Coarse Particulate Matter Exposure Research Articles

Japanese Nationwide Study on the Association Between Short-term Exposure to Particulate Matter and Mortality.

BackgroundFrom around 2012, the use of automated equipment for fine particulate matter (PM2.5) measurement with equivalence to a reference method has become popular nationwide in Japan. This enabled us to perform a national health effect assessment employing PM2.5 concentrations based on the standardized measurement method. We evaluated the association between non-accidental mortality and short-term exposure to PM2.5 and coarse particulate matter (PM), with the latter estimated as the difference between suspended particulate matter and PM2.5, for the fiscal years 2012–2014.MethodsThis was a time-stratified case-crossover study in 100 highly-populated Japanese cities. Mortality data was obtained from the Ministry of Health, Labour and Welfare. City-specific estimates of PM-mortality association were calculated by applying a conditional logistic regression analysis, and combined with a random-effects meta-analysis.ResultsThe respective averages of daily mean concentration were 14.6 µg/m3 for PM2.5 and 6.4 µg/m3 for coarse PM. A 10 µg/m3 increase in PM2.5 concentrations for the average of the day of death and the previous day was associated with an increase of 1.3% (95% confidence interval (CI), 0.9–1.6%) in total non-accidental mortality. For cause-specific mortality, PM2.5 was positively associated with cardiovascular and respiratory mortality. After adjustment for PM2.5, we observed a 1.4% (95% CI, 0.2–2.6%) increase in total mortality with a 10 µg/m3 increase in coarse PM.ConclusionThe study revealed that short-term exposure to PM2.5 had adverse effects on total non-accidental, cardiovascular, and respiratory mortality in Japan. Coarse PM exposure also increased the risk of total mortality.

Obesity as a susceptibility factor to indoor particulate matter health effects in COPD

Our goal was to investigate whether obesity increases susceptibility to the adverse effects of indoor particulate matter on respiratory morbidity among individuals with chronic obstructive pulmonary disease (COPD). Participants with COPD were studied at baseline, 3 and 6 months. Obesity was defined as a body mass index ≥30 kg·m(-2). At each time point, indoor air was sampled for 5-7 days and particulate matter (PM) with an aerodynamic size ≤2.5 μm (PM2.5) and 2.5-10 μm (PM2.5-10) was measured. Respiratory symptoms, health status, rescue medication use, exacerbations, blood biomarkers and exhaled nitric oxide were assessed simultaneously. Of the 84 participants enrolled, 56% were obese and all were former smokers with moderate-to-severe COPD. Obese participants tended to have less severe disease as assessed by Global Initiative for Chronic Obstructive Pulmonary Disease stage and fewer pack-years of smoking. There was evidence that obesity modified the effects of indoor PM on COPD respiratory outcomes. Increases in PM2.5 and PM2.5-10 were associated with greater increases in nocturnal symptoms, dyspnoea and rescue medication use among obese versus non-obese participants. The impact of indoor PM on exacerbations, respiratory status and wheeze also tended to be greater among obese versus non-obese participants, as were differences in airway and systemic inflammatory responses to indoor PM. We found evidence that obesity was associated with exaggerated responses to indoor fine and coarse PM exposure among individuals with COPD.

Hemodynamic, Autonomic, and Vascular Effects of Exposure to Coarse Particulate Matter Air Pollution from a Rural Location

Background: Fine particulate matter (PM) air pollution is associated with numerous adverse health effects, including increased blood pressure (BP) and vascular dysfunction. Coarse PM substantially contributes to global air pollution, yet differs in characteristics from fine particles and is currently not regulated. However, the cardiovascular (CV) impacts of coarse PM exposure remain largely unknown.Objectives: Our goal was to elucidate whether coarse PM, like fine PM, is itself capable of eliciting adverse CV responses.Methods: We performed a randomized double-blind crossover study in which 32 healthy adults (25.9 ± 6.6 years of age) were exposed to concentrated ambient coarse particles (CAP; 76.2 ± 51.5 μg/m3) in a rural location and filtered air (FA) for 2 hr. We measured CV outcomes during, immediately after, and 2 hr postexposures.Results: Both systolic (mean difference = 0.32 mmHg; 95% CI: 0.05, 0.58; p = 0.021) and diastolic BP (0.27 mmHg; 95% CI: 0.003, 0.53; p = 0.05) linearly increased per 10 min of exposure during the inhalation of coarse CAP when compared with changes during FA exposure. Heart rate was on average higher (4.1 bpm; 95% CI: 3.06, 5.12; p < 0.0001) and the ratio of low-to-high frequency heart rate variability increased (0.24; 95% CI: 0.07, 0.41; p = 0.007) during coarse particle versus FA exposure. Other outcomes (brachial flow-mediated dilatation, microvascular reactive hyperemia index, aortic hemodynamics, pulse wave velocity) were not differentially altered by the exposures.Conclusions: Inhalation of coarse PM from a rural location is associated with a rapid elevation in BP and heart rate during exposure, likely due to the triggering of autonomic imbalance. These findings add mechanistic evidence supporting the biological plausibility that coarse particles could contribute to the triggering of acute CV events.Citation: Brook RD, Bard RL, Morishita M, Dvonch JT, Wang L, Yang HY, Spino C, Mukherjee B, Kaplan MJ, Yalavarthi S, Oral EA, Ajluni N, Sun Q, Brook JR, Harkema J, Rajagopalan S. 2014. Hemodynamic, autonomic, and vascular effects of exposure to coarse particulate matter air pollution from a rural location. Environ Health Perspect 122:624–630; http://dx.doi.org/10.1289/ehp.1306595

Historical trends in the mass and chemical species concentrations of coarse particulate matter in the Los Angeles Basin and relation to sources and air quality regulations

To assess the impact of past, current and proposed air quality regulations on coarse particulate matter (CPM), the concentrations of CPM mass and its chemical constituents were examined in the Los Angeles Basin from 1986 to 2009 using PM data acquired from peer-reviewed journals and regulatory agency database. PM10 mass levels decreased by approximately half from 1988 to 2009 at the three sampling sites examined- located in downtown Los Angeles, Long Beach and Riverside. Annual CPM mass concentrations were calculated from the difference between daily PM10 and PM2.5 from 1999 to 2009. High CPM episodes driven by high wind speed/stagnant condition caused year-to-year fluctuations in the 99th/98th percentile CPM levels. The reductions of average CPM levels were lower than those of PM10 in the same period, therefore the decrease of PM10 level was mainly driven by reductions in the emission levels of PM2.5 (or fine) particles, as demonstrated by the higher annual reduction of average PM2.5 (0.92 µg/m3) compared with CPM (0.39 µg/m3) from 1999 to 2009 in downtown Los Angeles despite their comparable concentrations. This is further confirmed by the significant decrease of Ni, Cr, V, and EC in the coarse fraction after 1995. On the other hand, the levels of several inorganic ions (sulfate, chloride and to a lesser extent nitrate) remained comparable. From 1995 to 2008, levels of Cu, a tracer of brake wear, either remained similar or decreased at a smaller rate compared with elements of combustion origins. This differential reduction of CPM components suggests that past and current regulations may have been more effective in reducing fugitive dust (Al, Fe and Si) and combustion emissions (Ni, Cr, V, and EC) rather than CPM from vehicular abrasion (Cu) and inorganic ions (NO3 −, SO4 2− and Cl−) in urban areas. Implications Limited information is currently available to provide the scientific basis for understanding the sources and physical and chemical variations of CPM, and their relations to air quality regulations and adverse health effects. This study investigates the historical trends of CPM mass and its chemical components in the Los Angeles Basin to advance our understanding on the impact of past and current air quality regulations on the coarse fraction of PM. The results of this study will aid policy makers to design more targeted regulations to control CPM sources to ensure substantial protection of public health from CPM exposure. Supplemental Materials Supplemental materials are available for this article. Go to the publisher's online edition of the Journal of the Air & Waste Management Association for (1) details of the sampling sites and (2) the daily concentrations of high CPM/PM10 episodes.

Effects of inhalable particulate matter on blood coagulation.

Particulate matter (PM) exposure has been linked to increased risk of cardiovascular disease, possibly resulting from hypercoagulability and thrombosis. Lung and systemic inflammation resulting from PM inhalation may activate blood coagulation, but mechanisms for PM-related hypercoagulability are still largely unknown. To identify coagulation mechanisms activated by PM in a population with well-characterized exposure. We measured prothrombin time (PT), activated partial thromboplastin time, endogenous thrombin potentials (ETPs) with/without exogenous triggers and with/without soluble thrombomodulin, tissue-type plasminogen activator (t-PA) antigen, D-dimer and C-reactive protein (CRP) in 37 workers in a steel production plant with well-characterized exposure to PM with aerodynamic diameter of < 1 mum (PM(1)) and coarse PM (PM(10) - PM(1)). Blood samples were collected from each subject on the first (baseline) and last (postexposure) day of a 4-day work week. We analyzed differences between baseline and postexposure levels using a paired Student's t-test. We fitted multivariate mixed-regression models to estimate the associations of interquartile range PM(1) and coarse PM exposure with parameter levels. None of the parameters showed any significant changes from baseline in postexposure samples. However, exposure levels were associated with shorter PT (beta[PM(1)] = -0.33 s, P = 0.08; beta[PM(coarse)] = - 0.33 s, P = 0.01), and higher ETP without exogenous triggers and with thrombomodulin (beta[PM(1)] = + 99 nm min, P = 0.02; beta[PM(coarse)] = + 66 nm min, P = 0.05), t-PA (beta[PM(1)] = + 0.72 ng mL(-1), P = 0.01; beta[PM(coarse)] = + 0.88 ng mL(-1), P = 0.04), and CRP (beta[PM(1)] = + 0.59 mg L(-1), P = 0.03; beta[PM(coarse)] = + 0.48 mg L(-1), P = 0.01). PM exposure did not show any short-term effect within the week of the study. The association of PM exposure with PT, ETP and CRP provides some evidence of long-term effects on inflammation and coagulation.

Lung response to coarse PM: Bioassay in mice

Particulate matter (PM) elicits inflammatory and toxic responses in the lung specific to its constituents, which can vary by region, time, and particle size. To identify the mechanism of toxicity in PM collected in a rural area in the San Joaquin Valley of Central California, we studied coarse particles of 2.5–10 μm diameter (PM 2.5–PM 10). Potential pro-inflammatory and toxic effects of PM 2.5–PM 10 in the lung were investigated using intratracheally instilled mice. We determined total and differential cell profiles and inflammatory chemokines in lung lavage fluid, and biomarkers of toxicity resulting from coarse PM exposure. Responses of the mice were readily observed with total doses of 25–50 μg of PM per mouse. Changes in pro-inflammatory cellular profiles and chemokines showed both dose and time responses; peak responses were observed 24 h after PM instillation, with recovery as early as 48 h. Furthermore, macrophage inflammatory protein (MIP-2) profiles following PM exposures were correlated to levels of measured macrophages and neutrophils recovered from lung lavage fluid of PM-treated animals. Our data suggest that pro-inflammatory effects observed from coarse PM collected during the summer months from California's hot and dry Central Valley are driven largely by the insoluble components of the PM mixture, and are not caused by endotoxin.