Measures Of PM2 Research Articles

Inter-continental variability in the relationship of oxidative potential and cytotoxicity with PM2.5 mass

Most fine ambient particulate matter (PM2.5)-based epidemiological models use globalized concentration-response (CR) functions assuming that the toxicity of PM2.5 is solely mass-dependent without considering its chemical composition. Although oxidative potential (OP) has emerged as an alternate metric of PM2.5 toxicity, the association between PM2.5 mass and OP on a large spatial extent has not been investigated. In this study, we evaluate this relationship using 385 PM2.5 samples collected from 14 different sites across 4 different continents and using 5 different OP (and cytotoxicity) endpoints. Our results show that the relationship between PM2.5 mass vs. OP (and cytotoxicity) is largely non-linear due to significant differences in the intrinsic toxicity, resulting from a spatially heterogeneous chemical composition of PM2.5. These results emphasize the need to develop localized CR functions incorporating other measures of PM2.5 properties (e.g., OP) to better predict the PM2.5-attributed health burdens.

Long-term Exposure to Oxidant Gases and Mortality: Effect Modification by PM 2.5 Transition Metals and Oxidative Potential.

Background:Populations are simultaneously exposed to outdoor concentrations of oxidant gases (i.e., O3 and NO2) and fine particulate air pollution (PM2.5). Since oxidative stress is thought to be an important mechanism explaining air pollution health effects, the adverse health impacts of oxidant gases may be greater in locations where PM2.5 is more capable of causing oxidative stress.Methods:We conducted a cohort study of 2 million adults in Canada between 2001 and 2016 living within 10 km of ground-level monitoring sites for outdoor PM2.5 components and oxidative potential. Ox exposures (i.e., the redox-weighted average of O3 and NO2) were estimated using a combination of chemical transport models, land use regression models, and ground-level data. Cox proportional hazards models were used to estimate associations between 3-year moving average Ox and mortality outcomes across strata of transition metals and sulfur in PM2.5 and three measures of PM2.5 oxidative potential adjusting for possible confounding factors.Results:Associations between Ox and mortality were consistently stronger in regions with elevated PM2.5 transition metal/sulfur content and oxidative potential. For example, each interquartile increase (6.27 ppb) in Ox was associated with a 14.9% (95% CI = 13.0, 16.9) increased risk of nonaccidental mortality in locations with glutathione-related oxidative potential (OPGSH) above the median whereas a 2.50% (95% CI = 0.600, 4.40) increase was observed in regions with OPGSH levels below the median (interaction P value <0.001).Conclusion:Spatial variations in PM2.5 composition and oxidative potential may contribute to heterogeneity in the observed health impacts of long-term exposures to oxidant gases.

Fine Particulate Matter Pollution and Risk of Community-Acquired Sepsis.

While air pollution has been associated with health complications, its effect on sepsis risk is unknown. We examined the association between fine particulate matter (PM2.5) air pollution and risk of sepsis hospitalization. We analyzed data from the 30,239 community-dwelling adults in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort linked with satellite-derived measures of PM2.5 data. We defined sepsis as a hospital admission for a serious infection with ≥2 systemic inflammatory response (SIRS) criteria. We performed incidence density sampling to match sepsis cases with 4 controls by age (±5 years), sex, and race. For each matched group we calculated mean daily PM2.5 exposures for short-term (30-day) and long-term (one-year) periods preceding the sepsis event. We used conditional logistic regression to evaluate the association between PM2.5 exposure and sepsis, adjusting for education, income, region, temperature, urbanicity, tobacco and alcohol use, and medical conditions. We matched 1386 sepsis cases with 5544 non-sepsis controls. Mean 30-day PM2.5 exposure levels (Cases 12.44 vs. Controls 12.34 µg/m3; p = 0.28) and mean one-year PM2.5 exposure levels (Cases 12.53 vs. Controls 12.50 µg/m3; p = 0.66) were similar between cases and controls. In adjusted models, there were no associations between 30-day PM2.5 exposure levels and sepsis (4th vs. 1st quartiles OR: 1.06, 95% CI: 0.85–1.32). Similarly, there were no associations between one-year PM2.5 exposure levels and sepsis risk (4th vs. 1st quartiles OR: 0.96, 95% CI: 0.78–1.18). In the REGARDS cohort, PM2.5 air pollution exposure was not associated with risk of sepsis.

Protecting children from secondhand smoke: a mixed-methods feasibility study of a novel smoke-free home intervention.

BackgroundGlobally, 40 % of children under 14 years are regularly exposed to secondhand smoke (SHS), typically in their homes. There is limited evidence of the effectiveness of interventions to reduce children’s SHS exposure, and so the aim of this study was to test the feasibility and acceptability of a novel intervention to help parents and carers (caregivers) to reduce their children’s exposure to SHS at home.MethodsA novel multi-component intervention to support caregivers to reduce their children’s SHS exposure at home was tested in a two-phase feasibility study. The 12-week intensive intervention delivered in the home consisted of three components: behavioural support, nicotine replacement therapy (NRT) for temporary abstinence and feedback on levels of SHS exposure in the form of children’s salivary cotinine (phase 1) or home air quality (PM2.5) (phase 2). Participants were caregivers who smoked inside their homes and had at least one child under the age of 5 years living with them the majority of the time. Mixed-methods were used to explore the acceptability and feasibility of the intervention as well as processes, particularly around recruitment and retention, for an exploratory efficacy trial.ResultsTwelve caregivers completed the study, all received personalised feedback on SHS exposure and behavioural support to help them to make their homes smoke-free and the majority at least tried NRT. Saliva cotinine results were variable in phase 1, and therefore, measures of PM2.5 were used for feedback in phase 2. Behavioural support was well received with personalised feedback reported as being the key motivator for initiating and maintaining behaviour change.ConclusionsRecruiting disadvantaged caregivers was labour intensive, but once recruited, this novel intervention was both feasible and acceptable in supporting caregivers to reduce their children’s exposure to SHS at home. It is appropriate to test the efficacy of this novel intervention in an exploratory randomised controlled trial.Trial registrationThis is not applicable for the current study; however, a registered exploratory randomised controlled trial linked to this manuscript is currently ongoing (ISRCTN81701383).Electronic supplementary materialThe online version of this article (doi:10.1186/s40814-016-0094-7) contains supplementary material, which is available to authorized users.

Particulate Matter Exposure and Cardiopulmonary Differences in the Multi-Ethnic Study of Atherosclerosis.

Background:Particulate matter (PM) exposure may directly affect the pulmonary vasculature. Although the pulmonary vasculature is not easily measurable, differential associations for right ventricular (RV) and left ventricular (LV) mass may provide an indirect assessment of pulmonary vascular damage.Objectives:We tested whether long-term exposure to PM < 2.5 μm (PM2.5) is associated with greater RV mass and RV mass/end-diastolic volume ratio relative to the LV.Methods:The Multi-Ethnic Study of Atherosclerosis performed cardiac magnetic resonance (CMR) imaging among participants 45–84 years old without clinical cardiovascular disease in 2000–2002 in six U.S. cities. A fine-scale spatiotemporal model estimated ambient PM2.5 exposure in the year before CMR; individually weighted estimates accounted for indoor exposure to ambient PM2.5. Linear regression models were adjusted for demographics, anthropometrics, smoking status, cardiac risk factors, and LV parameters, with additional adjustment for city.Results:The 4,041 included participants had a mean age of 61.5 years, and 47% were never smokers. The mean ambient PM2.5 was 16.4 μg/m3 and individually weighted PM2.5 was 11.0 μg/m3. PM2.5 exposure was associated with greater RV mass [ambient: 0.11 g per 5 μg/m3 (95% CI: –0.05, 0.27); individually weighted: 0.20 g per 5 μg/m3 (95% CI: 0.04, 0.36)] and a greater RV mass/end-diastolic volume ratio conditional on LV parameters. City-adjusted results for RV mass were of greater magnitude and were statistically significant for both measures of PM2.5, whereas those for RV mass/end-diastolic volume ratio were attenuated.Conclusions:Long-term PM2.5 exposures were associated with greater RV mass and RV mass/end-diastolic volume ratio conditional on the LV; however, additional adjustment for city attenuated the RV mass/end-diastolic volume findings. These findings suggest that PM2.5 exposure may be associated with subclinical cardiopulmonary differences in this general population sample.Citation:Aaron CP, Chervona Y, Kawut SM, Diez Roux AV, Shen M, Bluemke DA, Van Hee VC, Kaufman JD, Barr RG. 2016. Particulate matter exposure and cardiopulmonary differences in the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 124:1166–1173; http://dx.doi.org/10.1289/ehp.1409451

AIR POLLUTION AND INFLAMMATORY MARKERS IN BLOOD

ISEE-22 Introduction: The adverse cardiovascular health effects of air pollution may be caused in part by systemic inflammation triggered by oxidative stress to the lungs. Recent studies have suggested that these associations may be strongest for traffic-related particles. In order to examine the associations between traffic-related particles and systemic inflammation, we conducted a study in which a panel of senior citizens was exposed to elevated traffic-related pollutant exposures through a series of bus trips. Methods: Repeated blood samples were collected from forty-four non-smoking participants living at one of four suburban independent senior living facilities. Blood samples were obtained between April and June of 2002, approximately 18-hours after study subjects participated in a field trip that included two hours aboard a diesel bus. Each subject participated in approximately four field trips, about once every 3-weeks. Blood samples were analyzed for red and white cell parameters using a CBC with differential analyses. Samples were also tested for interleukin-6, c-reactive protein, intracellular adhesion molecule–1, fibrinogen, and von willebrand’s factor. Particulate exposures of the participants were assessed using two mobile carts that followed the subjects throughout each field trip. Micro-environmental exposure measurements included continuous readings of fine particle mass (PM2.5), ultra-fine, fine, and coarse particle counts, and black carbon. Carbon monoxide and nitric oxide concentrations were also measured continuously during the bus rides. These exposure measures were supplemented with ambient air concentrations of gases, particle mass and number, and meteorological parameters measured at a local USEPA-funded Supersite. Results: Among the 138 blood samples analyzed, levels of circulating inflammatory markers were found to be comparable to the values reported by previous studies. Evaluation of the air monitoring data indicates that the bus trips successfully elevated hourly exposures above levels observed at the residence facilities and central site. The mean hourly black carbon concentration during the bus trip periods was 3,400 (SD: 1,200) ng/m3 as compared to mean hourly concentrations of 350 (SD: 450) ng/m3 during facility periods and 750 (SD: 370) ng/m3 at the Supersite during times concurrent with the bus trip. Measures of PM2.5 and particle counts were also substantially elevated during periods when subjects were aboard the bus. The impacts of these micro-environmental changes on circulating inflammatory markers will be presented using the results of longitudinal mixed models.