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Background: Human controlled-exposure studies have assessed the impact of ambient fine particulate matter on cardiac autonomic function measured by heart rate variability (HRV), but whether these effects are modified by concomitant ozone exposure remains unknown.
Objective: In this study we assessed the impact of O3 and particulate matter exposure on HRV in humans.
Methods: In a crossover design, 50 subjects (19–48 years of age) were randomized to 2-hr controlled exposures to filtered air (FA), concentrated ambient particles (CAPs), O3, or combined CAPs and ozone (CAPs + O3). The primary end point was change in HRV between the start and end of exposure. Secondary analyses included blood pressure (BP) responses, and effect modification by asthmatic status.
Results: Achieved mean CAPs and O3 exposure concentrations were 121.6 ± 48.0 μg/m and 113.9 ± 6.6 ppb, respectively. In a categorical analysis, exposure had no consistent effect on HRV indices. However, the dose–response relationship between CAPs mass concentration and HRV indices seemed to vary depending on the presence of O3. This heterogeneity was statistically significant for the low-frequency component of HRV (p = 0.02) and approached significance for the high-frequency component and time-domain measures of HRV. Exposure to CAPs + O3 increased diastolic BP by 2.0 mmHg (SE, 1.2; p = 0.02). No other statistically significant changes in BP were observed. Asthmatic status did not modify these effects.
Conclusion: The potentiation by O3 of CAPs effects on diastolic BP and possibly HRV is of small magnitude in young adults. Further studies are needed to assess potential effects in more vulnerable populations.
Background: Research has suggested an association with ambient air pollution and sperm quality.
Objectives: We investigated the effect of exposure to ozone (O3) and particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) on sperm quality.
Methods: We reexamined a previous cohort study of water disinfection by-products to evaluate sperm quality in 228 presumed fertile men with different air pollution profiles. Outcomes included sperm concentration, total sperm per ejaculate (count), and morphology, as well as DNA integrity and chromatin maturity. Exposures to O3 and PM2.5 were evaluated for the 90–day period before sampling. We used multivariable linear regression, which included different levels of adjustment (i.e., without and with season and temperature) to assess the relationship between exposure to air pollutants during key periods of sperm development and adverse sperm outcomes.
Results: Sperm concentration and count were not associated with exposure to PM2.5, but there was evidence of an association (but not statistically significant) with O3 concentration and decreased sperm concentration and count. Additionally, a significant increase in the percentage of sperm cells with cytoplasmic drop [β = 2.64; 95% confidence interval (CI), 0.21–5.06] and abnormal head (β = 0.47; 95% CI, 0.03–0.92) was associated with PM2.5 concentration in the base model. However, these associations, along with all other sperm outcomes, were not significantly associated with either pollutant after controlling for season and temperature. Overall, although we found both protective and adverse effects, there was generally no consistent pattern of increased abnormal sperm quality with elevated exposure to O3 or PM2.5.
Conclusions: Exposures to O3 or PM2.5 at levels below the current National Ambient Air Quality Standards were not associated with statistically significant decrements in sperm outcomes in this cohort of fertile men. However, some results suggested effects on sperm concentration, count, and morphology.
Background: Ground-level concentrations of ozone (O3) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM2.5)] have increased since preindustrial times in urban and rural regions and are associated with cardiovascular and respiratory mortality.
Objectives: We estimated the global burden of mortality due to O3 and PM2.5 from anthropogenic emissions using global atmospheric chemical transport model simulations of preindustrial and present-day (2000) concentrations to derive exposure estimates.
Methods: Attributable mortalities were estimated using health impact functions based on long-term relative risk estimates for O3 and PM2.5 from the epidemiology literature. Using simulated concentrations rather than previous methods based on measurements allows the inclusion of rural areas where measurements are often unavailable and avoids making assumptions for background air pollution.
Results: Anthropogenic O3 was associated with an estimated 0.7 ± 0.3 million respiratory mortalities (6.3 ± 3.0 million years of life lost) annually. Anthropogenic PM2.5 was associated with 3.5 ± 0.9 million cardiopulmonary and 220,000 ± 80,000 lung cancer mortalities (30 ± 7.6 million years of life lost) annually. Mortality estimates were reduced approximately 30% when we assumed low-concentration thresholds of 33.3 ppb for O3 and 5.8 μg/m for PM2.5. These estimates were sensitive to concentration thresholds and concentration–mortality relationships, often by > 50%.
Conclusions: Anthropogenic O3 and PM2.5 contribute substantially to global premature mortality. PM2.5 mortality estimates are about 50% higher than previous measurement-based estimates based on common assumptions, mainly because of methodologic differences. Specifically, we included rural populations, suggesting higher estimates; however, the coarse resolution of the global atmospheric model may underestimate urban PM2.5 exposures.
Background: The Yangtze River Delta (YRD) in China is a densely populated region with recent dramatic increases in energy consumption and atmospheric emissions.
Objectives: We studied how different emission sectors influence population exposures and the corresponding health risks, to inform air pollution control strategy design.
Methods: We applied the Community Multiscale Air Quality (CMAQ) Modeling System to model the marginal contribution to baseline concentrations from different sectors. We focused on nitrogen oxide (NOx) control while considering other pollutants that affect fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] and ozone concentrations. We developed concentration–response (C-R) functions for PM2.5 and ozone mortality for China to evaluate the anticipated health benefits.
Results: In the YRD, health benefits per ton of emission reductions varied significantly across pollutants, with reductions of primary PM2.5 from the industry sector and mobile sources showing the greatest benefits of 0.1 fewer deaths per year per ton of emission reduction. Combining estimates of health benefits per ton with potential emission reductions, the greatest mortality reduction of 12,000 fewer deaths per year [95% confidence interval (CI), 1,200–24,000] was associated with controlling primary PM2.5 emissions from the industry sector and reducing sulfur dioxide (SO2) from the power sector, respectively. Benefits were lower for reducing NOx emissions given lower consequent reductions in the formation of secondary PM2.5 (compared with SO2) and increases in ozone concentrations that would result in the YRD.
Conclusions: Although uncertainties related to C-R functions are significant, the estimated health benefits of emission reductions in the YRD are substantial, especially for sectors and pollutants with both higher health benefits per unit emission reductions and large potential for emission reductions.
Background: The mechanisms underlying ozone (O3)-induced pulmonary inflammation remain unclear. Interleukin-10 (IL-10) is an anti-inflammatory cytokine that is known to inhibit inflammatory mediators.
Objectives: We investigated the molecular mechanisms underlying interleuken-10 (IL-10)–mediated attenuation of O3-induced pulmonary inflammation in mice.
Methods: Il10-deficient (Il10) and wild-type (Il10) mice were exposed to 0.3 ppm O3 or filtered air for 24, 48, or 72 hr. Immediately after exposure, differential cell counts and total protein (a marker of lung permeability) were assessed from bronchoalveolar lavage fluid (BALF). mRNA and protein levels of cellular mediators were determined from lung homogenates. We also used global mRNA expression analyses of lung tissue with Ingenuity Pathway Analysis to identify patterns of gene expression through which IL-10 modifies O3-induced inflammation.
Results: Mean numbers of BALF polymorphonuclear leukocytes (PMNs) were significantly greater in Il10 mice than in Il10 mice after exposure to O3 at all time points tested. O3-enhanced nuclear NF-κB translocation was elevated in the lungs of Il10 compared with Il10 mice. Gene expression analyses revealed several IL-10–dependent and O3-dependent mediators, including macrophage inflammatory protein 2, cathepsin E, and serum amyloid A3.
Conclusions: Results indicate that IL-10 protects against O3-induced pulmonary neutrophilic inflammation and cell proliferation. Moreover, gene expression analyses identified three response pathways and several genetic targets through which IL-10 may modulate the innate and adaptive immune response. These novel mechanisms of protection against the pathogenesis of O3-induced pulmonary inflammation may also provide potential therapeutic targets to protect susceptible individuals.
Background: Mechanisms of cardiovascular injuries from exposure to gas and particulate air pollutants are unknown.
Objective: We sought to determine whether episodic exposure of rats to ozone or diesel exhaust particles (DEP) causes differential cardiovascular impairments that are exacerbated by ozone plus DEP.
Methods and results: Male Wistar Kyoto rats (10–12 weeks of age) were exposed to air, ozone (0.4 ppm), DEP (2.1 mg/m), or ozone (0.38 ppm) + DEP (2.2 mg/m) for 5 hr/day, 1 day/week for 16 weeks, or to air, ozone (0.51 or 1.0 ppm), or DEP (1.9 mg/m) for 5 hr/day for 2 days. At the end of each exposure period, we examined pulmonary and cardiovascular biomarkers of injury. In the 16-week study, we observed mild pulmonary pathology in the ozone, DEP, and ozone + DEP exposure groups, a slight decrease in circulating lymphocytes in the ozone and DEP groups, and decreased platelets in the DEP group. After 16 weeks of exposure, mRNA biomarkers of oxidative stress (hemeoxygenase-1), thrombosis (tissue factor, plasminogen activator inhibitor-1, tissue plasminogen activator, and von Willebrand factor), vasoconstriction (endothelin-1, endothelin receptors A and B, endothelial NO synthase) and proteolysis [matrix metalloprotease (MMP)-2, MMP-3, and tissue inhibitor of matrix metalloprotease-2] were increased by DEP and/or ozone in the aorta, but not in the heart. Aortic LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1) mRNA and protein increased after ozone exposure, and LOX-1 protein increased after exposure to ozone + DEP. RAGE (receptor for advanced glycation end products) mRNA increased in the ozone + DEP group. Exposure to ozone or DEP depleted cardiac mitochondrial phospholipid fatty acids (DEP > ozone). The combined effect of ozone and DEP exposure was less pronounced than exposure to either pollutant alone. Exposure to ozone or DEP for 2 days (acute) caused mild changes in the aorta.
Conclusions: In animals exposed to ozone or DEP alone for 16 weeks, we observed elevated biomarkers of vascular impairments in the aorta, with the loss of phospholipid fatty acids in myocardial mitochondria. We conclude that there is a possible role of oxidized lipids and protein through LOX-1 and/or RAGE signaling.
Background: Evidence suggests that increased ambient air pollution concentrations are associated with health effects, although relatively few studies have specifically examined infants.
Objective: We examined associations of daily ambient air pollution concentrations with central apnea (prolonged pauses in breathing) and bradycardia (low heart rate) events among infants prescribed home cardiorespiratory monitors.
Methods: The home monitors record the electrocardiogram, heart rate, and respiratory effort for detected apnea and bradycardia events in high-risk infants [primarily premature and low birth weight (LBW) infants]. From August 1998 through December 2002, 4,277 infants had 8,960 apnea event-days and 29,450 bradycardia event-days in > 179,000 days of follow-up. We assessed the occurrence of apnea and bradycardia events in relation to speciated particulate matter and gaseous air pollution levels using a 2-day average of air pollution (same day and previous day), adjusting for temporal trends, temperature, and infant age.
Results: We observed associations between bradycardia and 8-hr maximum ozone [odds ratio (OR) = 1.049 per 25-ppb increase; 95% confidence interval (CI), 1.021–1.078] and 1-hr maximum nitrogen dioxide (OR =1.025 per 20-ppb increase; 95% CI, 1.000–1.050). The association with ozone was robust to different methods of control for time trend and specified correlation structure. In secondary analyses, associations of apnea and bradycardia with pollution were generally stronger in infants who were full term and of normal birth weight than in infants who were both premature and LBW.
Conclusions: These results suggest that higher air pollution concentrations may increase the occurrence of apnea and bradycardia in high-risk infants.
Background: Concerns regarding the health impact of urban air pollution on asthmatic children are pronounced along the U.S.–Mexico border because of rapid population growth near busy border highways and roads.
Objectives: We conducted the first binational study of the impacts of air pollution on asthmatic children in Ciudad Juarez, Mexico, and El Paso, Texas, USA, and compared different exposure metrics to assess acute respiratory response.
Methods: We recruited 58 asthmatic children from two schools in Ciudad Juarez and two schools in El Paso. A marker of airway inflammation [exhaled nitric oxide (eNO)], respiratory symptom surveys, and pollutant measurements (indoor and outdoor 48-hr size-fractionated particulate matter, 48-hr black carbon, and 96-hr nitrogen dioxide) were collected at each school for 16 weeks. We examined associations between the pollutants and respiratory response using generalized linear mixed models.
Results: We observed small but consistent associations between eNO and numerous pollutant metrics, with estimated increases in eNO ranging from 1% to 3% per interquartile range increase in pollutant concentrations. Effect estimates from models using school-based concentrations were generally stronger than corresponding estimates based on concentrations from ambient air monitors. Both traffic-related and non–traffic-related particles were typically more robust predictors of eNO than was nitrogen dioxide, for which associations were highly sensitive to model specification. Associations differed significantly across the four school-based cohorts, consistent with heterogeneity in pollutant concentrations and cohort characteristics. Models examining respiratory symptoms were consistent with the null.
Conclusions: The results indicate adverse effects of air pollution on the subclinical respiratory health of asthmatic children in this region and provide preliminary support for the use of air pollution monitors close to schools to track exposure and potential health risk in this population.
Background: Toll-like receptor 4 (TLR4) is involved in ozone (O3)-induced pulmonary hyperpermeability and inflammation, although the downstream signaling events are unknown.
Objectives: The aims of our study were to determine the mechanism through which TLR4 modulates O3-induced pulmonary responses and to use transcriptomics to determine potential TLR4 effector molecules.
Methods: C3H/HeJ (HeJ; Tlr4 mutant) and C3H/HeOuJ (OuJ; Tlr4 normal) mice were exposed continuously to 0.3 ppm O3 or filtered air for 6, 24, 48, or 72 hr. We assessed inflammation using bronchoalveolar lavage and molecular analysis by mRNA microarray, quantitative RT-PCR (real-time polymerase chain reaction), immunoblots, immunostaining, and ELISAs (enzyme-linked immunosorbent assays). B6-Hspa1a/Hspa1btm1Dix/NIEHS (Hsp70–/–) and C57BL/6 (B6; Hsp70+/+ wild-type control) mice were used for candidate gene validation studies.
Results: O3-induced TLR4 signaling occurred through myeloid differentiation protein 88 (MyD88)-dependent and -independent pathways in OuJ mice and involved multiple downstream pathways. Genomewide transcript analyses of lungs from air- and O3-exposed HeJ and OuJ mice identified a cluster of genes that were significantly up-regulated in O3-exposed OuJ mice compared with O3-exposed HeJ mice or air-exposed controls of both strains; this cluster included genes for heat-shock proteins (e.g., Hspa1b, Hsp70). Moreover, O3-induced inflammation, MyD88 up-regulation, extracellular-signal–related kinase-1/2 (ERK1/2) and activator protein-1 (AP-1) activation, and kerotinocyte-derived chemokine (KC) protein content were significantly reduced in Hspa1a/Hspa1b (Hsp70) compared with Hsp70 mice (p < 0.05).
Conclusions: These studies suggest that HSP70 is an effector molecule downstream of TLR4 and is involved in the regulation of O3-induced lung inflammation by triggering similar pathways to TLR4. These novel findings may have therapeutic and preventive implications for inflammatory diseases resulting from environmental exposures.
Background: Our previous work demonstrated that the extracellular matrix protein mindin contributes to allergic airways disease. However, the role of mindin in nonallergic airways disease has not previously been explored.
Objectives: We hypothesized that mindin would contribute to airways disease after inhalation of either lipopolysaccharide (LPS) or ozone.
Methods: We exposed C57BL/6J and mindin-deficient () mice to aerosolized LPS (0.9 μg/m for 2.5 hr), saline, ozone (1 ppm for 3 hr), or filtered air (FA). All mice were evaluated 4 hr after LPS/saline exposure or 24 hr after ozone/FA exposure. We characterized the physiological and biological responses by analysis of airway hyperresponsiveness (AHR) with a computer-controlled small-animal ventilator (FlexiVent), inflammatory cellular recruitment, total protein in bronchoalveolar lavage fluid (BALF), proinflammatory cytokine profiling, and ex vivo bronchial ring studies.
Results: After inhalation of LPS, mindin mice demonstrated significantly reduced total cell and neutrophil recruitment into the airspace compared with their wild-type counterparts. Mindin mice also exhibited reduced proinflammatory cytokine production and lower AHR to methacholine challenge by FlexiVent. After inhalation of ozone, mice had no detectible differences in cellular inflammation or total BALF protein dependent on mindin. However, mindin mice were protected from increased proinflammatory cytokine production and AHR compared with their C57BL/6J counterparts. After ozone exposure, bronchial rings derived from mindin mice demonstrated reduced constriction in response to carbachol.
Conclusions: These data demonstrate that the extracellular matrix protein mindin modifies the airway response to both LPS and ozone. Our data support a conserved role of mindin in production of proinflammatory cytokines and the development of AHR in two divergent models of reactive airways disease, as well as a role of mindin in airway smooth muscle contractility after exposure to ozone.
Background: A critical question regarding the association between short-term exposure to ozone and mortality is the extent to which this relationship is confounded by ambient exposure to particles.
Objectives: We investigated whether particulate matter < 10 and < 2.5 μm in aerodynamic diameter (PM10 and PM2.5) is a confounder of the ozone and mortality association using data for 98 U.S. urban communities from 1987 to 2000.
Methods: We a) estimated correlations between daily ozone and daily PM concentrations stratified by ozone or PM levels; b) included PM as a covariate in time-series models; and c) included PM as a covariate as in d), but within a subset approach considering only days with ozone below a specified value.
Results: Analysis was hindered by data availability. In the 93 communities with PM10 data, only 25.0% of study days had data on both ozone and PM10. In the 91 communities with PM2.5 data, only 9.2% of days in the study period had data on ozone and PM2.5. Neither PM measure was highly correlated with ozone at any level of ozone or PM. National and community-specific effect estimates of the short-term effects of ozone on mortality were robust to inclusion of PM10 or PM2.5 in time-series models. The robustness remains even at low ozone levels (< 10 ppb) using a subset approach.
Conclusions: Results provide evidence that neither PM10 nor PM2.5 is a likely confounder of observed ozone and mortality relationships. Further investigation is needed to investigate potential confounding of the short-term effects of ozone on mortality by PM chemical composition.
Background: There is growing evidence for the role of oxidative damage in chronic diseases. Although ozone (O3) is an oxidant pollutant to which many people are exposed, few studies have examined whether O3 induces oxidative stress in humans.
Objectives: This study was designed to assess the effect of short-and long-term O3 exposures on biomarkers of oxidative stress in healthy individuals.
Methods: Biomarkers of lipid peroxidation, 8-isoprostane (8-iso-PGF), and antioxidant capacity ferric reducing ability of plasma (FRAP) were analyzed in two groups of healthy college students with broad ranges of ambient O3 exposure during their lifetimes and previous summer recess either in Los Angeles (LA, n = 59) or the San Francisco Bay Area (SF, n = 61).
Results: Estimated 2-week, 1-month, and lifetime O3 exposures were significantly correlated with elevated 8-iso-PGF. Elevated summertime exposures resulted in the LA group having higher levels of 8-iso-PGF than the SF group (p = 0.02). Within each location, males and females had similar 8-iso-PGF. No regional difference in FRAP was observed, with significantly higher FRAP in males in both groups (SF: p = 0.002; LA: p = 0.004). An exposure chamber substudy (n = 15) also showed a significant increase in 8-iso-PGF as well as an inhibition of FRAP immediately after a 4-hr exposure to 200 ppb O3, with near normalization by 18 hr in both biomarkers.
Conclusions: Long-term exposure to O3 is associated with elevated 8-iso-PGF, which suggests that 8-iso-PGF is a good biomarker of oxidative damage related to air pollution.
Objective: Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States.
Methods: We linked county-specific monitoring data for particles with aerodiameter of ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10), ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS), and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity), percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths.
Results: After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI), 1.06–1.27] for a 10-μg/m increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09–1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category).
Conclusions: This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.
Background: Asthma is the most important chronic disease of childhood. The U.S. Environmental Protection Agency has concluded that children with asthma continue to be susceptible to ozone-associated adverse effects on their disease.
Objectives: This study was designed to evaluate time trends in associations between declining warm-season O3 concentrations and hospitalization for asthma in children.
Methods: We undertook an ecologic study of hospital discharges for asthma during the high O3 seasons in California’s South Coast Air Basin (SoCAB) in children who ranged in age from birth to 19 years from 1983 to 2000. We used standard association and causal statistical analysis methods. Hospital discharge data were obtained from the State of California; air pollution data were obtained from the California Air Resources Board, and demographic data from the 1980, 1990, and 2000 U.S. Census. SoCAB was divided into 195 spatial grids, and quarterly average O3, sulfurdioxide, particulate matter with aerodynamic diameter ≤ 10 μm, nitrogen dioxide, and carbon monoxide were assigned to each unit for 3-month periods along with demographic variables.
Results: O3 was the only pollutant associated with increased hospital admissions over the study period. Inclusion of a variety of demographic and weather variables accounted for all of the non-O3 temporal changes in hospitalizations. We found a time-independent, constant effect of ambient levels of O3 and quarterly hospital discharge rates for asthma. We estimate that the average effect of a 10-ppb mean increase in any given mean quarterly 1-hr maximum O3 over the 18-year median of 87.7 ppb was a 4.6% increase in the same quarterly outcome.
Conclusions: Our data indicate that at current levels of O3 experienced in Southern California, O3 contributes to an increased risk of hospitalization for children with asthma.
Background: There are few studies on associations between children’s respiratory heath and air pollution in schools in China. The industrial development and increased traffic may affect the indoor exposure to air pollutants in school environment. Moreover, there is a need to study respiratory effects of environmental tobacco smoke (ETS) and emissions from new building materials in homes in China.
Objectives: We studied the associations between pupils’ asthmatic symptoms and indoor and outdoor air pollution in schools, as well as selected home exposures, in a coal-burning city in north China.
Methods: A questionnaire survey was administered to pupils (11–15 years of age) in 10 schools in urban Taiyuan, collecting data on respiratory health and selected home environmental factors. Indoor and outdoor school air pollutants and climate factors were measured in winter.
Results: A total of 1,993 pupils (90.2%) participated; 1.8% had cumulative asthma, 8.4% wheezing, 29.8% had daytime attacks of breathlessness. The indoor average concentrations of sulfur dioxide, nitrogen dioxide, ozone, and formaldehyde by class were 264.8, 39.4, 10.1, and 2.3 μg/m, respectively. Outdoor levels were two to three times higher. Controlling for possible confounders, either wheeze or daytime or nocturnal attacks of breathlessness were positively associated with SO2, NO2, or formaldehyde. In addition, ETS and new furniture at home were risk factors for wheeze, daytime breathlessness, and respiratory infections.
Conclusions: Indoor chemical air pollutants of mainly outdoor origin could be risk factors for pupils’ respiratory symptoms at school, and home exposure to ETS and chemical emissions from new furniture could affect pupils’ respiratory health.
Background: Although several previous studies have found a positive association between ambient ozone and mortality, the observed effect may be confounded by other secondary pollutants that are produced concurrently with ozone.
Objectives: We addressed the question of whether the ozone–mortality relationship is entirely a reflection of the adverse effect of ozone, or whether it is, at least in part, an effect of other secondary pollutants.
Methods: Separate time-series models were fit to 3–6 years of data between 2000 and 2005 from 18 U.S. communities. The association between nonaccidental mortality was examined with ozone alone and with ozone after adjustment for fine particle mass, sulfate, organic carbon, or nitrate concentrations. The effect estimates from each of these models were pooled using a random-effects meta-analysis to obtain an across-community average.
Results: We found a 0.89% [95% confidence interval (CI), 0.45–1.33%] increase in nonaccidental mortality with a 10-ppb increase in same-day 24-hr summertime ozone across the 18 communities. After adjustment for PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) mass or nitrate, this estimate decreased slightly; but when adjusted for particle sulfate, the estimate was substantially reduced to 0.58% (95% CI, –0.33 to 1.49%).
Conclusions: Our results demonstrate that the association between ozone and mortality is confounded by particle sulfate, suggesting that some secondary particle pollutants could be responsible for part of the observed ozone effect.
Background: Ozone exposure induces airway neutrophilia and modifies innate immune monocytic cell-surface phenotypes in healthy individuals. High-dose inhaled corticosteroids can reduce O3-induced airway inflammation, but their effect on innate immune activation is unknown.
Objectives: We used a human O3 inhalation challenge model to examine the effectiveness of clinically relevant doses of inhaled corticosteroids on airway inflammation and markers of innate immune activation in healthy volunteers.
Methods: Seventeen O3-responsive subjects [> 10% increase in the percentage of polymorphonuclear leukocytes (PMNs) in sputum, PMNs per milligram vs. baseline sputum] received placebo, or either a single therapeutic dose (0.5 mg) or a high dose (2 mg) of inhaled fluticasone proprionate (FP) 1 hr before a 3-hr O3 challenge (0.25 ppm) on three separate occasions at least 2 weeks apart. Lung function, exhaled nitric oxide, sputum, and systemic biomarkers were assessed 1–5 hr after the O3 challenge. To determine the effect of FP on cellular function, we assessed sputum cells from seven subjects by flow cytometry for cell-surface marker activation.
Results: FP had no effect on O3-induced lung function decline. Compared with placebo, 0.5 mg and 2 mg FP reduced O3-induced sputum neutrophilia by 18% and 35%, respectively. A similar effect was observed on the airway-specific serum biomarker Clara cell protein 16 (CCP16). Furthermore, FP pretreatment significantly reduced O3-induced modification of CD11b, mCD14, CD64, CD16, HLA-DR, and CD86 on sputum monocytes in a dose-dependent manner.
Conclusions: This study confirmed and extended data demonstrating the protective effect of FP against O3-induced airway inflammation and immune cell activation.
Background: Automobile exhaust contains precursors to ozone and fine particulate matter (PM ≤ 2.5 µm in aerodynamic diameter; PM2.5), posing health risks. Dependency on car commuting also reduces physical fitness opportunities.
Objective: In this study we sought to quantify benefits from reducing automobile usage for short urban and suburban trips.
Methods: We simulated census-tract level changes in hourly pollutant concentrations from the elimination of automobile round trips ≤ 8 km in 11 metropolitan areas in the upper midwestern United States using the Community Multiscale Air Quality (CMAQ) model. Next, we estimated annual changes in health outcomes and monetary costs expected from pollution changes using the U.S. Environmental Protection Agency Benefits Mapping Analysis Program (BenMAP). In addition, we used the World Health Organization Health Economic Assessment Tool (HEAT) to calculate benefits of increased physical activity if 50% of short trips were made by bicycle.
Results: We estimate that, by eliminating these short automobile trips, annual average urban PM2.5 would decline by 0.1 µg/m and that summer ozone (O3) would increase slightly in cities but decline regionally, resulting in net health bene-fits of $4.94 billion/year [95% confidence interval (CI): $0.2 billion, $13.5 billion), with 25% of PM2.5 and most O3 bene-fits to populations outside metropolitan areas. Across the study region of approximately 31.3 million people and 37,000 total square miles, mortality would decline by approximately 1,295 deaths/year (95% CI: 912, 1,636) because of improved air quality and increased exercise. Making 50% of short trips by bicycle would yield savings of approximately $3.8 billion/year from avoided mortality and reduced health care costs (95% CI: $2.7 billion, $5.0 billion]. We estimate that the combined benefits of improved air quality and physical fitness would exceed $8 billion/year.
Conclusion: Our findings suggest that significant health and economic benefits are possible if bicycling replaces short car trips. Less dependence on automobiles in urban areas would also improve health in downwind rural settings.
Background: Air pollution has been a topic of intense concern and study for hundreds of years. During the second half of the 20th century, the United States implemented regulations and controls to reduce the levels of criteria air pollutants and achieve the National Ambient Air Quality Standards (NAAQS) for the protection of human health, while concurrently reducing the levels of toxic air pollutants.
Objective: In this commentary we trace the changes in air pollution in New Jersey as a case study, demonstrating the impact of local, state, and federal strategies to control emissions of pollutants and pollutant precursors from the 1950s until today.
Discussion: The original NAAQS (1970–1995) have been achieved, and significant progress has been made to achieve revised standards for ozone and particulate matter (PM) < 2.5 µm in aerodynamic diameter (PM2.5) in New Jersey, which in the past was considered a highly polluted industrial state.
Conclusions: Assuming no reversals on current regulations because of some major event or energy infrastructure disruption, outdoor air pollution reductions will continue to address health risks among specific segments of the general population affected by ozone/PM and pollution caused by neighborhood, local, and regional point and mobile sources.
Background: Diabetes increases the risk of hypertension and orthostatic hypotension and raises the risk of cardiovascular death during heat waves and high pollution episodes.
Objective: We examined whether short-term exposures to air pollution (fine particles, ozone) and heat resulted in perturbation of arterial blood pressure (BP) in persons with type 2 diabetes mellitus (T2DM).
Methods: We conducted a panel study in 70 subjects with T2DM, measuring BP by automated oscillometric sphygmomanometer and pulse wave analysis every 2 weeks on up to five occasions (355 repeated measures). Hourly central site measurements of fine particles, ozone, and meteorology were conducted. We applied linear mixed models with random participant intercepts to investigate the association of fine particles, ozone, and ambient temperature with systolic, diastolic, and mean arterial BP in a multipollutant model, controlling for season, meteorological variables, and subject characteristics.
Results: An interquartile increase in ambient fine particle mass [particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 μm (PM2.5)] and in the traffic component black carbon in the previous 5 days (3.54 and 0.25 μg/m, respectively) predicted increases of 1.4 mmHg [95% confidence interval (CI): 0.0, 2.9 mmHg] and 2.2 mmHg (95% CI: 0.4, 4.0 mmHg) in systolic BP (SBP) at the population geometric mean, respectively. In contrast, an interquartile increase in the 5-day mean of ozone (13.3 ppb) was associated with a 5.2 mmHg (95% CI: –8.6, –1.8 mmHg) decrease in SBP. Higher temperatures were associated with a marginal decrease in BP.
Conclusions: In subjects with T2DM, PM was associated with increased BP, and ozone was associated with decreased BP. These effects may be clinically important in patients with already compromised autoregulatory function.