ライフサイエンスコーパス: PM2.5

1 er (PM) with aerodynamic diameter < 2.5 mum (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 exposure to ambient fine particulate matter (PM2.5).

6 O2) and decreased methylation in cg17629796 (PM2.5).

7 and cause-specific mortality associated with PM2.5.

8 f the outcome and lagged exposure effects of PM2.5.

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

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

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

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

13 ung cancer were consistently associated with PM2.5.

14 per 3 parts per billion [95% CI, 0.03-0.24]; PM2.5: 0.11 per 2 mug/m3 [95% CI, 0.03-0.19]; NOx: 0.06

15 exposed to real-world inhaled, concentrated PM2.5 (~10 times ambient levels/~60-120 mug/m3) or filte

16 verage HOMA-IR values when lagged 6-18 h for PM2.5, 15-19 h for BC, and 6-15 h for UFPs, with positiv

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

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

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

20 We ran Cox proportional hazards models for PM2.5 adjusted for eight subject-level indicators of soc

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

22 cted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also expl

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

24 (CI): 1.041, 1.065] per 10-mug/m3 change in PM2.5 after pooling the three cohort-specific hazard rat

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

26 Exposure to PM2.5 air pollution contributes to lung cancer incidence

27 association between fine particulate matter (PM2.5) air pollution and lung cancer.

28 Whether PM2.5 alters brain structure and accelerates the preclin

29 ve association between a 3-y running mean of PM2.5 and an overall incident MI with an HR = 1.20 (95%

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

31 s were used to estimate associations between PM2.5 and cancer incidence for selected cancers while co

32 PM2.5 and carbonaceous particle concentrations have been

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

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

35 Associations between PM2.5 and FeNO were consistently higher among individual

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

37 the exposure-response relationships between PM2.5 and hospital admissions was observed.

38 that examines potential associations between PM2.5 and incidence of non-lung cancers is limited.

39 sources through changes in concentrations of PM2.5 and its major components [nitrates, sulfates, elem

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

41 coronary heart disease, although evidence on PM2.5 and myocardial infarction (MI) incidence is mixed.

42 PM2.5 and NO2 were associated with breast cancer overall

43 concentration-response relationship between PM2.5 and nonaccidental mortality in three Canadian Cens

44 concentration-response relationship between PM2.5 and nonaccidental mortality.

45 Mean ambient concentrations of PM2.5 and NOx, but not O3, decreased substantially durin

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

47 Mortality associated with long-term PM2.5 and ozone exposure increased substantially at low

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

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

50 e, but we observed positive associations for PM2.5 and PM10 with fatal MI.

51 .5 mum and < 10 mum in aerodynamic diameter (PM2.5 and PM10, respectively) and nitrogen dioxide (NO2)

52 < 2.5 and < 10 mum in aerodynamic diameter (PM2.5 and PM10, respectively) and the above psychiatric

53 yses suggested stronger associations between PM2.5 and poor cognitive impairment in men than women.

54 sociation between acute exposures to ambient PM2.5 and psychiatric emergency department (ED) utilizat

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

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

57 ot observe a significant interaction between PM2.5 and sex.

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

59 pecific short-term association between daily PM2.5 and years of life lost (YLL); at the second stage,

60 erved significant associations between daily PM2.5 and YLL: each 10 mug/m3 increase in three-day-aver

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

62 re to fine particulate matter < 2.5 microns (PM2.5) and physical activity in the association with CVD

63 matter with aerodynamic diameter <= 2.5 mum (PM2.5) and poor cognitive function is lacking in develop

64 tter with an aerodynamic diameter <=2.5 mum (PM2.5)) and risk of gestational diabetes mellitus (GDM),

65 with diameters of <= 10 mum (PM10), 2.5 mum (PM2.5), and 1 mum (PM1) using satellite remote-sensing b

66 amic diameter less than or equal to 2.5 mum (PM2.5), and mortality from renal failure (RF) among part

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

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

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

70 1.32) for PM1, 1.52 (95% CI: 1.46, 1.58) for PM2.5, and 1.22 (95% CI: 1.17, 1.27) for PM10] than thos

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

72 ddition, higher exposures to acid vapor, EC, PM2.5, and non-freeway NOx were all associated with high

73 analyses, particulate (PNC, PM10, PMcoarse, PM2.5, and PM2.5abs) and gaseous (NOx, NO2) pollutants w

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

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

76 ain air pollutants (fine particulate matter [PM2.5] and ozone) and cause-specific risk of hospital ad

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

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

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

80 ual variables and 3-y moving-average ambient PM2.5 at a 1 x 1 km spatial resolution from 1988 to 2015

81 a, decreases in ambient nitrogen dioxide and PM2.5 between 1993 and 2014 were significantly associate

82 with an aerodynamic diameter of <= 2.5 mum (PM2.5), black carbon (BC), ultrafine particles (UFPs), a

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

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

85 matter with aerodynamic diameter <= 2.5 mum (PM2.5), carbon monoxide (CO), and black carbon (BC), and

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

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

88 assign participants to clusters derived from PM2.5 component profiles to evaluate the impact of heter

89 For an interquartile-range increase in PM2.5 concentration (3.22 mug/m3), hazard ratios for RF

90 PM2.5 concentration at the residential address of each p

91 stimate the annual average satellite-derived PM2.5 concentration for the geocoded location of the par

92 At any PM2.5 concentration, life expectancy loss was, on averag

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

94 utable to a higher-than-standards daily mean PM2.5 concentration.

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

96 the health and longevity impacts of current PM2.5 concentrations and the benefits of reductions from

97 For households boiling with biomass, modeled PM2.5 concentrations averaged 79 mug/m3 (standard deviat

98 ug/m3 increase in three-day-averaged (lag02) PM2.5 concentrations corresponded to an increment of 0.4

99 We used calculated changes in ambient PM2.5 concentrations for the period 2009-2014, with newl

100 cal variables from 5 monitoring stations and PM2.5 concentrations from 11 sites were used to estimate

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

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

103 The annual average PM2.5 concentrations ranged from 1.6 to 9.0 mug/m3, whic

104 013, with satellite-retrieved annual average PM2.5 concentrations to each postcode.

105 County-level PM2.5 concentrations were estimated using integrated emp

106 PM1 and PM2.5 concentrations were significantly associated with

107 Ambient O3 and NOx concentrations, but not PM2.5 concentrations, during follow-up were also signifi

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

109 ld be achieved by a reduction in the ambient PM2.5 concentrations.

110 evel population characteristics and baseline PM2.5 concentrations.

111 to log-transformed fine particulate matter (PM2.5) concentrations among cooks (beta = -0.089, p = 0.

112 e to a low level of fine particulate matter (PM2.5) concentrations.

113 e matter <= 2.5 mum in aerodynamic diameter (PM2.5) concentrations.

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

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

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

117 te matter <=2.5 mum in aerodynamic diameter (PM2.5)) during pregnancy is associated with preterm birt

118 (95% CI: 1.0% to 30.3%) of the total adverse PM2.5 effects on Trials 1-3 and List B, respectively.

119 PM2.5 emission factors were approximately 3 times higher

120 An interquartile-range increase in PM2.5 exposure (33.84 mug/m3 for trimester 1 and 33.23 m

121 ariable linear regression to examine average PM2.5 exposure across pregnancy in relation to PNS withd

122 investigating associations between long-term PM2.5 exposure and anxiety also reported statistically s

123 s of possible associations between long-term PM2.5 exposure and anxiety and between short-term PM10 e

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

125 associations between long-term ( > 6 months) PM2.5 exposure and depression (n = 5 studies), the poole

126 pothesis of an association between long-term PM2.5 exposure and depression, as well as supporting hyp

127 us (GDM), while the association between high PM2.5 exposure and GDM risk has not been well studied.

128 e associations were found between short-term PM2.5 exposure and hospital admissions for 7 major disea

129 has quantified the association between daily PM2.5 exposure and life expectancy.

130 atistically significant interactions between PM2.5 exposure and physical activity (overall, walking,

131 ions of 24-months moving average residential PM2.5 exposure and physical activity updated every 4 y a

132 multiplicative interaction between long-term PM2.5 exposure and physical activity; higher physical ac

133 dentify critical exposure windows for weekly PM2.5 exposure and PTB in California using California bi

134 %-0.54%) of YLL could be attributable to the PM2.5 exposure at the national level.

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

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

137 PM2.5 exposure during pregnancy for each participant was

138 Our findings suggest that high PM2.5 exposure during pregnancy increases blood glucose

139 We investigated the association of high PM2.5 exposure during pregnancy with blood glucose level

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

141 An interquartile-range increment of PM2.5 exposure during trimester 1 increased 1-hour and 2

142 The same increment of PM2.5 exposure during trimester 2 increased fasting gluc

143 help characterize potential contributions of PM2.5 exposure from background concentration.

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

145 nblinded nature of the intervention, limited PM2.5 exposure measurement, and a reliance on reported i

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

147 For a 10-mug/m3 increase in PM2.5 exposure over the entire period of gestation, PTB

148 tiotemporal model to estimate 3-year average PM2.5 exposure preceding MRI-1.

149 The mean 3-y annual average estimate of PM2.5 exposure ranged from 6.7 to 8.0 mug/m3 over the th

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

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

152 others may be more susceptible to effects of PM2.5 exposure than non-Hispanic white mothers, particul

153 heatwaves may also act synergistically with PM2.5 exposure to increase risk of preterm birth, which

154 ch 1-mug/m3 increase in long- and short-term PM2.5 exposure was associated with 35.4 (95% confidence

155 Long-term PM2.5 exposure was associated with increased Alzheimer's

156 In fully adjusted models, PM2.5 exposure was associated with modest increased risk

157 tude of transcriptional change detected with PM2.5 exposure was lower than that observed with a HFD,

158 alteration in chromatin accessibility after PM2.5 exposure was significant.

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

160 to investigate the association of long-term PM2.5 exposure with total mortality and cause-specific (

161 WI/SNF complex) was regulated in response to PM2.5 exposure, the cessation of which was associated wi

162 t spatial-temporal variations in relation to PM2.5 exposure.

163 by the unavailability of data on individual PM2.5 exposure.

164 e associated with increased vulnerability to PM2.5 exposure.

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

166 causally or likely to be causally related to PM2.5 exposure.

167 risk and overall mortality at all levels of PM2.5 exposure.

168 atter [PM < 2.5 mum in aerodynamic diameter (PM2.5)], exposure during the final gestational week on p

169 Combined effects of PM2.5 exposures and heatwaves appeared to be synergistic

170 sed to estimate the effects of heatwaves and PM2.5 exposures during the final week on preterm birth,

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

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

173 r a psychiatric ED visit 0-3 d after ambient PM2.5 exposures, estimated at residential addresses usin

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

175 ate ratios (IRRs), per 10-mug/m3 increase in PM2.5, for all and lung cancer were 1.09 (95% CI: 1.03,

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

177 e incidence rates from 1992-2016 and average PM2.5 from 1988-2015 were estimated.

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

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

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

181 e expectancy (PGLE) by assuming that ambient PM2.5 has met the Chinese National Ambient Air Quality S

182 te matter < 2.5 mum in aerodynamic diameter (PM2.5) has been associated with adult psychiatric exacer

183 adults, exposure to fine particulate matter (PM2.5) has been associated with reduced heart rate varia

184 t concentrations of fine particulate matter (PM2.5) have contributed to reductions in cardiovascular

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

186 uce a total burden of 33 DALYs, dominated by PM2.5 impacts from rail transport emissions (32 DALYs).

187 Exposure to PM2.5 impaired glucose and insulin tolerance and reduced

188 ficantly positively associated with same-day PM2.5 in both single- and 2-pollutant models, including

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

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

191 ed models we found that a 1-unit increase in PM2.5 (in micrograms per cubic meter) was associated wit

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

193 ss than 10 mum (PM10) and less than 2.5 mum (PM2.5) in the baseline year for each of 3 cohorts.

194 he pooled odds ratio was 1.102 per 10-mug/m3 PM2.5 increase (95% CI: 1.023, 1.189; I2 = 0.00%).

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

196 wered mortality in all but 14 counties where PM2.5 increased slightly.

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

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

199 lution with aerodynamic diameter <= 2.5 mum (PM2.5) is an important contributor to the global burden

200 posure to fine particulate matter pollution (PM2.5) is hazardous to health.

201 Ambient fine particulate matter pollution (PM2.5) is one leading cause of disease burden, but no st

202 iculate matter smaller than 2.5 mum in size (PM2.5) is the world's leading environmental risk factor

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

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

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

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

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

208 ry mortality in Queensland, Australia, where PM2.5 levels were measured well below the WHO air qualit

209 3-2010; (ii) long-term black carbon [BC] and PM2.5 levels, serum calcium homeostasis biomarkers (para

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

211 Compared to the lowest quartile of PM2.5 ( < 41.4 mug/m3), adjusted HR values were 1.20 (95

212 Prenatal exposure to PM2.5 may disrupt cardiac vagal tone during infancy.

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

214 e matter with aerodynamic diameter <2.5 mum (PM2.5) may increase the risk for Alzheimer's disease and

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

216 Long-term exposure to atmospheric PM2.5 might be an important risk factor for RF mortality

217 evaluate the impact of heterogeneity in the PM2.5 mixture.

218 Our findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of

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

220 Ambient concentrations of O3, PM2.5, NOx, and black carbon at study baseline were sign

221 e-specific air pollutant concentrations (O3, PM2.5, NOx, and black carbon) were estimated by validate

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

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

224 We investigated the effects of PM2.5 on phenotype, the transcriptome, and chromatin acc

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

226 Invasive breast cancer was associated with PM2.5 only in the Western United States [HR = 1.14 (95%

227 the nurses' residences since 1990 (PM10 and PM2.5) or 1970 (NO2 and NOx) were estimated using the Da

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

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

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

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

232 amic diameter less than or equal to 2.5 mum (PM2.5), ozone, and nitrogen dioxide with all-cause morta

233 We found that long- and short-term PM2.5, ozone, and nitrogen dioxide exposures were all as

234 e matter <= 2.5 mum in aerodynamic diameter (PM2.5) partially mediated the estimated associations.

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

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

237 te matter (PM) with a diameter < 2.5 mug/m3 (PM2.5), PM10, nitrogen dioxide (NO2), and nitrogen oxide

238 reases of 5.3, 5.5, 8.1, and 11.5 mug/m3 for PM2.5, PM10, NO2, and NOx, respectively.

239 no association between long-term exposure to PM2.5, PM10, NO2, or NOx and overall MI incidence, but w

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

241 lity and life expectancy loss due to current PM2.5 pollution and the benefits of reductions since 199

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

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

244 he use of county-specific random intercepts, PM2.5 pollution in excess of the lowest observed concent

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

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

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

248 PM2.5 precursor emissions have declined over the course

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

250 PM2.5 reductions represented 5.7% of the overall decline

251 cal study of emission sector contribution to PM2.5-related mortality, we found that reductions in sul

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

253 mass index (aircraft, road traffic Lden, and PM2.5), renal function and "allostatic load" (all exposu

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

255 ), and fourth ( >= 60.7 mug/m3) quartiles of PM2.5, respectively (p for trend < 0.001).

256 c diameter of <= 10 mum or 2.5 mum (PM10 and PM2.5, respectively), nitrogen dioxide, ozone, and black

257 ft, railway, and road traffic Lden; NO2; and PM2.5, respectively, with minimally overlapping signals.

258 Reductions in PM2.5 since 1999 have lowered mortality in all but 14 co

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

260 hts the need to formulate a stricter ambient PM2.5 standard at both national and regional levels of C

261 ts in life expectancy by attaining the daily PM2.5 standards in 72 cities of China during 2013-2016.

262 ach interquartile increment (2.81 mug/m3) of PM2.5, the annual decline rate was significantly acceler

263 For PM2.5, the IRR was 0.81 (95% CI, 0.67-0.98) for a median

264 1-h lagged exposures (ranging from 21.3% for PM2.5 to 74.7% for BC).

265 unity Multiscale Air Quality model estimated PM2.5 total and component concentrations, we calculated

266 We estimated PM2.5 total- and component-related CV mortality, adjuste

267 ween the incidence of cancer and exposure to PM2.5 using > 8.5 million cases of cancer incidences fro

268 We estimated daily residential PM2.5 using satellite data in combination with land-use

269 posures to PCBs and fine particulate matter (PM2.5), using disability-adjusted life years (DALYs) as

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

271 For example, a 10-mug/m3 increase in PM2.5 was associated with a 0.21% (95% CI 0.15% to 0.27%

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

273 Each 10-mug/m3 increase in PM2.5 was associated with a 5.1% increased risk of poor

274 PM2.5 was associated with a higher risk of invasive brea

275 A 10-mug/m3 increase in PM2.5 was associated with a significant increase in any

276 In multilevel structural equation models, PM2.5 was associated with greater declines in immediate

277 Long-term exposure to PM2.5 was associated with increased total mortality and

278 n-based cohort with up to 25 y of follow-up, PM2.5 was associated with nonaccidental mortality at con

279 Long-term exposure to PM2.5 was associated with total, non-accidental, cardiov

280 amining RSAc change between episodes, higher PM2.5 was generally associated with reduced PNS withdraw

281 PM2.5 was identified as a risk factor for poor cognitive

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

283 The life expectancy loss due to PM2.5 was largest around Los Angeles and in some souther

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

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

286 t-term exposure to air pollution, especially PM2.5, was associated with increased risk of hospitaliza

287 For each 1 mug/m3 increase in annual PM2.5, we found a 2.02% (95% CI 1.41%-2.63%; p < 0.01) i

288 For PM2.5, we investigated effect measure modification by co

289 gged moving averages of annual estimates for PM2.5 were also estimated.

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

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

292 iations with a 10-mug/m3 increase in PM1 and PM2.5 were significantly lower among women who initiated

293 particles with aerodynamic diameter <2.5 um (PM2.5)] were measured at central monitoring stations.

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

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

296 luated associations of long-term exposure to PM2.5 with poor cognitive function in a diverse, nationa

297 were performed to explore the association of PM2.5 with poor cognitive function.

298 ions of exposure to fine particulate matter (PM2.5) with HRV as an indicator of cardiac autonomic con

299 atter [PM < 2.5 mum in aerodynamic diameter (PM2.5)] with the Enhanced Children's MicroPEM(TM) (RTI I

300 trong association with a 3-y running mean of PM2.5, with an HR = 1.69 (95% CI: 1.33, 2.13), which att