Two important facets of cardiac disease as it relates to health at work. Agents used in the workplace may produce toxic effects manifested as heart disease or dysfunction. Possibly more important, however, is the effect that heart disease (common in Western society) has on the ability to work.

1. OCCUPATIONAL HEART DISEASES
Dr. Dalia Abdallah El-Shafei
Lecturer, Community medicine department, Zagazig
University

2. OCCUPATIONAL HEALTH & THE HEART
 Primary causes of
disease
 Exacerbations of
underlying disease
 Attribution & workers’
compensation
 Work capacity &
abilities
 Workplace as focus for
prevention efforts
Workplace
exposures & their
effects on the heart
Cardiovascular
health & its
effects on work
1-3% of CVD deaths are work-related.

3. PROBLEMS IN IDENTIFICATION OF
OCCUPATIONAL ETIOLOGIES OF CVD
 Common in our society:
Increased risks superimposed on high baseline
 Multifactorial etiology:
Work contributions difficult to tease out
 Long latency
 No accurate noninvasive tests for early disease
 Similar Clinical expressions with non-
occupational cause

4. AGENT & WORK EFFECTS ON THE HEART
Angina
CO + Nitrates+ Temp
Atherogenesis
CS2
Dysrhythmias
Solvents
Cardiomyopathy
Co + As
Hypertension
Pb + CS2 + Noise

5. • Extremes of Temperature
• Noise - Vibration.
• Radiation - Electricity.
Physical
• CO - CS2
• Nitrates - Solvents -
OPC+Carbamates
• Heavy metals (As, Pb, An, Co, Cd)
Chemical
Biological
• Psychological Stress + Shift Work
• Sedentary Work
Psychologic
al
• Brucellosis (Subacute bacterial endocarditis)

7. When you smell an odorless gas,
it is probably carbon monoxide.

9. Sources of incomplete combustion:
• Furnaces, boilers
• Internal combustion engine
(warehouses, auto plants)
Hazards increased in COLD
weather with closed doors &
windows

10. AT RISK OCCUPATIONS
 Fire fighters
 Garage mechanics
 Aircraft refuelers
 Truck Drivers
 Kiln & furnace operators
 Forklift operators
 Janitorial staff
 Disaster relief workers
 Miners
 Parking garage attendants
 Agricultural workers

11. Chronic exposure to CO associated with
cardiovascular mortality:
NYC bridge & tunnel officers
??? Atherosclerosis

12. DIHALOMETHANES
”“METHYLENE CHLORIDE & BROMIDE

13.  Solvent: degreasing, paint stripping
 Absorption through respiratory route or
through skin
 Metabolized in bloodstream to …… CO
METHYLENE CHLORIDE (CH2CL2)

14. May elevate COHb to 10% or more especially in
poorly ventilated space
Probably not significant to healthy person; may
become mildly symptomatic
Cigarette smokers, those with angina or current CHD
a concern: excess CO may trigger symptoms
METHYLENE CHLORIDE

15. Methylene Chloride
OSHA Standard: 25 ppm/ TWA8: STEL 125 ppm
NIOSH: As low as can be achieved (carcinogen)
Because of metabolic conversion to
CO, the biological life of COHb from
methylene chloride is longer than that
from direct CO exposure
!

16. CO HALF LIFE
Ambient air
5 hs.
100% O2
1 h.
Hyperbaric O2
15-30 min.

18. % COHb = % CO in air X Time X K
At Rest
3
Light physical work
5
Heavy physical work
11

19. CARBON MONOXIDE  CARBOXYHEMOGLOBIN
 Binds to Hb more avidly
than O2 (200x)
 Shifts oxygen dissociation
curve to “left”: Tissue anoxia
 Binds mitochondrial enzymes &
myoglobin (50x)
 Increases platelet stickiness
 Deceases arrhythmia threshold

22. CARDIOVASCULAR PHYSIOLOGICAL CHANGES
↓COP + Threshold for
VF.
↑Myocardial LDH

23.  2-4%→↓exercise
tolerance esp. in
COPD.
 6%→↑ Multiple vent.
Premature cont. after
exercise + arrhythmias
in MI.

25. Carbon monoxide: Exposure limits
NIOSH REL: 35 ppm for 10-hour TWA
Equivalent to 5% COHgb level
OSHA PEL: 50 ppm /TWA8
ACGIH: TLV®
: 25 ppm/ TWA8
.

27. NITRATES

28. Explosive industry:
- Ammonium
- Na nitrate
- Ethylene glycol dinitrate
- Nitroglycerine.
- Di- & Tri-nitrotoluene

29. Acute effects in workers noted in early 1960s:
Sudden death:
24-96 hours after exposure ceased
(weekends/holidays)
“Monday Morning Angina”:
Relieved by RTW, nitrate meds: coronary spasm
in absence of CAD
3 -fold increase in acute deaths in
younger men from IHD

30.  Potent VD → Throbbing headache ("NG head" or
"bang head“ or “ Powder head”) + Tachycardia +
Palpitation → Tolerance → Withdrawal (Weekend,
vacations) → Rebound VS → Monday Morning
Angina + Monday Morning death.
 Family members (Take home exposure)
 MetHb → IHD
 PN

31. CARBON DISULFIDE (CS2)

32. • Cellulose-derived materials
• Rayon
• Cellophane
• Solvent for rubber, oils
• Pesticides
• Fumigant for grain, books
• Microelectronics industry

33. Wood
Flakes
Raw
Cellulose
Cellulose
Xanthate
Viscose
Filtering
“Ripening”
SpinningRayon
Filaments
Zn++
H2SO4
CS2
CS2Lye
CS2
H + Solution
Viscose process for Rayon manufacture

34. Cellulose flakes after lye treatment
Viscose emerging from
spinneret. CS2 is given
off when viscose cross-
links to form rayon

35. RR of 2 to 5x for death from CAD
Direct role in atherogenesis in blood vessels
↑ LDL
Enzyme inhibition by metabolites of CS2
{Dithiocarbamates & carbonyl sulfate (COS)}.
• React with amino acids to form dithiocarbamates: these
chelate trace metals & react with enzyme cofactors
• Interfere to ↑ elastase activity, disrupting Bl.vessel walls
• ↓ fibrinolytic activity & enhance thrombosis
CARBON DISULFIDE & ATHEROGENESIS

36. Japanese CS2 workers
Retinal hemorrhages
Retinal microaneurysms

37. CARBON DISULFIDE
OSHA Standard: 20 ppm TWA8 ?????
NIOSH REL: 1 ppm TWA10
STEL: 15 ppm/15 minutes

38. NOISE
Bulldozer:
85dBA
Quite Room:
30 dBA
Normal Conversation:
50 dBA
Normal City Noises:
65 dBA
Artillery/Good Rock Band:
120 dBA

40. ↑EPINEPHERINE +
HYPERLIPEDAEMI
A

41. Each ↑5 dB → ↑ 0.5 mmHg in systolic Bl.pr

42. 42
Moderate vibration
High vibration
 impact wrenches
 carpet strippers
 chain saws
 percussive tools
 jack hammers
 scalers
 riveting or chipping
hammers
• grinders
• sanders
• jig saws
HAND ARM VIBRATION SYNDROME “HAVS”

43. 43
HAV SYMPTONS
 Attacks of whitening (Blanching) of one or
more fingers when exposed to cold/wet
 Tingling & Numbness in the fingers
 Loss of light touch
 Pain & cold sensations between periodic white
finger attacks
 Loss of grip strength
 Bone cysts in fingers and wrists

45. PERIPHERAL VASCULAR DISEASE
 Amplification of response of α2-
adrenoreceptors, norepinepherine constriction
receptors on vascular smooth muscle cells in
hand blood vessels.
 Chronic PN.
 ↑ Blood viscosity.

46. HVlab

48. EXTREMES OF TEMPERATURE
 Acute coronary artery disease
→ IHD → Angina + MI
 Exacerbate heart problems.
 Atherosclerosis
 Idiopathic dilated cardiomyopathy.
 Cold → Slow myocardial repolarization +
VF

49. CFC & SOLVENTS & PESTICIDES
 Chlorofluorocarbons (Freon® etc)
• Refrigeration, air conditioning,
propellants.
• ↑ Myocardial sensitiivity to
catecholamines effects
(↑ with Noise)
• Direct myotoxic action
• Occasional deaths (excess physical
activity near leaking refrigerants).

50.  Other solvents implicated in sudden death
(first noted in solvent abusers & glue
sniffers):
 Trichloroethylene, Trichloromethan,
Perchloroethylene, Toluene, Benzene, Xylene,
Gasoline.
 Halogenated derivatives of aliphatic
hydrocarbons are more active than corresponding
hydrocarbons (Tetrachloroethan more active than
Ethan)

51. Arrhythmias
Sinus brady- or -
tachycardia
HB
Vent. Tachycardia
(torsade de pointes)
Prolonged
Q-T
segment

52. ↓ FEV1
Hypoxic
effect on
heart
Co-
inflammation
in Coronary
artery
Atherosclerosis
Pre-
existing
HF
Cigarette
smoking
Obesity
Sedentary
life

53. Asbestosis (3-fold ↑ for IHD risk),
mainly with calcified plaques.

54. COBALT
 Cobalt: used to stabilize beer foam
(1960’s: Canada, Belgium)
 Cardiomyopathy reported in beer
drinkers several months afterward
(Quebecois beer drinkers)

55. Dose-related: seen in heavy drinkers
greatest risk in those drinking >10L/day (!)
22 - 50% mortality in some series
Why this group?????
CM not seen in cobalt therapy for
anemia
Probable synergistic effect with Alcohol
& Poor Diet

56. ARSENIC
 Cardiomyopathy (beer drinkers of As contaminated
beer “2-4 ppm”) → congestive HF
 Peripheral vascular disease:
- 0.8-1.8 ppm As contamination of drinking water in
Chile & Taiwan “Normal <0.01” → Black foot
syndrome “Arteriosclerosis + Thrombangitis
obliterans + Hyperpigmentations + Keratosis +
Gangrene”
 HTN
 IHD “2-3 fold ↑”
 Vasospastic “Raynaud” disease.
 Arrhythmias “ Torsade de pointes”

58. ANTIMONY&CADMIUM&LEAD
Lead:
 HTN, probable mechanism is via renal injury
 May also increase vascular tone and
resistance
Chelation may improve HTN in acute
intoxication, but not reverse with longstanding
renal damage Cadmium
 HTN; occur at levels below nephrotoxic dose
Antimony

59. JOB STRAIN
Main associations are with exposure to high
psychological demands and low control over
job

61.  10% of CVD.
 HTN “ Bus drivers”

62. Shift work

63. SEDENTARY WORK
Physical Activity
Work- time
(Anaerobic)
↑CAD
Leisure-time
(Aerobic)
↓CAD

64. SOCIAL CLASS & CVD
Increased CHD mortality
related to social status.
Unskilled manual workers
(Class V) have
considerably increased
risk when compared with
professionals (Class I)
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