (1973) Mainly belt sanding : 14 <5 

25 5-9 

25 10-19 

38 >20 

Hounam and Williams (1974) Sanding 9 2.0-22 .6 7.2 

Andersen et al. (1977) Sanding 41 14.3 

levy (1976) Sanding 2 4.3-6 .8 5.5 .... Gunter (1977a) Sanding 1 90 90 N 

0 Fr iar (1978) IoIachine sanding 45 1-75 6 

Weaver (1979) Drum sanding 2.5 2.5 

Ele I t sand i ng 1.6-56.6 

Edge sanding 2.4-20.7 

Whitehead et al. (1981b) Sanding on hardwood 12 1.4-11.4 4.5 

Sanding on softwood 13 0.6-14.3 3.2 

Jones and Smith (1986) IoIachine sanding : 1976-1977 36 2.1-6 .3 3.7 

1983 49 0.7-53 5.7 

Hand sanding: 1976-1977 33 5.8-32 16 .9 

1983 42 0.5-27.2 6.9 

McCawley (1983) large sander 8 1.0-5 .6 2.9 

Sma I I sande r 5 1.7-4.5 2.9 

Sass-Kortsak et al. (1986) Sanding 7 2.9 

Holl iday et al. (1986) Sanding 2.3 
-

Table 8.--Summary of total dust concentrations in sawing operations 

Reference Oescr ipt ion Number of TWA's, mg/m3 

Samples Range Mean 

Imbus (1978) Sawing 6 0.6-4.7 1.9 

Hounam and Williams (1974) Band sawin9 6 1.0-7.3 4.3 

Kominsky and Anstadt (1976) Sawing 17 0.1-416 38.1 

Levy (1916) Sawing 2 1. 1-3.4 2.2 

Friar (1978) Band sawing 13 2-127 18 

Other sawing 21 2-35 8 

Apo I (1919b) Panel sawing 2 0.9-1.6 1.3 

Weaver (1919) Rip/cutoff sawing 8.4-11.2 

Double trim sawing 6.0 6.0 

AI Zuhair et al. (1981) Sawmi II department 15 3.5 

-

N Jones and Smith (1986) Sawing: 1916-1911 29 4.7-13.1 1.4 

- 1983 49 1.0-30.3 3.4 

Lindroos (1983) Sawing 11 0.3-2.0 0.8 

Sass-Kortsak et al. (1986) Sawing 12 1.1 

Holliday et al. (1986) Sawi ng/cutt i ng 2.2 
-

Table 9.--Summary of total dust concentrations in woodworking operations (excluding sanding/sawing) 

Reference Description Nulllber of TWA's, mg/m3 

Samples Range Mean 

Paustovskaya (1968) Hand fin i sh i ng 1 23.5 23.5 

Imbus (197B) Gr i nd i ng 2 1.3-4 .9 3.1 

Rout ing 2 1.0-2.2 1.6 

Molding 2 1.1-2 .7 1.9 

Lathe/tenoner/shaper 3 3.3-4.5 3.7 

Hounam and Williams (1974) Planing 9 1.B- l0 .9 5.0 

Rout ing 6 1.B-B.6 4.1 

Spindle moulding B 1.5-B.4 5.1 

Assembly 10 2.1-25 .5 7.5 

- Turning 2 4.6-12.5 8.6 

N 

N Rosensteel (1974) Roundtable shaper 2 8.6-8.9 8.8 

Kominsky and Anstadt (1976) Routin9/grooving 5 1.2-48 .5 12.5 

Gunter (1917a) Mi II worker 1 4 4 

Friar (1978) Assembly 35 2-41 8 

Weaver (1979) Bor ing 4.8 4.8 

Rout in9 3.1-15.5 

Hand shaping 15.3-21.1 

Whitehead et al . (1981b) Rough mi II ing 12 0.2-2 .6 0.7 

Detai led mi II ing 18 0.2-6 .3 1.7 

Assembly 5 1.1-3.1 2.0 

Enright (1980) Rout ing 1 2.4 2.4 

Shaping 4 2.0-10.2 5.2 

Omni mi II ing 3 0.1-0.4 0.2 

McCawley (1983) Rout ing 5 1.7-8.1 4.0 

Lindroos (1983) Unloading wood 10 0 .5-28 .0 4.3 

Planing 20 0.02-1 .8 0.4 

(Continued) 
-

N 

w 

Table 9 (Continued).--Summary of total dust concentrations in woodworking operations (excluding sanding/sawing) 

Reference Oescr i pt ion Number of TWA's, mg/m3 

Samples Range Mean 

McCammon et al. (1985) Sweeper 5 0.1-6.1 1.6 

Shaping 7 0.3-13.9 2.7 

Multi-axis machining 4 0.2-1.0 0.5 

Jones and Smith (1986) Cutting (excluding sawing): 

1976- 1977 44 2.0-10.8 6.9 

1983 70 0.3-8 .8 2.3 

Sass-Kortsak et al . (1986) Assembly 19 1.9 

Laminating/gluing 3 1.1 

M isce II aneous 7 1.2 

Holliday et al . (1986) Planing 3.3 

Shaping/routing 1.9 

-
-

Table 10 .--Summary of general area sanples for tctal dust collected in woodworking 

operat ions 

Reference Description Number of TWA's, mg/m3 

Samples Range Mean 

Paustovskaya (1968) Remote areas 5-6 

Levy (1976) Sawing/sanding/planing 1 2.5 

AI Zuhair et al. (1981) Sawmi II Department 6 1.4 

Assembly Department 2 0.8 

Mach i ne floor 16 0.7 

Cabinet shop 14 4.4 

McCammon et al . (1985) Wood mi II 10 0.05-0 .5 0.3 

Mini mi II 4 0.3-0.6 0.4 

Lindroos (1983) Pretreatment Department 9 0.2-1.0 0.6 ... Woodworking Department 14 0.1-0.4 0.3 N 

4>- Holl iday et al. (1986) Secondary Industries 12 0.8 

Tertiary Industries 28 1.2 
..... 

N 

U1 

, 

Table 11.--Sumaary of respirable dust concentrations in woodworking operations 

Reference Descr i pt ion 

Imbus (1978) Sanding 

Rosensteel (1974) Roundtable shaper 

Kominsky and Anstadt (1976) Saw 

Router/groover 

Weaver (1979) Cutoff sawi ng 

Router 

Enright (1980) Orb ita I sander 

Hand sanding 

AI Zuhair et al. (1981) Mach i ne f 100 r 

Cabinet shop 

McCammon et al. (1985) 18-61% of dust (mass) 

is respirable 

Ellenbecker and Wegman (1985) Sander 

Lind roos (1983) Pretreatment Dept. 

Woodworking Dept. 

Holness et al. (1985) Sawing/sanding 

Sass-Kortsak et al. (1986) Sawing 

Sanding 

Assembly 

Laminating/gluing 

Miscellaneous 

Number of 

Samples 

1 

2 

13 

3 

1 

1 

4 

4 

3 

7 

6 

12 

7 

18 

3 

7 

TWA's, mg/m3 

Range Mean 

0.7 0.7 

0.02-0.4 0.2 

0.07-4.4 0.7 

0.3-0.8 0.5 

2.1 

1.5 

0.5 0.5 

(2.2% of total dust) 

0.4 0.4 

(4.8% of total dust) 

0.19 

0.44 

0.5-0.9 0.6 

0.14-0.19 0.16 

0.11-0.20 0.14 

0.3 

0.1 

0.6 

0.3 

0.3 

0.3 

-
-

Table 12.--Summary of particle size data in woodworking operations 

Reference Oescr ipt ion '-'MO, um 

Hounam and Ii Iliams (1974) Sanding 8.4 

NOTE: More than 75% of Band sawing 11.5 

the dust (mass) was Planing 9.2 

>5 um in size. Rout ing 10.0 

Spindle moulding 10.0 

Assembly 7.6 

Turning 11.5 

Andersen et al. (1977) 33% (mass) was in particles <5 m 

41% (mass) was in range 

6-10 um 

11% (mass) was in range 

... 11-15 um 

N 15% (mass) was in particles en >16 um 

Kominsky (1976) Saw and routerlgroover >10 

Whitehead et al. (1981b) Relatively little dust was in 

smallest size ranges 

AI Zuhair et al. (1981) Machine floor 9.3 

Cabinet shop 12.5 

Sawmi II 17.3 

Assembly 18.0 

McCammon et al. (1985) Wood Mill A (9/25180) 10 

Wood Mill A (1/9180) 9.8 

Wood Mill A (3/4/80) 6.6 

Wood Mi II A (9/4/80) 8.4 

Wood Mi II C (3/4/80) 6.1 

Mini Mi II A (1/9/80) 9.0 

Mini Mi II A (1/10/80) 5.2 

Shaper Room C (3/5/80) 6.1 

Shaper Room C (3/5/80) 7.8 

(Continued) 
.... 

N 

...... 

Table 12 (Continued) .--Summary of particle size data in woodworking operations 

Reference 

Jones and Smith (1986) 

McCawley (1983) 

Descr i pti on 

Sanding 

54% (mass) was in the range 

4-10 um 

45-60% (mass) was in particles 

<3 .5 um 

30-35% (mass) was in range 

3.5-20 um 

5-20% (mass) was in particles 

>20 um 

IlIAD, um 

9 

-
, 

Table 13.--Recommended exhaust volumes for woodworking machinery* 

Type of machinery 

Saws 

Band 

Table (including rip, mitre, 

and variety saws) 

Swing 

Gang rip 900-2,060 

Self-feed table rip 

Sanders 

Disc 

Hor i zonta I Be It 

Vertical belt 

Drum (single) 

Drum (multiple) 

Swing arm 

Planers 

Single 

Double 

Routers 

Jointers 

Molders, matchers, sizers 

Lathes 

Automat i c 

Forming 

*Adapted from ACGIH (1986) 

Exhaust volume (cfm) 

128 

700-1,950 

350-550 

350-440 

790-1,350 

350-1,250 

790-1,650 

440-1,100 

350-1,400 

550-1,400 

440 

785-2,200 

1,335-3,600 

350-800 

350-800 

1,690-5,370 

800-5,000 

350-1,400 
, 

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