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ELECTRONIC ARTICLE |
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* Division of General Internal Medicine Fellowship Program
Center for Tobacco Control Research and Education
|| Institute for Health Policy Studies, Cardiovascular Research Institute, University of California, San Francisco, California
Division of Reproductive Health, Centers for Disease Control and Prevention, Department of Health and Human Services, Atlanta, Georgia
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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The tobacco industry has used scientific consultants to attack the evidence that SHS causes disease, most often lung cancer. Little is known about the industry’s strategies to contest the evidence on maternal and child health. In 2001, a review was published on SIDS that acknowledged funding from the Philip Morris (PM) tobacco company. Tobacco industry documents related to this review were examined to identify the company’s influence on the content and conclusions of this review.
Methods. Tobacco industry documents include 40 million pages of internal memos and reports made available to the public as a result of litigation settlements against the tobacco industry in the United States. Between November 2003 and January 2004, we searched tobacco industry document Internet sites from the University of California Legacy Tobacco Documents Library and the Tobacco Documents Online website. Key terms included "SIDS" and names of key persons. Two authors conducted independent searches with similar key terms, reviewed the documents, and agreed on relevancy through consensus. Thirty documents were identified as relevant. Two drafts (an early version and a final version) of an industry-funded review article on SIDS were identified, and 2 authors independently compared these drafts with the final publication. Formal comments by PM executives made in response to the first draft were also reviewed. We used Science Citation Index in July 2004 to determine citation patterns for the referenced SIDS reviews.
Results. PM executives feared that SHS and maternal and child health issues would create a powerful and emotional impetus for smoke-free areas in the home, public areas, and the workplace. In response to the 1992 US EPA report on SHS, the Science and Technology Department of PM’s Switzerland subsidiary, Fabriques de Tabac Reunies, searched for "independent" consultants to publish articles addressing SHS. The first industry-funded article was a literature review focusing on smoking and SIDS, conducted by consultant Peter Lee and co-author Allison Thornton, which stated that the association between parental smoking and SIDS could have been attributable to the failure to control fully for confounders. That first review has only been cited once, in the subsequent industry-funded review.
In 1997, PM commissioned a consultant, Frank Sullivan, to write a review, with coauthor Susan Barlow, of all possible risk factors for SIDS. The first draft concluded that prenatal and postnatal smoking exposures are both independent risk factors for SIDS. After receiving comments and meeting with PM scientific executives, Sullivan changed his original conclusions on smoking and SIDS. The final draft was changed to emphasize the effects of prenatal maternal smoking and to conclude that postnatal SHS effects were "less well established." Changes in the draft to support this new conclusion included descriptions of Peter Lee’s industry-funded review, a 1999 negative but underpowered study of SIDS risk and urinary cotinine levels, and criticisms of the conclusions of the National Cancer Institute report that SHS was causally associated with SIDS. In April 2001, the Sullivan review was published in the United Kingdom journal Paediatric and Perinatal Epidemiology, with a disclosure statement that acknowledged financial support from PM but did not acknowledge contributions from PM executives in the preparation of the review. By 2004, the Sullivan SIDS review had been cited at least 19 times in the medical literature.
Conclusions. PM executives responded to corporate concerns about the possible adverse effects of SHS on maternal and child health by commissioning consultants to write review articles for publication in the medical literature. PM executives successfully encouraged one author to change his original conclusion that SHS is an independent risk factor for SIDS to state that the role of SHS is "less well established." These statements are consistent with PM’s corporate position that active smoking causes disease but only public health officials conclude the same for SHS. The author’s disclosure of industry funding did not reveal the full extent of PM’s involvement in shaping the content of the article. This analysis suggests that accepting tobacco industry funds can disrupt the integrity of the scientific process.
The background of this SIDS review is relevant for institutions engaged in the debate about accepting or eschewing funding from the tobacco industry. Those who support acceptance of tobacco industry funds argue that academic authors retain the right to publish their work and maintain final approval of the written product, but this argument fails to recognize that the tobacco industry funds work to ensure that messages favorable to the industry are published and disseminated.
Clinicians, parents, and public health officials are most vulnerable to the changed conclusions of the SIDS review. The national SIDS "Back to Sleep" campaign has been very successful in reducing SIDS rates. However, estimates of SIDS risk from SHS (odds ratios range from 1.4 to 5.1) have considerable overlap with estimates of risk from prone sleep positioning (odds ratios range from 1.7 to 12.9). With the Back to Sleep campaign well underway, efforts to address parental smoking behavior in both the prenatal and postnatal periods should be intensified. The tobacco industry’s disinformation campaign on SHS and maternal and child health can be counteracted within clinicians’ offices.
Key Words: secondhand smoke • tobacco industry • sudden infant death syndrome
Abbreviations: SIDS, sudden infant death syndrome • EPA, Environmental Protection Agency • SHS, secondhand smoke • PM, Philip Morris • FTR, Fabriques de Tabac Reunies • NCI, National Cancer Institute • ETS, environmental tobacco smoke
Prenatal and postnatal exposure to tobacco smoke adversely affects maternal and infant health. Adverse outcomes that have been causally associated with prenatal tobacco exposure include premature rupture of membranes, preterm delivery, fetal growth restriction, and impaired pulmonary function among infants.1 Exposure of infants and children to secondhand smoke (SHS) has also been associated with a number of adverse health outcomes, including induction and exacerbation of asthma, otitis media, and sudden infant death syndrome (SIDS). National estimates of annual pediatric morbidity and mortality rates associated with SHS exposure include 1900 to 2700 SIDS deaths, 0.7 to 1.6 million office visits for treatment of otitis media, 8000 to 26 000 new cases of asthma, 400 000 to 1 000 000 asthma exacerbations, and 150 000 to 300 000 cases of bronchitis or pneumonia among infants and toddlers.2
SHS has been causally linked with SIDS in a number of major health reports. The landmark 1992 report from the US Environmental Protection Agency (EPA)3 not only confirmed that SHS causes lung cancer among nonsmokers4,5 but also noted an association between SHS exposure and an increased risk of SIDS. Subsequent research on SIDS and smoking explored the roles of in utero exposure (prenatal), exposure to SHS after birth (postnatal), or both. In 1997, the California EPA concluded that both prenatal exposure and postnatal SHS exposure are independent risk factors for SIDS.2 The California EPA report was republished by the National Cancer Institute (NCI) as part of its Smoking and Health Monograph Series in 1999,6 with a preface by the US Surgeon General endorsing the report’s conclusions. In 1999, a World Health Organization report called for the elimination of exposure to tobacco smoke in utero and exposure to SHS in childhood.7 Most recently, the 2004 Surgeon General’s report on smoking concluded that there is"a causal relationship between SIDS and maternal smoking during and after pregnancy."1(pp4–5)
The tobacco industry has fought to counteract the scientific consensus that SHS is dangerous since the first evidence that SHS causes disease began to emerge in the 1970s.8 In 1988, Philip Morris (PM), working with other multinational tobacco companies, developed an International Environmental Tobacco Smoke (ETS) Consultant Program to "keep the controversy alive" on SHS by recruiting consultants to develop and promote scientific viewpoints favorable to the industry.9,10 The industry’s law firm, Covington and Burling, managed the consultants’ work for the tobacco industry so that the consultants’ relationship with the industry could be denied or downplayed, in effect allowing consultants to be portrayed as independent third parties. The industry commissioned reports and implemented strategies to confuse or undercut the mainstream scientific literature on SHS, particularly the evidence on lung cancer.11–15 Little is known about the tobacco industry’s influence on maternal and child health issues.
In 2001, a scientific review of SIDS was published that acknowledged funding from PM.16 We identified and compared 2 drafts of the review in previously secret, internal tobacco industry documents that have been made available as a result of litigation against the industry, and we noted changes made after communications between the PM scientific executives and the authors. In response to the suggestions of PM, the authors removed SHS from their original conclusion that both prenatal exposure and postnatal exposure to tobacco smoke are independent risk factors for SIDS. This industry-commissioned article may undermine efforts by clinicians, parents, and public health officials to promote the elimination of infant exposure to SHS as an important prevention strategy for SIDS.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Two of the authors independently searched the documents and agreed on relevance through consensus. We determined that 30 documents were relevant, in that they provided either contextual information on PM’s interest in SIDS or were related to the commissioning and writing of the SIDS review article.
Two drafts, namely, an early version17 and a final version,18 of a SIDS review by Frank Sullivan and Sue Barlow were found in the documents. The contents of these 2 drafts were compared with each other and with the final published version,16 and changes in the text were noted. Formal comments by PM executives made in response to the first draft and submitted to Frank Sullivan were also reviewed. We used Science Citation Index in July 2004 to determine citation patterns for the referenced SIDS reviews.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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In each case we have tried, without going into too much detail, to define the problem; our proposals for addressing the problem: and what we expect would be the benefits stemming from such work. In some cases, the ideal would be to commit to external research projects, whereas in others we feel the work could be covered by a suitable consultant, or maybe even internally.20
The proposals for research addressing maternal and child health issues were meant to address concerns that maternal and child health issues could be used to promote the establishment of smoke-free areas.
The issues of maternal, spousal and work-place smoking all come together when considering pregnancy. In addition, women of childbearing age constitute a significant part of our market, not to mention a powerful political force. Directly mobilizing such a significant segment of the adult population around such an emotional issue has the potential for providing tremendous impetus to all sorts of restrictive legislation in the home, in public areas as well as in the workplace. There is perhaps no other issue as powerful facing the industry [emphasis added].21
PM wanted consultants to develop a series of literature reviews on issues such as "ETS and Pregnancy"21 and "ETS and Physical Development in Childhood."22 Heading each proposed topic was a description of an appropriate consultant, "To be identified [emphasis added], Head of Obstetrics, Private Practice, Regional Hospital-Pediatric Polyclinic"21 or "Head of Pediatrics."22 PM would be heavily involved. "Support will have to be given in terms of the definition and measurement of ETS exposure, compilation and analysis of the data, and publication."21
The first industry-funded SIDS literature review focused only on smoking and SIDS and was written by long-time tobacco industry consultant Peter Lee and his associate Alison Thornton.23 Lee and Thornton examined 27 studies from 1966 to 1996 and described associations between parental smoking and SIDS risk. The authors concluded that study weaknesses, in particular the failure to control properly for numerous potential confounders, "mean that a causal relationship for parental smoking in SIDS remains unproven."23 In 1993, Lee charged the United Kingdom Tobacco Manufacturer’s Association Advisory Council £12 000 for reviews on SHS and SIDS, childhood cancer, and middle ear disease.24 In February 1997, PM paid Lee at least $2120 to publish his SIDS article.25
However, Lee and Thornton initially encountered difficulties. In August 1997, Lee reported to the FTR Science and Technology Department26 that he had submitted the article to Public Health Reviews but "they had rejected our SIDS paper ‘considering it not sufficiently unbiased.’ "27 Because of the general difficulty of "getting tobacco industry funded studies published,"27 Lee suggested sending
the [manuscript] to a more minor journal which is more likely to give acceptance. One possibility is Indoor and Built Environment [a journal set up by PM consultants28], edited by [tobacco industry consultant29] John Hoskins, whom I know, which has published review papers on ETS-related issues in the past.27
In 1998, Indoor and Built Environment published the Thornton and Lee article,23 which acknowledged that "support was provided by several companies of the tobacco industry." (Other articles by Thornton and Lee were also published in Indoor and Built Environment.30–32) The SIDS review by Thornton and Lee has had little direct impact on the medical literature. As of July 2004, it had been cited only once, and that citation was by the next consultant hired by PM to write about SIDS, Frank Sullivan.
PM Commissions Toxicologist Frank Sullivan
In February 1997, as the California EPA presented its draft SHS report for public comment, PM began its search for a consultant to review the literature on SHS and SIDS. An attorney at Covington and Burling notified PM executives that the California EPA was moving toward concluding that there was a causal relationship between SHS and SIDS and that there was a "need to continue SA’s [PM Scientific Affairs] ongoing work in this area."33 Covington and Burling sent the curriculum vitae of toxicologist consultant Frank Sullivan to Ted Sanders (FTR Scientific Affairs) and asked how PM would like to proceed.34,35
Sanders expressed reservations about Sullivan’s qualifications to Richard Carchman (director of PM Scientific Affairs), because Sullivan had no prior experience in SIDS research.36 Previously, Sullivan had served in multiple other capacities as an industry consultant. He was listed in 1988 as one of the industry’s first potential "international ETS consultants,"37,38 and he participated in tobacco industry activities downplaying the health effects of SHS.39,40
In March 1997, Sanders reported to Carchman that Sullivan had expressed an interest in conducting the SIDS review.36 PM and Sullivan agreed that literature searches would be supplied by PM and "[w]ork would be reviewed by the appropriate PM personnel on a periodic basis and the final manuscript would also be reviewed. However, Dr Sullivan would remain free to publish the final version without restriction by Philip Morris."36 They also agreed that "[a]ppropriate attribution for PM’s support would be made,"36 which in the published article was described as only financial support.16 In 1998, PM budgeted $50 000 to $100 000 for completion of Sullivan’s review.41,42
The Sullivan review article was part of PM’s overall scientific strategic plan for addressing SHS and childhood health issues. In January 1998, PM Worldwide Scientific Affairs described in an "Impact Assessment" how Sullivan’s review would meet PM’s goals: "a thorough analysis of all of the literature, not simply a review of those studies which implicate ETS ... in order to determine if it is likely that ETS truly does play a role in the etiology of SIDS."41 Another Worldwide Scientific Affairs project was to review the literature on SHS in childhood and organize a database of datasets for future statistical analysis.43 The "Impact Assessment" for this project was as follows: "Should provide the necessary scientific background for a policy on the acceptability of smoking around children." In 1999, PM Worldwide Scientific Affairs listed the scientific issues of greatest importance to the company and described strategies to develop reviews for establishing PM’s scientific positions. "ETS and Health" was listed as one such priority issue, with Sullivan’s review being noted as already covering SIDS.44 Besides SIDS and adult diseases such as lung cancer and cardiovascular diseases, other topics were being internally reviewed, including childhood respiratory disease and asthma. Otitis media had been covered previously by the publication by Thornton and Lee.31
Sullivan and PM Work Together
Sullivan worked on the SIDS review from 1997 to 2000, with his coauthor Sue Barlow; Sullivan was the direct link to PM’s scientific executives. In July 1998, Sullivan wrote to Sanders that he was nearly finished with the review except for the smoking section,45 and the 2 met soon after.46 Sullivan’s initial draft17 was 101 pages long and reviewed 20 risk factors for SIDS. Later, in June 1999, Sanders apologized to Sullivan, as he had "just not had the opportunity to complete my work on your draft [emphasis added]"47 and provided detailed comments from himself and Carchman (Table 1).48 Regarding the summary and conclusions section, Sanders’ only comment on Sullivan’s original conclusions was in disagreement with the role of SHS: "I would like to discuss some of the wording on this page with you. It seems that you have been less cautious in interpreting the data on postnatal ETS exposure than you were with prone sleeping position [emphasis added]."48 Sullivan and Sanders again planned a London meeting,47 after which Sanders sent a July 1999 memo to tobacco industry consultant Peter Lee, requesting that Lee analyze certain sections of Sullivan’s draft.49 Sanders passed on Lee’s commentary to Sullivan.50,51
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Comparison of Sullivan’s Drafts
PM’s Carchman had approved the comprehensive nature of Sullivan’s initial draft in 1999. Handwritten at the end of this draft, Carchman summarized his suggestions for the review.
Overall—excellent job—complete data capture
—I would have like [sic] some more creativity—bottle/breast—age—immune infection [emphasis added]17
Sullivan’s draft discussed 20 categories of SIDS risk factors. Despite Carchman’s desire for "more creativity," Sullivan made few changes to these sections. However, in response to specific PM comments on smoking,48 Sullivan incorporated some suggestions, such as noting that anemia among smoking mothers who have SIDS infants might suggest "other underlying problems" of the mother (Table 1).18
The comments solicited from Lee by PM were incorporated into the manuscript to downplay population attributable risks for maternal smoking in SIDS. Sullivan had described a meta-analysis of 11 studies by DiFranza and Lew54 and its calculation of population attributable risks for maternal smoking, but Sanders wrote to Sullivan, "Dr Carchman wondered if you could provide some individual critical analysis of the population attributable risks provided in this paragraph."48 Subsequently, Sanders asked Lee for comments, which Sanders forwarded to Sullivan.50,51 Lee stated that the attributable risk from maternal smoking could be explained mostly by confounding. Sullivan revised his final version18 to include Lee’s comments (Table 1), but the comments were not attributed to Lee and Lee’s contributions to the article were not acknowledged. Moreover, Sullivan deleted a sentence in his conclusion stating that the population attributable risk of maternal smoking was estimated to be between 27 and 66% (Table 1).
Sullivan’s original draft did not include the 1998 SIDS article by Thornton and Lee,23 but the final draft18 incorporated a descriptive paragraph about the article, stating that much of the association between tobacco exposure and SIDS appeared to be attributable to confounding (Table 3). The article by Thornton and Lee23 stated that the relative risks from SHS could be reduced with multiple statistical adjustments, which suggests that parental smoking and SIDS are not independently associated. In making this argument, however, Sullivan ignored the fact that, whereas proper adjustment for confounders generates a more accurate estimate of odds ratios, including excess adjustments can lead to an overspecified model and mask real associations by diluting their statistical significance.55
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Two additional paragraphs were added to describe a 1999 Tasmanian prospective study of SIDS and cotinine (a nicotine metabolite) by Dwyer et al,56 with an accompanying editorial by Spiers,57 in which sources of SHS exposure at 1 month of age and subsequent risks of SIDS were examined. Sanders wrote to Sullivan, "I think that this paper is extremely important, and I also think that if at all possible it ought to be included in your review."47 The study by Dwyer et al,56 in which parental smoking patterns predicted urinary cotinine concentrations among the infants but not the risks of SIDS, included only 34 cases. Nevertheless, Sullivan twice emphasized the article’s negative but underpowered findings as providing no evidence of an independent postnatal effect of smoking (Table 3). The accompanying commentary by Spiers57 discussed the difficulty of separating prenatal and postnatal smoking effects and debated the relative contributions and mechanisms of each effect. However, Sullivan cited only Spiers’ comments on the possible mechanisms for a prenatal effect (Table 3). (No documents connect Dwyer or Spiers personally with PM.)
In the summary and conclusions section of the final draft,18 Sullivan made a number of revisions that served to downplay the potential effects of SHS on the risks of SIDS. He deleted his original conclusion that SHS is an independent risk factor for SIDS and replaced it with statements emphasizing the prenatal effects of smoking (Tables 1 and 2). He deleted the sentence, "The evidence overall suggests that both prenatal and postnatal maternal smoking exert independent effects [emphasis added]." He also changed the statement, "Consistent associations have been found between SIDS and maternal smoking, whether smoking habits were ascertained prenatally or postnatally," by deleting the last phrase. He added the conclusion, "In considering modifiable maternal risk factors, smoking is among the most important," but he indicated that this does not necessarily include postnatal smoking exposure and inserted criticisms of studies of postnatal SHS exposure several times in the body of his article (Tables 1 and 2). He also expanded the summary and conclusions section by almost a whole paragraph to emphasize more strongly the effects of prenatal exposure on fetal development, stating that postnatal effects were "less well established" (Table 1).18 In summary, Sullivan substantially altered his article to focus more on abnormal infant development and the role of prenatal maternal smoking, while raising doubts about the certainty of SHS as a risk factor for SIDS.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Our analysis of the Sullivan SIDS review is relevant for institutions engaged in the debate regarding accepting or eschewing funding from the tobacco industry. Those who support acceptance of tobacco industry funds argue that academic authors retain the right to publish their work and maintain final approval of the written product,62 but this argument fails to recognize that the tobacco industry funds work to ensure that messages favorable to the industry are published and disseminated. For example, in 1988, PM led other tobacco companies in designing and controlling an airline indoor air quality study63 that downplayed exposure to SHS and its potential health effects when smoking restrictions on airlines were being debated.64 In 1995, the industry generated and controlled the conduct and content of a study, eventually published under Peter Lee’s name,65 that was designed specifically to refute a landmark study on lung cancer and SHS among nonsmoking women.13 In addition, the industry funded15 a 2003 British Medical Journal article66 that reported no causal relationship between SHS and lung cancer, which was criticized for being conducted in a way that almost ensured negative conclusions.67 In each of these cases, "independent" industry consultants played a critical role in providing scientific credibility in promoting the industry’s goals.
The tobacco industry’s long and consistent history of manipulating the content and presentation of scientific results raises questions about publishing work funded by the tobacco industry. The International Committee of Medical Journal Editors has recommended that, in addition to identification of financial support, the role of the funding organization in the design and control of a study should be specified.68 Paediatric and Perinatal Epidemiology, which published the article by Sullivan and Barlow,16 requires that acknowledgments include "details of funding." The Sullivan review,16 as well as the other cases described above,15,63,64,66,67 illustrates the need for journals to require complete disclosure of all sponsor involvement in the conduct of a study and the preparation of the manuscript. However, such disclosure guidelines have been demonstrated repeatedly not to be effective with the tobacco industry, which seeks actively to minimize its role.9,69
Clinicians, parents, and public health officials may be the most vulnerable to the conclusions in Sullivan’s article that SHS does not appear to be an important risk factor for SIDS. The national SIDS prevention campaign ("Back to Sleep"), sponsored by a coalition including the National Institute of Child Health and Human Development and the American Academy of Pediatrics,70,71 has focused mainly on the infant’s sleep position. Creating a smoke-free zone around the infant is one of many secondary messages. The Back to Sleep campaign has been very successful in reducing SIDS rates, and efforts to educate parents about the importance of sleep positioning must continue. Now that the campaign is well underway, efforts to address parental smoking behavior in both the prenatal and postnatal periods should be intensified. An example of a strengthened smoke-free message is found in the US EPA "Smoke-Free Home Pledge" 2001 campaign72 to reduce children’s diseases.
Clinicians need to address SHS exposure more effectively with their patients and parents. In 2001, according to a national survey of parents, only one half of all parents who visited pediatricians or family practitioners reported that they were asked about smoking status, and less than one half of the smoking parents said they were counseled about SHS or received advice to quit.73 Although quit rates during pregnancy have been increasing in the past decade, one half of the women who quit later experience relapses in the postpartum period, and these rates have not changed with time.74 One clinician barrier may be the perception that, as an American Academy of Pediatrics task force71 noted in 2000, "changing [maternal smoking] behavior has been far more difficult to accomplish than changing infant sleep position." However, estimates of SIDS risks from SHS (odds ratios range from 1.4 to 5.175) have considerable overlap with estimates of risks from prone sleep positioning (odds ratios range from 1.7 to 12.975). Therefore, efforts to promote smoking cessation and reduction of SHS exposure for infants and children, particularly in discussions of SIDS prevention, should be intensified.
Clinical interventions designed to reduce SHS exposure among infants and children may be effective. A review of 19 studies (from 1987 to 2002) to reduce SHS exposure among youth concluded that these interventions can be effective.76 In a randomized trial of a motivational intervention that included educating smoking parents, ambient nicotine concentrations in children’s homes were reduced by 25 to 30%, compared with concentrations in homes where self-help material was provided, which resulted in no change.77 Also encouraging is the finding that, in another study, more than one half of smoking parents tried to quit after being counseled at their children’s clinic and offered nicotine replacement therapy and quit-line referrals.78
The tobacco industry’s disinformation campaign regarding SHS and maternal and child health can be counteracted within clinicians’ offices. SHS must be recognized as an established, controllable, risk factor for SIDS, like prone sleep positioning. Clinicians and public health officials should intensify their efforts to promote reducing infant exposure to SHS as an effective strategy for reducing SIDS.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Address correspondence to Stanton A. Glantz, PhD, Center for Tobacco Control Research and Education, 530 Parnassus, Suite 366, University of California, San Francisco, CA 94143-1390. E-mail: glantz{at}medicine.ucsf.edu
No conflict of interest declared.
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REFERENCES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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This article has been cited by other articles:
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  E. K. Tong and S. A. Glantz Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease Circulation, October 16, 2007; 116(16): 1845 - 1854. [Abstract] [Full Text] [PDF]
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 S. F Schick and S. A Glantz Old ways, new means: tobacco industry funding of academic and private sector scientists since the Master Settlement Agreement Tob. Control, June 1, 2007; 16(3): 157 - 164. [Abstract] [Full Text] [PDF]
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 J. R. Lynch, M. R.A. Cunningham, W. J. Warme, D. C. Schaad, F. M. Wolf, and S. S. Leopold Commercially Funded and United States-Based Research Is More Likely to Be Published; Good-Quality Studies with Negative Outcomes Are Not J. Bone Joint Surg. Am., May 1, 2007; 89(5): 1010 - 1018. [Abstract] [Full Text] [PDF]
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 G Ottaviani, L Matturri, R Mingrone, and A M Lavezzi Hypoplasia and neuronal immaturity of the hypoglossal nucleus in sudden infant death J. Clin. Pathol., May 1, 2006; 59(5): 497 - 500. [Abstract] [Full Text] [PDF]
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Part 11: Pediatric Basic Life Support Circulation, December 13, 2005; 112(24_suppl): IV-156 - IV-166. [Full Text] [PDF]
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