Dear Editor,

I am writing in response to the research paper, “Clearing the airways: advocacy and regulation for smoke-free airlines” by Holm and Davis, published in the March supplement of Tobacco Control, 2004. While Holm and Davis present an apparently comprehensive narrative of the events that lead to the legislative prohibition of smoking in aircraft cabins, one is left with the sense from their research of “historical documents, journal and popular press articles, the world wide web and some tobacco industry documents” that the successful passage of the legislation was due to clever political maneuvering and the actions of “health advocates”. I would like to suggest that the flight attendants themselves, as individuals and members of unions, played a more central role in the passage of the legislation than was represented by the paper. In fact, the flight attendants were the critical element in getting congressional action.

Prior efforts to pass federal legislation on smoke-free worksites had not found Congress a friendly environment for such bills. One would therefore question why health advocates had failed to get federal legislation for smoke-free worksites but were successful in the airlines case? What was so different about the airline smoking ban case? Holm and Davis did not answer this question, nor did they bring any insight into the relationship between the tobacco industry and unions, key players in this battle. Rather, the paper simply painted a picture of flight attendants and the Association of Flight Attendants (AFA) as “scenery”, presenting personal testimonies of their ailments due to years of exposure to tobacco smoke. Union involvement in the issue is absent from the discussion and conclusions of this paper. Yet the presence and participation of the AFA was critical because with the unquestionable hazards to flight attendants on board, the issue was successfully reframed as one of “worker health and safety”, rather than the industry’s approach of “smokers’ rights” and accommodation.

The AFA has had a long history of concern over air quality in aircraft cabins. The AFA reasoned that advocating for smoking bans was an avenue to bring forth flight attendant health and safety concerns, since they feared that “without the intervention of Congress, the National Academy of Sciences study [on Cabin Air Quality] will end up on one of the (FAA’s) burners that is so far back you cannot even tell if it is on.”(1)

The authors of this paper attribute the defeat of the tobacco industry to (i) the industry’s limited leverage over the CAB and FAA, (ii) their inability to mobilize on a grassroots level and (iii) the lack of scientific basis to support their position. Absent from Holm and Davis’ discussion is the key role that the AFA played in thwarting industry efforts to win allies within organized labor. Industry documents reveal years of strategizing to woo organized labor and in the airlines case, the AFA and the Air Line Pilots Association (ALPA). The industry had actually underestimated the power of the flight attendants as they were duly warned in 1993 in light of smoking bans in bars and restaurants that “an anti- smoking position developed by HERE (Hotel Employees and Restaurant Employees International Union), similar to that adopted by the Association of Flight Attendants could present a major setback. However, HERE as an ally in this effort, would be a very powerful voice.”(2)

Holm and Davis conclude that the “single-issue focus” in advocacy work should be a lesson for future health advocacy work. The ownership of this success is debatable and, perhaps a more important “lesson” to reflect upon is how a single-issue focus in this instance has helped to create an alliance between health advocates and unions, while this has not always been the case. Perhaps a more valuable lesson is that unions are key players in tobacco policies in the workplace and that health advocates must consider how this coalition may be strengthened in future battles over workplaces such as restaurants and bars.

Charles Levenstein, Ph.D., M.Sc. Professor Emeritus of Work Environment Policy; and Co-Director, Organized Labor and Tobacco Control Network University of Massachusetts Lowell Lowell, MA

References

1. Achenbaugh N, Finucane M. FAA Should Create An Office To Address Crewmember And Passenger Health. R.J. Reynolds. September 19, 1986. Access Date: October 23, 2002. Bates No.:506294126/4131. URL: http://legacy.library.ucsf.edu/tid/hje71d00.

2. Ogilvy Adams & Rhinehart, Savarese and Associates. Restaurant Smoking Ban Strategy. Tobacco Institute. August 23, 1993. Access Date: July 8, 2003. Bates No.:TI01621153/1159. URL: http://legacy.library.ucsf.edu/tid/cyr30c00.

McAlister and his co-authors make an extremely valuable contribution to the ongoing debates of health care costs in the form of their estimate of the cost efficacy of a telephone quit line. The publication of this data should provide new evidence to convince payors to cover cessation.

However, since recruitment costs were excluded, it is difficult to make broader public health decisions based on these estimates. The decision not to include the costs from a controlled clinical trial is undoubtably correct, as they are not generalizable to larger scale promotion efforts. Most state funded quit lines in operations use multiple outreach methods, including television, radio, print and physician outreach to recruit patients into treatment.

To date there have been no estimates published of recruitment costs into these large-scale quit lines, despite the proliferation of state programs. This may be due to the fact that it is difficult to break out costs for recruitment from overall costs for cessation promotion and the normalization of quitting. None the less, until we have concrete estimates of the actual cost to recruit participants into such programs it will be impossible to actually calculate the true cost efficacy.

But as the authors say, there is good reason to stop tobacco companies having a free hand to do whatever product engineering they like. They have been given a unique exemption from virtually every law and norm of consumer protection and product safety. It is entirely right to stop them making products much more attractive than they would otherwise be - ie. systematically narrow the terms of the broad exemption they have.

But are there also dangers with the new proposal? If smoking is a behaviour based on seeking satisfaction from nicotine, isn't there a danger that reducing the addictiveness (ie. the pharmacological impact) will mean smokers seeking more nicotine for the same satisfaction? If more nicotine is required, then more toxins would be likely to be absorbed along with it, and so more harm caused.

Is there any evidence that, over time, it has become harder to quit smoking because the products have been engineered to be more 'addictive'? (I realise this might be difficult to gather). Have temporary withdrawal symptoms become more severe over time? These are the real harms associated with the addictiveness itself (as opposed to the co-exposure to toxins), so I think we ought to know what the behavioural changes have been before advocating a regulatory change.

Have all the strategies for subverting regulatory interventions available to smokers who are seeking a nicotine fix been considered...? Breaking off filters, switching to hand-rolled or cigars, compensatory smoking behaviour, bootlegging etc.

I don't know the answers to these questions. But to me, they say "not so fast". An approach to harm reduction that reduces the potency of the drug delivery system must consider the behavioural responses to these modifications, and this seems to me to be even more complex and risky than a more straightforward harm reduction strategy focussed on reducing toxins (which is probably pointless for combustible tobacco anyway).

Finally, is reducing addictiveness always right? If you could find a way to increase the addictiveness of medicinal nicotine or even smokeless tobacco, so that they compete better with cigarettes in nicotine delivery while doing orders of magnitude less harm, you may be able on to something that really would save millions of lives.

If blood lipid profile improves and weight increases with smoking cessation (1) smoking might be causally related to both the development of an abnormal blood lipid profile and the avoidance of weight gain or even weight loss. How then might smoking have increased the risk of non-fatal myocardial infarction in this study (2)? By reducing the capacity to respond to reductive stress with a further increase in the degree of blood lipid shift (3)?

The answer may lie in the next step in respoding to a progressive increase in the degree of reductive stress. If this is reverting to glucose as the preferred substrate for anaerobic glycolysis that would mean reversing the increase in nutrient energy density achieved by the antecedent lipid shift. In the case of an acute reductive stress equivalent to 25% of dysoxia that could mean having to increase a cardiac output of 4.7L/min that had been able to meet the tissues needs to as much as 16.2 L/min to achieve the same objective. A cardiac output of that magnitude is far in excess of the cardiovascular capacity of even a healthy fit athlete.

There is another possibility. Anaerobic glycolysis might be averted after the capacity for increasing nutrient energy density per unit volume of flowing blood had plateaued by using amino acids for acetyl coenzyme A synthesis in providing the substrate needed for oxidative phosphorylation to proceed at the rate needed to meet the tissues needs for ATP resynthesis at the time(4). But if NH3 is produced in the process the pH could rise inhibitng oxidative phosphorylation and stimulating anaerobic glycolysis and with it the demand of glucose(5). This too could incease the demand for ATP resynthesis far in excess of the cardiovascular capacity to meet the tissues energy needs.

Smoking might, therefore, have increased the risk of non-fatal myocardial infarction in this study by limiting the capacity for accommodating an acute reductive stress with a blood lipid shift and increasing the likelihood of acute cardiovascular decompensation. In which case smoking cessation can be expected to eliminate that risk once the blood lipid profile had been restored to normality even though weight was gained. What is more the gain in weight might be a compensatory response that enhanced the capacity to mount a lipid response to acute reductive stress. In other words a blood lipid shift revealed in blood lipid profiles may conceal the real capacity for mounting a fatty acid response to acute reductive stress.

If it is the capacity for mounting a fatty acid rsponse rather than a shift in blood lipid profile per se that is the primary determinant in meeting the metabolic demands of an acute reductive stress within cardiovascular capacity then it may be compromised by the administration of statins. Not only might the size of the mobile pool of fatty acids be reduced by statins by the ability to release it in a timely manner in acute reductive stress might be reduced by an accompanying reduction in the capacity for steroid hormone synthesis. In which case the risk of non- fatal acute myocardial infarction might be greatest in smokers taking statins or even confined to them.

1. Botella-Carretero JI, Escobar-Morreale HF, Martin I, Valero AM, Alvarez F, Garcia G, Varela C, Cantarero M. Weight gain and cardiovascular risk factors during smoking cessation with bupropion or nicotine. Horm Metab Res. 2004 Mar;36(3):178-82.

2. M S Mähönen, P McElduff, A J Dobson, K A Kuulasmaa, and A E Evans Current smoking and the risk of non-fatal myocardial infarction in the WHO MONICA Project populations Tob Control 2004; 13: 244-250

3. Successful evolutionary adaptation to environmental stress? Richard G Fiddian-Green Heart Online, 14 Jul 2004 eLetter re: D A Lawlor, G Davey Smith, R Mitchell, and S Ebrahim Temperature at birth, coronary heart disease, and insulin resistance: cross sectional analyses of the British women’s heart and health study Heart 2004; 90: 381-388

4. Might biochemical fermionic complexities be dictated by antecedent bosonic simplicities? Richard G Fiddian-Green (26 August 2004) eLetter re: Rodrigo B. Cavalcanti Does perioperative lipid-lowering therapy reduce in-hospital mortality after major noncardiac surgery? CMAJ 2004; 171: 328

5. pNH3: a relevant pulmonary variable? Richard G Fiddian-Green Chest Online, 11 Aug 2004 eLetter re: pNH3: a relevant pulmonary variable? Richard G Fiddian-Green Chest Online, 11 Aug 2004