How Much Ongoing Smoking Reduction is an Echo of the Initial Mass Education?

Objectives: In this paper, we attempt to quantify the "echo" effects of the downward shock in US smoking prevalence from mass education starting about 1965 through 2010. Methods: An agent- based population simulation replicates the observed effects of the initial education shock on smoking prevalence, and then estimates ongoing echo effects based on empirical estimates of the effects of parental smoking on initiation and peer-group quitting contagion. Further simulations estimate what additional echo effects would explain the entire historical reduction. Results: About one-third of the observed prevalence decline through 2010 can be attributed solely to fewer parents smoking after the initial education shock. Combining peer-group cessation contagion explains well over one-half of the total historical prevalence reduction. Plausible additional echo effects could explain the entire historical reduction in smoking prevalence. Conclusions: Ongoing anti-smoking interventions are credited with ongoing reductions in smoking, but most, or perhaps all that credit really belongs to the initial education and its continuing echoes. Ensuring that people understand the health risks of smoking causes large and ongoing reductions. The effect of all other interventions (other than introducing appealing substitutes) is clearly modest, and quite possibly, approximately zero, after accounting for the echo effects.

Potential effects of using non-combustible tobacco and nicotine products during pregnancy: a systematic review.

BACKGROUND: The range of risk reduced alternatives to smoking tobacco is increasing and so is use among pregnant women. The substantial harms of smoking during pregnancy are well established and there is reason to believe that nicotine alone is somewhat harmful. Differences in the exposure chemistry strongly suggest that the effects of using smoke-free nicotine products (including pharmaceutical nicotine products, smokeless tobacco, and electronic cigarettes containing nicotine) fall somewhere in the range between zero risk to the risk from smoking. How much lower risk these consumption choices are in terms of pregnancy outcomes, however, remains uncertain. METHODS: We reviewed the literature on smoke-free nicotine and tobacco product exposure and birth-outcome endpoints. Studies were included if they compared outcomes to either no nicotine use or smoking. We searched Google Scholar using broad search terms and additional articles were snowballed from citations. We report what could be learned from each study, given its methods. RESULTS: Of the 21 studies reviewed, 12 reported on the use of nicotine replacement therapies, 7 on Swedish snus, 1 on Alaskan iq'mik, and 1 on e-cigarettes. The range of results tends to support the prediction that smoke-free product use during pregnancy probably increases the risk of some negative birth outcomes, but that any effect is less than that from smoking. However, the limitations of epidemiology are such that no more-precise a conclusion is possible. DISCUSSION: The available epidemiology does not change our prior beliefs, based on other evidence and knowledge, that the risks from smoke-free nicotine and tobacco are lower than those for smoking, though it suggests they are non-zero. However, it also demonstrates that the epidemiology is unlikely to provide precise quantitative estimates. This is not just a matter of lack of studies; given the inherent limitation of these studies, doubling or tripling the corpus of available studies would add little precision. For the foreseeable future, decisions about using these products will need to be made based on rough estimates, based on a variety of forms of evidence, and qualitative comparisons.

Gateway Effects: Why the Cited Evidence Does Not Support Their Existence for Low-Risk Tobacco Products (and What Evidence Would).

It is often claimed that low-risk drugs still create harm because of "gateway effects", in which they cause the use of a high-risk alternative. Such claims are popular among opponents of tobacco harm reduction, claiming that low-risk tobacco products (e.g., e-cigarettes, smokeless tobacco) cause people to start smoking, sometimes backed by empirical studies that ostensibly support the claim. However, these studies consistently ignore the obvious alternative causal pathways, particularly that observed associations might represent causation in the opposite direction (smoking causes people to seek low-risk alternatives) or confounding (the same individual characteristics increase the chance of using any tobacco product). Due to these complications, any useful analysis must deal with simultaneity and confounding by common cause. In practice, existing analyses seem almost as if they were designed to provide teaching examples about drawing simplistic and unsupported causal conclusions from observed associations. The present analysis examines what evidence and research strategies would be needed to empirically detect such a gateway effect, if there were one, explaining key methodological concepts including causation and confounding, examining the logic of the claim, identifying potentially useful data, and debunking common fallacies on both sides of the argument, as well as presenting an extended example of proper empirical testing. The analysis demonstrates that none of the empirical studies to date that are purported to show a gateway effect from tobacco harm reduction products actually does so. The observations and approaches can be generalized to other cases where observed association of individual characteristics in cross-sectional data could result from any of several causal relationships.

Retailers' knowledge of tobacco harm reduction following the introduction of a new brand of smokeless tobacco.

BACKGROUND: Tobacco retailers are potential public health partners for tobacco harm reduction (THR). THR is the substitution of highly reduced-risk nicotine products, such as smokeless tobacco (ST) or pharmaceutical nicotine, for cigarettes. The introduction of a Swedish-style ST product, du Maurier snus (dMS) (Imperial Tobacco Canada Limited), which was marketed as a THR product, provided a unique opportunity to assess retailers' knowledge. This study examined retailers' knowledge of THR and compliance with recommendations regarding tobacco sales to young adults. METHODS: Male researchers, who may have looked younger than 18 years old, visited 60 stores in Edmonton that sold dMS. The researchers asked the retailers questions about dMS and its health risks relative to those from other tobacco products. They also attempted to purchase dMS to ascertain whether retailers would ask for identification to verify that they were at least 18 years old. RESULTS: Overall, the retailers were only moderately knowledgeable about THR and the differences between dMS and other tobacco products. About half of the retailers correctly indicated that snus is safer than cigarettes; half of whom knew it is safer because it is smoke-free. Fifty percent incorrectly believed that snus causes oral cancer. Less than fifty percent indicated that dMS differs from chewing tobacco because it is in pouches and is used without spitting or chewing (making it more promising for THR). Most (90%) of the retailers asked the researchers for identification when selling dMS. CONCLUSION: Tobacco retailers are potentially important sources of information about THR, particularly since there are restrictions on the promotion of all tobacco products (regardless of the actual health risks) in Canada. This study found that many retailers in Edmonton do not know the relative health risks of different tobacco products and are therefore unable to pass on accurate information to smokers.

Exposure to Helicobacter pylori-positive siblings and persistence of Helicobacter pylori infection in early childhood.

OBJECTIVES: Cross-sectional studies suggest that Helicobacter pylori may be transmitted between siblings. The present study aimed to estimate the effect of an H pylori-infected sibling on the establishment of a persistent H pylori infection. MATERIALS AND METHODS: The authors used data collected from a Texas-Mexico border population from 1998 to 2005 (the "Pasitos Cohort Study"). Starting at age 6 months, H pylori and factors thought to be associated with H pylori were ascertained every 6 months for participants and their younger siblings. Hazard ratios were estimated from proportional hazards regression models with household-dependent modeling. RESULTS: Persistent H pylori infection in older siblings always preceded persistent infection in younger siblings. After controlling for mother's H pylori status, breast-feeding, antibiotic use, and socioeconomic factors, a strong effect was estimated for persistent H pylori infection in an older sibling on persistent infection in a younger sibling (hazard ratio 7.6, 95% confidence interval 1.6-37], especially when the difference in the age of the siblings was less than or equal to 3 years (hazard ratio 16, 95% confidence interval 2.5-112). CONCLUSIONS: These results suggest that when siblings are close in age, the older sibling may be an important source of H pylori transmission for younger siblings.

Dichotomization: 2 x 2 (x2 x 2 x 2...) categories: infinite possibilities.

BACKGROUND: Consumers of epidemiology may prefer to have one measure of risk arising from analysis of a 2-by-2 table. However, reporting a single measure of association, such as one odds ratio (OR) and 95% confidence interval, from a continuous exposure variable that was dichotomized withholds much potentially useful information. Results of this type of analysis are often reported for one such dichotomization, as if no other cutoffs were investigated or even possible. METHODS: This analysis demonstrates the effect of using different theory and data driven cutoffs on the relationship between body mass index and high cholesterol using National Health and Nutrition Examination Survey data. The recommended analytic approach, presentation of a graph of ORs for a range of cutoffs, is the focus of most of the results and discussion. RESULTS: These cutoff variations resulted in ORs between 1.1 and 1.9. This allows investigators to select a result that either strongly supports or provides negligible support for an association; a choice that is invisible to readers. The OR curve presents readers with more information about the exposure disease relationship than a single OR and 95% confidence interval. CONCLUSION: As well as offering results for additional cutoffs that may be of interest to readers, the OR curve provides an indication of whether the study focuses on a reasonable representation of the data or outlier results. It offers more information about trends in the association as the cutoff changes and the implications of random fluctuations than a single OR and 95% confidence interval.

Debunking the claim that abstinence is usually healthier for smokers than switching to a low-risk alternative, and other observations about anti-tobacco-harm-reduction arguments.

Nicotine is so desirable to many people that when they are given only the options of consuming nicotine by smoking, with its high health costs, and not consuming nicotine at all, many opt for the former. Few smokers realize that there is a third choice: non-combustion nicotine sources, such as smokeless tobacco, electronic cigarettes, or pharmaceutical nicotine, which eliminate almost all the risk while still allowing consumption of nicotine. Widespread dissemination of misleading health claims is used to prevent smokers from learning about this lifesaving option, and to discourage opinion leaders from telling smokers the truth. One common misleading claim is a risk-risk comparison that has not before been quantified: A smoker who would have eventually quit nicotine entirely, but learns the truth about low-risk alternatives, might switch to an alternative instead of quitting entirely, and thus might suffer a net increase in health risk. While this has mathematical face validity, a simple calculation of the tradeoff -- switching to lifelong low-risk nicotine use versus continuing to smoke until quitting -- shows that such net health costs are extremely unlikely and of trivial maximum magnitude. In particular, for the average smoker, smoking for just one more month before quitting causes greater health risk than switching to a low-risk nicotine source and never quitting it. Thus, discouraging a smoker, even one who would have quit entirely, from switching to a low-risk alternative is almost certainly more likely to kill him than it is to save him. Similarly, a strategy of waiting for better anti-smoking tools to be developed, rather than encouraging immediate tobacco harm reduction using current options, kills more smokers every month than it could possibly ever save.

Smokeless tobacco: the epidemiology and politics of harm.

The health burden from tobacco smoking results almost entirely from inhalation of the components of smoke, although this is not widely known. The primary benefit of smoking is nicotine delivery, but nicotine can be obtained without combustion. Thus there is potential for tobacco harm reduction (THR), the substitution of lower-risk nicotine products for smoking. Epidemiological evidence suggests that smokeless tobacco causes about one one-hundredth the health risk of smoking. Despite the practice of harm reduction being widely accepted in public health, however, THR has faced fierce opposition from antitobacco activists. These activists have effectively misled the public about what aspect of smoking cigarettes causes the harm, convincing them that nicotine and tobacco themselves are harmful, ignoring the smoke. In the interests of promoting public health and rescuing science from politics, experts on inhalation hazards and health could play an important role in educating the public and policy makers about THR.

Survey of smokers' reasons for not switching to safer sources of nicotine and their willingness to do so in the future.

Despite the well-known risks of smoking, policy, social pressure, and accessible cessation programs, tens of millions of North American adults continue smoking rather than quitting or switching to less harmful non-combustion nicotine products. We surveyed people smoking in public in Edmonton, Canada (n = 242, year = 2007) to investigate smokers' reasons for resisting switching to low-risk nicotine sources. 43% had used low-risk products (mostly pharmaceutical nicotine). 75% indicated willingness to consider switching to low-risk products. Smokers cited similar reasons for not switching to smokeless tobacco and pharmaceutical nicotine, largely based on misinformation. Accurate risk information may lead many to try low-risk nicotine products.

Antibiotics taken for other illnesses and spontaneous clearance of Helicobacter pylori infection in children.

PURPOSE: Factors that determine persistence of untreated Helicobacter pylori (H. pylori) infection in childhood are not well understood. We estimated risk differences for the effect of incidental antibiotic exposure on the probability of a detected clearance at the next test after an initial detected H. pylori infection. METHODS: The Pasitos Cohort Study (1998-2005) investigated predictors of H. pylori infection in children from El Paso, Texas, and Juarez, Mexico. Children were screened for infection at 6-month target intervals from 6 to 84 months of age, using the 13C-urea breath test corrected for body-size-dependent variation in CO2 production. Exposure was defined as courses of any systemic antibiotic (systemic) or those with anti-H. pylori action (HP-effective) reported for the interval between initial detected infection and next test. Binomial regression models included country of residence, mother's education, adequacy of prenatal care, age at infection, and interval between tests. RESULTS: Of 205 children with a test result and antibiotic data following a detected infection, the number of children who took > or =1 course in the interval between tests was 74 for systemic and 33 for HP-effective. The proportion testing negative at the next test was 66% for 0 courses, 72% for > or =1 systemic course, and 79% for > or =1 HP-effective course. Adjusted risk differences (95%CI) for apparent clearance, comparing > or =1 to 0 courses were 10% (1-20%) for systemic and 11% (0-21%) for HP-effective. CONCLUSIONS: Incidental antibiotic exposure appears to influence the duration of childhood H. pylori infection but seems to explain only a small portion of spontaneous clearance.

Interpreting data in the face of competing explanations: assessing the hypothesis that observed spontaneous clearance of Helicobacter pylori was all measurement error.

BACKGROUND: We previously reported frequent transient positive urea breath tests for Helicobacter pylori infection in a cohort study of young children, and interpreted this as evidence of frequent spontaneous clearance of this infection. In a commentary, Perry and Parsonnet suggested that all transient positive tests we observed could be false positives and thus the appearance of transient infection could be an artifact. METHODS: We address the logic of the implicit argument that the transient infections were an artifact and we demonstrate a simple likelihood calculation to assess the plausibility of competing explanations. We calculate the likelihood of observing our data based on a range of clearance and measurement error rates and then how this updates a set of prior beliefs. RESULTS: The likelihood calculations and resulting posterior probabilities show strong support for the hypothesis of spontaneous clearance, after allowing for measurement error, even starting with a very high prior probability of no spontaneous clearance. The scenario Perry and Parsonnet present is incompatible with our data, and thus not a plausible explanation for our observations. Attributing most observed transient infections to measurement error requires assuming a high false positive rate and a very low infection rate and/or a high false negative rate, alternatives that are not supported by evidence. CONCLUSIONS: Acknowledgment of plausible levels of measurement error does not change the strong support our data provides for the hypothesis of frequent transient infection. Debate about competing explanations for observations should be accompanied by quantitative analysis that shows which is more plausible. We demonstrate one method for doing such analysis.

(Errors in statistical tests)3.

In 2004, Garcia-Berthou and Alcaraz published "Incongruence between test statistics and P values in medical papers," a critique of statistical errors that received a tremendous amount of attention. One of their observations was that the final reported digit of p-values in articles published in the journal Nature departed substantially from the uniform distribution that they suggested should be expected. In 2006, Jeng critiqued that critique, observing that the statistical analysis of those terminal digits had been based on comparing the actual distribution to a uniform continuous distribution, when digits obviously are discretely distributed. Jeng corrected the calculation and reported statistics that did not so clearly support the claim of a digit preference. However delightful it may be to read a critique of statistical errors in a critique of statistical errors, we nevertheless found several aspects of the whole exchange to be quite troubling, prompting our own meta-critique of the analysis.The previous discussion emphasized statistical significance testing. But there are various reasons to expect departure from the uniform distribution in terminal digits of p-values, so that simply rejecting the null hypothesis is not terribly informative. Much more importantly, Jeng found that the original p-value of 0.043 should have been 0.086, and suggested this represented an important difference because it was on the other side of 0.05. Among the most widely reiterated (though often ignored) tenets of modern quantitative research methods is that we should not treat statistical significance as a bright line test of whether we have observed a phenomenon. Moreover, it sends the wrong message about the role of statistics to suggest that a result should be dismissed because of limited statistical precision when it is so easy to gather more data.In response to these limitations, we gathered more data to improve the statistical precision, and analyzed the actual pattern of the departure from uniformity, not just its test statistics. We found variation in digit frequencies in the additional data and describe the distinctive pattern of these results. Furthermore, we found that the combined data diverge unambiguously from a uniform distribution. The explanation for this divergence seems unlikely to be that suggested by the previous authors: errors in calculations and transcription.

Switching to smokeless tobacco as a smoking cessation method: evidence from the 2000 National Health Interview Survey.

BACKGROUND: Although smokeless tobacco (ST) use has played a major role in the low smoking prevalence among Swedish men, there is little information at the population level about ST as a smoking cessation aid in the U.S. METHODS: We used the 2000 National Health Interview Survey to derive population estimates for the number of smokers who had tried twelve methods in their most recent quit attempt, and for the numbers and proportions who were former or current smokers at the time of the survey. RESULTS: An estimated 359,000 men switched to smokeless tobacco in their most recent quit attempt. This method had the highest proportion of successes among those attempting it (73%), representing 261,000 successful quitters (switchers). In comparison, the nicotine patch was used by an estimated 2.9 million men in their most recent quit attempt, and almost one million (35%) were former smokers at the time of the survey. Of the 964,000 men using nicotine gum, about 323,000 (34%) became former smokers. Of the 98,000 men who used the nicotine inhaler, 27,000 quit successfully (28%). None of the estimated 14,000 men who tried the nicotine nasal spray became former smokers. Forty-two percent of switchers also reported quitting smoking all at once, which was higher than among former smokers who used medications (8-19%). Although 40% of switchers quit smoking less than 5 years before the survey, 21% quit over 20 years earlier. Forty-six percent of switchers were current ST users at the time of the survey. CONCLUSION: Switching to ST compares very favorably with pharmaceutical nicotine as a quit-smoking aid among American men, despite the fact that few smokers know that the switch provides almost all of the health benefits of complete tobacco abstinence. The results of this study show that tobacco harm reduction is a viable cessation option for American smokers.

Correspondence between Helicobacter pylori antibodies and urea breath test results in a US-Mexico birth cohort.

The uncertain accuracy of methods for detecting Helicobacter pylori infection in young children complicates research on this infection in early life. The aim of the present report was to describe the correspondence between positive serology and positive urea breath test (UBT) in children followed from age 0 to 24 months in the Pasitos Cohort Study, conducted along the US-Mexico border at El Paso and Juarez. Children were recruited before birth during 1998-2000 and examined at target ages of 6, 12, 18 and 24 months. H. pylori infection was detected using an enzyme immunoassay for serum immunoglobulin G antibodies and the (13)C-urea breath test corrected for age-dependent variation in CO(2) production. Of 472 children, 125 had one or more positive UBT results and 46 had one or more positive serology results. The prevalence of H. pylori infection at target ages of 6, 12, 18 and 24 months was 7%, 14%, 16% and 19%, respectively, by UBT and 8%, 2%, 3% and 3%, respectively, by serology. Few (<1%) of those tested on both tests were positive on both at any age. Among UBT-positive children, 6% were concurrently seropositive and 6% became seropositive later. Because UBT positivity cut points were selected to minimise false positives, these results suggest that H. pylori infection occurred frequently in this cohort, but rarely produced detectable antibodies. For clinical or epidemiological investigations, serology should not be used as the sole method for detecting H. pylori infection in children aged 2 years or less.

Warning: Anti-tobacco activism may be hazardous to epidemiologic science.

This commentary accompanies two articles submitted to Epidemiologic Perspectives & Innovations in response to a call for papers about threats to epidemiology or epidemiologists from organized political interests. Contrary to our expectations, we received no submissions that described threats from industry or government; all were about threats from anti-tobacco activists. The two we published, by James E. Enstrom and Michael Siegel, both deal with the issue of environmental tobacco smoke. This commentary adds a third story of attacks on legitimate science by anti-tobacco activists, the author's own experience. These stories suggest a willingness of influential anti-tobacco activists, including academics, to hurt legitimate scientists and turn epidemiology into junk science in order to further their agendas. The willingness of epidemiologists to embrace such anti-scientific influences bodes ill for the field's reputation as a legitimate science.