Passive Smoking and Lung Disease

Updated: Oct 07, 2021
  • Author: Timothy D Murphy, MD; Chief Editor: Girish D Sharma, MD, FCCP, FAAP  more...
  • Print

Practice Essentials

Environmental tobacco smoke (ETS), or secondhand smoke, is increasingly recognized as the direct cause of lung disease in adults and children. [1]  ETS is responsible for significant mortality in adults, causing approximately 3000 deaths per year from lung cancer. Passive smoking also causes significant effects on the lung health of adult nonsmokers, including reduced lung function, increased sputum production and cough, and chest discomfort.

In children, ETS is associated with an increased risk of lower respiratory tract infections (LRTIs), such as bronchitis and pneumonia. An estimated 150,000-300,000 cases of LRTIs in children younger than 18 months are attributed to ETS annually. ETS is causally associated with increased prevalence of fluid in the middle ear, upper respiratory tract irritation, and reduced lung function. It is also associated with increased severity of asthma in children [2] ; the asthma of an estimated 200,000-1,000,000 children is worsened by ETS.

Finally, passive smoke exposure is a risk factor for the development of asthma in children. A cross-sectional study, which included 71,811 families who participated in the 2016-2017 National Survey of Children’s Health, found that estimated prevalence rates of asthma were significantly higher among children who were exposed to ETS than among those who were not (10.7% vs 7.8%; P< .001). Children who lived in a home with a smoker were 30% more likely to receive a diagnosis of asthma, compared with children who did not live with a smoker. [3]




Direct exposure to ETS affects the physiology of the respiratory tract, with symptoms of disease depending on which specific mechanism predominates and which anatomic area is affected most in an individual. The physiologic response to ETS is generally the same as that of the smoker but with a diminished effect. Such changes include increased mucus production (as much as 7-fold); decreased ciliary movement, beat frequency, and transport; increased WBC production and movement to the airway lumen; and increased mucosal permeability to allergens, associated with increased total and specific immunoglobulin E (IgE) levels and increased blood eosinophil counts.

Smoking is associated with acute and long term structural changes in the airways and pulmonary parenchyma, including upper airway mucosal gland hypertrophy and hyperplasia. In 2-week-old children of mothers who smoke, increased lung compliance has been observed. This led the authors to conclude that prenatal  exposure to tobacco products negatively affects elastic properties of the fetal lung because 2 weeks of postnatal exposure was not thought to be enough to exert such an effect. Changes have been described in lung compliance and elasticity, including predisposition toward centrilobular emphysema in adults. A fifth-decade follow-up study of the Tasmanian Longitudinal Health Study cohort, which was first studied in 1968, found that heavy maternal smoking during childhood appears to predispose to spirometrically defined COPD in middle-age. [4]

In an animal model, tobacco exposure induced systemic and local responses, including elevation of plasma levels of C5a and brain-derived neurotrophic factor and increases in pulmonary tumor necrosis factor (TNF)-alpha, interleukin (IL)-5, monocyte chemoattractant protein (MCP)-1, and the density of substance P–positive nerves along the bronchial epithelium. [5] Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. ETS exposure was also associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavage fluid. The effects of ETS on the fetus and infant continue to be studied, and the effects are many and deleterious.



The cause of ETS exposure is straightforward; smokers are in the child's environment. [6, 7, 8, 9]  Sometimes this is difficult to discern, particularly if a primary caregiver is unavailable to provide a history.

The reasons for a caregiver's smoking are myriad but may include a physiologic or psychologic predilection for addiction, the effects of aggressive advertising campaigns by the tobacco industry, and family exposure.

Tobacco use by a parent is a risk factor for initiation of smoking.



United States statistics

Smokers comprise approximately 26% of the adult population, consuming more than 500 billion cigarettes annually. [10] Urinary cotinine levels, a marker of recent tobacco exposure, are present in 50-75% of adult nonsmokers, confirming that exposure to ETS is nearly ubiquitous. Approximately 9-12 million children younger than 5 years (50-66% of children this age) may be exposed to ETS in the home.

International statistics

Data are lacking regarding the prevalence of international ETS exposure, but trends of increased tobacco consumption in Asia, South America, and Africa will increase the frequency of ETS-related disease. [11, 8] Current estimates are that more than 3 million people die annually from tobacco-related disease worldwide. In 1970-1972, tobacco consumption in developed countries was 3.25 times higher than in the developing world. By 1980-1982, this ratio had decreased to 2.38 and, by 1990-1992, to 1.75.

Sex- and age-related demographics

Data are limited regarding sex and ETS-related lung disease. In adults, the historical preponderance of male smokers meant that most spousal studies of never-smokers and ETS have examined mostly women. No clear sex-based differences in susceptibility to the effects of ETS are described in the pediatric population. Evidence from many studies demonstrates that the risk of ETS-associated disease is higher in children of smoking mothers than in those of smoking fathers, presumably because of closer contact of children with the mother.

The risk of ETS to children has an inverse relationship to age. The reasons for this are not clear but may relate to a general decrease in illness frequency, physiological development of the lung anatomy or immunologic function, or decreased close contact between mother and child over time.



Improvements in associated acute illnesses (ie, asthma, otitis media) are documented in association with cessation of passive smoke exposure.


In diseases for which ETS has a known causal link or is a known risk factor, a population-attributable risk factor can be calculated. Approximately 8,000-26,000 new cases of asthma are reported in children of mothers who smoke more than 10 cigarettes a day; if lower levels of exposure are considered, the number of new asthma cases caused by ETS is 13,000-60,000 per year. Exposure to ETS is a major aggravating factor in 10%, or 200,000, of asthma cases in children. Harder to detect, nonthreshold exposure to lower levels of ETS could account for worsening more than 1 million cases of asthma in children. Approximately 150,000-300,000 cases of LRTIs in children younger than 18 months are attributed to ETS, accounting for 7,500-15,000 hospitalizations yearly. Data demonstrate a continued relationship of LRTI to ETS in infants as old as 2 years.

Gill et al conducted a study to assess the effects of exposure to low levels of environmental tobacco smoke on asthma control, spirometry, and inflammatory biomarkers in school-aged children with asthma whose parents either denied smoking or who only smoked outside the home. [12]  Their study cohort consisted of 48 patients (aged 8-18 years) with well-controlled, mild to moderate, persistent asthma that was treated with either inhaled corticosteroids or montelukast. Patients completed an age-appropriate asthma control test and a smoke exposure questionnaire. levels of exhaled nitric oxide, urinary cotinine, and leukotriene E(4) were measured, and spirometry was conducted. Comparisons were then made between findings for patients exposed to environmental tobacco smoke and those who were not exposed. Although only one parent admitted to smoking, 70% of the children had elevated urinary cotinine levels. Urinary leukotriene E(4) was higher in the children exposed to environmental tobacco smoke who were treated with inhaled corticosteroids but not in those treated with montelukast. The investigators concluded that a majority of school-aged children with persistent asthma may be exposed to environmental tobacco smoke, even if their parents insist that they do not smoke in the home. [12]

A population-attributable risk of LRTI for children older than 2 years has not been assessed, but cases of LRTI are expected to decrease. The Centers for Disease Control and Prevention (CDC) has calculated that exposure to maternal smoking accounts for more than 700 deaths from sudden infant death syndrome (SIDS), although the risk attributable to ETS exposure (vs in utero or lactation-related risk factors) is unknown. [13]  Data that link ETS to middle ear disease or upper respiratory tract infection (URTI) widely vary, precluding an estimation of the frequency of those problems. Overall, ETS is responsible for hundreds of thousands to millions of episodes of acute illness in children every year. No case-specific determination of deaths attributable to ETS has been calculated other than those related to SIDS.


Complications associated with passive smoke exposure are related to the illnesses associated with it.


Patient Education

The principal task of the care provider is to provide information to allow the parent to stop exposing the child to ETS. Because understanding the effects of passive smoke exposure on children is one of the most powerful motivating factors in smoking cessation, such information should be available in all primary care physician offices. Validation and comparison of different interventions remains an area of research, but separate studies have demonstrated the efficacy of an "intensive counseling" strategy. The time required to optimally educate the parent regarding ETS is unknown, but this education is commonly performed during a routine office visit.

Ortega Cuelva et al conducted a multicenter, open, cluster-randomized clinical trial to determine the effectiveness of a brief primary care intervention directed at parents who smoke. [14]  The purpose of the intervention is to reduce exposure to tobacco smoke in babies. The study included 83 primary health pediatric teams of the Catalan Health Service and 1,101 babies whose parents were smokers. The intervention group received a brief tobacco smoke pollution intervention; the control group received the usual care. Outcomes were measured by parents' reported strategies to avoid exposing their babies to tobacco smoke. Baseline clinical data and characteristics of each baby's tobacco smoke exposure were collected, along with infant hair samples and parents' tobacco use and related attitudes/behaviors. At 3-month and 6-month follow-up, behavioral changes to avoid infant tobacco smoke exposure were recorded. During follow-up, tobacco smoke avoidance strategies improved more in the intervention groupthan in the control group. Reduced nicotine concentration was associated with improved implementation of effective strategies reported by parents at home and in cars. The researchers concluded that the intervention produced behavioral changes to avoid babies' exposure to tobacco smoke. [14]

For excellent patient education resources, visit eMedicineHealth's Healthy Living CenterLung Disease and Respiratory Health Center, and Children's Health Center. Also, see eMedicineHealth's patient education articles Cigarette Smoking and Sudden Infant Death Syndrome (SIDS).

For more information on the pharmacology of nicotine and smoking cessation, go to Medscape Reference article Nicotine Addiction: Treatment & Medication.