Huang et al. applied principal component analysis to data from their study, which showed that controlled exposure to CAPS from the Chapel Hill area induced an increase in neutrophils in the bronchial and alveolar fraction and increased blood fibrinogen levels in young healthy adults . The results of this analysis indicated that among the water-soluble fraction of CAPS, a sulfate/ Fe/Se factor was associated with an increase in the percentage of neutrophils in BALF and a Cu/Zn/V factor was associated with increased blood fibrinogen. This suggests that soluble constituents of PM differentially affect target organs and systems, which is consistent with the findings of in vitro and animal studies suggesting that particle-associated metals differ in their ability to affect different cell types within the lung and in the mechanisms by which they operate . These analyses were restricted to outdoor particles. It has been suggested that ambient stationary site measurements, as used in time series and most panel studies, do not accurately reflect personal exposures because people spend approx 90% of their time indoors and the contribution of outdoor particles to indoor concentrations varies widely between homes. Ambient sampling has been shown to overestimate the exposures resulting from traffic-related and long-range transport sources and to underestimate some significant indoor sources . Additionally, the chemical composition of indoor and outdoor particles can differ markedly . Notably, some indoor and outdoor particles exhibited similar trace element composition,drying rack for weed but scanning electron microscopy revealed that spherical particles, usually indicative of combustion or other high temperature industrial processes, were present almost exclusively in outdoor and ambient samples .
Furthermore, indoor particles can have greater toxicity than outdoor particles . Then, the issue arises regarding whether indoor or outdoor exposures are more relevant to the observed health outcomes. In a study that assessed personal exposure to PM10 and PM2.5 in children with asthma along with residential indoor and outdoor as well as central-site PM concentrations, FEV1 was associated with the 5-d average of all measurements but was most strongly associated with personal exposure . Residential indoor levels of PM2.5 and PM10 showed stronger associations with FEV1 than residential outdoor or central-site concentrations. Assessment of indoor and outdoor PM2.5 levels in some of the HRV studies also indicated somewhat greater effects associated with indoor concentrations . Biomarkers of oxidative stress in blood were associated with personal exposure to PM2.5 and black smoke but not with ambient background concentrations . These studies do not clarify whether indoor or outdoor sources are most relevant to the observed health effects. In recent studies, different modeling approaches have been used to determine ambient and non-ambient exposures to then correlate them with observed health effects . In one of these studies , personal PM2.5 exposure was found to be composed mostly of non-ambient particle exposure, and neither total personal nor non-ambient exposure was associated with any of the investigated health outcomes, with the exception of an unexpected increase in FEV1 . Ambient exposures were associated with decreased FEV1 and systolic blood pressure and increased heart rate and supra ventricular ectopic heartbeats. In most cases, ambient exposures provided better effect estimates than ambient concentrations. In another study, increases in exhaled NO were more strongly associated with the ambient-generated component of personal exposure . Conversely, and also differing from the previously discussed results , indoor-generated PM2.5 were associated with FEV1 and FVC but not mid-expiratory flow . Note that this association was somewhat dependent on the model used for estimating the indoor-generated component of PM2.5 exposure.
Interestingly, lag 0 indoor home PM2.5 and PM10 concentrations were significantly associated with decreases in FEV1 , whereas residential outdoor and central site measurements showed some significant associations with FEV1 only at longer averaging periods in another panel of children with asthma . This also suggests that indoor and outdoor particles differ in the mechanisms through which they induce adverse effects on respiratory health. Although somewhat preliminary in nature, these results suggest that ambient and nonambient particles are differentially associated with various health outcomes.The first report of a cluster of people in the same building becoming ill at the same time occurred in 1976, when 182 attendees of a convention of the American Legion in Philadelphia developed a disease characterized by respiratory symptoms that proved fatal in 29 of the cases. The disease was named Legionnaires’ disease, and the organism responsible was eventually called Legionella pneumonia.In buildings, they grow in air conditioning cooling towers, hot water tanks, other parts of the plumbing systems, and hot tubs. The disease is contracted by the inhalation of aerosolized droplets of water that are contaminated with the bacteria, but it is not spread by person-to-person contact. The incubation period is 2 to 14 d. Every year, 8000 to 10,000 people are hospitalized with Legionnaires’ disease. Individuals over age 65 yr, those with chronic lung diseases, those who are immuno suppressed, and patients with chronic illness are more susceptible. The mortality rate ranges from 5 to 30%. A less severe, non-respiratory form of Legionnaires’ disease was named Pontiac fever because it was first described in 144 health department facility workers in Pontiac, Michigan . The illness is caused by a bacterium with characteristics similar to that of L. pneumonia; it is self-limiting, and the symptoms include headache, fever, malaise, and myalgias.
Although the etiology of these disease outbreaks associated with specific buildings was initially unknown, causative agents were eventually identified, making Legionnaires’ disease and Pontiac fever examples of specific building-related illnesses. Other microbial agents have also been reported to cause outbreaks of disease that are confined to a particular building. Examples include influenza virus infections in nursing homes and, more recently, clusters of severe acute respiratory syndrome cases in a hospital and an apartment complex . However, in these cases, the buildings were not reservoirs of the infectious agents. Rather, transmission from human to human within the building caused the outbreaks.Fungi are ubiquitous. They require moisture for growth and survival but can grow on various substrates, including dead or living plant and animal tissue, paint, paper products, and building materials. During reproduction, they become airborne as mold spores. Fungal spore concentrations in indoor environments are measured in either air or dust,trimming cannabis and the results are reported either as viable spore concentrations in colony-forming units per cubic meter or per gram of dust or as total spore counts expressed in spores per cubic meter. The total spore count can be up to two orders of magnitude higher than the number of viable microbes. Viable fungal spore concentrations in more than 12,000 samples from more than 1700 buildings in the United States ranged from below the detection limit to more than 8200 CFU/m3 in outdoor air and to more than 10,000 CFU/m3 in indoor air samples . Median indoor and outdoor concentrations were 80 and approx 500 CFU/m3 , respectively. Similarly, in 19studies from North America, Europe, Asia, and Australia, total viable spore counts varied between below the detection limit and 23,000 CFU/m3 in indoor air samples from buildings with visible mold growth . With one notable exception , the maxima in indoor air samples from buildings without signs of mold growth were lower. There is seasonal as well as regional variability in the number of airborne mold spores and in the ratio of outdoor to indoor concentrations . This applies not only to concentrations of total fungi but also to specific genera and species . Outdoor viable as well as total spore counts are generally higher than, but show a positive correlation with, indoor levels . Indoor mold spore concentrations can exceed those found outdoors in buildings with obvious water damage or signs of mold growth; however, several studies have reported similar mold spore counts in buildings with and without dampness and mold problems . The profile of indoor fungi also differs from that found outdoors, and the diversity of fungal species is frequently greater in damp buildings . Worldwide, the most common genera in indoor and outdoor air are Penicillium, Cladosporium, and Aspergillus . Species that require high water activity, such as Stachybotrys and Trichoderma, are reported much less frequently because of their more infrequent occurrence and because they are difficult to culture with the standard culture methods . Fungal spore release is irregular and depends on various environmental conditions. Additionally, fungal spores in settled dust can be resuspended by human activities. Consequently, there can be substantial temporal variation in airborne spore counts. Measurements of airborne fungal spores fail to capture this variability and poorly reflect actual exposure because they are usually based on very short sampling periods . There are few reports of longer term measurements . In one study, personal exposure of 81 Finnish schoolteachers to total as well as viable microbes was determined by 24- h sampling with a personal button particle sampler and was compared with residential and workplace indoor concentrations . Geometric mean concentrations of total fungi were higher in the work environment than in the home environment , and concentrations of fungi in the home environment were similar to personal exposure levels . The geometric mean concentrations of viable fungi were 2 to 3, 5 to 6, and 12 CFU/m3 in work, home, and personal samples, respectively.
Fungal spores settle with floor dust, which can be resuspended during walking and other human activities; therefore, fungal concentrations in floor dust are believed to be a surrogate for cumulative exposure. More recently, fungal components such as extracellular polysaccharides , β–D-glucans, and ergosterol have been measured in house dust and air . The results suggest that they may represent acceptable markers of fungal exposure. Statistically significant, although not very strong, correlations were detected between EPS of Aspergillus/Penicillium and β-glucan levels in house dust and total culturable fungi . The weakness of the association may reflect that both markers represent total fungal biomass rather than only culturable species. In one of the studies, EPSAsp/Pen levels in floor dust were found to correlate positively with occupant-reported, but not investigator-observed, mold and dampness problems in the living room . For bedrooms, the association was inverted, possibly because of allergen avoidance measures. In 110 homes in Canada, airborne β-glucan and ergosterol concentrations obtained via long term active sampling were highly correlated not only with each other but also with area covered by visible mold growth . The correlation between glucans and total spore counts was markedly weaker, although highly significant.Reviews performed by a committee of European scientists regarding the literature on health effects associated with building dampness have concluded that dampness in nonindustrial work and residential environments is associated with a variety of health effects . Such health effects include increased prevalence of self-reported and physician-diagnosed asthma, decreased lung function, increased prevalence and severity of asthmatic and allergic symptoms, allergic sensitization, and inflammatory markers in nasal lavage. There is also evidence for associations with other typical SBS symptoms, although it is weaker than evidence for respiratory symptoms. However, the agents responsible for the increased risk of health effects associated with exposure to dampness remain unclear. There is some evidence that house dust mites are involved but do not fully account for the observed effects. Additionally, it is possible that organic chemicals given off by degrading building materials mediate some of the health effects associated with building dampness. However, microbiological agents and/or some of their products are prime candidates. There have been numerous reports of significant associations of SBS symptoms and other health effects not only with self-reported visible mold growth, but also with viable fungal spore counts in air and dust . Similarly to building dampness, the associations are with respiratory symptoms, lung function, and asthma prevalence. Inconsistent results were reported for nasal, throat, eye, skin, and general symptoms. Recently, however, significant and dose-dependent associations were detected between levels of culturable fungi in floor dust and mucous membrane and general symptoms in female—but not in male—teachers from 15 Danish public schools . Specifically, the risk of experiencing difficulties in concentrating was increased more than 10-fold at the highest exposure levels. Otherwise, however, the strongest associations with symptoms were detected for recent airway infections, hay fever, psychosocial factors, and current smoking status.