Long-term ozone exposure attenuates 1-nitronaphthalene-induced cytotoxicity in nasal mucosa.
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ABSTRACT:
SUBMITTER: Lee MG
PROVIDER: S-EPMC2258449 | biostudies-other | 2008 Mar
REPOSITORIES: biostudies-other
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Project description:Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.
| S-EPMC4105969 | biostudies-literature
Project description:As one of the main environmental stressors commonly found in closed pig houses, ammonia poses high risks to the well-being of humans and animals. This study is aimed at assessing the toxicity of ammonia exposure (80 ppm for 12 days) on the nasal mucosa in piglets. Firstly, we found that after ammonia exposure, the number of white blood cells significantly increased and the serum levels of cytokine IL-4 were significantly decreased. Then, histological analyses showed significant thickening of nasal mucosa and excessive mucus production in the exposure group. Finally, RNA-seq analyses demonstrated that the ammonia exposure disturbed the transcriptome of nasal mucosa which revealed 176 upregulated genes and 426 downregulated genes. GO and KEGG pathway enrichment analysis of the DEGs showed that the upregulated genes were mainly related to neutrophil chemotaxis and immune response, while 80 out of the 426 downregulated genes including CCDCs, CFAPs, DNAHs, and TEKTs were enriched in the microtubule cytoskeleton and cilium morphogenesis/movement. All these results indicated that ammonia exposure induces nasal mucosal hyperplasia and cilia dysfunction, as well as a systemic inflammatory response in piglets. These findings provide new evidence for understanding the damage mechanism of ammonia on the nasal mucosa.
| S-EPMC7273420 | biostudies-literature
Project description: Not available
| S-EPMC6794103 | biostudies-literature
Project description:ImportanceFew studies have investigated the association of long-term ambient ozone exposures with respiratory morbidity among individuals with a heavy smoking history.ObjectiveTo investigate the association of historical ozone exposure with risk of chronic obstructive pulmonary disease (COPD), computed tomography (CT) scan measures of respiratory disease, patient-reported outcomes, disease severity, and exacerbations in smokers with or at risk for COPD.Design, setting, and participantsThis multicenter cross-sectional study, conducted from November 1, 2010, to July 31, 2018, obtained data from the Air Pollution Study, an ancillary study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). Data analyzed were from participants enrolled at 7 (New York City, New York; Baltimore, Maryland; Los Angeles, California; Ann Arbor, Michigan; San Francisco, California; Salt Lake City, Utah; and Winston-Salem, North Carolina) of the 12 SPIROMICS clinical sites. Included participants had historical ozone exposure data (n = 1874), were either current or former smokers (≥20 pack-years), were with or without COPD, and were aged 40 to 80 years at baseline. Healthy persons with a smoking history of 1 or more pack-years were excluded from the present analysis.ExposuresThe 10-year mean historical ambient ozone concentration at participants' residences estimated by cohort-specific spatiotemporal modeling.Main outcomes and measuresSpirometry-confirmed COPD, chronic bronchitis diagnosis, CT scan measures (emphysema, air trapping, and airway wall thickness), 6-minute walk test, modified Medical Research Council (mMRC) Dyspnea Scale, COPD Assessment Test (CAT), St. George's Respiratory Questionnaire (SGRQ), postbronchodilator forced expiratory volume in the first second of expiration (FEV1) % predicted, and self-report of exacerbations in the 12 months before SPIROMICS enrollment, adjusted for demographics, smoking, and job exposure.ResultsA total of 1874 SPIROMICS participants were analyzed (mean [SD] age, 64.5 [8.8] years; 1479 [78.9%] white; and 1013 [54.1%] male). In adjusted analysis, a 5-ppb (parts per billion) increase in ozone concentration was associated with a greater percentage of emphysema (β = 0.94; 95% CI, 0.25-1.64; P = .007) and percentage of air trapping (β = 1.60; 95% CI, 0.16-3.04; P = .03); worse scores for the mMRC Dyspnea Scale (β = 0.10; 95% CI, 0.03-0.17; P = .008), CAT (β = 0.65; 95% CI, 0.05-1.26; P = .04), and SGRQ (β = 1.47; 95% CI, 0.01-2.93; P = .048); lower FEV1% predicted value (β = -2.50; 95% CI, -4.42 to -0.59; P = .01); and higher odds of any exacerbation (odds ratio [OR], 1.37; 95% CI, 1.12-1.66; P = .002) and severe exacerbation (OR, 1.37; 95% CI, 1.07-1.76; P = .01). No association was found between historical ozone exposure and chronic bronchitis, COPD, airway wall thickness, or 6-minute walk test result.Conclusions and relevanceThis study found that long-term historical ozone exposure was associated with reduced lung function, greater emphysema and air trapping on CT scan, worse patient-reported outcomes, and increased respiratory exacerbations for individuals with a history of heavy smoking. The association between ozone exposure and adverse respiratory outcomes suggests the need for continued reevaluation of ambient pollution standards that are designed to protect the most vulnerable members of the US population.
| S-EPMC6902160 | biostudies-literature
Project description:Rationale: Many studies have linked short-term exposure to ozone (O3) with morbidity and mortality, but epidemiologic evidence of associations between long-term O3 exposure and mortality is more limited.Objectives: To investigate associations of long-term (annual or warm season average of daily 8-h maximum concentrations) O3 exposure with all-cause and cause-specific mortality in the NIH-AARP Diet and Health Study, a large prospective cohort of U.S. adults with 17 years of follow-up from 1995 to 2011.Methods: The cohort (n = 548,780) was linked to census tract-level estimates for O3. Associations between long-term O3 exposure (averaged values from 2002 to 2010) and multiple causes of death were evaluated using multivariate Cox proportional hazards models, adjusted for individual- and census tract-level covariates, and potentially confounding copollutants and temperature.Measurements and Main Results: Long-term annual average exposure to O3 was significantly associated with deaths caused by cardiovascular disease (per 10 ppb; hazard ratio [HR], 1.03; 95% confidence interval [CI], 1.01-1.06), ischemic heart disease (HR, 1.06; 95% CI, 1.02-1.09), respiratory disease (HR, 1.04; 95% CI, 1.00-1.09), and chronic obstructive pulmonary disease (HR, 1.09; 95% CI, 1.03-1.15) in single-pollutant models. The results were robust to alternative models and adjustment for copollutants (fine particulate matter and nitrogen dioxide), although some evidence of confounding by temperature was observed. Significantly elevated respiratory disease mortality risk associated with long-term O3 exposure was found among those living in locations with high temperature (Pinteraction < 0.05).Conclusions: This study found that long-term exposure to O3 is associated with increased risk for multiple causes of mortality, suggesting that establishment of annual and/or seasonal federal O3 standards is needed to more adequately protect public health from ambient O3 exposures.
| S-EPMC6794108 | biostudies-literature
Project description:RationaleChronic air pollutant exposure has been associated with development of Acute Respiratory Distress Syndrome (ARDS) in patients at risk, particularly from severe trauma. We recently reported that shorter peripheral blood leukocyte (PBL) telomere length (TL) was associated with worse outcomes and higher severity of ARDS in critically ill patients. Since most major air pollutants are potent oxidants that can induce cellular oxidative stress, and oxidative stress can accelerate telomere shortening, we hypothesized that higher levels of chronic air pollutant exposure would be associated with shorter telomere length in critically ill patients including patients with ARDS.MethodsPBL-TL was measured in genomic DNA collected on the morning of ICU day 2 in 772 critically ill patients enrolled in a prospective observational study. Exposures to air pollutants including ozone (warm-season only), particulate matter < 2.5 µm (PM2.5), particulate matter < 10 µm (PM10), CO, NO2 and SO2, were estimated by weighted average of daily levels from all monitors within 50 km of each patient's residential address for the 3 years prior to admission. Associations of each air pollutant exposure and PBL-TL were investigated by multivariable linear regression models adjusting for age, ethnicity, sex, smoking history, alcohol abuse, insurance status, median household income, history of malignancy and APACHE II.ResultsContrary to our hypothesis, TL increased across exposure quartiles in both ozone and PM2.5 analyses (p < 0.05). In a regression model controlling for potential confounders, long term ozone exposure was significantly associated with an increase in TL in the entire cohort (0.31 kb per 10 ppb), as well as in subgroups with sepsis, trauma and ARDS (all p < 0.05). In multivariable models, entire-year exposure to PM2.5, PM10, CO, NO2 and SO2 was not associated with TL after adjustment for potential confounders. In an analysis restricted to warm-season levels to assess the effect of seasonality, higher warm-season PM2.5 and CO exposures were independently associated with longer TL.ConclusionsLong-term exposure to ozone is associated with longer peripheral blood TL in critically ill patients. Further studies are needed to investigate the potential underlying mechanisms for this unexpected positive association between telomere length and air pollution exposure in critical illness.
| S-EPMC7535086 | biostudies-literature
Project description:Numerous studies have demonstrated that exposure to ambient ozone (O3) could have adverse effects on children's respiratory health. However, previous studies mainly focused on asthma and wheezing. Evidence for allergic rhinitis and bronchitic symptoms (e.g., persistent cough and phlegm) associated with O3 is limited, and results from existing studies are inconsistent. This study included a total of 59,754 children from the seven northeastern cities study (SNEC), who were aged 2 to 17 years and from 94 kindergarten, elementary and middle schools. Information on doctor-diagnosed allergic rhinitis (AR), persistent cough, and persistent phlegm was collected during 2012-2013 using a standardized questionnaire developed by the American Thoracic Society (ATS). Information for potential confounders was also collected via questionnaire. Individuals' exposure to ambient ozone (O3) during the four years before the investigation was estimated using a satellite-based random forest model. A higher level of O3 was significantly associated with increased risk of AR and bronchitic symptoms. After controlling for potential confounders, the OR (95% CI) were 1.13 (1.07-1.18), 1.10 (1.06-1.16), and 1.12 (1.05-1.20) for AR, persistent cough, and persistent phlegm, respectively, associated with each interquartile range (IQR) rise in O3 concentration. Interaction analyses showed stronger adverse effects of O3 on AR in children aged 7-17 years than those aged 2-6 years, while the adverse association of O3 with cough was more prominent in females and children aged 7-12 years than in males and children aged 2-6 and 13-17 years. This study showed that long-term exposure to ambient O3 was significantly associated with higher risk of AR and bronchitic symptoms in children, and the association varies across age and gender. Our findings contribute additional evidence for the importance of controlling O3 pollution and protecting children from O3 exposure.
| S-EPMC8472948 | biostudies-literature
Project description:BackgroundEvidence shows that exposure to air pollutants can increase blood pressure in the short and long term. Some studies show higher levels of hypertension prevalence in areas of high pollution. Few data exist on the association of air pollution with hypertension incidence. The purpose of the present study was to prospectively assess the associations of the traffic-related nitrogen dioxide (NO2) and of ozone with the incidence of hypertension in the Black Women's Health Study (BWHS), a large cohort study of African American women.MethodsWe used Cox proportional hazards models to calculate hazard ratios (HRs) and 95% confidence intervals (CI) for hypertension associated with exposure to NO2 and ozone among 33,771 BWHS participants. NO2 and ozone levels at participant residential locations were estimated with validated models.ResultsFrom 1995 to 2011, 9,570 incident cases of hypertension occurred in a total of 348,154 person-years (median follow-up time, 11 years). The multivariable HRs per interquartile range of NO2 (9.7 ppb) and ozone (6.7 ppb) were 0.92 (95% CI = 0.86, 0.98) and 1.09 (95% CI = 1.00, 1.18).ConclusionsIn this large cohort of African American women, higher ozone levels were associated with an increase in hypertension incidence. Higher NO2 levels were not associated with greater hypertension incidence; indeed, incidence was lower at higher NO2 levels.
| S-EPMC5861564 | biostudies-literature
Project description:Ozone pollution is a damaging air pollutant that reduces maize yields equivalently to nutrient deficiency, heat, and aridity stress. Therefore, understanding the physiological and biochemical responses of maize to ozone pollution and identifying traits predictive of ozone tolerance is important. In this study, we examined the physiological, biochemical and yield responses of six maize hybrids to elevated ozone in the field using Free Air Ozone Enrichment. Elevated ozone stress reduced photosynthetic capacity, in vivo and in vitro, decreasing Rubisco content, but not activation state. Contrary to our hypotheses, variation in maize hybrid responses to ozone was not associated with stomatal limitation or antioxidant pools in maize. Rather, tolerance to ozone stress in the hybrid B73 × Mo17 was correlated with maintenance of leaf N content. Sensitive lines showed greater ozone-induced senescence and loss of photosynthetic capacity compared to the tolerant line.
| S-EPMC7756399 | biostudies-literature
Project description:BackgroundEpidemiologic studies on the effects of long-term exposure to ozone (O3) have shown inconclusive results. It is unclear whether to O3 has an effect on chronic kidney disease (CKD). We investigated the effects of O3 on mortality and renal outcome in CKD.MethodsWe included 61,073 participants and applied Cox proportional hazards models to examine the effects of ozone on the risk of end-stage renal disease (ESRD) and mortality in a two-pollutants model adjusted for socioeconomic status. We calculated the concentration of ozone exposure one year before enrollment and used inverse distance weighting (IDW) for interpolation, where the exposure was evenly distributed.ResultsIn the single pollutant model, O3 was significantly associated with an increased risk of ESRD and all-cause mortality. Based on the O3 concentration from IDW interpolation, this moving O3 average was significantly associated with an increased risk of ESRD and all-cause mortality. In a two-pollutants model, even after we adjusted for other measured pollutants, nitrogen dioxide did not attenuate the result for O3. The hazard ratio (HR) value for the district-level assessment is 1.025 with a 95% confidence interval (CI) of 1.014-1.035, while for the point-level assessment, the HR value is 1.04 with a 95% CI of 1.035-1.045. The impact of ozone on ESRD, hazard ratio (HR) values are, 1.049(95%CI: 1.044-1.054) at the district unit and 1.04 (95%CI: 1.031-1.05) at the individual address of the exposure assessment. The ozone hazard ratio for all-cause mortality was 1.012 (95% confidence interval: 1.008-1.017) for administrative districts and 1.04 (95% confidence interval: 1.031-1.05) for individual addresses.ConclusionsThis study suggests that long-term ambient O3 increases the risk of ESRD and mortality in CKD. The strategy to decrease O3 emissions will substantially benefit health and the environment.
| S-EPMC10900590 | biostudies-literature