ライフサイエンスコーパス: PM2.5

1 tion to atmospheric fine particulate matter (PM2.5).

2 CI: 1.11, 1.17 per 10 mug/m(3) increment in PM2.5).

3 [1.005-1.016] for a 10 mug/m(3) increase in PM2.5).

4 15-1.41; per interquartile range increase in PM2.5).

5 ectancy at birth, attributable to changes in PM2.5.

6 activity) and indoor particulate matter (PM) PM2.5.

7 nd little evidence of associations with dust PM2.5.

8 , driven by sulfur dioxide emissions forming PM2.5.

9 ack carbon, and the elemental composition of PM2.5.

10 in the majority of paired indoor and outdoor PM2.5.

11 n concentrations of nitrogen dioxide than of PM2.5.

12 mum) and even potentially more harmful than PM2.5.

13 ently valid surrogate measure of exposure to PM2.5.

14 t toxic can help guide targeted reduction of PM2.5.

15 CI): 1.00, 1.04 per 10 mug/m(3) increment in PM2.5].

16 iameter), PM2.5 (</=2.5mum in diameter), and PM2.5-10 (between 2.5 and 10mum in diameter)] up to 2 ye

17 [95% CI: (0.64, 1.22)] for hazard ratio (HR) PM2.5-10.

18 matter with aerodynamic diameter <2.5microm (PM2.5) (1999-2004), nitrogen dioxide (NO2) (2006), and o

19 ebo, PM2.5 (250 mug/m(3)) under placebo, and PM2.5 (250 mug/m(3)) under B-vitamin supplementation (2.

20 d-exposure-experiment to sham under placebo, PM2.5 (250 mug/m(3)) under placebo, and PM2.5 (250 mug/m

21 one interquartile increase in 1-year average PM2.5= -7.39; 95%CI -14.17, -0.61).

22 avings for primary cooks, a 72% reduction in PM2.5, a 78% reduction in PAH levels, and significant re

23 r (PM2.5, PM10, and PMcoarse, respectively); PM2.5 absorbance; nitrogen oxides (NO2 and NOx); traffic

24 Each short-term increase of 10 mug/m3 in PM2.5 (adjusted by ozone) and 10 parts per billion (10-9

25 otic vasculopathy (FTV) both with increasing PM2.5 [adjusted odds ratio (aOR) = 5.5; 95% CI: 1.1, 26.

26 For each 10-mug/m(3) increment in PM2.5, adjusted hazard ratio (HR) with 95% confidence in

27 Interestingly, the PM2.5 aerosol concentration usually increases abruptly f

28 a show that the annual mean concentration of PM2.5 aerosol has been increasing steadily since the beg

29 er limit of 0.25 mg/m(3) in the annual mean PM2.5 aerosols concentration in the Owens Lake basin tha

30 the relation between prevalence of T2D with PM2.5 after adjustment for confounding factors.

31 ework to provide a set of consistent primary PM2.5 aggregated exposure factors.

32 an aerodynamic diameter of 2.5 mum or less (PM2.5) amount to approximately 22.5 million premature de

33 ge study, with stronger associations between PM2.5 and both outcomes among lower- versus higher-incom

34 PM2.5 and carbonaceous particle concentrations have been

35 c regression, we explored the association of PM2.5 and CO exposure with placental pathology.

36 PM2.5 and CO exposures were moderate [geometric means (G

37 We examined the association between PM2.5 and current level of depressive and anxiety sympto

38 e first multicity studies of source-specific PM2.5 and ED visits.

39 d a significant positive association between PM2.5 and heart disease mortality (hazard ratio, 1.16; 9

40 presentative sample, the association between PM2.5 and heart disease mortality was elevated and simil

41 ments, and can contribute a large portion of PM2.5 and its elemental components to a metro commuter's

42 Ambient levels of PM2.5 and its elemental components were compared to thos

43 ve assessed the relationship between ambient PM2.5 and LC among never smokers.

44 h children concomitantly exposed to prenatal PM2.5 and maternal stress had increased risk of asthma.

45 We found significant associations between PM2.5 and mortality in every model; however, relative ri

46 re similar in two-pollutant models including PM2.5 and NO2 and in three-pollutant models with O3.

47 soline-fuelled vehicles to emissions of both PM2.5 and NO2 emphasises the importance of further contr

48 acts (premature mortalities) attributable to PM2.5 and O3 from RC and EGU emissions by precursor spec

49 mbient measurements, in particular secondary PM2.5 and O3, have some level of contribution from other

50 Increases of 10 mug per cubic meter in PM2.5 and of 10 ppb in ozone were associated with increa

51 association between short-term exposures to PM2.5 and ozone (mean of daily exposure on the same day

52 ce of adverse effects related to exposure to PM2.5 and ozone at concentrations below current national

53 Daily PM2.5 and ozone levels in a 1-km x 1-km grid were estima

54 ions of nitrogen oxides (NOx), which are key PM2.5 and ozone precursors.

55 e of less than 50 ppb, the same increases in PM2.5 and ozone were associated with increases in the ri

56 istorical trend in the long-term exposure to PM2.5 and PM2.5-related premature mortality (PM2.5-morta

57 stimate associations between source-specific PM2.5 and respiratory disease ED visits.

58 timated associations between source-specific PM2.5 and respiratory disease emergency department (ED)

59 significant association between exposure to PM2.5 and risk of incident CKD, eGFR decline, and ESRD.

60 We assessed the association between PM2.5 and risk of LC using the Adventist Health and Smog

61 Emissions of PM2.5 and UFP from kerosene were also low compared with

62 tion=0.005), whereas the association between PM2.5 and wheeze was limited to lower-income participant

63 aving an aerodynamic diameter of </=2.5 mum (PM2.5) and adult mortality.

64 rsonal exposures to fine particulate matter (PM2.5) and carbon monoxide (CO) over 72 hr among a cohor

65 of 45% and 47% for fine particulate matter (PM2.5) and carbon monoxide (CO), respectively.

66 ire-originated fine particulate matter (fire-PM2.5) and CHVI.

67 matter </= 2.5 mum in aerodynamic diameter (PM2.5) and incidence and mortality of lung cancer (LC),

68 t concentrations of fine particulate matter (PM2.5) and ozone (O3).

69 with aerodynamic diameter less than 2.5 mum (PM2.5) and ozone at an approximate 11 km x 11 km resolut

70 xposures to ambient fine particulate matter (PM2.5) and ozone, and at levels below the current daily

71 nd 24 h PM of <2.5 mum aerodynamic diameter (PM2.5) and total suspended particulate (TSP) samples.

72 surface ozone (O3), fine particulate matter (PM2.5), and maximum temperature (TX) over the eastern Un

73 c diameter less than or equal to 2.5 microm (PM2.5), and temperature with the development of metaboli

74 t diet to airborne fine particulate matters (PM2.5), and then investigated the complex effects and me

75 shold, by +7 ppb for O3, +6 microg m(-3) for PM2.5, and +1.7 degrees C for TX.

76 )] for PM10, 0.97 [95% CI: (0.72, 1.32)] for PM2.5, and 0.88 [95% CI: (0.64, 1.22)] for hazard ratio

77 alk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index wit

78 sses are used to estimate embedded NOx, SO2, PM2.5, and CO2 emissions on a cubic meter basis.

79 Estimating state-specific contributions to PM2.5- and O3-related health burden from residential com

80 llion tons) are associated with about 38,000 PM2.5- and ozone-related premature deaths globally in 20

81 rkets, avoiding approximately 174,000 global PM2.5- and ozone-related premature deaths in 2040.

82 Determining which sources of PM2.5 are most toxic can help guide targeted reduction o

83 matter <2.5 microm in aerodynamic diameter (PM2.5) are associated with increased risk of cardiovascu

84 We also found significant PM2.5-associated elevated risks for cardiovascular and l

85 atory disease ED visits with biomass burning PM2.5; associations with diesel and gasoline PM2.5 were

86 some of the largest estimated reductions in PM2.5-attributable deaths.

87 responding change in population exposure and PM2.5-attributable risk of death prior to the year 2000

88 strument for particulate matter </= 2.5 mum (PM2.5), black carbon (BC), or nitrogen dioxide (NO2) var

89 PM2.5-bound trace microbial elements, such as lipopolysa

90 ollution episodes, starting with a period of PM2.5 buildup and followed by a period with plateauing c

91 d with long-term exposure to fine particles (PM2.5), but to date, no such studies have been reported

92 d 0.5 mug m(-3) for fine particulate matter (PM2.5), but widespread.

93 67% (95% CI: 50% to 77%) reduction in indoor PM2.5, but no change was observed with the improved-tech

94 Subsequent daytime mixing enhances surface PM2.5 by dispersing the aerosol throughout the PCAP.

95 l soils could reduce O3 by up to 2.4 ppb and PM2.5 by up to 0.15 mug/m(3) in some regions.

96 annual estimates of fine particulate matter (PM2.5) by census tract.

97 late matter with diameter less than 2.5 mum (PM2.5) by up to 33.2 mug m(-3) (25.1%) and 11.0 mug m(-3

98 meters equal to or less than 2.5 mum, called PM2.5) can affect the surface energy balance and atmosph

99 F1 mice were exposed to concentrated ambient PM2.5 (CAPs) or filtered air (FA) throughout pregnancy [

100 Exposure to PM2.5 caused 4.2 million (95% uncertainty interval [UI]

101 TAPI PM2.5 CEM measurements were statistically similar to the

102 Reported PM2.5-CO correlations (r) were lower for personal exposu

103 old air pollution and the consistency of the PM2.5-CO relationship across different study settings an

104 s suggest that most of the health effects of PM2.5 come from PM1.

105 ls, we estimated associations of mean annual PM2.5 concentration and temperature with risk of inciden

106 80 microg/m(3), which is double the average PM2.5 concentration in Xiamen during the winter.

107 A 1-mug/m(3) increase in mean annual PM2.5 concentration was associated with a higher risk of

108 ] microg/m(3)), a 10-microg/m(3) increase in PM2.5 concentration was associated with increased risk o

109 rying analyses, a 10-microg/m(3) increase in PM2.5 concentration was associated with similarly increa

110 ed for each 10-mug/m(3) increment in ambient PM2.5 concentration.

111 the association remained when all days with PM2.5 concentrations > 30 mug/m3 were excluded from the

112 rvival models to evaluate the association of PM2.5 concentrations and risk of incident eGFR <60 ml/mi

113 nalyses showed a linear relationship between PM2.5 concentrations and risk of kidney outcomes.

114 We estimated annual mean county-level PM2.5 concentrations in 1980, 1990, 2000, and 2010 using

115 as defined at baseline as the annual average PM2.5 concentrations in 2004, and separately as time-var

116 stimate the effects of ambient daily PM1 and PM2.5 concentrations on emergency hospital visits in Chi

117 to estimate daily 24 h averaged ground-level PM2.5 concentrations over the conterminous United States

118 The observations showed that higher PM2.5 concentrations over the urban area corresponded to

119 he UHI intensity due to PM2.5 via the higher PM2.5 concentrations present in the urban region than th

120 chical framework to explain the variation of PM2.5 concentrations together with other factors, such a

121 PM1 and PM2.5 concentrations were significantly associated with

122 used a new technique to estimate historical PM2.5 concentrations, and estimated the effects of chang

123 To estimate PM2.5 concentrations, many parametric regression models

124 faces, can have complex impacts on ozone and PM2.5 concentrations.

125 exposure to ambient fine particulate matter (PM2.5) concentrations has been associated with increased

126 to the local soil both in indoor and outdoor PM2.5 demonstrating their noncrustal origins.

127 orological data of China in 2015 showed that PM2.5 driven by cold surges from the ground level could

128 s by testing the hypothesis that exposure to PM2.5 during discrete periods of pregnancy results in PT

129 associated with average weekly exposures to PM2.5 during pregnancy, allowing the identification of c

130 inhalation of fine-sized particulate matter (PM2.5) during pregnancy with preterm birth (PTB) and low

131 B-vitamin supplementation attenuated PM2.5 effect on HR by 150% (P = 0.003), low-frequency po

132 whether B vitamin supplementation mitigates PM2.5 effects on cardiac autonomic dysfunction and infla

133 min metro commute to daily mean exposure to PM2.5 elemental and mass concentrations.

134 PM2.5 emission factors were approximately 3 times higher

135 er year from RC emissions, driven by primary PM2.5 emissions.

136 tified using well-established cutoffs; daily PM2.5 estimates were obtained using spatiotemporal model

137 l to improve the accuracy of satellite-based PM2.5 estimates.

138 mortality was ten-fold greater than that of PM2.5 even before the widespread use of diesel particle

139 PM2.5 explained 6.3% of the spatial variation in obesity

140 we examined the association between chronic PM2.5 exposure and cause-specific mortality.

141 association between both long-term ozone and PM2.5 exposure and depression onset.

142 Based on the directly measured PM2.5 exposure and questionnaire data of indoor pollutio

143 e then estimated the association between the PM2.5 exposure and skin aging manifestations by linear r

144 The mean level of PM2.5 exposure during 2000-2005 was 43.7 mug/m(3) (rangi

145 significantly and inversely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord

146 We investigated PM2.5 exposure during pregnancy and lifetime and postneo

147 Maternal residential PM2.5 exposure during pregnancy was estimated using a hi

148 Prenatal PM2.5 exposure during sensitive windows is associated wi

149 A 5-microg/m3 increment in PM2.5 exposure during the entire pregnancy was associate

150 , we built a regression model to predict the PM2.5 exposure in larger datasets including an initial e

151 rovide important new evidence that long-term PM2.5 exposure is significantly related to increased mor

152 examination group, we showed that the indoor PM2.5 exposure levels were positively associated with sk

153 s to identify sensitive windows for prenatal PM2.5 exposure on children's asthma by age 6 years, and

154 The counteractive effect of PM2.5 exposure on high-fat diet-induced hepatic steatosi

155 However, PM2.5 exposure relieved hepatic steatosis in high-fat di

156 In healthy adults, two-hour PM2.5 exposure substantially increases HR, reduces HRV,

157 tile-range increase (1.3 mug/m3) in lifetime PM2.5 exposure were 2.66 (95% confidence interval (CI):

158 antified the individual and joint effects of PM2.5 exposure with MPBMI on COWO, defined as the child'

159 public health policy relevance of early life PM2.5 exposure.

160 eased between-subject variability in chronic PM2.5 exposure.

161 ips particularly in the context of long-term PM2.5 exposure.

162 the relationship of long-term fine particle (PM2.5) exposure and DNA methylation age (DNAm-age)-a nov

163 tive associations of 12-month moving average PM2.5 exposures (per 10-mug/m3 increase) with respirator

164 Our estimates suggest that declines in PM2.5 exposures between 1980 and 2010 have benefitted pu

165 Between 1980 and 2010, population-weighted PM2.5 exposures fell by about half, and the estimated nu

166 Higher NO2 and PM2.5 exposures over follow-up were also associated with

167 ple, an elevation in 60-month moving average PM2.5 exposures was linked to 1.33 times the lung cancer

168 Daily PM2.5 exposures were estimated using the Community Multi

169 ly concentrations of primary source-specific PM2.5 for four U.S. cities.

170 n ranging between 0.3 and 6.5 ng/m(3) in the PM2.5 fraction.

171 We found that PM2.5 from biomass burning, diesel vehicle, gasoline veh

172 in chemical composition between cities, but PM2.5 from coal combustion and metal sources varied acro

173 Exposure to fine particulate matter (PM2.5) from indoor and outdoor sources is a leading envi

174 Mothers who were exposed to higher levels of PM2.5 gave birth to newborns with shorter telomere lengt

175 providing evidence that indoor metal-bearing PM2.5 had predominantly outdoor origins.

176 n of obese mothers exposed to high levels of PM2.5 had the highest risk of COWO [RR>/=2.0, relative e

177 ulate matter with aerodynamic diameter <2.5 (PM2.5) had adverse effects on longitudinal measures of i

178 decades, correlations between population and PM2.5 have become weaker in Europe and North America due

179 1.00, 1.12; per 10-mug/m3 increase in 1-year PM2.5, HR = 1.08; 95% CI: 0.97, 1.20).

180 or ozone, HR = 1.08; 95% CI: 1.02, 1.14; for PM2.5, HR = 1.12; 95% CI: 1.00, 1.25).

181 prevalence was significantly associated with PM2.5 in males (R(2) = 11.1%, P < 0.0001) and females (R

182 a temporary increase in the concentration of PM2.5 in Shanghai.

183 exposure to CO as a surrogate of exposure to PM2.5 in studies of household air pollution and the cons

184 s been widely used as a surrogate measure of PM2.5 in studies of household air pollution.

185 Subsequently, the concentration of PM2.5 in Xiamen increased to a high of 80 microg/m(3), w

186 -3) for annual mean fine particulate matter (PM2.5) in northern Vietnam and up to 15 ppb for seasonal

187 Deaths attributable to ambient PM2.5 increased from 3.5 million (95% UI 3.0 million to

188 upportive evidence that lifetime exposure to PM2.5 increases risk of infant mortality.

189 igation revealed that inhalation exposure to PM2.5 induced hepatic autophagy in mouse livers in a man

190 duced hepatic steatosis was mediated through PM2.5-induced hepatic autophagy.

191 Adverse PM2.5-induced outcomes such as PTB and LBW are dependent

192 ty deterioration were examined by collecting PM2.5 inside and outside a mechanically ventilated high

193 d behavioral covariates and decomposition of PM2.5 into 2 spatiotemporal scales.

194 statistical models to estimate ground-level PM2.5 is a promising way to fill the areas that are not

195 ties with population >/= 50,000, exposure to PM2.5 is associated with increased risk for respiratory

196 rth outcomes, the individual contribution of PM2.5 is comparable in magnitude to any single individua

197 sources is difficult because source-specific PM2.5 is not directly measured, and source chemical comp

198 s mechanism has not been well explained yet, PM2.5 is recognized to exacerbate asthma.

199 Ambient fine particulate matter (PM2.5) is among the most prevalent sources of environmen

200 exposure to ambient fine particulate matter (PM2.5) is associated with mortality.

201 Fine particulate matter (PM2.5) is thought to be responsible for many of these he

202 le range [1.7 mug/m(3)] increase in prenatal PM2.5 level) during which children concomitantly exposed

203 showed a dose-response relationship between PM2.5 levels and COWO after a threshold near the median

204 s and PM2.5 to evaluate associations between PM2.5 levels and hospitalization risk in single-pollutan

205 hborhoods with worse air quality-with higher PM2.5 levels and/or temperatures than average-showed inc

206 Of all case and control days, 93.6% had PM2.5 levels below 25 mug/m3, during which 95.2% of deat

207 sting blood glucose remained significant for PM2.5 levels below the Environmental Protection Agency's

208 Annual average PM2.5 levels for the years 1990, 1995, 2000, and 2005 we

209 ants followed from 1982 to 2004 and assigned PM2.5 levels to all participants using seven different e

210 ongitudinal BACH/Bone study, baseline BC and PM2.5 levels were associated with lower serum PTH (Estim

211 3-2010; (ii) long-term black carbon [BC] and PM2.5 levels, serum calcium homeostasis biomarkers (para

212 ntary studies of: (i) long-term PM <2.5 mum (PM2.5) levels and osteoporosis-related fracture hospital

213 of PM [PM10 (</=10mum microns in diameter), PM2.5 (</=2.5mum in diameter), and PM2.5-10 (between 2.5

214 ndestructive analysis of particulate matter (PM2.5) mass concentration.

215 These results suggest that urban PM2.5 may exacerbate allergic inflammation in the murine

216 and 2.21 ppm (1.47) respectively]; 88.6% of PM2.5 measurements exceeded World Health Organization ai

217 utional layers for land use terms and nearby PM2.5 measurements increase CV R(2) by approximately 0.0

218 ere statistically similar to the other three PM2.5 methods.

219 from diseases of the circulatory system for PM2.5 modeled from RS with that for PM2.5 modeled using

220 stem for PM2.5 modeled from RS with that for PM2.5 modeled using ground-level information.

221 e year 2000 is made difficult by the lack of PM2.5 monitoring data.

222 ill the areas that are not covered by ground PM2.5 monitors.

223 PM2.5-mortalities in developed regions (i.e., Europe and

224 Estimated PM2.5-mortalities in East Asia and South Asia increased

225 erms were used to examine differences in the PM2.5-mortality association by race/ethnicity.

226 (NH3), and primary PM are estimated from the PM2.5-mortality responses to the emission variations.

227 PM2.5 and PM2.5-related premature mortality (PM2.5-mortality) and its response to changes in emission

228 by Health Effects Institute to estimate the PM2.5-mortality.

229 te matter with aerodynamic diameter <2.5mum (PM2.5), nitrogen oxides], greenness [Normalized Differen

230 In summary, PM2.5 noticeably impacts UHI intensity, which should be

231 restricted to person-years with exposure to PM2.5 of less than 12 mug per cubic meter and ozone of l

232 cts and mechanisms of inhalation exposure to PM2.5 on hepatic steatosis, a precursor or manifestation

233 amic diameter less than or equal to 2.5 mum (PM2.5)) on respiratory disease and lung cancer mortality

234 ticulate matter with a diameter of <2.5 mum [PM2.5] or 2.5-10 mum [PM10]), lag, and outcome, and pres

235 In WT mice, PM2.5 + OVA exacerbated OVA-related lung eosinophilia.

236 /c mice were intratracheally challenged with PM2.5 +/- ovalbumin (OVA) four times at 2-week intervals

237 cific mortality due to long-term exposure to PM2.5 over the exposure range experienced in China and o

238 Measurements of aerosol concentration (PM2.5 particle matter) in the Owens Lake salty playa sho

239 Maternal residential PM2.5 (particles with an aerodynamic diameter </=2.5 mum

240 l smoking during pregnancy; season of birth; PM2.5 (particulate matter </=2.5mm in aerodynamic diamet

241 m the off-road sector and (b) an increase in PM2.5 (particulate matter 2.5 mum or less in diameter) e

242 diameter <1 mum), which are a major part of PM2.5 (particulate matter with aerodynamic diameter <2.5

243 Pollutants measured included PM2.5 (PM = particulate matter), PM10, ultrafine particl

244 2.5mum, </=10mum, and 2.5-10mum in diameter (PM2.5, PM10, and PMcoarse, respectively); PM2.5 absorban

245 sts are based on emissions of CO2, CH4, N2O, PM2.5, PM10, NOx, SO2, VOC, CO, NH3, Hg, Pb, Cd, Cr (VI)

246 mic diameter <2.5mum, 2.5-10mum, and <10mum (PM2.5, PMcoarse, and PM10, respectively) and nitrogen di

247 ational exports and interprovincial trade on PM2.5 pollution and public health across China.

248 eal that the transboundary health impacts of PM2.5 pollution associated with international trade are

249 This leads to distinct stages of PM2.5 pollution episodes, starting with a period of PM2.

250 the 3.45 million premature deaths related to PM2.5 pollution in 2007 worldwide, about 12 per cent (41

251 ated 1.10 million premature deaths caused by PM2.5 pollution throughout China, nearly 19% (208,500 de

252 Slightly higher RRs of ambient PM1 and PM2.5 pollution were noted among women and children than

253 China could be attributed to ambient PM1 and PM2.5 pollution, respectively.

254 mortality caused by fine particulate matter (PM2.5) pollution as a result of atmospheric transport an

255 Ambient fine particle (PM2.5) pollution triggers acute cardiovascular events.

256 ons, and estimated the effects of changes in PM2.5 population exposures on mortality in adults (age >

257 PM2.5 precursor emissions have declined over the course

258 Exposures were estimated from PM2.5-prediction models based on satellite imagery.

259 High levels of PM2.5 probably contribute to increased T2D prevalence in

260 trend in the long-term exposure to PM2.5 and PM2.5-related premature mortality (PM2.5-mortality) and

261 Historical trends in PM2.5-related premature mortality during 1990-2010 acros

262 Exposure to high environmental levels of PM2.5 (relative to the USA) may explain the disproportio

263 mice fed normal chow to concentrated ambient PM2.5 repressed hepatic transcriptional regulators invol

264 h for comparing the chemical compositions of PM2.5 sources across cities and conducted one of the fir

265 Across four U.S. cities, among the primary PM2.5 sources assessed, biomass burning PM2.5 was most s

266 the chemical composition of primary ambient PM2.5 sources varies across cities.

267 l model predictions of both O3 and secondary PM2.5 species.

268 y, race, poverty, education and temperature, PM2.5 still explained 8.3% of the residual variation in

269 n of PM2.5 sulfate ion to the sum of SO2 and PM2.5 sulfate ion by distance from the source compared w

270 imilar patterns of an increasing fraction of PM2.5 sulfate ion to the sum of SO2 and PM2.5 sulfate io

271 omparing the highest and lowest quartiles of PM2.5, the adjusted relative risks (RRs) [95% confidence

272 For PM2.5, the risk of death among men, blacks, and people w

273 in the areas where the contribution of fire-PM2.5 to annual average ambient PM2.5 was high (>1.5 mug

274 series analysis of hospitalization rates and PM2.5 to evaluate associations between PM2.5 levels and

275 occur in the most polluted countries unless PM2.5 values are decreased substantially, but there is p

276 ed the weakening of the UHI intensity due to PM2.5 via the higher PM2.5 concentrations present in the

277 ll cities was 42.5 mug/m(3) (SD 34.6) and of PM2.5 was 51.9 mug/m(3) (41.5).

278 A 10 mug/m(3) increase in same-day PM2.5 was associated with a 0.47% (95% CI 0.34-0.61) inc

279 PM2.5 was associated with depressive and anxiety symptom

280 Long-term exposure to PM2.5 was associated with nonaccidental, CVD, lung cance

281 tion of fire-PM2.5 to annual average ambient PM2.5 was high (>1.5 mug/m(3)) and that 10.3 million ind

282 en-induced lung eosinophilia caused by urban PM2.5 was investigated.

283 mary PM2.5 sources assessed, biomass burning PM2.5 was most strongly associated with respiratory heal

284 adjusting for socioeconomic measures (SES); PM2.5 was positively associated with depressive symptoms

285 An increase in PM2.5 was significantly associated with anxiety symptoms

286 idering mental health as chronic conditions, PM2.5 was significantly associated with incident depress

287 ness of breath and a 5-mug/m(3) increment in PM2.5 was significantly higher for individuals from lowe

288 PM2.5 was significantly positively associated with death

289 Ambient PM2.5 was the fifth-ranking mortality risk factor in 201

290 4.30%) increase per 10-mug/m(3) increase in PM2.5, was observed in the least-urban counties; in the

291 Higher NO2 and PM2.5 were associated with a faster decline in SI and a

292 PM2.5; associations with diesel and gasoline PM2.5 were frequently imprecise or consistent with the n

293 talization risk per 10-mug/m(3) increment in PM2.5 were observed in the least-urban and most-urban co

294 amic diameter less than or equal to 2.5 mum (PM2.5) were predicted at each participant's residence us

295 ion (10-9) in warm-season ozone (adjusted by PM2.5) were statistically significantly associated with

296 relative risks (RRs) for the association of PM2.5 with circulatory mortality and ischemic heart dise

297 ear mixed-effects models, the association of PM2.5 with DNAm-age (in years) was significantly diminis

298 bundance, mediated 12% of the association of PM2.5 with DNAm-age.

299 cardiovascular hospitalizations and same-day PM2.5 with higher risk in urban counties: 0.35% [95% pos

300 he association between long-term exposure to PM2.5 with nonaccidental and cause-specific mortality in