Prenatal exposure to fine particles and polycyclic aromatic hydrocarbons and birth outcomes : a two-pollutant approach

Background Previous epidemiologic studies have considered the effects of individual air pollutants on birth outcomes, whereas a multiple-pollutant approach is more relevant to public health policy. Objectives The present study compared the observed effect sizes of prenatal fine particulate matter ( PM2.5) and polycyclic aromatic hydrocarbons (PAH) (a component of PM2.5) exposures on birth outcome deficits, assessed by the single vs. two-pollutant approaches. Methods The study sample included 455 term infants born in Krakow to non-smoking mothers, among whom personal exposures to PM2.5 and PAH were monitored in the second trimester of pregnancy. The exposure effect estimates (unstandardized and standardized regression coefficients) on birth outcomes were determined using evant covariates. Results In the single-pollutant approach, each pollutant was inversely associated with all birth outcomes. The effect size of prenatal PAH exposure on birth weight and length was twice that of PM2.5, in terms of standardized coefficients. In the two-pollutant approach, the negative effect of PM2.5 on birth weight and length, adjusted for PAH exposure, lost its significance. The standardized effect of PAH on birth weight was 10-fold stronger ($\beta$ = -0.20, $\rho$ = 0.004) than that estimated for PM2.5 ($\beta$ = -0.02, $\rho$ = 0.757). Conclusion The results provide evidence that PAH had a greater impact on several measures of fetal development, especially birth weight, than PM2.5. Though in the singlepollutant models PM2.5 had a significant impact on birth outcomes, this effect appears to be mediated by PAH

Dose-dependent relationship between prenatal exposure to fine particulates and exhaled carbon monoxide in non-asthmatic children : a population-based birth cohort study

Objectives: The main goal of the study was to assess possible association between fetal exposure to fi ne particulate matter (PM2.5) and exhaled carbon monoxide (eCO) measured in non-asthmatic children. Material and Methods: The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków. Personal samplers of PM2.5 were used to measure fi ne particle mass in the fetal period and carbon monoxide (CO) in exhaled breath from a single exhalation effort at the age of 7. In the statistical analysis of the effect of prenatal PM2.5 exposure on eCO, a set of potential confounders, such as environmental tobacco smoke (ETS), city residence area, sensitization to house dust allergens and the occurrence of respiratory symptoms monitored over the seven-year follow-up was considered. Results: The level of eCO did not correlate with the self-reported ETS exposure recorded over the follow-up, however, there was a positive signifi cant relationship with the prenatal PM2.5 exposure (non-parametric trend p = 0.042). The eCO mean level was higher in atopic children (geometric mean = 2.06 ppm, 95% CI: 1.58–2.66 ppm) than in non-atopic ones (geometric mean = 1.57 ppm, 95% CI: 1.47–1.73 ppm) and the difference was statistically signifi cant (p = 0.036). As for the respiratory symptoms, eCO values were associated positively only with the cough severity score recorded in the follow-up (nonparametric trend p = 0.057). In the nested multivariable linear regression model, only the effects of prenatal PM2.5 and cough severity recorded in the follow-up were related to eCO level. The prenatal PM2.5 exposure represented 5.1%, while children’s cough represented only 2.6% of the eCO variability. Conclusion: Our study suggests that elevated eCO in non-asthmatic children may result from oxidative stress experienced in the fetal period and that heme oxygenase (HO) activity in body tissues may be programmed in the fetal period by the exposure to fi ne particulate matter