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.
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)
6.
7. When you smell an odorless gas,
it is probably carbon monoxide.
8.
9. Sources of incomplete combustion:
• Furnaces, boilers
• Internal combustion engine
(warehouses, auto plants)
Hazards increased in COLD
weather with closed doors &
windows
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
!
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
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
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
44.
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.
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)
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”
57.
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
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)
50
70
90
110
130
150
170
190
I II III IV VSTANDARDIZEDMORTALITYRATIO