Mitochondrial toxicity of tobacco smoke and air pollution.
Ontology highlight
ABSTRACT:
SUBMITTER: Fetterman JL
PROVIDER: S-EPMC5681398 | biostudies-literature | 2017 Nov
REPOSITORIES: biostudies-literature
Publications
Mitochondrial toxicity of tobacco smoke and air pollution.
Fetterman Jessica L JL Sammy Melissa J MJ Ballinger Scott W SW
Toxicology 20170822
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Project description:BackgroundTobacco smoking, passive smoking, and indoor air pollution from biomass fuels have been implicated as risk factors for tuberculosis (TB) infection, disease, and death. Tobacco smoking and indoor air pollution are persistent or growing exposures in regions where TB poses a major health risk. We undertook a systematic review and meta-analysis to quantitatively assess the association between these exposures and the risk of infection, disease, and death from TB.Methods and findingsWe conducted a systematic review and meta-analysis of observational studies reporting effect estimates and 95% confidence intervals on how tobacco smoking, passive smoke exposure, and indoor air pollution are associated with TB. We identified 33 papers on tobacco smoking and TB, five papers on passive smoking and TB, and five on indoor air pollution and TB. We found substantial evidence that tobacco smoking is positively associated with TB, regardless of the specific TB outcomes. Compared with people who do not smoke, smokers have an increased risk of having a positive tuberculin skin test, of having active TB, and of dying from TB. Although we also found evidence that passive smoking and indoor air pollution increased the risk of TB disease, these associations are less strongly supported by the available evidence.ConclusionsThere is consistent evidence that tobacco smoking is associated with an increased risk of TB. The finding that passive smoking and biomass fuel combustion also increase TB risk should be substantiated with larger studies in future. TB control programs might benefit from a focus on interventions aimed at reducing tobacco and indoor air pollution exposures, especially among those at high risk for exposure to TB.
| S-EPMC1769410 | biostudies-literature
Project description:Tobacco smoke air pollution (TSAP) measurement may persuade parents to adopt smoke-free homes and thereby reduce harm to children from tobacco smoke in the home. In a pilot study involving 29 smoking families, a Sidepak was used to continuously monitor home PM(2.5) during an 8-h period, Sidepak and/or Dylos monitors provided real-time feedback, and passive nicotine monitors were used to measure home air nicotine for one week. Feedback was provided to participants in the context of motivational interviews. Home PM(2.5) levels recorded by continuous monitoring were not well-accepted by participants because of the noise level. Also, graphs from continuous monitoring showed unexplained peaks, often associated with sources unrelated to indoor smoking, such as cooking, construction, or outdoor sources. This hampered delivery of a persuasive message about the relationship between home smoking and TSAP. By contrast, immediate real-time PM(2.5) feedback (with Sidepak or Dylos monitor) was feasible and provided unambiguous information; the Dylos had the additional advantages of being more economical and quieter. Air nicotine sampling was complicated by the time-lag for feedback and questions regarding shelf-life. Improvement in the science of TSAP measurement in the home environment is needed to encourage and help maintain smoke-free homes and protect vulnerable children. Recent advances in the use of mobile devices for real-time feedback are promising and warrant further development, as do accurate methods for real-time air nicotine air monitoring.
| S-EPMC4690906 | biostudies-literature
Project description:IntroductionTobacco smoke pollution (TSP) has been identified as a serious public health threat. Although the number of jurisdictions that prohibit smoking in public places has increased rapidly, just a few successful attempts have been made to pass similar laws prohibiting smoking in cars, where the cabin space may contribute to concentrated exposure. In particular, TSP constitutes a potentially serious health hazard to children because of prolonged exposure and their small size.MethodsThe present study investigated the levels of TSP in 18 cars via the measurement of fine respirable particles (<2.5 microns in diameter or PM(2.5)) under a variety of in vivo conditions. Car owners smoked a single cigarette in their cars in each of five controlled air-sampling conditions. Each condition varied on movement of the car, presence of air conditioning, open windows, and combinations of these airflow influences.ResultsSmoking just a single cigarette in a car generated extremely high average levels of PM(2.5): more than 3,800 microg/m3 in the condition with the least airflow (motionless car, windows closed). In moderate ventilation conditions (air conditioning or having the smoking driver hold the cigarette next to a half-open window), the average levels of PM(2.5) were reduced but still at significantly high levels (air conditioning = 844 microg/m3; holding cigarette next to a half-open window = 223 microg/m3).DiscussionThis study demonstrates that TSP in cars reaches unhealthy levels, even under realistic ventilation conditions, lending support to efforts occurring across a growing number of jurisdictions to educate people and prohibit smoking in cars in the presence of children.
| S-EPMC2688598 | biostudies-literature
Project description:BackgroundAir pollution is associated with asthma exacerbations. We examined the associations of exposure to ambient particulate matter (PM10) and nitrogen dioxide (NO2) with the risk of wheezing in preschool children, and assessed whether these associations were modified by tobacco smoke exposure.MethodsThis study was embedded in the Generation R Study, a population-based prospective cohort study among 4,634 children. PM10 and NO2 levels were estimated for the home addresses using dispersion modeling. Annual parental reports of wheezing until the age of 3 years and fetal and infant tobacco smoke exposure was obtained by questionnaires.ResultsAverage annual PM10 or NO2 exposure levels per year were not associated with wheezing in the same year. Longitudinal analyses revealed non-significant tendencies towards positive associations of PM10 or NO2 exposure levels with wheezing during the first 3 years of life (overall odds ratios (95% confidence interval): 1.21 (0.79, 1.87) and 1.06 (0.92, 1.22)) per 10 μg/m3 increase PM10 and NO2, respectively). Stratified analyses showed that the associations were stronger and only significant among children who were exposed to both fetal and infant tobacco smoke (overall odds ratios 4.54 (1.17, 17.65) and 1.85 (1.15, 2.96)) per 10 μg/m3 increase PM10 and NO2, respectively (p-value for interactions <0.05).ConclusionsOur results suggest that long term exposure to traffic-related air pollutants is associated with increased risks of wheezing in children exposed to tobacco smoke in fetal life and infancy. Smoke exposure in early life might lead to increased vulnerability of the lungs to air pollution.
| S-EPMC3533997 | biostudies-literature
Project description:Background and aimsThere is increasing evidence indicating that air pollution exposure is associated with neuronal damage. Since pregnancy is a critical window of vulnerability, air pollution exposure during this period could have adverse effects on neurodevelopment. This study aims 1) to analyze associations of prenatal exposure to indoor air pollution (particulate matter with diameters ≤10 μm, PM10) and tobacco smoke with neurodevelopment and 2) to determine whether these associations are mediated by deviations of epigenetic gestational age from chronological gestational age (ΔGA).MethodsData of 734 children from the South African Drakenstein Child Health Study were analyzed. Prenatal PM10 exposure was measured using devices placed in the families' homes. Maternal smoking during pregnancy was determined by maternal urine cotinine measures. The Bayley Scales of Infant and Toddler Development III (BSID-III) was used to measure cognition, language and motor development and adaptive behavior at two years of age. Linear regression models adjusted for maternal age, gestational age, sex of child, ancestry, birth weight/length, and socioeconomic status were used to explore associations between air pollutants and BSID-III scores. A mediation analysis was conducted to analyze if these associations were mediated by ΔGA using DNA methylation measurements from cord blood.ResultsAn increase of one interquartile range in natural-log transformed PM10 (lnPM10; 1.58 μg/m3) was significantly associated with lower composite scores in cognition, language, and adaptive behavior sub-scores (composite score β-estimate [95%-confidence interval]: -0.950 [-1.821, -0.120]). Maternal smoking was significantly associated with lower adaptive behavior scores (-3.386 [-5.632, -1.139]). Associations were not significantly mediated by ΔGA (e.g., for PM10 and cognition, proportion mediated [p-value]: 4% [0.52]).ConclusionWe found an association of prenatal exposure to indoor air pollution (PM10) and tobacco smoke on neurodevelopment at two years of age, particularly cognition, language, and adaptive behavior. Further research is needed to understand underlying biological mediators.
| S-EPMC9177804 | biostudies-literature
Project description:IntroductionWaterpipe tobacco smoking continues to show increasing popularity, especially among individuals between 18 and 22 years old. Waterpipe tobacco smoke (WTS) is a mixture of particulates and gases formed from the combustion of the charcoal and volatilisation and humidification of the tobacco+humectant+flavouring substrate known as shisha or mu'assel. As such, variation in the configuration of the waterpipe may affect the particles produced. Our study focuses on the effects of waterpipe size on the physical properties and cytotoxicity of the smoke produced.MethodsShisha type and headspace volume were held constant and a modified Beirut puff protocol was followed while the size of the waterpipe was varied. Particle concentrations and size distributions were measured using a TSI Engine Exhaust Particle Sizer. Type II alveolar cells were exposed to smoke at the air-liquid interface and two metrics of cell health analysed.ResultsIn a 30 min session, we observed a decrease in total particle concentration (1014-1013) and mass (10 000-2800 mg/m3) and an increase in particle size (125-170 nm) as pipe height increases from 22 to 55 cm and bowl size from 300 to 1250 mL. Smoke from all pipe sizes caused decreases in lysosomal function (>40%) and membrane integrity (>60%) 24 hours post 57 min exposure, and meet the National Institutes of Health definition of a cytotoxic agent (≥30% decrease in cell viability).ConclusionSmoke from waterpipes of all sizes causes significant alveolar cellular harm, indicating that this device needs regulation as a hazard to human health.
| S-EPMC7839942 | biostudies-literature
Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.
2020-11-01 | GSE136945 | GEO
Project description:Smoking may modify the lung response to silica exposure including cancer and silicosis. Nevertheless, the precise role of exposure to tobacco smoke (TS) on the lung response to crystalline silica (CS) exposure and the underlying mechanisms need further clarification. The objectives of the present study were to determine the role of TS on lung response to CS exposure and the underlying mechanism(s). Male Fischer 344 rats were exposed by inhalation to air, CS (15 mg/m3, 6 h/day, 5 days), TS (80 mg/m3, 3 h/day, twice weekly, 6 months), or CS (15 mg/m3, 6 h/day, 5 days) followed by TS (80 mg/m3, 3 h/day, twice weekly, 6 months). The rats were euthanized 6 months and 3 weeks following initiation of the first exposure and the lung response was assessed. Silica exposure resulted in significant lung toxicity as evidenced by lung histological changes, enhanced neutrophil infiltration, increased lactate dehydrogenase levels, enhanced oxidant production, and increased cytokine levels. The TS exposure alone had only a minimal effect on these toxicity parameters. However, the combined exposure to TS and CS exacerbated the lung response, compared with TS or CS exposure alone. Global gene expression changes in the lungs correlated with the lung toxicity severity. Bioinformatic analysis of the gene expression data demonstrated significant enrichment in functions, pathways, and networks relevant to the response to CS exposure which correlated with the lung toxicity detected. Collectively our data demonstrated an exacerbation of CS-induced lung toxicity by TS exposure and the molecular mechanisms underlying the exacerbated toxicity.
| S-EPMC7825013 | biostudies-literature
Project description:Ambient air pollution is a leading environmental cause of morbidity and mortality globally with most of the outcomes of cardiovascular origin. While numerous mechanisms are proposed to explain the link between air pollutants and cardiovascular events, the evidence supports a role for oxidative stress as a critical intermediary pathway in the transduction of systemic responses in the cardiovascular system. Indeed, alterations in vascular function are a critical step in the development of cardiometabolic disorders such as hypertension, diabetes, and atherosclerosis. This review will provide an overview of the impact of particulate and gaseous pollutants on oxidative stress from human and animal studies published in the last five years. We discuss current gaps in knowledge and evidence to date implicating the role of oxidative stress with an emphasis on inhalational exposures. We conclude with the identification of gaps, and an exhortation for further studies to elucidate the impact of oxidative stress in air pollution mediated effects.
| S-EPMC7327965 | biostudies-literature
Project description:Background and objectiveIndoor air pollution (IAP) and tobacco smoke exposure (ETS) are global health concerns contributing to the burden of childhood respiratory disease. Studies assessing the effects of IAP and ETS in preschool children are limited. We assessed the impact of antenatal and postnatal IAP and ETS exposure on lung function in a South African birth cohort, the Drakenstein Child Health Study.MethodsAntenatally enrolled mother-child pairs were followed from birth. Lung function measurements (oscillometry, multiple breath washout and tidal breathing) were performed at 6 weeks and 3 years. Quantitative antenatal and postnatal IAP (particulate matter [PM10 ], volatile organic compounds [VOC]) and ETS exposures were measured. Linear regression models explored the effects of antenatal and postnatal exposures on lung function at 3 years.ResultsFive hundred eighty-four children had successful lung function testing, mean (SD) age of 37.3 (0.7) months. Exposure to antenatal PM10 was associated with a decreased lung clearance index (p < 0.01) and postnatally an increase in the difference between resistance at end expiration (ReE) and inspiration (p = 0.05) and decrease in tidal volume (p = 0.06). Exposure to antenatal VOC was associated with an increase in functional residual capacity (p = 0.04) and a decrease in time of expiration over total breath time (tE /tTOT ) (p = 0.03) and postnatally an increase in respiratory rate (p = 0.05). High ETS exposure postnatally was associated with an increase in ReE (p = 0.03).ConclusionAntenatal and postnatal IAP and ETS exposures were associated with impairment in lung function at 3 years. Strengthened efforts to reduce IAP and ETS exposure are needed.
| S-EPMC10947154 | biostudies-literature