The current study demonstrated that active maternal smoking throughout pregnancy poses a statistically significant increased risk for SGA, especially in male newborns. However, in this study, we found that active maternal smoking only in the first trimester, or active maternal smoking in the second and/or third trimesters did not pose a statistically significant risk for SGA. The abovementioned three categories in relation to active maternal smoking were not significantly related to the risk of preterm birth, although the positive linear trend was statistically significant. There was no significant relationship between active maternal smoking and LBW. Active maternal smoking throughout pregnancy was significantly associated with a decrease in birth weight, with an adjusted mean reduction in birth weight of 169.6 g. No significant associations were found between maternal ETS exposure at home or work and any of the birth outcomes we studied.
A prebirth cohort study in Greece showed that active maternal smoking at 12 weeks of gestation was significantly positively related to the risk of LBW and SGA, but not preterm birth, while smoking cessation before 12 weeks of gestation was not associated with the risk of preterm birth, LBW, or SGA . In a prebirth cohort study conducted in New Zealand and Australia, women who were still smoking at 15 weeks of gestation had a significantly increased risk for preterm birth and SGA compared with those who had stopped smoking before 15 weeks gestation . The same study found that for those who stopped smoking before 15 weeks of gestation had the same risk of preterm birth and SGA as women who did not smoke at all during pregnancy. Continued active smoking after conception is known to be significantly positively associated with the risk of preterm birth and LBW, while smoking until conception was found not to be related to the risk of preterm birth or LBW in the Generation R Study conducted in The Netherlands . In a historical cohort study in Brazil, active maternal smoking during the whole pregnancy was significantly associated with an increased risk of LBW and SGA, but not preterm birth, while smoking cessation during the first trimester was found to have no statistically significant relationship with increased risk of preterm birth, LBW, or SGA . A prebirth cohort study conducted in the USA found that women who smoked throughout their pregnancy had a significantly increased risk of SGA, while the risk of SGA for those who had smoked only during the first trimester was similar to that of non-smokers . In a retrospective cohort analysis of US birth certificates, which compared women who smoked throughout pregnancy with those who quit during their pregnancy, those who quit smoking in the first trimester had lower risk of delivering preterm non-SGA, term SGA, and preterm SGA newborns, and this risk was similar in magnitude to those who never smoked . The present results concerning active maternal smoking during pregnancy are in partial agreement with these observations. In particular, the current results confirm prior research that has demonstrated that those who quit smoking in early pregnancy can achieve the same low risk of adverse birth outcomes as those who never smoke during pregnancy.
The difference we found in the effect of maternal smoking on male and female babies differs from the findings of a study in Germany that found that, particular in heavy smokers, the adverse effect of maternal smoking during pregnancy on the mean birth weight and risk of SGA was greater in girls than in boys .
With respect to maternal ETS exposure during pregnancy among mothers who never smoked during pregnancy, the current results are consistent with those of some previous studies that showed no relationship between passive maternal smoking during pregnancy and birth outcomes [12, 18, 26]. In the Generation R Study, however, maternal ETS exposure of more than 3 hours per day in late pregnancy (≥ 25 weeks’ gestation) was significantly associated with an increased risk of LBW, but not preterm birth . A case–control study in New Zealand showed a significant positive relationship between the risk of SGA and maternal ETS exposure in the workplace or while socializing, but not between the risk of SGA and paternal or other household smoking . Women whose partner smoked during pregnancy had a significantly increased risk of SGA, but not LBW or preterm birth in the previously cited Brazilian study . Our results are in partial agreement with these findings. The discrepancies among studies may be explained, at least in part, by differences in characteristics, smoking habits, and lifestyle of the populations examined.
According to a review by Jauniaux and Burton, tobacco toxins interfere with the trophoblastic and biological functions of fetal cells that regulate protein metabolism and enzyme activity, leading to an impact on fetal growth, with a reduction of weight, body fat, and many other anthropometric parameters . We have no ready explanation as to why the detrimental effect of active maternal smoking on the risk of SGA was more evident in male babies than in female babies in the present study. The greater male susceptibility might be explained by a different hormonal milieu.
Several weaknesses of the present study warrant mention. Information on tobacco exposure was obtained with self-administered questionnaires and was not validated by objective measurements such as cotinine levels. However, Pickett et al. reported that urinary cotinine measures and self-reported number of cigarettes were highly correlated at any given time point in pregnant women in the USA . Although data on maternal smoking status at different trimesters were available, such data were collected using the second questionnaire after birth. Consequently, the possibility of recall bias should be considered; however, any resulting exposure misclassification would be non-differential and would have yielded an underestimation of values in our results.
In the first questionnaire, we could not estimate the participation rate because we do not have exact figures for the number of pregnant women who were provided with a set of leaflets explaining the KOMCHS, an application form, and a self-addressed and stamped return envelope by the 423 collaborating obstetric hospitals. This situation made it impossible to assess the differences between participants and non-participants, because no information on personal characteristics such as maternal age and socioeconomic status was available for non-participants. Our subjects were probably not representative of Japanese women in the general population. For example, a population census conducted in 2000 in Fukuoka Prefecture found that the percentages of women aged 30 to 34 years with < 13, 13–14, ≥ 15, and an unknown number of years of education were 52.0%, 31.5%, 11.8%, and 4.8%, respectively . The corresponding figures for this study were 23.1%, 33.4%, 43.5%, and 0.0%, respectively. Thus, our study subjects were more educated and probably more aware of health topics than women in the general population. Nevertheless, cigarette-smoking status in our study population was likely to be similar to that of the general population. In the National Health and Nutrition Survey in Japan of 2007, the percentages of currently-smoking, formerly-smoking, and non-smoking women aged 30 to 39 years were 17.2%, 11.4%, and 71.4%, respectively, although data specific to pregnant women were not available . At baseline, 31.7% of the present study subjects had ever smoked.
The current study did not have substantial statistical power although significant associations were detected. Although adjustment was made for several confounding factors, residual confounding effects could not be ruled out.