CORE CLINICAL CONCEPTS OCCUPATIONAL ENVIRONMENTAL MEDICINE

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