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LECTURE AGENDA:. Cardiopulmonary AssessmentPulmonary AssessmentCommon toxidromescardiacpulmonaryrenalneurotoxins. Cardiopulmonary Assessment. Thorough history and physicalStatic electrocardiographyDynamic electrocardiographyPulmonary function testing. Cardiopulmonary Assessment. Important
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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