Academic journal article Environmental Health Perspectives

International Studies of Prenatal Exposure to Polycyclic Aromatic Hydrocarbons and Fetal Growth

Academic journal article Environmental Health Perspectives

International Studies of Prenatal Exposure to Polycyclic Aromatic Hydrocarbons and Fetal Growth

Article excerpt

OBJECTIVES: Polycyclic aromatic hydrocarbons (PAHs) are ubiquitously distributed human mutagens and carcinogens. However, lack of adequate air monitoring data has limited understanding of the effects of airborne PAHs on fetal growth. To address this gap in knowledge, we examined the association between prenatal exposure to airborne PAHs and birth weight, birth length, and birth head circumference, respectively, in Krakow, Poland, and New York City (NYC).

METHODS: The parallel prospective cohort studies enrolled nonsmoking, healthy, and nonoccupationally exposed women and their newborns. Personal air monitoring of pregnant women was conducted over 48 hr. To control for maternal environmental tobacco smoke (ETS) exposure, we excluded those with umbilical cord plasma cotinine concentrations > 25 ng/mL. Mean cord plasma cotinine concentrations in both ethnic groups were [less than or equal to] 0.5 ng/mL.

RESULTS: Prenatal PAH exposure was 10-fold higher in Krakow than in NYC. Prenatal PAH exposure was associated with significantly reduced birth weight in both Krakow Caucasians (p < 0.01) and in NYC African Americans (p < 0.01), controlling for known and potential confounders, but not in NYC Dominicans. Within the lower exposure range common to the two cities (1.80-36.47 ng/[m.sup.3]), the effect per unit PAH exposure on birth weight was 6-fold greater for NYC African Americans than for Krakow Caucasians (p = 0.01).

CONCLUSIONS: These results confirm the adverse reproductive effect of relatively low PAH concentrations in two populations and suggest increased susceptibility of NYC African Americans. Fetal growth impairment has been linked to child developmental and health problems. Thus, substantial health benefits would result from global reduction of PAH emissions.

KEY WORDS: birth outcomes, birth weight, fetal toxicity, personal air monitoring, polycyclic aromatic hydrocarbons, prenatal. Environ Health Perspect 114:1744-1750 (2006). doi:10.1289/ehp.8982 available via http://dx.doi.org/ [Online 3 August 2006]

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Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants generated by combustion sources that include diesel- and gasoline-powered motor vehicles, coal-fired power plants, residential heating, cooking, and tobacco smoking (Bostrom et al. 2002). An estimated > 80% of airborne PAHs results from the combustion of fossil fuels and biomass (Bostrom et al. 2002). There is growing concern about the adverse effects of air pollution from fossil fuel combustion on public health (Bostrom et al. 2002; Brunekreef and Holgate 2002) and the global climate (National Academy of Sciences 2001). PAHs are human mutagens and carcinogens (Bostrom et al. 2002) and are potentially significant reproductive and developmental toxicants (Dejmek et al. 2000; Perera et al. 2003). For example, prenatal exposure of rats to 25-100 [micro]g/[m.sup.3] of the representative PAH, benzo[a]pyrene (BaP), through maternal inhalation significantly decreased the fetal survival rate and birth weight in a dose-dependent manner (Archibong et al. 2002). In humans, associations between PAHs or PAH-DNA damage and fetal growth reduction have been reported in some but not all studies (Dejmek et al. 2000; Perera et al. 1998, 2003; Sram et al. 2005). In the Czech Republic, ambient PAHs significantly increased the risk of intrauterine growth retardation (IUGR) both in Teplice and Prachatice (Dejmek et al. 2000). An earlier study in Poland found that the infants who had higher than median leukocyte PAH-DNA adduct level had significantly reduced birth weight, length, and head circumference (Perera et al. 1998). In New Jersey, USA, the risk of fetal death, premature birth, and low birth weight was significantly higher for those with a high prenatal polycyclic organic matter exposure (Vassilev et al. 2001). However, the limitations of most prior studies [retrospective or cross-sectional design, reliance on ambient air monitoring data, failure to account for co-exposure to other sources of PAHs such as environmental tobacco smoke (ETS)] have prevented definitive causal inferences regarding airborne PAHs and impaired fetal growth (Sram et al. …

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