The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies. This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air 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 due to 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 disease. 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.

In our present study we tested the health effects among women of controlled exposures to volatile organic compounds (VOCs), with and without ozone (O3), and psychological stress. Each subject was exposed to the following three conditions at 1-week intervals (within-subject factor): VOCs (26 mg/m3), VOCs + O3 (26 mg/m3 + 40 ppb), and ambient air with a 1-min spike of VOCs (2.5 mg/m3). As a between-subjects factor, half the subjects were randomly assigned to perform a stressor. Subjects were 130 healthy women (mean age, 27.2 years; mean education, 15.2 years). Health effects measured before, during, and after each 140-min exposure included symptoms, neurobehavioral performance, salivary cortisol, and lung function. Mixing VOCs with O3 was shown to produce irritating compounds including aldehydes, hydrogen peroxide, organic acids, secondary organic aerosols, and ultrafine particles (particulate matter with aerodynamic diameter < 0.1 μm). Exposure to VOCs with and without O3 did not result in significant subjective or objective health effects. Psychological stress significantly increased salivary cortisol and symptoms of anxiety regardless of exposure condition. Neither lung function nor neurobehavioral performance was compromised by exposure to VOCs or VOCs + O3. Although numerous epidemiologic studies suggest that symptoms are significantly increased among workers in buildings with poor ventilation and mixtures of VOCs, our acute exposure study was not consistent with these epidemiologic findings. Stress appears to be a more significant factor than chemical exposures in affecting some of the health end points measured in our present study.

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, 25 th , 50 th , 75 th and 95 th 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.

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 M.tb, were both taken up by the same peripheral human blood monocytes. To examine the effects of DEP on M.tb-induced production of cytokines, PBMC were stimulated with DEP and M.tb or PPD (purified protein derivative). The production of M.tb and PPD-induced IFN-γ, TNF-α, IL-1β, 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.tb infection altered the expression of TLR 3, 4, 5, 7 and 10 mRNAs and of a subset of M.tb-induced host genes including inhibition of expression of many NF-κB (e.g. CSF3, IFNG, IFNA, IFNB, IL1A, IL6, NFKBIA) and IRF (e.g. IFNG, IFNA1, IFNB1, CXCL10) pathway target genes. We propose that DEP down-regulate M.tb-induced host gene expression via MyD88-dependent (IL6, IL1A, PTGS2) as well as MyD88-independent (IFNA, IFNB) pathways. Pre-stimulation of PBMC with DEP suppressed the expression of proinflammatory mediators upon M.tb infection inducing a hypo-responsive cellular state. Therefore, DEP alters crucial components of antimycobacterial host immune responses, providing a possible mechanism by which air pollutants alter antimicrobial immunity.

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.

Diesel exhaust (DE) is a significant source of air pollution that has been linked to respiratory and cardiovascular morbidity and mortality. Many components in DE, such as polycyclic aromatic hydrocarbons, are present in the environment from other sources. 1-Nitropyrene appears to be a more specific marker of DE exposure. 1-Nitropyrene is partially metabolized to 1-aminopyrene and excreted in urine. We developed a practical, sensitive method for measuring 1-aminopyrene in human urine using a HPLC-fluorescence technique. We measured 1-aminopyrene concentrations in spot urine samples collected prior to and during 24 h following the start of 1 h controlled exposures to DE (target concentration 300 μg m−3 as PM10) and clean air control. Time-weighted-average concentrations of urinary 1-aminopyrene were significantly greater following the DE exposure compared to the control (median 138.7 ng g−1 creatinine vs. 21.7 ng g−1 creatinine, p < 0.0001). Comparing DE to control exposures, we observed significant increases in 1-aminopyrine concentration from pre-exposure to either first post-exposure void or peak spot urine concentration following exposure (p = 0.027 and p = 0.0026, respectively). Large inter-individual variability, in both the concentration of urinary 1-aminopyrene and the time course of appearance in the urine following the standardized exposure to DE, suggests the need to explore subject variables that may affect conversion of inhaled 1-nitropyrene to urinary excretion of 1-aminopyrene.

d-Limonene is an unsaturated volatile organic chemical found in cleaning products, air fresheners and soaps. It is oxidized by ozone to secondary organic aerosols consisting of aldehydes, acids, oxidants and fine and ultra fine particles. The lung irritant effects of these limonene ozone reaction products (LOP) were investigated. Female F344 rats (2- and 18-month-old) were exposed for 3 h to air or LOP formed by reacting 6 ppm d-limonene and 0.8 ppm ozone. BAL fluid, lung tissue and cells were analyzed 0 h and 20 h later. Inhalation of LOP increased TNF-alpha, cyclooxygenase-2, and superoxide dismutase in alveolar macrophages (AM) and Type II cells. Responses of older animals were attenuated when compared to younger animals. LOP also decreased p38 MAP kinase in AM from both younger and older animals. In contrast, while LOP increased p44/42 MAP kinase in AM from younger rats, expression decreased in AM and Type II cells from older animals. NF-kappaB and C/EBP activity also increased in AM from younger animals following LOP exposure but decreased or was unaffected in Type II cells. Whereas in younger animals LOP caused endothelial cell hypertrophy, perivascular and pleural edema and thickening of alveolar septal walls, in lungs from older animals, patchy accumulation of fluid within septal walls in alveolar sacs and subtle pleural edema were noted. LOP are pulmonary irritants inducing distinct inflammatory responses in younger and older animals. This may contribute to the differential sensitivity of these populations to pulmonary irritants.