The average concentration of total airborne PAHs (of adequate monitoring quality) in personal air samples was 39.5 ± 48.1 ng/m3, with a median of 17.96 ng/m3 (n = 344). Among all the children tested for RCPM at the 5-year follow-up (n = 329), the average RCPM score was 21.8 ± 4.1.
compares the basic demographic characteristics of fully enrolled subjects having prenatal airborne PAH monitoring data and RCPM data at 5 years of age with fully enrolled subjects having PAH monitoring data but no RCPM. The characteristics of the two groups did not differ significantly except for newborn birth weight and maternal age. On average, the children with RCPM data were 133.2 g lighter at birth, and mothers were older by 1 year. The differences in the means are modest but statistically significant.
Subset with airborne PAH monitoring data and RCPM data (n = 219)a versus subset with airborne PAH monitoring data but missing RCPM data in the Krakow cohort (n = 139).
Correlations between airborne PAHs and ETS exposure, between airborne PAHs and dietary PAHs, and between airborne PAHs and maternal or cord cotinine were examined using Spearman rank-order correlation. None was found to be significant, either in the Krakow cohort as a whole or the subset studied here (n = 214) (). As expected, ETS exposure during pregnancy was significantly correlated with maternal and cord cotinine levels both in the entire cohort and in the present subset, supporting self-reported ETS as a reliable measure of ETS exposure. ETS exposure and dietary PAHs were correlated in the present subset (n = 214) but not in the larger cohort.
Spearman correlations [correlation coefficient r; p-value in the Krakow cohort (n)].
High prenatal airborne PAH exposure levels were associated with a significant, albeit modest, reduction in child intelligence in models with either dichotomous or Ln-transformed continuous variables for PAH exposure (). The estimated effect of prenatal airborne PAH was significant after adjusting for prenatal ETS in the home and other potential confounders. The inverse relationship between airborne PAH level and RCPM score remained after adjusting for trimester of monitoring (second or third).
Association between prenatal exposure to airborne PAHs and RCPM score at 5 years of age in the Krakow cohort (n = 214).
Prenatal ETS in the home was a significant predictor of RCPM score, as shown in . Excluding prenatal ETS from the model did not materially alter the estimated effect size or p-value of PAH on child RCPM score [β= −1.3, p = 0.03 in the PAH high/low model; β = −0.5, p = 0.03 in the Ln(PAH) model after excluding ETS (n = 214)], indicating that prenatal ETS exposure is not a potential confounder of this association.
In the smaller subset having data for maternal intelligence (n = 171), the estimated effect of PAH exposure remained consistent and significant [β = −1.4, p = 0.04 for PAH high/low; β = −0.6, p = 0.05 for continuous Ln(PAH)]. Prenatal exposure to ETS in the home and maternal intelligence were significant or borderline-significant covariates in this model (data not shown).
Neither lead nor dietary PAHs was a significant predictor of RCPM scores (< 0.1) when included individually in the model. Lead (computed as a Ln-transformed variable) was not a significant predictor in the model after controlling for prenatal ETS exposure in the home, sex of the child, and maternal education; the effect of prenatal airborne PAH exposure remained significant with lead included in the model. The dietary route of exposure to PAHs was not a significant contributor to the effect of airborne PAHs, which remained significant after including dietary PAH in the model. The magnitude of the association between PAHs and RCPM was unchanged when either lead or dietary PAH exposure was included in the model.
Including birth head circumference or birth weight separately in the model did not alter the estimated effect of airborne PAH [adjusted for birth head circumference: β = −1.4, p = 0.02 for PAH high/low; β = −0.6, p = 0.02 for continuous Ln(PAH), n = 214; adjusted for birth weight: β = −1.3, p = 0.03 for PAH high/low; β = −0.5, p = 0.02 for continuous Ln(PAH), n = 214].
With respect to postnatal exposure to PAHs, we found no effect of postnatal urinary PAH metabolites on the magnitude of the effect of PAHs on RCPM. Twenty-three percent of families changed neighborhood of residence in the child’s first 3 years of life, with a likely though unmeasured change in airborne PAH exposure. Adjusting for change in neighborhood of residence did not alter the strength of the inverse association found between prenatal airborne PAHs and RPCM score. Controlling for postnatal exposure to ETS in the home (22% of mothers reported exposure during at least one of the 10 follow-up interviews given between birth and the child’s follow-up at 5 years of age) did not alter the estimated effect of PAHs.
There was no evidence of an interaction between trimester of PAH monitoring, PAH monitoring season, or season of birth. The p-values of interaction terms were > 0.38 in the models with dichotomized PAH and > 0.25 in the models with ln-transformed PAH.
Finally, to better compare the Krakow cohort with the NYC cohort, we restricted analysis to the Krakow participants within the common PAH exposure range seen in Krakow and NYC (0.27–44.81 ng/m3) and to the subset of women for whom data on maternal intelligence were available (so that the models would be directly comparable). In this comparison, the estimated effect sizes in both the dichotomous and continuous models were similar to those observed in the entire Polish cohort (over the full exposure range: 1.8–272.2 ng/m3) ().
Table 4 Association between prenatal exposure to airborne PAHs and RCPM score at 5 years of age in the Krakow cohort including only subjects whose PAH exposure was within the common exposure range between the NYC and Krakow cohorts (0.27–44.81 ng/m3) (more ...)