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Irritations of the airways and lungs can vary from mild to acute and the agents are numerous. Corrosive gases and fumes are obvious candidates. Ammonia, sulphur dioxide, nitrous fumes, phosgene, chlorine and fluorine are well known for their irritant effects. Depending on their solubility in water and the concentrations encountered they vary in the effects they have on the respiration system. Ammonia, being very soluble tends not to penetrate beyond the upper airways whereas nitrogen dioxide exerts its effects on the alveoli and is much more dangerous as a consequence. However, the system may be “swamped” by gases like ammonia and they may penetrate to the deeper levels causing a chemical burn of the entire system with life threatening effects appearing any time up to 48 hours later.
Certain cases of these irritations are a prescribed disease under the Department of Social Welfare Occupational Injuries Benefit scheme.
Metal fumes, tiny liquified metal droplets given off by heating metal, either in soldering, heating or cutting metal with an oxyacetylene torch can cause a chemical pneumonitis. Prior to that it can cause “metal fume fever”. It resembles a ‘flu with fever-like symptoms. Zinc, cadmium, copper, megnesium, aluminium, antimony, iron and silver can all produce this condition.

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The pneumoconioses are caused by the inhalation of dust. This can be silica dust, coal dust, asbestos or a large number of other dusts. The effects of inhaling these dusts varies. In some cases, the dust causes fibrotic reactions of varying degrees and in the case of asbestos, cancerous growth known as malignant mesothelioma. However, pneumoconiosis strictly is a condition arising directly from the effects of the dusts. Dust is not necessarily visible. To ascertain that a workplace is free of injurious dust may require a technical assessment.

Silica dust causes Silicosis which is the commonest form of pneumoconiosis world-wide. Apart from causing the development of fibrous nodules in the lungs, an increased vulnerability to lung cancer is evident in effected workers. Uniquely, silicosis increases the incidence of tuberculosis in victims. The fibrous nodules themselves may take a form (conglomerate silicosis or progressive massive fibrosis) resulting in serious and progressive lung deterioration. Silicosis is a serious disease in that a considerable proportion of persons effected develop the conglomerate form.

Workers handling rock containing silica are principally effected. Flint and quartz are the major sources of free silica. Granite is another such a rock but it is also found in slate, sand and sandstone and is encountered generally in mining. Quarry men are at risk as silica is one of the commonest ingredients in the earth’s crust. Sand-blasting of stone produces large quantities of silica dust and should be avoided by using silica-free grit. Grindstones containing silica are a serious danger and should be replaced by carborundum.

Symptoms vary but breathlessness and cough are typical. The period of exposure before symptoms appear varies with the quantity of dust inhaled. In some cases one year of inhalation has proved lethal but ten years is usual.

Coal dust is a well known cause of pneumoconiosis in coal miners. Fibrous nodules of coal dust and collagen gather in the lungs and can again take the form of progressive massive fibrosis as in silicosis although the toxic mechanisms and effects of these two substances differ. On occasions these nodules burst and large quantities of black sputum are coughed up over several days. Needless to say, in addition to coal miners, any person exposed to inhalation of coal dust for the necessary period will contract the disease. Exposure times vary with the degree of dust inhaled and the susceptibility of the individual. Again, breathlessness is a symptom. The appearance of small individual nodules may switch with great rapidity to a progressive massive fibrosis with unrelenting fatal development.

Asbestos has only recently been recognised as one of the most serious hazards in the development of pneumoconiosis. While the industry was aware of some of this hazard over a period of at least 60 years the occurrence of asbestosis in the general population and the frequency of malignant mesothelioma in workers exposed to asbestos came relatively late, in the 1960’s. It appears that not every form of asbestos has this effect and crocidolite (“blue asbestos”) is the significantly dangerous form. Although its importation into the U.K. has been banned since 1970 its use was previously unrestricted in every area of industry including widespread application as an insulation material in construction. Theoretically even one fibre can cause cancer. The demolition of buildings containing such material is a very hazardous operation for workers and the public.

As a result of its widespread use, every resident of New York in the U.S.A. is permanently exposed to asbestos in the environment. In Manhattan, levels of 25-60 mg/cu.m. have been measured in the air.
Levels of exposure resulting in asbestosis as opposed to mesothelioma are in excess of 2 fibres per millilitre of air or higher for at least ten years. This level can and has been achieved by the dust falling from the clothing of workers on their return home, causing asbestosis in the family of the worker.

In the U.K. the use of new asbestos products has been banned and the management of “second hand” asbestos is controlled. In 1986 the U.S.A. commenced a ten-year phasing out of manufacture and use of asbestos materials in the U.S.