Ilow

Not that I am deluded enough to think that any amount of information will convince those who don't wish to be comitted, but here are some interesting things that I found in a quick search: (Mods, please delete if you feel that this is too long for this area, and i can PM it to people individually)

1) Here is an interesting article that among other things documents that the "flawed" EPA study that KMA complains about so vociferously was actually found not to be "flawed" in 2002. It also speaks to the lengths that the tobacco industry will go to in order to protect itself.

Researchers Discover Documents Outlining Tobacco Industry's Political Efforts to Delay Environmental Protection Agency Report on Indoor Second-Hand Smoke

Dateline: ROCHESTER, Minn., April 2 (AScribe Newswire) —
Using previously secret tobacco industry documents, researchers in the current issue of the American Journal of Preventive Medicine, outline the strategies used by the tobacco industry to try to derail the Environmental Protection Agency (EPA) report that led to smoke-free indoor air requirements.
The researchers show for the first time how the tobacco industry attempted to mobilize political pressure on the EPA to delay or stop it from issuing its 1992 risk assessment on environmental tobacco smoke. The assessment concluded that second hand smoke was a Group A human carcinogen and had adverse effects on respiratory health, particularly in children. It also estimated that environmental tobacco smoke causes approximately 3,000 lung cancer deaths annually in nonsmokers.
The documents show the tobacco industry will expend whatever effort is necessary to protect itself from public health policy that would adversely affect cigarette consumption, says Richard Hurt, M.D., director of the Mayo Clinic Nicotine Dependence Center, and an author of the report. In this manuscript, we show that the tobacco industry is constantly trying to stymie public health efforts with regard to second hand smoke and tobacco consumption.
The authors call the environmental tobacco smoke report a seminal event that led to the development of the movement to create smoke-free indoor air.
The researchers obtained the information on the tobacco industry's political strategies based on tobacco company internal documents made public through litigation in the United States. The documents are available at the Minnesota Tobacco Document Depository in Minneapolis and the British American Tobacco (BAT) Document Depository in London. Strategies that are outlined in the journal's report include:
— Lobbying the first Bush Administration to approve an executive order that would impose new risk assessment standards for federal agencies, thus delaying the release of the EPA report.
— Urging the first Bush Administration transfer jurisdiction over environmental tobacco smoke from the EPA to the Occupational Safety and Health Administration, which would have squelched the EPA report.
— Applying enormous political pressure directly by alleging improper procedure and policy at EPA.
Most of the strategies eventually failed, but the authors say the political pressure from U.S. Rep. Thomas Bliley, Jr., R-Va., was a success.
This is the first report showing how a single member of Congress in conjunction with his staff, tobacco industry attorneys and executives worked very aggressively to advance the tobacco industry's interests, Dr. Hurt says.
Bliley, who served 20 years in the U.S. House of Representatives before retiring in 2000, wrote at least 11 letters to EPA Administrator William Reilly touting industry messages of faulty science and flawed procedures, the research says. The letters included attacks on James Repace, one of the journal article's authors, who was then an EPA air policy analyst and staff scientist.
The authors note that the tactics to slow the process were referred to by tobacco industry officials as sand in the gears.
Eventually, the tobacco industry sued the EPA in federal court to nullify the risk assessment as it related to lung cancer. The proceedings took seven years before the suit reached an appeals court hearing. These tactics successfully delayed the EPA risk assessment and placed a cloud over its validity that was not fully vindicated until December 2002 when the U.S. 4th Circuit Court of Appeals overturned the tobacco industry's suit, the authors report.
Ironically, the EPA report and the publicity surrounding its release accelerated the consideration of smoke-free public places and the passage of smoke-free laws in cities, states and even entire countries.
Co-authors of the report are Monique Muggli, an independent tobacco control consultant in St. Paul, Minn., and Repace, visiting clinical professor, Tufts University School of Medicine and Repace Associates, Inc.
American Journal of Preventive Medicine is a journal of the American College of Preventive Medicine and the Association of Teachers of Preventive Medicine. The American Journal of Preventive Medicine publishes articles in the areas of prevention research, teaching, practice and policy.


2)Here are a couple studies that show that you are misinformed in your thinking that second-hand smoke in the home is not harmful. The first relates to children and the second is a detailed study on the effects of briefexposure (I have the references and charts, but cut them out here.)

Title: Kids' Year-Round Asthma Symptoms Triggered by Parent's Second-Hand Smoke; Children's Doctors Should Ask Parents of Asthmatic Children If They Smoke, Counsel Them on Quitting, Researchers Recommend , Ascribe Newswire: Health, 5/5/2004Database: Health Source - Consumer Edition

Kids' Year-Round Asthma Symptoms Triggered by Parent's Second-Hand Smoke; Children's Doctors Should Ask Parents of Asthmatic Children If They Smoke, Counsel Them on Quitting, Researchers Recommend
Dateline: SAN FRANCISCO, May 4 (AScribe Newswire) —Children with asthma whose parents smoke at home are twice as likely to have asthma symptoms all year long than children of non-smokers, a new study shows.Overall, in a nationwide sample of children with asthma, about 13 percent of parents of asthmatic children still smoke - even though second-hand smoke is known to trigger asthma attacks and symptoms in kids.Those findings, made by University of Michigan researchers and scheduled to be presented here on May 4 at the Pediatric Academic Societies Annual Meeting, reinforce the importance of educating parents about how their own smoking can affect their children with asthma. The study is based on data from in-depth phone interviews with 896 parents of asthmatic children ages 2 to 12 years in 10 states.Those interviews were done as part of the Physician Asthma Care Education (PACE) project, which is designed to improve asthma education for physicians, and consequently the health of their young patients who have asthma. The chronic condition affects one in every seven children.The new analysis was conducted by Kathryn Slish, a researcher in the U-M Department of Pediatrics, with assistant professor of pediatrics Michael Cabana, M.D., M.P.H., M.A. The PACE project is led by U-M School of Public Health Dean Noreen Clark, Ph.D., and funded by the Robert Wood Johnson Foundation.We set out to look at children who have seasonal asthma symptoms, but found that a substantial percentage have symptoms year-round, says Slish. We looked more closely and found a strong relationship between parents' smoking status and the likelihood that their child would have problems all year long.It's not rocket science, since it's well known that second-hand smoke can trigger asthma in children, Slish continues. But it's astounding that so many parents smoke around their asthmatic kids, and don't stop even though their children are having trouble breathing all year.The study echoes findings of previous research by the Centers for Disease Control and Prevention, which looked at whether children had had severe asthma symptoms on more or less than 300 days per year, and found a strong correlation to parent smoking among those with more than 300 days.We used a different approach than the CDC, and looked at 90-day blocks of time corresponding to a season, says Cabana. The only other factor that was associated with year-round symptoms was Medicaid insurance coverage.Slish and Cabana note that their findings should provide even more reason for pediatricians, family physicians and nurses to broach the subject of smoking with the parents of any child diagnosed with asthma, and to steer parents who smoke toward resources that can help them quit.By addressing the issue directly, and reminding parents how second-hand smoke can affect their children, perhaps we can cut down on the number of kids having symptoms throughout the year, Cabana says.Even a very brief intervention with physicians encouraging patients to quit smoking has been shown to be successful, adds Clark.Part of the PACE project is teaching physicians how to counsel asthmatic patients and their parents on avoiding asthma triggers - substances in the air that can bring on an asthma attack or lesser symptoms. Triggers include dust, pollen, pet dander, stress, cockroach droppings, mold, air pollution, exercise, cold air - and second-hand smoke. Some triggers, such as pollen, occur only during some times of the year, while others are present year-round and are mainly linked to indoor exposure.The interviews conducted for the current study were part of the baseline data-gathering effort for the PACE project. Parents of young patients of participating doctors were interviewed at length about many factors. They were asked to recall the number of days during each three-month period of the last year that their child experienced daytime asthma symptoms, nighttime asthma symptoms, or limits on their daily activity due to asthma-related precautions or symptoms.If a child had had symptoms on 27 or more days, or seven or more nights, in a 90-day season, he or she was considered to be in peak or persistent asthma symptoms during that time - a definition laid out by the National Heart, Lung, and Blood Institute of the National Institutes of Health.Most of the children - 84 percent - in the study had peaks in none, one, two or three seasons of the past year. But 16 percent of the children had peaks in all four seasons - meaning they were experiencing symptoms nearly one-third of the entire year regardless of what seasonal triggers might be present.Two-thirds of the children in the study were boys, and 12 percent were African-American. The mean age was around 7, and 61 percent used some sort of daily medication to control their asthma. More than 90 percent of the parents interviewed were mothers. Parents were asked directly if they smoked, and 13 percent answered yes.Three-quarters of the households had private insurance, while 14 percent were insured through Medicaid. The remainder had other government insurance or paid for healthcare themselves. Just over 40 percent of the children lived in temperate climates, where differences between seasons were not dramatic.When the researchers performed a statistical analysis to look at which factors were most associated with year-round symptoms, Medicaid status and parental smoking both were linked to a more-than-doubled likelihood.The researchers hope to continue their evaluation of parental smoking behavior as the PACE project continues, and follow-up interviews with parents take place after their children's doctors receive training in evidence-based asthma care and patient communication.For more information, contact Kara Gavin or Krista Hopson, University of Michigan Health System Media Coordinators, at 734-764-2220, or kegavin@umich.edu or khopson@umich.edu.

Transient Decrease of Exhaled Nitric Oxide after Acute Exposure to Passive Smoke in Healthy Subjects



Contents
Materials and Method
Results
Discussion
References
ABSTRACT. Nitric oxide (NO) is produced and detected in the
exhalate from the respiratory tract where it plays important
regulatory functions. Exhaled nitric oxide (eNO) concentrations
are reduced in active cigarette smokers between cigarettes and
in nonsmoking subjects during short-term exposure to
environmental tobacco smoke. In this study, the authors evaluated
eNO before and after an acute exposure to environmental tobacco
smoke in healthy, nonsmoking subjects (n= 12). Baseline eNO
levels were measured by chemiluminescence at baseline (1 hr
before exposure), shortly after the end of exposure, and 10 and
30 min after the end of exposure. Mean room air NO concentration
increased from 3 ppb to 4 ppm (range, 560 ppb-8.5 ppm) during the
exposure period. Carboxyhemoglobin levels were assessed before
and after the exposure with spectrophotometry. All subjects had
decreased eNO with exposure to environmental tobacco smoke (mean
± standard error of the mean: 16.65 ± 1.35 ppb to
13.86 ± 1.33 ppb;p < .001). These concentrations
remained significantly decreased at 10 min and recovered within
30 min. No modifications in airway resistance or increase in
carboxyhemoglobin levels were observed. Exposure to environmental
tobacco smoke transiently—but consistently—decreased
eNO concentration in healthy, nonsmoking subjects, suggesting
that second-hand smoke can directly affect NO in the airway
environment.
<Key words: environmental tobacco smoke, lung, nitric oxide>
CHRONIC EXPOSURE to environmental tobacco smoke (ETS) is a recognized risk factor for respiratory and cardiovascular disease in healthy subjects.[1,2] Second-hand smoke contains several toxic substances that may produce harmful biological effects in exposed subjects—both in airways and in the circulation.[2,3] There is recent evidence linking short-term, acute passive cigarette smoking to endothelial dysfunction in healthy nonsmokers.[4] Nitric oxide (NO), the most important endothelium-derived relaxing factor, is produced and detected in measurable amounts in the respiratory tract, where it plays a part in pulmonary vascular regulation, bronchomotor tone, and host nonspe-cific defense.[5] Exhaled nitric oxide (eNO) is a simple, noninvasive measure of airway NO, which is particularly sensitive to environmental pollution or to pro-inflammatory airway challenges.[6] Decreased eNO has been reported in habitual smokers,[7,8] and reverts after smoking cessation,[9] suggesting an interference of NO-rich cigarette smoke with local antioxidant defenses. The effects of acute, passive smoking on eNO in nonsmokers are not well known; 1 recent study reported decreased eNO levels in nonsmoking subjects during a brief period of smoke exposure.[10] The current study measured eNO in non-smokers after an acute exposure to second-hand cigarette smoke.
Materials and Method
Twelve nonsmoking subjects with no history of disease, asthma, or other chronic airway disorders were recruited from hospital personnel and were enrolled in the study. All subjects lived in smoke-free homes and were advised to avoid environmental smoke exposure during their free time for at least 24 hr before entering the study. The study protocol was approved by the hospital ethics committee, and all subjects gave written informed consent.
NO was detected with a chemiluminescent analyzer (280 NOA Sievers Instruments, Sievers [Boulder, Col-orado]), characterized by a lower limit of detection of 1 ppb and a NO sampling rate of 200 ml/min. Daily 2-point calibration was performed with zero gas (Zero Air Filter, Sievers [Boulder, Colorado]) and a certified NO gas mixture at 1.01 ppm (SIAD [Osio, Italy]). NO was measured from exhaled air with the subjects performing a single, slow, vital capacity maneuver against an expiratory resistance in accordance with the American Thoracic Society guidelines. The breathing circuit comprised a mouthpiece connected to a Hans-Rudolph valve, through which air was inhaled and then exhaled via an expiratory resistance, while targeting a fixed-mouth pressure of 20 mm Hg displayed on a pressure gauge. This technique allows for closure of the velum, thus excluding nasal NO contamination during expiration. All subjects performed a vital capacity maneuver and then a slow (20-sec) exhalation against a 20-cm H[sub2]O mouth resistance, with a resulting expiratory flow rate of 45 ml/sec. The single-breath pattern of eNO showed an initial washout phase followed by a steady plateau.
Airway resistance, expressed as specific airway conductance (SG[subaw]) was determined by a compensated whole-body plethysmograph (6200 Autobox, Sensor Medics [Milan, Italy]). The technique has been described elsewhere.[11] Measurements were made in triplicate, with the subjects panting at 2 Hz.
We assessed baseline eNO concentrations every 20 min for 1 hr to calculate the coefficient of variation for each subject. We also measured SG[subaw] at baseline and again at the end of the exposure period. At the completion of baseline measurements, subjects entered a room with active smokers, where ventilation was 80 m[sup3]. Smokers consumed 22 cigarettes during the 30-min exposure period, during which time we assessed NO levels in the room. At the end of the exposure period, smokers left the room and we assessed eNO concentrations shortly thereafter, and at 10 and 30 min postexpo-sure. Furthermore, we took blood samples at baseline and at the end of the exposure to passive smoke from 5 subjects by venipuncture, using a heparinized syringe for determination of plasma carboxyhemoglobin level (COHb) by spectrophotometry.
Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using analysis of variance (ANOVA) and Student's paired t tests. A value ofp < .05 was considered statistically significant.
Results
NO room levels in the ambient air increased from 3 ppb to 4 ppm (range = 560 ppb-8.5 ppm) during the exposure period. At baseline, the mean eNO concentration was 16.65 ± 1.35; the individual coefficient of variation was < 10% (Table 1). All subjects had a decrease in eNO concentration immediately after the 30-min exposure to passive smoke (13.86 ± 1.33 ppb;p < .001) (Fig. 1); levels remained significantly lower than the baseline value at 10 min (14.93 ± 1.24 ppb;p = .006). Levels of eNO returned to baseline 30 min after the end of the exposure period (16.95 ± 1.47 ppb; p = .452). SG[subaw] did not change significantly between baseline and the end of the passive smoke exposure (0.279 ± 0.009 versus 0.290 ± 0.014 cm H[sub2]O/sec, respectively; p = .174). We observed no significant change in COHb levels following passive smoke exposure.
Discussion
The results of the present study show that passive exposure to cigarette smoke is associated with a reduction in eNO in healthy, nonsmoking subjects. Reductions in eNO occurred after a short (30 min) period of ETS exposure; reductions were completely reversed within 30 min after the exposure was stopped. ETS exposure did not yield significant changes, however, in the COHb blood levels in our subjects. Yates et al.10 recently reported a rapid fall in eNO, both during active smoking and passive cigarette smoke inhalation in normal subjects. The authors noted eNO remained low for 60 min. Our findings generally agree with and further refine those results.
We measured eNO using a single-breath, restricted technique. This method eliminates the contribution of the upper airway, the most important site of NO production in humans,[12] and allows for reproducible NO sampling from the lower airways. Moreover, we calculated eNO values from the plateau curve of the NO concentration, obtained by exhaling against a constant pressure and at a constant expiratory flow rate of 45 ml/sec. This rate is easy to sustain and yields reproducible measurements in the same subject, an important feature as a change in flow rates from 1,000 to 5 ml/sec could cause a 35-fold increase in eNO.[12] During baseline conditions, the technique yielded individual coefficients of variation in eNO in our subjects of < 10%.
It is unlikely that changes in humidity or oxygen ambient tension affected eNO measurement during the smoke exposure period. Nafion drying tubing in the exhalation apparatus minimized an increase in water vapor pressure, which may quench and decrease NO concentration during repeated measurements by chemiluminescence.[13] Inhalation of a hypoxic gas mixture could decrease eNO in humans, but only at very low oxygen concentrations.[14]
The reduction of eNO following smoke exposure could not be related to changes in airway caliber or to the effect of the forced expiratory maneuver.[15] We did not observe a significant change in airway conductance, a sensitive measurement of bronchial tone. The reduction of eNO did not appear to result from carbon monoxide, as the eNO decrease following smoke exposure was not associated with significant changes in COHb absorption. Inhalation of cigarette smoke in concentrations sufficient to raise exhaled carbon monoxide levels to 12 ppm should result in no change in eNO level.[8]
The mechanism for the decrease in eNO with exposure to tobacco smoke remains uncertain. Cigarette smoke contains high concentrations of nitrogen oxides,[16] and the reduction in eNO may result from down-regulation of NO synthase by a negative feedback mechanism.[8] During active smoking in the room, the low baseline ambient NO concentration increased to a median value of 4 ppm. Moreover, in vitro regulation of airway epithelium NO synthesis by smoke extracts takes several hours to change protein expression and is usually irreversible[17]; on the other hand, inhaled heated smoke may lead to a local change in airway osmolarity, which could decrease airway NO concentration.[18]
A recent in vitro study on porcine pulmonary endo-thelial cells suggests that the decreased NO generation seen in response to a solution of cigarette smoke could be related to the NOS gene or to NOS activity.[19] Other possible mechanisms include inactivation of NO by oxidants in cigarette smoke. Perhaps NO reacts rapidly with superoxide, yielding the harmful oxidant peroxyni-trite. Cigarette smoking is associated with lung recruitment and activation of neutrophils[20,21] that produce increased capabilities for the generation of nitrated protein. It is also possible that the decrease in eNO is related to some other substance or combination of substances in cigarette smoke.[4]
Exposure to passive smoke is associated with a number of adverse health effects, and several of these may be explained by reduced NO production. NO production by airway epithelial cells may be important in defending the respiratory tract against infectious agents, because NO has antimicrobial properties.[22] Reduction in the endogenous production of NO by the respiratory tract may increase the risk of infection by several mechanisms; it may contribute to the increased risk of respiratory infection after exposure to passive cigarette smoke.[1]
In conclusion, acute passive smoke exposure causes a transient—but consistent— decrease of lower airway NO in normal subjects, but its clinical significance is unknown. The measurement of eNO after passive smoke exposure may, however, provide a sensitive method for exploring airway response to ETS.


3)And finally for those of you thinking about having kids:

Title: EVEN SECOND-HAND SMOKE IMPAIRS FERTILITY , Better Nutrition, 0405668X, Dec2000, Vol. 62, Issue 12Database: Health Source - Consumer Edition

Section: Health Notes EVEN SECOND-HAND SMOKE IMPAIRS FERTILITY
Studies show that tobacco smoke impairs women's ability to conceive and reduces sperm count in men, and even second-hand smoke can prove damaging to fertility. Dr. Michael Hull and his research team reported in Fertility and Sterility that of the over 14,000 pregnancies looked at in the study, women exposed to smoke were about 15 percent less likely to conceive within the period of a year as those in smoke-free atmospheres. In light of this, Dr. Hull and his colleagues concluded that in couples where the woman is pregnant and in those trying to conceive, smoking by either partner is dangerous.

If anyone is interested in MORE documents on how the tobacco industry is subverting research, let me know.

__________________
"Religion is the one area of our discourse in which it is considered noble to pretend to be certain about things no human being could possibly be certain about"
--Sam Harris