Essential respiratory medicine. Shanthi Paramothayan

Chapter 15. Occupational, environmental, and recreational lung disease

Learning objectives

 To understand occupational, environmental, and recreational causes of lung disease

 To recognise the diagnosis and management of occupational asthma

 To understand the diagnosis and management of asbestosis

 To understand the diagnosis and management of other pneumoconiosis

 To understand the damage to lungs from inhalation of recreational drugs

 To appreciate the impact of air pollution on the lungs

 To appreciate the impact of the weather on the lungs


ALI acute lung injury

ARDS adult respiratory distress syndrome

BAL bronchoalveolar lavage

COPD chronic obstructive pulmonary disease

CXR chest X-ray

DAD diffuse alveolar damage

DNA deoxyribonucleic acid

DPLD diffuse parenchymal lung disease

FDG-PET fluoro-deoxyglucose positron emission tomography

FEV1 forced expiratory volume in one second

FVC forced vital capacity

HRCT high-resolution computed tomography

IPF idiopathic pulmonary fibrosis

LTOT long term oxygen therapy

MCE mucociliary escalator

NRT nicotine replacement therapy

PEF peak expiratory flow

RADS reactive airways disease syndrome

THC tetrahydrocannabinol

TLC total lung capacity

TLCO diffusing capacity to carbon monoxide

VC vital capacity

Occupational, environmental, and recreational lung diseases

Many respiratory diseases occur after exposure to dust particles, smoke, fumes, chemical irritants, and biological agents arising from the environment, at work, in a social setting, or at home. Inhalation of smoke particles and irritant fumes can occur because of air pollution, contributed to by vehicle emissions and factory fumes. Individuals may be exposed to chemicals in their home or be exposed to organic particles when carrying out their hobbies. Individuals can be exposed to chemical and biological substances at work that cause lung damage, or allergens that can provoke asthma. A significant proportion of the population deliberately inhale drugs for recreational purposes and these can cause damage to the lungs. The consequences of inhalation will depend on the size, solubility, and toxicity of the particles inhaled, and the intensity and duration of exposure.

It is important to consider an occupational, environmental, or recreational cause for the patient’s presentation, especially if the symptoms are new or unexplained. It is essential to take a detailed history of the patient’s occupation, hobbies, and home environment. History taking is discussed in Chapter 5.

The commonest occupational lung disease is asthma. Individuals can also develop bronchitis, hypersensitivity pneumonitis (see Chapter 7), pneumoconiosis, malignancy (see Chapter 9) and acute lung injury (see Chapter 17) after exposure to a variety of substances.

Occupational lung disease

Occupational lung diseases have been a common cause of morbidity and mortality in the industrialised, urban population for decades. In the past 50 years, recognition of these conditions by employers and the government has resulted in the identification of risk factors, early detection of work-related illnesses, preventative measures at work, and strict health and safety regulations and legislation. For certain occupational lung diseases, the employee can seek compensation from the employer.

When considering an occupational lung disease, it is important to identify a temporal relationship between exposure to a substance and the development of symptoms. Other diseases that could be responsible for the symptoms need to be excluded. The accurate diagnosis and management of occupational lung diseases may be difficult for non-specialists. Most patients, particularly if they wish to get compensation for their illness, will be referred to a specialist in Occupational Lung Diseases.

Occupational asthma

Occupational asthma is the commonest occupational lung disease, with an incidence of 3000 cases each year. It is estimated that 10—15% of those with adult-onset asthma have an occupational cause. Occupational asthma can develop for the first time in an individual exposed to an irritant or sensitizer. Occupational exposure can also exacerbate symptoms in patients who have a known diagnosis of asthma (work-exacerbated asthma), and the estimated prevalence of this is 21%. A history of atopy or asthma has a poor positive predictive value for developing occupational asthma.

Occupational asthma, just like non-occupational asthma (see Chapter 6), is characterised by reversible and variable airflow obstruction. Exposure to a variety of substances at work can result in sensitization, resulting in inflammation of the airways and bronchospasm. Non-immunological agents can irritate the nose and upper airways, resulting in symptoms within minutes or hours of inhalation. The rapidity with which symptoms develop depends on the size of the substance; low molecular weight agents have a shorter latency period. A single exposure to highly soluble toxic gases, for example, sulphur dioxide, ammonia, or chlorine gas, can directly damage the upper airways, and cause reactive airways disease syndrome (RADS), the symptoms of which include persistent dry cough, dyspnoea, and wheeze. More severe or prolonged exposure can result in damage to the alveolar epithelial cells and the development of acute lung injury (ALI) and adult respiratory distress syndrome (ARDS). The long term consequence of this might be the development of bronchiolitis obliterans.

Exposure to immunologic stimuli will result in a period of sensitization and the development of symptoms at a later stage: this latent period may vary from a few weeks to several years. Further exposure to the same agent in a sensitised individual can result in an early (30 minutes) or late (12 hours) response.

Individuals with occupational asthma will develop symptoms of cough, wheeze, chest tightness, and breathlessness while at work, usually within several hours of being in that environment. Their symptoms will generally improve when they are away from the workplace, for example, at weekends or during holidays, and return when they go back to work. This temporal relationship between exposure and symptoms is important in making a diagnosis of occupational asthma. The agent that is likely to be causing the symptoms should be sought by careful evaluation of all the products that the individual is being exposed to. Prolonged and recurrent exposure to the agent could result in chronic asthma and irreversible lung damage, with the individual developing persistent symptoms even when they are away from the workplace.

It is important to remember that other conditions, such as COPD, hypersensitivity pneumonitis and non-occupational asthma will present with similar symptoms, and will need to be excluded when making a diagnosis of occupational asthma.

Individuals suspected of having an occupational cause for their asthma should have careful monitoring of their peak expiratory flow (PEF) and spirometry at work and when away from work. They may require bronchial hyper-responsiveness testing using histamine or methacholine in some cases. If these investigations are normal, then occupational asthma is unlikely. Additional investigations that may be useful include skin prick testing and measurement of immunoglobulin E RAST to specific allergens, as discussed in Chapter 6.

Once a diagnosis of occupational asthma has been confirmed, the most important thing is to reduce exposure to the agent provoking it. Ideally, this might mean removing the individual from the workplace altogether. If this is not possible, the employer will have to ensure that safety measures are in place to reduce exposure. This would include adequate ventilation, the wearing of protective masks, screening of other workers, and regular health checks.

Table 15.1 lists some common causes of occupational asthma. This list is not exhaustive. These agents can also result in exacerbation of COPD and other lung diseases.


Pneumoconiosis is lung fibrosis occurring as the result of inhalation of a variety of inorganic particles and mineral dusts at work. Asbestos, silica, and talc are fibrogenic, beryllium causes non-caseating granuloma, and iron, tin and barium are inert metals. In the last 50 years, recognition of the harmful effects of these dusts has led to strict regulations in the work-place and compensation for those affected, at least in developed countries.

As most of the pneumoconiosis have a characteristic radiological appearance, tissue biopsy is not usually required to make a diagnosis. HRCT has a higher sensitivity and specificity for classifying pneumoconiosis than CXR. FDG-PET may be helpful when lung malignancy is of concern (see Chapter 9).

The International Labour Organisation uses a standardised system for classifying the radiological abnormalities associated with pneumoconiosis which is used in research, for screening of workers and for determining disability claims.

Table 15.1 Common causes of occupational asthma.

Occupation Agent

Healthcare workers


Car paint sprayers

Toluene di-isocyanate Acrylates



Sodium hypochlorite in bleach



Potassium hydroxide in oven and drain cleaners Sodium hydroxide in oven and drain cleaners


Hair spray


Persulfate salts


Wood dust

Painters and decorators

Paint and varnish solvents: turpentine, xylene, toluene, methanol, methylene, acetone, chlorine

Toxic pigments: arsenic, cadmium, chromium, lead, mercury, acrylic emulsion




Hydroquinone, acetic acid, chromium, acetic acid-sulfur dioxide, formaldehyde


Colophony from electronic soldering flux


Antibiotics: penicillin



Plastic manufacture



Colours and glazes: barium carbonate, lead, chromium, uranium, cadmium, manganese


Malathion, dichlorvos, carbaryl and methoxychlor in pesticides



Source: Adapted from Goldman and Peters (1981: 2831).


Asbestos is a naturally occurring fibre composed of hydrated magnesium silicate. Prior to the recognition that inhalation of asbestos fibres was harmful, asbestos was widely used without any protective measures in a variety of industries, as listed in Box 15.1.

Since the early 1970s, strict regulations in developed countries have resulted in banning the use of asbestos, and the implementation of health and safety measures to reduce exposure in those who might be exposed to it. However, the long lag period between exposure and developing the disease means that patients exposed to asbestos many decades ago are still presenting with asbestosis and mesothelioma. Therefore, it is important to take a full occupational history. In less developed countries, asbestos, which is a cheap material, is still widely used without any regulation.

Box 15.1 Occupations associated with asbestos exposure.

• Plumbers

• Construction workers

• Firefighters

• Mechanics • Blacksmiths

• Builders

• Shipyard workers

• Carpenters

• Chemical plant workers

• Roofers

• Cement plant workers

• Electricians

• Power plant workers

Asbestos occurs in natural sources, such as rocks, so those living in certain geographical regions are exposed to low levels. Those living or working in a building which contains asbestos, for example, a house or school, are also exposed. Those who breathe in asbestos fibres from the work- clothes of partners are also at risk. This type of exposure increases the risk of mesothelioma but does not increase the risk of asbestosis.

Asbestos comes in two main forms: serpentine and amphibole. Chrysotile, or white asbestos, is serpentine and accounts for most of the asbestos used commercially. Chrysotile is composed of curly fibres, 2 cm long and 1—2 μm wide. These fibres do not penetrate the lung tissue as much as crocidolite and are therefore less toxic. Crocidolite, blue asbestos, is composed of stiff amphibole fibres, 50 μm long and 102 μm wide. These shorter fibres penetrate the lung tissue, are not easily broken down and result in damage to the lung tissue. Amosite (brown asbestos) and tremolite are also amphiboles but are less prevalent.

Asbestos fibres, which contain iron molecules, have a direct toxic effect on pulmonary parenchymal cells. Alveolar macrophages, neutrophils, lymphocytes, and eosinophils accumulate around the fibres and release proteases, cytokines, reactive oxygen species, and free radicals which damage DNA causing genetic mutations and malignancy. These inflammatory cells also release cytokines that cause fibroblast proliferation and collagen formation. Inhaled asbestos fibres are deposited in the respiratory bronchioles and at the bifurcation of alveolar ducts. Some of the asbestos fibres are removed by mucociliary clearance mechanisms.

The remaining fibres are removed by alveolar macrophages and type 1 alveolar cells.

Inhalation of asbestos fibres can cause several types of damage to the lungs. Pleural disease and mesothelioma are discussed in Chapter 10 and bronchogenic carcinoma is discussed in Chapter 9. Asbestosis, which is pulmonary fibrosis resulting from inhalation of asbestos fibres, is a slowly progressive, irreversible disease resulting in respiratory failure and death. The lag period between exposure and development of asbestosis is 10—25 years, which is less than the lag period for developing mesothelioma. Heavy and more intense exposure to asbestos fibres will result in development of fibrosis in a shorter period.

The clinical and radiological presentation is identical to that of other Diffuse Parenchymal Lung Diseases (DPLDs), particularly idiopathic pulmonary fibrosis (IPF), which is discussed in Chapter 7. Patients with asbestosis will have bibasal, fine crackles and a third will have finger clubbing. They will become hypoxaemic and, in the late stages, develop cor pulmonale. Pulmonary function tests will show a restrictive picture, with reduced lung volumes (VC and TLC) and reduced diffusing capacity (TLCO), which are the most sensitive measures.

CXR may appear normal in the early stages but will progress to show bilateral, basal, reticulonodular shadowing (Figure 15.1). With progressive disease, these changes will involve the mid and upper zones, and with advanced disease there will be honeycombing. HRCT is more sensitive than CXR at detecting early changes and will show sub-pleural linear densities, peribronchiolar, intralobular, and interlobular septal fibrosis. The presence of benign pleural plaques on the chest X-ray is pathognomonic of asbestos exposure (Figure 15.2). Images of pleural plaques are shown in Chapter 10.

If the history of asbestos exposure is clear, and the clinical and radiological features are typical of asbestosis, a histological diagnosis is not required. A bronchoalveolar lavage (BAL) and lung biopsy will be required if there is uncertainty about the diagnosis or if concurrent infection is suspected. Lung biopsy will reveal asbestos bodies which are transparent asbestos fibres coated with iron and protein. The presence of asbestos fibres and asbestos bodies in sputum, a BAL and lung biopsy only indicates asbestos exposure. Patients with asbestosis will have 10—20 times more asbestos fibres than found in normal lung, with more than 1000 asbestos bodies g-1 of lung tissue, which correlates to more than one asbestos body ml-1 of BAL fluid. These ‘ferruginous bodies’, as they are also called, can also be found in individuals exposed to glass, talc, iron, and carbon.

Figure 15.1 Chest X-ray of asbestosis and mesothelioma.

Figure 15.2 CT thorax of asbestosis.

There is no specific treatment for individuals who develop asbestosis. Management is symptomatic and supportive, with long term oxygen therapy (LTOT) and ambulatory oxygen when patients develop respiratory failure. Smoking cessation should be strongly encouraged as smoking is an additional risk factor for developing mesothelioma and asbestosis.

Individuals who develop asbestosis are eligible for compensation, as are those who develop malignant mesothelioma. This is discussed in Appendix 2 of Chapter 10.

Coal worker’s pneumoconiosis

Coal worker’s pneumoconiosis, which results from the inhalation of carbon or coal dust, was a significant problem in the early part of the twentieth century among coal miners, many of whom died from respiratory failure. The risk of developing lung fibrosis is directly related to the amount of exposure to coal dust. Coal dust is taken up by alveolar macrophages in the lungs and cleared by the mucociliary escalator and by lymphatic drainage. If these systems are overwhelmed by the amount of dust inhaled, then the macrophages within the respiratory bronchioles ingest the dust and die, releasing cytokines which induce fibrosis.

In simple coal worker’s pneumoconiosis, there is accumulation of small, < 4 mm particles throughout the lung parenchyma, particularly in the upper lobes, giving a mottled appearance on CXR. These particles contain coal dust, dust-laden macrophages, and fibroblasts. The individual is not usually symptomatic, despite the abnormal CXR, unless they are concurrent smokers; in smokers, focal emphysema is often present.

Progressive massive fibrosis (PMF) is a serious condition with significant morbidity and mortality. It results in severe breathlessness, and can progress to respiratory failure (Figure 15.3). The CXR will show large (> 1 cm) fibrotic masses in the upper zones of the lung fields composed of collagen and coal dust. These masses may cavitate, resulting in the patient coughing up black sputum, which is called melanoptysis. Lung function tests will demonstrate reduced lung volumes, decreased diffusing capacity, and irreversible airflow obstruction.

Figure 15.3 CXR showing progressive massive fibrosis.

Caplan’s syndrome is a pneumoconiosis which occurs in coal miners with rheumatoid arthritis. Less commonly, it can occur after exposure to asbestos and silica. Patients develop multiple nodules, 0.5—2 cm in size, and may have symptoms of breathlessness and cough. Patients may also develop subcutaneous rheumatoid nodules.

Coal miners who develop respiratory disease because of their occupation are eligible for compensation from the Department of Social Security if they have worked for more than 20 years and have abnormal lung function. With fewer people working in the coal industry and the introduction of health and safety measures at work (better ventilation in coal mines and the wearing of protective masks), fewer deaths are associated with this industry these days.


Inhalation of free silica (silicon dioxide) results in lung injury. Box 15.2 lists industries that are associated with silica exposure. As with other pneumoconiosis, stringent health and safety measures in the UK have reduced the incidence of silicosis, although it remains a problem worldwide.

Individuals who have inhaled silica may be asymptomatic, even when they have CXR changes.

Box 15.2 Industries with exposure to silica.

 Mining for: gold, tin, iron, copper, nickel, silver, coal, tungsten, and uranium

 Tunnelling through rock with high silica content


 Stone cutting


 Foundry work



Figure 15.4 CXR showing silicosis and progressive massive fibrosis.

Significant exposure results in symptoms of chronic productive cough and breathlessness, progressively worsening to respiratory failure. Unlike asbestosis, finger clubbing and crackles do not occur.

In the early stages, the CXR typically shows eggshell calcification of the hilar lymph nodes and upper zone nodular fibrosis, with pleural thickening in some cases (Figure 15.4, Figure 15.5). With advanced disease, there will be extensive fibrosis, mainly in the upper zones. Pulmonary function tests will be consistent with a restrictive process, with reduction in VC, TLC and TLCO. Histology of the silicotic nodules characteristically reveals dust, bi-refringent quartz crystals, and macrophages surrounded by concentric layers of collagen. Silica is highly toxic to macrophages and is fibrogenic. Silicosis therefore predisposes to mycobacterium tuberculosis infection and an increased risk of lung cancer.

Figure 15.5 CT thorax showing silicosis and progressive massive fibrosis.

Figure 15.6 CT thorax showing changes associated with hard metal sensitivity.

Management of silicosis is the immediate removal of exposure, smoking cessation in smokers and symptomatic treatment. LTOT may be required in end-stage disease.


Individuals working in the iron and steel industry, especially those welding metals, may inhale iron oxide. These individuals are usually asymptomatic, with normal lung function, but CXR may have a characteristic mottled appearance because of the high radio-density of iron. Exposure to antimony, tin and other metals can result in similar radiological changes (Figure 15.6).


Byssinosis develops due to chronic inhalation of raw cotton, hemp, or flax. This can cause broncho- constriction with symptoms of breathlessness, cough, chest tightness, wheeze, and fever. Symptoms develop within hours of starting work, but gradually improve over the next few days. The CXR is usually normal, but with regular exposure, pulmonary function tests will show airflow limitation.


Beryllium is a lightweight metal used in the dental, computer, and aerospace industries. It has a latency period of 3—30 years and affects 5—20% of exposed workers. Beryllium causes non-caseating granuloma, almost identical to that seen in sarcoidosis. The CXR shows multiple, small, calcified nodules in the upper lobes which may coalesce causing parenchymal distortion, volume loss and bullae formation, with an increased risk of pneumothorax. Mediastinal and hilar lymph node enlargement is common. As with sarcoidosis (discussed in Chapter 7), HRCT shows nodular beading along bronchovascular bundles in a peri-lymphatic distribution and ground glass opacities. Beryllium produces a specific immune response, which can be used to differentiate berylliosis from sarcoidosis.

Hypersensitivity pneumonitis

Individuals exposed to organic dusts, for example, from avian droppings or mouldy hay, may develop hypersensitivity pneumonitis, also called extrinsic allergic alveolitis. This is discussed in Chapter 7.

Recreational drugs and the lungs

Inhalation of substances for recreational purposes is widespread. Cigarette, cigar, and pipe smoking is legal, although recent legislation has restricted the places where these can be smoked. Many young people sniff glue and solvents as these are cheap and easily obtainable. There were 1700 deaths from inhaling solvent and sniffing glue and paint thinners between 1983 and 2000. Cannabis smoking is common, especially in young people. Inhalation of crack cocaine, amphetamines and heroin is carried out by 2% of the population. Insufflation of poppers, amyl nitrites, and toluene (fine spray inhaled quickly) can damage the lungs. The use of aerosol propellant gases with a plastic bag held over the mouth has a high risk of hypoxia, aspiration, suffocation, and respiratory arrest.

Lungs have a large surface area and can absorb large quantities of inhaled drugs within seconds. These drugs are carried swiftly in the bloodstream to the brain, having immediate effects. Rapid inhalation of powders and solvents can result in pneumonitis, bronchitis, and pneumonia. Crack cocaine and heroin, which are snorted through the nostrils, can cause epistaxis, and destroy the nasal cartilage.


Smoking tobacco products is the single, greatest preventable cause of death in the UK, responsible for 120 000 deaths every year. Worldwide, approximately two billion people smoke, and smoking is responsible for five million deaths each year. In the UK, 17.7% of men and 15.8% of women smoke. Children whose parents smoke, and who are more socially deprived, tend to take up smoking. The pressure to smoke is compounded by peers and tobacco advertising. Cigarette smoking increases the risk of lung cancer, bladder cancer, renal cell cancer, COPD, interstitial lung disease, ischaemic heart disease, peripheral vascular disease, stroke, and respiratory infections. Smoking during pregnancy results in foetal growth retardation.

Smoking cigarettes is the main risk factor for developing lung cancer. Cigarette smoke contains a variety of carcinogens which cause genetic mutations, thus increasing the risk of lung cancer. The link between smoking and lung cancer was first considered in 1912 and clearly established in 1950 by Richard Doll. Passive smoking, which is inhaling ‘second-hand smoke’, also increases the risk of lung cancer. Smoking cessation decreases the risk of lung cancer within the first five years after cessation, but remains higher than in a never smoker. Individuals who stop smoking gain 6—10 years of life. Cigar smoking is associated with an increased risk of lung cancer, with a relative risk of 2.1. Pipe smoking also increases the risk of lung cancer with a relative risk of five. Lung cancer is discussed in Chapter 9.

Tobacco smoke contains carbon monoxide, which has a great affinity for haemoglobin, thus displacing oxygen to form carboxyhaemoglobin. Smokers have CO levels of 15% compared to nonsmokers who have levels of <3%. Cigarette smoke destroys the cilia lining the respiratory epithelium and impairs the function of the mucociliary escalator. It also causes hyperplasia of the goblet cells, resulting in an increase in the amount of mucus production, one of the key symptoms in patients with COPD. The diagnosis and management of obstructive airways disease is discussed in Chapter 6. Exposure to cigarette smoke can irritate the airways and cause exacerbation of asthma. Children exposed to cigarette smoke have an increased risk of developing asthma.

The main reason people continue to smoke cigarettes, even when they know of its detrimental effects, is because nicotine, one of the key components of tobacco, binds to the nicotinic acetylcholine receptors in the brain, resulting in the release of a variety of neurotransmitters, including dopamine, serotonin, P-endorphins, vasopressin, and noradrenaline. These neurotransmitters increase the sensation of pleasure, reduce anxiety, and suppress appetite, among other things. Nicotine leads to dependence, therefore smoking cessation results in severe physical and psychological withdrawal symptoms.

All healthcare professionals should advise and assist smokers to stop smoking by offering them pharmacological products and by offering them counselling and support. Box 15.3 lists the approach for counselling for smoking cessation. It has been shown that a simple counselling session results in a one year quit rate of 1—3%, whereas more intense counselling, including group counselling, can improve this up to 20%, especially when nicotine replacement therapy (NRT), Bupropion or Varenicline are prescribed. E-cigarettes are also now being use by many smokers to help them quit. The pharmacological agents available for smoking cessation is discussed in Chapter 3.

Box 15.3 Counselling for smoking cessation.

 Ask how many cigarettes the individual smokes every day and calculate pack years

 Assess the risk of smoking

 Advise how to stop smoking and refer to the smoking cessation counsellor

 Assist with pharmacological and behavioural therapy

 Arrange follow-up



Cocaine, an alkaloid, is a commonly used illegal drug. It is derived from the leaves of Erythroxylon coca, found mainly in Central and South America. Cocaine stabilises cell membranes and has local anaesthetic properties. Cocaine interferes with the re-uptake of catecholamines and serotonin in the brain, resulting in stimulation and a sensation of euphoria. Due to its potent sympathomimetic effects, cocaine also causes cardiovascular complications.

Cocaine hydrochloride, a white powder, can be snorted or injected intravenously. Crack cocaine, which is formed by boiling cocaine with baking soda and water and then extracted with alcohol or ether, can be smoked (free-basing). Crack cocaine is often mixed with either marijuana or tobacco and smoked. Cocaine is quickly absorbed into the pulmonary circulation and reaches the central nervous system within a few seconds. It has a halflife of 60—90 minutes in blood.

Crack cocaine has acute pulmonary toxicity by a variety of mechanisms. Thermal injury and cellular toxicity can result in diffuse alveolar damage (DAD), hyaline membrane formation, acute alveolitis, and pulmonary oedema within hours of inhalation. Acute eosinophilic pneumonia can occur within days of inhalation. Patients present with severe dyspnoea, pleuritic chest pain, fever, haemoptysis, and cough. Occasionally, patients may cough up black sputum, called melanoptysis. CXR and HRCT will show ground-glass changes. Those inhaling crack cocaine often use the Valsalva manoeuvre which can result in life-threatening pneumothorax, pneumopericardium, and pneumomediastinum.

Management of ‘acute crack lung’, which can progress to acute lung injury (ALI) and adult respiratory distress syndrome (ARDS), is supportive and includes supplemental oxygen, non-invasive ventilation, or intubation and ventilation. Bronchodilators and antibiotics may be required. Steroids are only indicated when there is an acute eosinophilic picture. ALI and ARDS are discussed in Chapter 17.

Chronic cocaine use can result in bronchiectasis, foreign body granulomatosis, bronchiolitis obliterans and recurrent alveolar haemorrhage with haemosiderosis. CXR and HRCT will show ground-glass or consolidative changes. Vasospasm can result in ventilation-perfusion mismatch which can progress to pulmonary hypertension, and which can be confused with acute pulmonary embolism. Those who smoke cocaine and cigarettes together have a higher risk of developing bullous emphysema.


Cannabis (marijuana) is used by many as a recreational drug. It is also reported to have benefit in relieving the pain of multiple sclerosis and in certain types of epilepsy. Cannabis is a Class B drug (under the Misuse of Drugs Act, 1971) and individuals can be sent to prison for five years for possessing cannabis, and up to 14 years for supplying it.

Marijuana is made from the Cannabis sativa hemp plant. It can be smoked after being rolled into joints, smoked in pipes, in bongs (water pipes), or in blunts, which are hollowed out cigars filled with a mixture of tobacco and marijuana. It can also be ground into hash and eaten as hash cakes or cookies.

Cannabis smoking is almost as prevalent as cigarette smoking in the young; 20% of the population are estimated to have used cannabis at least once. Cannabis is addictive, with one in six regular users becoming dependent.

Cannabis contains a chemical called delta-9- tetrahydrocannabinol (THC) which stimulates the secretion of dopamine in the brain, causing feelings of euphoria. The concentration of THC in cannabis joints varies considerably from 2.3% to 8%. Cannabis contains 33 carcinogens and tar, which is deposited in the lungs. As cannabis joints are unfiltered, more tar is deposited than with cigarette smoke and deposited more deeply into the lungs. Inhaling cannabis also results in an increase in the concentration of carbon monoxide in the blood.

The average cannabis user will smoke it two to three times a month, therefore is much less exposed to toxic substances than a tobacco smoker who usually smokes daily. Cannabis irritates the lungs, resulting in a productive cough, chest tightness, bronchospasm, and wheezing. These individuals may be predisposed to chest infections. Heavier and regular use of cannabis will result in a decline in pulmonary function. Studies have not found an increased risk of lung cancer with cannabis use alone, but it is difficult to find the evidence as most heavy cannabis smokers also smoke cigarettes.

Users of cannabis often inhale deeply and breath- hold, with an increased risk of pneumothorax or a pneumomediastinum and will present with sharp, pleuritic chest pain and breathlessness. Cannabis is associated with an increased risk of psychotic symptoms, increase in the risk of road traffic accidents, and foetal growth retardation if smoked by a pregnant woman.

The environment and the lungs


Air pollution has been shown to increase morbidity and mortality by increasing the risk of cardiovascular and respiratory illnesses. Air pollution also adversely affects lung development in children.

Individuals living in urban areas with high amounts of road traffic may be more susceptible to lung diseases. Exposure to traffic fumes containing high concentrations of particulate matter, including carbon, sulphite, and carbon monoxide can cause respiratory symptoms, especially in individuals with underlying lung disease. An increase in the amount of carbon particles in lung macrophages correlates with a reduction in lung function. A reduction in the number of fine particles in the atmosphere results in increased life expectancy. Reducing diesel in cars may reduce the risk of pollution-related respiratory disease. Environmentalists are calling for the use of electric cars and for stricter regulations on traffic fumes in urban areas.

Toxic substances

Toxic drugs in the environment may predispose to the development of malignancies, including lung cancer. These agents act synergistically with tobacco smoke to increase the risk of lung cancer. Box 15.4 lists some of the agents which have been implicated.

Radon is a gaseous decay product of Uranium-238 and radium-226 which is found in soil, rock, and groundwater. Radon emits alpha particles, which damage the respiratory epithelium. Radiotherapy used to treat malignancies can also increase the risk of primary lung cancer. Patients who have had radiotherapy for breast cancer have a relative risk of 3—4 of developing lung cancer, and those who have had radiotherapy for Hodgkin’s lymphoma have a relative risk of 3—7 of developing lung cancer. Exposure to particulate matter in polluted air increases the risk of lung cancer, as does inhalation of smoke from indoor wood and coal burning fires.

Box 15.4 Environmental agents associated with malignancies.

• Air pollution

• Asbestos

• Chromium

• Formaldehyde

• Hard metal dust

• Ionising radiation

• Polycyclic aromatic hydrocarbons

• Vinyl chloride

• Nickel

• Bis-chloromethyl ether

• Arsenic

• Radon

Inhaled allergens and irritants

Inhaled allergens and respiratory irritants, both indoor and outdoor, can trigger an acute exacerbation of asthma and COPD. Box 15.5 lists some common environmental allergens.

Fumes from unvented fireplaces, gas stoves, heaters, chlorine-based cleaning products, and volatile organic compounds, including formaldehyde, can cause bronchoconstriction, wheezing, and dyspnoea. Individuals with asthma can develop symptoms of cough, wheezing and breathlessness when exposed to aerosol sprays, including air fresheners and perfumes.


Changes in temperature and weather are associated with asthma and COPD exacerbations. Inhalation of cold, dry air can result in bronchoconstriction, possibly due to loss of water from the airways. Breathing hot, humid air can cause bronchoconstriction secondary to vagal mechanisms.

Thunderstorms result in increased concentrations of pollen debris which can cause an allergic exacerbation of asthma, as can an increase in the level of ozone on hot, sunny days. Damp weather results in increased levels of dust mites, moulds, and carbon dioxide levels, resulting in bronchoconstriction. Desert dust, containing particles of crystalline silica, can be blown across continents during storms, causes respiratory symptoms and an increase in hospitalisation with acute exacerbation of asthma and COPD. Weather forecasts now warn patients with respiratory disease about high pollen count and thunderstorms, and this may help to reduce the risk of exacerbations.

Box 15.5 Common indoor and outdoor allergens and irritants.





House dust mite


Grass pollen

Tree pollen



Tobacco smoke


Aerosol spray

Fumes from gas stoves

Chlorine-based cleaning products Paint sprays


Cold, dry air




Carbon particles

Desert dust (crystalline silica)


 Occupational lung diseases are a common cause of morbidity and mortality.

 A comprehensive history of ALL the jobs the individual has done is required.

 Occupational asthma is the commonest occupational lung disease, affecting 3000 new individuals each year.

 To make a diagnosis of occupational asthma, a temporal association between exposure to an agent and the development of new symptoms needs to be established.

 Individuals with occupational lung disease develop symptoms of cough, dyspnoea, and wheeze while at work or soon afterwards, with symptoms improving at weekends or during holidays.

 Management of occupational asthma includes removal from the workplace or measures to reduce exposure to the allergen, such as wearing a mask.

 Pneumoconioses are restrictive lung disorders that result from the inhalation of inorganic dust particles.

 Pneumoconiosis can progress to severe pulmonary fibrosis and respiratory failure in some cases.

 Asbestosis is associated with the inhalation of Crocidolite, or blue asbestos fibres, and has a lag period of 10-20 years.

 Asbestosis increases the risk of lung cancer.

 Silicosis, caused by exposure to silica, can also result in the development of silicotic nodules, pulmonary fibrosis, increased risk of pulmonary tuberculosis, and lung cancer.

 Smoking tobacco is the single, greatest preventable cause of pulmonary disease worldwide.

 Tobacco is addictive, with smokers getting withdrawal symptoms on cessation.

 Healthcare professionals should advise smokers about cessation, prescribe pharmacological therapy, and refer for counselling.

 Smoking causes malignancies, COPD, peripheral vascular disease, ischaemic heart disease, and stroke.

 Cannabis can cause significant damage to the lungs, with reduction in lung function and an increased risk of pneumothorax.

 Inhaling crack cocaine can result in thermal injury, risk of pneumothorax and acute lung injury.

 Particulate matter, particularly carbon particles in the atmosphere, can result in reduction in lung function and increased mortality.

 Many environmental agents increase the risk of malignancies: radon, chromium, nickel, and hard metal dust.

 The temperature and weather patterns can result in exacerbations of lung disease.


15.1 Which of the following has NOT been shown to be strongly associated with cannabis inhalation?

A Chest infection

B Cough

C Euphoria

D Lung cancer

E Pneumothorax

Answer: D

Inhaling cannabis causes cough, chest infections, euphoria and, if inhaled deeply with breath-holding (Valsalva manoeuvre), can result in a pneumothorax and a pneumopericardium. Although cannabis contains several carcinogens, there is no clear evidence that it causes lung cancer. Studies are made difficult by the fact that most heavy users of cannabis also smoke cigarettes and are young.

15.2 Which of the following is NOT associated with crack cocaine use?

A Bronchiolitis obliterans

B Diffuse alveolar damage

C Eosinophilic pneumonia

D Pneumothorax

E Sarcoidosis

Answer: E

Snorting cocaine or smoking crack cocaine can cause acute and chronic lung injury. It can result in all the above conditions as well as alveolar haemorrhage, haemosiderosis and foreign body granulomatosis. However, cocaine abuse is not associated with sarcoidosis.

15.3 Which of the following statements about occupational asthma is true?

A The latency period for developing asthma is longer with low molecular weight agents

B Symptoms of asthma always improve when the individual is away from work

C A history of atopy is accurate at predicting the likelihood of developing occupational asthma

D Occupational asthma is an extremely rare diagnosis

E If spirometry, peak expiratory flow monitoring, and bronchial hyperresponsiveness tests are normal then occupational asthma is unlikely

Answer: E

The latency period for developing occupational asthma is longer with high molecular weight agents. Individuals exposed over a long period of time may develop chronic asthma and become symptomatic even when away from work. A history of atopy is not good at predicting the risk of developing occupational asthma. Occupational asthma is the commonest occupational lung disease, accounting for 10—15% of adult- onset asthma.

15.4 Which of the following statements about asbestosis is true?

A Chrysotile is more likely to cause asbes- tosis than crocidolite

B Chest X-ray may be normal in up to 30% of patients with asbestosis

C Corticosteroid treatment is effective in asbestosis

D FEV1/FVC ratio will be reduced in asbestosis

E Pulmonary fibrosis develops 30—40 years after exposure to asbestos

Answer: B

Crocidolite, blue asbestos, is more likely to cause asbestosis and malignant mesothelioma as it is composed of short fibres which are cleared less easily from the lungs and are more toxic. Asbestosis results in a restrictive lung process, with an increase in the FEV1/FVC ratio, reduced VC, TLC and TLCO. Pulmonary fibrosis (asbestosis) develops 10—20 years after exposure to asbestos, unlike mesothelioma which develops 30—40 years after exposure. The CXR may appear normal in the early stages in approximately a third of patients.

15.5 Which of the following radiological features is most likely to be found in someone who works quarrying sandstone?

A Ground-glass opacification

B Eggshell calcification of hilar lymph nodes

C Massive fibrotic nodules

D Mottled micronodules

E Reticulonodular opacities at the lung bases

Answer: B

Working with sandstone increases the risk of silicosis, which typically presents with eggshell calcification of the hilar lymph nodes. Ground-glass opacification is nonspecific, usually associated with non-specific interstitial pneumonia. Massive fibrotic nodules are seen in coal worker’s pneumoconiosis and reticulonodular opacities at the bases can be seen in idiopathic pulmonary fibrosis.

15.6 Which of the following statements about occupational asthma is NOT true?

A Occupational asthma can occur after one exposure

B Occupational asthma can only occur in someone with known asthma

C Occupational asthma can occur after exposure to a variety of substances

D Occupational asthma is the commonest occupational lung disease

E Occupational asthma will improve if the individual is removed from the workplace

Answer: B

Occupational asthma can occur for the first time after exposure to an allergen in the workplace. All the other statements are true.

15.7 Non-caseating granulomas are associated with inhalation of which substance?

A Beryllium

B Cadmium

C Iron

D Nickel

E Silica

Answer: A

Berylliosis presents with non-caseating granuloma which is like that in sarcoidosis. Individuals who worked with fluorescent lights and work with dental material and in the computer and aerospace industry may be exposed.

15.8 Patients with which one of the following conditions are NOT eligible for compensation?

A Asbestosis B Benign pleural plaque C Occupational asthma

D Progressive massive fibrosis E Silicosis

Answer: B

The development of benign pleural plaque indicates exposure to asbestos, but the individual is asymptomatic and does not progress to either asbestosis or malignant mesothelioma. All the other conditions are eligible for compensation.

15.9 Which of the following is NOT associated with an increased risk of lung cancer?

A Asbestosis

B Massive pulmonary fibrosis

C Passive smoking

D Siderosis

E Silicosis

Answer: D

Siderosis is the result of inhalation of iron. Although there are chest X ray changes, the individual is asymptomatic, with no increased risk of lung cancer.

15.10 Which of the following features of a particle does not determine its risk of deposition in the lungs?

A Molecular weight of particle

B Origin of particle

C Shape of particle

D Size of particle

E Solubility of particle

Answer: B

The origin or source of the particle (inorganic dust, organic material) does not influence deposition in the lungs. All the other factors do influence deposition.


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