No abstract

Maternal exposure to ambient air pollution has been associated with preterm birth (PTB), however, entire pregnancy or trimester-specific associations were generally reported, which may not sufficiently identify windows of susceptibility. Using birth registry data from Guangzhou, a megacity of southern China (population ~14.5 million), including 469,975 singleton live births between January 2015 and July 2017, we assessed the association between weekly air pollution exposure and PTB in a retrospective cohort study. Daily average concentrations of PM, PM, NO, SO, and O from 11 monitoring stations were used to estimate district-specific exposures for each participant based on their district residency during pregnancy. Distributed lag models (DLMs) incorporating Cox proportional hazard models were applied to estimate the association between weekly maternal exposure to air pollutant and PTB risk (as a time-to-event outcome), after controlling for temperature, seasonality, and individual-level covariates. We also considered moderate PTB (32-36 gestational weeks) and very PTB (28-31 gestational weeks) as outcomes of interest. Hazard ratios (HRs) and 95% confidential intervals (95% CIs) were calculated for an interquartile range (IQR) increase in air pollutants during the study period. An IQR increase in PM exposure during the 20th to 28th gestational weeks (27.0 μg/m) was significantly associated with PTB risk, with the strongest effect in the 25th week (HR = 1.034, 95% CI:1.010-1.059). The significant exposure windows were the 19th-28th weeks for PM, the 18th-31st weeks for NO, and the 23rd-31st weeks for O, respectively. The strongest associations were observed in the 25th week for PM (IQR = 37.0 μg/m; HR = 1.048, 95% CI:1.034-1.062), the 26th week for NO (IQR = 29.0 μg/m; HR = 1.060, 95% CI:1.028-1.094), and in the 28th week for O (IQR = 90.0 μg/m; HR = 1.063, 95% CI:1.046-1.081). Similar patterns were observed for moderate PTB (32-36 gestational weeks) and very PTB (28-31 gestational weeks) for PM, PM, NO exposure, but the effects were greater for very PTB. We did not observe any association between pregnancy SO exposure and the risk of PTB. Our results suggest that middle to late pregnancy is the most susceptible air pollution exposure window for air pollution and PTB among women in Guangzhou, China.

No abstract

Ambient air pollution has been linked to small for gestational age (SGA); however, the relationship with large for gestational age (LGA) is unclear and very few studies have investigated seasonal effects on the association between air pollution and SGA or LGA. Using birth registry data of 506,000 singleton live births from 11 districts in Guangzhou, China between January 2015 and July 2017, we examined associations between ambient air pollutants (PM, PM, NO, SO, and O) and SGA/LGA, and further assessed the modification effect of season. Daily concentrations of air pollutants from 11 monitoring stations were used to estimate district-specific exposures for each participant based on their district of residence during pregnancy. Two-level binary logistic regression models were used to evaluate associations between air pollution and SGA/LGA. Stratified analyses by season and a Cochran Q test were performed to assess the modification of season. Exposure to PM, NO, SO, and O was significantly associated with increased risk of SGA, especially for exposure during the second and third trimester. For an interquartile range (IQR) increase in PM (6.5 μg/m), NO (12.7 μg/m), SO (2.8 μg/m) and O (20.8 μg/m) during the entire pregnancy, SGA risk increased by 2% (OR = 1.02, 95% CI: 1.00-1.04), 8% (OR = 1.08, 95% CI: 1.04-1.12), 2% (OR = 1.02, 95% CI: 1.01-1.03), and 14% (1.14, 1.11-1.17), respectively. A decreased risk of LGA was found for PM, PM, SO, and O during the first trimester or entire pregnancy. When examined by season, significant associations between air pollutants and SGA were observed for women who conceived during summer or fall, and the patterns were consistent for all pollutants. Our study suggests that conception during different seasons might modify the association between ambient air pollution and SGA.

Long-term exposure to airborne PM2.5 is associated with increased lung cancer risk but the underlying mechanism remains unclear. We characterized global microRNA and mRNA expression in human bronchial epithelial cells exposed to PM2.5 organic extract and integrally analyzed microRNA-mRNA interactions. Foci formation and xenograft tumorigenesis in mice with NIH3T3 cells expressing genes targeted by microRNAs were performed to explore the oncogenic potential of these genes. We also detected plasma levels of candidate microRNAs in subjects exposed to different levels of air PM2.5 and examined the aberrant expression of genes targeted by these microRNAs in human lung cancer. Under our experimental conditions, treatment of cells with PM2.5 extract resulted in downregulation of 138 microRNAs and aberrant expression of 13 mRNAs (11 upregulation and 2 downregulation). In silico and biochemical analyses suggested SLC30A1, SERPINB2 and AKR1C1, among the upregulated genes, as target for miR-182 and miR-185, respectively. Ectopic expression of each of these genes significantly enhanced foci formation in NIH3T3 cells. Following subcutaneous injection of these cells into nude mice, fibrosarcoma were formed from SLC30A1- or SERPINB2-expressing cells. Reduced plasma levels of miR-182 were detected in subjects exposed to high level of PM2.5 than in those exposed to low level of PM2.5 (P = 0.043). Similar results were seen for miR-185 although the difference was not statistically significant (P = 0.328). Increased expressions of SLC30A1, SERPINB2 and AKR1C1 were detected in human lung cancer. These results suggest that modulation of miR-182 and miR-185 and their target genes may contribute to lung carcinogenesis attributable to PM2.5 exposure.