[Gabz]

you dismiss the medical evidence of harmful effects of tobacco smoke including second hand smoke.

What evidence of harmful effects of SHS other than to those with pre-existing conditions?????

We all know you dislike smoke, smoking and smokers (excluding your beloved mother, may she rest in peace) but your attitude makes you look so petty, so scrawly.....so I can't even begin to define it.

Car crashes, building fires, falling down stairs, parkinson's disease and diabetes all can possibly cause very elongated and unpleasant deaths for the sufferer and the loved ones - do we abolish all of those things, or the "possible" causes of them?

[dallasgop]

GABZ asked "What evidence of harmful effects of SHS other than to those with pre-existing conditions?????"

Planet Earth to GABZ where have you been for the last 25+ years?


"Passive smoking" is the term used for breathing in other people’s
tobacco smoke. This form of smoking is usually involuntary and is
particularly dangerous because the smoke that drifts from the end of a lit
cigarette contains far greater amounts of cancer-causing chemicals and
other toxic substances than the smoke inhaled by the smoker. These
chemicals include ammonia, benzene, carbon monoxide, nicotine and five
different compounds known to cause cancer.The smoke particles involved in
passive smoking are also smaller, so they can be inhaled more deeply into
the non-smoker’s lungs. It has only come to light over the last 20 years,
through rigorous scientific research, that passive smoking is dangerous.
Now, it would be irresponsible not to acknowledge the wealth of evidence on
the subject and take appropriate action to protect the health of employees
and the general public.Years ago people unknowingly worked with asbestos
but, now, no-one willingly exposes themselves to this deadly substance.
Like asbestos, cigarette smoke is now classified as a "Group A" cancer
causing agent in the US.Renowned British medical researcher Professor Sir
Richard Doll has said that the risk of developing lung cancer from passive
smoking is as much as 90 times higher than the risk of developing an
asbestos-related cancer due to asbestos in buildings.
What does cigarette smoke do to the non-smoker?
assive smoking is known to cause the following health problems:
Lung cancer - Non smokers living with a smoker have a 30%increase in the
risk of developing lung cancer.Heart disease - Non smokers living with a
smoker have a 24%increase in the risk of heart attack or death from
coronary heart disease.Asthma, respiratory illness, glue ear and an
increase in the risk of sudden infant death in children. Estimated 46,500
cases of asthma caused annually in Australia by passive smoking.
Irritation of the eyes, nose and throat.Health effects are greatest for
people working in hospitality areas because this is where concentrations of
environmental tobacco smoke are greatest. Some of these workers inhale the
equivalent of smoking two packs of cigarettes per day.
Who says it’s so dangerous?
There are hundreds of studies on the effects of passive smoking but, more
importantly, there have been major reviews conducted on the scientific
evidence by national and international research authorities including:
International Agency for Research on Cancer. Tobacco Smoking. Lyon:
International Agency for Research on Cancer, 1985 (IARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Humans, Volume
38) US Department of Health and Human Services. The Health Consequences
of Involuntary Smoking. A report of the Surgeon General.Rockville,
Maryland: US Department of Health and Human Services,Public Health Service,
Centres for Disease Control, Centre for Health Promotion and Education,
Office on Smoking and Health, 1986. DHHS Publication No (CDC)87-8398.
Committee on Passive Smoking. Environmental Tobacco Smoke – Measuring
exposures and assessing health effects. Committee on PassiveSmoking, Board
on Environmental Studies and Toxicology, National Research Council.
Washington: National Academy Press, 1986.National Research Council
Committee on Passive Smoking.enviornmental tobacco smoke: Measuring
exposures and assessing health effects. Board on Environmental Studies and
Toxicology, National Research Council. Washington DC: National Academy
Press, 1986:241-242.

National Health and Medical Research Council. Effects of Passive
Smoking on Health. Report of the NH & MRC Working Party on the
Effects
of Passive Smoking on Health. Adopted at the 101st Session of the
Council,
June 1986. Canberra: Australian Government Publishing Service, 1987.

Fourth Report of the Independent Scientific Committee on Smoking
and Health. (Chairman: Sir Peter Froggatt). London: HMSO, 1988.

United States Environmental Protection Agency. Respiratory health
effects of passive smoking: Lung cancer and other disorders.
Publication
EPA/600/6-90/006F. Washington DC: United States Environmental
Protection Agency. December, 1992.

Working Party on Smoking and the Young. Royal College of Physicians
of London. Smoking and the Young. London: Royal College of
Physicians of
London, 1992.

Environmental tobacco smoke and cardiovascular disease. A position
paper from the Council on Cardiopulmonary and Critical Care,
American
Heart Association. Circulation 1992: 86:699-702.

Californian Environmental Protection Agency. Health effects of
exposure
to environmental tobacco smoke. Dunn A, Zeise L (eds). Office of
Environment Hazard, California USA, September 1997.

National Health and Medical Research Council. The Health Effects of
Passive Smoking: A Scientific Information Paper. Adopted at the
125th
Session of the Council, November 1997. Canberra: Australian
Government
Publishing Service, 1997.

The UK Scientific Committee on Tobacco and Health. Report of the
Scientific Committee on Tobacco and Health (Chaired by Prof David
Poswillo). Department of Health. The Stationery Office, March 1998.

[dallasgop]

GABZ asked "What evidence of harmful effects of SHS other than to those with pre-existing conditions?????"

Sidestream smoke (smoke that drifts off the end of a burning cigarette) and passive smoke (smoke exhaled by someone who is smoking) both describe types of secondhand smoke. Nonsmokers are unwittingly being forced to engage in a "smoking" habit by inhaling, secondhand, the smoke of others. Smoking family members and friends of nonsmokers may be exposing their loved ones to an increased risk of illness or disease, and more and more evidence points to the fact that this kind of indirect exposure to smoke is harmful.

Consider these facts that the American Association for Respiratory Care has learned in its search for information about secondhand smoke:

As reported in the 1989 "25 Years of Progress" report of the Surgeon General, a 1986 study titled "The Health Consequences of Involuntary Smoking" concluded that:
Involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers.

The children of parents who smoke have an increased frequency of respiratory infections and symptoms.

Separation of smokers and nonsmokers within the same air space reduces--but does not eliminate-- exposure of nonsmokers to environmental tobacco smoke.



A San Diego study showed that nonsmokers exhibited a functional change in their airways directly related to the amount of smoke they passively inhaled at work.


Children of nonsmoking and smoking parents were studied in research reported in the American Journal of Epidemiology. Results showed that children with nonsmoking parents demonstrated normal lung function, while those with one smoking parent demonstrated impaired function. The worst lung function test results were found in children from households in which both parents smoked.


Likewise, nonsmoking spouses of smokers demonstrated measurable lung function abnormalities.


Pregnant women who smoke are at greater risk for low-birthweight infants, fetal problems, infant deformities, and miscarriages.
Cigarette smoke contains dangerous chemicals that are a hazard when inhaled --either directly or indirectly. Carbon monoxide, which is found in smoke, starves your blood of oxygen and increases the work your heart must perform. Nicotine raises your blood pressure and heart rate, and tar, which also builds up in your lung tissue, contains cancer-causing substances. These dangerous chemicals increase your risk of several kinds of cancer, heart disease, heart attack, and chronic respiratory illness and disease.

[dallasgop]

GABZ asked "What evidence of harmful effects of SHS other than to those with pre-existing conditions?????"

Effects Of Environmental Tobacco Smoke
(ETS) on Children.

---

Excerpts from chapter 1 of the Environmental Protection Agency's report entitled
Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders,
EPA/600/6-90/006F. The report is dated December 1992 and was publicly released on January 7, 1993.

---

Environmental tobacco smoke (ETS) in the United States presents a
serious and substantial public health impact...

In children:

ETS exposure is causally* associated with an increased risk of lower respiratory tract infections (LRIs) such as bronchitis and pneumonia. This report estimates that 150,000 to 300,000 cases annually in infants and young children up to 18 months of age are attributable to ETS.

ETS exposure is causally associated with increased prevalence of fluid in the middle ear, symptoms of upper respiratory tract irritation, and a small but significant reduction in lung function.

ETS exposure is causally associated with additional episodes and increased severity of symptoms in children with asthma. This report estimates that 200,000 to 1,000,000 asthmatic children have their condition worsened by exposure to ETS.

ETS exposure is a risk factor for new cases of asthma in children who have not previously displayed symptoms.

In 1986, the National Research Council (NRC) and the Surgeon General of the U.S. Public Health Service independently assessed the health effects of exposure to ETS (NRC, 1986;

U.S. DHHS, 1986). Both of the 1986 reports conclude that ETS can cause lung cancer in adult nonsmokers and that children of parents who smoke have increased frequency of respiratory symptoms and acute lower respiratory tract infections, as well as evidence of reduced lung function.

Population estimates of ETS health impacts are also made for certain noncancer respiratory endpoints in children, specifically lower respiratory tract infections (i.e., pneumonia, bronchitis, and bronchiolitis) and episodes and severity of attacks of asthma. Estimates of ETS-attributable cases of LRI in infants and young children are thought to have a high degree of confidence because of the consistent study findings and the appropriateness of parental smoking as a surrogate measure of exposure in very young children...

1. Exposure of children to ETS from parental smoking is causally associated with:

a. increased prevalence of respiratory symptoms of irritation (cough, sputum, and wheeze),

b. increased prevalence of middle ear effusion (a sign of middle ear disease), and

c. a small but statistically significant reduction in lung function as tested by objective measures of lung capacity.

2. ETS exposure of young children and particularly infants from parental (and especially mother's) smoking is causally associated with an increased risk of LRIs (pneumonia, bronchitis, and bronchiolitis). This report estimates that exposure to ETS contributes 150,000 to 300,000 LRIs annually in infants and children less than 18 months of age, resulting in 7,500 to 15,000 hospitalizations. The confidence in the estimates of LRIs is high.

Increased risks for LRIs continue, but are lower in magnitude, for children until about age 3; however, no estimates are derived for children over 18 months...

. a. Exposure to ETS is causally associated with additional episodes and increased severity of asthma in children who already have the disease. This report estimates that ETS exposure exacerbates symptoms in approximately 20% of this country's 2 million to 5 million asthmatic children and is a major aggravating factor in approximately 10%.

b. In addition, the epidemiologic evidence is suggestive but not conclusive that ETS exposure increases the number of new cases of asthma in children who have not previously exhibited symptoms. Based on this evidence and the known ETS effects on both the immune system and lungs (e.g., atopy and airway hyperresponsiveness), this report concludes that ETS is a risk factor for the induction of asthma in previously asymptomatic children. Data suggest that relatively high levels of exposure are required to induce new cases of asthma in children. This report calculates that previously asymptomatic children exposed to ETS from mothers who smoke at least 10
cigarettes per day will exhibit an estimated 8,000 to 26,000 new cases of asthma annually. The confidence in this range is medium and is dependent on the conclusion that ETS is a risk factor for asthma induction.

1.3.2. ETS and Noncancer Respiratory Disorders

Exposure to ETS from parental smoking has been previously linked with increased respiratory disorders in children, particularly in infants. Several studies have confirmed the exposure and uptake of ETS in children by assaying saliva, serum, or urine for cotinine. These cotinine concentrations were highly correlated with smoking (especially by the mother) in the child's presence. Nine to twelve million American children under 5 years of age, or onehalf to two-thirds of all children in this age group, may be exposed to cigarette smoke in the home
(American Academy of Pediatrics, 1986; Overpeck and Moss, 1991).

With regard to the noncancer respiratory effects of passive smoking, this report focuses on epidemiologic evidence appearing since the two major reports of 1986 (NRC and U.S. DHHS) that bears on the potential association of parental smoking with detrimental respiratory effects in their children. These effects include symptoms of respiratory irritation (cough, sputum production, or wheeze); acute diseases of the lower respiratory tract (pneumonia, bronchitis, and bronchiolitis); acute middle ear infections and indications of chronic middle ear infections (predominantly middle ear effusion); reduced lung function (from forced expiratory volume and flow-rate measurements); incidence and prevalence of asthma and exacerbation of symptoms in asthmatics; and acute upper respiratory tract infections (colds and sore throats). The more than 50 recently published studies
reviewed here essentially corroborate the previous conclusions of the 1986 reports of the NRC and Surgeon General regarding respiratory symptoms, respiratory illnesses, and pulmonary function, and they strengthen support for those conclusions by the additional weight of evidence (Chapter 7). For example, new data on middle ear effusion strengthen previous evidence to warrant the stronger conclusion in this report of a causal association with parental smoking. Furthermore, recent studies establish associations between parental smoking and increased incidence of childhood asthma. Additional research also supports the hypotheses that in utero exposure to
mother's smoke and postnatal exposure to ETS alter lung function and structure, increase bronchial
responsiveness, and enhance the process of allergic sensitization, changes that are known to predispose children to early respiratory illness. Early respiratory illness can lead to long-term pulmonary effects (reduced lung function and increased risk of chronic obstructive lung disease).

This report also summarizes the evidence for an association between parental smoking and SIDS, which was not addressed in the 1986 reports of the NRC or Surgeon General. SIDS is the most common cause of death in infants ages 1 month to 1 year. The cause (or causes) of SIDS is unknown; however, it is widely believed that some form of respiratory pathogenesis is generally involved. The current evidence strongly suggests that infants
whose mothers smoke are at an increased risk of dying of SIDS, independent of other known risk factors for SIDS, including low birthweight and low gestational age, which are specifically associated with active smoking during pregnancy. However, available studies do not allow this report to conclude whether that increased risk is related to in utero versus postnatal exposure to tobacco smoke products, or to both.

The 1986 reports of the NRC and Surgeon General conclude that both the prevalence of respiratory symptoms of irritation and the incidence of lower respiratory tract infections are higher in children of smoking parents. In the 18 studies of respiratory symptoms subsequent to the 2 reports, increased symptoms (cough, phlegm production, and wheezing) were observed in a range of ages from birth to midteens, particularly in infants and preschool children. In addition to the studies on symptoms of respiratory irritation, 10 new studies have addressed the topic of parental smoking and acute lower respiratory tract illness in children, and 9 have reported statistically significant associations. The cumulative evidence is conclusive that parental smoking, especially the mother's,
causes an increased incidence of respiratory illnesses from birth up to the first 18 months to 3 years of life, particularly for bronchitis, bronchiolitis, and pneumonia. Overall, the evidence confirms and strengthens the previous conclusions of the NRC and Surgeon General.

Recent studies also solidify the evidence for the conclusion of a causal association between parental smoking and increased middle ear effusion in young children. Middle ear effusion is the most common reason for hospitalization of young children for an operation.

Regarding the effects of passive smoking on lung function in children, the 1986 NRC and Surgeon General reports both conclude that children of parents who smoke have small decreases in tests of pulmonary output function of both the larger and smaller air passages when compared with the children of nonsmokers. As noted in the NRC report, if ETS exposure is the cause of the observed decrease in lung function, the effect could be due to the direct action of agents in ETS or an indirect consequence of increased occurrence of acute respiratory illness related to ETS.

Results from eight studies on ETS and lung function in children that have appeared since those reports add some additional confirmatory evidence suggesting a causal rather than an indirect relationship. For the population as a whole, the reductions are small relative to the interindividual variability of each lung function parameter.

However, groups of particularly susceptible or heavily exposed children have shown larger decrements. The studies reviewed suggest that a continuum of exposures to tobacco products starting in fetal life may contribute to the decrements in lung function found in older children. Exposure to tobacco smoke products inhaled by the mother during pregnancy may contribute significantly to these changes, but there is strong evidence indicating that postnatal exposure to ETS is an important part of the causal pathway.

For diseases for which ETS has been either causally associated (LRIs) or indicated as a risk factor (asthma cases in previously asymptomatic children), estimates of population-attributable risk can be calculated. A population risk assessment (Chapter 8) provides a probable range of estimates that 8,000 to 26,000 cases of childhood asthma per year are attributable to ETS exposure from mothers who smoke 10 or more cigarettes per day. The confidence in this range of estimates is medium and is dependent on the suggestive evidence of the database. While the data show an effect only for children of these heavily smoking mothers, additional cases due to lesser ETS exposure also are a possibility. If the effect of this lesser exposure is considered, the range of estimates of new cases
presented above increases to 13,000 to 60,000. Furthermore, this report estimates that the additional public health impact of ETS on asthmatic children includes more than 200,000 children whose symptoms are significantly aggravated and as many as 1,000,000 children who are affected to some degree.

This report estimates that ETS exposure contributes 150,000 to 300,000 cases annually of lower respiratory tract illness in infants and children younger than 18 months of age and that 7,500 to 15,000 of these will require hospitalization. The strong evidence linking ETS exposure to increased incidence of bronchitis, bronchiolitis, and pneumonia in young children gives these estimates a high degree of confidence. There is also evidence suggesting a smaller ETS effect on children between the ages of 18 months and 3 years, but no additional estimates have been
computed for this age group. Whether or not these illnesses result in death has not been addressed here.

In the United States, more than 5,000 infants die of SIDS annually. It is the major cause of death in infants between the ages of 1 month and 1 year, and the linkage with maternal smoking is well established. The Surgeon General and the World Health Organization estimate that more than 700 U.S. infant deaths per year from SIDS are attributable to maternal smoking (CDC, 1991a, 1992b). However, this report concludes that at present there is not enough direct evidence supporting the contribution of ETS exposure to declare it a risk factor or to estimate its
population impact on SIDS.

[dallasgop]

GABZ asked "What evidence of harmful effects of SHS other than to those with pre-existing conditions?????"

Asthmatic kids' lungs react fast to 2nd-hand smoke

---

Last Updated: 2003-03-12 12:00:18 -0400 (Reuters Health)

DENVER (Reuters Health) - Children with asthma have worse lung function just a day after being exposed to second-hand smoke, according to a new study by Colorado researchers.

But when parents don't smoke at home or in the family car, the effect of smoke on their child's lungs is less severe, noted Dr. Nathan Rabinovitch of the National Jewish Medical and Research Center in Denver.

"The good news is that keeping the smoke outside the home makes a difference, although children will still get some tobacco exposure," he told Reuters Health. Rabinovitch presented the findings here this week at the American Academy of Allergy, Asthma, and Immunology's annual meeting.

He studied the effects of second-hand smoke by recruiting 40 schoolchildren with moderate to severe asthma and observing them over a four-month period.

Children wore a small, portable monitor that measured tiny airborne particles to gauge their second-hand smoke exposure. Their lung function was tested twice daily, at which time the filters in the monitors were weighed to gauge smoke exposure.

Rabinovitch and his colleagues found that children living with smokers were exposed to more airborne particles than were kids from non-smoking households.

But when parents only smoked outside of the house, their children were exposed to 30 percent fewer particles than were children whose parents smoked indoors.

On the day after the exposure, a child's lung function was lower in proportion to the amount of second-hand smoke he or she had inhaled. The investigators documented no such changes in the children in non-smoking households.

These findings show that banishing smoke from the house may decrease asthma severity in children whose family members smoke, Rabinovitch said.


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