Occupational lung disease

CM Barber

Consultant Respiratory Physician

Introduction

• What is occupational lung disease?

• What are the common conditions?

• Why is it important?

• What happens to people who get it?

• How should it be prevented?

Introduction

• What is occupational lung disease?

OLD – response to inhaling something at work

• Fume

OLD – response to inhaling something at work

• Dust

OLD – response to inhaling something at work

• Gas or vapour

OLD – response to inhaling something at work

• Mist/aerosol

Wide range of mechanisms • Direct injury (eg acute irritant asthma, pulmonary oedema)

• Infection (eg silicotuberculosis)

• Allergy (eg asthma, EAA)

• Chronic inflammation (eg COPD, bronchiolitis)

• Destruction of lung tissue (eg emphysema)

• Lung or pleural fibrosis (eg asbestos related disease)

• Carcinogenesis (eg lung cancer, mesothelioma)

Minutes

Years

Decades

OLD

Current exposure – Early recognition

– Accurate diagnosis

– Cessation of exposure

– Prognosis improved

– Health versus income

– Loss of employment

– Eg allergic OA

Historical exposure – Recognised years later

– Accurate diagnosis

– Supportive measures

– Little/no impact on prognosis

– Benefits advice

– Often retired

– Eg asbestosis

Wide range of effects

• Effects may be immediate or after a latent interval of months, years or decades

• Variable depending on individual susceptibility (? genetic)

• May occur whilst still at work or after retirement – E.g. silicosis and asbestosis may progress despite not being

exposed, due to lung retention of dust/fibres

• Effects range from mild to very severe (death)

• May be reversible or irreversible

• Some very old, some only recently described

Georgius Agricola.

De Re Metallica (16th Century)

• “If the dust has corrosive qualities, it eats away at the lungs, and implants consumption in the body. In the mines of the Carpathian mountains women are found who have married seven husbands, all of whom this terrible consumption has carried off to a premature death”

OLD

• What are the common conditions?

UK reporting figures

OLD cases

• Why is it important?

• What happens to people who get it?

Occupational

asthma

Occupational asthma - definition

• 90%- asthma induced by

sensitisation (allergy) to an

agent inhaled at work

OR

• 10%- asthma induced by

massive accidental irritant

exposure at work (direct

airway injury)

Occupational asthma

• 9-15% of all adult onset asthma

• UK estimate 1500-3000 new cases per year

• Risk of unemployment (up to one third)

• Loss of earnings

• Chronic ill health

• Early recognition

• Reduce/prevent exposures

Airway inflammation in farmers

Intervention n=32 Control n=10

Dressel et al, Eur Respir J 2007; 30: 545–548

Case study occupational asthma

• 42 male

• Adult-onset asthma

• Increasing severity and treatment

• Symptoms started 2 years after starting new job

• Symptoms better at weekend

• Worked as a baker

• Symptoms recognised within a year of onset due to health surveillance at work

• Normal spirometry

• Work-effect confirmed by PEF

• Positive immunology (flour IgE)

• Diagnosis of baker’s asthma

• OH dept advised to avoid exposure if possible

• Relocated to despatch room

• Asthma improved

• Medication reduced, remained employed

• i.e. good outcome with early diagnosis

Occupational COPD

Case study COPD

• 68 year old male

• Progressive dyspnoea over 5 years

• Breathless on one flight of stairs or carrying groceries

• Smoked age 14-30, max 25 pack years

• Irreversible airflow obstruction, low gas transfer

• CT - emphysema

Case study COPD

• Extremely dusty work (concrete dust)

• Grinding large concrete display tanks as an exhibit

preparatory in an aquarium.

• Also exposed to epoxies and fibreglass.

• Did 6-8 tanks per year x 7 years (1989-94)

• Less exposure 1994-1998, then retired.

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EF

25-7

5

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0.5

1

1.5

2

2.5

3

3.5

4

4.5

5

88

89

90

91

92

93

94

95

96

97

98

99

00

01

02

03

04

05

06

07

08

FVC

FEV

FEF

Case study - COPD • Patient found to be deficient in alpha 1 antitrypsin

• Genetic condition with increased risk of COPD

• Accelerated lung function decline due to dust exposure

• Fixed airway obstruction

• Permanent disability

• No longer working at time of presentation

• Bad outcome (opportunity to cease exposure missed)

FE

V1 (

% o

f valu

e a

t age 2

5) 100

75

50

25

0

25 50 75

Not exposed or

not susceptible

Stopped at 65

Stopped at 45

Disability

Exposed regularly to

FDGV and susceptible

Death

Age (years)

Lung function decline with time

FDGV = fume/dust/gas/vapour

EAA or HP

ppppppppppppppppppp

EAA or hypersensitivity pneumonitis

• Recognised since 1932 in farmers

• Allergic sensitisation

• Occupational or environmental

• Acute (self-limiting febrile response)

• Sub-acute

• Chronic (irreversible pulmonary fibrosis)

Occupational causes

• Microorganisms

– Farmers, wood pulp workers, sewage workers, mapple bark

strippers, cheese washers, paprika splitters, mushroom

workers, sequoiosis, suberosis, bagassosis, dog house

disease

• Animals

– Birds, wheat weevil, fish meal, rodent handlers

• Vegetation

– Coffee, wood

• Chemicals

– Vineyard sprayers, insecticide, isocyanates, anhydrides,

plastics

Bird Fanciers lung • 22 year old non-smoker

• SOBOE on exertion 2 years

• Weight loss of 1 stone

• Parrot in student house

• +ve avian precipitins

• HRCT sub-acute EAA

• Improvement over 3 years

• Gas transfer 52% to 78%

• Prognosis depends on early

recognition and avoiding exposure

Remove allergen to avoid irreversible fibrosis

Asbestos-related lung disease

• Benign pleural disease

• Pulmonary fibrosis

• Cancer

• Asbestos imported since 1880s

• Asbestosis described in 1920s

• Asbestos used widely in UK until 1980s

Pleural plaques

• Layers of collagen, often calcified

• Latency 30 years

• Harmless marker of exposure

• Not pre-malignant

• Aetiology unclear

Diffuse pleural thickening

• Follows benign effusion

• Obliteration of costophrenic angle

• Long latency

• Lung expansion restricted by thickened pleura

• Breathlessness, respiratory failure

• No effective treatment

• May progress slowly (without further exposure)

Asbestosis

• Scarring of lung tissue

• Long latency (decades)

• History of heavy exposure

• No effective treatment

• May progress (without further exposure)

• Progressive breathlessness

• Respiratory failure

Case study lung cancer

• 84 year old man

• GP abnormal CXRay

• Increasing breathlessness

• Ex-smoker (30 pack years)

• Retired electrician - 30 years

exposure to asbestos

• CT asbestosis and lung

cancer

Smoking, asbestos and lung

cancer risk

GB asbestos workers 1971-2005

Smoking status Asbestos exposure RR lung cancer 95% CI

Never Low

Medium

High

1.0

1.9

1.6

-

(0.8-4.3)

(0.6-4.2)

Former Low

Medium

High

5.6

6.5

9.7

(2.7-11.7)*

(3.2 -13.3)*

(4.7-20.0)*

Current Low

Medium

High

18.8

22.7

26.2

(9.4-37.9)*

(11.3-45.6)*

(13.0-53.1)*

Mesothelioma

• Long latency (decades)

• Rapidly progressive and incurable

pleural cancer

• Lung encased by tumour

• Often presents as an unexplained

pleural effusion

• Progressive breathlessness, chest

pain, weight loss

• Average survival 8-14 months

Annual total number of mesothelioma deaths in GB was predicted to

peak at a level of 1950 to 2450 deaths during the period 2011 to 2015

Latest predictions peak 2025

OLD

• How should it be prevented?

Preventing OLD

• Risk assessment

• Legal requirement under COSHH

• Prevent or minimise exposures to harmful substances

– Elimination (eg asbestos)

– Substitution (eg latex to nitrile gloves)

– Engineering controls (eg exhaust ventilation)

– RPE (masks and respirators)

Preventing OLD

• If residual risk, monitor workers health (surveillance)

– Identify health problems early

– (eg yearly questionnaire/spirometry/CXR)

– Prevent further harm by reducing/preventing

exposure

– Review control measures to protect other

workers

Summary

• Avoidable

• Morbidity, mortality, loss of income

• Easily missed

• Seek specialist advice early

• Cure if early recognition and cease exposure

• Balance health and employment

Occupational asthma:

evidence based diagnosis and management

Interactive e-learning online module

Author: Chris Barber and Timothy Frank

Target audience:

Foundation programme

International

Practice nurse CPD

Hospital doctor CPD

GP CPD

GP trainee

Practice manager CPD