Occupational/Env'al Lung Disease Flashcards
What is an Occupational/ Env’al Lung Disease? (Define)
Respiratory system dysfunction CAUSED BY or EXACERBATED BY contact with antigens or irritants that are inhales, resulting in acute or chronic illness
What factors determine the pathological result of a toxic inhalation
- Size: smaller travels further
- Solubility: more soluble travels less
- Concentration: potency
- Duration of exposure: also kind of potency
- Host factors: age, genetics, smoker?, co-morbid conditions, use of protective gear?
What sizes of particles travel where, what fraction do they qualified as,
and what type disease do they cause?
<100µm : “Inhalable fraction” : enters throat
Irritation
<10µm : “thoracic fraction” : past the bronchus
Acute disease
<4µm : “Respirable fraction” : Alveoli
Chronic disease
What solubility of irritants get where, and give an example of each
High: nose, pharynx, larynx
Ammonia, Chlorine, Sulfur dioxide
Medium: Trachea, Bronchi
Oozone
Low: Bronchiole, Alveoli
Nitrogen dioxide, Phosgene (spelled phosgen in slide deck)
Common Occupational/ Env’al Diseases 5 categories
- Airway diseases: Asthma, Reactive Airway Dysfunction Syndrome (RADS), Bronchiolitis Obliterans (BO), Bronchiolitis Obliterans Organizing Pneumonia (BOOP)
- Pneumoconiosis: Silicosis, Coal Workers Pneumoconiosis (PWC), asbestosis
- Hypersensitivity pneumonitis
- Cancer
- Burn
Upper airway exposure characteristics
What’s affected, how, and what to do
- Lg, very water soluble damaging nasopharynx and larynx (edema to epithelial ulceration and frank hemorrhage)
- Symptoms are short, burning, cough, sputum, sneezing, SOB, bronchospasm (reflex) and hemorrhage
- remove pt from exposure, irrigation, supplemental al O2, secure airway, give steroid if appropriate, racemic epi
- example would be ammonia, chlorine gas,
slide 9 shows burns from anhydous ammonia exposure from gas tank on truck
What can you do for BO, what causes it
no, not deodorant, I’m talking about bronchiolitis obliterans:
can’t do anything, but systemic steroids may help
sulfur dioxide, Nitrogen oxide gas exposure
What does BO look like?
Signs and symptoms
dyspnea on exertion,
early inspiratory crackle on exam (OR NORMAL)
CXR may be normal
PFTs may be obstructive pattern (rarely also restrictive)
Diagnose via lung biopsy
(also History will tell about exposure)
What’s an example of Lower Airway Disease, and how does it present?
BOOP
- fever, dry cough, dyspnea on exertion (like pnemonia)
- late inspiratory crackle on exam
- CXR with bilateral patchy infiltrate (BO has none)
- PFTs typical with restrictive pattern and low DLCO (diffusion of Lung for CO2)
- Diagnosis is via lung biopsy
What can cause BOOP?
How do you treat?
Chronic sequel of irritant gas exposure
Systemic steroid is usually very helpful for 6-7 months
What does RADS stand for, and what does it look like?
(natural history of RADS)
Reactive Airway Dysfunction Syndrome
Looks like asthma, but not immune mediated,
Burn-like damage to airway epithelium
- short-term exposure with high intensity to respiratory irritant. with onset in hrs-a day
- cough, wheeze, SOB
- symptoms last for months, but may remain permanently, in which case the diagnosis changes to asthma.
Tx for RADS
Bronchodilators may help
Occupational Asthma is the same as __________ _______ Asthma
What percentage of adult asthma is this?
Cause?
Work Related Asthma (WRA)
15-20%
Over 450 agents known and growing
Prodromal symptoms of UA irritation for some
With OA/ WRA, name two pathways to get it
With latency: immunologic bases:
High molecular weight >5000 KD, low molecular weight <5000 KD
With out latency: irritant asthma/RADS
faster development than allergen
Symptoms/Risks for OA with latency
Risk factors, and how to make it better
- After chronic daily exposure:
UA irritation, rhinorrhea, eye itching,
Cough mostly while at work/ after workday, wheezing, SOB
- improves when away from work (weekends)
- Risk factors include allergies in family (“Atopy”), smoking, genetics
Pathophysiology of OA with Latency
Two types of agents
High molecular weight agents: animal producs, plants, insects, gum, latex, detergents
IgE dependent classic immediate hypersensitivity reactions
IgE attacks inhaled Lg molecule (usually protein)
Low molecular weight agents: diisocyanates (foam, pneumonic for occupational exposure), anhydrides, fluxes, wood dust, pharmaceuticals
IgE against LMW + protein (needs protein to respond cuz otherwise it’s too small)
Legal Dx of OA/WRA
- Physician diagnosis of asthma
- Onset OR WORSENING of asthma after entering workplace
- Association between symptoms of asthma and work
- Need 1-3 plus One of the following
- workplace exposure to agent known to cause occupational asthma
- work related changes (wrc) in FEV1, or PEF
- or wrc in bronchial responsiveness
- Positive response to specific inhalation challenge test
- Onset of asthma with a clear association with a symptomatic exposure to an inhaled irritant agent in the workplace
Tx for OA/ WRA
avoid exposure (change job, living place)
protective devices (masks, respirators)
usual asthma meds NOT SO HELPFUL
Continuous exposure may cuase progressive damage
Byssinosis
“Monday morning fever and chest tightness”
From cotton processing (around the Mississippi river/ Nile river), also yarn, flax, and hemp
may become chronic symptoms of cough, tightness of chest, and SOB
Monday morning fever is called that because…
What causes it?
Byssinosis= Brown lung= Monday morning fever
symptoms improve upon repeated exposures
from exposure to endotoxins produced by microbial agents contaminating cotton plant
Coal Workers Pneumoconiosis (CWP)
- aka black lung
- relatively high exposure from a long exposure 20-30 years
- Parenchymal lung disease due to inhalation of coal dust
- cilia try to get it out, but eventually get overwhelmed
- excess dust precipitate in µ0 and release cytokines–> fibroblasts accumulate around µ0 and make reticulin, ultimately collagen formation :coal macule
- Cole macule–> coal nodule
- More common with Anthracite, than Bituminous
