The guidelines also offer qualitative statements on good practices for the management of certain types of particulate matter (PM), for example black carbon/elemental carbon, ultrafine particles, and particles originating from sand and dust storms, for which there is insufficient quantitative evidence to derive AQG levels.
Particle pollution refers to a mix of tiny solid and liquid particles that are in the air we breathe. Many of the particles are so small as to be invisible, but when levels are high, the air becomes opaque. Nothing about particle pollution is simple. In fact, it is so dangerous that it can shorten your life.
Size matters. Particles themselves are different sizes. Some are one-tenth the diameter of a strand of hair. Many are even tinier; some are so small they can only be seen with an electron microscope. Because of their size, you cannot see the individual particles. You can only see the haze that forms when millions of particles blur the spread of sunlight.
Researchers categorize particles according to size, grouping them as coarse, fine and ultrafine. Coarse particles (shown as blue dots in the illustration) fall between 2.5 microns and 10 microns in diameter and are called PM 10-2.5. Fine particles (shown as pink dots in the illustration) are 2.5 microns in diameter or smaller and are called PM2.5. Ultrafine particles (not shown) are smaller than 0.1 micron in diameter1 and are small enough to pass through the lung tissue into the blood stream, circulating like the oxygen molecules themselves. No matter what the size, particles can harm your health.
The differences in size make a big difference in where particles affect us. Our natural defenses help us to cough or sneeze some coarse particles out of our bodies. However, those defenses do not keep out smaller fine or ultrafine particles. These particles get trapped in the lungs, while the smallest are so minute that they can pass through the lungs into the bloodstream, just like the essential oxygen molecules we need to survive.
The mixtures differ between different regions in the United States and in different times of the year. Much of that comes from the sources that produce the particles. For example, nitrate particles from motor vehicle exhaust form a larger proportion of the unhealthful mix in the winter in western states, especially California and portions of the Midwest. By contrast, eastern states have more sulfate particles than the West on average, largely due to the high levels of sulfur dioxide emitted by large, coal-fired power plants.3
Even low levels of particles can be deadly. A 2016 study found that people aged 65 and older in New England faced a higher risk of premature death from particle pollution, even in places that met current standards for short-term particle pollution.2 Another study in 2017 looked more closely at Boston and found a similar higher risk of premature death from particle pollution in a city that meets current limits on short-term particle pollution.3 Looking nationwide in a 2017 study, researchers found more evidence that older adults faced a higher risk of premature death even when levels of short-term particle pollution remained well below the current national standards. This was consistent whether the older adults lived in cities, suburbs or rural areas.4 Some of the strongest research has documented that short-term exposure to particle pollution causes premature death from respiratory and cardiovascular causes.5
In 2013, the International Agency for Research on Cancer (known as IARC), part of the World Health Organization, concluded that particle pollution causes lung cancer. The IARC based its decision on the review of multiple studies from the U.S., Europe, and Asia and the presence of carcinogens on the particles.5
With so many sources of particles, researchers want to know if some particles pose greater risk than others. Researchers are exploring possible differences in health effects of the sizes of particles and particles from different sources, such as diesel particles from trucks and buses or sulfates from coal-fired power plants. Recent studies have tried to answer this question. So far, the answers are complicated.
Each particle may have many different components. The building blocks of each can include several biological and chemical components. Bacteria, pollen and other biological ingredients can combine in the particle with chemical agents, such as heavy metals, elemental carbon, dust and secondary species like sulfates and nitrates. These combinations mean that particles can have complex effects on the body.1
Other studies have identified the challenges of exploring all the kinds of particles and their health effects with the limited monitoring across the nation.5,6Some particles serve as carriers for other chemicals that are also toxic, and the combination may worsen the impact.7,8
Lepeule J, Laden F, Dockery D, Schwartz J. Chronic exposure to fine particles and mortality: An extended follow-up of the Harvard Six Cities Study from 1974 to 2009. Environ Health Perspect. 2012; 120: 965-970. U.S. EPA, 2019, Section 6.1.9.
Background: Ambient fine particulate matter with aerodynamic diameter less than 2.5 µm (PM2.5) has been associated with deteriorated respiratory health, but evidence on particles in smaller sizes and childhood respiratory health has been limited.
Methods: We collected time-series data on daily respiratory emergency room visits (ERVs) among children under 14 years old in Beijing, China, during 2015-2017. Concurrently, size-fractioned number concentrations of particles in size ranges of 5-560 nm (PNC5-560) and mass concentrations of PM2.5, black carbon (BC) and nitrogen dioxide (NO2) were measured from a fixed-location monitoring station in the urban area of Beijing. Confounder-adjusted Poisson regression models were used to estimate excessive risks (ERs) of particle size fractions on childhood respiratory ERVs, and positive matrix factorisation models were applied to apportion the sources of PNC5-560.
The association between particulate air pollution and asthma medication use and symptoms was assessed in a panel study of 53 adult asthmatics in Erfurt, Germany in winter 1996/1997. Number concentrations of ultrafine particles, 0.01-0.1 microm in diameter (NC(0.01-0.1), mean 17,300 x cm(-3), and mass concentrations of fine particles 0.01-2.5 microm in diameter (MC(0.01-2.5)), mean 30.3 microg x m(-3), were measured concurrently. They were not highly correlated (r=0.45). The associations between ambient particle concentrations and the prevalence of inhaled beta2-agonist, corticosteroid use and asthma symptoms, were analysed separately with logistic regression models, adjusting for trend, temperature, weekend, holidays, and first order autocorrelation of the error. Cumulative exposures over 14 days of ultrafine and fine particles were associated with corticosteroid use. Beta2-agonist use was associated with 5-day mean NC(0.01-0.1) and MC(0.01-2.5). The prevalence of asthma symptoms was associated with ambient particle concentrations. The results suggest that reported asthma medication use and symptoms increase in association with particulate air pollution and gaseous pollutants such as nitrogen dioxide.
Due to its increasing production, durability and multiple applications, plastic is a material we encounter every day. Small plastic particles from the μm to the mm range are classified as microplastics and produced for cosmetic and medical products, but are also a result of natural erosion and decomposition of macroplastics. Although being omnipresent in our environment and already detected in various organisms, less is known about the effects of microplastics on humans in general, or on vascular biology in particular. Here we investigated the effects of carboxylated polystyrene microplastic particles (PS, 1 μm) on murine endothelial and immune cells, which are both crucially involved in vascular inflammation, using in vitro and in vivo approaches. In vitro, PS induced adhesion molecule expression in endothelial cells with subsequent adhesion of leukocytes both under static and flow conditions. In monocytic cells, PS enhanced pro-inflammatory cytokine expression and release. Accordingly, administering mice with PS led to enhanced aortic expression of cytokines and adhesion molecules. Furthermore, we identified neutrophils as the PS-clearing blood leukocyte population. The findings from this study for the first time indicate polystyrene microplastic as a new environmental risk factor for endothelial inflammation.
For in vitro experiments, we used murine cell lines: endothelial MyEND cells (myocardial endothelial cells, RRID: CVCL_2131) which we recently characterized in regard to endothelial markers and properties  as well as monocytic J774A.1 cells (CVCL_0358), which were cultured in a humidified incubator at 37°C and 5% CO2. MyEND cells were cultured using Dulbecco´s Modified Eagle´s Medium (DMEM, Gibco, Darmstadt, Germany) supplemented with 10% fetal calf serum (FCS, PAN-Biotech, Aidenbach, Germany) and 1% Penicillin/Streptomycin (PenStrep, 100 U/mL and 100 mg/mL, Sigma-Aldrich, Seelze, Germany). For J774A.1, DMEM GlutaMAX (Gibco) supplemented with 10% FCS and 1% PenStrep was used. PS particles conjugated with tetramethylrhodamine isothiocyanate (TRITC) or unconjugated (1 μm, carboxylated, Kisker Biotech, Steinfurt, Germany,) were used as a representative of microplastics abundantly occurring in our environment. Polystyrene as polymer component of the particles was confirmed by Raman spectroscopy (S1A and S1B Fig) and size distribution of the PS particles were measured by dynamic light scattering (1108±185.6 nm, Zetasizer Nano ZS90, Malvern Pananalytical, Malvern, UK) (S1C Fig). Using the above mentioned medium supplemented with 1% FCS, J774A.1 (sub-confluent) and MyEND (confluent) cells were starved for 2 hours and subsequently stimulated with PS particles (103, 105 and 107 particles/mL, which corresponds to 0.54 ng/mL, 54 ng/mL and 5.4 μg/mL) for 3 and 6 hours in a 12-well plate, respectively. RNA and supernatant were used for further real-time PCR and ELISA analysis. 2b1af7f3a8