Particles with a 50% cut-off aerodynamic diameter of 10 µm can be inhaled into the lungs and, therefore, are referred to as thoracic, respirable, or inhalable particles. Since 1987, mass concentration of PM10 has been used in setting the US National Ambient Air Quality Standard for particulate air pollution . PM10 consists of fine particles with an aerodynamic diameter of 2.5 µm and coarse particles , and the contribution of PM2.5 to PM10 was relatively constant in a given area but varied between 35 and 80% by region . In 1997, the EPA proposed standards for PM2.5 . PM2.5 can be further divided into nucleation mode or ultrafine particles with an aerodynamic diameter less than 0.1 µm and accumulation mode particles . Whereas measurements of larger particles are commonly based on their mass concentration, UFPs have very little mass but comprise the vast majority of the total number of particles. Therefore, they are measured as number concentration. In Europe, there is a rather longstanding tradition of assessing levels of black smoke, which consists of black particles with an aerodynamic diameter less than 4.5 µm and measures elemental carbon . Based on the once valid assumption that black smoke originated mostly from burning coal, the OECD defined a standard of converting reflectance of these black soot particles into mass concentration. These standards are no longer appropriate because coal burning has decreased considerably in most industrialized countries over recent decades. Today, an estimated 60 to 90% of the atmospheric EC content is produced by diesel-powered vehicles. It is estimated that more than 80% of diesel exhaust particles have an aerodynamic diameter of 1 µm or less . Nonetheless, compared with purely gravimetric methods, measuring reflectance has the major advantage of providing some important information on the composition of particles.Coarse particles are generated from soil and other crustal materials mostly by the mechanical processes of agriculture, mining, construction, and road traffic,drying room but they also include particles of biological origin, such as pollen and fungal spores.

The most important sources of fine particles are incomplete combustion processes, formation of secondary particles via gas-to-particle reactions, and coagulation processes in the atmosphere. To varying degrees, ambient urban PM levels depend on both primary regional emissions and long-range transport. Indoor particle concentrations are determined by the concentration of particles outside and the generation of particles indoors. The contribution of outdoor PM2.5 to indoor levels has been estimated to average between 30 and 80% for homes from different geographical areas of the United States and Europe but can vary from 0 to 100% between individual buildings within these areas . This large variability results from the fact that the fraction of indoor PM derived from outdoor sources depends on various factors. These factors include particle penetration efficiency, particle deposition rate, air exchange rate, and the extent of particle generation during indoor activities of the residents, which, in turn, are subject to circadian and seasonal variation . The penetration efficiency of outdoor particles has been found to be close to one independent of particle size, indicating that building shells essentially do not filter particles nor do they provide protection from inhalation exposure to ambient PM . However, the effective penetration efficiency or infiltration efficiency depends on particle size because larger particles have higher deposition rates, whereas resuspension involves almost exclusively particles greater than 1 µm . The most important indoor source of particles is ETS . Considerable generation of particles also occurs during cooking and certain cleaning activities; vacuuming and the overall movement of people resuspend particles and contribute to indoor concentrations . Notably, one of these studies has provided evidence that terpeneozone reactions can result in pronounced elevations in fine particles and UFPs . As previously discussed, the products of terpene-O3 reactions have been shown to act as strong airway irritants . ETS results in elevated particle counts in all size ranges, but appears to more strongly affect the size fraction smaller than 1.0 µm . Cooking is one of the major indoor sources of UFP, with frying, toasting, baking, and barbecuing generating particles mostly in the ranges of 0.02 to 0.1 µm and 0.1 to 0.5 µm . Sautéing produces particles both in the ultra fine and coarse modes .

Although dusting, vacuuming, and walking constitute important sources of PM2.5, they predominantly raise the concentrations of coarse particles . Note that indoor particle events are brief and intermittent and not only have a pronounced effect on the size distribution of particles but can also raise particle number concentrations up to 100-fold and can result in peak mass concentrations that are several orders of magnitude higher than the values obtained from time-integrated samples .Inhalation is the major pathway of exposure to airborne particles, and adverse health effects can occur when particles are deposited in the lung or enter the systemic circulation via the lung. The fractional deposition of fine particles and UFPs is fairly high, generally ranging from approx 0.4 to 0.7 for UFPs, depending on the nature and size of the test aerosol and the breathing pattern . Total lung as well as peak deposition within certain regions of the lung depend on particle size, becoming greater with decreasing particle size for particles less than 0.5 µm and with increasing particle size for particles greater than 0.5 µm . The site of peak deposition also depends on particle size, with the site of maximal deposition shifting proximally with decreasing particle size for particles less than 0.1 µm and with increasing particle size for particles greater than 1 µm. This entails that local deposition dose can greatly exceed the average dose of the entire lung. Whereas fine and coarse particles deposit by gravitational sedimentation and inertial impaction, diffusion is the predominant mechanism of deposition of particles for the UFP range and up to a diameter of approx 0.3 to 0.5 µm. Peak deposition of UFP was observed in a volumetric lung region corresponding to the transition zone between the conducting airways and alveolar regions . Similarly, autopsy studies of lung tissue from subjects who had lived in areas with high particulate air pollution have indicated that tissue retention of fine particles is mostly observed in this transition zone . There is some evidence that UFPs are not necessarily retained in the lung but can diffuse directly into the systemic circulation . In healthy subjects, the magnitude of the total deposition fraction for fine particles and UFPs mainly depends on tidal volume and respiratory time and does not differ significantly between young and elderly subjects using the same controlled breathing patterns. Consistent with these observations, deposition of UFPs increases markedly with exercise as a result of both increased minute ventilation and an increase in the depositional fraction .

The influence of lung function parameters on the deposition fraction appears to be essentially negligible in healthy subjects . However, this is not applicable to patients with obstructive airway disease. Results from several recent studies indicate that deposition of fine particles as well as UFPs is greater in patients with asthma or chronic obstructive pulmonary disease than in healthy subjects , whereas clearance does not differ significantly . Examination of autopsy lungs indicates that particles are retained in lung parenchyma from residents of areas with low-to-moderate air pollution and that particle burden is significantly higher in lungs from residents of more highly polluted areas . A vast majority of these particles have aerodynamic diameters smaller than 2.5 µm, but UFPs constitute only a small fraction of the total . Such studies further show that retention of fine particles occurs primarily in terminal and respiratory bronchioles and is associated with inflammatory changes and small airway remodeling that may contribute to chronic airflow obstruction .In an ever-growing number of time series studies from around the world,trimming marijuana plants short-term increases in PM10 are statistically associated with increased cardiopulmonary morbidity and mortality . Conversely, there are indications that reduction of particulate air pollution is associated with a significant decrease in daily mortality . Fewer studies have addressed the effects of fine particles, but studies that have analyzed both PM10 and PM2.5 have provided evidence of much stronger associations of morbidity and mortality with the fine fraction . High correlations between PM and other air pollutants have been reported in some locations, and other criteria pollutants have also been linked to increased morbidity and mortality . However, at least part of the effect of PM appears to be independent of other air pollutants, and it remains a matter of debate whether gaseous pollutants are confounders, effect modifiers, or actual surrogates for PM exposure . Effect estimates for the increase in overall mortality associated with a 10 µg/m3 increase in PM10 range from approx 0.2 to approx 0.7% . Corresponding estimates for cardio respiratory mortality are usually considerably higher, and there is a markedly greater increase in respiratory compared with cardiovascular mortality . However, because cardiovascular disease affects far more people, the absolute number of cardiovascular deaths associated with particulate air pollution is substantially greater than that of respiratory deaths. Cross-sectional time series suffer from the inability to control for confounding factors such as smoking, alcohol consumption, diet and nutrition, body mass index, occupational exposure, and socioeconomic factors. However, the results from several large prospective cohort studies, in which such corrections are possible, have not only confirmed that higher ambient particulate pollution levels are associated with significant increases in deaths from lung cancer and cardiopulmonary disease but have yielded much larger effect estimates .

In a recent extended follow-up of one of the American Cancer Society cohorts, an increase in annual mean PM2.5 concentration was found to correlate with increases in all cause, cardiopulmonary, and lung cancer mortality of at least 4, 6, and 8% of subjects, respectively; the estimate depended on the time period during which PM2.5 levels were measured . All other causes of mortality were not associated with particulate air pollution. In partial contrast, in a cohort of nonsmoking Seventh-Day Adventists, ambient concentrations of PM10 were significantly associated with all-cause mortality in both genders and with lung cancer deaths in males only but were not associated with cardiopulmonary mortality . However, there was a significant association with deaths for which the death certificate made any mention of nonmalignant respiratory disease as an underlying or contributing cause of death. There are indications that the elderly and people with underlying heart disease, respiratory disease, or diabetes are more susceptible to the adverse effects of particulate and other air pollution . Nonetheless, the increase in daily mortality associated with particulate air pollution does not appear to be simply “ premature harvesting”—that is, the advancement of death by a few days in individuals with severe illness. Instead, some recent analyses have suggested that particulate air pollution shortens life expectancy by at least several months . Additionally, consistent with the results of prospective studies, the effect size estimates become considerably larger when longer lag periods are considered . We emphasize that although the effects of acute PM exposure on mortality are very small, a vast majority of the world population is exposed to this type of pollution, making the number of premature deaths associated with this exposure substantial. A recent estimate stated that 800,000 deaths worldwide are attributable to particulate pollution alone, of which approx 65% occur in Asia . Note that adverse effects associated with particulate air pollution are evident at levels below the standards set by various governmental and supra governmental agencies. Furthermore, the relationship between PM concentrations and adverse health effects is essentially linear, and there does not appear to be a threshold below which exposure can be considered safe . The biological plausibility of a causal association between particulate air pollution and adverse cardiovascular and respiratory health effects is supported by the fact that adverse effects of particulate and other air pollution on mortality and morbidity have rather consistently been reported from numerous areas worldwide with widely differing mixtures of air pollutants, absolute levels of PM, particle sources, and, therefore, particle composition. However, there are considerable differences in the size of the effect estimates. This is most likely attributable to differences in absolute exposure levels, particle sources, and their size distribution and composition, but may also include differences in the subjects and in the definitions of outcome measures.