Nitrogen Dioxide Exposure May Be Associated with Poststroke Emotional Symptoms.
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ABSTRACT:
SUBMITTER: Kwon HS
PROVIDER: S-EPMC8053548 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:RationaleChronic exposure to indoor nitrogen dioxide (NO2) is a public health concern. Over half of U.S. households have a source of NO2, and experimental data suggest potential for adverse respiratory effects.ObjectiveTo examine associations of indoor NO2 exposure with respiratory symptoms among children with asthma.MethodsNO2 was measured using Palmes tubes, and respiratory symptoms in the month before sampling were collected during home interviews of mothers of 728 children with active asthma. All were younger than 12 yr, lived at the sampled home for at least 2 mo, and had asthma symptoms or used maintenance medication within the previous year.MeasurementsRespiratory symptoms (wheeze, persistent cough, shortness of breath, chest tightness).ResultsMean (SD) NO2 was 8.6 (9.1) ppb in homes with electric ranges and 25.9 (18.1) ppb in homes with gas stoves. In models stratified by housing type (a factor associated with socioeconomic status), gas stove presence and elevated NO2 were each significantly associated with respiratory symptoms, controlling for age, ethnicity, medication, mold/mildew, water leaks, and season of sampling. Among children in multifamily housing, exposure to gas stoves increased likelihood of wheeze (odds ratio [OR], 2.27; 95% confidence interval [95% CI], 1.15, 4.47), shortness of breath (OR, 2.33; 95% CI, 1.12, 5.06), and chest tightness (OR, 4.34; 95% CI, 1.76, 10.69), whereas each 20-ppb increase in NO2 increased both likelihood of any wheeze (OR, 1.52; 95% CI, 1.04, 2.21) or chest tightness (OR, 1.61; 95% CI, 1.04, 2.49), and days of wheeze (rate ratio (RR), 1.33; 95% CI, 1.05, 1.68) or chest tightness (RR, 1.51; 95% CI, 1.18, 1.91).ConclusionExposure to indoor NO2 at levels well below the Environmental Protection Agency outdoor standard (53 ppb) is associated with respiratory symptoms among children with asthma in multifamily housing.
| S-EPMC2662932 | biostudies-literature
Project description:Rationale: Lung function and growth are adversely associated with nitrogen dioxide (NO2) exposure. Lower levels of circulating club cell secretory protein (CC16) in childhood are also associated with subsequent decreased lung function. NO2 exposure may induce epithelial damage in lungs and alter club cell proliferation and morphology.Objectives: To determine if increased ambient NO2 levels at participants' home addresses in early life were associated with decreased levels of CC16 from age 6 to 32 years.Methods: Participants were enrolled at birth in the Tucson Children's Respiratory Study and had circulating CC16 measured at least once between age 6 and 32. Linear mixed models were used to determine the association between estimated ambient NO2 exposure at participants' home address at birth or age 6 with CC16 levels from age 6 to 32.Measurements and Main Results: NO2 exposures at birth or age 6 were available for 777 children with one or more CC16 measurement. We found a negative association between NO2 exposure and CC16 levels, with a 4.7% (95% confidence interval, -8.6 to -0.7) decrease in CC16 levels from age 6 to 32 per interquartile range increase in NO2 exposure (6.0 ppb) at the participants' birth address. We observed modification by race (p interaction = 0.04), with stronger associations among participants with at least one black parent (-29.6% [95% confidence interval, -42.9% to -13.2%] per interquartile range). NO2 at participant's age 6 address was not significantly associated with CC16 levels (-1.9%; 95% confidence interval, -6.3 to 2.6).Conclusions: Higher exposure to NO2 at birth is associated with persistently low levels of CC16 from 6 to 32 years.
| S-EPMC6727155 | biostudies-literature
Project description:BACKGROUND:Ambient and home exposure to nitrogen dioxide (NO2) causes asthma symptoms and decreased lung function in children with asthma. Little is known about the health effects of school classroom pollution exposure. OBJECTIVE:We aimed to determine the effect of indoor classroom NO2 on lung function and symptoms in inner-city school children with asthma. METHODS:Children enrolled in the School Inner-City Asthma Study were followed for 1 academic year. Subjects performed spirometry and had fraction of exhaled nitric oxide values measured twice during the school year at school. Classroom NO2 was collected by means of passive sampling for 1-week periods twice per year, coinciding with lung function testing. Generalized estimating equation models assessed lung function and symptom relationships with the temporally nearest classroom NO2 level. RESULTS:The mean NO2 value was 11.1 ppb (range, 4.3-29.7 ppb). In total, exposure data were available for 296 subjects, 188 of whom had complete spirometric data. At greater than a threshold of 8 ppb of NO2 and after adjusting for race and season (spirometry standardized by age, height, and sex), NO2 levels were associated highly with airflow obstruction, such that each 10-ppb increase in NO2 level was associated with a 5% decrease in FEV1/forced vital capacity ratio (? = -0.05; 95% CI, -0.08 to -0.02; P = .01). Percent predicted forced expiratory flow between the 25th and 75th percentile of forced vital capacity was also inversely associated with higher NO2 exposure (? = -22.8; 95% CI, -36.0 to -9.7; P = .01). There was no significant association of NO2 levels with percent predicted FEV1, fraction of exhaled nitric oxide, or asthma symptoms. Additionally, there was no effect modification of atopy on lung function or symptom outcomes. CONCLUSION:In children with asthma, indoor classroom NO2 levels can be associated with increased airflow obstruction.
| S-EPMC5886827 | biostudies-literature
Project description:Epigenetic influence plays a role in the association between exposure to air pollution and attention deficit hyperactivity disorder (ADHD); however, research regarding sulfur dioxide (SO2) is scarce. Herein, we investigate the associations between prenatal SO2 exposure and ADHD rating scale (ARS) at ages 4, 6 and 8 years repeatedly in a mother-child cohort (n = 329). Whole blood samples were obtained at ages 2 and 6 years, and genome-wide DNA methylation (DNAm) was analyzed for 51 children using the Illumina Infinium HumanMethylation BeadChip. We analyzed the associations between prenatal SO2 exposure and DNAm levels at ages 2 and 6, and further investigated the association between the DNAm and ARS at ages 4, 6 and 8. Prenatal SO2 exposure was associated with ADHD symptoms. From candidate gene analysis, DNAm levels at the 6 CpGs at age 2 were associated with prenatal SO2 exposure levels. Of the 6 CpGs, cg07583420 (INS-IGF2) was persistently linked with ARS at ages 4, 6 and 8. Epigenome-wide analysis showed that DNAm at 6733 CpG sites were associated with prenatal SO2 exposure, of which 58 CpGs involved in Notch signalling pathway were further associated with ARS at age 4, 6 and 8 years, persistently. DNAm at age 6 was not associated with prenatal SO2 exposure. Changes in DNAm levels associated with prenatal SO2 exposure during early childhood are associated with increases in ARS in later childhood.
| S-EPMC9977725 | biostudies-literature
Project description:Study objectivePrior studies have shown that children are particularly sensitive to air pollution. This study examined whether children of low socioeconomic status suffered greater exposure to outdoor nitrogen dioxide than more affluent ones, both at their place of residence and at school, in a country with widespread state intervention for social equity.DesignLocal scale data on outdoor nitrogen dioxide obtained from a validated air pollution model were analysed, along with all school children accurately geocoded to their building of residence and school.ParticipantsAll 29,133 children in grades one through nine (aged 7 to 15 years) residing and attending school in Malmö, Sweden, in 2001.Main resultsDefining the socioeconomic status of children according to the mean income in their residential building, the spatial scan statistic technique allowed the authors to identify eight statistically significant clusters of low socioeconomic status children, all of which were located in the most polluted areas of Malmö. Four clusters of high socioeconomic status children were found, all of them located in the least polluted areas. The neighbourhood socioeconomic status better predicted the nitrogen dioxide exposure of children than the socioeconomic status of their building of residence. Exposure to nitrogen dioxide at the place of residence and school of attendance regularly increased as the socioeconomic status of a child's neighbourhood of residence decreased.ConclusionsEvidence of environmental injustice was found, even in a country noted for its egalitarian welfare state. Enforcement of environmental regulations may be necessary to achieve a higher level of environmental equity.
| S-EPMC2465552 | biostudies-literature
Project description:BackgroundAmbient air pollution is among the greatest environmental risks to human health. However, little is known about the health effects of nitrogen dioxide (NO2), a traffic-related air pollutant. Herein, we aimed to conduct a meta-analysis to investigate the long-term effects of NO2 on mortality.MethodsWe conducted a systematic search for studies that were published up to February 2020 and performed a meta-analysis of all available epidemiologic studies evaluating the associations between long-term exposure to NO2 with all-cause, cardiovascular, and respiratory mortality. Overall pooled effect estimates as well as subgroup-specific pooled estimates (e.g. location, exposure assessment method, exposure metric, study population, age at recruitment, and key confounder adjustment) and 95% confidence intervals were calculated using random-effects models. Risk of bias assessment was accessed by following WHO global air quality guidelines. Publication bias was accessed by visually inspecting funnel plot and Egger's liner regression was used to test of asymmetry.ResultsOur search initially retrieved 1349 unique studies, of which 34 studies met the inclusion criteria. The pooled hazard ratio (HR) for all-cause mortality was 1.06 (95%CI: 1.04-1.08, n = 28 studies, I2 = 98.6%) per 10 ppb increase in annual NO2 concentrations. The pooled HRs for cardiovascular and respiratory mortality per 10 ppb increment were 1.11 (95%CI: 1.07-1.16, n = 20 studies, I2 = 99.2%) and 1.05 (95%CI: 1.02-1.08, n = 17 studies, I2 = 94.6%), respectively. The sensitivity analysis pooling estimates from multi-pollutant models suggest an independent effect of NO2 on mortality. Funnel plots indicate that there is no evidence for publication bias in our study.ConclusionWe provide robust epidemiological evidence that long-term exposure to NO2, a proxy for traffic-sourced air pollutants, is associated with a higher risk of all-cause, cardiovascular, and respiratory mortality that might be independent of other common air pollutants.
| S-EPMC8499020 | biostudies-literature
Project description:BackgroundSince 1971, the annual National Ambient Air Quality Standard (NAAQS) for nitrogen dioxide (NO2) has remained at 53 ppb, the impact of long-term NO2 exposure on mortality is poorly understood.ObjectivesWe examined associations between long-term NO2 exposure (12-month moving average of NO2) below the annual NAAQS and cause-specific mortality among the older adults in the U.S.MethodsCox proportional-hazard models were used to estimate Hazard Ratio (HR) for cause-specific mortality associated with long-term NO2 exposures among about 50 million Medicare beneficiaries living within the conterminous U.S. from 2001 to 2008.ResultsA 10 ppb increase in NO2 was associated with increased mortality from all-cause (HR: 1.06; 95% CI: 1.05-1.06), cardiovascular (HR: 1.10; 95% CI: 1.10-1.11), respiratory disease (HR: 1.09; 95% CI: 1.08-1.11), and cancer (HR: 1.01; 95% CI: 1.00-1.02) adjusting for age, sex, race, ZIP code as strata ZIP code- and state-level socio-economic status (SES) as covariates, and PM2.5 exposure using a 2-stage approach. NO2 was also associated with elevated mortality from ischemic heart disease, cerebrovascular disease, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, and lung cancer. We found no evidence of a threshold, with positive and significant HRs across the range of NO2 exposures for all causes of death examined. Exposure-response curves were linear for all-cause, supra-linear for cardiovascular-, and sub-linear for respiratory-related mortality. HRs were highest consistently among Black beneficiaries.ConclusionsLong-term NO2 exposure is associated with elevated risks of death by multiple causes, without evidence of a threshold response. Our findings raise concerns about the sufficiency of the annual NAAQS for NO2.
| S-EPMC8810665 | biostudies-literature
Project description:The effects of exposure of animals to 100% O2 and NO2 on the rate of prostaglandin metabolism by lung and kidney were studied in vitro. Exposure of guinea pigs to 100% O2 for 48 h inhibited the metabolism of prostaglandin F2 alpha by both NAD+- and NADP+-dependent prostaglandin dehydrogenase in lung, but had no effect on the metabolism in kidney. Succinate dehydrogenase, but not glucose 6-phosphate dehydrogenase, in guinea-pig lung was inhibited by exposure to 100% O2. Exposure to 46 p.p.m. but not 16 or 29 p.p.m. NO2 for 6 h inhibited guinea-pig lung prostaglandin dehydrogenase in vitro. The inhibition of pulmonary prostaglandin dehydrogenase by exposure to 100% O2 or to 49 p.p.m. NO2 was dependent on the duration of exposure, but returned to control values within 7 days after cessation of the exposure. The pulmonary transport system responsible for removing circulating prostaglandins from the blood was not affected by exposure to 100% O2 as measured by using the isolated perfused lung. Kinetic analysis of the inhibition of pulmonary prostaglandin dehydrogenase activity in guinea pig exposed to 100% O2 showed non-competitive inhibition with respect to both prostaglandin F2 alpha and NAD+, which suggests destruction or inactivation of the enzyme. Pulmonary prostaglandin dehydrogenase appears to be inhibited by exposure to oxidant gases, which may lead to elevated prostaglandin concentrations in the lungs or in the systemic circulation.
| S-EPMC1161673 | biostudies-other
Project description:Numerous studies have linked air pollution with adverse birth outcomes, but relatively few have examined differential associations across the socioeconomic gradient. To evaluate interaction effects of gestational nitrogen dioxide (NO2) and area-level socioeconomic deprivation on fetal growth, we used: (1) highly spatially-resolved air pollution data from the New York City Community Air Survey (NYCCAS); and (2) spatially-stratified principle component analysis of census variables previously associated with birth outcomes to define area-level deprivation. New York City (NYC) hospital birth records for years 2008-2010 were restricted to full-term, singleton births to non-smoking mothers (n=243,853). We used generalized additive mixed models to examine the potentially non-linear interaction of nitrogen dioxide (NO2) and deprivation categories on birth weight (and estimated linear associations, for comparison), adjusting for individual-level socio-demographic characteristics and sensitivity testing adjustment for co-pollutant exposures. Estimated NO2 exposures were highest, and most varying, among mothers residing in the most-affluent census tracts, and lowest among mothers residing in mid-range deprivation tracts. In non-linear models, we found an inverse association between NO2 and birth weight in the least-deprived and most-deprived areas (p-values<0.001 and 0.05, respectively) but no association in the mid-range of deprivation (p=0.8). Likewise, in linear models, a 10 ppb increase in NO2 was associated with a decrease in birth weight among mothers in the least-deprived and most-deprived areas of -16.2g (95% CI: -21.9 to -10.5) and -11.0 g (95% CI: -22.8 to 0.9), respectively, and a non-significant change in the mid-range areas [?=0.5 g (95% CI: -7.7 to 8.7)]. Linear slopes in the most- and least-deprived quartiles differed from the mid-range (reference group) (p-values<0.001 and 0.09, respectively). The complex patterning in air pollution exposure and deprivation in NYC, however, precludes simple interpretation of interactive effects on birth weight, and highlights the importance of considering differential distributions of air pollution concentrations, and potential differences in susceptibility, across deprivation levels.
| S-EPMC4715366 | biostudies-literature
Project description:Background and objectiveExposure to traffic-related air pollutants is an important public health issue. Here, we present a systematic review and meta-analysis of research examining the relationship of measures of nitrogen oxides (NOx) and of various measures of traffic-related air pollution exposure with lung cancer.MethodsWe conducted random-effects meta-analyses of studies examining exposure to nitrogen dioxide (NO2) and NOx and its association with lung cancer. We identified 20 studies that met inclusion criteria and provided information necessary to estimate the change in lung cancer per 10-?g/m3 increase in exposure to measured NO2. Further, we qualitatively assessed the evidence of association between distance to roadways and traffic volume associated with lung cancer.ResultsThe meta-estimate for the change in lung cancer associated with a 10-?g/m3 increase in exposure to NO2 was 4% (95% CI: 1%, 8%). The meta-estimate for change in lung cancer associated with a 10-?g/m3 increase in NOx was similar and slightly more precise, 3% (95% CI: 1%, 5%). The NO2 meta-estimate was robust to different confounding adjustment sets as well as the exposure assessment techniques used. Trim-and-fill analyses suggest that if publication bias exists, the overall meta-estimate is biased away from the null. Forest plots for measures of traffic volume and distance to roadways largely suggest a modest increase in lung cancer risk.ConclusionWe found consistent evidence of a relationship between NO2, as a proxy for traffic-sourced air pollution exposure, with lung cancer. Studies of lung cancer related to residential proximity to roadways and NOx also suggest increased risk, which may be attributable partly to air pollution exposure. The International Agency for Research on Cancer recently classified outdoor air pollution and particulate matter as carcinogenic (Group 1). These meta-analyses support this conclusion, drawing particular attention to traffic-sourced air pollution.CitationHamra GB, Laden F, Cohen AJ, Raaschou-Nielsen O, Brauer M, Loomis D. 2015. Lung cancer and exposure to nitrogen dioxide and traffic: a systematic review and meta-analysis. Environ Health Perspect 123:1107-1112; http://dx.doi.org/10.1289/ehp.1408882.
| S-EPMC4629738 | biostudies-literature