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Smoking during pregnancy: the dose dependence of birthweight deficits
G A Ellard1, F D Johnstone, R J Prescott
1National Institute for Medical Research, Mill Hill, London.
Objective:
To assess whether a simple urine based estimate of relative daily nicotine intake could predict smoking related birthweight deficits more accurately than self-reported cigarette consumption.
Design:
Active smokers were identified by a simple qualitative colorimetric urine test procedure and their relative nicotine intakes assessed by determining the ratios of the urinary concentrations of nicotine plus its metabolites to creatinine using automated colorimetric methods.
Setting:
A large teaching hospital.
Participants:
Three thousand and thirty-eight mothers from whom smoking histories had been elicited and who gave birth to live singleton babies after 28 weeks of gestation.
Main Outcome Measures:
Birthweights (adjusted for maternal weight, maternal age, baby's sex, parity and length of gestation), maternal weight gains during pregnancy and placental weights.
Results:
The adjusted birthweight deficits of babies born to proven active smokers averaged 226 g (95% confidence interval 194 g to 258 g), but dose dependent effects were only apparent when nicotine intake was based on urinary nicotine metabolites/creatinine ratios. Among the smokers, adjusted birthweights fell linearly with increasing nicotine intakes but gave a predicted mean birthweight for nonsmokers that was 102 g (95% CI 50 g to 154 g) lighter than that actually found (P < 0.0001). Maternal weight gains during pregnancy were substantially reduced in smokers and correlated more closely with urinary nicotine metabolite excretions than with reported daily cigarette consumptions. Placental weights were unaffected by smoking.
Conclusion:
There was a closer dose-effect relationship between birthweight deficits and urinary nicotine metabolites/creatinine ratios than with self-reported daily cigarette consumptions. The influence of nicotine exposure on birthweight appears to be biphasic, with one mechanism operating at very low levels of tobacco smoke intake and the other causing seemingly linearly related effects over the whole range of nicotine intakes of active smokers. These findings support recent evidence that passive smoking can cause substantial birthweight deficits.