1. Environmental Lung Disease
The next lecture provides perspectives on ways to assess pulmonary diseases for which environmental or occupational causes are suspected
Assessment is important because removal of the patient from harmful exposure is often the only intervention that might prevent further significant deterioration or lead to improvement in a patient's condition.
Identification of an environment-associated disease in a single patient may lead to primary preventive strategies affecting other similarly exposed people who have not yet developed disease.
Hilario M. Tamondong Jr. M.D.
Fellow, Philippine College of Physicians
Diplomate, Philippine College of Chest Physicians
July 30, 2010

2. Environmental Lung Disease: History and Physical Examination
Inquiry into specific work practices should include questions about :
specific contaminants involved
availability and use of personal respiratory protection devices
size and ventilation of workspaces
whether co-workers have similar complaints
alternative sources for exposure to potentially toxic agents including:
Hobbies
home characteristics
exposure to second-hand smoke
proximity to traffic or industrial facilities.
The patient's history is important in assessing any potential occupational or environmental exposure.
Inquiry into specific work practices should include questions about specific contaminants involved, the availability and use of personal respiratory protection devices, the size and ventilation of workspaces, and whether co-workers have similar complaints.
The temporal association of exposure at work and symptoms may provide clues to occupation-related disease
In addition, the patient must be questioned about alternative sources for exposure to potentially toxic agents, including hobbies, home characteristics, exposure to secondhand smoke, and proximity to traffic or industrial facilities.
Short-term and long-term exposures to potential toxic agents in the distant past must also be considered.

3. Spirometry and Lung Volumes
Many mineral dusts produce characteristic alterations in the mechanics of breathing and lung volumes that clearly indicate a restrictive pattern
Similarly, exposures to a number of organic dusts or chemical agents may result in occupational asthma or COPD.
Measurement of change in forced expiratory volume (FEV1) before and after a working shift can be used to detect an acute bronchoconstrictive or inflammatory response.
For example, an acute decrement of FEV1 over the first work shift of the week is a characteristic feature of cotton textile workers with byssinosis (an obstructive airway disorder with features of both asthma and chronic bronchitis).

4. The chest radiograph is useful in detecting and monitoring the pulmonary response to mineral dusts, certain metals, and organic dusts capable of inducing hypersensitivity pneumonitis.
The International Labour Organisation (ILO) International Classification of Radiographs of Pneumoconioses classifies chest radiographs according to the nature and size of opacities seen and the extent of involvement of the parenchyma.
Asbestosis
Silicosis

5. In general, small rounded opacities are seen in silicosis or coal worker's pneumoconiosis
and small, linear opacities are seen in asbestosis.
Ironically, dusts causing rounded opacities, the degree of involvement on the chest radiograph may be extensive, while pulmonary function may be only minimally impaired.
In contrast, in pneumoconiosis causing linear, irregular opacities like those seen in asbestosis, the radiograph may lead to underestimation of the severity of the impairment until relatively late in the disease.
Asbestosis
Silicosis

6. For the individual patient with a history of exposure, conventional CT and high-resolution CT (HRCT) have improved the sensitivity of identifying diffuse parenchymal abnormalities of the lung as well as pleural thickening characteristic of asbestos exposure.

7. Non-Invasive Diagnostic Test to Identify Environment Exposures
heavy metal concentrations in urine (cadmium in battery plant workers)
skin prick testing or specific IgE antibody titers for evidence of immediate hypersensitivity to agents capable of inducing occupational asthma (flour antigens in bakery workers)
Other procedures that may be of use in identifying the role of environment exposures in causing lung disease include
evaluation of heavy metal concentrations in urine (cadmium in battery plant workers)
skin prick testing or specific IgE antibody titers for evidence of immediate hypersensitivity to agents capable of inducing occupational asthma (flour antigens in bakery workers)

8. Non-Invasive Diagnostic Test to Identify Environment Exposures
specific IgG precipitating antibody titers for agents capable of causing hypersensitivity pneumonitis (pigeon antigens in bird handlers)
assays for specific cell-mediated immune responses (beryllium lymphocyte proliferation testing in nuclear workers or tuberculin skin testing in health care workers)
specific IgG precipitating antibody titers for agents capable of causing hypersensitivity pneumonitis (pigeon antigens in bird handlers)
assays for specific cell-mediated immune responses (beryllium lymphocyte proliferation testing in nuclear workers or tuberculin skin testing in health care workers)

9. Invasive Diagnostic Test to Identify Environment Exposures
Bronchoscopy with Bronchoalveolar Lavage
Transbronchial Biopsy
Video-assisted Thoracoscopic Surgery (VATS)
Sometimes, a bronchoscopy to obtain bronchoalveolar lavage fluid and transbronchial biopsy of lung tissue may be required for histologic diagnosis (chronic beryllium disease)
Rarely, video-assisted thoracoscopic surgery to obtain a larger sample of lung tissue may be required to determine the specific diagnosis of environment-induced lung disease (hypersensitivity pneumonitis or giant cell interstitial pneumonitis due to cobalt exposure).

10. Measurement of Environmental Exposure: Particle Size
>10–15 m in diameter, do not penetrate beyond the upper airways
<10 m in size are deposited below the larynx
Particle size of air contaminants must also be considered.
Particles >10–15 m in diameter, because of their settling velocities in air, do not penetrate beyond the upper airways.
Particles <10 m in size are deposited below the larynx and are primarily created by the burning of fossil fuels or high-temperature industrial processes resulting in condensation products from gases, fumes, or vapors.

11. Measurement of Environmental Exposure: Particle Size
>10–15 m in diameter, do not penetrate beyond the upper airways
<10 m in size are deposited below the larynx
~2.5–10 m (coarse-mode fraction), deposit relatively high in the tracheobronchial tree
<2.5m (fine-mode fraction), deposit to the lower airways
<0.1 m (ultrafine fraction ), contact with alveolar wall
These particles are divided into three size fractions on the basis of their size characteristics and sources.
Particles of ~2.5–10 m (coarse-mode fraction) contain crustal elements, such as silica, aluminum, and iron. These particles mostly deposit relatively high in the tracheobronchial tree. Although the total mass of an ambient sample is dominated by these larger respirable particles, the number of particles, and therefore the surface area on which potential toxic agents can deposit and be carried to the lower airways, is dominated by particles <2.5 m (fine-mode fraction).
The smallest particles, those <0.1 m in size, represent the ultrafine fraction and make up the largest number of particles, which tend to remain in the airstream and deposit in the lung only on a random basis as they come into contact with the alveolar walls.
Besides the size characteristics of particles and the solubility of gases, the actual chemical composition, mechanical properties, and immunogenicity or infectivity of inhaled material determine in large part the nature of the diseases found among exposed persons.

12. Categories of Occupational Exposure and Associated Respiratory Conditions

13. Categories of Occupational Exposure and Associated Respiratory Conditions

14. Asbestos Chrysolite Amosite Anthophyllite Crocidolite
Asbestos is a generic term for several different mineral silicates, including chrysolite, amosite, anthophyllite, and crocidolite.

15. Who are exposed to Asbestos?
Production of Asbestos (mining, milling, manufacturing)
Workers in the ship-building and construction trades, including pipe fitters and boilermakers
Manufacturing of
fire-smothering blankets and safety garments
filler for plastic materials
cement and floor tiles
friction materials, such as brake and clutch linings.
In addition to workers involved in the production of asbestos products (mining, milling, and manufacturing)
many workers in the ship-building and construction trades, including pipe fitters and boilermakers, were occupationally exposed because asbestos was widely used for its thermal and electrical insulation properties.
Asbestos also was used in the manufacture of fire-smothering blankets and safety garments, as filler for plastic materials, in cement and floor tiles, and in friction materials, such as brake and clutch linings.

16. Asbestos Related Disease/s
Asbestosis
Lung Cancer, most frequent cancer associated with asbestos exposure
Mesothelioma, not associated with smoking
Asbestosis
Lung cancer is the most frequent cancer associated with asbestos exposure. The excess frequency of lung cancer (all histologic types) in asbestos workers is associated with a minimum latency of 15–19 years between first exposure and development of the disease. Persons with more exposure are at greater risk of disease. In addition, there is a significant multiplicative effect of smoking and asbestos exposure than would be expected from the additive effect of each factor. The use of HRCT in such at-risk individuals to detect lung cancer at an earlier stage is currently under investigation.
Mesotheliomas, both pleural and peritoneal, are also associated with asbestos exposure.
In contrast to lung cancers, these tumors do not appear to be associated with smoking. Relatively short-term asbestos exposures of 1–2 years or less, occurring up to 40 years in the past, have been associated with the development of mesotheliomas (an observation that emphasizes the importance of obtaining a complete environmental exposure history). While the risk of mesothelioma is much less than for lung cancer among asbestos-exposed workers, over 2,000 cases were reported in the U.S. per year at the start of the 21st century.

17. Asbestosis: Spirometry and Lung Volumes
Restrictive Pattern
decrease in both lung volumes and diffusing capacity.
Mild airflow obstruction (due to peribronchial fibrosis)
Physiologic studies reveal a restrictive pattern with a decrease in both lung volumes and diffusing capacity. There may also be evidence of mild airflow obstruction (due to peribronchiolar fibrosis).

18. Asbestosis Pathophysiology
fibrotic lesions are the end result of oxidative injury due to the generation of reactive oxygen species by the transition metals on the surface of the fibers as well as from cells engaged in phagocytosis
The fibrotic lesions are the end result of oxidative injury due to the generation of reactive oxygen species by the transition metals on the surface of the fibers as well as from cells engaged in phagocytosis.
Irregular or linear opacities, usually first noted in the lower lung fields and spreading into the middle and upper lung fields, occur as the disease progresses. An indistinct heart border or a "ground glass" appearance in the lung fields is seen in some cases. In cases in which the x-ray changes are less obvious,

19. Asbestosis Early stage
fibrosis around alveolar ducts and respiratory bronchioles
Fibres incite a firbrogenic response
Thus may produce obstructive as well as restrictive defect.
Advance stage – fibrosis spreads honey comb lung.

20. Asbestos bodies Found in bronchiolar walls or in alveoli.
Clear thin asbestos fibre
( 10-50m) surrounded by beaded iron-protein coat which appears golden brown.
Blue with Prussian blue stain for iron. (REMEMBER THIS)

21. Asbestosis Pleural plaques, exposure, not pulmonary impairment
Pleural effusion (serous or bloody exudate), benign
The clinical and pathological features of acute silicosis are similar to those of pulmonary alveolar proteinosis
The CXR can be used to detect a number of manifestations of asbestos exposure.
Past exposure is specifically indicated by pleural plaques, which are characterized by either thickening or calcification along the parietal pleura, particularly along the lower lung fields, the diaphragm, and the cardiac border. Without additional manifestations, pleural plaques imply only exposure, not pulmonary impairment.
Benign pleural effusions may also occur. The fluid is typically a serous or bloody exudate. The effusion may be slowly progressive or may resolve spontaneously.
Irregular or linear opacities, usually first noted in the lower lung fields and spreading into the middle and upper lung fields, occur as the disease progresses. An indistinct heart border or a "ground glass" appearance in the lung fields is seen in some cases. In cases in which the x-ray changes are less obvious,

22. Asbestosis
Frontal chest radiograph shows bilateral calcified pleural plaques consistent with asbestos-related pleural disease
Poorly defined linear and reticular abnormalities are seen in the lower lobes bilaterally T

23. Asbestosis
Axial high-resolution CT of the thorax obtained through the lung bases shows bilateral, subpleural reticulation (black arrows), representing fibrotic lung disease due to asbestosis.
Subpleural lines are also present (arrowheads), characteristic of, though not specific for, asbestosis.
Calcified pleural plaques representing asbestos-related pleural disease (white arrows) are also evident.

24. Asbestosis: Pleural Plaque
Occur in parietal and diaphragmatic pleura often 10 – 20 years after exposure.
Pearly white with smooth or nodular surface.

25. Free Silica (SiO2): Silicosis
Occupational Exposure:
Mining
Stonecutting
Employment in abrasive industries; stone, clay, glass and cement

26. Silicosis
Silica toxic to macrophages, leads to their death with release of proteolytic enzymes and silica particles- cycle continues
Nodules (2-4mm) form in lungs after many years of exposure
Some develop reactivation of tuberculosis
Pathway - diffuse pulmonary fibrosis with numerous silicotic nodules.
Tuberculosis more common in patients with silicosis
Macrophages illicit fibrogenic factors which produce marked fibrotic nodules in the lung (parenchyma).

27. Silicosis Silicotic nodules may be identified more readily by HCRT
The nodular fibrosis may be progressive in the absence of further exposure, with coalescence and formation of nonsegmental conglomerates of irregular masses >1 cm in diameter (complicated silicosis).

28. Silicosis
Acute silicosis. The high-resolution CT scan shows multiple small nodules consistent with silicosis but also diffuse ground-glass densities with thickened intralobular and interlobular septa, producing polygonal shapes. This has been referred to as "crazy paving."

29. Silicosis
Silicosis.
Frontal chest radiograph in a patient with silicosis shows variably sized, poorly defined nodules (arrows) predominating in the upper lobes

30. Coal Worker's Pneumoconiosis (CWP)
Occupational exposure to coal dust can lead to CWP
Prolonged exposure to coal dust (i.e., 15–20 years), small, rounded opacities similar to those of silicosis may develop.

31. Coal Workers Pneumoconiosis (CWP)
Anthracosis – presence of coal dust pigment
Macular CWP – aggregates of laden macrophages
Nodular CWP – no obvious scarring or functional respiratory impairment nodules less than 10mm in a background of macular CWP
Simple radiographically identified CWP is seen in ~10% of all coal miners and in as many as 50% of anthracite miners with more than 20 years' work on the coal face.
With prolonged exposure to coal dust (i.e., 15–20 years), small, rounded opacities similar to those of silicosis may develop. As in silicosis, the presence of these nodules (simple CWP) is not usually associated with pulmonary impairment. Much of the symptomatology associated with simple CWP appears to be due to the effects of coal dust on the development of chronic bronchitis and COPD
The effects of coal dust are additive to those of cigarette smoking.

32. Coal Workers Pneumoconiosis (CWP)
Progressive massive fibrosis (PMF) :
-large (2cm or more) irregular nodules usually midzonal or in upper lobes, bilateral
-associated with emphysema
-eventually honeycomb lung with RF
Caplan’s syndrome – Seropositive rheumatoid disease with CWP having firm nodules with central necrosis.
Complicated CWP is manifested by the appearance on the chest radiograph of nodules ranging from 1 cm in diameter to the size of an entire lobe, generally confined to the upper half of the lungs. As in silicosis, this condition can progress to PMF which is accompanied by severe lung function deficits and associated with premature mortality.
Caplan's syndrome , first described in coal miners but subsequently found in patients with silicosis, includes seropositive rheumatoid arthritis with characteristic pneumoconiotic nodules. Silica has immunoadjuvant properties and is often present in anthracitic coal dust.

33. CWP
PMF
Activation of macrophages results in release of several mediators
Free radicals – reactive oxygen species
Chemotactic factors – TNF, IL-6, IL-8
Fibrogenic cytokines – IL-1, TNF, PDGF

35. Environmental/ Occupational Exposure
Disease
Antigen
Source
Farmer’s lung
Faeni rectivirgula
Moldy hay, grain, silage
Humidifier lung
Thermoactinomyces
Contaminated water reservoirs
Bagassosis
Thermoactinomyces vulgaris
Moldy sugarcane
Pigeon breeder’s lung
Avian droppings, feathers, serum
Parakeets, pigeons, chickens, turkeys
Woodworkers lung
Alternaria sp., wood dust
Oak, cedar, mahogany dust, pine and spruce pulp

36. Common Toxic Chemical Agents Affecting the Lung

37. Common Toxic Chemical Agents Affecting the Lung

38. Common Toxic Chemical Agents Affecting the Lung

39. Common Toxic Chemical Agents Affecting the Lung