Childhood exposure to ambient air pollution and predicting individual risk of depression onset in UK adolescents.
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SUBMITTER: Latham RM
PROVIDER: S-EPMC8412033 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectivesAir pollution has been associated with increased mortality and morbidity in several studies with indications that its effect could be more severe in children. This study examined the relationship between short-term variations in criteria air pollutants and occurrence of sudden infant death syndrome (SIDS).DesignWe used a case-crossover study design which is widely applied in air pollution studies and particularly useful for estimating the risk of a rare acute outcome associated with short-term exposure.SettingThe study used data from the West Midlands region in the UK.ParticipantsWe obtained daily time series data on SIDS mortality (ICD-9: 798.0 or ICD-10: R95) for the period 1996-2006 with a total of 211 SIDS events.Primary outcome measuresDaily counts of SIDS events.ResultsFor an IQR increase in previous day pollutant concentration, the percentage increases (95% CI) in SIDS were 16 (6 to 27) for PM10, 1 (-7 to 10) for SO2, 5 (-4 to 14) for CO, -17 (-27 to -6) for O3, 16 (2 to 31) for NO2 and 2 (-3 to 8) for NO after controlling for average temperature and national holidays. PM10 and NO2 showed relatively consistent association which persisted across different lag structures and after adjusting for copollutants.ConclusionsThe results indicated ambient air pollutants, particularly PM10 and NO2, may show an association with increased SIDS mortality. Thus, future studies are recommended to understand possible mechanistic explanations on the role of air pollution on SIDS incidence and the ways in which we might reduce pollution exposure among infants.
| S-EPMC5898297 | biostudies-literature
Project description:The association between air pollution and childhood respiratory disease is inconsistent. In the present study, we investigated a short-term effect of ambient air pollutants and daily childhood lower respiratory diseases (CLRD). Daily air pollutants, weather data, and CLRD data were collected from January 2014 to April 2015 (452 days) in Nanjing, China. Time-series regression and generalized additive models were used to assess the effects of air pollutants (PM10, PM2.5, NO2, SO2, O3, and CO) on CLRD. We observed that an interquartile range (IQR) increase in concentrations of PM10, NO2, and SO2 significantly increased the daily CLRD with 6 days cumulative effects (difference of estimates: 2.8%, 95% CI: 0.6-5.0%; 4.1%, 1.2-7.0%; 5.6%, 2.6-8.6%, respectively). However, no significant association was found in IQR concentrations of PM2.5, O3, and CO. Specifically, elevated PM10, PM2.5, NO2, and SO2 significantly increased the numbers of CLRD in cool season (3.6%, 1.5-5.7%; 2.4%, 0.3-4.5%; 4.9%, 2.9-7.0%; 6.3%, 3.7-9.0%, respectively). Additionally, the effect estimates of PM10, NO2, and SO2 in female and age >27 months were more pronounced than in male and age ≤27 months. This study suggested that short-term exposure to ambient PM10, NO2, and SO2 were associated with the increased CLRD numbers.
| S-EPMC5493680 | biostudies-literature
Project description: Not available
| S-EPMC4276028 | biostudies-literature
Project description:ObjectiveMigraine is a common recurrent headache disorder affecting 14% American adults. Although weather and air pollution are often reported by patients with migraine as precipitating factors, previous studies have had mixed results.MethodsWe prospectively collected migraine headache onset data using electronic questionnaires from 98 adults with episodic migraine in the Greater Boston area (2016-2017). Each participant was followed for an average of 45 days for a total of 4406 days of observation. Temperature, relative humidity, and barometric pressure data were obtained from local weather station. Daily average fine particulate matter, daily maximum 1-hour sulfur dioxide, daily maximum 1-hour nitrogen dioxide, daily maximum 8-hour ozone, and daily maximum 8-hour carbon monoxide from local air pollution monitors. We conducted a repeated measures analysis using fixed effects logistic regression models. In the models we adjusted for day of week, a natural cubic spline term of day of the year with 4 degrees of freedom, and a participant identifier. We additionally adjusted for linear terms of temperature and relative humidity in the air pollution analyses. We also applied logistic regression models with generalized estimating equation (GEE) and autoregressive correlation structure in the sensitivity analysis.ResultsThe mean age was 35 years and 88% were women. Mean temperature was 56.9 °F, relative humidity 67.3%, and fine particulate matter 7.3 μg/m3. Higher relative humidity was associated with higher odds of migraine headache, but the association was only observed in warm season (April-September). Higher levels of daily maximum 8-hour ozone and daily maximum 8-hour carbon monoxide appeared to be associated with higher odds of migraine headache onset in cold season (October-March). Although the associations for ozone and relative humidity were attenuated and no longer statistically significant in the overall GEE analysis, the differing associations by season remained.ConclusionsWe found that higher relative humidity was associated with higher odds of migraine headache onset in warm season, and traffic-related gaseous pollutants may be associated with higher odds of migraine headache onset in cold season.
| S-EPMC7523027 | biostudies-literature
Project description:BACKGROUND: The effect of ambient air pollution on global variations and trends in asthma prevalence is unclear. OBJECTIVES: Our goal was to investigate community-level associations between asthma prevalence data from the International Study of Asthma and Allergies in Childhood (ISAAC) and satellite-based estimates of particulate matter with aerodynamic diameter < 2.5 µm (PM?.?) and nitrogen dioxide (NO?), and modelled estimates of ozone. METHODS: We assigned satellite-based estimates of PM?.? and NO? at a spatial resolution of 0.1° × 0.1° and modeled estimates of ozone at a resolution of 1° × 1° to 183 ISAAC centers. We used center-level prevalence of severe asthma as the outcome and multilevel models to adjust for gross national income (GNI) and center- and country-level sex, climate, and population density. We examined associations (adjusting for GNI) between air pollution and asthma prevalence over time in centers with data from ISAAC Phase One (mid-1900s) and Phase Three (2001-2003). RESULTS: For the 13- to 14-year age group (128 centers in 28 countries), the estimated average within-country change in center-level asthma prevalence per 100 children per 10% increase in center-level PM?.? and NO? was -0.043 [95% confidence interval (CI): -0.139, 0.053] and 0.017 (95% CI: -0.030, 0.064) respectively. For ozone the estimated change in prevalence per parts per billion by volume was -0.116 (95% CI: -0.234, 0.001). Equivalent results for the 6- to 7-year age group (83 centers in 20 countries), though slightly different, were not significantly positive. For the 13- to 14-year age group, change in center-level asthma prevalence over time per 100 children per 10% increase in PM?.? from Phase One to Phase Three was -0.139 (95% CI: -0.347, 0.068). The corresponding association with ozone (per ppbV) was -0.171 (95% CI: -0.275, -0.067). CONCLUSION: In contrast to reports from within-community studies of individuals exposed to traffic pollution, we did not find evidence of a positive association between ambient air pollution and asthma prevalence as measured at the community level.
| S-EPMC3440118 | biostudies-literature
Project description:BackgroundAmbient air pollution is associated with systemic increases in oxidative stress, to which sperm are particularly sensitive. Although decrements in semen quality represent a key mechanism for impaired fecundability, prior research has not established a clear association between air pollution and semen quality. To address this, we evaluated the association between ambient air pollution and semen quality among men with moderate air pollution exposure.MethodsOf 501 couples in the LIFE study, 467 male partners provided one or more semen samples. Average residential exposure to criteria air pollutants and fine particle constituents in the 72 days before ejaculation was estimated using modified Community Multiscale Air Quality models. Generalized estimating equation models estimated the association between air pollutants and semen quality parameters (volume, count, percent hypo-osmotic swollen, motility, sperm head, morphology and sperm chromatin parameters). Models adjusted for age, body mass index, smoking and season.ResultsMost associations between air pollutants and semen parameters were small. However, associations were observed for an interquartile increase in fine particulates ≤2.5 µm and decreased sperm head size, including -0.22 (95% CI -0.34, -0.11) µm2 for area, -0.06 (95% CI -0.09, -0.03) µm for length and -0.09 (95% CI -0.19, -0.06) µm for perimeter. Fine particulates were also associated with 1.03 (95% CI 0.40, 1.66) greater percent sperm head with acrosome.ConclusionsAir pollution exposure was not associated with semen quality, except for sperm head parameters. Moderate levels of ambient air pollution may not be a major contributor to semen quality.
| S-EPMC5878741 | biostudies-literature
Project description:Whether exposure to outdoor air pollution increases the prevalence of rhinoconjunctivitis in children is unclear. Using data from Phase Three of the International Study of Asthma and Allergies in childhood (ISAAC), we investigated associations of rhinoconjunctivitis prevalence in adolescents with model-based estimates of ozone, and satellite-based estimates of fine (diameter?<?2.5 ?m) particulate matter (PM2.5) and nitrogen dioxide (NO2). Information on rhinoconjunctivitis (defined as self-reported nose symptoms without a cold or flu accompanied by itchy watery eyes in the past 12 months) was available on 505,400 children aged 13-14 years, in 183 centres in 83 countries. Centre-level prevalence estimates were calculated and linked geographically with estimates of long-term average concentrations of NO2, ozone and PM2.5. Multi-level models were fitted adjusting for population density, climate, sex and gross national income. Information on parental smoking, truck traffic and cooking fuel was available for a restricted set of centres (77 in 36 countries). Between centres within countries, the estimated change in rhinoconjunctivitis prevalence per 100 children was 0.171 (95% confidence interval: -?0.013, 0.354) per 10% increase in PM2.5, 0.096 (-?0.003, 0.195) per 10% increase in NO2 and -?0.186 (-?0.390, 0.018) per 1 ppbV increase in ozone. Between countries, rhinoconjunctivitis prevalence was significantly negatively associated with both ozone and PM2.5. In the restricted dataset, the latter association became less negative following adjustment for parental smoking and open fires for cooking. In conclusion, there were no significant within-country associations of rhinoconjunctivitis prevalence with study pollutants. Negative between-country associations with PM2.5 and ozone require further investigation.
| S-EPMC6097066 | biostudies-literature
Project description:BackgroundRecent studies suggest potential interactions of air pollutants with dietary factors and genetic susceptibility on mortality risk; however, evidence from prospective studies is still lacking. We aimed to assess the association between air pollution and mortality, and investigate the modification effects of a healthy diet and genetic susceptibility.MethodsA total of 386 937 participants were enrolled from 2006 to 2010 and followed up to 2018 in the UK Biobank study. The annual average air pollutant concentrations of particulate matter (PM) with diameters ≤2.5 (PM2.5), ≤10 (PM10) and between 2.5 and 10 µm (PM2.5-10) and nitrogen oxides (NO2 and NOx) were calculated and linked to participants' residential addresses. Healthy dietary patterns were evaluated by a healthy diet score (HDS) based on intakes of vegetables, fruit, fish, unprocessed red meat and processed meat. We also calculated genetic risk score (GRS) of the lifespan. We examined potential interactions by setting variable cross-product terms of air pollutants with diets or GRS in the models.ResultsWe identified 11 881 deaths [2426 from cardiovascular diseases (CVD), 1211 from coronary heart disease (CHD) and 466 from stroke] during a median follow-up of 8.9 years. We found that PM2.5 [hazard ratio (HR), 1.27; 95% CI, 1.05-1.55], PM10 (HR, 1.18; 95% CI, 1.04-1.34), NO2 (HR, 1.05; 95% CI, 1.01-1.08), and NOx (HR, 1.02; 95% CI, 1.01-1.03) were associated with all-cause mortality. PM2.5 was also associated with increased risks of CVD mortality (HR, 1.68; 95% CI, 1.10-2.56) and CHD mortality (HR, 2.08; 95% CI, 1.16-3.75). In addition, we found that adherence to healthy dietary patterns modified associations of PM2.5, NO2 and NOx with all-cause mortality (P-interaction = 0.006, 0.006 and 0.02, respectively). Among the individual dietary components, vegetable intakes showed interactions with PM2.5, NO2 and NOx (P-interaction = 0.007, 0.004 and 0.02, respectively). The associations between air pollutants and increased risks of all-cause mortality were attenuated among participants with higher vegetable intakes. We did not observe interactions between air pollutants and HDS on CVD, CHD or stroke mortality (P-interaction > 0.05). Besides, we did not find interactions between air pollutants and genetic risk for lifespan on mortality risk.ConclusionThis study provides evidence linking long-term exposure to various air pollutants to the risk of all-cause, CVD and CHD mortality, and the potential attenuation of a healthy diet, especially high vegetable intakes, on such relations. Our findings highlight the importance of adherence to a healthy diet in lowering ambient air-pollution-related mortality risk.
| S-EPMC9365625 | biostudies-literature
Project description:Purpose of reviewDuring the past century, exposure to particulate matter (PM) air pollution < 2.5 μm in diameter (PM2.5) has emerged as an all-pervading element of modern-day society. This increased exposure has come at the cost of heightened risk for cardiovascular (CV) morbidity and mortality. Not only can short-term PM2.5 exposure trigger acute CV events in susceptible individuals, but longer-term exposure over years augments CV risk to a greater extent in comparison with short-term exposure. The purpose of this review is to examine the available evidence for how ambient air pollution exposure may precipitate events at various time frames.Recent findingsRecent epidemiological studies have demonstrated an association between ambient PM2.5 exposure and the presence and progression of atherosclerosis in humans. Multiple animal exposure experiments over two decades have provided strong corroborative evidence that chronic exposure in fact does enhance the progression and perhaps vulnerability characteristics of atherosclerotic lesions. Evidence from epidemiological studies including surrogates of atherosclerosis, human translational studies, and mechanistic investigations utilizing animal studies have improved our understanding of how ambient air pollution may potentiate atherosclerosis and precipitate cardiovascular events. Even so, future research is needed to fully understand the contribution of different constituents in ambient air pollution-mediated atherosclerosis as well as how other systems may modulate the impact of exposure including adaptive immunity and the gut microbiome. Nevertheless, due to the billions of people continually exposed to PM2.5, the long-term pro-atherosclerotic effects of this ubiquitous air pollutant are likely to be of enormous and growing global public health importance.
| S-EPMC8379601 | biostudies-literature
Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.
| S-EPMC5089873 | biostudies-other