Long-term Particulate Matter Exposure Research Articles

Particulate Matter Concentration and Microbial Load in Heavy Traffic Areas of District Lahore, Pakistan

A major threat to the environment and public health is air pollution. Previous research has looked at the harmful health impacts of both short- and long-term particulate matter exposure. In addition, PM (particulate matter) of fine or coarse size (PM 2.5 and PM 10) was linearly related with mortality, with PM 2.5 being associated with long-term mortality and PM10 being connected with short-term mortality. Traffic congestion is one of the foremost problems. Objective: To characterize gram positive and gram negative airborne bacteria from air samples of heavy traffic areas. Methods: These were assessed using direct as well as indirect sampling technique. A total of 40 samples 10 from each traffic areas (i.e., Bhatti Gate, Bohr wala chowk, Chauburji and Railway Station) were collected. These were collected with the help of Mini Vol portable air sampler. Filter papers containing particulate matter 2.5 and 10 were placed on prepared petri dishes. The petri dishes were then kept in an incubator for 24 hours at 37 °C, the appearances of colonies were characterized and proceeded for morphological and biochemical identification. Results: The results showed the presence of different bacteria including Bacillus spp., Micrococcus spp. Streptococcus and Staphylococcus aureus, Pseudomonas aeroginosa. Conclusion: It was found that air was heavily polluted with PM 10 and micrococcus aureus.

Long-term exposure to particulate air pollution and incidence of Parkinson's disease: A nationwide population-based cohort study in South Korea

There has been increasing interest in the neurological impact of particulate matter (PM). However, its association with the incidence of Parkinson's disease (PD) remains unclear. We selected 313,355 participants satisfying inclusion criteria from the National Health Insurance Service-National Sample Cohort based on the nationwide population of South Korea, and followed them up from January 2007 through December 2015. Individual-level long-term PM exposure was assessed as the five time-varying average concentrations estimated for the previous 1, 2, 3, 4 and 5 years on each year (until censored or event occurred) at the district-level residential addresses of participants using a previously validated prediction model. Incident PD was defined as the first diagnosis accompanied by anti-PD medication prescription from 2007 through 2015. Time-varying Cox proportional hazards models were employed to estimate the hazard ratio (HR) of incident PD for long-term PM exposure, adjusting for individual- and area-level covariates. During the 8 years (2,745,389 person-years) of follow-up for a total of 313,355 participants (mean [range] age, 48.9 [19–87] years; 169,571 males [54.1%]), 2621 participants (0.8%) developed PD. The HR of incident PD per interquartile range (3.3 μg/m3) increase in fine PM (PM2.5) for the previous 1 year was 1.08 (95% confidence interval: 1.01–1.19). In subgroup-specific analyses, HRs for PM2.5 were significant among older participants, males, participants living in metropolitan cities, ibuprofen users, and participants with comorbidities (HR: 1.10–1.20). Long-term exposure to PM2.5 might play a role in PD development.

Long-term particulate matter exposure and bone mineral density in the Women’s Health Initiative

BACKGROUND AND AIM: Ambient particulate matter air pollution 10 μm (PM10) concentrations have been associated with several outcomes, but few studies have examined their association with bone mineral density (BMD). Previous studies have suggested an effect of air pollution on bone health, but none has evaluated its impact in postmenopausal women. METHODS: We studied the longitudinal PM10-BMD association among 5,080 postmenopausal women in the Women’s Health Initiative Clinical Trials (WHI-CT). We used log-normal, ordinary kriging to estimate daily mean PM10 concentrations (μg/m3) at geocoded participant addresses. We averaged the means over 1-, 3-, and 5-year periods before triennial, dual energy X-ray absorptiometry (DXA) exams. We estimated total hip, lumbar spine, and total body BMD (in g/cm2) and their corresponding T-scores. We estimated the association of PM10 with BMD and T-scores using multivariable linear mixed models while controlling for correlation of repeated measures among participants and adjusting for age at DXA, race/ethnicity, income, body mass index (kg/m2), smoking status, coffee consumption, physical activity, CT randomization arm, US region of residence, and DXA equipment serial number. Multiple imputation was done for missing data. RESULTS:At baseline, women were aged 50-79 years, 78% were White, 40% were college graduates, and 71% earned $40,000/year. PM10 concentrations at baseline were cross-sectionally associated with both hip, lumbar spine, and whole-body BMD and T-scores (p 0.05). Longitudinally, lumbar spine BMD decreased 0.052 (95% confidence interval [95%CI]: 0.067, 0.037) g/cm2/year per 10% (2.21 ug/m3) increase in 5-year mean PM10 concentration. Lumbar spine T-scores also decreased with increasing duration of the 3- and 5-year mean PM10 concentrations: -0.362 Standard Deviations (SD) (-0.490, -0.235) and -0.512 SD (-0.649, -0.375), respectively. No association was seen with changes in hip or total body BMD. CONCLUSIONS:This is the first study suggesting an inverse association of ambient PM10 with BMD among postmenopausal women. KEYWORDS: Air pollution, long-term, PM10, bone mineral density, t-score, osteoporosis.

Climate change, environmental factors, and COVID-19: Current evidence and urgent actions

Climate change, environmental factors, and COVID-19: Current evidence and urgent actions

Letter to the Editor regarding Wang Y, Liu Y, Yan H. 2020. Effect of long-term particulate matter exposure on Parkinson’s risk

Letter to the Editor regarding Wang Y, Liu Y, Yan H. 2020. Effect of long-term particulate matter exposure on Parkinson’s risk

Particulate matter air pollution, neighborhood socio-economic status, and leukocyte telomere length

Background: Telomeres cap and protect chromosomes from degradation and risk factors for telomere attrition include aging and environmental factors. Although exposure to some air pollutants and neighborhood socio-economic factors (nSES) have been associated with telomere length, evidence of associations between exposure to particulate matter (PM) air pollution, nSES, and the interaction between the two in relation to telomere length is limited and inconclusive. Our objective was to examine the associations between exposure to short-, intermediate-, and long-term (1-, 3-, and 12-month) exposure to different size fractions of PM (<2.5 microns [PM2.5], 2.5-10 microns [PM10-2.5], and <10 microns [PM10]) and nSES at blood draw, and leukocyte telomere length.Methods: We used generalized linear regression models to examine the associations between each of the PM exposure metrics, nSES, and z-scores of log-transformed telomere length in 10,212 female participants of the nationwide Nurses’ Health Study, after adjusting for demographics and telomere attrition risk factors. Using participants’ address history, we applied spatio-temporal prediction models to estimate monthly PM exposures.Results: In adjusted models, PM2.5 exposure per 10 μg/m3 increase was not associated with relative telomere length: 1-month exposure: β: 0.01, standard error (SE): 0.01, p: 0.40; 3-month exposure: β: 0.01, SE: 0.01, p: 0.37; 12-month exposure: β: 0.01, SE: 0.01, p: 0.34. Results for exposure to PM10-2.5, and PM10 were similar. nSES at blood draw was also not associated with telomere length: β: -0.001, SE: 0.001, p: 0.28. We observed no multiplicative interactions between 1-, 3-, and 12-month PM exposures and nSES.Conclusions: In this study of U.S. women, short-, intermediate-, and long-term PM exposures were not associated with telomere attrition for any size fraction of PM; nSES was also not associated with telomere length. Additionally, we observed no interactions between PM exposures and nSES in association with telomere length.

Association of particulate matter air pollution with leukocyte mitochondrial DNA copy number

BackgroundAmbient particulate matter (PM) has been associated with mitochondrial damage and dysfunction caused by excessive oxidative stress, but the associations between long-term PM exposure and leukocyte mitochondrial DNA copy number (mtDNAcn), a biomarker of mitochondrial dysfunction due to oxidative stress, are less studied. ObjectivesTo investigate the associations between short-, intermediate- and long-term exposure (1-, 3- and 12-months) to different size fractions of PM (PM2.5, PM2.5-10 and PM10) and leukocyte mtDNAcn in a cross-sectional study. MethodsThe associations between each of the PM exposure metrics with z scores of log-transformed mtDNAcn were examined using generalized linear regression models in 2758 female participants from the Nurses’ Health Study (NHS). Monthly exposures to PM were estimated from spatio-temporal prediction models matched to each participants’ address history. Potential effect modification by selected covariates was examined using multiplicative interaction terms and subgroup analyses. ResultsIn single-size fraction models, increases in all size fractions of PM were associated with decreases in mtDNAcn, although only models with longer averages of PM2.5 reached statistical significance. For example, an interquartile range (IQR) increase in 12-month average ambient PM2.5 (5.5 μg/m3) was associated with a 0.07 [95% confidence interval (95% CI): −0.13, −0.01; p-value = 0.02] decrease in mtDNAcn z score in both basic- and multivariable-adjusted models. Associations for PM2.5 were stronger after controlling for PM2.5-10 in two size-fraction models. ConclusionsOur study suggests that long-term exposure to ambient PM2.5 is associated with decreased mtDNAcn in healthy women.

Effect of long-term particulate matter exposure on Parkinson's risk.

Environmental pollution is a critical predisposing factor underlying neurodegenerative diseases, but the association between particulate matter (PM) exposure and Parkinson's disease (PD) remains unclear. This study aimed to evaluate the association between long-term PM2.5/PM10 exposure and PD risk. We searched the PubMed, Ovid Medline, EMBASE, Cochrane Library, and Web of Science citation databases to select studies about the relationship between long-term PM exposure and PD risk. The association was assessed using meta-analysis, and subgroup analysis was carried out on the basis of the types of PM (PM2.5 and PM10). Among the 611 articles identified from the databases, we selected six articles, including three cohort studies and three case-control studies, which collectively involved 10,077,029 participants. With every 10μg/m3 increment, the relative risks (RRs) and 95% confidence intervals (CIs) were 1.03 (0.98, 1.07), 1.21 (0.95, 1.54), and 1.01 (0.97, 1.05) for the total PM, PM2.5, and PM10, respectively. In the current study, no statistically substantial association was observed between long-term PM2.5/PM10 exposure and PD incidence. However, further large-scale prospective studies are needed to determine the association.

Long-term particulate matter exposure increases the mortality risk of patients with end-stage renal disease

Long-term particulate matter exposure increases the mortality risk of patients with end-stage renal disease

Particulate matter air pollution and blood glucose in children and adolescents: A cross-sectional study in China.

The health effects of particulate matter (PM) air pollution on glucose metabolism have been rarely examined in children and adolescents. We aimed to investigate the associations between long-term PM exposure and blood glucose and prevalence of impaired fasting glucose in a large population of Chinese children and adolescents. In 2013, a total of 11,814 children and adolescents aged 7 to 18 years were recruited from seven provinces/municipalities in China. Fasting blood sample was taken for the measurement of blood glucose. Satellite-based spatial-temporal models were used to estimate exposure to ambient submicrometer particles (PM1), fine particles (PM2.5) and thoracic particles (PM10). Cross-sectional analyses were performed using mixed-effects multivariable linear and logistic regression models. After adjustment for a range of covariates, every 10 μg/m3 increment in PM1, PM2.5 and PM10 concentrations was associated with 0.160 [95% confidence interval (CI): 0.039, 0.280], 0.150 (95% CI: 0.044, 0.256) and 0.079 (95% CI: -0.009, 0.167) mmol/L higher blood glucose levels, respectively. PM exposure was also associated with higher prevalence of impaired fasting glucose, but the associations did not reach statistical significance [odds ratio per 10 μg/m3 increment in PM1, PM2.5 and PM10: 1.30 (95% CI: 0.86,1.96), 1.20 (95% CI: 0.85,1.69) and 1.08 (95% CI: 0.83,1.41)]. We found that long-term exposure to PM air pollution was associated with increased levels of blood glucose in children and adolescents. The associations were more evident for PM1 and PM2.5.

Long-Term Particulate Matter Exposure and Onset of Depression in Middle-Aged Men and Women.

Background:Long-term exposure to particulate matter (PM) air pollution is associated with all-cause mortality and adverse cognitive outcomes, but the association with developing depression remains inconsistent.Objective:Our goal was to evaluate the prospective association between PM air pollution and developing depression assessed using the Center for Epidemiological Studies Depression (CES-D) scale.Methods:Subjects were drawn from a prospective cohort study of 123,045 men and women free of depressive symptoms at baseline who attended regular screening exams in Seoul and Suwon, South Korea, from 2011 to 2015. Exposure to PM with an aerodynamic diameter of ( and , respectively) was estimated using a land-use regression model based on each subject’s residential postal code. Incident depression was defined as a CES-D score during follow-up. As a sensitivity analyses, we defined incident depression using self-reports of doctor’s diagnoses or use of antidepressant medications during follow-up.Results:The mean baseline 12-month concentrations of and were 50.6 (4.5) and , respectively. The hazard ratios (HRs) and 95% confidence intervals (CIs) for developing depression associated with a increase in 12- and 60-month exposure were 1.11 (95% CI: 1.06, 1.16) and 1.06 (95% CI: 1.01, 1.11), respectively. The corresponding HRs for 12-month exposure was 0.96 (95% CI: 0.64, 1.43). Similar results were obtained when incident depression was identified using self-reports of doctor’s diagnoses or the use of antidepressant medications.Conclusion:In this large cohort study, we found a positive association between long-term exposure to outdoor air pollution and the developing depression. We did not find an association for outdoor air pollution; however, we had a much shorter follow-up for subjects’ exposure to . https://doi.org/10.1289/EHP4094

Personal exposure to particulate matter in peri-urban India: predictors and association with ambient concentration at residence.

Scalable exposure assessment approaches that capture personal exposure to particles for purposes of epidemiology are currently limited, but valuable, particularly in low-/middle-income countries where sources of personal exposure are often distinct from those of ambient concentrations. We measured 2 × 24-h integrated personal exposure to PM2.5 and black carbon in two seasons in 402 participants living in peri-urban South India. Means (sd) of PM2.5 personal exposure were 55.1(82.8) µg/m3 for men and 58.5(58.8) µg/m3 for women; corresponding figures for black carbon were 4.6(7.0) µg/m3 and 6.1(9.6) µg/m3. Most variability in personal exposure was within participant (intra-class correlation ~20%). Personal exposure measurements were not correlated (Rspearman < 0.2) with annual ambient concentration at residence modeled by land-use regression; no subgroup with moderate or good agreement could be identified (weighted kappa ≤ 0.3 in all subgroups). We developed models to predict personal exposure in men and women separately, based on time-invariant characteristics collected at baseline (individual, household, and general time-activity) using forward stepwise model building with mixed models. Models for women included cooking activities and household socio-economic position, while models for men included smoking and occupation. Models performed moderately in terms of between-participant variance explained (38-53%) and correlations between predictions and measurements (Rspearman: 0.30-0.50). More detailed, time-varying time-activity data did not substantially improve the performance of the models. Our results demonstrate the feasibility of predicting personal exposure in support of epidemiological studies investigating long-term particulate matter exposure in settings characterized by solid fuel use and high occupational exposure to particles.

Particulate Matter Triggers Depressive-Like Response Associated With Modulation of Inflammatory Cytokine Homeostasis and Brain-Derived Neurotrophic Factor Signaling Pathway in Mice

Particulate matter (PM) exposure may contribute to depressive-like response in mice. However, few studies have evaluated the adaptive impacts of long-term PM exposure on depressive-like response associated with systemic inflammation and brain-derived neurotrophic factor (BDNF) signaling pathway. We studied the association among depressive-like behaviors, mRNA levels of pro and anti-inflammatory cytokines, and the expression of BDNF signaling pathway in mice by long-term PM exposure. C57BL/6 male mice were exposed to ambient air alongside control mice breathing air filtered through a high-efficiency air PM (HEPA) filter. Depressive-like behaviors were assessed together with proinflammatory, anti-inflammatory cytokine mRNA levels and the modulation of BDNF pathway in hippocampus and olfactory-bulb of mice exposed to PM for 4, 8, and 12 weeks. Exposure to HEPA-filtered air for 4 weeks may exert antidepressant like effects in mice. Proinflammatory cytokines were up-regulated while the expression of BDNF, its high-affinity receptor tropomyosin-related kinase B (TrkB), and the transcription factor (cyclic adenosine monophosphate)-response element-binding protein (CREB) were down-regulated in ambient air mice. However, after 8 weeks, there was no significant difference in the rate of depressive-like behaviors between the 2 groups. After 12 weeks, mice exposed to ambient air again had a higher rate of depressive-like behaviors, significant up-regulation of proinflammatory cytokines, down-regulation of interleukin-10, BDNF, TrkB, and CREB than HEPA mice. Ultrafine PM in brain tissues of mice exposed to ambient air was observed. Our results suggest continuous high-level PM exposure alters the depressive-like response in mice and induces a damage-repair-imbalance reaction.

The Association of Long-Term Exposure to Particulate Matter Air Pollution with Brain MRI Findings: The ARIC Study.

Background:Increasing evidence links higher particulate matter (PM) air pollution exposure to late-life cognitive impairment. However, few studies have considered associations between direct estimates of long-term past exposures and brain MRI findings indicative of neurodegeneration or cerebrovascular disease.Objective:Our objective was to quantify the association between brain MRI findings and PM exposures approximately 5 to 20 y prior to MRI in the Atherosclerosis Risk in Communities (ARIC) study.Methods:ARIC is based in four U.S. sites: Washington County, Maryland; Minneapolis suburbs, Minnesota; Forsyth County, North Carolina; and Jackson, Mississippi. A subset of ARIC participants underwent 3T brain MRI in 2011–2013 (). We estimated mean exposures to PM with an aerodynamic diameter less than 10 or ( and ) in 1990–1998, 1999–2007, and 1990–2007 at the residential addresses of eligible participants with MRI data. We estimated site-specific associations between PM and brain MRI findings and used random-effect, inverse variance–weighted meta-analysis to combine them.Results:In pooled analyses, higher mean and exposure in all time periods were associated with smaller deep-gray brain volumes, but not other MRI markers. Higher exposures were consistently associated with smaller total and regional brain volumes in Minnesota, but not elsewhere.Conclusions:Long-term past PM exposure in was not associated with markers of cerebrovascular disease. Higher long-term past PM exposures were associated with smaller deep-gray volumes overall, and higher exposures were associated with smaller brain volumes in the Minnesota site. Further work is needed to understand the sources of heterogeneity across sites. https://doi.org/10.1289/EHP2152

Particulate Matter and Respiratory Diseases: How Far Have We Gone?

Air pollution is a potential threat to public health worldwide, especially in South Asia. The Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016) reported that most of global deaths attributable to ambient particulate matter occurred in China and India. Particulate matter (PM), as the main air pollutant, is receiving increasing attention due to its specific biological properties. PM is a complicated mixture and varies in sizes, compositions and sources. Increasing epidemiological studies have shown that both short- and long-term PM exposure are associated with the morbidity and mortality of respiratory diseases, including chronic obstructive pulmonary disease (COPD), asthma, lung cancer, and pneumonia, especially in the elderly and children. Several potential biological mechanisms have been proposed to explain the adverse effect of PM on the respiratory diseases, including oxidant stress, pro-inflammation, epigenetic modifications, DNA damage and carcinogenesis. However, there are still some contradictions with regard to the role of PM in the development of these respiratory diseases. Thus, this review made a summary of results from epidemiological studies about the association between PM and COPD, asthma, lung cancer, and pneumonia, and elucidated its potential biological mechanisms.

Abstract P070: Glucose, Insulin, Insulin Resistance and Exposure to Ambient Air Pollution

Background: Numerous studies suggest that long-term exposure to ambient particulate matter (PM) and nitrogen oxide (NOx) air pollution may be diabetogenic, but little is known about the effects of shorter-term exposures on markers of diabetes risk. Therefore, our objective was to determine whether short- and long-term ambient PM and NOx exposures are associated with glucose, insulin, and insulin resistance measures. Methods: We studied a stratified, random minority oversample of non-diabetic Women’s Health Initiative (WHI) clinical trials participants for whom estimates of fasting glucose, fasting insulin, insulin resistance, and geocoded address-specific daily mean concentrations of PM &lt; 10 μm (PM 10 ), PM &lt; 2.5 μm (PM 2.5 ), and NOx were available at screening and up to three follow-up visits between 1993-2004 (total n=4,019; mean age: 62.2 yr; 24% black; 12% Hispanic; 51% white). We measured insulin resistance using the homeostatic model assessment [HOMA], triglyceride to high-density lipoprotein cholesterol ratio, and the triglyceride-glucose index. We log-transformed the glucose, insulin, and insulin resistance measures, then used multi-level, mixed, longitudinal models weighted for sampling design / attrition and adjusted for sociodemographic, clinical, and meteorological covariates to estimate their associations with 2- and 365-day mean PM 10 and NOx and 365-day mean PM 2.5 concentrations. Results: Measures of glucose homeostasis decreased with short-term exposure to ambient PM 10 . For example, we found a -0.2% (95% confidence interval: -0.4%, 0.1%), -0.9% (-1.7%, -0.1%), and -1.1% (-2.0%, -0.3%) change in glucose, insulin, and HOMA per 10 μg/m 3 increase in the 2-day mean PM 10 concentration. In contrast, we found generally null results per 10 μg/m 3 increase in 365-day mean PM 10 concentration. Measures of glucose homeostasis similarly did not appear to be associated with short- and long-term increases in mean NOx or PM 2.5 concentrations. Conclusion: The findings suggest that responses to ambient exposure to PM 10 in women may be adaptive (i.e. capable of re-establishing normal glucose homeostasis and improving insulin sensitivity) over the short-term. Endoplasmic reticulum stress-response mechanisms involving decreases in protein misfolding may help explain this observed phenomena. Contrary to previous studies, results also suggest that sustained exposure to ambient PM and NOx has nominal influence on glucose homeostasis.

Associations between Long-Term Particulate Matter Exposure and Adult Renal Function in the Taipei Metropolis.

Background:Studies on the effect of air pollutions on kidney diseases are still limited.Objective:We aimed to investigate the associations between particulate matter (PM) exposures and renal function among adults.Methods:We recruited 21,656 adults as participants from 2007 to 2009. The Taiwanese Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation was used to derive the estimated glomerular filtration rate (eGFR). Subjects with an eGFR lower than 60 mL/min/1.73 m2 were defined as having chronic kidney disease (CKD). Land use regression (LUR) models were used to estimate individual exposures to PM with an aerodynamic diameter < 10 μm (PM10), coarse particles (PMCoarse), fine particles (PM2.5), and PM2.5Absorbance. Generalized linear and logistic regression models were used to estimate the associations between PM exposure and renal function.Results:An IQR increase in PM10 (5.83 μg/m3) was negatively associated with eGFR by –0.69 (95% CI: –0.89, –0.48) mL/min/1.73 m2 and positively associated with the prevalence of CKD with adjusted OR = 1.15 (95% CI: 1.07, 1.23). An IQR increase in PMCoarse (6.59 μg/m3) was significantly associated with lower eGFR by –1.07 (95% CI: –1.32, –0.81) mL/min/1.73 m2 and CKD with OR = 1.26 (95% CI: 1.15, 1.38). In contrast, neither outcome was significantly associated with PM2.5 or PM2.5Absorbance. Stratified analyses indicated that associations of CKD with both PM10 and PMCoarse were limited to participants < 65 years of age, and were stronger (for PM10) or limited to (PMCoarse) women. Associations also appeared to be stronger in those without (vs. with) hypertension, and in normal versus overweight participants.Conclusions:Exposure during the previous year to PM10 and PMCoarse, but not PM2.5 or PM2.5Absorbance, was associated with reduced renal function among Taiwanese adults.Citation:Yang YR, Chen YM, Chen SY, Chan CC. 2017. Associations between long-term particulate matter exposure and adult renal function in the Taipei metropolis. Environ Health Perspect 125:602–607; http://dx.doi.org/10.1289/EHP302

Long-term Particulate Matter Exposures during Adulthood and Risk of Breast Cancer Incidence in the Nurses' Health Study II Prospective Cohort.

There is increasing concern that environmental exposures, such as air pollution, may be related to increasing rates of breast cancer; however, results from cohort studies have been mixed. We examined the association between particulate matter (PM) and measures of distance to roadway with the risk of incident breast cancer in the prospective nationwide Nurses' Health Study II (NHSII) cohort. Incident invasive breast cancer from 1993 to 2011 (N = 3,416) was assessed among 115,921 women in the NHSII cohort. Time-varying Cox proportional hazards models were used to calculate HRs and 95% confidence intervals (95% CI) for increases in ambient exposures to PM10, PM2.5-10, and PM2.5 and residential roadway proximity categories. In multivariable adjusted models, there was little evidence of an increased risk of breast cancer (or any of the receptor-specific subtypes) overall or by menopausal status with PM exposure. There was, however, a suggestion of increased risks among women living <50 m of the largest road type (HR = 1.60; 95% CI, 0.80-3.21) or within <50 m of the two largest road types (1.14; 95% CI, 0.84-1.54) compared with women living farther (≥200 m) away. Among women in the NHSII, we found no statistically significant associations between particulate matter exposures and incidence of breast cancer overall, by menopausal status, or by hormone receptor subtype. There was, however, a suggestion that residential proximity to major roadways may be associated with increased risk. These results suggest no elevated breast cancer risk with increasing exposures to particulate matter air pollution, but that other traffic-related exposures may be important. Cancer Epidemiol Biomarkers Prev; 25(8); 1274-6. ©2016 AACR.

Biomolecular Markers within the Core Axis of Aging and Particulate Air Pollution Exposure in the Elderly: A Cross-Sectional Study.

Background:Telomere length and mitochondrial DNA (mtDNA) content are markers of aging and aging-related diseases. There is inconclusive evidence concerning the mechanistic effects of airborne particulate matter (PM) exposure on biomolecular markers of aging.Objective:The present study examines the association between short- and long-term PM exposure with telomere length and mtDNA content in the elderly and investigates to what extent this association is mediated by expression of genes playing a role in the telomere–mitochondrial axis of aging.Methods:Among 166 nonsmoking elderly participants, we used qPCR to measure telomere length and mtDNA content in leukocytes and RNA from whole blood to measure expression of SIRT1, TP53, PPARGC1A, PPARGC1B, NRF1, and NFE2L2. Associations between PM exposure and markers of aging were estimated using multivariable linear regression models adjusted for sex, age, BMI, socioeconomic status, statin use, past smoking status, white blood cell count, and percentage of neutrophils. Mediation analysis was performed to explore the role of age-related markers between the association of PM exposure and outcome. Annual PM2.5 exposure was calculated for each participant’s home address using a high-resolution spatial–temporal interpolation model.Results:Annual PM2.5 concentrations ranged from 15 to 23 μg/m3. A 5-μg/m3 increment in annual PM2.5 concentration was associated with a relative decrease of 16.8% (95% CI: –26.0%, –7.4%, p = 0.0005) in telomere length and a relative decrease of 25.7% (95% CI: –35.2%, –16.2%, p < 0.0001) in mtDNA content. Assuming causality, results of the mediation analysis indicated that SIRT1 mediated 19.5% and 22.5% of the estimated effect of PM2.5 exposure on telomere length and mtDNA content, respectively.Conclusions:Our findings suggest that the estimated effects of PM2.5 exposure on the telomere–mitochondrial axis of aging may play an important role in chronic health effects of PM2.5.Citation:Pieters N, Janssen BG, Dewitte H, Cox B, Cuypers A, Lefebvre W, Smeets K, Vanpoucke C, Plusquin M, Nawrot TS. 2016. Biomolecular markers within the core axis of aging and particulate air pollution exposure in the elderly: a cross-sectional study. Environ Health Perspect 124:943–950; http://dx.doi.org/10.1289/ehp.1509728

Long-Term Exposure to Particulate Matter Air Pollution Is a Risk Factor for Stroke: Meta-Analytical Evidence.

Epidemiological studies suggest an association between stroke incidence and stroke mortality and long-term exposure to particulate matter (PM) air pollution. However, the magnitude of the association is still unclear. We searched the Pubmed citation database for epidemiological studies and reviews on stroke and PM exposure. Then, we carried out a meta-analysis to quantify the pooled association between stroke incidence and mortality and long-term exposure to PM. Meta-analyses were performed for stroke events and stroke mortality and for PM10 and PM2.5 separately and jointly. We identified 20 studies, including a total of >10 million people, on long-term PM exposure and stroke event or stroke mortality. For exposure to PM10 (including estimated exposure to PM10 from studies using PM2.5), the pooled hazard ratio for each 10-μg/m3 increment in PM10 was 1.061 (95% confidence interval, 1.018-1.105) and 1.080 (0.992-1.177) for overall stroke events and stroke mortality, respectively. A stratified analysis by continent revealed that the association between stroke and long-term PM10 exposure was positive in North America (1.062 [1.015-1.110]) and Europe (1.057 [0.973-1.148]), but studies in Asia (1.010 [0.885-1.153]) showed a high degree of heterogeneity. Considering exposure to PM2.5 (Europe and North America combined), the hazard ratios for a 5-μg/m3 increment were 1.064 (1.021-1.109) and 1.125 (1.007-1.256) for stroke events and mortality, respectively. The scientific evidence of the past decade identifies long-term exposure to PM, and PM2.5 in particular, as a risk factor for stroke. However, we found some currently unexplained geographical variability in this association.