Full-text resources of CEJSH and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl

Results found: 2

first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  fine particulate matter
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1
Publication available in full text mode
Content available

Dose-dependent relationship between prenatal exposure to fine particulates and exhaled carbon monoxide in non-asthmatic children. A population-based birth cohort study

100%
Jędrychowski W. A., Maugeri U., Spengler J., Mróz E., Flak E., Klimaszewska-Rembiasz M., Jacek R., Sowa A.
International Journal of Occupational Medicine and Environmental Health
|
2013
|
vol. 26
|
issue 1
73-82
EN
Objectives: The main goal of the study was to assess possible association between fetal exposure to fi ne particulate matter ($\text{PM}_\text{2.5}$) and exhaled carbon monoxide (eCO) measured in non-asthmatic children. Material and Methods: The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków. Personal samplers of $\text{PM}_\text{2.5}$ were used to measure fi ne particle mass in the fetal period and carbon monoxide (CO) in exhaled breath from a single exhalation effort at the age of 7. In the statistical analysis of the effect of prenatal $\text{PM}_\text{2.5}$ exposure on eCO, a set of potential confounders, such as environmental tobacco smoke (ETS), city residence area, sensitization to house dust allergens and the occurrence of respiratory symptoms monitored over the seven-year follow-up was considered. Results: The level of eCO did not correlate with the self-reported ETS exposure recorded over the follow-up, however, there was a positive signifi cant relationship with the prenatal $\text{PM}_\text{2.5}$ exposure (non-parametric trend p = 0.042). The eCO mean level was higher in atopic children (geometric mean = 2.06 ppm, 95% CI: 1.58–2.66 ppm) than in non-atopic ones (geometric mean = 1.57 ppm, 95% CI: 1.47–1.73 ppm) and the difference was statistically signifi cant (p = 0.036). As for the respiratory symptoms, eCO values were associated positively only with the cough severity score recorded in the follow-up (nonparametric trend p = 0.057). In the nested multivariable linear regression model, only the effects of prenatal $\text{PM}_\text{2.5}$ and cough severity recorded in the follow-up were related to eCO level. The prenatal $\text{PM}_\text{2.5}$ exposure represented 5.1%, while children’s cough represented only 2.6% of the eCO variability. Conclusion: Our study suggests that elevated eCO in non-asthmatic children may result from oxidative stress experienced in the fetal period and that heme oxygenase (HO) activity in body tissues may be programmed in the fetal period by the exposure to fi ne particulate matter.
2
Publication available in full text mode
Content available

Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells

75%
Ru Q., Xiong Q., Chen L., Tian X., Yue K., Ma B., Liu L., Wu R., Xu C., Pi M., Li C.
International Journal of Occupational Medicine and Environmental Health
|
2017
|
vol. 31
|
issue 2
173-183
EN
Objectives The aim of the study has been to investigate the effect of the Standard Reference Material of fine particulate matter (SRM 2786) on cytotoxicity and apoptosis in human lung bronchial epithelial cells (16HBE cells). Whether the lipopolysaccharide (LPS)-induced inflammation could further accelerate cell apoptosis induced by SRM 2786 stimulation has also been determined. Material and Methods 16HBE cells were exposed to various doses of SRM 2786 with or without LPS. The following parameters: cytotoxicity, apoptotic rate, Bax/Bcl-2 expression, nitric oxide (NO) production, and reactive oxygen species (ROS) generation were measured. Results The results have shown that SRM 2786 induces cell damage and apoptosis of 16HBE cells as demonstrated by significant decrease in expression of Bcl-2 and increase in expression of Bax. When compared with the control cells, the apoptotic rate of cells treated by 500 μg/ml of SRM 2786 increased from 2.43±0.21% to 43.96±2.95% (p < 0.01). Further, there was an elevated production of NO and ROS post SRM 2786 treatment. The level of NO in cells treated with 500 μg/ml of SRM 2786 was 18.33±1.02 μmol/l whereas that of control cells was 1.58±0.31 μmol/l (p < 0.01). When compared with the control group, the level of intracellular ROS increased by 24% after treatment with 500 μg/ml of SRM 2786 (p < 0.05). In addition, LPS pre-treatment may accelerate cell apoptosis by increasing generation of NO and ROS followed by SRM 2786 stimulation. When compared to cells treated with 125 μg/ml of SRM 2786 alone, the levels of NO and ROS in cells pretreated with LPS increased by 28% and 11.6%, respectively (p < 0.05), and the apoptotic rate increased from 34.62±4.44% to 54.11±3.34% (p < 0.01). Conclusions These findings have suggested that in vitro exposure to SRM 2786 could induce 16HBE cells apoptosis probably by means of the mechanism involving the generation of free radicals, while the degree of apoptosis would be further aggravated under inflammation condition. Int J Occup Med Environ Health 2018;31(2):173–183
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.