Environmental tobacco smoke (ETS), commonly known as secondhand smoke, is the air pollution involuntarily inhaled by non-smokers. This harmful mixture is composed of two primary elements: sidestream smoke, which rises directly from the burning end of a cigarette, and mainstream smoke, the smoke exhaled by the person smoking. The air is contaminated with thousands of chemical compounds, including at least 70 known carcinogens. Due to the lower burning temperature of the tobacco between puffs, sidestream smoke contains higher concentrations of toxic substances like ammonia, carbon monoxide, and nicotine compared to the smoke directly inhaled by the smoker.
Developmental Hazards for Fetuses and Infants
Exposure to environmental tobacco smoke during pregnancy poses significant risks to the developing fetus, as the harmful chemicals are not blocked by the placenta. Both nicotine and carbon monoxide can cross the placental barrier and reach the fetal bloodstream via the umbilical cord. This exposure is associated with an increased risk of adverse pregnancy outcomes, including preterm delivery and fetal growth restriction, which often results in low birth weight.
One of the most documented effects of ETS on infants is the increased risk of Sudden Infant Death Syndrome (SIDS). Prenatal and postnatal exposure to smoke impairs the infant’s ability to arouse from sleep in response to reduced oxygen levels. The carbon monoxide inhaled forms carboxyhemoglobin, reducing the oxygen-carrying capacity of the blood and leading to chronic oxygen deprivation in the fetus. Nicotine acts as a neurotoxicant, affecting the autonomic nervous system and brainstem nuclei that regulate breathing and heart rate.
Infants exposed to ETS are at risk for long-term neurodevelopmental problems. The toxic components can interfere with the normal maturation of the nervous system, potentially leading to cognitive and behavioral issues later in childhood. Studies have linked early life smoke exposure to deficits in cognitive abilities and an increased likelihood of developing behavioral problems such as hyperactivity.
Respiratory and Infectious Illnesses in Children
Children exposed to environmental tobacco smoke after infancy experience higher rates of respiratory and infectious illnesses. ETS exposure is directly linked to both the development of new-onset asthma and the exacerbation of symptoms in children already diagnosed with the condition. The irritation and inflammation caused by smoke particles in the airways increase bronchial hyperresponsiveness, making asthma attacks more frequent and severe.
Exposure significantly increases a child’s susceptibility to acute respiratory infections, such as bronchitis and pneumonia. The smoke damages the protective lining of the airways and impairs the function of cilia, the tiny hair-like structures that sweep mucus and pathogens out of the lungs. This compromised defense mechanism allows viruses and bacteria to penetrate deeper into the respiratory tract, leading to more frequent and severe lower respiratory tract infections.
The increased incidence of middle ear infections, or otitis media, is a common effect. ETS can cause toxic injury to the mucosal lining of the nose and throat, leading to inflammation and congestion. The smoke impairs the mucociliary function of the Eustachian tube, which connects the middle ear to the back of the throat. When this tube becomes blocked or dysfunctional, fluid accumulates, creating an environment where bacteria and viruses can thrive, leading to recurrent acute otitis media.
Chronic exposure to smoke during childhood impairs the normal growth and development of the lungs. This exposure leads to measurable reductions in lung function, which can persist throughout life. This early impairment establishes a lifelong risk of poor lung health and may contribute to the development of chronic respiratory conditions in adulthood.
Chronic Disease Risk for Non-Smoking Adults
For adults who have never smoked, chronic exposure to environmental tobacco smoke significantly elevates the risk for diseases. The cardiovascular system is especially vulnerable, with ETS exposure increasing the risk of death from ischemic heart disease. The toxic components in ETS, such as carbon monoxide and fine particulates, cause immediate damage to the endothelium, which is the delicate inner lining of the blood vessels.
This damage promotes the formation of atherosclerotic plaques and accelerates the progression of existing artery hardening. ETS also promotes the aggregation of platelets, making the blood more prone to forming dangerous clots that can lead to heart attacks and stroke. Non-smokers exposed to secondhand smoke have been found to have elevated levels of fibrinogen, a protein that plays a central role in the clotting cascade and is an independent risk factor for thrombosis.
Environmental tobacco smoke has been classified as a Group A carcinogen, a designation reserved for substances proven to cause cancer in humans. This exposure is a known cause of lung cancer in non-smokers, with studies indicating an increased risk of developing the disease compared to unexposed non-smokers. The cancer-causing agents in the smoke, particularly from the more concentrated sidestream component, are inhaled deep into the lungs where they can damage cellular DNA.
Non-smoking adults exposed to ETS also experience other respiratory symptoms. This includes increased risk of developing general respiratory symptoms and, with long-term, high-level exposure, a potential increase in the risk for chronic obstructive pulmonary disease (COPD). The persistent airway inflammation caused by the smoke can contribute to a decline in lung function over time, mirroring the effects seen in active smokers.