Occupational heart diseases

OCCUPATIONAL HEART DISEASES

Dr. Dalia Abdallah El-ShafeiLecturer, Community medicine department, Zagazig

University

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.

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

AGENT & WORK EFFECTS ON THE HEART

Angina

CO + Nitrates+ Temp

Atherogenesis

CS2

Dysrhythmias

Solvents

Cardiomyopathy

Co + As

Hypertension

Pb + CS2 + Noise

• 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

Psychological

• Brucellosis (Subacute bacterial endocarditis)

When you smell an odorless gas,

it is probably carbon monoxide.

Sources of incomplete combustion:

• Furnaces, boilers

• Internal combustion engine

(warehouses, auto plants)

Hazards increased in COLD

weather with closed doors &

windows

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

Chronic exposure to CO associated with

cardiovascular mortality:

NYC bridge & tunnel officers

??? Atherosclerosis

DIHALOMETHANES

”“METHYLENE CHLORIDE & BROMIDE

Solvent: degreasing, paint stripping

Absorption through respiratory route or

through skin

Metabolized in bloodstream to …… CO

METHYLENE CHLORIDE (CH2CL2)

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

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!

CO HALF LIFE

Ambient air

5 hs.

100% O2

1 h.

Hyperbaric O2

15-30 min.

% COHb = % CO in air X Time X K

At Rest

3

Light physical work

5

Heavy physical work

11

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

CARDIOVASCULAR PHYSIOLOGICAL CHANGES

↓COP + Threshold for

VF.

↑Myocardial LDH

2-4%→↓exercise

tolerance esp. in

COPD.

6%→↑ Multiple vent.

Premature cont. after

exercise + arrhythmias

in MI.

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.

NITRATES

Explosive industry:

- Ammonium

- Na nitrate

- Ethylene glycol dinitrate

- Nitroglycerine.

- Di- & Tri-nitrotoluene

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

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

CARBON DISULFIDE (CS2)

• Cellulose-derived materials

• Rayon

• Cellophane

• Solvent for rubber, oils

• Pesticides

• Fumigant for grain, books

• Microelectronics industry

Wood

Flakes

Raw

CelluloseCellulose

Xanthate

Viscose

Filtering

“Ripening”

SpinningRayon

Filaments

Zn++

H2SO4

CS2

CS2Lye

CS2

H + Solution

Viscose process for Rayon manufacture

Cellulose flakes after lye treatment

Viscose emerging from

spinneret. CS2 is given

off when viscose cross-

links to form rayon

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

Japanese CS2 workers

Retinal hemorrhages

Retinal microaneurysms

CARBON DISULFIDE

OSHA Standard: 20 ppm TWA8 ?????

NIOSH REL: 1 ppm TWA10

STEL: 15 ppm/15 minutes

NOISE

Bulldozer:

85dBAQuite Room:

30 dBA

Normal Conversation:

50 dBA

Normal City Noises:

65 dBA

Artillery/Good Rock Band:

120 dBA

↑EPINEPHERINE +

HYPERLIPEDAEMI

A

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

42

Moderate vibrationHigh 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

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

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.

HVlab

EXTREMES OF TEMPERATURE

Acute coronary artery disease

→ IHD → Angina + MI

Exacerbate heart problems.

Atherosclerosis

Idiopathic dilated cardiomyopathy.

Cold → Slow myocardial repolarization +

VF

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).

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)

Arrhythmias

Sinus brady- or -tachycardia

HB

Vent. Tachycardia

(torsade de pointes)

Prolonged Q-T

segment

↓ FEV1

Hypoxic effect on

heart

Co-inflammation in Coronary

artery

Atherosclerosis

Pre-existing

HF

Cigarette smoking

ObesitySedentary

life

Asbestosis (3-fold ↑ for IHD risk),

mainly with calcified plaques.

COBALT

Cobalt: used to stabilize beer foam

(1960’s: Canada, Belgium)

Cardiomyopathy reported in beer

drinkers several months afterward

(Quebecois beer drinkers)

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

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 + Thrombangitisobliterans + Hyperpigmentations + Keratosis +

Gangrene”

HTN

IHD “2-3 fold ↑”

Vasospastic “Raynaud” disease.

Arrhythmias “ Torsade de pointes”

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

Direct myotoxic action

JOB STRAINMain associations are with exposure to high psychological demands and low control over

job

10% of CVD.

HTN “ Bus drivers”

Shift work

SEDENTARY WORK

Physical Activity

Work- time (Anaerobic)

↑CAD

Leisure-time (Aerobic)

↓CAD

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 VS

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