3.25 Smoking compared with or in combination with other pollutants

Last updated: Feb 2021
Suggested citation: Winnall, W, Bellew, B & Winstanley, MH. 3.25 Smoking compared with or in combination with other pollutants. In Greenhalgh, EM, Scollo, MM and Winstanley, MH [editors].  Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2021. Available from http://www.tobaccoinaustralia.org.au/3-25-air-pollution-cigarette-smoking-and-ill-healt


A preliminary note of caution about tobacco industry interference is appropriate before embarking on a discussion of other pollutants and health. Tobacco companies have historically sought to distract the public from the issue of the health effects of smoking (and later of secondhand smoke) by emphasising the dangers of other pollutants, including car exhaust and carpet glue fumes. A broader discussion of indoor air quality, ventilation and ‘sick building syndrome’ in some countries for many years drowned out concerns about the harms of secondhand smoke. The tobacco industry has manipulated information regarding the effects of secondhand smoke to avoid the development of smokefree environments—see  Section 15.3.1. It has, in the past, assembled a network of clinicians and scientists to divert attention away from secondhand smoke toward other indoor air pollutants.1 Tobacco companies have invested heavily in research on air quality issues. Substantial funds have been channelled to outside investigators through scientific organisations and companies focusing on indoor air research that were meant to appear independent and objective, but in fact were run by tobacco industry consultants—see Section 10A.3.2, 3 The tobacco industry and its interference tactics are discussed more fully in Chapter 10, Section 10.A.

3.25.1 Outdoor air pollution

Particulate matter (PM), also known as particle pollution, is the term commonly used in discussion of outdoor (ambient) air pollution. PM is a complex mixture of small particles and liquid droplets suspended in air. Sources of PM include dust, smoke, industry emissions, vehicle exhaust and wood fires.4, 5 It is made up of numerous particle types, including nitrates, sulphates, organic compounds (such as polycyclic aromatic hydrocarbons), metals, soil and dust particles and allergens (such as fragments of pollen or mould spores).6 The size of these particles is associated with their potential for causing health problems. The smaller a particle, the more deeply it can penetrate into the respiratory tract, and at an increasing rate.6 PM2.5 describes particulate matter that is 2.5 micrometres in diameter and smaller (about 1/30th the diameter of a human hair).7 The evidence points to PM2.5 as the most appropriate index of particulate air pollution for quantitative assessments of the effects of policy interventions.8 These very small particles emitted into the surrounding air by combustion and abrasion have a large effect on annual death rates.

Outdoor air pollution contributes substantially to the global burden of disease. Exposure to PM2.5 air pollution was estimated to be the 5th-highest ranking risk factor for global mortality in 2015.9 Smoking, however, was the 2nd-highest ranking risk factor for both mortality and health burden, measured as disability-adjusted life years.9 Worldwide, air pollution contributed to an estimated 4.2 million deaths and 103.1 million disability-adjusted life years in 2015.9 Mortality from air pollution is associated with lung cancer, cardiovascular diseases, lower respiratory tract infections and chronic obstructive pulmonary disease (COPD). Outdoor air pollution was classified as carcinogenic to humans by the International Agency for Research on Cancer in 2013.10

Outdoor air pollution is a cause of sickness and death in Australia. The 2015 Australia Burden of Diseases study estimated that 2,566 deaths (1.6% of the total) in Australia in 2015 were attributed to air pollution.11 Air pollution contributed to cancer, cardiovascular disease, respiratory disease and infections. However smoking creates an even bigger burden of disease. Whereas air pollution contributed to 0.8% of the total burden of health in 2015, tobacco use contributed to 9.3% - the highest risk factor in 2015.11  

A 2008 systematic review of the association of long-term exposure to ambient air pollution and mortality from chronic diseases12 showed that long-term exposure to PM2.5 increased the risk of non-accidental mortality by 6% per 10 μg/m3 PM2.5, regardless of age, gender and geographic region. Exposure to PM2.5 was associated with higher mortality from lung cancer (ranging from 15% to 21% per μg/m3 increase) and cardiovascular disease (ranging from 12% to 14% per 10 μg/m3 increase). Residing close to busy traffic was also associated with higher risks of non-accidental mortality, lung cancer mortality and cardiovascular mortality. The evidence also suggested that exposure to PM2.5 was more common in those who died from coronary heart disease and that exposure to sulphur dioxide increased mortality from lung cancer.12

Earlier in the 20th century, increasing pollution from vehicle exhaust and industry was erroneously proposed as a cause of the rising incidence of lung cancer.13 However, a case-control study by Doll and Hill from 1950 collected data on smoking as well as exposure to air pollution and many other potential risk factors for lung cancer, demonstrating that people with lung cancer were most likely smokers compared to other risk factors.13, 14

Just as studies on the effects of smoking need to factor in the effects of pollution, studies of the effects of outdoor air pollution need to be adjusted to account for the effects of smoking and, ideally, secondhand smoke exposure. The majority of studies reviewed by Chen 2008 measured smoking as a covariate, in their systematic review of air pollution exposure and mortality from chronic diseases.12, 15

Synergistic effects of outdoor pollution and tobacco exposure have been observed for the risks for cardiovascular disease and lung cancer. An analysis of the effects of PM2.5 and smoking on lung cancer risk showed an interaction – where the effects from both risk factors together were more than additive (synergistic).16 This study used data from the Cancer Prevention Study II, a large prospective cohort of almost 1.2 million people from the US starting in 1982. The results implied that reductions to lung cancer risks would be most efficient if interventions addressed both smoking and air quality.16 A small but significant excess risk was also found for cardiovascular mortality from both smoking and air pollution.17

Air pollution has recently been labelled “the new smoking”, but this analogy has drawn sharp criticism.18 Smoking remains the cause of a greater burden of health than air pollution, both globally9 and in Australia.11 Both ambient air pollution and smoking have been in decline over the past three decades.18 Air pollution is not obviously poised to overtake tobacco as a cause of illness and mortality. Ensuring a smokefree environment and promoting smoking cessation remain crucial to reducing the burden of lung disease, cardiovascular disease and many other conditions.

3.25.2 Occupational pollution Occupational pollution

Workplaces exposure people to pollution from a range of substances that can cause illness. For example, environments containing fine particulate matter from grains, flours, plants, coal dust, asbestos, silica, wood, feathers, insects and fungi, drugs and enzymes, chlorofluorocarbons, alcohols, metals and their salts and welding fumes can cause asthma, progressive lung damage and other serious respiratory disease.19, 20 Combining smoking with these exposures may greatly increase disease risk.20

The accumulation of evidence regarding workplace health hazards over previous decades has led to the introduction of industrial health and safety standards, which have greatly reduced exposures to carcinogenic and other toxic substances in developed countries. However the relocation of hazardous industry to less developed countries, where occupational safety may be less regulated (and where, incidentally, there is more likely to be a higher prevalence of smoking), is a major cause for concern.21

Past exposure to occupational carcinogens is judged an important determinant of the incidence of lung cancer and other cancers. Researchers have reported on occupational exposures and lung cancer; 4.9% (95% CI, 2.0 - 7.8) of lung cancers in men were attributable to occupation in known higher risk professions.22, 23

There is evidence that smoking has an additive or more than additive (synergistic) effect on disease risks for people exposed to some types of occupational pollution.  Current or previous occupational exposure to organic solvents has been found to double the smoking-related risk of chronic bronchitis.24 Another well-documented example is the interaction between workplace exposure to asbestos and cigarette smoking. Among those unexposed to asbestos, smoking increased the lung cancer rate approximately 10-fold in a study of 17,800 insulation workers from 1979.20, 25 In non-smoking workers, the lung cancer rate was increased 5-fold; but among asbestos workers who smoked, the lung cancer rate was increased 50-fold. In other words, for those workers who both smoked and were exposed to asbestos, the risk of developing and dying from lung cancer was 50 times greater than the risk for those who didn’t smoke and were unexposed to asbestos at work. The risk was also dose-responsive, varying with exposure to both contributing factors. Heavy smokers who were heavily exposed to asbestos had an even higher risk.20

Since this study, it has become apparent that the asbestos causes a type of lung cancer called mesothelioma, whereas tobacco is not a risk factor for mesothelioma by itself.26 The existence of a synergistic effect of tobacco and asbestos on lung cancer was verified by similar large studies from the UK, Europe and Canada.26-28 In Australia, most exposure to asbestos now occurs through the removal of asbestos from buildings, but the long lag-time for development of asbestos-caused disease means that death rates may continue to rise for over a decade.21

There is evidence that inhalation of particulates such as cigarette smoke and coal dust contribute to the development of chronic lung disease in coal miners.29-31 These studies provide evidence that (i) elemental carbon levels in the lungs and pack-years of cigarette smoking correlate significantly, and elemental carbon levels correlate with the severity of small airway disease;29 (ii) cumulative exposure to coal dust increases the risk of emphysema and has an additive effect to smoking;30, 31 (iii) exposure to coal mine dust leads to increased mortality, even in the absence of smoking;32 (iv) increased exposure to coal dust is associated with increased risk of death from chronic obstructive pulmonary disease;30 and (iv) that in newly employed coal miners, bronchitis symptoms are associated with a rapid decline in lung function within two years after starting work.30 Inhalation of coal dust and smoking are therefore significant risk factors for respiratory disease in miners but have an additive effects, rather than the synergism seen for asbestos workers.

Other studies of exposure to dust or fumes have reported associations with the incidence of chronic obstructive pulmonary disease,33 chronic bronchitis34 and asthma.35 Mineral dust is an airborne suspension of minerals that is often produced from human industry, as well as desert winds. Mineral dust contains compounds of minerals such as silicon, aluminium, iron, calcium and magnesium. Occupational exposure to mineral dust is a risk factor for chronic bronchitis and reduced lung function. These risks were further increased in smokers exposed to mineral dust, greater than the separate effects of mineral dust and smoking together.35

Exposure to silica dust as well as smoking may synergistically increase the risk of numerous respiratory and cardiovascular diseases. A study of miners and pottery workers in China found possible synergistic effects of smoking with silica dust exposure on mortality from respiratory and cardiovascular diseases. The strongest effect was seen for pneumoconiosis (an interstitial lung disease associated with dust exposure); people exposed to silica dust had a 5-fold higher risk, smokers had a 4.7-fold increased risk and smokers exposed to silica dust had a 12.5-fold increased risk of pneumoconiosis.36 Case-control studies from Canada found evidence in favour of a synergistic effect of smoking and silica dust exposure on lung cancer.37 Silica exposure and smoking had an synergistic effect on lung cancer risks in a study of European and Canadian workers.38 Exposure to silica dust and smoking caused a 7.4-fold increased risk of rheumatoid arthritis, which was greater than the additive effects of silica dust and smoking alone.39 In a study of Chinese iron mine workers, being exposed to silica dust and smoking accounted for 76% of mortality from non-malignant respiratory disease, 35.7% from cardiovascular disease, and 81.4% from lung cancer.40

Cigarette smoking accompanied by exposure to workplace noise has been associated with a 5-fold increase in risk of noise-induced hearing loss among smokers compared with non-smokers.41, 42 In a study of refinery workers in China, smoking and manganese exposure had a synergistic effect on decreasing lung function.43 Being a current smoker is a also risk factor for sensitisation to workplace allergens.44 Current or previous occupational exposure to organic solvents doubles the smoking related risk of chronic bronchitis.24 A synergistic relationship was described between arsenic exposure and smoking on mortality from ischemic heart disease.45 However, a 2017 meta-analysis found insufficient evidence for a synergistic effects of smoking and exposure to particular asbestos, crystalline silica and diesel engine exhaust emissions on lung cancer.46

Smoking status should be taken into account when measuring the risk of exposure to other types of pollution. For instance, exposure to low-level radiation in nuclear workers was found to be associated with diseases of all causes, non-cancerous diseases and liver cancer. However, when these results were adjusted to take into account smoking, these associations became statistically insignificant.47

The US Surgeon General has concluded that ‘for the majority of American workers who smoke, cigarette smoke represents a greater cause of death and disability than their workplace environment’.20 The Australian Burden of Disease Study confirms this for Australia. It is estimated that in 2015, occupational exposures and hazards accounted for 2.0% of the total burden of health, while tobacco use accounted for 9.3% of the total burden in Australia.48 Sick building syndrome

A potential syndrome described last century is termed "sick building syndrome". This term refers to situations in which building occupants experience acute health and comfort effects that appear associated with time spent in a building, but no specific illness or cause can be identified.49 The term sick building syndrome is used to refer to a heterogeneous group of symptoms, including irritation of the skin and mucous membranes of the eyes, nose and throat, headache, fatigue and difficulty concentrating. The existence of this syndrome is controversial, as many experts consider that the wide variety of symptoms and no identified cause means that no single syndrome exists.50

During the 1980s the tobacco industry took a particular interest in sick building syndrome, using it as a means of deflecting attention away from newly emerging evidence about the health consequences of exposure to environmental tobacco smoke. This is discussed further in Chapter 15, Section (10A.3.2.2).


Relevant news and research

For recent news items and research on this topic, click  here. ( Last updated September 2023)



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2. Lee C and Glantz S. The tobacco industry's successful efforts to control tobacco policy making in Switzerland. San Francisco: School of Medicine University of California, San Francisco, 2001. Available from: http://www.who.int/tobacco/media/en/InquirySwiss.pdf.

3. Drope J, Bialous SA, and Glantz SA. Tobacco industry efforts to present ventilation as an alternative to smoke-free environments in North America. Tobacco Control, 2004; 13 Suppl 1(Suppl 1):i41-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/14985616

4. Environmental Protection Authority Victoria. PM10 particles in the air. Melbourne, Australia: EPA VIC, 2021. Available from: https://www.epa.vic.gov.au/for-community/environmental-information/air-quality/pm10-particles-in-the-air.

5. Environmental Protection Authority Victoria. PM2.5 particles in the air. Melbourne, Australia: EPA VIC, 2021. Available from: https://www.epa.vic.gov.au/for-community/environmental-information/air-quality/pm25-particles-in-the-air.

6. Kim KH, Kabir E, and Kabir S. A review on the human health impact of airborne particulate matter. Environment International, 2015; 74:136-43. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25454230

7. US Environmental Protection Agency (EPA). EPA Website - Particulate matter.  2011. Available from: http://www.epa.gov/air/particlepollution/index.html.

8. Committee on the Medical Effects of Air Pollutants. Long-term exposure to air pollution: effect on mortality. Whitehall, London: Department of Health, 2009. Available from: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/304667/COMEAP_long_term_exposure_to_air_pollution.pdf.

9. Cohen AJ, Brauer M, Burnett R, Anderson HR, Frostad J, et al. Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the Global Burden of Diseases Study 2015. Lancet, 2017; 389(10082):1907-18. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28408086

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11. Australian Institute of Health and Welfare. Australian Burden of Disease Study: impact and causes of illness and death in Australia 2015. Australian Burden of Disease, Canberra: AIHW, 2019. Available from: https://www.aihw.gov.au/reports/burden-of-disease/burden-disease-study-illness-death-2015/contents/summary.

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16. Turner MC, Cohen A, Jerrett M, Gapstur SM, Diver WR, et al. Interactions between cigarette smoking and fine particulate matter in the Risk of Lung Cancer Mortality in Cancer Prevention Study II. American Journal of Epidemiology, 2014; 180(12):1145-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25395026

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18. Gao W, Sanna M, Hefler M, and Wen CP. Air pollution is not 'the new smoking': comparing the disease burden of air pollution and smoking across the globe, 1990-2017. Tobacco Control, 2020; 29(6):715-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31611424

19. Driscoll T, Steenland K, Imel Nelson D, and Leigh J. Occupational airborne particulates. Assessing the environmental burden of disease at national and local levels. Environmental burden of disease series, no. 7, Geneva: World Health Organization, 2004. Available from: http://www.who.int/quantifying_ehimpacts/publications/en/ebd7.pdf.

20. US Department of Health and Human Services. The health consequences of smoking: cancer and chronic lung disease in the workplace. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1985. Available from: https://profiles.nlm.nih.gov/spotlight/nn/catalog/nlm:nlmuid-101584932X452-doc.

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22. Consonni D, De Matteis S, Lubin JH, Wacholder S, Tucker M, et al. Lung cancer and occupation in a population-based case-control study. American Journal of Epidemiology, 2010; 171(3):323-33. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20047975

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30. Santo Tomas LH. Emphysema and chronic obstructive pulmonary disease in coal miners. Current Opinion in Pulmonary Medicine, 2011; 17(2):123-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21178627

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47. Kudo S, Ishida J, Yoshimoto K, Mizuno S, Ohshima S, et al. Direct adjustment for confounding by smoking reduces radiation-related cancer risk estimates of mortality among male nuclear workers in Japan, 1999-2010. Journal of Radiological Protection, 2018; 38(1):357-71. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29313822

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