Firsthand and secondhand smoke both cause pulmonary, heart, cell and fetal damage.
In a 2007 study, radiology physicist Chengbo Wang used helium-3 diffusion magnetic resonance imaging to prove that human lungs change when exposed to secondhand smoke. Tiny holes and extended spaces in the lung's structure showed abnormal microscopic changes before symptoms appeared. A 2004 British Medical Journal article reported results of a study using plasma cotinine, a metabolized nicotine. It found that secondhand smoke in any kind of smoke-filled environment carries a high risk of non-smokers there contracting coronary heart disease and stroke. The study concluded that secondhand smoke is a true health hazard.
Lung Disease
Harvard University reported that cancer symptoms take roughly 20 years to develop. Because the lungs are filled with blood and lymph vessels, cancer cells travel via these vessels to other tissues and organs. Cancer cells first invade an organ's tissue and then metastasize to invade and destroy other tissues and organs. Dangerous chemicals in secondhand smoke begin changing a non-smoker's lungs instantly by causing a normal cell's key genes to mutate. These abnormal cells or tumors change a normal cell's internal structure and shape-shift the external structure. The tumor's location determines the symptoms. If the tumor settles in lung tissue, it causes belabored breathing and wheezing; if it settles in a breathing tube, a person coughs up blood.
Heart Disease
Harvard also studied how secondhand smoke affects heart and blood vessels. Mid-1980s studies proved that passive smoke can cause clogged coronary arteries. These arteries are important because they are the oxygen and nutrient messengers of the heart muscle. Likewise, secondhand smoke causes similar damage to the carotid arteries by making the blood vessels stiffen.
Secondhand smoke immediately begins changing blood platelets by making them stick to one another. Eventually, they develop into clumps which can become clots. Blood clots can block arteries and cause a heart attack or stroke.
Fetal and Infant Risks
A 1999 Stanford University study on active- and passive-smoking mothers found that carbon monoxide and nicotine harmed fetuses and babies. When carbon monoxide combines with hemoglobin, the new compound decreases fetal oxygen supply. Decreased fetal oxygen makes the placenta grow larger and often leads to placenta previa. Nicotine crosses the placenta and competes with the mother's amniotic fluid, and that can cause spontaneous abortion. Carcinogens cross placental membranes and mutate fetal tissue; this can later cause childhood cancer, particularly leukemia and lymphoma. A 1995 Vanderbilt University study on fetal lambs showed that nicotine impairs an infant's ventilating and arousal ability, a factor in sudden infant death syndrome.
Deadly Chemicals
Chemical engineer Joe Zasadzinski believes the chemistry of primary and secondhand smoke to be the same. He explained that burning smoke contains more than 5,000 chemicals including carbon monoxide, cyanide, benzene, formaldehyde and arsenic. "When (smokers) suck cigarettes, (they expect) a hefty hit of nicotine," Zasadzinski reasoned. "It's tough to say who gets the worst of it--the active smoker or the passive bystander," he added.
University of California-Berkeley Tobacco Lab scientist Kamlesh Asotra stated that regular smokers develop a degree of resilience to the attack on their lungs; non-smokers don't. Therefore, secondhand smoke can cause more lung damage than direct smoke does.
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