Robert J. Laumbach

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.

Health Effects of a Mixture of Indoor Air Volatile Organics, Their Ozone Oxidation Products, and Stress

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.

A joint ERS/ATS policy statement: What constitutes an adverse health effect of air pollution? An analytical framework

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. Air pollution has many effects on health; this document provides guidance to judge the adversity of such effects http://ow.ly/T2xx304WTZp

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

Purpose of reviewSick 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 findingsEpidemiological 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. SummaryEpidemiological 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.

Acute exposure to elevated PM2.5 generated by traffic and cardiopulmonary health effects in healthy older adults

There are evidences for exposure to vehicular emissions and adverse cardiopulmonary health effects. This study attempted to further explore these effects on elderly. This study monitored personal PM2.5 concentrations and ambulatory electrocardiograms continuously for 24 h on 1 working day in 3 separate weeks for 11 school crossing guards. Spirometry was also performed before and after the morning shift. The traffic at each work location was video recorded during one of the three morning shifts. The increases in the average personal PM2.5 concentrations (baseline PM2.5 was subtracted) of 1.2–87 and 1.1–98 μg/m3 were observed during the 1-h morning (ΔPM2.5-ave-m) and afternoon shift (ΔPM2.5-ave-a), respectively. Traffic count was not a significant predictor of the ΔPM2.5-ave-m (P=0.78). Mean heart rate variability (HRV), measured as 5-min standard deviation of normal-to-normal (SDNN) beats during the 10-min rest periods, decreased 18–26% (P<0.02) 15 min, 2 and 4 h after the morning shift, but changes in SDNN (ΔSDNN) were insignificant post-afternoon exposure (−0.3 to −7% with P>0.53). ΔSDNN were negatively associated with ΔPM2.5-ave-m, with the strongest association at 2 h after the morning shift (P<0.01) but insignificant 4 h after the morning exposure. The peak PM2.5 concentration (ΔPM2.5-peak, baseline PM2.5 was subtracted) was not a significant predictor for ΔSDNN, and no clear effect of PM2.5 exposure on heart rate was observed. There was no effect of PM exposure on lung function (P>0.16), either. In conclusion, acute exposure to the PM2.5 resulting from mobile sources can cause acute decline in HRV in healthy older adults, suggesting one of the biological mechanisms for the adverse cardiovascular health effects associated with traffic-related air pollution. Traffic count may not be an appropriate surrogate measure of acute personal exposure to vehicular emission in traffic congested areas.

Acute effects of motor vehicle traffic-related air pollution exposures on measures of oxidative stress in human airways

Epidemiological studies have linked exposure to traffic‐related air pollutants to increased respiratory and cardiovascular morbidity and mortality. Evidence from human, animal, and in vitro studies supports an important role for oxidative stress in the pathophysiological pathways underlying the adverse health effects of air pollutants. In controlled‐exposure studies of animals and humans, emissions from diesel engines, a major source of traffic‐related air pollutants, cause pulmonary and systemic inflammation that is mediated by redox‐sensitive signaling pathways. Assessment of human responses to traffic‐related air pollution under realistic conditions is challenging due to the complex, dynamic nature of near‐roadway exposure. Noninvasive measurement of biomarkers in breath and breath condensate may be particularly useful for evaluating the role of oxidative stress in acute responses to exposures that occur in vehicles or during near‐roadway activities. Promising biomarkers include nitric oxide in exhaled breath, and nitrite/nitrate, malondialdehyde, and F2‐isoprostanes in exhaled breath condensate.

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-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. 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.

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/m3 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.

What can individuals do to reduce personal health risks from air pollution

In many areas of the world, concentrations of ambient air pollutants exceed levels associated with increased risk of acute and chronic health problems. While effective policies to reduce emissions at their sources are clearly preferable, some evidence supports the effectiveness of individual actions to reduce exposure and health risks. Personal exposure to ambient air pollution can be reduced on high air pollution days by staying indoors, reducing outdoor air infiltration to indoors, cleaning indoor air with air filters, and limiting physical exertion, especially outdoors and near air pollution sources. Limited evidence suggests that the use of respirators may be effective in some circumstances. Awareness of air pollution levels is facilitated by a growing number of public air quality alert systems. Avoiding exposure to air pollutants is especially important for susceptible individuals with chronic cardiovascular or pulmonary disease, children, and the elderly. Research on mechanisms underlying the adverse health effects of air pollution have suggested potential pharmaceutical or chemopreventive interventions, such as antioxidant or antithrombotic agents, but in the absence of data on health outcomes, no sound recommendations can be made for primary prevention. Health care providers and their patients should carefully consider individual circumstances related to outdoor and indoor air pollutant exposure levels and susceptibility to those air pollutants when deciding on a course of action to reduce personal exposure and health risks from ambient air pollutants. Careful consideration is especially warranted when interventions may have unintended negative consequences, such as when efforts to avoid exposure to air pollutants lead to reduced physical activity or when there is evidence that dietary supplements, such as antioxidants, have potential adverse health effects. These potential complications of partially effective personal interventions to reduce exposure or risk highlight the primary importance of reducing emissions of air pollutants at their sources.

Acute decreases in proteasome pathway activity after inhalation of fresh diesel exhaust or secondary organic aerosol.

Background Epidemiologic studies consistently demonstrate an association between acute cardiopulmonary events and changes in air pollution; however, the mechanisms that underlie these associations are not completely understood. Oxidative stress and inflammation have been suggested to play a role in human responses to air pollution. The proteasome is an intracellular protein degradation system linked to both of these processes and may help mediate air pollution effects. Objectives In these studies, we determined whether acute experimental exposure to two different aerosols altered white blood cell (WBC) or red blood cell (RBC) proteasome activity in human subjects. One aerosol was fresh diesel exhaust (DE), and the other freshly generated secondary organic aerosol (SOA). Methods Thirty-eight healthy subjects underwent 2-hr resting inhalation exposures to DE and separate exposures to clean air (CA); 26 subjects were exposed to DE, CA, and SOA. CA responses were subtracted from DE or SOA responses, and mixed linear models with F-tests were used to test the effect of exposure to each aerosol on WBC and RBC proteasome activity. Results WBC proteasome activity was reduced 8% (p = 0.04) after exposure to either DE or SOA and decreased by 11.5% (p = 0.03) when SOA was analyzed alone. RBCs showed similar 8–10% declines in proteasome activity (p = 0.05 for DE alone). Conclusions Air pollution produces oxidative stress and inflammation in many experimental models, including humans. Two experimental aerosols caused rapid declines in proteasome activity in peripheral blood cells, supporting a key role for the proteasome in acute human responses to air pollution.