Smoking and Occupational Health

1
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

2
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
• Chronic bronchitis
• COPD (Emphysema)
• Bronchiolitis
• Lung Cancer
• Affected by cigarette smoking
• Asthma
• Fibrosis

7
The Spectrum of Occupational Lung Disease
8
Past Smoking Prevalence in US Males by Birth
CohortUS 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 InteractionsAsbestos 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 DNAArrows 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 InteractionsAsbestos and Lung
Cancer

• Heavy (e.g. gt11/2 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 18822

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Smoking Workplace InteractionsLung 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 gt 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

• gt 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 299939.

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Asthma

• Smoking may increase risk of workplace
  sensitization to
• Acid Anhydrides Colophony
• Flour Antigens Lab Animals
• Platinum Salts
• Taylor, Int Arch Allergy Appl Immunol 198782435
• Venables, Br Med J 1989299939.

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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
  pack-year 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 1986315437

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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 197912075.

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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 130293-301

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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 130293-301.
• Barnhart, Am Rev Respir Dis 1990 1411102

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COPD Coal Dust and SmokingRetired 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 Coalworkers
Pneumoconiosis with Progressive Massive Fibrosis

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Smoking and Coal Dust Retired Coal Miners
Pulmonary Function Tests

• FVC 2.18 liters 71 of Predicted
• FEV1 0.95 40
• FEV1/FVC ratio 43
• 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 199741(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 19881276.

33
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 1990132453

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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.

36
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 work-related 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 1985132-137.

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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,
  199139432.