scholarly journals Air pollution exposure associates with increased risk of neonatal jaundice

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Liqiang Zhang ◽  
Weiwei Liu ◽  
Kun Hou ◽  
Jintai Lin ◽  
Changqing Song ◽  
...  
2020 ◽  
Vol 56 (1) ◽  
pp. 2000147 ◽  
Author(s):  
Ulrike Gehring ◽  
Alet H. Wijga ◽  
Gerard H. Koppelman ◽  
Judith M. Vonk ◽  
Henriette A. Smit ◽  
...  

BackgroundAir pollution is associated with asthma development in children and adults, but the impact on asthma development during the transition from adolescence to adulthood is unclear. Adult studies lack historical exposures and consequently cannot assess the relevance of exposure during different periods of life. We assessed the relevance of early-life and more recent air pollution exposure for asthma development from birth until early adulthood.MethodsWe used data of 3687 participants of the prospective Dutch PIAMA (Prevention and Incidence of Asthma and Mite Allergy) birth cohort and linked asthma incidence until age 20 years to estimated concentrations of nitrogen dioxide (NO2), particulate matter with a diameter <2.5 μm (PM2.5), <10 μm (PM10), and 2.5–10 μm, and PM2.5 absorbance (“soot”) at the residential address. We assessed overall and age-specific associations with air pollution exposure with discrete time-hazard models, adjusting for potential confounders.ResultsOverall, we found higher incidence of asthma until the age of 20 years with higher exposure to all pollutants at the birth address (adjusted odds ratio (95% CI) ranging from 1.09 (1.01–1.18) for PM10 to 1.20 (1.10–1.32) for NO2) per interquartile range increase) that were rather persistent with age. Similar associations were observed with more recent exposure defined as exposure at the current home address. In two-pollutant models with particulate matter, associations with NO2 persisted.ConclusionsExposure to air pollution, especially from motorised traffic, early in life may have long-term consequences for asthma development, as it is associated with an increased risk of developing asthma through childhood and adolescence into early adulthood.


2018 ◽  
Vol 33 (3) ◽  
pp. 247-264 ◽  
Author(s):  
Alexandra Grippo ◽  
Jun Zhang ◽  
Li Chu ◽  
Yanjun Guo ◽  
Lihua Qiao ◽  
...  

Abstract The developing fetus is particularly susceptible to environmental pollutants, and evidence has shown adverse effects of air pollutants on pregnancy and birth outcomes. Pregnancy loss, including spontaneous abortion (miscarriage) and stillbirth, is the most severe adverse pregnancy outcome. This review focuses on air pollution exposure during pregnancy in relation to spontaneous abortion and stillbirth. A total of 43 studies are included in this review, including 35 human studies and eight animal studies. Overall, these studies suggest that exposure to air pollutants such as particulate matter (PM), carbon monoxide (CO) and cooking smoke may be associated with higher risk for stillbirth and spontaneous abortion. PM10 exposure during an entire pregnancy was associated with increased risk of spontaneous abortion, and exposure to PM2.5 and PM10 in the third trimester might increase the risk of stillbirth. CO exposure during the first trimester of pregnancy was associated with an increased risk of spontaneous abortion and exposure during the third trimester was associated with an increased risk of stillbirth. Cooking smoke was found to increase the risk of stillbirths, and the evidence was consistent. Insufficient and conflicting evidence was found for various other pollutants, such as NO2 and SO2. Studies did not show clear evidence for associations between pregnancy loss and others pollutants such as heavy metals, organochlorine compounds, PAH and total dust count. Further research is warranted to better understand the relationship between air pollution exposure and pregnancy loss.


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.


Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 327
Author(s):  
Nichapa Parasin ◽  
Teerachai Amnuaylojaroen ◽  
Surasak Saokaew

Air pollution exposure has been identified as being associated with childhood obesity. Nevertheless, strong evidence of such an association is still lacking. To analyze whether air pollution exposure affects childhood obesity, we conducted a systematic review and meta-analysis utilizing the PRISMA guidelines. Of 7343 studies identified, eight studies that investigated the effects of air pollutant characteristics, including PM2.5, PM10, PMcoarse, PMabsorbance, NOx, and NO2, on childhood obesity were included. The polled effects showed that air pollution is correlated with a substantially increased risk of childhood obesity. PM2.5 was found to be associated with a significantly increased risk (6%) of childhood obesity (OR 1.06, 95% CI 1.02–1.10, p = 0.003). In addition, PM10, PM2.5absorbance, and NO2 appeared to significantly increase the risk of obesity in children (OR 1.07, 95% CI 1.04–1.10, p < 0.00; OR 1.23, 95% CI 1.06–1.43, p = 0.07; and OR 1.10, 95% CI 1.04–1.16, p < 0.001, respectively). PMcoarse and NOx also showed trends towards being associated with an increased risk of childhood obesity (OR 1.07, 95% CI 0.95–1.20, p = 0.291, and OR 1.00, 95% CI 0.99–1.02, p = 0.571, respectively). Strong evidence was found to support the theory that air pollution exposure is one of the factors that increases the risk of childhood obesity.


Author(s):  
Wasif Raza ◽  
Benno Krachler ◽  
Bertil Forsberg ◽  
Johan Nilsson Sommar

We aimed to assess a possible interaction effect between physical activity and particulate air pollution exposure on recurrence of ischemic heart disease (IHD) and stroke. We followed 2221 adult participants comprising first time IHD (1403) and stroke (818) cases from the Västerbotten Intervention Program between 1 January 1990 to 31 December 2013. During mean follow-up times of 5.5 years, 428 and 156 participants developed IHD and stroke recurrence, respectively. PM2.5 concentrations above the median (5.48 µg/m3) were associated with increased risk of IHD and stroke recurrence by 13% (95% CI −17–45%) and 21% (95% CI −19–80%), respectively. These risk increases were however only observed among those that exercised at most once a week at 21% (95% CI −5–50%) and 25% (95% CI −19–90%) for IHD and stroke recurrence, respectively. Higher frequency of exercise at recruitment was positively associated with IHD and stroke recurrence but only the association with IHD recurrence among participants with low residential PM2.5 was statistically significant (96% increased risk (95%-CI 22–215%)). However, no interaction effect between physical activity and PM2.5 exposure was found. Our findings suggest that physical activity may reduce the air pollution exposure associated risk for recurrent cardiovascular disease, likely by reducing the inflammatory response.


Atmosphere ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1039
Author(s):  
Hung-Lin Chen ◽  
Ruihong Zhang ◽  
Stella Chin-Shaw Tsai ◽  
Ruey-Hwang Chou ◽  
Yi-Chao Hsu ◽  
...  

(1) Background: Studies on the association between air pollution and developmental delay in children are limited. Therefore, we evaluated the risk of developmental delay in Taiwanese children exposed to air pollution. (2) Methods: We merged the two nationwide databases, and the annual average pollutant concentrations were grouped into tertiles to evaluate the risk of developmental delay (ICD-9 code 315.9). We identified the patients’ active residential locations based on the location of the clinic or hospital in which they sought treatment for acute upper respiratory infections (ICD 9 code 460). The two nationwide databases were linked for analysis based on the active residential locations of each participant and the locations of the 74 ambient air quality monitoring stations. (3) Results: We observed an increased risk of developmental delay in children and teenagers exposed to SO2, CO, and NO2. The adjusted odds ratios (ORs) of developmental delay for comparison among the tertiles with respect to SO2, CO, and NO2 exposures were 1.12 (95% confidence interval [CI], 1.01–1.24), 1.21 (95% CI, 1.09–1.34), and 1.40 (95% CI, 1.261.55), respectively. (4) Conclusions: The present findings suggest that air pollution exposure increases the risk of developmental delay in children and teenagers in Taiwan.


Hypertension ◽  
2019 ◽  
Vol 74 (2) ◽  
pp. 384-390 ◽  
Author(s):  
Carrie J. Nobles ◽  
Andrew Williams ◽  
Marion Ouidir ◽  
Seth Sherman ◽  
Pauline Mendola

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