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ENVIRONMENTAL LUNG DISEASES

Particle size is an important determinant of the impact of environmental

exposures on the respiratory system.

Particles >10 m in diameter typically are captured by the upper airway.

Particles 2.510 m in diameter will likely deposit in the upper tracheobronchial

tree, while smaller particles will reach the alveoli.

APPROACH TO THE PATIENT WITH ENVIRONMENTAL LUNG DISEASES

Obtaining careful occupational history is essential

Types of occupation performed by the patient, the specific environmental

exposures, use of protective respiratory devices, and ventilation of the work

environment can provide key information.

Assessing the temporal development of symptoms relative to the pts work

schedule also can be very useful. .

Pulmonary function tests should be used to assess the severity of impairment.

Some radiologic patterns are distinctive for certain occupational lung diseases

chest x-rays are widely used

Chest CT scans can provide more detailed evaluation.

OCCUPATIONAL EXPOSURES AND PULMONARY DISEASE

Categories of Occupational Exposure and Associated Respiratory Conditions

Occupational Exposures Nature of Respiratory

Responses

Comment

Inorganic Dusts

Asbestos: mining,

processing, construction,

ship repair

Fibrosis (asbestosis),

pleural disease, cancer,

mesothelioma

Virtually all new miningand construction with

asbestos done in

developing countries

Silica: mining, stone

cutting, sandblasting,

quarrying

Fibrosis (silicosis), PMF,

cancer, silicotuberculosis,

COPD

Improved protection in

United States,

persistent risk in


Coal dust: mining

Fibrosis (coal workers'

pneumoconiosis), PMF,

COPD

Risk dropping in United

States, increasing

where new mines open

Beryllium: processing

alloys for high-tech

industries

Acute pneumonitis, chronic

granulomatous disease,

lung cancer

Risk in high-tech

industries persists

Other metals: aluminum,chromium, cobalt, nickel,

titanium, tungsten carbide,

or "hard metal"

Wide variety of conditions

from acute pneumonitis to

lung cancer and asthma

New diseases appear

with new process

development

Organic Dusts

Cotton dust: milling,

processing

Byssinosis (an asthma-like

syndrome), chronic

bronchitis, COPD

Increasing risk in


with drop in United

States as jobs shift

overseas

Grain dust: elevator

agents, dock workers,

milling, bakers

Asthma, chronic bronchitis,

COPD

Risk shifting more to

migrant labor pool

Other agricultural dusts:

fungal spores, vegetable

products, insect

fragments, animal dander,

bird and rodent feces,

endotoxins,

microorganisms, pollens

Hypersensitivity

pneumonitis (farmers'

lung), asthma, chronic

bronchitis

Important in migrant

labor pool but also

resulting from in-home

exposures

Toxic chemicals: wide

variety of industries

Chronic bronchitis, COPD,

hypersensitivity

pneumonitis,

pneumoconiosis, andcancer

Reduced risk with

recognized hazards;

increasing risk for


where controlled laborpractices are less

stringent

Other respiratory

environmental agents

(proven or highly

suspect): uranium and

radon daughters,

environmental tobacco

smoke, polycyclic

hydrocarbons, biomass

fuels, diesel exhaust,

welding fumes, woods or

wood finishing products

Estimates vary from ~3 to

10% of all lung cancers; in

addition chronic bronchitis,

COPD, and fibrosis

In-home exposures

important, in developing

countries disease rates

as high or higher in

females compared to

males

INORGANIC DUSTS

Asbestos-Related Diseases

Exposures to asbestos may occur during the production of asbestos products

(from mining to manufacturing)

Common occupational asbestos exposures also occur in

o shipbuilding and other construction trades (e.g., pipefitting, boilermaking)

o manufacture of safety garments and friction materials (e.g., brake and

clutch linings)

Pleural plaques indicate that asbestos exposure has occurred, but they are

typically not symptomatic.

Interstitial lung disease

o often referred to as asbestosis

o pathologically and radiologically similar to idiopathic pulmonary fibrosis

o Typically accompanied by a restrictive ventilatory defect on pulmonary

function testing.

Asbestosis can develop after 10 years of exposure, and no specific therapy is

available.

Benign pleural effusions can also occur from asbestos exposure.

Lung cancer is clearly associated with asbestos exposure but does not typically

present for at least 15 years after initial exposure.

Lung cancer risk increases multiplicatively with cigarette smoking.

Environmental Lung Diseases

Dr. Carabeo + Harrisons 17th

Ed.

July 20, 2011

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Mesotheliomas (both pleural and peritoneal) are strongly associated with

asbestos exposure, but are not re lated to smoking

Brief asbestos exposures may lead to mesotheliomas, which typically do not

develop for decades after the initial exposure.

Biopsy of pleural tissue by thoracoscopic surgery, is required for diagnosing

mesothelioma.

Silicosis

Results from exposure to free silica (crystalline quartz)

o

occurs in mining, stone cutting, abrasive industries (e.g., stone, clay,

glass, and cement manufacturing), foundry work, and quarrying.

Heavy exposures over relatively brief time periods (as little as 10 months) can

cause acute silicosis

o pathologically similar to pulmonary alveolar proteinosis and associated

with a characteristic chest CT pattern known as crazy paving.

Acute silicosis can be severe and progressive

o whole lung lavage may be of some therapeutic benefit.

Longer-term exposures can result in simple silicosis, with small rounded pacities

in the upper lobes of the lungs.

Calcification of hilar lymph nodes can give a characteristic eggshell

appearance.

Progressive nodular fibrosis can result in masses >1 cm in diameter in

complicated silicosis

o When such masses become very large, the term progressive massive

fibrosis is used to describe the condition.

Silicosis patients are at increased risk of tuberculosis, atypical mycobacterial

infections, and fungal infections due to impaired cell-mediated immunity

Silica may also be a lung carcinogen.

Coal Workers Pneumoconiosis

Occupational exposure to coal dust predisposes to coal workers

pneumoconiosis (CWP)

1. Simple CWP

o Defined radiologically by small nodular opacities and is not typically

symptomatic.

2. Complicated CWP

o Characterized by the development of larger nodules (>1 cm indiameter), usually in the upper lobes

o Often symptomatic and is associated with reduced pulmonary

function and increased mortality.

Berylliosis

Beryllium exposure may occur in the manufacturing of alloys, ceramics, and

electronic devices.

acute beryllium exposure can rarely p roduce acute pneumonitis

a chronic granulomatous disease very similar to sarcoidosis is much more

common.

Chronic beryllium disease

characterized radiologically by pulmonary nodules along septal lines.

either a restrictive or obstructive ventilatory pattern on pulmonary function

testing can be seen.

Bronchoscopy with transbronchial biopsy is typically required to diagnose.

The most effective way to distinguish chronic beryllium disease from sarcoidosis

is to perform a beryllium lymphocyte proliferation test using blood or

bronchoalveolar lavage lymphocytes.

Removal from further beryllium exposure is required, and corticosteroids may be

beneficial.

ORGANIC DUSTS

Cotton Dust (Byssinosis)

Dust exposures occur in the production of yarns for cotton, linen, and rope

making.

Flax, hemp, and jute produce a similar syndrome.

At the early stages of byssinosis, chest tightness occurs near the end of the firs

day of the work week.

In progressive cases, symptoms are present throughout the work week.

After at least 10 years of exposure, chronic airflow obstruction can develop. Insymptomatic individuals, limiting further exposure is essential.

Grain Dust

Farmers and grain elevator operators are at risk for grain dust related lung

disease, which is similar to COPD.

Symptoms include cough, wheezing, and dyspnea.

Pulmonary function tests show airflow obstruction.

Farmers Lung

Exposure to moldy hay containing thermophilic actinomycetes can lead to the

development of hypersensitivity pneumonitis.

Acute presentation of farmers lung includes fever, cough, and dyspnea within

8hrs after exposure.

Chronic and patchy interstitial lung disease can develop with repeated

exposures

TOXIC CHEMICALS

Many toxic chemicals can affect the lung in the form of vapors and gases.

Carbon monoxide poisoning can cause life-threatening hypoxemia.

Combustion of plastics and polyurethanes can release toxic agents

including cyanide.

Occupational asthma can result from exposure to diisocyanates in

polyurethanes and acid anhydrides in epoxides.

Selected Common Toxic Chemical Agents Affecting the Lung

Agent(s)Selected

Exposures

Acute Effects

from High or

Accidental

Exposure

Chronic Effects

from Relatively

Low Exposure

Acid fumes:

H2SO4, HNO3

Manufacture of

fertilizers,

chlorinated organic

compounds, dyes,

explosives, rubber

products, metal

etching, plastics

Mucous

membrane

irritation, followed

by chemical

pneumonitis 23

days later

Bronchitis and

suggestion of mildly

reduced pulmonary

function in children

with lifelong

residential

exposure to high

levels; clinical

significance

unknown

Acrolein and

other aldehydes

By-product of

burning plastics,

woods, tobacco

smoke

Mucous

membrane

irritant, decrease

in lung function

Mutagen in

animals, no human

data

Ammonia

Refrigeration;

petroleum refining;

manufacture of

fertilizers,

explosives,

plastics, and other

chemicals

Mucous

membrane


by chemical

pneumonitis 23

days later

Chronic bronchitis


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Anhydrides

Manufacture of

resin esters,

polyester resins,

thermoactivated

adhesives

Nasal irritation,

cough

Asthma, chronic

bronchitis,

hypersensitivity

pneumonitis

Cadmium fumes

Smelting,

soldering, battery

production

Mucous

membrane

irritant, acute

respiratory

distress

syndrome

(ARDS)

COPD

Formaldehyde

Manufacture of

resins, leathers,

rubber, metals,

and woods;

laboratory

workers,

embalmers;

emission from

urethane foam

insulation

Mucous

membrane


by chemical

pneumonitis 23

days later

Cancers in one

species; no data on

humans

Halides and acid

salts (Cl, Br, F)

Bleaching in pulp,

paper, textile

industry;

manufacture ofchemical

compounds;

synthetic rubber,

plastics,

disinfectant, rocket

fuel, gasoline

Mucous

membrane

irritation,

pulmonaryedema; possible

reduced FVC 1

2 yrs after

exposure

Dryness of mucous

membrane,

epistaxis, dental

fluorosis,tracheobronchitis

Hydrogen sulfide

By-product of

many industrial

processes, oil,

other petroleum

processes and

storage

Increase in

respiratory rate

followed by

respiratory

arrest, lactic

acidosis,

pulmonary

edema, death

Conjunctival

irritation, chronic

bronchitis, recurrent

pneumonitis

Isocyanates (TDI,

HDI, MDI)

Production of

polyurethane

foams, plastics,

adhesives, surface

coatings

Mucous

membrane

irritation,

dyspnea, cough,

wheeze,

pulmonary

edema

Upper respiratory

tract irritation,

cough, asthma,

allergic alveolitis

Nitrogen dioxide

Silage, metal

etching,

explosives, rocket

fuels, welding, by-

product of burning

fossil fuels

Cough, dyspnea,

pulmonary

edema may be

delayed 412 h;

possible result

from acute

exposure:

bronchiolitis

obliterans in 26

wks

Emphysema in

animals, ?chronic

bronchitis,

associated with

reduced lung

function in children

with lifelong

residential

exposure, clinical

significance

unknown

Ozone

Arc welding, flour

bleaching,

deodorizing,

emissions from

copying

equipment,

photochemical air

pollutant

Mucous

membrane

irritant,

pulmonary

hemorrhage and

edema, reduced

pulmonary

function

Chronic eye

irritation and slight

excess in

cardiopulmonary

mortality in

susceptible

individuals

transiently in

children and

adults, and

increased

hospitalization

with exposure to

summer haze

Phosgene

Organic

compound,

metallurgy,

volatilization of

chlorine-containing

compounds

Delayed onset of

bronchiolitis and

pulmonary

edema

Chronic bronchitis

Sulfur dioxide

Manufacture of

sulfuric acid,

bleaches, coating

of nonferrous

metals, food

processing,

refrigerant, burning

of fossil fuels,

wood pulp industry

Mucous

membrane

irritant, epistaxis

?Chronic bronchitis

PRINCIPLES OF MANAGEMENT

Treatment involves limiting or avoiding exposures to the toxic substance

Chronic interstitial lung diseases (e.g., asbestosis, CWP) are not responsive to

glucocorticoids

Acute organic dust exposures may respond to corticosteroids.

Therapy of occupational asthma (e.g., diisocyanates) follows usual asthma

guideline

Therapy of occupationalCOPD (e.g., byssinosis) follows usual COPD guidelines

MNEMONICS of Differential Diagnosis

For DYSPNEA

Acute DYSPNEAA Asthma/Airway obstruction

C COPD

U UMN Lesion

T Tracheal Obstruction

E Endocrine/Environmental

D Deformed Chest Wall

Y hYperventilation Syndrome (labooo..)

S Sarcoid/Shock

P 5 Ps of pleuritic Pain (pericarditis, pulmonary Embolism,

pneumomediastinum, pleurisy/pneumonia, pneumothorax

N Neoplasm

E Edema

A Anemia/Acidosis

For Cough

HACKINGH Hilar adenopathy

A Aneurysm, Asthma, Aspiration

C CHF

K Killer Neoplasms

I Infections

N Nasal Drip

G Growth on vocal cord

i-9b.environmental lung dse

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