Unhealthy levels of air pollution are breathed by billions of people worldwide, and air pollution is the leading environmental cause of death and disability globally. Efforts to reduce air pollution at its many sources have had limited success, and in many areas of the world, poor air quality continues to worsen. Personal interventions to reduce exposure to air pollution include avoiding sources, staying indoors, filtering indoor air, using face masks, and limiting physical activity when and where air pollution levels are elevated. The effectiveness of these interventions varies widely with circumstances and conditions of use. Compared with upstream reduction or control of emissions, personal interventions place burdens and risk of adverse unintended consequences on individuals. We review evidence regarding the balance of benefits and potential harms of personal interventions for reducing exposure to outdoor air pollution, which merit careful consideration before making public health recommendations with regard to who should use personal interventions and where, when, and how they should be used.

Previous human exposure studies of traffic-related air pollutants have demonstrated adverse health effects in human populations by comparing areas of high and low traffic, but few studies have utilized microenvironmental monitoring of pollutants at multiple traffic locations while looking at a vast array of health endpoints in the same population. We evaluated inflammatory markers, heart rate variability (HRV), blood pressure, exhaled nitric oxide, and lung function in healthy participants after exposures to varying mixtures of traffic pollutants. A repeated-measures, crossover study design was used in which 23 healthy, non-smoking adults had clinical cardiopulmonary and systemic inflammatory measurements taken prior to, immediately after, and 24 hours after intermittent walking for two hours in the summer months along three diverse roadways having unique emission characteristics. Measurements of PM2.5, PM10, black carbon (BC), elemental carbon (EC), and organic carbon (OC) were collected. Mixed effect models were used to assess changes in health effects associated with these specific pollutant classes. Minimal associations were observed with lung function measurements and the pollutants measured. Small decreases in BP measurements and rMSSD, and increases in IL-1β and the low frequency to high frequency ratio measured in HRV, were observed with increasing concentrations of PM2.5 EC. Small, acute changes in cardiovascular and inflammation-related effects of microenvironmental exposures to traffic-related air pollution were observed in a group of healthy young adults. The associations were most profound with the diesel-source EC.

Sick building syndrome is a poorly understood condition that can be vexing to clinicians and public health investigators alike. Concerns about possible causes have recently shifted to bioaerosols, especially indoor mold contamination. Recently, controversy over the health effects of indoor bioaerosols has intensified in the media and in medical forums. Allergists and other clinicians are increasingly being asked to evaluate cases of sick building syndrome attributed to bioaerosol exposure. Although allergy may play a role, it is unlikely to fully explain the nonspecific symptoms of the condition. This review of recent literature will attempt to put into context the roles of allergy and nonallergic mechanisms in sick building syndrome. Epidemiological and toxicological studies have provided further evidence of a possible link between bioaerosol exposure and sick building syndrome, but continue to have methodological limitations. Cross-sectional studies of building occupants have found associations between bioaerosols and symptoms of the condition, but case definitions and exposure assessment remain problematic. Attempts to develop better exposure assessment and biomonitoring methods have made limited progress. Toxicological studies of inhalation of bioaerosols continue to indicate potential toxicity, but at doses that are not comparable to human exposures indoors. Epidemiological studies suggest an association between bioaerosols and sick building syndrome, and toxicological studies have provided some evidence supporting biological plausibility. However, the extent to which bioaerosol exposure may explain the nonspecific symptoms of the condition is unclear. Nonspecific inflammatory responses to bioaerosols, modified by psychosocial factors such as stress, may be a promising area for continued research.

For many individuals, daily commuting activities on roadways account for a substantial proportion of total exposure, as well as peak-level exposures, to traffic-related air pollutants (TRAPS) including ultrafine particles, but the health impacts of these exposures are not well-understood. We sought to determine if exposure to TRAPs particles during commuting causes acute oxidative stress in the respiratory tract or changes in heart rate variability (HRV), a measure of autonomic activity. We conducted a randomized, cross-over trial in which twenty-one young adults took two 1.5-hr rides in a passenger vehicle in morning rush-hour traffic. The subjects wore a powered-air-purifying respirator, and were blinded to high-efficiency particulate air (HEPA) filtration during one of the rides. At time points before and after the rides, we measured HRV and markers of oxidative stress in exhaled breath condensate (EBC) including nitrite, the sum of nitrite and nitrate, malondialdehyde, and 8-isoprostane. We used mixed linear models to evaluate the effect of exposure on EBC and HRV outcomes, adjusting for pre-exposure response levels. We used linear models to examine the effects of particle concentrations on EBC outcomes at post-exposure time points. Mean EBC nitrite and the sum of nitrite and nitrate were increased from baseline at immediately post-exposure comparing unfiltered to filtered rides (2.11 μM vs 1.70 μM, p = 0.02 and 19.1 μM vs 10.0 μM, p = 0.02, respectively). Mean EBC malondialdehyde (MDA) concentrations were about 10% greater following the unfiltered vs. filtered exposures, although this result was not statistically significant. We found no significant associations between exposure to traffic particles and HRV outcomes at any of the time points. At immediately post-exposure, an interquartile range increase in particle number concentration was associated with statistically significant increases in nitrite (99.4%, 95% CI 32.1% to 166.7%) and nitrite + nitrate (75.7%, 95% CI 21.5% to 130.0%). Increases in markers of oxidative stress in EBC may represent early biological responses to widespread exposures to TRAPs particles that affect passengers in vehicles on heavily trafficked roadways.

Individuals with COVID‐19 who do not require hospitalization are instructed to self‐isolate in their residences. Due to high secondary infection rates in household members, there is a need to understand airborne transmission of SARS‐CoV‐2 within residences. We report the first naturalistic intervention study suggesting a reduction of such transmission risk using portable air cleaners (PACs) with HEPA filters. Seventeen individuals with newly diagnosed COVID‐19 infection completed this single‐blind, crossover, randomized study. Total and size‐fractionated aerosol samples were collected simultaneously in the self‐isolation room with the PAC (primary) and another room (secondary) for two consecutive 24‐h periods, one period with HEPA filtration and the other with the filter removed (sham). Seven out of sixteen (44%) air samples in primary rooms were positive for SARS‐CoV‐2 RNA during the sham period. With the PAC operated at its lowest setting (clean air delivery rate [CADR] = 263 cfm) to minimize noise, positive aerosol samples decreased to four out of sixteen residences (25%; p = 0.229). A slight decrease in positive aerosol samples was also observed in the secondary room. As the world confronts both new variants and limited vaccination rates, our study supports this practical intervention to reduce the presence of viral aerosols in a real‐world setting.