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Methods. We examined socioeconomic, demographic, and clinical risk factors associated with maternal smoking in a nationally representative cohort of women (n = 8285) who were surveyed 175 months and again 355 months after delivery.
Results. Smoking rates among women with a college degree decreased 30% from before pregnancy to 35 months postpartum but did not change among the least educated women. Risk factors clustered, and a gradient linked the number of risk factors (0, 2, 4) to the percentage smoking (6%, 31%, 58%, P<.0001).
Conclusions. The period of pregnancy and early parenthood is associated with worsening education-related disparities in smoking as well as substantial clustering of risk factors. These observations could influence the targeting and design of maternal smoking interventions. (Am J Public Health. 2002;92:1801-1808)
Smoking poses a significant threat to women's health.1 Women are more likely to stop smoking during pregnancy than at other times,1 yet the majority who quit are smoking again within 1 year postpartum.2-8 The lack of sustained benefit from interventions during pregnancy and postpartum9-16 suggests that our understanding of the determinants of smoking before, during, and after pregnancy remains inadequate.
In the only national population-based longitudinal study to examine this issue, Fingerhut et al.2 found that although 39% of smokers quit during pregnancy, 70% of them relapsed within 1 year postpartum. The lowest quitting rates were among those who smoked most before pregnancy and who had the least education. No significant risk factors for smoking relapse were identified. Although this was an important early contribution to smoking cessation research, the study included only White women, had a small sample size for examining relapse rates (n= 191 quitters), and did not assess potentially important risk factors, such as income17 and the presence of other household smokers.3,5-7,18 A populationbased, cross-sectional study found similar quitting and relapse rates but also identified African American race, parity, stressful events, and pregnancy weight gain as predictors.8 Other studies have found additional significant factors, including marital status,19 alcohol use,12 and breastfeeding.3,4 Surprisingly few studies have examined maternal depression despite the link between depression and smoking outside the context of pregnancy20-26 and its prevalence among women with young children.27,28
This prior research offers a detailed but fragmented picture of the factors associated with maternal smoking. First the relative importance of any given risk factor is difficult to interpret, because past studies each examined different sets of covariates. Second, important clinical (e.g., depressive symptoms) and social (e.g., income) risk factors remain inadequately studied. Third, no study has examined the clustering of these risk factors or assessed their cumulative effects.29-31 Finally, small sample sizes,3,5-7 sample homogeneity,2 and a lack of longitudinal data17 have further limited interpretation. The present study used data from the 1988 National Maternal and Infant Health Survey (NMIHS) and 1991 Longitudinal Follow-Up (LF), a national cohort study designed to identify factors related to poor pregnancy outcomes.32,33 We investigated factors associated with maternal smoking trends over the course of pregnancy and the first 3 years postpartum. We examined a more comprehensive set of clinical and social factors than has been analyzed to date, for both their individual and their cumulative associations with maternal smoking behaviors.
METHODS
Sample
The 1988 NMIHS was a population-based survey of 9953 women giving birth in 1988. Sampling was based on birth certificates from 48 states and the District of Columbia; Black mothers and the mothers of low- and very low birthweight infants were oversampled. The 1988 NMIHS was administered 175 months after delivery, and questions about pregnancy behaviors were based on maternal recall. The 1991 LF was administered 355 months after delivery. Eighty-eight percent (n=82 85) of the women completed the LF, and these women constitute the sample for this study. Additional information on the NMIHS has been published elsewhere.34,35
Measures
Outcomes. We examined four outcome measures. The first three of these outcomes came from the 1988 NMIHS and were determined by the mother's response to the following questions: "Did you smoke cigarettes during the 12 months before delivery?"; "Did you quit smoking for at least a week during your pregnancy?"; and "Do you smoke cigarettes now?" The fourth outcome, smoking at the time of the 1991 LF (355 months postpartum), was determined by the question "Do you smoke cigarettes now at all?" All responses were dichotomous. The predictor variables that follow were recoded to accommodate nonlinear relationships, skewed distributions, and prior approaches in the literature.
Socioeconomic and demographic variables. Maternal education (< 12 years, 12 years, 13 to 15 years, >= 16 years), total household income (<$10 000, $10,000 to $19 999, $20000 to $34 999, $35 000 to $49 999, and >=$50,000), Hispanic ethnicity, and marital status (currently married, never married, formerly married) were reported by the mother in the 1988 NMIHS. Maternal age (<20, 20 to 29, >=30 years) and race came from the birth certificate. Race and ethnicity data were combined to create 4 groups (White, non-Hispanic; Black, non-Hispanic; Hispanic; other).
Clinical variables. Additional self-report measures from the 1988 NMIHS included amount smoked during the 3 months before conception (< 1, >=1 pack/day), number of drinks per week before learning of pregnancy (< 1, 1 to 2, >=3), number of drinks per week after learning of pregnancy (< 1, >=1), pregnancy intention (wanted to become pregnant at that time, did not want to become pregnant at that time), and being currently pregnant (at the time of the 1988 NMIHS). Parity (1, >=2) and infant birthweight (<2500 g, >=2500 g) also came from the birth certificate.
We used any intention to breastfeed as a predictor for quitting during pregnancy, and ever breastfeeding as a predictor for smoking relapse after pregnancy.4 Maternal weight gain during pregnancy was constructed from the self-report of maternal weight before pregnancy and before delivery and was coded as either in the top quartile (>=40 lb) or below the top quartile.8 Maternal depression was determined by the Center for Epidemiologic Studies Depression Scale, a 20-item selfreport instrument included in the 1988 NMIHS. Women who scored 16 or above (out of a possible 60) were classified as having significant depressive symptoms.36
Contextual variables. The number of smokers (0, >=1) living with the mother during pregnancy and the number of smokers (0,
FIGURE 1.
>=1) living with the mother at 175 months postpartum were ascertained in the 1988 NMIHS.
Analysis
In the cross-sectional bivariate and multivariate analyses of each outcome, we used all women with available data. In the description of maternal smoking patterns over time (Figure 1) and in our longitudinal analysis, we used only those women who had outcome data available at all 4 points in time. Therefore, there is slight variation in the reported prevalence of smoking at each time point. For cross-sectional analyses, associations between independent variables and smoking outcomes were first examined in bivariate analyses. Significance was determined by the X^sup 2^ statistic and associated P value. Multivariate logistic regression analyses were used to determine the independent associations of the covariates on smoking outcomes. In longitudinal analyses, we examined the association of depressive symptoms at 175 months postpartum with the change in smoking status between 175 and 355 months (i.e., between the 1988 and 1991 surveys). We report adjusted odds ratios (ORs) and 95% confidence intervals (CIs). All variables that were significant in the prior literature were included in the regression models and were maintained in the adjusted analyses.
We weighted analyses to reflect US women who had a live birth in 1988, using data provided by the National Center for Health Sta tistics. We used SAS Version 8.1 (SAS Institute Inc, Cary, NC) and SAS-callable SUDAAN Version 7.5.4A (Research Triangle Institute, Research Triangle Park, NC).
RESULTS
Twenty-nine percent of the women smoked during the 12 months before delivery, 56% quit smoking for at least 1 week during pregnancy, and the majority (72%) of women who quit were smoking again at 17+/5 months postpartum (Figure 1). At 355 months, an additional 367 women (approximately 17% of all 1991 LF smokers) reported smoking, despite reporting no history of smoking in the 12 months before delivery. The net result was that the prevalence of smoking decreased slightly, from 29% within the 12 months before delivery to 26% at 355 months postpartum.
Smoking During the 12 Months Before Delivery
Compared with women who had graduated from college, women who had not graduated from high school were more than 4 timesas likely to smoke during the 12 months before delivery, adjusting for covariates (Table 1). The presence of other household smokers and increased alcohol consumption had similarly strong, independent associations with increased smoking. Lower family income, unmarried status, White race, and increased maternal age were also significant predictors of smoking.
Quitting During Pregnancy
Women who had not completed high school were one third as likely to quit smoking during pregnancy compared with women who had graduated from college, after adjusting for covariates (Table 2). Consuming 1 or more drinks per week during pregnancy, greater parity, no intention to breastfeed, and presence of other smokers in household were all independently associated with a lower likelihood of quitting during pregnancy.
TABLE 1
Relapsing After Pregnancy
Women who lived with another smoker were 4 times as likely to relapse as women who did not live with another smoker (Table 3). Low income and less education were also significant predictors of relapse. Neither breastfeeding nor the experience of having a low- birthweight infant conferred protection against relapse. In contrast to their significant association with quitting, the amount smoked before delivery and prenatal alcohol consumption were not significant predictors of relapse. Pregnancy weight gain also had no association with relapse.
Summary of Predictors
Maternal education and household smoking had significant adverse associations with all three outcomes (Table 4). Income also had consistent, but more modest, associations across all outcomes. Black race was associated with a reduced likelihood of smoking during the 12 months before delivery but was not associated with increased quitting or lower relapse.
Depressive Symptoms and Maternal Smoking
Twenty-four percent of women screened positive for depression at 175 months postpartum. Depressive symptoms were significantly associated with concurrent smoking (odds ratio [OR] = 1.2; 95% confidence interval [CI] = 1.0, 1.4). However, they were not associated with any change in smoking status between 175 and 35+/ -5 months (the 1988 NMIHS and 1991 LF). Among women who were not smoking at 175 months (n=5746), depressive symptoms at that time did not predict smoking initiation (n = 307) between the 2 surveys (OR=0.9; 95% CI=0.6, 1.4). Similarly, among women who were smoking at 175 months, depressive symptoms were not associated with continued smoking between the 2 surveys (OR= 1.1; 95% CI=0.8, 1.7).
Disparities in Smoking Over Time and Across Risk Factors
Education-related disparities in smoking rates increased over time. This increasing disparity was the result of the independent association of low education with both reduced likelihood of quitting and increased likelihood of later relapse. Smoking rates among women with a college degree decreased 30% from within 12 months before delivery to 355 months postpartum (11.7%1.1 % to 8.3%+/1.0%). In contrast, smoking rates among women with less than a high school degree did not decrease (39.9%1.7% to 41.1%+/1.80%). The net effect, therefore, was an increase in the relative disparity in smoking over the approximately 4-year window of time.
We examined the clustering of 5 risk factors found to be independently associated with current smoking at the time of the 1988 NMIHS. The risk factors were low income (<$20,000/year), less education (<=high school), living with another smoker, depressive symptoms (Center for Epidemiclogic Studies-Depression Scale score >=16), and alcohol consumption (>=3 drinks/week). Twenty-seven percent of all women had 2 risk factors, 18% had 3, and 7% had 4 or 5. A more detailed examination of smokers with depressive symptoms (n= 849), for example, showed that 57% lived in households with another smoker, 67% lived in low-income households, and 83% had no education beyond high school. Women with 0, 2, and 4 of these risk factors smoked at rates of 5.7%, 30.7%, and 58.10% (P< .00001), respectively.
DISCUSSION
Using a national sample with comprehensive demographic and clinical data, this study offers the fullest accounting to date of the patterns and correlates of smoking before, during, and after pregnancy. Three central findings emerge from this study relating to (1) the salient independent predictors of smoking outcomes, (2) the surprising lack of association between depressive symptoms and a change in smoking status, and (3) the disparities in smoking rates over time and across risk factors.
Predictors of Smoking Outcomes
Women with less education were more likely to smoke before delivery, less likely to quit during pregnancy, and more likely to relapse after delivery. The strengths of these relationships were striking even after adjustment for household income and other demographic covariates. Fingerhut et al.2 found associations of a similar magnitude between education levels and smoking rates before pregnancy as well as quitting rates but, in contrast, did not find that education levels predicted a postpartum relapse. This discrepancy may be due to power differences between their study and the current one. Given that in 1988 approximately 75% of all women smokers with young children had a 12th-grade education or less, future intervention trials should include a greater focus on these women, ensuring representation in study samples and appropriate educational materials.
A strong relationship was confirmed between the presence of other household smokers and an increased risk of postpartum relapse. The effect of partner smoking has been documented in prior studies,3,5- 7,12,15,18 and the more complete accounting for covariates in this study made little difference to the estimated effect. Studies in the general adult population have shown that such contextual smoking cues produce a desire to smoke.37 Recent animal research and human neuroimaging studies of addiction have suggested that the contextual cues themselves become directly associated with powerful neurobiological responses.38,39 The association of household smokers with postpartum relapse stands in some contrast to the weaker association of household smokers with quitting. It is not surprising that factors uniquely related to quitting may play a moderating role. For example, other smokers' support for the woman's quitting during pregnancy is likely stronger than their support for relapse prevention after delivery.5,18 Intervention research directed at changing the behavior of other household smokers appears to be an important area for future work.
TABLE 2
TABLE 3.
Neither parity nor birthweight was associated with protective effects. Presumably, multiparous mothers have had increased contact with health providers and therefore an increased "dose" of health education about smoking. However, consistent with Cnattingius and Thorslund's results,19 increased parity was associated with a lower rate of quitting. Perhaps a third factor, such as a woman's attitude of diminished investment toward her own reproductive health and toward the health of the fetus, increases parity and reduces quitting. However, controlling for unintended pregnancy had no effect in the model of quitting. Women who have previously delivered a healthy infant despite smoking may also be less motivated to quit in subsequent pregnancies.
Having a low-birthweight infant did not protect against relapse, despite presumed contact with physicians after the pregnancy. One difficulty may lie in the relative elevation of prenatal quitting messages over messages that emphasize the risk associated with smoking outside the context of pregnancy. Women who deliver low- birthweight infants despite quitting (for at least a week) may have been given little reason to "stay quit" after pregnancy. The stress of caring for a low-birthweight baby may also promote relapse. Alternatively, women with a low-birthweight infant may be more inclined to overreport having quit during pregnancy; thus, these women would appear to have higher relapse rates. In contrast to other studies, this study did not find that postpartum breastfeeding4 protected against postpartum relapse and did not find that excessive pregnancy weight gain8 had an adverse effect on postpartum relapse. Controlling for a larger number of covariates in our analyses (e.g., including other household smokers) may in part explain the different findings.
Lack of Association Between Depressive Symptoms and Change in Postpartum Smoking Status
Maternal depressive symptoms were assodated with concurrent smoking status. Surprisingly, they were not associated with a change in smoking status. These results contrast with those of Anda et al.,20 who found that in the general population, depressive symptoms significantly decrease the likelihood of subsequent quitting. Studies focusing on the relationship between depression and smoking cessation during pregnancy have had mixed results.40-42 A postpartum relapse prevention trial found that poor mental health 12 months after delivery was associated with having relapsed.15 Hanna et al.,43 using the 1988 NMIHS data, suggested that depressive symptoms influence smoking during pregnancy, but their study examined fewer covariates than this study, and the depressive symptoms were assessed well after delivery. Nevertheless, the high rates of both postpartum depression and smoking relapse suggest that further additional prospective research is needed to clarify this complex relationship.
This study demonstrates that the relative health disadvantage associated with low maternal education is dynamic and continues to accrue over a time period that is rich in health care contacts. The elimination of health disparities is now a major national health goal.44,45 As more efficacious treatments for smoking emerge,46 however, there is a risk that social disparities in smoking rat\es may actually increase if there are persistent differentials in knowledge about and access to these treatments.47 The rising Black- to-White differential in sudden infant death syndrome is one example of an increased health disparity between these groups that has resulted from an intervention (in this case, a campaign to change infants' sleep position).48
TABLE 3
TABLE 4
Our findings support the prior literature in delineating a series of independent risk factors associated with maternal smoking. However, the results also demonstrate that these "independent" risk factors cluster together. This clustering suggests the need for a more comprehensive and integrated approach across women's many health care contacts. It may also suggest the need for a broader notion of "well-women's care" with the goal of maintaining the positive health trajectory achieved during pregnancy. Specifically, the clustering of risk factors suggests that new interventions may be required for long-term success. This may include, for example, removing financial barriers to nicotine replacement therapy, focusing on the treatment of comorbid depression or alcohol problems, and changing the behavior of other household smokers.
Several limitations of this study exist. All smoking behaviors were by maternal selfreport, and behaviors during pregnancy were recalled approximately 17 months after delivery. Social desirability might lead to a biased recall of smoking. For example, underreporting of smoking might be more pronounced among highly educated women or women who had relapsed. However, self-reported smoking status, even well after the pregnancy, is reasonably accurate,49-51 and less educated women may actually be more likely to underreport smoking.52 Another limitation is that the outcomes lack detail. We cannot ascertain in which trimester the women quit smoking, whether the women did not smoke for the remainder of the pregnancy, and indeed whether some women quit before conception. The reported associations are not necessarily causal. An unobserved factor, such as a capacity to delay gratification, may jointly determine both the amount of education and smoking behavior.53 It is also important to note that the prevalence of smoking among pregnant women has decreased substantially since 1988. Nevertheless, the current social patterning of smoking may be as great, if not greater, than in 1988.54 Finally, the 88% response rate for the 1991 LF may bias the findings (e.g., relating to depressive symptoms), although the direction of the potential bias is unclear.
We used a nationally representative longitudinal cohort to examine the risk factors associated with smoking and relapse during the window of pregnancy and early parenthood. Of particular note was the powerful relationship between other household smokers and maternal relapse. In addition, we found that education-related disparities in smoking grew over a time period relatively rich in health care contacts and that the disparities rose sharply with an increasing number of clinical and social risk factors. Comprehensive interventions are needed that promote integration across health care contacts and that address the co-occurring morbidity that may constrain women's efforts to quit.
Copyright American Public Health Association Nov 2002
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Nov 23 02 8:20 PM
Feb 1 03 8:34 PM
From Join Together Online:
Many Women Return to Smoking After Pregnancy
1/31/2003
Although more women are quitting smoking during pregnancy, a new study finds that many return to cigarettes during the post-natal period, Health 24 reported Jan. 27.
The study analyzed surveys conducted from 1993 to 1999 involving 115,000 new mothers from 10 U.S. states. The data showed that 51 percent of pregnant women quit smoking in 1999, but half of them resumed smoking within six months of giving birth.
Those more likely to begin smoking again were teenagers and heavy smokers.
Based on the study's findings, author Dr. Gregory Colman of Pace University in New York recommended that doctors encourage women to stay away from cigarettes after their baby is born by emphasizing the dangers of secondhand smoke to infants.
The study is published in the January 2003 issue of the American Journal of Preventive Medicine.
Colman, G., & Joyce, T. (2003) Trends in smoking before, during, and after pregnancy in ten states. American Journal of Preventive Medicine, 24(1): 29-35.
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Study: Smoking During Pregnancy Impairs Fetal Development British research finds that women who smoke during pregnancy risk having smaller babies with smaller brains, Reuters reported March 24. According to researchers at University College London, smoking damages the placenta and reduces levels of a critical growth hormone. "The profound effects of smoking on fetal development are irreversible and may cause impairment in the health and well-being of the offspring in later life," said Dr. Peter Hindmarsh, lead author of the study. "In particular, the reduced brain size that we saw in smokers' babies could lead to impaired cognitive ability of the child." The study involved 1,650 expectant mothers, including 200 who smoked throughout their pregnancy. The researchers measured blood flow between the fetus and placenta and monitored levels of insulin-like growth factors (IGF), a group of hormones essential to fetal growth and organ development. After birth, the researchers weighed the newborns and measured their head size to determine brain size. The study found that blood flow in the artery joining the fetus to the placenta was lower in women who smoked. This resulted in damage to the placenta and restricted the delivery of essential nutrients. In addition, there was a lower amount of IGF in umbilical-cord blood among women who smoked. The levels varied, based on how many cigarettes the mother smoked. "What we're talking about are reductions of about 10 to 15 percent in IGF levels, producing rather similar reductions in overall birth size, birth length, and head growth," said Hindmarsh. Hindmarsh presented the study's findings at the annual meeting of the British Endocrine Societies, held recently in Glasgow, Scotland.
Jun 14 04 2:54 PM
SIDS prevention--good progress, but now we need to focus on avoiding nicotine. Acta Paediatr. 2004 April;93(4):450-2. Sundell HW. Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2585, USA. hakan.sundell@vanderbilt.edu Chong et al. examined risk factors for sudden infant death syndrome (SIDS) before and after the start of the Swedish campaign to reduce the risk of SIDS. They found that maternal smoking was the strongest risk factor for SIDS in the post-campaign compared to the pre-campaign period. CONCLUSION: After successful results of the SIDS campaigns to prevent prone sleeping, strong efforts need to be undertaken to eliminate maternal smoking during pregnancy altogether without replacing cigarette smoking with other nicotine delivery devices such as snuff, gum or patches. Publication Types: PMID: 15188968 [PubMed - in process] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15188968
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Mar 5 05 2:27 AM
From above:
July 2001
SMOKING, SEX & REPRODUCTION
Introduction
Cigarette smoking can affect women's fertility; men's fertility; sexual function in men; pregnant women's health; the health of an unborn child; and the health of young children.
Fertility
Women who smoke may have reduced fertility. One study found that 38% of non-smokers conceived in their first cycle compared with 28% of smokers. Smokers were 3.4 times more likely than non-smokers to have taken more than one year to conceive. It was estimated that the fertility of smoking women was 72% that of non-smokers.[1] A recent British study found that both active and passive smoking was associated with delayed conception.[2] Cigarette smoking may also affect male fertility: spermatozoa from smokers has been found to be decreased in density and motility compared with that of non-smokers.[3]
Male sexual impotence
Impotence, or penile erectile dysfuntion, is the repeated inability to have or maintain an erection. One US study of men between the ages of 31 and 49 showed a 50% increase in the risk of impotence among smokers compared with men who had never smoked.[4] Another US study, of patients attending an impotence clinic, found that the number of current and ex-smokers (81%) was significantly higher than would be expected in the general population (58%).[5]
Overall smoking increases the risk of impotence by around 50% for men in their 30s and 40s. ASH and the British Medical Association have calculated that around 120,000 UK men in this age group are needlessly impotent as a result of smoking.[6]
Smoking and oral contraceptives
For younger women, smoking and the use of oral contraceptives increases the risk of a heart attack, stroke or other cardiovascular disease by tenfold. This effect is even more marked in women over 45.[7] It is therefore important that all women who take the contraceptive pill be advised not to smoke.
Smoking and pregnancy
Approximately one-quarter of pregnant women in the UK smoke. Women who smoke in pregnancy are more likely to be younger, single, of lower educational achievement and in unskilled occupations. The male partner is more likely to smoke. Only one in four women who smoke succeed in stopping at some time during pregnancy. Almost two-thirds of women who succeed in stopping smoking in pregnancy restart again after the birth of their baby.[8] In December 1998, the Government set a target to reduce the percentage of women who smoked during pregnancy from 23% to 15% by the year 2010, with a fall to 18% by 2005.[9] This will mean approximately 55,000 fewer women in England who smoke during pregnancy.
Foetal growth and birth weight
Babies born to women who smoke are on average 200 grams (8 ozs) lighter than babies born to comparable non-smoking mothers. Furthermore, the more cigarettes a woman smokes during pregnancy, the greater the probable reduction in birth weight. Low birth weight is associated with higher risks of death and disease in infancy and early childhood. The adverse effects of smoking in pregnancy are due mainly to smoking in the second and third trimesters. Therefore, if a woman stops smoking within the first three months of pregnancy, her risk of having a low‑weight baby will be similar to that of a non-smoker. 8
Spontaneous abortion
The rate of spontaneous abortion (miscarriage) is substantially higher in women who smoke. This is the case even when other factors have been taken into account.8
Other complications of pregnancy
On average, smokers have more complications of pregnancy and labour which can include bleeding during pregnancy, premature detachment of the placenta and premature rupture of the membranes.[10] Some studies have also revealed a link between smoking and ectopic pregnancy 10 and congenital defects in the offspring of smokers.[11]
Perinatal mortality
Perinatal mortality (defined as still‑birth or death of an infant within the first week of life) is increased by about one-third in babies of smokers. This is equivalent to approximately 420 deaths per year in England and Wales. The increased perinatal mortality in smoking mothers occurs particularly among manual socio-economic groups and in groups that are already at high risk of perinatal death, such as older mothers or those who have had a previous perinatal death. More than one-quarter of the risk of death due to Sudden Infant Death Syndrome (cot death) is attributable to maternal smoking (equivalent to 365 deaths per year in England and Wales).8
Passive smoking and pregnancy
Exposure by the mother to passive smoking has also been associated with lower birth weight, a higher risk of perinatal mortality and spontaneous abortion.[12]
Breast feeding
Research has shown that smoking cigarettes may contribute to inadequate breast milk production. In one study, fat concentrations were found to be lower in the milk from mothers who smoked and milk volumes were lower.[13]
Health and long‑term growth
Infants of parents who smoke are twice as likely to suffer from serious respiratory infection than the children of non-smokers. (See also Fact Sheet No. 8, Passive Smoking.) Smoking in pregnancy may also have implications for the long term physical growth and intellectual development of the child. It has been associated with a reduced height of children of smoking mothers as compared with non-smoking mothers, with lower attainments in reading and mathematics up to age 16 and even with the highest qualification achieved by the age of 23.[14] One study has demonstrated a link between maternal smoking during pregnancy and adult male crime.[15] There is also evidence that smoking interferes with women's hormonal balance during pregnancy and that this may have long-term consequences on the reproductive organs of her children.[16]
Smoking and cervical cancer
Epidemiological studies have found that women who smoke have up to four times higher risk of developing cervical cancer than non-smokers and that the risk increases with duration of smoking. Studies have demonstrated biochemical evidence that smoking is a causal factor in cervical cancer.[17][18]
Smoking and the menopause
The natural menopause occurs up to two years earlier in smokers. The likelihood of an earlier menopause is related to the number of cigarettes smoked, with those smoking more than ten cigarettes a day having an increased risk of an early menopause.[19] New research suggests that polycyclic aromatic hydrocarbons found in tobacco smoke can trigger premature egg cell death which may in turn lead to earlier menopause. [20]
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Mode of action: disruption of brain cell replication, second messenger, and neurotransmitter systems during development leading to cognitive dysfunction--developmental neurotoxicity of nicotine. Critical Reviews in Toxicology 2005 Oct-Nov;35(8-9):703-11. Slikker W Jr, Xu Z, Levin ED, Slotkin TA. Division of Neurotoxicology, NCTR/FDA, Jefferson, Arkansas 72079, USA. wslikker@nctr.fda.gov Developmental exposure to nicotine in rats results in neurobehavioral effects such as reduced locomotor and cognitive function. Key events in the animal mode of action (MOA) include binding to the nicotinic cholinergic receptor during prenatal and/or early postnatal development. This leads to premature onset of cell differentiation at the expense of cell replication, which leads to brain cell death or structural alterations in regional brain areas. Other events include an initial increase followed by a decrease in adenyl cyclase activity, as well as effects on the noradrenergic, dopaminergic, and serotonergic neurotransmitter systems. Because the nicotine receptor is also present in the developing human brain and the underlying biology for DNA synthesis and cell signaling is comparable, this MOA is likely to be relevant for humans. Although the effects of nicotine exposure in developing humans is not well documented, nicotine exposure as a result of cigarette smoking during pregnancy is associated with several physiological and behavioral outcomes that are reminiscent of the effects of nicotine alone in animal models. As data become available with the advent of the use of the nicotine patch in pregnant humans, the question as to the relative importance of smoking per se versus nicotine alone may be determined. PMID: 16417037 [PubMed - in process] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16417037&query_hl=8&itool=pubmed_docsum
Jan 31 06 6:58 AM
If you are pregnant and reading this message Dr. Slotkin of Duke Medical University, who is referenced in the above study, has a few words he wants to read and think about. Please keep in mind that Dr. Slotkin is one of the world's lead toxicologists studying nicotine's path of destruction during fetal animal development. From: Theodore Slotkin t.slotkin@duke.edu To: John R. Polito john@whyquit.com Sent: Monday, January 09, 2006 11:33 AM Subject: Re: NRT pregnancy use I certainly have no objections to your sharing my comments - I'm on record for this information in a number of reviews and primary research papers, and I think it's important to get that information out to practitioners and to smokers. One of my main concerns is that, although NRT is fine for smoking cessation in nonpregnant smokers, the assumption that it is safe in pregnancy leads people away from thinking about more effective (albeit more costly) ways of addressing the issue. It's easy to dispense drugs (even if they don't work and cause damage to the fetus, and damage to the developing brain doesn't show up as an obvious "birth defect") and although it's harder to go one-on-one with a pregnant smoker to try to get the desired results, it's probably more effective. Also, the patch is the "easiest" NRT approach, and it turns out that this is the absolute worst form of nicotine administration for the fetus. Essentially, achieving a continuous steady-state plasma level of nicotine in the mother removes the protective effect of the placenta (delay of entry to fetus, partial catabolism of nicotine) because all water spaces become saturated with nicotine. A recent paper from Walter Lichtensteiger's group showed that the brains of fetal mice wound up with 3x the nicotine concentration found in maternal plasma when a continuous administration paradigm was used. So NRT might be OK, but not on a continuous basis - at the very least, removing the patch at night would allow for some "wash-out" from the fetus (but probably not much, since fetal clearance of nicotine is lower than in mom). Beyond that, there is still the nagging problem that the only two controlled studies on quit rate in pregnant smokers found no help from NRT. So promoting NRT in pregnancy still needs someone to show that the benefits outweigh the risks. Regards, Ted Slotkin
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Critical Review" Nicotine for the Fetus, the Infant and the Adolescent?
Mar 23 07 5:16 PM
Study: Nicotine reduces attention capacity NEW HAVEN, Conn., March 22 (UPI) --U.S. scientists have determined exposure to nicotine might diminish a person's attention capacity. Yale University researchers led by Leslie Jacobsen found teenage smokers who were also exposed to nicotine before birth showed a dramatic reduction in attention capacities related to vision and hearing. The scientists also demonstrated male and female attention capacities are affected by the exposure in different ways. Jacobsen's team determined girls who smoke and were subject to nicotine exposure in the womb performed most poorly in both visual and auditory attention tasks. In boys, nicotine exposure had a greater effect on auditory attention, suggesting brain regions involved in auditory attention might be more vulnerable to nicotine in males. The researchers believe the gender-specific effects may result from differences in hormonal control of nicotine's actions. The study appears in the journal Neuropsychopharmacology. Source link: http://www.upi.com/NewsTrack/Science/20070322-082351-1235r/ © Copyright 2007 United Press International, Inc. All Rights Reserved. ---------------------------- Gender-Specific Effects of Prenatal and Adolescent Exposure to Tobacco Smoke on Auditory and Visual Attention. Neuropsychopharmacology. 2007 March Volume 21 Jacobsen LK, Slotkin TA, Mencl WE, Frost SJ, Pugh KR. [1] 1Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA [2] 2Department of Pediatrics, Yale University School of Medicine, New Haven, CT, USA [3] 3Haskins Laboratories, New Haven, CT, USA. Prenatal exposure to active maternal tobacco smoking elevates risk of cognitive and auditory processing deficits, and of smoking in offspring. Recent preclinical work has demonstrated a sex-specific pattern of reduction in cortical cholinergic markers following prenatal, adolescent, or combined prenatal and adolescent exposure to nicotine, the primary psychoactive component of tobacco smoke. Given the importance of cortical cholinergic neurotransmission to attentional function, we examined auditory and visual selective and divided attention in 181 male and female adolescent smokers and nonsmokers with and without prenatal exposure to maternal smoking. Groups did not differ in age, educational attainment, symptoms of inattention, or years of parent education. A subset of 63 subjects also underwent functional magnetic resonance imaging while performing an auditory and visual selective and divided attention task. Among females, exposure to tobacco smoke during prenatal or adolescent development was associated with reductions in auditory and visual attention performance accuracy that were greatest in female smokers with prenatal exposure (combined exposure). Among males, combined exposure was associated with marked deficits in auditory attention, suggesting greater vulnerability of neurocircuitry supporting auditory attention to insult stemming from developmental exposure to tobacco smoke in males. Activation of brain regions that support auditory attention was greater in adolescents with prenatal or adolescent exposure to tobacco smoke relative to adolescents with neither prenatal nor adolescent exposure to tobacco smoke. These findings extend earlier preclinical work and suggest that, in humans, prenatal and adolescent exposure to nicotine exerts gender-specific deleterious effects on auditory and visual attention, with concomitant alterations in the efficiency of neurocircuitry supporting auditory attention. Neuropsychopharmacology advance online publication, 21 March 2007; doi:10.1038/sj.npp.1301398. PMID: 17375135 [PubMed - as supplied by publisher] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17375135
Yale University researchers led by Leslie Jacobsen found teenage smokers who were also exposed to nicotine before birth showed a dramatic reduction in attention capacities related to vision and hearing. The scientists also demonstrated male and female attention capacities are affected by the exposure in different ways.
Jacobsen's team determined girls who smoke and were subject to nicotine exposure in the womb performed most poorly in both visual and auditory attention tasks. In boys, nicotine exposure had a greater effect on auditory attention, suggesting brain regions involved in auditory attention might be more vulnerable to nicotine in males.
The researchers believe the gender-specific effects may result from differences in hormonal control of nicotine's actions.
The study appears in the journal Neuropsychopharmacology.
Source link:
http://www.upi.com/NewsTrack/Science/20070322-082351-1235r/
© Copyright 2007 United Press International, Inc. All Rights Reserved.
----------------------------
Gender-Specific Effects of Prenatal and Adolescent Exposure to Tobacco Smoke on Auditory and Visual Attention.
Neuropsychopharmacology. 2007 March Volume 21
Jacobsen LK, Slotkin TA, Mencl WE, Frost SJ, Pugh KR. [1] 1Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA [2] 2Department of Pediatrics, Yale University School of Medicine, New Haven, CT, USA [3] 3Haskins Laboratories, New Haven, CT, USA.
Prenatal exposure to active maternal tobacco smoking elevates risk of cognitive and auditory processing deficits, and of smoking in offspring. Recent preclinical work has demonstrated a sex-specific pattern of reduction in cortical cholinergic markers following prenatal, adolescent, or combined prenatal and adolescent exposure to nicotine, the primary psychoactive component of tobacco smoke.
Given the importance of cortical cholinergic neurotransmission to attentional function, we examined auditory and visual selective and divided attention in 181 male and female adolescent smokers and nonsmokers with and without prenatal exposure to maternal smoking. Groups did not differ in age, educational attainment, symptoms of inattention, or years of parent education. A subset of 63 subjects also underwent functional magnetic resonance imaging while performing an auditory and visual selective and divided attention task.
Among females, exposure to tobacco smoke during prenatal or adolescent development was associated with reductions in auditory and visual attention performance accuracy that were greatest in female smokers with prenatal exposure (combined exposure). Among males, combined exposure was associated with marked deficits in auditory attention, suggesting greater vulnerability of neurocircuitry supporting auditory attention to insult stemming from developmental exposure to tobacco smoke in males. Activation of brain regions that support auditory attention was greater in adolescents with prenatal or adolescent exposure to tobacco smoke relative to adolescents with neither prenatal nor adolescent exposure to tobacco smoke.
These findings extend earlier preclinical work and suggest that, in humans, prenatal and adolescent exposure to nicotine exerts gender-specific deleterious effects on auditory and visual attention, with concomitant alterations in the efficiency of neurocircuitry supporting auditory attention.
Neuropsychopharmacology advance online publication, 21 March 2007; doi:10.1038/sj.npp.1301398.
PMID: 17375135 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17375135
Apr 22 07 5:35 AM
Jun 6 07 5:44 AM
Nicotine alters lung branching morphogenesis through the {alpha}7 nicotinic acetylcholine receptor Journal: American journal of physiology. Lung cellular and molecular physiology, June 1, 2007 Authors: Wongtrakool C, Roser-Page S, Rivera HN, Roman J. Pulmonary, Emory University School of Medicine, Atlanta, Georgia, United States. There is abundant epidemiologic data linking prenatal environmental tobacco smoke with childhood asthma and wheezing, but the underlying molecular and physiologic mechanisms that occur in utero to explain this link remain unelucidated. Several studies suggest that nicotine, which traverses the placenta, is a causative agent. Therefore, we studied the effects of nicotine on lung branching morphogenesis using embryonic murine lung explants. We found that the expression of alpha7 nicotinic acetylcholine receptors, which mediate many of the biological effects of nicotine, is highest in pseudoglandular stage lungs when compared to later stages. We then studied the effects of nicotine in the explant model and found that nicotine stimulated lung branching in a dose-dependent fashion. alpha-bungarotoxin, an antagonist of alpha7 nicotinic acetylcholine receptors, blocked the stimulatory effect of nicotine, whereas GTS-21, a specific agonist, stimulated branching thereby mimicking the effects of nicotine. Explants deficient in alpha7 nicotinic acetylcholine receptors did not respond to nicotine. Nicotine also stimulated the growth of the explant. Altogether, these studies suggest that nicotine stimulates lung branching morphogenesis through alpha7 nicotinic acetylcholine receptors and may contribute to dysanaptic lung growth which, in turn, may predispose the host to airways disease in the postnatal period. Key words: nicotine, branching morphogenesis, lung growth, nicotinic receptors. PMID: 17545491 [PubMed - as supplied by publisher] Source link: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17545491
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