Studies over the past few decades have showed a clear association between cigarette smoking and the development of chronic airway obstruction. Yet, only a minority of smokers is affected so that in many, even heavy, smokers, pulmonary function remains within normal limits. While carcinogens have been well characterized, there is only limited information about the constituents of cigarette smoke responsible for inducing chronic airway obstruction. In addition, the associated risks factors for airway obstruction in smokers have not been totally identified. The present paper is a review of the recently accumulated facts concerning the intimate action of cigarette smoke at the level of large and small airways and lung parenchyma. The role of classical inflammatory cells such as neutrophils and alveolar macrophages is reviewed, but emphasis is put on recent evidence indicating the involvement of CD8 + T-lymphocytes and possibly eosinophils in the genesis of the structural changes leading to airways obstruction. The mechanisms by which airway inflammation and remodelling cause airway narrowing and airflow limitation are discussed, along with the associated loss of lung elasticity secondary to destructive emphysema. Other biological, epidemiological, physiopathological, and clinical aspects are analyzed, stressing such fundamental aspects as the defence mechanisms, the morpho-functional correlations, the identification of susceptible smokers, and the early detection of airway obstruction, both in specialized laboratories and in primary care.

A cross sectional study was conducted on 513 employees at three hard metal plants: 425 exposed workers (351 men, 74 women) and 88 controls (69 men, 19 women). Cough and sputum were more frequent in workers engaged in "soft powder" and presintering workshops compared with controls (12-5% and 16X5% v 3 5%). Spirometric abnormalities were more frequent among women in sintering and finishing workshops compared with control women (56-8% v 23-8%) and abnormalities of carbon monoxide test were more frequent in exposed groups than in controls; this difference was more pronounced in women (31[4% v 5-6%) than in men (18-5% v 13%). No significant correlation was observed between duration ofexposure and age adjusted lung function tests. Slight abnormalities of chest radiographs (0/1, 1/1 according to ILO classification) were more frequent in exposed men than controls (12-8% v 1-9%) and mostly in soft powder workers. In subjects with abnormal chest radiographs FVC, FEV1 and carbon monoxide indices (fractional uptake of CO or CO transfer index or both) were lower compared with those with normal chest radiographs. Although relatively mild, the clinical, radiological, and functional abnormalities uncovered call for a regular supervision of workers exposed to hard metal dust.The industrial use of hard metal tools began in Germany in 1922. Owing to their hardness and resistance to wear and high temperatures they are used to make cutting tools, drill tips, and armament components. Their qualities are due mainly to tungsten carbide which, with cobalt (Co), constitutes the essential part of this alloy. They are produced according to the powder metallurgy technique in specialised factories in relatively large quantities (in France 300 tons a year at present).About 20 years later, hard metals were suspected of being responsible for bronchopulmonary disorders, first in Germany, then in the other industrialised countries. Despite a certain heterogeneity of the symptoms and signs, the condition progresses towards a diffuse pulmonary fibrosis and leads to severe respiratory insufficiency. Except for sporadic case reports, the frequency and intensity of clinical and functional respiratory disorders which can be observed among a group of workers exposed to hard metal dust are not well known. Thus a cross sectional survey was conducted among a group of 425 workers exposed to hard metal dusts and of 88 controls who worked in three factories.

Cedex, and Lormines, 57703 Hayange, France ABSTRACr Eleven hundred and nine iron mine workers aged 35 to 55 with normal chest radiographs were submitted to a pulmonary examination consisting of a questionnaire, a clinical examination, and pulmonary function testing including an acetylcholine challenge test. A positive response (decrease of FEV, of more than 10%) was observed in 210 subjects (Ace+). The remaining 899 had a negative response (Ace-). Bronchitis, asthma, dyspnoea, and obstructive syndrome were more frequent in the Ace+ group. Five years later, 820 subjects were reexamined: occasional cough and sputum and chronic bronchitis appeared more frequently among subjects without symptoms at the first examination but with a positive acetylcholine challenge test. The obstructive syndrome was more often observed and regressed more rarely in the Ace+ group. The results confirm the use of a test of bronchial hyperreactivity as a means of identifying subjects at risk from chronic obstructive lung disease.The concept that bronchial hyperreactivity was important in the evolution of chronic obstructive lung disease (COLD) was introduced by Dutch investigators.' 2 Pharmacodynamic tests using acetylcholine, metacholine, or histamine may be used to evaluate the degree of hyperreactivity.36 Initial work by Tiffeneau et a13-6 on the ventilatory effect of acetylcholine concerned asthmatic subjects during remission. It is now known, however, that bronchial hyperreactivity may occur not only in asthma but also in other conditions as a response to inhaled irritants and infections. The mechanism of this hyperreactivity is complex and not yet fully understood; nevertheless, it remains a criterion to be taken into account when evaluating the diagnosis and prognosis of COLD, the decrease in forced expiratory volume in one second (FEV,) being correlated with the degree of methacholine reactivity as was pointed out by Barter and Campbell7 and Minette8 in their longitudinal studies of bronchitic patients.In 1973 a recommendation was made by the working group on "functional respiratory tests in

Lung function was studied in 354 coke oven plant workers in the Lorraine collieries (Houilleres du Bassin de Lorraine, France) who retired between 1963 and 1982 The aim of this work was to study the long term effect of occupational exposure on lung function in retired coke oven workers from the HBL. This work is part of a study on mortality and morbidity in survivors.'7 It continues a previous study carried out in 1983 on mortality which showed an excess of mortality from lung cancer (standardised mortality ratio (SMR) = 2 51) with reference to the French male population.'8 Material and methodsThe study sample consisted of all the male workers from the two coke oven plants who had retired between 1 January 1963 and 31 December 1982 (536 subjects) and who were still alive on 1 January 1988 (354 subjects). They were born between 1902 and 1935. Executives were excluded from the study.The subjects were asked to attend a medical examination at the firm's occupational health centre. The protocol included a standard questionnaire, conducted by the occupational physician, concerning diseases treated or followed up for more than five years (cardiovascular, respiratory, digestive, infectious, and psychiatric diseases, traumas, cancers, etc), the questionnaire for the study of chronic bronchitis and pulmonary emphysema of the European Steel and Coal Commission (ECSC) of the EC,'9 and the notion of "regular overconsumption" of alcoholic drink. Because of low numbers we did not distinguish between smokers and ex-smokers. The respiratory symptoms taken into account were chronic bronchitis defined by a daily cough and phlegm for three consecutive months each year over a period of two years, wheezing or chest noises heard daily, day and night, and dyspnoea classified into five stages.To be aware of the respiratory symptoms in the period nearing retirement we sought information 316 on 12 May 2018 by guest. Protected by copyright.

A case report of a patient in which exercise and cough induced asthmatic attacks is presented. Besides exercise, maximal voluntary hyperventilation, and repeated forced expirograms yielded each time an asthmatic attack. Coughing, spontaneously or imposed, precipitated also an asthmatic attack. A high flow rate is considered to be responsible for triggering asthmatic attacks through stimulation of airway receptors.