Even stratification into more sensitive subgroups did not yield any significant findings

Further evidence of plausibility comes from the finding that PM associated adverse health effects cover a continuous spectrum of severity . In addition to increased mortality, this spectrum includes increased hospitalizations for cardiovascular and respiratory diseases , emergency department and other health care visits for asthma and other respiratory symptoms , prevalence of atherosclerosis , decreased lung function and lung function growth , and increased respiratory infections and respiratory symptoms .In addition to cross-sectional and prospective cohort studies, panel studies have become an important tool for assessing the effects of particulate pollution on respiratory and other health outcomes. Such studies use repeated measurements of the outcome of interest in a fairly small group of subjects and correlate them with daily changes in ambient concentrations of PM and other air pollutants, which are generally obtained from central monitoring sites. A significant association between particulate pollution and declines in PEFRs as well as increased prevalence of cough and lower respiratory symptoms has been reported in some panels of unselected children but not in others . In other studies, only children with asthma or asthmatic symptoms appeared to be susceptible to the effects of particulate air pollution . Similarly, in panels of unselected adults, associations of PM and other air pollutants with increases in the prevalence of decrements in PEFR greater than 20 or in respiratory symptoms were only observed in those with chronic respiratory symptoms or increased airway lability but not in those without . Such findings suggest that patients with obstructive airway disease are more susceptible to the adverse effects of particulate air pollution. Therefore,vertical farming units most panel studies have focused on children and adults with asthma or, more rarely, COPD. Significant negative associations between daily fluctuations in PM10 and PEF deviation or prevalence of PEF decrements greater than 10 and 20% have been reported in asthmatic children . An association of borderline significance was also noted in one panel of patients with COPD .

These are not entirely consistent findings . Notably, no effect of PM10 on PEFR were observed in the Pollution Effects on Asthmatic Children in Europe study, one of the largest panel studies on air pollution and respiratory health in children with chronic respiratory symptoms, involving more than 2000 children in 14 European centers .The association between exposure to PM10 and other lung function measures, such as FEV1 or FVC, has been investigated more rarely. Significant negative associations between residential outdoor and, to a lesser extent, central site PM10 values and FEV1 were observed in children with asthma from southern California . In a panel of 86 children with asthma from Detroit, PM10 and 8-h peak O3 levels with a 2-d lag showed a significant negative correlation with diurnal variability in FEV1 and lowest daily FEV1 value . However, others were unable to detect an effect of PM10 on FEV1 or FVC . In numerous panel studies of children and adults with asthma, a significant association has been detected between elevations in PM10 concentrations and increased incidence and prevalence of cough, phlegm, specific respiratory symptoms, or symptom scores . Similar associations have been reported in patients with COPD . Again, there have been studies that have not confirmed these findings, including the large PEACE study . Some panel studies with asthmatic children and adults have indicated that the prevalence of asthma medication use rises during, or shortly after, periods of elevated PM pollution . Associations have been reported between both bronchodilator and maintenance medication use and various PM size fractions, including PM10 and PM2.5 as well as UFPs. However, others failed to observe a significant effect of PM on the prevalence of asthma medication intake or the daily dose . Several studies have analyzed potential interactions between the effects of anti-inflammatory medication use and exposure to ambient PM on asthma symptoms and lung function .

In some investigations, associations between PM and increased symptoms and/or decreased lung function were only noted, or were stronger, in those subjects who were taking anti-inflammatory medication . This was even reported from panels whose prevalence of asthma medication use increased in association with elevated particulate pollution . Note that this increased overall medication use did not necessarily affect the associations of PM with lung function in the same way it influenced the association with symptoms . Others were unable to detect a significant interaction between the effects of anti-inflammatory medication use at baseline and PM10 exposure on asthma symptoms or lung function . Finally, there have also been studies in which particulate air pollution significantly affected lung function, exhaled NO , or symptoms to a much greater extent, or exclusively in children who did not take inhaled corticosteroids. Some of these discrepancies may have resulted from the fact that some studies assessed medication use only at baseline, whereas others assessed medication use during the entire follow-up period. Additionally, the effects of particulate pollution on lung function and symptoms were observed at different lag and averaging times in the various studies. The averaging time for particulate concentrations, symptom severity of the subjects, and medication use were all found to have a major impact on the association between PM pollution and increased symptom scores in a study of 25 children and adolescents with asthma in southern California . The largest effect of 24-h mean PM10 concentrations was noted in less symptomatic children who did not take anti-inflammatory medications, whereas more symptomatic asthmatics showed the greatest increase in symptoms in association with short-term PM10 excursion . No association between PM10 at any averaging or lag time could be detected in subjects who took anti-inflammatory medications, whereas non-medicated subjects exhibited large and significant increases in symptom scores in association with same day 8-h maximum and 24-h mean PM10 levels as well as with their 5-d moving averages. Overall, the available data suggest that anti-inflammatory medication and possibly bronchodilator use provide some protection from the effects of particulate pollution on lung function and symptoms in patients with asthma.

Protection may be incomplete if the type or dose of medication is inadequate. In some patient groups, however, medication use appears to be a marker of asthma severity, which confounds the protective effects of anti-inflammatory therapy. Interactions have been observed not only with medication use but also with respiratory infections. In a panel of 86 children with asthma living in Detroit, both PM2.5 and PM10 were significantly associated with decreased lung function in children with upper respiratory infections with a 3- to 5-d lag, whereas PM2.5 did not show significant effects in the absence of upper respiratory infections . Others did not detect a significant interaction between the effects of respiratory infections and concentrations of particulate air pollution on percent predicted FEV1 . When symptom severity was the outcome of interest, however, the same investigators found significantly stronger associations with various averaging times of PM10, O3 , and NO2 during respiratory infections, with some of the ORs increasing up to fivefold .Numerous panel and some cross-sectional population-based studies have investigated the association of PM10 and PM2.5 with time- and frequency-domain parameters of heart rate variability . In panel studies, small, but significant, decreases in time domains, such as the standard deviation of all normal-to normal intervals and the square root of the mean of the sum of the squares of differences between adjacent NN intervals were observed in association with daily fluctuations in centrally monitored PM2.5 and PM10 concentrations as well as in association with personal exposure to UFPs . Frequency domains of HRV,weed drying room such as high- and low-frequency power, also showed small but significant inverse associations with daily changes in outdoor and indoor PM2.5 concentrations or the time-weighted total exposure derived from them . They also decreased significantly in association with fluctuation in personal exposure to sub-micrometer particles . The inability to detect significant effects of PM2.5 and PM10 on HRV in some other panel studies likely results from the small sample sizes, low absolute pollution levels in both of the locations, low variability of PM2.5 measurements for most subjects, and, possibly, differences in the composition of particles from these cities compared with other metropolitan areas. Most of these panel studies were conducted in elderly subjects, and there are indications that the elderly are more susceptible to the effects of particulate pollution on HRV than younger adults . Susceptibility appears to be further enhanced in subjects with underlying cardiovascular disease and hypertension , although others did not observe a significant effect modification by CVD . However, some effects on HRV have also been reported in young subjects in association with personal PM2.5 and UFP exposure , with the effects of UFPs being smaller in young subjects than in older subjects studied simultaneously . Additionally, brief occupational and environmental exposures to PM2.5 were significantly associated with decreased SDNN in relatively young cohorts of boilermakers . In striking contrast to the fairly consistent finding of decreased HRV, in nine North Carolina State Highway Patrol troopers, PM2.5 exposure inside their vehicles was associated with increased HRV and other changes suggestive of increased vagal tone . Principal factor analysis of components of PM2.5 and associated pollutants indicated that these changes were associated most strongly with PM resulting from brake wear and engine emissions .

This type of PM may exert different effects than ambient particles from other sources. The results of controlled exposure studies are also not entirely consistent with these findings . Note that particle concentrators used to generate CAPS concentrate fine particles but not UFPs. This could account for some of the differences between the results of controlled exposure studies with CAPS compared with those of panel studies because UFPs were shown to exert significant effects on HRV . Overall, however, there is rather consistent evidence that exposure to PM results in changes in cardiac autonomic control, and the decreases in SDNN in r-MSSD suggest reduced parasympathetic tone. Exposure to particulate air pollution is also associated with a decrease in heart rate , which is consistent with an increase in sympathetic tone; however, an association has not been evident in all studies .Specific rotation factor analysis of the elemental composition of fine and course PM measured in six US cities indicated that PM2.5 from mobile sources showed the strongest association with overall daily mortality, followed by particles from coal combustion sources . Fine particles from crustal sources were not associated with mortality. Interestingly, a 10-µg/m3 increase in particles from mobile sources was associated with a 2% increase in deaths from ischemic heart disease, but this was not statistically significant. An adverse effect of traffic-related particles on respiratory deaths was not evident. Conversely, deaths from COPD and pneumonia increased with increased exposure to particles from coal combustion sources, whereas this factor did not affect deaths from ischemic heart disease. Similarly, analysis of data from 14 US cities regarding PM10 emissions by source category indicated that hospital admissions for CVD were most strongly correlated with increasing percentage of PM10 from highway vehicles and highway diesels . A correlation between percentage of PM10 from highway vehicles/ diesels and hospitalization for COPD was not observed for the entire data set but became significant after exclusion of two cities . These findings are consistent with reports of increased mortality and morbidity in association with indicators of traffic and traffic-related air pollution, such as black smoke and NO2 . Additionally, in several studies, , including some analyses of the effects of air pollution on respiratory health , some investigators found black smoke to be more strongly associated with adverse health effects compared with PM10 or PM2.5 . EC and organic carbon are also likely to be derived largely from traffic emissions. In Hispanic children living in an area of Los Angeles with high traffic density, an asthma symptom score was more strongly associated with EC and OC than with PM10 . In two-pollutant models that included EC and OC along with PM10, the OR for PM10 was reduced to 1.0, whereas the ORs of EC and OC remained unchanged. The composition of PM does not vary only by emission source; even ambient particles used for CAPS studies show considerable day to-day variation in their OC, EC, and elemental composition .

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