The effect of maternal alcohol consumption on fetal growth and preterm birth

DOI: 10.1111/j.1471-0528.2008.02058.x Epidemiology www.blackwellpublishing.com/bjog The effect of maternal alcohol consumption on fetal growth and preterm birth CM O’Leary,a N Nassar,a JJ Kurinczuk,b C Bowera a Division of Population Sciences, Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, Perth, WA, Australia b National Perinatal Epidemiology Unit, University of Oxford, Headington, Oxford, UK Correspondence: Ms CM O’Leary, Division of Population Sciences, Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, PO Box 855, West Perth, WA 6872, Australia. Email colleeno@ichr.uwa.edu.au Accepted 26 October 2008. Objective To investigate the relationship between prenatal alcohol exposure and fetal growth and preterm birth and to estimate the effect of dose and timing of alcohol exposure in pregnancy. Design A population-based cohort study linked to birth information on the Western Australian Midwives Notification System. Setting Western Australia. Population A 10% random sample of births restricted to nonindigenous women who had delivered a singleton infant (n = 4719) in 1995–1997. Methods The impact of alcohol consumption in pregnancy on fetal growth (small-for-gestational-age [SGA] and large-forgestational-age infants [LGA]) and preterm birth (<37 weeks of gestation) was assessed using multivariate logistic regression analysis and adjusting for confounding factors. Main outcome measures Odds ratios and 95% CI, attributable risk, and population attributable risk were calculated. Results The percentage of SGA infants and preterm birth increased association between alcohol intake and SGA infants was attenuated after adjustment for maternal smoking. Low levels of prenatal alcohol were not associated with preterm birth; however, binge drinking resulted in a nonsignificant increase in odds. Preterm birth was associated with moderate and higher levels of prenatal alcohol consumption for the group of women who ceased drinking before the second trimester. This group of women was significantly more likely to deliver a preterm infant than women who abstained from alcohol (adjusted OR 1.73 [95% CI 1.01–3.14]). Conclusions Alcohol intake at higher levels, particularly heavy and binge drinking patterns, is associated with increased risk of preterm birth even when drinking is ceased before the second trimester. This finding, however, is based on small numbers and needs further investigation. Dose and timing of prenatal alcohol exposure appears to affect preterm delivery and should be considered in future research and health education. Keywords Fetal growth, high risk, pregnancy, prenatal alcohol exposure, preterm birth, RASCALS, small for gestational age. with higher levels of prenatal alcohol exposure; however, the Please cite this paper as: O’Leary C, Nassar N, Kurinczuk J, Bower C. Impact of maternal alcohol consumption on fetal growth and preterm birth. BJOG 2009;116:390–400. Introduction The evidence surrounding the effect of low to moderate intake of alcohol during pregnancy on fetal growth and preterm birth is inconclusive. While there is a large body of literature on the issue, the evidence base has many weaknesses limiting our ability to reach definitive conclusions. In their systematic review of the literature, Henderson et al. (2007)1 reported that many studies did not control for known confounding factors, such as cigarette smoking and ethnicity. In their more detailed report,2 the authors found that the studies that had adjusted for confounding factors had other limita- 390 tions, which prevented their results from being generalised to the wider community. In the few studies that have reported an association between low levels of prenatal alcohol exposure and fetal growth, the direction of the association has not been consistent. While the majority of studies have reported no association with less than 72 g of alcohol per week (equivalent to seven standard drinks per week in Australia; six in the USA, Canada, and Europe; and nine units in the UK) and low birthweight,3–9 intrauterine growth restriction,5,10,11 and preterm birth,8,10,12–17 a small number of studies found an increased risk at low levels18–20 and, conversely, others have ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology The effect of prenatal alcohol on fetal outcomes reported a possible protective effect of low levels of alcohol consumption in pregnancy.10,13,18,21–23 At higher levels of prenatal alcohol exposure, the findings of an association between prenatal alcohol exposure and fetal growth are not consistent, with around half of studies reporting no significant association3,4,10,18,24–31 and half reporting a significant association.9,20,32–40 Uncertainty also exists about the impact of binge drinking on intrauterine growth and questions remain as to whether the increased risk from binge drinking, if one truly exists, is due to the pattern of binge drinking per se or rather a result of heavy alcohol intake.2 Using data from a population-based cohort study of nonindigenous women in Western Australia (WA), this study examines the impact of maternal alcohol consumption, taking into account the quantity per occasion, frequency of consumption, and total quantity consumed during the 3 months before and during each trimester of pregnancy on preterm birth and fetal growth. Materials and methods The details of the study used for this analysis have been described previously.41–43 Briefly, a 10% random sample of all women giving birth in WA between 1995 and 1997 was invited by letter at 12 weeks postpartum to participate in a postal survey of health-related behaviours and events during pregnancy and infancy (subsequently known as the RASCALS study), designed to survey health-related behaviours and events before and during pregnancy and early infancy. Data were collected using a postal questionnaire sent with the letter of invitation. Mothers whose infants were stillborn (n = 20) or given up for adoption (n = 5) were excluded. An 81% response rate resulted in 4861 completed questionnaires of which 4860 were able to be linked to their corresponding birth information on the WA Midwives’ Notification System, a statutory population-based surveillance system of all births in WA. The analysis reported here was restricted to women with singleton births (multiples n = 66) and nonindigenous mothers (indigenous n = 75), giving a sample size of 4719. Comparison with data available for all births in WA in this period44 showed that the respondents were representative of mothers of all singleton live births with the exception of a slight underrepresentation of mothers with low-birthweight babies (5.3% overall versus 4.7% respondents) and mothers aged less than 20 years (6.0% overall versus 3.6% respondents; 2.5% in this sample). Ethics approval for the conduct of this study was granted by the Princess Margaret Hospital Research Ethics Committee and the WA Confidentiality of Health Information Committee. Information about maternal alcohol consumption was collected retrospectively for the 3-month period prepregnancy and for each trimester separately. For each period, women were asked how often they drank alcohol (5 or more, 3–4, or 1–2 days/week; 1–2 days/month; less than once per month; or never) and the quantity consumed (e.g. number of cans, glasses, bottles) on a typical occasion for each of four types of alcoholic beverages (beer, wine/champagne, spirits/liqueurs, and fortified wines). Consumption frequency calculations used the lower of the days marked, for example 3–4 days/week was included as 3 days/week to calculate total weekly dose of alcohol. However, there were a small number of women (n = 7 in first trimester and n = 1 in third trimester) who reported a frequency of drinking of one to two times per week and who consumed two or more types of beverages each at less than 50 g per occasion, but with a total weekly consumption of 70+ g. As we could not be confident that the women had consumed only once per week, and therefore, at binge levels, we coded them as heavy drinkers. Where respondents used a tick mark instead of indicating a numeric value, a minimum level for the type of beverage, time period, and frequency was applied. Standard drink calculations were derived during the data analysis stage and covered a range of measures for each type of beverage;42 more details are available on request from the authors. To examine the impact of the pattern of drinking by women before and during pregnancy, we took into account the frequency, quantity per occasion, and total quantity consumed. The level of alcohol consumption was categorised into five mutually exclusive groups; none, low, moderate, binge (less than weekly up to twice per week), and heavy (including women who binged more than twice per week) (Table 1). For the analyses, abstinence during pregnancy refers to women who reported not drinking at any stage during pregnancy. One standard drink in Australia is equal to 10 g of alcohol. The ‘low’ category was defined in line with the 2001 recommendation to women who are pregnant or might soon become pregnant set out by the Australian National Health and Medical Research Council alcohol guideline 11, which recommends that ‘If women choose to drink, over a week, should have less than 7 standard drinks, AND, on any one day, no more than 2 standard drinks’.45 To assess the overall impact of alcohol intake greater than the low level, moderate, heavy, and binge drinking were also combined. The primary outcomes of the study were the effect of alcohol consumption in pregnancy on fetal growth and preterm birth. Appropriate fetal growth was ascertained using the proportion of optimal birthweight (POBW), where optimal birthweight was determined after taking into account infant sex, gestational age, maternal height, and parity. The POBW was then calculated by taking the ratio of observed birthweight to optimal birthweight.46 The population selected to define optimal birthweight was the total 1998–2002 WA population of singleton, Caucasian births, not exposed to factors known to influence fetal growth pathologically. We used a POBW score less than the 10th percentile to define small-for-gestational-age (SGA) infants. Preterm birth was defined as infants born at less than 37 weeks of gestation. Gestational age was estimated using an ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology 391 O’Leary et al. Table 1. Classification of maternal alcohol consumption Alcohol consumption (g) Low Moderate* Binge <weekly to one to two times per week Heavy Frequency per week <Weekly** to <daily <Weekly** to daily <Weekly** to 2 days 21 days Grams per occasion*** •20 20–<50 501 >10–501 Grams per week*** •60 •70 ‚5 ‚68 9.3 3.8 0.5 60.0 21.5 12.5 2.1 70.0 60.3 50.6 5.0 320.0 208.7 141.0 68.0 3685.0 6.2 2.5 0.5 60.0 16.6 8.0 2.1 67.5 58.0 50.0 5.0 270.0 192.5 150.0 71.0 1453.0 6.0 2.5 0.5 60.0 14.6 7.5 2.1 66.0 48.0 25.3 5.0 265.0 161.1 120.0 75.0 540.0 6.0 2.5 0.5 60.0 15.2 7.6 3.0 70.0 47.0 25.0 5.0 265.0 143.2 105.0 74.0 540.0 Prepregnancy Mean Median Minimum Maximum Trimester 1 Mean Median Minimum Maximum Trimester 2 Mean Median Minimum Maximum Trimester 3 Mean Median Minimum Maximum *Women reporting consuming 10 g of alcohol per occasion on a daily basis are included in the moderate group. **,Weekly 5 one to two times per month to once every 8–10 weeks. ***10 g 5 one standard drink in Australia and 50 g per occasion 5 binge drinking. algorithm taking into account two independent estimates of gestational duration from routinely collected data (last menstrual period, expected due date, ultrasound fetometry, baby’s date of birth, and neonatal estimate of gestational age) by the WA Midwives’ Notification System.47 The effect of alcohol consumption in specific periods of pregnancy was examined by investigating infant outcomes for women who only drank in the first trimester, those who drank in the first trimester regardless of whether they stopped or continued drinking later in pregnancy, and the outcomes for women who drank in either trimesters 2 and/or 3 irrespective of whether they drank in first trimester, referred to as ‘late’ pregnancy. The maximum alcohol intake in each respective period was used to assign the level of drinking and where alcohol consumption was missing for the third trimester (n = 27), the second trimester alcohol consumption information was assigned. This study had 80% power at a 95% level of confidence to detect a 50% increase in the odds of preterm birth or poor fetal growth (OR 1.50) for infants of women consuming a low 392 level of alcohol and a 70% increase in the odds for the offspring of women consuming a moderate level of alcohol. Due to the small numbers in the specific categories, there was only limited power to detect a statistically significant difference for heavier drinking levels. The association between alcohol consumption both before and during pregnancy and risk of SGA infants compared with infants of abstinent women was assessed using logistic regression analysis. In addition, we used the same method to assess the association between prenatal alcohol and large-for-gestational-age (LGA) infants, using a POBW score greater than the 90th percentile to define LGA infants. We also conducted generalised linear regression analysis of POBW to ensure we had not missed any information by categorising the variable. Cox regression was used to determine independent risk factors for preterm birth. The analyses were adjusted for potential confounders: maternal smoking and illicit drug use (tranquillizers, marijuana, ecstasy, amphetamines, heroin, methadone, cocaine, lysergic acid diethylamide [LSD], and ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology The effect of prenatal alcohol on fetal outcomes volatile substances) during pregnancy, maternal age, parity, ethnicity, marital status and income (all self-reported), and maternal medical conditions (essential hypertension, preexisting diabetes mellitus, asthma, and genital herpes); pregnancy complications (threatened miscarriage, threatened preterm labour, urinary tract infection, pre-eclampsia, placenta praevia, abruption, antepartum haemorrhage, prelabour rupture of membranes, and gestational diabetes); or pregnancy procedures (ultrasound, fertility treatments, cervical suture, chorionic villus sampling/placental biopsy, amniocentesis, and antepartum and intrapartum cardiotocogram), identified from the WA Midwives’ Notification System. As self-reported income was missing for 17% of the cohort, the relative Index for Socio-Economic Disadvantage48 was applied as a proxy for missing cases. Interaction terms were tested for but were not included in the analysis as they did not make a statistically significant (r < 0.01) contribution to the fit of the data. Data analyses were conducted using SPSS version 15.0, and results are presented as odds ratios with 95% CI. The population attributable risk (PAR) and the attributable risk (AR)49 for preterm birth were calculated for alcohol exposure in the group of women who stopped drinking at moderate, heavy, and binge levels before second trimester. Results The quantity of alcohol consumed per week during pregnancy is presented in Table 1. Levels of alcohol intake decreased from the prepregnancy period to trimester 2 for each level of alcohol exposure, particularly the maximum intake for women with a binge or heavy drinking pattern. The median intake for women drinking at low to moderate levels decreased by approximately one-third between prepregnancy and first trimester but did not decrease markedly in late pregnancy. Conversely, there was little change in the median intake at higher levels of intake until late pregnancy when the median for binge drinkers halved and decreased by onethird for heavy drinkers. Around 9% of women drinking at heavy levels during prepregnancy consumed more than 400 g/week (data not shown). The distribution of maternal alcohol consumption before and during pregnancy is shown in Table 2. While fewer than 20% of women abstained during the prepregnancy period, this increased to 57% in the first two trimesters, decreasing to 54% in the third trimester. Only 41% of women abstained throughout each trimester of pregnancy (results not shown). Approximately one-third of women consumed a low level of alcohol before and during pregnancy. There was a marked reduction at higher levels of consumption with the percentage of women drinking at heavy and binge levels dropping from around 10– 3% between the prepregnancy and the first trimester. There were 421 (8.9%) infants who were SGA (POBW less than 10th percentile) and 265 (5.7%) infants were delivered before 37 weeks of gestation. Overall, there was little difference between the outcomes for infants of women who drank low levels of alcohol during pregnancy and those of women who were abstinent during pregnancy (Table 3). The percentage of growth-restricted infants was highest among those exposed to either maternal binge or heavy drinking during pregnancy, around 13% for each group. For preterm births, the percentage of infants born before 37 weeks was highest among those exposed to binge drinking during late pregnancy (9.5%) and for children born to mothers who drank heavily but stopped drinking before the second trimester (13.6%). The distribution of maternal characteristics by alcohol use is shown in Table 4. The prevalence of smoking in the whole cohort was 24.6%, with 10.6% of women smoking >10 cigarettes per day. Women who reported smoking at any time during pregnancy were less likely to abstain from alcohol during their pregnancy and to comprise a larger percentage of the women who continued to drink during late pregnancy (27.7%). Predictive factors for continuing to drink during late pregnancy were maternal age 30 years and older, higher income, other drug use, Caucasians, and married women. A higher percentage of women who stopped drinking before the second trimester reported that the pregnancy had been unplanned (55%) than women who were abstinent during pregnancy (47%). Table 5 shows the elevated odds of SGA infants with moderate to heavy alcohol consumption in pregnancy and how, after adjustment for smoking status, this effect is eliminated. There was, however, an increased odds of infants being born SGA following low levels of alcohol in the prepregnancy period (adjusted OR [aOR] 1.34, 95% CI 0.99–1.82) that attained significance in the fully adjusted generalised linear model Table 2. Pattern of maternal alcohol consumption before and during pregnancy Pattern of drinking Abstinent Low Moderate Binge two times per week Heavy Prepregnancy, n (%) Trimester 1, n (%) Trimester 2, n (%) Trimester 3, n (%) 919 (19.5) 1557 (33.0) 1282 (27.2) 512 (10.8) 449 (9.5) 2707 (57.4) 1326 (28.1) 446 (9.5) 131 (2.8) 108 (2.3) 2688 (57.0) 1542 (32.7) 367 (7.8) 56 (1.2) 66 (1.4) 2537 (53.8) 1668 (35.3) 402 (8.50) 43 (1.0) 69 (1.5) ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology 393 O’Leary et al. Table 3. Distribution of SGA and gestational age by maternal alcohol consumption before and during pregnancy Abstinent, n (%) Low, n (%) Drank during prepregnancy Percentage optimal birthweight 10% 844 (91.8) 1398 (89.9) SGA ,10% 75 (8.2) 157 (10.1) Gestational age 37 weeks 865 (94.1) 1426 (93.9) Preterm delivery ,37 weeks 54 (5.9) 93 (6.0) Drank during trimester 1 Percentage optimal birthweight 10% 1752 (91.2) 1199 (90.6) SGA ,10% 170 (8.8) 125 (9.4) Gestational age 37 weeks 1812 (94.3) 1252 (94.6) Preterm delivery ,37 weeks 110 (5.7) 72 (5.4) Alcohol consumed in trimester 1 with abstinence in late pregnancy* Percentage optimal birthweight 10% 1752 (91.2) 208 (90.0) SGA ,10% 170 (8.8) 23 (10.0) Gestational age 37 weeks 1812 (94.3) 219 (94.8) Preterm delivery ,37 weeks 110 (5.7) 12 (5.2) Drank during late pregnancy* Percentage optimal birthweight 10% 1752 (91.2) 1640 (91.3) SGA ,10% 170 (8.81) 157 (8.7) Gestational age 37 weeks 1812 (94.3) 1700 (94.6) Preterm delivery ,37 weeks 110 (5.7) 97 (5.4) Moderate, n (%) Binge •two times per week, n (%) Heavy, n (%) 1177 (92.0) 103 (8.0) 1210 (94.5) 70 (5.5) 464 (90.6) 48 (9.4) 489 (95.5) 23 (4.5) 410 (91.5) 38 (8.5) 423 (94.4) 25 (5.6) 408 (91.5) 38 (8.5) 424 (95.1) 22 (4.98) 114 (87.0) 17 (13.0) 121 (92.4) 10 (7.6) 94 (87.0) 14 (13.0) 102 (94.4) 6 (5.6) 80 (88.9) 10 (11.1) 82 (91.1) 8 (8.9) 33 (89.2) 4 (10.8) 33 (89.2) 4 (10.8) 20 (90.9) 2 (9.1) 19 (86.4) 3 (13.6) 436 (92.4) 36 (7.6) 452 (95.8) 20 (4.2) 55 (87.3) 8 (12.7) 57 (90.5) 6 (9.5) 69 (86.3) 11 (13.8) 75 (93.8) 5 (6.3) *Second and/or third trimesters. (adjusted b –1.66, 95% CI –2.94 to –0.39) (results not shown), but this association was not observed at higher levels of alcohol in prepregnancy or in any other analyses investigating the other time periods during pregnancy. The odds of an infant being LGA were close to or below one for all levels of alcohol exposure in each time period; however, none was statistically significant. There was no evidence of an increased likelihood of preterm birth at low levels of alcohol after adjusting for covariates (Table 6). There was a nonsignificant increase in the odds of preterm birth with binge drinking in pregnancy, aOR 1.31 (95% CI 0.67–2.58) in first trimester and aOR 1.61 (95% CI 0.68– 3.77) in late pregnancy, although the results lack precision due to small numbers. Combining all women who drank at greater than low levels during late pregnancy resulted in a masking of the association at higher levels, aOR 0.90 (95% CI 0.60–1.37). Women with a heavy pattern of alcohol intake in the first trimester and who stopped drinking by the second trimester had a nonsignificant, two-fold increased odds of preterm birth (aOR 2.30, 95% CI 0.69–7.72). There was a trend for moderate or higher levels of alcohol to increase the odds of preterm birth. Analysis combining moderate and higher levels of alcohol consumption yielded a 78% increased odds of preterm birth (aOR 1.78, 95% CI 1.01–3.14). The PAR and AR for preterm birth for combined moderate, heavy, and binge exposure in the group of women who stop- 394 ped drinking before second trimester were 11.4 and 19.4%, respectively. Discussion This study has been able to investigate the effect of different levels of alcohol consumption on fetal growth and preterm birth taking into account the quantity per occasion, frequency of consumption, and total quantity consumed. The findings of our study demonstrate that low levels of alcohol consumed during pregnancy at levels less than 60 g/week and not more than two standard drinks per occasion were not associated with preterm birth or SGA infants. Moderate to heavy alcohol intake resulted in an increased risk of preterm birth only in women who stopped drinking before the second trimester. There was no association between alcohol consumption during pregnancy and SGA infants after taking into account smoking status. Our results highlight an increasing trend in the risk of preterm birth with increasing levels of alcohol exposure, although findings were imprecise due to small numbers. Many previous studies have not differentiated the pattern of alcohol consumption. By combining infrequent and weekly binge drinking with drinking at low levels (an average of less than one drink per day), the association was (likely to be) masked.1,40 The tendency for researchers to group together all women ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology The effect of prenatal alcohol on fetal outcomes Table 4. Maternal characteristics by alcohol consumption before and during pregnancy Alcohol consumption Whole Cohort (%), n 5 4719 Prepregnancy Abstinent (%), n 5 919 During pregnancy Abstinent (%), n 5 1924 Drank trimester 1 (%), n 5 2011 Stopped before trimester 2 (%), n 5 380 Drank during late* pregnancy (%), n 5 2415 34.4 3.2 16.6 45.9 2.3 30.4 13.2 54.1 3.4 22.1 30.9 43.6 1.8 11.5 30.6 56.0 81.0 10.4 8.6 67.6 18.4 14.0 64.6 17.7 17.7 71.8 16.6 11.1 86.6 13.4 96.7 3.3 96.3 3.7 97.4 2.6 77.4 16.4 6.2 72.5 20.4 7.1 60.6 25.6 13.4 77.3 17.2 5.1 29.5 30.2 40.3 29.8 30.9 39.3 37.2 30.3 32.4 27.5 32.3 40.2 95.8 4.2 90.0 10.0 91.8 8.2 90.8 9.2 22.8 39.9 36.2 32.4 38.4 28.2 23.4 41.5 34.0 34 39.3 25.7 80.9 19.1 82.3 17.7 80.3 19.7 81.8 18.2 7.1 58.1 34.9 7.5 35.5 57.0 5.1 58.5 36.4 8.2 56.2 35.6 71.8 28.2 73.1 29.0 69.4 30.6 73.1 26.9 47.1 47.2 43.8 49.7 38.3 55.3 41.2 38.6 Maternal age group (n 5 4717) ,20 2.5 2.4 20–24 14.4 17.0 25–29 32.3 34.8 30–44 50.8 45.8 Smoking** (n 5 4688) None 74.7 83.3 10 per day 14 8.0 .10 per day 10.6 8.8 Ethnic group (n 5 4714) Caucasian 92.8 78.6 Other 7.1 21.4 Marital status (n 5 4700) Married 75.9 81.0 Defacto 17.5 13.4 Single 6.2 5.6 Parity (n 5 4714) First 29.1 24.6 Second 31.2 30.3 Third1 39.6 45.2 Drug use during pregnancy (n 5 4719) No 92.9 95.9 Yes 7.1 4.1 Income (n 5 4666) Most advantaged .$40 000 28.5 19.9 $25 001–40 000 30.8 39.5 Most disadvantaged $25 001 39.6 39.5 Maternal medical conditions (n 5 4717) None 81.3 80.8 Any 18.7 19.2 Procedures and treatments during pregnancy (n 5 4717) None 7.5 6.2 Ultrasound 57.2 57.6 Other 35.4 36.2 Pregnancy complications (n 5 4719) None 72.3 71.1 One or more 27.7 28.9 Unplanned pregnancy (n 5 4395) No 46.9 46.2 Yes 46.2 47.4 *Second and/or third trimesters. Note that numbers may vary due to missing covariate data. **Smoking at any stage during pregnancy. consuming an average of one drink or more per day also appears to conceal the association between dose and outcome. The potential risk of preterm birth for women who ceased alcohol consumption before the second trimester was signif- icantly increased when consumption at moderate and higher levels was combined. These results are similar to those reported by Jaddoe et al.40 who found an adjusted 2.5-fold increase in the risk of preterm birth with an average of one or ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology 395 O’Leary et al. Table 5. OR (and 95% CI) for the association between alcohol consumption categories before and during pregnancy and SGA (POBW <10%) Alcohol consumption and timing of exposure Frequency n SGA Unadjusted OR Prepregnancy Abstinent 919 75 Low 1557 157 1.27 Moderate 1282 103 0.99 Binge occasional 512 48 1.16 Heavy 449 38 1.04 Alcohol consumption during trimester 1 Abstinent 1924 170 Low 1326 125 1.07 Moderate 446 38 0.96 Binge occasional 131 17 1.54 Heavy 108 14 1.54 Alcohol consumed in trimester 1 with abstinence in late pregnancy Abstinent 1924 170 Low 231 23 1.14 Moderate 90 10 1.29 Binge occasional 37 4 1.25 Heavy 22 2 1.03 Maximum consumption during late pregnancy** Abstinent 1924 170 Low 1800 157 0.98 Moderate 472 36 0.85 Binge occasional 63 8 1.50 Heavy 80 11 1.64 Adjusted for smoking 95% CI OR 0.95–1.69 0.72–1.34 0.80–1.70 0.69–1.57 1.24 0.96 0.82 0.81 0.84–1.36 0.67–1.38 0.90–2.62 0.86–2.75 95% CI Fully adjusted* OR 95% CI Referent 1.0 0.92–1.66 0.70–1.32 0.55–1.22 0.53–1.24 1.34 1.05 0.93 0.83 0.99–1.82 0.75–1.46 0.62–1.40 0.53–1.30 1.05 0.85 0.91 0.84 Referent 1.0 0.82–1.35 0.58–1.23 0.52–1.59 0.44–1.59 1.08 0.87 0.98 0.82 0.84–1.40 0.59–1.29 0.55–1.71 0.42–1.59 0.72–1.80 0.66–2.53 0.44–3.57 0.24–4.45 1.06 1.11 0.83 0.75 Referent 1.0 0.66–1.68 0.56–2.20 0.29–2.43 0.17–3.31 1.09 1.10 0.91 0.72 0.68–1.75 0.55–2.21 0.31–2.72 0.16–3.26 0.79–1.24 0.59–1.24 0.70–3.20 0.85–3.17 0.96 0.75 0.86 1.04 Referent 1.0 0.76–1.21 0.51–1.10 0.40–1.88 0.51–2.09 1.00 0.79 0.86 1.03 0.78–1.28 0.53–1.17 0.39–1.92 0.50–2.10 *Adjusted for maternal age, smoking, ethnicity, marital status, parity, drug use, income, maternal medical conditions, procedures, and treatments during pregnancy and pregnancy complications. **Second and/or third trimesters. Note that numbers may not add up to the total due to women who abstained in First Trimester but drank in Late Pregnancy (n5784, 17%) and those who abstained in Late Pregnancy but drank in First Trimester (n5380, 8%). more drinks of alcohol per day until pregnancy recognition. There are several possible explanations for the greater risk of adverse infant outcomes among women who ceased drinking before the second trimester that we have not been able to investigate in this study. Although we adjusted for maternal medical complications in general, there may be specific health problems for which women stop consuming alcohol and that predispose them to preterm birth that we were unable to investigate. Another potential reason may be that cessation of alcohol consumption before second trimester may trigger an inflammatory or other metabolic response resulting in elevation of inflammatory cytokines and thereby increasing the risk of preterm birth.50,51 Furthermore, it is possible that some or all the women reporting cessation actually continued to drink during late pregnancy, although given the lack of dose response observed in late pregnancy, this is unlikely to explain our findings. It should be noted that the finding of increased odds of preterm delivery in women ceasing alcohol consumption before second trimester is based on small numbers and a type 396 1 error cannot be ruled out. It is, however, an issue warranting further investigation as our results indicate that, if this is a true finding, around 11% of preterm births would be attributable to this pattern of drinking. Prevention of high-risk drinking in early pregnancy could potentially minimise preterm birth and associated adverse developmental outcomes for the child and reduce costs on the healthcare system. Our study highlights that fetal growth appears to be much more influenced by the effects of smoking than alcohol. The negative association between low levels of alcohol in prepregnancy and SGA infants was not observed with higher levels of exposure in prepregnancy. This association is likely to reflect the influence of unmeasured confounding factors rather than a true association. Our results are consistent with the majority of studies investigating low to moderate prenatal alcohol exposure and the power of our study to detect a difference at these levels was reasonable. While our study is in agreement with half of the studies examining higher levels of prenatal alcohol exposure, the lack of power in our study at higher levels of prenatal alcohol exposure precludes firm conclusions ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology The effect of prenatal alcohol on fetal outcomes Table 6. OR (and 95% CI) for the association between alcohol consumption categories before and during pregnancy and preterm birth (<37 weeks) Alcohol consumption and timing of exposure Frequency n Preterm birth Prepregnancy Abstinent 919 54 Low 1557 93 Moderate 1282 70 Binge two times per week 512 23 Heavy 449 25 Alcohol consumption during trimester 1 Abstinent 1924 110 Low 1326 72 Moderate 446 22 Binge two times per week 131 10 Heavy 108 3 Alcohol consumed in trimester 1 with abstinence in late pregnancy Abstinent 1924 110 Low 231 12 Moderate 90 8 Binge two times per week 37 4 Heavy* 22 3 .Low combined 149 15 Maximum consumption during late pregnancy** Abstinent 1924 110 Low 1800 97 Moderate 472 20 Binge two times per week 80 6 Heavy 63 5 .Low combined 615 30 Unadjusted Adjusted for smoking OR 95% CI OR 0.89 0.71 0.77 0.83 0.73–1.43 0.66–1.33 0.47–1.25 0.59–1.53 1.00 0.94 0.75 0.94 0.95 0.86 1.31 0.97 0.71–1.28 0.55–1.37 0.69–2.51 0.43–2.21 0.91 1.59 1.89 2.59 1.81 0.94 0.74 1.65 1.08 0.88 95% CI Fully adjusted* OR 95% CI Referent 1.0 0.72–1.41 0.66–1.35 0.46–1.23 0.58–1.51 1.13 1.05 0.83 1.05 0.79–1.59 0.72–1.52 0.50–1.38 0.64–1.74 0.96 0.90 1.27 0.93 Referent 1.0 0.71–1.30 0.56–1.42 0.65–2.49 0.40–2.13 1.04 0.93 1.31 1.09 0.76–1.41 0.58–1.49 0.67–2.58 0.46–2.54 0.50–1.65 0.78–3.26 0.70–5.11 0.82–8.15 1.05–3.10 0.91 1.60 1.73 2.26 1.73 Referent 1.0 0.50–1.65 0.78–3.29 0.63–4.79 0.71–7.23 1.00–3.00 0.91 1.67 1.65 2.30 1.78 0.49–1.66 0.80–3.46 0.58–4.69 0.69–7.72 1.01–3.14 0.72–1.24 0.46–1.19 0.72–3.75 0.44–2.64 0.59–1.24 0.95 0.75 1.52 1.03 0.87 Referent 1.0 0.72–1.24 0.47–1.21 0.66–3.51 0.42–2.55 0.58–1.30 0.99 0.77 1.61 1.09 0.90 0.75–1.32 0.48–1.26 0.68–3.77 0.44–2.72 0.60–1.37 *Adjusted for maternal age, smoking, ethnicity, marital status, parity, drug use, income, maternal medical conditions, procedures, and treatments during pregnancy and pregnancy complications. **Second and/or third trimesters. Note that numbers may not add up to the total due to women who abstained in First Trimester but drank in Late Pregnancy (n=784, 17%) and those who abstained in Late Pregnancy but drank in First Trimester (n=380, 8%). from being made for very heavy alcohol consumption. A significantly increased risk for women drinking an average of three or more drinks per day across pregnancy has been reported by one study.39 The relatively small numbers of women drinking at these levels in our study, particularly in late pregnancy, limited our ability to look at this group separately, so we cannot rule out that a higher risk is associated with this level of exposure. The key strengths of this study are that it includes a randomly selected population-based cohort with a high response rate, thereby enabling the results to be generalised to the wider population, and we were able to adjust for a comprehensive range of known confounding factors including maternal behaviours and socio-demographic factors. While there may have been factors associated with heavy drinking that we were not able to account for, adjustment for known confounders such as smoking and socio-economic status is likely to have accounted, at least in part, for their effect. Our results have allowed us to address some of the main limitations identified in the recent systematic review by Henderson et al.,1 specifically, to examine the impact of low levels of alcohol consumption during pregnancy with sufficient power to detect a 50% increase in the odds of an effect for women drinking at low to moderate levels. Underreporting of alcohol consumption is always a potential concern to epidemiological studies and although we cannot confirm if underreporting occurred in this study, there are a number of factors that we believe would have limited underreporting. In Australia, alcohol consumption during pregnancy is very prevalent with almost 50% of women in our study consuming alcohol during pregnancy; this percentage is similar to earlier Australian studies.52 Screening for alcohol use during pregnancy and information on the risks from prenatal alcohol exposure are not routinely undertaken by WA health professionals53 and there were no public health campaigns on this issue either before or during the study. ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology 397 O’Leary et al. Reporting of prenatal alcohol consumption is influenced by the method and the timing of the questions.54–59 In this study, information on alcohol consumption during pregnancy was collected after the outcome of pregnancy was known so it is possible that recall bias may have occurred in some instances. Our data, however, were collected by selfadministered questionnaire, which has been shown to elicit more valid responses on socially sensitive issues and reveal more unwanted behaviour than interviews.56 Studies have indicated that misclassification of prenatal alcohol consumption collected retrospectively is rare54,58–60 and thus is unlikely to have had a profound influence on our findings,58,60 although we accept this remains a possibility. Although self-administered questionnaires have been reported to underestimate prenatal binge drinking,55 estimation of binge drinking in our survey was not obtained through a specific question on binge drinking. Instead, it was calculated from responses to questions on frequency, quantity consumed type of beverage, and measure (e.g. cans, glasses), which were asked together with questions on a range of prenatal maternal behaviours and family factors, so the focus of the survey was not exclusively upon alcohol consumption. However, if alcohol intake was underestimated in our study, the bias would likely be towards the null. The trend to increased risk of preterm birth when mothers binge or drink heavily during pregnancy, even occasionally, highlights the importance of screening all women of childbearing age for alcohol use and promoting abstinence or less risky patterns of drinking. The increasing tendency for young women in general to drink at risky levels, including binge drinking,61,62 should be recognised as an important modifiable cause of preterm birth and efforts need to be made to reverse this trend especially before women conceive. Conclusions Our results highlight the importance of taking into account the pattern of maternal drinking when estimating risk. This population-based cohort study showed no evidence of an association between low levels of prenatal alcohol consumption and SGA infants or preterm birth and showed that smoking accounts for the association between alcohol intake and SGA births. There was a significant increased likelihood of preterm delivery in women who were drinking at moderate or higher levels in first trimester but stopped drinking before second trimester. Future studies with larger sample sizes and which take into account the pattern and timing of maternal drinking are necessary. In particular, to investigate the effects of heavy alcohol intake and binge drinking and the effect of ceasing alcohol intake after the first trimester on preterm birth. Disclosure of interests statement All authors declare that there are no competing interests and therefore we have nothing to declare. 398 Contribution to authorship J.J.K. designed, obtained funding, and ran the original cohort study from which these data arose. Ms C.M.O. was the primary contributor to the paper in relation to the concept and design, analysis and interpretation of the results, and drafting of the article. N.N. and C.B. supervised Ms C.M.O. in the analysis of the data. All authors contributed to the interpretation of results, reviewing the article and provided final approval for the version to be published. Ethics approvals Ethics approval for the conduct of this study was granted by the Princess Margaret Hospital Research Ethics Committee and the WA Confidentiality of Health Information Committee. Funding The Western Australian survey of health-related behaviours and events during pregnancy and early infancy was funded by a grant from Healthway (the Western Australian Health Promotion Foundation 8016). J.J.K. was partially funded by a National Public Health Career Scientist award from the Department of Health and National Health Services Research and Development (PHCS022) when this analysis was conducted. This study was supported by the Australian National Health and Medical Research Council (NHMRC) program grant numbers 353514 (2005–2009), NHMRC Research Fellowship (353628) (C.B.) and NHMRC Public Health (Australia) Fellowship (404118) (N.N.). Acknowledgements The authors thank Margaret Wood, Peter Cosgrove, and Vivien Gee for maintenance of the databases. j References 1 Henderson J, Gray R, Brocklehurst P. Systematic review of effects of low-moderate prenatal alcohol exposure on pregnancy outcome. BJOG 2007;114:243–52. 2 Gray R, Henderson J. Review of the Fetal Effects of Prenatal Alcohol Exposure. Oxford, UK: National Perinatal Epidemiology Unit, University of Oxford, 2006. 3 Shu XO, Hatch MC, Mills JJ, Clemens JJ, Susser MM. Maternal smoking, alcohol drinking, caffeine consumption, and fetal growth: results from a prospective study. Epidemiology 1995;6:115–20. 4 Sulaiman ND, Florey CD, Taylor DJ, Ogston SA. Alcohol consumption in Dundee primigravidas and its effects on outcome of pregnancy. Br Med J (Clin Res Ed) 1988;296:1500–3. 5 Verkerk PH, van Noord-Zaadstra BM, Florey CD, de Jonge GA, VerlooveVanhorick SP. The effect of moderate maternal alcohol consumption on birth weight and gestational age in a low risk population. Early Hum Dev 1993;32:121–9. 6 Virji SK. The relationship between alcohol consumption during pregnancy and infant birthweight. An epidemiologic study. Acta Obstet Gynecol Scand 1991;70:303–8. 7 Day NL, Richardson G, Robles N, Sambamoorthi U, Taylor P, Scher M, et al. Effect of prenatal alcohol exposure on growth and morphology of offspring at 8 months of age. Pediatrics 1990;85:748–52. 8 Passaro K, Little R, Savitz D, Noso J. The effect of maternal drinking before conception and in early pregnancy on infant birthweight. The ALSPAC Study Team. Avon Longitudinal Study of Pregnancy and Childhood. Epidemiology 1996;7:377–83. ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology The effect of prenatal alcohol on fetal outcomes 9 Mills JL, Graubard BI, Harley EE, Rhoads GG, Berendes HW. Maternal alcohol consumption and birth weight. How much drinking during pregnancy is safe? JAMA 1984;252:1875–9. 10 McDonald A, Armstrong B, Sloan M. Cigarette, alcohol, and coffee consumption and prematurity. Am J Public Health 1992;82:87–90. 11 Whitehead N, Lipscomb L. Patterns of alcohol use before and during pregnancy and the risk of small-for-gestational-age birth. Am J Epidemiol 2003;158:654–62. 12 Berkowitz GS, Holford TR, Berkowitz RL. Effects of cigarette smoking, alcohol, coffee and tea consumption on preterm delivery. Early Hum Dev 1982;7:239–50. 13 Lazzaroni F, Bonassi S, Magnani M, Calvi A, Repetto E, Serra F, et al. Moderate maternal drinking and outcome of pregnancy. Eur J Epidemiol 1993;9:599–606. 14 Marbury M, Linn S, Monson R, Schoenbaum S, Stubblefield P, Ryan K. The association of alcohol consumption with outcome of pregnancy. Am J Public Health 1983;73:1165–8. 15 Ogston SA, Parry GJ. EUROMAC. A European concerted action: maternal alcohol consumption and its relation to the outcome of pregnancy and child development at 18 months. Results–strategy of analysis and analysis of pregnancy outcome. Int J Epidemiol 1992;21:(Suppl 1):S45–71. 16 Peacock JL, Bland JM, Anderson HR. Preterm delivery: effects of socioeconomic factors, psychological stress, smoking, alcohol, and caffeine. BMJ 1995;311:531–6. 17 Albertsen K, Andersen AM, Olsen J, Grønbaek M. Alcohol consumption during pregnancy and the risk of preterm delivery. Am J Epidemiol 2004;159:155–61. 18 Lundsberg LS, Bracken MB, Saftlas AF. Low-to-moderate gestational alcohol use and intrauterine growth retardation, low birthweight, and preterm delivery. Ann Epidemiol 1997;7:498–508. 19 Windham GC, Fenster L, Hopkins B, Swan SH. The association of moderate maternal and paternal alcohol consumption with birthweight and gestational age. Epidemiology 1995;6:591–7. 20 Jacobson JL, Jacobson SW, Sokol RJ, Martier SS, Ager JW, Shankaran S. Effects of alcohol use, smoking, and illicit drug use on fetal growth in black infants (see comment). J Pediatr 1994;124:757–64. 21 Bell R, Lumley J. Alcohol consumption, cigarette smoking and fetal outcome in Victoria, 1985. Community Health Stud 1989;13:484–91. 22 Primatesta P, Del Corno G, Bonazzi MC. Alcohol consumption as a fetal risk factor in a group of pregnant women of Northern Italy. J Prev Med Hygiene 1994;35:89–94. 23 Kesmodel U, Olsen SF, Secher NJ. Does alcohol increase the risk of preterm delivery? Epidemiology 2000;11:512–18. 24 Tennes K, Blackard C. Maternal alcohol consumption, birth weight, and minor physical anomalies. Am J Obstet Gynecol 1980;138:774–80. 25 Hingson R, Alpert JJ, Day N, Dooling E, Kayne H, Morelock S, et al. Effects of maternal drinking and marijuana use on fetal growth and development. Pediatrics 1982;70:539–46. 26 Wright JT, Waterson EJ, Barrison IG, Toplis PJ, Lewis IG, Gordon MG, et al. Alcohol consumption, pregnancy, and low birthweight. Lancet 1983;321:663–5. 27 Ernhart CB, Wolf AW, Linn PL, Sokol RJ, Kennard MJ, Filipovich HF. Alcohol-related birth defects: syndromal anomalies, intrauterine growth retardation, and neonatal behavioral assessment. Alcohol Clin Exp Res 1985;9:447–53. 28 Coles CD, Platzman KA, Smith I, James ME, Falek A. Effects of cocaine and alcohol use in pregnancy on neonatal growth and neurobehavioral status. Neurotoxicol Teratol 1992;14:23–33. 29 Geva D, Goldschmidt L, Stoffer D, Day NL. A longitudinal analysis of the effect of prenatal alcohol exposure on growth. Alcohol Clin Exp Res 1993;17:1124–9. 30 Faden VB, Graubard BI. Alcohol consumption during pregnancy and infant birth weight. Ann Epidemiol 1994;4:279–84. 31 Yang Q, Witkiewicz BB, Olney RS, Liu Y, Davis M, Khoury MJ, et al. A case-control study of maternal alcohol consumption and intrauterine growth retardation. Ann Epidemiol 2001;11:497–503. 32 Little RE. Moderate alcohol use during pregnancy and decreased infant birth weight. Am J Public Health 1977;67:1154–6. 33 Ouellette EM, Rosett HL, Rosman NP, Weiner L. Adverse effects on offspring of maternal alcohol abuse during pregnancy. N Engl J Med 1977;297:528–30. 34 Little RE, Asker RL, Sampson PD, Renwick JH. Fetal growth and moderate drinking in early pregnancy. Am J Epidemiol 1986;123:270–8. 35 Day NL, Jasperse D, Richardson G, Robles N, Sambamoorthi U, Taylor P, et al. Prenatal exposure to alcohol: effect on infant growth and morphologic characteristics. Pediatrics 1989;84:536–41. 36 Kaminski M, Rumeau C, Schwartz D. Alcohol consumption in pregnant women and the outcome of pregnancy. Alcohol Clin Exp Res 1978;2: 155–63. 37 Lumley J, Correy JF, Newman NM, Curran JT. Cigarette smoking, alcohol consumption and fetal outcome in Tasmania 1981–82. Aust N Z J Obstet Gynaecol 1985;25:33–40. 38 Covington CY, Nordstrom-Klee B, Ager J, Sokol R, Delaney-Black V. Birth to age 7 growth of children prenatally exposed to drugs: a prospective cohort study. Neurotoxicol Teratol 2002;24:489–96. 39 Chiaffarino F, Parazzini F, Chatenoud L, Ricci E, Sandretti F, Cipriani S, et al. Alcohol drinking and risk of small for gestational age birth. Eur J Clin Nutr 2006;60:1062–6. 40 Jaddoe VW, Bakker R, Hofman A, Mackenbach JP, Moll HA, Steegers EA, et al. Moderate alcohol consumption during pregnancy and the risk of low birth weight and preterm birth. The Generation R Study. Ann Epidemiol 2007;17:834–40. 41 Kurinczuk JJ, Parsons DE, Dawes V, Burton PR. The relationship between asthma and smoking during pregnancy. Women Health 1999;29:31–47. 42 Colvin L, Payne J, Parsons DE, Kurinczuk JJ, Bower C. Alcohol consumption during pregnancy in non-Indigenous west Australian women. Alcohol Clin Exp Res 2007;31:276–84. 43 Straker LM, Pollock CM, Zubrick SR, Kurinczuk JJ. The association between information and communication technology exposure and physical activity, musculoskeletal and visual symptoms and socio-economic status in 5-year-olds. Child Care Health Dev 2006;32:343–51. 44 Stanley F, Read A, Kurinczuk JJ, Croft M, Bower C. A population maternal and child health research database for research and policy evaluation in Western Australia. Semin Neonatol 1997;2:195–201. 45 National Health and Medical Research Council. Australian Alcohol Guidelines: Health risks and Benefits. Canberra: NHMRC, 2001. 46 Blair E, Liu Y, de Klerk N, Lawrence D. Optimal fetal growth for the Caucasian singleton and assessment of appropriateness of fetal growth: an analysis of a total population perinatal database. BMC Pediatr 2005;5:13. 47 Blair E, Liu Y, Cosgrove P. Choosing the best estimate of gestational age from routinely collected population-based perinatal data. Paediatr Perinat Epidemiol 2004;18:270–6. 48 ABS. Socio-Economic Indexes for Areas. Canberra: Australian Bureau of Statistics; 2001. January 2004. Report No.: ABS Catalogue No. 2039.0. 49 Hennekens C, Buring J. Epidemiology in Medicine, 1st edn. Boston/ Toronto: Little, Brown and Company, 1987. 50 Catov J, Bodnar L, Ness R, Barron S, Roberts J. Inflammation and dyslipidemia related to risk of spontaneous preterm birth. Am J Epidemiol 2007;166:1312–19. 51 Lohsoonthorn V, Qiu C, Williams MA. Maternal serum C-reactive protein concentrations in early pregnancy and subsequent risk of preterm delivery. Clin Biochem 2007;40:330–5. 52 O’Callaghan FV, O’Callaghan M, Najman JM, Williams GM, Bor W. Maternal alcohol consumption during pregnancy and physical outcomes up to 5 years of age: a longitudinal study. Early Hum Dev 2003;71:137–48. ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology 399 O’Leary et al. 53 Payne J, Elliott E, D’Antoine H, O’Leary CM, Mahony A, Haan E, et al. Health professionals’ knowledge, practice and opinions about fetal alcohol syndrome and alcohol consumption in pregnancy. Aust N Z J Public Health 2005;29:558–64. 54 Jacobson SW, Chiodo LM, Sokol RJ, Jacobson JL. Validity of maternal report of prenatal alcohol, cocaine, and smoking in relation to neurobehavioral outcome (see comment). Pediatrics 2002;109:815–25. 55 Kesmodel U. Binge drinking during pregnancy-is it possible to obtain valid information on a weekly basis? Am J Epidemiol 2004;159:803–8. 56 Alvik A. Consistency of reported alcohol use by pregnant women: Anonymous versus confidential questionnaires with item nonresponse differences. Alcohol Clin Exp Res 2005;29:1444–9. 57 Kesmodel U, Olsen SF. Self reported alcohol intake in pregnancy: comparison between four methods. J Epidemiol Commun Health 2001;55: 738–45. 400 58 Greene T, Ernhart CB, Martier S, Sokol R, Ager J. Prenatal alcohol exposure and language development. Alcohol Clin Exp Res 1990;14: 937–45. 59 Da Costa Pereira A, Olsen J, Ogston S. Variability of self reported measures of alcohol consumption: implications for the association between drinking in pregnancy and birth weight. J Epidemiol Commun Health 1993;47:326–30. 60 Verkerk P. Differential misclassification of alcohol and cigarette consumption by pregnancy outcome. Int J Epidemiol 1994;23: 1218–25. 61 White V, Hayman J. Australian Secondary School Students’ Use of Alcohol in 2002. Melbourne: The Cancer Council, Victoria, 2004. 62 ABS. Alcohol consumption in Australia: a snapshot, 2004–05. Canberra: Commonwealth Government. 2006 [www.abs.gov.au/ AUSSTATS/abs@.nsf/mf/4832.0.55.001/]. Accessed 14 February 2008. ª 2009 The Authors Journal compilation ª RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology