B23- Occupational Lung Diseases Flashcards
What substance in buttery popcorn caused 2-3% of workers to get obliterative broncholitis
Diacetyl ketone
Nake 6 occupation lung diseases
Asthma Infection Acute lung injury Interstitial lung disease Copd Lung cancer (asbestos)
How many deaths in europe per year due to fumes or dust
39000
Why is it hard to diagnose
Because has a long latency period. Develops overtime
What is the most common old
Asthma
What % of all asthma cases
15
Give examples
Proteins from animals, favrics, detergents, metalic agents or chemicals can cause an asthmatic response
What is exacerbation at work of already caused asthma called
Work aggrevated asthma
Give 2 examples where occupation cuases risk of infrction
TB in healthworkers
Legionnaires disease in air ventilated areas eg schools, leisure centres
What are acute inhalation injuries
Where 1 major expsure eg to dist, gas fumes, fire cwn trigger lung injuries eg ards onset
Give an example
Bhopal disaster, isocyanate gas fumes
What % had resitrcitive diseases
13.3%
What is the proper name for dust diseases
Pneumoconiosis
Give 4 examples
Coal workers lung
Silicosis
Asbestosis
Asbestos cancer
Give some mineral dust examples vs organic
Coal, silica, asbestos
Vs
Cotton, hay
What is an inert response to dust
Where it needs to be overtime collection to have effect eg cml
What is a fibrous reactikn
Reaxtikn to fibrous dust eg asbestosis
Why are fibrous reactions ahrd to get rid of by immunity
Macrophages cant digest them
Five an example of an allergic response to dust
Extrinsic allergic alveolitis
What is an example of a neoplastic effect (abnormal change eg cancer)
Mesothelioma (by asbestos)
Particles of what size are not likely to get to lower airways
10 um
What suze are small enough to diffuse wirh has across to blood
0.5um
Which particles are most dnagetous and why eg asbestos
1-5um because they deposit in lungs overtime and damage
What does parhogensis of pneumocioniosis via 1-5um dust depend on
Conc of dust Duration of exposure Type of dust (asbestos is worse) Genetic susceptibility of woker Other inhaled irritants
Which kind of dust needs to be dposited a llng time for pneumoconiosis occur
Inert eg coal
Where sre particles going after being englufed by mscrophegaes
Either out by mucociliaty or to lymph/blood
What do most reactive patticles allow
Killing of macrophage and subsequent release of them eg in the blood
How does rhis cause emphysema
By sm ateophy and sm breakdown
Sre these pneumoconiosis effects localised
Yes
When dust builds up up to 10um forming nodules what can this cause
Chronic fibrosis (because of damage) and honeycombing, sitffness, hypoxia, deposition in capillaries
What is the first stage of pneumocionsis called (not too bad)
Pulmonary anthracosis
What is pulmonary anthrocosis
Carbon rxposure and deposition eg in smokers, urban dwellers, cw.
What happens to the carbon/coal build ip
Ingested by macrophages in alveoli and deposits in connrcgive tissue or lymphatics
Its harmeless at first but what can happen
Emphysema eventually at connectivr tissue/smooth muscle
What is simple cwp and what can it cause
Coal laege nodules forming in lungs ans overtime causes dilation of adjacent alvoeli and centrilobulsr emphysema
(Coal also causes things like fibrosis)
What is complicated cwp aslincalled
Progressive massive fibrosis
What % of cwp ends up at pmf
10
What is rhe pathogenssis of this
2-10cm balckened scars due to fibrosis effects of dust psrtickes building up overtime
What is the centre of the blackened scars in pmf
Necrotic tissue/dead tissue
Which dust causes silocosis
Crystalline silicon dioxide dust
How mayy yesrs does it take gi develop
20-30 years
How small ste they so depositied
1um
Name some sources
Mining, quarrying , tunneling
Is it inert
No. Has damaging effect such as pmf/silicosis
What is silociss a type of
Pm fibrosis
Silica is reactive enough to activate macrophages. What does this do
Allow macrophage release of ros and cytokines eg il1(recruits neutrohils)
Which group in silica in macrophages xan intersct with macromolecules luke carbs,lipids and NA
Silanol Sioh group
What does this do
Kill macrophages cussing more silica rleease and also dmaahe to epithelial/lung membrnaes
What do these effects all have
Fibrogenesis
A fibrotic nodule forms which is what
Finrotic matedial eg collagen and surrounding inflammatort cells (activated because silica is so reactive)
Which article discusses silicosis more
Hamilton et al 2009
Can silica produce ros itself or just induce macorphages to
Can produce it itself which is fibrogenic as it dsmshes epithelia
Which inflammasome is activated by these radicals causing activation of cytokines like il1b = lmyphocyte involvemnet
Nalp3
How else does silica allow t lymphocyte induction
Increase ag presentstikn by mscrophages and also induce migration of dc to alveoli for apc
Where can asbestos be
Insulation, roofing material
It causes diffuse ipf. Where does this start the spread
Respiratory bronchioles
Where does fibrosis gradually extend to (kawabata 2019)
To pleura ie causing mesothelioma cancer in pleura
Which cancer has a 5x risk due to asbestos
Bronchogenic carcinoma
What other thing with asbestos causes bronchogenic c
Smoking together
What x risk does asbestos have on mesothelioma
1000x (90% of causes are asbestos)
Where is mesothelioma tumour
In pleura which causes subseqeuent restirction
Which article discusses asbestos related diseases including asbestosis
Kamp 2009
What was the synergistic effect of smoking and abestos on bc
Dna damage and impaired fibre clearance
What do mac execesdivelt cause when exposed to asbestos
Oxidatice stress ie causing fibrosis
How do lung epithelia take up asbestos causing damage
Avb5 integrin
Which pathway due to excessive ros (caused dna damage)release in asbestosis caused aec apoltosis
P53 pathway
