Adverse Effects Of Maternal Smoking Research Articles

The effect of maternal tobacco smoking and second-hand tobacco smoke exposure on human milk oxidant-antioxidant status

BackgroundMany women who smoke tobacco continue to do so during lactation, and many non-smoking women are exposed to second-hand tobacco smoke (SHS) during the period that she wishes to breastfeed. There are reports documenting the adverse effects of maternal smoking during lactation on their infant's health; however, the pathophysiological mechanisms underlying these effects are incompletely understood. ObjectivesOur study purpose was to examine the influence of tobacco smoke on biochemical markers reflecting the intensity of oxidative stress using concentration of total protein (TP), trolox equivalent antioxidant capacity (TEAC), S-nitrosothiols (RSNO), nitric oxide (NO), thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) in the plasma, colostrum, and mature milk of women who smoke, those only exposed to SHS, and non-smokers. MethodsQuestionnaire data on the tobacco smoking status were verified based on the determination of cotinine by high performance liquid chromatography with diode array detector (HPLC-DAD). Relevant markers of oxidative stress and biochemical parameters were determined using spectrophotometric methods. ResultsWe found that tobacco smoking during lactation increases oxidative stress in the mother's plasma, colostrum, and mature milk, and lesser so in those exposed to SHS. Tobacco smoke significantly increase TBARS and decrease TEAC in colostrum and mature milk. In response to ROS generated by tobacco smoke increase the activity of antioxidant enzymes (SOD, GST, GPx and CAT), p < 0.05. DiscussionSuch exposure to tobacco smoke influences the antioxidant barrier of human colostrum and mature milk that can adversely affect their infant's health. Greater public health awareness of the adverse effects of tobacco smoking during lactation on breast milk quality and its protective effects is urgently needed.

MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring

To investigate the effect of maternal MitoQ treatment on renal disorders caused by maternal cigarette smoke exposure (SE). We have demonstrated that maternal SE during pregnancy increases the risk of developing chronic kidney disease (CKD) in adult offspring. Mitochondrial oxidative damage contributes to the adverse effects of maternal smoking on renal disorders. MitoQ is a mitochondria-targeted antioxidant that has been shown to protect against oxidative damage-related pathologies in many diseases. Female Balb/c mice (8 weeks) were divided into Sham (exposed to air), SE (exposed to cigarette smoke) and SEMQ (exposed to cigarette smoke with MitoQ supplemented from mating) groups. Kidneys from the mothers were collected when the pups weaned and those from the offspring were collected at 13 weeks. Maternal MitoQ supplementation during gestation and lactation significantly reversed the adverse impact of maternal SE on offspring’s body weight, kidney mass and renal pathology. MitoQ administration also significantly reversed the impact of SE on the renal cellular mitochondrial density and renal total reactive oxygen species in both the mothers and their offspring in adulthood. Our results suggested that MitoQ supplementation can mitigate the adverse impact of maternal SE on offspring’s renal pathology, renal oxidative stress and mitochondrial density in mice offspring.

Genome-wide DNA methylation study in human placenta identifies novel loci associated with maternal smoking during pregnancy.

We conducted an epigenome-wide association study (EWAS) of DNA methylation in placenta in relation to maternal tobacco smoking during pregnancy and examined whether smoking-induced changes lead to low birthweight. DNA methylation in placenta was measured using the Illumina HumanMethylation450 BeadChip in 179 participants from the INfancia y Medio Ambiente (INMA) birth cohort. Methylation levels across 431 311 CpGs were tested for differential methylation between smokers and non-smokers in pregnancy. We took forward three top-ranking loci for further validation and replication by bisulfite pyrosequencing using data of 248 additional participants of the INMA cohort. We examined the association of methylation at smoking-associated loci with birthweight by applying a mediation analysis and a two-sample Mendelian randomization approach. Fifty CpGs were differentially methylated in placenta between smokers and non-smokers during pregnancy [false discovery rate (FDR) < 0.05]. We validated and replicated differential methylation at three top-ranking loci: cg27402634 located between LINC00086 and LEKR1, a gene previously related to birthweight in genome-wide association studies; cg20340720 (WBP1L); and cg25585967 and cg12294026 (TRIO). Dose-response relationships with maternal urine cotinine concentration during pregnancy were confirmed. Differential methylation at cg27402634 explained up to 36% of the lower birthweight in the offspring of smokers (Sobel P-value < 0.05). A two-sample Mendelian randomization analysis provided evidence that decreases in methylation levels at cg27402634 lead to decreases in birthweight. We identified novel loci differentially methylated in placenta in relation to maternal smoking during pregnancy. Adverse effects of maternal smoking on birthweight of the offspring may be mediated by alterations in the placental methylome.

L-Carnitine reverses maternal cigarette smoke exposure-induced renal oxidative stress and mitochondrial dysfunction in mouse offspring.

Maternal smoking is associated with metabolic disorders, renal underdevelopment, and a predisposition to chronic kidney disease in offspring, yet the underlying mechanisms are unclear. By exposing female Balb/c mice to cigarette smoke for 6 wk premating and during gestation and lactation, we showed that maternal smoke exposure induced glucose intolerance, renal underdevelopment, inflammation, and albuminuria in male offspring. This was associated with increased renal oxidative stress and mitochondrial dysfunction at birth and in adulthood. Importantly, we demonstrated that dietary supplementation of l-carnitine, an amino acid shown to increase antioxidant defenses and mitochondrial function in numerous diseases, in smoke-exposed mothers during pregnancy and lactation significantly reversed the detrimental maternal impacts on kidney pathology in these male offspring. It increased SOD2 and glutathione peroxidase 1, reduced ROS accumulation, and normalized levels of mitochondrial preprotein translocases of the outer membrane, and oxidative phosphorylation complexes I-V in the kidneys of mouse progeny after intrauterine cigarette smoke exposure. These findings support the hypothesis that oxidative stress and mitochondrial dysfunction are closely linked to the adverse effects of maternal smoking on male offspring renal pathology. The results of our study suggest that l-carnitine administration in cigarette smoke-exposed mothers mitigates these deleterious renal consequences.

Characterization of the adverse effects of nicotine on placental development: in vivo and in vitro studies

In utero exposure to nicotine is associated with increased risk of numerous adverse fetal and neonatal outcomes, which suggests that it acts directly to affect placental development and the establishment of the fetomaternal circulation (FC). This study used both in vivo [Wistar rats treated with 1 mg/kg nicotine from 2 wk prior to mating until gestational day (GD) 15] and in vitro (RCHO-1 cell line; treated with 10(-9) to 10(-3)M nicotine) models to examine the effects of nicotine on these pathways. At GD 15, control and treated placentas were examined for the impact of nicotine on 1) trophoblast invasion, proliferation, and degree of hypoxia, 2) labyrinth vascularization, 3) expression of key genes of placental development, and 4) expression of placental angiogenic factors. The RCHO-1 cell line was used to determine the direct effects of nicotine on trophoblast differentiation. Our in vivo experiments show that nicotine inhibits trophoblast interstitial invasion, increases placental hypoxia, downregulates labyrinth vascularization as well as key transcription factors Hand1 and GCM1, and decreases local and circulating EG-VEGF, a key placental angiogenic factor. The in vitro experiments confirmed the inhibitory effects of nicotine on the trophoblast migration, invasion, and differentiation processes and demonstrated that those effects are most likely due to a dysregulation in the expression of nicotine receptors and a decrease in MMP9 activity. Taken together, these data suggest that adverse effects of maternal smoking on pregnancy outcome are due in part to direct and endocrine effects of nicotine on the main processes of placental development and establishment of FC.

High cotinine levels are persistent during the first days of life in newborn second hand smokers

BackgroundDespite the adverse effects of maternal smoking during pregnancy on the newborn's health are well-known, in the pediatric population, a high prevalence exists that is very much affected by second hand smoke (SHS). This study aims to investigate the impact of maternal smoking habits during pregnancy on cotinine levels in newborns during the first days of life. The high association between cotinine concentration in maternal and umbilical cord blood (UCB) has been previously reported, but the levels of blood cotinine that remain in infants born to smokers is unknown. MethodsCotinine concentration was measured in UCB, in maternal and newborn peripheral blood. Data from UCB sample dyads of ninety mothers and from seventy-one newborns were analyzed. ResultsCotinine levels were significantly different among non-smokers (9.9±5.9ng/ml), moderate (67.3±7.4ng/ml), and heavy smokers (137.7±19.5ng/ml) (p<0.0001). Significant correlations were found between maternal and UCB cotinine (r=0.748; p<0.001), and between UCB and newborn plasma cotinine at 48h after birth (r=0.541; p<0.001). The smokers exposed their infants to cotinine with a median of 31.7±8.6ng/ml (moderate) or 59.1±13.3ng/ml (heavy smokers) until at least, 48h after birth. Reduced birth weight and length were significantly related with UCB cotinine levels. ConclusionsA positive association between UCB and plasmatic cotinine in newborns was found. The high cotinine levels detected in newborns from smoker mothers indicates that their infants are subjected to elevated SHS from birth. These results can help to reinforce the awareness of the adverse effects of smoking during pregnancy.

Application of causal model to maternal smoking cessation intervention in pregnancy

The adverse effects of maternal smoking during pregnancy on both the offspring and women are well known. The main objective of this research article is to provide health professional causal modelling approach to make a more comprehensive assessment of major determinants of smoking behaviour during and after pregnancy and consequently the outcomes of pregnant women smoking which are adversely affecting both the offspring and pregnant women. The causal model based on theory and evidence was modified and applied to material smoking cessation intervention to control the adverse effects of smoking on offspring obesity and neurodevelopment. In this approach a generic model links behavioural determinants, causally through behaviour, to physiological and biochemical variables, and health outcomes. It is tailored to context, target population, behaviours and health outcomes. The model provides a rational guide to appropriate measures, intervention points and intervention techniques, and can be tested quantitatively. The causal modelling approach showed promising results which can be used to help maternal smoking women to understand the risk of smoking and help them to quit smoking. The regression analysis of maternal smoking women BMI (n = 1000) on offspring BMI was statistically significant, p 0.05). This supported the hypothesis that maternal smoking women BMI during pregnancy is an important determinant of offspring obesity and consequently the risk factors of cardiovascular development. The causal modelling approach is unique as it provides an incentive to health professional to use these models to target any important and modifiable determinants of the maternal smoking behaviour and decrease the risk of adverse pregnancy outcomes for the offspring and the mother.

Combined adverse effects of maternal smoking and high body mass index on heart development in offspring: evidence for interaction?

ObjectiveTo study the influence of a possible interaction between maternal smoking and high body mass index (BMI) on the occurrence of specific congenital heart anomalies (CHA) in offspring.DesignCase-control study.SettingData from...

Folic Acid Supplements Modify the Adverse Effects of Maternal Smoking on Fetal Growth and Neonatal Complications

Maternal smoking during pregnancy leads to increased risks of neonatal complications. The use of folic acid supplements might reduce the adverse effects of smoking. We examined whether folic acid supplement use modifies the associations of maternal smoking with first trimester plasma homocysteine concentrations, fetal growth characteristics, and risks of neonatal complications. The associations were studied in 6294 mothers participating in a prospective population-based cohort study in The Netherlands. Main outcomes measurements were first trimester plasma homocysteine concentrations, fetal growth characteristics, and neonatal complications, including preterm birth, low birth weight, and small-size-for-gestational-age. Continued maternal smoking was associated with higher first trimester plasma homocysteine concentrations [difference 0.52 γ mol/L (95% range = 0.20, 2.14)], lower third trimester fetal weight (difference -44 g (95% CI = -57, -31)], and birth weight [difference -148 g (95% CI = -179, -118)]. There were significant interactions between maternal smoking and folic acid supplements on all outcome measures (all P -interaction < 0.040). Among mothers who continued smoking during pregnancy, those who did not use folic acid supplements had the highest risk of delivering a child with low birth weight [OR = 3.45 (95% CI = 1.25, 9.54)] compared to those who did use periconceptional folic acid supplements. No significant effects were observed for the risks of preterm birth and small-size-for-gestational-age at birth. Our results suggest that some adverse effects of maternal smoking on fetal growth and neonatal outcomes might be reduced by the use of folic acid supplements. The observed interaction seems to be mainly driven by smoking in the first trimester only.

Smoking During Pregnancy Increases Risks of Various Obstetric Complications: A Case-Cohort Study of the Japan Perinatal Registry Network Database

BackgroundThe adverse effects of maternal smoking on the health of pregnant women have been examined mostly on a disease-by-disease basis. The aims of this study were to evaluate simultaneously the effects of smoking during pregnancy on various obstetric complications, using data from a large medical database, and to investigate the expediency of using a case-cohort design for such an analysis.MethodsA case-cohort study was conducted within the Japan Perinatal Registry Network database. Perinatal information on infant deliveries was entered into the database at 125 medical centers in Japan. The base population of the study was 180 855 pregnant women registered in the database from 2001 through 2005. The outcome measures were the incidences of 11 different obstetric complications. Logistic regression models were used to estimate age-adjusted risk ratios (aRRs) and relative excess incidence proportions (REIs).ResultsThe overall prevalence of smoking during pregnancy was 5.8% in the base cohort, and the prevalence was higher among younger women. A comparison of the cases and control cohort showed that smokers during pregnancy had statistically significant higher risks for preterm rupture of the membrane (aRR: 1.67, 95% confidence interval [CI]: 1.43–1.96; REI: 40.2%, 95% CI: 29.9%–49.1%), chorioamnionitis (1.65, 1.36–2.00; 39.4%, 26.4%–50.0%), incompetent cervix (1.63, 1.35–1.96; 38.5%, 25.8%–49.1%), threatened premature delivery (1.38, 1.17–1.64; 27.7%, 14.5%–38.9%), placental abruption (1.37, 1.10–1.72; 27.1%, 8.8%–41.7%), and pregnancy-induced hypertension (1.20, 1.01–1.41; 16.4%, 1.2%–29.3%).ConclusionsMaternal smoking was associated with a number of obstetric complications. This highlights the importance of smoking cessation during pregnancy. In addition, case-cohort analysis proved useful in estimating RRs for multiple outcomes in a large database.

Maternal smoking during pregnancy predicts nicotine disorder (dependence or withdrawal) in young adults – a birth cohort study

To investigate whether maternal smoking during pregnancy predicts offspring nicotine disorder (dependence or withdrawal) at 21 years. Participants comprised a prospective birth cohort involving 7,223 singleton children whose mothers were enrolled between 1981 and 1983 at the first antenatal visit to the Mater Mothers' Hospital, Brisbane, Queensland. The present sub-cohort consisted of 2,571 youth who completed the Composite International Diagnostic Interview-computerised version (CIDI-Auto) that assesses nicotine dependence and withdrawal according to DSM-IV diagnostic criteria at the 21-year follow-up. 12.8% of offspring met criteria for nicotine dependence and 8.5% met criteria for withdrawal. 16.6% met criteria for either dependence or withdrawal. Smoking during pregnancy resulted in offspring being more likely to have dependence or withdrawal at 21 years than offspring of mothers who never smoked (age adjusted odds ratio 1.53 (95% CI: 1.19-1.96). Findings emphasise the long-term adverse effects of maternal smoking during pregnancy, including nicotine dependence in young adult offspring. Public health approaches should strengthen arguments for mothers to cease smoking during pregnancy in view of the long-term health implications for offspring, and reinforce measures to help smokers among pregnant women and women of childbearing age to stop.

Adverse Birth Outcomes of Maternal Smoking During Pregnancy and Genetic Polymorphisms: Exploiting Gene-Environment Interaction

It has been recognized that metabolic enzymes mediating genetic susceptibility to environmental chemicals such as polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls might be related to adverse human health. Recent studies, including the Hokkaido Study of Environmental and Children's Health, have shown that metabolic enzymes mediating genetic susceptibility to environmental chemicals including tobacco smoke might be related to adverse birth outcomes. Certain maternal genetic polymorphisms in the polycyclic aromatic hydrocarbons (PAHs)-metabolizing enzymes have been shown to enhance the association between maternal smoking and infant birth weight in both Caucasians and Japanese. For maternal genetic polymorphisms encoding the N-nitrosamine-metabolizing enzymes, we found that infant birth weight, birth length and birth head circumference were significantly smaller among infants of smokers than among those of nonsmokers and quitters. The adverse effects of maternal smoking on infant birth size may be modified by maternal genetic polymorphisms. Further study is required to clarify the potential association between genetic polymorphisms and cognitive function in childhood, becauae it has been reported that a small birth length or a small head circumference at birth might affect neurobehavioral development during early childhood. It is necessary to elucidate additive impacts of genetic factors on adverse effects of various chemicals commonly encountered in our daily lives, follow up the development of children, and carry out longitudinal observation.

Adverse Birth Outcomes Associated with Maternal Smoking and Polymorphisms in the N-Nitrosamine-Metabolizing Enzyme Genes NQO1 and CYP2E1

Maternal smoking during pregnancy can result in both pregnancy complications and reduced size of the fetus and neonate. Among women who smoke, genetic susceptibility to tobacco smoke also is a likely causative factor in adverse pregnancy outcomes. A prospective cohort study was conducted among 460 pregnant women who delivered live singletons in Sapporo, Japan, from 2002 to 2005. Multiple linear regression models were used to estimate associations of maternal smoking and polymorphisms in two genes encoding N-nitrosamine-metabolizing enzymes-NAD(P)H: quinone oxidoreductase 1 (NQO1) and cytochrome P-450 2E1 (CYP2E1)-with birth size. Among infants born to smokers with the NQO1 homozygous wild-type allele, birth weight, birth length, and birth head circumference were significantly reduced (p < 0.01 for each factor). For the homozygous wild-type CYP2E1 allele, birth weight was lower by an estimated 195 g (standard error, 55; p < 0.001) among smokers. These genotypes did not confer adverse effects among women who had never smoked or who quit smoking during the first trimester. The adverse effects of maternal smoking on infant birth size may be modified by maternal genetic polymorphisms in N-nitrosamine-metabolizing enzymes among Japanese subjects. These results may help in directing smoking cessation interventions during pregnancy, especially among susceptible women.

Chronic nicotinein uteroselectively suppresses hypoxic sensitivity in neonatal rat adrenal chromaffin cells

Nicotine in cigarette smoke has been linked to several deleterious side effects on the offspring of smoking mothers, including impaired development of the sympathoadrenal system, abnormal arousal reflexes, and sudden infant death syndrome. Catecholamine (CA) release from adrenomedullary chromaffin cells (AMCs) in response to asphyxial stressors, e.g., low O(2) (hypoxia) and elevated CO(2) (hypercapnia), is critical for adaptation to extrauterine life and occurs before splanchnic innervation. Here, we investigated the effects of prenatal nicotine bitartrate exposure on the ability of neonatal (P0) rat AMCs to respond appropriately to asphyxial stressors. Control AMCs isolated from pups born to saline-treated dams displayed typical responses to hypoxia and hypercapnia, including inhibition of outward K(+) current, membrane depolarization, increased cytosolic calcium, and CA secretion. In contrast, P0 AMCs from pups born to nicotine-treated dams showed a marked suppression or loss of hypoxic sensitivity, although hypercapnic sensitivity and the expression of CO(2) markers (i.e., carbonic anhydrase I and II) appeared normal. Moreover, isolated saline-treated P0 AMCs lost their hypoxic sensitivity when grown in culture for approximately 1 wk in the presence of a subsaturating concentration of nicotine base (50 microM), and this effect was abolished by the nicotinic acetylcholine receptor (nAChR) blocker mecamylamine (100 microM). Taken together, these data suggest that the adverse effects of maternal smoking on sympathoadrenal function in the offspring are due in part to a loss or suppression of acute hypoxic sensitivity in adrenal chromaffin cells, triggered by the direct action of nicotine on endogenous nicotinic acetylcholine receptors.

Adverse effects of maternal smoking during pregnancy on innate immunity in infants

The potentially fatal effects of maternal smoking on infants have been recognised since the 1800s 1. In the latter half of the 1900s, the link between maternal smoking and the increased rate of lower respiratory infection (LRI) in early life was described 2. Given the high rates of smoking in many societies 3, the burden of the increase in LRI is substantial. In a meta-analysis of relationships between parental smoking and respiratory disease, Li et al. 4 calculated that the odds ratio (OR) for hospitalisation of LRI in infancy or early childhood for those exposed to parental environmental tobacco smoke (ETS) compared with those not exposed was 1.93 (95% confidence interval (CI) 1.66–2.25). The risk was age related, as the ORs of prevalence of serious LRI were 1.71 (95% CI 1.33–2.20) and 1.25 (95% CI 0.88–1.78) for children aged 0–2 and 3–6 yrs, respectively. Li et al. 4 concluded that the results of community and hospital studies were broadly consistent, and showed that the child of a parent who smokes is at approximately twice the risk of having a serious respiratory tract infection requiring hospitalisation in early life. Indeed, early respiratory infection is not only a major cause of morbidity in developed countries, but, in developing countries, respiratory infection is also the leading cause of death in children 5. There have been a large number of studies showing the relationships between maternal smoking and impaired lung function and increases in respiratory symptoms in infants and young children. An effect of maternal smoking on neonatal lung function has been demonstrated in a study …

The adverse effects of maternal smoking on the human placenta: A review

Studies of placental pathologies associated with maternal cigarette smoking have led to many interesting observations. For example, maternal smoking impairs human placental development by changing the balance between cytotrophoblast (CTB) proliferation and differentiation. It is likely that chronic exposure to tobacco constituents in early pregnancy can affect placental development directly or indirectly by reducing blood flow, which creates a pathologically hypoxic environment. To understand this process at a molecular level, tissue samples from non-smoking and smoking mothers were studied to determine whether active and/or passive cigarette smoke exposure affects CTB expression of molecules that govern cellular responses to oxygen tension: the von Hippel-Lindau tumor suppressor protein (pVHL), hypoxia-inducible transcription factors (HIFs) and vascular endothelial growth factor-A (VEGF). The results show that maternal smoking dysregulates CTB expression of all three types of molecules. In addition, cell columns and proliferating cells were reduced while there was a corresponding increase in cell islands. All three phenomena were most obvious in the placentas of heavy smokers. Interestingly, a subset of the aforementioned effects can be detected in samples obtained from women who were passively exposed to cigarette smoke during pregnancy. These observations suggest that tobacco constituents exert direct effects on CTB proliferation and differentiation and help to explain the mechanisms by which smoking negatively effects human pregnancy outcome.

Neonatal health care costs related to smoking during pregnancy.

Much of the work on estimating health care costs attributable to smoking has failed to capture the effects and related costs of smoking during pregnancy. The goal of this study is to use data on smoking behavior, birth outcomes and resource utilization to estimate neonatal costs attributable to maternal smoking during pregnancy. We use 1995 data from the Center for Disease Control's (CDC) Pregnancy Risk Assessment Monitoring System (PRAMS) database. The PRAMS collects representative samples of births from 13 states (Alabama, Alaska, California, Florida, Georgia, Indiana, Maine, Michigan, New York (excluding New York City), Oklahoma, South Carolina, Washington, and West Virginia), and the District of Columbia. The 1995 PRAMS sample is approximately 25 000. Multivariate analysis is used to estimate the relationship of smoking to probability of admission to an NICU and, separately, the length of stay for those admitted or not admitted to an NICU. Neonatal costs are predicted for infants 'as is' and 'as if' their mother did not smoke. The difference between these constitutes smoking attributable neonatal costs; this divided by total neonatal costs constitutes the smoking attributable fraction (SAF). We use data from the MarketScantrade mark database of the MedStattrade mark Corporation to attach average dollar amounts to NICU and non-NICU nursery nights and data from the 1997 birth certificates to extrapolate the SAFs and attributable expenses to all states. The analysis showed that maternal smoking increased the relative risk of admission to an NICU by almost 20%. For infants admitted to the NICU, maternal smoking increased length of stay while for non- NICU infants it appeared to lower it. Over all births, however, smoking increased infant length of stay by 1.1%. NICU infants cost $2496 per night while in the NICU and $1796 while in a regular nursery compared to only $748 for non-NICU infants. The combination of the increased NICU use, longer stays and higher costs result in a positive smoking attributable fraction (SAF) for neonatal costs. The SAF across all states is 2.2%. Across the states, the SAF varied from a low of 1.3% in Texas to a high of 4.6% in Indiana. These results further confirm the adverse effects of smoking. Among mothers who smoke, smoking adds over $700 in neonatal costs. The smoking attributable neonatal costs in the US represent almost $367 million in 1996 dollars; these costs vary from less than a million in smaller states to over $35 million in California. These costs are highly preventable since the adverse effects of maternal smoking occur in the short-run and can be avoided by even a temporary cessation of maternal smoking. These cost estimates can be used by managed care plans, state and local public health officials and others to evaluate alternative smoking cessation programs.

Involuntary smoking and pregnancy

Attention has recently been focused on the effect of involuntary smoking on health [1,2]. The 1986 Surgeon General Report asserted for the first time that the involuntary inhalation of cigarette smoke by nonsmokers causes disease [3]. One of the best described associations is the risk of lung cancer among women married to smoking husbands [4,5]. The adverse effects of maternal smoking during pregnancy on the fetus have been convincingly established [6-81. The offspring of smoking mothers tends to be smaller in size [6,7] and at an increased risk for low birth weight [7,8] perinatal mortality [9] and congenital malformations [lo]. The aim of the present study is to review the current epidemiological data on the influence of environmental exposure to tobacco smoke during pregnancy on the fetus.

Carboxyhemoglobin Concentration in Fetal Cord Blood and in Blood of Mothers Who Smoked During Labor

It has been established beyond doubt that maternal cigarette smoking is associated with increased perinatal morbidity (prematurity, failure to grow, vaginal bleeding of pregnancy) and perinatal mortality (abortion and fetal or neonatal death).1,2 Various mechanisms have been implicated to explain these adverse effects of maternal smoking on the fetal outcome and among these, chronic carbon monoxide intoxication of the fetus induced by maternal smoking is identified as a major cause of the fetal toxicity of smoking.3,4 In animal studies, chronic exposure to a low level of carbon monoxide produced perinatal complications similar to those reported in pregnant smokers,1,3,4 In humans, accidental carbon monoxide poisoning from sources other than smoking caused fetal death or fetal brain damage.5