Transcript Occupational lung disease - University of California, Irvine

Occupational Lung Disease
Marion J. Fedoruk MD, CIH, DABT, FACMT, FACOEM
December 8, 2014, University of California , Irvine
Medical Center
Objectives
Identify major types of occupational lung
disease in US
 Describe clinical characteristics of work
related asthma
 Provide description of preventive
measures that can be taken for
occupational asthma
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Case presentation
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38 year old male presents with 11 month history of rhinitis,
followed by cough, shortness of breath and chest tightness.
No environmental (seasonal) medication or aspirin allergy
Ex-smoker: 5 pack years, occasional marijuana - no change
Occupation: automobile painter for 3 years
Otherwise well
Symptoms: worse at end of the workday – improves on
weekends and vacations
Physical exam: un-remarkable. Cardiac and lung sounds were
normal. There were no inspiratory or expiratory wheezes,
nor a prolonged expiratory phase.
Thoughts?
Clues for occupational association
The temporal variation of symptoms in association with
work, the absence of pre-existing asthma
 Physical exam findings are normal which is not uncommon
between episodes of asthma
 When did he last work when you saw him?
 Paint can contain both irritants and sensitizers that cause or
aggravate asthma
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Asthma
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Approximately 7.5% of all US adults have a
diagnosis of asthma
Work-related asthma is the most commonly
reported occupational lung disease in the United
States
Work-related asthma is often under recognized and
misdiagnosed
Source: Dykewicz MS. Occupational asthma: current concepts in pathogenesis, diagnosis,
and management J Allergy Clin Immunol. 2009;123(3):519.
Work-Related Asthma
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Occupational asthma
a) Occupational asthma with latency
(immunologic)
b) Occupational asthma without latency Reactive
Airways Dysfunction Syndrome (RADS) or
irritant-induced asthma (non immunologic)
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Work aggravated asthma
exacerbation as a result of a workplace exposure
in an individual with a prior history of asthma
Occupational Asthma
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Form of work-related asthma characterized by
variable airflow obstruction, airway hyper
responsiveness, and airway inflammation
attributable to a particular exposure in the
workplace and not due to stimuli encountered
outside the workplace
Tarlo et al. Diagnosis and management of work-related asthma: American College
Of Chest Physicians Consensus Statement Chest. 2008;134(3 Suppl):1S.
Work-exacerbated asthma
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Proportion of individuals with asthma who have
worsening asthma symptoms at work (workexacerbated asthma) is approximately 10
percent meta-analysis of 43 risk estimates from
19 different countries that suggested that 10
percent of all adult-onset asthma cases appear
to be occupationally related
Source: Torén K, Blanc PD Asthma caused by occupational exposures is
common - a systematic analysis of estimates of the population-attributable
fraction. BMC Pulm Med. 2009;9:7. Epub 2009 Jan 29.
Work up: occupational history
Workplace Exposure History: Obtain
employment history, including past and present
jobs. Carefully document both job tasks and
production processes
 Did symptoms change (improve/deteriorate)
with the introduction of a new chemical, new
production process, or the institution of
administrative and engineering controls?
 Obtain material safety data sheets from the
employer
 Are or have co-workers been affected?
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Objective testing to verify asthma
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Medical history alone insufficent
Objective Testing to verify work
related
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Pre and post shift monitoring of lung function
Spirometry
PEF at and off work for period of several weeks
- 4 times daily, preferable every 2 hours
NSBH related to work cycle
Gold standard specific inhalation challenge
generally available
Patterns of response
PEF monitoring
False positive
 Subjects not exposed
 Poor compliance
 False negative
 Change of medications
 Bronchitis
 Malingering
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PEF issues
Sensitizers
High molecular weight agents (e.g., wheat flour)
sensitize a worker via an IgE mediated process.
Atopy is known to increase the risk of OA to
high molecular weight agents.
 Low molecular weight agents (e.g., diisocyanates)
often sensitize a worker via interactions with
endogenous proteins inducing a physiologic
response
 High exposures in the workplace to known
sensitizers, can increase the risk of sensitization
and the development of occupational asthma
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Isocyanates
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Family of highly reactive, low molecular weight
chemicals
Widely used: flexible and rigid foams, fibers, coatings
such as paints and varnishes, elastomers, automobile
industry, autobody repair, building insulation
materials,
Spray-on polyurethane products containing
isocyanates for wide range of retail, commercial, and
industrial uses to protect cement, wood, fiberglass,
steel and aluminum, including protective coatings for
truck beds, trailers, boats, foundations, and decks.
How should we manage our case:
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Primary treatment: removal of exposure
If not removed?
Can exposure be controlled to control disease
Personal protective measures
Keep in position with medication control
Desensitization?
Occupational lung disease-how big a
problem?
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What type of disease?
Spectrum
What is size of affected population?
Where can I find this out?
Lack of standardized reporting, and issues with case
identification/misdiagnosis
The Spectrum of Occupational Lung Disease
COPD Overview
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2003, 10.7 million United States adults were estimated
to have COPD.
About 14 % of the U.S. adult population (25+ years)
have been diagnosed with COPD
About 24 million adults were estimated to have
impaired lung function, suggesting under-diagnosis of
COPD.
Leading cause of morbidity and mortality in the United
States and world-wide
Fourth leading cause of death
Tobacco smoking is overwhelmingly the most important
risk factor for COPD
Other risk factors operative: COPD non smokers
Source: Braman, S. Update on the ATS Guidelines for COPD. Medscape Pulmonary Medicine. 2005;9(1):1.
Occupational COPD
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15% of COPD is attributable to occupation
Long term exposure
Dusts: (inorganic) and organic; chemicals
Chemicals-vapors irritants , fumes
3rd NHANES: increased risk for COPD - number of
industries: rubber, plastics, leather manufacturing;
utilities; building services; textile manufacturing;
construction
Establish work relatedness of
COPD
Mostly based upon epidemiological evidence
 In individual patient, work relatedness is difficult
to establish
 Diagnosis by exclusion. Easier if patient is non
smoker
 In smoker, often not possible to apportion
effect of smoking from occupational exposure
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Bronchiolitis and bronchiolitis obliterans
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General terms used to describe a nonspecific
inflammatory injury that primarily affects the small
airways (eg, less than 2 mm in diameter), often sparing
a considerable portion of the interstitium
Describe both a clinical syndrome and a constellation
of histopathologic abnormalities: found in variety of
disorders
Much of the literature about bronchiolitis consists of
isolated case reports or small case series.
Tissue confirmation of the diagnosis has not been
described in many of these reports
Uncertainties remain regarding the epidemiology,
pathophysiology, long-term sequelae, and therapy of
bronchiolitis.
Clinical classification:
based primarily upon etiology
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Inhalational injury, nitrogen oxides, ammonia, welding fumes,
or food flavoring fumes (eg, diacetyl);
Infections: respiratory syncytial virus, adenovirus,
Mycoplasma pneumoniae; Legionella
Drug-induced reaction: e.g. busulfan, gold, penicillamine.
Post Transplant
HIV associated
Idiopathic cases are often characterized by the insidious
onset of cough or dyspnea. An obstructive ventilatory
defect, without significant responsiveness to
bronchodilators, may be present. These cases are frequently
confused with more common causes of these symptoms,
such as asthma or chronic obstructive pulmonary disease
(COPD).
Popcorn lung: bronchiolitis obliterans in
workers in a microwave-popcorn plant
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Eight former employees of a microwavepopcorn plant were reported to have severe
bronchiolitis obliterans (between 1993-2000)
Diacetyl was flavoring agent thought to cause
disease
Newer term: Flavorings-Related Lung Disease
California OSHA passes diacetyl standard
calling for medical surveillance of exposed
workers
Diacetyl diagnostic issues
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Symptoms cough (usually without phlegm), wheezing, and dyspnea
on exertion
Spirometry: fixed airways obstruction
Lung volumes: hyperinflation
High-resolution CT (inspiration/expiration) may reveal
heterogeneous air trapping on the expiratory view as well as
haziness and thickened airway walls
Lung biopsies: constrictive bronchiolitis obliterans (i.e., severe
narrowing or complete obstruction of the small airways).
An open lung biopsy, such as by thoracoscopy, is required for a
pathologic diagnosis (in contrast to a transbronchial biopsy).
Special processing, staining, and review of multiple tissue sections
may be necessary for a diagnosis. However, even open lung biopsy
appears to be insensitive because of the patchiness of the
pathologic abnormality and the ease with which the diagnosis has
been initially missed even by experienced chest pathologists
What about interstitial lung disease
Hypersensitivity pneumonitis: allergic
alveolitis
 Pneumoconiosis (mineral dusts)
 Beryllium
 Hard metal disease
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Hypersensitivity pneumonitis
Hypersensitivity pneumonitis is a
spectrum of granulomatous,
interstitial, and alveolar-filling lung
diseases that result from repeated
inhalation of and sensitization to a
wide variety of organic dusts
Clinical findings
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Acute: abrupt onset (four to six hours following
exposure) of fever, chills, malaise, nausea, cough, chest
tightness, and dyspnea without wheezing. Physical
examination is notable for tachypnea and diffuse fine
crackles. Wheezing is rarely present. Confused with a viral
or bacterial infection, patients are frequently treated
initially with antibiotics Arterial blood gases may show
mild hypoxemia fever
Subacute or intermittent — Subacute HP is characterized
by the gradual development of productive cough, dyspnea,
fatigue, anorexia, and weight loss. Similar findings may
occur in patients who suffer repeated, infrequent acute
attacks of HP characterized by cough and malaise
Chronic HP may lack a history of acute episodes and
usually reports the insidious onset of cough, dyspnea,
fatigue, and weight loss.
Pneumoconioses
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Group of interstitial lung diseases caused by the
inhalation of certain dusts and the lung tissue’s
reaction to the dust
Primary pneumoconiosis are asbestosis, silicosis,
and coal dust
Other forms aluminum, antimony, barium, graphite,
iron, kaolin, mica, talc, among other dusts. There is
also a form called mixed-dust pneumoconiosis.
Typically many years
Some cases – silicosis, particularly – rapidly
progressive forms can occur after only short
periods of intense exposure
Crystalline silica
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At least 1.7 million U.S. workers are exposed to
respirable crystalline silica in a variety of industries
and occupations, including construction, sandblasting,
and mining.
Silicosis, with occupational exposure to the material,
which also is known as silica dust.
Occupational exposures to respirable crystalline
silica are associated with the development of
silicosis, lung cancer, pulmonary tuberculosis, and
airways diseases.
May be related to development of autoimmune
disorders, chronic renal disease
A Bangladeshi garment laborer works in a
sandblasting factory in Dhaka, 2011
(MUNIR UZ ZAMAN/AFP/Getty Images)
Coal workers pneumoconiosis
Inhalation and deposition of silica-free
coal dust particles that induce the
formation of coal macules, once they
reach the alveoli.
 Radiographic features to silicosis, but is
classified as a separate disease due to its
rather characteristic pathologic findings
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Asbestos exposure
Asbestosis = parenchymal disease
interstitial fibrosis
 Malignant mesothelioma (pleural, parietal ,
testicular - (tunica vaginalis not shown to
be related)
 Lung cancer: all types
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Hard metal disease
Cobalt-tungsten carbide alloy – sintered
 Abrasion resistance - high temperature
machine cutting tools-cut through stainless
steel, bridal jewelry, surgical instruments,
armor piercing ammunition,
 Pneumoconiosis (fibrosis)- dust and fumes
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Lung Cancer Epidemiology
Occupational Exposure
 Several occupational carcinogens
 Attributable risk 7.4% males and 3.1% females
Environmental exposures
 Outdoor particulate matter
 Residential radon exposure (attributable risk 7% in US)
 Environmental tobacco smoke
 Enviromental exposure to occupational carcinogens
 low dietary intake; other factors
Sources: Samet J. J Natl Cancer Inst 1989
and Steenland K et al. Am J Ind Med 1996
Occupational lung cancer agents
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Arsenic
Asbestos
BCME
Beryllium
Cadmium
Chromium 6
Silica dust
Nickel
Ionizing radiation
Occupational exposure to strong inorganic acids
Sulfur mustard
Polycyclic aromatic hydrocarbons
Soot
Coal tar pitch
Diesel exhaust
Source :IARC
Occupational lung cancer occupations
Aluminium production
 Coal gasification
 Coke production
 Hematite mining
 Iron and steel founders
 Painting
 Rubber production
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Source :IARC