scholarly journals Effects of Involuntary Smoking and Vaping on the Cardiovascular System

2019 ◽  
Author(s):  
Manfred Neuberger
Keyword(s):  
Tobacco Smoke ◽  
Social Acceptance ◽  
Animal Experiments ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Second Hand Smoke ◽  
Coronary Syndrome ◽  
Acute Changes ◽  
Tobacco Specific Nitrosamines

In deaths and diseases attributed to tobacco smoke cardiovascular events exceed cancer and respiratory diseases. Second hand smoke (SHS) promotes the development of arteriosclerosis and can also trigger acute changes of endothelial function and of blood coagulability. Indoor smoking bans reduced coronary syndrome and myocardial infarction 10-20% within one year and were followed by sustainable decreases of stroke and diabetes. With a smoke-free hospitality industry people recognized tobacco smoke as an air pollutant, smoking in public was denormalized and social acceptance of smoking in front of children and pregnant women decreased also in homes and in cars. Combined effects with ambient air pollution are proven for active smoking and suspected for SHS. Contamination with third hand smoke (THS, “cold smoke”)  persists for months in homes and cars, creating secondary pollutants that in some cases are more toxic (e.g., tobacco-specific nitrosamines).  Remnants found in air, dust, and on surfaces (carpets, wallpapers, upholstery, soft toys) were associated with their metabolites in saliva and urine of children and with elevated levels of nicotine on hands and cotinine in urine of nonsmokers residing in homes previously occupied by smokers. In animal experiments effects of THS were found on thrombogenesis, insulin resistance through oxidative stress, on the developing immune system, lipid metabolism and alterations in liver, lung, skin and behavior. Much less is known about health effects for bystanders from the aerosols exhaled during “vaping” of e-cigarettes, but nicotine and other toxins from e-cigarettes are certainly a hazard, which should be prevented by the use of dermal and oral nicotine products, which are safer for nicotine replacement and without risk for bystanders.

scholarly journals Relationship between Air Pollutant Exposure and Gynecologic Cancer Risk

2021 ◽  
Vol 18 (10) ◽  
pp. 5353
Author(s):  
Qiwei Yu ◽  
Liqiang Zhang ◽  
Kun Hou ◽  
Jingwen Li ◽  
Suhong Liu ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cancer Risk ◽  
Air Pollutants ◽  
Gynecological Cancer ◽  
Gynecologic Cancer ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Short Term Exposure ◽  
Increased Risk

Exposure to air pollution has been suggested to be associated with an increased risk of women’s health disorders. However, it remains unknown to what extent changes in ambient air pollution affect gynecological cancer. In our case–control study, the logistic regression model was combined with the restricted cubic spline to examine the association of short-term exposure to air pollution with gynecological cancer events using the clinical data of 35,989 women in Beijing from December 2008 to December 2017. We assessed the women’s exposure to air pollutants using the monitor located nearest to each woman’s residence and working places, adjusting for age, occupation, ambient temperature, and ambient humidity. The adjusted odds ratios (ORs) were examined to evaluate gynecologic cancer risk in six time windows (Phase 1–Phase 6) of women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the highest ORs were found in Phase 4 (240 days). Then, the higher adjusted ORs were found associated with the increased concentrations of each pollutant (PM2.5, CO, O3, and SO2) in Phase 4. For instance, the adjusted OR of gynecological cancer risk for a 1.0-mg m−3 increase in CO exposures was 1.010 (95% CI: 0.881–1.139) below 0.8 mg m−3, 1.032 (95% CI: 0.871–1.194) at 0.8–1.0 mg m−3, 1.059 (95% CI: 0.973–1.145) at 1.0–1.4 mg m−3, and 1.120 (95% CI: 0.993–1.246) above 1.4 mg m−3. The ORs calculated in different air pollution levels accessed us to identify the nonlinear association between women’s exposure to air pollutants (PM2.5, CO, O3, and SO2) and the gynecological cancer risk. This study supports that the gynecologic risks associated with air pollution should be considered in improved public health preventive measures and policymaking to minimize the dangerous effects of air pollution.

scholarly journals Insulin sensitizers prevent fine particulate matter-induced vascular insulin resistance and changes in endothelial progenitor cell homeostasis

2016 ◽  
Vol 310 (11) ◽  
pp. H1423-H1438 ◽  
Author(s):  
Petra Haberzettl ◽  
James P. McCracken ◽  
Aruni Bhatnagar ◽  
Daniel J. Conklin
Keyword(s):  
Insulin Resistance ◽  
Bone Marrow ◽  
Particulate Matter ◽  
Insulin Sensitivity ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Endothelial Progenitor ◽  
Insulin Sensitizer ◽  
Circulating Levels

Exposure to fine particular matter (PM2.5) increases the risk of developing cardiovascular disease and Type 2 diabetes. Because blood vessels are sensitive targets of air pollutant exposure, we examined the effects of concentrated ambient PM2.5 (CAP) on vascular insulin sensitivity and circulating levels of endothelial progenitor cells (EPCs), which reflect cardiovascular health. We found that CAP exposure for 9 days decreased insulin-stimulated Akt phosphorylation in the aorta of mice maintained on control diet. This change was accompanied by the induction of IL-1β and increases in the abundance of cleaved IL-18 and p10 subunit of Casp-1, consistent with the activation of the inflammasome pathway. CAP exposure also suppressed circulating levels of EPCs (Flk-1+/Sca-1+ cells), while enhancing the bone marrow abundance of these cells. Although similar changes in vascular insulin signaling and EPC levels were observed in mice fed high-fat diet, CAP exposure did not exacerbate diet-induced changes in vascular insulin resistance or EPC homeostasis. Treatment with an insulin sensitizer, metformin or rosiglitazone, prevented CAP-induced vascular insulin resistance and NF-κB and inflammasome activation and restored peripheral blood and bone marrow EPC levels. These findings suggest that PM2.5 exposure induces diet-independent vascular insulin resistance and inflammation and prevents EPC mobilization, and that this EPC mobilization defect could be mediated by vascular insulin resistance. Impaired vascular insulin sensitivity may be an important mechanism underlying PM2.5-induced vascular injury, and pharmacological sensitization to insulin action could potentially prevent deficits in vascular repair and mitigate vascular inflammation due to exposure to elevated levels of ambient air pollution. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/particulate-matter-induced-vascular-insulin-resistance/ .

scholarly journals Ambient Air Pollution and Hospital Admissions for Peptic Ulcers in Taipei: A Time-Stratified Case-Crossover Study

2019 ◽  
Vol 16 (11) ◽  
pp. 1916 ◽  
Author(s):  
Shang-Shyue Tsai ◽  
Hui-Fen Chiu ◽  
Chun-Yuh Yang
Keyword(s):  
Air Pollution ◽  
Peptic Ulcer ◽  
Crossover Study ◽  
Air Pollutants ◽  
Hospital Admissions ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Research Database ◽  
Case Crossover

Very few studies have been performed to determine whether there is a relationship between air pollution and increases in hospitalizations for peptic ulcer, and for those that have occurred, their results may not be completely relevant to Taiwan, where the mixture of ambient air pollutants differ. We performed a time-stratified case-crossover study to investigate the possible association between air pollutant levels and hospital admissions for peptic ulcer in Taipei, Taiwan. To do this, we collected air pollution data from Taiwan's Environmental Protection Agency and hospital admissions for peptic ulcer data for the years 2009–2013 from Taiwan's National Health Insurance's research database. We used conditional logistic regression to analyze the possible association between the two, taking temperature and relative humidity into account. Risk was expressed as odds ratios and significance was expressed with 95% confidence intervals. In our single pollutant model, peptic ulcer admissions were significantly associated with all pollutants (PM10, PM2.5, SO2, NO2, CO, and O3) on warm days (>23 °C). On cool days (<23 °C), peptic ulcer admissions were significantly associated with PM10, NO2, and O3. In our two-pollutant models, peptic ulcer admissions were significantly associated NO2 and O3 when combined with each of the other pollutants on warm days, and with PM10, NO2, and O3 on cool days. It was concluded that the likelihood of peptic ulcer hospitalizations in Taipei rose significantly with increases in air pollutants during the study period.

scholarly journals Second-Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

2003 ◽  
Vol 10 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Brian W. P. Seymour ◽  
Edward S. Schelegle ◽  
Kent E. Pinkerton ◽  
Kathleen E. Friebertshauser ◽  
Janice L. Peake ◽  
...  
Keyword(s):  
Tobacco Smoke ◽  
Murine Model ◽  
Airway Hyperresponsiveness ◽  
Allergic Bronchopulmonary Aspergillosis ◽  
Ambient Air ◽  
Airway Hyperreactivity ◽  
Second Hand Smoke ◽  
Th2 Response ◽  
Allergic Lung Disease ◽  
Public Areas

Involuntary inhalation of tobacco smoke has been shown to aggravate the allergic response. Antibodies to fungal antigens such asAspergillus fumigatus(Af) cause an allergic lung disease in humans. This study was carried out to determine the effect of environmental tobacco smoke (ETS) on a murine model of allergic bronchopulmonary aspergillosis (ABPA). BALB/c mice were exposed to aged and diluted sidestream cigarette smoke to simulate 'second-hand smoke'. The concentration was consistent with that achieved in enclosed public areas or households where multiple people smoke. During exposure, mice were sensitized to Af antigen intranasally. Mice that were sensitized to Af antigen and exposed to ETS developed significantly greater airway hyperreactivity than did mice similarly sensitized to Af but housed in ambient air. The effective concentration of aerosolized acetylcholine needed to double pulmonary flow resistance was significantly lower in Af + ETS mice compared to the Af + AIR mice. Immunological data that supports this exacerbation of airway hyperresponsiveness being mediated by an enhanced type 1 hypersensitivity response include: eosinophilia in peripheral blood and lung sections. All Af sensitized mice produced elevated levels of IL4, IL5 and IL10 but no IFN-γ indicating a polarized Th2 response. Thus, ETS can cause exacerbation of asthma in ABPA as demonstrated by functional airway hyperresponsiveness and elevated levels of blood eosinophilia.

scholarly journals Ambient air pollution and pulmonary vascular volume on computed tomography: the MESA Air Pollution and Lung cohort studies

2019 ◽  
Vol 53 (6) ◽  
pp. 1802116 ◽  
Author(s):  
Carrie P. Aaron ◽  
Eric A. Hoffman ◽  
Steven M. Kawut ◽  
John H.M. Austin ◽  
Matthew Budoff ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Air Pollution ◽  
Black Carbon ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Second Hand Smoke ◽  
Oxides Of Nitrogen ◽  
Vascular Volume ◽  
Pulmonary Vessels

BackgroundAir pollution alters small pulmonary vessels in animal models. We hypothesised that long-term ambient air pollution exposure would be associated with differences in pulmonary vascular volumes in a population-based study.MethodsThe Multi-Ethnic Study of Atherosclerosis recruited adults in six US cities. Personalised long-term exposures to ambient black carbon, nitrogen dioxide (NO2), oxides of nitrogen (NOx), particulate matter with a 50% cut-off aerodynamic diameter of <2.5 μm (PM2.5) and ozone were estimated using spatiotemporal models. In 2010–2012, total pulmonary vascular volume was measured as the volume of detectable pulmonary arteries and veins, including vessel walls and luminal blood volume, on noncontrast chest computed tomography (TPVVCT). Peripheral TPVVCTwas limited to the peripheral 2 cm to isolate smaller vessels. Linear regression adjusted for demographics, anthropometrics, smoking, second-hand smoke, renal function and scanner manufacturer.ResultsThe mean±sdage of the 3023 participants was 69.3±9.3 years; 46% were never-smokers. Mean exposures were 0.80 μg·m−3black carbon, 14.6 ppb NO2and 11.0 μg·m−3ambient PM2.5. Mean±sdperipheral TPVVCTwas 79.2±18.2 cm3and TPVVCTwas 129.3±35.1 cm3. Greater black carbon exposure was associated with a larger peripheral TPVVCT, including after adjustment for city (mean difference 0.41 (95% CI 0.03–0.79) cm3per interquartile range; p=0.036). Associations for peripheral TPVVCTwith NO2were similar but nonsignificant after city adjustment, while those for PM2.5were of similar magnitude but nonsignificant after full adjustment. There were no associations for NOxor ozone, or between any pollutant and TPVVCT.ConclusionsLong-term black carbon exposure was associated with a larger peripheral TPVVCT, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population.

scholarly journals Long-term ambient air pollutant exposure and risk of migraine and recurrent headache in children: A 12-year cohort study

2020 ◽  
Author(s):  
Syuan-Yu Hong ◽  
Lei Wan ◽  
Hui-Ju Lin ◽  
Cheng-Li Lin ◽  
Chang-Ching Wei
Keyword(s):  
Air Pollution ◽  
Cohort Study ◽  
Sulfur Dioxide ◽  
Incidence Rate ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Research Database ◽  
Migraine Headaches

Abstract Background Although research has suggested environmental factors to be triggers of headache, the contribution of long-term air pollution exposure to migraine and recurrent headaches (migraine/headaches) is poorly understood. Hence, we executed this nationwide cohort study to investigate the association of levels of ambient air pollution with the incidence and the risk of migraine/headaches in Taiwan children from 2000 to 2012. Methods We collected data from the Taiwan National Health Insurance Research Database and linked them to the Taiwan Air Quality Monitoring Database. Overall 218,008 children aged <18 (0-17) years old were identified from January 1, 2000 and then followed until they were diagnosed by a physician >=3 times with migraine/headaches or until December 31, 2012. We categorized the annual average concentration of each air pollutant (fine particulate matter, total hydrocarbon, methane, sulfur dioxide, and nitrogen dioxide) into quartiles (Q1-Q4). We measured the incidence rate, hazard ratios (HRs), and the corresponding 95% confidence intervals for migraine/headaches stratified by the quartiles. Results A total of 28037 children (12.9%) were identified with migraine/headaches. The incidence rate and adjusted HR for migraine/headaches increased with higher-level exposure of air pollutants, except sulfur dioxide. Conclusions We herein demonstrate that long-term ambient air pollutant exposure might be a risk factor for childhood migraine/headaches.

scholarly journals Prenatal PM2.5 Exposure in Relation to Maternal and Newborn Telomere Length at Delivery

Toxics ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 13
Author(s):  
Teresa Durham ◽  
Jia Guo ◽  
Whitney Cowell ◽  
Kylie W. Riley ◽  
Shuang Wang ◽  
...  
Keyword(s):  
Telomere Length ◽  
Statistical Significance ◽  
Negative Relationship ◽  
Newborn Health ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Maternal And Newborn Health ◽  
Pm2.5 Exposure ◽  
Maternal And Newborn

Particulate matter with an aerodynamic diameter of 2.5 μm or less (PM2.5) is a ubiquitous air pollutant that is increasingly threatening the health of adults and children worldwide. One health impact of elevated PM2.5 exposure is alterations in telomere length (TL)—protective caps on chromosome ends that shorten with each cell division. Few analyses involve prenatal PM2.5 exposure, and paired maternal and cord TL measurements. Here, we analyzed the association between average and trimester-specific prenatal PM2.5 exposure, and maternal and newborn relative leukocyte TL measured at birth among 193 mothers and their newborns enrolled in a New-York-City-based birth cohort. Results indicated an overall negative relationship between prenatal PM2.5 and maternal TL at delivery, with a significant association observed in the second trimester (β = −0.039, 95% CI: −0.074, −0.003). PM2.5 exposure in trimester two was also inversely related to cord TL; however, this result did not reach statistical significance (β = −0.037, 95% CI: −0.114, 0.039), and no clear pattern emerged between PM2.5 and cord TL across the different exposure periods. Our analysis contributes to a limited body of research on ambient air pollution and human telomeres, and emphasizes the need for continued investigation into how PM2.5 exposure during pregnancy influences maternal and newborn health.

scholarly journals Association of Ambient Air Pollution with Perceived Stress in Pregnant Women: A Prospective Cohort Study

2021 ◽  
Author(s):  
Dirga Kumar Lamichhane ◽  
Dal-Young Jung ◽  
Yee-Jin Shin ◽  
Kyung-Sook Lee ◽  
So-Yeon Lee ◽  
...  
Keyword(s):  
Air Pollution ◽  
Pregnant Women ◽  
Perceived Stress ◽  
Regression Models ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Linear Regression Models ◽  
Third Trimester ◽  
The Third

Abstract Background: Air pollution is associated with perceived stress in the general population, but its influence on maternal perceived stress during pregnancy has not been investigated.We aimed to investigate the relationship between air pollution and non-specific perceived stress among pregnant women.Methods: Our analysis included2162 pregnant women who had participated in the cohort for childhood origin of asthma and allergic disease study between 2008 and 2015. Maternal exposures to particulate matter with an aerodynamic diameter < 2.5 µm (PM2.5) and < 10 µm (PM10), as well as to nitrogen dioxide (NO2) and ozone (O3) for each trimesterand the entire pregnancy were determined using land-use regression models. Maternal perceived stress during the third trimester was assessed using the 14-item Perceived Stress Scale (PSS): scores ranged from 0-56 with higher scores indicating increased stress. Linear regression models were applied to estimate associations between PSS scores and each air pollutant, after adjusting for socio-demographic and behavioral covariates.Results: In single-pollutant models,after adjustment, an IQR increase in the whole pregnancy exposure to PM2.5 and PM10 and O3 in the third trimester was related to 0.37 (95% confidence interval [CI]: 0.01, 0.74) and 0.55 (95% CI: 0.12, 0.98) and 0.29 (95% CI: 0.05, 0.52) points increase in the PSS score, respectively.This association was more evident in women with child-bearing age and lower levelofeducation, and the association of PM10was stronger in thespring season.In multi-pollutant models, exposures to PM10 and O3 were associated with higher perceived stress. Conclusion:Our findings suggest that pregnancy exposure to PM2.5, PM10and O3 is positively associated with maternal PSS score during the third trimester.

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