Environmental and Occupational Lung Diseases

Dr. Yeşim YASİN Fall-2013

Outline

• Description of occupational lung diseases• Basic classifications• Major occupational lung diseases• Prevention• Occupational history

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Ramazzini

• He published De Morbis Artificum Diatriba in 1700 (Treatise on the Diseases of Workers). He described:• Dyspnea and metal poisoning in miners• Bronchitis from irritant fumes• Lung fibrosis in potters• Asthma from exposure to corn &flour• Silicosis in stonemasons

Description

Occupational lung diseases are a group of diseases that are caused by either repeated, extended exposure or a single, severe exposure to irritating or toxic substances present in the work environment that leads to acute or chronic respiratory ailments.

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Main difference:

• Occupational diseases: Diseases related to a specific occupation, such as asbestosis, coal worker’s pneumoconiosis (black lung), beryllosis (brown lung), silicosis• Work-related diseases: Diseases that are not

occupation-specific, but are aggravated at work, such as occupational asthma, industrial bronchitis

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Major classification

1. Diseases due to physical agents:a. Heat b.Cold c. Light d. Pressure e. Noise f. Radiation

2. Diseases due to chemical agents: a. Gases: Gas poisoning b. Pneumoconiosis c. Metals and their compounds: Chemicals & solvents3. Diseases due to biological agents: Leptospirozis, anthrax,

actinomycosis, tetanus4. Occupational cancers: Cancer of skin, lungs, bladder

5. Occupational dermatosis: Dermatitis, eczema

6. Diseases of psychological origin: Industrial neurosis, hypertension, peptic ulcer, etc.

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Major Type of Exposure Associated with Clinical Disease• Gases• Corrosive substances (acids, alkalis)• Dyes and stains• Dusts and powders• Asbestos and other fibers• Infectious agents• Insecticides and pesticides• Metal and metal fumes• Organic dusts (cotton, wood, biologic matter)• Plastics• Solvents• Petrochemicals (coal, petroleum distillates)• Physical factors (noise, lifting, thermal stress, vibration, repetitive

motion)• Emotional factors (stress)• Radiation (electromagnetic fields, X-ray radiation,ultraviolet

radiation)

Induction Periods

• Short:• Asthma• Infections • Allergic alveolitis• Toxic poisonings

• Long:• Pneumoconioses• Neoplasms

Classification of OLD

• Inflammation of airways• Inflammation of lining of respiratory

system

• Obstructive lung disease• Reversible: Occupational asthma,

Byssinosis• Irreversible: Industrial bronchitis,

Emphysema

• Restrictive lung disease• Pneumoconiosis: Silicosis, Asbestosis• EAA: Farmer’s lung

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Agent Examples of agents Disease/responseInorganic dusts Crystalline silica Silicosis

Asbestos Asbestosis, lung cancer, mesothelioma

Coal dust Coal workers’ pneumoconiosis

Organic and metallic dusts

Cotton, flax, hemp Byssinosis

Proteins, metallic salts, antibiotics, chemicals

Occupational asthma

Moldy hay, grain, sugar cane, contaminated humidifiers

Hypersensitivity pneumonitis

Gases and fumes Nitrogen, CO2, CO, methane, ozone

Asphyxiation, irritation, pulmonary edema

Viable aerosols Bacteria, viruses Brucellosis, psitticosis, anthrax

Fungi Histoplasmosis, aspergillosisRespiratory carcinogens Arsenic, asbestos,

chromium, nickelLung cancer 10

Inflammation/irritation of airways• Main substances• Soluble in water• Can produce inflammatory effect

• The site of the effect depends on the degree of solubility• Highly soluble Upper respiratory tract • Moderately soluble middle respiratory tract• Sparingly soluble lower respiratory tract

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Occupational asthma and rhinitis• Caused by immunological sensitization to agents in the

workplace• Approx. 10% of adult onset of asthma is occupational.• Asthma symptoms: wheeze, chest tightness and dyspnea.

Classically, symptoms are worse at work or soon after work, and better during weekends and holidays.

• Rhinitis and conjunctivitis symptoms: rhinorrhea, nasal stuffiness and itching of the eye/nose, sneezing; often associated by asthma and may precede chest symptoms.

• When sensitized, symptoms can be precipitated by non-specific irritation (e.g smoking or cols air)

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Causal exposure/industries

Exposure Industry/uses

Isocyanates Car body shops

Platinum salts Platinum industry

Acid anhydrides Manufacturing use of epoxy resins

Rosin flux Electronics (soldering)

Proteolytic enzymes Manufacturing of biological washing powders

Animal proteins (urine/dander) Laboratory animal research

Grain dust, flour Bakeries, agriculture

Antibiotics, cimettidine, isphagula Pharmaceutical manufacturing

Glutaraldehyde, natural rubber latex Health care

Wood dust Construction, forestry, carpentry

Persulphate salts or henna Hairdressing

Fish proteins, soya bean, tea dust Fish preparation, food industry

Reactive dyes Cosmetic and rubber manufacture

Metal working fluids Manufacturing

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Asthma and rhinitis-prognosis

• Symptoms usually resolve after removal from exposure, but the practical constraints of exposure control can be a real threat to employment.• Where exposure cannot be controlled

completely, individuals are sometimes allowed to continue to work wearing PPE. However, they must be informed about risk, and have a frequent health surveillance.

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Byssinosis• Associated with the exposure to cotton dust.• Symptoms: wheezing and chest tightness. Typically worse after

a break from work (Mondays!), improving with return to exposure (better towards the end of the working week). Temporal relationship can be obscured after prolonged exposure.

• Textile and rope making industries• Development of disease is rare if the exposure is < 10 years; in

general 20 years or more• Prevention: exposure controls include enclosure of carding

operations, and steaming of raw cotton to reduce particle formation. 15

Hypersensitivity pneumonitis (HP)• Also known extrinsic allergic alveolitis (EAA)• Inflammatory disorder of the lower RS results from an

immunological reaction to specific allergens in moldy organic material.

• The most prevalent form is Farmer’s hypersensitivity pneumonitis (FHP) or Farmer’s lung.

• Clinical Features• Acute form: Fever, chills, cough, dyspnea, myalgia, headache;

Onset 4-8 hours after exposure to antigen; Resolution after 1-3 days

• Subacute/chronic form: Gradual onset of dyspnea over months or years; Recurrent acute attacks; Chronic productive cough

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HP (Cont.)• Causal exposures/industries:• Agricultural workers, Forestry workers, Mushroom workers, Bird

handlers, Sugar cane producers, Distillery workers• Prevention:• Reduction of exposure to moldy organic material• PPE for high exposure activities

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COPD• Characterized by generally irreversible airflow limitation, with

impairment of lung function and debility in severe cases.• Causal exposures/industries:• Mineral dusts; i.e. coal mining, construction, cement, silica• Organic dusts; i.e. farming, cotton textile work, wood.• Chemicals; i.e. cadmium, welding fumes, isocyanates

• Prevention: exposure controls, ventilation, dust reduction measures, and use of PPE.

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Pneumoconiosis

• The term is currently defined by the International Labor Organization (ILO) as the accumulation of dust in the lungs and the tissue reactions to its presence. • Tissue reaction may be non-collagenous

(minimal stromal reaction) or collagenous (when scarring is permanent).

Pneumoconiosis (Cont.)

Etiologic Determinants:• Size of inhaled particle• 1 to 5 μm reach the alveoli

• Chemical nature of the particle• Concentration of the particle• Length of exposure• Individual’s susceptibility

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Pneumoconiosis (Cont.)

•Asbestosis• Silicosis• Coal Worker’s pneumoconiosis• Berylliosis

ILO radiologic classification

• Rounded opacities: p (<1.5mm), q, and r (>3 mm)• Irregular opacities: s, t, or u• Profusion: 12 point scale (0/0 thru 3/3)•Grading of pleural thickening

Asbestos and related diseases• Asbestos is a generic term for a group of six mineral silicates• Asbestos fibers are: • Very strong• Highly flexible• Resistant to breakdown by acid, alkali, water, heat, and flame• Non-biodegradable• Environmentally persistentSERPENTINE (93% commercial use) AMPHIBOLE (7% commercial

use)

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Asbestos related diseases

•Asbestosis• Pleural disorders• Mesothelioma• Diffuse pleural thickening• Benign pleural effusion• Pleural plagues

• Lung cancer• Laryngeal cancer

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Asbestosis-industry/uses

• Acoustic products• Automobile undercoating• Brake lining• Cements• Clutch casings• Dockyards• Floor tiles

• Fire-fighting suits• Fireproof paints• Insulation• Roofing materials• Ropes • Steam pipe material

Asbestosis

• Diffuse fibrosis caused by a persistent alveolar inflammation• Irregular opacities predominately in the

lung bases• Rales invariably present• Clubbing is common

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Asbestos-Related Pleural Abnormalities

Disease Description

Typical Symptoms

Asbestos-related pleural abnormalities

Occurs when asbestos fibers reach the lining of the lungs; pleura.

Presence of asbestos fibers can cause various reactions in the lung linings, many which are pretty mild.

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Asbestos-related Lung Cancer

Disease Description Typical Symptoms

Lung cancer

The same type of cancer caused by smoking and other factors

None (until late stage)Sometimes: Cough, wheezing, and difficulty breathing

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Asbestos-related Laryngeal Cancer

Disease Description Typical Symptoms

Laryngeal cancer

The same type of cancer caused by smoking and other factors

Persistent hoarseness, chronic sore throat, painful swallowing, pain in the ear, lump in the neck

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Mesothelioma

Disease Description

Typical Symptoms

Mesothelioma

A type of cancer that affects the lining of the lungs or the lining of the abdomen

None (until late stage) Sometimes: Cough, chest pain, and difficulty breathing

Coal Worker’s Pneumoconiosis (CWP)• Coal dust is inert and not particularly

fibrogenic. • Can cause industrial bronchitis, emphysema,

and progressive massive fibrosis.• Xray looks worse than patient• Many symptomatic coal miners have silicosis or

tobacco induced COPD• The onset of CWP normally occurs after 10

years, and son incidence and mortality reflects past exposures.

CWP (Cont.)

• Mortality is declining in developed countries• Cases are still common in China, and there is low but

significant incidence in India.• Two forms: Simple CWP (often asymptomatic with

minor impairment in pulmonary capacity); Complicated CWP (Progressive Massive Fibrosis-PMF, development of large or confluent solid fibrotic nodules in the lung parenchyma, dyspnea and productive cough. • Prevention: exposure controls in the mining industry

including ventilation, dust reduction measures, and use of PPE.

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Silicosis• A type of pneumoconiosis associated with the exposure to

respirable crystalline silica. • Clinical forms: • Acute: early onset of dyspnea and dry cough within a few months

of heavy exposure to fine dusts (i.e. Sandblasting)• Subacute: graduate onset of dyspnea and dry cough over years

after moderate exposure.• Chronic: slow development of nodules on CXR over many years

after lower exposure.• Prevention: Control of exposure through substitution of low-

silica sand for molding and sandblasting, dust control measures (ventilation, suppression) and use of PPE.

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Silicosis-Industry/uses

• Tunneling • Hard-rock mining• Sandblasting• Quarrying • Stonecutting• Foundry work• Ceramics work

• Abrasive work• Brick making• Paint making• Polishing• Stone drilling• Well drilling

Prevention• Primary prevention is concerned with preventing the initiation

of disease by controlling the exposure to its causes.• control of the source,• control at the transmission path,• control at the level of the worker.

• Secondary prevention is concerned with preventing disease complications early in its natural history by early diagnosis and intervention

• Tertiary prevention is concerned with preventing and compensating permanent disability.

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A few examples• Pre-employment screening• Atopy• Genetic factors• Cigarette smoking

• Education • Engineering measures• Indoor air quality control

• Reduce exposure• If doable, replace the substance• Medical monitoring/surveillance• Screen for potential respiratory sensitizers

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The Occupational History

• All jobs held in their lifetime and the duration• Do symptoms improve with weekends and

vacations?• What they did, not their title:• “brusher” drills into hard rock• “rodeo sander” Sandblasts jeans through compressed-

air

The Occupational History (Cont.)

• Toxic exposures can produce airway symptoms or an alveolitis.• If everyone in the workplace is affected in a

dose-dependent manner, the etiology is likely to be toxic rather than immunologic.• Toxic reactions can occur on the first exposure.

Immunologically-mediated diseases require re-exposure.

• Common denominator through which all occupational lung diseases aggravate:

Tobacco smoking!

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Summary

• Awareness of occupational exposure as a cause of disease is important

• Occupational history is crucial • To establish a work relationship, objective evidence of

exposure and occurrence of symptoms or changes in lung function is necessary

• Reduction of exposure is the key to prevention• Engineering measures as well as medical monitoring • Prohibition of smoking in the workplace is necessary• Education/awareness raising

THANK YOU!

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