3.25 Smoking compared with or in combination with other pollutants

Last updated: 2011
Suggested citation:Bellew, B & Winstanley, MH. 3.25 Smoking compared with or in combination with other pollutants. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2011. 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 secondhand smoke by emphasising the dangers of other pollutants, including carpet glue fumes and car exhaust. A broader discussion of indoor air quality, ventilation and 'sick building syndrome' has served, in some cases, to drown out concerns about the harms of secondhand smoke. According to a Philip Morris publication developed for Europe, the range of pollutants found in offices which cause sick building syndrome include fumes and gases emitted from carpets, computer screens, photocopiers, etc., with the problem often augmented by bacteria, moulds and dusts from ventilation equipment. It has even been argued that tobacco smoke can be a useful visual marker of bad ventilation inside buildings. 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.1-3 The tobacco industry and its interference tactics are discussed more fully in Chapter 10, Section 10.12.

3.25.1 Outdoor air pollution 

Particulate matter (PM), also known as particle pollution, is the term commonly used in discussion of outdoor air pollution. PM is a complex mixture of extremely small particles and liquid droplets suspended in air. It is made up of a number of components, including acids (such as nitrates and sulphates), organic chemicals, metals, and soil or dust particles and allergens (such as fragments of pollen or mould spores). The size of particles is directly linked to their potential for causing health problems; it is now generally accepted that the very small particles emitted into the surrounding air by combustion and abrasion have a large effect on annual death rates. The evidence points to PM2.5 as the most satisfactory index of particulate air pollution for quantitative assessments of the effects of policy interventions.4 Fine particle pollution or PM2.5 describes particulate matter that is 2.5 micrometres in diameter and smaller (about 1/30th the diameter of a human hair).5 A 2008 systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases was conducted by Chen and colleagues.6 The analysis showed that long-term exposure to PM2.5 increases the risk of non-accidental mortality by 6% per 10 microg/m3 increase, independent of age, gender and geographic region. Exposure to PM2.5 was found to be associated with an increased risk of mortality from lung cancer (range: 15% to 21% per 10 microg/ m3 increase) and total cardiovascular mortality (range: 12% to 14% per 10 microg/ m3 increase). Living close to busy traffic is associated with elevated risks of these three outcomes. Evidence suggested that exposure to PM2.5 is positively associated with mortality from coronary heart diseases and that exposure to sulphur dioxide (SO2) increases mortality from lung cancer. For other pollutants and health outcomes, there are insufficient data to make solid conclusions.6 Studies examined in the systematic review are available as an online appendix.7 Virtually all studies covering non-accidental mortality and exposure to PM2.5 have adjusted for the effects of active smoking; in other words, researchers used statistical techniques that attempted to allow for the adverse health effects of this exposure when estimating the risk from air pollution. One of these studies adjusted for exposure to secondhand smoke; McDonnell et al provided a risk estimate of 1.09 (95% CI, 0.98–1.21) for men, which is only on the cusp of statistical significance while there was a non-significant finding for women. Lung cancer mortality was also examined in this secondhand smoke adjusted study whereby a (non-significant) risk estimate of 1.39 (95% CI, 0.79–2.46) was obtained.8

A number of studies provide insights into road traffic-specific component of outdoor air pollution. As noted earlier, a systematic review has concluded that living close to busy traffic is associated with elevated risks of the adverse outcomes associated with exposure to PM2.5.6 Other recent studies have found that long-term exposure to traffic-related air pollution may contribute to the development of chronic obstructive pulmonary disease with possibly enhanced susceptibility in people with diabetes and asthma;9 that medium-term exposure to traffic-related air pollution may induce an increased inflammatory/endothelial response, especially among diabetics and those not using statins;10 and that traffic intensity near the home is associated with natural-cause mortality (highest relative risks for respiratory mortality).11

The National Pollutant Inventory holds data for all sources of particulate matter emissions in Australia.12 Overall, air quality in Australia is relatively good, but for some places, such as large cities and mining areas, air quality can be an issue. The 'headline indicator' for atmosphere in Measures of Australia's Progress has generally regressed compared with 10 years ago.13 In recognition of the effects of these pollutants on health and climate, a range of standards has been introduced across Australia over recent decades. The National Environment Protection Measures describe standards for six main pollutants, including PM10 (particulate matter, or inhalable particles, more than 10 microns in diameter). The maximum PM10 concentration allowed under the standard is 50 microg /m3 and for a maximum of five days a year. (In 2003 the National Environment Protection Measures was varied to add an advisory reporting standard for PM2.5; the advisory standard for PM2.5 is a maximum concentration of 25 microg /m3 in one day and 8 microg /m3 per year.) All capital cities except Hobart had PM10 concentrations above the standard between 1991 and 2001. In Melbourne the levels of PM10 remained above the standard from 2001 to 2006, with concentration peaks seen in 2003 and 2006. New South Wales also recorded PM10 levels above the standard from 2001 to 2006, with a peak in 2003. The peaks can be attributed to severe bushfires and dust storms in those years. Most capital cities have shown a fairly steady rate of sulphur dioxide emissions and met the National Environment Protection Measures standards for highest daily average and highest daily maximum between 1991 and 2001. This trend was maintained in Sydney and Melbourne from 2002 to 2006. Until 1996, Adelaide exceeded the standards but since then the levels have been below the standard.14

Outdoor air pollution is a significant cause of sickness and death in Australia. It is estimated that in 2003, about 2000 deaths in Australia were attributable to long-term exposure to urban air pollution, and a further 1000 deaths were caused by short-term exposure through exacerbation of pre-existing illness.15 Most deaths were due to ischaemic heart disease, followed by stroke, lung cancer and chronic obstructive pulmonary disease. In total, urban air pollution caused 2.3% of all deaths in Australia in 2003. Tobacco caused almost five times that amount.15

Tobacco smoke is, of course, also a source of environmental particulate matter. A study comparing the output of particulate matter from three single cigarettes burning consecutively over 30 minutes showed that the total delivery of particulate matter was up to 10 times greater than emissions of particulate matter from the exhaust of a modern turbo diesel motor car with the engine left idling for the same amount of time.16 Tobacco smoke is also a major source of indoor carbon monoxide pollution17–see following section.

Policy action to reduce levels of air pollutants is important and it is reasonable to assume that a reduction in air pollution will lead to considerable health benefits.18 However, since the adverse effects of outdoor air pollution may also be used by the tobacco industry to distract attention from policy measures for secondhand smoke, it is worth noting the recent report by the World Health Organization, which provides risk estimates for exposure to secondhand smoke across a wide range of adverse health outcomes for both children and adults.19 These well quantified risks from secondhand smoke exposure,19 the relative ease and low cost of policy measures to reduce or eliminate the risks, and the immediacy of their impact20 are all powerful arguments that should help ensure a clearer focus in the attention of policy-makers and members of the public alike.

3.25.2 Indoor pollution Indoor pollution: generic

With Australians spending up to 90% of their time indoors,21 indoor air quality, whether it be domestic or workplace, is an important health consideration. Sources of indoor pollution in Australia include asbestos products, radon gas, secondhand tobacco smoke, house dust mite allergens, formaldehyde (used in production of pressed wood products such as particleboard, or insulation products), nitrogen dioxide emissions from unflued gas appliances, and pesticides applied under buildings.22 Moulds, dust, animal fur or dander (tiny flakes from fur, skin or feathers), and chemicals arising from paint, glues or other household solvents are also a cause of irritation. 'Off-gassing', the emission of toxic fumes from furniture, carpets, paints, glues and sealants in newer buildings and houses may remain at high levels for several months.21 Of course, outdoor pollutants may also infiltrate the indoor environment. Exposures to these agents may cause a variety of responses, from mild irritation through to asthma and disease.

Of all these pollutants, the three most significant in Australia are asbestos fibres, radon gas and secondhand tobacco smoke.22 As already noted, asbestos fibres are a cause of lung cancer and other respiratory disease, and although it is no longer mined and its use in building products has been phased out, asbestos remains present in many structures. Radon gas is also a known human carcinogen that occurs naturally in soil and rocks, collecting in buildings from the soil beneath. Radon levels in Australian buildings are, for the most part, well below internationally recommended indoor levels, and significantly lower than for buildings in the US and the UK, probably due to different soils, building practices and the coastal proximity for much housing.22 Secondhand tobacco smoke causes lung cancer, as well as a range of other respiratory symptoms and illnesses among non-smoking adults and children.23 In past decades, exposure to secondhand smoke has been ubiquitous. Restrictions on smoking in the workplace and in many public places have reduced exposure to secondhand smoke for many Australians over the past 20 years, although exposure in recreational facilities and establishments such as hotels and nightclubs has remained high. A significant number of adults and children also remain exposed in the home (see Chapter 4, Section 4.14). For further information on secondhand smoke refer to Chapter 4. Smokefree environments are discussed in Chapter 15. Indoor pollution: workplace exposure

Workplace exposures to a range of substances 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.24, 25 Combining smoking with these exposures may greatly increase disease risk.25

A well-documented example is the interaction between workplace exposure to asbestos and cigarette smoking. Among the population not exposed to asbestos, smoking increases the lung cancer rate approximately 10-fold. In non-smoking asbestos workers, the lung cancer rate is increased five-fold; but among asbestos workers who smoke, the lung cancer rate is increased 50-fold. In other words, for those workers who both smoke and are exposed to asbestos, the risk of developing and dying from lung cancer is 50 times greater than the risk for individuals who neither smoke nor are exposed to asbestos at work. The risk is also dose-responsive, varying with exposure to both contributing factors. Heavy smokers heavily exposed to asbestos will have a higher than 50-fold increase.25 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 will continue to rise for the next two decades.26 There is also ample evidence suggesting that exposures to petrochemicals, aromatic amines, ionising radiation and pesticides interact with tobacco smoke.25

Evidence on occupational exposures and health effects has further expanded in recent years. 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; past exposure to occupational carcinogens is judged an important determinant of lung cancer incidence 27, 28. A follow up study of 15 million people in Denmark, Finland, Iceland, Norway and Sweden showed that male waiters and tobacco workers had the highest risk of lung cancer, probably attributable to active and passive smoking. Miners and quarry workers also had a high risk, which might be related to their exposure to silica dust and radon daughters. Among women, tobacco workers and engine operators had a more than four-fold risk as compared with the lung cancer risk among farmers, gardeners and teachers. Waiters had the highest risk of bladder cancer among men; tobacco workers had the highest risk among women; the low-risk categories were the same ones as for lung cancer. The researchers stated that all of this could be accounted for by smoking.29 A systematic review found consistent evidence that exposure to benzene at work increases the risk of leukaemia with a dose–response pattern.30 Studies have also demonstrated negative consequences from inhaling fumes during welding,31 and the impact of silica exposure on the risk of developing rheumatoid arthritis32 and lung cancer,33 with greatly increased risk for these diseases among smokers. Current or previous occupational exposure to organic solvents has been found to double the smoking-related risk of chronic bronchitis.34 Cigarette smoking accompanied by exposure to workplace noise has also been associated with a five-fold increase in risk of noise induced hearing loss among smokers compared with non-smokers.35, 36 The risk of infertility and spontaneous abortion has been found to be 30% higher among female hairdressers than among women in other occupations, thought to be due to their occupational chemical exposure and found primarily among never smokers.37 Being a current smoker is a risk factor for sensitisation to workplace allergens. Smokers are more than twice as likely as non-smokers to have positive tests of allergic reactions (OR 2.39; 95% CI, 1.01–5.65).38

Inhalation exposure to particulates such as cigarette smoke and coal dust is known to contribute to the development of chronic lung disease and several studies of the health and wellbeing of coal miners have been reported.39-42 These studies provide evidence that:
(i) elemental carbon levels in the lungs and pack-years of cigarette smoking correlate significantly, as do elemental carbon levels and the severity of small airway disease;39
(ii) cumulative exposure to coal dust is a significant risk factor for the development of emphysema and has an additive effect to smoking;40, 41
(iii) exposure to coal mine dust leads to increased mortality, even in the absence of smoking42;
(iv) increased exposure to coal dust is associated with increased risk of death from chronic obstructive pulmonary disease;40 and
(v) that in newly employed coal miners, bronchitis symptoms are associated with a rapid decline in lung function within two years after starting work.40 Other studies of exposure to dust or fumes have reported associations with the incidence of chronic obstructive pulmonary disease,44 and asthma45; chronic bronchitis occurs more frequently among individuals exposed to mineral dust, and smoking doubles this risk.45

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'.25 The Australian Burden of Disease Study confirms this. It is estimated that in 2003, occupational exposures and hazards accounted for 2% of the total disease and injury burdeni and 1.3% of all deaths, while tobacco use accounted for 7.8% of the total disease and injury burden and 11.7% of all deaths.15

The accumulation of evidence about 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.26 Sick building syndrome

Over the past 15 to 20 years awareness has risen about 'sick building syndrome'.22 The term sick building syndrome is used to refer to a heterogeneous group of work-related symptoms, including irritation of the skin and mucous membranes of the eyes, nose and throat; headache; fatigue; and difficulty concentrating. These are considered illnesses because of the occurrence of symptoms, even though affected workers do not have objective clinical or laboratory abnormalities and causative agents cannot be found. The clinical symptoms of sick building syndrome, although not life-threatening, are disruptive: they reduce productivity and increase absenteeism from work.46 It is likely that the cause of sick building syndrome is multifactorial, involving ventilation, airborne particulates from a wide range of sources (including chemicals, micro-organisms and non-organic matter) and other vectors in the indoor environment. A recent update review concluded that sick building syndrome is related to both personal and environmental risk factors and, in the office environment, may have important economic implications.47 United States Environmental Protection Agency studies have identified four distinct groups of symptoms, representing 'tiredness', 'mucosal irritation', 'neuropsychological' and 'lower respiratory' conditions. Rather than a dichotomy of healthy versus unhealthy ('sick') buildings the Environmental Protection Agency found that the prevalence of health problems related to buildings spans a continuum; the distribution of work-related symptoms and identification of symptom groups can help in identification of problems.48

A recent review of the literature on ventilation rates and health found biological plausibility for an association of health outcomes with ventilation rates, but a lack of clear evidence on particular agent(s) for the effects.49 Higher ventilation rates in offices, up to about 25 litres per person, are associated with reduced prevalence of sick building syndrome symptoms.

The limited available data suggest that inflammation, respiratory infections, asthma symptoms and short-term sick leave increase with lower ventilation rates. Home ventilation rates above 0.5 air changes per hour (h(–1)) have been associated with a reduced risk of allergic manifestations among children in a Nordic climate.49 Improved ventilation practices and reduction of pollutants are key factors in alleviating sick building syndrome, along with adherence to building and maintenance standards and improved controls over temperature, humidity and lighting.22 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.1 This is discussed further in Chapter 15, Section 15.3.1.

Recent news and research

For recent news items and research on this topic, click here (Last updated March 2018) 

The measure used to express total burden of disease and injury is the 'disability-adjusted life year' (DALY). The DALY 'describes the amount of time lost due to both fatal and non-fatal events; that is, years of life lost due to premature death coupled with years of 'healthy' life lost due to disability'.(p2) (ref is Begg, S et al - AIHW 2007).


1. 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):i41-7. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/13/suppl_1/i41.pdf

2. Pan American Health Organization/ World Health Organization. Second-hand smoke and the tobacco industry - factsheet. Washington DC: World Health Organization, 2001, viewed 1 September 2011. Available from: www.paho.org/english/ad/sde/ra/wntd-factsheet3.doc

3. 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, [viewed 1 September 2011]. Available from: http://www.who.int/tobacco/media/en/InquirySwiss.pdf

4. Committee on the Medical Effects of Air Pollutants. Long-term exposure to air pollution: effect on mortality. Whitehall, London: Department of Health, 2009, [viewed 1 September 2011]. Available from: http://www.advisorybodies.doh.gov.uk/comeap/pdfs/finallongtermeffectsmort2009report.pdf

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

6. Chen H, Goldberg MS and Villeneuve PJ. A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases. Reviews on Environmental Health 2008;23(4):243-97. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19235364

7. Chen H, Goldberg MS and Villeneuve PJ. A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases: On-line Appendix. Reviews on Environmental Health 2008 Available from: http://www.med.mcgill.ca/epidemiology/goldberg/Review%20of%20Outdoor%20Air%20Pollution.pdf

8. McDonnell WF, Nishino-Ishikawa N, Petersen FF, Chen LH and Abbey DE. Relationships of mortality with the fine and coarse fractions of long-term ambient PM10 concentrations in nonsmokers. Journal of Exposure Analysis and Environmental Epidemiology 2000;10(5):427-36. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11051533

9. Andersen Z, Hvidberg M, Jensen S, Ketzel M, Loft S, Sorensen M, et al. Chronic obstructive pulmonary disease and long-term exposure to traffic-related air pollution: a cohort study. American Journal of Respiratory and Critical Care Medicine 2011;183(4):455–61. Available from: http://ajrccm.atsjournals.org/cgi/content/full/183/4/455

10. Alexeeff SE, Coull BA, Gryparis A, Suh H, Sparrow D, Vokonas PS, et al. Medium-term exposure to traffic-related air pollution and markers of inflammation and endothelial function. Environmental Health Perspectives 2011;119(4):481-6. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080929/pdf/ehp-119-481.pdf

11. Brunekreef B, Beelen R, Hoek G, Schouten L, Bausch-Goldbohm S, Fischer P, et al. Effects of long-term exposure to traffic-related air pollution on respiratory and cardiovascular mortality in The Netherlands: the NLCS-AIR study. Research Report (Health Effects Institute) 2009(139):5-71; discussion 73-89. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19554969

12. Australian Government Department of Sustainability E, Water, Population and Communities,. National Pollutant Inventory - Particulate matter (PM10 and PM2.5): . Available from: http://www.npi.gov.au/substances/particulate-matter/index.html

13. Australian Bureau of Statistics. 1370.0 Measures of Australia's progress. Atmosphere and progress. Canberra: ABS, 2010. Available from: http://www.abs.gov.au/ausstats/abs@.nsf/mf/1370.0

14. Australian Institute of Health and Welfare. Australia's health 2010. Australia's health series no. 12, cat. no. AUS 122. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=6442452962&libID=6442452962

15. Begg S, Vos T, Barker B, Stevenson C, Stanley L and Lopez A. The burden of disease and injury in Australia 2003. AIHW cat. no. PHE 82. Canberra: Australian Institute of Health and Welfare, 2007. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10317

16. Invernizzi G, Ruprecht A, Mazza R, Rossetti E, Sasco A, Nardini S, et al. Particulate matter from tobacco versus diesel car exhaust: an educational perspective. Tobacco Control 2004;13(3):219–21. Available from: http://tc.bmjjournals.com/cgi/content/abstract/13/3/219

17. Department of the Environment and Heritage. Carbon monoxide. Air quality fact sheet. Canberra: Department of the Environment and Heritage, 2005. Available from: http://www.environment.gov.au/atmosphere/airquality/publications/carbonmonoxide.html

18. World Health Organization - Regional Office for Europe. Health Aspects of Air Pollution: results from the WHO project "Systematic Review of Health Aspects of Air Pollution in Europe". 2004. Available from: http://www.euro.who.int/__data/assets/pdf_file/0003/74730/E83080.pdf

19. Öberg M, Jaakkola MS, Prüss-Üústün A, Schweizer C and Woodward A. Second-hand smoke: assessing the environmental burden of disease at national and local levels. WHO Environmental Burden of Disease Series, no.18. Geneva, : World Health Organization, 2010. Available from: http://www.who.int/quantifying_ehimpacts/publications/SHS.pdf

20. Hopkins DP, Razi S, Leeks KD, Priya Kalra G, Chattopadhyay SK and Soler RE. Smokefree policies to reduce tobacco use. A systematic review. American Journal of Preventive Medicine 2010;38(suppl. 2):S275-89. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20117612

21. Australian Bureau of Statistics. 1301.0 Australia now. Environment. Air Pollution Canberra: ABS, 2004. Available from: http://www.abs.gov.au/ausstats/abs@.nsf/0/8f1a0bea81c1d6eeca256dea00053a5e?OpenDocument

22. Brown S. Indoor air quality, Australia: State of the Environment Technical Paper Series (Atmosphere). Canberra: Department of the Environment, Sport and Territories, 1997. Available from: http://www.deh.gov.au/soe/techpapers/series1/pubs/12indora.pdf

23. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm

24. 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 Organisation, 2004. Available from: http://www.who.int/quantifying_ehimpacts/publications/en/ebd7.pdf

25. 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: http://profiles.nlm.nih.gov/NN/B/C/B/N/segments.html

26. Stewart B, Kleihues P and Editors. IARC World Cancer Report. Lyon, France: International Agency for Research on Cancer, 2003.

27. Consonni D, De Matteis S, Lubin J, Wacholder S, Tucker M, Pesatori A, et al. Lung cancer and occupation in a population-based case-control study. American Journal of Epidemiology 2010;171(3):323–33. Available from: http://aje.oxfordjournals.org/cgi/content/full/171/3/323

28. Paris C, Clement-Duchene C, Vignaud J, Gislard A, Stoufflet A, Bertrand O, et al. Relationships between lung adenocarcinoma and gender, age, smoking and occupational risk factors: a case-case study. Lung Cancer 2010;68(2):146–53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19586681

29. Pukkala E, Martinsen JI, Lynge E, Gunnarsdottir HK, Sparen P, Tryggvadottir L, et al. Occupation and cancer - follow-up of 15 million people in five Nordic countries. Acta Oncologica 2009;48(5):646-790. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19925375

30. Khalade A, Jaakkola MS, Pukkala E and Jaakkola JJ. Exposure to benzene at work and the risk of leukemia: a systematic review and meta-analysis. Environmental Health 2010;9:31. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20584305

31. Gube M, Ebel J, Brand P, Goen T, Holzinger K, Reisgen U, et al. Biological effect markers in exhaled breath condensate and biomonitoring in welders: impact of smoking and protection equipment. International Archives of Occupational and Environmental Health 2010;83(7):803–11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20130903

32. Stolt P, Yahya A, Bengtsson C, Kallberg H, Ronnelid J, Lundberg I, et al. Silica exposure among male current smokers is associated with a high risk of developing ACPA positive rheumatoid arthritis. Annals of the Rheumatic Diseases 2010;69(6):1072–6. Available from: http://ard.bmj.com/content/69/6/1072.long

33. Vida S, Pintos J, Parent M, Lavoue J and Siemiatycki J. Occupational exposure to silica and lung cancer: pooled analysis of two case-control studies in Montreal, Canada. Cancer Epidemiology, Biomarkers & Prevention 2010;Epub ahead of print Available from: http://cebp.aacrjournals.org/content/early/2010/05/21/1055-9965.EPI-10-0015.full.pdf+html

34. Ebbehoj NE, Hein HO, Suadicani P and Gyntelberg F. Occupational organic solvent exposure, smoking, and prevalence of chronic bronchitis-An epidemiological study of 3387 men. Journal of Occupational & Environmental Medicine 2008;50(7):730 – 5. Available from: http://www.joem.org/pt/re/joem/abstract.00043764-200807000-00002.htm;jsessionid=LLwQJLvnJThFbhJQv1mpvDhmtJpMB0pt2TzCRN7YysQ1Xxh29l4H!523807009!181195628!8091!-1

35. Mohammadi S, Mazhari MM, Mehrparvar AH and Attarchi MS. Effect of simultaneous exposure to occupational noise and cigarette smoke on binaural hearing impairment. Noise Health 2010;12(48):187-90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20603575

36. Mohammadi S, Mazhari MM, Mehrparvar AH and Attarchi MS. Cigarette smoking and occupational noise-induced hearing loss. European Journal of Public Health 2010;20(4):452-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19887518

37. Baste V, Moen B, Riise T, Hollund B and Oyen N. Infertility and spontaneous abortion among female hairdressers: the Hordaland Health Study. Journal of Occupational and Environmental Medicine 2008;50(12):1371–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19092492

38. Adisesh A, Gruszka L, Robinson E and Evans G. Smoking status and immunoglobulin E seropositivity to workplace allergens. Occupational Medicine 2011;61(1):62–4. Available from: http://occmed.oxfordjournals.org/content/61/1/62.full

39. Saxena R, McClure M, Hays M, Green F, McPhee L, Vallyathan V, et al. Quantitative assessment of elemental carbon in the lungs of never smokers, cigarette smokers, and coal miners. Journal of Toxicology and Environmental Health 2011;74(11):706–15. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21480045

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

41. Kuempel ED, Wheeler MW, Smith RJ, Vallyathan V and Green FH. Contributions of dust exposure and cigarette smoking to emphysema severity in coal miners in the United States. American Journal of Respiratory and Critical Care Medicine 2009;180(3):257-64. Available from: http://ajrccm.atsjournals.org/cgi/reprint/180/3/257.pdf

42. Attfield MD and Kuempel ED. Mortality among US underground coal miners: a 23-year follow-up. American Journal of Industrial Medicine 2008;51(4):231-45. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18247381

43. Blanc PD, Menezes AM, Plana E, Mannino DM, Hallal PC, Toren K, et al. Occupational exposures and COPD: an ecological analysis of international data. European Respiratory Journal 2009;33(2):298-304. Available from: http://erj.ersjournals.com/content/33/2/298.full.pdf

44. Sunyer J, Zock JP, Kromhout H, Garcia-Esteban R, Radon K, Jarvis D, et al. Lung function decline, chronic bronchitis, and occupational exposures in young adults. American Journal of Respiratory and Critical Care Medicine 2005;172(9):1139-45. Available from: http://ajrccm.atsjournals.org/cgi/reprint/172/9/1139

45. de Meer G, Kerkhof M, Kromhout H, Schouten JP and Heederik D. Interaction of atopy and smoking on respiratory effects of occupational dust exposure: a general population-based study. Environmental Health 2004;3(1):6. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC443511/pdf/1476-069X-3-6.pdf

46. Epstein Y. Sick building syndrome. Harefuah 2008;147(7):607-8, 662. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18814520

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