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LECTURE AGENDA:. Session 1I. Occupational DermatosesII. Occupational Eye InjuriesIII. Noise-Induced Hearing Loss. LECTURE AGENDA,cont.:. Session 2I. Cardiopulmonary AssessmentII. Occupational PneumoconiosisIII. Common
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1. CORE CLINICAL CONCEPTSOCCUPATIONAL &ENVIRONMENTAL MEDICINE
3. LECTURE AGENDA,cont.: Session 2
I. Cardiopulmonary Assessment
II. Occupational Pneumoconiosis
III. Common “toxidromes” and toxins
IV. Occupational Cancer
4. Occupational Dermatoses Occupational association first made by Ramazzini
Percival Pott -- occupational induced cancer of the scrotum in chimney sweeps in 1775
Leading cost of time off work
35% of work-related illness
5. Occupational Skin Disorders Protective role played by skin
Constant contact with external environment
physical
chemical
biologic
mechanical
6. Occupational Dermatoses Seven common conditions
1. irritant contact dermatitis
2. allergic contact dermatitis
3. photosensitive dermatitis
4. pigment alterations
5. acneiform conditions
6. contact uticaria
7. malignancies
7. Contact Dermatitis 90% of skin lesions seen in wp
80% -- irritant
20% -- allergic
8. Irritant Contact Dermatitis Erythema to eczematous changes to papules, vesicles
Caused by chronic exposure to mild irritants Fissuring
Hyperpigmentation
Hardening
9. I’ve Got you Under My Skin Common household irritants
bleach, detergents, fertilizers, furniture polish, oven cleaner, pet and rug shampoos. Window and toilet bowl cleaners
Common workplace irritants
acids & alkali, cleaning products, epoxy resins, organic solvents
10. Irritant Contact Dermatitis Diagnosis
difficult to distinguish from allergic cd
temporal relationship
agent is know irritant
pt. improves after removal
biopsy not useful
11. Irritant Contact Dermatitis Treatment
modification of work practice
elimination of offending agent
worker may have to change job
domeboro’s soak
topical or systemic coticosteriods
antipuritics
12. Allergic Contact Dermatitis Plants
poison ivy/oak/sumac
Common chemicals
formaldehyde, aromatic amines, caine-type anesthetics, phenol compounds
Metals
nickels, chromium, cobalt
13. Allergic Contact Dermatitis Rubber products
Plastic resins
Fragrances
Food/spices
carrot, coffee, lettuce, vanilla
14. Photodermatitis Synergistic relationship between a chemical and uv light and causes photoirritation
Examples-
coal tar, limes, dyes, pitch, creosote
others produce photoallergic cutaneous reaction
tetracycline
15. Pigmentary Changes
Organic phenols inhibit melanin synthesis
toxic vitiligo (depigmented lesions)
Post inflammatory changes
result from melanin synthesis and leads to hyperpigmentation
16. Acneiform Conditions Chloracne
caused by numerous petroleum products
dioxin
pcb’s
17. Occupational Uticaria Rare
Onset shortly after exposure
Examples-
penicillin
coffee bean dust
citrus fruit
18. Malignancies Types
basal
squamous
melenoma
19. Melenoma Screening is crucial
ABCD rule
aymmetry
border irregularity
color variegation
diameter
thickness determines survivability <.76 mm--->96% survival
3mm bad news
20. Skin Cancers Etiology
sun exposures
chemicals; arsenic tar, phenol compounds
treatment
PREVENTION + sunscreen
surgery
21. Occupationally Related Skin Cancers Farmers
Fishermen
Construction workers
22. Management of Occupational Dermatoses Careful History
Patch Testing
Removal From Exposure
Medications
Barrier Creams -- may worsen exposure at times
Protective Equipment
23. Other Occupational Dermatoses Vinyl chloride
Cutaneous scleroderma-like leisons
Raynaud’s phenomenon
sclerodactyly
acro-osteolysis
hepatic angiosarcoma
24. Other Occupational Dermatoses Chromate associated with chronic non-healing ulcers
Infectious conditions associated with the workplace
herpes simplex
anthrax
brucellosis
25. Other Occupational Dermatoses Arsenic
smelting, orchard spraying, sheep-dipping, grapevine growing, forestry
irritant or allergic cd
basal and squamous cell
hyper-pigmentation to hyper-keratosis
mees lines after 6 weeks of exposure
26. Nail Changes May follow
trauma, infection, vibration, radiation
chemicals
silver exposure ---> blue lunulae
PCB’s ---> brown discoloration
arsenic ---> white bands
27. Health Care Facilities Use of germicidal uv lamps
Latex gloves
contact dermatitis
latex asthma
28. Vibration White Finger Mimics cold-induced vaso-spasm seen in Raynaud’s
Early recognition is important to prevent progression
vibration mitigation
or removal from further exposure
29. Vibration Whole body vrs segmental
Whole body
motion sickness
prostatitis
gi disturbances
ddd
30. Vibration Segmental (VWF)
sensory and motor neuropathy
Raynaud’s
bone cysts
trophic finger changes
31. Vibration Greatest risk for hand-arm is 30-300 hz
Prevention
tool design’
anti-vibration gloves
standard enforcement
32. Occupational Eye Disease Common work-related problems
uv keratitis
corneal abrasions
foreign bodies
chemical injuries
33. Chemical Eye Injuries Alkalis are especially dangerous
ability to rapidly penetrate
Acid
usually less severe than alkalis
sulfuric acid can however result in permanent corneal scarring
34. Occupational Eye Injuries KEY IS PREVENTION
use of appropriate safety glasses
if welding, use of welder’s hood
contacts provide didley against uv keratitis
worker’s exposed to laser radiation
need eye protection designed for the wavelength of the laser
35. Noise- Induced Hearing Loss Overview What is it and why do we care?
Who does it affect?
How do we measure it?
How do we prevent it?
36. Sensorineural Hearing Loss Noise-induced
Meniere’s
Aminoglycosides
Aging
Unilateral think acoustic neuroma, Meniere’s, childhood mumps
37. What is NIHL? Several types
Acoustic trauma
Acute onset, painful, clear cause/effect relationship
Typically after sound level greater than 140 dBA
Temporary threshold shift
Short-term change from baseline after loud noise exposure
NIHL
Related to long-term noise exposure
Insidious onset
Arrestable but not reversible
38. What is NIHL? Sensorineural hearing loss
Pathology is damage to cochlear hair cells
Eventually lose hair cells and may have resultant changes in cochlear nucleus
Usually bilaterally symmetric
May be asymmetric, especially if related to shooting
Moderate hearing loss
40-75 dB
39. Why do I care about NIHL? Predominantly affects frequencies associated with speech
Speech is 500-5000 Hz
NIHL worst at 3000-6000 Hz with early peak at 4000 Hz
Inability to hear related to social isolation and depression in elderly
“Doc, I can hear, but I can’t understand what they are saying.”
40. NOISE-INDUCED HEARING LOSS Sensorineural Hearing Loss-Noise induced:
begins at 3000-6000Hz range
max loss initially 4000 Hz with a dip or notch
4K notch
continued exposure spreads hearing loss to lower frequencies
41. NIHL, cont. If loss is confined above 3000 Hz speech intelligibility in quiet surroundings is normal
Compensation awards (impairment) use 500, 1000, 3000 Hz
42. NIHL, cont. Noise Attenuation
improving maintenance
substitution
sound absorption materials
isolation of process
43. NIHL, cont. It is 100% preventable
Hearing Protection
Ear plugs
Ear muffs
44. How loud is it? 115 dBA
95 dBA
85 dBA
60 dBA
40 dBA ZZ Top in the 4th row
Pneumatic chipper
Lawnmower
Newspaper press
Truck at 40 mph 50 feet away
Milling machine
Conversation at 3 feet
Quiet room
45. Audiometry 101: Normal
46. Audiology 101: Early NIHL
47. Audiology 101: Sensorineural Hearing Loss
48. Who gets NIHL? 30 million Americans at risk
Estimated that 25% will develop NIHL
Workers in manufacturing, mining, construction, transportation are most at risk
Shooting is largest non-occupational source of hazard
50% of workers in above industries also hunt and shoot
At 90 dBA most hearing loss is due to presbycusis; at 100 dBA most hearing loss is NIHL
49. How do we prevent NIHL? Hearing conservation programs
Required by OSHA if 8-hour TWA exceeds 85 dBA
Monitor workers at 85 dBA and provide hearing protection
Workers must wear hearing protection if 8-hour TWA exceeds 90 dBA
Programs consist of monitoring exposure, controlling exposure, audiometric evaluation, hearing protection, worker education, records (this is the government), and evaluation
50. How do we prevent NIHL? Exposure monitoring
Sound pressure level (instantaneous)
Dosimeter (TWA)
Exposure control
Engineering controls
Noise reduction, vibration isolation, equipment isolation
Management controls
Adjust work schedule or reassign workers
51. How do we prevent NIHL? Audiometric evaluation
Pre-exposure to develop baseline
Must be within six months of exposure
Must have hearing protection if it will be more than six months until test
Must not be exposed to workplace noise for 14 hours prior to test
Annually thereafter
Looking for standard threshold shift (STS)
>10dB change in average of 2,3, and 4K Hz
52. How do we prevent NIHL? Hearing protection
Earplugs, canal caps, ear muffs
Must be properly fitted and must be USED
Compliance is an issue
Objective is to reduce noise at ear to below 85 dBA