[Virginia GASP]   ENVIRONMENTAL TOBACCO SMOKE --
HARMS & KILLS

Updated January  17, 2005
Special thanks to Dr. K. Heinz Ginzel for making this update possible!


Topics considered on this page.


OVERVIEW:

There may be many things that people will accept secondhand -- but smoke is NOT one of them.  Tobacco Smoke is so dangerous, it can even kill secondhand.

Tobacco companies do not allow smoking around tobacco seedlings -- because it kills them
-- tobacco mosaic virus.
Tomato plants are also susceptible to this. 

People are also hurt and killed by secondhand smoke.
  For this reason, more and more workplaces are going smoke-free.  This protects both the nonsmoker and the smoker from the devastating health effects of secondhand smoke.

Smoking is hazardous -- to the smoker, and to those who are forced to breathe the smoke.  This smoke is called secondhand smoke (SHS), passive smoke, and environmental tobacco smoke (ETS). 

ETS has immediate impacts on health, and it can kill through triggering severe asthma attacks, heart attacks, several cancers, and other illnesses. 

ETS impacts the brain and can disorient the breather, lowering test scores, affecting reasoning and hand--eye relationships.  There is no safe level of exposure to ETS.

A most informative governmental report from Ireland in 2002 on ETS in the workplace, based on worldwide research, concluded that the weight of evidence for lung cancer, cardiovascular, and respiratory disease, and for adverse effects on reproduction calls for legislative measures to protect employees from exposure to ETS at work.

A research team at Health Canada found that working in bars and restaurants can triple lung cancer risk.  They also observed a dose-response relation between the degree of exposure and lung cancer risk.

In the city of Helena, Montana (USA), the number of heart attacks decreased substantially after the city banned indoor smoking, but then rose quickly to its former level after the law was struck down in court six months later.  This event prompted the US Centers of Disease Control and Prevention (CDC) for the first time to warn people at risk of heart disease to avoid all buildings and gathering places that allow indoor smoking.

In Western New York State (USA) air pollution of RSPs (PM2.5) in a sample consisting of seven bars, six bar/restaurants, five restaurants, two bowling alleys, a pool hall, and a bingo hall dropped by 84% after implementation of the Clean Indoor Air Law in 2003.

In New York City (USA), "The city's bar and restaurant industry is thriving and its workers are breathing cleaner, safer air," said a report issued by the Economic Development Corporation and the Departments of Finance, Health & Mental Hygiene and Small Business Services.  Mike O'Neal, who served as president of the N.Y. State Restaurant Association for 17 years, supported legislation for a comprehensive smoking ban.  "I feel strongly," he said, "that it is pro-business and pro-health to eliminate smoking in all workplaces.  We owe our workers a safe, healthy work environment."

In the state of California (USA), the strict smoking bans have led to a substantial decline in smoking prevalence and also in the state's rates of heart disease, lung cancer, and chronic obstructive pulmonary disease (COPD), which have fallen well below the national average.


In this Fact Sheet on secondhand smoke the following topics are considered:
Overview
Nations going smoke-free
What is ETS?
Ventilation does not protect people from ETS
Immediate impacts of ETS
Children -- Dental Decay caused by ETS
ETS Kills
Cancers
Cardiovascular
Repiratory
Fetus and ETS
Some Poisons in ETS
Some Carcinogens in ETS
Tobacco industry loses lawsuit challenging scientific report
Tobacco companies do not show corporate responsibility
Tobacco industry strategy to undermine research
Tobacco industry strategy continues in 2005
Agencies stating ETS is carcinogenic
References
Pets and ETS:
Articles may be searched at the web site of the American Journal of Epidemiology
For example, cats have an increased risk of lymphoma from breathing secondhand smoke.



Several nations recognize the lethal health dangers of tobacco smoke and prohibit smoking in most workplaces, including restaurants and bars. These nations are
Bhutan
Ireland
Italy
New Zealand
Norway
Uganda
and in July, 2005, Sweden

Austria -- The new law exempts bars and restaurants; enforcement begins 2007.

The county of Brondby in Denmark prohibits smoking in all public buildings.

NATIONS considering requiring smoke-free workplaces:
England -- November, 2004, the British Medical Association (BMA) has called for smoke-free workplaces
Scotland -- November 2004, Scotland is considering smoke-free workplaces
Jack McConnell, Scotland's first minister, has stated in the Scottish Parliament that, "We will introduce a comprehensive ban on smoking in enclosed public places," which he say should come into force in 2006.
Portugal -- although Portugal is considering exempting bars, restaurants, and nightclubs
Wales

The United States of America (USA) does not have a plan to protect people from the deadly effects of secondhand smoke.

STATES in the USA which now require smoke-free workplaces are as follows:
California   
Connecticut
Delaware
Maine
Massachusetts
Many cities, including New York City, also require smoke-free workplaces.



Environmental tobacco smoke (ETS) results primarily from sidestream smoke and partly from exhaled mainstream smoke.   Sidestream smoke is the smoke emitted by the burning end of the cigarette, cigar, pipe, etc. between puffs.  Mainstream smoke is the smoke the smoker inhales. 

There is no safe level of exposure to ETS.

ETS is the single most important source of harmful indoor air pollution.
There is no safe level of exposure to tobacco smoke.

The simple separation of smokers and nonsmokers within the same air space is not sufficient to protect nonsmokers.

Smoke cannot read signs, and it does not stay in the "smoking" section.
Picture a swimming pool filled with water -- now, which part is not chlorinated?  Would you put up signs saying "Chlorinated Area" and "Unchlorinated Area"?

If people are swimming at one side of the swimming pool, and a child is urinating at the other side of the swimming pool, would you put up signs saying, "Swimming Area" and "Peeing Area"?

So it is with smoke in the air.

The US Environmental Protection Agency has concluded that "Research indicates that total removal of tobacco smoke through ventilation is both technically and economically impractical."

Ventilation is not the answer to protecting people from ETS.


The British Medical Association has declared that:
Research in America found that there was 50 times more air pollution in a smoky bar than in New York's Holland tunnel at rush hour, and studies have found that ventilation in bars does not reduce the risk to the health of customers or staff.

The tobacco industry has proposed that ventilation is the solution to the problem of passive smoke, however, scientific evidence proves that conventional ventilation and air-cleaning systems do not provide effective protection against the health hazards of second hand smoke.

Ventilation systems use a filtration method to re-circulate air. However, while this method can clear the smoky atmosphere, the toxins present in the gas of second hand smoke remains.

Particulate matter and toxic gases of ETS remain suspended in the air of a room, a car, and/or attached to walls, furnishings, and materials in the room, long after smoking has ceased.  This can trigger health problems for people who enter that room, car, etc.


The abstract on a Fact Sheet on Secondhand Smoke, available at http://www.repace.com states:
Breathing secondhand-smoke causes morbidity and mortality from cancer, heart disease, and respiratory disease, as well as acute sensory irritation.  It causes the premature death of hundreds of thousands of nonsmokers worldwide.  Smoke-free buildings are the only remedy.  Secondhand smoke cannot be controlled by ventilation, air cleaning, or spatial separation of smokers from nonsmokers.

Environmental tobacco smoke contains more than 4,000 chemicals and approximately 60 carcinogens (cancer causing agents).
Normally, people are not sufficiently aware of their breathing, a largely automatic process, to pay attention to what they breathe or how much they breathe. 
For an adult male, for example,
the average daily intake of food is 1.5 kg,
of water is 2.5 kg,
but the amount of air exchanged by the lungs is as high as 15.0 kg
It is estimated that each year an estimated 2.25 million metric tons of gaseous and inhalable particulate matter of ETS are discharged into our personal air space.  
Smoking creates a toxic waste dump in the air that lingers long after the smoker has left the room, automobile, etc.

A low-tar filter cigarette may increase health hazards for nonsmokers exposed to its smoke, as more mutagens may be released through the burning end rather than through the filter tip.


The following are among the powerful poisons in ETS:

Nicotine is a potent poison and is the precursor of the lung carcinogen NNKNonsmokers exposed to ETS carry the lung cancer causing NNK, one of the most potent organ-specific lung carcinogens known, in their bodies.  The damage done by carcinogens is permanent and may be cumulative.  This is one of the tobacco-specific nitrosamines which arise from nicotine.  The Clinical Toxicology of Commercial Products, 5th edition, describes nicotine as "one of the most toxic of all poisons acting with great rapidity."

Carbon Monoxide is highly toxic and disables the oxygen carrying capacity of the hemoglobin in red blood cells, and is associated with heart disease and fetal damage, for example.

Nitrogen oxide is needed for nitrosamine formation.

Ammonia is a respiratory and eye irritant.

Acrolein is a ciliotoxic agent, and it is a respiratory irritant.

Methyl isocyanate is the lung poison known from the Bhopal disaster.

Hydrogen cyanide was used in rat poisons and in Nazi gas chambers.

Phenol was a toilet bowl disinfectant.

Respirable Suspended Particulates constitute the visible smoke which is even less than 5% of the total effluent from a burning cigarette, and carries the bulk of the carcinogens (cancer causing agents) which number approximately 60.  The damage done to the body by the carcinogens is permanent.

Air polluted by tobacco smoke contains more than a hundred times the concentrations of endotoxins that are present in average smoke free indoor air.  These endotoxins arise from bacteria and can induce serious inflammatory reactions and lead to bronchitis and asthma.

Among the carcinogens (cancer causing agents) in ETS are
Benzo [a] pyrene  -- indicated in lung cancer

Nitrosamines -- cancer of lung, respiratory system, and other organs

Aromatic amines -- cancer of the bladder, cancer of the breast

Benzene -- leukemia

Formaldehyde -- nasal cancer; used in embalming fluid

Polonium-210 -- radioactive -- yes, radioactive!



IMMEDIATE impacts of ETS on health
ETS immediately impacts the respiratory system and can trigger asthma attacks which may be severe enough to cause death.  ETS can also lead to pneumonia, bronchitis, and bronchiolitis.

ETS can trigger migraine headaches, earaches, eye and throat irritation, and middle ear infections.

ETS can trigger heart attacks and strokes.

Nicotine is changed into cotinine in the body.  In a study of 4,399 children aged 6 to 16, even the lowest exposure of ETS, as monitored by the levels of cotinine, a metabolite of nicotine, in blood, urine, saliva, and hair, was found to significantly impair, in a dose related manner, the children's reading, math, and reasoning scores. 
In other words, in children and teenagers, even low amounts of ETS can significantly lower test scores by as much as 2-5 or more points and demonstrate a decline in the skills of reading, math, reasoning, and logic.  No safe level of exposure to ETS exists.  Quoting from that recent study, the authors stated:
"We estimate that more than 33 million children in the United States are exposed to levels consistent with the adverse effects seen in this study."
 

"In the United States, 43% of children are exposed to environmental tobacco smoke in their own homes, and 85% of children have detectable levels of cotinine in their blood."
(K.Yolton, et al.  Exposure to environmental tobacco smoke and cognitive abilities among U.S. children and adolescents.  Environmental Health Perspectives 113 (1): 98-103, 2005.)
http://ehp.niehs.nih.gov/members/2004/7210/7210.html


ETS KILLS
Cancer
Cardiovascular Disease
Respiratory Disease
Perinatal death, miscarriage, low birth weight, Sudden Infant Death Syndrome (SIDS)
 
Cancer
Carcinogens cause damage to the body which is permanent and can lead to cancer.  There is no safe level for carcinogens.  Approximately 60 carcinogens are present in tobacco smoke.

ETS has been definitely linked to several types of cancers including:

Lung Cancer

Breast Cancer -- the California EPA 2004 report conclusively links breast cancer to ETS.
  Earlier studies on breast cancer had been inconclusive because of the complexity of variables that needed to be controlled before statistical significance could be achieved, such as menopausal status, age of exposure to ETS, genetic susceptibility, and the hormone receptor status of the tumor.

Nasal Sinus Cancer


Cervical Cancer
A new study reveals that women exposed to ETS may be at greater risk for cervical cancer.  Published in the Obstetrics & Gynecology Journal, 2005, the Johns Hopkins School of Medicine study noted that women who did not smoke but who lived with someone who did smoke were twice as likely to develop cervical tumors as women not exposed to smoke.

There is strong evidence that ETS is a cause of

nasopharyngeal cancer,
and of brain cancer and lymphomas in children. 
(California EPA Report Update 2004 Draft)

A recent study from the Johns Hopkins Bloomberg School of Public Health states that the current EPA Assessment System for Population Exposure Nationwide (ASPEN), which is being used nationally to assess the public health impact of ambient air toxins, underestimates their cancer risk by a factor of as high as three, when compared to directly measuring indoor, outdoor, and personal exposures.  (T.J. Buckley, et al.  Cancer health risk significantly underestimated by EPA's ambient model estimates.  Journal of Environmental Health Perspectives  112: 589-598, 2004.)

Please note:  The tobacco industry lost its lawsuit challenging the 1992 U.S. Environmental Protection Agency Report which classified ETS as a Group A Human Carcinogen.  
First, however, Federal Middle District Judge William Osteen in 1998 ruled in favor of the industry.  As a private attorney in 1974, Osteen had worked for tobacco growers as a lobbyist. 

The EPA appealed his ruling.  The Fourth Circuit Court of Appeals not only dismissed Judge Osteen's ruling, but threw out the case against the EPA altogether. 

The tobacco companies had the option to appeal to the U.S. Supreme Court, but failed to do so, probably because they knew they would lose with so many credible scientific studies that had reaffirmed that ETS causes cancer. 

The nicotine cartel had succeeded, however, in clouding media reporting and the understanding of the general public who still seemed to think there was doubt about ETS causing cancer. 

There are a variety of web sites which could have hidden ties to the tobacco companies and which continue to cultivate doubt about health hazards with articles sneering at reputable studies and maintaining the "right" of smokers to smoke wherever they please and to blow smoke in other people's airspace.

ETS Kills, continued:
Cardiovascular Diseases
One out of every six deaths from cardiovascular disease is caused by smoking, the leading preventable risk factor.  Smoke-free workplaces would significantly reduce heart disease.

Coronary Heart Disease (CHD) is causally associated with ETS exposure. 
The latest estimate of the annual death toll from ETS-related CHD in the USA ranges from 22,700 to 69,600.  Underlying conditions such as diabetes, hypertension, or vascular disease worsen the risk.

Stroke -- ETS can contribute to stroke due to atherosclerosis of the carotid artery and the large arteries of the brain as well as the degeneration of intracerebral arteries.

The mechanisms by which ETS affects the heart and blood vessels comprise
arterial wall thickening,
lesion formation,
decrease in aortic distensibility and reactivity, and
endothelial dysfunction which has emerged as a major factor in CHD.

ETS induced endothelial dysfunction, that is, a functional impairment of the linings of blood vessels, may finally explain why ETS can cause much greater damage to the cardiovascular system than one would have expected simply by comparing the quantities of cigarette smoke to which active and passive smokers are exposed. 

A recent landmark experiment in healthy young nonsmokers revealed that a mere 30 minute exposure to ETS causes changes in coronary blood flow, specifically a substantial reduction in the coronary flow velocity reserve, that are indistinguishable from those of habitual smokers.  These changes are caused by nicotine which inhibits the self-regulatory widening of the coronary blood vessels (vasodilatation) in response to nitric oxide, an endogenous agent released by endothelial cells.  Since this effect of nicotine reaches its maximum already in the small amounts present in ETS, the difference between passive and active smoking as to their effects on blood vessels is greatly narrowed.  By the same token, smoking of only 1 to 3 cigarettes per day can cause heart disease by this mechanism.

Other factors contributing to heart disease and stroke are the adverse effect of ETS on blood lipids:  increase in "bad" cholesterol, LDL, decrease in "good" cholesterol, HDL, as well as platelet activation and elevated fibrinogen levels, all of which are associated with endothelial damage and plaque formation leading to atherosclerosis that, in turn, predisposes to coronary heart disease and stroke.

ETS Kills, continued:
Respiratory Disease
Asthma in children and in adults can be induced and exacerbated by exposure to ETS.
ETS aggravates episodes and severity of asthma attacks.
ETS causes more than 8,000 new cases of asthma in children each year.
As children grow, ETS significantly reduces their lung capacity and exercise tolerance.

The fetus and ETS -- Children and ETS
ETS from either parent hurts the fetus.  The fetus is hurt by smoke from the pregnant mother who smokes, and the ETS breathed by the mother.

ETS from either parent hurts infants and children.

Pregnant women who smoke, or who are around ETS, may find serious consequences for the fetus and later for the infant, such as:
perinatal death
miscarriage
low birth weight, a predictor of frequent illness in the first year of life
asthma
otitis
sudden infant death syndrome (SIDS)
childhood leukemia
cancer of the brain or lungs later in life
conduct disorder
emotional as well as intellectual deficits which have been traced past age 20

This damage can be manifested in impaired lung development, decreased lung function, sudden infant death syndrome (SIDS), acute and chronic respiratory illnesses (including otitis media), and the induction and exacerbation of asthma.

ETS  exposure in pregnancy is responsible for a reduction in birth weight which is associated with respiratory problems and perinatal mortality.

The danger of SIDS, the most common cause of death in the first year of life, greatly increases for infants whose parents smoke near them.

Nicotine, which impacts the brain during critical stages of its intrauterine development in experimental animals, is a likely cause for the deficits in learning and memory, and the emotional and behavioral problems seen in childhood and later in life.


Prenatal nicotine also primes the adolescent brain for addiction.


Carcinogens reaching the fetus via the placental circulation can cause cancer later in life.


Experimental findings in mice suggest that prenatal ETS exposure may also promote development of adult cardiovascular disease.

ETS increases the incidence of middle ear effusion in children.

Heart disease risks go up as ETS lowers kids' "good" cholesterol [HDL] and increases the "bad" cholesterol [LDL].

Children suffer great physical and psychological distress from ETS exposure.



ETS causes Dental Decay
Association of Pediatric Dental Caries With Passive Smoking
Conclusions:  There is an association between environmental tobacco smoke and risk of caries among children. Reduction of passive smoking is important not only for the prevention of many medical problems, but also for the promotion of children's dental health.
JAMA, Journal of the American Medical Association.  2003;289:1258-1264
Vol. 289 No. 10, March 12, 2003 http://jama.ama-assn.org/cgi/content/short/289/10/1258
C. Andrew Aligne, MD, MPH; Mark E. Moss, DDS, PhD; Peggy Auinger, MS; Michael Weitzman, MD



The British Medical Association (BMA) has called for smoke-free workplaces and smoke-free enclosed public places.  Noting on their web site, http://www.bma.org.uk,
"The politicians in Ireland, Norway, and New York have decided to put the health of their citizens first by banning smoking in enclosed public places.  Surely we have a right to ask the same from our Governments?"

Below are EXCERPTS from the press release from the British Medical Association (BMA), November 9, 2004, calling on the English Health Secretary, John Reid, to set a date to ban workplace smoking in the United Kingdom.

In a stark BMA report, The Human Cost of Tobacco, published today (9 November 2004), doctors chronicle individual stories behind the statistics to show how second-hand smoke destroys lives and health.

Every year [in England] at least 1000 people die from the effects of passive smoking. The BMA believes the biggest single step governments can take to improve the health of the public is to take action at national level to stop smoking in enclosed workplaces.

In his foreword to the report, BMA Chairman, Mr. James Johnson, offers the Health Secretary, John Reid, the same advice as smokers get:
There is no doubt that giving up smoking can be extremely difficult – like any addiction kicking the habit is no easy task. When smokers decide to quit they are often advised to set a date, bin the fags and then just do it. Support from a doctor or health professional during this time can be invaluable. I am going to give the same advice to John Reid.

In the forthcoming White Paper for England, he should set a date for banning smoking in all enclosed public places, this will give the bars and restaurants time to bin their ash-trays and then these workplaces will just have to abide by the law. John Reid already has the support of the medical profession.

The report charts around 70 cases throughout the United Kingdom of doctors’ experiences of dealing with patients who have been exposed to second-hand smoke. For example:

Lung Cancer
“I have had three confirmed cases of inoperable primary lung cancer in life-long non-smokers in the last two years. The biopsies showed the type of lung cancer only seen in smokers, and all three worked in public places where they were heavily exposed to secondary cigarette smoke. All three died within weeks of diagnosis.”

Respiratory Disease
"I have recently seen a thirty-four year old landlady with severe bronchial irritation and a history of recurrent wheezy chest infections caused by her work environment in a smoky pub. She now needs regular inhaled drugs including steroids to control her symptoms. She herself has never smoked.”

Children
“I saw a young boy on a number of occasions suffering from severe asthma attacks. His mother said she could not think of anything that brought on the attack, but the young boy said 'I always get sick after seeing granddad'. Apparently his grandfather owns a small and usually smoke filled restaurant.”

Pregnancy
“In my current post in obstetrics I see numerous cases of low-birth weight babies and difficult pregnancies exacerbated by passive smoking."

The BMA has been calling for legislation to ban smoking in enclosed public places since 1986.



Several agencies classify ETS as a human carcinogen including:
The International Agency for Research on Cancer (IARC) classified tobacco smoke as a human carcinogen -- a global recognition
The World Health Organization -- another global recognition
The Surgeon General's Report on the Health Consequences of Involuntary Smoking, United States Department of Health and Human Services (USDHHS), 1986
The National Academy of Sciences, USA
The National Cancer Institute, USA
The National Institute for Occupational Safety and Health (NIOSH), USA
The National Research Council of the National Academy of Sciences, Report on Environmental Tobacco Smoke, 1986, USA
U.S. Environmental Protection Agency, 1992 Report, endorsed and reprinted by the National Cancer Institute, USDHHS, as Smoking and Tobacco Control Monograph 4, 1993.
California EPA, 1997, endorsed and reprinted by the National Cancer Institute, USDHHS, as Smoking and Tobacco Control Monograph 10, 1999, USA
California EPA Update, 2004 Draft Report
The U.S. Public Health Service




The tobacco industry is the only industry which when confronted with the illness, death, and devastation it causes to people and the environment, refuses to stop manufacturing and marketing the product. 
Instead, as greedy drug pushers, they continue to promote their products and refuse to accept responsibility for their actions, blaming the user, not the manufacturer, blaming the addict, not the ones who made the product addictive. 

They post so-called information on their web sites stating that the products they make have been deemed by others to be harmful.  Since they continue to manufacture and advertise their products, this is apparently a legal ploy to try to say that they have sufficiently warned every consumer, so that no one can then sue them for any illness or death resulting from the use of their products.  This is immoral, obscene, and shows a total lack of compassion for both their consumers -- the smokers -- and those bystanders, including children and adults, who are forced to breathe the tobacco smoke.

This is not an industry that exhibits corporate responsibility.

Furthermore, as evidenced by the items given below on this page, they have in the past and continue to this day to try to intimidate scientists and to discredit peer reviewed studies.



Press release from the International Agency for Research on Cancer (IARC)
January 14, 2005
TOBACCO INDUSTRY UNDERMINING THE BASIS OF TRUST IN SCIENCE
IARC Press Releases http://www.iarc.fr, 2005

Tobacco industry undermining the basis of trust in Science

Bitton and colleagues publish in the current issue of Lancet further revelations about Tobacco Industry subterfuge employed to discredit scientific research, including work conducted at the International Agency for Research on Cancer (IARC), and to target specific scientists.

"The use of consultants, who fail to declare their associations with the tobacco industry, to publish purchased critiques of scientific research appears to remain one of the key strategic approaches of the Tobacco Industry" said Dr Peter Boyle, Director of the IARC. "Strategically coordinated attacks by hired guns, hiding behind undisclosed paid associations with industry, on the personal research of independent scientists by such means is at best unethical and at worst cowardly."

Mutations in p53 tumour suppressor gene have been reported in 60% of lung tumours. Work published from 1996 onwards, based to a large extent on IARC's p53 Database (http://www-p53.iarc.fr/index.html), demonstrated patterned mutagenic effect of benzo[a]pyrene, a carcinogen present in tobacco smoke. "The tobacco industry tried to tamper with this evidence because of the implications in the recognition of tobacco smoke as the cause of individual cases of lung cancer. Their strategy of infiltrating the scientific community to undermine the normal process of peer review and publication is distressing for the scientists whose work is targeted. It is also damaging for outstanding journals and academic institutions whose record with respect to tobacco research might appear to be blurred by the actions of a few individuals who maintained undisclosed tobacco industry ties."

"Such activity was supposed to be a thing of the past following the U.S. Master Settlement in the late 1990s, but obviously this is not the case" noted Dr Boyle. "The Tobacco companies claim that they are now working with the public health community to support a single, consistent public health message on the role played by cigarette smoking in the development of disease in smokers."

"If the Tobacco Industry is genuine in their recently proclaimed desire to work with the Public Health community then they cannot expect any cooperation if they continue to be involved in this and other similar activities. This Industry needs to demonstrate true corporate social responsibility. Until then, the public health community can have no confidence in the actions of the Tobacco Industry, and academic institutions should refuse any involvement with them, no matter how loudly the industry claims that they will not interfere in the research."

Nicolas Gaudin, Ph.D.
Chief, IARC Communications Group
International Agency for Research on Cancer
World Health Organization
France



Tobacco Industry Strategy to Undermine Research

Excerpted from EurekAlert, November 1, 2001 http://www.eurekalert.org/pub_releases/2001-11/uoc--idr110101.php

ID: 77768   Contact: Wallace Ravven, wravven@pubaff.ucsf.edu, 415-476-2557, University of California - San Francisco

Philip Morris tobacco company launched a hidden campaign in the 1990s to change the standards of scientific proof needed to demonstrate that secondhand smoke was dangerous, according to an analysis of internal tobacco industry documents by researchers at the University of California, San Francisco (UCSF). The "sound science" standards they promoted through a variety of industry groups would have made proving the hazards of secondhand smoke virtually impossible, according to the study.

The tobacco industry strategy involved a seemingly noble calling for "sound science", while rejecting so-called "junk science" on secondhand smoke that actually threatened the industry's business interests.

Working through lawyers and public relations firms, Philip Morris sought to organize other industries to participate in the "sound science" movement, masking its own involvement. It also hired public relations and marketing firms to help form The Advancement for Sound Science Coalition (TASSC), developed to look like a grassroots organization of scientists and policymakers. Phillip Morris hoped TASSC would seem like an independent body rejecting evidence that secondhand smoke caused significant lung cancer and heart disease risk, according to the analysis of the documents.

In Europe, where secondhand smoke restrictions had not yet been put in place, Philip Morris promoted a set of standards originally proposed by the Chemical Manufacturers Association called "Good Epidemiology Practices." By modifying the proposal and developing new opportunities to introduce it, Philip Morris sought to establish an arbitrary threshold for identifying health risk from secondhand smoke - a threshold higher than what scientists had found for secondhand smoke.

The proposal would have revoked conclusions that an environmental toxin such as secondhand smoke was a public health problem. This effort was particularly focused on undermining a large European epidemiologic study of passive smoking and lung cancer being conducted by the International Agency for Research on Cancer at the time, the researchers found.

The analysis appears in the November issue of The American Journal of Public Health.

First author is Elisa K. Ong, MD, a medical resident at Santa Clara Valley Medical Center who conducted the research while a medical student working in the Institute for Health Policy Studies at UCSF.  Her co-author is Stanton Glantz, PhD, a core faculty member of the Institute and a professor of medicine at UCSF.

Between 1994 and 2000, seemingly independent seminars involving other industries and issues on the so-called "Good Epidemiology Practices" (GEP) were conducted in the United States, United Kingdom, European Union and China, yet in all cases Philip Morris was connected to these events, the documents show.

Essentially, Philip Morris appropriated the "sound science" concept to shape the standards of epidemiology and to prevent increased smoking restrictions, the authors state.

"Phillip Morris has gone beyond 'creating doubt' and 'controversy' about the scientific evidence, to attempting to change the scientific standards of proof," they write.

The approach, the report states, ignores the fact that a comprehensive assessment of risk involves considering all the evidence related to a toxin, not just the epidemiology.

"While every practicing scientist agrees that scientific work should be rigorously done, the scientific, public health and regulatory community need to be more aware that the 'sound science' and 'GEP' movement is not simply an indigenous effort from within the profession, but also reflects sophisticated public relations campaigns controlled by industry executives and lawyers to manipulate the scientific standards of proof for the corporate interests of their clients," the authors conclude.

The research was supported by the National Cancer Institute and the Richard and Rhoda Goldman Fund.

The full text of the article is available online at the American Journal of Public Health web site http://www.ajph.org/cgi/content/abstract/91/11/1749

Two editorials commenting on the significance of this work are also in the journal: http://www.ajph.org/cgi/content/abstract/91/11/1742

http://www.ajph.org/cgi/content/abstract/91/11/1745




REFERENCES used in preparing this Fact Sheet include:

C.A. Aligne, et al., Association of Pediatric Dental Caries With Passive Smoking, Journal of the American Medical Association.  289 (10):1258-1264, March 12, 2003.

C.A. Aligne and J.J. Stoddard. An economic evaluation of the medical effects of parental smoking. Archives of Pediatrics and Adolescent Medicine 161:648-653, 1997.

C.B. Ambrosone, et al. Cigarette smoking, n-acetyltransferase 2 genetic polymorphisms, and breast cancer risk. Journal of the American Medical Association 276:1494-1501, 1996.

Anderson and Arias (2003). National Vital Statistics Report 51(9), Table 2 for yr 2000 Ischemic heart diseases including AMI.

Associated Press, "Judge Once Worked as Tobacco Lobbyist," New York Times, August 23, 1995, p. D3.

P. Brennan, et al.  Secondhand smoke exposure in adulthood and risk of lung cancer among never smokers: A pooled analysis of two large studies.  International Journal of Cancer 109 (1):12-131, 2003.

British Medical Association, November 9, 2004, Press Release calling for a date to set a ban on workplace smoking, http://www.bma.org.uk

T.J. Buckley, et al. Cancer health risk significantly underestimated by EPA's ambient model estimates. Journal of Environmental Health Perspectives 112: 589-598, 2004.

California EPA. Health Effects of Exposure to Environmental Tobacco Smoke, 1997.
California EPA Report Update 2004 Draft at http://www.arb.ca.gov/toxics/ets/dreport/dreport.htm.

CDC Advisory on Heart Disease from ETS , Washington Post, April 23, 2004.

J. Cherner. http://www.smokefree.net/JoeCherner-announce/messages/247185.html.

C.D. Drews, et al. The relationship between idiopathic mental retardation and maternal smoking during pregnancy. Pediatrics 97:547-553, 1996.

J.R. DiFranza and R.A. Lew. Effect of maternal cigarette smoking on pregnancy complications and sudden infant death syndrome. Journal of Family Practice 40:385-394, 1995.

Tobacco Industry Strategy to Undermine Research, EurekAlert, November 1, 2001

W. Farone, former Director of Applied Research for Philip Morris from 1976 to 1984. Prepared statement, "Toxic Gas for the Masses," July 13, 1998.

C. Fichtenberg and S. A. Glantz. Association of the California Tobacco Control Program with declines in cigarette consumption and mortality from heart disease.  New England Journal of Medicine 343: 1772-1777, 2000.

G. Filippi, et al. Mothers' active and passive smoking during pregnancy and risk of brain tumours in children. International Journal of Cancer 57:769-774, 1994.

E.A. Gilpin, et al. Clean Indoor Air: Advances in California, 1990–1999.  American Journal of Public Health 92: 785-791, 2002.

K.H. Ginzel. Testimony presented at the CDC Public Comments Meeting, National Conference on the Healthy People 2010 Tobacco Objectives, San Francisco, California, November 18, 2002.

K.H. Ginzel. Hazards smokers impose. New Jersey Medicine 87:311-317, 1990.

S.A. Glantz and W.W. Parmley. Passive smoking and heart disease: epidemiology, physiology, and biochemistry. Circulation 83:1-12, 1991.

Health Benefits of Snuffing out Workplace Smoking Detailed by Stanford Researcher, Ong. Business Wire, June 22, 2004.

S.S. Hecht. Carcinogen derived biomarkers: applications in studies of human exposure to secondhand tobacco smoke. Tobacco Control 13: 148, 2004.

S.S. Hecht. Body turns nicotine into cancer chemical. Proceedings of the National Academy of Sciences 97:12493, 2000.
http://tobacconews.org/?StoryID=53228 OR

http://www.pnas.org/cgi/content/abstract/97/23/12493

S.S. Hecht. NNK-metabolites in first urine of infants born to smoking mothers. American Chemical Society Press Release, August 23, 1998.

S.S. Hecht, et al. Metabolites of a tobacco-specific lung carcinogen in the urine of elementary school-aged children. Cancer Epidemiology Biomarkers & Prevention 10: 1109-1116, 2001.

D. Hoffmann and I. Hoffmann. The changing cigarette 1950-1995. Journal of Toxicology and Environmental Health 50:307-364, 1997.

G. Howard, et al. Cigarette smoking and progression of atherosclerosis. Journal of the American Medical Association 279:92-124 and 157-158, 1998.

Indoor Air Quality in Hospitality Venues Before and After Implementation of a Clean Indoor Air Law in Western New York, 2003. Office on Smoking and Health, MMWR 53 (44), 11/12/04.

International Agency for Research on Cancer, IARC, 1986, 2002.

International Agency for Research on Cancer, Press Release, January 14, 2005, IARC Press Releases http://www.iarc.fr

International Journal of Cancer 109 (1):125-131, 2003.

G. Invernizzi, et al. Particulate matter from tobacco versus diesel car exhaust: an educational perspective. Tobacco Control 13: 219-21, 2004.

D.T. Janerich, et al. Lung cancer and exposure to tobacco smoke in the household. New England Journal of Medicine 323:632-636, 1990.

L. Larsson of Lund University, Sweden. Rooms where people smoke contain higher air concentrations of endotoxins. News-Medical in Medical Research News, 23-Aug-2004. http://thestar.com.my/lifestyle/story.asp?file=/2004/9/29/features/8994786&sec=features.

J. Laurance. The link between industry, authors and their results. The Independent (UK), April 23, 2004.

R. Maneckjee and J.D. Minna. Opioids induce while nicotine suppresses apoptosis in human lung cancer cells. Cell Growth and Differentiation 5:1033-1040, 1994.

A. Morabia, et al. Relation of breast cancer with passive and active exposure to tobacco smoke. American Journal of Epidemiology 143:918-928, 1996.

W. Moskowitz, et al. Circulation 81:586-592, 1990.

National Cancer Institute, Centers for Disease Control and Prevention, reported in Tobacco Control, October 1997.

New York Times,  January 11, 2005.

R. Otsuka, et al. Acute effects of passive smoking on the coronary circulation in healthy young adults. Journal of the American Medical Association 286: 436-441, 2001; S.A. Glantz and W.W. Parmley. Editorial - Even a little secondhand smoke is dangerous. Journal of the American Medical Association 286: 462-463, 2001.

F.P. Perera. Environment and cancer: who are susceptible? Science 278:1068-1073, 1997.

J. Peto and R. Doll. Passive smoking. British Journal of Cancer 54:382, 1986.

Andreas Picard, Public Health Reporter. Globe and Mail, July 16, 2002, p.A1

A. Picard (Health Reporter). Second-hand smoke can triple lung cancer risk. Globe and Mail, July 12, 2001 ( published in the International Journal of Cancer).

C. Arden Pope III, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of the American Medical Association 287: 1132-1141, 2002.

J.L. Repace. The problems of passive smoking. Bulletin of the New York Academy of Medicine 57: 936-946, 1981.

J.L. Repace. Risk management of passive smoking at work and at home. St. Louis University Public Law Review XIII 2:763-785, 1994.

J.L. Repace and A.H. Lowrey. An indoor air quality standard for ambient tobacco smoke based on carcinogenic risk. New York State Journal of Medicine 85:381-383, 1985.

J.L. Repace, et al. Airborne nicotine and salivary cotinine as indicators of passive smoking exposure in the workplace. Risk Analysis 18:71-83, 1998.

Report on the Health Effects of Environmental Tobacco Smoke (ETS) in the Workplace, Health and Safety Authority, Office of Tobacco Control, 62 pages, Dublin, Ireland, December 2002.

D.P. Sandler, A.J. Wilcox, and R.B. Everson. Cumulative effects of lifetime passive smoking on cancer risk. Lancet I:312-315, 1985.

R. P. Sargent, R. M. Shepard , S. A. Glantz. Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study. British Medical Journal. April 5, 2004. doi:10.1136bmj.38055.715683.55v1.

M. Siegel. Involuntary smoking in the restaurant workplace. A review of employee exposure and health effects, Journal of the American Medical Association, 270: 490-493, 1993.

T.A. Slotkin. Fetal nicotine or cocaine exposure: Which one is worse? Journal of Pharmacology and Experimental Therapeutics 285: 951-945, 1998.

Smokefree ordinances:  Go to http://www.no-smoke.org and click on Smokefree Ordinances Lists.

Surgeon General's Report on the Health Consequences of Involuntary Smoking, 1986.

E.L. Sweda, Jr., Esq. Summary of Legal Cases Regarding Smoking in the Workplace and Other Places, for Tobacco Control Resource Center, Inc., Boston, MA. Dec. 1997; Updated 2004, Tobacco Control

UC DAVIS Study: Fewer Californians dying of lung cancer, pulmonary disease as smoking decreases. EurekAlert May 21, 2001.

U.S. Environmental Protection Agency [EPA] Report Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders, 1992.

USDA Tobacco Quality and Safety Research Laboratory. Cigarettes: the low-tar irony. Science News 136:398, 1989.

U.S. EPA http://www.epa.gov/ttn/oarpg/naaqsfin/pmfact.html

L.S. Wakschlag, et al. Maternal smoking during pregnancy and the risk of conduct disorder in boys. Archives of General Psychiatry 54:670-676, 1997.

Z. Yang, et al. Prenatal environmental tobacco smoke exposure promotes adult atherogenesis and mitochondrial damage in apolipoprotein E. Circulation 110: 3715-3720, 2004.

K. Yolton, et al. Exposure to environmental tobacco smoke and cognitive abilities among U.S. children and adolescents. Environmental Health Perspectives 113 (1), 98-103, 2005.
http://ehp.niehs.nih.gov/members/2004/7210/7210.html



[Virginia GASP]   Updated 17th January 2005