FIOH / Tampere Pneumoconiosis Tööga seotud kopsuhaigused Tartu 8.-9. oktoober 2003 PNEUMOCONIOSES Panu Oksa Soome Töötervishoiu Instituut Tampere, Soome

FIOH / Tampere Pneumoconiosis

Tööga seotud kopsuhaigusedTartu 8.-9. oktoober 2003

PNEUMOCONIOSES

Panu OksaSoome Töötervishoiu Instituut

Tampere, Soome

Finnish Institute of Occupational HealthTampere, Finland


Pneumoconiosis

pneumon = lung

konis = dust

Pneumoconiosis = accumulation of inorganic dust in lungs, following non-neoplastic tissue reaction.


Falling of dust

Particle size (m)

1005010

510.20.1

Falling speed

100 cm/s

20 - " -

0.8 cm/s=48 cm/min

0.18 cm/s=48 cm/min

3.5 cm/h

1.1 - " -

0.8 - " -

Mineral dust = 2.6 g/m3, no wind




diffusion collision

falling on surface

Dust in airways, effect of particle size

Acc

um

ula

t io

n i

n a

irw

ays

100

80

60

40

20

0,01 0,1

%

1,0 10 100 m

Alveoli

Upper airways

Nose


During rest0,5 l x 20 min = 4800 l/8 t

During heavy work2 l x 40 min = 38400 l/8 t

If there are 0.5 fibers/cm3 in the breathing zone, a worker in heavy work will inhale 1 920 000 fibers in 8 hours.

Fibers thinner than 10 µm can reach the terminal bronchioles and alveoli.

Breathing


• nose: blowing, wiping, sneezing

• ciliated airways from trachea to terminal

bronchioles: mucociliary clearance

• terminal bronchioles and alveoli: alveolar

clearance with pneumocytes,

macrophages, via lymphatic vessels

Clearing of airways


• If there is a large number of fibers in the airways, clearance mechanisms may be insufficient, especially in the alveolar region.• Fibers cause an inflammatory reaction and finally: normal lung tissue will be replaced with fibrosis

Lung fibrosis 1/2


• number, size, shape and solubility of fibers

• individual features of person (immunological mechanism)

Lung fibrosisfactors affecting the fibrosing process

2/2


• asbestosis

• silicosis

• hard metal disease

• aluminum fibrosis, Shaver's disease

• berylliosis

• talcosis

• kaolin pneumoconiosis.

• coal workers' pneumoconiosis

Fibrogenic pneumoconioses"true pneumoconioses"


Causes:

• antimony

• barium

• boric acid

• manganese

• iron

• tin

• titanium

• bismuth

Non-fibrogenic pneumoconioses

benign pneumoconioses


Pneumoconiosis caused by crystalline silicon dioxide (quartz (silica), tridymite, cristobalite)

Exposure

Most common mineral in earth: in granite, sand, ore, kaolin etc. in most rocks. Finnish TLV 0.2 mg/m3 does not protect from possibility to develop silicosis. Latency period is long, median 19 years.5 % of diseases develop in 10 years.

Silicosis 1/5


PathogenesisUnknown. Silicon dioxide is toxic for macrophages. Collagen fibers develop and are hyalinized.

Clinical forms of silicosis, symptomsTypical and most common is the chronic nodular

form.Rheumatoid silicosis and silicoproteinosis seldom

occur.First symptom is shortness of breath in exercise.

Silicosis 2/5


Findings

X-ray: 1 - 2 mm round nodules at first only in upper parts of the lungs, will spread to lower parts, grow and melt together.

Lung functions react later: reduction of lung volumes, VC, FVC decreas first, and finally also TLC, RV and FRC

Silicosis 3/5


Diagnosis

Typical radiographic changes and sufficient exposure to silica.

Differential diagnosis: tuberculosis, sarcoidosis, siderosis, histoplasmosis, alveolar microlitiasis, complication of measles.

Silicosis 4/5



Complications, prognosis

• lower tolerance to mycobacteria, silicotuberculosis

• recurrent bronchitis, cor pulmonale• lung cancer (IARC classification 2A, probably

carcinogenic for humans)• silicosis may progress even in the absence of

further exposure

Follow-upThorax x-ray and lung function measurements in

two (1 - 3) year intervals also after cessation of exposure

Silicosis 5/5


Asthma is the most common disease caused by hard metal.Hard metal disease can be acute fibrosing alveolitisor the slow progressing symptomless form leading to

chronic pneumoconiosis within years (rarely).

Exposure• hard metal always contains cobalt and wolfram carbide• other agents, like titan, molybdenum and vanadin, may

be needed, depending on technical demands.• acute form can develop in a few years• latency of chronic form is usually over 10 years

Hard metal disease 1/4


Pathogenesis• cause of hard metal disease is probably

exposure to cobalt. • repeated acute diseases lead to

desquamative fibrosing alveolitis • alveolar walls thicken and are infiltrated

by plasma cells, lymphocytes and macro-phages. Later progressive fibrosing occurs between cells.

Hard metal disease 2/4


Hard metal disease

Clinical picture• dry cough and shortness of breath• lung auscultation: crepitation

X-ray: irregular spotty shading, in chronic state irregular opacities in lower parts of lungs

lung function: restriction and later also lower diffusion capacityBAL: typically multinuclear giant cells

PrognosisAcute disease can be cured with steroids; chronic lung

fibrosis is irreversible.

3/4


ExposureIn 1977 - 1989 blade grinder in

furniture factory, 3 x 5 m workroom

in the beginning sharpened 10 disc saw blades in a day

In 1980 new bigger workroom, same machines and filters. Wet grinding 15 blades/day and dry grinding 5 - 6 disc saw and drill blades

In 1989: occupational hygienic measurements: cobalt 3 x TLV, wolfram 2 x TLV

ExposureIn 1977 - 1989 blade grinder in

furniture factory, 3 x 5 m workroom

in the beginning sharpened 10 disc saw blades in a day

In 1980 new bigger workroom, same machines and filters. Wet grinding 15 blades/day and dry grinding 5 - 6 disc saw and drill blades

In 1989: occupational hygienic measurements: cobalt 3 x TLV, wolfram 2 x TLV

DiseaseNon-smoker who after 2 years of work

in factory, developed dry cough Cooling agent "Kemso" suspected.

In 1981 diffuse opacity in thorax x-ray,

FEV1 60%, VC 57%, DL 55%, DLVA 94%. No diagnosis. Did not come to re-examinations.

In 1989 spotty infiltration in thorax X ray, cor pulmonale. VC 22%, FEV1 25%, DL 18% and DL/VA 66%.

Corticosteroids did not help.Oxygen enricher was used.Lung transplantation was suggested,

Deceased 1991.PAD: dust in lungs, 80% wolfram,

fibrosis. Occupational disease.

DiseaseNon-smoker who after 2 years of work

in factory, developed dry cough Cooling agent "Kemso" suspected.

In 1981 diffuse opacity in thorax x-ray,

FEV1 60%, VC 57%, DL 55%, DLVA 94%. No diagnosis. Did not come to re-examinations.

In 1989 spotty infiltration in thorax X ray, cor pulmonale. VC 22%, FEV1 25%, DL 18% and DL/VA 66%.

Corticosteroids did not help.Oxygen enricher was used.Lung transplantation was suggested,

Deceased 1991.PAD: dust in lungs, 80% wolfram,

fibrosis. Occupational disease.

Hard metal disease42-year-old blade grinder

4/4


Exposure levels:

in production usually under 0.1 fibers/cm3 also in "usual" work tasks.

• in using MMMF without adhesive medium over 10 fibers/cm3

• blowing MMMF about 1 fibers/cm3

Man-made mineral fibers, MMMF 1/2


Dangers

Animal studies:• fibrosis and cancerHuman experience and studies• irritation of skin and mucous

membrane, eczema, fibrosis?, cancer???

Man-made mineral fibers, MMMF 2/2

Documents

FIOH / Tampere Pneumoconiosis Tööga seotud kopsuhaigused Tartu 8.-9. oktoober 2003 PNEUMOCONIOSES Panu Oksa Soome Töötervishoiu Instituut Tampere, Soome