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

3. 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.

4. Overview: Smoking/Workplace Interactions A. Lung Diseases 1. Malignant 2. Non-malignant B. Cardiovascular Disease C. Urologic (Bladder, Kidney) Diseases D. Injuries and mortality

5. Outcome Measures for Interactions • Disease Incidence • Disease severity -- Symptoms -- Pulmonary Function (FEV1,Diffusing capacity) -- X-ray changes • Premature Mortality

6. 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

9. 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.

10. 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

11. Smoking/Workplace Interactions: Lung Diseases A. Malignant (Cancer) B. Non-malignant Asthma COPD Pulmonary Fibrosis

12. 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

13. 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

14. 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

15. 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

16. 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.

17. 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.

18. Asthma Smoking may increase risk of workplace sensitization to: Acid Anhydrides Colophony Flour Antigens Lab Animals Platinum Salts Taylor, Int Arch Allergy Appl Immunol 1987;82:435 Venables, Br Med J 1989;299:939.

19. 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 1986;315:437

20. 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.

21. Asbestos and Cigarette Smoking: Autopsy Lung of a Patient Who Died with Asbestosis

22. 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)

23. Interaction of Asbestos and Cigarette Smoking to Increase X-ray Markings (Normal Chest X-Ray ILO Category 0/0)

24. 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

25. 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

26. COPD: Coal Dust and SmokingRetired coal miner and former smoker demonstrates “melanoptysis” – expectoration of coal dust from lungs

27. COPD: Smoking and Coal Dust: Chest X-ray of retired coal miner demonstrates Coalworker’s Pneumoconiosis with Progressive Massive Fibrosis

28. Smoking and Coal Dust: Retired Coal Miner’s 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)

29. COPD: Coal Dust Lung with Coalworkers’ Pneumoconiosis: Nodular fibrosis with focal emphysema

30. 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

31. 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

32. 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.

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 1990;132:453

34. 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.

35. 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

37. 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

38. 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 inUnited States coalminers. Thorax 1985;132-137.

39. 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.