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

CHAPTER 3
Developmental Toxicity I: Perinatal Manifestations

3.2 Fetal Growth

This report claims that "Smoking by the mother during pregnancy has long been considered an important independent risk factor for decreased infant birthweight," and that "the weight of the evidence indicates a causal effect." (3.2.1, page 3-1).

We contest this claim on the grounds that the studies upon which it is 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.

3.3 Spontaneous Abortion and Perinatal Mortality

Spontaneous abortion:

Physical activity is not mentioned as an important confounder. Reference: Florack EIM, Zielhuis GA, Pellegrino JEMC, Rolland R. Occupational physical activity and the occurrence of spontaneous abortion. Int J Epidemiol 1993 Oct;22(5):878-884. 170 pregnancies. Smoking 0.9 (0.4-1.9). Work involving bending 3.2 (1.3-9.8). Violence is not mentioned as an important confounder. In fact, there are virtually no studies directly investigating violence. Alcohol use (also not mentioned), which has been associated in some studies with spontaneous abortion, may be a proxy variable for violence. References: Adams Hillard PJ. Physical abuse in pregnancy. Obstet Gynecol 1985 Aug;66 (2):185-190. 918 prenatal care patients, 29 reported current physical abuse. 55% of abused used tobacco, versus 36% of controls. "The association with adverse pregancy outcome has been suggested frequently in the psychiatric literature with statements to the effect that blows to the abdomen often lead to abortions and premature births." Seven percent of the women interviewed by Bowker reported that they had suffered miscarriages as a result of beating. Amaro H, Fried LE, Cabral H, Zuckerman B. Violence during pregnancy and substance use. Am J Public Health 1990 May;80(5):575-579. Berenson AB, San Miguel VV, Wilkinson GS. Violence and its relationship to substance use in adolescent pregnancy. J Adolesc Health 1992 Sep;13(6): 470-474. Helton AS, McFarlane J, Anderson ET. Battered and pregnant: A prevalence study. Am J Public Health 1987 Oct;77(10):1337-1339. "One retrospective chart review of 2676 women with injuries at an emergency department found 21 per cent of the women's injuries positive, probable, or suggestive of battering. The battered women were more likely to have been pregnant or to have miscarried than the non-battered women....battered women have reported spontaneous abortions and stillbirths following episodes of battering."

Perinatal mortality:

This report claims that "Low birthweight is associated with many well-recognized problems for infants and is strongly associated [sic] with perinatal mortality," (3.5 Chapter Summary and Conclusions, page 3-35), without being specific about those problems, and attributes low birthweight deaths to ETS on this basis. This is epidemiologic malpractice and fraud. It deliberately evades the fact that poor perinatal outcome is really most strongly related to certain specific clinical causes, which are demonstrably not caused even by active smoking, and are not due to low birth-weight per se. These poor perinatal outcomes are actually due to chorioam-nionitis, and include preterm birth, premature rupture of membranes, still-birth, septicemia, neonatal otitis media, meningitis, septic arthritis, and neonatal pneumonia. References which should be included in this report: Naeye RL. Acute chorioamnionitis and the disorders that produce placental insufficiency. In: Monographs in Pathology No.33, Pathology of Reproductive Failure. FT Kraus et al, eds. Williams and Wilkins 1991. Ch 10, pp 286-307. Naeye RL. Editorial. The investigation of perinatal deaths. NEJM 1983;309 (10):611-612. Naeye RL. Disorders of the placenta, fetus, and neonate, diagnosis and clinical significance. New York: CV Mosby Co., 1992. Naeye RL, et al. The clinical significance of placental villous edema. Pediatrics 1983;71(4):588-594.

In "Disorders of the placenta, fetus, and neonate, diagnosis and clinical significance," Naeye states:

"In the CPS the uncorrected relative risk of maternal smoking for the death of fetuses and neonates was 1.22, which is close to the 1.28 value of the British Perinatal Mortality Survey. The British survey did not collect information on the other risk factors on which information is needed to do a credible study of the reasons.... When these risk factors were taken into consideration, mothers' smoking during pregnancy was no longer a risk factor for fetal or neonatal death.... Based on these findings, it cannot be taken for granted that persuading women to stop smoking during pregnancy will reduce perinatal mortality." [Page 85].

There is quite clearly an anti-smoker conspiracy in this report, as well as throughout the literature as a whole, to ignore the work of RL Naeye, which exposes the methodological defects of the work they rely upon, in order to deliberately continue using that defective methodology to deceive the public and falsely blame smoking and passive smoking.

3.4 Congenital Malformations

This report claims that "The most consistent association appears to be with central nervous system or neural tube defects; this association was observed in all but one of the five studies that provided sufficient data." (3.5 Chapter Summary and Conclusions, page 3-35). Despite recent highly-publicized recommendations that pregnant women get adequate folic acid during pregancy in order to prevent CNS / neural tube defects, this report makes no mention whatsoever of this as a necessary factor for valid study results. In fact, there is no consistent association even with active smoking. Nor are there associations between active smoking and chromosome anomalies, congenital heart defects, musculoskeletal or urogenital birth defects. (Summaries of study results enclosed).