Association between Residential Tobacco Smoking Bans, Smoke Exposure, and Pulmonary Function: A Survey of Latino Children with Asthma

2003 ◽  
Vol 16 (4) ◽  
pp. 305-317 ◽  
Author(s):  
Ana P. Martinez-Donate ◽  
Melbourne F. Hovell ◽  
Dennis R. Wahlgren ◽  
Susan B. Meltzer ◽  
Eli O. Meltzer ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Tobacco Smoking ◽  
Smoke Exposure ◽  
Latino Children ◽  
Smoking Bans ◽  
Children With Asthma

scholarly journals Comparison of Levels of Three Tobacco Smoke Exposure Biomarkers in Children of Smokers

2021 ◽  
Vol 18 (22) ◽  
pp. 11803
Author(s):  
E. Melinda Mahabee-Gittens ◽  
Georg E. Matt ◽  
Lili Ding ◽  
Ashley L. Merianos
Keyword(s):  
African American ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Smoking Bans ◽  
Convenience Sample ◽  
Targeted Interventions ◽  
Exposure Biomarkers ◽  
Lower Education ◽  
Pearson Correlations

Objectives: Cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and N-oxides are biomarkers of tobacco smoke exposure (TSE) used to assess short- and longer-term TSE. The objective of this study was to assess the associations between these TSE biomarkers, sociodemographics, parental smoking, and child TSE patterns among 0–17-year-olds. Methods: A convenience sample of 179 pediatric patients (mean (SD) age = 7.9 (4.3) years) who lived with ≥1 smoker and who had parental assessments completed and urine samples analyzed for the three TSE biomarkers of interest were included. Biomarker levels were log-transformed, univariate regression models were built and Pearson correlations were assessed. Results: In total, 100% of children had detectable levels of cotinine and >96% had detectable NNAL and N-oxide levels. The geometric means of cotinine, NNAL, and N-oxide levels were 10.1 ng/mL, 25.3 pg/mL, and 22.9 pg/mL, respectively. The mean (SD) number of daily cigarettes smoked by parents was 10.6 (6.0) cigarettes. Child age negatively correlated with urinary cotinine (r = −0.202, p = 0.007) and log NNAL levels (r = −0.275, p < 0.001). The highest log-cotinine levels were in children who were younger, of African American race, and whose parents had a lower education, an annual income ≤USD15,000, and no smoking bans. The highest log-NNAL and N-oxide levels were in children whose parents had a lower education, had no smoking bans, and were around higher numbers of cigarettes. Conclusion: Children of smokers who were younger, African American, and had no smoking bans had the highest TSE biomarker levels. Targeted interventions are needed to reduce TSE levels among high-risk children.

The Effect of Physical Training in Children With Asthma on Pulmonary Function, Aerobic Capacity and Health-Related Quality of Life: A Systematic Review of Randomized Control Trials

2012 ◽  
Vol 24 (3) ◽  
pp. 472-489 ◽  
Author(s):  
Alison Crosbie
Keyword(s):  
Quality Of Life ◽  
Pulmonary Function ◽  
Aerobic Capacity ◽  
Physical Training ◽  
Health Related Quality ◽  
Children With Asthma ◽  
Related Quality ◽  
Health Related ◽  
Randomized Control

ObjectiveAsthma is a leading cause of chronic illness in children, impacting heavily on their daily life and participation in physical activity. The purpose of this systematic review was to investigate the evidence for the use of physical therapy to improve pulmonary function and aerobic capacity in children with asthma. Furthermore, the review aims to update previous literature on the effect of exercise on health related quality of life.MethodsA search was conducted for randomized control trials (RCTs) using the electronic databases Medline, Embase, SPORTDiscus, AMED, CINAHL, and The Cochrane Central Register of Controlled Trials. Studies were included if the participants were asthmatic children aged 6–18 years participating in any mode of physical exercise. Studies were reviewed for study quality, participant details, exercise intervention details, and intervention outcomes.ResultsA total of 16 studies and 516 subjects met inclusion criteria for review. Severity of asthma ranged from mild to severe. No improvement in pulmonary function was observed. Physical training led to an increase in aerobic capacity as measured by VO2max (mL/kg/min).ConclusionsFindings suggest that physical training does not improve pulmonary function in children with asthma, but does increase aerobic capacity. The small number of studies investigating quality of life suggests that physical training does improve health related quality of life; however further well designed randomized control trials are needed to verify these findings.

scholarly journals In utero tobacco smoke exposure, DNA methylation, and asthma in Latino children

2019 ◽  
Vol 3 (3) ◽  
pp. e048 ◽  
Author(s):  
Andreas M. Neophytou ◽  
Sam S. Oh ◽  
Donglei Hu ◽  
Scott Huntsman ◽  
Celeste Eng ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Tobacco Smoke ◽  
In Utero ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Latino Children

scholarly journals Tobacco smoking induces cardiovascular mitochondrial oxidative stress, promotes endothelial dysfunction, and enhances hypertension

2019 ◽  
Vol 316 (3) ◽  
pp. H639-H646 ◽  
Author(s):  
Sergey Dikalov ◽  
Hana Itani ◽  
Bradley Richmond ◽  
Liaison Arslanbaeva ◽  
Aurelia Vergeade ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Tobacco Smoking ◽  
Smoke Exposure ◽  
Metabolic Reprogramming ◽  
Wild Type ◽  
Mitochondrial Oxidative Stress

Tobacco smoking is a major risk factor for cardiovascular disease and hypertension. It is associated with the oxidative stress and induces metabolic reprogramming, altering mitochondrial function. We hypothesized that cigarette smoke induces cardiovascular mitochondrial oxidative stress, which contributes to endothelial dysfunction and hypertension. To test this hypothesis, we studied whether the scavenging of mitochondrial H2O2 in transgenic mice expressing mitochondria-targeted catalase (mCAT) attenuates the development of cigarette smoke/angiotensin II-induced mitochondrial oxidative stress and hypertension compared with wild-type mice. Two weeks of exposure of wild-type mice with cigarette smoke increased systolic blood pressure by 17 mmHg, which was similar to the effect of a subpresssor dose of angiotensin II (0.2 mg·kg−1·day−1), leading to a moderate increase to the prehypertensive level. Cigarette smoke exposure and a low dose of angiotensin II cooperatively induced severe hypertension in wild-type mice, but the scavenging of mitochondrial H2O2 in mCAT mice completely prevented the development of hypertension. Cigarette smoke and angiotensin II cooperatively induced oxidation of cardiolipin (a specific biomarker of mitochondrial oxidative stress) in wild-type mice, which was abolished in mCAT mice. Cigarette smoke and angiotensin II impaired endothelium-dependent relaxation and induced superoxide overproduction, which was diminished in mCAT mice. To mimic the tobacco smoke exposure, we used cigarette smoke condensate, which induced mitochondrial superoxide overproduction and reduced endothelial nitric oxide (a hallmark of endothelial dysfunction in hypertension). Western blot experiments indicated that tobacco smoke and angiotensin II reduce the mitochondrial deacetylase sirtuin-3 level and cause hyperacetylation of a key mitochondrial antioxidant, SOD2, which promotes mitochondrial oxidative stress. NEW & NOTEWORTHY This work demonstrates tobacco smoking-induced mitochondrial oxidative stress, which contributes to endothelial dysfunction and development of hypertension. We suggest that the targeting of mitochondrial oxidative stress can be beneficial for treatment of pathological conditions associated with tobacco smoking, such as endothelial dysfunction, hypertension, and cardiovascular diseases. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/mitochondrial-oxidative-stress-in-smoking-and-hypertension/ .

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