Environmental Tobacco Smoke - Secondhand Smoke
Environmental tobacco smoke has been identified as increasing the risk of coronary heart disease and lung cancer. The increase in the risks have been estimated by various studies at 15-35%.
In a study of 72,829 women who never smoked in Shanghai, China, 83.1% of the women were exposed to tobacco smoke from their husbands, at work, or early in life. The study lasted 5.7 years and found that deaths from all illnesses was significantly higher in women whose husbands smoked. In particular, deaths from cardiovascular disease and stroke was significantly higher when the husband smoked. Deaths due to cancer, especially lung cancer, were significantly higher among women exposed to tobacco smoke at work.
A study of French non-smoking workers exposed to tobacco smoke noted a significantly increased risk of lung cancer on the order of 12% to 39%.
Smoking has long been know to cause genetic mutations and chromosomal damage to cells. Cells cannot function properly in a damaged state. If the rate of damage exceeds the rate of repair, the cell may die or produce a cancer.
DNA damage typically consists of broken strands of DNA. For example, active smokers show significantly more chromosomal damage in lymphocytes (a type of while blood cell) than non-smokers. Also, those exposed to environmental tobacco smoke in an indoor workplace (both non-smokers and ex-smokers) show significantly more chromosomal damage than non-smokers not exposed to secondhand smoke Chromosomal damage was greatest among active smokers. And, the damage increased as the number of daily cigarettes increased.
There was more chromosomal damage due to passive smoking among ex-smokers than among those who had never smoked. Analyzing the number of years since the ex-smokers had actively smoked showed that for ex-smokers to reach the same lower level of damage of never-smokers would require being an ex-smokers for 17 years.
DNA damage can be repaired within the cell. Researchers induced chromosomal damage in lymphocytes to determine how quickly repairs took place. The lymphocytes from never-smokers not exposed to passive smoking were completely repaired within 60 minutes. In active smokers, 45 to 60% of the lymphocytes remained damaged after 60 minutes. Similar long lasting damage was observed in passive smokers (both never-smokers and ex-smokers). Repair speed can be stated in terms of half-life or the time to repair half the damage. In non-smokers half the chromosomal damage was repaired within a few minutes. For active smokers, half-life was between 67 and 110 minutes.
Maternal exposure to environmental tobacco smoke also exposes the fetus to constituents of the smoke through the mother's blood system. After birth, tobacco smoke affects infants in approximately 36% of homes. Side-steam smoke contains higher concentrations of toxins than mainstream smoke and these toxins can easily enter the infant's bloodstream.
Exposure to tobacco smoke during pregnancy can cause reduced fetal growth. Exposure to tobacco smoke after birth can cause cognitive deficits, increased number of nicotine receptors in the brain, and behavior problems.
Further, altered neurobehavioral functions involving heart rate are related to exposure to tobacco smoke. The resting heart rate of 2-4 week old infants is significantly higher when the mother smoked during pregnancy. And, as the number of daily cigarettes increases, the infant heart rate increases. Smoking cigarettes smoked during pregnancy or exposure postnataly to tobacco smoke also predicts reduced RSA (respiratory sinus arrhythmia measured as the difference between the maximum interbeat interval during expiration and the minimum interbeat interval on inspiration). Lower RSA may make it harder for infants to respond to environmental challenges.
Infants are not unique in experiencing negative effects of tobacco smoke. Studies seem to indicate that exposure to tobacco smoke has lasting effects on children and include such symptoms as behavior problems, conduct disorder and delinquency.
Attention Deficit Hypereactivity Disorder (ADHD) affects between 3 and 8% of U.S. children. It is the most common childhood disorder. Children with ADHD are at risk of conduct disorder, antisocial behavior and drug abuse later in life.
Prenatal exposure to tobacco smoke has been found to increase risk of ADHD by a factor of 2 to 4 times. One study found an 4.6-fold increased risk for ADHD for females and a 2.1-fold increased risk for males when the mother was exposed to tobacco smoke during pregnancy. Compare this to a 4.1-fold increased risk of ADHD for children with high lead levels in their blood.
While some studies have found behavior problems associated with postnatal exposure to tobacco smoke, postnatal exposure to tobacco smoke has not been found to predict ADHD.
Studies have estimated that between 35-80% of inner-city children are exposed to environmental tobacco smoke. Detrimental health effects include reduced birth weight, neurodevelopmental problems, various respiratory diseases such as asthma, increased risks for cancer and cardiovascular diseases. These effects are seen from early childhood through adulthood.
In a New York City study, researchers tested 226 infants, 40.2% of the non-smoking mothers were exposed to tobacco smoke before delivery. The Mental Development Index of the Baley Scales of Infant Intelligence was administered at 24 months. Those infants exposed to tobacco smoke showed an average 4.8 point deficit in test score with 32.3% of the children showing a high rate of developmental delay. The authors estimate that the cost for remedial services (Early Intervention Services) because of development delay due to environmental tobacco smoke is $99 million across all of New York City.
Environmental tobacco smoke is an important cause of respiratory illness in children, especially pre-school children. Childhood exposure to tobacco smoke is associated with the development of asthma, allergies, nasal and sinus diseases, tooth decay, and behavior problems. Nicotine is metabolized or broken down in the body and produces a chemical called cotinine. The amount of cotinine in the blood, saliva or urine is good measure of the exposure to nicotine. It take about 20 hours for half the continine to be metabolize to other products.
One study investigated the relationship between young student's continine levels and reports of parental smoking. It was clear that smoking in the home significantly increased the continine levels of children in the home.
Overall, the effects of tobacco smoke on those who do not smoke are staggering. This is especially true of the most vulnerable, our youth.
References
- Hasim Boyaci, Nilay Etiler, Can Duman, Ilknur Basyigit & Ayse Pala, Environmental tobacco smoke exposure in school children: parent report and urine continine measures, Pediatrics International, v 48, 2006, 382-389.
- Wanqing Wen, Xiao Shu, Yu-Tang Gao, Gong Yang, Qi Li Honglan Li & Wei Zheng, Environmental tobacco smoke and mortality in Chinese women who have never smoked: prospective cohort study, BMJ, doi:10.1136/bmj.38834.522894.2F (published 12 July 2006)
- Thaddeus Miller, Virginia A Rauh, Sherry A M Glied, Dale Hattis, Andrew Rundle, Howard Andrews & Frederica Perera, The Economic Impact of Early Life Environmental Tobacco Smoke Exposure: Early Intervention for Developmental Delay, Environmental Health Perspectives, 114(10), October 2006, 1585-1588. >
- Shahryar Alipour, Fredric Deschamps, Francois-Xavier Lesage & Framcois Lebargy, Estimation of Annual Incidence of Lung Cancer Associated wtih Work Place Exposure to Passive Smoking in France, Journal of Occupational Health, v 49, 2006, 329-331.
- Maria Enrica Fracasso, Denise Doria, Paola Franceschetti, Luigi Perbelline & Luciano Romeo, DNA damage and repair capacity by comet assay in lymphocytes of white-collar active smokers and passive smokers (non- and ex-smokers) at workplace, Toxicology Letters, v 167, 2006, 131-141.
- Pamela Schuetze & Rina D Eiden, The association between maternal smoking and secondhand exposure and autonomic function at 2-4 weeks of age, Infant Behavior & Development, v 29, 2006, 32-43.
- Joe M Braun, Robert S Kahn, Tanya Froehlich, Peggy Auinger & Bruce P Lanphear, Exposures to Environmental Toxicants and Attention Deficit Hyperactivity Disorder in U.S. Children, Environmental Health Perspectives, 114(12), December 2006, 1904-1909.
The following are resources for ETS:
- S.A.F.E. Smokefree Air For Everyone
- S.A.F.E. is a network of individuals injured or disabled by secondhand smoke. Our members include adults and children with chronic illnesses and/or hypersensitivity to secondhand smoke or other environmental pollutants.
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