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.
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).
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.
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)|
|Inorganic nonfibrous dusts|
|Carbon compounds (graphite, carbon black, oil shale)|
|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).
|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|
|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
|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
|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|
|Haematite mining (underground)||Welding fumes|
|Iron and steel founding|
|MOPP (vincristine-prednisone-nitrogen mustardprocarbazine
|Radon-222 and its decay products|
|Rubber production industry|
|Silica dust, crystalline|
|Tobacco smoke, secondhand|
|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).