During studies of postnatal developmental physiology of human infants, in which deep body temperature was monitored over night, we collected information on parental smoking habits and urine samples from the babies for cotinine estimation. Details of parental reported smoking were recorded and validated by direct observation by a trained researcher.
The studies were carried out over a period of five years up to and including 1998,20
and for this study, infants were recruited sequentially from the database according to whether the parents smoked (in the original studies, infants who met the inclusion criteria were selected at random from the Birth Notification Register). Infants with insufficient physiological data were excluded. For the purpose of this study, a smoking household was defined as one in which either parent (or main carer) smoked. Co‐sleeping was defined as an infant who routinely bed shared with the carer(s) for the main night‐time sleep over the duration of the study.
The database contained 493 infants. We sequentially selected the first 104 infants who provided a cotinine urine sample and for whom full physiological data were available. The infants were split into those from smoking and non‐smoking households for analysis. All infants were monitored during the same period. Their weight, record of feeding and care practices, and evidence of illness or immunisation were obtained from the database. In the original study, at bedtime, a paediatric urine collector (Hollister U bag), which was modified to reduce the risk of detachment, was attached to the infant to collect the evening urine sample. Samples were frozen within four hours of collection. Care was taken to avoid contamination of the specimen containers with any suspected source of nicotine.
The infants were approximately 10–12 weeks of age at the time of the study. The local ethics committee approved the study, and informed consent was obtained from all parents.
We report on the infants' cotinine levels, in relation to the reported smoking habits of parents, social circumstances and the care practices applied to the infant.
We used the cotinine:creatinine ratio as the measure of exposure to smoke. It was estimated by the enzyme‐linked immunosorbent assay (ELISA) method (Cosazt Bioscience Ltd, UK), a competitive enzyme immunoassay. The logarithm transformation was used to attain normal distribution. All analyses on the ELISA kit were carried out in duplicate and we used cotinine standards from 0 μg/l to 880 μg/l for calibration. All samples with cotinine levels greater than 880 μg/l were reanalysed after diluting in deionised water. Creatinine levels were determined by the Jaffe reaction on a Cobas Fara analyser (Roche Diagnostics, UK). The results were expressed as μg/l of cotinine per mmol/l creatinine. All analyses were performed blind (standards and reagents, Sigma Chemical Co, UK).
We used Student's t test to compare birth weight, gestational age and other approximately normally distributed variables, according to the smoking status of parents. Cotinine and creatinine levels were found to be largely positively skewed; they were therefore logarithm transformed for analysis. The geometric means are presented here. Homogeneity of variance was formally tested. The residual plots were examined visually and found to be satisfactory. The χ2 test was used to examine the association between parental smoking status and sex, feeding methods, social class of the family and other characteristics.
We used general linear models to examine the association between combinations of characteristics, primarily smoking status and the cotinine:creatinine ratio (on a logarithmic scale). Effects of potential confounders were examined by building models using forwards and backwards selection procedures. The pool of variables used for this consisted of: feeding method; father's employment status; social class; whether the baby co‐slept; inadequate heating in the home; the time of maturation of the adult core body temperature pattern and whether this was delayed; the minimum room temperature where baby slept; and the season.
All analyses were undertaken using SPSS for Windows (version 14.0). The level for statistically significant results was set at 5% (p<0.05), and 95% confidence intervals are presented for the main results.
What is already known on this topic
- Smoking is related to cot death.
- Babies are able to metabolise nicotine secondary to exposure to environmental tobacco smoke.
What this study adds
- If parents smoke, the baby smokes.
- Mother smoking is the most important contributing factor.
- Co‐sleeping and the temperature of the room the baby sleeps in are also contributory factors.