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Dr. BALAMUGESH.T
Professor
Dept. of Pulmonary Medicine
CMC, Vellore
Scenario
 33 yr
 Nursing staff
 Past h/o allergic rhinitis
 Itching skin lesions, followed by cough, chest tightness
and breathlessness with wheeze in ward
 Following handling Inj Piptaz.
Occupational respiratory diseases
 Occupational allergies
 At risk population
 Diagnosis
 Smoke inhalation
 Infections
 Tuberculosis
 Influenza
Occupational allergies
 Under recognized
 Under diagnosed
 Under treated
 Under reported
 Common Occupational allergies
 Occupational asthma
 Occupational dermatitis
 Occupational rhinitis
 Occupational conjunctivitis
Occupational asthma
 Accounts for 5-10% of asthma in young adults
 New‐onset asthma:
 Hospital technicians (RR 4.63; 95% CI 1.87 to 11.5)
 Those using ammonia and/or bleach at work (RR 2.16;
95% CI 1.03 to 4.53).
Kogevinas M et al.
Lancet. 1999
Occupational asthma
 Of 182 cases of OA in HCWs over 10 years.
 75% - nursing, operating theatre, endoscopy and
radiology staff.
 70% - glutaraldehyde, latex and cleaning products
G. I. Walters et al. Occupational Medicine 2013;63:513–
516
Definition – occupational asthma
 Occupational asthma (OA) refers to
 de novo asthma or the recurrence of previously
quiescent asthma
 induced by
 sensitization to a specific substance, which is termed
sensitizer-induced OA, or
 exposure to an inhaled irritant at work, which is termed
irritant-induced OA (reactive airways dysfunction syndrome).
 Work related asthma
 Work exacerbated asthma + OA
OA
Agents causing OA
NEJM:
July
1995
Risk factors
 Level and duration of exposure
 Smoking
 Atopy
 Occupational rhinitis and conjunctivitis
 Genetic factors
Irritant-induced OA
 Exposure to airway irritants, in the absence of
sensitization
 New-onset asthma after exposure to very high levels of
alkaline dust from the collapse of the World Trade
Center
 16% of persons with high exposures at 1 year
 At 9 years 36% of them recovered.
Lower airway disease symptoms -
WTC dust exposure
 Irritant-induced asthma (of subacute onset),
 Nonspecific chronic bronchitis,
 Chronic bronchiolitis, or
 Aggravated preexistent obstructive pulmonary disease
Symptoms OA
 Cough,
 Breathlessness,
 Wheeze
Diagnosis
 History
 Examination
 PEFR
 Spirometry
 Serum IgE
 Skin prick test
 Methacholine challenge test
The Peak Flow Meter
like a thermometer for asthma
 Inexpensive clinic
instrument
 Monitoring
 Builds confidence in
treatment
 One ‘hard, fast blow’
Occupational asthma diagnosis
• Compatible history
• Detailed exposure history
• Spirometry with reversibility
• Bronchoprovocation test
• Establish the relationship
• Serial peak flow, BPT after exposure, Skin tests,
Immunoassay
Environmental Health Perspectives August 2000
 An estimated prevalence of sensitization among the
general healthcare worker population - 12.1 %
 4-7% : powder-free gloves
 It can be assumed that rates have decreased even
further with the increased use of non-latex gloves.
Latex allergy
Diagnostic tests for latex allergy
 Skin testing
 Extracts prepared with Hevea latex B and C serum
proteins
 Sensitivity 65 -96 % and specificity – 88-94 %
 Serology testing
 Hevea latex-specific IgE antibody
 Sensitivity – 70%, specificity - >95%
Glutaraldehyde induced asthma
 Cidex
 Agent used for disinfection
 The odour threshold of glutaraldehyde has been
reported to be 0.04 parts per million (ppm),
 Odour detection is a potential indicator that the
engineering controls are inadequate.
 Odour detection - unreliable
 Glutaraldemeter
 United Kingdom Health and Safety Executive which
also has established a 0.05 ppm Workplace Exposure
Limit (WEL)
Prevention
 Primary prevention
 reducing workplace exposure to potential
causal agents
 Substitution,
 Process modification,
 Respirator use,
 Engineering control with monitoring of
airborne exposure levels.
Secondary prevention
identify early evidence of subclinical
disease
 periodic medical surveillance by using tools such as
questionnaires, spirometry
Tertiary prevention
minimize effects of the workplace
environment on clinically manifest
disease
 Control of specific factors responsible for
disease onset or exacerbation/aggravation
 Change the person to another job.
Treatment
 Medical management of asthma
 Controller inhalers
 Rescue inhalers
Outcomes
 Factors predicting a worse outcome
 Smoking
 Lower PC20 at baseline, longer duration of exposure, and
the interval since removal of the patient from exposure
 Subjects with OA to HMW agents
 Typical plateau for improvement in spirometry is
around 1 year, whereas the plateau for improvement in
BPT occurs around 2 years
Smoke inhalation
Three types of injuries:
 Thermal injury to the upper airways,
 Chemical injury to the tracheobronchial tree, and
 Systemic poisoning due to carbon monoxide and/or
cyanide.
95 people, including members of the staff
Thermal injury: airway compromise
 Intubation is justified if any of the following signs are
present:
 Stridor,
 Use of accessory respiratory muscles,
 Respiratory distress,
 Hypoventilation,
 Deep burns to the face or neck, or blistering or edema of
the oropharynx.
 Oropharygeal examination -if erythema
 Do Larygoscopy
 Upper airway edema or blistering seen during
laryngoscopic exam should prompt intubation.
 Bronchoscopy instead of laryngoscopy
 if there is a history of inhalation
of superheated particles or steam,
Carbon monoxide poisoning
 Headache, nausea, malaise, altered cognition,
dyspnea, angina, seizures, coma, cardiac
dysrhythmias, heart failure, or bright "cherry red" lips.
 Detected by co-oximetry
 Treatment
 100% oxygen
 Hyperbaric oxygen.
Cyanide poisoning
 Burning of certain compounds (eg, polyurethane,
acrylonitrile, nylon, wool, and cotton)
 Clinical suspicion for cyanide poisoning should be
high
 Unexplained lactic acidosis, low arterial carbon
dioxide tension
 Treatment
 high flow oxygen,
 use of antidotes ( eg, sodium thiosulfate PLUS
hydroxocobalamin)
Prevention
Influenza in HCW
Olga Anikeeva et al, Am J Public Health. 2009
Additional benefits of vaccination
 Prevent sickness absenteeism
 Protect transmission to patients
SUMMARY
 High index of suspicion required for occupational
respiratory diseases
 Preparedness for smoke inhalation management.
THANK YOU
Cleveland clinic,
Nov 2013
Features of Irritant-Induced
Occupational Asthma.
ASSOCIATIONS BETWEEN OCCUPATIONAL EXPOSURES
AND ASTHMA AMONG TEXAS HEALTH CARE WORKERS:

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Vaccination of healthcare workers,

  • 1. Dr. BALAMUGESH.T Professor Dept. of Pulmonary Medicine CMC, Vellore
  • 2. Scenario  33 yr  Nursing staff  Past h/o allergic rhinitis  Itching skin lesions, followed by cough, chest tightness and breathlessness with wheeze in ward  Following handling Inj Piptaz.
  • 3. Occupational respiratory diseases  Occupational allergies  At risk population  Diagnosis  Smoke inhalation  Infections  Tuberculosis  Influenza
  • 4. Occupational allergies  Under recognized  Under diagnosed  Under treated  Under reported  Common Occupational allergies  Occupational asthma  Occupational dermatitis  Occupational rhinitis  Occupational conjunctivitis
  • 5. Occupational asthma  Accounts for 5-10% of asthma in young adults  New‐onset asthma:  Hospital technicians (RR 4.63; 95% CI 1.87 to 11.5)  Those using ammonia and/or bleach at work (RR 2.16; 95% CI 1.03 to 4.53). Kogevinas M et al. Lancet. 1999
  • 6. Occupational asthma  Of 182 cases of OA in HCWs over 10 years.  75% - nursing, operating theatre, endoscopy and radiology staff.  70% - glutaraldehyde, latex and cleaning products G. I. Walters et al. Occupational Medicine 2013;63:513– 516
  • 7. Definition – occupational asthma  Occupational asthma (OA) refers to  de novo asthma or the recurrence of previously quiescent asthma  induced by  sensitization to a specific substance, which is termed sensitizer-induced OA, or  exposure to an inhaled irritant at work, which is termed irritant-induced OA (reactive airways dysfunction syndrome).  Work related asthma  Work exacerbated asthma + OA OA
  • 8.
  • 10. Risk factors  Level and duration of exposure  Smoking  Atopy  Occupational rhinitis and conjunctivitis  Genetic factors
  • 11. Irritant-induced OA  Exposure to airway irritants, in the absence of sensitization  New-onset asthma after exposure to very high levels of alkaline dust from the collapse of the World Trade Center  16% of persons with high exposures at 1 year  At 9 years 36% of them recovered.
  • 12. Lower airway disease symptoms - WTC dust exposure  Irritant-induced asthma (of subacute onset),  Nonspecific chronic bronchitis,  Chronic bronchiolitis, or  Aggravated preexistent obstructive pulmonary disease
  • 13. Symptoms OA  Cough,  Breathlessness,  Wheeze
  • 14. Diagnosis  History  Examination  PEFR  Spirometry  Serum IgE  Skin prick test  Methacholine challenge test
  • 15. The Peak Flow Meter like a thermometer for asthma  Inexpensive clinic instrument  Monitoring  Builds confidence in treatment  One ‘hard, fast blow’
  • 16. Occupational asthma diagnosis • Compatible history • Detailed exposure history • Spirometry with reversibility • Bronchoprovocation test • Establish the relationship • Serial peak flow, BPT after exposure, Skin tests, Immunoassay
  • 18.  An estimated prevalence of sensitization among the general healthcare worker population - 12.1 %  4-7% : powder-free gloves  It can be assumed that rates have decreased even further with the increased use of non-latex gloves. Latex allergy
  • 19. Diagnostic tests for latex allergy  Skin testing  Extracts prepared with Hevea latex B and C serum proteins  Sensitivity 65 -96 % and specificity – 88-94 %  Serology testing  Hevea latex-specific IgE antibody  Sensitivity – 70%, specificity - >95%
  • 20. Glutaraldehyde induced asthma  Cidex  Agent used for disinfection
  • 21.
  • 22.  The odour threshold of glutaraldehyde has been reported to be 0.04 parts per million (ppm),  Odour detection is a potential indicator that the engineering controls are inadequate.  Odour detection - unreliable
  • 23.  Glutaraldemeter  United Kingdom Health and Safety Executive which also has established a 0.05 ppm Workplace Exposure Limit (WEL)
  • 24. Prevention  Primary prevention  reducing workplace exposure to potential causal agents  Substitution,  Process modification,  Respirator use,  Engineering control with monitoring of airborne exposure levels.
  • 25. Secondary prevention identify early evidence of subclinical disease  periodic medical surveillance by using tools such as questionnaires, spirometry
  • 26. Tertiary prevention minimize effects of the workplace environment on clinically manifest disease  Control of specific factors responsible for disease onset or exacerbation/aggravation  Change the person to another job.
  • 27. Treatment  Medical management of asthma  Controller inhalers  Rescue inhalers
  • 28. Outcomes  Factors predicting a worse outcome  Smoking  Lower PC20 at baseline, longer duration of exposure, and the interval since removal of the patient from exposure  Subjects with OA to HMW agents  Typical plateau for improvement in spirometry is around 1 year, whereas the plateau for improvement in BPT occurs around 2 years
  • 29. Smoke inhalation Three types of injuries:  Thermal injury to the upper airways,  Chemical injury to the tracheobronchial tree, and  Systemic poisoning due to carbon monoxide and/or cyanide.
  • 30. 95 people, including members of the staff
  • 31. Thermal injury: airway compromise  Intubation is justified if any of the following signs are present:  Stridor,  Use of accessory respiratory muscles,  Respiratory distress,  Hypoventilation,  Deep burns to the face or neck, or blistering or edema of the oropharynx.
  • 32.  Oropharygeal examination -if erythema  Do Larygoscopy  Upper airway edema or blistering seen during laryngoscopic exam should prompt intubation.  Bronchoscopy instead of laryngoscopy  if there is a history of inhalation of superheated particles or steam,
  • 33. Carbon monoxide poisoning  Headache, nausea, malaise, altered cognition, dyspnea, angina, seizures, coma, cardiac dysrhythmias, heart failure, or bright "cherry red" lips.  Detected by co-oximetry  Treatment  100% oxygen  Hyperbaric oxygen.
  • 34. Cyanide poisoning  Burning of certain compounds (eg, polyurethane, acrylonitrile, nylon, wool, and cotton)  Clinical suspicion for cyanide poisoning should be high  Unexplained lactic acidosis, low arterial carbon dioxide tension  Treatment  high flow oxygen,  use of antidotes ( eg, sodium thiosulfate PLUS hydroxocobalamin)
  • 36. Influenza in HCW Olga Anikeeva et al, Am J Public Health. 2009
  • 37. Additional benefits of vaccination  Prevent sickness absenteeism  Protect transmission to patients
  • 38. SUMMARY  High index of suspicion required for occupational respiratory diseases  Preparedness for smoke inhalation management.
  • 41.
  • 43. ASSOCIATIONS BETWEEN OCCUPATIONAL EXPOSURES AND ASTHMA AMONG TEXAS HEALTH CARE WORKERS: