Papers on occupational lung disease 1989-94

Author: Stenton S C 1995

INTRODUCTION:

The lungs present a surface area to the environment of about 70m2 and the average adult inhales about 15,000 L of air each day1. It is hardly surprising therefore that those who work in contaminated environments develop respiratory diseases, or that these were among the first occupational disorders to be recognised.

The history of occupational lung disease over the 20th century has been one of constant change. Mechanisation in mines led to epidemics of coal workers pneumoconiosis and silicosis. The increasing use of asbestos for thermal insulation led to asbestosis and a variety of other conditions. The industrial processes which led to these diseases are now carefully controlled (at least in developed countries), although because of long latency periods, a legacy of ill health will remain for several more decades. At the same time other diseases have emerged or become recognised. Airflow obstruction in miners2, occupational asthma in a wide variety of industries3, pneumonia amongst welders4, legionellosis in those working close to contaminated water systems5, multiply resistant tuberculosis among hospital staff6, and others. The following collection of papers reviews and describes a number of developments in the field of occupational lung disease over the last decade.

Pneumoconiosis in coal miners has been recognised as an industrial disease for $ decades. In the past, simple pneumoconiosis was considered to be a benign disorder though complicated pneumoconiosis has always been known to be associated with impaired lung function. More recently, a debate has emerged over whether coal dust can cause airflow obstruction in the absence of complicated pneumoconiosis. The scientific issues have become interwoven with political considerations leading to the ‘Black Lung’ legislation in the USA, and to the recognition of airflow obstruction amongst miners as a prescribed industrial disease in the UK in 1993. Airflow obstruction and mining2 reviews the scientific background to this disease.

Whilst the incidence of coal workers pneumoconiosis has decreased steadily since the 1960s, occupational asthma appears to be increasing in prevalence. It is a disease which was rarely mentioned 40 years ago, but it is now the most commonly reported occupational lung disease. This might represent increased recognition, an increased incidence due to increased exposures to low molecular weight asthmagenic chemicals, or even an amplifying effect of occupational exposures on an increasingly propensity to develop asthma amongst the population. It is an important area of research not only because of the morbidity and economic loss which it engenders, but because occupational asthma presents a very useful model of asthma in general. Occupational asthma3 reviews the current state of knowledge in this field.

The increasing prevalence of asthma in westernised countries is now a matter of considerable public concern and research effort. Investigation of cases of occupational asthma might be able to offer some clues. The Barcelona epidemics illustrate how an recognised occupational asthmagen (soy dust) can cause sensation and a localised high incidence of asthma in non working populations7. Formaldehyde8 looks at another issue – the health risks of formaldehyde in indoor environments – and shows how information derived from relatively heavily exposed working populations can be used to place risks to non-working populations in context.
To obtain useful results from scientific research requires careful attention to methodology. Statistical aids in the recognition of late asthmatic reactions9 describes two novel techniques for recognising late asthmatic reactions. When used in place of traditional and entirely arbitrary techniques for recognising late reactions (eg defining any fall in ventilatory function of 15% or more from baseline as a late reaction10), they allow much smaller late reactions to be detected, whilst offering protection against false positive diagnosis.

Glutaraldehyde, asthma, and work – a cautionary tale11 illustrates one case in which the statistical techniques were applied. It shows how after careful investigation, a diagnosis of occupational asthma can appear much less convincing than the history or even the results of an uncontrolled, unblended challenge test might suggest. It illustrates the need for caution in diagnosing a new or relatively new occupational disease, particularly when irritant or pungent chemicals are under investigation, when the level of concern is high, or when litigation is contemplated.

The value of questionnaires and spirometry in asthma surveillance programmes in the workplace12 illustrates how similar caution needs to be applied in epidemiological investigations of working populations. Symptoms recorded on a respiratory questionnaire which was designed to detect asthma performed very poorly. Airway responsiveness measurements were a much better guide to previous diagnoses of asthma and to the use of medication. This outcome was not found in a similar study of the general population13 and was probably a consequence of biases which are peculiar to working populations, such as a reluctance to admit symptoms or an exaggerated awareness of symptoms when there are concerns about occupational exposures. It illustrates the importance of objective tests in establishing a diagnosis if it is likely to result in important management decisions.

Asthmagenic properties of a newly developed detergent ingredient: sodium iso-nonanoyl oxybenzene sulphate14 and Occupational asthma due to a repair process for polyethylene cables15 describe two new causes of occupational asthma. The SINOS studies were one of the first to demonstrate a log-linear dose response relationship for late asthmatic reactions and were an important testing ground for the statistical techniques described above. Initially it was suspected that the log-linear dose-response relationships indicated an unusual mechanism for SINOS asthma, though ultimately SINOS asthma was found to bear all the hallmarks of typical occupational and was presumed to have an immunological basis. The polyethylene cable repair process involved the liberation of the reactive chemical agent dicumyl peroxide which acted as a cross linking agent. It was typical of a low molecular weight asthma inducer.

It is sometimes felt that modern occupational medicine is merely a matter of applying legislation and controlling exposures, and that clinical skills are of secondary importance16. The lessons from occupational lung disease are that new conditions will continue to arise and will pose diagnostic problems in individuals and in groups of workers. The refinement of clinical investigative and epidemiological skills is therefore no less important to this than to any other field of medicine.


1. Gardner DE, Kennedy DL. Methodologies and technology for animal inhalation toxicology studies. In: Gardner DE, Crapo JD, McClennan RO (eds). Toxicology of the lung. New York, Raven Press, 1993.

2. Stenton SC, Hendrick DJ. Airflow obstruction and mining. Occupational Medicine: State of the Art Reviews 1993; 8: 155-70.

3. Stenton SC, Hendrick DJ. Occupational asthma. Postgrad Med J 1991; 67:271-77.

4. Coggan D, Inskip H, Winter P, Pannett B. Lobar pneumonia: an occupational disease in welders. Lancet 1994; 344:41-3

5. Tyndall RL, Solomon JA, Christenson SW. Legionnaires’ disease bacteria in power plant cooling systems: Downtime report. Oak Ridge National Laboratory, Tennesee, 1985.

6. Cauthen C, Jarvis JR. Hospital outbreak of multidrug-resistant Mycobacterium tuberculosis infections. Factors in transmission to staff and HIV-infected patients. JAMA 1992; 268: 1280-6.

7. Hendrick DJ. Asthma: epidemics and epidemiology. Thorax 1989; 44: 609-13

8. Stenton SC, Hendrick DJ. Immunology and allergy clinics of North America 1994; 14: 35-57

9. Stenton SC, Avery AJ, Walters EH, Hendrick DJ. Statistical approaches to the identification of late asthmatic reactions. Eur Respir J 1994; 7: 806-12

10. Boulet LP, Roberts RS, Dolovitch J, Hargreave FE. Prediction of late asthmatic responses to inhaled allergen. Clin Allergy 1984; 14: 379-85.

11. Stenton SC, Beach JR, Dennis JH, Keaney NP, Hendrick DJ. Glutaraldehyde, asthma and work – a cautionary tale. Occup Med 1994; 44;95-8

12. Stenton SC, Beach JR, Avery AJ, Hendrick DJ. The value of questionnaires and spirometry in asthma surveillance programmes in the workplace. Occup Med 1993; 43: 203-6

13. Devereux G, Ayatollahi SMT, Bourke SJ, Hendrick DJ. Effects of gender and geography on the prevalence of asthma symptoms and airway responsiveness. Am Rev Respir Dis 1994; 149: A915

14. Stenton SC, Avery AJ, Walters EH, Hendrick DJ. Asthmagenic properties of a newly developed detergent ingredient: sodium iso-nonanoyl oxybenzene sulphonate. Br J Indust Med 1990; 47: 405-10.

15. Stenton SC, Kelly CA, Walters EH, Hendrick DJ. Occupational asthma due to a repair process for polyethylene-coated electrical cables. J Soc Occup Med 1989; 39; 33-4.

16. Seaton A. Occupational medicine – let’s keep our white coats and stethoscopes. Occup Med 1993; 43: 63-4.
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