Occupational and Environmental Lung Disease

I found this article at Health, Environment & Work – some interesting info on how lungs function and the health effects of dust and gasses.

“The lungs and skin (including nose and eyes) are the organs of first contact for most environmental exposures (excluding ingestion). This aid to learning also includes an introduction to wider harmful consequences as exemplified by the effects on cellular respiration. It will exclude infection and consequences of radioactivity. It complements other modes of learning in the module.

Relevant Fundamentals of Lung Structure and Function

The airways of the lung derive from the trachea (wind pipe) downwards by progressive division into two (or more) branches. Those airways beyond the trachea that contain cartilage are called bronchi. The airways lacking in cartilage beyond the bronchi are the bronchioles. These lead into hollow spaces called alveoli which have a diameter of about 0.1 mm each. There are approximately 300 million alveoli and their total surface area is about 140 m2. The conducting airways are lined by cells with cilia (small motile surface projections). Interspersed between these cells are mucus secreting cells. Secreted mucus spreads over the cilia which direct it upwards to the larger airways by rhythmic undulating movements, thus helping to clear deposited dusts.
The respiratory units, i.e. the alveoli and the smallest bronchioles called respiratory bronchioles are responsible for the exchange of gases. They are lined mainly by flat, extremely thin cells which permit easy diffusion of oxygen through them from the air in the alveolar spaces to the blood in the capillaries and easier diffusion of carbon dioxide in the opposite direction. Alveolar macrophages are very abundant, mobile and phagocytic cells mainly responsible amongst other functions for the ingestion of foreign matter. The lining of the outside of the lung and the inside of the chest wall is called the pleura.

Deposition and host defence of inhaled dusts and mists

Aerosol is an all-embracing term including all airborne particles small enough to float in the air. Dusts are solid particles dispersed in air. Mists are liquid droplets formed by the condensation of vapours, usually around appropriate nuclei or the ‘atomisation’ of liquids. The aerodynamic diameter of a particle is the diameter of a sphere of unit density that would settle at the same rate.
When airborne particles come in contact with the wall of the conducting airway or a respiratory unit they do not become airborne again. This constitutes deposition and can be achieved in one of four ways:
Sedimentation is settlement by gravity and tends to occur in larger airways.

Inertial impaction occurs when an airstream changes direction especially in the nose but also in other large airways.

Interception applies mainly to irregular particles such as asbestos or other fibrous dusts which by virtue of their shape can avoid sedimentation and inertial impaction. However they are intercepted by collision with walls of bronchioles especially at bifurcations or if the fibres are curved.

Diffusion is the behaviour of very small aerosol particles which are randomly bombarded by the molecules of air. It significantly influences deposition beyond the terminal bronchioles.

Most compact particles larger than 20 microns aerodynamic diameter and about half of those of 5 micron aerodynamic diameter are filtered within the nose during breathing at rest. However there is a wide variation in the efficiency of this among apparently normal subjects.

Moreover conditions which favour mouth breathing, (e.g. high ventilation rates and obstructive disease of the nasal airways) will cause large particles to bypass this filter. Alveolar deposition is appreciable at particle diameters of between 1 and 7 microns (respirable particles) and probably maximal at aerodynamic diameter of between 2 and 4 microns. During regular breathing at rest only about 10% of compact particles of 0.5 to 1 micron diameter are deposited in the lung (alveoli), the bulk being again exhaled.

During exertion, increase in tidal volume (i.e. the volume of air inspired with each breath) and particularly in respiratory minute volume (i.e. the product of tidal volume and the number of breaths per minute) is the single most important determinant of the total load of particles in the alveoli and hence the total volume of particles deposited for a given aerosol. Several other factors may influence particle deposition. Insoluble particles deposited in the conducting airways are propelled towards the larger airways by the cilia and then rapidly coughed or swallowed. This may be delayed by factors such as tobacco smoking. In the respiratory units, ingestion by macrophages is necessary before the particles are carried to the larger airways. Particles may also penetrate the deeper lung tissue where they may stay for years or be transported by macrophages to the lymph nodes.

Vapours and gases

Vapours are substances in the gaseous phase at a temperature below their boiling point. Gases produce their harmful effects in the following ways (as described below):
(1) They can cause asphyxiation (deprivation of oxygen to the tissues);

(2) They can cause irritation of the airways and the lungs;

(3) After entering the body through the lungs they can cause damage to other tissues of the body.

Health Effects of Dusts, Gases and Vapours

Nuisance dusts are relatively inert and, by definition, cause no serious health effects although they may be irritant to the upper airways. Examples include chalk, limestone, and titanium dioxide (provided they are free of toxic impurities). They may cause radiographic changes without disease. Dusts should be considered as nuisance dusts only when there is good evidence that they are inert and free from significant health effects not when evidence for an effect is lacking. Moreover there is now good evidence that ultrafine particles of dusts previously considered inert, such as titanium dioxide can be toxic.
Diseases Mainly of the Respiratory Units


Pneumoconiosis is the non-neoplastic (i.e. excludes cancer) reaction of the lungs to inhaled mineral or organic dust and the resultant alteration in their structure. It also excludes diseases mainly of the airways like asthma, bronchitis and emphysema (although destruction of alveoli as in emphysema can be caused by dusts). Two important pneumoconioses are coal workers pneumoconiosis and silicosis.
Coalworkers’ pneumoconiosis (cwp) is a pneumoconiosis caused by inhalation of coal dust and is more prevalent in underground workers exposed to higher concentrations of dust than in surface workers. The lung is destroyed by fibrosis and emphysema.

Silicosis is a pneumoconiosis caused by inhalation of quartz (or some other crystalline forms of silicon dioxide) which is lethal to macrophages that ingest it and releases their enzymes. In its early stages it is similar to cwp but the nodules in the lung tend to be denser. It is a serious and progressive disease. A number of exposures such as grit / sand-blasting with silica have essentially been banned because of the risk of this serious condition.

The term mixed dust fibrosis describes the pulmonary disorder caused by the inhalation of silica dust simultaneously with another non-fibrogenic dust. Other mineral pneumoconiosis may be caused by beryllium, talc, kaolin and mica.

The image alongside shows a quarry worker gently pushing an explosive charge down a hole bored in the rock. The reel next to his right foot contains a cable to permit detonation from a safe distance. As well as the obvious trauma hazard, this procedure (shot-blasting) can generate large concentrations of silica dust.

Environmental Lung Disease

Asbestosis, and other asbestos-related lung disease

Asbestos is such an important cause of lung disease that it is now discussed on a separate page in this website: Asbestos and Disease.

The accompanying image shows asbestos bodies in human bronchoalveolar fluid obtained through bronchoalveolar lavage by the author for diagnostic and research purposes from a symptomatic worker who had significant exposure to asbestos (note alveolar macrophage cells adherent to the larger body, close to a large multinucleated giant cell, while in the bottom right hand corner a smaller body has probably been engulfed by a couple of the cells).
Asbestosis is often classified separately from pneumoconiosis even though asbestos is a dust -but it is a special form of fibrous dust. Like silicosis, asbestosis is a serious condition which is incurable and can result in death at an early age. However, as is the case with many harmful substances it does require a certain inhaled dose of asbestos before there is a measurable risk of asbestosis.

Extrinsic allergic alveolitis

Extrinsic allergic alveolitis can be caused by sensitisation to many organic dusts mainly fungal spores, e.g. farmer’s lung and malt worker’s lung. It tends to affect the respiratory units of the lung rather than the conducting airways and may have ‘flu’ like symptoms in addition. In some respects it is similar to humidifier fever which might be caused by sensitisation to amoebae or algae.
Inhalation of oil mists may cause asthma, airways irritation, lipid pneumonia or other conditions depending on their composition.

Diseases Mainly of the Airways

Irritant effects of gases

Examples: Sulphur dioxide, Nitrogen dioxide, Ozone, Ammonia and Chlorine
These gases produce their harmful effect by irritating eyes, airways and even the respiratory units of the lungs. Many of them may be detected by their smell and irritant effect, but if evasive action is not taken in time, and if exposure is high enough they can produce severe damage throughout the lungs.

Occurrence: Exposure to ammonia and chlorine occurs as a result of industrial accidents. High levels of nitrogen dioxide can be encountered in agriculture (silo filling), during arc welding, as a result of shot firing in the mines and in the chemical industry. It can achieve high levels in the vicinity of internal combustion exhausts. Ozone is usually a secondary pollutant. Sulphur dioxide results from the combustion of sulphur containing substances.

Symptoms: Sulphur dioxide, chlorine, and Ammonia are highly irritant and cause pain in the eyes, mouth and chest. In high concentrations they can produce inflammation of the lining of the lungs and this causes breathlessness and may be fatal. (See chronic effects below).

Nitrogen dioxide has less effect on the eyes, nose and mouth but can cause severe inflammation of the lungs. It is important to realise that although symptoms at first may be mild, serious breathing problems may follow later if the exposure is high enough.


Asthma is a condition characterised by inflammation of the lining of the airways and intermittent spasm of the underlying smooth muscle. Comparatively more is known about the cause of asthma caused by work (occupational asthma) than about other forms of asthma. It is often but not always the result of allergy to an inhaled dust or vapour in the workplace. Its symptoms include cough, wheeze, chest tightness and shortness of breath which improve on days off work or longer holidays but the association with work may be difficult to establish in some cases. In the UK there are probably more than 2000 new cases every year and there have been a few fatalities from agents such as isocyanates or reactive dyes.
Important causative agents include:-

Isocyanates (e.g. in twin-pack spray paints), Hardening/curing agents e.g. anhydrides, Rosin (colophony) fumes from soldering flux, Dusts from various cereals (including flour), Animals such as mammals (rats, mice) but also arthropods (such as locusts), Wood dusts – various e.g. Canadian red cedar, Aldehydes e.g. formaldehyde or glutaraldehyde, Cyanoacrylates (as in “superglue”), and Antibiotics.

In the home, exposure to allergens from house dust mites can be a contributing factor in the development of asthma as well as a cause of its symptoms. Other allergens from pollen, moulds, animal dander etc can cause asthmatic symptoms. Outside the home in the general environment increase in asthmatic symptoms has been attributed to exposure to soya bean dust and to oil seed rape. The contribution to the causation of asthma by irritant gases such as sulphur dioxide, nitrogen dioxide and ozone is still unclear, although it is known that these substances can certainly aggravate symptoms in those who are already asthmatic.

Chronic Bronchitis

The best documented and probably most important environmental cause of chronic bronchitis is tobacco smoke. Other substances could cause bronchitis but this is not yet clear. Certainly many substances (such as sulphur dioxide) can aggravate the symptoms of bronchitis and cause premature deaths from this condition, as occurred in the smogs that affected many big cities in the early 1950’s.

Bronchial cancer

(“lung” cancer)
The single most important known environmental respiratory carcinogen by far in man is tobacco smoke. However lung cancer may also be caused by other agents e.g. asbestos, certain compounds of nickel, polycyclic aromatic hydrocarbons (PAH) e.g. benzpyrene, arsenic trioxide and chromates.


Exposure to asbestos dusts probably of all kinds but especially of blue asbestos (crocidolite) causes mesothelioma which is a cancer of the pleural lining of the lung (besides an increased risk of lung cancer in the bronchus as with smokers). Hundreds of ex-workers still die of these diseases in the UK every year.
Cancer of the nose or nasal sinuses might be caused by certain dusts from hard woods, leather processes and nickel refining.

Systemic Effects


Some dusts e.g. lead of its salts can be absorbed into the body after inhalation or skin contact. They can then have harmful effects on other organs e.g. the nerves or the blood forming organs. Ultrafine particles might travel through the alveoli to produce harmful effects elsewhere.
Systemically toxic gases and vapours

Examples: Methylene chloride, various chloroethanes and chloroethylenes. The effect of methylene chloride is similar to the effect of vapours given off by organic solvents (e.g. trichlorethylene). Initially they might cause a feeling of well being similar to that produced by alcohol. At higher concentrations they cause unconsciousness. Repeated exposure can lead to permanent brain damage.
Simple Asphyxiant gases

Life depends on an adequate supply of oxygen reaching the tissues of the body. Oxygen present in the air breathed into the lungs passes into the blood and is carried to the tissues. Simple asphyxiants may interfere with this process either by displacing oxygen from the air breathed in. Examples: Methane, Nitrogen. This happens usually in enclosed, poorly ventilated spaces particularly underground where methane can be produced by naturally occurring processes or where natural oxygen has been depleted. Symptoms include breathlessness due to lack of oxygen. Carbon dioxide also causes rapid breathing, headache and sweating. Eventually, loss of consciousness and death can result.
Chemical asphyxiants gases

These cause asphyxia by interfering with oxygen transport. Examples: Carbon monoxide, Hydrogen cyanide, Hydrogen sulphide. See toxicology – toxicodynamics.


Companion page on Occupational and Environmental Skin Disease

Information about the reported incidence of occupational lung disease in the UK and the Republic of Ireland is collected by SWORD and other surveillance schemes which are part of the THOR network at the University of Manchester.”

Have a great day!  Regards, Chris

Dust Monitoring Equipment – providing equipment, services and training in dust fallout management to the mining industry.


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