Shorter telomere length in cord blood associated with prenatal air pollution exposure: Benefits of intervention

2018 ◽  
Vol 113 ◽  
pp. 335-340 ◽  
Author(s):  
Frederica Perera ◽  
Chia-jung Lin ◽  
Lirong Qu ◽  
Deliang Tang
Toxics ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 169
Author(s):  
Seyram Kaali ◽  
Darby Jack ◽  
Jones Opoku-Mensah ◽  
Tessa Bloomquist ◽  
Joseph Aanaro ◽  
...  

Background: Associations between prenatal household air pollution exposure (HAP), newborn telomere length and early childhood blood pressure are unknown. Methods: Pregnant women were randomized to liquefied petroleum gas (LPG) stove, improved biomass stove or control (traditional, open fire cook stove). HAP was measured by personal carbon monoxide (CO) (n = 97) and fine particulate matter (PM2.5) (n = 60). At birth, cord blood mononuclear cells (CBMCs) were collected for telomere length (TL) analyses. At child age four years, we measured resting blood pressure (BP) (n = 97). We employed multivariable linear regression to determine associations between prenatal HAP and cookstove arm and assessed CBMC relative to TL separately. We then examined associations between CBMC TL and resting BP. Results: Higher prenatal PM2.5 exposure was associated with reduced TL (β = −4.9% (95% CI −8.6, −0.4), p = 0.03, per 10 ug/m3 increase in PM2.5). Infants born to mothers randomized to the LPG cookstove had longer TL (β = 55.3% (95% CI 16.2, 109.6), p < 0.01)) compared with control. In all children, shorter TL was associated with higher systolic BP (SBP) (β = 0.35 mmHg (95% CI 0.001, 0.71), p = 0.05, per 10% decrease in TL). Conclusions: Increased prenatal HAP exposure is associated with shorter TL at birth. Shorter TL at birth is associated with higher age four BP, suggesting that TL at birth may be a biomarker of HAP-associated disease risk.


2019 ◽  
Vol 172 ◽  
pp. 495-501 ◽  
Author(s):  
Maria José Rosa ◽  
Hsiao-Hsien Leon Hsu ◽  
Allan C. Just ◽  
Kasey J. Brennan ◽  
Tessa Bloomquist ◽  
...  

2020 ◽  
Vol 142 ◽  
pp. 105860
Author(s):  
Maria Tsamou ◽  
Tim S. Nawrot ◽  
Riccardo M. Carollo ◽  
Ann-Julie Trippas ◽  
Wouter Lefebvre ◽  
...  

2019 ◽  
Vol 168 ◽  
pp. 507-513 ◽  
Author(s):  
Janneke G.F. Hogervorst ◽  
Narjes Madhloum ◽  
Nelly D. Saenen ◽  
Bram G. Janssen ◽  
Joris Penders ◽  
...  

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Chloe Friedman ◽  
Dana Dabelea ◽  
Lizan D. Bloemsma ◽  
Deborah SK Thomas ◽  
Jennifer L. Peel ◽  
...  

2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Lifang Hou ◽  
Chang Dou ◽  
Umakanth Avula ◽  
Sheng Wang ◽  
Yue Yu ◽  
...  

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 808
Author(s):  
Michele Carugno ◽  
Elisa Borroni ◽  
Luca Fedrizzi ◽  
Mirjam Hoxha ◽  
Luisella Vigna ◽  
...  

Reduced telomere length (TL) has been associated with increased risk of age-related diseases, most likely through oxidative stress and inflammation, which have also been claimed as mechanisms underlying health effects of air pollution exposure. We aimed to verify whether exposure to particulate matter with diameter ≤10 µm (PM10) affects TL. We recruited 1792 participants with overweight/obesity in Milan (Italy) in 2010–2015 who completed a structured questionnaire on sociodemographic data, gave a blood sample for TL measurement by real-time PCR, and were assigned air pollution and meteorological data of their residential address. In multivariate mixed-effects linear models (with a random intercept on PCR plate), we observed a −0.51% change in TL (95% confidence interval (CI): −0.98; −0.05)) per 10 µg/m3 increase in PM10 at the day of recruitment. A similar decreasing trend in TL was observed up to two weeks before withdrawal, with percentage changes as low as −1.53% (average exposure of the 12 days before recruitment). Mean annual exposure to PM10 was associated with −2.57% TL reduction (95%CI: −5.06; −0.08). By showing consistent associations between short- and long-term PM10 exposures and reduced TL, our findings shed light on the potential mechanisms responsible for the excess of age-related diseases associated with air pollution exposure.


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