Personal Interventions to Reduce Exposure to Outdoor Air Pollution.

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.

Portable air cleaners and residential exposure to SARS-CoV-2 aerosols: A real-world study.

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.

Severe Obstructive Sleep Apnea Is Associated with Alterations in the Nasal Microbiome and an Increase in Inflammation.

RATIONALE: Obstructive sleep apnea (OSA) is associated with recurrent obstruction, subepithelial edema, and airway inflammation. The resultant inflammation may influence or be influenced by the nasal microbiome. OBJECTIVES: To evaluate whether the composition of the nasal microbiota is associated with obstructive sleep apnea and inflammatory biomarkers. METHODS: Two large cohorts were used: 1) a discovery cohort of 472 subjects from the WTCSNORE (Seated, Supine and Post-Decongestion Nasal Resistance in World Trade Center Rescue and Recovery Workers) cohort, and 2) a validation cohort of 93 subjects rom the Zaragoza Sleep cohort. Sleep apnea was diagnosed using home sleep tests. Nasal lavages were obtained from cohort subjects to measure: 1) microbiome composition (based on 16S rRNA gene sequencing), and 2) biomarkers for inflammation (inflammatory cells, IL-8, and IL-6). Longitudinal 3-month samples were obtained in the validation cohort, including after continuous positive airway pressure treatment when indicated. MEASUREMENTS AND MAIN RESULTS: In both cohorts, we identified that: 1) severity of OSA correlated with differences in microbiome diversity and composition; 2) the nasal microbiome of subjects with severe OSA were enriched with Streptococcus, Prevotella, and Veillonella; and 3) the nasal microbiome differences were associated with inflammatory biomarkers. Network analysis identified clusters of cooccurring microbes that defined communities. Several common oral commensals (e.g., Streptococcus, Rothia, Veillonella, and Fusobacterium) correlated with apnea-hypopnea index. Three months of treatment with continuous positive airway pressure did not change the composition of the nasal microbiota. CONCLUSIONS: We demonstrate that the presence of an altered microbiome in severe OSA is associated with inflammatory markers. Further experimental approaches to explore causal links are needed.

World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung.

Exposure to World Trade Center (WTC) dust has been linked to respiratory disease in humans. In the present studies we developed a rodent model of WTC dust exposure to analyze lung oxidative stress and inflammation, with the goal of elucidating potential epigenetic mechanisms underlying these responses. Exposure of mice to WTC dust (20µg, i.t.) was associated with upregulation of heme oxygenase-1 and cyclooxygenase-2 within 3days, a response which persisted for at least 21days. Whereas matrix metalloproteinase was upregulated 7days post-WTC dust exposure, IL-6RA1 was increased at 21days; conversely, expression of mannose receptor, a scavenger receptor important in particle clearance, decreased. After WTC dust exposure, increases in methylation of histone H3 lysine K4 at 3days, lysine K27 at 7days and lysine K36, were observed in the lung, along with hypermethylation of Line-1 element at 21days. Alterations in pulmonary mechanics were also observed following WTC dust exposure. Thus, 3days post-exposure, lung resistance and tissue damping were decreased. In contrast at 21days, lung resistance, central airway resistance, tissue damping and tissue elastance were increased. These data demonstrate that WTC dust-induced inflammation and oxidative stress are associated with epigenetic modifications in the lung and altered pulmonary mechanics. These changes may contribute to the development of WTC dust pathologies.

Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity.

Epidemiological studies suggest that chronic exposure to air pollution increases susceptibility to respiratory infections, including tuberculosis in humans. A possible link between particulate air pollutant exposure and antimycobacterial immunity has not been explored in human primary immune cells. We hypothesized that exposure to diesel exhaust particles (DEP), a major component of urban fine particulate matter, suppresses antimycobacterial human immune effector cell functions by modulating TLR-signaling pathways and NF-κB activation. We show that DEP and H37Ra, an avirulent laboratory strain of Mycobacterium tuberculosis, were both taken up by the same peripheral human blood monocytes. To examine the effects of DEP on M. tuberculosis-induced production of cytokines, PBMC were stimulated with DEP and M. tuberculosis or purified protein derivative. The production of M. tuberculosis and purified protein derivative-induced IFN-γ, TNF-α, IL-1ß, and IL-6 was reduced in a DEP dose-dependent manner. In contrast, the production of anti-inflammatory IL-10 remained unchanged. Furthermore, DEP stimulation prior to M. tuberculosis infection altered the expression of TLR3, -4, -7, and -10 mRNAs and of a subset of M. tuberculosis-induced host genes including inhibition of expression of many NF-κB (e.g., CSF3, IFNG, IFNA, IFNB, IL1A, IL6, and NFKBIA) and IFN regulatory factor (e.g., IFNG, IFNA1, IFNB1, and CXCL10) pathway target genes. We propose that DEP downregulate M. tuberculosis-induced host gene expression via MyD88-dependent (IL6, IL1A, and PTGS2) as well as MyD88-independent (IFNA, IFNB) pathways. Prestimulation of PBMC with DEP suppressed the expression of proinflammatory mediators upon M. tuberculosis infection, inducing a hyporesponsive cellular state. Therefore, DEP alters crucial components of antimycobacterial host immune responses, providing a possible mechanism by which air pollutants alter antimicrobial immunity.

A controlled trial of acute effects of human exposure to traffic particles on pulmonary oxidative stress and heart rate variability.

BACKGROUND: 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. METHODS: 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. RESULTS: 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%). CONCLUSIONS: 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.

Real-World Effectiveness of Portable Air Cleaners in Reducing Home Particulate Matter Concentrations.

Portable air cleaners (PACs) equipped with HEPA filters are gaining attention as cost-effective means of decreasing indoor particulate matter (PM) air pollutants and airborne viruses. However, the performance of PACs in naturalistic settings and spaces beyond the room containing the PAC is not well characterized. We conducted a single-blinded randomized cross-over interventional study between November 2020 and May 2021 in the homes of adults who tested positive for COVID-19. The intervention was air filtration with PAC operated with the HEPA filter set installed ("filter" condition) versus removed ("sham" condition, i.e., control). Sampling was performed in 29 homes for two consecutive 24-hour periods in the primary room (containing the PAC) and a secondary room. PAC effectiveness, calculated as reductions in overall mean PM2.5 and PM10 concentrations during the filter condition, were for the primary rooms 78.8% and 63.9% (n = 23), respectively, and for the secondary rooms 57.9% and 60.4% (n = 22), respectively. When a central air handler (CAH) was reported to be in use, filter-associated reductions of PM were statistically significant during the day (06:00-22:00) and night (22:01-05:59) in the primary rooms but only during the day in the secondary rooms. Our study adds to the literature evaluating the real-world effects of PACs on a secondary room and considering the impact of central air systems on PAC performance.

Respiratory health effects of air pollution: update on biomass smoke and traffic pollution.

Mounting evidence suggests that air pollution contributes to the large global burden of respiratory and allergic diseases, including asthma, chronic obstructive pulmonary disease, pneumonia, and possibly tuberculosis. Although associations between air pollution and respiratory disease are complex, recent epidemiologic studies have led to an increased recognition of the emerging importance of traffic-related air pollution in both developed and less-developed countries, as well as the continued importance of emissions from domestic fires burning biomass fuels, primarily in the less-developed world. Emissions from these sources lead to personal exposures to complex mixtures of air pollutants that change rapidly in space and time because of varying emission rates, distances from source, ventilation rates, and other factors. Although the high degree of variability in personal exposure to pollutants from these sources remains a challenge, newer methods for measuring and modeling these exposures are beginning to unravel complex associations with asthma and other respiratory tract diseases. These studies indicate that air pollution from these sources is a major preventable cause of increased incidence and exacerbation of respiratory disease. Physicians can help to reduce the risk of adverse respiratory effects of exposure to biomass and traffic air pollutants by promoting awareness and supporting individual and community-level interventions.

Personal Interventions for Reducing Exposure and Risk for Outdoor Air Pollution: An Official American Thoracic Society Workshop Report.

Poor air quality affects the health and wellbeing of large populations around the globe. Although source controls are the most effective approaches for improving air quality and reducing health risks, individuals can also take actions to reduce their personal exposure by staying indoors, reducing physical activity, altering modes of transportation, filtering indoor air, and using respirators and other types of face masks. A synthesis of available evidence on the efficacy, effectiveness, and potential adverse effects or unintended consequences of personal interventions for air pollution is needed by clinicians to assist patients and the public in making informed decisions about use of these interventions. To address this need, the American Thoracic Society convened a workshop in May of 2018 to bring together a multidisciplinary group of international experts to review the current state of knowledge about personal interventions for air pollution and important considerations when helping patients and the general public to make decisions about how best to protect themselves. From these discussions, recommendations were made regarding when, where, how, and for whom to consider personal interventions. In addition to the efficacy and safety of the various interventions, the committee considered evidence regarding the identification of patients at greatest risk, the reliability of air quality indices, the communication challenges, and the ethical and equity considerations that arise when discussing personal interventions to reduce exposure and risk from outdoor air pollution.

Outdoor air pollutants and patient health.

Almost 160 million persons live in areas of the United States that exceed federal health-based air pollution standards. The two air pollutants that most commonly exceed standards are ozone and particulate matter. Ozone and particulate matter can harm anyone if levels are sufficiently elevated, but health risk from air pollution is greatest among vulnerable populations. Both ozone and particulate matter can cause pulmonary inflammation, decreased lung function, and exacerbation of asthma and chronic obstructive pulmonary disease. Particulate matter is also strongly associated with increased cardiovascular morbidity and mortality. Children, older adults, and other vulnerable persons may be sensitive to lower levels of air pollution. Persons who are aware of local air pollution levels, reported daily by the U.S. Environmental Protection Agency as the Air Quality Index, can take action to reduce exposure. These actions include simple measures to limit exertion and time spent outdoors when air pollution levels are highest, and to reduce the infiltration of outdoor air pollutants into indoor spaces.

Lack of association between estimated World Trade Center plume intensity and respiratory symptoms among New York City residents outside of Lower Manhattan.

Researchers have reported adverse health effects among rescue/recovery workers and people living near the World Trade Center on September 11, 2001. The authors investigated the occurrence of respiratory symptoms among persons living outside of Lower Manhattan in areas affected by the World Trade Center particulate matter plume. Using a novel atmospheric dispersion model, they estimated relative cumulative plume intensity in areas surrounding the World Trade Center site over a 5-day period following the collapse of the buildings. Using data from a telephone survey of residents (n = 2,755) conducted approximately 6 months after the event, the authors evaluated associations between the estimated plume intensities at individual residence locations and self-reported respiratory symptoms among nonasthmatics, as well as symptoms and nonroutine care among asthmatics. Comparing persons at or above the 75th percentile of cumulative plume intensity with those below it, there was no statistically significant difference in self-reported new-onset wheezing/cough after September 11 (16.1% vs. 13.3%; adjusted odds ratio = 1.0, 95% confidence interval: 0.7, 1.7) and no worsening of asthma from before September 11 to the 4 weeks prior to the survey (13.9% vs. 16.6%; odds ratio = 1.0, 95% confidence interval: 0.3, 2.8). These results suggest that the plume was not strongly associated with respiratory symptoms outside of Lower Manhattan, within the limitations of this retrospective study.

Pulmonary effects of inhaled diesel exhaust in aged mice.

Pulmonary morbidity and mortality resulting from exposure to fine particulate matter (PM) increases with age. The present studies analyzed potential mechanisms underlying increased susceptibility of the elderly to PM using diesel exhaust (DE) as a model. Mice (2 m and 18 m) were exposed to DE (0, 300, and 1000 microg/m(3)) for 3 h once (single) or 3 h/day for 3 days (repeated). Bronchoalveolar lavage fluid (BAL), serum and lung tissue were collected 0 and 24 h later. Exposure to DE resulted in structural alterations in the lungs of older but not younger mice, including patchy thickening of the alveolar septa and inflammatory cell localization in alveolar spaces. These effects were most pronounced 24 h after a single exposure to the higher dose of DE. Significant increases in BAL nitrogen oxides were also noted in older mice, as well as expression of lipocalin 24p3, an oxidative stress marker in the lung with no effects in younger mice. Following DE inhalation, expression of Tumor Necrosis Factor alpha (TNFalpha) was upregulated in lungs of both younger and older mice; however, this was attenuated in older animals. Whereas exposure to DE resulted in increases in lung Interleukin-6 (IL-6) expression in both older and younger mice, IL-8 increased only in older animals. In younger mice, constitutive expression of manganese superoxide dismutase (MnSOD) decreased after DE exposure, while in older mice, constitutive MnSOD was not detectable and DE had no effect on expression of this antioxidant. Taken together, these results suggest that altered generation of inflammatory mediators and MnSOD may contribute to increased susceptibility of older mice to inhaled DE.

Per and polyfluoroalkyl substances (PFAS) blood levels after contamination of a community water supply and comparison with 2013-2014 NHANES.

INTRODUCTION: Per and polyfluoroalkyl substances (PFAS), including perfluorononanoic acid (PFNA) and perfluorooctanoic acid (PFOA), were detected in the community water supply of Paulsboro New Jersey in 2009. METHODS: A cross-sectional study enrolled 192 claimants from a class-action lawsuit, not affiliated with this study, who had been awarded a blood test for 13 PFAS. Study participants provided their blood test results and completed a survey about demographics; 105 participants also completed a health survey. Geometric means, 25th, 50th, 75th, and 95th percentiles of exposure of PFNA blood serum concentrations were compared to that of the 2013-2014 NHANES, adjusted for reporting level. Associations between PFNA, PFOA, PFOS, and PFHxS and self-reported health outcomes were assessed using logistic regression. RESULTS: PFNA serum levels were 285% higher in Paulsboro compared with U.S. residents. PFNA serum levels were higher among older compared with younger, and male compared to female, Paulsboro residents. After adjustment for potential confounding, there was a significant association between increased serum PFNA levels and self-reported high cholesterol (OR: 1.15, 95% CI: 1.02, 1.29). DISCUSSION/CONCLUSION: Further investigation into possible health effects of PFAS exposure in Paulsboro and other community settings is warranted. Since exposure has ceased, toxicokinetics of PFAS elimination should be explored.

Bioaerosols and sick building syndrome: particles, inflammation, and allergy.

PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.

Nasal effects of a mixture of volatile organic compounds and their ozone oxidation products.

OBJECTIVE: Our objective was to determine if low levels of a mixture of volatile organic compounds (VOCs) and their ozone (O3) oxidation products, similar to what might be found in "sick buildings," cause nasal irritation and inflammation under controlled exposure conditions. METHODS: Healthy, nonsmoking women (n=130) completed 2-hour controlled exposures to VOCs, VOCs and O3, and a masked air "MA" control in random order at least 1 week apart. VOCs and O3 concentrations were approximately 25 mg/m and approximately 40 ppb, respectively. Nasal symptoms were rated before, during, and after exposure. Nasal lavage fluid was analyzed for polymorphonuclear cells, total protein, interleukin-6, and interleukin-8. RESULTS: We found no significant differences in symptoms or markers of nasal inflammation between exposure conditions. CONCLUSIONS: Results suggest that VOCs and their oxidation products may not cause acute nasal effects at low concentrations.