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Luther Lazaro
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Maternal exposure to fine particulate matter (PM2.5) was associated with pregnancy complications. However, we still lack comprehensive evidence regarding which specific chemical components of PM2.5 are more harmful for maternal and foetal health.
Exposure to fine particulate matter (PM2.5) in the ambient atmosphere has adverse health effects across all generations [1]. Women of reproductive age are not exceptions. There is evidence that exposure to PM2.5 during pregnancy is associated with obstetric complications that threaten the health of pregnant mothers, such as hypertensive disorders of pregnancy (including preeclampsia) and placental abruption [2,3,4,5]. In addition, maternal exposure to PM2.5 appears to have harmful effects on the next generation; for example, PM2.5 exposure during pregnancy was associated with foetal growth restriction that resulted in the birth of small for gestational age (SGA) children [6, 7], and was linked to the occurrence of stillbirths [8]. Although the accumulating findings suggest that total PM2.5 (general mixture) influences maternal and foetal health, we still lack comprehensive evidence regarding which specific chemical components of PM2.5 are more harmful for their health [9]. Thus, understanding the association between individual PM2.5 components and perinatal health may provide information of value to policy making for environmental health.
The placenta is a temporal organ, and normal placentation is absolutely essential for foetal development and growth, while also contributing to maternal health [10]. Conversely, abnormal placentation during the first trimester is related to adverse maternal and foetal conditions called placenta-mediated pregnancy complications, including SGA, preeclampsia, placental abruption, and stillbirth [11,12,13]. As aforementioned, each of these four complications has been reported to be individually associated with maternal exposure to PM2.5 [2, 5,6,7,8]. Therefore, in the present study, we focused on PM2.5 exposure over the first trimester, which is an important period of placentation, and investigated the association with placenta-mediated pregnancy complications, with the aim of elucidating the relationship between PM2.5 exposure and placental toxicity, and seeking a pathogenic foundation common to individual complications. In light of the fact that PM2.5 may be a common risk factor for four individual complications, few studies have examined the association between PM2.5 exposure and placenta-mediated pregnancy complications as a composite outcome. Also, it seems likely that ozone is a risk factor for placenta-mediated pregnancy complications, because the potential maternal and foetal health effects of ozone exposure were indicated [14].
We collected data on all the live births and stillbirths after 22 weeks of gestation at 39 cooperating hospitals within the study area, from January 2013 to December 2015 (a total of 89,417 births), which were extracted from the Japan Perinatal Registry Network database, a hospital-based registry (mainly university hospitals and local general hospitals) managed by the Japan Society of Obstetrics and Gynaecology. Details of the database are described elsewhere [17]. The database included roughly two-fifths of the total births in the study area for the study period. The data are routinely input by attending physicians via a standardised electronic form, and checked with respect to uniform coding specifications and diagnostic criteria for complications by the Perinatal Committee of the Society [18]. We used anonymised information on maternal age, height, weight, parity, gestational age, smoking habits and alcohol drinking, infertility treatment, medical history, diagnoses of obstetric complications, such as preeclampsia and placental abruption, mode of delivery, neonatal records, and the hospital at which the woman delivered.
The women were categorised into five groups according to their level of exposure to total PM2.5, its chemical components and ozone during the first trimester. The data in this study had a hierarchical structure that the participants were nested within hospitals. To explore the association between exposure to pollutants during the first trimester, and placenta-mediated pregnancy complications, as a composite outcome and in terms of individual complications, we considered this hierarchical structure, and applied a multilevel logistic regression model with the hospital as a random effect. With the lowest concentration group as the reference, first the odds ratios (ORs) and 95% confidence intervals (CIs) of placenta-mediated pregnancy complications were estimated, after adjustment for maternal age at delivery (
We investigated in detail the association of carbon and sodium with placenta-mediated pregnancy complications (Fig. 1). Overall, the tendency towards a positive association persisted. For example, the multi-component model suggested that carbon and sodium were independently associated with outcome. Also, exposure to these components from 8 to 12 weeks was positively associated with outcome.
The odds ratios (ORs) per interquartile range increase in the concentrations of each component were adjusted for maternal age, birth year, season of conception, smoking, alcohol drinking, prepregnancy body mass index, current history of diabetes/gestational diabetes, infertility treatment and parity. The error bars indicate 95% confidence intervals.
In the analysis of singleton pregnant women in Tokyo between 2013 and 2015, exposure to total PM2.5 was not associated with placenta-mediated pregnancy complications (mixed outcome of SGA, preeclampsia, placental abruption and stillbirth). In the latest report by the US Environmental Protection Agency, the evidence for the association between maternal exposure to total PM2.5 and pregnancy and birth outcomes, including SGA, preeclampsia and stillbirth, was not consistent [9]. In contrast, we here observed that an increase in the concentrations of some PM2.5 chemical components, such as total carbon and sodium, was clearly associated with an elevated occurrence of pregnancy complications. This positive association was observed for exposure over the first trimester, but not for exposure over the 3 months before pregnancy or over the second trimester.
Our findings suggested that the first trimester was susceptible to pollutants exposure associated with placenta-mediated pregnancy complications. The first trimester of pregnancy, especially the latter half, is a crucial period in placentation [11]. Abnormal placentation and failure of trophoblast invasion into the placental bed are considered to be involved in the pathogenesis of preeclampsia, and to lead to foetal growth restriction related to SGA [11, 32]. Further, it has been noted that impaired placentation is the basis for the development of placental abruption [33]. Inflammation, hypoxia and coagulation in the intrauterine environment appears to contribute to the pathophysiology of abnormal placental development [12, 32]. These biological reactions are on the biological pathway of exposure to PM2.5 [34], and short-term exposure to OC was associated with an elevated level of inflammatory biomarkers, such as tumour necrosis factor alpha, in healthy adults [35]. Furthermore, a birth cohort study in Canada reported that hyperhomocysteinemia, which is related to inflammation and increased coagulation [36], was associated with an elevated risk of placenta-mediated pregnancy complications [37]. Plasma levels of homocysteine were higher in taxi drivers, who were routinely exposed to air pollutants, such as PAHs as carbonaceous constituent of PM2.5, than in non-occupationally exposed individuals [38]. Therefore, it is likely that first-trimester exposure to pollutants, such as OC, has a role in abnormal placentation. Incidentally, the OR point estimates for the association with exposure to some components over the second trimester showed below unity. Since we did not have reason to believe that the direction of this association was biologically plausible, we interpreted this to mean that second trimester exposure had little influence on pregnancy complications.
Irrespective of these limitations, to the best of our knowledge, this is the first study focused on the association between exposure to PM2.5 chemical components over the first trimester and placenta-mediated pregnancy complications as a composite outcome. Another strength is that we used continuous filter-based measurements of PM2.5 components in a megacity, Tokyo, and this allowed us to analyse a relatively large sample size. In addition, we analysed data derived from a good-quality clinical database, including information on major confounding factors related to placenta-mediated pregnancy complications, such as smoking habits, prepregnancy overweight, and past history of pregnancy complications.
In conclusion, we found that exposure to some components of PM2.5 over the first trimester was positively associated with placenta-mediated pregnancy complications in Tokyo, a highly urbanised major global city. Our findings suggest that specific components of PM2.5 have harmful effects on placentation in urbanised settings.
The authors thank Ms. Hitomi Matsushita and Ms. Emi Yamazaki (Department of Environmental and Occupational Health, School of Medicine, Toho University) for research assistance. Data of PM2.5 components were provided from Type II joint research between the National Institute for Environmental Studies and the local environmental research institutes in Japan.
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