The document discusses two occupational health hazards: noise and carbon monoxide. It describes the auditory and non-auditory effects of noise exposure, including temporary and permanent hearing loss. It also discusses the signs and symptoms of acute and chronic carbon monoxide poisoning, how carbon monoxide binds to hemoglobin, and its clinical effects like headache and nausea. Diagnosis involves measuring carboxyhemoglobin levels and treatment requires removal from exposure and supplying oxygen.

1. Occupational diseases -VII
Group B

2. Contents Occupational health hazards of noise
 Auditory
 Non-auditory
Carbon monoxide and occupational health
Contents

3. Noise and
occupational
hazards
 Noise is an unwanted sound, causing disturbance or
annoyance to the hearer.Therefore, noise is a
‘nuisance’.
 The term ‘Noise pollution’ signifies the cacophony of
sounds that are being produced in the modern life,
leading to health hazards.

5. Auditory
Effects
A. Quantifiable:
 Threshold shift (temporary, later
permanent).Auditory fatigue
(associated with whistling and
buzzing)The temporary hearing loss
occurs in frequency range between
4,000 to 6,000 Hz.
 Repeated or continuous exposure to
the noise around 100 dB may result in
permanent deafness.
 Exposure to noise above 160 dB may
cause rupture of tympanic membrane
and cause permanent deafness.
B. Non-quantifiable:
 Tinnitus (ringing or buzzing or
whistling
 Vertigo

7.  Acoustic trauma: Sudden hearing damage caused by short burst of
extremely loud noise such as a gun shot.
 Tinnitus: Ringing or buzzing in the ear.
 Temporary hearing loss:Also known as temporary threshold shift
(TTS) which occurs immediately after exposure to a high level of
noise.There is gradual recovery when the affected person spends
time in a quiet place.Complete recovery may take several hours or
days (up to 48 hours).
 Permanent hearing loss: Permanent hearing loss, also known as
permanent threshold shift (PTS), usually progresses constantly as
noise exposure continues month after month and year after year.
Most individuals do not notice the impairment at first.The hearing
impairment is noticeable only when it is substantial enough to
interfere with routine activities.At this stage, permanent and
irreversible hearing damage has occurred. Noise-induced hearing
damage cannot be cured by medical treatment and worsens as the
noise exposure continues.

8.  When the noise exposure stops, the person does not regain the
lost hearing sensitivity.As the employee ages, hearing may
worsen as "age-related hearing loss" adds to the existing noise-
induced hearing loss.
 Permanent hearing loss can also occur from a single traumatic
event.

10. NonAuditory
Effects
 Fatigue
 Irritability
 Nervousness
 Interference with speed and communication
 Annoyance
 Increased intracranial tension
 Hypertension
 Peptic ulcer
 Higher environmental stress

11. a. Reference with speech-
 Noise interferes with speech communication .In everyday life ,the
frequencies causing most disturbance to speech communication lie
in the 300-500Hz.Such frequencies are commonly present in noise
produced by road and air traffic.
 For good speech intelligibility, it is considered that the speech sound
level must exceed the SIL ( speech interference level)by
approximately 12dB.
b. Annoyance:
 This is primarily a psychological response. Neurotic people are more
sensitive to noise than balanced people.
 Workmen exposed to higher intensity of noise in occupational
capacities, were often irritated, short tempered and impatient and
more likely to resort to agitation and disrupt production.
c. Efficiency:
 Reduction in noise has been found to increase work output.

12. c. Physiological changes:
 A number of temporary physiological changes occur in the human
body as a direct result of noise exposure.These are- a rise in blood
pressure, a rise in intracranial pressure, an increase heart rate and
breathing and an increase in sweating.
 Noise interferes sleep. Noise is also said to cause visual disturbance.
It is said to cause a narrowing of pupil, affect color perception and
reduce night vision.
d. Besides affecting health ,noise is also a significant factor in
economic losses.The potential cost of noise induced hearing
loss to industry is quite great.
e. Lack of concentration.

13. Occupations commonly
involved in loud noises
• Agriculture
• Mining
• Construction
• Manufacturing
• Public utilities
• Transportation
• Military drill/warfare

14. Carbon
monoxide &
occupational
health
 Carbon monoxide (CO) is a colorless, odorless, and tasteless
flammable gas that is slightly less dense than air.
 It is toxic to animals that use hemoglobin as an oxygen carrier
(both invertebrate and vertebrate) when encountered in
concentrations above about 35 ppm.
 It is a byproduct of combustion reaction, or the burning of certain
fuels.
 CO can be emitted from gasoline powered engine; natural gas
heating system; oil, coal, propane; wood and other material which
may also release CO when burned.

15. EFFECTS OF CO
 CO binds more readily to hemoglobin (Hb B) displacing oxygen
and forming carboxyhaemoglobin.
 premature release of O2 prior to reaching distal tissue leads to
hypoxia at the cellular level.
 inflammatory response is initiated due to poor and inadequate
tissue perfusion.
 myocarxial depression from CO
exposure;dysrhythemia,MI,myocardial ischaemia.
 vasodilation-from increased release of nitric oxide worsening
tissue perfusion and leading to syncope.

16. Clinical
features
ACUTE POISONING: Early (non
specific); 2 classic features: Cherry
red colour (blood, tissue) &
Cutaneous blister.
Based on severity
1) Mild:
 Headache
 Nausea
 Vomiting
 Dizziness
 exertional dyspnoea
2) Moderate:
 chest pain
 blurred vision
 Confusion
 Weakness
 tachycardia
 tachypnoea
3) severe:
 Trismus
 muscle spasm
 Convulsion
 Palpitation
 Hypotension
 MI
 respiratory failure
 coma

17. CHRONIC POISONING
 headache ,dizziness, confusion.
 weakness, nausea, vomiting, abdominal pain.
 Paraesthesia
 visual disturbance
 Hypertension
 Hyperthermia
 cherry red skin
 Palpitation
 aggravation of angina

18. DIAGNOSIS:
 estimation of CO Hb level
 pulse oximetry
 arterial blood gases
 ECG-chest X-ray
TREATMENT:
 immediate removal from contaminated environment
 100%O2
 endotracheal tube
 monitor C&D
 neurologic exam + CAT scan + fundoscopic exam
 if ICT increased  Hyperventilation, head elevation, mannitol.

19. References
 K Park’s PSM
 A H Suryakantha’s PSM
 www.bing.com/images

20. Group
Members
 Roll no. 11  Pranshu Dwivedi
 Roll no. 12  Siddharth Gurung
 Roll no. 13  Mohsin Ahmed Ansari
 Roll no. 14  Gemin Langkam
 Roll no. 15  Radhe Nampi
 Roll no. 16 Yanu Kodak
 Roll no. 17  Nani Kuru
 Roll no. 18  Marjum Haji
 Roll no. 19 Tiling Rema
 Roll no. 20 Tadar Matma