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

CHAPTER 4
Developmental Toxicity II: Postnatal Manifestations

4.2 Sudden Infant Death Syndrome

This report commits a reprehensible sophistry. By definition, the causes of SIDS are unknown. It is definitely not just one single entity. The variety of different risk factors which have been identified, from sleeping position to recent illnesses, illustrate this. It is ludicrous to claim that "There is adequate epidemiological evidence of a causal relationship between maternal smoking in general and risk of SIDS" (4.6 Chapter Summary and Conclusions, page 4-29) when this actually amounts to asserting that smoking "caused" their own ignorance! This report pretends that, just because they can plug numbers into a computer program, "the unknown" is an actual clinical entity! Predictably, these unknown factors are more common among the socioeconomically disadvantaged, which the anti-smoking movement has always eagerly exploited. This report ignores the experience of The Netherlands, where the SIDS rate was very low during the highest rates of maternal smoking, then rose precipitously while maternal smoking declined; and similar experiences in other countries. References: Engelberts AC, de Jonge GA. Choice of sleeping position for infants: possible association with cot death. Arch Dis Childhood 1990;65:462-467. Notes increased SIDS during smoking decline in Holland. Engelberts AC, de Jonge GA, Kostense PJ. An analysis of trends in the incidence of sudden infant death in The Netherlands 1969-89. J Paediatr Child Health 1991;27:329-333. "Maternal smoking ... was on a stable high level in the period 1967-75: in those years the percentage of smoking women aged 20-34 years was 58%. It showed a slow but steady decline in subsequent years until it reached 35% in 1989. The percentage of smoking during pregnancy followed the same trend on a somewhat lower level (in 1988 27%). "Meanwhile, SIDS rose swiftly around 1974, as prone sleeping position increased from around 10% to peak at 55-65%, then declined, most swiftly in 1987-88 as prone sleeping fell to 27%. After a slight rise in 1989, prone sleeping fell to 15% in 1990." Court C. (news) Cot deaths. Britain: Incidence reduced by two thirds in five years. BMJ 1995 Jan 7;310(6971):7-8. Gilman EA, Cheng KK, Winter HR, Scragg R. Trend in rates and seasonal distribution of sudden infant deaths in England and Wales, 1988-92. BMJ 1995 Mar 11;310(6980):631-632. "sudden infant death rates rose more or less continuously from 1971 to a peak of 2.30 deaths per 1000 live births in 1988. Rates then fell steadily to 1.44 in 1991 and abruptly to 0.70 in 1992." Meanwhile, maternal smoking declined during the increase, which is not mentioned. Dwyer T, Ponsonby A-L, Blizzard L, Newman NM, Cochrane JA. The contribu- tion of changes in the prevalence of prone sleeping position to the decline in Sudden Infant Death Syndrome in Tasmania. JAMA 1995 Mar 8;273(10):783-789. In 1975 3.8/1k, 1990 1.5/1k. Position = 70% of the reduction; "Other factors examined individually contributed to less than 10% of the SIDS rate reduction." Antenatal maternal smoking after/before 0.93 (0.84-1.04) [about the same]. "Mother never smokes in room with infant" supposedly contributed to 4.0% of reduction [sic, in view of studies showing higher risks from never smoking inside the house]. Guntheroth WG, Spiers PS. Sleeping prone and the risk of sudden infant death syndrome. JAMA 1992 May 6;267(17):2359-2362. Review. Notes that in the Netherlands, SIDS increased during a period when smoking decreased, prone position. The bottom line is that changes in sleeping position have produced dramatic changes in SIDS death rates. Changes in maternal smoking have produced no such changes. It is utterly criminal for this report to pretend that 30% of SIDS deaths are caused by a whiff of secondhand smoke.

4.3 Cognition and Behavior in Children

Those who are not just culturally biased but explicitly hostile members of an aggressor subculture should not even attempt to pass off their judgments as science. We have never seen any studies treating smokers and smokers' children as daily victims of hate propaganda and attempted cultural genocide by anti-smoking demagogues, the government and their media collaborators. "Controlling for social class" does not address this issue. Thus they are in a state of complete denial of the harm they are wantonly inflicting on others.

4.4 Postnatal Physical Development

As in Chapter 3, we point out that the studies upon which claims of height growth reduction are based are systematically methodologically deficient. New evidence has been found which links Helicobacter pylori infection in children to reduced growth:

Patel P, Mendall MA, Khulusi S, Northfield TC, Strachan DP. Helicobacter pylori infection in childhood: risk factors and effect on growth. BMJ 1994 Oct 29;309(6962):1119-1123. 554 schoolchildren age 7, followup at age 11. "Growth in height between 7 and 11 was diminished in infected children by a mean of 1.1 cm (0.3 to 2.0 cm) over four years. This growth reduction was largely confined to girls (1.6 cm over four years), among whom it correlated with salivary IgG (p=0.015)." Girls grow more than boys from ages 7 to 11.

Helicobacter pylori infection has also been associated with diminished adult height (Mendall M, Molineaux N, Levy J, Strachan D, Northfield TC. Association of H pylori with diminished adult height. Gut 1994;35:S4). Immune responses to infection may nonspecifically interefere with growth, or may disturb endocrine ovarian function or gonadal sex steroids (Patel). People of lower socioeconomic class are more likely to have been infected by H pylori, and smokers, along with ETS-exposed non-smokers, are more likely to be of lower socioeconomic class than non-exposed non-smokers, and therefore share this risk factor. The similarity of the magnitude of the differences in birthweight between smokers and passive smokers, versus non-exposed non- smokers, despite immensely different exposure levels, points to socioeconomic factors, not biochemical exposure, as the cause.