Exposures and their effects

Acute inhalation injuries

Acute inhalation injury can have various clinical manifestations and may injure both the airways and the lung parenchyma. In principle, the site of damage depends on the nature of the inhaled agent. Causes of chemical pneumonitis may be grouped into four categories (table 1).

In addition, certain organic agents may cause (mainly) inhalation fever. Characteristically, high exposure to bacteria, fungi, and (endo)toxins in cotton mills, grain-handling facilities, livestock farming and comparable settings is responsible for toxic pneumonitis due to organic agents.

Occupational infections

Compared with occupational lung diseases caused by exposure to gases, fumes and dusts at work, occupationally acquired lung infections received little attention until the 2003 epidemic of the viral infection severe acute respiratory syndrome (SARS), which affected more than 8000 individuals globally, one-fifth of whom were healthcare workers.

Many occupational infections have, however, been recognised for a long time. In recent years, some ‘old’ infections such as tuberculosis – particularly multidrug-resistant tuberculosis – and anthrax have re-emerged. Another occupational viral infection which has emerged in the past decade is avian influenza (H5N1) (table 2).

Occupational asthma

Workplace agents that are known to cause allergic occupational asthma include high-molecular-weight (glyco)proteins of vegetable or animal origin and low-molecular- weight compounds. High-molecular-weight proteins and a few low-molecular-weight compounds (such as platinum salts, reactive dyes, acid anhydrides, sulfonechloramide and some wood species) act via a recognised IgE-mediated mechanism. However, the immunological mechanisms underlying the effects of most low-molecular-weight agents (such as isocyanates, persulphate salts, aldehydes and wood dusts) have not been fully characterised.

The distribution of causal agents varies widely across geographical areas, depending on the pattern of industrial and/or agricultural activities. Between 350 and 400 agents have been reported to cause occupational asthma. Updated lists of causal agents and occupations are available online (see, for instance, www.asthme.csst.qc.ca ). The commoner occupational causes of asthma are listed in table 3.

A major problem with occupational asthma is that the relevant agents are identified mainly by nonregulatory organisations, and most are not regulated with the aim of preventing asthma. About 10 new agents are recognised each year.

Occupational COPD

Some work-related obstructive airway disorders may be classified as COPD, but do not fit neatly into this category. For example, work-related variable airway limitation may occur with occupational exposure to organic dusts such as cotton ( i.e . byssinosis), flax, hemp, jute, sisal and various grains (table 4). Such organic dust-induced airway disease is sometimes classified as an asthma-like disorder, but both chronic bronchitis (chronic cough and sputum production) and poorly reversible airflow limitation can develop with chronic exposure. Bronchiolitis obliterans and irritant-induced asthma are other conditions that may overlap clinically with work-related COPD.

The term ‘nuisance dust’ is frequently used to characterise exposures generally thought to be without adverse health effects. There is, however, abundant evidence that this is an inappropriate term. Although, a priori, there is no biological reason why a similar response to inhaled workplace irritants should not occur, it has until recently been somewhat more difficult to demonstrate an association between occupational exposures and COPD in epidemiological studies. For COPD, a population-attributable risk (PAR) of approximately 15–20% has been estimated to be due to occupational factors.

Inorganic fibrous dusts  
Palygorskites (attapulgite and sepiolite)
Silicon carbide (carborundum)
Aluminium oxide
Nylon flock
Inorganic nonfibrous dusts  
Crystalline silica
Coal dust
Carbon compounds (graphite, carbon black, oil shale)
Diatomaceous earth
Inhaled metals and metal compounds  
Rare earths (lanthanides)
Iron, tin, barium (causes of ‘benign’ pneumoconioses)
Table 5 – Causes of pneumoconiosis.

Occupational interstitial lung diseases

Many different agents are reported to cause occupational interstitial lung disease, some well described and others poorly characterised, and the list of causative agents continues to expand. These diseases were formerly thought of as the ‘pneumoconioses’, but the list of known causes of occupational interstitial lung disease extends far beyond the traditional coal, asbestos and silica (table 5). In large studies, about 10–15% of cases of interstitial lung disease turn out to be caused by occupational agents.

Another important form of interstitial lung disease is extrinsic allergic alveolitis (aka hypersensitivity pneumonitis – see also chapter 24 ). A large and expanding range of occupational agents are recognised as causes of this disease (table 6).

Disease Exposure
Air conditioner lung Humidifier water
Animal handlers’ lung Dust of dander, hair particles, dried urine of rats
Bagassosis Mouldy sugar cane
Bird fanciers’ lung Droppings and feathers
Cheese washers’ lung Cheese mould
Farmers’ lung Mouldy hay, straw, grain
Hot tub lung Bacteria in mist from hot tub
Maltworkers’ lung Mouldy malt
Maple bark strippers’ disease Mouldy maple bark
Mushroom workers’ lung Mouldy mushroom compost
Sequoiosis Mouldy sawdust
Sewage sludge disease Dust of heat-treated sludge
Wheat weevil lung Mouldy grain, flour, dust
Suberosis Mouldy cork dust
Wood pulp workers’ disease Mouldy wood chips

Table 6 – Causes of extrinsic allergic alveolitis/hypersensitivity pneumonitis.

Sufficient evidence Limited evidence
Aluminium production Acid mists, strong inorganic
Arsenic and inorganic arsenic compounds Art glass, glass containers and pressed ware
(manufacture of)
Asbestos (all forms) Biomass fuel (primarily wood), indoor emissions
from household combustion
Beryllium and beryllium compounds Carbon electrode manufacture
bis(chloromethyl)ether Alpha-chlorinated toluenes and benzoyl chloride
(combined exposures)
Chloromethyl methyl ether (technical grade) Cobalt metal with tungsten carbide
Cadmium and cadmium compounds Creosotes
Hexavalent chromium compounds Engine exhaust, diesel
Coal, indoor emissions from household combustion Frying, emissions from high-temperature
Coal gasification Insecticides, nonarsenical (occupational
exposures in spraying and application)
Coal tar pitch Printing processes
Coke production 2,3,7,8-tetrachlorodibenzo-para-dioxin
Haematite mining (underground) Welding fumes
Iron and steel founding  
MOPP (vincristine-prednisone-nitrogen mustardprocarbazine
Nickel compounds  
Radon-222 and its decay products  
Rubber production industry  
Silica dust, crystalline  
Sulfur mustard  
Tobacco smoke, secondhand  
Tobacco smoking  
X radiation, gamma radiation

Table 7 – Occupational causes of lung cancer. Adapted from Cogliano et al., 2011, with permission from the publisher.

Occupational lung cancer

Following thorough scientific discussion, the International Agency for Research on Cancer has classified agents with sufficient and those with limited evidence of causing lung cancer (table 7). As can be seen, a huge variety of industries and occupations increase the risk of lung cancer. However, most occupational lung cancer is still caused by asbestos.

Occupational pleural diseases

Asbestos causes both malignant mesothelioma and various nonmalignant pleural diseases (diffuse thickening, noncalcified and calcified plaques, and benign pleural effusion). Even very low exposures and short periods of time are sufficient to cause malignant mesothelioma. Malignant mesothelioma is a signal tumour of asbestos exposure, both in an occupational and in an environmental setting, and, as discussed above, its latent period is up to 50 years. Therefore, a detailed occupational history is of highest importance in the work-up of patients with malignant mesothelioma. Checklists are helpful for patients and physicians (see also chapter 24).

See the entire Occupational risk factors Chapter