Toxicity by inhalation is the most frequent route of exposure in the workplace.  Additionally, there exist factors that increase the risk of respiratory toxicity, including 1) the tissues are exposed directly to the environment, 2) the lungs receive 100% of the cardiac output (from the right heart) and they hold approximately 60% of the body's entire blood volume at any given time point, and 3) there is an expansive (50-70 sq m) surface area that allows extensive absorptive capability.

Toxicants that may be inhaled are generally classified as one of the following two types:

Vapours and Gases -- generally, the more water soluble the vapour/gas the greater its distribution in the upper respiratory tract (nose, trachea, bronchus).  Examples include sulphur dioxide (SO₂) discussed below, and ozone (O_3, from welding and bleaching processes).  The more lipid soluble, the greater the distribution in the lower respiratory tract (bronchioles, alveoli).

Particulate matter -- Distribution of particles is size dependent.  Smaller particles may penetrate to the deep lung (lower respiratory tract) while larger particles will deposit in the upper tract.  Particulate matter may be man-made (coal dust, asbestos, silica, fly ash) or natural (volcanic activity, wildfires) in origin.

Damage to the pulmonary system may present as one of the following types

Irritation of the air passage -- causing bronchoconstriction, oedema, secondary infection
Ammonia (NH₄), chloride ions, and sulphur dioxide (SO₂) are all examples of inhalants that directly irritate the passage.
Sulphur dioxide is a major air pollutant resulting from both the chemical industry and automobile exhaust (NOTE that it is also a causative agent of acid rain, through its conversion to sulphuric acid with the moist cloud cover).  Sulphur dioxide will cause a proliferation and redistribution (from the upper tract to deeper within the pulmonary tree) of ciliated goblet cells within the respiratory tract, causing increased mucus secretion and ciliary overload within the lower tract, thus inhibiting gas exchange.
 
Damage to the cell lining of the airway -- resulting in cellular necrosis (by the various mechanism discussed previously), increased permeability and subsequent œdema.  Examples of agents that may directly cause cellular necrosis include the solvent xylene and phosgene. (It was primarily for this effect that phosgene was employed as a poison gas in the Great War.  The moisture in the lungs will hydrolise the chlorine liberated from phosgene to hydrochloric acid, thus causing direct acid damage and necrosis to the lungs.)

Fibrosis -- in a mechanism similar to that described for hepatic fibrosis, this will result in massive, obliterated respiratory capacity with large amounts of scar tissue formation.  Various silicates, aluminium dust and coal dust are classic examples of toxicants that produce pulmonary fibrosis. (Coal dust pulmonary fibrosis is specifically referred to as pneumoconiosis).

Allergic responses -- these are typical types of allergic reactions that may result from pollens or chemicals to which the individual has been previously exposed, initiating the immune response cascade.

Oncogenesis -- tumour formation may occur as a direct or indirect result of exposure to asbestos, arsenic, or hexavalent chromium.

Asbestos -- A naturally occurring mineral that is mined primarily in the U.S.A. and Canada (especially Ontario Province).   It occurs as a large number of hydrated silicates that may be formed into small flexible fibres.  Chrysotile is the most common form of asbestos used.  Other forms include amusite, crosidolite, anthophylite, tremolite, and actinolite.
Asbestosis, as a specific consequence of asbestos exposure, was recognised early in the mining and use of the mineral (which supports the routine measurement of asbestos dust in the workplace).  It initially presents as interstitial fibrosis that proceeds to calcification (calcium deposition in areas of fibrosis, thus limiting the elasticity of the alveoli and bronchial passages).  Bronchogenic carcinoma and mesothelioma present late (up to 30 years) after exposure and are more likely a result of cellular irritation rather than direct interaction with DNA within the cells.


Silica -- Silicosis -- Exposure to silicates other than asbestos may also cause pulmonary fibrosis.

Talc -- Talcosis -- Another form of silicate that causes fibrosis

Cotton Dust -- Byssinosis -- Inhalation of cotton dust affects the upper respiratory tract, causing tightness and wheezing that may progress to decreased function and chronic bronchitis.

Dried Sugar Cane (Bagasse) Dust -- Bagassosis -- Chronic inhalation will cause shortness of breath, black sputum, fever, chills, weight loss.

Kaolin -- Persons who are employed in pottery works may suffer from chronic inhalation of the clay kaolin, which causes fibrosis.

Paraquat -- Paraquat is a herbicide that causes pulmonary toxicity NOT by inhalation but by ingestion.  Paraquat will concentrate in the type II (surfactant-producing) epithelial cells of the respiratory tract, causing a frothy exudate and pulmonary œdema.

Drugs -- Some drugs, even those administrered systemically, may cause pulmonary toxicity.  Amiodarone, Busulfan, and Bleomycin may all cause pulmonary fibrosis that may be irreversible.

Many occupations may pre-expose individuals to pulmonary disease that is, strictly speaking, not due to toxicant exposure.

Farmer's Lung -- Primarily caused by inhalation of Actinomyces spores, resulting in a chronic pulmonary fungal infection, characterised by dyspnea, fever, malaise, chills, aches, pain, and weight loss.