Passive smoking is the inhalation of tobacco smoke, called secondhand smoke, or environmental tobacco smoke, by persons other than the intended active smoker.

Increases risk of cardiac death or morbidity by 30% compared with a doubling to quadrupling of risk associated with active smoking.

Exposure to secondhand smoke activates platelets nearly to the extent that they are activated by smokers.

Cigarette smoke contains approximately 7000 chemicals, including 60 to 70 known carcinogens.

Estimated 41,000-53,000 annual deaths attributed to involuntary smoking in the U.S.

The WHO states that passive smoking causes about 600,000 deaths a year, and about 1% of the global burden of disease.

Passive smoking causes about about 1/8 of all deaths caused by smoking.

Secondhand smoke increases coronary heart disease in smokers in a non-linear dose relationship such that exposure has a larger than expected adverse effect at low levels (Barnoya J, Glantz SA).

Secondhand smoke causes many of the same diseases as direct smoking, including cardiovascular diseases, lung cancer, and respiratory diseases.

These diseases include:

Cancer: secondhand tobacco smoke is carcinogenic to humans, with about 70 chemicals present in secondhand smoke being carcinogenic.

In the United States passive smoke is estimated to cause more than 7,000 deaths from lung cancer a year among non-smokers, with a quarter of all cases occur in people who’ve never smoked.

Passive smoking may increase the risk of breast cancer in younger, primarily premenopausal females.

Systematic reviews found that exposure to secondhand smoke increased the risk of cervical cancer.

Bladder cancer: A review and meta-analysis found that secondhand smoke exposure is associated with a significant increase in the risk of bladder cancer.

Both active and passive cigarette smoking increase the risk of atherosclerosis.

Passive smoking is strongly associated with an increased risk of stroke.

Exposure to secondhand smoke is associated with an increased risk of depressive symptoms.

Maternal secondhand smoke exposure increased the risk of miscarriage by 11%.

Children absorb much less nicotine from secondhand e-cigarette vapor than from secondhand tobacco smoke.

Women exposed to environmental tobacco smoke and non-exposed females, demonstrate that females exposed while pregnant have higher risks of delivering a child with congenital abnormalities, longer lengths, smaller head circumferences, and low birth weight.

Passive smoking is associated with a slightly increased risk of allergic diseases among children and adolescents.

Passive smoking was associated with a higher rare of atopic dermatitis.

There is evidence to infer a causal relationship between exposure to secondhand smoke and sudden infant death syndrome:estimated to be associated with 430 SIDS deaths in the United States annually.

Secondhand smoke exposure is also associated with an almost doubled risk of hospitalization for asthma exacerbation among children with asthma.

Secondhand smoke exposure associated with lung infections, more severe illness with bronchiolitis and bronchitis, and worse outcomes as well as increased risk of developing tuberculosis if exposed to a carrier.

In the United States, secondhand smoke has been associated with between 150,000 and 300,000 lower respiratory tract infections in infants and children under 18 months of age, resulting in between 7,500 and 15,000 hospitalizations each year.

Maternal passive smoking increases the risk of non-syndromic orofacial clefts by 50% among their children.

An increase in tooth decay is associated with passive smoking in children.

Passsive smoking associated with Increased risk of middle ear infections, and invasive meningococcal disease.

Exposure to secondhand smoke during pregnancy is associated with an increased risk of neural tube defects.

Exposure to secondhand smoke associated with anesthesia complications, and negative surgical outcomes.

There is a suggestion of significant association between passive smoking and sleep disordered breathing in children.

Epidemiological findings show that non-smokers exposed to secondhand smoke are at risk for many of the health problems associated with direct smoking.

Secondhand smoke exposure increases the risk of heart disease by a quarter.

Inhaled sidestream smoke, the main component of secondhand smoke, is about four times more toxic than mainstream smoke.

There is a relative risk of lung cancer of 1.29 for women exposed to secondhand smoke from their spouses.

Secondhand smoke is not simply a diluted version of mainstream smoke, but has a different composition with more toxic substances per gram of total particulate matter.

Passive smoking appears to be capable of precipitating the acute cardio-vascular diseases and may also have a negative impact on the outcome of patients who have acute coronary syndromes.

Secondhand smoke is probably the most important indoor pollutant, especially for young children

Smoking by either parent, particularly by the mother, increases the risk of asthma in children.

The outlook for early childhood asthma is less favorable in smoking households.

Among people with asthma, higher secondhand exposure is associated with a greater risk of severe attacks.

Smoke-free legislation reduces the number of hospital admissions for heart disease.

There is evidence that secondhand smoke caused cancer in humans, especially for those who work in environments where smoke is not regulated.

Parrticular risk of exposure includes those in installation repair and maintenance, construction and extraction, and transportation.

Living or working in a place where smoking is permitted increases the non-smokers’ risk of developing heart disease by an estimated 25–30% and lung cancer by an 20–30%.

Children exposed to environmental tobacco smoke experience a range of adverse effects and a higher risk of becoming smokers later in life.

Reducing of exposure to environmental tobacco smoke is a key element to encourage healthy child development.

The prevalence of secondhand smoke exposure among U.S. nonsmokers has declined significantly.

Environmental tobacco smoke can be evaluated either by directly measuring tobacco smoke pollutants in the air or by using biomarkers, which are indirect measures of exposure.

Biologic markers of tobacco smoke exposure include: breath carbon monoxide, body levels of nicotine, cotinine, thiocyanates, and proteins.

Biochemical tests are a much more reliable biomarker of secondhand smoke than surveys of exposure.

Biological levels of nicotine from secondhand smoke exposure are equivalent to nicotine levels from active smoking and levels that are associated with behavior changes due to nicotine consumption.

Cotinine is the metabolite of nicotine, and is a biomarker of secondhand smoke exposure.

Cotinine can be measured in the blood, saliva, urine, and hair.

Cotinine accumulates in hair, and is a

measure of long-term, cumulative exposure to tobacco smoke.

Cotinine levels found in the urine reflect exposure only over the preceding 48 hours.

Cotinine levels of the skin, hair and nails, reflect tobacco exposure over the previous three months and are a more reliable biomarker.

Carbon monoxide monitored via breath is a reliable biomarker of secondhand smoke exposure as well as tobacco use.

It not only provides an accurate non-invasive measure, and is highly reproducible.

Breath CO monitoring measures the concentration of CO in an exhalation in parts per million, and this can be directly correlated to the blood CO concentration.

World Health Organization has concluded that non-smokers are exposed to the same carcinogens as active smokers.

Passive smoke contains more than 4,000 chemicals, including 69 known carcinogens: particularly polynuclear aromatic hydrocarbons, tobacco-specific N-nitrosamines, and aromatic amines, known to be highly carcinogenic.

Carcinogens have been shown to be present at higher concentrations in sidestream smoke than in mainstream smoke.

Secondhand smoke has been shown to produce more particulate-matter (PM) pollution than an idling low-emission diesel engine.

Secondhand tobacco smoke exposure effects on blood and blood vessels that increase the risk of a heart attack, particularly in people already at risk.

Exposure to tobacco smoke for 30 minutes significantly reduces coronary flow velocity reserve in healthy nonsmokers.

Secondhand smoke is also associated with impaired vasodilation among adult nonsmokers, affects platelet function, vascular endothelium, and myocardial exercise tolerance at levels commonly found in the workplace.

Third-hand smoke identifies the residual tobacco smoke contamination that remains after the cigarette is extinguished and secondhand smoke has cleared from the air: third-hand smoke poses a special danger for the developing brains of infants and small children.

Lung cancer has linked the primary factors closely tied to lung cancer in non-smokers as exposure to secondhand tobacco smoke, carcinogens including radon, and other indoor air pollutants.

Smoke-free policies reduce tobacco use among workers when implemented in worksites or by communities.

The vast majority of the public supports restricting smoking in various outdoor settings.

Engineering approaches, such as ventilation, are ineffective and do not protect against secondhand smoke exposure.

Secondhand smoke exposure associated with lung cancer, with an increased relative risk of lung cancer among those exposed to secondhand smoke is 1.19, 1.48 for lung cancer among men exposed to secondhand smoke, and a relative risk of 1.16 among those exposed to it at work.

Passive smoke associated with an increased risk of death in both adults, where it is estimated to kill 53,000 nonsmokers per year, making it the third leading cause of preventable death in the U.S, and in children.

Passive smoking may increase the risk of tuberculosis infection and accelerate its progression of the disease: but the evidence remains weak.

Studies have found a significant association between secondhand smoke and sinusitis.

Exposure to secondhand smoke may increase the risk of cognitive impairment and dementia in adults 50 and over.

Children exposed to secondhand smoke show reduced vocabulary and reasoning skills when compared with non-exposed children as well as more general cognitive and intellectual deficits.

Since implementation of smoke free laws there has been a 10% reduction in admissions for MI.

A 100% smoke-free policy in workplaces, restaurants, and bars significantly decrease the incidence of myocardial infarction and a trend to decreased sudden cardiac death (Hurt RD. et al).

Smoke free environments have caused decline in nose, eye, throat irritation and in cough, wheeze and shortness of breath.

Bar workers have a 4-6 times higher exposure to secondhand smoke compared to other workplaces.

Exposure to secondhand smoke in non-smokers is associated with the lowering of the high density lipoprotein cholesterol, increased markers of inflammation, increased serum fibrinogen levels, increased homocysteine levels, decreased antioxidant levels, and increased insulin resistance.

Secondhand smoke exposure has nearly as large effects on the cardiovascular system as those with the active smoking (NCI).

Children exposed to secondhand smoke have a greater risk of sudden death infant syndrome.

Children exposed to secondhand smoke have increased risk of adverse respiratory difficulties during surgery.

Associated with exacerbation of respiratory illness in children exposed to secondhand smoke.

When tobacco smoke enters the environment, it causes inhalation by people within that environment.

Secondhand tobacco smoke causes disease, disability, and death.

Associated with lung cancer, coronary artery disease, lower respiratory illness, middle ear disease and childhood asthma.

Because smoking prevalence is higher in men, women are disproportionately harmed by secondhand smoke.

Relative risk for ischemic heart disease in non-smokers exposed to secondhand smoke with those not exposed is 1.31 based on a meta-analysis of 29 studies (Barnooya J , Glantz SA).

Smoking exposure is measured by cotinine levels, a metabolite of nicotine, has a hazard ratio for coronary artery disease of 1.57 in the highest quartile of exposure compared to the lowest quartile of exposure (Whincup PH et al).

Associated with increased white blood count, C reactive protein, homocysteine, fibrinogen, and LDL-cholesterol.

It is found that there is no risk free level of secondhand smoke exposure.