Subject: Re: Please post any DATA from research on SECOND HAND SMOKE DANGERS.
From: prupp@ix.netcom.com (Rob)
Date: Tue, 22 Oct 1996 01:02:17 GMT
To Ms. Brophy and all thread participants:
sci.data.formats has *ABSOLUTELY NOTHING* to do with medicine, the
body, cigarettes, or cancer. Please remove it from any followups.
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>Subject: Re: Please post any DATA from research on SECOND HAND SMOKE DANGERS.
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>
>Tim R. Benson wrote in article
><3260AB3B.FF6@iastate.edu>...
>> I WOULD LIKE TO SEE SOME DATA ON SECOND HAND SMOKING OR SMOKING EFFECTS
>> PERIOD.
>
>Please stop shouting we are not deaf.
>
> THERE IS ALOT OF PEOPLE OUT THERE THAT DO NOT BELIEVE IT CAUSES
>> CANCER. THANK YOU! PLEASE POST REPLY
>
>This is only a minor fraction of research available.....
>Look the rest up on your own.....
>
>ETS (Environmental tobacco smoke): The Problem
>
>As even a brief glance at the research will confirm, ETS is a public health
>challenge of staggering proportions. It is estimated that 330 Canadians die
>every year from lung cancer caused by exposure to ETS. The total number of
>ETS-related deaths among otherwise healthy non-smokers in Canada is
>currently estimated to range from 3,000 to 3,500 annually. Though this
>figure clearly underscores the threat ETS poses to public health, it does
>not convey the full extent of illness and disability resulting from ETS and
>thus furnishes only an initial and partial description of the overall
>health hazards of ETS. [3]
>
>Most nonsmoking Canadians are regularly exposed to the hazards of ETS. It
>is estimated that Canadians generally spend about 90% of their time
>indoors, and that about 55% to 70% of those who do not smoke regularly
>inhale ETS in either the workplace or the home.[4] The amount of exposure
>depends on such variables as the number of cigarettes smoked, room size,
>tar level, duration of exposure, and ventilation rates. [5]
>
>The smoker's immediate surroundings are often shared by nonsmokers, who are
>then obliged, often unwillingly, to suffer the effects of the smoker's
>addiction. Breathing in other people's smoke, called passive or involuntary
>smoking, exposes nonsmokers to the myriad carcinogens and toxins found in
>tobacco smoke.
>
>Harmful constituents of ETS can be dispersed throughout a home or workplace
>even though smoking is restricted to a single room and that room appears to
>contain all of the visible remnants of the smoke. [6]
>
>It is a serious yet common error to regard ETS as consisting solely of the
>visible smoke occupying the immediate vicinity of the smoker. Many of the
>constituents of ETS, and indeed many of its more dangerous constituents,
>are not visible. The carbon monoxide in ETS, for instance, is not visible.
>
>ETS Constituents
>
>ETS is a potent combination of harmful gases, liquids, and inhalable
>particles. It consists of mainstream smoke, the smoke inhaled and exhaled
>by the smoker, and sidestream smoke, the smoke released directly from the
>end of a burning cigarette.
>
>The distinction between sidestream and mainstream smoke is critical. Both
>kinds of smoke contain the same compounds, but they contain these compounds
>in different proportions. For instance, sidestream smoke contains almost
>twice as much nicotine as mainstream smoke.
>
>The differences may be even greater in certain cases. To illustrate, the
>amount of 4-aminobiphenyl, a constituent of ETS linked to bladder cancer,
>is almost 31 times greater in sidestream than in mainstream smoke. (ETS is
>currently the only known environmental source of this carcinogen.) There is
>3 times as much benzo(a)pyrene, 6 times as much toluene, and 50 times as
>much dimethylnitrosamine. Chemically, sidestream smoke contains these
>carcinogens and toxins regardless of the brand that is smoked, the amount
>that is puffed by the smoker, or whether the cigarette is filtered. [7]
>
>In many cases, involuntary smokers cannot avoid these chemical hazards. A
>non-smoking bartender in a poorly ventilated bar may breathe as much
>benzo(a)pyrene and carbon monoxide in eight hours as if he or she had
>smoked about 36 cigarettes. [8] An involuntary smoker at 50 cm distance
>from a burning cigarette may inhale 10 times the amount of toxic carbonyl
>compounds inhaled by the smoker. Roughly two thirds of all tobacco smoke is
>sidestream smoke. [9]
>
>All told, tobacco smoke contains over 4,000 chemicals, of which at least 50
>are known carcinogens. Benzene, formaldehyde, and hydrazine are examples of
>leading carcinogens. Toxins include ammonia, hydrogen sulphide, carbon
>monoxide, nitrogen oxide, and, not least, tar and nicotine. Tobacco smoke
>also contains immunogens, i.e., substances that trigger the immune system.
>Approximately half of allergy-prone individuals react to tobacco leaf
>extracts. [10]
>
>These carcinogens and toxins not only enter the surrounding air, they also
>enter the human bloodstream of involuntary smokers, posing serious health
>risks.[11] Cotinine measurements have shown that nicotine is also absorbed
>through exposure to ETS. (Cotinine is a metabolite of nicotine found in the
>blood, urine and saliva of nonsmokers, providing a reliable biomarker of
>the effects of ETS exposure on nonsmokers.) Cotinine has been detected in
>50-75% of reported nonsmokers tested, and it has been estimated that
>one-half to two-thirds of all children are exposed to ETS in the home.
>Worse, many of the harmful ETS constituents cannot be removed by
>ventilation or filtration. Tobacco smoke, in short, is the single largest
>source of harmful air pollution for the nonsmoking population.[12]
>
>Cardiovascular and Cerebrovascular Disease
>
>Like active smoking, passive smoking is commonly associated with lung
>cancer. In fact, heart and stroke disease are a much more frequent result
>of passive smoking than lung cancer. Studies estimate that there are as
>many as ten times more deaths due to ETS-related heart disease than to
>ETS-related lung disease. [13]
>
>The harmful effects of ETS on the cardiovascular and cerebrovascular system
>are apparent even after short-term exposure. Exposure lasting even as
>briefly as 8 to 20 minutes has measurable effects linked with heart and
>stroke disease. The heart rate increases, the heart's oxygen supply
>decreases, and the blood vessels constrict. [14] In short, the heart is
>required to do more work at precisely the same time that it is being
>deprived of oxygen, its key source of energy. Exposure to ETS causes
>platelet aggregation, making blood "sticky" and causing blockages in veins
>and arteries that can lead to heart attacks and strokes. The accumulation
>of arterial plaque caused by such ETS carcinogens as benzo(a)pyrene also
>clogs arteries, again leading to heart and stroke diseases, for instance,
>atherosclerosis and arteriosclerosis. [15]
>
>While passive smokers receive smaller doses of the toxins in ETS, evidence
>shows that their hearts and vascular systems are less able to adapt to the
>barrage of toxins. Active smokers adapt in a way that passive smokers do
>not; small doses have a more harmful effect on passive smokers.[16]
>
>Exposure to ETS is characterized by a dose-response effect: The greater and
>more prolonged the exposure, the more harmful the consequences for those
>exposed. In other words, increased exposure means increased risk of
>cardiovascular and cerebrovascular disease. It has been estimated, for
>instance, that nonsmoking spouses living with smokers face a 20 - 30%
>increase in the risk of death from ischemic heart disease or heart attack.
>It is estimated that in the United States approximately 62,000 deaths are
>attributable to ischemic heart disease caused by exposure to ETS. [17]
>
>Cancer
>
>Tobacco smoke is full of carcinogens and toxins. It is hardly surprising to
>find that it has been linked with numerous types of cancer.
>
>ETS is the third largest known cause of lung cancer deaths. [18] A landmark
>1992 study by the EPA, based on a comprehensive and detailed review of 30
>different epidemiological studies, concluded that passive smoking is
>causally associated with lung cancer in adults. The risk of lung cancer has
>been estimated to increase by 30% for nonsmoking spouses of smokers. [19]
>It is known, moreover, that certain compounds in ETS, such as hydrogen
>cyanide and nitrogen dioxide, damage the lungs and impair respiratory
>activity. [20]
>
>ETS compounds have been linked to other types of cancer as well.
>Beta-naphthylamine, for instance, has been linked to bladder cancer.
>Tobacco-specific N-nitrosamines have been linked to cancer of the liver,
>pancreas, and aerodigestive tract in various animal studies. Several of the
>aldehydes in ETS, including formaldehyde and acetaldehyde, are known animal
>carcinogens and are thought to be linked to human cancers. Benzene, a
>hydrocarbon in ETS, is a recognized occupational carcinogen linked to
>various forms of leukemia. Benzo(a)pyrene, one of the 80 to 100 polynucleur
>aromatic hydrocarbons in tobacco smoke, is a major carcinogen. [21]
>
>Exposure to ETS is an independent risk factor for cervical cancer, with
>high levels of ETS exposure estimated to result in twofold to threefold
>increased risks. [22] Several studies have noted an increased risk of
>cancer in children of smokers, especially lymphocyte leukaemia and
>lymphoma. An association has also been drawn to brain cancer. [23]
>
>All told, the EPA estimates that the risk of developing cancer from
>exposure to ETS is about 57 times greater than the total risk posed by all
>outdoor air contaminants regulated under U.S. environmental law. [24]
>
>Respiratory Disease and Related Disorders
>
>Much of the recent research focuses on ETS-related respiratory conditions
>in children. The cumulative evidence shows that parental smoking causes an
>increased incidence of respiratory diseases from birth to the third year of
>life. It is estimated that in Canada approximately 2.8 million children, or
>47% of all children, are exposed to tobacco smoke at home.[25]
>
>The burden of ETS-related illness encompasses a wide range of acute and
>chronic conditions, including such respiratory irritations as coughing,
>wheezing, and excessive sputum production; acute diseases of the lower
>respiratory tract, such as pneumonia, bronchitis, branchiolitis[26]; acute
>and possibly chronic middle ear infections[27]; reduced lung function [28];
>increased incidence of asthma and exacerbation of existing asthmatic
>conditions [29]; and acute upper respiratory tract infections, such as
>colds and sore throats. [30] In the United States it is estimated 150,000
>to 300,000 cases of bronchitis and pneumonia in infants and young children
>are attributable to ETS exposure. In addition, U.S. researchers estimate
>that ETS exacerbates the asthma of 200,000 to 1,000,000 asthmatic children.
>[31]
>
>Infants of mothers who smoke are at greater risk of dying from Sudden
>Infant Death Syndrome (SIDS), a condition widely believed to be linked to
>an underlying but as yet unknown respiratory deficiency. U.S. researchers
>estimate that maternal smoking accounts for approximately 1,900 SIDS cases
>a year. In all, smoking during pregnancy triples the risk of SIDS. [32]
>More than three times as many infants die from ETS-related SIDS as from
>child abuse or homicide. [33] On a related point, it has also been
>estimated that maternal smoking causes 115,000 miscarriages in the U.S.
>each year, or 19% of all miscarriages experienced by smoking women.
>
>Exposure to ETS has been linked to low birth weight, and low birth weight
>has in turn been linked to increased risk of respiratory illness.[34]
>Recent evidence suggests that fetal exposure to tobacco smoke reduces lung
>capacity in early infancy.[35] Generally, children whose mothers smoke are
>admitted more frequently to hospital and may be more likely to become
>smokers themselves. [36]
>
>Exposure to ETS has also been linked to a variety of other diseases and
>ailments. In children it has been linked, for instance, to increased risk
>of toncillitis, adenoiditis, and inflammatory bowel disease. [37]
>
>Though there is less evidence available on ETS-related respiratory diseases
>in adults, recent studies show that exposure to ETS may increase the risk
>of such airway obstructive diseases as asthma, chronic bronchitis, and
>emphysema in adults. [38] Recent evidence also shows that exposure to ETS
>reduces lung function, and that damage to lung function increases with
>increased levels of exposure. [39]
>
>Conclusion
>
>ETS poses a substantial risk to human health. It has been linked to
>cardiovascular and cerebrovascular disease, various kinds of cancer, and
>numerous respiratory diseases. Removing the health risks of ETS exposure
>will require a concerted effort to remove tobacco smoke from public places,
>the workplace, the home, and any other enclosed environments that human
>beings occupy.
>
>
>------------------------------------------------------------------------
>
>
>References
>
>
>
>1. It has recently been estimated that the number of Canadian
>municipalities with smoking control by-laws is 367, more than five times
>the 1991 estimate of 66. For recent information on Canadian by-laws, see
>Smoking By-laws in Canada 1995, Health Canada, Health Protection Branch,
>Office of Tobacco Control.
>
>2. U.S. Environmental Protection Agency (EPA), Respiratory health effects
>of passive smoking: Lung cancer and other disorders, USEPA, Document
>No./600/6-90/006F. This EPA report is the third in a series of seminal
>research reports, the other two being the U.S. Surgeon General's report
>(The Health Consequences of Involuntary Smoking. US DHHS (PHS), 1986) and
>the National Research Council report (Environmental Tobacco Smoke in the
>United States. Washington, DC, National Academy Press, 1986). Taken
>together, these two reports articulate three principal findings: (1) ETS
>causes disease in healthy non-smokers; (2) children exposed to ETS in the
>home are more likely to suffer respiratory infections and impaired lung
>function; (3) ETS is the leading source of indoor respirable suspended
>particulate matter. Another report that deserves mention here is that of
>the National Institute for Occupational Safety and Health (Current
>Intelligence Bulletin #54 Environmental Tobacco Smoke in the Workplace,
>Lung Cancer and Other Health Effects, U.S. Department of Health and Human
>Services, Cincinnati, OH, June 1991). This report classifies ETS as an
>"occupational carcinogen." Other major research reports include the
>National Health and Medical Research Council: Effects of Passive Smoking on
>Health (1986) and (1995) (Australian Government Publishing Service,
>Canberra) as well as Smoking and the Young (Royal College of Physicians of
>London, London, 1992).
>
>3. For the lung cancer mortality estimate, see Wigle et al, "Deaths in
>Canada from lung cancer due to involuntary smoking," Canadian Medical
>Association Journal, Vol. 136, May 1, 1987. American researchers estimate
>ETS causes ten times more deaths from heart disease than from lung cancer
>(Note 2). If this factor is applied to lung cancer mortality in Canada, the
>result is approximately 3,300 ETS-related deaths. For its part, the tobacco
>industry has been aware of the hazards of ETS for some time, as early as
>1975 perhaps, more than ten years before the U.S. Surgeon General's report.
>For detailed discussion see Barnes et al, "Enviromental Tobacco Smoke: The
>Brown and Williamson Documents," in Journal of the American Medical
>Association, 274 (3), July, 1995.
>
>4. J.L. Repace and A.H. Lowry, "Indoor Air Pollution, tobacco smoke, and
>public health," Science, (208) pp. 464-472, 1980. The estimate of 90% is an
>American figure, but the Canadian figure is most likely similar. For the
>range estimate of 55% to 70%, Karen M. Emmons et al "An Evaluation of the
>Relationship between Self-Report and Biochemical Measures of Environmental
>Tobacco Smoke Exposure," Preventive Medicine, 23, 1994, pp. 35-39./
>
>5. J.E. Fielding & K.J. Phenow, "Health effects of involuntary smoking,"
>New England Journal of Medicine, Vol. 319, 1988, 1452-1460.
>
>6. Hammond et. al.; "Relationship Between Environmental Smoke Exposure and
>Carcinogen-Hemoglobin Adduct Levels in Nonsmokers," Journal of the National
>Cancer Institute, Vol. 85, No. 6, March 17, 1993. The use of 4-ABP, once a
>common ingredient in industrial dyes, was discontinued when the link to
>bladder cancer was uncovered. Its presence in ETS, however, is subject to
>no ban. See also The health consequences of smoking -- cancer: A Report of
>the Surgeon General. DHHS, (PHS) 82-50179, 1982. For a recent discussion of
>the physical chemistry of mainstream and sidestream smoke, see Indoor Air
>Quality: A Comprehensive Reference Book, Maroni, Seifert, & Lindvall eds.,
>Elsevier, Amsterdam, 1995, especially Chapter 4.
>
>7. K. H. Ginzel, MD, "Hazards Smokers Impose," New Jersey Medicine, April
>1990, p. 312. Ginzel's figure is based on earlier work by American
>researchers. See J.E. Cuddleback, J.R. Donavan, W.R. Burg, "Occupational
>aspects of passive smoking," American Industrial Hygiene Association
>Journal, 37, 1976, pp. 263-267. Sidestream smoke particles are smaller than
>those of mainstream smoke. These particles can therefore be inhaled more
>deeply into the lungs (see The Health Consequences of Involuntary Smoking,
>cited above).
>
>8. For further discussion, see Indoor Air Quality: A Comprehensive
>Reference Book, Air Quality Monograph Series, Eds. M. Marconi, B. Seifert,
>and T. Lindvall, Elsevier, Amsterdam, 1995, especially Chapters 4, 6, 7, &
>17.
>
>9. Goran Lofroth, "Environmental tobacco smoke: multicomponent analysis and
>room-to-room distribution in homes," Tobacco Control, 1993, 2, pp. 222-5.
>
>10. op. cit., Indoor Air Quality: A Comprehensive Reference Book, Chapter
>4.
>
>11. Maclure et. al, "Elevated blood levels of carcinogens in passive
>smokers," Am. J. Public Health, 79, 1989, p. 1381.The number and individual
>amounts of carcinogens, mutagens, and other toxins depend on the rate at
>which the tobacco burns, its pH level, and on other technical
>considerations. Recent evidence suggests that sidestream smoke from low tar
>cigarettes may be more dangerous than sidestream from high tar cigarettes.
>See O.T. Chortyk and W.S. Schlotzhauer, "The Contribution of Low Tar
>Cigarettes to Environmental Tobacco Smoke," Journal of Analytical
>Toxicology, Vol 13, 1989, pp. 129-134.
>
>12. op. cit. K. H. Ginzel, p. 311. Two related facts should be noted here.
>First, indoor air pollution consistently exceeds outdoor air pollution;
>second, tobacco smoke is the leading indoor air contaminant. Given that
>human beings typically spend more of their time indoors than outdoors, ETS
>is in effect the main source of air pollution for human beings. It is
>therefore not surprising that ETS causes more cancer deaths than all other
>regulated industrial air pollutants combined (James L. Repace and W.
>Lowrey, "Nonsmokers' Lung Cancer Risk from Passive Smoking," Journal of the
>Air Pollution Control Association, May 1985). For a more detailed
>discussion of ETS as an indoor air pollutant, see James L. Repace, "Tobacco
>Smoke Pollution"; in Nicotine Addiction: Principles and Management, Ed. C.
>Tracy Orleans, Ph.D. and John Slade, M.D., Oxford University Press, 1993,
>pp.9-142. See also Moroni, Seifert, & Lindvall, Eds. p. 133. For the
>cotinine estimate, see p. 327; for the estimate on child exposure, see. p.
>329. For information regarding the difficulties in ventilation and
>filtration, see Martin Dewey, Smoke in the Workplace, Non-Smokers' Rights
>Association, Toronto, 1985.
>
>13. S. Glantz and W. Parmley, "Passive smoking and heart disease:
>Epidemiology, physiology, and biochemistry," Circulation, 1991, 83, pp.
>1-12. See also: K. Steenland, "Passive smoking and the risk of heart
>disease," Journal of the American Medical Association, 267, 1992, pp.
>94-99. A.J. Wells, "Passive smoking as a cause of heart disease," Journal
>of the American College of Cardiology, 24, 1994, pp. 546-554. For a recent
>discussion of ETS and heart attack, see J. Muscat and E. Wynder, "Exposure
>to Environmental Tobacco Smoke and the Risk of Heart Attack," International
>Journal of Epidemiology, Vol. 24, No. 4, 1995, pp. 715-719.
>
>14. A. Judson Wells, PhD, "Passive Smoking as a Cause of Heart Disease,"
>Journal of the American College of Cardiology, Vol 24, August 1994, pp.
>546-554.
>
>15. A. V. Diez-Roux, M.D., M.P.H., et al, "The Relationship of Active and
>Passive Smoking to Carotid Atherosclerosis 12-14 Years Later," Preventive
>Medicine, 24, 1995, pp. 48-55. Recent animal studies have linked ETS to the
>development of arteriosclerotic plaques, a leading factor in heart disease.
>See A. Penn et al, "Inhalation of Steady-State Sidestream Smoke From One
>Cigarette Promotes Arteriosclerotic Plaque Development." Circulation, Vol.
>90, No. 3, September, 1994. For a useful guide to the short and long-term
>effects of ETS on the cardiovascular and cerebrovascular systems, see B.
>Ford, Smokescreen, Halycon Press, 1994, Chapter 11.
>
>16. A. Wu-Williams and J. Samet, "Environmental tobacco smoke:
>Exposure-response relationships in epidemiologic studies," Risk Analysis,
>10, 1990, pp. 39-48.
>
>17. S. Glantz and W. Parmley, Passive Smoking and Heart Disease; Clinical
>Progress Series. It has been known for some time that ETS can have dramatic
>effects on those who share homes with smokers. Glantz and Parmley (1991)
>arrive at the estimate of 20 - 30 % of lung cancer, based on an overview of
>ten separate epidemiologic studies. This estimate is confirmed in a recent
>review of 25 different epidemiological studies. See Göran Perschagen,
>"Passive Smoking and Lung Cancer," Epidemiology of Lung Cancer, Vol. 74,
>1994, pp. 109-130. For the estimates of 62,000 see J. Fledman et al.,
>"Passive smoking alters lipid profiles in adolescents," Pediatrics, Vol.
>88, 1991, pp. 259-64.
>
>18. D.T. Wigle, N.E. Collishaw, J. Kirkbride, "Exposure of Involuntary
>Smokers to Toxic Components of Tobacco Smoke," Canadian Journal of Public
>Health, 78(3), 1987, pp. 151-154. Active smoking is the leading cause.
>
>19. See, for instance, T. Hirayama, "Non-smoking wives of heavy smokers
>have a higher risk of lung cancer: a study from Japan," British Medical
>Journal, 282, 1981, pp. 183-185. The report of the National Research
>Council (1986, Note 1) also estimated increased risk at about 30%. See also
>E. Fontham, "Lung Cancer in Nonsmoking Women: A Multicenter Case-Control
>Study," Cancer Epidemiology, Biomarkers and Prevention, Vol. 1,
>November/December, 1991, pp. 35-43. For a more recent assessment of health
>risks, see Morris, P.D., "Lifetime excess risk of death from lung cancer
>for a U.S. female never-smoker exposed to environmental tobacco smoke,"
>Environmental Research, 68, 1995, pp. 3-9. Morris calculates lifetime
>excess risks for home, social, and overall workplace exposures, finding in
>each case that the estimated risks exceed acceptable risk levels.
>
>20. Dietrich Hoffmann, Ph.D., "Analysis of Toxic Smoke Ingredients," in
>Toxicity Testing Plan, U.S. Consumer Product Safety Commission and
>Department of Health and Human Services, August, 1993, D1-D38. See also
>S.S. Heght, PhD, et al "A Tobacco-Specific Lung Carcinogen In The Urine Of
>Men Exposed To Cigarette Smoke," New England Journal of Medicine, Vol. 329,
>1993, pp. 1543-1546.
>
>21. ibid. See also M. Maclure, ScD, et al, "Elevated Blood Levels of
>Carcinogens in Passive Smokers," American Journal of Public Health, Vol.
>79, No. 10, 1989, pp. 1381-1384.
>
>22. M. L. Slattery, PhD, MPH; L. M. Robinson, MSPH; et al, "Cigarette
>Smoking and Exposure to Passive Smoke Are Risk Factors for Cervical
>Cancer," Journal of the American Medical Association, Vol. 261, No. 11,
>March, 1989, pp. 1593-1598.
>
>23. D.P. Sandler, A.J. Wilcox, & R.B. Everson, "Cumulative Effects Of
>Lifetime Passive Smoking On Cancer Risk," The Lancet, February, 1985,
>312-314.
>
>24. Tobacco In Australia: Facts and Issues, 1995.
>
>25. Health Canada, Survey of Smoking in Canada, Cycle 4. 1995 (a).
>
>26. E. Rylander, G. Pershagen, et al, "Parental Smoking, Urinary Cotinine,
>and Wheezing Bronchitis in Children," Epidemiology, Vol. 6, No. 3, May,
>1995, 289-293. See also Respiratory health effects of passive smoking,
>cited above.
>
>27. G. Kitchens, MD., "Relationship of Environmental Tobacco Smoke to
>Otitis Media in Young Children'" Laryngoscope, Vol. 105, May, 1995, pp
>1-13. See also R. Stenstrom, P.A.M. Bernard, and Haim Ben-Simhon, "Exposure
>to environmental tobacco smoke as a risk factor for recurrent otitis media
>in children under the age of five years," International Journal of
>Pediatric Otolaryngology, 27, 1993, pp. 127-136.
>
>28. X. Wang, D. Wypij, et al, "A Longitudinal Study of the Effects of
>Parental Smoking on Pulmonary Function in Children 6-18 Years," American
>Journal of Respiratory Critical Care Medicine, Vol 149, 1994, pp.
>1420-1425.
>
>29. J. Stoddard and T. Miller, "Impact of Parental Smoking on the
>Prevalence of Wheezing Respiratory Illness in Children," American Journal
>of Epidemiology, Vol. 141, No. 2,1995, 96-102. Stoddard and Miller estimate
>that maternal smoking may be responsible for as much 7.5% of all asthma and
>other wheezing respiratory illness in children. For another recent study
>linking parental smoking to increased prevalence of asthma, see J. Kay.
>M.R.C.G.P. et al, "Do Both Paternal and Maternal Smoking Influence the
>Prevalence of Childhood Asthma? A Study into the Prevalence of Asthma in
>Children and the Effects of Parental Smoking," Journal of Asthma, 32 (1),
>1995, pp. 47-55. See also B. A. Chilmonczyk, M.D., et al., "Association
>Between Exposure to Environmental Tobacco Smoke And Exacerbation Of Asthma
>In Children," New England Journal of Medicine, Vol. 328, June, 1993, pp.
>1665-1669.
>
>30. For a comprehensive review of the relationship between ETS exposure and
>the incidence of various respiratory diseases, see Respiratory Health
>Effects of Passive Smoking and Effects of Passive Smoking on Health, cited
>above. See also I. Tager, M.D., M.P.H., "Health Effects of 'Passive
>Smoking' in Children," Chest, Vol. 96, No. 5, 1989. The Royal College of
>Physicians (cited above) estimate that infants of smoking parents are twice
>as likely to suffer from serious respiratory infection.
>
>31. op. cit. Respiratory Health Effects of Passive Smoking: Lung Cancer and
>other Disorders, U.S. EPA
>
>32. For recent figures, see J.R. DiFranza, MD, and R.A. Lew, PhD, "Effect
>of Maternal Cigarette Smoking on Pregnancy Complications and Sudden Infant
>Death Syndrome," Journal of Family Practice, Vol. 40, 1995, pp. 385-394.
>H.S. Klonoff-Cohen et al, "The Effect of Passive Smoking and Tobacco
>Exposure Through Breast Milk on Sudden Infant Death Syndrome," Journal of
>the American Medical Association, Vol 273, No. 10, March, 1995. See also
>Effects of Passive Smoking on Health. For the U.S. figures on maternal and
>SIDS, see Indoor Air Quality: A Comprehensive Reference Book, Chapter 17.
>The Royal College of Physicians report (cited above) estimates that over
>one-quarter of Sudden Infant Death Syndrome mortality risk is attributable
>to ETS exposure.
>
>33. ibid. DiFranza & Lew, 1995.
>
>34. Y. Chen, "Environmental Tobacco Smoke, Low Birth Weight, and
>Hospitalization for Respiratory Disease," American Journal of Critical Care
>Medicine, Vol. 150, 1994, pp. 54-58. For more recent studies, see B.
>Eskenazi, PhD, et. al., "Passive and Active Maternal Smoking as Measured by
>Serum Cotinine: The Effect on Birthweight," American Journal of Public
>Health, Vo. 85, No. 3, March, 1995; and X. O. Shu et al, "Maternal Smoking,
>Alcohol Drinking, Caffeine Consumption, and Fetal Growth: Results from a
>Prosepective Study," Epidemiology, Vol.6, No. 2, March, 1995, pp. 115-119.
>For a recent discussion of the birthweight effects of ETS exposure from
>paternal smoking, see F.D. Martinez, et al, "The Effect of Paternal Smoking
>on the Birthweight of Newborns Whose Mothers Did Not Smoke," American
>Journal of Public Health, Vol. 84, No. 9, September, 1994, pp.1489-1491.
>
>35. R. W. Brown et al, "Effect of Maternal Smoking During Pregnancy on
>Passive Respiratory Mechanics in Early Infancy," Pediatric Pulmonology,
>Vol. 19, 1995, pp. 23-28. See also F.D. Martinez et. al., "Asthma and
>Wheezing In The First Six Years Of Life," The New England Journal of
>Medicine, Vol. 332, No. 3, January, 1995, pp. 133-138. The Royal College of
>Physicians (cited above) also estimate that the children of smokers are
>more at risk for chronic obstructive airway disease and lung cancer
>
>36. Robertson, P. Pattemore, et al, "The effect of maternal smoking on
>admission to hospital in infancy," New Zealand Journal of Medicine, (106),
>1993, pp. 476-477). Almost twenty years earlier, Harlap and Davies also
>found that that the admission rates for ETS-exposed infants were
>significantly higher than those for infants not so exposed, especially for
>such respiratory complaints as bronchitis and pneumonia. See S. Harlap and
>A.M. Davies, "Infant Admissions to Hospital and Maternal Smoking," Lancet,
>Vol. 1, 1974, 529-532. For the tendency of children of smokers to become
>smokers themselves, see M. Osler et al, "Maternal Smoking during Childhood
>and Increased Risk of Smoking in Young Adulthood," International Journal of
>Epidemiology, Vol. 24, No. 4, 1995.
>
>37. B.A. Lashner, M.D., M.P.H., F.A.C.G., et al, "Passive Smoking is
>Associated with an Increased Risk of Developing Inflammatory Bowel Disease
>in Children," The American Journal of Gastroenterology, Vol. 88, No. 3,
>1993. For a recent study on tonsillectomy and ETS exposure, see A.E.
>Hinton, et al, "Parental cigarette smoking and tonsillectomy in children,"
>Clinical Otolaryngology, Vol. 18, 1993, pp. 178-180.
>
>38. A. S. Robbins et al, "Passive Smoking and Chronic Respiratory Disease
>Symptoms in Non-Smoking Adults," International Journal of Epidemiology,
>Vol. 22, No. 5, pp. 809-817. See also X. Xu and B. Li, "Exposure-Response
>Relationship between Passive Smoking and Adult Pulmonary Function,"
>American Journal of Respiratory Critical Care Medicine, Vol. 151, 1995, pp.
>41-46.
>
>39. A. S. Robbins et al, "Passive Smoking and Chronic Respiratory Disease
>Symptoms in Non-Smoking Adults," International Journal of Epidemiology,
>Vol. 22, No. 5, pp. 809-817. See also X. Xu and B. Li, "Exposure-Response
>Relationship between Passive Smoking and Adult Pulmonary Function,"
>American Journal of Respiratory Critical Care Medicine, Vol. 151, 1995, pp.
>41-46.
>for further details
>http://www.ccsh.ca/ncth/docs/ets_e.html