Part 2: Non-Asbestos occupational Respiratory Disease

Unlike asbestos-related respiratory conditions there has been less emphasis on the importance of occupational asthma, silicosis and work-related chronic obstructive respiratory disease in New Zealand until recent years. Nevertheless, there is a historical base to non-asbestos occupational respiratory disease as reference to the following brief summary indicates.

1938: Silicosis report of interdepartmental committee bulletin No 57, Department of Scientific and Industrial Research, Wellington.⁽¹⁾
This report noted that since the Miners' Phthisis Act of 1915, 1,576 miners had been granted pensions as a result of silicosis, 1,508 were described as gold miners and 68 as coal miners.

The 1940s: A record of tuberculosis morbidity in hospital nurses is recorded in the book Challenge for Health, by Dr F S McLean⁽²⁾, and 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 1524 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 has seen a significant output of publications on non-asbestos occupational respiratory disease, to a large extent due to the energy and drive of Professor Neil Pearce of the Massey Uuniversity Centre, together with that of Dr David Fishwick and Lisa Bradshaw. Over this period occupational asthma has been investigated nationally⁽⁴⁾ and among farmers⁽⁵⁾, sawmill workers⁽⁶⁾ and aluminium potroom workers⁽⁷⁾, while respiratory symptoms, lung function and dust levels have been measured in the wood industry^(8/9), plywood mill workers⁽¹⁰⁾, hairdressers⁽¹¹⁾, mussel openers⁽¹²⁾, welders^(13-18), and quarry workers⁽¹⁹⁾. Of this group, welders in particular have been intensely investigated.

At a 2005 scientific meeting in Christchurch, Rumball outlined concern at exposure to beryllium among aircraft engineering and maintenance workers, as well as cleaners and even the families of the workers. His presentation reinforced, if reinforcement was necessary, that dirty workplace air remains a major work environment issue and its consequences occupational lung disease is a continuing health hazard. At the same meeting, Short⁽²⁰⁾ presented a paper indicating that woollen mill workers showed significant across-shift changes in FEVv1, and other lung function indices.

Occupational asthma

In the Colt Lecture given by Anthony Newman Taylor at the Ninth International Symposium on Inhaled Particles at Cambridge Uuniversity in 2001⁽²¹⁾, Professor Taylor noted some pertinent points about this disease as follows:

• Asthma is the most prevalent cause in the Uunited 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 higher 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 clean up dirty workplaces can thus be seen as a practical response to the accumulating evidence relating to the causes of work-related asthma. In New Zealand a debate frequently ensues between 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, as both work-aggravated asthma 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 and the possibility 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.

Chronic obstructive pulmonary disease

Chronic obstructive respiratory disease (CORD), or as it is now more commonly referred to as Chronic Obstructive Pulmonary Disease (COPD), "is the fourth leading cause of death worldwide"⁽²²⁾. It is defined as a condition with airflow limitation which is not fully reversible and which is progressive and 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 is linked to the development of this disease. It is, thus, now recognised as an occupational disease in certain situations with likely additive effects occurring between smoking and some workplace exposures.

Contaminants of air, which have been associated in studies with work-related COPD, include welding fumes, silica, coal, oil mist, Portland cement, cotton, grain and wood dusts.⁽²³⁾

Diagnosis of COPD requires both a clinical and occupational approach, and as far as the latter is concerned, a careful occupational history is required. That is, a chronological list of jobs, what the job entailed, what respiratory exposures occurred, to what extent and for how long. The exposure index methodology used for asbestos and, as illustrated, is an example.

Silica and silicosis - one agent, many outcomes

In a review of the outcome of silica exposure Steenland⁽²⁴⁾ 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 currently 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⁽²⁵⁾. 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 0.2 mg/m³ (the current New Zealand workplace exposure standard).

References

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

2. Maclean, ES. Challenge for Health 1964. Government Printer, Wellington.

3. de Hamel, FA. 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. Occup. Environ. Med. 1997; 54: 301-306.

5. Asthma and allergy in New Zealand farmers. M. Kimbell-Dunn, L.M. Bradshaw et al Am. J. Industrial. Med. 1999; 35: 51-57.

6. Asthma and other respiratory symptoms in New Zealand pine processing sawmill workers. J. Douwes, D. McLean et al. Am. J. Industrial Med. 2001; 39:608-615.

7. Potroom asthma: New Zealand experience and follow-up. T.Vv. O'Donnell, B. Welford and E.D. Coleman. Am. J. Industr. Med. 1989; 15:43-49.

8. Worker exposures to airborne dust, endotoxin and B (1, 3) - glucan in two New Zealand sawmills. J. Douwes, D. McLean etc al. Am. J. Industrial. Med. 2000; 38:426-430.

9. Wood dust exposure in small New Zealand woodworking companies. D McBride, K. Nelsen. J. Occupational. Health Safety Aust. NZ. 2004; 20: 465-472.

10. Respiratory symptoms and occupational exposures in New Zealand plywood mill workers. W Fransman, D. McLean et al. Am. Occup. Hyg. 2003; 42: 287-295.

11. Occupational respiratory symptoms in New Zealand hairdressers. T Slater, L. Bradshaw et al. Occup. Med. 2000; 50: 586-590.

12. Work-related respiratory symptoms and lung function in New Zealand mussel openers. WI. Glass, P. Power et al. Am. J. Industr. Med. 1998; 34: 163-168.

13. Chronic interstitial lung disease in a welder of galvanised steel. WI. Glass, D.B. Taylor, A.M. Donoghue. Occup. Med. 1994; 44:158-160.

14. Transient changes in the pulmonary function of welders: A cross-sectional study of Monday peak expiratory flow. A.M. Donoghue, WI. Glass, G.P. Herbison. Occup. Environmental. Med. 1994; 51:553-556.

15. Chronic bronchitis, work-related respiratory symptoms, and pulmonary function in welders in New Zealand. L.M. Bradshaw, D. Fishwick et al. Occup. Environmental. Med. 1998; 55:150-154.

16. Two year follow-up of pulmonary function values among welders in New Zealand. R Erkinjuntti-Pekkanen, T. Slater et al. Occup. Environmental. Med. 1999; 56:328-333.

17. Exposure to fumes in typical New Zealand welding operations. E. Dryson, D. Rogers. New Zealand Med. J. 1991; 104:365-367.

18. Respiratory symptoms, across-shift lung function charges and lifetime exposures of welders in New Zealand. D. Fishwick, L. Bradshaw et al. Scand J. Work. Environmental. Health. 1997; 23:351-358.

19. Respiratory health and silica dust levels in the extractive industry in New Zealand. WI. Glass, D. McLean et al. Occ. Health Report Series, No. 9. 2003; 25.

20. Respiratory symptoms and airflow limitations in woollen mill workers: Are they associated with workplace exposures? M.T. Short, Dissertation for MFOM(I) 2005.

21. Asthma and work. Anthony Newman Taylor. Ann. Occup. Hyg. 2002; 46:563-574.

22. Occupation and COPD. D.C. Christiari. Occup. Environmental Med. 2005; 62:215.

23. Occupational contribution to the burden of chronic obstructive pulmonary disease. John Balmes. J.O.E.M. 2005; 47:154-160.

24. One agent, many diseases: exposure-response data and comparative risks of different outcomes following silica exposure. K. Steerland. Am. J. Industr Med. 2005; 48:16-23.

25. Exposure to alpha quartz dust in New Zealand Industries. E. Nicol, Occ. Health 1982; 4:1, 30-36.

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