Smoke Signals – Nothing is the Only Safe Bet

Chronic Obstructive Pulmonary Disease or COPD is a leading cause of death in the US. COPD is generally the result of smoking tobacco. Years of exposure to tobacco smoke can damage the airways and result in either emphysema or chronic bronchitis together with a persistent progressive reduction in lung function that ends in death. Tobacco companies have fought hard to prevent the exposure of data that clearly indicates the dangers of tobacco smoke, not only to the smoker but also to anyone in the smoker’s environment. 

The danger to tobacco smokers is very clear. They are constantly exposed to toxins and carcinogens that flood the blood stream and result in a variety of effects that include:

  • loss of the senses of smell and taste
  • reduced oxygen levels and increased blood carbon monoxide levels
  • increased risk of sudden heart attack, stroke and coronary heart disease
  • poor circulation
  • raised blood pressure and pulse
  • reduced lung function
  • increased risk of death from lung cancer
  • increased risk of cancer of the mouth, throat, esophagus, cervix, bladder, kidney and pancreas
  • cataracts
  • reduced fertility in women
  • reduced health status

Epidemiologic studies have clearly illustrated the dose-response relationship between cigarette smoking and adverse health outcomes. Smoking intensity and duration are leading contributors to negative outcomes.(1)

Gender differences in smoking behaviour

Nicotine is metabolized to cotinine which can be measured in serum or urine. The cotinine levels can distinguish between non-smokers, passive and active tobacco smokers.(2) Cotinine is used as a biomarker for evaluating active and passive exposure to cigarette smoke toxins. 

Meilkian and colleagues (3) examined gender differences with respect to smoking behaviour and emissions of toxins from mainstream tobacco smoke. Data from 129 female and 129 male smokers were analyzed. The team found that women:

  • took smaller puffs
  • inhaled for a shorter duration
  • drew more puffs/cigarette
  • smoked less of each cigarette (left longer butts)
  • had 1.92 mg/cigarette emission of nicotine
  • inhaled 139.5 ng/cigarette of specific toxins
  • emitted 18 ng/cigarette emission of BaP emissions

Men, on the other hand, not only took longer puffs, inhaled more and left shorter butts but had 2.20 in nicotine and 20.5 ng BaP emission for each cigarette smoked. Further, they inhaled 170.3 specific toxins per cigarette. 

An interesting observation in this study involved the gender difference in cigarette smoke. The yields of toxins was greater in European Americans than in African Americans. Further, African American men produced the highest emissions of select toxins while European American females showed the lowest self-exposure to carcinogens and toxins. 

Second hand smoke

Sadly, the danger is not restricted to smokers. Exposure to environmental tobacco smoke (ETS), commonly referred to as second-hand smoke or SHS, can also lead to death from lung cancer. SHS exposure at home, work or both is strongly associated with increased acute respiratory symptoms.(3) This study by Lam and colleagues, involving 9,923 current smokers, found that the percentage of smokers exposed to SHS was:

  • 5% at home only
  • 53% at work only
  • 30% at home and at work

The prevalence of respiratory symptoms such as cough, phlegm, wheeze, throat and nasal problems, together with physician consultation and self-medication, were higher for those exposed to SHS at home and at work. After adjusting for age, education, marital status, exposure to pollutants and total dose of active smoking, researcher found that the odds ratio of reporting one or more respiratory symptoms for SHS exposure at home or at work was 1.33 and 1.66 respectively. There was a dose-response relationship between SHS exposure at home, at work or both places. 

Effect of SHS on smokers in confined areas

In the past research has concentrated on the effect of SHS on non-smokers. It has been assumed that SHS would have a negligible effect on smokers. Recent research has indicated that smokers exposed to SHS in a confined area increased their daily carcinogenic intake.(4)

Published in Environmental Health, this study was the first to analyze the effects of ETS on active smokers. It involved newsagents in Italy who were chosen because they work in small newsstands where any tobacco smoke in the air they breathe is strictly correlated to the number of cigarettes they smoke. Results showed that, in terms of carcinogen exposure, SHS accounted for

  • 15% to 23% for regular cigarettes (> 10mg tar)
  • 21% to 34% for light cigarettes (5 - 10 mg tar)

The average smoker smoked 14 cigarettes a day. Smoking in a confined environment or closed area added the carcinogenic equivalent of smoking another 2.6 cigarettes. If there were other smokers in the closed environment, then the carcinogen exposure becomes the equivalent of an additional 1.3 cigarettes. Thus SHS is an additional danger to smokers.

SHS and Youth

Whether in utero or early life, exposure to parental smoking has a significant impact on lung function. The question as to the effects of SHS on healthy male adolescents was answered by Rizzi et al(5) who surveyed 80 adolescent boys (21 smokers, 30 nonsmokers and 29 passive smokers). Assay of urinary cotinine levels and lung function tests were conducted together with a standardized questionnaire on the smoking habits of the adolescents and their parents. The team found that passive smokers had a higher residual volume than non-smokers as well as a lower maximal expiratory flow at 25% of FVC (MEF25) and DLCO. Their MEF25, DLCO and carbon monoxide transfer coefficient were lower if their mothers had smoked during pregnancy than those adolescents whose mothers had not smoked during pregnancy. A statistically significant correlation was found between the cotinine/creatine ratio and DLCO in both smokers and in passive smokers but not in nonsmokers. The researchers concluded that current exposure to SHS in health male adolescents was associated with lung function impairment regardless of the effects of maternal smoking during pregnancy. 

There is some good news in that SHS exposujre in cars and rooms declined significantly between 2000 and 2009. Data from the National Youth Tobacco Survey showed that the reduction in exposure rate was greater for males than females.(6)

Third-Hand Smoke

The American Cancer Society defines third-hand smoke as the post-smoking toxic residue left behind in the air, which settles on surfaces once the smoke has dissipated. Tobacco-smoke residue can be found on carpets, upholstered furniture, clothing, curtains, car interiors and everyday surfaces exposed to a smoker.

The researchers investigated the result of contact between nicotine from tobacco smoke and nitrous acid. Nitrous acid, a compound typically found in indoor environments, is commonly emitted by household appliances or cigarette smoke. They found the result to be compounds called tobacco-specific nitrosamines, which are known carcinogens. More than half the nitrosamines lingered in the environment for more than two hours after the tobacco smoke had dissipated.

Researchers exposed a piece of paper to smoke and found that three hours later, in the presence of nitrous acids, the level of newly formed carcinogens had increased by a factor of 10. 

The researchers stress that the health impacts of such compounds were uncertain but noted that non-smokers and infants could face health risks from exposure to contamination of surfaces and dust from third-hand smoke residue.


There is no good news related to smoking. The asthma educator must:

  • ask patients of all ages if they smoke and if they are exposed to cigarette/pipe or cigar smoke 
  • ascertain where the exposure takes place. 

Infants, children and adolescents are particularly susceptible because their lungs are going through a period of growth. Confined spaces, whether indoors or in automobiles, increase the exposure to the ill-effects of SHS, in particular the carcinogens present in tobacco smoke.



BaP        benzo(a)pyrene
DLCO    diffusing capacity of carbon monoxide
ETS        environmental tobacco smoke, also called SHS
FVC        forced vital capacity
MEF        mid expiratory flow
SHS        second hand smoke
COPD    chronic obstructive pulmonary disease

1) U.S. Department of Health and Human Services. The health consequences of smoking: a report of the surgeon general. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Smoking and Health, Superintendent of Documents. Washington (DC): U.S. Government Printing Office; 2004.

2) Zielinska-Danch W, Wardas W, et al. Estimation of urinary cotinine cut-off points distinguishing non-smokers, passive and active smokers. Biomarkers. 2007;12(5):484–96.
Lam TH, Ho LM, Hedley AJ, et al. Secondhand smoke and respiratory ill health in current smokers. Tob Control. 2005;14(5):307–14.

3) Melikian AA, Djordjevic MV, et al. Gender differences relative to smoking behavior and emissions of toxins from mainstream cigarette smoke. Nicotine Tob Res. 2007;9(3):377–87.

4) Piccardo MT, Stella A, Valerio F. Is the smokers exposure to environmental tobacco smoke egligible? Environ Health. 2010 Jan 29;9:5.

5) Rizzi M, Sergi M et al. Environmental tobacco smoke may induce early lung damage in healthy male adolescents. Chest 2004; 125(4): 1387–93

6) McIntire RK, Macy JT et al. Secondhand smoke exposure in cars and rooms: trend comparisons of nonsmoking U.S. middle and high school students. Nicotine Tob Res. 2013 Dec 24 (Epub ahead of print) Abstract.