Maternal fine particulate matter (PM2.5) exposure and adverse birth outcomes: an updated systematic review based on cohort studies

Background: Preterm birth contributes to the morbidity and mortality of newborns and infants. Recent studies have shown that maternal exposure to particulate matter and extreme temperatures results in immune dysfunction, which can induce preterm birth. This study aimed to evaluate the association between fine particulate matter (PM2.5) exposure, temperature, and preterm birth in Seoul, Republic of Korea. Methods: We used 2010–2016 birth data from Seoul, obtained from the Korea National Statistical Office Microdata. PM2.5 concentration data from Seoul were generated through the Community Multiscale Air Quality (CMAQ) model. Seoul temperature data were collected from the Korea Meteorological Administration (KMA). The exposure period of PM2.5 and temperature were divided into the first (TR1), second (TR2), and third (TR3) trimesters of pregnancy. The mean PM2.5 concentration was used in units of ×10 µg/m3 and the mean temperature was divided into four categories based on quartiles. Logistic regression analyses were performed to evaluate the association between PM2.5 exposure and preterm birth, as well as the combined effects of PM2.5 exposure and temperature on preterm birth. Result: In a model that includes three trimesters of PM2.5 and temperature data as exposures, which assumes an interaction between PM2.5 and temperature in each trimester, the risk of preterm birth was positively associated with TR1 PM2.5 exposure among pregnant women exposed to relatively low mean temperatures (<3.4 °C) during TR1 (OR 1.134, 95% CI 1.061–1.213, p < 0.001). Conclusions: When we assumed the interaction between PM2.5 exposure and temperature exposure, PM2.5 exposure during TR1 increased the risk of preterm birth among pregnant women exposed to low temperatures during TR1. Pregnant women should be aware of the risk associated with combined exposure to particulate matter and low temperatures during TR1 to prevent preterm birth.

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Short-term and long-term exposures to fine particulate matter constituents and health: A systematic review and meta-analysis

Environmental Pollution ◽

10.1016/j.envpol.2018.12.060 ◽

2019 ◽

Vol 247 ◽

pp. 874-882 ◽

Cited By ~ 53

Author(s):

Yang Yang ◽

Zengliang Ruan ◽

Xiaojie Wang ◽

Yin Yang ◽

Tonya G. Mason ◽

...

Keyword(s):

Systematic Review ◽

Particulate Matter ◽

Meta Analysis ◽

Fine Particulate Matter ◽

Short Term ◽

Fine Particulate

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Impact of long-term temporal trends in fine particulate matter (PM2.5) on associations of annual PM2.5 exposure and mortality

Environmental Epidemiology ◽

10.1097/ee9.0000000000000009 ◽

2018 ◽

Vol 2 (2) ◽

pp. e009 ◽

Cited By ~ 1

Author(s):

Ki-Do Eum ◽

Helen H. Suh ◽

Vivian Chit Pun ◽

Justin Manjourides

Keyword(s):

Particulate Matter ◽

Fine Particulate Matter ◽

Temporal Trends ◽

Fine Particulate ◽

Pm2.5 Exposure

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Association between fire smoke fine particulate matter and asthma-related outcomes: Systematic review and meta-analysis

Environmental Research ◽

10.1016/j.envres.2019.108777 ◽

2019 ◽

Vol 179 ◽

pp. 108777 ◽

Cited By ~ 18

Author(s):

Nicolas Borchers Arriagada ◽

Joshua A. Horsley ◽

Andrew J. Palmer ◽

Geoffrey G. Morgan ◽

Rachel Tham ◽

...

Keyword(s):

Systematic Review ◽

Particulate Matter ◽

Meta Analysis ◽

Fine Particulate Matter ◽

Fine Particulate ◽

Fire Smoke

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Different exposure levels of fine particulate matter and preterm birth: a meta-analysis based on cohort studies

Environmental Science and Pollution Research ◽

10.1007/s11356-017-9363-0 ◽

2017 ◽

Vol 24 (22) ◽

pp. 17976-17984 ◽

Cited By ~ 18

Author(s):

Chenchen Liu ◽

Jiantao Sun ◽

Yuewei Liu ◽

Hui Liang ◽

Minsheng Wang ◽

...

Keyword(s):

Particulate Matter ◽

Preterm Birth ◽

Cohort Studies ◽

Meta Analysis ◽

Fine Particulate Matter ◽

Fine Particulate ◽

Exposure Levels

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In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring

Cellular Physiology and Biochemistry ◽

10.1159/000488418 ◽

2018 ◽

Vol 46 (1) ◽

pp. 148-159 ◽

Cited By ~ 7

Author(s):

Zhengmeng Ye ◽

Xi Lu ◽

Yi Deng ◽

Xinquan Wang ◽

Shuo Zheng ◽

...

Keyword(s):

Blood Pressure ◽

Particulate Matter ◽

Sodium Excretion ◽

Fine Particulate Matter ◽

In Utero ◽

D1 Receptor ◽

In Utero Exposure ◽

Fine Particulate ◽

Pm2.5 Exposure ◽

Renal Dopamine

Background/Aims: Adverse environment in utero can modulate adult phenotypes including blood pressure. Fine particulate matter (PM2.5) exposure in utero causes hypertension in the offspring, but the exact mechanisms are not clear. Renal dopamine D1 receptor (D1R), regulated by G protein-coupled receptor kinase type 4 (GRK4), plays an important role in the regulation of renal sodium transport and blood pressure. In this present study, we determined if renal D1R dysfunction is involved in PM2.5–induced hypertension in the offspring. Methods: Pregnant Sprague–Dawley rats were given an oropharyngeal drip of PM2.5 (1.0 mg/kg) at gestation day 8, 10, and 12. The blood pressure, 24-hour sodium excretion, and urine volume were measured in the offspring. The expression levels of GRK4 and D1R were determined by immunoblotting. The phosphorylation of D1R was investigated using immunoprecipitation. Plasma malondialdehyde and superoxide dismutase levels were also measured in the offspring. Results: As compared with saline-treated dams, offspring of PM2.5-treated dams had increased blood pressure, impaired sodium excretion, and reduced D1R-mediated natriuresis and diuresis, accompanied by decreased renal D1R expression and GRK4 expression. The impaired renal D1R function and increased GRK4 expression could be caused by increased reactive oxidative stress (ROS) induced by PM2.5 exposure. Administration of tempol, a redox-cycling nitroxide, for 4 weeks in the offspring of PM2.5-treated dam normalized the decreased renal D1R expression and increased renal D1R phosphorylation and GRK4 expression. Furthermore, tempol normalized the increased renal expression of c-Myc, a transcription factor that regulates GRK4 expression. Conclusions: In utero exposure to PM2.5 increases ROS and GRK4 expression, impairs D1R-mediated sodium excretion, and increases blood pressure in the offspring. These studies suggest that normalization of D1R function may be a target for the prevention and treatment of the hypertension in offspring of mothers exposed to PM2.5 during pregnancy.

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Ambient Fine Particulate Matter and Preterm Birth in California: Identification of Critical Exposure Windows

American Journal of Epidemiology ◽

10.1093/aje/kwz120 ◽

2019 ◽

Vol 188 (9) ◽

pp. 1608-1615 ◽

Cited By ~ 12

Author(s):

Paige Sheridan ◽

Sindana Ilango ◽

Tim A Bruckner ◽

Qiong Wang ◽

Rupa Basu ◽

...

Keyword(s):

Particulate Matter ◽

Preterm Birth ◽

Proportional Hazards ◽

Fine Particulate Matter ◽

Cox Proportional Hazards ◽

Distributed Lag ◽

Fine Particulate ◽

Cox Proportional Hazards Models ◽

Pm2.5 Exposure ◽

Exposure Windows

Abstract Exposure to ambient fine particulate matter (particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5)) during pregnancy is associated with preterm birth (PTB), a leading cause of infant morbidity and mortality. Results from studies attempting to identify etiologically relevant exposure periods of vulnerability have been inconsistent, possibly because of failure to consider the time-to-event nature of the outcome and lagged exposure effects of PM2.5. In this study, we aimed to identify critical exposure windows for weekly PM2.5 exposure and PTB in California using California birth cohort data from 2005–2010. Associations were assessed using distributed-lag Cox proportional hazards models. We assessed effect-measure modification by race/ethnicity by calculating the weekly relative excess risk due to interaction. For a 10-μg/m3 increase in PM2.5 exposure over the entire period of gestation, PTB risk increased by 11% (hazard ratio = 1.11, 95% confidence interval: 1.09, 1.14). Gestational weeks 17–24 and 36 were associated with increased vulnerability to PM2.5 exposure. We find that non-Hispanic black mothers may be more susceptible to effects of PM2.5 exposure than non-Hispanic white mothers, particularly at the end of pregnancy. These findings extend our knowledge about the existence of specific exposure periods during pregnancy that have the greatest impact on preterm birth.

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