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Journal of the New Zealand Medical Association, 21-July-2006, Vol 119 No 1238

Maternal smoking: risks related to maternal asthma and reduced birth weight in a Pacific Island birth cohort in New Zealand

Sarnia Carter, Teuila Percival, Janis Paterson, Maynard Williams

Abstract

Aims This study investigated associations between smoking and maternal asthma and two indicators of pregnancy outcome: birth weight and preterm delivery.

Methods Data were gathered as part of the Pacific Islands Families (PIF) Study. Mothers of a cohort of 1398 Pacific infants born in South Auckland, New Zealand during 2000 were interviewed when their infants were 6 weeks old. Mothers were questioned regarding maternal health and lifestyle behaviours such as cigarette smoking. Additional data were obtained from hospital records. Analyses focused on 1368 biological mothers.

Results Approximately 20% of mothers reported smoking during their last trimester of pregnancy. Logistic regression analyses showed that smokers had over twice the risk of having maternal asthma as well as a low birth weight (LBW) or small for gestational age (SGA) infant than non-smokers. Smoking significantly reduced mean birth weight from between 149.2 grams (1–9 cigarettes) to 204.3 grams (10+ cigarettes). No significant association was found between smoking and preterm birth.

Conclusions Smoking is preventable, yet continues to have negative consequences for mothers and their offspring. Findings can inform public health policy and smoking cessation programmes for Pacific families.

Little data exist pertaining to smoking behaviour and associated consequences among the Pacific population in New Zealand (i.e. mostly people of Samoan, Tongan, Niuean, and Cook Islands origin). As Pacific infants tend to weigh more than other ethnic groups in New Zealand,1 it is possible that the effects of smoking on birth weight may go largely undetected until such associations are specifically examined. Thus further understanding of the effects of smoking among this relatively socioeconomically disadvantaged group is important given the potential harm in regard to both child and adult health.

Evidence is sufficient to suggest a causal relationship exists between active smoking and acute respiratory illnesses and symptoms including wheeze.2 The relationship between smoking and asthma is less clear with underlying causes of asthma not well understood.

Although some studies show an association between smoking and increased likelihood of asthma or asthma symptoms,3–4 it is possible that smoking aggravates airways in susceptible people, exacerbating symptoms rather than causing development of the disease.5 Smoking has serious implications for asthmatics, being repeatedly linked to greater severity of symptoms, poorer control, increased use of hospital services, impaired lung function, and asthma-related morbidity and mortality.2,6,7

Smoking carries additional risk to women with greater likelihood of reproductive complications.2,10,11 The heightened risk of foetal and neonatal mortality among offspring of smoking mothers is thought to stem mostly from increased incidence of low birth weight infants (LBW) weighing less than 2500 grams, infants with intrauterine growth retardation (and thus abnormally small for their gestational age [SGA]), or from pregnancy complications including abruptio placentae.12

Research has consistently shown mothers who smoke during pregnancy are more likely (than non-smoking mothers) to have preterm births,13,14, LBW, or SGA infants.10-11,15,16 A mean weight reduction of approximately 150–250 grams is frequently observed in infants of smoking mothers.11,12,16–18 Prevention of LBW is crucial as it continues to be the most important determinant of perinatal mortality and impaired later development.16 Many LBW and/or preterm infants require admission to high-cost neonatal intensive care units resulting in a significant economic burden.10

Smoking in New Zealand

New Zealand has one of the highest prevalences of asthma in the World, and available data indicate that Māori and Pacific adults are more likely than other groups to have asthma.19 Asthma has been estimated to cost the country at least NZ$825 million annually.19 A significant number of female smokers are endangering their own health, and (in parallel) a sizeable proportion of pregnancies may be at risk for adverse outcome. In 2001, 55.9% of Māori, 26.3% of Pacific, and 20.7% of European/other New Zealand women were smokers.20

Smoking rates specific to pregnancy closely mirror rates seen for female smoking in the general population. Although small fluctuations over time have been observed, pregnancy smoking has remained fairly stable at approximately 30% for 20 years.21 A study in the Canterbury region during 1993–94 showed the overall prevalence of smoking during pregnancy to be 33.0%; smoking prevalence was substantially higher (close to 50%) in areas associated with socioeconomic disadvantage.21

In 1997, 26.8% of participants smoked during the first, 25.0% smoked during the second, and 23.0% smoked during the third trimester of pregnancy.22

Smoking among Pacific women

Pacific people comprise approximately 6.5% of the New Zealand population,23 and (largely due to high fertility rates) are one of the fastest growing groups, projected to be 12% of the population by 2051.24

Pacific peoples have generally fared worse than the New Zealand population as a whole on a range of health and social indicators.24,25 For instance, compared with national rates, Pacific children have high rates of hospitalisation as well as a higher incidence of respiratory infections, meningococcal disease, and common infectious diseases such as measles.25,26

Few studies document smoking among Pacific women. Smoking prevalence for Pacific women in 2002 was 28.5% compared with 25.5% for all New Zealand women,25 while research conducted approximately 10 years ago revealed 23.6% of Pacific mothers smoked during pregnancy compared with 33.2% for the whole population sampled.27

In an Australian study, 16% of Pacific mothers smoked during pregnancy, substantially lower than the 36% indicated for Caucasian mothers.28 However, the study contained only 80 Pacific mothers and it is possible that smoking behaviours and other characteristics differ between Pacific mothers residing in Australia and New Zealand.

Findings from our New Zealand cohort study of Pacific infants (the Pacific Islands Families [PIF] Study) supports this view, with 24.9% of mothers smoking during pregnancy.29 Using data from the PIF Study, this study investigated associations between smoking and maternal asthma and two indicators of pregnancy outcome: birth weight and preterm delivery.

Methods

Data collection—Data were collected as part of the PIF Study, a longitudinal investigation of a cohort of 1398 infants born at Middlemore Hospital, South Auckland, New Zealand during the year 2000. The majority (67%) of Pacific communities reside in the Auckland area.23 Middlemore Hospital was chosen for recruitment as it has the largest number of Pacific births and is representative of the major Pacific ethnicities (Samoan, Cook Island Māori, and Tongan). Eligibility criteria for entry to the PIF Study included having at least one parent who self-identified as being of Pacific ethnicity and being a New Zealand permanent resident. Thus, infants of non-Pacific mothers were eligible in cases where the father was of Pacific descent.

Potential participants were identified in conjunction with Middlemore’s Pacific Islands Cultural Resource Unit and the Birthing Unit. Following delivery, study personnel approached potential participants, provided brief information, and obtained permission for later contact. All procedures and interview protocols were granted ethical approval from the National Ethics Committee. Detailed information about the cohort and procedures is described elsewhere.30

Approximately 6-weeks postpartum, Pacific interviewers fluent in English and a Pacific language visited the mothers at home. Of the 1376 mothers, 1368 were biological and 8 were foster or adoptive mothers. Eligibility criteria were confirmed and informed consent was gained for participation in an interview and access to Middlemore Hospital discharge records. For the present study, responses based on the 1368 biological mothers and first-born twin for twin pairs were utilised in analyses.

Mothers participated in 1-hour interviews concerning the health and development of the child and family functioning. As part of this interview, mothers approximated how many cigarettes they had smoked per day prior to pregnancy, during the three trimesters of pregnancy, and yesterday (current smoking).

Mothers were asked whether they currently had any of a range of health problems (including asthma) that had been diagnosed by a doctor or for which the mother was presently taking medications. Sociodemographic data were also collected—including maternal age, ethnicity (self-identified), education, marital status, and household income. Birth weight (grams) and preterm delivery status (<37 weeks of completed gestation) were extracted from hospital birth records. Data were coded and double-entered into the SPSS (version 12.0.1) statistical software package.31

Smoking during the last trimester of pregnancy was categorised into three groups: non-smoking, light/moderate smoking (1–9 cigarettes daily), and heavy smoking (10+ cigarettes daily).

The associations between smoking and three outcome variables (maternal asthma, preterm birth, and birth weight) were examined in the following manner:

Maternal asthma—Univariate logistic regression analyses were initially performed with the measure of effect being the odds ratio (OR) with its 95% confidence interval (CI). As it is likely that other factors also contribute to a heightened risk of asthma, a multiple logistic regression analysis was then undertaken to control for potential confounding effects. Five demographic variables (maternal age, education, ethnicity, marital status, and household income) along with the smoking variable were therefore entered into a multiple regression model.

Preterm birth—Univariate and multivariate logistic regression analyses also were conducted to determine any associations between smoking during pregnancy and preterm birth. The five demographic variables (maternal age, education, ethnicity, marital status, and household income) were again entered as control variables in the multivariate model.

Birth weight—To examine the effect of third-trimester smoking on birth weight, three sets of analyses were conducted:

First, differences between means were tested using analysis of variance. Cuzick’s non parametric test was employed to test for a significant trend of decreasing birth weight with increasing smoking dosage.32 Multiple regression analyses were then performed to control for potential confounding effects of maternal age, ethnicity, marital status, education, household income, twin birth, and gestational age (<37, 37–40, >40 weeks).
Second, LBW was examined using births of 37 or more weeks of gestation (i.e. excluding preterm births). Due to the small number of LBW infants, smoking-dose categories were combined into smoking and non-smoking during the third trimester. Logistic regression was used to determine whether smoking increased risk of LBW (<2500 grams). However, multiple logistic regression analyses controlling for other factors were not possible due to small numbers of LBW infants.
Third, a SGA variable was created using births of 37 or more weeks of gestation categorised into five groups (37-38, 39, 40, 40+ weeks) and tested against each groups’ sex-specific 10th percentile weight to determine if they were small or of appropriate weight for their gestational age grouping. Due to small frequency counts in some weeks of gestation, it was necessary to group ages. Univariate logistic regression analyses were conducted to determine any associations between smoking during pregnancy and SGA. To control for potential confounding effects a multiple logistic regression analysis was then undertaken. The same five demographic variables used previously, along with twin status and smoking, were entered into the model.

Results

Initially, 1708 mothers of Pacific infants (born between 15 March 2000 and 17 December 2000) were identified as potentially meeting eligibility criteria. After excluding cases where the infant died or non-resident status was confirmed whilst the mother was in hospital, a potential group of 1657 mothers were then invited to participate in the study.

Ninety-six percent (N=1590) of these potentially eligible mothers gave consent to be visited at 6 weeks postpartum. Ten (1%) mothers were then determined as ineligible, 103 (6%) mothers were of indeterminate eligibility (largely due to leaving Auckland or being untraceable), and 1477 mothers were contacted and confirmed eligible. Of these 1477 mothers, 1376 (93.2%) agreed to participate in the PIF Study.

The study presented here is based on data obtained for the 1368 biological mothers in the PIF study. Table 1 presents the basic demographic characteristics of the biological mothers.

During the third trimester of pregnancy, 1089 (79.7%) mothers reported to be non-smokers, 194 (14.2%) smoked an average of 1–9 cigarettes daily, and 84 (6.1%) smoked 10 or more cigarettes daily (smoking data were missing for one mother).

Table 1. Frequencies (percentages) of basic demographic variables measured at 6-weeks postpartum for biological mothers (N=1368) in 2000

Variable	N	(%)
Ethnicity Samoan Cook Island Māori Tongan Niuean Other Pacific* Non-Pacific	647 229 287 59 47 99	(47.3) (16.7) (21.0) (4.3) (3.4) (7.2)
Age (years) <20 20-29 30+	110 750 538	(8.0) (52.6) (39.3)
Marital status Partnered Non-partnered	1100 268	(80.4) (19.6)
New Zealand-born Yes No	452 916	(33.0) (67.0)
Highest educational qualifications No formal qualifications Secondary Post-secondary	533 460 375	(39.0) (33.6) (27.4)
Household income (annual) $0–$20,000 $20,001–$40,000 > $40,000 Unknown	454 708 159 47	(33.2) (51.8) (11.6) (3.4)

*Includes mothers identifying equally with two or more Pacific groups, equally with Pacific and Non-Pacific groups, or with Pacific groups other than Tongan, Samoan, Cook Island or Niuean

Maternal asthma

99 (7.2%) mothers reported having asthma (as diagnosed by a medical professional or for which they were taking medication). Table 2 shows the association between smoking (in the third trimester of pregnancy) and maternal asthma. The numbers and percentages of mothers who reported smoking are given along with the univariate and adjusted OR (95% CI) indicating likelihood of asthma.

Table 2. Association between daily cigarette dose and incidence of maternal asthma (N=1366)

Daily cigarette dose	Maternal asthma n (%)		Univariate odds ratio (95% CI)		Adjusted odds ratio (95% CI)
0 1–9 10+	58 23 18	(5.3) (11.9) (21.4)	1.00 2.41 4.85	(1.45–4.00)† (2.70–8.70)‡	1.94 3.63	(1.14–3.30)* (1.93–6.85)‡

*p<0.05; †p<0.01; ‡p<0.001.

Compared to non-smokers, univariate analyses depicted in Table 2 show that mothers who smoked 1–9 cigarettes daily had over twice the risk (and mothers who smoked 10+ cigarettes daily had almost five times the risk) of having asthma. Table 2 also shows that smoking remained significantly associated with maternal asthma for both cigarette doses levels following adjustment for demographic variables. The degree of risk was reduced, however, once these factors were controlled for.

The adjusted OR for 1–9 cigarettes was 1.9 (95%CI=1.1–3.3; p<0.05), and for the heavier smoking dose, the adjusted OR was 3.6 (95%CI=1.9–6.9; p<0.001). Ethnicity and age were also independently associated with maternal asthma, with younger mothers (<20 years) being just over two times more likely (OR=2.1; 95%CI=1.0–4.4; p<0.05) to have asthma than older mothers aged 30 or more years; ‘Other Pacific’ (OR=0.2; 95%CI=0.1–0.6) and Cook Islands (OR=0.4; OR=0.2–0.8) women less likely to exhibit asthma than Samoan women (p<0.01).

Preterm birth

Of the 1346 births for which data were available, 106 (7.9%) were considered preterm (less than 37 weeks gestation). As indicated in Table 3, no significant association between smoking during pregnancy and preterm birth was found.

Table 3. Association between daily cigarette dose and preterm births (<37 weeks) (N=1346)

Daily cigarette dose	Preterm birth n (%)		Univariate odds ratio (95%CI)		Adjusted odds ratio (95%CI)
0 1–9 10+	87 15 4	(8.1) (7.9) (4.8)	1.00 0.96 0.57	(0.54–1.71) (0.20–1.58)	1.00 0.97 0.60	(0.54–1.75) (0.21–1.72)

Odds ratios adjusted for mother’s age, education, ethnicity, social marital status, and household income.

Birth weight

Mean birth weight—Smoking was significantly associated with reduced birth weight (p<0.001). The mean birth weight of infants born to non-smoking mothers was 3636.2 (n=1073; SD=619.8). The corresponding mean weights of infants born to light-to-moderate smoking mothers was 3392.6 grams (n=191; SD=553.3), and 3358.4 grams (n=84; SD=551.0) for heavy smokers.

There was a significant trend: decreasing birth weight with increasing smoking dose (p<0.001). On average, infants born to light-to-moderate smokers weighed 243.5 grams less and infants born to heavy smokers weighed 277.7 grams less than infants born to non-smokers.

Adjusting for potential confounders reduced the strength of the associations between smoking during pregnancy and birth weight. Bonferroni tests confirmed that the associations remained significant (p<0.01) with mothers who smoked 1–9 cigarettes daily having infants that weighed on average 149.2 grams less and mothers who smoked 10 or more cigarettes daily delivering infants weighing 204.3 grams less than their non-smoking counterparts.

Low birth weight (<2500 grams)—Univariate analyses conducted on births of 37 or more weeks of gestation (n=1240) showed that smokers were significantly (p<0.01) more likely to deliver LBW infants compared to non-smokers (OR=6.3; 95%CI=2.1–19.5).

Small for gestational age (SGA)—Table 4 shows that (compared to non-smoking mothers) mothers who smoked 1–9 cigarettes daily had over twice the risk (and mothers who smoked 10+ cigarettes daily had over three times the risk) of delivering an infant considered SGA.

Table 4. Numbers (row percentages) as well as univariate and adjusted odds ratios of small for gestational age (SGA) and low birth weight (LBW) babies by smoking dose of mothers (N=1240)

Variable		SGA n (%)		Univariate OR (95%CI)		Adjusted OR (95%CI)
Daily cigarette dose	0 1–9 10+	76 29 18	(7.7) (16.5) (22.5)	1.00 2.36 3.47	(1.49–3.74)‡ (1.95–6.16)‡	2.10 2.72	(1.30–3.41)† (1.44–5.20)†
		LBW n (%)
Smoked last trimester of pregnancy	No Yes	5 8	(0.5) (3.1)	1.00 6.32	(2.05–19.48)†

†p<0.01; ‡p<0.001

Multiple logistic regression analyses showed that smoking remained significantly associated with increased likelihood of SGA. The adjusted OR for 1–9 cigarettes was 2.1 (95%CI=1.3–3.4; p<0.01)—and for the heavier smoking dose, the adjusted OR was 2.7 (95%CI=1.4–5.1; p<0.01).

Income and twin status were also independently associated with SGA. Compared to those with household incomes <$20,000 per annum, mothers with incomes $20,001–$40,000 per annum were at a reduced risk of SGA (OR=0.4; 95%CI=0.3–0.7; p<0.01). Mothers delivering twins exhibited over 15 times the risk of SGA than singleton births (OR=15.8, 95%CI=4.2–59.3; p<0.001).

Discussion

Three health indicators were examined in relation to maternal smoking among Pacific communities, two pertinent to infant wellbeing (preterm birth and birth weight) and one to maternal wellbeing (asthma).

Prior to discussing findings, some limitations are acknowledged. Measurement of smoking was based on use during a specific timeframe, thus data regarding non-smokers may also include former smokers. Maternal reporting may have underestimated smoking and recall bias cannot be ruled out.

Studies comparing the use of self-report versus biomarkers of smoking such as cotinine tests have shown self-report to be an accurate measure of smoking status, although dose may be underreported.33 Thus, it is possible that cigarette consumption data could be conservative. However, bias was minimised with smoking questions forming a small part of the overall interview and interviewers not being health workers.

Birth data were extracted from hospital records recognising that estimation of some gestational ages may lack precision without confirmation by ultrasound scans. Inaccuracies may also have occurred with asthma data, as it was not feasible to confirm diagnoses through testing or review of records.

As many Pacific people do not have a regular doctor or use preventive medication,34 estimates of asthma are likely to be conservative, especially given that measurement was based on diagnosis and medication rather than the presence of symptoms. Data pertaining to onset and duration of asthma and other known risk factors such as family history or personal atopy2 were not available so it is not known how these and other unmeasured factors would have influenced the relationships observed between smoking and asthma. Recognising possible limitations, this study adds to the overwhelming, accumulating evidence that smoking has adverse consequences for both the smoker and their offspring.

The link between smoking and negative health consequences (including respiratory illness) is widely accepted. Furthermore, exposure to tobacco smoke is a recognised risk factor for asthma symptoms in children,9 however, inconsistent findings have been reported for adults.4–7

Although research indicates that smoking negatively affects asthma, direct causation has not been confirmed due to methodological differences in measurement coupled with biases arising from alterations in smoking habits by asthmatics.2 In this study, analyses controlling for sociodemographic factors revealed a significant association between current smoking and maternal asthma. Dose response effects were evident, with light-to-moderate smokers being approximately twice as likely (and heavy smokers being over three and a half times as likely) to have asthma than non-smokers.

Little is known about the mechanisms of how smoking influences asthma morbidity, although genetic and environmental factors are thought to underlie the development of the disease.35 Smoking may heighten or suppress inflammatory responses of the airways and may modify immunological responses.8 Thus smoking cessation is important, particularly for those with compromised respiratory health. Along with the need to reduce individual suffering from asthma morbidity, the economic impact of the condition could be reduced.19

In addition to adverse consequences of smoking for maternal respiratory health, research has consistently shown smoking to be associated with negative pregnancy outcomes, including preterm delivery and lower birth weight.2,11–14,16,36

In New Zealand, Pacific women tend to have fewer preterm deliveries compared to women of other ethnic groups.1,25 When risk of preterm delivery from smoking was examined in our cohort, no association (contrary to most research) between increased smoking and increased preterm deliveries was found. Our findings are in line with others who have also failed to find an association.18,37

It is possible that other factors not measured, such as pregnancy complications, are stronger predictors of preterm delivery than smoking. Others have suggested that methodological differences in estimation of gestational age and possible publication biases may contribute to the occasional observed lack of association between smoking and preterm birth.18

Pacific infants tend to weigh more than infants of other ethnic groups in New Zealand, possibly masking the effects of smoking. Analyses examining mean birth weight, LBW, and SGA were used to investigate the relationship between birth weight and smoking. Irrespective of which birth weight variable was examined, an adverse association with smoking was found. Despite controlling for potential confounders and corroborating previous research,11,12,16–18 smoking was significantly associated with reduced birth weight with a trend towards a dose-response effect.

In line with previous research,10,12,15,36 smokers were significantly more likely to deliver LBW infants compared to non-smokers. Although it was not possible to control for other factors, smoking was associated with a six-fold increased risk of a LBW infant. Consistent with the literature,14,15,38 mothers who smoked 1–9 cigarettes daily had just over twice the risk (and mothers who smoked 10+ cigarettes daily had almost three times the risk) of delivering an infant considered SGA compared to non-smoking mothers.

Adverse risks associated with a lower birth weight or being SGA can be significant and include compromised immunocompetence, subnormal growth, increased morbidity and mortality in infancy, with some risks persisting over several years39 (including increased risk of childhood obesity ,type 2 diabetes, and cardiovascular disease).40 Maternal smoking is a preventable contributor to poor foetal growth that precedes the development of these conditions.

Evidence is sufficient to regard the relationship between smoking and intrauterine growth restriction and LBW as causal,2,14 although specific mechanisms remain unclear. Smoking during pregnancy exposes the foetus to higher concentrations of nicotine than present in the mother and carbon monoxide interferes with the release of oxygen into foetal tissues, retarding growth.41,42

Although attention has been directed at nicotine and carbon monoxide, there are thousands of chemicals in cigarettes and little known about the interaction among these components.43

This study of Pacific families provides further evidence that smoking confers increased risk to both maternal and reproductive health and these results reinforce the need to commit additional effort into smoking prevention and cessation initiatives.

Author information: Sarnia Carter, Research Fellow, Pacific Islands Families Study, Auckland University of Technology; Teuila Percival, Paediatrician, South Auckland Health—and Co-Director, Pacific Islands Families Study, Auckland University of Technology; Janis Paterson, Co-Director, Pacific Islands Families Study, Auckland University of Technology; Maynard Williams, Senior Research Fellow and Statistician, Auckland University of Technology; Auckland

Acknowledgments: The PIF Study is supported by the Foundation for Science, Research and Technology, the Health Research Council of New Zealand and the Maurice and Phyllis Paykel Trust. The authors gratefully acknowledge the families who have participated in the study, the Pacific Peoples Advisory Board and the other members of the research team.

Correspondence: Sarnia Carter, Division of Public Health & Psychosocial Studies, Faculty of Health & Environmental Sciences, Auckland University of Technology, Private Bag 92006, Auckland. Fax: (09) 917 9877; email: sarnia.carter@aut.ac.nz

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