Transcript No Slide Title

Smoking
and Occupational Health
Association of Occupational and Environmental Clinics
(AOEC)
National Institute for Occupational Safety and Health
(NIOSH)
Curriculum Models in Occupational Health
Developed by
William S. Beckett M.D., M.P.H., Dina Markowitz Ph.D.
Occupational Medicine and Pulmonary and Critical Care Divisions
University of Rochester School of Medicine and Dentistry
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Introduction
• Many cases of occupational lung disease
formerly attributed to smoking alone
• Occupational hazards and smoking remain
common; both pose risks to workers.
• Interactions may be additive, or greater than
additive.
• Most smokers do not develop significant lung
disease, but interaction with occupational
exposures increases risk
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Interactions Between Occupational
Exposures and Smoking
• Additive: the effect of combination of
agents is the same as the sum of
individual effects
• Greater than additive (multiplicative
synergistic): effect is more than the sum
of individual effects
• Antagonistic: one factor reduces the
excess disease caused by another.
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Overview:
Smoking/Workplace Interactions
A. Lung Diseases
1. Malignant
2. Non-malignant
B. Cardiovascular Disease
C. Urologic (Bladder, Kidney)
Diseases
D. Injuries and mortality
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Outcome Measures for Interactions
•
•
•
Disease Incidence
Disease severity
-- Symptoms
-- Pulmonary Function
(FEV1,Diffusing capacity)
-- X-ray changes
Premature Mortality
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Smoking Related Respiratory
Disease
Caused by cigarette smoking:
1. Chronic bronchitis
2. COPD (Emphysema)
3. Bronchiolitis
4. Lung Cancer
Affected by cigarette smoking:
1. Asthma
2. Fibrosis
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The Spectrum of Occupational Lung Disease
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Past Smoking Prevalence in US Males by Birth Cohort
US Dept of Health and Human Services . The Health Consequences of Smoking.
A Report of the Surgeon General. 1985
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Current Workplace Smoking
Prevalence
• Smoking prevalence lowest among White
Collar Workers, highest among Blue Collar
and Service Workers
• Gap between White and Blue Collar Workers
appears to be widening
• Blue Collar and Service Workers less likely to
quit
• Blue Collar Workers are heavier smokers
Giovino GA, NIOSH Scientific Workshop on Work, Smoking and
Health, 2000.
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Smoking / Workplace Interactions:
Mechanisms
1. Toxins in smoke may also be present in
workplace (e.g. carbon monoxide)
2. Chemicals may be transformed into more
harmful agents by smoking
3. Smoking may increase delivery or retention
of agents
4. Presence of COPD may increase the amount
of workplace particulate retained in the lung
Adapted from Dement, NIOSH Scientific Workshop,
Work, Smoking and Health, 2000
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Smoking/Workplace
Interactions: Lung Diseases
A. Malignant (Cancer)
B. Non-malignant
Asthma
COPD
Pulmonary Fibrosis
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Smoking Workplace Interactions:
Asbestos and Lung Cancer
• A multiplicative interaction has been found for
asbestos and cigarette smoking.
• This may occur for other known occupational
causes of lung cancer: arsenic, bis- and
chloro-chloromethyl ether, cadmium,
chromiumVI, silica (crystalline), mustard gas,
nickel, radon, ionizing radiation, soots, tars,
mineral oils
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Inhaled Asbestos Fibers And Cigarette Smoke Penetrate
Airway Epithelial Cells to Cause Mutations in DNA
Arrows: asbestos fiber; M: macrophage; Ep: Airway epithelial cell
(Illustration from a mouse inhalation model using asbestos fibers)
Brody et al. Am Rev Respir Dis 1981; 123: 670-9
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Smoking Workplace Interactions:
Asbestos and Lung Cancer
Heavy (e.g. >11/2 packs per day)
lifetime cigarette smoking increases
risk for lung cancer 10-fold or more;
heavy career-long asbestos
exposure increases lung cancer
risk 5-fold; combination is
multiplicative (10 x 5 = 50 fold).
Selikoff et al. J. Am. Med Assoc. 1964; 188:22
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Smoking Workplace Interactions:
Lung Cancer
• Intervention: Smoking cessation reduces risk
for lung cancer; risk drops progressively over
10 years of disease-free follow-up, but
excess risk may be lifelong for heavy
smokers
• Smoking cessation has been found to reduce
risk for lung cancer in heavily-exposed
asbestos workers
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Non-Malignant Lung
Diseases
Asthma: > 200 occupational substances cause
asthma; smoking can make disease worse
Chronic Bronchitis: smoking and dusts are
additive
COPD: Multiple occupational substances
interact with smoke
Pulmonary Fibrosis: Smoking a risk factor for
some forms and interacts with occupational
exposures in some forms.
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Asthma: Interactions
• > 200 workplace substances known to cause
asthma
• Smoking increases asthma severity, but
association with causation inconsistent
• Smoking increases risk for occupational
asthma caused by some substances
• Smoking accelerates lung function loss in
asthmatics
Venables et al: Br Med J 1989; 299:939.
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Asthma
Smoking may increase risk of
workplace sensitization to:
Acid Anhydrides
Flour Antigens
Platinum Salts
Colophony
Lab Animals
Taylor, Int Arch Allergy Appl Immunol 1987;82:435
Venables, Br Med J 1989;299:939.
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Case Report: Combined Effects of Asbestos
(Fibrosis) and Cigarettes (Emphysema)
History: 74 year old retired laborer who worked
in shipyard, welding, and demolition; 67 packyear smoking
X-Ray: emphysema, pleural plaque, linear
opacities both bases
Pulmonary Function: FEV1 47% predicted, FVC
81% predicted, FEV1/FVC 44%, DLCO 11%
predicted,
Autopsy: Asbestosis and emphysema
Case 32-1986 the Mass. Gen. Hospital; New Engl J Med 1986;315:437
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Combined Effects of Asbestos and Cigarettes
on Lung Function
• 383 employed shipyard and manufacturing
workers, mean age 41-45
• Effects of asbestos exposure and
smoking tested in multivariate statistical
models
• Additive, independent effects of asbestos
and cigarette smoking were seen on
decreased forced vital capacity and on
single breath diffusing capacity
Samet et al., Am Rev Respir Dis 1979;120:75.
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Asbestos and Cigarette Smoking:
Autopsy Lung of a Patient Who Died with Asbestosis
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COPD (Chronic Obstructive Pulmonary Disease):
Occupational Causes
Examples of workplace exposures that
interact with smoking to cause chronic
obstructive pulmonary disease:
Coal Dust
Silica
Cotton Dust
Cadmium
Diisocyanates (MDI, HDI, TDI)
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Interaction of Asbestos and Cigarette Smoking to
Increase X-ray Markings
(Normal Chest X-Ray ILO Category 0/0)
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Interaction of Asbestos and Cigarette Smoking to
Increase X-ray Markings (Asbestosis, ILO Category 2/2)
Smoking increases the profusion of small opacities on
x-rays in asbestosis Weiss W. Am Rev Respir Dis 1984; 130:293-301
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Asbestos and Cigarette Smoking Interaction on
Chest X-ray ILO Category
• Asbestos causes pulmonary fibrosis, while
smoking usually causes emphysema
(destruction of alveolar surface area).
• In those with asbestosis who have also been
heavy smokers, there is (on average) an
increase in the profusion of small linear
opacities on chest x-ray.
• A smoker may have one half category higher
profusion than a non-smoker with equivalent
asbestos exposure
Weiss, Am Rev Respir Dis 1984; 130:293-301.
Barnhart, Am Rev Respir Dis 1990; 141:1102
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COPD: Coal Dust and Smoking
Retired coal miner and former smoker
demonstrates “melanoptysis” – expectoration of
coal dust from lungs
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COPD: Smoking and Coal Dust: Chest X-ray of retired
coal miner demonstrates Coalworker’s Pneumoconiosis
with Progressive Massive Fibrosis
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Smoking and Coal Dust: Retired Coal
Miner’s Pulmonary Function Tests
FVC 2.18 liters
FEV1 0.95
FEV1/FVC ratio
71% of Predicted
40%
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TLC 4.89
93%
VC
2.22
73%
FRC 3.37
104%
RV
2.67
121%
DLCO 8.6
45%
(Severe obstructive abnormality, gas transfer defect)
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COPD: Coal Dust
Lung with Coalworkers’ Pneumoconiosis:
Nodular fibrosis with focal emphysema
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COPD: Smoking and Coal Dust
In an epidemiologic study of autopsy lungs
from coal miners for whom smoking histories
were available, pathologic degree of
emphysema was associated both with coal
dust and smoke exposure, independent of the
effects of coal dust causing nodular fibrosis.
Conclusion: Smoking/Coal Dust Additive
Interaction Causes Emphysema
Vallyathan et al. Ann Occ Hyg 1997;41(Suppl 1):352
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Cardiovascular Disease
• Smoking a major risk factor for
myocardial infarction, death, peripheral
vascular disease
• Multiple workplace factors (carbon
monoxide, carbon disulphide, and
possibly workplace stress) may
contribute to risk
• Combinations of smoking and
workplace factors may increase risk
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Cardiovascular Disease:
Carbon Monoxide
Carbon monoxide in cigarette smoke is
suspected of contributing to excess
cardiovascular mortality in smokers.
A mortality study of New York City tunnel
workers exposed to 50 (mean) up to 400
parts per million carbon monoxide (before
ventilation improvements in 1970) had 35%
increased cardiovascular mortality compared
to control bridge workers.
Stern et al. Am J Epidemiology 1988;1276.
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Urologic Disease:
Bladder Cancer
• After lung, bladder cancer is the most
common fatal, occupational malignancy
• Proportion of bladder cancer attributable to
occupational exposures has been estimated
at 21 to 25% for males and 11% for females
in U.S.
Silverman DT. Am J Epidemiol 1990;132:453
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Bladder Cancer
• Causative factors (recognized or strongly
suspected): smoking, benzidine, benzidine
dyes, 3,3-dichlorobenzidine, nitrobiphenyl,
4,4-methylene-bis(2-chloroaniline) (MOCA),
4,4-methylene dianiline (MDA).
Goldstein et al., Bladder Carcinogens, in
Environmental and Occupational Medicine, W. Rom,
ed., Lippincott, 1998.
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Integration of smoking cessation with
occupational health and safety programs
• Workplaces may be either enabling or
discouraging to healthy behaviors such
as smoking cessation
• Integrating tobacco control program into
a comprehensive occupational health
and safety program may be more
effective than having separate
programs.
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Effects of workplace smoking
bans
• Studies of smoking among employees
after implementation of workplace
smoking bans show reduced total
cigarette consumption in employees
• Benefits included reduced active
smoking and reduced passive smoke
exposure to non-smokers
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Interventions to prevent occupational
inhalation exposures:
• Substitution of less hazardous materials
• Process containment (prevention of
release of hazards into breathing air)
• Local exhaust ventilation
• General area ventilation
• Respiratory protective devices
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Disability and Workers’
Compensation
• State Workers’ Compensation rules may
require physician to “apportion” the per
cent of pulmonary disability that is workrelated and non-work related.
• Relative effects of smoking and
occupational exposures in population
studies may be helpful in apportionment
decisions.
Attfield. Longitudinal decline in FEV1 in United
States coalminers. Thorax 1985;132-137.
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Resources for Reading
• Work, Smoking and Health. Proceedings of a
NIOSH Scientific Workshop
• Strasser PB. Smoking Cessation Programs in
the Workplace: Review and
recommendations for Occupational Health
Nurses. American Association of
Occupational Health Nurses Journal,
1991;39:432.
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