The air pollution scare industry is at it again -- in a very timely manner to help the Environmental Protection Agency impose more dubious regulations on us.
Second Hand Smoke and Health
January 27th, 2009 By Terry Simpson, M.D., F.A.C.S. The 1964 Surgeon General Report, which declared that the inhalation of cigarettes would likely cause lung cancer and heart disease, had a profound impact in the United States. This report started America thinking that the practice of inhaling cigarette smoke was unhealthy and began a long series of studies, lawsuits, and laws, that changed the face of America from a primary smoking society—where over 60 percent of adults in the U.S. smoked—to a number that is now about 30 percent. On June 27, 2006, long after the first Report and yet likely based on its long-lasting impact, Surgeon General Richard Carmona issued the following statements regarding second hand smoke: (a) The scientific evidence is now indisputable: secondhand smoke is not a mere annoyance. It is a serious health hazard that can lead to disease and premature death in children and nonsmoking adults. (b) Secondhand smoke contains more than 50 cancer-causing chemicals, and is itself a known human carcinogen (c) There is no risk-free level of exposure to secondhand smoke. Nonsmokers exposed to secondhand smoke at home or work increase their risk of developing heart disease by 25 to 40 percent and lung cancer by 20 to 30 percent. The Surgeon General also stated that 49,000 deaths per year were caused by second hand smoke. As a surgeon, I was stunned, because I had never seen an autopsy report listing second hand smoke as the cause of death. Nor had I seen this as a secondary cause of death. So I asked six pathologists if they had ever listed second hand smoke as a cause of death – not one had. In my years of clinical practice, I have seen patients die from many devastating diseases, and yet I have never seen anyone who has been disabled by, or has died as a result of, second hand smoke. This was my first clue that perhaps there was more hyperbole than science involved in the reports issuing from the Surgeon General’s Office. To give a contrast: 33,000 people die per year of pancreatic cancer – all of the pathologists have listed pancreatic cancer as a cause of death. Composition of Smoke
Second hand smoke, also called Environmental Tobacco Smoke, is a combination of Mainstream Smoke, which is exhaled by smokers and Sidestream Smoke, which is released directly from the burning tip of cigarettes or cigars. Sidestream smoke is the primary constituent of environmental tobacco smoke, providing most of the vapor phase and over half the particles. Hence, at events such as “The Big Smoke”, the majority of particulate matter comes from sidestream smoke. Exhaled mainstream smoke contributes between 15 and 43 percent of the particulate matter in environmental tobacco smoke. Sidestream smoke is generated at lower temperatures and a higher alkalinity than mainstream smoke, and as a result has a different chemical composition. During environmental tobacco smoke formation, both sidestream smoke and exhaled mainstream smoke are diluted by many orders of magnitude and subsequently undergo physical transformation and alterations in chemical composition. For example, nicotine and many other semi-volatile compounds of tobacco smoke tend to be present in the particle phase of inhaled mainstream smoke, but evaporate into the vapor phase as exhaled mainstream smoke is rapidly diluted during the formation of environmental tobacco smoke. Second Hand Smoke and Lung Cancer
If second hand smoke exposure is a significant risk factor for developing lung cancer, then we should expect to see increased numbers of cancer cases in non-smokers who are exposed to regular doses of second hand smoke. Has there been an increase in the incidence of lung cancer among nonsmokers over the last 40 years? The answer is quite simply… No. Data from national mortality studies show that rates of lung cancer among non-smoking women remained stable between the 1950’s to the 1980’s (very few women smoked during those years) and didn’t rise until substantial numbers of women started smoking in more recent years. These non-smoking women were included in numerous studies as control groups for examining lung cancer rates in their smoking spouses. As anti-smoking logic would dictate, the longer one is exposed to second hand smoke the more we should see a rise in lung cancer. However, when we examine the data from the studies noted above, we do not see such a rise in cancer rates for these non-smoking women. In 1992, second hand smoke was labeled a Class A carcinogen: one that causes lung cancer and is responsible for the deaths of 3,000 Americans annually (U.S. EPA, 1993). However, there were no autopsies, no bodies, nor one person that could be claimed as a victim. The EPA did not base their classification on their own independent study but examined over thirty epidemiological studies (i.e., studies that attempt to correlate various risk factors with early death in different populations). Eleven of those studies were done in the United States, and of those eight found a positive risk, three found a negative risk but none of them were statistically significant (that is, none of the U.S. studies could make the statement that there was a causal relationship between second hand smoke and cancer). In medical research, a statistical confidence level of 95% means that there is only a five percent chance that a significant finding could be due to chance (i.e., a random result). In their interpretation of the epidemiological studies, the EPA made a critical procedural statistical alteration. They changed the confidence level to 90%. This statistical manipulation made it more likely that their findings would show significant negative health effects of second hand smoke, but also made more likely the potential for erroneous conclusions. Furthermore, the EPA did not take into consideration the factors independently associated with both the development of lung cancer and exposure to second hand smoke, factors that certainly could account for the purported relationship between second hand smoke and early death. Finally, they did not attempt to assure that the subjects were properly identified into the correct experimental group. The EPA left several important questions unanswered such as: Were the exposed cases truly ill with primary lung cancer? Had the subjects been smokers previously? Were they truly exposed to second hand smoke? And, did the subjects accurately report their exposure levels? The EPA also classified second hand smoke as a carcinogen based on chemical “similarities” between inhaled mainstream smoke and environmental tobacco smoke. Their logic was that since inhaled tobacco smoke is a carcinogen, environmental tobacco smoke must also be. Inhaled mainstream smoke, however, contains chemicals at concentrations of up to one million times those found in environmental tobacco smoke (which is a combination of exhaled mainstream smoke and sidestream smoke). Further, deep inhalation affects the degree of exposure to those chemicals, as well as the deposition of those chemicals into the respiratory passages of the smoker. One of the frustrating issues is we do not know the chemical, or chemical compounds responsible for the link to lung cancer and/or heart disease. This leads to another difficult issue – the length of exposure to the chemical might not yield a linear relationship to the formation of cancer (also known as the exposure-risk relationship). Single dose exposure likely does not yield 100 percent incidence of carcinoma. For example, low exposures of materials in drinking water does not yield disease, but higher and longer exposures of materials – such as arsenic, certainly produce disease. Much as a single aspirin may produce the effect of headache relief, a large dose of aspirin will be toxic. What was not evident in many of these studies was a dose-response curve to second hand (passive) smoking and disease. At the behest of Congressman Henry Waxman (D-Ca), the Congressional Research Service (CRS) spent two years examining reports and came up with the following conclusions regarding second hand smoke and lung cancer (Redhead and Rowberg, 1995): (a) The statistical evidence does not appear to support a conclusion that there are substantial health effects of passive smoking. (b) It is possible that very few or even no deaths can be attributed to second hand smoke. (c) If there are any lung cancer deaths from second hand smoke, they are likely to be concentrated among those subjected to the highest exposure levels (e.g., spouses). (d) The absolute risk, even to those with the greatest exposure levels, is uncertain. The CRS found that, what was considered an “obvious” conclusion by the EPA was, in fact, flawed. The EPA reasoned that if the smoke inhaled by a smoker was close enough in composition to that which is exhaled, then if one was carcinogenic the other must also be carcinogenic. This assumption is chemically incorrect and was rejected. The CRS examination of the various studies concluded that someone exposed to significant second hand smoke—a spouse for example—might increase their risk of dying from lung cancer to 2/10 of one percent, while those who are exposed on the job would have less risk: 7/100 of one percent. The most devastating opinion about the EPA’s decision to classify second hand smoke as a class A carcinogen, came from Federal Judge William Osteen who interviewed scientists for four years and in 1998 opined, The Agency disregarded information and made findings based on selective information… [The EPA] deviated from its risk assessment guidelines; failed to disclose important (opposing) findings and reasons; and left significant questions without answers… Gathering all relevant information, researching and disseminating findings, were subordinate to EPA’s [goal of] demonstrating [that] ETS was a Group A carcinogen… In this case, the EPA publicly committed to a conclusion before research had begun; adjusted established procedure and scientific norms to validate the Agency’s public conclusion, and aggressively utilized the Act’s authority to disseminate findings to establish a de facto regulatory scheme…and to influence public opinion… While doing so, [the EPA] produced limited evidence, then claimed the weight of the Agency’s researched evidence demonstrated ETS causes cancer. (Osteen, 1998) Because the EPA report was “advisory” and not “regulatory,” Judge Osteen’s indictment was reversed. However, it is important to note that the decision was reversed on a technical distinction, not the merits of the EPA’s report. In another large-scale study, and in contradistinction to the EPA conclusions, the World Health Organization International Agency on Cancer published a report concluding that there was no statistically significant risk of lung cancer in non-smokers who lived or worked with smokers (Boffetta, et al, 1998). This study was the product of ten years of data gathered from seven European countries. Health Risks of Second Hand Smoke
In a study spanning 16 U.S. cities, the U.S. Department of Energy researchers placed monitors on nonsmoking bartenders and waiters who worked in smoke-filled bars and restaurants to measure the amount of environmental tobacco. The conclusion was that the monitors detected minuscule amounts of tobacco products. (Jenkins, et al, 1999) The harm that might come from such minuscule amounts of exposure was calculated as “none” to “improbable harm”. The anti-tobacco forces have condemned this study because it was partly funded by the R.J. Reynolds Company. Later, a group of individuals visited the establishments and concluded that since they saw few individuals smoking, the study was flawed. In spite of this study being done by Oak Ridge National Laboratories, it was painted with a broad brush because of the funding from the tobacco industry. Environmental tobacco smoke (ETS) is considered by many authorities to be an important component of indoor air pollution in part because it is often viewed as being equivalent to mainstream cigarette smoke (MS). It has been clearly demonstrated that ETS is not the same as MS. Side stream cigarette smoke (SS) is a major contributor to ETS. Side-stream smoke is generated under different conditions than MS, and as a result, has a different relative chemical composition. Exhaled MS, the second primary contributor to ETS, is a different material from that which leaves the cigarette butt and enters the lungs. Exhaled MS has been substantially depleted in vapor-phase constituents, and the particulate matter is likely to have increased its water content in the high-humidity environment of the respiratory tract. As the cigarette smoke, both SS and exhaled MS, enters the atmosphere, it is diluted by many orders of magnitude and subsequently undergoes both physical transformation and alterations in its chemical composition. Upon standing, or during air exchange from other sources, ETS continues to change… (Guerin, et al, 2000) The science and chemistry of this field of research are complex, and if the conclusions reached do not meet with current public policy, the research scientist is often stereotyped as being “pro-tobacco”. Because these studies are expensive, and because tobacco companies often supply the grant funds to purchase the supplies, anti-tobacco advocates will often say this is equivalent to bribing the researchers. They sometimes fail to mention, however, the anti-tobacco-funded individuals who personally receive thousands of dollars to vent anti-tobacco research and lend their name to the anti-tobacco movement. One of those individuals, Stanton Glantz, a Ph.D. whose field of expertise is aerospace engineering, attempted to convince the EPA to accept that there were over 50,000 deaths a year, from cardiac events, attributed to second hand smoke. The Congressional Research office examined the statistics related to second hand smoke and cardiac events and determined that those numbers were implausible (Gravelle and Redhead, 1994) And yet, the anti-smoking advocates continue to march their cause… The Occupational Safety and Health Administration (OSHA) withdrew a 12-year-old petition that smoking be banned from all indoor workplaces. The withdrawal was based on a lack of evidence. The decision was taken to court in an attempt to force OSHA to reverse its decision. OSHA stated that it would regulate based on permissible levels of the various ingredients in environmental tobacco smoke, and the lawsuit was withdrawn on the grounds that OSHA would do nothing. (Henshaw, 2001) It’s no wonder OSHA decided to withdraw its complaint, since even its own people couldn’t agree on a position. In 1997, Acting Assistant Secretary of OSHA, Greg Watchman aired his own view: Field studies of environmental tobacco smoke indicate that under normal conditions, the components in tobacco smoke are diluted below existing Permissible Exposure Levels (PELS) as referenced in the Air Contaminant Standard (29 CFR 1910.1000). It would be very rare to find a workplace with so much smoking that any individual PEL would be exceeded. (Letter from Greg Watchman, 1997) As with arsenic content in drinking water, for example, setting scientific numbers to permissible levels would compel the scientific community to make real statements as to levels that are acceptable. Given that science had already answered the question with a number of chemicals in tobacco, such a regulation would be a blow to all anti-smoking advocates and their contention that there is no “safe” level of second hand smoke. With no scientific evidence to back his statement, Mayor Bloomberg of New York City proclaimed that bartenders inhale the equivalent of half a pack of cigarettes a day. In fact, a study from the U.K. showed that the average London bartender inhaled the equivalent of six cigarettes annually (about one quarter of a pack). (Matthews and MacDonald, 1998) Perhaps one of the better studies was published in the British Medical Journal by epidemiologist James Enstrom and Geoffrey Kabat (2003). Their study of 35,000 Californians showed that lifelong exposure to a husband or wife’s smoke produced no increased risk of coronary heart disease or lung cancer among the non-smoking spouses. As with most who oppose the anti-tobacco lobby, Enstrom was forced to defend his study on the basis that it had received funding from a tobacco company. The study was condemned as biased, even though it was published in a peer-reviewed journal, the statistics were not flawed, and the conclusions were sound. When the cigar lounge at Seattle’s El Gaucho restaurant was closed because smoking in public places in the state of Washington became illegal, one of the reasons cited was to “protect the workers”. The premise of this law has no evidence. Suffice it to say, there is far more evidence to ban the sale of alcohol in bars and restaurants than cigar smoking. Every day in every major city there are deaths from people who have consumed alcohol and driven. Alcohol is directly responsible for about 100,000 deaths a year and an estimated 2.3 million years of lost life. Alcohol prohibition didn’t work. So why attempt to prohibit tobacco? The press frequently overlooks inconsistent data when reporting about environmental tobacco smoke. The most recent example was when a group of radiologists noted that one-third of patients who had never smoked, but were exposed to “high levels” of second hand smoke, showed MRI changes in their lungs similar to the changes seen in smokers. What failed to make the mainstream news was that two-thirds of the patients who were listed as non-smokers, but exposed to “high levels” of second hand smoke, paradoxically, had lower diffusion through the lungs than the “low exposure” group. That is, they showed the opposite of changes seen with heavy smokers. Again, what made the news in most circles was that this was more proof about the negative effects of environmental tobacco smoke. What did not make the news was that the paradoxical report might prove the opposite of their conclusion. (Science Daily, 2007) The Surgeon General was incorrect. Second hand smoke may be an irritant and an annoyance, but it’s not a cause of death. There are no body bags filled with those who have developed tumors or heart disease as a result of second-hand smoke. The body bags are filled, however, with scientists and physicians who dare go against the anti-smoking lobby and state the obvious—the science isn’t there. As much as they want to ban all smoking in all places, the health risk is grossly overstated. Whenever someone dies of lung cancer, such as Diane Reeves, the late wife of Christopher Reeves, the anti-smoking lobby uses the news as a media circus. They want to relate the unfortunate death to something… even if such a relationship has no basis in solid scientific research. In 1633, the Catholic church condemned Galileo for asserting that the Earth revolves around the sun. Galileo was forced to recant his scientific findings to avoid being burned at the stake. This was a clear conflict between faith and science. References
Boffetta, P., Agudo, A., Ahrens, W., et al. (1998). “Multicenter Case-Control Study of Exposure to Environmental Tobacco Smoke and Lung Cancer in Europe.” Journal of the National Cancer Institute. Vol. 90, No. 19:1440–50. Enstrom, J. E. and Kabat, G. C. (2003, May 17) “Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98.” British Medical Journal, 326(7398): 1057. Available: www. pubmedcentral.nih.gov/articlerender.fcgi?artid=155687id=”d11j90″> Gravelle, J. G., and Redhead, C. S. (1994, March 23). Congressional Research Office Memorandum “Discussion of Source of Claims of 50,000 Deaths from Passive Smoking.” “in response to request for information on the possible source of an estimated premature 50,000 deaths from passive smoking effects.” Available: www .nycclash.com/Cabinet/CRSDiscusses_50000_Deaths.htmlid=”d11j92″> Guerin, M. R., Jenkins, R. A., Tomkins, B. A. (2000). “The Chemistry of Environmental Tobacco Smoke: Composition and Measurement.” (Second Ed.) CRC Press. Henshaw, J. L. (2001). “Withdrawal of Proposal.” U.S. Department of Labor, OSHA, Notice, Indoor Air Quality – Federal Register #66:64946. Available: http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=FEDERAL_REGISTER&p_id=16954 Jenkins, R. A., Palausky, A., Counts, R. W., Bayne, C. K., Dindal, A. B., and Guerin, M. R. (1999). “Exposure to Environmental Tobacco Smoke in Sixteen Cities in the United States as Determined by Personal Breathing Zone Air Sampling.” Journal of Exposure Analysis and Environmental Epidemiology. Oct-Dec;6(4):473-502. Letter from Greg Watchman, Acting Ass’t Sec’y, OSHA, to Leroy J Pletten, PhD, July 8, 1997. Matthews, R., and MacDonald, V. (1998). “Passive Smokers Inhale Six Cigarettes a Year.” UK News Electronic Telegraph, Issue 1178. Available http://www.forces.org/evidence/files/passmok2.htm Osteen, W. L., United States District Judge (1998). “Flue-Cured Tobacco Cooperative Stabilization Corporation, et al v. United States Environmental Protection Agency, et al.” United States District Court for the Middle District of North Carolina, Winston-Salem Division, 6:93CV00370, 89-90. Available: www.forces.org/evidence/epafraud/files/osteen.htm id=”d11j106″> Redhead, C. S. and Rowberg, R. E. (1995, November 14) CRS Report for Congress. “Environmental Tobacco Smoke and Lung Cancer Risk.” Retrieved November 2007 from the WWW. Available: www.forces.org/evidence/files/crs11-95.htm id=”d11j108″> Science Daily. (November 27, 2007). “Second hand smoke damages lung, MRIs show.” Available: www.sciencedaily.com/releases/2007/11/071126104424.htm id=”d11j110″> U.S. Environmental Protection Agency. (1993) “Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. ” National Institutes of Health. Monograph 4, NIH Publication No. 93-3605, August 1993. Read: http://yourdoctorsorders.com/?p=9
Secondhand Smoke is No Danger: The Heartland Institute featured on Rush Limbaugh As Rush Limbaugh noted on his nationally syndicated radio program Tuesday, July 8, fear-mongers unfairly have made an article of faith out of the charge that second-hand tobacco smoke can cause disease in humans. Rush spent a major portion of his Tuesday program discussing an article in the July issue of The Heartland Institute s Environment & Climate News written by Dr. Jerome Arnett Jr., a pulmonologist who lives in Helvetia, W.Va. Dr. Arnett wrote that the basis for the second-hand smoke scare an EPA report in 1992 is not supported by reliable scientific evidence. The report has been largely discredited and, in 1998, was legally vacated by a federal judge. The full article is available here and copied below: http://www.heartland.org/Article.cfm?artId=23399Scientific Evidence Shows Secondhand Smoke Is No Danger Author: Jerome Arnett, Jr., M.D. Published by: The Heartland Institute Published in: Environment & Climate News Publication date: July 2008 Exposure to secondhand smoke (SHS) is an unpleasant experience for many nonsmokers, and for decades was considered a nuisance. But the idea that it might actually cause disease in nonsmokers has been around only since the 1970s. Recent surveys show more than 80 percent of Americans now believe secondhand smoke is harmful to nonsmokers. Federal Government Reports A 1972 U.S. surgeon general's report first addressed passive smoking as a possible threat to nonsmokers and called for an anti-smoking movement. The issue was addressed again in surgeon generals' reports in 1979, 1982, and 1984. A 1986 surgeon general's report concluded involuntary smoking caused lung cancer, but it offered only weak epidemiological evidence to support the claim. In 1989 the Environmental Protection Agency (EPA) was charged with further evaluating the evidence for health effects of SHS. In 1992 EPA published its report, "Respiratory Health Effects of Passive Smoking," claiming SHS is a serious public health problem, that it kills approximately 3,000 nonsmoking Americans each year from lung cancer, and that it is a Group A carcinogen (like benzene, asbestos, and radon). The report has been used by the tobacco-control movement and government agencies, including public health departments, to justify the imposition of thousands of indoor smoking bans in public places. Flawed Assumptions EPA's 1992 conclusions are not supported by reliable scientific evidence. The report has been largely discredited and, in 1998, was legally vacated by a federal judge. Even so, the EPA report was cited in the surgeon general's 2006 report on SHS, where then-Surgeon General Richard Carmona made the absurd claim that there is no risk-free level of exposure to SHS. For its 1992 report, EPA arbitrarily chose to equate SHS with mainstream (or firsthand) smoke. One of the agency's stated assumptions was that because there is an association between active smoking and lung cancer, there also must be a similar association between SHS and lung cancer. But the problem posed by SHS is entirely different from that found with mainstream smoke. A well-recognized toxicological principle states, "The dose makes the poison." Accordingly, we physicians record direct exposure to cigarette smoke by smokers in the medical record as "pack-years smoked" (packs smoked per day times the number of years smoked). A smoking history of around 10 pack-years alerts the physician to search for cigarette-caused illness. But even those nonsmokers with the greatest exposure to SHS probably inhale the equivalent of only a small fraction (around 0.03) of one cigarette per day, which is equivalent to smoking around 10 cigarettes per year. Low Statistical Association Another major problem is that the epidemiological studies on which the EPA report is based are statistical studies that can show only correlation and cannot prove causation. One statistical method used to compare the rates of a disease in two populations is relative risk (RR). It is the rate of disease found in the exposed population divided by the rate found in the unexposed population. An RR of 1.0 represents zero increased risk. Because confounding and other factors can obscure a weak association, in order even to suggest causation a very strong association must be found, on the order of at least 300 percent to 400 percent, which is an RR of 3.0 to 4.0. For example, the studies linking direct cigarette smoking with lung cancer found an incidence in smokers of 20 to around 40 times that in nonsmokers, an association of 2000 percent to 4000 percent, or an RR of 20.0 to 40.0. Scientific Principles Ignored An even greater problem is the agency's lowering of the confidence interval (CI) used in its report. Epidemiologists calculate confidence intervals to express the likelihood a result could happen just by chance. A CI of 95 percent allows a 5 percent possibility that the results occurred only by chance. Before its 1992 report, EPA had always used epidemiology's gold standard CI of 95 percent to measure statistical significance. But because the U.S. studies chosen for the report were not statistically significant within a 95 percent CI, for the first time in its history EPA changed the rules and used a 90 percent CI, which doubled the chance of being wrong. This allowed it to report a statistically significant 19 percent increase of lung cancer cases in the nonsmoking spouses of smokers over those cases found in nonsmoking spouses of nonsmokers. Even though the RR was only 1.19--an amount far short of what is normally required to demonstrate correlation or causality--the agency concluded this was proof SHS increased the risk of U.S. nonsmokers developing lung cancer by 19 percent. EPA Study Soundly Rejected In November 1995 after a 20-month study, the Congressional Research Service released a detailed analysis of the EPA report that was highly critical of EPA's methods and conclusions. In 1998, in a devastating 92-page opinion, Federal Judge William Osteen vacated the EPA study, declaring it null and void. He found a culture of arrogance, deception, and cover-up at the agency. Osteen noted, "First, there is evidence in the record supporting the accusation that EPA 'cherry picked' its data. ... In order to confirm its hypothesis, EPA maintained its standard significance level but lowered the confidence interval to 90 percent. This allowed EPA to confirm its hypothesis by finding a relative risk of 1.19, albeit a very weak association. ... EPA cannot show a statistically significant association between [SHS] and lung cancer." The judge added, "EPA publicly committed to a conclusion before the research had begun; adjusted established procedure and scientific norms to validate its conclusion; and aggressively utilized its authority to disseminate findings to establish a de facto regulatory scheme to influence public opinion." In 2003 a definitive paper on SHS and lung cancer mortality was published in the British Medical Journal. It is the largest and most detailed study ever reported. The authors studied more than 35,000 California never-smokers over a 39-year period and found no statistically significant association between exposure to SHS and lung cancer mortality. Propaganda Trumps Science The 1992 EPA report is an example of the use of epidemiology to promote belief in an epidemic instead of to investigate one. It has damaged the credibility of EPA and has tainted the fields of epidemiology and public health. In addition, influential anti-tobacco activists, including prominent academics, have unethically attacked the research of eminent scientists in order to further their ideological and political agendas. The abuse of scientific integrity and the generation of faulty "scientific" outcomes (through the use of pseudoscience) have led to the deception of the American public on a grand scale and to draconian government overregulation and the squandering of public money. Millions of dollars have been spent promoting belief in SHS as a killer, and more millions of dollars have been spent by businesses in order to comply with thousands of highly restrictive bans, while personal choice and freedom have been denied to millions of smokers. Finally, and perhaps most tragically, all this has diverted resources away from discovering the true cause(s) of lung cancer in nonsmokers. ________________________________________ Dr. Jerome Arnett Jr. ( jerry.arnett@gmail.com) is a pulmonologist who lives in Helvetia, West Virginia. ________________________________________ 19 South LaSalle Street #903 * Chicago, IL 60603 312/377-4000 phone * 312/377-5000 fax * http://www.heartland.org
Secondhand data on secondhand smoke October 8, 2007 HELVETIA, W.Va.--The federal government's 30-year anti-smoking crusade has been so successful that there are now more ex-smokers than smokers in the United States. But about a quarter of the population continues to smoke cigarettes, and over the past decade a new health hazard has been fabricated and publicized. The news media have parroted the idea that secondhand smoke is harmful, and a recent survey finds that more than 80 percent of adults now believe this. But the secondhand-smoke scare is based largely on speculation reminiscent of superstitions from the Middle Ages, before the discovery of the scientific method. The 2006 surgeon general's 709-page report "The Health Consequences of Involuntary Exposure to Tobacco Smoke" further promotes this sham. The report claims that even brief exposure to secondhand smoke can cause immediate harm and cites reports that estimate secondhand smoke causes approximately 3,000 lung cancer deaths and tens of thousands of heart disease deaths among nonsmokers each year. It concludes that there is no risk-free level of exposure, and recommends "smoke-free policies" to eliminate all indoor smoking. Surgeon General Richard Carmona himself stated at a June 27, 2006, press conference, "The science is clear: [secondhand smoke] is a serious health hazard that causes premature death and disease in children and non-smoking adults." The Environmental Protection Agency, American Lung Association, American Public Health Association, and American Cancer Society all concur. The California Air Pollution Authority has labeled secondhand smoke a toxin and the EPA has initiated a "Smoke-Free Home Pledge Campaign." Marriott has announced that its 2,300 hotels will become totally smoke-free by October 15 of this year. In June, a California state Senate committee approved a bill to ban smoking in private cars with children. But the science is not "clear." In fact, there is no credible scientific evidence to support any of this. Whereas the association of cigarette smoking with heart disease and lung cancer in epidemiologic studies is strong--an increase of 100 to 300 percent and 900 percent respectively--the association found between secondhand-smoke exposure and heart disease and lung cancer in the studies cited by the surgeon general is very weak, an increase of about 30 percent for each. In addition, the report cherry-picks studies that support its claims and ignores other important ones that do not. For example, it cites a 1993 EPA meta-analysis of 30 studies, that has since been discredited, and ignores an excellent 1998 World Health Organization large single study that showed a reduced association for children of smokers and no association for spouses and co-workers. The largest single study of all, a 39-year analysis of over 35,000 Californians published in 2003 in the British Medical Journal, found no connection between passive smoking and mortality. It was not cited. Epidemiology is the study of disease in populations. Epidemiologists collect data using poorly controlled observational studies and evaluate it by using statistical methods. These methods are not adequate to test the hypotheses required by the scientific method, so epidemiology can never prove or disprove anything. It uses "relative risk" to report its findings of association. An RR of 1.0 is average, while an RR of 3.0 or more--a 300 percent increase--is required to suggest causation. The epidemiologic studies cited by the surgeon general's report cannot determine causation largely because they are unable to control for inherent systematic errors. These include measurement errors, confounding factors, and at least 56 different biases, including "recall bias." In the studies cited by the surgeon general, not only do the researchers have no control over the exposures to secondhand smoke, they don't even know what the data are. A weak association is a fortuitous finding. Converting it into a causal link bypasses the scientific method, and has been termed "statistical malpractice" in the literature. This unethical application of statistics to the imperatives of health policy is a common occurrence in politically motivated science. The report claims that the weak statistical associations found in the studies "were not determinant" in making causal inferences, but instead, "judgments were based on an array of considerations." What these considerations were, and why they were more important than the results of the studies cited, is not apparent. Finally, a basic principle of toxicology is that "the dose makes the poison." The surgeon general's report admits that secondhand smoke "is rapidly diluted as it travels away from the burning cigarette," and that it cannot be defined or measured. It takes many years of persistent exposure for cigarette smoking to cause disease. For example, a patient's smoking one pack of cigarettes (22 cigarettes) a day for 10 years alerts a physician to search for lung disease. But even in the smokiest of smoke-filled rooms, nonsmokers inhale only a fraction of one cigarette a day. To be beneficial, public policy must be based on good science. Bad science inevitably leads to bad public policy. All government bureaucracies have one hidden agenda--to increase their funding and power. This leads to misrepresentations like the secondhand-smoke scare. The 2006 surgeon general's report reminds us that one ongoing peril for citizens is being misled by government bureaucrats seeking to expand their power. We need to shape our policies on the basis of good science, instead of shaping the science to fit the policies. ----------- JEROME ARNETT JR. is a pulmonologist and writer. He wrote this commentary for the Competitive Enterprise Institute. Read
Airborne Dead Skin Cells 2/24/07 Human skin is constantly regenerating, and in the process a single person will shed billions of dead skin cells each day. About 80% of the visible airborne particles in a room (for example highlighted in a ray of sunshine) is comprised of dead skin cells. These dead skin cells contain bacteria, and can cause allergic reactions in some people. Therefore, remove a large percentage of people from an establishment by passing smoking bans and you will also remove up to 80% of the airborne pollution from the PM 2.5 micron range. As this testing data by the pro-smoking ban Minnesota organization MPAAT/ClearWay MN proved... Read More and See Charts
Living close to heavy industry may increase risk of lung cancer 27-Sep-2006 Emma Dickinson A case control study using life grid interviews online first Thorax 2006 Living close to heavy industry may increase the risk of developing lung cancer, although the effect is relatively modest, suggests research published ahead of print in Thorax. Over 200 women under the age of 80 with primary lung cancer were compared with 339 healthy women matched for age and sex in Teeside, north east England. Rates of lung cancer among women are high in this particular area of England, where heavy industry expanded rapidly throughout the nineteenth and twentieth centuries, and where poverty and deprivation are common. By 1945, Billingham on Teeside was the larges single chemical production complex in the world, and houses for the workforce were built as close as possible to the industrial sites. All the study participants were interviewed at length about their lives, including full histories of where they had lived, their employment, as well as their smoking habits, and exposure to second hand smoke. The distances from heavy industry sites were grouped into three zones: less than 5 km (zone A) away; 5 to 10 km away (Zone B); and more than 10 km away (Zone C). The average length of time that all participants had lived in the area was over 55 years. After taking account of smoking and other factors likely to influence the results, the data showed that women who had lived in zone A for more than 25 years were almost twice as likely to develop lung cancer as those who had not lived there. The findings are broadly consistent with those of other studies, say the authors, who suggest that the impact of air pollution on the development of lung cancer warrants further study. Read
The EPA's Fine Particulate Matter (PM2.5) Standards, Lung Disease, and Mortality
September 7, 2006 Jerome Arnett
Congress passed the Clean Air Act of 1970 based on the belief that reducing air pollution levels saves lives and improves health. The Act mandated the Environmental Protection Agency (EPA) to base its regulatory policies on good science. In 1997, EPA promulgated standards for fine particulate matter that were the most stringent and expensive in the agency’s 35-year history. The standards were widely criticized, and even EPA’s own science advisory committee did not endorse them. Instead of preventing 20,000 deaths and saving $69 to $144 billion a year at a cost of $6.3 billion (for partial attainment), as claimed, the standards have cost at least $70 billion a year to implement, eliminated hundreds of thousands of jobs a year, and likely have cost lives (because of the huge cost) without providing any public health benefit.
One reason for this failure of public policy lies with the epidemiological environmental studies used. Two large studies served as the scientific basis for the standards promulgated—the 1993 Harvard Six Cities Study and the 1995 American Cancer Society Study. These and other studies showed only a weak association between exposure and disease or death—an increased relative risk of 1.26 and 1.17 respectively—and yielded several discrepant results.
Epidemiology is the study of health in populations. With air pollution studies, as a practical matter, exposure is estimated at the group level, while health outcomes are measured at the individual level. In addition, observational epidemiological studies, unless they show overwhelmingly strong associations—on the order of an increased relative risk of 3.0 or 4.0—do not indicate causation because of the inherent systematic errors that can overwhelm the weak associations found. These errors include confounding factors, methodological weaknesses, statistical model inconsistencies, and at least 56 different biases.
In order to show causation, environmental epidemiological studies showing strong associations must be accompanied by experimental animal toxicologic studies that provide evidence for a plausible biological mechanism. But dozens of such animal studies performed over the past 30 years all have been negative.
The introduction of causal assumptions into observational epidemiological studies that show only weak statistical associations is a problem that has been recognized for many years, and has been well documented in the literature. Since this process bypasses the scientific method, it has been labeled “statistical malpractice.” In addition, the improper use of science to promote political agendas is rightly considered unethical.
EPA’s PM2.5 regulations are a tragic failure of public policy that are shown to have no basis in science and thus are not saving lives or preventing illness. Instead they are imposing billions of dollars of net cost each year on the American people. Read
Study: Death rates drop after air cleanup
March 26, 2006 By Nicholas Bakalar, The New York Times
When air pollution in a city declines, the city benefits with a directly proportional drop in death rates, a new study has found. For each decrease of 1 microgram of soot per cubic meter of air, death rates from cardiovascular disease, respiratory illness and lung cancer decrease by 3 percent -- extending the lives of 75,000 people a year in the United States. The association held even after controlling for smoking and body-mass index. The work, described in a paper in the March 15 issue of The American Journal of Respiratory and Critical Care Medicine, was carried out in six metropolitan areas: Watertown, Mass.; Kingston and Harriman, Tenn.; St. Louis; Steubenville, Ohio; Portage, Wyocena and Pardeeville, Wis.; and Topeka, Kan. The participants, ages 25-74 at enrollment, were followed from 1974 through 1998. The scientists periodically measured concentrations of soot, or particulate air pollution, in each city. At the same time, they tracked disease and mortality among 8,096 residents. Particulate air pollution consists of a mixture of liquid and solid particles, mostly a result of fossil fuel combustion and high-temperature industrial processes. By definition, the particles have a diameter less than 2.5 microns, or about one ten-thousandth of an inch. "For the most part, pollution levels are lower in this country than they were in the '70s and '80s," said Francine Laden, the study's lead author, "and the message here is that if you continue to decrease them, you will save more lives." Further declines in air pollution are within reach, said Laden, an assistant professor of environmental epidemiology at Harvard. "The technology is out there," she said. "The cities that we've covered have cleaned up considerably." Laden said the study supported what the federal scientific advisers had advocated: tightening the air quality standard below the present 15 micrograms per cubic meter. "There was discussion about lowering it to 12," she said, "and this study supports that." Read
Harvard Six Cities Study Follow Up: Reducing Soot Particles Is Associated with Longer LivesFor immediate release: Wednesday, March 15, 2006 Boston, MA - An eight-year follow up to the landmark Harvard Six Cities Study has found an association between people living longer and cities reducing the amount of fine particulate matter, or soot, in their air. The study has been published in the March 15 issue of the American Journal of Respiratory and Critical Care Medicine. The follow-up study found that an average of three percent fewer people died for every reduction of one ug/m3 in the average levels of PM2.5 fine particulate matter, defined as having a diameter of 2.5 microns or less -- narrower than the width of a human hair. This decreased death rate is approximate to saving 75,000 people per year in the U.S., said lead author Francine Laden, HSPH Assistant Professor of Environmental Epidemiology. The largest drops in mortality rates were in cities with the greatest reduction in fine particulate air pollution. The findings remained valid after controlling for the general increase in adult life expectancy in the U.S. during both the original and follow-up study periods (1979 to 1989 and 1990 to 1998). Particulate matter is a complex mixture of extremely small particles and liquid droplets that can be directly emitted, as in smoke from a fire, or it can form in the atmosphere from reactions of gases such as sulfur dioxide, according to the Environmental Protection Agency (EPA). The original Harvard Six Cities Study evaluated the effects of pollution on adults in the 1970s and 1980s. The results found a strong, positive correlation between levels of air pollution and mortality. The study led to a revision of existing air quality standards by the EPA. The follow-up study population consisted of nearly 8,100 white participants residing in Watertown, Massachusetts; Kingston and Harriman, Tennessee; St. Louis, Missouri; Steubenville, Ohio; Portage, Wyocena, and Pardeeville, Wisconsin; and Topeka, Kansas. The annual mean concentration of fine particulate matter declined during the study period by seven micrograms ug/m3 of air per decade in Steubenville, five micrograms in St. Louis, three micrograms in Watertown, two micrograms in Harriman, one microgram in Portage, and less than a microgram in Topeka. Recently, the EPA's external science advisors recommended that the agency back new air quality standards that would reduce by one to two ?g/m3 of air the acceptable standard of average levels of PM2.5. The EPA proposed lowering the level of the 24-hour fine particle standard but keeping unchanged the annual standard, set in 1997. "Our study supports the science advisors' position," said Laden. "When cities make those reductions, the results save lives." A public comment period on the proposals will end on April 17, and the EPA is expected to make a final ruling in September. For more information about the proposals, visit here. In addition to Laden, the study's authors are Joel Schwartz, HSPH Professor of Environmental Epidemiology; Frank Speizer, Edward H. Kass Professor of Medicine at Harvard Medical School and HSPH Professor of Environmental Science; and Douglas Dockery, chair of the HSPH Department of Environmental Health and lead author on the original Six Cities study. For more information about the original study, see Harvard Public Health Review. An editorial on the follow up has been published in the same issue of the American Journal of Respiratory and Critical Care Medicine. The EPA and the National Institute of Environmental Health Sciences funded this follow up.
EPA Whips Up Air Pollution Scare
March 09, 2006 Steven Milloy
The air pollution scare industry is at it again -- in a very timely manner to help the Environmental Protection Agency impose more dubious regulations on us.
“When the air is filled with increased levels of soot and other tiny particles, more people end up in the hospital with heart and lung problems, according to the largest study yet on the health effects of such pollutants,” reported the Chicago Sun-Times on March 8.
Published in the Journal of the American Medical Association, the study reports that “short-term exposure to [fine particulate air pollution or soot] increases the risk for hospital admission for cardiovascular and respiratory diseases.”
The researchers estimated that reducing average ambient soot levels by almost 75 percent would have reduced the total number of hospital admissions for a variety of heart and lung problems during 2002 in the 204 mostly urban counties studied from1,394,441 admissions down to 1,383,282 – a difference of 11,159 admissions or 0.8 percent.
Before we get to the question of whether the benefits of such a reduction would exceed the costs – let alone whether such a reduction is even possible -- we ought to examine the “air worthiness” of this estimate.
First, the researchers’ results are derived through purely statistical methods in which soot levels recorded by geographically-dispersed Environmental Protection Agency-operated air monitoring stations were matched with local hospital admissions records. Higher levels of soot were slightly correlated with increased hospital admissions, according to the researchers.
But there are several major drawbacks to the researchers’ methodology which, in the parlance of epidemiologists, is termed an “ecological study.”
First, no one knows how much soot any of the hospitalized patients were exposed to. The researchers simply assumed that people are exposed to the level of soot measured by the closest EPA monitoring stations, a distance of 5.9 miles from their residences on average. But the likelihood of varying environmental conditions over such distances and time spent indoors-versus-outdoors raises significant doubts about the validity of their assumption.
Next, not a single patient’s hospitalization was diagnosed by an attending physician as being due to air pollution. The researchers simply assumed that, for a specified level of soot, any “extra” hospital admissions were due to soot.
Since the population studied consisted entirely of elderly Medicare patients and since there is no biological explanation for how short-term exposure to low-levels of soot could possibly cause acute heart and lung problems, its quite likely that the hospitalizations had nothing whatsoever to do with soot.
The researchers know very well that ecological studies, at best, may be useful for designing future studies, but are not capable of proving cause-and-effect relationships. Study author Jonathan Samet of the Johns Hopkins University once even discouraged the use of ecological studies, stating in the context of indoor radon, “The methodologic limitations inherent in the ecologic method may substantially bias ecologic estimates of risk...”
So why claim such a certain connection between soot and health when the data and study method are so deficient?
As it turns out, the study was funded by the U.S. Environmental Protection Agency, which conveniently just started a rulemaking process in January that would make outdoor air quality standards more stringent.
The study was released on March 7, in time for the March 8 newspapers – the same day that the EPA held a public hearing in Chicago on the need for new air pollution standards.
The need for more stringent air pollution regulation is certainly open to debate, if for no other reason than that current EPA air pollution rules were issued in 1997 and have not yet been fully implemented – much less, evaluated in terms of benefits and costs.
The EPA claims that hundreds of studies show that current air quality levels harm the public’s health. But virtually all of these studies, however, have been funded by the EPA -- an agency once famously accused by its own Science Advisory Board of “adjusting science to fit policy” – conducted by the same clique of EPA-funding-dependent researchers, and suffer from the exact same weaknesses as the study published this week.
You would think that if the case was so clear-cut concerning current air quality and public health, it would take only a few good studies to sufficiently make the link. Instead, we’re barraged with hundreds of studies that prove nothing except that, if there is some risk to health from current levels of air pollution and public health, it is exceedingly small and difficult to detect.
Technology exists to significantly improve studies on air pollution and health. Study author Francesca Dominci told me that personal monitors exist that could more precisely indicate what levels of air pollution people actually experience. But, she said, that would cost millions of dollars.
Given that national compliance with the last round of EPA air quality rules costs an estimated $10 billion annually, it make sense for the agency to spend a few million dollars to improve the exposure data on which such costly regulation is based – but don’t hold your breath waiting for that to happen.
Exposure to fine particle air pollution linked with risk of respiratory and cardiovascular diseasesBeing exposed to fine particle matter air pollution increases a person's risk for hospital admission for cardiovascular and respiratory diseases, according to a study in the March 8 issue of JAMA.
Numerous studies have shown associations of chronic exposure to airborne particles and increased health risks. Recent evidence on adverse effects of particulate air pollution on public health has motivated the development of more stringent standards for levels of particulate matter in outdoor air in the United States and in other countries, according to background information in the article. In 1997, the standard for airborne particulate matter was revised, maintaining the previous indicator of particulate matter of less than or equal to 10 µm in aerodynamic diameter (PM10) and creating a new indicator for fine particulate matter of less than or equal to 2.5 µm in aerodynamic diameter (PM2.5). Particles in this size range have a much greater probability of reaching the small airways and the alveoli (air sacs) of the lung than do larger particles. Evidence is limited on the health risks of this size range of particulate matter.
Francesca Dominici, Ph.D., of Johns Hopkins University, Baltimore, and colleagues conducted a study to estimate the risk for cardiac and respiratory diseases from exposure to fine particulate air pollution. The researchers analyzed data from a national database for 1999 through 2002 on hospital admission rates (constructed from the Medicare National Claims History Files) for cardiovascular and respiratory outcomes and injuries for 11.5 million Medicare enrollees (aged 65 years or older) who lived in 204 U.S. urban counties (population greater than 200,000). The individuals lived an average of 5.9 miles from a PM2.5 monitor.
The researchers found there was a short-term increase in hospital admission rates associated with exposure to PM2.5 for all of the health outcomes except injuries. The largest association was for heart failure, which had a 1.28 percent increase in risk per 10-µg/m3 increase in same-day PM2.5. Cardiovascular risks tended to be higher in counties located in the Eastern region of the United States, which included the Northeast, the Southeast, the Midwest, and the South.
"In the lung, particulate matter may promote inflammation and thereby exacerbate underlying lung disease and reduce the efficacy of lung-defense mechanisms. Cardiovascular effects may reflect neurogenic [arising in or stimulated by nerve tissues] and inflammatory processes," the authors write.
"Our findings indicate an ongoing threat to the health of the elderly population from airborne particles and provide a rationale for setting a PM2.5 National Ambient Air Quality Standard that is as protective of their health as possible," the researchers write. "The sources of particles contributing to the observed risks need to be identified so that control strategies can be targeted efficiently."
###
|