OCCUPATIONAL EXPOSURE TO WOOD DUST

by

KURUPPUGE UDENI ALWIS

A thesis submitted in fulfilment

of the requirements for the degree of

Doctor of Philosophy

DEPARTMENT OF PUBLIC HEALTH AND COMMUNITY MEDICINE

FACULTY OF MEDICINE

THE UNIVERSITY OF SYDNEY

NEW SOUTH WALES, AUSTRALIA August, 1998 DECLARATION

The investigations undertaken and described in this thesis were carried out during 1995-1998 in the National Occupational Health and

Safety Commission (NOHSC), and the Department of Public Health

and Community Medicine, the University of Sydney, under the

supervision of Dr. John Mandryk. Unless otherwise stated or except

where due acknowledgement has been made, the materials

embodied in this thesis are the result of my own original work and

have not been submitted fully or in part to any other university or

institution for the award of any other degree or diploma.

The following five papers have been submitted for publication, from the results of field and experimental investigations described in this thesis:

· Mandryk J, Alwis KU, Hocking AD (1999): Work-related symptoms and dose-response

relationships for personal exposures and pulmonary function among woodworkers. Am. J. Ind.

Med. 35, 481-490.

· Alwis KU, Mandryk, J, Hocking AD, Lee J, Mayhew T, Baker W (1999): Dust exposures in

wood processing industry. Am. Ind. Hyg. Assoc. J. (in press).

· Alwis KU, Mandryk J, Hocking AD (1999): Exposure to biohazards in wood dust – bacteria,

fungi, endotoxin and (1->3)-b-D-glucan. Appl. Occup. Environ. Hyg. (in press). · Mandryk J, Alwis KU, Hocking AD (1999): Effects of personal exposures on pulmonary

function and work-related symptoms among sawmill workers. Ann. Occup. Hyg. (submitted).

· Alwis KU, Mandryk J (1999): Occupational exposure to wood dust in joineries. Ann. Occup.

Hyg. (submitted).

In addition, a report has been prepared for the Timber Industry:

· Alwis KU, Mandryk J (1998): Wood dust exposure. A study of the timber industry in NSW.

Department of Public Health and Community Medicine, The University of Sydney, Australia.

KURUPPUGE UDENI

ALWIS

ACKNOWLEDGMENTS I am deeply indebted to my supervisor, Dr. John Mandryk for all his

efforts in making a peaceful environment for me to do this research

and helping me to overcome all the barriers I encountered

throughout this study. His advice, continuous support, and

encouragement throughout the study are gratefully acknowledged. I

would like to thank him especially for his help in literature survey,

organizing and planning field studies, his advice on data

interpretation and statistical analyses, and proof reading

manuscripts, reports and my thesis. It was a great privilege being a

student of such a knowledgeable, helpful and patient supervisor.

I also gratefully acknowledge my associate supervisor, Dr. Ailsa D.

Hocking, Research Food Mycologist, Food Science Australia, for her

support in carrying out this research. Dr. Hocking carried out the speciation of Penicillium and Aspergillus and also helped me identify other fungi from the airborne samples collected from the worksites. I

profoundly thank her also for her advice throughout the study, as

well as for proof reading manuscripts, reports, and my thesis.

Prof. Geoffrey Berry, Head, Department of Public Health and Community Medicine, University of

Sydney is gratefully acknowledged for his support and encouragement to progress this study.

Mr. John Lee and Mr. Trevor Mayhew, Occupational Hygienists,

WorkCover Authority (NSW), are deeply acknowledged, for their training and provision of air sampling equipment for the study, as

well as giving their time for discussion, proof reading of

manuscripts, and providing me with necessary information.

Mr. Warren Baker, Organizer, CFMEU (Construction, Forestry, Mining, and Energy Union, NSW) is gratefully acknowledged, for his helps in

getting access to joineries in NSW.

I would like to thank Mr. Jim Morton, Occupational Health and Safety

Advisory Officer, the Timber Trade Industrial Association (TTIA,

NSW) for his helps in getting access to sawmills and the

woodchipping mill in this study.

Mr. Steve Dobbin, Mr. Kevin Mainey, Forestry Officers of the State

forest Authority, Kempsey and Mr. Peter Dixon, Forestry Officer, the

State Forest Authority, Walcha are gratefully acknowledged for

giving permission and providing facilities to study two logging sites

at Kalatheenee State Forest, Kunda Bung and Styx River Forest,

Armidale.

I am deeply indebted to the management and the employees of the

companies, for participating in this study, for their cooperation, and

spending time demonstrating the different woodworking processes,

machinery, and ventilation systems. I would also like to thank:

Prof. Ragnar Rylander, Department of Environmental Medicine,

University of Gothenburg, Sweden for resolving my doubts regarding

sampling and analysis of airborne endotoxin;

Dr. Wijnand Eduard, National Institute of Occupational Health,

Norway, for his advice on sampling of airborne wood dust and microorganisms, and for providing copies of his published research;

Prof. Taminori Obayashi, Department of Clinical Pathology, Jichi

Medical College, Japan, for advising me on endotoxin-specific and

glucan-specific assays and providing copies of his published

research;

Dr. Hiroshi Tamura, Seikagaku Co., Tokyo, Japan, for advising me on

the technical details of the above assays;

Dr. Jim Leigh, Head, Research Unit, the National Occupational Health and Safety Commission

(NOHSC), for his advice on lung function;

Mr. Carl Bragg, formerly of Department of Public Health and Community Medicine, University of

Sydney, for providing me with SPSS software for the data analysis; Mr. Robert van der Hoek, Disease Registers Unit, Australian Institute

of Health and Welfare, Canberra for providing me with nasal cancer

statistics of NSW;

Mr. Mahinda Seneviratne, formerly of the Occupational Medicine Unit, the NOHSC for assisting me with basic microbiological methods and his help in making contacts with relevant organizations;

Mrs. Linda Apthorpe, formerly of the Occupational Hygiene Unit, the

NOHSC for allowing me to use laboratory facilities and for her help in taking photographs of pure cultures of microorganisms;

The library staff of NOHSC, especially Ms. Julie Hill, Ms. Verena Hunt, Ms.

Heather Macleod and Ms. Wendy Chan, former staff Ms. Theresa

Laxamana, and Ms. Claudette Taylor for their help in getting required information;

Prof. Graham Budd, formerly of the Occupational Medicine Unit, the NOHSC, for his encouragement and advice; and,

Ms. Joanne O’ Brian, Ms. Bhadra Illangakoon (NOHSC) and Ms. Patricia Davidson (NOHSC) for their support and encouragement. I would like to express my sincere gratitude to the University of

Sydney, for awarding me an Australian Post-Graduate Award

Scholarship and the National Occupational Health and Safety

Commission (NOHSC) for providing me with facilities during the

study.

At last, but not the least I respectfully acknowledge my parents, my mother and my late father, for everything they have done for the betterment of my life. DEDICATION

This thesis is dedicated to woodworkers

in Australia.

ABBREVIATIONS ACGIH American Conference of Governmental Industrial Hygienists

AM arithmetic mean

EAA extrinsic allergic alveolitis

ELISA enzyme-linked-immunosorbent assay

FEF25%-75% forced expiratory flow during the middle half of the FVC

FEV1 forced expiratory volume in one second

FVC forced vital capacity

GM geometric mean

GSD geometric standard deviation

HSE Health and Safety Executive

IgE immunoglobulin E

IgG immunoglobulin G

IOM Institute of Occupational Medicine

IPM inhalable particulate mass sampling

ISO International Standard Organization

LAL limulus amebocyte lysate

LPS lipopolysaccharide

MMAD mass median aerodynamic diameter

MMF maximum mid flow rate

MMI mucous membrane irritation

NIOSH National Institute of Occupational Safety and Health

NSW New South Wales

ODTS organic dust toxic syndrome

OR odds ratio

OSHA Occupational Safety and Health Administration

PEF peak expiratory flow

RAST radioallergosorbent test

RPM respirable particulate mass sampling

SD standard deviation TLV threshold limit value

TWA time weighted average

UKAEAUnited Kingdom Atomic Energy Authority

VC vital capacity

ABSTRACT

Occupational exposure to wood dust and biohazards associated with wood dust (endotoxins, (1-

>3)-b-D-glucans, Gram (-)ve bacteria and fungi), their correlation to respiratory function, and symptoms among woodworkers have been investigated in the present study.

Wood dust, endotoxins, and allergenic fungi are the main hazards found in woodworking environments. Relatively very few studies have been done on wood dust exposure. The present study was designed to comprehensively investigate the health effects of wood dust exposure, and in particular provide new information regarding:

· Exposure to (1->3)-b-D-glucans in an occupational environment; · Levels of exposure to wood dust and biohazards associated with wood dust in different

woodworking environments;

· Correlations among personal exposures, especially correlations between (1->3)-b-D-glucans

and fungi exposures, and endotoxins and Gram (-)ve bacteria exposures;

· Effects of personal exposure to biohazards on lung function;

· Effects of personal exposure to biohazards on work-related symptoms; and

· Determinants of inhalable exposures (provide which factors in the environment influence the

personal inhalable exposures).

Workers at four different woodworking processes; two logging sites, four sawmills, one major woodchipping operation and five joineries situated in the state of New South Wales in Australia were studied for personal exposure to inhalable dust (n=182) and respirable dust (n=81), fungi

(n=120), Gram (-)ve bacteria (n=120), inhalable endotoxin (n=160), respirable endotoxin (n=79), inhalable (1->3)-b-D-glucan (n=105), and respirable (1->3)-b-D-glucan (n=62). The workers

(n=168) were also tested for lung function. A questionnaire study (n=195) was carried out to determine the prevalence of work-related symptoms.

The geometric mean inhalable exposure at logging sites was 0.56 mg/m3 (n=7), sawmills 1.59 mg/m3 (n=93), the woodchipping mill 1.86 mg/m3 (n=9) and joineries 3.68 mg/m3 (n=66). Overall, sixty two percent of the exposures exceeded the current standards. Among joineries, 95% of the hardwood exposures and 35% of the softwood exposures were above the relevant standards.

Compared with green mills, the percentage of samples, which exceeded the hardwood standard was high for dry mills (70% in dry mills, 50% in green mills).

The respirable dust exposures were high at the joineries compared with the other worksites.

Exposure levels to fungi at logging sites and sawmills were in the range 103-104 cfu/m3, woodchipping 103-105 cfu/m3 and joineries 102-104 cfu/m3. The predominant fungi found at sawmills were Penicillium spp. High exposure levels of Aureobasidium pullulans were also found at two sawmills. At the woodchipping mill the predominant species were Aspergillus fumigatus, Penicillium spp., and Paecilomyces spp. The sawmills, which employed kiln drying processes, had lower exposure levels of fungi compared with the green mills. Those workplaces which had efficient dust control systems showed less exposure to fungi and bacteria. Although mean endotoxin levels were lower than the suggested threshold value of 20 ng/m3, some personal exposures at sawmills and joineries exceeded the threshold limit value. The mean inhalable (1->3)- b-D-glucan level at the woodchipping mill was 2.32 ng/m3, at sawmills 1.37 ng/m3, at logging sites 2.02 ng/m3, and at joineries 0.43 ng/m3. For the respirable size fraction, mean endotoxin and mean (1->3)-b-D-glucan concentrations were much lower, being similar to observed dust concentrations. Significant correlations were found between mean inhalable endotoxin and Gram

(-)ve bacteria levels (p<0.0001), and mean airborne inhalable (1->3)-b-D-glucan and fungi levels

(p=0.0003). The correlations between mean respirable endotoxin levels vs Gram (-)ve bacteria exposure levels (p=0.005), and respirable (1->3)-b-D-glucan exposure levels vs total fungi levels

(p=0.005) were also significant.

Significant correlations were found between lung function and personal exposures. Multivariate analyses showed that the effect of all the personal exposures on cross-shift decrements in lung function was more prominent among sawmill and chip mill workers compared with joinery workers.

Woodworkers had markedly high prevalence of cough, phlegm, chronic bronchitis, frequent headaches, throat and eye irritations, and nasal symptoms compared with controls. Among the woodworkers, smokers had a high prevalence of chronic bronchitis (20%) compared with non- smokers (10%). Some workers also reported a variety of allergy problems due to exposure to various types of wood dust.

Both joinery workers and sawmill and chip mill workers revealed significant correlations between work-related symptoms and personal exposures. Chronic bronchitis was significantly correlated with personal exposure to wood dust, endotoxin, (1->3)-b-D-glucan, fungi, and Gram (-)ve bacteria among joinery workers. Whereas among sawmill workers chronic bronchitis was significantly correlated with personal exposure to endotoxin, (1->3)-b-D-glucan, and fungi.

Woodworkers showed significant positive correlations between percentage cross-shift change

(decrease) in lung function and respiratory symptoms. Significant inverse correlations were also found among percentage predicted lung function and respiratory symptoms.

The elevated inhalable dust exposures observed in this study can be explained by a combination of factors, including: lack of awareness of potential health effects of wood dust exposure among both management and workers, aging equipment, inadequate and ineffective dust extraction systems or usually none especially for hand held tools, poor maintenance of the ventilation system in some, non-segregation of dusty processes, dry sweeping, and the use of compressed air jets.

The determinant-of-exposure analysis confirmed the field observations. The significant determinants of personal inhalable dust exposures (n=163) were found to be: local exhaust ventilation, job title, use of hand-held tools, cleaning method used, use of compressed air, and green or dry wood processed. Type of wood processed was not found to be statistically significant.

A majority of workers (~90%) did not wear appropriate respirators approved for wood dust, while the workers who did wear them, used them on average less than 50% of the time. Workers should be protected by controlling dust at its source. When exposure to wood dust cannot be avoided, engineering controls should be supplemented with the use of appropriate personal protective equipment. xvii

CONTENTS

DECLARATION ii

ACKNOWLEDGMENTS iv

DEDICATION ix

ABBREVIATIONS x

ABSTRACT xii

CHAPTER 1: INTRODUCTION AND LITERATURE REVIEW

1.1 Wood and Wood Processing 1

1.2 Occupational Exposure to Wood Dust 3

1.2.1 Toxicity 3

1.2.2 Non-allergic Respiratory Effects 16

1.2.3 Sinonasal Effects Other than Cancer 18

1.2.4 Nasal and Other Types of Cancer 20

1.2.5 Lung Fibrosis 25

1.2.6 Wood Dust Exposure Standards and

Recommendations 25

1.3 Occupational Exposure to Biohazards Associated with

Wood Dust 27

1.3.1 Endotoxin 29

1.3.2 Wood Moulds 32

1.3.3 (1->3)-b-D-Glucan 39

1.4 Sampling and Analysis 41 xviii

1.4.1 Wood Dust 41

1.4.2 Endotoxin 46

1.4.3 (1->3)-b-D-Glucan 50

1.4.4 Microorganisms 51

1.5 Summary 53

1.6 Timber Industry in Australia 54

1.6.1 The Aim of the Research 56

1.6.2 The Main Objectives 58

CHAPTER 2: EXPERIMENTAL INVESTIGATION

2.1 Field Investigation 59

2.2 Personal Dust Sampling 69

2.3 Endotoxin and (1->3)-b-D-Glucan Assays 73

2.4 Sampling and Culturing of Microorganisms 74

2.5 Lung Function Test 76

2.6 Questionnaire Study 77

2.7 Data Analysis 77

CHAPTER 3: RESULTS AND DISCUSSION

3.1 Distribution of Exposure Data 82

3.2 Personal Exposure to Wood Dust 84

3.2.1 Inhalable Dust

84 xix

3.2.2 Respirable Dust 97

3.2.3 Discussion 98

3.3 Personal Exposure to Biohazards Associated with

Wood Dust 103

3.3.1 Personal Exposure to Fungi and Bacteria 103

3.3.2 Personal Exposure to Endotoxin and

(1->3)-b-D-Glucan 109

3.3.3 Correlations among Personal Exposures (Dust,

Fungi, Bacteria, (1->3)-b-D-Glucan, and Endotoxin) 112

3.3.4 Discussion 117

3.4 Effects of Mean Personal Exposures, Number of Years of

Exposure to Wood Dust, and Cumulative Dust Indices on

Lung Function 120

3.4.1 Among Joinery Workers and Sawmill and

Chip Mill Workers 120

3.4.1.1 Effects on Cross-shift Change in Lung Function 120

(Acute Effects)

3.4.1.2 Effects on Percentage Predicted Lung Function 122

(Chronic Effects)

3.4.2. Among Non-smokers and Smokers 128

3.4.2.1 Effects on Cross-shift Change in Lung Function 128

(Acute Effects)

3.4.2.2 Effects on Percentage Predicted Lung Function 132

(Chronic Effects) xx

3.4.3 Discussion 133

3.5 Questionnaire Study 136

3.5.1 Use of Respirators 136

3.5.2 Prevalence of Work-Related Symptoms 137

3.5.3 Correlations among Personal Exposures and

Work-related Symptoms 143

3.5.4 Effects of Work-related Respiratory Symptoms on

Lung Function 146

3.5.4.1 Effects on Cross-shift Change in Lung Function 146

3.5.4.2 Effects on Percentage Predicted Lung Function 147

3.5.5 Wood Allergies 148

3.5.6 Discussion 149

3.6 Other Occupational Health Related Problems Observed at

Sawmills and Chipping mills 152

3.7 Nasal Cancer Statistics of NSW 154

CHAPTER 4: GENERAL DISCUSSION 155

4.1 Recommendations for the Timber Industry 161

4.2 Future Research 162

BIBLIOGRAPHY 165

APPENDIX A - Eucalypt Hardwood Forest 189

APPENDIX B - Logging Sites 197 xxi

APPENDIX C - Woodworking Processes Carried out in Sawmills 208

APPENDIX D - Woodworking Processes Carried out at

the Woodchipping mill 231

APPENDIX E - Joinery Operations 238

APPENDIX F - Process Flow Diagrams 248

APPENDIX G - Fungi Identified from the Personal Airborne

Samples Collected from the Worksites 263

APPENDIX H - Colony Morphology of the Pure Cultures

Prepared from Aspergillus and some Other

Mould Species Isolated from Airborne Samples 277 1

CHAPTER 1

INTRODUCTION AND LITERATURE REVIEW

1.1 WOOD AND WOOD PROCESSING

Wood is one of the most important renewable resources in the world. Wood is the hard fibrous substance composing most of the stem and branches of a tree or shrub, and covered by the bark. The inner core of the wood is called heartwood and the outer layer is called sapwood. For industrial purposes, wood is classified into two types; hardwoods and softwoods (Fengel and Wegner,

1989). Softwoods are derived from coniferous trees (botanically named as

Gymnospermae with exposed seeds), whereas hardwoods are from deciduous trees (botanically named as Angiospermae with encapsulated seeds).

The essential chemical constituents of wood are cellulose, polyoses

(hemicellulose), and lignin. Cellulose, which is built up exclusively of D-

Glucose units joined by b(1->4) glycosidic linkages, is the major component

(40-50%) of both hardwood and softwood. The proportion and chemical composition of lignin and polyoses differ in softwood and hardwood. Polyoses are present in larger amounts in hardwood than softwood and differ in their sugar composition. Softwood has a higher proportion of mannose and more galactose units than hardwood, whereas hardwood has a higher proportion of xylose units. The lignin content of softwood is higher than that of hardwood.

The “extractives” (organic matter, which can be extracted from wood with non- 2 polar or polar solvents) may have toxic, irritant or sensitising properties.

Comparatively, hardwoods tend to be denser and have a higher content of polar extractives than softwood. A detail description of the types, properties and uses of wood used in Australia is given in Bootle (1993) and about hardwoods of Australia and their economics is given in Baker (1919).

The major wood working processes are debarking, sawing, sanding, milling, lathing, drilling, veneer cutting, chipping and mechanical defibrating. From the tree felling stage onwards through the various stages of wood working and manufacturing processes, workers are exposed to airborne dust of different particle sizes, concentrations and compositions. Sawing and sanding both shatter lignified wood cells and break out whole cells and groups of cells

(chips) (Hinds, 1988). The more cell shattering that occurs the finer the dust particles that are produced. Sawing and milling are mixed cell shattering and chip forming processes, whereas sanding is almost exclusively cell shattering.

In hardwoods, the cells are tightly bound resulting in more shattering and more dust. Similarly, dry wood leads to more dust formation. Softwood particles are more fibrous and usually larger and as a result less capable of becoming airborne (Walker, 1988). Considerably high heat generation during sawing, machining and sanding may change the chemical composition of wood dust

(Gulzow, 1975). It has been reported (Thorpe and Brown, 1995), that hardwoods give rise to finer airborne dust at a lower rate during sanding than softwoods, but that the total amount of airborne dust produced depends only on the total mass of wood removed, and not the type of wood.

1.2 OCCUPATIONAL EXPOSURE TO WOOD DUST 3

The health effects of occupational exposure to wood dust can be summarised under five headings:

· toxicity (including dermatitis and allergic respiratory effects)

· non-allergic respiratory effects

· sinonasal effects other than cancer (nasal mucociliary clearance and

mucostasis)

· nasal and other types of cancer

· lung fibrosis

1.2.1 TOXICITY

The toxicity of wood, the irritant effects of wood on the skin and respiratory system of man are well documented (Senear, 1933; Bolza, 1976; Woods and

Calnan, 1976; Hausen, 1981; ILO, 1983; Goldsmith and Shy 1988a; HSE,

1995).

The structural components of wood are cellulose, hemi-cellulose and lignin.

The accessory substances or extractives (alkaloids, saponins, phenolic compounds especially catechols, quinones, stilbenes, terpenes, furocoumarins etc.) are found mainly in the heartwood and are responsible for most toxic, irritant, and sensitising effects (Woods and Calnan, 1976). Most of these constituents are considered as by-products and end-products of the biological functions of a living tree, which are of no further use for the tree, and therefore 4 are stored in the dead cells of the heartwood, giving it a different colour

(Hausen, 1981). Bark and sapwood may contain different or the same constituents as found in heartwood, but in different amounts. Wood dermatitis is mainly caused by the heartwood constituents of tropical species. The amounts of the responsible sensitisers vary seasonally, geographically and even among the same species growing in the same place. The more rare cases of contact dermatitis in woodcutters and debarkers are mainly due to compounds found in the outer sapwood and lichens growing on the bark.

Although freshly cut wood is as a rule quite toxic, the wood can become even more toxic on seasoning (Senear, 1933).

The toxic effects associated with wood or wood dust include skin irritation, sensitisation dermatitis (allergic dermatitis), allergic respiratory effects, nasal and eye irritations and splinter wounds (HSE, 1995). Splinter wounds are slow to heal and often turn septic. The reason may be partly due to the wood species and partly due to secondary infections, from bacteria and fungi entering through the skin.

1.2.1.1 Skin Irritation and Skin Sensitisation

Skin irritation can be caused by contact with the wood itself, dust, bark, sap or lichens growing on the bark. Symptoms subside once the irritant is removed.

Some species of wood can cause nettle rashes or irritant dermatitis on the forearm, back of the hands, the face, neck, scalp and the genitals. Sensitisation dermatitis is usually caused by exposure to the fine dust from certain wood species. This exposure produces symptoms similar to skin irritation. Once 5 sensitised, the body sets up an allergic reaction, and will react severely when exposed even to a small amount of wood dust.

Inhalation of fine wood dust causes a number of effects on the respiratory tract.

The nasal symptoms are rhinitis (runny nose), continuous sneezing, blocked nose, and nose bleeds. Eye symptoms are soreness, watering and conjunctivitis.

1.2.1.2 Allergic Respiratory Effects

The most commonly reported allergic respiratory effect due to wood dust is asthma (“woodworker’s asthma”). It may occur alone or in conjunction with dermatitis. The hypersensitivity reaction may be immediate or delayed or dual.

The presence of alkaloids, acids and other natural constituents, which give colour and grain to the timber, produces the pulmonary sensitivity (Goldsmith and Shy, 1988a).

Occupational asthma and rhinitis due to exposure to western red cedar has been studied extensively. It is one of the most common types of occupational asthma prevailing in British Colombia. In cedar sawmill workers, the prevalence of asthma is reported to be more than twice than that of the un-exposed reference population (Enarson and Chan-Yeung, 1990). Occupational asthma occurs in 5% of exposed workers in British Colombia (Chan-Yeung, 1982).

Western red cedar (Thuja plicata) is a softwood, widely used in indoor and outdoor constructions in coastal areas of British Colombia, because of its high 6 durability (Chan-Yeung, et al., 1971). The clinical features associated with red cedar asthma include cough, wheeze and dyspnoea developing after a period of steady exposure to red cedar, usually of about 3 years (Chan-Yeung, 1982;

Chan-Yeung et al., 1982; Tse et al., 1982). Initially these symptoms develop after work, but with continued exposure, the symptoms tend to develop during work as well. The persistence of asthma among workers after removal from exposure has also been described (Chan-Yeung et al., 1982; 1987). Plicatic acid, a low molecular weight substance, unique to Thuja plicata, has been identified as the causative agent for red cedar asthma (Chan-Yeung et al.,

1973; 1980; Chan-Yeung and Lam, 1986). It has been reported that inhalation provocation tests using plicatic acid, a major fraction in the red cedar non- volatile extractives, produce immediate, late or dual bronchial reactions similar to those produced by the whole wood extract (Chan-Yeung et al., 1973).

Symptoms of work-related asthma in red cedar workers are more common after

10 years of exposure (Vedal et al., 1986). Prevalence of cough, dyspnoea, persistent wheeze, and asthma increased with increase in dust exposure level.

Levels of FVC and FEV1 were lower with dust concentrations greater than 2 mg/m3. An eight hour time-weighted-average dust level below 3.5 mg/m3 of western red cedar is necessary in order to reduce the incidence of occupationally related asthma (Brooks et al., 1981). In the US, OSHA established an exposure limit of 2.5 mg/m3 for western red cedar based on allergenic properties of the dust (Federal Register, 1989). 7

A summary of previous case studies on wood dermatitis and allergic respiratory effects due to exposure to various types of wood is given in Table 1.1.

1.2.1.3 Wood Allergy Reported from Australia

There is far less published information on wood allergy (especially due to native woods) reported from Australia. Much of the information is found in very old descriptive literature or case reports dating back to the 1920’s.

Radiata pine (Pinus radiata) - A native tree of Southern California, which was introduced to Australia in 1876, is a softwood used mostly in home construction. About 15 cases of allergic contact dermatitis have been reported by Burry (Burry et al., 1973; Burry, 1976; 1977). The subjects had shown positive skin patch reactions to sawdust and in some cases to colophony or to wood turpentine. Terpenoid components of the wood may be responsible for the allergies. A previous study (Burge, 1979) described an association between woodworker’s asthma and colophony exposure, confirmed by positive bronchial challenge to wood dust as well as colophony. An animal study has also confirmed that pine dust (colophony) can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells of lungs (Ayars et al., 1989). Table 1.1 Summary of Case Studies on Wood Allergy type of wood number of duration of reported health effects reference cases exposure prior to symptoms

RESPIRATORY EFFECTS

Kejaat wood 1 wood machinist from the dyspnoea, chest tightness Ordman, 1949a (Pterocarpus angolensis) first day cough, sneezing, severe headache, (confirmed by a positive skin test)

Kejaat wood 1 cabinet maker three asthma, rhinitis, sneezing, wheezing Ordman, 1949b (Pterocarpus angolensis) months (confirmed by positive skin patch test) Iroko (Chlorophora excelsa) Patridge or Panga Panga (Millettia stuhlmanii) Western red cedar (Thuja plicata), Congo

Oak 1 mill worker 12 yrs asthma, cough, rhinitis, dyspnoea Sosman et al., Mahogany 1 pattern maker 16 yrs (confirmed by decline in FEV1 and FVC 1969 Cedar 2 carpenter 17-18 yrs immediate for Oak, dual for Mahogany delayed for Cedar, positive serum antibodies

Western red cedar 2 carpenters, 1 week to asthma, wheezing, coughing, rhinitis Milne and (Thuja plicata) 2 joiners, 1 yr (nocturnal symptoms) Gandevia, 1969 1 wood mechanist 1 sign writer type of wood number of duration of reported health effects reference cases exposure prior to symptoms

Western red cedar 6 joiners 1 month to asthma and rhinitis, nocturnal cough Gandevia and (Thuja plicata) six year sneezing, dyspnoea, wheezing, persistence of Milne, 1970 symptoms after cessation of exposure (confirmed by decline in FEV1 to bronchial provocation test, mild or absent skin test, negative precipitin test)

Western red cedar 1 carpenter 1 yr asthma with dyspnoea (confirmed by a positive Pickering et al., (Thuja plicata) skin patch test and a positive serum antibodies 1972 Iroko (Chlorophora excelsa) 1 carpenter unknown for iroko only and a decline in FEV1 for both wood)

Cedar of Lebanon 6 joinery workers 3 months asthma, rhinitis, chest tightness, cough, dyspnoea Greenberg, 1972 (Cedra libani) negative skin testing and precipitin testing

Cocabolla 3 furniture makers day to chest tightness, wheeze, dry cough Eaton, 1973 (Dalbergia retusa) 18 months nasal obstruction, frontal headache dermatitis (positive skin patch test)

Western red cedar 22 woodworkers not stated asthma, rhinitis, cough (confirmed by inhalation Chan-Yeung et al., (Thuja plicata) provocation test, immediate reaction (4) and late 1973 (8) and dual (6), positive skin patch test in (3), negative precipitin test, the (4) subjects not reacted to inhalation provocation test, not recovered on cessation of exposure

Abiruana 2 furniture makers days to asthma, nocturnal dyspnoea and cough (decline in Booth et al., 1976 (Lucuma species) 1 yr FEV1, FVC, MMF when provoked, positive skin test, positive precipitin test)

California redwood 2 carpenters 2-3 yrs asthma, dyspnoea, wheezing (confirmed by Chan-Yeung and (Sequoia sempervirens) immediate, delayed and dual decline in FEV1) Abboud, 1976 type of wood number of duration of reported health effects reference cases exposure prior to symptoms

Ramin 1 woodworker not stated hypersensitivity, dyspnoea, cough, shivering Howie et al., 1976 (Gonystylus bancanus) sweating, tiredness (confirmed by decline in FEV1 positive serum antibody, negative skin patch test)

African Zebra wood 1 woodworker 5 months asthma, cough, dyspnoea (confirmed by a positive skin Bush et al., 1978 (Microberlinia species) skin patch test, dual decline in FEV1 for bronchial challenge test, a positive RAST

Quillaja bark (soap bark) 1 spray drier operator 3 months asthma, rhinitis, lacrimation, itchiness of eye, Raghuprasad, (Quillaja saponaria) saponin dust factory sneezing, dyspnoea, wheezing (confirmed by immediate et al., 1980 bronchoconstriction, faintness, diffuse erythema hypotension)

Tanganyike anigré 3 woodworkers days to asthma, dyspnoea, cough, wheezing, itchiness, Paggiaro, et al., 3 months rhinorrhea (confirmed by positive skin patch test and 1981 decline in FEV1 in two subjects, negative precipitin test or specific IgE)

Central American Walnut 1 woodworker not stated rhinorrhea, cough, wheezing, dyspnoea Bush and (Juglans olanchana) (confirmed by decline in FEV1, negative Clayton, 1983 skin patch test and RAST)

African maple 2 carpenter 2 months dyspnoea, wheezing, sneezing, rhinitis Hinojosa et al, (Triplochiton scleroxylon) nasal itching (confirmed by immediate decline 1984 in FEV1 for bronchial provocation test. positive skin patch test and specific IgE

Eastern white cedar 1 sawmill worker after a few asthma (confirmed by change in PEF and bronchial Cartier et al., (Thuja occidentalis) weeks responsiveness to histamin and inhalation challenge 1986 test, late decline in FEV1, specific IgE) type of wood number of duration of reported health effects reference cases exposure prior to symptoms

DERMAL EFFECTS

Iroko (African teak) 9 woodworkers 1 -2 hrs itching of exposed skin areas, oedema of the face Davidson, 1941 (Chlorophora excelsa) acute coryza, headache, pharyngitis, dry cough, dyspnoea simulating asthma

Iroko (Mvule) 3 joiners 1 -2 weeks dermatitis of face, neck and arms, legs and feet, rhinitis Piorkowski, 1944 (Chlorophora excelsa) 1 cabinet maker 10 days and conjunctivitis (3 joiners); dermatitis face, hand and Cedar (Juniperus procera) 1 owner of a carpenter 6 months and fore arms (cabinet maker); eczematous dermatitis, Podo (Podocarpus milanjianu) shop face, hand, fore arms, pruritus (slight positive skin patch Camphor (Ocotea usambarensis) test in 4 subjects for Iroko) Burma teak (Tectona grandis)

African mahogany 7 furniture makers not stated dermatitis in face, fore arms and back of the Morgan and (Khaya anthotheca) hands, swollen eyelids Wilkinson, 1965

Ayan wood 1 woodworker not stated dermatitis in arms, chest, legs, crutch region Morgan and (Distemonanthus (coffin manufacture) feet (confirmed by positive skin patch test) Thomsan, 1967 benthamianus) Oak, Elm

African mahogany 5 furniture makers not stated dermatitis in ear lobs, sides of the neck, forearms Morgan et al., (Khaya anthotheca) and other exposed part of the body 1968 Machaerium scleroxylon 7 furniture makers 4 days - 3 eczematous dermatitis in hands, cheeks, lips weeks forehead, neck, all exposed area (confirmed by positive skin patch test in all)

type of wood number of duration of reported health effects reference cases exposure prior to symptoms Rio rosewood 1 woodworker 1 week dermatitis (erythema multiform like) Holst et al., (Dalbergia nigra) face, arm, thighs, upper trunk 1976 Pao ferro 1 woodworker 1 week (confirmed by positive skin patch tests) (Mackerium scleroxylon) Blue gum (E. saligna) 1 frameworker 2 weeks

Machaerium scleroxylon 4 joiners 2 - 12 days dermatitis, itching, swellings and redness of face, Beck et al., scrotum, hands, sore mouth, throats and eyes 1984 (positive skin patch test)

MDF - Medium density fibre 11 furniture not stated occupational irritant dermatitis (exposed areas) Vale and (MDF consisted of 85% sore eyes, sore nose, dryness of mouth, slight Rycroft, 1988 softwood chip fibre, 8.5% urea- scaling over the back of the hands, and patchy formaldehyde resin, 0.5% red scaly eczema over the upper limbs, and in paraffin wax, and 6% water) some cases on the face (skin patch testing was not carried out)

Table 1.3 Summary of Wood Dust Surveys (dust concentrations in mg/m3) type of type of sampling nb sawing planing/milling sanding overall comments reference industry wooda furniture (5) H personal (total) 58 7.5 (1-20) 5.1 (1-25) 9.0 (2.4-25.2) 5.9 (1-25) 75% of the samples Hounam area (total) 40 20.1 (0.8-100) 3.6 (0.5-100) 8.0 (0.5-34.3) 3.6 (1.7-9.4) in the range of and 4.15-13.65 Williams, equivalent diameter 1974 furniture H area (total) 35 4.5 (1.4-11.4) 2.4 (0.2-11.4) 60% of the samples Whitehead S 35 3.2 (0.6-14.3) 2.1 (0.2-14.3) >22.5 µm equi. dia. et al., 1981b P 32 0.9 (0.1-3.2) plywood factory area (total) 49 2.5 (0.4-12) 3.2 (0.8-9.5) background level: Kauppinen 0.9 mg/m3 et al., 1984 wood model H/S personal (total) 23 0.79 (0.16-8.33) MMAD -(5.2-10mm) Mccammon shop (3) S 04 0.34 (0.2-0.51) average - 7.7 mm et al., 1985 H 12 0.64 (0.16-0.25) cabinet S personal (total) 2.23 (0.28) Sass-Kortsak making (4) H 2.02 (0.34) et al., 1986 S/H 1.32 (0.36) 48 1.72 (0.11) 2.91 (0.63) 1.83 (0.29) furniture (7) H personal (inh.) 210 3.4 (1-30.3) 2.3 (0.3-8.8) 6.9 (0.5-27.2)c 4.3 (0.3-53) 54% of the weight Jones and 5.7 (0.7-53)d of the dust in the range Smith, 1986 of 4-10 µm equi. dia. woodworking H personal (total) 56 3.2 (0.3-57.8) 44-73% of the total Lehmann operations (17) area (total) 32 1.9 (0.1-12) mass in the range of and Fröhlich >9 µm equi. dia. 1988 sawmills (2) H personal (total) 11 1.5 (0.5-3.3) 80% of the samples Archer, exceeded the hardwood 1988 standard of 1 mg/m3 aS: softwood, H: hardwood, P: particle boards. bnumber of samples. chand-held tools. dmachine handled. (Table 1.3) continued -> page 45 Table 1.3 continued ->

type of type of sampling nb sawing planing/milling sanding overall comments reference industry (no.) wooda furniture (15) H/S personal (inh.) 171 3.7 (1-24) 5.5 (2-10)c 3.7 (0.4-24) inhalable dust Pisaniello 3.0 (0.7-5.6)d 3.8 (H) MMAD (µm) et al., 3.3 (S) 16-19 (sanding) 1991 17-22 (sawing) 15-23 (mixed) machine shop (3) H/S personal (inh.) 07 0.5-5.1 inhalable dust Hamill woodworking (24) H/S 51 0.5-33 et al., woodworking (12) S 37 0.3-55.2 1991 sawmills (20) personal (inh.) 85 0.54 inhalable dust Vinzents and furniture (27) 118 0.63 40-50% of the dust Laursen, factory (96) 396 1.12 in the range of 1993 (doors/windows) 4-14 µm equi. dia. others (49) 153 0.90 sawmills (2) S personal (total) 224 0.09 0.22 0.51 (0.08-52) total dust Teschke personal (resp.) 217 0.09-20 respirable dust et al., 1994 furniture (1) personal (inh.) 36 4.7 (2.69-9.79) 3.3 (1.52-6.05) 4.60c inhalable dust Scheeper joinery (1) 23 5.0 (3.05-6.59) 2.8 (0.91-10.08) 10.00 (3.02-28.78)c inhalable dust et al., 1995 04 4.23 (2.01-5.60) respirable dust joinery (1) 39 1.6 (0.44-3.93) 1.4 (0.44-3.45) inhalable dust

Wood mill (6) S/H six-stage 7 12.00 (4.4-22.4) total dust (grinding) Liou et al., cascade (0.30-11.24) resp. dust (grinding) 1996 impactor 2.90 2.90 total dust (sawing) 0.23 0.23 resp. dust (sawing) aS: softwood, H: hardwood. bnumber of samples. chand-held tools. dmachine handled. 13

Blackwood (Acacia melanoxylon) - Australian blackwood which is native to

Western Australia is a hardwood species of commercial value which may induce allergy (allergic contact dermatitis) among the workers handling it. The wood is dark brown in colour, with black annual rings giving it a decorative appearance, used in Australia not only for high quality furniture, panelling, joinery, and turnery, but also for coach and boat building and even for parts of musical instruments.

Cases of allergic contact dermatitis as well as outbreaks of bronchial asthma after handling and inhalation of fine wood dust and shavings have been described since 1925. Workers in joinery shops and motor-boat factories have been mainly affected, developing severe dermatitis, circumscribed skin lesions on the forearms, the neck, face and eyebrows (Cleland, 1925; Pulleine, 1925).

Robertson reported 10 cases, one of which had bronchial asthma and the rest had contact dermatitis (Robertson, 1927). Hurst (1942) and Cleland (1931) have described further cases without detailed descriptions. It has been found that the quinonoid constituents (benzoquinones and furanquinones) are the contact sensitisers in Australian blackwood (Hausen and Schmalle, 1981). 14

Red bean (Dysoxylon muelleri) - Red bean is a commercially valuable hardwood in New South Wales used for furniture, joinery, turnery, carving, veneer, and panelling. Maiden (1910) has reported the sawdust of red bean as exceedingly irritating, inducing eczema and irritation of the mucous membrane among cabinet makers. It was also reported that the more seasoned the wood is, the worse it becomes.

Queensland maple (Flindersia chatawaiana) - MacPherson (1925) reported a cabinet maker suffering from acute dermatitis caused by working with the wood of Queensland maple. The initial symptoms were irritation of the back of the hands and between the fingers. Exposed parts were later affected,

“weeping” occurred in the lesions and a condition resembling acute exfoliative dermatitis followed with desquamation of epidermis particularly on the dorsal and lateral aspects of the fingers and hand, also about the wrist and nape.

Eucalyptus species - Eucalyptus is the most abundant hardwood species, native to Australia. The timber of E. hemiphloia (grey box) and E. maculata

(spotted gum) are known to cause skin irritation among bushworkers (Morris,

1943). A previous report has stated that these plants (grey box and spotted gum) excited irritation of the skin not only by contact, but even by proximity

(Maiden, 1904). Nasal irritation and temporary spasmodic rhinorrhea among workers in a joinery and a furniture shop exposed to South Australian blue gum

(E. leucoxylon) and red pine (Sequoia semperviren-imported wood) have also been reported (Cleland, 1925). 15

Indian teak (Tectona grandis) - Indian teak is an imported hardwood used mainly for furniture manufacture and also for ship’s decking. A carpenter suffering from dermatitis with nettle-rash and irritation lasting for several days, caused by handling Indian teak or when saw dust was contacted, has been reported from Sydney. The affected areas were the hands and forearms as well as the scrotum (Cleland, 1914).

Western red cedar (Thuja plicata) - Western red cedar or Canadian red cedar is an imported softwood (native to North America). It is widely used in the joinery trade in Australia because of its durability, good appearance in natural finish, the ease with which it takes paints and its resistance to attack by white ants. The occupational asthma and rhinitis resulting from exposure to red cedar dust was first described by Milne and Gandevia (1969) among joinery workers in Australia.

Many of the woods described above are highly prized for durability and quality of appearance, making exposure to dust and the resulting respiratory and dermal effects a major occupational health issue for the industry. It has also been reported that many chemicals which are introduced into timber while it is being processed, (eg. preservatives such as pentachlorophenol and other chlorinated phenols, potassium dichromate, urea-formaldehyde and epoxy resins, turpentine, polishes, varnishes and dyes) cause more dermatitis problems than does the wood itself (Woods and Calnan, 1976). 16

1.2.2 NON-ALLERGIC RESPIRATORY EFFECTS

Exposure to wood dust can cause chronic obstructive lung diseases (Carosso et al., 1987), even in the absence of reported asthma (Enarson and Chan-

Yeung, 1990).

Many of the epidemiological studies of wood dust associated health hazards are focused on the furniture industry. A number of studies have demonstrated a reduction in pulmonary function due to wood dust exposure (Al Zuhair et al.,

1981; Whitehead et al., 1981a; Holness et al., 1985; Carosso et al., 1987;

Goldsmith and Shy, 1988b; Rastogi et al., 1989; Shamssain, 1992; Liou et al.,

1996). Dose-response relationships were reported among percentage predicted lung function values and cumulative dust index (given by mean area dust level multiplied by number of years of exposure) (Holness et al., 1985), and reduction in lung function indices with wood dust exposure, classified by job titles (Goldsmith and Shy, 1988b; Liou et al., 1996).

Exposure to sawfumes containing terpenes also causes a chronic obstructive impairment in lung function (Hedenstierna et al., 1983; Dalqvist et al., 1994;

1996). Sawfumes are generated when lumber is sawn in bandsaws or framesaws, and when the battens are edged. a-pinene, b-pinene and D-3- carene are the main terpene constituents of pine. Airborne terpene levels in

Swedish sawmills have been reported to be in the range of 80-550 mg/m3. It 17 has been reported that workers exposed to an average about 250 mg/m3 of a- pinene, b-pinene and D-3-carene had decreased lung function (Hedenstierna et al., 1983). In Sweden there are no specific exposure limits for individual terpenes, but the exposure limit for turpentine (450 mg/m3) is used when assessing exposure to saw fumes (Eriksson and Levin, 1990). Terpenes also cause irritation of skin and mucous membrane, and also allergic and non- allergic contact dermatitis. The verbenols (metabolites from a-pinene) in urine

(Eriksson and Levin 1990) can be used as a biological exposure index of sawfumes (Eriksson et al., 1996).

1.2.2.1 Respiratory, Nasal, Eye and Other Symptoms

Respiratory, nasal and eye symptoms are the most common symptoms reported by woodworkers (Holness et al., 1985; Li et al., 1990; Pisaniello et al.,

1991; Shamssain, 1992; Liou et al., 1996). Chronic bronchitis is more prevalent among smokers than non-smokers (Li et al., 1990; Liou et al, 1996). A study on woodmill workers making joss sticks reported that the prevalence of chronic bronchitis was 15% among smokers and 8% among non-smokers (Liou et al.,

1996). Another similar woodworking study reported chronic bronchitis among

33% of smokers and 17% of non-smokers (Li et al., 1990).

A South Australian study (Pisaniello et al., 1991) reported that the prevalence of regular blocked nose was 51%, sneezing 41%, regular runny nose and excess nasal secretion 45% and eye irritation 35% among furniture workers.

Hardwood users reported more nasal symptoms than users of reconstituted wood. This latter study also reported that the woodworkers with the least 18 experience were more likely to report symptoms than more experienced workers. A South African study reported that the prevalence of nasal symptoms was 49%, cough 43%, and phlegm 15% among furniture workers (Shamssain,

1992). In contrast to the previous South Australian study, the South African study reported that the prevalence of cough and nasal symptoms increased with increase in the number of years of employment. A Canadian study reported high prevalence of cough (38%), sputum (30%), wheeze (18%), rhinitis (32%) and eye irritation (20%) among woodworkers compared with the controls (Holness et al., 1985). Significant correlations have also been reported between frequent sneezing and eye irritation with wood dust exposed jobs

(Goldsmith and Shy, 1988b)

1.2.3 SINONASAL EFFECTS OTHER THAN CANCER

1.2.3.1 Nasal Mucociliary Clearance

Chronic exposure to wood dust can cause impaired mucociliary clearance among woodworkers. A British furniture industry study reported that nasal mucociliary function is significantly impaired in workers who have been exposed to wood dust in the furniture industry for more than 10 years (Black et al., 1974). A Swedish furniture industry study reported that 20% of workers had nasal hypersecretion, nasal obstruction (40%), and impaired nasal clearance

(54%) compared to controls (Wilhelmsson and Drettner, 1984). Work-related impairment of nasal mucociliary clearance among woodwork teachers exposed to dust concentrations below the TLV of 2 mg/m3 has been reported from

Sweden (Ahman et al., 1996). Among them 55% had work-related nasal 19 obstruction, runny nose (27%), sneezing (39%), nose bleed, and impaired smell (22%), the prevalence being significantly higher than in the controls.

1.2.3.2 Nasal Mucostasis

It has been reported that the mucostatic factor in wood dust is of importance in the development of nasal adenocarcinoma because of the prolonged retention of dust in the nasal cavity (Andersen et al., 1977). The study found that the number of workers with nasal mucostasis was directly proportional to the wood dust concentration. This study also reported that at a wood dust concentration of 25.5 mg/m3, 63% of workers had mucostasis and at 2.2 mg/m3 only 11% showed mucostasis.

A number of studies showed that cuboidal metaplasia with dysplasia was a possible precursor to nasal adenocarcinoma among workers exposed to wood dust (Boysen and Solberg, 1982; Wilhelmsson et al., 1985; Boysen et al.,

1986). The histological examination of biopsies for nasal dysplasia can be used as an appropriate tool in identifying occupational groups with an increased incidence of sinonasal carcinoma (Boysen et al., 1986).

1.2.4 NASAL AND OTHER TYPES OF CANCER 20

1.2.4.1 Nasal Cancer

The association between nasal cancer and occupational exposure to wood dust, especially in the furniture industry, was first noted in the late 1960’s in the

UK (Macbeth, 1965; Acheson, 1976), where the annual incidence of nasal adenocarcinoma was 0.7 cases per 1000 and is estimated as 500 times the level found in the general population (Acheson et al., 1968). Nasal cancer is a significant hazard of woodworking, particularly associated with furniture making and hardwoods (Acheson et al., 1981; Rang and Acheson, 1981). Australian studies have confirmed that not only furniture workers but also sawmillers and carpenters are at risk (Ironside and Matthews, 1975; Franklin, 1982). Hardwood dust exposure has been shown to be associated with nasal adenocarcinoma

(Acheson et al., 1981) while softwood dust exposure has been shown to increase the risk of both sinonasal and nasopharyngeal squamous cell cancers

(Voss et al., 1985; Vaughan and Davis, 1991). The aetiological factors for nasal adenocarcinoma are still unknown. A review has stated that it is possible that the health hazards of hardwoods are related more to physical properties than to any chemical constituents (Walker, 1988). The period of latency on average for nasal cancer is about 41 years (Andersen et al., 1977). The

International Agency of Research on Cancer (IARC) in their monograph on the

“Evaluation of Carcinogenic Risks to Humans”, has concluded that wood dust is carcinogenic to humans (group 1) (IARC, 1995). 21

The carcinogenic aspects of exposure to wood dust have been reviewed by

Wills (1982), HSE (1986), Walker (1988), Nylander and Dement (1993), and in more detail in an IARC monograph, 1995.

The association between nasal cancer and wood dust exposure has been confirmed to varying degrees in France (Luce et al., 1993; Leclerc et al., 1994); the Netherlands (Hayes et al., 1986); a pooled case-control study of seven countries - France, China, Germany, Italy, the Netherlands, Sweden, the US

(Demers et al., 1995); Australia (Ironside and Matthews, 1975; Franklin, 1982), the United Kingdom (Macbeth, 1965; Acheson et al., 1981); Denmark, Finland and Sweden (Hernberg et al., 1983a; 1983b), British Colombia (Elwood, 1981),

Japan (Fukuda and Shibata, 1988), and Norway (Voss et al., 1985). The studies reported from the US are less convincing (Imbus and Dyson, 1987;

Viren and Imbus 1989). These two studies have shown that there was no overall excess of deaths from nasal cancer in wood-related industries including furniture manufacturing in the US.

The size-selective sampling of wood dust in US furniture plants has shown that

85-90% of the dust by weight is >15µm aerodynamic diameter (Whitehead et al., 1981b). Whereas a UK study (Hounam and William, 1974) found only 30-

40% wood dust in furniture plants to be >13.7µm aerodynamic diameter. A

Danish furniture study found only 15% of the dust to be 15µm in size

(Anderson et al., 1977). The three European studies indicated that the airborne dust particle sizes found in European furniture plants were finer compared with those of the US. This might be one reason for the high prevalence of nasal 22 adenocarcinoma observed among furniture workers in European countries compared with the US. Larger wood dust particles are not retained in the nose, since the deposited larger particles are removed by mucociliary clearance.

Only the finer particles are trapped in nasal passages, causing mucostasis, which may in turn lead to nasal cancer.

It has been reported that the much lower risk observed in British Colombia compared with English furniture makers is most probably due to the use of softwood rather than hardwood, or the use of coarse and unseasoned timber rather than kiln dried timber, or the use of rough sawing rather than fine finishing, or outdoor or large indoor workplaces rather than small shops or a combination of these factors. The study also reported that in British Colombia, forestry and sawmills employ a large proportion of the population while furniture manufacturing is very limited. Workers performing sanding operations may have an especially high risk of development of cancers within the sinonasal area because the mean airborne wood dust concentration in the breathing zone of workers engaged in hand or machine sanding has been found to be nearly three times the concentration found in the breathing zone of persons employed in sawing, planing and drilling (Anderson et al., 1977; Wills, 1982).

Excess risk of nasal cancer is associated with high levels of exposure to airborne wood dust. One review has suggested that nasal adenocarcinoma can be eliminated in Europe and it’s occurrence can be prevented in the US if wood dust exposures do not exceed an 8 hr time-weighted-average (TWA) of 5 mg/m3 (Blot et al., 1997). 23

1.2.4.2 Nasal Adenocarcinoma Reported from Australia

Nasal adenocarcinoma among woodworkers has been reported from Tasmania

(Franklin, 1982) and Victoria (Ironside and Matthews, 1975). Both studies have stated that males are at a greater risk than females and occupation as the possible factor for the difference. The annual incidence of nasal cancer is 5 per million per annum for Tasmania (Franklin, 1982) and 7 per million per annum for South Australia (Pisaniello and Muriale, 1990), incidences which are similar to the annual incidence of 7-10 per million in the UK. The proportion of nasal adenocarcinoma to total nasal cancer was 20% in Victoria, and 65% in

Tasmania whereas in High Wycombe (UK) the proportion was 25% (Franklin,

1982). In South Australia, the proportion is 20%, similar to Victoria. The relatively greater risk found in Tasmania may be due to the more extensive use of hardwoods, especially blackwood (Acacia melanoxylon) (Pisaniello and

Muriale, 1990). In Tasmania, blackwood is the most common wood (65% of total solid wood) processed among furniture manufacturing companies

(Ozarska, 1988). The British studies reported that only furniture workers were at a greater risk of nasal adenocarcinoma (Acheson et al., 1981). The

Tasmanian and Victorian studies confirmed that not only furniture workers but also all woodworkers including sawmillers and carpenters are at risk. The possible reasons given are, different varieties of timber processed; the drier wood processed by Australian sawmillers and carpenters (because of climate or treatment of timber) compared with their English counterparts; and sawmilling being proportionately a larger industry in Australia, whereas the 24 furniture industry is the larger industry in the UK (Ironside and Matthews,

1975).

1.2.4.3 Other Types of Cancers

A variety of cancers have been described: increased risks of Hodgkins disease among woodworkers (Milham and Hesser, 1967); non-Hodgkins lymphoma among furniture workers (Miller et al., 1989); leukaemia among furniture makers (Miller et al., 1989) and sawmillers (Jappinen et al., 1989); nasopharyngeal cancer among foresters and loggers (Kawachi et al., 1989), furniture makers (Moulds and Bakowski, 1976), and sawmillers (Hardell et al.,

1982); lung cancer among sawmillers (Kawachi et al., 1989), plywood workers

(Kauppinen et al., 1993), carpenters (Robinson et al., 1996); liver cancer among sawmillers (Kawachi et al., 1989), stomach cancer among carpenters

(Robinson et al, 1996); skin cancer among sawmillers (Jappinen et al., 1989); lip cancer among carpenters (Kawachi et al., 1989) and sawmillers (Jappinen et al., 1989); mouth and pharynx cancer among sawmillers (Jappinen et al.,

1989) and male breast cancer and malignant mesothelioma among carpenters

(Robinson et al., 1996). Some of these studies reported that the possible risk factors included; wood dust, terpenes, organic solvents, chemical preservatives, and fungicides used during wood processing. A Swedish study has reported an increased risk of lung cancer, malignant mesothelioma and malignant lymphoma among pulp and paper mill workers, and has suggested that exposure to fresh wood is the probable risk factor (Toren et al., 1996).

1.2.5 LUNG FIBROSIS 25

Inhaled wood dust can cause lung fibrosis (Michaels, 1967). Results of an animal study also have suggested that wood dust has a very weak fibrogenetic effect on lungs (Yuan et al., 1990). A British study (Hubbard et al., 1996) has given evidence of cryptogenic fibrosing alveolitis (CFA) among workers associated with exposure to metal or wood dust. CFA is characterised by progressive dyspnoea, dry cough, inspiratory crackles on auscultation of the chest, and restrictive lung function.

1.2.6 WOOD DUST EXPOSURE STANDARDS AND RECOMMENDATIONS

A number of countries have set occupational exposure standards or guidelines for wood dust (Table 1.2). Some countries have classified standards according to the type of wood dust (eg. "hardwood” and “softwood”) (Australia, the US) or according to carcinogenic potential of wood dust (Germany). In Denmark,

Finland, and the USSR, wood dust is regulated under more general categories of particulate matter (as organic dust, or dust of vegetable or animal origin).

Switzerland has no specific standards for wood dust, but control “total dust” and “fine dust” (NIOSH, 1987). The ACGIH (1994) recommended the TLVs: 1 mg/m3 for 8 hr TWA for certain hardwoods such as beech and oak; and 5 mg/m3 TWA for softwoods, with the notation that the substance has been identified elsewhere as a suspected human carcinogen. Australia and New-

Zealand have adopted the similar exposure limits for wood dust.

Table 1.2 Wood Dust Exposure Standards

country level (mg/m3) remarks TWAa STELb 26

Australia 1 hardwood (beach and oak) (Worksafe, 1995) 5 10 softwood

Canada 1 hardwood (NIOSH, 1987) 5 20 softwood

Denmark organic dust (notified to be (Vinzents and Laursen, 1993) 4 decreased to 1.0 mg/m3)

Finland 5 10 organic dust (NIOSH, 1987)

Germany 2 total wood dust (IARC, 1995) oak and beach-group IIIA1 human carcinogen group IIIB other wood species suspected of human carcinogen

New Zealand 1 hardwood (NIOSH, 1987) 5 10 softwood

The Netherlands 5 total wood dust (Scheeper et al., 1995) 0.2 health-based limit (Dutch Expert Committee for Occupational Standards)

Norway 1 tropical hardwood (Direktoratet of Arbeidstilsynet, 1996) 2 Nordic species

Sweden 2 wood dust (Arbetarskyddsstyrelsen, 1996)

Switzerland 20 total dust (NIOSH, 1987) 8 fine dust

UK 5 hardwood (HSE, 1992; 1996) 5 softwood

US 1 hardwood (beach and oak) (ACGIH, 1994) 5 10 softwood (Federal Register, 1989) 2.5 western red cedar

USSR 2 dust of vegetable or animal origin (NIOSH, 1987) (>10% of free silica) 4 dust of vegetable or animal origin (<10% of free silica)

aTWA – time-weighted-average.

bSTEL – short-term exposure limit. 27

1.3 OCCUPATIONAL EXPOSURE TO BIOHAZARDS ASSOCIATED WITH

WOOD DUST

Bacteria and actinomycetes are the most common wood-inhabiting microorganisms (Greaves, 1971), and together with fungal colonisation on wood (Butcher, 1975; Levy, 1975) they may initiate the process of decaying

(Kaarik, 1975). Therefore, while processing wood in sawmills, chip mills, pulp and paper mills, joineries and furniture factories (and also when wood chips are used as fuels), the workers may be exposed to a variety of potentially allergenic or toxic microorganisms. Endotoxins of Gram (-)ve bacteria and the allergenic fungi growing on timber are the main hazardous agents found in wood processing workplaces (Dutkiewicz et al., 1988).

Most wood mould grows in the areas between the bark and the wood (Levy,

1975) which is consistent with the finding of high concentrations of fungal spores near to the automatic debarker and in the green mill (Halpin et al.,

1994a). The drying of sawn timber takes place in kilns, which produces relatively high humidity and temperature, creating favourable conditions for the growth of thermophilic and thermotolerant fungi (Wimander and Belin, 1980;

Land et al., 1987).

A study of microorganisms growing on stored woods (Dutkiewicz, 1989;

Dutkiewicz, et al., 1989) reported that the concentrations of fungi, Gram (-)ve bacteria, and endotoxins were extremely high in the sapwood as compared to the heartwood. One study reported that the concentrations of Gram (-)ve 28 bacteria in the sapwood samples were in the range of 107-109 cfu/g and 104 cfu/g in the heartwood samples. In contrast, endotoxin levels of the samples of sapwood varied between 50-2000 µg/g, while in the heartwood it was 0.02-0.04

µg/g. Fungi was identified only in the sapwood (Dutkiewicz, 1989).

Chip piles and wood dust provide an easily accessible food supply for wood attacking organisms since the wood is finely divided and the protective lignin shield around the cellulose may be broken (Rossell et al., 1973). The temperature in a chip pile can reach up to 700C, and thus the growth of thermophilic and thermotolerant fungi occurs (Jappinen et al., 1987). The most prevalent species were Aspergillus fumigatus, other Aspergillus species and

Penicillum species. The fungal spore concentration at chip piles varied between

104 to 105 spores/m3. Hardwood chips are more easily infected by fungi than chips of coniferous wood (Thörnqvist and Lundstrom, 1982). A study of biohazards in composted wood chips (Olenchock et al., 1991) found that the endotoxin levels of the bulk material ranged from 98.92 to 934.68 EU/mg, while the airborne levels of endotoxins were 636.52 EU/m3 in inspirable dust and

771.79 EU/m3 in respirable dust. The concentration of Gram (-)ve bacteria in bulk were 7.9x109 CFU/g and in airborne dust 2.9x105 CFU/m3. Predominant fungi identified in the bulk material were Aspergillus fumigatus, Aspergillus niger, Penicillium spp., Rhizopus microsporus, and Absidia sp. The predominant fungi in the dust were Aspergillus fumigatus, Aspergillus niger, Penicillum spp.,

Rhizopus stolonifer, Cladosporium sp. and Trichoderma sp.

1.3.1 ENDOTOXIN 29

Endotoxins are the lipopolysaccharide-protein complexes which are integral parts of the outer membrane of Gram (-)ve bacteria. In viable bacteria, the endotoxin is firmly bound to the outer cell membrane and released only during multiplication or disintegration of microbial organisms. Gram (-)ve bacteria and their endotoxins are ubiquitous in nature, and are commonly found in those agricultural industries where large amounts of organic dusts are generated.

Endotoxin is a biologically active material, known to interact with both cellular and humoral systems of the host. Cell types that are responsive to endotoxic lipopolysaccharides (LPS) include, macrophages, monocytes, endothelial cells, platelets, mast cells, polymorphonuclear leucocytes, lymphocytes and fibroblasts (Bradley, 1979; Ryan and Morrison, 1992; Brigham, 1994). An animal inhalation study with LPS from different bacteria isolated from cotton revealed that only some endotoxins have the capacity to induce leucocyte invasion into the airways (Helander et al., 1980). The major cell type responsible for initiating pulmonary reactions after inhalation of organic dusts is the macrophage (Rylander, 1989). Human alveolar macrophages are extremely sensitive to endotoxin in vitro (Davis et al., 1980). Symptoms suggestive of exposure to airborne endotoxins are chest tightness, cough, shortness of breath, fever and wheezing (Olenchock, 1994). Endotoxins may contribute for developing chronic bronchitis among those exposed to organic dust (Rylander,

1985).

Endotoxins have been quantified mainly in agricultural environments, such as industries processing vegetable fibres (Rylander and Morey, 1982); the grain industry (Olenchock et al., 1989); wood and wood processing plants 30

(Wilhelmsson et al., 1984; Dutkiewicz, 1989; Dalqvist et al., 1992; Liesivuori et al., 1994); the cotton industry (Rylander et al., 1985; Castellan et al., 1987;

Rylander, 1987) swine and poultry confinement units (Attwood et al., 1987;

Donham et al., 1989; Lenhart et al., 1990; Reynolds et al., 1994; Donham et al.,

1995; Preller et al., 1995a; Reynolds et al., 1996); brewery (Carvalheiro et al.,

1994); and the potato processing industry (Zock et al., 1995; 1998). Endotoxins have also been found in other industrial settings associated with humidifiers

(Rylander et al., 1978; Flaherty et al., 1984); air-conditioners, cooling towers, waste disposal systems (Laitinen et al., 1992; 1994); pharmaceutical industry

(Palchak et al., 1988); and a fibreglass manufacturing facility (Milton et al.,

1996).

Only a few studies have reported on endotoxins in wood dust. A Polish study

(Dutkiewicz, 1989) found concentrations of airborne endotoxins ranging from

0.24-40 µg/m3 in wood processing plants. A Swedish study reported endotoxin levels of 1.2-350 ng/m3 in furniture factories (Wilhelmsson et al.,

1984). Liesivuori et al. (1994) reported airborne endotoxin levels of 0.1-79 ng/m3 in sawing departments and 0.1-56 ng/m3 in trimming departments of sawmills. A Swedish sawmill study (Dalqvist et al., 1992), found airborne endotoxin levels ranging from 1.5-2.5 ng/m3.

Dose-response relationships between lung function indices and endotoxin exposure have most commonly been reported from cotton and swine production facilities. Dose-response relationships of endotoxin levels with reduction in

FEV1, prevalence of byssinotic symptoms (Cinkotai et al., 1977), and increase 31 in blood neutrophil counts have been reported in the cotton industry (Haglind and Rylander, 1984; Rylander et al., 1985; Petsonk et al., 1986; Castellan et al., 1987). Similar dose-response relationships between personal exposure levels of endotoxins with percentage decrease in lung function (Donham et al.,

1995.) and also with percentage predicted lung values (Reynolds et al., 1996) have been reported among swine production workers and also from potato processing industry (Zock et al., 1998). A significant inverse association between baseline lung function and endotoxin exposure among asymptomatic pig farmers has been reported from the Netherlands (Preller et al., 1995b). A

US study has reported an exposure-response relationship between the number of years of exposure with increased amplitude of PEF among workers in a fiber- glass manufacturing facility (Milton et al., 1996). This study further reported that the endotoxin exposure above 4 ng/m3 (8 hr-TWA) was associated with a decline in lung function across the workshift. Such dose-response relations have not been reported in woodworking industry.

A workgroup report has suggested that in any environment, the total number of

Gram (-)ve bacteria should not exceed 103/m3 (Clark, 1986). The suggested threshold limit value for airborne endotoxin is 20 ng/m3 (8 hr-TWA) (Rylander,

1990).

1.3.2 WOOD MOULDS

Exposure to microorganisms associated with wood dust can cause airways inflammation, extrinsic allergic alveolitis, and organic dust toxic syndrome

(ODTS). Wood trimmers are exposed to moulds that periodically grow on 32 timber and which may induce alveolitis and obstructive lung diseases (Dalqvist et al., 1992). A Swedish study has reported restrictive pulmonary dysfunction among wood trimmers and its association with duration and degree of exposure to moulds and dust (Hedenstierna et al., 1986). Both studies have shown dose- response relationships between reduction in lung function and personal exposure levels to moulds (Hedenstierna et al., 1986; Dalqvist et al., 1992).

1.3.2.1 Extrinsic Allergic Alveolitis (EAA)

Allergic alveolitis, or hypersensitivity pneumonitis, is used to describe a spectrum of lymphocytic and granulomatous alveolar filling and interstitial pulmonary diseases associated with repeated, intense exposure to a wide variety of inhaled organic dusts and related occupational antigens (Salvaggio,

1990). The clinical features of extrinsic allergic alveolitis are the symptoms of cough, chest tightness, fever, headache, aches and pains in the extremities, and malaise (Terho, 1982). Acute symptoms appear about 4 to 8 hours after antigen exposure. An insidious onset without distinct acute attacks also occurs commonly, with symptoms of dry cough, gradually increasing shortness of breath, and loss of weight. The diagnostic criteria for EAA are given by Terho

(1986).

Animal studies of the histopathology of lungs of guinea pigs exposed to mouldy hay or different microorganisms, have shown alveolar cell infiltrates and early granulomas which were similar to allergic alveolitis (Fogelmark and Rylander,

1993; Fogelmark et al., 1989; 1991). 33

Extrinsic allergic alveolitis occurs more often in non-smokers than smokers

(Belin, 1980; Terho, 1982). Whether this is due to the effects of smoking on particle handling or the immune response in the lung is unknown (Warren,

1977). Smoking has been reported to interfere with the immune response system of the lungs (Holt and Keast, 1977; Hocking and Golde, 1979).

Total spore concentration higher than 109 spores/m3 or higher than 107 CFU/m3 is hazardous (Clark, 1986). The insidious subacute development of allergic alveolitis can result from prolonged exposure to low concentrations of fungi

(Jappinen et al., 1987). EAA in wood workers is primarily caused by inhalation of the spores of contaminating fungi, but inhaled wood dust may exert a synergistic effect (Halpin et al., 1994b).

The fungi predominantly associated with EAA are dry spored species with spore size less than 5µm, in the respirable range, and which includes most species of Aspergillus and Penicillium (Lacey and Crook, 1988). Allergic alveolitis may also be caused by slimy spored species (such as Graphium sp.,

Aureobasidium pullulans, Phoma violacea and Acremonium spp.) which become airborne in aerosols (eg. humidifiers and sawmills). Wood associated

EAA may be caused by fungi of either spore type (Halpin et al., 1994b).

Wood trimmers disease occurs among workers trimming wood that has been dried in kilns, which produce favourable conditions for mould growth

(Wimander and Belin, 1980). The concentration around 108 -109 spores/m3 34 predominantly of Rhizopus rhizopodiformis were found to occur in the trimming departments of Swedish sawmills (Belin, 1980).

Wood-borne fungi are potential sources of mycotoxins (Land et al., 1987).

Aspergillus fumigatus was found on the surface of wood dried in kilns. Extracts of fungus, when orally administered induced tremorgenic reactions in rats.

HPLC analysis revealed two tremorgenic mycotoxins, verruculogen and fumitremorgen C. Since the symptoms produced by tremorgens resemble the acutely toxic phase of wood trimmers disease, it was concluded that wood trimmers disease was at least in part a form of mycotoxicoses.

Symptoms consistent with allergic alveolitis in wood workers were first described in 1932 in bark peelers stripping bark from maple logs (Acer saccharum) (Towey et al., 1932). The predominant symptoms reported were dyspnoea, cough, loss of weight, and varying amounts of expectoration. The maple bark disease is caused by the inhalation of the spores of Cryptostroma corticale, which is found growing beneath the bark of maple logs (Wenzel and

Emanuel, 1967).

Cases of acute EAA have been reported in a woodman cutting live oak

(Quercus robustus) and maple (Acer saccarum) trees (Dykewicz et al., 1988), and a sawmill worker exposed to sawdust from redwood (Sequoia sempervirens) (Cohen et al., 1967). Precipitating antibodies in serum were found against Penicillium spp. in the case of woodman’s disease and against

Graphium spp, Aureobasidium pullulans and Trichoderma spp. in the case of 35 sequoisis. Pulmonary histoplasmosis caused by Histoplasma capsulatum has been described among people who cut decayed wood (Pladson et al., 1984).

The prevalence of wood trimmers disease among Swedish wood trimmers is estimated at 5-10% (Belin, 1987). In British Colombia, an annual incidence of

4.3 per 10,000 is reported (Enarson and Chan-Yeung, 1990). Wood associated

EAA is also reported among sawmill workers in Britain (Halpin et al., 1994a), in

Finland (Terho et al., 1980), in Norway (Eduard et al., 1993); among wood-pulp workers in the US (Schlueter et al., 1972); and among cork workers in Portugal

(Avila and Lacey, 1974); and Trichoderma koningii; Thermoactinomyces vulgaris or Aspergillus fumigatus; Rhizopus microsporus and Paecilomyces variotii; Alternaria; and Penicillium frequentans respectively were found to be the causative agents.

Penicillum induced hypersensitivity pneumonitis among farmers handling fuel chips has been reported from Finland (van Assendelft et al., 1985) and Sweden

(Malmberg et al., 1985; Kolmodin-Hedman et al., 1987). Microorganisms associated with fuel woodchips and their impact on indoor air quality have been reviewed by Hellenbrand and Reade (1992).

Most of the above studies have used precipitin testing or inhalation challenge test against particular moulds to confirm diagnosis of EAA. A correlation between the prevalence of precipitins against P. frequentans and the number of cork particles was found among the workers exposed to cork dust (Avila and

Lacey, 1974). A Norwegian sawmill study showed an exposure-response 36 relationships between exposure levels to mould spores and symptoms, and also antibody levels to moulds and symptoms (Eduard et al., 1993). Although precipitins have no pathogenic role in disease, they can be used to identify the agents in the environments to which the subject has been exposed (Burrell and

Rylander, 1981). Serum IgG antibodies against mould and actinomycetes are biomarkers indicating exposure at workplaces and may also be useful in evaluating preventive measures (Eduard, 1995a).

The presence of antibodies against wood allergens can be assayed by the double diffusion gel technique (Belin, 1980; 1987; Dalqvist et al., 1992), enzyme linked immunosorbent assay-ELISA (Sandven and Eduard, 1992;

Eduard et al., 1992; 1993; 1994) and the radioallergosorbent test - RAST

(Halpin et al., 1994a; Virtanen and Mäntyjärvi, 1994). The double diffusion gel technique (first described by Ouchterlony, 1953) is basically a qualitative method whereas ELISA and RAST are quantitative techniques.

1.3.2.2 Organic Dust Toxic Syndrome (ODTS)

ODTS is an acute respiratory illness reported among agricultural workers, which is caused by inhaled contaminated organic dust. The effects of organic dust exposure are caused by biologically active, specific agents in the dust

(Rylander, 1985). The agent can either be a constituent of the dust itself (eg. plicatic acid from red cedar, Thuja plicata) or a microbiological component in the dust such as fungal spores, endotoxin from Gram (-)ve bacteria etc.

Organic dust has the potential to cause lung disease if a) the particle size allows penetration into the lung and/or the alveoli, b) the agents are water or 37 lipid-soluble, and c) reactions occur at concentrations of the agent as evaluated either in provocation tests with human or animal experiments. A new set of postulates has been developed to define the determinants for disease-causing agents in organic dusts (Donham and Thorne, 1994). A questionnaire evaluating organic dust exposure is given in Rylander et al. (1990).

ODTS has been characterised as an influenza like syndrome with or without respiratory symptoms and usually without clinical or radiological evidence of

EAA (doPico et al., 1986). EAA appears to require repeated exposure, whereas febrile reactions (ODTS) are associated with occasional heavy exposure to mouldy dust (Malmberg and Rask-Andersen, 1988). In particular, ODTS occurs more frequently than EAA among agricultural workers. In 1994, NIOSH (US) published an “Alert” on ODTS, requesting assistance to prevent it.

ODTS has been described in Swedish sawmills (Belin, 1980), where the fungal spore concentrations ranged from 108 - 109 spores/m3. A Norwegian sawmill study indicated that the symptoms suggestive of mucous membrane irritation, chronic non-specific lung disease, allergic alveolitis, and organic dust toxic syndrome were more frequently reported by wood trimmers than by planing operators (Eduard et al., 1993). ODTS has also been described among grain handlers (doPico et al., 1977) and among brewery workers (Carvalheiro et al.,

1994). The study on brewery workers concluded that the prevalence of mucous membrane irritation (MMI) and ODTS was 39% and 18% respectively and that the causative agent was the airborne endotoxin (ranging from 0.40-0.6 mg/m3) in the brewery environment. The Swedish studies have shown that ODTS to be 38 very common among farmers handling mouldy materials (Malmberg et al.,

1986; 1990; Rask-Andersen, 1989; Kolmodin-Hedman and Stjernberg, 1986). A clinical investigation of a worker shovelling composted wood chips and leaves concluded that in a clinical setting, even with extensive environmental measurements, separation of ODTS and EAA may not be possible (Weber et al., 1990).

1.3.3 (1->3)-b-D-GLUCAN

Although the health effects of airborne moulds have been recognised centuries ago, the health implications of the cell wall component, (1->3)-b-D-glucan have only been recognised recently (ICOH, 1994).

Most of the studies on (1->3)-b-D-glucans have been done on indoor environments (Rylander et al., 1992; Rylander, 1996; 1997). Dose-response relationships between (1->3)-b-D-glucan and symptoms (sneezing, eye and throat irritation, dry cough and itching skin) have been described for sick buildings (Rylander et al., 1992). The effects were found at very low levels of 39

(1->3)-b-D-glucan and endotoxin. The results support the hypothesis that endotoxin and (1->3)-b-D-glucan play a role in sick buildings.

The results of an animal study (Goto et al., 1994) to determine the biological activity of (1->3)-b-D-glucan show that macrophages expressed (1->3)-b-D- glucan specific receptors on their surface, and that the release of TNF-a from cells is modulated by the presence of (1->3)-b-D-glucan. Inhalation experiments have also demonstrated that (1->3)-b-D-glucan interferes with the normal inflammatory reaction, in that, it depresses the formation of antibodies and reacts synergistically with endotoxin and other inflammatory agents

(Rylander, 1994). Inhaled endotoxin and (1->3)-b-D-glucan influence the cell kinetics of the airways and lung walls in different ways (Fogelmark et al., 1992).

The effect of endotoxin is a rapid increase in the number of inflammatory cells, particularly neutrophils with a return to normal values within few days. In contrast (1->3)-b-D-glucan causes a prolonged depression of inflammatory cells, particularly lymphocytes. Water-soluble types of (1->3)-b-D-glucans can induce airway inflammation, whereas non-soluble types do not cause an acute reaction (Rylander, 1989).

(1->3)-b-D-glucans are potential inflammatory agents as well as modulators of the immune system which can also produce granulomas (Cook et al., 1980). An animal study has shown that (1->3)-b-D-glucan and endotoxin together cause a histology resembling hypersensitive pneumonitis with alveolar infiltrates and early granulomas (Fogelmark, et al., 1994). 40

An experimental study of human exposure to (1->3)-b-D-glucan, has shown that it causes nose and throat irritation (Rylander, 1996). A relationship was also observed between the intensity of throat irritation and an increase in airway responsiveness. Studies on (1->3)-b-D-glucans in occupational environments have not been reported yet.

1.4 SAMPLING AND ANALYSIS

1.4.1 WOOD DUST

Wood dust operations generate dusts of different particle sizes, concentrations, and compositions. Particle-size distribution studies have shown that the major portion of airborne wood dust is contributed by particles larger than 10 µm size

(Hounam and Williams, 1974; Whitehead et al., 1981b; Lehmann and Fröhlich,

1988; Pisaniello et al., 1991) which can be trapped effectively in the nasal passages on inhalation and for which inhalable mass sampling is mostly appropriate. Inhalable particulate matter (IPM) sampling is the environmental measurement which is most closely predictive of the risk of developing nasal 41 cancer (Hinds, 1988). Hinds has recommended IPM sampling for wood dust, and also that personal sampling be used for monitoring, as concentration and size distribution vary with position due to the presence of local sources.

According to the ISO (International Standard Organisation), inhalable dust is defined as the “mass fraction of total airborne particles which is inhaled through the nose and mouth” [ISO 7708: 1995 (E)] (ISO, 1995). The ACGIH has defined inhalable particulate mass (TLV-IPM) as those materials that are hazardous when deposited anywhere in the respiratory tract (ACGIH, 1991). Particulate aerodynamic diameter for inhalable dust ranges from 0-100 µm.

In 1986, a new personal sampler (IOM sampler) was developed by Mark and

Vincent (Mark and Vincent, 1986), to collect the inhalable fraction of airborne dust. The device has a cylindrical body 37 mm. in diameter and 27 mm. long, incorporated with a 15 mm. circular orifice. The inlet is directed forward. The dust collecting cassette is located inside the body of the sampler. This sampler uses a 25 mm filter. The filter and cassette are weighed together. The advantage of the cassette is that it minimises errors due both to particle blow- off from the external surface and to internal wall losses. This sampler is operated at a flow rate of 2 L/min.

The Casella seven-hole sampler (Modified UKAEA sampler) is the one originally recommended by the Health and Safety Executive (HSE, 1983) for measurements of inhalable dust. A comparison study (Vaughan et al., 1990) of

Cassella seven hole and IOM personal samplers, indicated that the differences between sampler performances demonstrated in laboratory wind tunnel studies, 42 were not significant when assessed in real industrial environments. The latest revision of the HSE (1993) and Standards Australia (1989) recommend either the Casella seven hole sampler or the IOM sampler for personal sampling of inhalable fraction of airborne dust.

Some investigators have used the seven hole samplers (Jones and Smith,

1986; Hamill et al., 1991) while others have used the IOM samplers (Vinzents,

1988; Vinzents and Laursen, 1993; Scheeper et al., 1995). The Australian wood dust exposure study (Pisaniello et al., 1991) used both the Casella seven hole and IOM samplers for inhalable dust monitoring. Some woodworking processes produce appreciable quantities of coarse dust, chips and shavings, which can be projected towards the breathing zone of worker. The IOM sampler has a more open face than the seven-hole sampler, and would therefore be more prone to the collection of projectiles, whereas the seven-hole has a partially shrouded front face which tends to reduce the collection of projected dust (Hamill et al., 1991).

Polyvinyl chloride (PVC) filters are recommended as the collective medium for gravimetric analysis, since the PVC filters are less hygroscopic than other filters. Desiccation of PVC filters prior to weighing is an unnecessary step as the differences in weight is insignificant when the filter is weighed after keeping in a desiccator (Sass-Kortsak et al., 1989). Sampling and gravimetric determination of inhalable dust is given in Australian Standard AS 3640-1989

(Standards Australia, 1989). 43

The previous wood dust surveys reported in Table 1.3, show that the major portion of wood dust mass is contributed by particles larger than 10 µm (for which the use of inhalable mass sampling is necessary and important), but most of the studies have used traditional “total dust” sampling, which is not appropriate for wood dust. Respirable mass sampling (RPM) should be used when the health concern is occupational asthma (eg. a plant processing western red cedar, Thuja plicata) (Hinds, 1988).

1.4.2 ENDOTOXIN

Monitoring of endotoxins involves air sampling, followed by extraction of the endotoxins from the filters followed by quantitative analysis. Endotoxins appear to bind to varying degrees to different filter materials (Milton et al., 1990), and the effects of different filter types and extraction media on the analysis of the endotoxins are strongly dependent on the organic dust matrix containing the endotoxins (Gordon et al., 1992). Glass fibre, teflon, or polycarbonate filters yield higher extractable endotoxin concentrations than do cellulose mixed ester filters (Douwes et al., 1995). A blank filter must be analysed as a control, in parallel with the filters containing samples.

After post weighing the filters, it is recommended that the filters be placed in

50 ml sterile plastic conical centrifuge tubes with screw caps so that when transported to the laboratory, the extract can be made directly in the transport tube and no dust will be lost (Olenchock, 1990). For longer and more difficult transportation times, the process may require additional handling such as freezing or cold shipment to prevent possible bacterial growth. The standard 47 procedure for extracting the filters starts with rocking the filters in sterile, non- pyrogenic water (approximately 250 mg of dust in 10 to 25 ml of water) for 60 minutes at room temperature, followed by centrifugation of the decanted fluid for 10 minutes at 1000xg. The supernatant fluids can be frozen at -850C or assayed immediately, in duplicate (Olenchock, 1988; Olenchock et al., 1989;

Olenchock, 1990).

There are a number of methods available for quantifying endotoxin levels. The original method is the limulus amebocyte lysate (LAL) gelation method (Tai and

Liu, 1977; Tai et al., 1977; Rylander and Morey, 1982, Dalqvist et al., 1992).

The modified methods which have been developed based on the latter method are the spectrophotometric modification of the LAL test (Castellan et al., 1987), kinetic turbidimetric limulus test with resistant-parallel-line estimate - KLARE

(Milton et al., 1990; 1992; Walters et al., 1994), and the quantitative end point chromogenic modification of the limulus test (Scully et al., 1980; Friberger,

1982; Olenchock, 1988; Olenchock et al., 1989; 1991; Liesivuori et al., 1994).

The gas chromatography-mass spectrometry, GC-MS methods were also used to quantify endotoxins (Sonesson et al., 1990). A workgroup on Agents in

Organic Dusts in the Farm Environment recommended the use of the quantitative chromogenic modification of the LAL test as the standard test for the determination of endotoxins in occupational environments, because of its high accuracy and reproducibility (Popendorf, 1986).

Comparisons of the chromogenic limulus assay with gas-chromatography mass-spectrometry (Sonesson et al., 1990); and KLARE method and chromogenic endpoint limulus assay (Reynolds and Milton, 1993), have 48 demonstrated poor correlation, although the KLARE and gas-chromatography mass spectrometry methods have shown good correlation (Walters et al.,

1994). Epidemiological studies need to employ more than one method and should compare the relative utility of various methods for predicting the respiratory toxicity of inhaled endotoxin (Reynolds and Milton, 1993).

The principle of the “limulus test” for detection of endotoxins is based on the endotoxin-induced coagulation reaction, using amebocyte lysate. The limulus amebocyte lysate in horseshoe crab (Limulus polyphemus) hemolymph contains a coagulation system, which is activated by 10-9g of Gram (-)ve bacterial endotoxins (Levin and Bang, 1968). Gram (-)ve bacterial endotoxin catalyzes the activation of a proclotting enzyme in the limulus amebocyte lysate

(LAL). The initial rate of activation is determined by the concentration of endotoxin present. The activated enzyme catalyses the splitting of p- nitroaniline (pNA) from chromogenic substrate. The chromogenic version of the gelation test is more sensitive to very low concentrations of endotoxins than the gelation test itself. Since LAL reactivity may be enhanced or inhibited by other constituents of the dust, it is suggested that dilution curves of a sample with both high and low dust concentrations be determined, including spiking different dilutions of these samples with a known concentration of endotoxin standard (Hollander et al., 1993; Boleij et al., 1995).

It used to be thought that the limulus test was highly specific for endotoxins. It now appears that this is not so, as lysate is affected by substances other than endotoxin through factor G, one of the coagulin factors, causing false positive results. The fungal polysaccharides, (1->3)-b-D-glucans cross react in the 49 limulus assay reacting through factor G (Morita et al., 1981). Based on this finding, a group of researchers developed two separate methods; endospecy

(for endotoxin specific assay) by removing factor G from lysate, and gluspecy which is specific for (1->3)-b-D-glucan (Obayashi, 1990; ICOH, 1994). The reaction schemes of both methods are given in Fig. 1.1.

The storage of commercially available LPS dissolved in pyrogen free water can be stored for a period of 1 year at 70C without any effect on endotoxin level, but it is not recommended for environmental samples as microbial growth may affect the endotoxin content (Douwes et al., 1995). It is recommended that sterile non-pyrogenic siliconized glass or polystyrene be used to prepare standards or making dilutions of samples since LPS adsorb onto untreated glass and polypropylene surfaces (Novitsky et al., 1986). A recent study has demonstrated however, that the use of borosilicate glass, soft glass, and polypropylene as containers did not result in different endotoxin levels (Douwes et al., 1995).

Reaction Scheme for Gluspecy Reaction Scheme for Endospecy

(1->3)-b-D-Glucan Endotoxin

Factor C activated Factor C

activated Factor G activated Factor B Factor G Factor B

proclotting clotting proclotting clotting enzyme enzyme enzyme enzyme

Boc-Leu-Gly-Arg-pNA Boc-Leu-Gly-Arg-OH Boc-Leu-Gly-Arg-OH Boc-Leu-Gly-Arg-pNA (chromogenic substrate) + + (chromogenic substrate) pNA (A405) pNA (A405)

diazo-coupling diazo-coupling

azodye azodye (A545) (A545) 50

Fig. 1.1 Reaction scheme for Glucan-specific and Endotoxin-specific assays.

1.4.3 (1->3)-b-D-GLUCAN

Measurement of (1->3)-b-D-glucan using gluspecy has been described by

Obayashi (1990) and ICOH (1994). The principal of the test is that

(1->3)-b-D-glucan activates factor G in limulus amebocyte lysate to form activated factor G, and activated factor G further activates proclotting enzyme to produce clotting enzyme. Clotting enzyme then hydrolyzes chromogenic substrate to release p-nitroaniline (pNA) (Fig. 1.1). By measuring the absorbance of released pNA at 405 nm by spectrophotometer, the concentration of (1->3)-b-D-glucan) can be determined. When higher sensitivity is desired or when the sample is yellowish, it is better to take the measurements at 545 nm after diazo-coupling.

Previous studies have demonstrated the importance of (1->3)-b-D-glucan in clinical assays. Determination of plasma (1->3)-b-D-glucans with factor G is a highly sensitive and specific test for invasive deep mycosis and fungal febrile episodes (Obayashi et al., 1995). The assay is one of the most promising tests for the diagnosis of pulmonary Aspergillosis (Yuasa and Goto, 1994), and is more sensitive than ID (immunodiffusion), or ELISA (enzyme linked immunoassay) or RAST (radioallergosorbent test). Moreover this newer assay 51 is a better indicator of the clinical causes. The plasma (1->3)-b-D-glucan assay has been described in Obayashi et al. (1995).

1.4.4 MICROORGANISMS

The most common methods for sampling microbial aerosols are gravity collection, impaction onto agar or adhesive surfaces (Blomquist et al., 1984;

Kotimaa et al., 1984; Halpin et al., 1994a), liquid impingement (Morey, 1990) and membrane filtration (Eduard et al., 1990; Dalqvist et al., 1992; Halpin et al.,

1994a; Hanhela et al., 1995). The details of the operation, advantages and disadvantages of these methods are given in Hellenbrand and Reade (1992) and Popendorf (1986). The appropriate sampler or sampling technique will depend on a number of factors, such as, the objective of the survey, the types and characteristics of microorganisms, concentration of microorganisms, sampling frequency, and location. Filtration and impaction methods have been widely used to evaluate microbes in agricultural environments (Popendorf,

1986). CAMNEA method (Collection of airborne microorganisms on nucleopore filters, estimation, and analysis) is widely used for both area and personal sampling in highly contaminated occupational environments (Palmgren et al.,

1986a; 1986b). A modified CAMNEA method using an improved resuspension and destaining technique has been described recently (Heldal et al., 1996).

Measurement of the actual amount of allergen inhaled by individuals (breathing zone) is probably more meaningful than measurement of the general 52 concentration in the environment (Virtanen and Mäntyjärvi, 1994; Eduard,

1995b).

Information on the choice of culture media, incubation temperature, enumeration and classification of microorganisms is given in Lacey et al.

(1980). The use of scanning electron microscopy for identification and quantification of mould spore collection on filters is given in Eduard et al.

(1988), and Eduard and Aalen (1988). Scanning electron microscopy is better than the cultivation method for estimating total spore concentration as both viable and non-viable spores have been implicated as causative agents of allergy (Heikkilä et al., 1988).

A Norwegian sawmill study recommended the use of polystyrene filter monitoring loaded with polycarbonate or cellulose acetate membrane filters for sampling of aerosolised micro-organisms from highly contaminated occupational environments (Eduard et al., 1990). A Swedish sawmill study

(Dalqvist et al., 1992) has used personal sampling for airborne mould spores

(using polycarbonate filters of 0.4µm pore size, 37mm in diameter). The filters were analysed by scanning electron microscopy. A British sawmill study (Halpin et al., 1994a) used both personal and static samplers for the sampling of microorganisms. To assess spore concentrations at different sites around the sawmill, air was sampled with an Andersen sampler (Andersen, 1958), which was placed 1.5 meters above the floor level, at a flow rate of 25 l/min. Personal samples were collected in the breathing zone of workers using seven-hole filter holders containing polytetrafluoroethylene (PTFE) filters (1.2 µm pore size, 25 53 mm). A Polish study (Dutkiewicz, 1989), used a particle-sizing slit sampler for sampling microorganisms in wood processing plants.

1.5 SUMMARY

Woodworkers from the tree felling stage onwards through various manufacturing processes, are exposed to wood dust of different particle sizes, concentrations, and compositions. Endotoxins of Gram (-)ve bacteria and the allergenic fungi growing on timber are the main biohazardous agents found in wood processing workplaces.

Wood dust exposure causes extrinsic allergic alveolitis, organic dust toxic syndrome, occupational asthma, non-asthmatic chronic airflow obstruction, and chronic bronchitis. Wood dust is carcinogenic to humans. It is estimated at least two million people worldwide are occupationally exposed to wood dust

(IARC, 1995).

IPM sampling is the most appropriate sampling technique for airborne wood dust. Only very few studies have employed inhalable dust monitoring for workplace assessments. The information about occupational exposure to biohazards associated with wood dust is far less. Experimental investigations on (1->3)-b-D-glucans in organic dust environments have not been reported previously. Studies on dose-response relationships among pulmonary function indices and personal exposures to endotoxins and (1->3)-b-D-glucans, and relations between personal exposures to biohazards and work-related symptoms have not been reported for the woodworking industry. 54

1.6 TIMBER INDUSTRY IN AUSTRALIA

The forest in Australia is comprised of rainforests and mangroves (8%),

Eucalyptus (60%) and native pine and open forests (32%) (Forest Industries,

1992), and it is the Eucalypt forests that are the major resource of timber production. Australia has one of the lowest percentages of forest area to total area (4%) compared with other principal timber producing countries in the world [Finland 69%, Canada 45%, Soviet Union 34%, USA 32% and UK 7.2%]

(Wallis, 1970).

Of all the Australian genera the genus Eucalyptus probably covers at least two thirds of the forest area and it is these trees that supply the bulk of the hardwoods of the timber trade locally and internationally. Eucalyptus is derived from the Greek eu, means “well”, and kalyptos, “covered” (Pyne, 1992).

Eucalypts being a scleromorph have hardened leaves that reduce moisture loss. Some of their greatest attributes are rapid growth rate, significant differences in physical properties (colour, texture, grain, weight) and their high durability.

The wood processing industry is the second largest manufacturing industry in

Australia and consists of a number of sectors, including 23 pulp and paper mills, 1785 sawmills, 15 veneer and plywood plants, and 9 woodchip operations. Native hardwood species are used widely for many purposes, from heavy timber bridges to home construction, and also for fine furniture, 55 decorative applications and high quality paper. Plantation softwood is exclusively used for home construction. As the demand for native timber products is higher than the supply, the industry imports 30% of the need.

Woodchips represent an important economic commodity for Australia, with an annual production of 5 million tonnes, earning approximately $400 million per year.

As the woodchips will be processed into pulp, the logs used for chipping are called pulplogs. Eucalyptus pulps make high quality paper. Paper made from the pulp of pine is used for newsprint, tissue and cardboard production. The sources of wood used for the production of woodchips are as follows:

· native pulplogs (diseased, weak or defective native trees),

· plantation pulplogs (young trees removed to promote the growth of

bigger sawlogs, usually in softwood plantations; or the harvest of

short rotation pulp log crops in hardwood plantations),

· forest residues (branches and other waste material from both native

and plantation forest harvesting) and

· sawmill residues (sawlog offcuts and waste)

There are 2119 people employed in logging in NSW (State Forest Authority,

1997). At a logging site, normally 3-5 people are employed on contract basis for tree cutting, tractor-trailing logs to the logging site and trimming. There are

628 licensed sawmills in New South Wales, greatly varying in size, with small mills employing around 5 workers up to large mills employing about 40 workers. 56

Joineries are small scale operations, employing around 3 workers in a small joinery up to a large joinery employing around 60 workers. The average number of workers in a joinery is about 10.

The production yields of sawlogs and pulpwood during 1995-1996 (both hardwood and softwood) were 2,360,386 cubic meters and 1,389,512 tonnes respectively in New South Wales (State Forest Authority, 1997). As the native hardwood timber is expensive, most of the joineries process imported timber together with reconstituted particle boards (eg. MDF - medium density fibre boards).

Hence, the industrial use of wood is of significant economic importance for

Australia. The industry employs around 85,000 people; of which 73,900 are in the manufacturing and 11,400 are in forestry and logging operations (Forest

Industries, 1992). Any work-related symptoms or diseases due to industrial association are therefore of importance to the Australian economy, as well as affecting the lives of a substantial proportion of the working population.

1.6.1 THE AIM OF THE RESEARCH

“To investigate occupational exposure to wood dust and biohazards associated with wood dust, their correlation to respiratory function, and symptoms among woodworkers.”

Wood dust, endotoxins, and allergenic fungi are the main hazards found in woodworking environments. Relatively very few studies have been undertaken 57 on wood dust exposure. The present study was designed to comprehensively investigate the health effects of wood dust exposure, and in particular provide new information regarding:

· Exposure to (1->3)-b-D-glucans in an occupational environment;

· Levels of exposure to wood dust and biohazards associated with

wood dust in different woodworking environments;

· Correlations among personal exposures, especially correlations

between (1->3)-b-D-glucans and fungi exposures, and endotoxins

and Gram (-)ve bacteria exposures;

· Effects of personal exposure to biohazards on lung function;

· Effects of personal exposure to biohazards on work-related

symptoms; and

· Determinants of inhalable exposures (provide which factors in the

environment influence the personal inhalable exposures).

The above information, together with field observations (awareness of health effects, the use and maintenance of exhaust ventilation systems, the use of personal protective equipment, etc.) were used to make recommendations to improve the existing occupational health conditions of the timber industry. This study was the first organic dust exposure study conducted in Australia.

1.6.2 THE MAIN OBJECTIVES

The main objectives were to investigate and evaluate: 58

· personal airborne wood dust levels (both inhalable and respirable

dust) at different woodworking operations in NSW; determinants of

wood dust exposures for different woodworking processes; and

present status of local exhaust ventilation systems

· levels of exposure to biohazards in wood dust (fungi, Gram (-)ve

bacteria, and their cell wall components (1->3)-b-D-glucans and

endotoxins respectively) and correlations among them

· effects of personal exposures (wood dust, Gram (-)ve bacteria, fungi,

endotoxins, (1->3)-b-D-glucans), number of years of exposure to

wood dust on lung function, and dose-response relationships

· prevalence of work-related symptoms; correlations between personal

exposures and work-related symptoms; and effects of work-related

respiratory symptoms on pulmonary function

· nasal cancer statistics in New South Wales

· recommendations for the timber industry 59

CHAPTER 2

EXPERIMENTAL INVESTIGATION

2.1 FIELD INVESTIGTION

Two logging sites, four sawmills, one major woodchipping operation, and five joineries located in NSW were investigated during Sept. 1996 to June 1997

(Table 2.1). The worksites were randomly selected in consultation with the

Timber Trade Industrial Association (TTIA, NSW) and the Construction,

Forestry, Mining and Energy Union (CFMEU, NSW). The logging sites were studied with the permission of the State Forest Authority of the area investigated.

Prior to the field study (except for logging sites), the worksites were inspected and assessed for a preliminary occupational hygiene survey, in order to study the lay-out, the woodworking processes, and to identify the zones for personal sampling of wood dust and microorganisms. The background information for each worksite is presented below.

2.1.1 WORKSITES

Logging Site A and Logging Site B

Both logging sites studied, A and B, were located in natural Eucalypt forests in

Northern New South Wales (Appendices A and B). About 3-5 contract workers 60 were employed at these logging sites for tree felling, tractor-trailing logs to the logging site, and debarking and trimming logs into appropriate lengths. All the cutting processes carried out at the logging sites were with portable chain saws. The chain saw, which has a continuous articulated chain with teeth along its outer edge, is powered by a gasoline engine.

Initially, the state forest officer marked specific trees for retention: habitat trees, species which were less abundant or rare, as well as high quality trees for propagation. One of the main responsibilities of the forestry officer was to check the protective clothing and equipment of the employees. The required protective clothing for the workers were helmets (“hard hats”), ear muffs, boots, chaps or cut-proof trousers, and high visibility vests. The officer also had to check whether vehicles and machines were properly equipped, safety guarded and permitted, that log truck loads were correctly chained, and whether all the safety equipment and first-aid kits on-site were in working condition (State

Forest Authority, 1996).

At logging site B, a jacking technique was used for directional felling of trees.

The jacking technique is a safe practice, as without it sometimes the falling tree might collide with another tree and could then fall backwards. This might even kill the tree feller. Such incidents have been reported in NSW (Driscoll et al.,

1995). The tree feller’s job is extremely dangerous. 61

Table 2.1 Description of Worksites

worksite type of wood common name of major product number. of workers species processed employed logging site A hard eucalypt logs for sawmilling 04 logging site B hard eucalypt logs for sawmilling 04 sawmill C hard eucalypt green timber and 25 (green mill + chip mill) woodchips sawmill D hard eucalypt kiln dried timber for 20 (dry mill) flooring sawmill E hard eucalypt green timber and 26 (green mill + chip mill) woodchips sawmill F hard eucalypt green timber and kiln 23 (green mill + dry mill) dried timber (for flooring) woodchipping mill G hard eucalypt woodchips 30a joinery H hard and soft radiata pine, meranti, MDFb staircases 12 joinery I soft western red cedar window frames 40 joinery J hard and soft sugar pine, radiata pine, meranti mouldings 12 brush box joinery K hard and soft radiata pine, meranti, MDF staircases and handrails 18 joinery L mostly hard Tasmanian oak, American oak, jarrah pantry cupboard doors 11 Tasmanian blackwood, brush box a6 workers in processing, 24 workers in transportations and maintenance. bMDF – medium density fibre. 62

Tree felling, sawing, and cutting were usually done with chainsaws accompanied by axes and metal wedges. When the tree feller sawed the felled tree into log lengths (bucking), trimming off branches and clearing the brush, he was most likely to be exposed to dust (although such exposures might be very low). The mechanical removal of bark from a log is now performed at logging sites using excavators. This was previously carried out in sawmills. In general, debarking involves no exposure to wood dust as the excavator removes only the bark of the log leaving the wood intact, and the operator performs the task from inside the vehicle. After debarking, the logs are cut into appropriate sizes.

The measuring and grading of each log is then done by the state forest officer, before the logs are loaded into trucks. A tree feller in the bush cuts around 120 logs per day.

Sawmill C

Sawmill C was a fairly large mill producing approximately 40,000 m3 of green timber (hardwood) and 32,000 tonnes of wood chips per year. This mill, which was one of the biggest mills in NSW, was a modern mill using computerised cutting of logs with enclosed booths for the operators. Woodchips were produced from the waste wood, which accumulated in the mill. This sawmill processed around 250-350 logs per day. The main processes carried out in this sawmill were, sawing (the head rig saw - a jig saw, and a canter-chipper twin saw), edging (circular saws), resawing (a circular saw), sorting, chipping, planing (using a planer machine), auto-docking, auto-stacking (stacks for kiln drying) and grading (green timber). The canter-chipper-twin saw, which was computer operated, was a machine consisting of two rotating cutters followed 63 by the band saw. The rotating cutters or chippers removed the sapwood, converting the log into a cant and then the band saw cut one board from each side of the cant. Side boards were then cut into proper widths with edgers.

Edgers consisted of two circular saws. The jig saw, canter-chipper-saw, edger, and the resaw were operated from inside the enclosed booths. The auto- docking and auto-stacking processes were mechanically operated, while the grading and stacking of green timber was carried out manually at the rotating table.

Sawmill D

Sawmill D was a medium size dry mill with an annual production of 12,000m3 kiln dried hard timber. The process involved air drying of green timber for 3 months followed by kiln drying for 3-8 days depending on the moisture content required. Steam was used for kiln drying of timber. Sawdust was used as the fuel for boilers to generate steam. After kiln drying, the stacks were kept in another chamber for a day, at a temperature around 890C, to recondition the wood. Reconditioning relieved the internal stresses and tension of the timber.

After this, the stacks were further processed in the sawmill before transport to the market. This sawmill was studied twice, before and after the replacement of both the moulder and the central exhaust ventilation system. The processes carried out in this sawmill were moulding, docking (using radial arm saws), end- matching (tenoning), ripsawing, grading (using a rotating table), and stacking.

Tenoning involved both milling and sawing actions, producing tongue-groove cuts. This mill produced kiln dried timber for flooring. 64

Sawmill E

Sawmill E was a green mill, which also processed woodchips. This mill produced 5,800 m3 of sawn green timber and 20,000 tonnes of woodchips annually. The headrig saws were Canadian saws (two circular saws operating on top of each other) for bigger logs and a twin band saw for smaller logs. The processes carried out in this sawmill were sawing, bench sawing (table saw), edging, docking (cross-cut saws or radial arm saws), and grading (using a rotating table). Also carried out were planing, picket machining, and moulding processes. The table saw was a circular saw fixed to the middle of the table, with about half of the saw protruding to the outside. This was used to further cut the logs, which had been already ripped by the headrig saw.

Sawmill F

Sawmill F consisted of a green mill and a dry mill with an annual production of

4500m3 of sawn hardwood timber. Solar energy was used for kiln drying at this sawmill. The process consisted of air drying of green timber for 3 months followed by kiln drying for 4-5 days. The processes carried out at the green mill were sawing (the headrig saw - two circular saws in parallel), bench sawing, multi-cut sawing (mechanically operated), docking (using cross-cut saws) and grading at the table. The multi-cut saw consisted of six circular saws in parallel, which cut large pieces of logs lengthwise into a number of planks. The processes carried out in dry mill were, planing, moulding, end-matching, auto- docking, grading and packing. Sawmill F produced green timber as well as kiln dried timber mainly for hardwood flooring. 65

The photographs showing the main woodworking processes carried out in sawmills and the woodchipping mill are given in Appendix C and Appendix D respectively. The process flow diagrams of sawmills and the woodchipping mill are given in Appendix F.

Woodchipping mill G

Wood chipping mill G was one of the major wood chipping operations in

Australia, exporting around 790,000 tonnes of wood chips per annum. The process involved log washing, chipping (enclosed), screening (separating chips from saw dust and waste wood by automatic sieving) and transferring through overhead conveyer belts to the chip pile. The process was completely controlled from enclosed booths. Approximately 25% of the woodchips processed came from the neighbouring sawmills. About 50 large trucks per day unloaded chips into the underground hopper, which then passed from the underground tunnel by conveyer belt to the chip pile. The workers here were exposed to wood dust mainly during cleaning of the underground tunnel and during truck unloading as well as from over-head conveyer belts which carried chips from the screen house to the chip pile.

Joinery Operations

The processes carried out in joineries are shown in Appendix E.

Sawing and planing: Planing smooths one or more sides of a piece of wood.

The planer head consisted of a series of cutting blades mounted on a cylinder, which revolved at high speed. The planing operation was generally performed 66 parallel to the wood grain, therefore producing relatively low concentrations of airborne dust. Sawing and planing were carried out in all the joineries.

Moulding: Moulders are used to cut and shape mouldings. Moulders (joinery I and joinery L) consisted of a number of cutter heads. The cutter heads were staggered spindles of various designs.

Shaping: Shapers are similar to moulders, but used to cut and shape the outer surface of wood products (joinery L). The shaper consisted of a table through which protruded a rotating spindle with blades arranged to produce the desired contours.

Wood turning (lathing): Wood turning is used to produce cylindrical shapes.

The point of operation was a sharp edged tool for the larger wood items and sandpaper for the smaller items. Tool point operation produced a large volume of chips, whereas sandpaper application produced very fine airborne dust. The operator held the cutting tool or the sandpaper in his hands, pressed it against the revolving work, and shaped it to the desired design. Joinery K employed wood turning and copy lathing processes.

Boring (drilling) and routing: Boring machines are designed to drill holes for dowel joists, screws and for various other purposes. Routers are used to shape the edges and corners of wood items and also to cut grooves of various shapes. The routing action is a combined action of boring and milling. Hand 67 held routers and stationary automatic routers were used at joinery H and joinery K.

Sanding: All joineries employed sanding to obtain the final finish or smoothness to the surface of the product. This is one of the major processes carried out in the joinery and furniture industry. The sanders can be either hand held or machine operated. Some of the joineries used horizontal band sanders

(joineries H and K), broad-belt sanders (joineries I, K and L), and disc sanders

(joinery J). The hand-held sanders used were belt-sanders and orbital sanders.

Orbital sanders are operated with an elliptical, vibrating motion. A belt sander consisted of a continuous strip of sandpaper rotated around two rollers.

The horizontal belt-sander consists of a strong paper belt faced on one side with carborundum powder. It is placed over two pulley wheels, and runs horizontally over a table. The work to be sanded is placed on the table, and the running belt is pressed onto it. The disc sander is sandpaper, which is fastened to a circular vertically positioned rotating disc.

2.1.2 TYPES OF WOOD PROCESSED

Eucalyptus, the most abundant hardwood native to Australia, was the major wood species processed at sawmills (blue gum - E. saligna, blackbutt - E. pilularis, ribbon gum - E. viminalis, tallowwood - E. microcorys, spotted gum - E. maculata, brown barrel - E. fastigata, messmate - E. obliqua etc.) and woodchipping mills (silvertop ash - E. sieberana, mountain gum - E. dalrympleana, cuttail or brown barrel, grey gum - E. cypellocarpa, yellow stringy 68 bark - E. muellerana, white stringy bark - E. eugenioides etc.). Radiata pine

(Pinus radiata) which is grown as a plantation softwood is also used widely in the wood processing industry.

As native hardwoods are expensive, some joinery operations used imported timber together with reconstituted softwood (typically, MDF - Medium Density

Fibre) for processing. Joineries H and K used the same type of wood for processing (meranti - Shorea spp., radiata pine - Pinus radiata and MDF), whereas Joinery I processed Western red cedar (Thuja plicata), a softwood imported from North America. The most common species used at Joinery J were brushbox (Tristania conferata), radiata pine and sugar pine (Pinus lambertiana). Joinery L mostly used native timber (Tasmanian oak -

E. delegatensis, Tasmanian blackwood - Acacia melanoxylon, jarrah -

E. marginata, and brush box) and also imported species such as American oak

- (Quercus sp.), nyotoh (Payena sp. and Palanquim sp.) and douglas fir

(Pseudotsuga menziesii).

2.2 PERSONAL DUST SAMPLING

Personal dust monitoring for airborne inhalable dust and respirable dust was conducted at each worksite. Although inhalable particulate sampling (IPM) has been recommended to monitor airborne wood dust (Hinds, 1988), respirable fractions were sampled as well, in order to quantify biohazards in both fractions. Sampling for inhalable dust was done on all the woodworking jobs at all the worksites (except joinery I, where sampling was done on randomly selected workers of each job title). The other jobs of possible exposure (eg. 69 supervisor, maintenance worker) were also sampled, if such jobs were associated with woodworking or working in the vicinity of a woodworking operation throughout the day. Sampling for respirable dust was done on randomly selected workers from each worksite.

Casella-seven-hole samplers (Fig. 2.1 and Fig. 2.2) (modified UKAEA sampler)

(Vaughan et al., 1990) were used for the inhalable dust sampling (Standards

Australia, 1989) and Casella Higgins cyclones (Fig. 2.1 and Fig. 2.3) were used for the sampling of respirable dust (Standards Australia, 1987). The flow rates of the portable pumps (Gilian, model HFS 513A, Gilian Instruments

Corporation, USA) were calibrated to 2 L/min for inhalable dust sampling, and

1.9 L/min for respirable dust sampling according to Standards Australia, using the flow rate calibrator (Ametex, Mansfield & Greens Division, USA). 70

Fig. 2.1 Personal samplers used: A - Casella seven-hole sampler (for inhalable dust), B - Higgins cyclone sampler (for respirable dust), C – 3-piece filter cassette (for microorganisms). 71

Fig. 2.2 Casella seven-hole sampler (consisting of end cap with seven equispaced inlet holes [diameter 4 mm], filter [dia. 25 mm], filter support grid, ‘O’ ring seal, and exhaust port for connection to pump).

Fig. 2.3 Higgins cyclone sampler (consisting of outer metallic holder, filter [dia. 25 mm], ‘O’ ring, filter support grid, cassette/inlet/grit port). The monitor was attached to the worker’s clothing (lapel) within the breathing zone. The flow rates were recorded before and after sampling. The duration of sampling was 6-8 hours except at logging sites (~4 hrs). The work pattern of a worker was consistent throughout the day except for joineries H and K, and sawmill C where some workers did multi task jobs during the day.

For each person sampled, information was recorded by the investigators regarding job title, type of wood processed, green or dry wood processed, local exhaust ventilation, use of respirators, use of compressed air, and cleaning method used. At each worksite, dust monitoring was personally supervised by the investigators. Sawmill E was studied twice, before, and after replacing of 72 both the moulder and the central exhaust ventilation system. The local exhaust ventilation systems fitted to woodworking machines were assessed by visual inspection of connecting ductworks and maintenance of dust collectors.

Polycarbonate filters (Millipore, 25 mm, 0.8 mm) were used as the collection media as the same sample filters were utilised for the extraction of endotoxins from wood dust (due to their high extractability of endotoxins) (Douwes et al.,

1995). Filters were weighed before and after sampling with a Cahn electrobalance (detection limit ± 0.01 mg) (model Cahn 25, Cahn Instruments

Inc, USA). The weight of the sample filters was corrected by the average weight change of a number of field blanks. The time-weighted average (TWA) exposure for each worker was calculated.

2.3 ENDOTOXIN AND (1->3)-b-D-GLUCAN ASSAYS

After weighing, the filters were extracted with 2.5-20 ml of endotoxin/glucan free water (depending on the weight of dust) (Douwes et al., 1995) for 60 min at room temperature, followed by centrifugation of the decanted fluid for 10 min at

1000 x g (Olenchock, 1990). The supernatant was analysed immediately for endotoxin and (1->3)-b-D-glucan using quantitative end-point chromogenic limulus assay (Obayashi, 1990) using endotoxin specific [Endospecy test kit, standard endotoxin - E. coli 0111:B4 (Westphal), Seikagaku Co., Japan] and glucan specific (Gluspecy test kit, standard (1->3)-b-D-glucan - pachyman,

Seikagaku Co., Japan) lysates respectively. Assay procedures for Endospecy and Gluspecy are shown in Fig. 2.4. Both Endospecy and Gluspecy were 73 sensitive to very low concentrations (1 pg/ml) of endotoxin and

(1->3)-b-D-glucan respectively. Only the water-soluble fraction of

(1->3)-b-D-glucans was measured, as this is the fraction important symptomatically (Rylander, 1989). Sterile polystyrene tubes were used for the extraction and chemical assay (Novitsky et al., 1986). For each assay, blank filters were utilised as controls.

To keep the reaction temperature at 370C a dry block heater (Thermoline

Scientific Equipment, Aust., Model DB3) was used. The absorbance after diazo-coupling was read using a UV/VIS spectrophotometer (Pye Unicam, PU

8800). With each set of samples a calibration was carried out (correlation coefficient r ³ 0.98).

sample 0.1ml

lysate for Endospecy or 0.1ml lysate for Gluspecy 370C, 30 min

0.5ml 0.04% NaNO2/0.48m HCl diazo-coupling 0.5ml 0.3% Ammonium Sulfamate 0.5ml 0.07% N-1-Naphthylethylene- diamine dihydrochloride

A 545 nm

Fig. 2.4 Assay procedure for Endospecy and Gluspecy.

2.4 SAMPLING AND CULTURING OF MICROORGANISMS 74

2.4.1 PERSONAL SAMPLING

Personal samples of airborne bacteria and fungi were collected using pre- sterilised three-piece cellulose ester membrane filter cassettes (Fig. 2.1 - C)

(37 mm, 0.45 µm, Millipore) connected to a constant flow personal pump calibrated to 1.5 L/min. The duration of sampling was 4-6 hours.

Microorganisms were extracted from the collected filter cassettes using a suspension fluid (0.1% bacteriological peptone with 0.05% Tween 80 and 2% inositol) as described by Eduard et al., (1990). Serial dilutions of the suspension were then prepared using 1/4-strength Ringer’s solution (Oxoid,

U.K.) and 0.1 ml of the dilutions were plated in different media. The plates were incubated at two temperatures (250C and 400C). The following culture media were used: for the isolation of fungi 2% malt extract agar, for xerophilic fungi dichloran-glycerol agar (Oxoid, U. K.), for bacteria and actinomycetes 1/2- strength nutrient agar (Oxoid, U.K.) and for Gram (-)ve bacteria, a selective medium, violet red bile glucose agar (Amyl media, Australia).

2.4.2 AREA SAMPLING

A single-stage Andersen sampler (model 5KH10GGR38T, Andersen Sampler

Inc., Atlanta, USA) (flow rate 25 L/min) was used for the area (static) sampling of microorganisms. The samples were collected about 1.5 m above the floor from different wood processing sections of each workplace. The collection media were same as for personal sampling. The duration of sampling was 10-

60 sec. 75

The colonies were identified by their appearance and microscopic morphology from standard texts (Larone, 1995; Murray et al., 1995; Lacey et al., 1980).

Aspergillus and Penicillium species were identified using media and methods described by Pitt and Hocking (1997), with reference to more detailed tests where necessary (Pitt, 1979; Pitt, 1988; Klich and Pitt, 1988).

For Aspergillus the cultures were inoculated onto Czapek yeast extract agar

(CYA), malt extract agar (MEA), and 25% glycerol nitrate agar (G25N) and plates were incubated at 250C for 7 days. For Penicillium, the cultures were also inoculated onto CYA, MEA, and G25N and the plates were incubated at

250C and 370C for 7 days. After incubation, colony morphology was noted and the cultures were examined microscopically.

Microscopic photographs of the isolated fungi were taken using Olympus microscope (model BH2) attached to Olympus automatic photographic system

(model PM-10ADS, Olympus Optical Co. Ltd., Tokyo). Photographs of the pure cultures of microorganisms were taken using Olympus (model OM-2, 35 mm) manual camera.

2.5 LUNG FUNCTION TEST

Lung function testing followed the guidelines given by the American Thoracic

Society (1979) for measuring respiratory function. The Vitalograph Alpha portable spirometer (serial no: AL 06993, Vitalograph Ltd., U.K.) was used. The 76 measurement of expired air was made on the Vitalograph-Alpha using a Fleisch type pneumotach while the attached microprocessor displayed the data on the screen.

The vital capacity and forced vital capacity tests of workers were conducted before and after a workshift. The workers at each worksite were tested for lung function and monitored for personal exposures during the same workshift. The spirometer was calibrated with a one litre precision syringe (cat. no. 20.408,

Vitalograph Ltd., UK) before testing. Each worker was requested to perform 3-5 attempts, until maximum effort was obtained. The “best test” (highest FVC +

FEV1) was recorded as the lung function capacity of the worker. All measurements were expressed in standard units (BTPS) (ILO, 1989). For each worker age, height, number of years of exposure to wood dust, ethnic origin, and smoking status were also recorded. The maintenance workers at the woodworking sites were used as controls (comparison group) as their ethnic and social backgrounds were similar to the woodworkers. The job tasks of the maintenance workers did not involve wood dust exposure under normal circumstances.

2.6 QUESTIONNAIRE STUDY

The “Organic Dusts Questionnaire” (Rylander et al., 1990), together with appropriate questions on respiratory, nasal, and conjunctival symptoms from the British Medical Research Council’s respiratory questionnaire (Medical

Research Council, 1960) were used to assess work-related symptoms. A 77 majority of the workers and the management were interviewed to obtain information on their awareness of the potential health effects of wood dust.

2.7 DATA ANALYSIS

a) Determinants-of-Exposure Analysis for Inhalable Wood Dust Exposure

A preliminary analysis of determinants-of-exposure (Teschke et al., 1994) was done using one-way analysis of variance (ANOVA) to determine which factors of the occupational environment influenced wood dust exposure levels. The independent variables used were job title, type of wood processed (softwood or hardwood), green or dry wood processed (dry: kiln dried or air dried), use of compressed air, whether the woodworking machine was fitted with local exhaust ventilation, use of hand-held tools, and cleaning method used (dry sweeping or vacuum cleaning). The dust exposures at the logging sites were not included for the analysis as the jobs were done outdoors.

A multi-factor analysis of covariance (ANCOVA) was also done using all the factors used in the preliminary ANOVA one-way analyses. For the ANCOVA analysis of the sawmills exposures, the variables used were ventilation, job title, and green or dry wood processed (the sawmills studied processed only hardwood, did not use hand-held tools and compressed air, and used only dry sweeping). For the joineries the variables used were ventilation, job title, use of hand-held tools, use of compressed air, cleaning method used, and type of wood processed (the joineries processed dry wood only). As wood dust exposure data were log-normally distributed, log transformed dust 78 concentrations (inhalable dust) were used as the dependent variable (for the

ANOVA one-way and multi-factor analyses). The statistical analyses were done using SPSS software (SPSS for Windows, Release 6.1.3 standard version,

SPSS Inc., USA).

b) Correlations among Personal Exposures (Dust, Fungi, Bacteria

Endotoxins, (1->3)-b-D-Glucans)

Correlations (Pearson’s R) among personal exposures (geometric mean values) were analyzed using the natural logarithms of exposure (as the data were log normally distributed). Data analyses were performed using the

GraphPad InStat (version 2.04a. USA) statistical program.

c) Dose-Response Relationships between Personal Exposures and Lung

Function

All the woodworkers participated in this study were males (Caucasians). As the ex-smokers (6) were a few in numbers, they were counted as non-smokers.

The workers having a past history of asthma (4) were excluded in the data analysis. At joinery I the two workers having mild asthma, due to exposure to western red cedar dust, did not participate in the lung function test.

Among Joinery Workers and Sawmill and Chip Mill Workers: 79

Lung function parameters (VC, FVC, FEV1, %FEV1/FVC, PEF, FEF25-75%) of joinery workers, sawmill and chip mill workers, and controls were adjusted for age, height and smoking by multiple linear regression analysis (using Microsoft

Excel, version 5.0, Microsoft Co., USA). The smoking status was specified as 1 for smokers and 0 for non-smokers (Donham et al., 1995). The lung function indices of woodworkers and controls were compared with unpaired T test.

Among Smokers and Non-smokers:

The workers were stratified into two groups according to smoking status. Lung function parameters (VC, FVC, FEV1, FEV1/FVC, PEF, FEF25-75%) were adjusted for age and height by multiple linear regression analysis (using Microsoft Excel, version 5.0, Microsoft Co., USA).

Predicted normal values were calculated using the formulae of Gibson et al.

(1979) for FVC, FEV1, FEV1/FVC and of Lazarus (1982) for VC and FEF25-75%.

Percentage cross-shift change (decrease) in lung function and percentage predicted lung function indices were calculated (adjusted values) as follows;

{% cross-shift change in FEV1 = 100 x [FEV1(morning)-FEV1(afternoon)/FEV1 (morning)]}

{% predicted FEV1 = 100 x observed FEV1 (morning)/predicted FEV1}

Dose-response relationships among personal exposures and lung function were computed by regression analysis (Pearson’s R). Personal exposure data 80 were log normally distributed, and hence the natural logarithms of exposure were used for linear regression and correlations (GraphPad InStat, version

V2.04a, USA).

Stepwise multiple regression was used to develop models for prediction of pulmonary function changes from independent variables among joinery workers and sawmill and chip mill workers (using Microsoft Excel, version 5.0, Microsoft

Co., USA). Cross-shift change in each pulmonary function variable (VC, FVC,

FEV1, FEV1/FVC, PEF, FEF25-75%) was treated individually as the dependent variable. Independent variables tested in the regression models included age, height, smoking, number of years of exposure to wood dust, and personal exposure data for inhalable dust, respirable dust, inhalable endotoxin, respirable endotoxin, inhalable (1->3)-b-D-Glucans), and respirable

(1->3)-b-D-Glucans). The mean percentage cross-shift changes in lung function were compared with controls (unpaired t-test).

d) Questionnaire Analysis

The SPSS statistical program was used for the questionnaire analysis (SPSS for Windows, version 6.1.3, SPSS Inc., USA). Logistic regression analysis was used to adjust the symptoms prevalence data for age and smoking among woodworkers and controls. The comparison of the prevalence of work-related symptoms among woodworkers and controls were tested by chi-square analysis. 81

The correlations among work-related symptoms and personal exposures were computed by logistic regression analysis (confounders adjusted age and smoking). The correlations between work-related respiratory symptoms and lung function were computed by linear regression analysis. 82

CHAPTER 3

RESULTS AND DISCUSSION

3.1 DISTRIBUTION OF EXPOSURE DATA

Occupational exposures are often log-normally distributed (Rappaport, 1991).

In theory, lognormal distributions arise from multiplicative effects of random influences on exposure levels (Waters et al., 1991). These random influences include the mobility of the worker, the generation rate of the contaminant

(source), and the rate of contaminant concentration dilution (ventilation). The distribution of data is positively right-skewed with a long tail.

A lognormal distribution is completely determined by the median or geometric mean (GM) and the geometric standard deviation (GSD) (NIOSH, 1977). For lognormally distributed data, a logarithmic transformation of the original data is normally distributed. The GM and GSD of the lognormal distribution are the antilog of the mean and standard deviation of the logarithmic transformation.

In this study, the exposure data were lognormally distributed as shown in Fig.

3.1. Therefore in statistical analyses (determinants-of-exposure, correlations and regressions), log-transformed data were used (Fig. 3.2). 83

80

70 ) 3 60 m / g

m 50 (

t s

u 40 d

e l

b 30 a l a

h 20 n i

10

0 0 10 20 30 40 50 60 70 80

inhalable endotoxin (ng/m3)

Fig. 3.1 Inhalable dust vs. inhalable endotoxin - a lognormal distribution (data skewed to the right side with a long tail) (n=160, with 95% confidence interval).

5

) 4 3 m /

g 3 m (

t s 2 u d

e l

b 1 a l a

h 0 n i

g o l -1

-2 4 5 6 7 8 9 10 11 12

log inhalable endotoxin (ng/m3)

Fig. 3.2 Inhalable dust (log) vs. inhalable endotoxin (log) - a normal distribution for log transformed Data (n=160, with 95% confidence interval).

3. 2 PERSONAL EXPOSURE TO WOOD DUST 84

3.2.1 INHALABLE DUST

A total of 182 inhalable dust samples were collected. Twelve samples collected at logging sites, sawmills and the woodchipping mill were not included in the study as there was evidence of contamination and tampering of the samples, despite the fact that the sampling was personally supervised by the investigator.

Inhalable dust exposure levels at each worksite are given in Table 3.1. The frequency distribution of inhalable exposures is presented in Fig. 3.3. Overall,

62% of the personal inhalable dust exposures exceeded the current exposure standards (57% at sawmills and woodchipping, and 71% at the joineries). The

Worksafe Australia standards (1995) for wood dust exposure are for hardwood:

1 mg/m3 and softwood: 5 mg/m3 (8 hr. time weighted average for inhalable particle-size fraction). Table 3.2 and Table 3.3 present the personal exposures by job titles (only woodworking jobs) at sawmills and joineries respectively. The job title itself describes the primary task of each worker (unless otherwise mentioned in the footnotes of Table 3.2 and Table 3.3). The frequency distributions of inhalable dust exposures at sawmills and joineries are shown in

Fig. 3.4 and Fig. 3.5.

Table 3.1 Mean Inhalable Exposure Levels (mg/m3)

worksite inhalable dust 85

na AMb GMc range GSDd

logging site A 4 0.50 0.49 (0.38-0.59) 1.23 logging site B 3 0.68 0.67 (0.57-0.84) 1.22 logging site (total) 7 0.58 0.56 (0.38-0.84) 1.29

sawmill C 22 0.83 0.74 (0.25-2.63) 1.60 sawmill D 29 2.99 1.91 (0.55-11.22) 2.62 sawmill E 25 12.32 2.44 (0.26-74.05) 5.42 sawmill F 17 2.02 1.68 (0.56-4.55) 1.89 sawmill (total) 93 4.81 1.59 (0.25-74.05) 3.19

woodchipping mill G 4 3.17 2.86 (1.80-5.66) 1.66 woodchipping (total)e 9 2.16 1.86 (0.98-5.66) 1.72

joinery H 13 15.33 11.47 (4.85-50.65) 2.02 joinery I 12 0.68 0.61 (0.21-1.31) 1.68 joinery J 12 2.53 1.80 (0.37-7.79) 2.47 joinery K 18 11.35 7.32 (0.73-35.86) 2.86 joinery L 11 5.33 4.84 (2.60-10.90) 1.57 joinery (total) 66 7.59 3.68 (0.21-50.65) 3.67

Total 170 5.68 2.14 (0.21-74.05) 3.59

ano. of workers sampled. barithmetic mean. cgeometric mean. dgeometric standard deviation. eincluding personal exposures at the chippers of sawmills C/E.

70

60

50 s e l

p 40 m a s

f

o 30

. o n 20

10 Std. Dev = 11.45 Mean = 6 0 N = 170.00 1 11 21 31 41 51 61 71

inhalable dust concentration (mg/m3)

Fig. 3.3 Frequency distribution of inhalable exposures. 86

Compared with green mills, the percentage of samples, which exceeded the hardwood standard was high for dry mills (70% in dry mills, 50% in green mills).

The extremely high levels observed at sawmills were either due to the use of defective machines fitted with poorly maintained ventilation systems, ineffectively ventilated machines, or the use of machines not fitted to any local exhaust ventilation system. At green mills, none of the machines was fitted with a local exhaust ventilation system.

At sawmill C, the workers doing multi-task jobs (operating a saw inside an enclosed booth and sorting timber) had slightly lower exposures compared with those of the sorters (Table 3.2). There was no significant difference observed in the geometric mean exposure levels before (1.88 mg/m3, range: 0.55-7.69 mg/m3) and after (1.94 mg/m3, range: 0.58-11.22 mg/m3) the replacement of the moulder and the central exhaust ventilation system at sawmill D. As the joints of the ventilation system were not properly sealed, dust leaking into the work environment was observed. The old ripsaw was a defective machine and holes and leakages were observed in the flexible ducts and in the joints of the attached dust extraction system. When the ripsaw was in operation, the whole area was clouded with wood dust, which affected not only the operator, but also other workers within 5 meters who were sorting and grading timber. The end- matcher was not fitted with a local dust extraction system.

At Sawmill E, the picket machine and the moulder produced very high concentrations (51 mg/m3 and 67 mg/m3 respectively) of wood dust as both machines were not enclosed and were ineffectively ventilated. Table 3.2 Exposure Levels to Inhalable Dust (mg/m3) by Job Titles at Sawmills job title na AMb GMc GSDd job title n AM GM GSD

Green Mill Dry Mill mill C mill D (before replacing of the moulder and exhaust vent. system) band saw operatore 2 0.79 0.78 1.07 moulder operator 3 1.54 1.45 1.57 jig saw operatore 2 0.84 0.83 1.03 cross-cut saw operator 2 3.98 3.69 1.74 edger operatore 2 0.87 0.86 1.11 end-matcher operator 2 3.39 3.23 1.54 resaw operatore 2 0.82 0.82 1.09 rip saw operatorf 1 5.99 5.99 sorter 3 1.60 1.46 1.67 grader 6 0.78 0.75 1.33 chipper operator 2 1.08 1.08 1.14 stacker 2 7.10 7.07 1.13 planer operator 1 0.70 0.70 auto-docker operator 1 0.54 0.54 mill D (after replacing of the moulder and exhaust vent. system) auto-stacker operator 1 0.46 0.46 moulder operator 3 2.17 2.11 1.31 grader 4 0.52 0.51 1.30 cross-cut saw operator 1 3.36 3.36 end-matcher operator 2 10.35 10.31 1.13 mill E grader 6 0.82 0.79 1.34 Canadian saw operator 2 1.87 1.87 1.07 stacker 1 7.09 7.09 bench saw operator 4 1.74 1.49 1.96 band saw operator 1 45.22 45.22 mill E docking saw operator 4 1.00 0.99 1.21 planer operator 2 1.96 1.92 1.32 chipper operator 3 1.52 1.50 1.20 moulder operator 2 50.94 50.83 1.10 grader 2 0.31 0.31 0.36 picket machine operator 2 67.41 67.08 1.15 mill F mill F band saw operator 2 2.61 2.54 1.40 planer operator 1 0.83 0.83 bench saw operator 5 2.22 1.82 1.98 moulder operator 2 2.25 2.24 1.10 cross-cut saw operator 2 3.88 3.85 1.19 end-matcher operator 2 1.28 1.26 1.25 auto-docker operator 2 0.96 0.95 1.18 grader 1 0.56 0.56 ano. of workers sampled. barithmetic mean. cgeometric mean. dgeometric standard deviation. einvolved operating a saw inside an enclosed booth and sorting timber. foperation removed following the replacement. Table 3.3 Exposure Levels to Inhalable Dust (mg/m3) by

Job Titles at Joineries

job title na AMb GMc GSDd joinery H wood machinist 2 5.14 5.13 1.08 belt sander (hand held) operatore 5 11.19 11.18 1.06 horizontal band sander operator 2 49.34 49.32 1.04 automatic router operator 2 9.48 9.48 1.04 router (hand held) operator 2 7.70 7.70 1.03 joinery I sawing operator 3 0.45 0.43 1.48 planer operator 2 0.73 0.73 1.15 belt sander (hand held) operator 3 0.69 0.69 1.09 broad belt sander operator 1 1.31 1.31 cross-cut saw operator 1 1.16 1.16 spindling machine operator 1 0.58 0.58 assembler 1 0.21 0.21 joinery J wood machinist 5 1.81 1.56 1.79 router (hand held) operator 3 2.48 2.45 1.20 cross-cut saw operator 2 0.46 0.45 1.35 disc sander operator 1 5.21 5.21 orbital sander operator 1 7.79 7.79 joinery K spindling machine operator 1 0.73 0.73 wood turner operator 2 14.17 14.14 1.10 copy lathe operator 2 34.61 34.59 1.05 automatic router operator 2 2.20 2.20 1.03 belt sander (hand held) operator If 4 7.83 7.75 1.18 inverted router operatore 2 4.64 4.61 1.18 belt sander (hand held) operator IIe 3 18.10 18.03 1.11 broad-belt sander operator 1 2.04 2.04 belt sander (hand held) operator III 1 4.72 4.72 joinery L planer operator 2 3.05 3.02 1.23 moulder operator 1 10.90 10.90 wood shaper operator 2 3.42 3.41 1.06 panel saw operator 1 4.95 4.95 cross-cut saw operator 1 3.44 3.44 orbital sander operator (hand held) 2 7.79 7.75 1.15 horizontal belt sander operator 2 5.44 5.39 1.21 ano. of workers sampled. barithmetic mean. cgeometric mean. dgeometric standard deviation. einvolved trenching. finvolved routing.

88

sawmill C - hardwood sawmill D - hardwood 11 14 10 13 12 9 11 8 10 s s e e l l 7 9 p p 8 m m 6 a a 7 s s

f f 5 6 o o

. . 4 5 o o n n 3 4 3 2 Std. Dev = .47 2 Std. Dev = 2.97 Mean = 3 1 Mean = .83 1 0 N = 22.00 0 N = 29.00 .25 .50 .75 1.00 1.25 1.50 1.75 2.00 2.25 2.50 2.75 1 3 5 7 9 11

inhalable dust concentration (mg/m3) inhalable dust concentration (mg/m3)

sawmill E - hardwood sawmill F - hardwood 20 10 18

16 8

s 14 s e l e l p 12 p 6 m m a a

s 10

s f

f o

8 o .

4 . o o n 6 n

4 2 Std. Dev = 22.99 Std. Dev = 1.28 2 Mean = 12 Mean = 2 0 N = 25.00 0 N = 17.00 1 11 21 31 41 51 61 71 1 2 3 4 5 inhalable dust concentration (mg/m3) inhalable dust concentration (mg/m3)

all the sawmills 40

30 s e l p m

a 20 s

f o

. o n 10 Std. Dev = 12.75 Mean = 5 0 N = 93.00 1 6 11 16 21 26 31 36 41 46 51 56 61 66 71 76 inhalable dust concentration (mg/m3)

Fig. 3.4 Frequency distribution of inhalable dust concentrations at sawmills. 89

The band saw at this mill also gave rise to high dust exposure (45 mg/m3) as the machine was not fitted to any local exhaust ventilation system. The operator was standing close to the saws.

Among joinery operations, 95% of the personal hardwood exposures and 35% of the softwood exposures exceeded the relevant standards. Fig. 3.6 and

Fig. 3.7 present the frequency distribution of hardwood dust and softwood dust exposures respectively of the joineries. Hand-held sanding operations with or without integral dust extraction systems nearly always resulted in exposures above 5 mg/m3 (Table 3.3). Joinery H had a very dusty work environment with poor hygiene practices. Mounds of dust were observed not only on the ground, but up to the rooftop and on horizontal surfaces. Dust particles falling from the roof was a frequent sight. The ineffectively ventilated horizontal band sander resulted in high exposure levels (49 mg/m3). The exhaust hood was fitted only to the head pulley of the horizontal band sander and the work pieces processed were large in size. This did not effectively control airborne dust when the sanding could not be done close to the head pulley, or when the workpiece was large. Holes and leaks were observed in cyclone bags and the flexible ducts. None of the hand-held tools (for trenching, sanding, routing) was fitted with integral dust extraction systems. The use of compressed air to clean the surface of machines to remove dust from stored timber, workpieces and from clothing, made dust airborne. Dry sweeping further aggravated the situation. 91

joinery I - softwood joinery H - hard/softwood 7 6

6 5 5 s s e l

e 4 l p

p 4 m m a a s

3 s f

f 3 o

o .

. o o 2 n

n 2

Std. Dev = .32 1 Std. Dev = 15.27 1 Mean = .7 Mean = 15 N = 12.00 0 N = 13.00 0 .2 .5 .7 1.0 1.2 1.5 4 12 20 28 36 44 52

inhalable dust concentration (mg/m3) inhalable dust concentration (mg/m3)

joinery J - hard/softwood joinery K - hard/softwood 5 4

3 4 3 s s e e l l p p 3 2 m m a a s s

f f

o 2 o

2 . . o o n n 1 1 Std. Dev = 2.18 1 Std. Dev = 10.30 Mean = 3 Mean = 11 0 N = 12.00 0 N = 18.00 1 2 3 4 5 6 7 8 1 5 9 13 17 21 25 29 33 37

Inhalable dust concentration (mg/m3) inhalable dust concentration (mg/m3)

all the joineries joinery L - hardwood 16 4 14

3 12 s s e l e

l 10 p p m m a a

s 8

2 s f

f o o . 6 . o o n n 1 4 Std. Dev = 2.59 2 Std. Dev = 10.81 Mean = 5 Mean = 8 0 N = 11.00 0 N = 66.00 2 4 6 8 10 12 1 5 9 13 17 21 25 29 33 37 41 45 49 53

inhalable dust concentrations (mg/m3) inhalable dust concentration (mg/m3)

Fig. 3.5 Frequency distribution of inhalable dust concentrations at joineries. 92

6

5

s 4 e l p m

a 3 s

f o

. o 2 n

1 Std. Dev = 9.42 Mean = 8 0 N = 40.00 1 11 21 31 41 51 inhalable dust concentration (mg/m3)

Fig. 3.6 Frequency distribution of hardwood dust exposures at joineries.

16

14

12 s e l 10 p m

a 8 s

f o

. 6 o n 4

Std. Dev = 11.22 2 Mean = 6 0 N = 26.00 1 7 13 19 25 31 37 43 49 inhalable dust concentration (mg/m3)

Fig. 3.7 Frequency distribution of softwood dust exposures at joineries. 93

Joinery I was a large size woodworking site employing around 40 workers.

Here all the machines, both static and portable were either fitted through flexible ducts to the central exhaust ventilation system or attached to dust collection bags. A vacuum cleaner similar to household cleaners was used to clean the floor. The dust filled bags attached to the hand held sanders were emptied frequently. The mean exposure level was (0.6 mg/m3).

At joinery J, although the disc sander was fitted with an annular exhaust hood surrounding the disc, it still gave high dust levels (5.2 mg/m3). The workpieces sanded were mostly hollow items. This system was not effective when sanding flat or hollow workpieces as the dust cloud was drawn towards the operator when the item was removed from the sander. The dust from hand-held routers and orbital sanders was also not controlled and gave high dust exposures

(router - 2.5 mg/m3, orbital sander - 7.8 mg/m3).

At joinery K, the copy lathe machine, the wood turner, and the hand-held tools

(trenching, routing, and sanding) were the main sources of airborne dust.

Although the copy lathe machine was fitted with a movable dust extraction hood, it did not extract all the airborne dust from the breathing zone of the worker (35 mg/m3). The process produced very fine airborne dust and the worker had to work very close to the source of emission.

Although the operators were provided with plastic goggles, they were reluctant to wear them because they get rapidly covered with dust, blurring their vision.

Although all the workers were provided with respirators, only some of the 94 operators wore respirators, and even then not throughout the entire workshift.

The wood turner produced a large volume of chips and dust. The dust collection hood was permanently fitted only to one end of the machine although the worker worked all along the length of the wood (~1.5 m). A sharp edged tool was used as the point of operation together with applying sand paper along the wood item. While tool point operation produced a large volume of chips, the sanding process liberated fine dust into the work environment. High personal dust exposures were observed at the wood turning machine (14 mg/m3). A compressed air jet was used to remove the dust from automatic router. This method was unsatisfactory for removing fine dust as it disturbed the laden dust, making it airborne and projecting it into the general work environment behind the machine. Although the hand-held belt sanders were fitted with dust bags, the airborne levels were still very high (4.7 mg/m3). It was observed that the workers would use sanders for the whole day and the next day, without replacing or emptying the filled bags. This too, must have contributed to higher airborne concentrations due to lower capture efficiency of the integral system.

Joinery L was a small woodworking site which carried out a lot of sanding operations, which resulted in a high geometric mean concentration of airborne dust (4.8 mg/m3). The airborne level at the moulding machine was high (11 mg/m3) as it was not enclosed properly and the operator very often used a compressed air jet to remove the dust from the table and timber.

All the static machines were connected through flexible ducts to a central exhaust ventilation system (consisting of cyclone bags and a dust hopper, 95 which were placed inside the workplace). The dust filled hoppers were replaced

2-3 times per day. During disconnection of such hoppers, thick clouds of dust were liberated into the work environment. Since there were no openings except for the front entrance in the building, dust laden air kept on circulating inside for a significant period of time. The operators of the cross-cut saws and moulder were thus more exposed to dust as their machinery was located close to the hopper. Thick layers of dust could also be seen on top of stored timber nearby.

Compressed air jets were used to remove dust from stored timber, work pieces

(especially after sanding), the tops of the benches and the machines. Dry sweeping further aggravated the situation. The dust from hand-held orbital sanders was not controlled and gave high exposure levels (7.8 mg/m3).

3.2.1.1 Determinants of Wood Dust Exposure

Table 3.4 shows the significance of individual factors on the personal inhalable dust exposures (using ANOVA). For the total exposures (n=163), the type of wood processed was not an influential factor determining dust exposures.

Table 3.4 Influence of Individual Factors on Wood Dust Exposures

(ANOVA one-way analyses) 96

determinants sawmillsa joinery totalb (n=97)c (n=66) (n=163)

job title <0.001*** <0.001*** <0.001*** local exhaust ventilation 0.72 <0.001*** 0.042* use of hand-held tools 0.22 <0.001*** cleaning method used <0.001*** <0.001*** use of compressed air <0.001*** <0.001*** green or dry wood processed 0.01** <0.001*** type of wood processed 0.001*** 0.52

aincluding chip mills. bsawmills + chip mills + joineries.

cn – number of workers sampled. *p<0.05; **p<0.01; ***p<0.001.

Table 3.5 shows the results of the multi-factor analysis, which considers the influence of all the factors together. For the ANCOVA analysis, both significant and non-significant factors in the ANOVA one-way analysis were used. For the total exposures (n=163), the important determinants of exposure were local exhaust ventilation, job title, use of hand-held tools, cleaning method used, use of compressed air, and green or dry wood processed, while type of wood processed was not. The influential factors on wood dust levels for the joineries

(n=66) were local exhaust ventilation, job title, use of hand-held tools, use of compressed air, and cleaning method used. For the sawmills (n=97), the important determinants were local exhaust ventilation, job title, and green or dry wood processed. 97

Table 3.5 Significance of Determinants on Wood Dust Exposure

(ANCOVA model)

determinants sawmillsa joinery totalb (n=97)c (n=66) (n=163)

job title <0.001*** <0.001*** <0.001*** local exhaust ventilation 0.001*** <0.001*** <0.001*** use of hand-held tools <0.001*** <0.001*** cleaning method used 0.001*** 0.011* use of compressed air 0.033* 0.045* green or dry wood processed 0.025* 0.001*** type of wood processed 0.468 0.869

2 r (r-correlation coefficient) 0.43 0.90 0.68

aincluding chip mills. bsawmills + chip mills + joineries.

cn – number of workers sampled. *p<0.05; **p<0.01; ***p<0.001.

3.2.2 RESPIRABLE DUST

The respirable dust levels at different worksites are given in Table 3.6.

Table 3.6 Personal Respirable Dust Levels (mg/m3)

worksite na AMb GMc range GSDd

logging sites 4 <0.1 <0.1 (0.03-0.05) 1.29 sawmills 37 0.4 0.3 (0.05-1.05) 2.17 woodchipping mille 4 0.3 0.3 (0.12-0.40) 1.71 joinery 39 0.7 0.5 (0.03-2.55) 2.49 total 82 0.5 0.3 (0.03-2.55) 2.72

ano. of workers sampled. barithmetic mean.

cgeometric mean. dgeometric standard deviation.

eincluding personal exposures at the chippers of sawmills C/E.

Mean personal respirable dust exposures were higher at joineries compared with the other worksites. 98

3.2.3 DISCUSSION

This evaluation of a variety of woodworking operations has confirmed that woodworkers from the tree felling stage onwards through various manufacturing processes are exposed to wood dust of different particle sizes, concentrations, and compositions.

The overall geometric mean personal inhalable dust exposure was 2.14 mg/m3

(n=170, GSD=3.59). For logging sites it was 0.56 mg/m3 (n=7, GSD=1.29), sawmills 1.59 mg/m3 (n=93, GSD=3.19), woodchipping 1.86 mg/m3 (n=9,

GSD=1.72) and for joineries 3.68 mg/m3 (n=66, GSD=3.67). The variability in concentrations appeared to be relatively high for joineries and sawmills as indicated by their high GSDs.

The mean inhalable exposures found in some of our joineries were significantly higher than the levels found in the Dutch study (Scheeper et al., 1995) and also the South Australian furniture study (Pisaniello et al., 1991). Among joinery operations, there was a greater degree of over exposure to hardwood dust

(95%) than to softwood dust (35%). Hardwood dust exposure has been shown to be associated with nasal adenocarcinoma (Acheson et al., 1968; Franklin,

1982; Leclerc et al., 1994).

The determinants of exposure analysis were consistent with the field observations. The influential factors on wood dust levels for the sawmills

(n=97) were local exhaust ventilation (p=0.001), job title (p<0.001), and green 99 or dry wood processed (p=0.025). The extremely high levels observed at sawmills were either due to the use of defective machines fitted with poorly maintained ventilation systems (sawmill D, rip saw operator - 6 mg/m3), ineffectively ventilated machines (drymill E, moulder operator - 51 mg/m3, picket machine operator - 67 mg/m3), or the machines not fitted to any local exhaust ventilation system (green mill E, band saw operator - 45 mg/m3). At the green mills, none of the machines was fitted with a local exhaust ventilation system. Compared with green mills, the percentage of samples, which exceeded the hardwood standard was much higher for dry mills (70% in dry mills and 50% in green mills). One reason for this difference is that fresh wood dust contains a higher percentage of moisture and so becomes less airborne. A second reason is that in hardwoods the cells are tightly bound and kiln drying makes them less elastic, leading to cell shattering producing fine airborne dust

(Hinds, 1988).

For the joineries (n=66), local exhaust ventilation system (p<0.001), job title

(p<0.001), use of hand-held tools (p<0.001), use of compressed air (p=0.033), and cleaning method used (p=0.001) were the important determinants, while type of wood processed was not. Sanding operations nearly always resulted in exposures above 5 mg/m3. Hand-held orbital sanders and routers produced high airborne levels, as they were not fitted to any dust extraction system. With or without integral dust extraction systems, the belt sanders (hand held) produced very high concentrations of airborne dust (except joinery I) which is consistent with the findings of the study of dust extraction systems of hand sanders used on wood by Thorpe and Brown (1994). The belt sanders, which 100 were attached to dust bags in joinery I gave, rise to low dust levels (0.7 mg/m3) even though sanding was restricted to the edges. Frequent replacement of bags also took place at this workplace. At joinery H and K, the workers doing multi-task jobs, which were mainly involved with hand-held tools, had elevated exposures. Copy lathes (35 mg/m3) and wood turners (14 mg/m3) also contributed to elevated exposures. At joinery H, the ineffectively ventilated horizontal band sander resulted in high exposure levels (49 mg/m3). The use of compressed air to clean the surface of machines to remove dust from stored timber, workpieces and from clothing, made dust airborne. Dry sweeping further aggravated the situation. Joinery I had a low mean exposure level (0.6 mg/m3), as the static machinery and the hand-held tools were efficiently ventilated and vacuum cleaning was used to clean the floor and the surface of machines.

The elevated exposures observed in this study are explained by a combination of factors, including:

· lack of awareness of potential health effects of wood dust exposure

among both management and workers

· aging equipment

· inadequate and ineffective dust extraction systems or usually none

especially for hand held tools

· poor maintenance of the ventilation system at some worksites

· non-segregation of dusty processes

· dry sweeping, and

· the use of compressed air jets 101

One US study reported that the primary work practice contributing significantly to personal exposures is the use of compressed air to remove laden dust from the machinery and surfaces (Mazurkiewicz and Festa, 1989). Although the peak exposures produced by the use of compressed air for sweeping or cleaning (where the concentration may rise above 50 mg/m3 on a 10-20 min basis) are of short duration, they still contribute to a significantly elevated TWA exposure over an 8 hr work shift (Scheeper et al., 1995).

For some machines, more effective enclosure and ventilation must be devised.

Improved designs are available for some but still need to be introduced into the workplace. An external source of extraction rather than integral bags is recommended for belt sanders and orbital sanders as it gives higher dust capture efficiency and thus results in less airborne dust (Thorpe and Brown,

1994). A recent study has demonstrated a prototype sanding table to extract dust during hand sanding as an effective dust control option for small and flat workpieces (Martin and Zalk, 1997). Other woodworking machines such as copy lathes, wood turners, and routers also contributed to the higher exposure levels. However, lathes are difficult to enclose and ventilate (Hamill et al.,

1991).

Methods for the control of dust from a number of wood processing machines and hand-held tools (rotational hand-held sanders [Hampl et al., 1992], disc sanders [Hampl and Johnston, 1991], automated routers [Hampl et al., 1990], shapers [Huebener, 1987], horizontal belt sanders [Hampl and Johnston, 102

1985], and table saws) are given in NIOSH (1996) Hazard Control series, and the Health and Safety Executive as well (Sykes, 1988; Fletcher, 1988). The

ACGIH manual (1995) also provides a comprehensive account of industrial ventilation systems. Enclosed booths have been shown to be an effective control technique, which prevent worker exposure to both noise and dust

(Teschke et al., 1994).

Complete control of dust during processing is often not possible, (a) because of strong localized air movements created by the movement of blades, cutters, drums, pulleys etc., (b) because of difficulty of enclosing these moving parts, and (c) because of the size of the workpiece (dust control is easier when machining small workpieces) (Sykes, 1988). Although it is difficult to control dust completely, it is usually possible to control the levels to within the occupational exposure limits with a well designed, efficient, properly used and maintained exhaust ventilation system. Where this is not possible, suitable respiratory protection equipment should be provided for the workers.

Furthermore, apart from direct health risks, excessive amounts of dust, if allowed to accumulate inside equipment and in work areas, can cause fire or explosion hazards. Dusty surfaces and machinery should be cleaned regularly using a dustless technique such as vacuum cleaning. 103

3.3 PERSONAL EXPOSURE TO BIOHAZARDS ASSOCIATED WITH WOOD

DUST

3.3.1 PERSONAL EXPOSURE TO FUNGI AND BACTERIA

Table 3.7 summarises the personal exposures to fungi, total bacteria and Gram

(-)ve bacteria observed at each worksite. At logging sites, Aspergillus fumigatus and Penicillium were the predominant fungi. Among sawmills, Penicillium was the dominant species. High concentrations of Aureobasidium pullulans at dry mills, and Aspergillus fumigatus and Paecilomyces spp. at the woodchipping mill, were also found. Total concentrations of fungi were lower at joineries than at logging sites, sawmills, and the woodchipping mill. The percentage distributions of personal airborne fungi levels at different worksites are also presented graphically in Fig. 3.8-3.10.

Higher concentrations of Penicillium were found at woodchipping mill G

(41 x 103 cfu/m3) and the green mills (sawmill C - 38 x 103 cfu/m3; sawmill E - 30

3 3 3 x 10 cfu/m , sawmill Fg - 22 x 10 ) than at the dry mills. Among Penicillium spp. identified in personal samples collected at each worksite, Penicillium glabrum

(previously known as Penicillum frequentans) was the predominant species.

Penicillium chrysogenum was also found at low concentrations at most of the sites. At sawmills D and F, two Penicillium species, which grew strongly at 370C Others others 5.1% 6.6% (Penicillium purpurogenumAcremonium sp. and another unidentified Penicillium sp.), both 6.5% Fusarium sp. belonging to subgenus6.1% Biverticillium, were also found at low levels.

Penicillium spp. Asp. fumigatus 3 3 a 39.9% logging53.5% site A (64 x 10 cfu/m ) Penicillium spp. 20.2% Asp. fumigatus 62.0% 106

logging site B (34 x 103 cfu/m3)

woodchipping mill G (74 x 103 cfu/m3) atotal mean exposure level

Fig. 3.8 Percentage distribution of mean personal exposure to fungi at logging sites and the woodchipping mill.

Asp. fumigatus 22.0%

Others 1.7%

Penicillium spp. 56.0%

Paecilomyces sp. 20.4% 106

others Asp. fumigatus 9.1% 10.3% Cladosporium sp. 4.9%

Penicillum spp. 75.7%

Others 14.9% Asp. fumigatus 24.4%

Aureobasidium sp. 9.8%

Cladosporium sp. 11.6%

Paecilomyces sp. Penicillium spp. 8.8% 30.5%

sawmill C (50 x 103 cfu/m3)a

sawmill D (26 x 103 cfu/m3)

sawmill E (54 x 103 cfu/m3) atotal mean exposure level sawmill F (27 x 103 cfu/m3)

Fig. 3.9 Percentage distribution of mean personal exposure to fungi at sawmills.

Asp. fumigatus Others 3.0% 13.3%

Others Asp. fumigatus 8.0% 8.4%

Aureobasidium sp. 22.4%

Penicillium spp. Aureobasidium sp. 55.7% 31.2% Paecilomyces sp. 5.6%

Penicillium spp. 52.4% 107

Others 8.9% others Asp. fumigatus Paecilomyces spp. 25.6% 25.2% 10.4%

Penicillium spp. 4.9%

Other Asp. spp. 10.3%

Asp. fumigatus Fonsecaea sp. 27.3% Penicillium spp. 75.8% 11.6%

joinery H (14 x 103 cfu/m3)a joinery I (4 x 103 cfu/m3)

Others Others 11.6% Asp. fumigatus 17.1% Asp. fumigatus 20.7% 25.6% Paecilomyces sp. 8.7%

Penicillium spp. Cladosporium sp. 18.9% 38.4%

Penicillium spp. 59.0%

joinery J (17 x 103 cfu/m3) joinery K (8 x 103 cfu/m3)

Penicillium spp. 55.2%

Paecilomyces sp. 17.8%

Aureobasidium sp. 4.6% Asp. fumigatus others 12.0% 10.4%

joinery L (19 x 103 cfu/m3) atotal mean exposure level

Fig. 3.10 Percentage distribution of mean personal exposure to fungi at joineries. 108

High mean airborne levels of Aureobasidium pullulans were found at sawmill E

3 3 3 3 (12 x 10 cfu/m ) and sawmill Fg (13 x 10 cfu/m ). Eurotium species, which are teleomorps of the genus Aspergillus, were found in some of the personal samples collected at two sawmills and the woodchipping mill, and were identified as Eurotium amstelodami, Eurotium repens, Eurotium rubrum and

Eurotium chevalieri. Aspergillus fumigatus concentrations were high at the logging sites (A - 40 x 103 cfu/m3, B - 18 x 103 cfu/m3), the woodchipping mill G

(16 x 103 cfu/m3) and joinery H (10 x 103 cfu/m3). The other Aspergillus species identified were, at logging site A, Aspergillus niger; sawmills, Aspergillus ochraceus, Aspergillus niger, Aspergillus candidus and Aspergillus sydowii; at the woodchipping mill, Aspergillus niger, Aspergillus sydowii and Aspergillus ochraceus; and at the joineries, Aspergillus niger, Aspergillus nidulans,

Aspergillus sydowii, Aspergillus flavipes and Aspergillus flavus. The microscopic photographs of the moulds identified are given in Appendices G and H.

High concentrations of Gram (-)ve bacteria were found at the green mills

(sawmills C and E - 12 x 103 cfu/m3), the woodchipping mill (14 x 103 cfu/m3), the joinery H (15 x 103 cfu/m3), and joinery K (13 x 103 cfu/m3). A work group report has suggested that in any environment, the total number of Gram (-)ve bacteria should not exceed 103 cfu/m3 (Clark, 1986). A high variability in concentrations of Gram (-)ve bacteria was found at the logging sites (GSD -

7.11) compared with the sawmills (GSD - 3.84), the woodchipping mill (GSD -

3.52) and the joineries (GSD - 4.55). The geometric standard deviation (GSD) for fungi levels at the logging sites was 3.72, the sawmills 2.77, the woodchipping mill 3.41 and the joineries 3.18. 109

Mean area airborne fungi and bacteria levels are given in Table 3.8. High concentrations of Penicillium spp. were found at logging sites (A: 17 x 103 cfu/m3; B: 25 x 103 cfu/m3), sawmill C (66 x 103 cfu/m3), sawmill E (18 x 103 cfu/m3) and the woodchipping mill G (16 x 103 cfu/m3). Similar to personal exposures, total airborne fungi levels were high at logging sites, sawmills and the woodchipping mill compared with joineries. The mean concentrations of

Gram (-)ve bacteria were high at the logging sites and the woodchipping mill.

3.3.2 PERSONAL EXPOSURE TO ENDOTOXIN AND (1->3)-b-D-GLUCAN

High personal exposure to endotoxins was found in the inhalable fraction relative to the respirable fraction (Table 3.9). Although mean exposures were lower than the 8 hr-TLV for airborne endotoxins (20 ng/m3) (Rylander, 1990), some of the inhalable exposures at sawmills (sawmills C, E and F) and the joinery H exceeded the standard. The variability of inhalable endotoxin concentrations as expressed by the geometric standard deviation (GSD), was high for sawmills (4.77) and joineries (3.66), compared with logging sites (1.32) and the woodchipping mill G (1.55). 112

Similarly, the (1->3)-b-D-glucan concentrations were found to be high in the inhalable fraction compared with the respirable fraction (Table 3.10). The inhalable (1->3)-b-D-glucan exposures were much lower at the joineries than those found at the sawmills, the woodchipping mill and the logging sites, which is comparable to the exposure levels of fungi. High GSDs of inhalable exposures were found for sawmills (4.42) and the woodchipping mill G (4.71), compared with those at the logging sites (2.71) and the joineries (2.01).

3.3.3 CORRELATIONS AMONG PERSONAL EXPOSURES (DUST, FUNGI,

BACTERIA, (1->3)-b-D-GLUCAN, AND ENDOTOXIN)

The exposure data were log normally distributed. Therefore, log transformed data was used for correlation analysis. Both inhalable and respirable endotoxins had highly significant positive correlations with both total bacteria and Gram (-)ve bacteria (Table 3.11). Also, the correlations among inhalable dust, inhalable endotoxin and inhalable (1->3)-b-D-glucan levels, respectively with respirable dust, respirable endotoxin and respirable (1->3)-b-D-glucan levels were significant. Positive correlations were found between personal airborne mean inhalable endotoxins with Gram (-)ve bacteria (p<0.0001) and mean inhalable (1->3)-b-D-glucans with total fungi (p=0.0003). Also the correlations between personal mean respirable endotoxins vs Gram (-)ve bacteria (p=0.005) and respirable (1->3)-b-D-glucans vs total fungi (p=0.005) were significant. Fig. 3.11 and Fig. 3.12 present the scatter plots of mean Gram

(-)ve bacteria levels with mean respirable and mean inhalable endotoxin levels. 115

7.5 ) 3 m /

g 7.0 n (

n i x o

t 6.5 o d n e

e

l 6.0 b a r i p

s 5.5 e r

n a e 5.0 m

g o l 4.5 Rsq = 0.5698 5 6 7 8 9 10

log mean Gram (-)ve bacteria (cfu/m3)

Fig. 3.11 Mean respirable endotoxin levels vs. mean Gram (-)ve bacteria levels

(n=12).

9.5 ) 3 9.0 m / g n ( 8.5 n i x o t

o 8.0 d n e 7.5 e l b a l

a 7.0 h n i

n 6.5 a e m

g 6.0 o l 5.5 Rsq = 0.8079 5 6 7 8 9 10

log mean Gram (-)ve bacteria (cfu/m3)

Fig. 3.12 Mean inhalable endotoxin levels vs. mean Gram (-)ve bacteria levels

(n=12). 116

Scatter plots of mean respirable glucan and mean inhalable glucan levels with mean fungi levels are given in Fig. 3.13 and Fig. 3.14.

7.0 ) 3 m /

g 6.5 n (

n a c u l 6.0 g

e l b a r i

p 5.5 s e r

n a e

m 5.0

g o l

4.5 Rsq = 0.5736 7.5 8.0 8.5 9.0 9.5 10.0 10.5 11.0

log mean fungi (cfu/m3)

Fig. 3.13 Mean respirable (1->3)-b-D-Glucan levels vs. mean fungi levels (n=12).

8.0 ) 3 m /

u 7.5 f c (

n a c u

l 7.0 g

e l b a l

a 6.5 h n i

n a e

m 6.0

g o l

5.5 Rsq = 0.7472 7.5 8.0 8.5 9.0 9.5 10.0 10.5 11.0

log mean fungi (cfu/m3)

Fig. 3.14 Mean inhalable Glucan levels vs. mean fungi levels (n=12). 117

3.3.4 DISCUSSION

Personal exposure levels to fungi at logging sites and sawmills were in the range 103-104 cfu/m3, at the woodchipping mill 103-105 cfu/m3 and at joineries

102-104 cfu/m3. The predominant species at logging sites were Aspergillus fumigatus and Penicillium spp; at sawmills, Penicillium spp. and also

Aureobasidium pullulans; while at the woodchipping mill, Penicillium spp.,

Paecilomyces spp., and Aspergillus fumigatus. Penicillium glabrum was dominant among the Penicillium species found. While these levels may appear low, it is important to note that the insidious subacute development of allergic alveolitis can result from prolonged exposure to low concentrations of fungi

(Jappinen et al., 1987).

The fungi implicated in allergic alveolitis are mainly the dry spored species which produce abundant spores of respirable size, less than 5 µm (Aspergillus and Penicillum species) (Lacey and Crook, 1988). EAA can also be caused by slimy spored species such as Graphium sp., Aureobasidium pullulans, Phoma violacea and Acremonium species. Aspergillus fumigatus and Fusarium spp. are known pathogens, which can cause infection or toxicosis in humans and animals (Murray et al., 1995). Some species of Paecilomyces are also pathogenic.

Penicillium glabrum has been implicated in the aetiology of suberosis, a form of

EAA caused by inhaling dust from mouldy cork, being reported among workers at a Portuguese cork factory (Avila and Lacey, 1974). Non-occupational allergic 118 alveolitis caused by Penicillium chrysogenum due to faulty installation of central heating has been reported (Fergusson et al., 1984). Penicillium has also been reported as the causative agent in fuel-chip induced hypersensitivity pneumonities (van Assendelft et al., 1985), woodman’s disease (Dykewicz et al., 1988), hypersensitivity pneumonities from cutting live trees, and cheese worker’s hypersensitivity pneumonitis (Campbell et al., 1983). Aureobasidium pullulans is considered as the cause of Sequoiosis, extrinsic allergic alveolitis associated with redwood sawdust (Sequoia sempervirens) (Cohen et al., 1967).

Swedish studies have identified kiln drying as the cause of high mould exposure at trimming departments in Swedish sawmills (Belin, 1987; Land et al., 1987). In contrast, in this study, the sawmills, which employed kiln drying processes, had low mould exposure levels. Although the Scandinavian studies mostly use non-culture based methods compared with the culture based method used in the present study to enumerate microorganisms, the observed large difference in exposures cannot mainly be due to the methodology

(Eduard et al., 1990). The type of wood processed and the employing of air drying process (3-5 months) prior to kiln drying (which reduces the moisture content considerably, thus preventing excessive growth of microorganisms) would be the most probable explanations for the low fungi exposures found in

Australian dry mills.

Personal exposure levels to microorganisms were also found to be very low at those workplaces with efficient dust control systems. The lowest concentrations

3 3 3 of total fungi were found at sawmill Fd (3 x 10 cfu/m ) and joinery I (4 x 10 119 cfu/m3), where efficient dust extraction systems have been installed. Dust exposures were also relatively lower for these worksites (sawmill Fd - 1.2 mg/m3, joinery I - 0.6 mg/m3).

Although the mean endotoxin levels observed were generally lower than the threshold level value (TLV) for endotoxins (20 ng/m3), some personal exposures at sawmills and a joinery did exceed the TLV. The mean exposure levels of (1->3)-b-D-glucan were higher at the woodchipping mills, green mills and the logging sites compared with the joineries. Significant positive correlations were found between personal airborne mean inhalable endotoxin and Gram (-)ve bacteria and mean inhalable (1->3)-b-D-glucan with total fungi.

The correlations between personal mean respirable endotoxin vs Gram (-)ve bacteria and respirable (1->3)-b-D-glucans vs total fungi were also significant.

The measurement of airborne constituents, such as endotoxins from Gram (-)ve bacteria and (1->3)-b-D-glucan from moulds can have practical advantages over the counting of viable microorganisms, as the former are often stable and can be measured over longer sampling periods. Furthermore, these constituents have been found to be of etiologic relevance (Eduard, 1995b). 120

3.4 EFFECTS OF MEAN PERSONAL EXPOSURES, NUMBER OF YEARS OF

EXPOSURE TO WOOD DUST, AND CUMULATIVE DUST INDICES ON LUNG

FUNCTION

3.4.1 AMONG JOINERY WORKERS AND SAWMILL AND CHIP MILL

WORKERS

3.4.1.1 Effects on Cross-shift Change in Lung Function

(Acute Effects)

Compared with controls, both the joinery workers and sawmill and chip mill workers showed remarkably high, statistically significant mean cross-shift change (decrease) in lung function (Table 3.12). Furthermore, the effects of dust, endotoxin, Gram (-)ve bacteria and, (1->3)-b-D-glucan on cross-shift decreases in lung function (given by significant positive correlation coefficients) were more prominent among the joinery workers compared with the sawmill and chip mill workers (Table 3.13). The significant positive correlation coefficients indicated that an increase in the percentage cross-shift change (decrease) in lung function was associated with increasing levels of personal exposures.

The cross shift decreases in VC and FEF25-75% were positively correlated with number of years of exposure among both joinery workers and sawmill and chip mill workers (Table 3.14). Significant positive correlations were also found among inhalable dust indices and cross shift decreases in VC and FEF25-75% respectively for the sawmill and chip mill workers and joinery workers. The 121 joinery workers showed significant positive correlations among percentage cross shift decreases in lung function (VC, FVC, and FEF25-75%) and respirable dust indices. The sawmill and chip mill workers have also shown significant effects of respirable dust indices on the percentage cross shift decrease in VC and FEF25-75%.

The mean percentage cross-shift decrease in lung function adjusted for age, height, smoking, number of years of exposure to wood dust, and personal exposures was significantly high in both joinery workers and sawmill and chip mill workers compared with controls (Table 3.15). Sawmill and chip mill workers had a high mean percentage cross-shift decrement in FEV1 adjusted for number of years of exposure to wood dust (15%) compared with that of joinery workers (4%). An 11% mean cross-shift change in FEF25-75% adjusted for inhalable endotoxin was also observed among sawmill and chip mill workers.

Joinery workers had a high percentage of cross-shift changes in VC (10%) and

FEV1 (15%) adjusted for respirable endotoxin levels compared with those of sawmill and chip mill workers. Effects of inhalable and respirable

(1->3)-b-D-glucan on the percentage cross-shift decrements in lung function were more prominent among sawmill and chip mill workers compared with those of joinery workers. The total group of woodworkers (joinery workers plus sawmill and chip mill workers) had marked effects of inhalable dust exposures on mean percentage cross-shift change in VC (29%), respirable dust exposure on mean percentage cross-shift change in FEV1/FVC (15%) and inhalable endotoxin exposures on mean percentage cross-shift change in FVC (38%) compared with those of controls. The effect of all the personal exposures on 122 cross-shift decrements in lung function was more prominent among sawmill and chip mill workers compared with joinery workers.

3.4.1.2 Effects on Percentage Predicted Lung Function

(Chronic Effects)

The woodworkers had low percentage predicted lung function compared with controls (Table 3.12). Similar to the effects on the cross-shift decrease in lung function, the effects of personal exposures on the percentage predicted lung function indices were more pronounced among joinery workers compared with the sawmill and chip mill workers (Table 3.16). The sawmill and chip mill workers showed an inverse correlation among percentage predicted FEV1 and inhalable dust exposures only (a decrease in percentage predicted FEV1 with increasing levels of inhalable dust). The sawmill and chip mill workers showed an inverse relationship between percentage predicted VC and inhalable dust indices (Table 3.14).

The relationships between percentage predicted lung function and the number of years of exposure to wood dust were positively correlated. This may be because some workers developed tolerance to high dust exposures after working for a number of years with wood, and/or the “healthy worker effect”, where those workers who were sensitive to wood dust had left the jobs. Table 3.12 Mean Cross-shift Change (decrease) in Lung Function and Mean Percentage

Predicted Lung Function among Joinery Workers and Sawmill and Chip Mill Workers

Compared with Controls (mean ± SD)

joinery sawmill/chip mill total controls workers workers no: 63 105 168 30 age (yr): 34 ± 13.6 38 ± 12.1 37 ± 12.8 39 ± 11.7 height (cm): 176 ± 9.3 175 ± 7.8 175.9 ± 8.2 175.3 ± 7.8 years exposed: 14 ± 13.1 9 ± 8.3 11 ± 10.6 11 ± 7.7 smoking status: 30% 40% 33% 30% mean % cross-shift decrease in lung functiona VC 6.27 ± 0.42 (0.0001)b 6.36 ± 0.36 (0.0001) 6.33 ± 0.38 (0.0001) 2.37 ± 0.35 FVC 4.49 ± 0.74 (0.0001) 4.34 ± 0.63 (0.0001) 4.40 ± 0.68 (0.0001) 2.12 ± 0.30 FEV1 6.40 ± 0.29 (0.0001) 6.31 ± 0.30 (0.0001) 6.34 ± 0.30 (0.0001) 1.78 ± 0.45 FEV1/FVC 2.96 ± 0.60 (0.0001) 2.80 ± 0.66 (0.0001) 2.86 ± 0.64 (0.0001) 0.75 ± 0.48 FEF25-75% 7.62 ± 0.58 (0.0001) 7.81 ± 0.67 (0.0001) 7.74 ± 0.65 (0.0001) 1.42 ± 1.12 PEF 7.12 ± 2.41 (0.001) 6.32 ± 2.66 (0.05) 6.61 ± 2.59 (0.0087) 5.25 ± 2.20 mean % predicted lung functionc VC 83.95 ± 3.02 (0.0001) 83.16 ± 3.15 (0.0001) 83.45 ± 3.12 (0.0001) 95.35 ± 7.93 FVC 84.65 ± 1.43 (0.0001) 84.68 ± 1.05 (0.0001) 84.66 ± 0.72 (0.0001) 94.90 ± 3.85 FEV1 84.59 ± 0.82 (0.0001) 84.71 ± 0.65 (0.0001) 84.67 ± 1.20 (0.0001) 93.11 ± 2.81 FEV1/FVC 99.61 ± 0.64 (0.0096) 99.82 ± 0.72 (ns) 99.74 ± 0.70 (ns) 99.90 ± 0.34 FEF25-75% 100.49 ± 8.97 (ns) 101.23 ± 7.00 (ns) 100.96 ± 7.76 (ns) 101.63 ± 5.17 a eg, {% decrease in FEV1 = 100 x [FEV1 (morning) – FEV1 (afternoon)/FEV1 (morning)]} (lung function adjusted for age, height and smoking). b two-tailed p values compared with controls (unpaired T test) (*p<0.05, **p<0.01, ***p<0.001, ns-not significant). c [% predicted lung function = 100 x observed/predicted lung function] (adjusted values). Table 3.13 Dose-Response Relationships (Pearson’s R)a between Cross-shift Change (decrease) in Lung Function and Mean Personal Exposures (log transformed) among Joinery Workers and Sawmill and Chip Workers group of % cross-shift decrease inhalable respirable inhalable respirable Gram (-)ve respirable workersb in lung functionc dust dust endotoxin endotoxin bacteria glucan joinery VC -0.66*** -0.42*** -0.61*** -0.56*** -0.31* 0.28* sawmill/chip mill 0.26** ns ns ns ns 0.20* total -0.29*** -0.28*** -0.32*** ns ns 0.23**

*** *** *** *** *** joinery FEV1 0.55 0.35 0.51 0.47 0.54 ns sawmill/chip mill -0.26** ns ns ns ns -0.21* total 0.21** 0.25*** 0.24** ns ns -0.24** joinery FVC 0.67*** 0.42*** 0.61*** 0.56*** 0.67*** -0.28* sawmill/chip mill -0.25** ns ns ns ns -0.20* total 0.29*** 0.28*** 0.33*** ns 0.23** -0.22**

** * * *** joinery FEF25-75% -0.33 ns -0.31 -0.28 -0.66 ns sawmill/chip mill 0.22* ns ns ns ns 0.19* total ns -0.20* ns ns -0.22** 0.23** joinery PEF 0.43*** 0.27* 0.39** 0.36*** 0.41*** ns sawmill/chip mill -0.25* ns ns ns ns -0.21* total 0.16** 0.22** 0.19* ns ns -0.24** aR (+)ve: indicates an increase in percentage cross-shift change (decrease) in lung function with increasing exposure levels. two-tailed p values: *p<0.05, **p<0.01, ***p<0.001, ns-not significant. bjoinery: n = 63; sawmill/chipping: n = 105; total: n = 168. clung function indices were adjusted for age, height, and smoking by multiple linear regression. Table 3.14 Effects of Number of Years of Exposure to Wood Dust (yr) and Cumulative Dust Indicesa (mg-yr/m3) on

Lung Function among Joinery Workers and Sawmill and Chip Mill Workers (Pearson’s R)

no. of years of exposure cumulative inhalable dust index cumulative respirable dust index b group of workers total joinery sawmill/chip mill total joinery sawmill/chip mill total joinery sawmill/chip mill

% cross-shift decrease in lung functionc

VC 0.59*** 0.81*** 0.48*** 0.21** ns 0.46*** 0.41*** 0.59*** 0.45*** FVC -0.60*** -0.80*** -0.48*** -0.21** ns -0.46*** -0.41*** 0.43*** -0.45*** *** *** *** ** * *** *** ** *** FEV1 -0.50 -0.77 -0.39 -0.22 -0.26 -0.42 -0.33 -0.57 -0.36 * * * * * FEV1/FVC -0.17 -0.28 ns -0.16 -0.26 -0.24 ns ns ns *** *** ** * * * ** *** ** FEF25-75% 0.35 0.57 0.28 0.19 0.26 -0.24 0.21 0.41 0.26 PEF -0.40*** -0.32*** -0.65*** -0.21** -0.29* -0.38* -0.26*** -0.49** -0.30** % predicted lung functiond VC ns ns ns ns ns -0.24* ns ns ns FVC 0.48*** 0.59*** 0.38*** ns ns 0.28** 0.35*** 0.43*** 0.36*** *** *** *** * *** *** *** *** FEV1 0.59 0.77 0.49 0.19 ns 0.44 0.41 0.56 0.46 *** *** ** * ** *** ** *** *** %FEV1/FVC 0.34 0.56 0.27 0.19 0.29 0.34 0.21 0.43 0.36 *** *** *** * *** *** *** *** FEF25-75% 0.58 0.73 0.48 0.18 ns 0.40 0.41 0.53 0.45 a[cumulative dust index = geometric mean personal dust exposure of the worksite x number of years of exposure to wood dust] bjoinery: n = 63; sawmill/chip mill: n = 105; total: n = 168. c eg, {% cross-shift change (decrease) in FEV1 = 100 x [FEV1 (morning)-FEV1(afternoon)/FEV1 (morning)]}. lung function values were adjusted for age, height, and smoking by multiple linear regression. d[% predicted lung function = 100 x observed/predicted lung function] (adjusted values). two-tailed p value: *p<0.05, **p<0.01, ***p<0.001, ns-not significant. Table 3.15 Percentage Cross-shift Decrements in Lung Function among Woodworkers

lung function A/H/Sm/Y A/H/Sm/Y/Id A/H/Sm/Y/Rd A/H/Sm/Y/Ie A/H/Sm/Y/Re A/H/Sm/Y/Ig A/H/Sm/Y/Rg A/H/Sm/Y/P (% decrease) C Jn Sc Jn Sc Jn Sc Jn Sc Jn Sc Jn Sc Jn Sc Jn Sc

VC 2.37 5.30*** 7.56*** 7.09*** 8.47*** 7.97*** 4.35*** 3.97*** 5.30*** 10.44*** 6.88*** 4.33*** 25.39*** 7.87*** 13.81*** 5.17*** 7.67*** FVC 2.12 4.51*** 3.21*** 4.50*** 2.53* 3.72*** 4.91*** 4.41*** 3.75*** 3.64*** 9.28*** 3.08** 3.19*** 3.50*** 3.35*** 5.85*** 19.21*** *** *** * *** ** *** *** *** *** *** *** *** *** *** * *** FEV1 1.78 4.24 14.66 9.11 4.42 2.52 4.66 5.07 5.50 14.97 5.93 7.44 5.28 7.05 11.74 2.72 8.80 *** *** *** *** *** *** *** *** ns *** *** *** *** *** *** *** FEV1/FVC 0.06 2.34 3.62 2.13 3.58 1.77 5.81 1.78 3.42 2.15 2.35 1.75 3.53 0.69 3.41 1.76 3.76 *** *** *** *** *** *** *** *** ns ns *** *** *** *** ns *** FEF25-75% 2.22 3.83 8.31 6.05 9.68 6.21 2.85 4.13 10.62 1.64 2.63 5.61 8.57 9.09 5.55 2.67 8.83 PEF 5.20 3.48* 9.09*** 3.40* 8.98*** 3.21* 8.59*** 3.42* 8.50*** 3.55* 8.62*** 3.79ns 8.92*** 3.27* 9.15*** 3.69ns 8.60***

C total total total total total total total total

VC 2.37 6.32*** 29.24*** 6.34*** 6.10*** 6.32*** 6.33*** 6.32*** 4.36*** FVC 2.12 4.40*** 3.52** 4.33** 38.23*** 4.40*** 4.40*** 4.39*** 4.56*** *** *** *** *** *** *** *** *** FEV1 1.78 6.34 5.71 6.30 6.34 6.34 6.34 6.35 7.10 *** *** *** *** *** *** *** *** FEV1/FVC 0.06 2.86 2.87 14.84 2.86 2.86 2.86 2.86 2.66 *** *** *** *** *** *** *** *** FEF25-75% 2.22 7.74 7.76 8.00 7.75 7.75 7.75 7.76 11.38 PEF 5.20 6.62* 6.70*** 6.69*** 6.62* 6.62* 6.61* 6.63* 6.79*

A/H/Sm/Y = Lung function adjusted for age, height, smoking, duration of exposure to wood dust. A/H/Sm/Y/Id = Lung function adjusted for age, height, smoking, duration of exposure to wood dust, and inhalable dust. A/H/Sm/Y/Rd = Lung function adjusted for age, height, smoking, duration of exposure to wood dust, and respirable dust. A/H/Sm/Y/Ie = Lung function adjusted for age, height, smoking, duration of exposure to wood dust, and inhalable endotoxin. A/H/Sm/Y/Re = Lung function adjusted for age, height, smoking, duration of exposure to wood dust, and respirable endotoxin. A/H/Sm/Y/Ig = Lung function adjusted for age, height, smoking, duration of exposure to wood dust, and inhalable glucan. A/H/Sm/Y/Rg = Lung function adjusted for age, height, smoking, duration of exposure to wood dust, and respirable glucan. A/H/Sm/Y/P = Lung function adjusted for age, height, smoking, duration of exposure to wood dust, and all personal exposures (Id, Rd, Ie, Re, Ig, Rg). C = Controls (n = 30). Jn = Joinery workers (n = 63). Sc = Sawmill/chip mill workers (n = 105). total = Both joinery workers and sawmill/chip mill workers (n = 168). *p<0.05; **p<0.01; ***p<0.001; ns = not significant. Table 3.16 Dose-Response Relationships (Pearson’s R)a between Percentage Predicted Lung Function and Mean

Personal Exposures (log transformed) among Joinery Workers and Sawmill and Chip Mill Workers

group of % predicted inhalable respirable inhalable respirable Gram (-)ve respirable workersb lung functionc dust dust endotoxin endotoxin bacteria glucan

*** *** *** *** *** * joinery FEV1 -0.65 -0.41 -0.60 -0.55 -0.66 0.28 sawmill/chip mill -0.26** ns ns ns ns ns total -0.30*** -0.27*** -0.33*** ns -0.24** 0.18* joinery FVC -0.57*** -0.36** -0.52*** -0.48*** -0.58*** ns sawmill/chip mill ns ns ns ns ns ns total -0.27*** -0.19* -0.30*** ns -0.26*** ns

** * * *** joinery FEV1/FVC -0.34 ns -0.31 -0.28 -0.64 ns sawmill/chip mill 0.22* ns ns ns ns 0.19* total ns -0.20** ns ns -0.24** 0.24**

*** ** *** *** * * joinery FEF25-75% -0.63 -0.40 -0.58 -0.53 -0.32 0.27 sawmill/chip mill ns ns ns ns ns ns total -0.29*** -0.24** -0.32*** -0.16* -0.26*** ns aR (-)ve indicates a decrease in percentage predicted lung function with increasing personal exposure levels. two-tailed p value: *p<0.05, **p<0.01, ***p<0.001, ns-not significant. bjoinery: n = 63; sawmill/chipping: n = 105; total: n = 168. cadjusted for age, height, smoking by multiple linear regression.

128

3.4.2 AMONG NON-SMOKERS AND SMOKERS

3.4.2.1 Effects on Cross-shift Change in Lung Function

(Acute Effects)

Table 3.17 presents the mean percentage cross-shift decrease in lung function and mean percentage predicted lung function indices separately for non- smokers and smokers, after adjusting for age and height. Smokers showed high mean percentage cross-shift decreases in lung function compared with non-smokers. The mean percentage cross-shift decrease in lung function among smokers and non-smokers were significantly high compared with controls.

Positively correlated dose-response relationships were found between the percentage cross-shift decrease in FVC, FEV1, and PEF with mean personal exposures among non-smokers (Table 3.18). Smokers showed significant correlations between the cross-shift decrease in FVC and mean personal respirable dust and Gram (-)ve bacteria levels. Mean personal respirable exposures were also significantly correlated with the cross-shift decrease in

PEF among smokers.

Dose-response relationships were also found between percentage cross-shift decrease in FEF25-75%, and mean exposure levels of fungi (r=0.19, p=0.04) and also with mean personal respirable (1->3)-b-D-glucan levels (r=0.22, p=0.02) among non-smokers. 129

Table 3.17 Mean Cross-shift Change (decrease) in Lung Function and

Mean Percentage Predicted Lung Function among Non-smokers and

Smokers compared with Controls (mean ± SD)

smokers non-smokers controls no: 56 112 30 age (yr): 36 ± 11.5 37 ± 13.6 39 ± 11.7 height (cm): 176 ± 7.6 175.6 ± 8.6 175.3 ± 7.8 years exposed: 11 ± 9.6 12 ± 11.0 11 ± 7.7

a mean % cross-shift decrease in lung function VC 8.01 ± 1.11 5.14 ± 0.83 2.37 ± 0.35 FVC 4.93 ± 0.47 4.59 ± 0.61 2.12 ± 0.30 FEV1 7.85 ± 0.10 5.41 ± 0.42 1.78 ± 0.45 FEV1/FVC 5.46 ± 0.55 5.02 ± 0.60 0.75 ± 0.48 FEF25-75% 12.16 ± 1.50 5.70 ± 1.50 1.42 ± 1.12 PEF 10.11 ± 4.98 3.35 ± 1.37 5.25 ± 2.20

b mean % predicted lung function VC 82.47 ± 3.78 83.72 ± 2.71 95.35 ± 7.93 FVC 84.56 ± 0.96 85.02 ± 1.70 94.90 ± 3.85 FEV1 83.28 ± 1.79 84.03 ± 2.11 93.11 ± 2.81 FEV1/FVC 98.25 ± 0.58 104.85 ± 1.36 99.90 ± 0.34 FEF25-75% 97.40 ± 2.45 103.28 ± 0.80 101.63 ± 5.17 a eg, {% change in FEV1 = 100 x [FEV1 (morning) – FEV1 (afternoon)/FEV1 (morning)]} smokers and non-smokers - lung function values were adjusted for age, and height and number of years of exposure to wood dust; controls – lung function values were adjusted for age, height and smoking, by multiple linear regression.

Mean percentage cross-shift decrease in lung function indices among smokers and non- smokers were significant compared with controls (two-tailed p<0.0001; unpaired T test).

b[% predicted lung function = 100 x observed/predicted lung function]

Mean percentage predicted lung function indices of smokers and non-smokers

(except % predicted FEF25-75%) were significant compared with controls.

(two-tailed p<0.0001; unpaired T test). 130

Table 3.18 Dose-Response Relationships (Pearson’s R)a between Cross-shift Change (decrease) in Lung Function and Mean Personal Exposures (log transformed) among Non-smokers and Smokers

% cross-shift inhalable respirable inhalable respirable Gram(-)ve decrease in dust dust endotoxin endotoxin bacteria b lung function

c *** * *** * *** FEV1 - NS 0.32 0.21 0.39 0.21 0.35 d FEV1 - S ns ns ns ns ns

FVC - NS 0.40*** 0.29** 0.42*** 0.19* 0.35*** FVC - S ns 0.29* ns ns 0.22**

PEF - NS 0.22* ns ns ns ns PEF - S ns 0.25* ns ns ns a R (+)ve indicates an increase in the cross-shift change (decrease) in lung function with increasing levels of personal exposures (*p<0.05, **p<0.01, ***p<0.001). badjusted for age and height by multiple linear regression. cnon-smokers, (NS): n = 112. dsmokers (S): n = 56.

Non-smokers showed significant correlations between cross-shift decrease in

VC with number of years of exposure, and cumulative respirable dust indices

(Table 3.19). Positive correlation coefficients obtained indicated that an increase in cross-shift change (decrease) in VC was associated with increasing number of years of exposure to wood dust, and cumulative respirable dust indices. Smokers showed correlations between cross-shift decrease in FEF25-

75% with number of years of exposure, and also cross-shift decrease in VC and cumulative inhalable dust indices. Table 3.19 Effects of Number of Years of Exposure to Wood Dust (yr), and Cumulative Dust Indicesa (mg-yr/m3) on Lung Function among Non-smokers and Smokers (Pearson’s R)b

no: of years of exposure cumulative inhalable dust index cumulative respirable dust index

c group of workers NS S NS S NS S

d % cross-shift decrease in lung function VC 0.44*** ns ns 0.24* 0.33*** ns FVC -0.57*** -0.34** ns ns -0.40*** ns *** ns *** FEV1 -0.46 ns ns -0.34 ns *** * *** FEV1/FVC ns -0.61 ns -0.30 ns -0.46 *** FEF25-75% ns 0.46 ns ns ns ns PEF -0.32*** -0.65*** ns ns -0.22* ns

e % predicted lung function VC ns -0.52*** ns -0.31* ns -0.41*** FVC 0.45*** -0.59*** ns ns 0.33*** -0.32** *** *** *** *** FEV1 0.60 -0.66 ns ns 0.42 -0.43 ** *** * * *** FEV1/FVC 0.30 -0.63 ns -0.29 0.19 -0.45 *** *** * *** ** FEF25-75% 0.60 -0.41 ns -0.31 0.42 -0.39 a [cumulative dust index = geometric mean personal dust exposure of the worksite x no. of years of exposure to wood dust]. b R (+)ve (with % cross-shift decrease in lung function) indicates an increase in percentage cross-shift change (decrease) in lung function with increasing no. of years of exposure to wood dust/cumulative dust indices. R (-)ve (with % predicted lung function) indicates a decrease in predicted lung function with increasing no. of years of exposure/cumulative dust indices. two-tailed p value: *p<0.05; **p<0.01; ***p<0.001; ns - not significant. c NS (non smokers): n = 112; S (smokers): n = 56. d eg, {% cross-shift decrease in FEV1 = 100 x [FEV1 (morning)-FEV1(afternoon)/FEV1 (morning]}. (NS/S: lung function adjusted for age and smoking by multiple linear regression analysis). e [% predicted lung function = 100 x observed/predicted lung function] (adjusted for age and height). 132

3.4.2.2 Effects on Percentage Predicted Lung Function (Chronic Effects)

The mean percentage predicted lung function was high for controls compared with the woodworkers (Table 3.17). The mean percentage predicted lung function (except percentage predicted FEF25-75%) among non-smokers and smokers were statistically significant compared with controls.

Significant inverse correlations were found between percentage predicted

FEV1, FVC, and FEF25-75% and personal exposures among non-smokers

(Table 3.20). In addition, the percentage predicted FVC with mean fungi levels

(r=-0.21, p=0.02) and mean personal respirable (1->3)-b-D-glucan levels

(r=-0.22, p=0.02) were also significant among non-smokers. Such correlations were not observed for smokers.

Table 3.20 Dose-Response Relationships (Pearson’s R)a between Percentage

Predicted Lung Function and Mean Personal Exposures (log transformed) among Non-smokers and Smokers

% predicted inhalable respirable inhalable respirable Gram (-)ve b lung function dust dust endotoxin endotoxin bacteria

c *** *** *** *** FEV1 - NS -0.39 -0.31 -0.40 ns -0.32 d FEV1 - S ns ns ns ns ns

FVC - NS -0.31*** -0.20* -0.40*** ns -0.36*** FVC - S ns ns ns ns ns

*** ** *** ** *** FEF25-75% - NS -0.37 -0.28 -0.42 -0.28 -0.34 FEF25-75% - S ns ns ns ns ns a R (-)ve indicates a decrease in % predicted lung function with increasing levels of personal exposures (*p<0.05, **p<0.01, ***p<0.001). badjusted for age and height by multiple linear regression. cnon-smokers: n = 112. dsmokers: n = 56. 133

Only smokers demonstrated inverse correlations between percentage predicted lung function (VC, FVC, FEV1, FEV1/FVC, and FEF25-75%) and number of years of exposure, and cumulative respirable dust indices (Table 3.19). The correlations among percentage predicted (VC, FEV1/FVC, and FEF25-75%) and cumulative inhalable dust indices were also significant among smokers.

3.4.3 DISCUSSION

Joinery Workers and Sawmill and Chip Mill Workers

The lung function changes observed among woodworkers were obstructive in nature. Both the joinery and sawmill and chip mill workers showed marked difference in the cross-shift decrease in lung function and the mean percentage predicted lung function compared with the controls. The effects of personal exposures on lung function were prominent among joinery workers compared with sawmill and chip mill workers. Similar dose-response relationship studies have been reported among swine production facility workers (Donham et al.,

1995; Reynolds et al., 1996).

Both sawmill and joinery workers showed significant effects of number of years of exposure, and cumulative dust indices on cross-shift decrease in lung function. The cumulative dust index for each worker was derived by multiplying the geometric mean personal dust exposure of the worksite by the number of years of exposure to wood dust. This index assumed that the current exposure measured during this cross-sectional study was representative of the worker’s 134 past exposure. A previous study has also shown exposure-effect relationships between percentage predicted lung function (FEV1 and FEF75) and dust indices

(respirable and total dust) (Holness et al., 1985).

In summary, the correlations found among lung function and personal exposures (dust, endotoxins, (1->3)-b-D-glucans, and Gram (-)ve bacteria), and lung function and the number of years of exposure to wood dust demonstrated that all these factors have deteriorating effects on the respiratory function among woodworkers. Such associations may be observed for exposure factors that are correlated with a causal factor for the actual effect. Multivariate analyses showed that the effect of all the personal exposures on cross-shift decrements in lung function was more prominent among sawmill and chip mill workers compared with joinery workers.

Non-Smokers and Smokers

The percentage decrease in lung function and percentage predicted lung function indices were shown to be significantly related to personal exposure to dust, endotoxins, (1->3)-b-D-glucans, Gram (-)ve bacteria and fungi. The correlations found between lung function indices and personal exposures indicated that airborne wood dust and biohazards associated with wood dust

(endotoxins, (1->3)-b-D-glucans, fungi and Gram (-)ve bacteria) have negative effects on the pulmonary function of woodworkers. 135

Only smokers demonstrated inverse correlations between percentage predicted lung function and the number of years of exposure, and cumulative dust indices

(for both inhalable and respirable dust). For non-smokers, the percentage predicted lung function was positively correlated with number of years of exposure. The most probable reasons for this might be that some workers developed tolerance to high dust exposure after working for a number of years with wood, and/or the “healthy worker effect”, where those workers who were sensitive to wood dust had left the jobs.

Non smokers had a marked deterioration in lung function on exposure to moulds compared with smokers. Previous studies have also shown that the symptoms associated with occupational mould exposure (eg. allergic alveolitis) are more common among non-smokers than smokers (Warren, 1977). Smoking has been reported to interfere with the immuno-responses of lungs (Holt and

Keast, 1977; Hocking and Golde, 1979) and this may explain why smokers are apparently less vulnerable to mould exposure. Table 3.7 Mean Personal Exposure Levels of Microorganisms (x103 cfu/m3) by Worksitea

A B C D E Fd Fg Fdg G H I J K L b microorganism n : (n=3) (n=3) (n=15) (n=10) (n=12) (n=5) (n=8) (n=13) (n=10) (n=10) (n=5) (n=6) (n=9) (n=11) fungi: Aspergillus fumigatus 39.86 18.09 5.16 6.45 1.63 .58 3.26 2.25 16.27 10.30 .99 3.51 1.99 2.34 Aspergillus versicolor 1.56 1.48 .61 .63 .41 .25 .20 .27 .20 .18 other Aspergillus spp. 0.23 .17 .68 .31 .14 .71 .06 .07 Eurotium spp. .22 .32 .19 Penicillium spp. 13.00 13.51 37.96 8.07 30.14 1.69 21.63 13.96 41.44 .66 .46 9.98 1.46 10.75 Paecilomyces spp. 0.50 .10 2.32 3.02 .22 .85 .61 15.07 1.41 .10 1.48 .40 3.46 Alternaria spp. 0.06 .17 .38 .12 .19 .11 .18 .15 .08 .17 Cladosporium spp. 2.46 3.07 1.14 .11 .24 .19 .19 .27 .10 2.97 .41 Aureobasidium pullulans .89 .48 .76 2.60 12.15 .11 13.42 8.30 .44 .90 Fusarium spp. 3.93 .88 1.34 1.55 2.47 .94 .58 .20 .94 .37 .13 Acremonium spp. 4.17 .41 1.50 .22 .11 yeast .89 .18 .47 .25 .63 .27 .40 .07 .34 .11 other fungi .06 .14 .55 .12 .16 .34 1.27 .08 .11 .79 total fungi 64.26 33.85 50.16 26.46 54.17 3.34 41.21 26.65 74.06 13.59 3.95 16.95 7.75 19.20 bacteria 8.86 9.96 21.43 5.19 22.40 9.19 17.56 14.34 20.56 25.72 2.86 3.00 23.00 4.40 Gram (-)ve bacteria 5.89 6.95 11.65 3.30 11.58 5.58 7.81 6.95 14.13 15.13 .44 1.53 12.86 2.08 a A, B - logging sites; C-F - sawmills (Fd-dry mill, Fg-green mill, Fdg – both dry mill and green mill); G - woodchipping mill; H-L – joineries. b number of workers sampled. Table 3.8 Mean Area Concentrations of Microorganisms (x103 cfu/m3) by Worksitea

A B C D E Fd Fg Fdg G H I J K L b microorganism n : (n=4) (n=2) (n=14) (n=16) (n=18) (n=5) (n=8) (n=13) (n=15) (n=5) (n=5) (n=5) (n=7) (n=10) fungi: Aspergillus fumigatus 7.02 5.15 1.58 0.37 0.30 0.33 0.69 0.49 1.10 1.16 0.29 0.40 0.21 0.13 Aspergillus versicolor 2.25 0.59 0.16 0.42 0.21 other Aspergillus spp. 0.50 0.52 0.21 0.15 0.12 0.14 0.19 0.20 0.92 0.81 0.11 Eurotium spp. 0.18 0.36 0.11 0.04 0.02 Penicillium spp. 17.20 24.63 65.88 8.62 18.07 2.51 5.86 4.00 15.76 0.40 0.19 1.48 0.46 8.46 Paecilomyces spp. 0.99 1.95 0.05 0.14 0.08 0.47 0.37 0.43 4.27 0.82 0.10 0.26 0.21 0.22 Alternaria spp. 1.88 0.49 0.40 0.12 0.11 0.14 0.12 0.11 0.33 0.07 0.05 0.06 0.02 Cladosporium spp. 6.85 6.12 2.76 0.82 2.14 1.41 0.15 0.73 0.52 0.18 2.09 0.56 Aureobasidium pullulans 0.92 1.09 0.04 2.28 1.69 2.02 0.21 0.06 0.11 Fusarium spp. 1.89 2.46 0.40 2.89 0.25 0.46 0.34 0.08 0.16 0.03 0.02 Acremonium spp. 0.46 0.24 4.67 0.19 0.40 yeast 6.12 0.58 1.20 1.73 1.43 0.21 0.13 0.03 0.03 other fungi 0.90 3.37 0.42 0.15 0.15 0.39 0.22 0.32 0.69 0.13 0.10 0.02 total fungi 30.71 46.65 76.35 8.81 30.07 8.52 13.42 10.70 22.99 4.17 2.33 3.38 3.38 9.75 bacteria 29.57 32.37 4.35 2.64 5.97 2.24 7.45 4.56 4.78 29.13 1.50 0.98 1.23 0.95 Gram (-)ve bacteria 10.12 13.34 2.23 1.76 1.29 0.89 1.24 2.18 3.10 19.28 0.23 0.18 0.65 0.11 a A, B - logging sites; C-F - sawmills (Fd-dry mill, Fg-green mill, Fdg- both dry mill and green mill); G - woodchipping mill; H-L – joineries. b number of samples. Table 3.9 Mean Personal Endotoxin Exposure Levels (ng/m3)

worksite inhalable endotoxin respirable endotoxin a b c AM GM GSD AM GM GSD logging site A 1.76 1.72 1.28 (1.29-2.28, n=4)d 0.16 0.15 1.44 (0.12-0.20, n=2) logging site B 1.30 1.28 1.27 (0.99-1.56, n=3) 0.13 0.13 1.12 (0.12-0.14, n=2) logging site (total) 1.56 1.52 1.32 (0.99-2.28, n=7) 0.14 0.14 1.28 (0.12-0.20, n=4) sawmill C 16.83 5.35 6.12 (0.19-78.40, n=22) 2.03 0.87 5.76 (0.1-5.25, n=6) sawmill D 2.27 1.95 1.78 (0.53-5.59, n=17) 0.18 0.16 1.49 (0.11-0.33, n=6) sawmill E 21.08 9.11 4.66 (0.39-73.63, n=24) 1.85 1.45 2.13 (0.61-4.45, n=11) sawmill F 8.09 2.69 4.42 (0.51-40.56, n=20) 1.20 0.50 5.02 (0.1-2.80, n=8) sawmill (total) 12.97 4.30 4.77 (0.19-78.40, n=83) 1.40 0.65 4.10 (0.1-5.25, n=31) woodchipping mill G 3.52 3.27 1.55 (2.00-4.87, n=5) 0.83 0.81 1.35 (0.49-1.02, n=5) joinery H 9.80 5.98 3.20 (0.60-27.88, n=13) 0.91 0.71 2.09 (0.30-2.04, n=12) joinery I 0.74 0.37 3.41 (0.10-2.36, n=12) 0.14 0.13 1.27 (0.10-0.20, n=8) joinery J 2.61 2.21 1.78 (1.30-7.04, n=12) 0.30 0.29 1.36 (0.18-0.40, n=5) joinery K 6.42 5.22 1.88 (2.37-17.88, n=17) 0.43 0.36 1.92 (0.15-0.83, n=7) joinery L 2.31 2.13 1.52 (1.18-4.72, n=11) 0.25 0.24 1.36 (0.19-0.44, n=7) joinery (total) 4.65 2.41 3.66 (0.10-27.88, n=65) 0.47 0.33 2.24 (0.10-2.04, n=39) a b arithmetic mean. geometric mean. c geometric standard deviation. d(range, number of workers sampled). Table 3.10 Mean Personal (1->3)-b-D-Glucan Exposure Levels (ng/m3)

worksite inhalable glucan respirable glucan a b c AM GM GSD AM GM GSD logging site A 3.35 1.98 3.62 (0.47-7.62, n=4)d 0.76 0.75 2.42 (0.64-0.88, n=2) logging site B 2.39 2.07 2.02 (0.95-3.74, n=3) 0.39 0.36 1.69 (0.25-0.53, n=2) logging site (total) 2.94 2.02 2.71 (0.47-7.62, n=7) 0.57 0.52 1.70 (0.25-0.88, n=4) sawmill C 4.33 2.13 3.98 (0.25-11.74, n=13) 0.52 0.31 2.25 (0.1-1.56, n=6) sawmill D 0.60 0.49 1.90 (0.20-1.46, n=11) 0.15 0.14 1.35 (0.1-0.25, n=6) sawmill E 4.78 2.75 4.02 (0.16-9.67, n=16) 0.40 0.29 2.47 (0.1-1.03, n=10) sawmill F 2.70 0.92 5.42 (0.16-7.65, n=14) 0.52 0.33 2.96 (0.1-1.24, n=6) sawmill (total) 3.28 1.37 4.42 (0.16-11.74, n=54) 0.40 0.26 2.53 (0.1-1.56, n=28) woodchipping mill G 4.63 2.32 4.71 (0.27-10.40, n=5) 0.85 0.76 1.64 (0.49-1.76, n=5) joinery H 0.51 0.50 1.22 (0.43-0.71, n=10) 0.12 0.12 1.19 (0.1-0.15, n=6) joinery I 0.33 0.33 1.11 (0.28-0.38, n=8) 0.11 0.11 1.15 (0.1-0.14, n=5) joinery J 0.71 0.59 1.86 (0.31-1.62, n=6) 0.21 0.20 1.16 (0.18-0.25, n=4) joinery K 0.35 0.30 1.73 (0.19-0.79, n=8) 0.12 0.12 1.12 (0.1-0.14, n=5) joinery L 1.09 0.49 4.01 (0.11-3.60, n=7) 0.18 0.16 1.69 (0.1-0.35, n=5) joinery (total) 0.57 0.43 2.01 (0.11-3.60, n=39) 0.14 0.14 1.39 (0.1-0.35, n=25) a b arithmetic mean. geometric mean. c geometric standard deviation. d(range, number of workers sampled). Table 3.11 Significant Correlations (Pearson’s R) among Mean Personal Exposure Levels of Dust, Bacteria, Fungi,

Endotoxin, and (1->3)-b-D-Glucan) (n = 62-160)

respirable inhalable respirable total Gram (-)ve inhalable respirable fungi dust endotoxin endotoxin bacteria bacteria glucan glucan inhalable dust 0.81** 0.58* 0.41 0.58* 0.58* -0.58* -0.60* -0.21 respirable dust 0.41 0.37 0.39 0.33 -0.52 -0.55 -0.25 inhalable endotoxin 0.84*** 0.84*** 0.90*** 0.31 0.11 0.50 respirable endotoxin 0.91*** 0.75** 0.38 0.45 0.46 total bacteria 0.90*** 0.21 0.06 0.27 inhalable glucan 0.86*** 0.86*** respirable glucan 0.76**

*p<0.05, **p<0.01, ***p<0.001 (two-tailed p). 136

3.5 QUESTIONNAIRE STUDY

3.5.1 USE OF RESPIRATORS

Only two worksites (joinery J and joinery K) provided all workers with appropriate respirators approved for wood dust by the WorkCover Authority,

NSW. Furthermore, the majority of workers did not wear respirators, and the workers, who did use them only wore them on average for less than 50% of the time during a workshift (Table 3.21). Interestingly, those who wore respirators in the sawmills and chip mills were mainly the maintenance staff and forklift drivers who did so primarily to avoid road dust exposure.

Table 3.21 Percentage of Workers Wearing Respirators

% of workers wearing respirators

80-100% 50-79% <50% total of the timec of the time of the time any respirator na sawmills 7.2 0.0 0.0 100.0 na woodchipping mill 36.7 18.2 9.1 72.7 a, na joinery 41.5 12.8 5.1 82.1 a, na all 25.8 12.3 5.3 82.5 approved respirator joinery 25.5 8.3 4.2 87.5 all 10.9 8.3 4.2 87.5 a na approved respirators. non-approved respirators. cno. of workers wearing respirators for 80-100% of the time during a workshift X 100%. total no. of workers wearing repirators 137

3.5.2 PREVALENCE OF WORK-RELATED SYMPTOMS

Table 3.22 presents the prevalence of work-related symptoms among woodworkers and controls. Woodworkers had markedly high prevalence of cough, phlegm, chronic bronchitis (persistent cough and phlegm for more than

3 months per year for more than 2 years), frequent headaches, sinus problems, throat and eye irritations, and nasal symptoms compared with controls

(Fig. 3.15). Particle-size distribution studies have shown that the major portion of wood dust is contributed by particles larger than 10 µm in diameter which can be easily trapped in the nasal passages (Hinds, 1988; Pisaniello et al.,

1991).

The prevalence of asthma, phlegm, wheezing, chest tightness, sinus problems, throat irritation, and nausea was high among joinery workers compared with sawmill and chip mill workers (Table 3.22, Fig. 3.16). Whereas the prevalence of eye irritation and regular ear inflammation and infections was high among sawmill and chip mill workers. Nasal problems were high in both groups compared with controls.

Table 3.23 represents the prevalence of work-related symptoms among high

(joineries H and K), medium (joineries J and L), and low (joinery I) dust exposure groups among joinery workers, and also dry mill and green mill workers of sawmills. Table 3.22 Percentage Prevalence of Work-related symptomsa among

Woodworkers and Controls

sawmill joinery woodworkersb controls and chipmill no.: 108 82 195 34 c age (yr) 38 ± 12.8 36 ± 14.7 37 ± 13.6 40 ± 11.3 years exposed (yr)c: 8 ± 8.7 12 ± 12.1 10 ± 10.5 9 ± 7.7 smoking: 40% 23% 33% 30%

Respiratory: asthma 8.3 13.4 10.8 5.9 dry cough 24.1 23.2 23.1 23.5 coughd 58.6*** 62.2*** 61.0*** 23.5 phlegme 46.0* 67.1*** 61.5*** 23.5 chronic bronchitis 29.6* 31.7 30.3* 11.8 breathlessness 18.5 18.3 17.4 14.7 wheezing 15.7 32.9* 22.6 11.8 chest tightness 21.3 36.6 27.2 17.6 dyspnoea 2.8 7.3 4.6 0.0

Nasal: regular dry nose 32.4 35.4 33.3 20.6 regular blocked nose 46.3* 63.4*** 42.6 29.4 regular itching or bleeding nose 25.9 22.0 23.6 14.7 regular runny nose 42.6** 51.2*** 54.4*** 17.6 regular sneezing 44.4** 46.3** 52.3*** 14.7 sinus problems 29.6* 35.4* 31.8* 11.8

Other: flu-like symptoms 29.6 29.3 28.7 14.7 frequent headaches 59.3*** 57.3*** 59.0*** 17.6 conjunctivitis 3.7 7.3 5.1 2.9 eye irritation 53.7*** 29.3 37.9* 17.6 regular ear inflammation/infections 16.7* 8.5 13.3 2.9 throat irritation 22.2* 51.2*** 32.8*** 5.9 vertigo 4.6 3.7 4.1 5.9 nausea 5.6 11.0 7.7 0.0 skin problems 15.7 25.6 20.0 14.7 aadjusted for age and smoking by logistic regression. bincluding workers at logging sites. cmean ± SD.

*p<0.05, **p<0.01,***p<0.001 (chi-square analysis; compared with controls). dusually cough during the day or at night? eusually bring up phlegm during the day or night? Table 3.23 Percentage Prevalence of Work-related Symptomsa among Joinery Workers and Sawmill Workers

joineryb sawmill

high med. low total dry mill green mill total no.: 30 20 32 82 34 53 87 age (yr)c: 25 ± 7.0 40 ± 15.7 45 ± 12.9 36 ± 14.7 38 ± 14.1 35 ± 11.6 36 ± 12.6 years exposed (yr)c: 5 ± 4.9 17 ± 15.0 15 ± 12.3 14 ± 12.1 5 ± 5.7 9 ± 10 7 ± 8.7 smoking: 17% 20% 31% 23% 44% 49% 46% Respiratory: asthma 16.7 10.0 12.5 13.4 11.8 7.5 9.2 dry cough 25.0 15.0 25.0 23.2 20.6 30.2 26.4 cough 66.7*** 40.0 40.6 62.2*** 29.4 50.9* 58.6*** phlegm 56.7* 38.1 18.8 67.1*** 29.4 43.3 46.0* chronic bronchitis 44.8** 30.0 21.9 31.7 11.8 37.7* 27.6 breathlessness 20.0 20.0 15.6 18.3 8.8 24.5 18.4 wheezing 30.0 25.0 40.6* 32.9* 8.8 24.5 17.2 chest tightness 36.7 35.0 37.5 36.6 11.8 28.3 21.8 dyspnoea 6.7 5.0 9.4 7.3 0.0 5.7 3.4

Nasal: regular dry nose 41.4 50.0* 25.0 35.4 29.4 41.5 35.6 regular blocked nose66.7** 60.0* 62.5** 63.4*** 41.2 49.1* 46.0 regular itching/bleeding nose 20.0 25.0 21.9 22.0 20.6 32.1 28.7 regular runny nose 46.7* 40.0 50.0** 51.2*** 44.1* 43.3* 43.7* regular sneezing 46.7** 50.0* 56.3*** 46.3** 47.1** 54.7*** 50.0*** sinus problems 53.3*** 40.0* 21.9 35.4* 23.5 34.0* 29.9

Other: flu-like symptoms 20.0 20.0 43.8* 29.3 17.6 35.8* 28.7 frequent headaches 56.7** 35.0 53.1** 57.3*** 52.9** 54.7*** 54.0*** conjunctivitis 10.0 10.0 3.1 7.3 2.9 3.8 3.4 eye irritation 20.0 25.0 40.6 29.3 29.4 49.1** 41.4* regular ear inflam./infections 13.3 10.0 0.0 8.5 8.8 5.7 6.9 throat irritation 50.0*** 40.0** 46.9*** 51.2*** 11.8 24.5* 19.5 vertigo 0.0 10.0 3.1 3.7 2.9 3.8 3.4 nausea 3.3 10.0 18.8* 11.0 8.8 5.7 6.9 skin problems 23.3 20.0 31.3 25.6 5.9 22.6 16.1 adata adjusted for age and smoking by logistic regression. *p<0.05, **p<0.01, ***p<0.001 (chi-square analysis; compared with controls). bhigh dust exposure group (GM: >6 mg/m3); medium dust exposure group (GM: <5 mg/m3); low dust exposure group (GM: <1mg/m3). cmean ± SD.

139

70

e 60 c n e l 50 a v e

r 40 p

e

g 30 a t n

e 20 c r

e 10 woodworkers p 0 controls c c e fr p ru s s th hr ou ye eq hl n in ne r o g . e n u e oa ni h irr h gm y s z t c it e n p in ir b a a o ro g ri ro tio da se b ta n n c le ti c h m on hi es s tis

symptom

Fig. 3.15 Prevalence of work-related symptoms among woodworkers compared with controls.

80

e 70 c n

e 60 l a

v 50 e r p 40 e g a

t 30 n

e joinery

c 20 r

e sawmill/chip mill p 10 0 control bl ch co ea ey fre ph ru si sn th w o r u r e q l n n e ro h ck o g i . eg n us e a ee e ni h nf irr h m y z t z d c la it e n p in ir in n b m a a o ro g ri g o ro m tio da se b ta s n a n c le ti e c t h m on hi io es s tis n

symptom

Fig. 3.16 Prevalence of work-related symptoms among joinery workers and sawmill and chip mill workers compared with controls. 140

Although the high dust exposure group had the least number of years of woodworking experience on average, low average age and low average smoking, they had high prevalence of most of the symptoms compared with the medium dust exposure group (Fig. 3.17). The prevalence of cough, phlegm, chronic bronchitis, regular blocked nose, regular runny nose and excess nasal secretion, regular sneezing, sinus problems, frequent headaches, and throat irritation was significant among the high dust exposure group compared with controls. Asthma, cough, phlegm, chronic bronchitis, and sinus problems had high prevalence in the high exposure group compared with those of medium or low dust exposure groups.

However, the low dust exposure group (joinery I), had high prevalence of wheezing, flu-like symptoms, eye irritation, skin problems and nausea compared with the medium or the high exposure groups. The personal dust exposure level of the low dust exposure group was very low (GM = 0.60 mg/m3) compared with that of the other two groups. The most probable reason for the high prevalence of some symptoms among the workers in the low dust exposure group may be because of their exposure to western red cedar (Thuja plicata), which is known to cause occupational asthma, dermatitis, and rhinitis among such populations (Vedal et al., 1986). 142

80

e 70 c n

e 60 l a

v 50 e r p 40 e

g high a

t 30 n

e medium

c 20 r

e low p 10 0 control bl ch co dr fre in ph ru si sn th w na o r u y q fl l n n e ro h u ck o g n . ue eg n us e a ee s e ni h o h n m y z t z e d c s e z n p in ir in a n b e a a o ro g ri g o ro da se b ta s n c le ti e c h m on hi es s tis

symptom

Fig. 3.17 Prevalence of work-related symptoms among high, medium, and low dust exposure groups of joineries compared with controls.

Among sawmill workers, the green mill workers had high prevalence of most of the respiratory symptoms except for asthma, when compared with the dry mill workers (Table 3.23). They also had high prevalence of sinus problems, flu-like symptoms, eye and throat irritation, and skin problems. As found for the joinery workers, the dry mill and green mill workers had high prevalence of nasal symptoms.

Compared with controls, the prevalence of cough, chronic bronchitis, regular blocked nose, regular runny nose and excess nasal secretion, regular sneezing, sinus problems, flu-like symptoms, frequent headaches, eye 143 irritation, and throat irritation was significant among green mill workers (Fig.

3.18).

60 e

c 50 n e l a

v 40 e r p 30 e g a t

n 20

e dry mills c r

e 10 green mills p 0 controls bl ch co ey fre in ru si sn th o r u e q fl n n e ro ck o g . ue n us e a e ni h irr h n y z t d c it e z n p in ir n b a a a o ro g ri o ro tio da se b ta s n n c le ti e c h m on hi es s tis

symptom

Fig. 3.18 Prevalence of work-related symptoms among dry mill and green mill workers compared with controls.

3.5.3 CORRELATIONS AMONG PERSONAL EXPOSURES AND WORK-

RELATED SYMPTOMS

Both the joinery workers and the sawmill and chip mill workers showed significant correlations between mean personal exposures and work-related symptoms after controlling for age and smoking (Table 3.24). The significant correlations indicated that the probability of getting work-related symptoms increases with increasing levels of personal exposures. 144

Table 3.24 Correlations among Mean Personal Exposures and Work-related

Symptoms among Joinery Workers and Sawmill and Chip Mill Workers

b d group of symptom exposure prevalence p value a c workers odds ratio joinery bronchitis inh..dust 2.26 (0.19-4.22) 0.009 phlegm 1.79 (1.05-3.04) 0.028 sawmill/chip mill ear inflam. 5.50 (1.07-28.29) 0.037 freq. headache 2.76 (1.01-7.57) 0.044 joinery bronchitis resp. dust 3.12 (1.23-7.96) 0.015 total eye irritation 1.94 (1.11-3.37) 0.017 joinery bronchitis inh. endotoxin 2.32 (1.25-4.30) 0.007 phlegm 1.76 (1.06-2.92) 0.026 total ear inflam. 1.81 (1.01-3.23) 0.040 throat irritation 1.53 (1.09-2.14) 0.012 joinery bronchitis resp. endotoxin 14.27 (3.36-60.58) <0.001 sawmill/chip mill bronchitis 2.34 (1.14-4.79) 0.018 ear inflam. 2.90 (1.07-7.86) 0.032 joinery bronchitis inh. glucan 20.00 (9.80-41.09) 0.007 sawmill/chip mill bronchitis 3.09 (1.37-6.98) 0.006 ear inflam. 7.49 (1.61-34.91) 0.009 total ear inflam 3.13 (1.70-5.73) <0.001 throat irritation 1.49 (1.00-2.23) 0.047 wheezing 1.58 (1.00-2.50) 0.048 joinery ear inflam. resp. glucan 29.99 (18.33-49.07) 0.016 sawmill/chip mill bronchitis 3.73 (1.37-10.11) 0.008 ear inflam. 33.22 (5.85-188.61) <0.001 throat irritation 2.79 (1.01-7.70) 0.044 total chest tightness 1.81 (1.02-3.22) 0.037 ear inflam. 7.29 (3.09-17.21) <0.001 wheezing 2.29 (1.19-4.39) 0.011 joinery bronchitis fungi 2.95 (1.31-6.65) 0.008 phlegm 2.00 (1.02-3.92) 0.041 sawmill/chi mill breathlessness 4.77 (1.36-16.69) 0.013 bronchitis 2.87 (1.14-7.23) 0.023 ear inflam. 13.32 (1.97-90.02) 0.007 total ear inflam. 2.69 (1.48-4.88) <0.001 throat irritaion 1.56 (1.15-2.10) 0.003 wheezing 1.41 (1.03-1.95) 0.031 joinery bronchitis Gram (-)ve bac. 4.16 (1.58-10.97) 0.003 sawmill/chip mill ear inflam. 5.36 (1.46-19.72) 0.010 total ear inflam. 2.78 (1.39-5.55) 0.003 a b joinery: n = 82, sawmill/chip mill: n = 108, total: n = 190. bronchitis = chronic bronchitis. 145 c odds ratio (95% confidence interval) using multiple logistic models (confounders adjusted: age and smoking), explogistic coefficient = odds ratio (OR). d *p<0.05, **p<0.01, ***p<0.001. Although personal exposure levels of respirable dust, (1->3)-b-D-glucans and endotoxins were very low, they still showed significant relationships with respiratory, throat, and ear problems among both groups. It has been reported that an increase in symptomatology occurs, when the (1->3)-b-D-glucan exposures are above 10 ng/m3 (Rylander, 1996). In the present study except for a few, a majority of the inhalable and all the respirable (1->3)-b-D-glucan exposures were much below 10 ng/m3. Previous studies on sick buildings have also reported dose-response relationships between low (1->3)-b-D-glucan exposures with eye and throat irritation, dry cough, and itching skin (Rylander et al., 1992) and with nose and throat irritation (Rylander, 1996). In the present study, dose-response relationships were found between mean personal respirable (1->3)-b-D-glucan exposures with chronic bronchitis (OR=3.73), throat irritation (OR=2.79), and regular ear inflammation and infections

(OR=33.22) among sawmill and chip mill workers. A significant correlation was found between mean personal inhalable (1->3)-b-D-glucan exposures and chronic bronchitis among joinery workers (OR=20). Frequent ear inflammation and ear infections was also significantly correlated with mean personal respirable glucan levels (OR=29.99) among joinery workers.

Significant correlations were also found between mean personal endotoxin exposures and bronchitis. Rylander (1985) reported that endotoxins contributed to develop bronchitis among those exposed to organic dust. Relationships were 146 also found between mean personal exposures of fungi and Gram (-)ve bacteria with respiratory, throat, and ear problems.

3.5.4 EFFECTS OF WORK-RELATED RESPIRATORY SYMPTOMS ON

LUNG FUNCTION

3.5.4.1 Effects on Cross-shift Change in Lung Function

Woodworkers showed statistically significant positive correlations between work-related respiratory symptoms and percentage cross-shift change

(decrease) in lung function (FVC, FEV1, FEV1/FVC, and PEF) (Table 3.25).

Positive correlation coefficients indicated that an increase in the percentage cross-shift change (decrease) in lung function was associated with respiratory symptoms. Among sawmill and chip mill workers, phlegm and regular blocked nose were significantly correlated with the percentage cross-shift decrease in

FVC. Such correlations were not observed among joinery workers.

Table 3.25 Significant Correlations between Percentage Cross-shift Change

(decrease) in Lung Function and Respiratory Symptoms among Joinery Workers and Sawmill and Chip Mill Workers group of % cross-shift decrease respiratory correlation- p valuee workersa in lung functionb symptomc coefficient (r)d total FVC phlegm 0.18 0.012 bronchitis 0.14 0.046 sawmill/chip mill phlegm 0.19 0.049 blocked nose 0.19 0.046 total FEV1 bronchitis 0.14 0.047 phlegm 0.17 0.017 total FEV1/FVC chest tightness 0.15 0.045 dyspnoea 0.15 0.034 total PEF phlegm 0.15 0.037 147 a b total: n = 168, sawmill/chip mill: n = 105. adjusted for age, height and smoking. c d e bronchitis = chronic bronchitis. by linear regression. *p<0.05, **p<0.01, ***p<0.001. 3.5.4.2 Effects on Percentage Predicted Lung Function

Both joinery and sawmill workers showed significant inverse relationships between respiratory symptoms and percentage predicted lung function

(Table 3.26). Among joinery workers percentage predicted lung function (FVC,

FEV1, FEV1/FVC, and FEF25-75%) were inversely correlated with phlegm.

Woodworkers (total) showed significant inverse correlations between percentage predicted lung function (FVC, FEV1, FEV1/FVC, and FEF25-75%) and chronic bronchitis and phlegm.

Table 3.26 Significant Correlations between Percentage Predicted

Lung Function and Respiratory Symptoms

group of % predicted respiratory correlation- p valuee workersa lung functionb symptomc coefficient (r)d

joinery FVC phlegm -0.22 0.045 sawmill/chip mill blocked nose -0.32 <0.001 total phlegm -0.17 0.018 bronchitis -0.14 0.046

joinery FEV1 phlegm -0.23 0.038 sawmill/chip mill blocked nose -0.26 0.007 total phlegm -0.18 0.011 bronchitis -0.16 0.024

joinery FEV1/FVC phlegm -0.26 0.020 sawmill/chip mill dyspnoea -0.20 0.038 phlegm -0.20 0.040 total phlegm -0.15 0.036 bronchitis -0.15 0.039

joinery FEF25-75% phlegm -0.22 0.050 sawmill/chip mill blocked nose -0.20 0.037 dry cough -0.20 0.043 phlegm -0.20 0.039 total phlegm -0.19 0.008 148

bronchitis -0.15 0.043

ajoinery: n = 63, sawmill/chip mill: n = 105, total: n = 168. badjusted for age, height, and smoking by multiple regression. cbronchitis = chronic bronchitis. dby linear regression. e*p<0.05, **p<0.01, ***p<0.001. 3.5.5 WOOD ALLERGIES

A number of workers complained about allergy problems, which they ascribed to exposure to various types of wood dust, during processing (Table 3.27).

Table 3.27 Wood Allergies reported by the Workers wood no. of workers (worksite) hazardous effects reported western red cedar 14 (joinery) skin, nasal (runny nose, continuous (Thuja plicata) sneezing) throat irritation, and mild asthmaa spotted gum 5 (sawmill) skin and nasal irritation (continuous (E. maculata) sneezing), sinus problems blue gum 3 (sawmill) nasal (runny nose) and throat (E. saligna) irritation, itchy arms and legs brush box 3 (joinery-1 nasal irritation (continuous sneezing, (Tristania conferata) sawmill-2) runny nose), frequent headache sinus problems, slight fever, clammy skin tallowwood 2 (sawmill) nasal and skin irritation (E. microcorys) splinter wounds getting infected

Oregon (Douglas fir) 2 (joinery) nasal irritation (continuous sneezing) (Pseudotsuga menziesii) white top box 1 (sawmill) nasal irritation (E. quadrangulata) tulip oak 1 (sawmill) nasal irritation (continuous sneezing) (Argyridendron sp.) camphor laurel 1 (sawmill) nasal irritation (runny nose, (Cinnamomum camphora) continuous sneezing), strong headache meranti (Shorea spp.) 1 (joinery) nasal irritation (blocked nose) and sinus problems pine (Pinus radiata) 1 (joinery) itchiness, clammy skin, slight fever 149 aonly two workers.

One worker reported an allergy to reconstituted wood. A joinery worker (at joinery H) complained that whenever he worked with MDF, any cuts, or scratches on his hands or arms would fester and take a long time to heal. He also reported eye irritation and excess nasal secretion problems. The major constituents of MDF particle boards are pulverized softwood and urea- formaldehyde resin, both of which are recognized as potential health hazards in the work environment (Priha, 1996). Wood dust and formaldehyde together have been reported to cause respiratory irritation with symptoms of dryness of throat, rhinitis, and eye irritation (Stump et al., 1986), as well as occupational skin disease (Vale and Rycroft, 1988).

3.5.6 DISCUSSION

Nasal problems, cough, phlegm, chronic bronchitis, frequent headache, eye and throat irritation were the most common symptoms reported by woodworkers. The high personal airborne dust exposure levels observed, as well as workers not wearing respirators might have contributed to the high prevalence of nasal symptoms. Overall, only 11% of the workers used appropriate respirators and among them, respirators were worn on average for less than 50% of the time during a workshift. Therefore, for exposure-response analyses, (irrespective of the use of respirators) all workers sampled were included. The South Australian study of Pisaniello et al. (1991) also reported a 150 high prevalence of nasal symptoms among furniture workers (regular blocked nose 51%, sneezing 41%, and regular runny nose and excess nasal secretion

45%), where the geometric mean exposure level was 2.9 mg/m3 (range 0.4-24 mg/m3). The prevalence of chronic bronchitis was significantly higher among the woodworkers than the controls. Among the woodworkers, smokers had a high prevalence of chronic bronchitis (20%) compared with the non-smokers

(10%). Previous studies have also reported a high prevalence of chronic bronchitis among woodworkers (Enarson and Chan-Yeung, 1990; Li et al.,

1990; Liou et al., 1996).

The prevalence of chest tightness at joineries was 37%, and at sawmills and chip mills, 21%. Among those having symptoms, 33% of joinery workers, 52% of sawmill and chip mill workers reported that they had symptoms on their first day back at work after weekend holidays. Monday-related chest tightness which was initially described among cotton workers, is now known to occur in other organic dust exposures such as swine confinement buildings, poultry plants and buildings with contaminated humidifiers (Rylander, 1989). The majority of sawmill workers and chip workers who had flu-like symptoms reported that once they had symptoms, it took several days to recover. Joinery workers also reported that they suffered from such symptoms when the airborne dust concentration was very high. Some workers reported that they had recovered by the next day, while others reported that their symptoms lasted for several days. 151

Among joinery workers, the high dust exposure group had high prevalence of asthma, cough, phlegm, chronic bronchitis and sinus problems compared with the medium or low exposure groups. The low dust exposure group (at joinery I) had high prevalence of wheezing, flu-like symptoms, eye irritation, skin problems and nausea compared with the medium or the high dust exposure groups. Joinery I processed only western red cedar. The dust level at this joinery (GM - 0.6 mg/m3) was much lower than the standard for softwood (5 mg/m3). This level is also below the OSHA standard (Federal Register, 1989) for western red cedar (2.5 mg/m3). A study of Vedal et al. (1986) reported that work-related eye irritation was seen more commonly with dust concentrations of

3 mg/m3. Joinery I imported red cedar timber from North America. Before processing, the timber stacks were air-dried outside for at least 3-5 months. It has also been reported that the wood can become more toxic on seasoning

(Senear, 1933). This could be one probable reason, for having symptoms at such relatively low exposures. Workers also reported a variety of allergy problems due to exposure to various types of wood dust (western red cedar, meranti, radiata pine, some eucalypt species, tulip oak, camphor, and Douglas fir) during wood processing.

Both the joinery workers and the sawmill and chip mill workers showed significant positive correlations between mean personal exposures and work- related symptoms. The effects of respiratory symptoms on percentage predicted lung function and percentage cross-shift decrease in lung function were also significant. These findings confirmed that wood dust is a potential health hazard. 152

3.6 OTHER OCCUPATIONAL HEALTH RELATED PROBLEMS OBSERVED

AT SAWMILLS AND CHIPPING MILLS

At sawmills and the woodchipping mill, forklift trucks made the road dust airborne. In particular, on windy days, the forklift operators, and those who worked in the timber and log yards were exposed to significant amount of airborne road dust (with personal dust concentrations ranging from 2-5 mg/m3).

Sometimes dust levels in the yard were so high that visibility was almost nil.

To increase the cutting life of the saw tips as well as to improve the surface finish of sawn timber, small cubes of stellite (IARC, 1991), a cobalt based alloy, containing a high percentage of cobalt and chromium, are welded by induction to the sharp edges of circular saws and band saws. Tungsten carbide cubes are also used for the same purpose.

Sawmill C did such welding without any exhaust hood, and the operator was not wearing any personal protective equipment. During such welding and grinding, the operator worked very close to the source. Some operators complained of continuous sneezing, sore throat and flu-like symptoms (perhaps

“metal fume fever”) (Morgan, 1989). None of the chip mills was fitted with an exhaust hood for the grinding of chipper blades. 153

To avoid the road dust problems, the following options should be considered:

- water sprinklers fitted to the ground

- sprinkling water to the ground with water bowsers

- providing forklifts with air-conditioned cabins

- providing the yard workers with appropriate dust masks and eye shields

Appropriate exhaust ventilation systems should be installed for the grinding process (ACGIH, 1995) and the operators should be provided with suitable personal protective equipment.

3.7 NASAL CANCER STATISTICS OF NSW 154

According to the National Institute of Health and Welfare, Canberra, Australia, during 1986-1993, 296 (212 male, 84 female) cases of nasal cancer (ICD 160, cancer of nasal cavity and paranasal sinuses) were reported in NSW. For a population of 5.8 million, this is about 6 cases per million per annum for NSW, which is similar to the UK (7-10 per million per annum) and Tasmania (5 per million per annum) (Franklin, 1982). Among the nasal cancer cases recorded for NSW, 85 cases (66 males and 19 females) were nasal adenocarcinoma.

The higher figures for males may implicate occupation as a major factor contributing to the cause of such cancers. The overall proportion of adenocarcinoma was 29% in NSW which is similar to Victoria (20%) and High

Wycombe, UK (25%), but much lower than that found in Tasmania (65%)

(Franklin, 1982). 155

CHAPTER 4

GENERAL DISCUSSION

This investigation of different woodworking processes (in New South Wales,

Australia) has confirmed that woodworkers from the tree felling stage onwards through various manufacturing processes are exposed to wood dust of different particle-sizes, concentrations, and compositions. Overall, 62% of the personal inhalable dust exposures exceeded the current exposure standards. Among joineries, 95% of the hardwood dust exposures and 35% of the softwood dust exposures were above the relevant standards. Sanding, wood turning, copy lathing, and routing were the main processes identified in the joineries which produced high personal airborne exposures. Among sawmills, 70% of the exposures from dry mills and 50% of the exposures from green mills exceeded the occupational standard for hardwood. None of the machines in the green mills was fitted with exhaust ventilation systems.

Personal exposure levels to fungi at logging sites and sawmills were in the range 103-104 cfu/m3 , at the woodchipping mill 103-105 cfu/m3 , and at joineries

102-104 cfu/m3 . The predominant species found at logging sites were

Aspergillus fumigatus and Penicillium spp.; at sawmills, Penicillium spp., and also Aureobasidium pullulans; at the woodchipping mill, Penicillium spp.,

Paecilomyces spp., and Aspergillus fumigatus. Penicillium glabrum was dominant among the Penicifflum species found. The sawmills, which employed kiln drying, had relatively low mould exposure levels. Although the levels of 156 fungi exposure found in this study were lower than those reported in Swedish (Belin,

1987) and Norwegian studies (Eduard et al., 1993), prolonged exposure to low concentrations can result in subacute development of allergic alveolitis (Jappinen et al., 1987). A British sawmill study (Halpin et al., 1994a) reported a 4.4% prevalence of symptomatic extrinsic allergic alveolitis among sawmill workers, in which the personal exposure levels to fungi were similar to those found in the present study.

Some personal exposures to endotoxins at the sawmills and a joinery exceeded the TLV of 20 ng/m3. The mean exposure levels of (1->3)-b-D-glucans were higher at the woodchipping mills, green mills, and the logging sites compared with the joineries. Significant positive correlations were found between personal airborne mean inhalable endotoxin levels with Gram (-)ve bacteria and for mean inhalable (1->3)-ß-D-glucan levels with total fungi. The correlations between personal mean respirable endotoxin levels vs. Gram (-)ve bacteria and personal mean respirable (1->3)-ß-D-glucan levels vs. fungi were also significant. The measurements of endotoxins and (1->3)-ß-D-glucans can have practical advantages over the counting of viable microorganisms, as they are more stable and can be measured over longer sampling periods.

The significant correlations found between lung function and personal exposures indicated that airborne wood dust, endotoxins, (1->3)-ß-D-glucans,

Gram (-)ve bacteria and fungi have negative effects on the pulmonary function of woodworkers. Significant correlations were also found between lung function 157 and number of years of exposure to wood dust and cumulative dust indices.

Multivariate analyses showed that the effect of all the personal exposures on cross-shift decrements in lung function was more prominent among sawmill and chip mill workers compared with joinery workers.

Woodworkers had significantly high prevalence of cough, phlegm, chronic bronchitis, frequent headaches, eye and throat irritations, and nasal symptoms compared with controls. The prevalence of chronic bronchitis was high among smokers (20%) compared with non-smokers (10%). The prevalence of asthma, phlegm, wheezing, chest tightness, sinus problems, throat irritation, and nausea was high among joinery workers compared with sawmill and chipmill workers.

The significant correlations found among personal exposures and work-related symptoms indicated that airborne wood dust, endotoxin, (1->3)-ß-D-glucan,

Gram (-)ve bacteria, and fungi have deteriorating effects on the health of woodworkers. Both joinery workers and sawmill and chip mill workers showed significant inverse correlations between percentage predicted lung function and respiratory symptoms.

Although inhalable dust exposures were high compared with the respirable dust exposures, some of the exposure-effects were associated with the lower airways of lungs. The inhalable fraction (0-100 pm in dia.) includes respirable fraction (<5 pm in dia.) as well, and most of the fungal spores are in the respirable range, which explains the effects in the lower airways. Furthermore, the dose-response relationships found shows that, not only the inhalable 158 fraction, but also the respirable fraction is important in evaluating the health effects of wood dust exposure.

Only 11% of the workers used appropriate respirators and among them, respirators were worn on average less than 50% of the time. Some workers reported a variety of allergy problems due to exposure to various types of wood dust during wood processing (western red cedar, meranti, pine, some

Eucalyptus species, tulip oak, camphor laurel and Douglas fir).

The elevated dust exposures observed are due to:

• lack of awareness of potential health effects of wood dust exposure among both management and workers

• aging equipment (in sawmills)

• inadequate and ineffective dust extraction systems or usually none (especially for hand-held tools)

• poor maintenance of the ventilation system at some worksites

• non-segregation of dusty processes

• dry sweeping, and

• the use of compressed air jets.

It was observed that there was a general lack of awareness of potential health effects among both the woodworkers and the management. When interviewed, a majority of workers indicated that they had no idea of potential health effects, 159

apart from occasional rare skin allergy to particular woods. Some answered

that, since wood is a natural cellulose substance, it wouldn't cause major health

effects. Similar responses were obtained from some of the management staff.

The determinant-of-exposure analysis was consistent with the field observations. The statistically significant determinants for personal airborne inhalable exposures were local exhaust ventilation, job title, use of hand-held tools, cleaning method used, use of compressed air, and green or dry wood processed.

It was observed that the larger companies usually had better control measures and hence lower exposure levels. The medium and small scale woodworking companies had the major dust exposure problems. Major dust problems were also observed at a worksite (investigated twice), which was graded for excellence in health and safety. The observed problems at the worksite included the use of aging equipment, poor maintenance of local exhaust ventilation systems, machines not fitted to any ventilation system, dust deposits on stored timber stacks and on all horizontal surfaces inside the mill, and leakage of dust from the joints (which were not properly sealed) of the central exhaust ventilation system.

For some machines, more effective enclosure and ventilation must be devised.

Improved designs do exist for some machines but these still need to be introduced into the workplace. Installation of enclosed booths should be 160 encouraged especially for sawmill operations, as these prevent worker exposure to both noise and dust, and ensure his safety as well. Personal behaviour can also influence an individual's exposure substantially. Behavioural differences are probably an important contributing factor to the wide range of exposures obtained at the same woodworking machines.

If at all possible, it is desirable to provide a safe and healthy work environment without the use of personal protective equipment. Although it is difficult to control dust completely, it is usually possible to control levels to within the occupational exposure limits with a well designed, efficient, properly used and maintained exhaust ventilation system. Personal protective equipment should only be used as a last resort. Worker comfort should also be considered, as the wearing of respirators (especially during hot summer months) makes the workers uncomfortable.

Both management and the workers showed great interest and co-operation

during this study. They want the relevant authorities to propose appropriate

control strategies and formally advise them on how to reduce exposures.

The present study has found that the personal dust exposures often exceeded

the current exposure standards (Worksafe, 1995). Moreover, this study

supports the contention that wood dust exposure is a major occupational health

hazard. The study also investigated the present status of ventilation systems

used in the different woodworking processes. The relevant authorities need to 161

help the industry take necessary steps to remedy the present situation,

especially regarding ventilation systems. A major conclusion of this study is that

appropriate control measures must be taken to reduce exposure at the source.

4.1 RECOMMENDATIONS FOR THE TIMBER INDUSTRY

The timber industry should:

• conduct awareness programs (eg. using booklets, video programs, etc.) of

potential health effects of wood dust exposure not only for woodworking

companies in the cities but also in rural areas throughout the country.

• make available appropriate and cost-effective wood dust control technologies for woodworking companies.

• educate both management and workers on the use and maintenance of exhaust ventilation systems, and also the use and maintenance of personal protective equipment.

• set up separate threshold limit values for allergenic wood (eg. the OSHA standard for western red cedar is 2.5 Mg/M3 [Federal register, 1989], which was established based on its allergenic properties). 162 4.2 FUTURE RESEARCH

Investigations should be carried out to further assess occupational health impacts and to improve the working conditions of woodworkers. The following areas should be considered:

• A thorough investigation of exhaust ventilation systems used in different woodworking processes should be carried out. In the present study, the ventilation systems were studied purely by visual inspection of the ductworks and the maintenance of the system. The adequacy, effectiveness, dust extraction efficiency, and connecting ductworks of ventilation systems should be studied technically in order to identify the major problems. This will help in determining appropriate remedial action in modifying or designing engineering controls.

• The seasonal variation of exposure to wood dust, microorganisms and their toxic constituents (endotoxin and (1->3)-ß-D-glucan) at woodworking places should be studied.

• Research on toxicity, especially of native hardwoods should be investigated as very little information exists regarding this field. The results will be useful in setting separate exposure standards for allergenic wood. 163

More research related to nasal mucostasis and pre-cancerous-lesions of the nasal mucosa of woodworkers should be undertaken in order to prevent serious nasal problems.

Nasal problems had remarkably high prevalence in the present study. It has been reported that the mucostatic factor in wood dust is of importance in the development of nasal adenocarcinoma because of the prolonged retention of dust in the nasal cavity (Andersen et al., 1977).

Immunoassay studies (Sandven and Eduard, 1990; Eduard et al., 1992;

1993; 1994) should be carried out to identify the specific agents in the environment (particularly moulds) to which the woodworkers have been exposed. This will help in identifying the prevailing work-related symptoms and in evaluating the prevalence of EAA and ODTS among woodworking populations. This may also be useful in evaluating control measures.

Epidemiological studies should be conducted to study long-term effects of exposure to dust and formaldehyde during the processing of reconstituted softwood (MIDF, particle boards) and plywoods. MIDIF is a wood based panel produced from wood fibre bonded with urea formaldehyde or melamine urea formaldehyde adhesives, which are recognized as potential health hazards in the work environment (Priha, 1996). Wood dust and formaldehyde together have been reported to cause respiratory irritation with symptoms of dryness of throat, rhinitis and eye irritation (Stump et al., 1986), as well as occupational skin disease (Vale and Rycroft, 1988). MIDF produces very fine 164

formaldehyde to the lower airways (Holmstorm and Wilheirrisson, 1988). A working group

of the IARC concluded that formaldehyde is probably carcinogenic to humans ([ARC,

1995). The evidence for formaldehyde carcinogenicity was strong for nasal and

nasopharyngeal cancer. A French study reported that exposure to both formaldehyde and

wood dust may increase the risk of nasal adenocarcinoma, compared with wood dust

exposure alone (Luce et al., 1993).

Occupational exposure to terpenes from sawfumes (generated during the

processing of coniferous logs) should be investigated. Sawfumes are

produced when lumber is sawn in bandsaws and when battens are edged.

Softwood sawlog production is a major woodworking operation in the timber

industry producing 978,621 cubic meter of sawlogs from softwood

plantations and 95,105 cubic meter from cypress pine annually (State Forest

Authority, 1997). Previous studies (Dalqvist et al., 1994; Hedenstierna et al.,

1983) have demonstrated that sawfumes can cause chronic obstructive

impairment in lung function.

Long term effects of occupational exposure to chemical preservatives,

organic solvents, and fungicides used during wood processing should be

investigated. 165

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Eucalypt Hardwood Forest

“Found virtually nowhere outside Australia, but within Australia found nearly everywhere, the eucalypt became the Universal Australian. Eucalptus is not only the Universal Australian, it is the ideal Australian-versatile, tough, sardonic, contrary, self-mocking, with a deceptive complexity amid the appearance of massive homogeneity, an occupier of disturbed environments, a fire creature.” - Stephen J. Pyne Burning Bush, A Fire History of Australia (1992) Fig. A2.1 Eucalypt hardwood forest in northern New South Wales.

Fig. A2.2 Spotted gum (Eucalyptus maculata).

Fig. A2.3 Blackbutt (Eucalyptus pilularis). Fig. A2.4 Ironbark (Eucalyptus paniculata). Fig. A2.5 Brush box (Tristania conferata). Fig. A2.6 Tallowwood (Eucalyptus microcorys). Fig. A2.7 Blue gum (Eucalyptus saligna). Fig. A2.8 Die-hard stringybark (Eucalyptus cameronii). Fig. A2.9 Ribbon gum (Eucalyptus viminalis). Fig. A2.10 Silver-top stringybark (Eucalyptus laevopinea). Fig. A2.11 and Fig. A2.12 Burning of a logged area of a hardwood forest (improves soil fertility and dispersal and germination of seeds). Descriptions of Fig. A2.1 - Fig. A2.10 (Forest Industries, 1992; Bootle, 1993)

Fig. A2.1 Eucalypt hardwood forest – Australia has approximately 43.2 million hectares of native forests. 7.1 million hectares of this are state forests managed specifically on a sustainable basis for wood production

Fig. A2.2 Spotted gum – Eucalyptus maculata; relatively common in NSW and Southern Queensland; use for heavy engineering construction, piles, poles, ship building, agricultural machinery, flooring, plywood; the main Australian species for handles subject to high impact forces (eg. axe handles).

Fig. A2.3 Blackbutt – Eucalyptus pilularis; A large hardwood growing in the coastal forests between Bega, New South Wales and Maryborough, Queensland. It is a major timber used in building framework and poles in NSW and Southern Queensland.

Fig. A2.4 Ironbark – Eucalyptus paniculata; A large hardwood relatively common in New South Wales and Queensland. It is used for heavy engineering construction, poles, sleepers, flooring, decking and shipbuilding.

Fig. A2.5 Brush box – Tristania conferata; A large hardwood, which grows on the edge of the rainforests from the central coast of New South Wales to Bowen, Queensland. The timber is used for flooring, cladding, panelling, mallets, pulley blocks and for bridge decking.

Fig. A2.6 Tallowwood – Eucalyptus microcorys; A large hardwood, which grows in the coast and coastal ranges between the Hunter River in New South Wales and the Maryborough district of Queensland. The timber is used for heavy engineering structures, sleepers, bridges, wharfage, flooring, cladding, sills, crossarms, poles, piles, cooling towers.

Fig. A2.7 Blue gum – Eucalyptus saligna; A large commonly occurring hardwood in coastal New South Wales. It is used for general building purposes, cladding, flooring, panelling and boat building.

Fig. A2.8 Die-hard stringybark – Eucalyptus cameronii; A large hardwood of occasional occurrence on the eastern edge of the Northern Tablelands of New South Wales. It is used for building framework.

Fig. A2.9 Ribbon gum (Manna gum) – Eucalyptus viminalis; A large hardwood, widely distributed in the cooler areas of Australia. The timber is used for internal joinery, furniture, panelling, flooring and for handles. The wood is of limited commercial availability because of seasoning problems.

Fig. A2.10 Silvertop stringybark – Eucalyptus laevopinea; A medium-sized hardwood, relatively common in Northern New South Wales. The timber is used for building framework, and for preservative treated posts and poles. APPENDIX B

Logging Sites

· logging during the olden days

· logging sites A and B Fig. A2.13 and Fig. A2.14 Logging during the olden days – the hard way ((photographs taken at Quambi Museum, Stroud, NSW).

Fig. A2.15 Marking a quality hardwood tree for retaining and propagation. Fig. A2.16 A habitat tree for retaining.

Fig. A2.17 Sharpening the teeth of a chain saw. Fig. A2.18 Protective clothing-chaps/cut-proof trouser, boots, ear-muffs, a hard hat, and a high visibility shirt. Fig. A2.19 Using a chain saw together with an axe and a wedge for tree cutting.

Fig. A2.20 Using jacking technique for directional felling of a tree (logging site B). Fig. A2.21 Tree felling at logging site A (without using a jack). Fig. A2.22 Cutting knots off a felled tree. Fig. A2.23 Tractor trailing logs to the logging site.

Fig. A2.24 Logging site A. Fig. A2.25 Debarking of logs using an excavator at logging site B.

Fig. A2.26 Trimming of logs at logging site B. Fig. A2.27 Measuring of logs at logging site B.

Fig. A2.28 Seal the date and the measurements on logs. Fig. A2.29 Grading a log by the state forest officer.

Fig. A2.30 Loading of logs to a truck. Fig. A2.31 Transport logs to sawmills. APPENDIX C

Woodworking Processes Carried out in Sawmills

· green mills

· dry mills

“Timber is the stuff of history. Timber kept us warm for a thousand centuries, saved Noah, built King Solomon’s temple, sacked Troy, symbolised our hopes of Heaven, discovered America and Australia, made Britain mistress of the seas, and keeps the flag flying still.” - O. D. A. Oberg C. M. G. Australian Timber Handbook, by Norman K. Wallis (1970) Processes Carried out in Green Mills

Fig. A2.32 A log yard - sawmill C.

Fig. A2.33 Graded logs according to the quality. Fig. A2.34 Safe unloading of logs (sawmill C).

Fig. A2.35 Unsafe unloading of logs (sawmill F). Fig. A2.36 Logs for the head rig saw (sawmill C).

Fig. A2.37 Head rig saw – circular saws (sawmill F). Fig. A2.38 Head rig saw – a Canadian saw (sawmill E). Fig. A2.39 Cutting a log using a Canadian saw (dust deposits on the roof). Fig. A2.40 Operating the band saw from an enclosed booth - sawmill C.

Fig. A2.41 Dust deposits near the band saw operation at sawmill C (the band saw operation was not segregated or fitted to a local exhaust ventilation system). Fig. A2.42 The jig saw operation - sawmill C. Fig. A2.43 The edging process - sawmill C.

Fig. A2.44 The resawing process (operated from an enclosed booth) – sawmill C. Fig. A2.45 The bench sawing at sawmill F (manually operated).

Fig. A2.46 The bench sawing (mechanically operated) – sawmill E. Fig. A2.47 Sorting process (manually operated) – sawmill C.

Fig. A2.48 The auto-docking process (consisted of no. of circular saws - mechanically operated).- sawmill C. Fig. A2.49 The sorting table - sawmill C.

Fig. A2.50 Sorting and manual stacking of timber - sawmill E. Fig. A2.51 Sawdust for fertiliser manufacture.

Fig. A2.52 Woodchips - to the export market or for landscaping. Fig. A2.53 A small chipper at sawmill E (1500 rounds/min).

Fig. A2.54 Dispose waste wood by burning - sawmill F.

Processes Carried out in Dry Mills Fig. A2.55 Air drying of green timber prior to kiln drying – sawmill F.

Fig. A2.56 Steam powered kilns at sawmill D (sawdust was used as the fuel to generate steam).

Fig. A2.57 An empty kiln chamber (steam pipes, dry and wet bulbs) Fig. 2.58 A steam powered kiln on operation – 390C Fig. A2.59 Inside the same kiln (temp. gradient – 55 0C). Fig. A2.60 Inside the same kiln (temp. gradient - 700C, high humidity). Fig. A2.61 A data monitor (relative humidity, wet and dry bulb temp. of kilns) Fig. A2.62 Reconditioning process (~890C, to release the internal stress and tension of timber).

Fig. A2.63 Solar-powered kilns at sawmill F (covered with polyethylene films, temp. inside - 600C, do not require data monitoring).

Fig. A2.64 An inside view of a solar-powered kiln (a natural de-humidification system). Fig. A2.65 A dry mill (effectively and efficiently exhaust ventilated) – sawmill F.

Fig. A2.66 A moulder (enclosed in a room, a noisy operation) – sawmill D. Fig. A2.67 A sawshop – sawmill D (moulder blades on the table).

Fig. A2.68 A moulder – sawmill F (enclosed and locally exhaust ventilated, a noisy operation). Fig. A2.69 The end-matcher - sawmill F (fitted to the central exhaust ventilation system through ducts).

Fig. A2.70 The end-matcher - sawmill D (not fitted to any dust extraction system). Fig. A2.71 The defective ripsaw – sawmill D. Fig. A2.72 The auto-docking machine - sawmill F.

Fig. A2.73 The cross-cut saw at sawmill D (not fitted to a local dust extraction system). 231

APPENDIX D

Woodworking Processes Carried out at

the Woodchipping Mill 232

Fig. A2.74 Defective logs (also called pulplogs) utilized for chipping.

Fig. A2.75 Logs for washing prior to chipping. 233

Fig. A2.76 Log washing (to remove dirt and mud).

Fig. A2.77 The Chipper (2000 rounds/min). 234

Fig. A2.78 Automatic sieving process (separates chips from saw dust and waste wood) – at the screen house.

Fig. A2.79 Saw dust for fertilizer manufacture. 235

Fig. A2.80 Waste wood pile.

Fig. A2.81 Burner – to burn waste wood (once in every six months). 236

Fig. A2.82 Woodchip pile.

Fig. A2.83 From the chip pile, chips are carried to ships by conveyor belts. 237

Fig. A2.84 Export woodchips to Japan by ships for the manufacture of high quality paper. 238

APPENDIX E

Joinery Operations

“Wood frames and sheaths our homes, furnishes the rooms, forms the fence, provides the gate. It spans the stream, supports the railroad, crates the goods, lifts the loads, carries the cargoes. It is the door of the house, the heat of the hearth, the board of the table, the frame of the bed, the wood of the cradle and the shell of the coffin. It is the gift of God and friend of man.” - Norman K. Wallis Australian Timber Handbook (1970) 239

Fig. A2.85 A large-scale joinery operation (joinery I) – low personal dust exposures.

Fig. A2.86 A medium scale joinery operation (joinery K) – although the static machinery and portable tools were fitted with local exhaust ventilation systems, the personal exposures were still high. 240

Fig. A2.87 A small scale joinery operation (joinery H) – personal dust exposures were very high (due to inefficient and inadequate exhaust ventilation, hand-held tools were not fitted to any dust extraction system).

Fig. A2.88 Hand routing process - joinery J (not fitted with an integral dust extraction system). 241

Fig. A2.89 Automatic router - joinery H.

Fig. A2.90 Use of compressed air to remove dust during routing process – Joinery K. 242

Fig. A2.91 The Inverted routing process - joinery K .

Fig. A2.92 Wood machining - joinery J. 243

Fig. A2.93 Trenching - joinery K.

Fig. A2.94 Docking (not fitted to any dust extraction system) – joinery H. 244

Fig. A2.95 Boring and drilling – joinery K.

Fig. A2.96 Horizontal band sander (the exhaust hood was fitted only to the head pulley) - joinery H. 245

Fig. A2.97 The copy lathing process (generates fine airborne dust) - joinery K.

Fig. A2.98 The copy lathing process (movable dust extraction hood was not fully efficient to extract all airborne dust) - joinery K. Fig. A2.99 Disc sander - joinery J. Fig. A2.100 Hand-held belt sander fitted to a dust collection bag - joinery I. Fig. A2.101 Hand routing process – joinery H. Fig. A2.102 Wood turning process – joinery K.

248

APPENDIX F

Process Flow Diagrams

· sawmills

· woodchipping mill G 249

·Armidale (l) ·Walcha (sm/wc) ·Kempsey (sm) New ·Kunda Bung (l) South ·Gloucester (sm) Wales ·Stroud (sm/wc)

·Sydney (j)

·Wollongong (j)

·Eden (wc)

Fig. A2.103 The locations of the worksites in NSW

(l) - logging site (sm) - sawmill (j) - joinery (wc) - woodchipping mill log yard

band saw chip pile screener

jig saw R

chipper resawing edger

waste wood

sorting auto docker table docker planer

saw dust

to sawmill D for kiln drying grading/stacking green timber for market

Fig. A2.104b Process flow diagram - sawmill C. 250

Logging Site

Debarked Logs

forest sawmill C Log Yard

Jig Saw Band Saw waste wood waste wood

Edger waste wood

waste wood Sorter Resaw waste wood

Docker waste wood Planer waste wood

Auto Stacker Auto Docker

waste wood

Sorting Table Chipper to sawmill D for Kiln Drying Screener Stacking/Grading

Chip Pile Market

to the Export Market

Fig. A2.104a Process flow diagram - sawmill C. 251 254

Debarked logs forest sawmill Canadian Saw

waste wood Bench Saw I

Planer Moulder waste wood Bench Saw II

Docker I Stacking Market waste wood

Dry Bench Docker II Table

waste wood Band Saw Chipper

Debarked Logs Screener

Wood Chips

Export Market

Fig. A2.106a Process flow diagram - sawmill E (mill I). 255

Debarked Logs

Canadian Saw

Bench Saw I

waste wood Docker I Stacking

Chipper waste wood Band Saw

Stacking Docker II Bench II

Debarked Logs

Fig. A2.106b Process flow diagram - sawmill E (mill II). 256 257 timber yard table

bench saw

wood chips screener defective R logs Canadian saw chipper

band saw sawlog offcuts

bench saw

log yard

stacking table timber yard

docker Fig. A2.106d Process flow diagram – sawmill E (mill II). wood chips saw dust

planer moulder timber yard screener table

R docker l docker

stacking/grading chipper bench saw II

waste wood

dry bench to the chipper

band saw

waste wood

Canadian saw bench saw I chipper Fig. A2.106c Process flow diagram of sawmill E (mill I). kiln dried timber for processing

Quality Kiln Dried Hard Wood

planer l Quality Kiln Dried Hard Wood Quality Kiln Dried Hard Wood

timber for flooring grader planer ll

end matcher

docker moulder auto docker

air drying of green timber

cyclone dust collectors solar powered kilns saw dust

Fig. A2.107c Process flow diagram – sawmill F (dry mill). auto docker Z K Z Q Q Z Q

saw dust pile K Z K Z Z Z Q Q K

docker lll log yard

stacks for kiln drying

Q Q Z K rechecking the logs Z graded by the Q docker ll forestry officer

circular saw

Q multi saw Q

K

Q

Q Q

bench saw ll

bench saw l

bench saw lll timber yard

grading and stacking timber from docker l

docker l Fig. A2.107b Process flow diagram – sawmill F (green mill). 258

Logging Site

Debarked Logs forest sawmill F

Log Yard

Band Saw

Multi Saw Bench Saw ll Bench Saw l

Docker l

Bench Saw lll

Grading and Stacking Market

Docker ll

Docker lll Docker lV Stacking for Kiln Drying

Stacking Stacking Air Drying (3-5 months)

Green Timber to the Market Kiln Drying (5 days)

Planer

End Matching

Moulding Kiln Dried Timber to the Market Auto Docker Grading for Flooring

Fig. A2.107a Process flow diagram - sawmill F. 259 260 reconditioner

air drying kiln 1, 2, 3 air drying

steam

kiln dried timber for processing

saw dust boiler crane rip saw moulder

stress grader

docker l

docker Il

table docker IIl docker

grading/stacking

storage of processed end matcher kiln dried timber

kiln dried timber kiln dried timber

Fig. A2.105b Process flow diagram – sawmill D. 252

Timber from sawmill C

Air Drying

Kiln Drying

steam Reconditioning Boiler

saw dust Moulder Stress Grader

saw dust Docker I

saw dust Docker II Rip Saw

End Matcher Sorting Table Docker

Grading/Stacking

Market

Fig. A2.105a Process flow diagram - sawmill D. 253 261

Logging Site forest ------woodchipping mill G Debarked Logs

Log Yard

Log Washing

Chipper

Chips from the neighbouring Screen House sawmills

Chips Waste Wood saw dust

Export Burner for fertilizer manufacture

Fig. A2.108a Process flow diagram - woodchipping mill G. 262 klinker

export chip pile burner wood chips from other sawmills

waste wood pile screen house

chipper R saw dust pile

washing logs

log yard

Fig. A2.108b Process flow diagram – woodchipping mill G. APPENDIX G

Fungi Identified from the Personal Airborne Samples

Collected from the Worksites

(medium: DG[18] – Dichloran glycerol agar,

SDA – Sabouraud dextrose agar,

PDA – Potato dextrose agar;

1 week old cultures) Fig. A3.1 Aspergillus fumigatus (DG, mag. x1000). Fig. A3.2 Aspergillus niger (SDA, mag. x100).

Fig. A3.3 Aspergillus flavus (PDA, mag. x 200). Fig. A3.4 Aspergillus nidulans (SDA, mag. x1000). Fig. A3.5 Hülle cells of Emericella nidulans (SDA, mag. x 200). Fig. A3.6 Aspergillus ochraceus (SDA, mag. x 200). Fig. A3.7 Eurotium chevalieri (SDA, mag. x 400). Fig. A3.8 Eurotium rubrum (SDA, mag. x1000).

Fig. A3.9 Cleistothecia of Eurotium rubrum (SDA, mag. x 200). Fig. A3.10 Eurotium amstelodami (SDA, mag. x 1000). Fig. A3.11 Eurotium repens (SDA, mag. x 100). Fig. A3.12 Penicillium glabrum (SDA, mag. x400).

Fig. A3.13 Penicillium glabrum (SDA, mag. x 1000). Fig. A3.14 Penicillium sp. (SDA, mag. x 400).

Fig. A3.15 Paecilomyces sp. (SDA, mag. x 400). Fig. A3.16 Aureobasidium pullulans (SDA, mag. x 400).

Fig. A3.17 Cladosporium sp. (SDA, mag. x 200). Fig. A3.18 Fusarium sp. (SDA, mag. x 1000).

Fig. A3.19 Fusarium chlamydosporum (SAB, mag. x 1000). Fig. A3.20 Curvularia sp. (SDA, mag. x 400).

Fig. A3.21 Drechslera sp. (SAB, mag. x 400). Fig. A3.22 Alternaria sp. (SDA, mag. x 400).

Fig. A3.23 Pseudallescheria boydii (SAB, mag. x 100). Fig. A3.24 Rhizopus sp. (SDA, mag. x 400).

Fig. A3.25 Syncephalastrum sp. (SAB, mag. x 400). 277

APPENDIX H

Colony Morphology of the Pure Cultures Prepared from

Aspergillus and Some Other Mould Species

Isolated from Airborne Samples

(medium: DG[18] - Dichloran glycerol agar

and SDA - Sabouraud dextrose agar

incubation temp.: 25-300C,

incubation period: <7 days) 278

Aspergillus species and their teleomorphs

Fig. A3.26 Asp. fumigatus (DG).

Fig. A3.27 Asp. niger (SDA). 279

Fig. A3.28 Asp. versicolor (SDA).

Fig. A3.29 Asp. flavus (DG). 280

Fig. A3.30 Asp. nidulans (SDA).

Fig. A3.31 Emericella nidulans (SDA). 281

Fig. A3.32 Asp. candidus (DG).

Fig. A3.33 Asp. wentii (DG). 282

Fig. A3.34 Asp. sydowii (DG).

Fig. A3.35 Asp. terreus (DG). 283

Fig. A3.36 Asp. flavipes (DG).

Fig. A3.37 Asp. ustus (DG). 284

Fig. A3.38 Asp. ostianus (DG).

Fig. A3.39 Asp. sclerotiorum (DG). 285

Fig. A3.40 Asp. ochraceus (DG).

Fig. A3.41 Eurotium repens (DG). 286

Fig. A3.42 Eurotium rubrum (DG).

Fig. A3.43 Eurotium chevalieri (DG). 287

Fig. A3.44 Eurotium amstelodami (DG - 4 days)

Fig. A3.45 Eurotium amstelodami (DG - 7 days). 288

Other moulds

Fig. A3.46 Penicillium sp. (SDA).

Fig. A3.47 Penicillium sp. (DG). 289

Fig. A3.48 Fusarium chlamydosporum (SDA).

Fig. A3.49 Paecilomyces sp. (SDA). 290

Fig. A3.50 Aureobasidium pullulans (SDA)

Fig. A3.51 Aureobasium pullulans (DG). 291

Fig. A3.52 Rhizopus sp. (SDA).

Fig. A3.53 Syncephalustrum sp. (SDA).