COMMENT ON "HEALTH EFFECTS OF EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE"

CHAPTER 6
Respiratory Health Effects

6.1.1 Asthma (exacerbation); 6.2.1 Asthma (induction)

This report claims that "ETS exposure produces a variety of acute effects involving the upper and lower respiratory tract. ETS exposure can exacerbate asthma in children, perhaps affecting 48,000 to 120,000 children annually in California; adults may also be affected." And, "There is consistent and compelling evidence that ETS is a risk factor for induction of new cases of asthma; in California, between 960 and 3,120 new cases per year may be ETS- related." Also, "Children are especially sensitive to the respiratory effects of ETS exposure." (6.4 Chapter Summary and Conclusions, page 6-60).

We categorically reject these claims, on the grounds that, since the anti-smoking movement began, the death rate from asthma has tripled in every age group above five years, while remaining the same in children under five. In fact, the death rates from asthma among children less than five years old are lowest of all age groups. This makes anti-smoking demagogues' habitual use of children to incite public hysteria doubly despicable. (Source: Vital Statistics of the US, 1977-89; Section 1, General Mortality, Table 1-10.) In fact, this evidence the authors did not see fit to consider is more consistent with more frequent exposure, after age five, to some unknown agent, among sociologically similar smokers and passive smokers than among non- smokers.

6.1.1.2 Evidence from chamber studies

This report admits that "The controlled exposure studies do not clearly demonstrate a consistent effect of acute ETS exposure on asthmatics as a whole," but cites "general design constraints" such as small sample size (page 6-15). Studies confirming such effects would be of great propaganda value to the anti-smokers. One can only suspect that they knew they wouldn't find any, and decided to rely upon anecdotes instead. However, this report also claims that "In summary, although the design constraints of the chamber studies limit the interpretation of the results, they do suggest that there is likely to be a subpopulation of asthmatics who are especially susceptible to ETS exposure. The physiological responses observed in these investigations appear to be reproducible in both 'reactors' and 'nonreactors'. It is unlikely that the physiological and symptomatic responses reported are due exclusively to either stress or suggestion" (page 6-16). No reason is given for this high-handed dismissal. In fact, differential diagnosis of ETS effects from hyperventilation is a requirement of good clinical and epidemiologic practice. The effects of hyperventilation can in fact be identical to nearly all supposed ETS effects, including "breathlessness," dizziness, palpitations, chest pain, and headache. Although hyperventilation syndrome is quite common, no studies have ever been done to differentiate the reported symptoms. References: Magarian GJ. Hyperventilation syndromes: Infrequently recognized common expressions of anxiety and stress. Medicine 1982;61(4):219-236.

Hyperventilators tend to have greater tendencies toward obsessional behavior with difficulties in handling everyday stresses resulting in frequent frustration. In adolescence they often harbor feelings of inadequacy and experience interpersonal maladjustments.... Hyperventilators are often overly body- and health-conscious with tendencies toward thoracic breathing.... Lazarus and Kostan have emphasized the frequency of phobias in hyperventilators and state that such individuals are "running scared" and is the cause for their frequent phobias relating toward disease, death, being alone, and of becoming psychotic.

Demeter SL, Cordasco EM. Hyperventilation syndrome and asthma. Am J Med 1986 Dec;81:989-994. In asthmatics, hyperventilation can trigger attacks. Golden GS, Golden LH, Beerel FR. Hyperventilation-induced T-wave changes in the limb lead electrocardiogram. Chest 1975 Jan;67(1):123-125. Jacobs WF, Battle WE, Ronan JA. False-positive ST-T-wave changes secondary to hyperventilation and exercise. Ann Intern Med 1974;81:479-482. Wheatley CE. Hyperventilation syndrome: A frequent cause of chest pain. Chest 1975 Aug;68(2):195-199.

Although they pant and wheeze and complain of being unable to breathe, their symptoms are actually caused by breathing too much and putting themselves into a state of respiratory alkalosis. With the anti-smoking demagogues egging them on and approving, these people are creating their physiologically abnormal state by overbreathing, then blaming innocent people for what they did to themselves. Bag rebreathing, not smoking bans, are the cure for their malady.

6.1.2 Respiratory Infections (children)

This report claims that "Parental smoking is associated with an increased risk of acute lower respiratory tract illnesses in children,..." (6.4 Chapter Summary and Conclusions, page 6-60). We categorically reject this claim on the grounds that the studies are systematically methodologically defective. They do not control for absolutely essential covariates, namely the touching and hand-washing practices of cases and those with whom they associate. Respiratory infections are not spread by particles in the air, they are spread by physical contact. References: Gwaltney JM, Moskalski PB, Hendley JO. Hand-to-hand transmission of rhino- virus colds. Ann Intern Med 1978 Apr;88(4):463-467. Gwaltney JM, Hendley JO. Transmission of experimental rhinovirus infection by contaminated surfaces. Am J Epidemiol 1982;116(5):828-833. Hendley JO, Wenzel RP, Gwaltney JM. Transmission of rhinovirus colds by self-inoculation. NEJM 1973 Jun;288(26):1361-1364.

The anti-smokers are simply exploiting the socioeconomic differences and similarities between smokers, passive smokers, and non-smokers, as usual. The same criticism applies to the 1986 NRC, 1986 Surgeon General, and 1992 US EPA, notwithstanding pompous pretensions that "It has been clearly estab- lished in nearly two dozen reports... that ETS exposure increases the risk of acute lower respiratory disease in young children by 1.5 to 2-fold" (page 6-16). Repeating defective studies over and over again because they serve a political agenda doesn't make them valid, nor does repeating a lie over and over again make it true.

6.1.3 Otitis Media (children)

This report claims that "Parental smoking is associated with an increased risk of... acute and chronic otitis media with middle ear effusions. In California, ETS-related otitis media cases may result in an estimated 78,000 to 188,000 office visits per year among children under three years of age" (6.4 Chapter Summary and Conclusions, page 6-60).

We categorically reject this claim on the grounds that the alleged "risk" is in large part derived from studies of persons at whose age otitis media rarely occurs. Of the 8859 subjects of studies examined by the EPA, 3290 were aged 10 to 20; 1615 were aged 6-13 and the outcome of interest was merely snoring; and 736 were aged 6+ to 7+. Barely 3000 were in the most important age group: Over 80% of episodes of otitis media occur in 0-6 year olds; fewer than 8% of 7 year olds experience it, and it virtually disappears with increasing age (Lundgren K, Ingvarsson L. Scand J Infect Dis 1983;39(suppl):19-25.) But there was virtually no "ETS risk" among those under 6 years old. EPA finessed this difficulty by rationalizing: "Iverson and coworkers ... suggested that the risk associated with passive smoking increased with age. This may explain the negative results of several studies based on preschool children." Then EPA projected the "ETS effect" from older school-age children to pre- schoolers. And, speculations on biological effects of ETS ought to include the observation that Hemophilus influenzae and Streptococcus pneumoniae, bacteria linked to acute otitis media, are reported to be very sensitive to growth inhibition by cigarette smoke in vitro (at 8 fg/ml). (Ertel A et al. Chest 1991;100(3):628-630). This report does not mention this analysis, presumably because their conclusion is Politically Incorrect: Blakley BW, Blakley JE. Smoking and middle ear disease: Are they related? A review article. Otolaryngol Head Neck Surg 1995 Mar;112(3):441-446. In addition to reviewing the literature and finding the evidence unconvincing, they pointed out: "We could find no articles in the literature that suggested that smoking caused middle ear disease in the actual smokers. This is unique in the smoking literature. Ear infections are more prevalent in children than in adults, but serous otitis media and ear infections are common events in adults, too. We expect that exposure to possible irritants in smoke would be an order of magnitude greater to the smoker than to the nonsmoker and thus a higher risk for actual smokers. It is possible that children's special physiology includes exquisite sensitivity to smoke, but it is hard to believe that this vanishes completely in adulthood. Lower respiratory and upper respiratory diseases are more common in smokers and less so in children exposed to second-hand smoke, but ear disease apparently is the only known disease with a 'first-pass miss' phenomenon, affecting only the second-hand smoker."

6.2.4 Chronic Pulmonary Disease and Respiratory Symptoms (adults) -----------------------------------------------------------------

This report claims that "The effect of chronic ETS exposure upon pulmonary function in otherwise healthy adults is likely to be small, and unlikely by itself to result in clinically significant chronic disease. However, in combination with other insults (e.g., prior smoking history, exposure to occupational irritants or ambient air pollutants), ETS exposure could contribute to chronic respiratory impairment in adults." (6.4 Chapter Summary and Conclusions, page 6-60). We consider this a gross exaggeration, and more appropriately describes the effects of active smoking. There is very poor correlation between death rates from the group of diagnoses called "Chronic Obstructive Pulmonary Disease," or COPD, which includes emphysema, bronchitis, asthma, and other lung diseases, and the percentage of smokers by state. There is no correlation with the percentage of smokers above age 65, either. A National Center for Health Statistics study (Gillum RF. J Natl Med Assoc 1994;86(2):105-112) from the National Health Interview Survey on the prevalence of COPD by region and urbanization found that it paralleled smoking only among men aged 45-64, who paradoxically had the lowest reported rates. Cigarette smoking also doesn't explain international differences in COPD mortality (Brown CA et al. J Epidemiol Commun Health 1994;48(2):134-139). "Mortality rates in men are, in general, two to four times those in women. Most countries show either a decrease or no change in COPD mortality over the period [1979-1988]. In women the opposite is true -- no clear relationships are seen when comparing rates and trends of COPD with measures of smoking." And, a study supported by the US Environmental Protection Agency (Whittemore AS, Perlin SA, DiCiccio Y. Chronic Obstructive Pulmonary Disease in Lifelong Nonsmokers: Results from NHANES. Am J Public Health 1995 May;85 (5):702-706) showed that 4% of male and 5% of female lifelong nonsmokers reported physician-diagnosed COPD. Also, by NHANES II there was a clear class gradient, with the most privileged at several times less risk than the least privileged. Contrary to what we have been told, "the disease is not vanishingly rare in lifelong nonsmokers." And this is in conflict with the anti-smoker claim that "Approximately 85% of chronic obstructive pulmonary disease mortality in men and 69% of its mortality in women can be attributed to cigarette smoking," and that smokers have 8 to 10 times the risk of COPD. Only about 5% of smokers die of COPD, and the alleged prevalence is closer to 10-12%, not 24%.

This report also claims that "From 18,000 to 36,000 cases of ETS-related bronchitis or pneumonia can be predicted to occur in children 18 months of age and under, based on national statistics." (6.4 Chapter Summary and Conclu- sions, page 6-60). This does not appear to have been discussed anywhere else in the chapter. Pneumonia in newborns is almost invariably a consequence of intraamniotic infection, i.e., chorioamnionitis (see Chapter 3 comments). Exposed neonates are also at greater risk of septicemia, and more rarely otitis media, meningitis, and septic arthritis. It may also cause late onset disease from 1 week to several months after birth, and typically affects apparently healthy infants. References: RL Naeye. Disorders of the placenta, fetus, and neonate, diagnosis and clinical significance. New York: CV Mosby Co., 1992. Schuchat A, Wender JD. Epidemiology of Group B Streptococcal disease. Risk factors, prevention strategies, and vaccine development. Epidemiologic Reviews 1994;16(2):374-402.