DOI: 10.1111/j.1471-0528.2008.02058.

Epidemiology

www.blackwellpublishing.com/bjog

The effect of maternal alcohol consumption on

fetal growth and preterm birth
CM OLeary,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 OLeary, 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 19951997.
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 1.013.14]).
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: OLeary C, Nassar N, Kurinczuk J, Bower C. Impact of maternal alcohol consumption on fetal growth and preterm birth. BJOG
2009;116:390400.

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,39 intrauterine growth restriction,5,10,11 and
preterm birth,8,10,1217 a small number of studies found an
increased risk at low levels1820 and, conversely, others have

2009 The Authors Journal compilation 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.10,13,18,2123 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 association3,4,10,18,2431 and half reporting a significant association.9,20,3240 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.4143 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, 34,
or 12 days/week; 12 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 34 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 19982002 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

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391

OLeary 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

>10501

Grams per week***

60

70

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 810 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, babys
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

2009 The Authors Journal compilation 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 0.991.82) 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)

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393

OLeary 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 0.672.58) 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 0.601.37).
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 0.697.72). 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 1.013.14).
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

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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
2024
14.4
17.0
2529
32.3
34.8
3044
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 00140 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

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OLeary 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

0.951.69
0.721.34
0.801.70
0.691.57

1.24
0.96
0.82
0.81

0.841.36
0.671.38
0.902.62
0.862.75

95% CI

Fully adjusted*
OR

95% CI

Referent 1.0
0.921.66
0.701.32
0.551.22
0.531.24

1.34
1.05
0.93
0.83

0.991.82
0.751.46
0.621.40
0.531.30

1.05
0.85
0.91
0.84

Referent 1.0
0.821.35
0.581.23
0.521.59
0.441.59

1.08
0.87
0.98
0.82

0.841.40
0.591.29
0.551.71
0.421.59

0.721.80
0.662.53
0.443.57
0.244.45

1.06
1.11
0.83
0.75

Referent 1.0
0.661.68
0.562.20
0.292.43
0.173.31

1.09
1.10
0.91
0.72

0.681.75
0.552.21
0.312.72
0.163.26

0.791.24
0.591.24
0.703.20
0.853.17

0.96
0.75
0.86
1.04

Referent 1.0
0.761.21
0.511.10
0.401.88
0.512.09

1.00
0.79
0.86
1.03

0.781.28
0.531.17
0.391.92
0.502.10

*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

2009 The Authors Journal compilation 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

0.731.43
0.661.33
0.471.25
0.591.53

1.00
0.94
0.75
0.94

0.95
0.86
1.31
0.97

0.711.28
0.551.37
0.692.51
0.432.21

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
0.721.41
0.661.35
0.461.23
0.581.51

1.13
1.05
0.83
1.05

0.791.59
0.721.52
0.501.38
0.641.74

0.96
0.90
1.27
0.93

Referent 1.0
0.711.30
0.561.42
0.652.49
0.402.13

1.04
0.93
1.31
1.09

0.761.41
0.581.49
0.672.58
0.462.54

0.501.65
0.783.26
0.705.11
0.828.15
1.053.10

0.91
1.60
1.73
2.26
1.73

Referent 1.0
0.501.65
0.783.29
0.634.79
0.717.23
1.003.00

0.91
1.67
1.65
2.30
1.78

0.491.66
0.803.46
0.584.69
0.697.72
1.013.14

0.721.24
0.461.19
0.723.75
0.442.64
0.591.24

0.95
0.75
1.52
1.03
0.87

Referent 1.0
0.721.24
0.471.21
0.663.51
0.422.55
0.581.30

0.99
0.77
1.61
1.09
0.90

0.751.32
0.481.26
0.683.77
0.442.72
0.601.37

*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.

2009 The Authors Journal compilation RCOG 2009 BJOG An International Journal of Obstetrics and Gynaecology

397

OLeary et al.

Reporting of prenatal alcohol consumption is influenced

by the method and the timing of the questions.5459 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 rare54,5860 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 (20052009), 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

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