Like Lemmings to the Sea – Part 2
In yesterday’s engrossing piece of journalism (oh right – boring), I pointed out the misuse of science and the willingness of the media to promote an agenda. I have also discussed correlative science and the need to recognize it is a projection of risk and not an absolute proof of cause and effect.
In 1998 the Environmental Protection Agency’s publication on the effects of secondhand smoke was thrown out at trial due to it’s a priori (before the fact) conclusions and attempt to cite only studies which showed that perspective. Finally, I should say the actual risk, (even by the most extreme measure) was slight, to say the least.
The study used by the State of Maryland to pass the smoking ban was The Health Consequences of Involuntary Exposure to Tobacco Smoke. This study was published by the U.S. Surgeon General in conjunction with the Center for Disease Control (CDC).
I would note first, that the term “secondhand smoke” has been changed to “involuntary smoking,” a very pregnant term which has little to do with science and a lot to do with political manipulation. Keep in mind that those which determine the argument win – hence words matter.
Like I said before, advocacy groups are fully aware of this technique. We may even find ourselves unable to order something like a “rare” hamburger – oops, that’s already the case. Guess we need to be protected against that as well.
“Exposure of nonsmokers to secondhand smoke has declined in the United States since the 1986 Surgeon General’s report, The Health Consequences of Involuntary Smoking.”
What?!?! Does this report actually state that exposure has declined even without this new state law regulating business? But wait, it further states that “[h]omes and workplaces are the predominant locations for exposure to secondhand smoke.”
So, if it is not businesses where people are exposed to secondhand smoke, what could possibly require a new law to limit that exposure?
Already we have seen that the study itself determines that further regulation is not necessary. But, let’s continue reading this study used by the state.
“In 2005, it was estimated that exposure to secondhand smoke kills more than 3,000 adult nonsmokers from lung cancer, approximately 46,000 from coronary heart disease, and an estimated 430 newborns from sudden infant death syndrome.”
Alright – let’s use the most extreme estimate to determine how many American’s may be affected by this “estimate.” Keep in mind that this estimate includes those who do not go to bars as well as children).
(3,000 + 46,000 + 430)/300 million = 1.647667; or a 0.017% risk that secondhand smoke could cause you lung cancer or death. That is a pretty small possibility.
Wouldn’t it be something if our tax rates were based upon these ratios? But, you need to recognize that this “increase in the risk of lung cancer from secondhand smoke exposure [is] associated with living with a smoker.” In other words, you must be exposed continuously for a long period of time.
The study used a model from 1964 for correlative comparison. “The criteria, offered in a brief chapter of the 1964 report entitled ‘Criteria for Judgment,’ included (1) the consistency of the association, (2) the strength of the association, (3) the specificity of the association, (4) the temporal relationship of the association, and (5) the coherence of the association. Although these criteria have been criticized (e.g., Rothman and Greenland, 1998), they have proved useful as a framework for interpreting evidence on smoking and other postulated causes of disease, and for judging whether causality can be inferred.”
Rothman and Greenland determined that multiple toxins influencing an analysis become extremely complicated. In other words, causal effects can be determined with one cause and one effect, but when you allow for multiple causes, (toxins) for even one effect, the analysis becomes quite difficult to narrow down.
“That same framework was used in this report on involuntary smoking and health. The criteria dating back to the 1964 Surgeon General’s report remain useful as guidelines for evaluating evidence (USDHEW 1964), but they were not intended to be applied strictly or as a “checklist” that needed to be met before the designation of “causal” could be applied to an association. In fact, for involuntary smoking and health, several of the criteria will not be met for some associations… The finding of only a small elevation in risk, as in the example of spousal smoking and lung cancer risk in lifetime nonsmokers, does not weigh against a causal association; however, alternative explanations for a risk of a small magnitude need full exploration and cannot be so easily set aside as alternative explanations for a stronger association… To address coherence, the report draws not only on the evidence for involuntary smoking, but on the even more extensive literature on active smoking and disease.”
In other words, the study allows for a wide berth on cause and effect and uses active smokers as an additional basis to make their conclusions.
There is also a liberal allowance for levels of causation. A “four-level hierarchy for classifying the strength of causal inferences based on available evidence.”
Level 1 Evidence is sufficient to infer a causal relationship.
Level 2 Evidence is suggestive but not sufficient to infer a causal relationship.
Level 3 Evidence is inadequate to infer the presence or absence of a causal relationship (which encompasses evidence that is sparse, of poor quality, or conflicting).
Level 4 Evidence is suggestive of no causal relationship.
Source: U.S. Department of Health and Human Services 2004.
Note that this has no basis for a “direct” causal effect – inference is the highest level attained. While this has been determined acceptable for this correlative study, it should be noted that even Level 1 allows for an “inference” of causal effects.
Now that we have established that methods to determine the effects of secondhand smoke are quite liberal, what was the mechanism used to determine some of these causalities?
“At this time, cotinine, the primary proximate metabolite of nicotine, remains the biomarker of choice for assessing secondhand smoke exposure.” One would assume that such a biomarker would be specific enough to ensure that its cause could be well determined.
"Up to 50% of nonsmokers may show urinary cotinine, demonstrating the ubiquity of the exposure." eMedicine (WebMD) Passive Smoking and Lung Disease. So, the indicator substance is ubiquitous; or present throughout our environment. Hence, with such high exposure rates, it becomes increasingly difficult to determine “cause.” But, let’s accept this measure for sake of argument.
The final death nail for this study are these highlights of the various chapters – not one sufficient inference, (even with the very liberal criteria) that secondhand smoke causes serious respiratory problems in adults:
“The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among persons with asthma.
“The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among healthy persons.
“The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and chronic respiratory symptoms.
“The evidence is suggestive but not sufficient to infer a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in persons with asthma.
“The evidence is inadequate to infer the presence or absence of a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in healthy persons.
“The evidence is suggestive but not sufficient to infer a causal relationship between chronic secondhand smoke exposure and a small decrement in lung function in the general population.
“The evidence is inadequate to infer the presence or absence of a causal relationship between chronic secondhand smoke exposure and an accelerated decline in lung function.
“The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and adult-onset asthma.
“The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and a worsening of asthma control.
“The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and risk for chronic obstructive pulmonary disease.
The evidence is inadequate to infer the presence or absence of a causal relationship between secondhand smoke exposure and morbidity in persons with chronic obstructive pulmonary disease.”
Read it, folks. I have been known to be wrong before, but in this case, I believe the state and federal government are once again infringing upon the rights of a business owner without substantial authority. Keep this in mind the next time you hear of a new study on TV which could limit yours or a businesses right to choose.