Abstract

The International Expert Meeting on Asbestos, Asbestosis, and Cancer was convened in Helsinki on 20-22 January 1997 to discuss disorders of the lung and pleura in association with asbestos and to agree upon state-of-the-art criteria for their diagnosis and attribution with respect to asbestos. The group decided to name this document The Helsinki Criteria. The requirement for diagnostic criteria was perceived
in part because of new developments in diagnostic methods, with better identification of asbestos-related disorders. Such developments enhance awareness of health
hazards imposed by asbestos, lead to practical prevention and appropriate compensation, and also provide an opportunity to carry out international comparisons. They also provide possible models for the risk assessment of other mineral dusts. The meeting was attended by 19 participants from 8 countries not producing asbestos. The chairmen were
Professor Douglas W Henderson (Flinders Medical Centre, Australia) and Professor Jorma Rantanen (Finnish Institute of Occupational Health, Finland). The group was a multidisciplinary gathering of pathologists, radiologists, occupational and pulmonary physicians, epidemiologists, toxicologists, industrial hygienists, and clinical and laboratory scientists specializing in tissue fiber analysis. Collectively, the group has published over 1000 articles on asbestos and associated disorders. This document is based on a more comprehensive report providing scientific evidence for the conclusions and recommendations (People ard Work Research Reports, no 14, Finnish Institute of Occupational Health, Helsinki, 1997).

Asbestosis is generally associated with relatively high exposure levels with radiological signs of parenchymal fibrosis. However, it is possible that mild fibrosis may occur at lower exposure levels, and the radiological criteria need not always be fulfilled in cases of histologically detectable parenchymal fibrosis. The recognition of asbestosis by chest radiography is best guided by standardized methods such as the classification of the International Labour Organisation (ILO) and its modifications. Standard films must always be used. For research and screening purposes, radiological
findings of small opacities, grade 110, are usually regarded as an early stage of asbestosis. Inspiratory basilar sales, restrictive impairment, small airway obstruction, and gas exchange disturbances in pulmonary function are considered valuable information for clinical diagnosis, for occupational health practice, and for
attribution purposes. HRCT can confirm radiological findings of asbestosis and show early changes not seen on chest X rays, but should be performed only in selected cases.
Smoking effects should be considered in the evaluation of early asbestosis, lung function tests, and respiratory symptoms.
A histological diagnosis of asbestosis requires the identification of diffuse interstitial fibrosis in well inflated lung tissue remote from a lung cancer or other mass lesion, plus the presence of either 2 or more asbestos bodies in tissue with a section area of 1 cm2 or a count of uncoated asbestos fibers that falls into the range recorded for asbestosis by the same laboratory.

There is evidence that rare cases of asbestosis occur without significant numbers of asbestos bodies. These cases are recognizable - and distinguishable from idiopathic pulmonary fibrosis - only by analysis of the uncoated fiber burden. Rare cases of asbestosis in relation to the inhalation of pure chrysotile can occur, with a
prolonged interval between the last exposure and the diagnosis and few or no detectable asbestos bodies and a low fiber burden. The existence of such cases is speculative and, if the diagnosis can be made, it must be done from other compelling clinical or radiological grounds combined with exposure data.
Fibro-inflammatory patterns other than conventional asbestosis have also been described for workers with occupational exposure to asbestos, including a DIP pattern

Estimates of the relative risk for asbestos-associated lung cancer are based on different-sized populations. Because of the high incidence of lung cancer in the general population, it is not possible to prove in precise deterministic terms that asbestos is the causative factor for an individual patient, even when asbestosis is present. However, attribution of causation requires reasonable medical certainty on a probability basis that the agent (asbestos) has caused or contributed materially to the disease.
The likelihood that asbestos exposure has made a substantial contribution increases when the exposure increases. Cumulative exposure, on a probability basis, should thus be considered the main criterion for the attribution of a substantial contribution by asbestos to lung cancer risk. For example, relative risk is roughly doubled for cohorts exposed to asbestos fibers at a cumulative exposure of 25 fiber-years or with an equivalent occupational history, at which level asbestosis may or may not be present or detectable. Heavy exposure, in the absence of radiologically diagnosed asbestosis, is sufficient to increase the risk of lung cancer. Cumulative exposures below 25 fiber-years are also associated with an increased risk of lung cancer, but to a less extent.
The presence of asbestosis is an indicator of high exposure. Asbestosis may also contribute some additional risk of lung cancer beyond that conferred by asbestos exposure alone. Asbestosis diagnosed clinically, radiologically (including HRCT), or histologically can be used to attribute a substantial causal or contributory
role to asbestos for an associated lung cancer. Pleural plaques are an indicator of exposure to asbestos fibers. Because pleural plaques may be associated with low levels of asbestos exposure, the attribution of lung cancer to asbestos exposure must be supported by an occupational history of substantial asbestos exposure or measures of asbestos fiber burden. Bilateral diffuse pleural thickening is often associated with moderate or heavy exposures, as seen in cases with asbestosis, and should be considered accordingly in terms of attribution.
A minimum lag-time of 10 years from the first asbestos exposure is required to attribute the lung cancer to asbestos.
Not all exposure criteria need to be fulfilled

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