While few people argue against the negative effects of smoking on health, the jury is still out regarding the long-term damage that can be inflicted by secondhand smoke. To be sure, there are plenty of news releases suggesting that thousands of cancers and other serious diseases can be attributed to environmental tobacco smoke (ETS). However, nearly all of these claims are based on statistical modeling, rather than hard data on actual patients.
We do know that most toxins have profoundly greater effects in utero. Thus, pregnant women are cautioned to avoid exposure to drugs and environmental chemicals—including ETS. Stephen G. Grant, Ph.D., of the University of Pittsburgh, has been studying the effects of ETS on newborns, who were exposed to it while in the womb.
In a 2005 paper, Grant examined the effects of ETS—as well as active smoking by the mother—on a particular gene (HPRT) of the newborns.
The disturbing findings of this research were that both active maternal smoking and secondary maternal exposure produce quantitatively and qualitatively indistinguishable increases in fetal HPRT mutation. More than that, Grant concluded that this effect is not lessened to any measurable degree if the mother stops smoking upon confirmation of pregnancy. He did posit that ETS could play a role in this phantom ongoing effect.
In a paper just published online in The Open Pediatric Medicine Journal, Grant confirms smoke-induced mutation in a completely different gene—glycophorin A. Here again, there was little difference in results between active smoking and passive exposure to ETS. And, there was also the finding that stopping smoking during pregnancy was of little benefit if the mother did not also limit exposure to ETS.
It is noted that the women studied categorized themselves into the four groups of unexposed, passive only, quit during pregnancy, and smoked throughout. This self-assessment was tested with further blood assays that checked for smoking metabolites and drugs of abuse. Still, various confounding factors including nutrition and exposure to other toxins could not be evaluated.
Grant seems to be the best promoter of his own work…
“These findings back up our previous conclusion that passive, or secondary, smoke causes permanent genetic damage in newborns that is very similar to the damage caused by active smoking. By using a different assay, we were able to pick up a completely distinct yet equally important type of genetic mutation that is likely to persist throughout a child’s lifetime. Pregnant women should not only stop smoking, but be aware of their exposure to tobacco smoke from other family members, work and social situations.”
How about a reality check?
Grant is certainly correct when he cautions pregnant women to stop smoking. As to ETS, a few points should be considered.
Any effect of toxins on genes would be dose-dependent, but Grant’s four categories of exposure hardly quantify dose. This alone should cast serious doubts on his conclusions. Is it possible that in nine months of pregnancy a woman can really be “unexposed” to environmental tobacco smoke? And imagine the variation in exposure that must have existed within the “passive only” cohort.
With some exceptions, the notion of a mutation persisting throughout life is absurd. Based on exposure to countless factors, mutations are occurring—by the millions—all the time. In fact, the inherent mechanism of DNA to repair itself is so prodigious that it directly correlates with the life expectancy of organisms. Inasmuch as Grant’s assays were run on newborn cord blood, they would not reflect in vivo repair modalities.
Finally, what are the public health implications of encouraging pregnant women to stop smoking, but then stating that it will do them no good if they cannot also avoid exposure to ETS? Perhaps the National Institute of Child Health and Human Development—one of the agencies that funded Grant’s work—should be asking themselves this question.
By Michael D. Shaw