...And They Call This "Science"!

The long list of methodological errors in the junk science of passive smoke

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PROLOGUE The long list of methodological errors in the junk science of passive smoke The questionnaires of the epidemiological fraud Downloadable list of all base studies on lung cancer and cardiovascular disease, including financing sources The list of all the lung cancer studies by category updated to 2006 on passive smoke: no dangers

Educate everyone!  Download this document in PDF format and give it to your family, relatives, friends and acquaintances... to everyone, that is, who is convinced that the smoker hurts the nonsmoker with his passive smoke because the health authorities say that science has demonstrated it.  Show them what kind of "science" on which our laws banning smoking in "public" places is based  - and what passes for credibility in public health today.

List of errors || What must an epidemiologic study warrant? || Hill's Criteria

PREFACE

May 4, 2005 - The public's growing awareness that the studies on passive smoke are statistical trash along with the knowledge that the health authorities are representing such trash as scientific evidence is a positive development. Many readers, however, have asked us for an exhaustive list of the reasons why these studies are trash.

The health authorities often state or imply that "smoking is indefensible." That statement is absurd.  Smoking is perfectly defensible because none of the alarms swirling about passive smoke have any scientific foundation, while those regarding active smoking are huge exaggerations as well.  Both are entirely based on incalculable factors. Let's set aside active smoking for now and consider the "dangers" of passive smoke that are the bases of smoking bans enacted to "protect the health of nonsmokers" - a protection that has no actual basis since passive smoke has never been demonstrated statistically or scientifically as dangerous, or risky. Thus what is indefensible is the false representation of evidence by authority. Such false representation is easily demonstrable.

THE LONG LIST OF METHODOLOGICAL ERRORS IN THE JUNK SCIENCE OF PASSIVE SMOKE

  1. The claims of exposure are not authentic. Exposure is not measured. The studies actually measure nothing, but rely on the vague and grossly imprecise recall of queried subjects who attempt to evoke in a few minutes their individual lifetime memories of passive smoking exposure.
  2. Errors in individual exposure recollection, most likely large, are unknown ,and are unknowable. Digitized numerical claims of exposure are, therefore, incongruous and impermissible. Their numerical representation gives an impression of reliability and precision that is demonstrably false and misleading.
  3. A recall bias has been demonstrated to be larger in subjects, who are more likely to amplify their recall of passive smoking exposure as a justification for their disease, with lung cancer or cardio vascular disease.
  4. A misclassification bias has been demonstrated to be larger in subjects with lung cancer or cardio vascular disease because they are more likely than healthy subjects to classify themselves as nonsmokers.
  5. A mismatch error of cases and controls is inevitable because the groups compared are not homogeneous and differ in many characteristics other than recall of passive smoking exposure.
  6. Confounding errors by definition are likely to be more prevalent among lung cancer and cardio vascular disease cases. Confounders are all other known and unknown potential causes of lung cancer and cardio vascular disease that interfere with the specific attribution of risk to passive smoking.
  7. Probable errors of disease diagnosis are seldom addressed by passive smoking studies.
  8. Publication errors have been found to favor the publication of studies that claim associations of increased risk.
  9. Statistical errors of sampling and statistical significance are grossly inconsistent among passive smoking studies owing to the feeble differentials of exposure recall and the small number of subjects in each study. A majority of studies have not reached statistical significance. In any event, significant or not, the statistical indices of all passive smoking studies are illusory because they are derived from the grossly illusory and misleading numerical renderings of vague individual exposure recalls.
  10. Results from different studies have not been consistent and reproducible.
  11. Epidemiologic criteria of causal inference (the Hill criteria) are not met by passive smoking studies.
  12. Attempts to summarize the results of different studies by meta-analysis statistical techniques are illegitimate. Results are obtained by pooling heterogeneous and selected studies, giving arbitrary preferential weights to certain studies, which, in any case, are handicapped by the sources of error listed above.

What must an epidemiologic study warrant?

  1. A study must warrant that its numerical representations of individual lifetime ETS exposure recalls are true measures of actual exposures.

  2. A study must warrant that an exposure recall bias affects cases and control groups, and exposed and non-exposed groups at the same rate.

  3. A study must warrant that subject selection and misclassification biases affect cases and control groups, and exposed and non-exposed groups at the same rate.

  4. A study must warrant that known causal confounders affect cases and control groups, and exposed and non-exposed groups at the same rate.

  5. A study must warrant the accuracy of pathological and diagnostic records.

  6. The results from different studies addressing the same subject must be consistently reproducible.
    In any study, the statistical margin of error of reported risks should reach no less than the 95% level of significance.

  7. If the above criteria are met, the results of a study should also be consistent with Hill's criteria of causality. (See below)

  8. Meta-analysis summations shall not be credible unless performed on the basis of all available studies. Such studies also must be of homogeneous design and conduct, and must have met the above criteria of validity.

Given that the above is universally and medically accepted as epidemiological practice:

  1. It is incontrovertible that no extant study can warrant that the numerical representation of individual lifetime ETS exposure recalls is a reliable measure of actual exposures.
  2. It is incontrovertible that no extant study can warrant that ETS exposure recall bias affects cases and control groups, and exposed and non-exposed groups at  the same rate.
  3. It is incontrovertible that no extant study can warrant that subject selection and misclassification biases (and other biases) affect cases and control groups, and exposed and non-exposed groups at the same rate.
  4. It is incontrovertible that no extant study can warrant that known causal confounders affect cases and control groups, and exposed and non-exposed groups at the same rate.
  5. It is incontrovertible that no extant study has warranted the accuracy of  pathological and diagnostic records.
  6. It is incontrovertible that results from different studies addressing the same subject have been grossly inconsistent and not reliably reproducible.
  7. It is incontrovertible that only for a random minority of studies has the numerical margin of error of reported risks been at or below the 95% confidence level of  statistical significance.
  8. It is incontrovertible that no study of ETS has met Hill’s criteria of causality.
  9. It is incontrovertible that no meta-analysis summation of ETS studies has been performed on the basis of all available studies, of studies that are of homogeneous design and conduct, and of studies that have met the above criteria of validity.

Hill's criteria

1) Strength of an association is a clue to causation, although a strong association is neither necessary nor sufficient to affirm causality, and a weak one is neither necessary nor sufficient to deny causality.

  • In the case of passive smoke it is clear that the associations are extremely weak, as confirmed by the authoritative opinions below:
     

National Cancer Institute - “In epidemiologic research, relative risks of less than 2 are considered small and usually difficult to interpret. Such increases may be due to chance, statistical bias or effects of confounding factors that are sometimes not evident.” – National Cancer Institute, “Abortion and possible risk for breast cancer: analysis and inconsistencies,” October 26, 1994.

Sir Richard Doll - " ... when relative risk lies between 1 and 2 ... problems of interpretation may become acute, and it may be extremely difficult to disentangle the various contributions of biased information, confounding of two or more factors, and cause and effect."
“The Causes of Cancer," by Richard Doll, F.R.S. and Richard Peto.  Oxford-New York, Oxford University Press, 1981, p. 1219.

WHO/IARC - “Relative risks of less than 2.0 may readily reflect some unperceived bias or confounding factor, those over 5.0 are unlikely to do so.”  - Breslow and Day, 1980, Statistical methods in cancer research, Vol. 1, The analysis of case control studies. Published by the World Health Organization, International Agency for Research on Cancer, Sci. Pub. No. 32, Lyon, p. 36

FDA - “Relative risks of 2 have a history of unreliability” - Robert Temple, M.D. Food and Drug Administration Journal of the American Medical Association (JAMA), Letters, September 8, 1999

FDA - "My basic rule is if the relative risk isn't at least 3 or 4, forget it." - Robert Temple, director of drug evaluation at the Food and Drug Administration.

Average cancer risk elevation for exposure to passive smoke: about 20% (relative risk=1.2)
Average cardiovascular disease risk elevation for exposure to passive smoke: about 30% (relative risk=1.3)
Quality of methodology and data gathering on passive smoke in all studies: trash

 

2) Consistency of results from different studies is an obvious attribute of true causal relationships.

  • Epidemiologic studies of passive smoke are grossly inconsistent, and epidemiologic associations that are inconsistent are quite unlikely to be true.

3) Specificity requires that a cause leads to a single effect, which is seldom the case in multi-factorial epidemiology.

  • Passive smoke has been claimed to cause many different effects.

4) Temporality. That effects must occur after the cause has a chance to act is a self-evident and trivial criterion of causality.

5) Dose-effect relationship is a useful criterion of causation, but does not resolve the matter.

  • Such an effect is the exception in passive smoke studies.

6) Plausibility. Whether an association is biologically plausible or not remains a matter of individual speculation and is far from being objective or conclusive.

7) Coherence. Agreement with other information may be a corollary attribute but not evidence of causation.

8) Experimental evidence. Experimental evidence in humans would indeed constitute proof of causation, but it is unavailable in the case of passive smoke.

9) Analogy is open to imagination and remains an invalid criterion of causation.

CASE CLOSED

The above are not opinions: these rules are the basis of science, epidemiology and statistics, rendering the supposed importance of the authority releasing the study - or the entity financing it - irrelevant.  These fundamental rules are systematically violated to "square the balance", justifying prohibition, fulfilling an ugly thirst for power, as well as enacting the pharmaceutical agenda.

Even setting aside the violations we have demonstrated, the studies still demonstrate nothing, but they are nevertheless touted by the health authorities as if they meant something.

This is the reason why anti-tobacco operatives at all levels continue to refuse public debates on the validity of their junk science and the truthfulness of their statements.


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