Intrauterine exposure to polycyclic aromatic hydrocarbons, fine particulate matter and early wheeze. Prospective birth cohort study in 4-year olds

Abstract

The main goal of the study was to determine the relationship between prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) measured by PAH-DNA adducts in umbilical cord blood and early wheeze. The level of PAH-DNA adducts in the cord blood is assumed to reflect the cumulative dose of PAHs absorbed by the fetus over the prenatal period. The effect of prenatal PAH exposure on respiratory health measured by the incidence rate ratio (IRR) for the number of wheezing days in the subsequent four year follow-up was adjusted for potential confounding factors such as personal prenatal exposure to fine particulate matter (PM2.5), environmental tobacco smoke (ETS), gender of child, maternal characteristics (age, education and atopy), parity, and mold/dampness in the home. The study sample includes 339 newborns of non-smoking mothers 18-35 years of age and free from chronic diseases, who were recruited from ambulatory prenatal clinics in the first or second trimester of pregnancy. The number of wheezing days during the first two years of life was positively associated with prenatal level of PAH-DNA adducts (IRR = 1.69, 95%CI = 1.52 – 1.88), prenatal particulate matter (PM2.5) level dichotomized by the median (IRR = 1.38; 95%CI: 1.25 – 1.51), maternal atopy (IRR = 1.43; 95%CI: 1.29 – 1.58), moldy/damp house (IRR = 1.43; 95%CI: 1.27 – 1.61). The level of maternal education and maternal age at delivery were inversely associated with the IRRs for wheeze. The significant association between frequency of wheeze and the level of prenatal environmental hazards (PAHs and PM2.5) was not observed at ages 3 or 4 years. Although the frequency of wheezing at ages 3 or 4 years was no longer associated with prenatal exposure to PAHs and PM2.5, its occurrence depended on the presence of wheezing in the first two years of life, which nearly tripled the risk of wheezing in later life. In conclusion, the findings may suggest that driving force for early wheezing (<24 months of age) are different to those leading to later onset of wheeze. As we reported no synergistic effects between prenatal PAH (measured by PAH-DNA adducts) and PM2.5 exposures on early wheeze, this suggests the two exposures may exert independent effects via different biological mechanism on wheeze.

The health burden of pollution: the impact of&nbsp;prenatal exposure to air pollutants

“…The highest levels of PAHs during pregnancy were associated with a reduced FEV 1 and a reduced FEV 25–75 40. The same authors have reported that the number of wheezing days during the first 2 years of life was positively associated with the prenatal level of PAH-adducts (incidence rate ratio [IRR] =1.69; 95% CI: 1.52–2.88) 41. Correlations among personal exposure, pre-and postnatal PAH, and the severity of wheezing and recurrent wheezing were also studied by the same group of researchers and suggested that prenatal exposure may trigger and intensify the symptoms resulting from postnatal exposure.…”

Seasonal Gradient Patterns of Polycyclic Aromatic Hydrocarbons and Particulate Matter Concentrations near a Highway

“…Eight nonvolatile PAHs (PAHs with more than 4 rings: MW 228-278) were selected as target compounds due to their abundance in traffic emissions and their adverse health effects observed in young children [5][6][7][8][24][25][26] [27]. Detailed analytical protocols employed for the measurement of PAHs have been reported elsewhere [28] and a brief summary is given here.…”

“…However, the uncertainties surrounding the precise physical and chemical components of PM, which are responsible for observed health risks, make it challenging to understand the causal relationships between PM exposure and health effects. Among numerous toxic chemical components of PM, polycyclic aromatic hydrocarbons (PAHs) have received particular attention because recent studies implicated that prenatal PAH exposure, specifically Σ 8 PAHs (the sum of 8 nonvolatile PAHs; ), were associated with respiratory symptoms, low birth weight, and deficits in neurodevelopment and cognition in young children [4][5][6][7][8].…”

A mouse model links asthma susceptibility to prenatal exposure to diesel exhaust

“…In support of the latter hypothesis, there are many epidemiological studies showing an association between various in utero exposures and asthma susceptibility 5–12 . Among prenatal insults with linkage to asthma, solid and consistent epidemiological evidence has been provided for exposure to traffic-related pollution, including diesel exhaust 5–8 . Mothers who lived near highways during pregnancy are more likely to have children with asthma 5 .…”