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On June 28, 2007 the Seattle Times published an article about use of antidepressants by women who are pregnant. The article downplayed the risks to a developing fetus attributable to antidepressant use that have been well-documented in several previous studies. The Times’ take-home message was that the U.S. Centers for Disease Control and Prevention believes study results are “generally reassuring” it is safe for pregnant women to continue taking drugs such as GlaxoSmithKline’s PAXIL. On the same day, June 28, 2007, The Times also published an article concerning exposure to secondhand smoke for pregnant women and the alleged risks that such exposure creates for a developing a fetus. That University of Washington study included data that purportedly demonstrates nicotine ingested through exposure to Environmental Tobacco Smoke (ETS) is strongly associated with later behavior problems in children and recommends further study on the subject. Those familiar with tobacco control advocacy are also aware that GlaxoSmithKline is the distributor for Nicotine Replacement Therapy (NRT) delivery device products NicoDerm CQ patches, Nicorette gum, and Commit lozenges.
 

The problems with the two news reports by the Seattle Times are manifold. Most glaringly apparent is the fact that many of the birth defects attributed to ETS by tobacco control advocates and in part by the University of Washington study are also attributed by other researchers to use of anti-depressants during pregnancy. Despite this confounding factor, the University of Washington study authors report no controls as to whether subjects were using prescribed antidepressants during their pregnancy. Moreover, if nicotine ingested due to ETS exposure is the alleged culprit that raises the risks of birth defects or behavioral problems then considerably greater quantities of nicotine ingested through use of NRT products necessarily imposes higher risks to fetal development. The University of Washington study authors also report no controls for use NRT products by study participants. In addition, careful examination of the University of Washington study data reveals that the calculations to establish an alleged strong association between ETS exposure and later behavioral problems for children are based on a numeric value assigned by the authors, to apparently quantify the amount of nicotine allegedly ingested. That is accomplished in the study by assigning a numeric value that corresponds to the mother being an occasional smoker, even though the participants in the secondhand smoke study declare themselves to be nonsmokers. In contrast, the antidepressant studies quantify to varying degrees the specific medications and dosage used plus duration of use by pregnant mothers. 
 

We observe the curious phenomenon of University of Washington study authors inventing analysis criteria and calculation variables concerning ETS to “prove” an association that does not plausibly exist, while ignoring well-documented and highly relevant confounding factors. As will become apparent in the policy discussion section of this work, many known causal factors that directly contribute to later child behavior problems are created or strongly amplified by tobacco control public advocacy. We therefore observe the repugnant pattern of conduct of tobacco control advocates and some university researchers apparently working hand-in-glove to document and report as legitimate scientific inquiry the adverse affects of anti-tobacco activism on families and children to justify its continued, aggressive expansion. Earnest social policy researchers who are genuinely concerned about legitimate public health policy should be alarmed and concerned about that pattern of conduct. Such conduct adversely influences the integrity of governing institutions and diminishes the credibility of university research, to say nothing of its negative consequences on children.
 

Downplaying the risks of antidepressants and pregnancy tends to increase use of such drugs by prospective mothers who may otherwise be sufficiently concerned to abstain. Adding yet another alleged risk of exposure to ETS, now for unborn children, tends to increase sales of Nicotine Replacement Therapy for use in “Smoke Free” environments advocated by tobacco control advocates who are directly funded by pharmaceutical special-interests. News articles published by The Times on June 28, 2007 therefore serve to increase the sale of both antidepressants and Nicotine Replacement Therapy products. It is transparent that increased drug sales also equals increased media advertising revenues. Notably, GlaxoSmithKline has two dogs in this fight about antidepressants and ETS: the first is named PAXIL and the second mongrel goes by aliases such as NicoDerm and Nicorette. We observe mainstream media aggressively peddling Social Marketing drug advertising as newsworthy content.

Consider the potential impact of the above described two news stories on a prospective mother suffering from depression who also smokes and is genuinely concerned about her baby’s well being. What is the predictable course of events that would unfold, were she to receive a recommendation from her physician to medicate depression and smoking conditions? The obvious response would be to continue use of PAXIL or a similar drug and begin using NicoDerm CQ Nicotine Replacement Therapy for smoking cessation. Just as physicians consider risk/reward factors in prescribing antidepressants they could also do so for Nicotine Replacement Therapy. According to the antidepressant and ETS studies that the Seattle Times reports about on June 28, 2007, however, that prospective mother would also dramatically increase the risks of adverse fetal development and later child behavior problems through use of two products strongly associated with those symptoms. Apparently, even babies in the womb are no longer safe from pharmaceutical sales practices.
 

Finally, the University of Washington study specifically attributes ETS exposure for pregnant women to home and work environments. The study reports an interview question about ETS exposure that states and example of “For instance partner at home, worked in a restaurant or bar where smoking regularly took place.” The consistency of the University of Washington study’s characterization of places where ETS exposure occurs transparently corresponds to the current tobacco control agenda to expand smoking bans to private residences, bars and restaurants. Accordingly, we also observe what appear to be university research studies-on-demand produced in a timely and efficient manner to support current pharmaceutical Social Marketing themes of the day to ban smoking in restaurants and bars. But at what cost to families, children and consumers are those mercantile themes employed?
 

The Times’ two news articles published on June 28, 2007 therefore merit careful examination. Such examination is necessary for those who are genuinely concerned about the integrity of our governing institutions and the fast-waning credibility university research. This work begins that examination by first looking at several previously-published facts about antidepressants and fetal development. We then proceeding to a detailed look at data in the University of Washington’s study about ETS and child development. From that point this commentary discusses conflicting news and views, a few important points about Environmental Tobacco Smoke and related public policy implications.
 

Pregnancy and Antidepressants 
 

From the Seattle Times, June 28, 2007, “Antidepressants’ Link to Birth Defects Small,” by Seattle Times News Service:

”Two new studies suggest that taking antidepressants during the first trimester of pregnancy may slightly increase the risk of some rare birth defects. But the studies, published in today's New England Journal of Medicine, found that the overall risks are quite small. And scientists cautioned women against stopping treatment, saying untreated depression can be even more of a danger to their offspring. "Overall, our results are generally reassuring with respect to the use of antidepressants during pregnancy," said Jennita Reefhuis, an epidemiologist at the Centers for Disease Control and Prevention (CDC) and one of the study authors. The studies were designed to find out if a class of drugs known as SSRIs (selective serotonin-reuptake inhibitors) posed a risk to developing fetuses early in pregnancy. They were prompted, in part, by a 2005 study suggesting that Paxil increased the rate of heart defects from about 1 percent to 2 percent. Other drugs in that class include Prozac, Zoloft and Celexa. Paxil maker GlaxoSmithKline sparked concern about SSRIs by issuing an alert in 2005 about possible heart defects in newborns whose mothers took Paxil early in pregnancy. The Food and Drug Administration then added its own warning. Together, the two studies looked at 19,471 newborns with birth defects and 9,952 without them. They then considered what SSRIs the mothers in both groups took during the first three months of pregnancy and mapped the patterns of birth defects. Neither study was able to tie SSRIs as a group to heart defects. However, one of the reports associated Zoloft with a nearly sixfold increase in cases of omphalocele, in which intestines or other abdominal organs protrude from the navel. The birth defect is rare, occurring in one of every 5,000 births, according to federal statistics. . . . The other study linked antidepressant use to a doubling of the risk of three congenital problems: anenecephaly, a defect in which a large portion of the brain and skull is missing; craniosynostosis, in which connections between skull bones close prematurely; and intestinal defects. The researchers, from the CDC and the University of British Columbia in Vancouver, B.C., cautioned that their findings were based on a handful of cases. "The take-home message is that we are talking about very small risks," said University of California, San Diego, epidemiologist Christina Chambers, who has studied the effects of antidepressants but wasn't involved in the new research. Experts say every pregnancy carries about a 3 percent chance of serious birth defects. About 10 percent of women experience depression during pregnancy, according to one of the studies. Left untreated, a woman's depression could lead to smoking, drinking and other behaviors that can harm fetuses. It also could lead to poor care, turmoil at home, a weaker maternal bond and other problems for a newborn. "The fetus and the newborn are almost always worse off if the mom is depressed than if ... exposed to the vast majority of antidepressants," said Dr. Stephan Quentzel, a psychiatrist who treats pregnant women at Beth Israel Medical Center in New York. Last year, a separate study linked SSRIs taken late in pregnancy to a lung disorder in newborns. The latest studies do not consider that disorder, known as persistent pulmonary hypertension.” (Underline, italic added.) 
 

From CBS, The Early Show, February 9, 2006, “Antidepressants During Pregnancy,” discussion with Dr. Emily Senay: 
 

“(CBS) Two new studies have linked the use of Prozac and other similar antidepressants during pregnancy to a higher risk of complications, such as serious respiratory disease, in newborns. The research involved antidepressants known as selective serotonin reuptake inhibitors, or SSRIs, which include familiar names like Prozac, Paxil and Zoloft. As Dr. Emily Senay reported on The Early Show, a study published in the New England Journal of Medicine looked at women who took these drugs late in pregnancy and found that their babies were six times more likely to develop a complication known as persistent pulmonary hypertension — which can, in rare occasions, be fatal. Another study published in this month's Archives of Pediatrics and Adolescent Medicine found that nearly one-third of newborns whose mothers took that same class of antidepressants during pregnancy experienced neonatal abstinence syndrome, which means they had withdrawal symptoms.” 
 

The first learning point about pharmaceutical studies-on-demand to support Social Marketing emerges. If studies such as the February 2006 report immediately above show that babies are “six times more likely to develop a complication known as persistent pulmonary hypertension” then produce a later study that quotes a Centers for Disease Control & Prevention co-author and reports "Overall, our results are generally reassuring with respect to the use of antidepressants during pregnancy." When CDC’s reassuring report is published on June 28, 2007 that mothers can continue to medicate depression with anti-depressants while pregnant that “The latest studies do not consider that disorder, known as persistent pulmonary hypertension” is mentioned as an afterthought. In short, exclude highly relevant information to produce new study conclusions that supports increased drug sales.  
 

From MayoClinic.com, “Antidepressants: Are They Safe during Pregnancy?” 
 

“Are some types of antidepressants safer than others? So far, bupropion (Wellbutrin) has not been associated with risks to a developing baby. But researchers have identified various risks with other types of antidepressants. For example:

 

• Paxil. Paroxetine (Paxil) — a type of antidepressant known as a selective serotonin reuptake inhibitor (SSRI) — has been linked to fetal heart defects when it's taken during the first three months of pregnancy. The American College of Obstetricians and Gynecologists recommends avoiding Paxil during pregnancy, if possible.
• Other selective serotonin reuptake inhibitors. Taking other SSRIs — including citalopram (Celexa), fluoxetine (Prozac) and sertraline (Zoloft) — in the last half of pregnancy increases the risk of a rare but serious lung problem known as persistent pulmonary hypertension of the newborn. This condition occurs when a newborn's circulation system doesn't adapt to breathing outside the womb. For some women, however, the benefits of continuing these drugs may outweigh the risks.
• Tricyclic antidepressants. These older antidepressants — including amitriptyline and nortriptyline (Aventyl, Pamelor) — are generally discouraged during pregnancy in favor of newer, more effective medications. Potential risks of tricyclic antidepressants to a baby may include damage to the central nervous system, physical deformities or developmental delays.

 

Are there any other risks for the baby? If you take an SSRI antidepressant throughout pregnancy or during the last trimester, your baby may experience temporary withdrawal symptoms at birth — including tremors, gastrointestinal problems, sleep disturbances and high-pitched cries.” (Underline added.)

 

Fetal heart defects, pulmonary hypertension, damage to the central nervous system, physical deformities, developmental delays (perhaps including ADHD) and withdrawal symptoms at birth. Such are the reported consequences of mothers using antidepressants during pregnancy.

 

From BabyCenter.com, December 2006, Ask the Experts, “Is It Safe To Take Antidepressants During Pregnancy?” by pharmacist clinical specialist Gerald Briggs: 
 

“Question: Is it safe to take any antidepressants during pregnancy?

Answer: Recent research is casting doubts on the safety of the drugs most commonly prescribed for depression — selective serotonin reuptake inhibitors (SSRIs) and some closely related drugs. SSRIs include fluoxetine (Prozac), paroxetine (Paxil), citalopram (Celexa), and sertraline (Zoloft), among others. Three closely related drugs are duloxetine (Cymbalta), nefazodone (Serzone), and venlafaxine (Effexor). . . . Past studies found no significant difference in the rates of miscarriages and stillbirth between women who took SSRIs and women who didn't. An older class of drugs known as tricyclics, which includes amitriptyline (Elavil) and imipramine (Tofranil), has also been considered safe, as have newer drugs such as bupropion (Wellbutrin). However, the most recent research analysis, published in 2006, showed that SSRIs are associated with a small increase in the risk of miscarriage. Another analysis showed that babies whose mothers take SSRIs during pregnancy may be more likely to be born prematurely, have low birth weight, spend time in a neonatal intensive care unit, and have trouble adapting to life outside the womb. This was particularly the case for babies of women who were also taking other drugs for mental conditions or who smoked or drank alcohol. Recent studies have noted withdrawal symptoms in nearly a third of newborns whose mothers were treated with SSRIs near the end of their pregnancy. The most commonly reported symptoms included tremors, convulsions, irritability, and increased crying.” (Underline added.)  
 

Premature birth, low birth weight, longer neonatal intensive care, and having trouble adapting to life outside the womb are also reported as fetal consequences of antidepressant use by mothers during pregnancy. However, many of those consequences are also attributed to smoking during pregnancy and Environmental Tobacco Smoke by tobacco control advocates. Are those antidepressant consequences important confounding factors for tobacco control research claims concerning smoking and now exposure to ETS? 
 

Pregnancy and Secondhand Smoke 
 

Needless to say, The Times’ report about pregnant mothers’ exposure to ETS is not reassuring. From the Seattle Times, June 28, 2007, “Secondhand Smoke May Affect Brain of Fetus:”
 

“Pregnant women who are chronically exposed to secondhand smoke may have children who are at greater risk of problems related to attention and emotion, University of Washington researchers believe. In a study released Wednesday, scientists found that children who have such psychological problems have a higher frequency of them -- or more severe troubles -- if their mothers were regularly exposed to tobacco smoke while pregnant. Those troubles include Attention Deficit Hyperactivity Disorder (ADHD), aggressive behavior, defiance and a behavior pattern called conduct disorder, which can include truancy, fighting, failing in school, substance abuse, theft and property destruction. "Parents should be really aware of the [fetal] brain development going on during pregnancy," said psychologist Lisa Gatze-Kopp, lead investigator of the study, which was reported in the current issue of the journal Child Psychiatry and Human Development. . . . Mothers exposed to nicotine -- the smoking mothers and the secondhand smoke mothers -- generally had children with more severe problems with attention or more severe emotional and behavioral problems than the children of nonsmokers, said Gatze-Kopp. She said the findings could extend to all children whose mothers were exposed to tobacco smoke during pregnancy. Gatze-Kopp said the data for the study were taken from a larger study of the relationship between depression and conduct disorder. She granted that the smoking study is as a small sample and needs additional research. . . . Previous research, cited in a 2006 U.S. Surgeon General's report, found that secondhand smoke may increase the risk of miscarriages and instances of babies with low birth weights. Gatze-Kopp said pregnant women should avoid any chronic exposure to secondhand smoke. "Mothers should know: 'If it's not safe for me, it's not safe for my baby,' " she said.” (Underline added.)

 

Gatzke-Kopp [according to UW sources the Seattle Times misspelled her name] do not reference fetal exposure to nicotine due to pregnant women using NicoDerm CQ patches to allegedly quit smoking while pregnant. NicoDerm CQ is manufactured for distributor GlaxoSmithKline by Johnson & Johnson subsidiary ALZA Corp. In comparison to the infinitesimal amount of nicotine that could possibly be ingested through exposure to secondhand smoke, the steady stream of nicotine delivered to a prospective mother’s blood stream by the patch mega tons.

 

The news story was widely published by June 29, 2007, including a United Press International report, “ADHD Linked to Prenatal Smoke Exposure,” published by Consumer Health Daily Briefing:

 

“A mother's exposure to tobacco smoke during pregnancy has been linked to attention deficit hyperactivity disorder and conduct disorder, says a U.S. study. The study, published in Child Psychiatry and Human Development, showed that those whose mothers had been exposed to tobacco smoke while pregnant -- either by smoking or by being around smokers -- did not show more symptoms of depression or anxiety than those children whose mothers were not exposed to smoke. However, University of Washington psychologists Lisa Gatzke-Kopp and Theodore Beauchaine did find that the children whose mothers were exposed to smoke showed more symptoms of ADHD and conduct disorder. "This is a matter of severity," Gatzke-Kopp said in a statement. "Children with these disorders have a range of behaviors that stretch from problematic to severe. It is a continuum based on the number of symptoms, and children who were exposed to smoke exhibited more symptoms." The Seattle researchers believe the nicotine in tobacco may affect brain development during pregnancy. (Underline added.)

 

Do we conclude from the above United Press International report that nicotine in patches, gums, lozenges, sprays and inhalers has no effect on fetal brain development? It bears repeating that pulmonary hypertension, problems with development of the central nervous systems, premature birth, low birth weight, neonatal intensive care, and having trouble adapting to life outside the womb are reported as fetal consequences of antidepressant use by mothers during pregnancy. Many of those symptoms are also attributed to Environmental Tobacco Smoke by tobacco control advocates.  
 

The full text of the original study “Direct and Passive Prenatal Nicotine Exposure and the Development of Externalizing Psychopathology” co-authored by Lisa M. Gatzke-Kopp and Theodore P. Beauchaine provides some interesting insights. The study was reportedly funded by grant R01 MH63699 awarded by the National Institute of Mental Health to Theodore P. Beauchaine. The abstract for that study says: 
 

“The association between maternal smoking during pregnancy and childhood antisocial outcomes has been demonstrated repeatedly across a variety of outcomes. Yet debate continues as to whether this association reflects a direct programming effect of nicotine on fetal brain development, or a phenotypic indicator of heritable liability passed from mother to child. In the current study, we examine relations between maternal smoking and child behavior among 133 women and their 7–15-year-olds, who were recruited for clinical levels of psychopathology. In order to disentangle correlates of maternal smoking, women who smoked during pregnancy were compared with (a) those who did not smoke, and (b) those who did not smoke but experienced significant second-hand exposure. Second-hand exposure was associated with increased externalizing psychopathology in participant mothers’ offspring. Moreover, regression analyses indicated that smoke exposure during pregnancy predicted conduct disorder symptoms, over and above the effects of income, parental antisocial tendencies, prematurity, birth weight, and poor parenting practices. This is the first study to extend the findings of externalizing vulnerability to second hand smoke exposure.” (Underline, italic added.) 
 

The above study authored by Gatzke-Kopp and Beauchaine appears to be seriously flawed for at least six very important reasons:
 

1. Those who read the study in full through the above link will find no reference for controls related to prospective mother’s use of antidepressants during pregnancy. Not only could those drugs have affects on fetal development that are confounding factors for the University of Washington study but the neurosis of the mothers that mandates their use could also predictably influence child behavior development.

 

2. Readers who search the entire study will also find no reference to controls for prospective mothers’ use of “Smoke Free” pharmaceutical Nicotine Replacement Therapy (NRT) nicotine delivery devices such as patches, gums, lozenges, nasal sprays and inhalers. If nicotine in secondhand smoke is the alleged culprit for adverse fetal development then the comparatively massive amounts of nicotine ingested through those devices would have a much larger impact. The NicoDerm CQ and Nicorette boxes distributed by GalxoSmithKline contain the following messages:

 

NicoDerm CQ (2006): “If you are pregnant or breast-feeding, only use this medicine on the advice of your health care provider. Smoking can seriously harm your child. Try to stop smoking without using any nicotine replacement medicine. This medicine is believed to be safer than smoking. However, the risks to your child from this mediation are not fully known.” (Underline added.)

 

Nicorette (2006): “If you are pregnant or breast-feeding, only use this medicine on the advice of your health care provider. Smoking can seriously harm your child. Try to stop smoking without using any nicotine replacement medicine. This medicine is believed to be safer than smoking. However, the risks to your child from this mediation are not fully known.” (Underline added.)

 

Nicorette (2000): “Nicotine can increase your baby’s heart rate; if you are pregnant or nursing a baby, seek the advice of a health professional before using this product.”

 

NOTE: In 2000 the active ingredient in Nicorette was clearly identified in the warnings for prospective mothers as “Nicotine” and mothers were warned that the substance could increase their baby’s heart rate – two facts a layperson mother could reasonably understand. By 2006 the identical warnings for Nicorette and NicoDerm CQ materially changed: “Nicotine” became “medicine;” warnings concerning the baby’s heart were removed; and the “medicine” was believed to be safer than smoking. The warnings changed from facts a layperson mother could reasonably understand to medical terminology and conclusions a prospective mother would necessarily trust her health care provider to interpret. A risk to the developing child that is not “fully known” could just as easily be interpreted by a layperson to be minimal and therefore justify use of NRT as it could be deemed sufficiently great to avoid using the product.

 

Consider the preceding warning messages and necessary reliance on physician’s advice by pregnant mothers in light of a recent article published by the journal Tobacco Control (2006;15:447-45), “The US Public Health Service ‘treating tobacco use and dependence clinical practice guidelines, as a legal standard of care:’” 

 

“There are four items that need to be considered in negligence torts: legal duty, a breach of that duty, causal relationship between breach and injury, and damages. . . . Although each case of medical malpractice depends on a multitude of factors unique to individual cases, a court could have sufficient basis to find that the failure to adequately treat the main cause of preventable disease and death in the US qualifies as a violation of the legal duty that doctors and hospitals owe to patients habituated to tobacco use and dependence.” (Underline added.)

 

Facing threats of malpractice law suits, what can physicians reasonably be expected to do, recommend or not recommend Nicotine Replacement Therapy for pregnant women? Add together changing the warnings on NRT product boxes to include a general belief that NRT is “safer” than smoking, downplaying the risks of antidepressant use while pregnant, creating new risks from ETS that are based on researchers inventing numeric values to produce study results, and escalating the malpractice risk for physicians that do not recommend or prescribe Nicotine Replacement therapy for patients who smoke. What emerges is what serves the economic mercantile interests of pharmaceuticals at patient, consumer and credible researchers’ expense: increased sales of both antidepressants and Nicotine Replacement therapy to pregnant women.

 

3. The confounding factors attributable to the absence of the two above controls – use of antidepressants and NRT during pregnancy -- may account for a curious phenomenon reported in the full text of the study: in some cases the development problems for children whose mother was exposed to secondhand smoke are higher than those of mothers who are reported smokers, which is implausible. This flaw in the study points directly to the probable impact of the first two fatal flaws. Do the study data in fact reveal the impact of confounding factors not associated with exposure to Environmental Tobacco Smoke?

 

4. Critical calculations in the study that produce the statistical results associating ETS with adverse fetal development are not based on any quantification of actual ETS exposure. Much like the Otsuka study that purportedly established a causal relationship between exposure to ETS and heart disease, this study also does not measure or quantify exposure to ETS. Instead, the authors state:

 

“Second hand exposure was coded as one because there was no reliable way to quantify exposure more specifically.”

 

Unknown ETS exposure therefore expediently equals firsthand smoking by study participants who state they do not and have not use cigarettes. In contrast, anti-depressant studies customarily identify specific medications, quantify the dosage used, and record the term of use during pregnancy. Exposure to the alleged causal agent is explicitly quantified. Absent quantification of the magnitude of exposure any conclusions regarding the impact of ETS on fetal development become rank speculation. That problem is compounded by the authors’ assignment of a numeric value of one, which according to the study criteria is “occasional smoking as one, smoking less that half a pack a day classified as two . . .” That numeric assignment is particularly curious in light of the statement in the study that the secondhand smoke exposure participant group consisted of “16 women who endorsed exposure at home or at work for the second or third trimester of pregnancy and also denied any personal use of cigarettes (even occasional use.) The preceding underline was added by this author. The study therefore falsely attributes occasional smoking to participants that deny occasional use of cigarettes to reach is ultimate conclusions about secondhand ETS.

 

5. The relative sizes of the three reported study groups are highly imbalanced. Nonsmoking is reported as n = 96, smoking as n = 21 and 2^nd hand exposures as n =  16, for a total of 133. The secondhand smoke exposure group therefore represents a mere 11.33 percent of the total study population. In contrast, antidepressant study populations are often reported to be in the thousands or tens of thousands.

 

6. The study fails to consider or adjust for fifteen years of tobacco control promoting false information about Environmental Tobacco Smoke (ETS). As explained below in policy discussions, that is highly relevant to both the study’s primary conclusions and recommendations for future research. 
 

Critical to evaluating this University of Washington study is the following text from its introduction: 
 

“Maternal smoking during pregnancy is associated with a wide range of externalizing outcomes among exposed children. This adversity is expressed across the lifespan, and includes conditions such as aggression in preschool [1], attention deficit/hyperactivity disorder (ADHD) in childhood [2–4], conduct disorder (CD) and delinquency in adolescence [5, 6] and criminality in adulthood [7]. Behavioral effects have been reported to increase linearly with the number of cigarettes smoked during pregnancy [8]. These associations appear specific to externalizing psychopathology, with no increased risk for internalizing outcomes among exposed children [9, 1]. While this observation has been supported consistently, the association cannot be considered causal, and the exact mechanism(s) through which maternal smoking affects behavioral outcomes remain(s) poorly understood. Retrospective research with human participants is replete with social, biological, and genetic confounds, weakening any assumptions of causality between smoking and externalizing outcomes [10]. (Underline, italic added.) 
 

We have therefore progressed to unknown exposures to ETS, for which a personal smoking figure is inserted, unquestionably causes a child behavioral problem for which credible researchers state the mechanism is poorly understood as to firsthand smoking. Footnote 10 cites in the above excerpt is for a study, “Prenatal Smoking and Early Childhood Conduct Problems,” published August 2004 in the Volume 61, No. 8 edition of the Archives of General Psychiatry (2004;61:836-843).

The abstract for that study, which addresses primary smoking, not Environmental Tobacco Smoke, says: 
 

“Conclusions Observed associations between prenatal smoking and childhood conduct problems are likely to be heavily confounded with other known risks for children's behavioral development. As a result, tests of any causal influence of prenatal smoking must await findings from experimental studies.” (Underline, italic added.) 

We confront the inescapable fact that the University of Washington study reported by the Seattle Times on June 28^th attempts to establish a causal relationship between secondhand ETS exposure and childhood development problems that cannot be established for a mother who personally smokes during her pregnancy. Even by tobacco control’s extremely loose standards for statistical manipulation that is a daunting test. As described below, the University of Washington study authors fail to do so. 

CURRICULUM VITAE for Associate Professor of Psychology Theodore P. Beauchaine at University of Washington lists several studies or articles coauthored with Gatzke-Kopp, who is identified as a student or post doctoral coauthor. Those studies co-authored with Gatze-Kopp tend to focus on youth behavior and contributing factors. According to his resume’, Beauchaine is a virtual rainmaker for grants to UW, including a National Institute of Mental Health grant in the reported amount of $1.4 million. Does the University of Washington measure the credibility of studies published under its banner by the depth and quality of genuinely probative inquiry or the magnitude of researched grants secured by the author?  
 

The following text and table from the University of Washington study is important: 
 

ANOVAs run for each diagnostic measure are presented in Table 1. Significant group differences were found only for externalizing measures of psychopathology, including CBCL attention problems, CBCL aggression, CSI CD, and CSI ADHD. The result for the CSI ODD scale was significant only at the trend level, P = .082. Because the MANOVA including internalizing measures approached significance, follow-up ANOVAs were examined, yet no significant univariate effects were found.

 

Table 1 Group means (and standard deviations) on measures of child psychopathology  

 

Notes. CBCL = Child Behavior Checklist (Achenbach, 1991); CSI = Child Symptom Inventory (Gadow &

Sprafkin, 1997) *P < .05. **P < .01 Child Psychiatry Hum Dev

 

There are two data lines in the above table high-lighted in red italic: CBCL Aggression and CBCL Anxious Depressed. Those items directly relate to crude, blunt-instrument stereotyping by tobacco control advocates, which associate smoking with higher levels of anger and violence. The former (Aggression) shows values for exposure to secondhand smoke (77.56) that are higher than those associated with smoking (77.14). The second, Anxious/Depressed, shows values for both nonsmoking and secondhand smoke (73.52 and 73.44 respectively) that are markedly higher than for smoking (71.57). In fact, the Anxious/Depressed data for nonsmokers is the highest of the three. 
 

Who is most likely to be using prescribed antidepressants: nonsmoking and nonsmoker exposed to ETS mothers whose children have the highest data for feelings of being anxious or depressed or smokers with the lowest? Indeed, the University of Washington study data appear to prove the opposite of what tobacco control claims. Judging by what Beauchaine and Gatzke-Kopp report in the above table, the way to assure offspring that do not exhibit behavior of being anxious or depressed would be to light up. If we believe  the data reported in this University of Washington study we necessarily conclude that nonsmokers have a greater impact on producing aggressive, anxious or depressed children than parents who choose to smoke. The obvious “protective” step to be taken would again be to light up.  
 

Notwithstanding the above factual observations, given the content of conclusions stated in the study abstract, Mr. Bueachaine has undoubtedly found a veritable goldmine of new grants for the University of Washington. The conclusions that he and Ms. Gatzke-Kopp reach not only unfavorably stereotype children of mothers who smoke as anti-social psychopaths but also extend negative labels to secondhand smoke.  
 

Studies-On-Demand 
 

There are at least two charges that Social Marketing researchers and tobacco control advocates will predictably level at anyone who opposes or questions the findings of self-serving research studies. The charges and appropriate responses are: 
 

1. Front for Big Tobacco: Those who question anti-tobacco dogma are charged with being a “Front for Big Tobacco, whether or not it is true, with absolutely no corroborating information. Merely making the charge is apparently sufficient to prove the offense. The appropriate response is that since the November 1998 tobacco settlement that has funneled billions to support anti-tobacco research at universities and tobacco control programs no two groups have been more awash in Big Tobacco money than universities and tobacco control groups. We therefore observe those who level the charge of “Front for Big Tobacco” to be the greatest recipients of Big Tobacco money. Far beyond being an exercise in a portly pot of Marlboro Man gold calling little kettles that do not enjoy such largess black, the charge itself is inherently fraudulent because it omits important material information. To which one adds that researchers such as myself who directly question tobacco control claims are not and could not be funded by Big tobacco because they also expose the direct links between Marlboro Man and allegedly anti-tobacco. See, for example, Tobacco Control Basic Information No. 1. 

 

2. Opponents are Unprofessional: In other words, “Trust professionals, we know what’s best for you.” This is most commonly accompanied by refusal to discuss the study or its related data. Peer review is the final hold-out bastion for Junk Science studies-on-demand. The first response to this charge is that if studies contain such sufficiently transparent flaws that layperson researchers can cite six examples (as in the preceding section) with clear reference to specific data then the problem certainly must be with the authors and not those reviewing the conclusions. Relying on credentials to overcome challenges to transparent flaws in research is the hallmark of those who cannot explain problems inherent in their work. Leveling charges of “unprofessional” while refusing to discuss the subject of earnest critique is unseemly conduct by researchers. Finally, if all peers reviewing a study share the same vested interest in preserving grant research funding sources then peer review will predictably support wild speculation and unfounded research conclusions. Few disciplines other than tobacco control demonstrate a greater propensity for peer review chicanery. The money is just too good. And why shouldn’t the money be good? With billions per year in antidepressant and Nicotine Replacement Therapy products on the line a few million here and a few million there for special-interest research soon adds up to serious drug sales money. 
 

Social engineering studies-on-demand, such as the University of Washington study about exposure to ETS and later child behavior problems, to support tobacco control Social Marketing claims are much-relished tactics consistently employed by one of the largest institutional shareholders of NicoDerm CQ patch manufacturer Johnson & Johnson, the Robert Wood Johnson Foundation. That foundation has awarded many grants to the University of Washington, including those for childhood obesity, E-Health Technologies, King County Asthma Forum, Healthy Eating Research, local health department costs, and intensive care.   
 

The Robert Wood Johnson Foundation has also committed at least $446 million to tobacco control grants since 1992, according to pages 5 and 6 of its 2005 publication “Taking on Tobacco: The Robert Wood Johnson Foundation’s Assault on Smoking.” And the foundation directly profits by doing so through capital appreciation and dividend streams derived from its $3.9 billion stock holdings in Johnson & Johnson, as reported by Yahoo Finance for December 31, 2006. Adding at least $446 million in pharmaceutical nicotine grants from the Robert Wood Johnson Foundation to tobacco control advocates also further diminishes the “Front for Nicotine” charges leveled at those who question research study conclusions.  
 

Considering the multi-million-dollar level of current grants from that foundation to the University of Washington, this study appears to be just more of the same business as usual in the “publish or perish,” research-grant-hungry environment of today’s universities. It is a tragedy that expectant mothers and their babies can fall victim to such Social Marketing dogma as substituted for credible public health research. Earnest researchers at the University of Washington should be deeply concerned about the adverse affects such studies have on the credibility of the institution to which their personal careers are attached.  

While such grant making is undoubtedly beneficial to many seeking recognition or tenure based in part on their ability to secure founding for their university, that money appears to come at a very high price for patients, consumers and credible researchers. GlaxoSmithKline indisputably has clear vested interests in downplaying the risks of antidepressant use during pregnancy to sell PAXIL and in artificially inflating the alleged risks of exposure to ETS to sell NicoDerm CQ, Nicorette and Commit. Does the fact that the source of millions in grants to the University of Washington – the Robert Wood Johnson Foundation – is also among the largest institutional shareholders of NicoDerm CQ manufacturer Johnson & Johnson account, at least in part, for the clear bias of the university’s latest conclusions about ETS? 
 

Conflicting Views and News  
 

If the previous research concerning antidepressants and pregnancy are true then it is not possible for the University of Washington’s research to also be true, as indicated by the six fatal flaws in the study noted above. On the other hand, if the University of Washington’s study about ETS exposure and fetal development is true then that data points to incompetence by antidepressant researchers who incorrectly attribute fetal developments caused by Environmental Tobacco Smoke to other medications. Either way we look at this unseemly display of unabashed Social Marketing studies-on-demand as news earnest university research inquiry and legitimate public health are apparently traded in for grant income and media advertising revenues.  

The above observations regarding Environmental Tobacco Smoke, adverse fetal development and later child development problems are the vicissitudes encountered when researchers begin to stretch the boundaries of statistical realities in hot pursuit of research grants versus truth. But there is a much greater matter at issue here than the credibility of research at the University of Washington or the professional reputation of other researchers associated with that institution. That matter is the well being of children born to mothers who necessarily trust their physicians who rely on such studies in making recommendation to their patients. Where do the interests of patients, consumers, and legitimate public health fit within this tawdry research paradigm?  

While tobacco control is certainly a rich and sustaining source of research grant funding it is also indisputably and inextricably intertwined with mercantile vested-interests to peddle pharmaceutical products. As noted above, the net effect of the two news articles published by the Seattle Times on June 28, 2007 is to increase sales of both antidepressants and Nicotine Replacement Therapy. We also observe GlaxoSmithKline as a notable beneficiary through increased sales of PAXIL and NicoDerm CQ, with Johnson & Johnson and the Robert Wood Johnson Foundation garnering their cut of the profits through at least manufacturing of NicoDerm CQ.  
 

Another net effect of the two articles is to divert – deflect – attention from legitimate concerns about antidepressants and pregnancy to artificially crafted issues that falsely and implausibly “blame” Environmental Tobacco Smoke for many of the adverse effects of antidepressants on fetal development. While that may be a short term tactical victory for pharmaceuticals and their research grantees, does it portend greater long term loss and harm in the theatre of legitimate public health? Time will tell, and the current dysfunctional state of our health care delivery system augurs for looming clouds on the horizon of both medical research and services. 
 

A Few Facts About Environmental Tobacco Smoke

 

I mention the latest from tobacco control about ETS, as published by Reuters last week. From MSNBC News, June 29, 2007, “Just One Night in Smoky Bar Can be Toxic,” by Reuters:

 

CHICAGO - Even brief exposure to secondhand smoke in bars and restaurants can result in measurable levels of a toxin in workers’ bodies that is known to cause lung cancer, U.S. researchers said on Thursday. They found nonsmoking workers in Oregon who worked a single shift in a bar or restaurant that allowed smoking were more likely to have a detectable level of NNK — a carcinogen linked with lung cancer — in their bodies than those who worked in nonsmoking establishments. “NNK is only found in the body as a result of either smoking or breathing other people’s smoke,” said Michael Stark of the Multnomah County Health Department in Portland, Ore., whose study appears in the American Journal of Public Health. . . . Other studies have shown that nonsmokers exposed to secondhand smoke have about a 20 percent higher risk of lung cancer. They are also at a higher risk of asthma and perinatal complications such as sudden infant death syndrome. . . . Secondhand smoke causes about 3,400 lung cancer deaths and 46,000 heart disease deaths in adult nonsmokers in the United States each year, according to the American Lung Association.”

 

It must be noted that the December 1992 EPA report on passive smoking stated 3,000 nonsmokers die from lung cancer caused by exposure to Environmental tobacco Smoke. According to the “statistic” cited in the above report by Reuters 3,400 Environmental Tobacco Smoke causes 3,400 lung cancer deaths among adult nonsmokers in the USA each year. The original EPA figure of 3,000 was based on a risk factor or 1.19 at a 90 percent level of confidence (versus the customary 95 percent level of confidence), which is the source the oft-repeated claim – as stated once again in the above article by Reuters -- that “nonsmokers exposed to secondhand smoke have about a 20 percent higher risk of lung cancer.”  

The current number quoted by Rueters is 14 percent higher than EPA’s statement of deaths in 1992. The obvious question to ask of the American Lung Association is “OK, you’ve been diligently working on anti-tobacco since at least 1992, so when are you going to get something done about that allegedly deadly problem?” 
 

U.S. district court judge William Osteen exquisitely defined the “problem” about ETS and lung cancer among nonsmokers in his July 17, 1998 order to vacate Chapters 1 to 6 and appendices of the December 1992 EPA report on passive smoking (see page 1 of EPAPOST.PDF  for a copy of that order and page 2 for EPA conclusions that it effected).   
 

1. On page 73 of his 90 page-plus Memorandum Opinion  Judge Osteen specifically referenced EPA’s use of a 90 percent confidence level in place of the customary 95 percent:

 

“The first contention is EPA switched, without explanation, from using standard 95% confidence intervals to 90% confidence intervals to enhance the likelihood that its meta-analysis would appear statistically significant. This shift assisted EPA in obtaining statistically significant results. Studies that are not statistically significant are "null studies"; they cannot support a Group A classification. See Brock v. Merrell Dow Pharm., Inc., 874 F.2d 307, 312 (5th Cir. 1989) ("If the confidence interval is so great that it includes the number 1.0, then the study will be said to show no statistically significant 'association between the factor and the disease."). EPA used a 95% confidence interval in the 1990 Draft ETS Risk Assessment, but later switched to a 90% confidence interval. Most prominently, this drew criticism from IAQC's epidemiologist, who was also a contributor to the ETS Risk Assessment:  The use of 90% confidence intervals, instead of the conventionally used 95% confidence intervals, is to be discouraged. It looks like a[n] attempt to achieve statistical significance for a result which otherwise would not achieve significance.” (Underline added.)

 

2. On page 72 of his Memorandum Opinion Judge Osteen’s conclusions included a statement that EPA cherry-picked data:

 

“EPA's study selection is disturbing. First, there is evidence in the record supporting the accusation that EPA "cherry picked" its data. Without criteria for pooling studies into a meta-analysis, the court cannot determine whether the exclusion of studies likely to disprove EPA's a priori hypothesis was coincidence or intentional. Second, EPA's excluding nearly half of the available studies directly conflicts with EPA's purported purpose for analyzing the epidemiological studies and conflicts with EPA's Risk Assessment Guidelines. See ETS Risk Assessment at 4-29 ("These data should also be examined in the interest of weighing all the available evidence, as recommended by EPA's carcinogen risk assessment guidelines . . . Third, EPA's selective use of data conflicts with the Radon Research Act. The Act states EPA's program shall "gather data and information on all aspects of indoor air quality.” (Underline added.)

 

3. On page 60 of his Memorandum Opinion Judge Osteen concluded that it was possible EPA adopted different methodologies for each chapter based on the outcome desired:

 

“The court is faced with the ugly possibility that EPA adopted a methodology for each chapter, without explanation, based on the outcome sought in that chapter. This possibility is most potent where EPA rejected MS-ETS similarities to avoid a "cigarette-equivalents" analysis in determining carcinogenicity of ETS exposure. Use of cigarette-equivalents analysis may have lead to a conclusion that ETS is not a Group A carcinogen." It is striking that MS and ETS were similar only where such a conclusion promoted finding ETS a carcinogen.” (Underline added.)

 

4. In December 2002 the 4^th Circuit Court of Appeals overturned Judge Osteen’s July 1998 decision. The full text of the 4th Circuit’s ruling makes it painfully obvious that important issues regarding the December 1992 EPA report on secondhand smoke remained (see, for example, pages 15 and 16 of that ruling.) The U.S. Court of Appeals for the 4th Circuit confirmed important issues remained about the EPA report and its methodologies when it overturned Judge Osteen’s July 1998 order on December 11, 2002, based on procedural grounds that our federal courts did not have authority to review the EPA report on secondhand smoke.

 

5. The federal 4^th circuit Court of Appeals did not criticize or vacate Judge Osteen’s conclusions as set forth in his Memorandum Opinion. That Memorandum Opinion, including the above quotes about the 1992 EPA report on secondhand smoke, stand as authoritative results of judicial review if the 1992 EPA report. The fact that neither Philip Morris nor any other tobacco company chose to carry the appeal to the U.S. Supreme Court changes neither Judge Osteen’s district court conclusions about fatal flaws in the EPA report on secondhand smoke nor the important issues regarding that report the 4th circuit expressed its concern about.  
 

It is alarming that tobacco control most often continues to tout – indeed, in some cases increase to 3,400 -- the same 3,000 figure for lung cancer deaths among nonsmokers that it calculated at a reduced confidence level in 1992, as if judge Osteen never spoke a word to the subject. It is embarrassing for taxpayers to observe now-multi-billion-dollar per year tobacco control advocacy braying in the press about increasing deaths from lung cancer among nonsmokers as the reason to continue their programs that have failed to produce any positive results over the past 15 years. If the risks of exposure to ETS are not as represented by EPA in 1992 how could ETS present the risk for pregnant mothers and their offspring that Beauchaine and Gatzke-Kopp report in their June 2007 University of Washington study?  
 

Judge Osteen’s July 1998 conclusions about the December 1992 report on passive smoking were later confirmed by the U.S. Occupational Safety and Health Administration (OSHA) in its August 2001 brief filed with the U.S. Court of Appeals for the Circuit of Washington D.C. (see OSHANOTES.PDF). Notable among OSHA’s conclusions included in that brief are the following:

 

Page 8: “In addition, although the participants did not address whether the proposal’s residential-analogy method of quantifying risk was sound, they made clear that accurate data on ETS exposures in workplaces would be a fundamental component of such an assessment of the occupational hazard.”

 

Page 8: “The participants found that by 1998, however, new approaches were available that might be used to assess the health effects of exposure to ETS at various levels in the workplace.

 

Page 8: “The June 1998 workshop on ventilation controls addressed the feasibility of the proposed rule in certain industry sectors. In industries where there is substantial contact between customers who smoke and workers, such as some sectors of the food, beverage and gaming industries (including bars and casinos), the proposed rule’s prohibition on smoking except in separately ventilated areas may not be economically feasible.” (Italic added.)

 

Page 9: “. . . it now appears that, contrary to the assumption in the proposal, it may be possible to perform dose-response analysis for the ETS risk assessment. This may allow selection of a permissible exposure level for ETS, something that was not possible at the time of the proposal.”

 

Page 10: “Similarly, it also appears that OSHA’s critical assumption that workplace exposures to ETS are similar to spousal exposure is simply wrong. (Underline added.)

 

Page 17: "Here, as we have explained above, the proposed rule appears to be based upon outdated information and methodology and its risk estimates are not supported by the weight of evidence now available." 

 

Page 17: “OSHA does not believe that over 74 million nonsmoking workers are exposed to ETS at work levels equivalent to those faced by a nonsmoking spouse at home.

 

Page 18: "Nor does OSHA believe that issuance of an ETS rule would prevent between 2,234 and 13,723 excess deaths annually, or anything like that."

 

Page 18: "This potential hazard is not, as ASH’s Petition suggests, so egregious as to demand instant action, . . .” (Underline added.)

 

Shortly after filing its August 2001 response with the U.S. Court of Appeals OSHA withdrew its proposed nationwide workplace smoking ban. In its December 14, 2001 press release, “OSHA Withdraws Indoor Air Proposal With Support Of Anti-Smoking Groups” , OSHA said, in part: 

 

“Assistant Secretary for Occupational Safety and Health John Henshaw announced that OSHA is withdrawing an inactive indoor air quality regulation proposed in 1994. The decision was reached with the support of major anti-smoking public health groups including the American Heart Association, the American Cancer Society, the American Lung Association, Americans for Nonsmokers' Rights and the Campaign for Tobacco-Free Kids.”  
 

If tobacco control and smoking bans are genuinely about public health, why would anti-smoking health groups such as the American Lung Association and the American Cancer Society support OSHA withdrawing comprehensive Indoor Air Quality regulations. The long-winded, contorted explanation of tobacco control advocates is provided by Action on Smoking and Health (ASH) in its  
 

The views of both Judge Osteen and OSHA about ETS were indirectly confirmed in a research article about human lung carcinogen hexavalent chromium published by Occupational Safety & Health Reporter, March 2, 2006, “Technological, Economic Feasibility Justifies Higher Limit in Final CrVI Rule, OSHA Says” 
 

“Under a final rule for hexavalent chromium, employee exposures must be under 5 micrograms per cubic meter of air, a higher limit than the 1 microgram per cubic meter the Occupational Safety and Health Administration first proposed, according to a final rule published in the Feb. 28 Federal Register (71 Fed. Reg. 10,100).

 

The new permissible exposure limit still leaves a significant health risk, OSHA said, but the new PEL is the lowest level that is technologically and economically feasible for all industry sectors. When it began the rulemaking, OSHA said, the agency believed a PEL of 1microgram per cubic meter was feasible, but the rulemaking process revealed otherwise. The "vast majority of commenters," OSHA said, did not believe the proposed PEL was appropriate. Under OSHA's previous limit, which was the equivalent of 52 micrograms per cubic meter of CrVI per eight-hour time-weighted average, the agency estimated that there were between 101 and 351 excess lung cancer deaths per 1,000 workers, assuming a 45-year workplace exposure. Under the PEL in the final rule, excess deaths are estimated at between 10 and 45 per 1,000 workers, OSHA said. A PEL of 1 microgram per cubic meter would have reduced the figure to between 2.1 and 9.1 deaths. 

 

                                                                    

* Range is based on maximum likelihood estimate (0.43, .0056) and upper 95% confidence limit (18.9, 2.64)
** No prior standard; reported risk is based on estimated exposures at the time of the rulemaking
Source: Occupational Safety and Health Administration 
 

In stark contrast, the median risk to hospitality trade workers in deaths per thousand is 1.31, assuming that EPA was absolutely correct in its claim that 3,000 nonsmokers die each year from exposure to ETS is 1.31. That figure is still less that the range of 2.1 to 9.1 estimated deaths per thousand established by OSHA for hexavalent chromium at a 1 microgram per cubic centimeter PEL (versus its 5 microgram PEL.)  Tobacco control’s most extreme and hyper-inflated claim about lung cancer and ETS, which has been directly challenged by both our federal district courts and OSHA, produce merely produce hospitality trade workers deaths per thousand that is less than that estimated by OSHA for eight other human lung carcinogens encountered in the workplace.  
 

If the facts about ETS above about OSHA Permissible Exposure Limits are true for hexavalent chromium and lung cancer, what impact does that have on conclusions concerning ETS exposure during pregnancy and child behavior problems? The facts about ETS say that University of Washington researchers Gatzke-Kopp and Beauchaine should return to the drawing board with dispatch.  
 

Will the Social Marketing gurus and their university research system next focus attention on banning other human lung carcinogens such as asbestos, benzene and formaldehyde in all workplaces in the name of pregnant mothers? What would be the economic and employment costs nationwide, were that to occur?  
 

Public Policy Implications 
 

From Journal of Clinical and Consulting Pshycology, abstract for “Explaining the Link Between Low Socioeconomic Status and Psychopathology,” (Vol. 73 No. 6 p1146-1153 Dec 2005) by Wadsworth ME and Achenbach, TM:  
 

Two mechanisms of the hypothesized social causation of psychopathology--differential incidence and cumulative prevalence--were tested over 9 years in a nationally representative sample of 1,075 children and youths, ages 8-17 at Time 1 (1986). Analyses using parental responses on behavior checklists at 4 time points showed significant increases in clinical elevations for those of the lowest socioeconomic status (SES) on anxious/depressed, somatic complaints, thought problems, delinquent, and aggressive syndromes. This SES-linked differential incidence supports the social causation hypothesis that factors associated with SES contribute to variations in levels of psychological problems. SES-linked differential cumulative prevalence was found for withdrawn and somatic complaints; this finding indicates that low-SES cases do not improve as much as do middle- and high-SES cases, which results in greater accumulation of low-SES cases. 
 

From MSNBCNews.com, July 2, 2007, “Depression in Kids of Divorce Blamed on Genes,” by Linda Carroll: 
 

“Numerous studies have found that growing up in a broken home increases a person’s risk of developing depression or having problems with anxiety later in life. But a new report suggests that divorce isn’t at the root of the offspring's depression after all. In fact, the study, published in the July issue of the Journal of Child Psychology and Psychiatry, found that the cause of the divorce and the depression might be the same: shared genes. ‘This study suggests that the increased risk of emotional problems in the offspring of divorced parents is due to genetic risk shared by parents and their offspring,’ says the study’s lead author, Brian D’Onofrio, an assistant professor of psychology at Indiana University. This is contrary to what a lot of people have assumed in sociology and psychology.’” 
 

From OhioNewsNow.com, June 2007, “Cleveland Clinic Bans Hiring of Smokers,” North East edition: 
 

“The Cleveland Clinic, which has targeted fatty foods at its lunch counters and scooted smokers away from its buildings and sidewalks, now will ban the hiring of anyone who smokes. The move is part of a healthy work force initiative that included the appointment Thursday of Dr. Michael Roizen, author of a series of best-selling books on making healthy lifestyles, as the first chief wellness officer of the research hospital. Beginning Sept. 1, Ohio's second-biggest employer with 36,300 employees will no longer hire smokers. The policy will not affect current employees, who can get free stop-smoking help from the clinic. Prospective employees will be tested for tobacco use along with drugs. The ban is "essentially a challenge to every other major health-care organization that we want them to focus on wellness as well as illness too," Roizen said Wednesday. The step comes after the clinic removed trans fats from its cafeteria menus and sugar-sweetened beverages from its vending machines.” (Underline added.)  
 

Consider a child that is born to a nonsmoker professional mother in the upper economic class. The child enjoys full, health care through premium health insurance and secure economic stability. In addition the child is accustomed to preference as to primary and secondary education, unlimited food choices, and a stable home. Finally, that child has the advantage of life-long mentoring by professional parents who understand higher education opportunities and challenges.  
 

In contrast, consider a child who is born to a mother who smokes and works as a hospitality waitress. What are the differences? 
 

Begin with the fact that the mother’s current employment is directly and persistently threatened by a nationwide tobacco control agenda to pass smoking bans for restaurants and bars that is financed by tens of millions in special-interest grants tied to Nicotine Replacement Therapy manufacturers and distributors. Should the mother be laid off or her place of employment close her prospects of finding similar employment are minimal. Finally, as noted for Cleveland clinics above, that mother also faces direct and increasing employment discrimination in any trade or industry due to the tobacco agenda to exclude smokers from employment. See, for example, MELBOURNE, FLORIDA, MAY BAN OFF-THE-JOB SMOKING BY EMPLOYEES  [02/09/06-1] posted by Action on smoking and Health.That agenda is also financed by pharmaceutical nicotine manufacturers and distributors through the Robert Wood Johnson Foundation.  
 

Next, consider that directly due to tobacco control advocacy the mother faces discriminatory premiums for health insurance coverage, if she can get it in the first place. Indeed, increasing health insurance costs for smokers – to provide discounts for nonsmokers – is a tobacco control agenda. See for example, the Washington Post, November 14, 2006, “Smokers, Obese Should Pay More Health Insurance: Poll,” by Kim Dixon: 
 

“CHICAGO (Reuters) - Most Americans believe smokers and obese people should pay more for health insurance . . . Sixty percent of those polled favored higher premiums for smokers while 30 percent felt the obese should pay more. ‘When it comes to personal responsibility, consumers increasingly support making people pay more for unhealthy behavior,’ said the report in the journal Health Affairs. . . . The rate of uninsured, now nearly 16 percent of Americans, has been climbing for years, driven by consumer demand and escalating prices for prescription drugs and hospital care. About 20 percent of large employers are already giving discounts to workers who do not smoke, according to Helen Darling, president of the National Business Group on Health, which lobbies for corporations on health issues. ‘The non-smoker's discount is growing in popularity and I think it is going to grow faster,’ she said. As to obesity, ‘I think it will be a while before we get to the point where people begin tying a financial discount to something like BMI (body mass index),’ she said.” (Underline added.) 
 

Tobacco control also advocates expanding higher costs for smokers to Medicaid, which could adversely effect lower economic class families, again to provide greater health care access for nonsmokers. From United Press International, October 14, 2006, “Insurance Plan Penalizes Smokers, Obese:”   

 

WASHINGTON, Oct. 23 (UPI) -- The director of a U.S. anti-smoking organization says smokers and obese people should pay substantially more for health insurance than others. John Banzhaf, director of the Washington organization Action on Smoking and Health said he's urging state governors to adopt his plan in reforming their Medicaid programs. Under the plan, obese people would pay a 10-percent increased health insurance premium, with smokers generally paying an even higher percentage. Those who are obese and smoke would pay nearly 30 percent more to obtain health insurance. ‘While a growing number of health insurance companies are now charging smokers higher premiums, and a few state governments have started charging employees who smoke more for health coverage, this may be the first situation in which the concept is applied to Medicaid," Banzhaf said in a release. While noting increasing the premium penalty beyond a certain point might cause some to do without insurance, Banzhaf said correspondingly lower rates for non-smokers would probably help many of them obtain coverage that was previously financially out of bounds.” (Underline added.)   
 

The mother, quite probably a renter and not a home owner, also faces direct discrimination for housing due to the Robert Wood Johnson Foundation’s tobacco control agenda to ban smoking – and therefore smokers – in rental housing. See, for example,  RWJF $74,901 grant to City of Portland to eliminate smoking in rental housing units, which is one of many such grants to cities and counties nationwide.  For additional information on housing and smoking see my January 16, 2007 commentary “Politics, Housing & Tobacco Control.”  
 

Now add an additional persistent, unrelenting agenda of pharmaceutical-financed anti-tobacco: to “Denormalize” smoking through public ostracization and escalating threats to employment, housing and medical insurance for persons who smoke.  

What are the cumulative effects of tobacco control on the stability of home life for that child of a waitress who smokes compare to those of the child born to a professional class mother?  
 

Consider that question in light of what Wadsworth and Achenbach report in their study excerpted above, “Explaining the Link Between Low Socioeconomic Status and Psychopathology,” The following portion from that excerpt is poignant in context of tobacco control advocacy: 
 

Analyses using parental responses on behavior checklists at 4 time points showed significant increases in clinical elevations for those of the lowest socioeconomic status (SES) on anxious/depressed, somatic complaints, thought problems, delinquent, and aggressive syndromes.” (Underline added.)  

Also consider that question in context of a simple reality: tobacco control advocacy intentionally and willfully creates the very economic and societal factors for its “Target Group” of choice, persons who smoke, that numerous studies say contribute to child development and behavior problems.  Credible university researchers should explore the extent to which child behavior problems are directly and materially influenced by tobacco control public policy. Judging by the stress factors on working parents that tobacco control advocacy predictably imposes on its mercantile “Target Group” it is particularly heinous – some would outright say filthy of spirit – for tobacco control researchers to use the very causal factors that anti-tobacco contributes to “justify” further expansion of tobacco control policy.  
 

Considering the above powerful social factors in child behavior and development, as well as tobacco cotnrl’s direct complicity in adding to them, by what stretch of remotely credible imagination do University of Washington researchers conclude that Environmental Tobacco Smoke is a contributing factor? Any one of the influencing factors described above – persistent threats employment, OR medical care, OR housing would impose vastly more powerful causal factors on family stability and child behavior than mere exposure to ETS at work.   
 

By what ethical standards can researchers at the University of Washington ignore such influencing and confounding factors as documented above to produce a study-on-demand for mercantile special-interests? Where is the adult supervision in university research?  
 

We arrive at a simple public policy formula and straightforward solution: