Part 2: Non-Asbestos Occupational Respiratory Disease

There has been little emphasis on the importance of occupational asthma, silicosis and work-related chronic obstructive respiratory disease in New Zealand until recent years. However, there is a historical base to non-asbestos occupational respiratory disease as referenced below:

1938

Silicosis: Report of Interdepartmental Committee, Bulletin No 57, Department of Scientific and Industrial Research, Wellington^[1].

This report noted that since the 1915 Miners' Phthisis Act, 1,576 miners had been granted pensions as a result of silicosis; of those, 1,508 were described as gold miners and 68 as coal miners.

1940s

A record of tuberculosis morbidity in hospital nurses recorded in the book Challenge for Health by Dr F.S. McLean^[2] showed a morbidity rate per 1,000 nursing staff which ranged from 8.9 to 20.3, averaging 16.5 over the years 1943-1949.

1961

The Grey Valley Survey^[3] in which Dr Francis de Hamel surveyed 1,524 miners and ex-miners in the coal industry during 1958 revealed only 32 cases of pneumoconiosis, not all of whom had worked in New Zealand coal mines.

The 1990s

This period saw a significant output of publications on non-asbestos occupational respiratory disease, to a large extent due to Professor Neil Pearce of the Centre for Public Health Research at Massey University, together with Dr David Fishwick and Lisa Bradshaw. Over this period occupational asthma was investigated nationally^[4] among farmers^[5], sawmill workers^[6] and aluminium workers^[7]; at the same time respiratory symptoms, lung function and dust levels were measured in the wood industry^{[8] [9]}, plywood mill workers^{[10] [11]}, hairdressers^[12], mussel openers^[13], welders^{[14] [15] [16] [17] [18] [19] [20] [21]} and quarry workers^[22].

2000

In 2000 Dr Jeroen Douwes joined the Centre, accelerating the interest in sawmill workers, wood dust and respiratory effects.

2.1 Occupational Asthma

In the Colt Lecture given by Anthony Newman Taylor at the Ninth International Symposium on Inhaled Particles at Cambridge University in 2001^[23], Professor Taylor noted some key points about this disease:

• Asthma is the most prevalent cause in the United Kingdom, and probably in the western world, of respiratory ill health during working life
• Asthma consists of variable airflow limitation, reversibility and hyper-responsiveness of the airways
• Asthma can be induced by direct toxic damage to the lining of the airways (irritant inducers) or the RADS phenomenon, or as a result of a specific hypersensitivity response to inhaled proteins and low molecular weight chemicals
• Asthma can be incited in persons who already have hyper-responsive airways when exposed to pollutants in the workplace air
• Evidence is strong that the risk of developing occupational asthma is determined more by the level of exposure to the risk factor than by individual susceptibility
• Asthma induced by work exposures carries a high risk of progression to chronic asthma
• There is evidence that the extent of occupational asthma can be reduced by reducing the airborne concentration of the causative agents.

The current programme of the Department of Labour to investigate dirty workplace air is a practical response to the accumulating evidence relating to the causes of work-related asthma.

In New Zealand a debate frequently occurs regarding work-aggravated asthma (WAA), and work-induced asthma (occupational asthma), largely related to whether a compensation claim is accepted or not. While this debate may be relevant to the issue of compensation, it is clearly not relevant to reducing and minimising the impact of asthma at work. This is because both work-aggravated and work-induced asthma are a consequence of exposure to dirty workplace air, and the outcome of both types of asthma is seen in lost time from work. The possibility is that what begins as asthma may in time, if exposure continues, lead to a lack of reversibility and the development of chronic obstructive respiratory disease.

In confirming a case of occupational asthma the Panel requires the following:

• A diagnosis of asthma
• Asthma occurring for the first time at work (work-induced asthma) or asthma made worse at work (work-aggravated asthma)
• A work history of exposure to an asthmagen or to a substance that can irritate the respiratory tract
• Supportive peak flow records indicating a temporal relationship between work and symptoms/peak flow
• Evidence of reversibility.

2.2 Occupational Asthma Case Studies

Case 1

This case concerned a 44 year old woman who began work as a hospital cleaner, then in mid 2003 worked in theatre as a sterile technician for 15 hours a week. She was exposed to "Shipshape" (a scourer), and "Epizyme" (a washing fluid which was heated, forming a mist). Epizyme contained cellulose, amylase, lipase and proteinase.

Some five to six months after beginning work, she noticed sneezing, reddened eyes and a cough, worse during work days and better in the weekend.

Four months later her symptoms worsened with breathlessness, wheeze and back pain. She had a nine-month period off work with improvement of her lower respiratory tract symptoms after about three months, but not her upper respiratory tract symptoms.

On returning to work to the hospital her symptoms returned and remained for the next two years.

Epizyme was ultimately identified as a potential cause and removed, with a gradual improvement of her chest symptoms, but persistence of her upper respiratory tract symptoms. Her past history indicated no childhood asthma, hay fever or eczema. She was an ex-smoker of 20 years.

Investigations showed normal lung function and chest X-ray. There were no work-related serial peak flow tests available. A methacholine bronchial provocation test with a PC20 of 1.4mg/ml showed moderate hyper-responsiveness. Reviewing her history there was latency between her first exposure and development of her upper respiratory tract symptoms, and a further latency before her lower respiratory tract symptoms occurred - a pattern typical in asthma due to enzyme exposure.

There was a work-relatedness with her symptoms in the initial stage of her exposure, and the chemicals are known asthmagens. Her outcome to date has not been one of recovery as she now has a non-specific bronchial hyper-responsiveness as a result returning to work even though the enzymes have been removed.

Case 2

This case concerned a 54 year old woodworker who used western red cedar, macrocarpa and occasionally rimu and Oregon pine in the manufacture of timber doors and windows. In the first two to three years he had no health problems. Over a Christmas holiday, he developed upper respiratory tract symptoms with sneezing and itchy eyes which continued on his return to work, gradually involving his lower respiratory tract with cough and phlegm, breathing difficulties and "chills". He noted that the symptoms were worse at work, improving when away from work. He now finds that cold winds and exercise act as respiratory irritants.

In his past history he had no childhood asthma or hay fever and is a very modest ex-smoker with a pack per year history of two to three.

His spirometry was normal, his skin tests for atopy negative apart from a small reaction to house dust. No peak flow measurements were available.

The diagnosis was made from his history and his exposure to a known asthmagen (western red cedar) which contained plicatic acid, a sensitising agent. The slow development of his condition, first upper airway symptoms then lower airway symptoms, was consistent with such exposure.

Case 3

This case involving a 27 year old male was less clear cut. He had a previous history of working in the boat building industry and cabinet making, but without symptoms. He then began a boilermaking apprenticeship where he worked in a large, dusty factory and was exposed to welding fumes. After some two months he developed a mild cough and tiredness. This improved over the two week Christmas break with the symptoms returning when he recommenced work.

He then had a job on a fishing boat below deck, removing steel tanks by grinding the steel into strips. Beneath the steel there was polyurethane foam which was caught up in the hot grinding disc. There were significant fumes in this confined space, and a fan had been installed and a paper filter mask provided. He worked for two hours then had a break. On his second "shift" he was the only individual doing this job and the fan had been removed. He felt unwell, dizzy, and had a nasty taste in his mouth. He went on deck for a break before returning to complete the task over the remaining four hours. That evening he had a blocked nose, headache, flu-like symptoms, cough and was short of breath, finding it difficult to breathe. He saw his General Practitioner who recorded "moist chest sounds".

Investigations showed a normal X-ray, normal spirometry, no bronchial hyperactivity (methacoline challenge), peak flows unconvincing, positive atopic skin test, negative isocyanate IgE.

The respiratory physician raised the possibility of asthma, but this could not be confirmed.

2.3 Metal Fume Fever

This condition which commonly occurs to welders cutting or welding galvanised steel, as well as less commonly to workers exposed to other freshly formed metal oxides produced during high temperature processes.

Metal fume fever is usually a self limiting systemic condition occurring four to 12 hours after exposure and characterised by fever, muscle aches and pains, malaise, cough and a metallic taste in the mouth. Recovery usually takes 24 hours and unless the doctor asks about a patient's occupation it is usually diagnosed as the common "flu".

In 2004 the Journal of Occupational and Environmental Medicine published a paper on the inflammatory responses and oxidative stress in a group of automotive welders in Taiwan. The main findings of this relatively small cross-sectional study were:

1. Higher values for average urine zinc, nickel and copper in full time welders than in a control group
2. A correlation between average urine zinc, nickel and copper levels and hours of welding per week
3. A finding that 17.7% of welders had experienced flu-like symptoms in the course of their career^[24]
4. Urine zinc levels were associated with white blood count, neutrophil count, eosinophal cancer and inter leukin-6, suggesting the inflammatory response might be mediated by cytokines
5. The results confirm other studies that welding fume exposure is associated with systemic inflammatory responses as indicated by increased levels of white blood cells and neutrophils while the raised eosinophal levels might suggest an allergic mechanism where local injury results in inflammation with the release of a histamine-like substance
6. It was also noted that smoking was significantly associated with urine zinc and nickel levels.

2.4 Chronic Obstructive Pulmonary Disease

Chronic obstructive respiratory disease (CORD), or Chronic Obstructive Pulmonary Disease (COPD), as it is now more commonly referred to, "is the fourth leading cause of death worldwide"^[25]. It is defined as a condition with airflow limitation which is not fully reversible, is progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Historically, and still, the major cause is cigarette smoking. However, there is increasing evidence indicating that exposure to dusts, gases, and fumes at work are linked to the development of COPD. As a result, it is now recognised as an occupational disease in certain situations, with likely additive effects occurring between smoking and some workplace exposures.

Contaminants of air associated in studies with work-related COPD, include welding fumes, silica, coal, oil mist, Portland cement, cotton, grain and wood dusts^[26].

Diagnosis of COPD requires both a clinical and occupational approach and as far as the latter is concerned, a careful occupational history. That is, a chronological list of jobs, what the job entailed, which respiratory exposures occurred, to what extent and for how long.

As a consequence, the panel is now not only recording the presence of COPD in asbestos diagnosed cases, but also in asbestos exposed and non-asbestos exposed cases.

2.5 Silica and Silicosis - One Agent, Many Outcomes

Silica is the most common element found in the earth's crust. When combined with other substances, silica is relatively harmless. Silicosis is a serious lung condition described by the ILO as an accumulation of dust in the lungs and the tissue reaction to its presence. It is caused by inhaling airborne crystalline silica dust in high concentrations over a period of time.

In a review of the outcome of silica exposure Steenland^[27] noted "evidence in recent years indicates that silica causes lung cancer, and probably renal disease, in addition to its well-known relationship to silicosis" and, as indicated in the previous section, it can also result in Chronic Obstructive Pulmonary Disease.

While silicosis is rarely diagnosed in New Zealand, there is evidence that most New Zealand rocks contain some quartz and with erosion and quarrying the quartose sands tend to contain a higher content of quartz than the parent material^[28]. This was re-affirmed in the extractive industry study where the dust measurements carried out by the Department of Labour showed that in 13% of the air samples collected, levels of respirable quartz exceeded 0.2mg/m³ (the current New Zealand workplace exposure standard).

2.6 Indoor Air Quality (IAQ)

An article on particle emission characteristics of office printers^[29] revealed that among 62 printers investigated, while 60% did not emit submicrometer particles, 40% did, among which 27% were high emitters. However, there is no data to link any harm to these exposures. Office-related respiratory conditions have been recognised for some years with pollutants entering the office environment from outdoor air, as well as pollutants arising form within the office environment. These include organic vapours (VOCs), fibres and inorganic gases. With increasing numbers of office workers, attention to indoor air quality is as important as attention to factory and outdoor (quarries, construction) air. The article makes the point that by identifying the high emitters and recognising emitting rates are printer-type specific and are affected by toner cartridge age, such contaminants of indoor air "can be reduced by a proper choice of printers".

2.7 Recent "New" Work-Related Occupational Respiratory Disease

In an editorial in Occupational Environmental Medicine Kreiss^[30] looked into the future. She noted recent, "new", occupational respiratory diseases such as flock workers' lung - an interstitial lung disease - hypersensitivity pneumonitis associated with bio-contaminated synthetic metal working fluids, asthma associated with 3-amino-5-mercapto-1, 2, 4-triazole (AMT) in herbicide manufacture, and bronchiolites obliterans from flavouring chemicals used in popcorn plant workers.

Kreiss wrote of barriers to recognition of new respiratory diseases, including:

• Clinicians too readily attributing lung disease to smoking
• The lack of work-related symptoms in some diseases, i.e. occupational industrial diseases
• Long latency of some diseases
• Lack of knowledge by physicians of patients' workplaces and hazards

With regard to recognition of new diseases, she instanced the value of a national state-based surveillance system for occupational asthma.

As to the future and emerging causes of occupational lung disease, Kreiss cites asthma related to damp offices. "Building dampness can be considered an emerging cause of occupational lung disease because we are still unsure of causal agents ..."

In addition, Kreiss raises the issue of COPD and states: "Although 80% of COPD is attributable to smoking, most of the remainder is likely to have occupational causes." She goes on to say that "control recommendations can be made, even when such relations are based on surrogate exposures and before specific aetiological agents or safe levels of exposure are known".

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References

1 Silicosis Report of Interdepartmental Committee Bulletin no. 57, Department of Scientific and Industrial Research 1937 Government Printer, Wellington.

2 McLean, E.S. Challenge for Health 1964. Government Printer, Wellington.

3 de Hamel, F.A. The Grey Valley Survey 1961. Department of Health, Wellington.

4 Occupational Asthma in New Zealanders: A Population-Based Study. D. Fishwick, N. Pearce et al. Occupational and Environmental Medicine 1997; 54: 301-306.

5 Asthma and Allergy in New Zealand Farmers. M. Kimbell-Dunn, L.M. Bradshaw et al. American Journal of Industrial Medicine 1999; 35: 51-57.

6 Asthma and Other Respiratory Symptoms in New Zealand Pine Processing Sawmill Workers. J. Douwes, D. MacLean et al. American Journal of Industrial Medicine 2001; 39: 608-615.

7 Potroom Asthma: New Zealand Experience and Follow-Up. T.V. O’Donnell, B. Wellford and E.D. Coleman. American Journal of Industrial Medicine 1989; 15: 43-49.

8 Worker Exposures to Airborne Dust, Endotoxin and B(1, 30 – Glucan) in Two New Zealand Sawmills. J. Douwes, D.MacLean et al. American Journal of Industrial Medicine 2000;38: 426-430.

9 Wood Dust Exposure in Small New Zealand Woodworking Companies. D. McBride, K. Nelse. The Journal of Occupational Health and Safety – Australia and New Zealand, 2004; 20: 465-472.

10 Respiratory Symptoms and Occupational Exposures in New Zealand Plywood Mill Workers. W. Fransman, D. MacLean et al. American Occupational Hygiene 2003; 42: 287-295.

11 Pine Dust, Atopy and Lung Function: A Cross-Sectional Study in New Zealand Sawmill Workers. J. Douwes, D. MacLean, T. Slater, N. Travier, S. Cheng, N. Pearce. European Respiratory Journa. 2006; 28: 791-798.

12 Occupational Respiratory Symptoms in New Zealand Hairdressers. T. Slater, L. Bradshaw et al. Occupational Medicine 2000; 50: 586-590.

13 Work-Related Respiratory Symptoms and Lung Function in New Zealand Mussel Openers. W.I. Glass, P. Power et al. American Journal of Industrial Medicine 1998; 34: 163-168.

14 Chronic Interstitial Lung Disease in a Welder of Galvanised Steel. W.I. Glass, D.B. Taylor, A.M. Donoghue. Occupational Medicine 1994; 44: 158-160.

15 Transient Changes in the Pulmonary Function of Welders: A Cross-Sectional Study of Monday Peak Expiatory Flow. A.M. Donoghue, W.I. Glass, G.P. Herbison. Occupational and Environmental Medicine. 1994; 51: 553-556.

16 Chronic Bronchitis, Work-Related Respiratory Symptoms, and Pulmonary Function in Welders in New Zealand. L.M. Bradshaw, D. Fishwick et al. Occupational and Environmental Medicine 1998;55: 150-154.

17 Two Year Follow-Up of Pulmonary Function Values among Welders in New Zealand. R. Erkinjuntti-Pekkanen, T. Slater et al. Occupational and Environmental Medicine 1999; 56: 328-333.

18 Exposure to Fumes in Typical New Zealand Welding Operations. E. Dryson, D. Rogers. New Zealand Medical Journal 1991; 23: 351-258.

19 Respiratory Symptoms, Across-Shift Lung Function Changes and Lifetime Exposures of Welders in New Zealand. D. Fishwick, L. Bradshaw et al. Scandinavian Journal of Work and Environmental Health. 1997; 23:351-358.

20 Changes in Work Practice after a Respiratory Health Survey among Welders in New Zealand. T. Slater, R. Erkinjuntti-Pekkanen, D. Fishwick, L. Bradshaw, N. Pearce, S. Cheng, H. Armstrong, D. McLean. New Zealand Medical Journal 2000 July 28; 113 (1114): 305-8.

21 Respiratory Symptoms and Lung Function Change in Welders: Are they associated with Workplace Exposures? D. Fishwick, L. Bradshaw, A. Curran, N. Pearce. New Zealand Medical Journal 2004 May 7; 117 (1193): U872.

22 Respiratory Health and Silica Dust Levels in the Extractive Industry in New Zealand. W.I. Glass, D. McLean et al. Occupational Health Report Series, No. 9 2003; 25.

23 Asthma and Work. Anthony Newman Taylor. Ann. Occupational Hygiene 2002; 46: 563-574.

24 Inflammatory Responses and Oxidative Stress from Metal Fume Exposure in Automobile Welders. Luo, Jiin-Chyuan John, Hsu, Kuang-Hung, Shen, Wu-Shiun. Journal of Occupational And Environmental Medicine 2009;51(1): 95-103.

25 Occupation and COPD. D.C. Christiani. Occupational and Environmental Medicine 2005; 62: 215.

26 Occupational Contribution to the Burden of Chronic Obstructive Pulmonary Disease. John Balmes. Journal of Occupational and Environmental Medicine 2005; 47: 154-160.

27 One Agent, Many Diseases: Exposure-Response Data and Comparative Risks of Different Outcomes Following Silica Exposure. K. Steenland. American Journal of Industrial Medicine 2005; 48: 16-23.

28 Exposure to Alpha Quartz Dust in New Zealand Industries. E. Nicol. Occupational Health 1982; 4:1, 30-36.

29 Particle Emission Characteristics of Office Printers. Congreve H. E. Congrong, L. Morawska, L. Taplia. Environmental Science and Technology 2007; 41:17 6039 – 6045.

30 Emerging Opportunities to Prevent Occupational Lung Disease. Kathleen Kreiss. Occupational and Environmental Medicine 2007; 64: 499-500.