CORE CLINICAL CONCEPTS OCCUPATIONAL ENVIRONMENTAL MEDICINE

1. CORE CLINICAL CONCEPTSOCCUPATIONAL &ENVIRONMENTAL MEDICINE Session Two

2. LECTURE AGENDA: Cardiopulmonary Assessment Pulmonary Assessment Common toxidromes cardiac pulmonary renal neurotoxins

3. Cardiopulmonary Assessment Thorough history and physical Static electrocardiography Dynamic electrocardiography Pulmonary function testing

4. Cardiopulmonary Assessment Important components of selected pre-placement and medical surveillance exams Individuals with routine use of air purifying respirators if no increased cardiac workload is expected thorough H & P static ECG and PFT�s

5. Cardiopulmonary Assessment Workers in fully encapsulated clothing and SCBA exert additional CV effort with severe heat stress haz mat workers, fire fighters, asbestos removal crews etc. Pre-placement and periodic dynamic electrocardiography and PFT�s are required For baseline & RTW evaluations when excellent CV fitness is required to ensure optimal worker safety and protection in the workplace Follow standards for assessment criteria

6. Cardiopulmonary Assessment Risk Factors for Morbidity and Mortality age prior infarction non-q wave infarction congestive heart failure persistent angina LV ejection fraction <40% complex ventricular ectopy

7. Cardiotoxins: Coronary Heart Disease Arrhythmias Cardiomyopathies Hypertension Cor pulmonale

8. Cardiovascular Toxins: I. CHD Carbon Monoxide Accounts for greatest # of intoxications and deaths in industry Also most frequent occupational cardiotoxin CO has stronger affinity for Hgb than does O2 Cigarette smoking additive to occupational exposures

9. Carbon Monoxide Occupations at risk firefighters police officers toll collectors parking garage attendants bridge and tunnel workers foundry and blast furnace workers

10. Carbon Monoxide Measure by carboxyhgb 10-20% headache 30% coma 50% death nl levels nonsmoker 4% smokers 8% Chronic exposure promotes atherosclerosis People with CAD are very sensitive

11. Cardiovascular Toxins: I. CHD Nitroglycerin and other nitrates Occupations at risk manufacturers of explosives, users (road builders, construction and military) and pharmaceutical industry Monday morning angina: long-term exposure, cessation of exposure, re-exposure---> rebound vasospasm and sudden V fib

12. Cardiovascular Toxins: I. CHD Noise >85dBA assoc with heart disease, htn, arteriosclerosis Carbon disulfide 5 fold increase risk of death from CHD

13. Cardiovascular Toxins: II. Arrhythmias Hydrocarbons: low level palpatations, myocardial irritability high levels SA blocks, AV blocks all levels PAT, V tach, SVT

14. Cardiovascular Toxins III. Cardiomyopathy Cobalt cardiomyopathy in Canadian beer drinkers lead in moonshine, arsenic in beer

15. Cardiovascular ToxinsIV. Hypertension Cadmium direct toxic effects , nephropathy Lead nephropathy, hyperuricemia, gout Psychosocial stress Thermal stress, noise, vibration

16. Cardiovascular ToxinsV. Cor Pulmonale Due to advances stages of pneumonconioses

17. Peripheral Vascular disease Vinyl chloride --- Raynaud�s syndrome Vibration--- vasospastic disease in small arteries of the hand -VWF

18. Pulmonary Function Assessment Critical parameter in cardio-respiratory assessment Valuable clinical parameter in assessment of exposures effects, monitoring, and impairment severity

19. Pulmonary Function Assessment Mandatory requirement of occupational assessment is some cases Asbestos (CFR 1910.1001) Cotton dust (CFR1910.10430 standards)

20. Pulmonary Assessment FEV1/FVC ratios of 70 or less require further assessment before respiratory clearance can be given

21. Occupational Asthma 5% of all asthma is occupationally related some occupations (flour milling, baking) incidence is 40%

22. Occupational Asthma NIOSH definition for occupational asthma dx of asthma assoc. between sxs and work

23. Occupational Asthma Airflow narrowing causally related in the work environment to dusts, vapors or fumes Type 1 IgE mediated cotton, wood dust, Western Red Cedars animal, bird dusts, excreta chemicals--diisocyanates metals--nickel, chromium, platinum, steel, cobalt

24. Occupational Asthma Byssinosis cotton dust, flax or hemp sxs occur dramatically on Monday after weekend of no exposure treatment at the the workplace -- exposure to steamed raw cotton eliminates the respiratory response

25. Occupational Asthma Hypersensitivity pneumonitis if asthma is the lung�s reaction to inhaled matter at the bronchial level, hypersensitivity pneumonitis is the reaction to inhaled material at the alveolar and terrminal bronchiole level

26. Hypersensitivity Pneumonitis Extrinsic allergic alveolitis resembles pneumonia mostly type 3 hypersensitivity Farmer�s lung, moldy hay bagassosis - moldy sugar cane suberosis - moldy cork

27. Hypersensitivity Pneumonitis Prototype is farmer�s lung onset fever and myalgias 4-8 hours after exp. cough and dyspnea sxs peak at 12 hours moderate cases x-ray-->infiltrate tx- remove from exposure repeated exposure -->fibrosis

28. Acute Respiratory Irritants Primarily caused by irritant gases and fumes ammonia chlorine sulfur dioxide nitric oxide ozone mercury vapor

29. Asbestosis Dose related disease with long latent period Asbestos body -- protein coated fiber which contains iron Cigarette smoke + asbestos ---> DNA damage Causes mesothelioma, lung cancer, pleural plaques and benign pleural effusions Spirometry ---> restrictive

30. Coal Worker�s Pneumonconiosis Typical lesion is pinhead sized macules loaded with black coal dust near alveolar ducts May progress rapidly from minor lesions to advanced forms Associated with centrolobular emphysema Spirometry ---> obstructive pattern

31. Silicosis Progresses slowly through increasingly severe disease May be carcinogenic Spirometry ---> restrictive

32. Neurotoxins Most common peripheral neurotoxins OP pesticides carbamates CS2 mercury lead arsenic antimony and acrylamide

33. Neurotoxins Most common CNS neurotoxins arsenic, lead (epilepsy) manganese (Parkinson�s) mercury CS2 Chlorinated hydrocarbons CO benzene, toulene, xylene

34. Neurotoxins Parkinson�s manganese CO CS2 MPTP n-methyl-4 phenyltetrahydropyridine

35. Arsenic Smelting, orchard spraying, sheep-dipping,grapevine growing, forestry Arsenic trioxide, arsenic pentoxide and arsine gas Exposure inhaltion ingestion skin

36. Arsenic Inhalation--nasal, pulmonary irritation Dermal irritant or allergic contact dermatitis Teratogenic, mutagenic, and carcinogenic

37. Arsenic Keratoses Keratoconjunctivits Myocardial damage (prolonged QT) Bone marrow hypoplasia Peripheral neuropathy sensory motor

38. Beryllium Used in aerospace industry, many alloys Exposure inhalation

39. Beryllium Chronic beryllium lung disease long latent period exertional dyspnea, cough hilar adenopathy rx: corticosteroids

40. Lead Plumbers, solderers, painters Batteries, glass, ceramics Exposure inhalation ingestion

41. Lead Storage compartments; blood/internal organs skin/muscles bone

42. Lead Organ systems affected gi bone marrow/circulating RBC�s CNS/PNS kidneys reproductive

43. Lead intoxication - effects In children almost all organs affected permanent damage at low levels nervous system and kidney ADD, learning disabilities, decrease intelligence, behavioral problems speech and language impairment decrease muscle and bone growth, hearing damage

44. Lead intoxication - effects In adults fetal damage/demise fertility problems hyptertension gi problems neurological disorders memory/concentration problems impotency

45. Lead poisoning - at what level? Childhood lead poisoning was redefined in 1990 by CDC blood lead level of 10 micrograms per deciliter or above

46. Lead Medical surveillance requirements Medical removal protection Role of chelation therapy

47. Lead intoxication -- action at what level? Blood lead level 0-9 10-14 15-19 20-44 45-69 >69 Action taken Routine testing Env/nutritional education, home lead check. Retest 3 months As above, referral, possible chelation chelation therapy emergency, chelation therapy and support

48. Cadmium Electroplating, fabrication,welding Colored pigments, batteries Exposure inhalation

49. Cadmium Storage sites: liver kidney Acute toxicity metal fume fever bronchial, pulmonary irritation rare, pulmonary edema

50. Cadmium Chronic toxicity renal proximal tubule damage impaired low MW protein absorption bone changes secondary to renal tubular dysfunction latent period of 10-20 years

51. Nickel Electroplating, production of catalysts, mining, smelting, refining Route of exposure inhalation dermal

52. Nickel Allergic contact dermatitis Respiratory tract irritant/asthma Carcinoma of lung and nasal sinus soluble nickel compounds--greatest risk metallic nickel--no increased risk

53. Nickel Carbonyl Acute Inhalation headache, fatigue, weakness, nausea influenza-like illness initial sxs clear--12-36 hour latent period, followed by severe SOB,CP

54. Vanadium Found in nature as insoluble salt, not metal Used in production of steel, alloys, catalysts, and dye manufacture Vanadium oxides--welding, brazing,cutting of steel

55. Vanadium Exposure inhalation eye Acute/chronic toxicity rhinorrhea, sneezing eye watering, sore throat cough, wheezing green tongue

56. Metal Fume Fever Associated with inhalation of metallo-oxides Zinc, copper, cadmium, magnesium Onset 4-6 hours after exposure

57. Metal Fume Fever Upper respiratory tract irritation Chest tightness, cough Headache, myalgias Fever, tachycardia Elevated WBC with shift

58. Reproductive Toxicity REPRODUCTIVE FUNCTION Women Who Are Pregnant Women of Child Bearing Age Men Teratogenicity

59. Reproductive Toxicity First occupational reproductive hazard Percival Pott but not taken seriously until 1975 lead exposed male workers in Romania 1977 DBCP in exposed male workers in California

60. Reproductive Toxicity Difficulty in studying repro toxicity in women nature of the female cycle relative frequency spontaneous abortions common occurrence of birth defects in general population

61. Male Reproductive Function Normal 70-80 days for spermatogenesis 20-350 million sperm/day 50-100 million sperm/ml Fertility Criteria >20 million sperm/ml >40% motile >70% normal morphology

62. Reproductive Function �Norms� Azospermai: 1/100 Low Birthweight (2.5kg): 7/100 Failure to conceive: 10-15/100 Spontaneous ab 10-20/100 Chromosomal abnormalities 30-40/100

63. Reproductive Function �Norms� Stillbirths: 2-4/100 Birth Defects: 2-3/100 Chromosomal abnormalities: 0.2/100 Severe retardation: 0.4/100

64. Regulated Agents in the Workplace Lead - seen at BLL of 40 mg/dl Ethylene oxide DCBP (dichlorobromopropane) banned by EPA

65. Summary of Repro Tox Studies Challenge arises due to: wide ranges of �normal reproductive variations� correlating exposure observed effect normal variation in critical outcome and birth-related factors