Newborns Of Smoking Mothers Research Articles

URINARY COTININE AS A MEASURE OF TOBACCO SMOKE EXPOSURE IN UTERO AND INFANCY

Maternal smoking during pregnancy and after birth has adverse effects on infants. However, studies to date have not used quantitative measures of infant tobacco smoke exposure. A RIA for cotinine, the major metabolite of nicotine, has been used for this purpose in adults. We studied whether urine cotinine could be detected in exposed newborns and young infants. Urine was collected every 12 hrs for the first 5 days of life from 7 newborns of smoking mothers and 1 control, all isolated from tobacco smoke after birth. Initial mean cotinine/creatinine in exposed newborns was 1884 ng/mg (range 364 to 3888 ng/mg); these are comparable to values found in non-smoking adults with workplace tobacco smoke exposure. The control infant had only 18 ng/mg. Cotinine elimination halftime was 56 hrs, more than twice that seen in adults. Urine cotinine was measured in 18 non-hospitalized, non-exposed infants and in 28 infants with at least 2 recent exposures. Mean cotinine/creatine from exposed infants was significantly greater (p<0.0001) than from non-exposed (459 vs 19 ng/mg), with a direct relationship between cotinine excretion and number of cigarettes consumed daily by the mother (r=0.64, p=0.0001). Urine cotinine is an easily obtainable and reliable measure of infant tobacco smoke exposure.

Carboxyhemoglobin Concentration in Fetal Cord Blood

To the Editor.— Bureau et al1 reported that the concentration of carboxyhemoglobin (HbCO) is increased more than twofold in cord blood of newborns of smoking mothers as compared to corresponding values in maternal venous blood. Data were obtained from an IL 282 (Instrumentation Laboratory, Lexington) Co-oximeter, an instrument using spectroscopic multicomponent analysis of HbO2, Hb, MetHb, and HbCO in whole blood. We are concerned that the data presented are due to an artifact of HbCO measurement as the instrument used is not suitable for the correct measurement of HbCO concentrations in fetal blood.

Genotoxicity of tobacco smoke and tobacco smoke condensate

This report reviews the literature on the genotoxicity of mainstream tobacco smoke and cigarette smoke condensate (CSC) published since 1985. CSC is genotoxic in nearly all systems in which it has been tested, with the base/neutral fractions being the most mutagenic. In rodents, cigarette smoke induces sister chromatid exchanges (SCEs) and micronuclei in bone marrow and lung cells. In humans, newborns of smoking mothers have elevated frequencies of HPRT mutants, translocations, and DNA strand breaks. Sperm of smokers have elevated frequencies of aneuploidy, DNA adducts, strand breaks, and oxidative damage. Smoking also produces mutagenic cervical mucus, micronuclei in cervical epithelial cells, and genotoxic amniotic fluid. These data suggest that tobacco smoke may be a human germ-cell mutagen. Tobacco smoke produces mutagenic urine, and it is a human somatic-cell mutagen, producing HPRT mutations, SCEs, microsatellite instability, and DNA damage in a variety of tissues. Of the 11 organ sites at which smoking causes cancer in humans, smoking-associated genotoxic effects have been found in all eight that have been examined thus far: oral/nasal, esophagus, pharynx/larynx, lung, pancreas, myeoloid organs, bladder/ ureter, uterine cervix. Lung tumors of smokers contain a high frequency and unique spectrum of TP53 and KRAS mutations, reflective of the PAH (and possibly other) compounds in the smoke. Further studies are needed to clarify the modulation of the genotoxicity of tobacco smoke by various genetic polymorphisms. These data support a model of tobacco smoke carcinogenesis in which the components of tobacco smoke induce mutations that accumulate in a field of tissue that, through selection, drive the carcinogenic process. Most of the data reviewed here are from studies of human smokers. Thus, their relevance to humans cannot be denied, and their explanatory powers not easily dismissed. Tobacco smoke is now the most extreme example of a systemic human mutagen.

Letter to the Editor

The valuable comments of Christoffel are much appreciated. It is said that newborns do adapt to carboxyhemoglobin poisoning (from smoking) by increasing their hemoglobin concentration in blood. Recently, we have further explored the adaptability of newborns to maternal smoking by a study of oxygen dissociation curves in newborns of smoking mothers. Our preliminary results showed that the newborn adapts to maternal and fetal increases in HbCO by a very small left shift in the Hb-O2 dissociation curve and by an increase in hemoglobin.1

Ultrastructural changes in preputial neural tissues: effects of maternal smoking.

The fetal prepuce was studied for neural changes due to maternal smoking during pregnancy. Prepuces from 10 newborns whose mothers smoked throughout pregnancy and from 4 newborns of nonsmoking mothers were examined by transmission electron microscope. Significant ultrastructural changes were seen in the neural tissues of the newborns of smoking mothers. The ultrastructural changes observed were: (1) local aggregation of mitochondria; (2) many myelin bodies, and (3) dilated Golgi apparatus and dilated endoplasmic reticulum of the Schwann cell. Similar changes have been reported in neuropathies due to various drugs, chemicals and deficiency states. These findings suggest adverse effects on fetal preputial neural tissue due to maternal smoking.