PM source apportionment for short-term cardiac function changes in ApoE-/- mice

Daily rates of cardiovascular mortality and morbidity are have been associated with daily variations in fine particulate matter (aerodynamic diameter < or = 2.5 microm, PM2.5), but little is known about the influences of the individual source-related PM2.5 categories or the temporal lags for the effects. We investigated heart rate (HR) and HR variability (HRV) data collected during a 5-month study involving 6 hr/day, 5 day/week exposures of normal (C57) mice and a murine model for atherosclerotic disease (ApoE-/-) in Sterling Forest (Tuxedo, New York, USA). The mice were exposed to concentrated ambient particles (PM2.5 concentrated 10-fold, producing an average of 113 microg/m3). Daily 6-hr PM2.5 air samples were analyzed by X-ray fluorescence, permitting attribution to major PM source categories [secondary sulfate (SS), resuspended soil (RS), residual oil (RO) combustion, and other, largely due to motor vehicle traffic]. We examined associations between these PM2.5 components and both HR and HRV for three different daily time periods: during exposure, the afternoon after exposure, and late at night. For HR there were significant transient associations for RS during exposure, and for SS in the afternoon after exposure. For HRV, there were comparable associations with RO in the afternoon after exposure and for both SS and RS late at night. The biologic bases for these associations and their temporal lags are not known but may be related to the differential solubility of the biologically active PM components at the respiratory epithelia and their access to cells that release mediators that reach the cardiovascular system. Clearly, further research to elucidate the underlying processes is needed.     

Night heart rate variability and particulate exposures among boilermaker construction workers

BACKGROUND: Although studies have documented the association between heart rate variability (HRV) and ambient particulate exposures, the association between HRV, especially at night, and metal-rich, occupational particulate exposures remains unclear. OBJECTIVE: Our goal in this study was to investigate the association between long-duration HRV, including nighttime HRV, and occupational PM(2.5) exposures. METHODS: We used 24-hr ambulatory electrocardiograms (ECGs) to monitor 36 male boilermaker welders (mean age of 41 years) over a workday and nonworkday. ECGs were analyzed for HRV in the time domain; rMSSD (square root of the mean squared differences of successive intervals), SDNN (SD of normal-to-normal intervals over entire recording), and SDNN(i) (SDNN for all 5-min segments) were summarized over 24-hr, day (0730-2130 hours), and night (0000-0700 hours) periods. PM(2.5) (particulate matter with an aerodynamic diameter 相似文献   

Obesity is a modifier of autonomic cardiac responses to fine metal particulates

BACKGROUND: Increasing evidence suggests that obesity may impart greater susceptibility to adverse effects of air pollution. Particulate matter, especially PM(2.5) (particulate matter with aero-dynamic diameter /= 30 kg/m(2) were classified as obese. Mixed-effect models were used for statistical analyses. RESULTS: Half (50%) of the study subjects were obese. After adjustment for confounders, each 1-mg/m(3) increase in 4-hr moving average PM(2.5) was associated with HR increase of 5.9 bpm [95% confidence interval (CI), 4.2 to 7.7] and with 5-min HRV reduction by 6.5% (95% CI, 1.9 to 11.3%) for SDNN, 1.7% (95% CI, -4.9 to 8.4%) for rMSSD, and 8.8% (95% CI, -3.8 to 21.3%) for HF. Obese individuals had greater PM(2.5)-mediated HRV reductions (2- to 3-fold differences) than nonobese individuals, and had more PM(2.5)-mediated HR increases (9-bpm vs. 4-bpm increase in HR for each 1-mg/m(3) increase in PM(2.5); p < 0.001). CONCLUSIONS: Our study revealed greater autonomic cardiac responses to metal particulates in obese workers, supporting the hypothesis that obesity may impart greater susceptibility to acute cardiovascular effects of fine particles.     

Out-of-hospital cardiac arrest and airborne fine particulate matter: a case-crossover analysis of emergency medical services data in Indianapolis, Indiana

BACKGROUND: Previous studies have found particulate matter (PM) < 2.5 microm in aerodynamic diameter (PM2.5) associated with heart disease mortality. Although rapid effects of PM2.5 exposure on the cardiovascular system have been proposed, few studies have investigated the effect of short-term exposures on out-of-hospital cardiac arrest (OHCA). OBJECTIVES: We aimed to determine whether short-term PM2.5 exposures increased the risk of OHCA and whether risk depended on subject characteristics or presenting heart rhythm. METHODS: A case-crossover analysis determined hazard ratios (HRs) for OHCAs logged by emergency medical systems (EMS) versus hourly and daily PM2.5 exposures at the time of the OHCA and for daily and hourly periods before it. RESULTS: For all OHCAs (n = 1,374), exposures on the day of the arrest or 1-3 days before arrest had no significant effect on the incidence of OHCA. For cardiac arrests witnessed by bystanders (n = 511), OHCA risk significantly increased with PM2.5 exposure during the hour of the arrest (HR for a 10-microg/m3 increase in PM2.5 exposure = 1.12; 95% confidence interval, 1.01-1.25). For the subsets of subjects who were white, 60-75 years of age, or presented with asystole, OHCA risk significantly increased with PM2.5 during the hour of the arrest (HRs for a 10-microg/m3 increase in PM2.5 = 1.18, 1.25, or 1.22, respectively; p < 0.05). HR generally decreased as the time lag between PM2.5 exposure and OHCA increased. CONCLUSION: The results suggest an acute effect of short-term PM2.5 exposure in precipitating OHCAs, and a need to investigate further the role of subject factors in the effects of PM on the risk of OHCA.     

Interaction effects of ultrafine carbon black with iron and nickel on heart rate variability in spontaneously hypertensive rats

BACKGROUND: Particulate matter (PM) has been reported to be associated with alterations in heart rate variability (HRV); however, the results are inconsistent. We propose that different components of PM cause the discrepancy. OBJECTIVE: In this study, our goal was to determine whether different types of exposure would cause different HRV effects, and to verify the interactions between co-exposing components. METHODS: Ultrafine carbon black (ufCB; 14 nm; 415 microg and 830 microg), ferric sulfate [Fe(2)(SO(4))(3); 105 microg and 210 microg], nickel sulfate (NiSO(4); 263 mug and 526 microg), and a combination of high-dose ufCB and low-dose Fe(2)(SO(4))(3) or NiSO(4) were intratracheally instilled into spontaneously hypertensive rats. Radiotelemetry data were collected in rats for 72 hr at baseline and for 72 hr the following week to determine the response to exposure. Effects of exposure on 5-min average of normal-to-normal intervals (ANN), natural logarithm-transformed standard deviation of the normal-to-normal intervals (LnSDNN), and root mean square of successive differences of adjacent normal-to-normal intervals (LnRMSSD) were analyzed using self-control experimental designs. RESULTS: Both high- and low-dose ufCB decreased ANN marginally around hour 30, with concurrent increases of LnSDNN. LnRMSSD returned to baseline levels after small initial increases. We observed minor effects after low-dose Fe and Ni instillation, whereas biphasic changes were noted after high-dose instillations. Combined exposures of ufCB and either Fe or Ni resulted in HRV trends different from values estimated from individual-component effects. CONCLUSIONS: Components in PM may induce different cardioregulatory responses, and a single component may induce different responses during different phases. Concurrent exposure to ufCB and Fe or Ni might introduce interactions on cardioregulatory effects. Also, the effect of PM may be mediated through complex interaction between different components of PM.     

Personal coronary risk profiles modify autonomic nervous system responses to air pollution

OBJECTIVE: We investigated whether PM2.5-mediated autonomic modulation depends on individual coronary risk profiles. METHODS: Five-minute average heart rate (HR) and heart rate variability (HRV, including standard deviation of normal-to-normal intervals [SDNN], square root of the mean squared differences of successive NN intervals [rMSSD], high frequency [HF]) were measured from 24-hour ambulatory electrocardiograms, and personal PM(2.5) exposures were monitored in a prospective study of 10 male boilermakers (aged 34.3 +/- 8.1 years). We used the Framingham score to classify individuals into low (score = 1-3) and high (score = 5-6) risk categories. Mixed-effect models were used for statistical analyses. RESULTS: Each 1-mg/m(3) increase in the preceding 4-hour moving average PM(2.5) was associated with HR increase (5.3 beats/min) and HRV reduction (11.7%, confidence interval [CI] = 6.2-17.1% for SDNN; 11.1%, CI = 3.1-19.1% for rMSSD; 16.6%, CI = 1.5-31.7% for HF). Greater responses (2- to 4-fold differences) were observed in high-risk subjects than in low-risk subjects. CONCLUSIONS: Our study suggests that adverse autonomic responses to metal particulate are aggravated in workers with higher coronary risk profiles.     

Ambient gas concentrations and personal particulate matter exposures: implications for studying the health effects of particles

BACKGROUND: Data from a previous study conducted in Baltimore, MD, showed that ambient fine particulate matter less than 2.5 mum in diameter (PM2.5) concentrations were strongly correlated with corresponding personal PM2.5 exposures, whereas ambient O3, NO2, and SO2 concentrations were weakly correlated with their personal exposures to these gases. In contrast, many of the ambient gas concentrations were reasonable surrogates of personal PM2.5 exposures. METHODS: Personal multipollutant exposures and corresponding ambient air pollution concentrations were measured for 43 subjects living in Boston, MA. The cohort consisted of 20 healthy senior citizens and 23 schoolchildren. Simultaneous 24-hour integrated PM2.5, O3, NO2, and SO2 personal exposures and ambient concentrations were measured. All PM2.5 samples were also analyzed for SO4 (sulfate). We analyzed personal exposure and ambient concentration data using correlation and mixed model regression analyses to examine relationships among (1) ambient PM2.5 concentrations and corresponding ambient gas concentrations; (2) ambient PM2.5 and gas concentrations and their respective personal exposures; (3) ambient gas concentrations and corresponding personal PM2.5 exposures; and (4) personal PM2.5 exposures and corresponding personal gas exposures. RESULTS: We found substantial correlations between ambient PM2.5 concentrations and corresponding personal exposures over the course of time. Additionally, our results support the earlier finding that summertime gaseous pollutant concentrations may be better surrogates of personal PM2.5 exposures (especially personal exposures to PM2.5 of ambient origin) than they are surrogates of personal exposures to the gases themselves. CONCLUSIONS: Particle health effects studies that include both ambient PM2.5 and gaseous concentrations as independent variables must be analyzed carefully and interpreted cautiously, since both parameters may be serving as surrogates for PM2.5 exposures.     

Controlled Exposure Study of Air Pollution and T-Wave Alternans in Volunteers without Cardiovascular Disease

Background: Epidemiological studies have assessed T-wave alternans (TWA) as a possible mechanism of cardiac arrhythmias related to air pollution in high-risk subjects and have reported associations with increased TWA magnitude.Objective: In this controlled human exposure study, we assessed the impact of exposure to concentrated ambient particulate matter (CAP) and ozone (O3) on T-wave alternans in resting volunteers without preexisting cardiovascular disease.Methods: Seventeen participants without preexisting cardiovascular disease were randomized to filtered air (FA), CAP (150 μg/m3), O3 (120 ppb), or combined CAP + O3 exposures for 2 hr. Continuous electrocardiograms (ECGs) were recorded at rest and T-wave alternans (TWA) was computed by modified moving average analysis with QRS alignment for the artifact-free intervals of 20 beats along the V2 and V5 leads. Exposure-induced changes in the highest TWA magnitude (TWAMax) were estimated for the first and last 5 min of each exposure (TWAMax_Early and TWAMax_Late respectively). ΔTWAMax (Late-Early) were compared among exposure groups using analysis of variance.Results: Mean ± SD values for ΔTWAMax were -2.1 ± 0.4, -2.7 ± 1.1, -1.9 ± 1.5, and -1.2 ± 1.5 in FA, CAP, O3, and CAP + O3 exposure groups, respectively. No significant differences were observed between pollutant exposures and FA.Conclusion: In our study of 17 volunteers who had no preexisting cardiovascular disease, we did not observe significant changes in T-wave alternans after 2-hr exposures to CAP, O3, or combined CAP + O3. This finding, however, does not preclude the possibility of pollution-related effects on TWA at elevated heart rates, such as during exercise, or the possibility of delayed responses.     

Acute effect of ambient ozone on heart rate variability in healthy elderly subjects

Acute ambient ozone (O(3)) exposure is associated with the increased mortality and morbidity of cardiovascular diseases. The dysfunction of cardiac autonomic nervous system (ANS), indicated by the disturbed heart rate variability (HRV), may be the most important underlying mechanism. Previous studies reported the heterogeneous associations between O(3) within several hours' exposure and HRV on general elderly subjects, in which poor surrogate of exposure evaluation and different health status of the subjects may be responsible for the heterogeneous associations. No studies were found focusing on the O(3)-mediated HRV effects within several minutes' exposure on healthy older subjects until recently. We measured the real-time 5-min ambient O(3) concentration and HRV frequency indices in 20 healthy elderly subjects in two surveys, with the 1st and 2nd survey in summer and winter, respectively. Mixed-linear model was used to evaluate the associations between the ambient 5-min average O(3) and concurrent 5-min HRV frequency indices measured during the outdoor period. After adjusting the co-pollutants (ambient PM(2.5) and nitrogen oxides concentrations) and subject characteristics, high frequency (HF) changed -4.87% (95% CI -8.62 to -0.97%) per 10?ppb increment of O(3), whereas decreased low frequency (LF) and increased LFHFR were found to be marginally associated with the elevated O(3) (P values were 0.092 and 0.069). We concluded that the ambient O(3) exert transient decrease effects on HRV, which may induce acute cardiac events.     

Effects of particle size fractions on reducing heart rate variability in cardiac and hypertensive patients

It is still unknown whether the associations between particulate matter (PM) and heart rate variability (HRV) differ by particle sizes with aerodynamic diameters between 0.3 microm and 1.0 microm (PM(0.3-1.0)), between 1.0 microm and 2.5 microm (PM(1.0-2.5)), and between 2.5 microm and 10 microm (PM(2.5-10)). We measured electrocardiographics and PM exposures in 10 patients with coronary heart disease and 16 patients with either prehypertension or hypertension. The outcome variables were standard deviation of all normal-to-normal (NN) intervals (SDNN), the square root of the mean of the sum of the squares of differences between adjacent NN intervals (r-MSSD), low frequency (LF; 0.04-0.15 Hz), high frequency (HF; 0.15-0.40 Hz), and LF:HF ratio for HRV. The pollution variables were mass concentrations of PM(0.3-1.0), PM(1.0-2.5), and PM(2.5-10). We used linear mixed-effects models to examine the association between PM exposures and log10-transformed HRV indices, adjusting for key personal and environmental attributes. We found that PM(0.3-1.0) exposures at 1- to 4-hr moving averages were associated with SDNN and r-MSSD in both cardiac and hypertensive patients. For an interquartile increase in PM(0.3-1.0), there were 1.49-4.88% decreases in SDNN and 2.73-8.25% decreases in r-MSSD. PM(0.3-1.0) exposures were also associated with decreases in LF and HF for hypertensive patients at 1- to 3-hr moving averages except for cardiac patients at moving averages of 2 or 3 hr. By contrast, we found that HRV was not associated with either PM(1.0-2.5) or PM(2.5-10). HRV reduction in susceptible population was associated with PM(0.3-1.0) but was not associated with either PM(1.0-2.5) or PM(2.5-10).     

Ambient Particulate Matter Air Pollution Exposure and Mortality in the NIH-AARP Diet and Health Cohort

Background:

Outdoor fine particulate matter (≤ 2.5 μm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains limited, especially at lower recent exposures.

Objectives:

We aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort.

Methods:

Individual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000–2009 follow-up period when matching census tract–level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 μg/m3 of PM2.5 exposure.

Results:

PM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-μg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality.

Conclusions:

Long-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5–mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels.

Citation:

Thurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484–490; http://dx.doi.org/10.1289/ehp.1509676     

Coarse particles and heart rate variability among older adults with coronary artery disease in the Coachella Valley, California

Alterations in cardiac autonomic control, assessed by changes in heart rate variability (HRV), provide one plausible mechanistic explanation for consistent associations between exposure to airborne particulate matter (PM) and increased risks of cardiovascular mortality. Decreased HRV has been linked with exposures to PM10 (PM with aerodynamic diameter相似文献   

Coarse particulate matter (PM2.5-10) affects heart rate variability, blood lipids, and circulating eosinophils in adults with asthma

INTRODUCTION: We investigated whether markers of airway and systemic inflammation, as well as heart rate variability (HRV) in asthmatics, change in response to fluctuations in ambient particulate matter (PM) in the coarse [PM with aerodynamic diameter 2.5-10 microm (PM(2.5-10))] and fine (PM(2.5)) size range. METHODS: Twelve adult asthmatics, living within a 30-mile radius of an atmospheric monitoring site in Chapel Hill, North Carolina, were followed over a 12-week period. Daily PM(2.5-10) and PM(2.5) concentrations were measured separately for each 24-hr period. Each subject had nine clinic visits, at which spirometric measures and peripheral blood samples for analysis of lipids, inflammatory cells, and coagulation-associated proteins were obtained. We also assessed HRV [SDNN24HR (standard deviation of all normal-to-normal intervals in a 24-hr recording), ASDNN5 (mean of the standard deviation in all 5-min segments of a 24-hr recording)] with four consecutive 24-hr ambulatory electrocardiogram measurements. Linear mixed models with a spatial covariance matrix structure and a 1-day lag were used to assess potential associations between PM levels and cardiopulmonary end points. RESULTS: For a 1-microg/m(3) increase in coarse PM, SDNN24HR, and ASDNN5 decreased 3.36% (p = 0.02), and 0.77%, (p = 0.05) respectively. With a 1-microg/m(3) increase in coarse PM, circulating eosinophils increased 0.16% (p = 0.01), triglycerides increased 4.8% (p = 0.02), and very low-density lipoprotein increased 1.15% (p = 0.01). No significant associations were found with fine PM, and none with lung function. CONCLUSION: These data suggest that small temporal increases in ambient coarse PM are sufficient to affect important cardiopulmonary and lipid parameters in adults with asthma. Coarse PM may have underappreciated health effects in susceptible populations.     

Effects of low sulfur fuel and a catalyzed particle trap on the composition and toxicity of diesel emissions

In this study we compared a "baseline" condition of uncontrolled diesel engine exhaust (DEE) emissions generated with current (circa 2003) certification fuel to an emissions-reduction (ER) case with low sulfur fuel and a catalyzed particle trap. Lung toxicity assessments (resistance to respiratory viral infection, lung inflammation, and oxidative stress) were performed on mice (C57Bl/6) exposed by inhalation (6 hr/day for 7 days). The engine was operated identically (same engine load) in both cases, and the inhalation exposures were conducted at the same exhaust dilution rate. For baseline DEE, this dilution resulted in a particle mass (PM) concentration of approximately 200 microg/m3 PM, whereas the ER reduced the PM and almost every other measured constituent [except nitrogen oxides (NOx)] to near background levels in the exposure atmospheres. These measurements included PM, PM size distribution, PM composition (carbon, ions, elements), NOx, carbon monoxide, speciated/total volatile hydrocarbons, and several classes of semivolatile organic compounds. After exposure concluded, one group of mice was immediately sacrificed and assessed for inflammation and oxidative stress in lung homogenate. Another group of mice were intratracheally instilled with respiratory syncytial virus (RSV), and RSV lung clearance and inflammation was assessed 4 days later. Baseline DEE produced statistically significant biological effects for all measured parameters. The use of low sulfur fuel and a catalyzed trap either completely or nearly eliminated the effects.     

Traffic-related occupational exposures to PM2.5, CO, and VOCs in Trujillo, Peru

A traffic-related exposure study was conducted among 58 workers (drivers, vendors, traffic police, and gas station attendants) and 10 office workers as controls in Trujillo, Peru, in July 2002. PM2.5 was collected, carbon monoxide (CO) was measured, volatile organic compounds (VOCs) were sampled and analyzed. Newspaper vendors had the highest full-shift CO exposures (mean +/- SD: 11.4 +/- 8.9 ppm), while office workers had the lowest (2.0 +/- 1.7 ppm). Bus drivers had the highest full-shift PM2.5 exposures (161 +/- 8.9 microg/m3), while gas station attendants (64 +/- 26.5 microg/m3) and office workers (65 +/- 8.5 microg/m3) were the lowest. Full-shift benzene/toluene/ethylbenzene/xylene exposures (BTEX) among gas station attendants (111/254/43/214 microg/m3) were much higher than those among van and taxi drivers. Several of the traffic-related occupational exposures studied were elevated and are of occupational health concern.     

Effects of air pollution on heart rate variability: the VA normative aging study

Reduced heart rate variability (HRV), a marker of poor cardiac autonomic function, has been associated with air pollution, especially fine particulate matter [< 2.5 microm in aerodynamic diameter (PM2.5)]. We examined the relationship between HRV [standard deviation of normal-to-normal intervals (SDNN), power in high frequency (HF) and low frequency (LF), and LF:HF ratio] and ambient air pollutants in 497 men from the Normative Aging Study in greater Boston, Massachusetts, seen between November 2000 and October 2003. We examined 4-hr, 24-hr, and 48-hr moving averages of air pollution (PM2.5, particle number concentration, black carbon, ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide). Controlling for potential confounders, HF decreased 20.8% [95% confidence interval (CI), 4.6-34.2%] and LF:HF ratio increased 18.6% (95% CI, 4.1-35.2%) per SD (8 microg/m3) increase in 48-hr PM2.5. LF was reduced by 11.5% (95% CI, 0.4-21.3%) per SD (13 ppb) increment in 4-hr O3. The associations between HRV and PM2.5 and O3 were stronger in people with ischemic heart disease (IHD) and hypertension. The associations observed between SDNN and LF and PM2.5 were stronger in people with diabetes. People using calcium-channel blockers and beta-blockers had lower associations between O3 and PM2.5 with LF. No effect modification by other cardiac medications was found. Exposures to PM2.5 and O3 are associated with decreased HRV, and history of IHD, hypertension, and diabetes may confer susceptibility to autonomic dysfunction by air pollution.     

Exposure to fuel-oil ash and welding emissions during the overhaul of an oil-fired boiler

The health effects of exposure to vanadium in fuel-oil ash are not well described at levels ranging from 10 to 500 microg/m(3). As part of a larger occupational epidemiologic study that assessed these effects during the overhaul of a large oil-fired boiler, this study was designed to quantify boilermakers' exposures to fuel-oil ash particles, metals, and welding gases, and to identify determinants of these exposures. Personal exposure measurements were conducted on 18 boilermakers and 11 utility workers (referents) before and during a 3-week overhaul. Ash particles < 10 microm in diameter (PM(10), mg/m(3)) were sampled over full work shifts using a one-stage personal size selective sampler containing a polytetrafluoroethylene filter. Filters were digested using the Parr bomb method and analyzed for the metals vanadium (V), nickel (Ni), iron (Fe), chromium (Cr), cadmium (Cd), lead (Pb), manganese (Mn), and arsenic (As) by inductively coupled plasma mass spectrometry. Nitrogen dioxide (NO(2)) was measured with an Ogawa passive badge-type sampler and ozone (O(3)) with a personal active pump sampler.Time-weighted average (TWA) exposures were significantly higher (p < 0.05) for boilermakers than for utility workers for PM(10) (geometric mean: 0.47 vs. 0.13 mg/m(3)), V (8.9 vs. 1.4 microg/m(3)), Ni (7.4 vs. 1.8 microg/m(3)) and Fe (56.2 vs. 11.2 microg/m(3)). Exposures were affected by overhaul time periods, tasks, and work locations. No significant increases were found for O(3) or NO(2) for boilermakers or utility workers regardless of overhaul period or task group. Fuel-oil ash was a major contributor to boilermakers' exposure to PM(10) and metals. Vanadium concentrations sometimes exceeded the 2003 American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value.     

Particulate matter exposures, mortality, and cardiovascular disease in the health professionals follow-up study

Background: The association of all-cause mortality and cardiovascular outcomes with air pollution exposures has been well established in the literature. The number of studies examining chronic exposures in cohorts is growing, with more recent studies conducted among women finding risk estimates of greater magnitude. Questions remain regarding sex differences in the relationship of chronic particulate matter (PM) exposures with mortality and cardiovascular outcomes.Objectives: In this study we explored these associations in the all-male Health Professionals Follow-Up Study prospective cohort.Methods: The same spatiotemporal exposure estimation models, similar outcomes, and biennially updated covariates were used as those previously applied in the female Nurses’ Health Study cohort.Results: Among 17,545 men residing in the northeastern and midwestern United States, there were 2,813 deaths, including 746 cases of fatal coronary heart disease (CHD). An interquartile range change (4 µg/m³) in average exposure to PM ≤ 2.5 µm in diameter in the 12 previous months was not associated with all-cause mortality [hazard ratio (HR) = 0.94; 95% confidence interval (CI), 0.87–1.00] or fatal CHD (HR = 0.99; 95% CI, 0.87–1.13) in fully adjusted models. Findings were similar for separate models of exposure to PM ≤ 10 µm in diameter and PM between 2.5 and 10 µm in diameter and for copollutant models.Conclusions: Among this cohort of men with high socioeconomic status living in the midwestern and northeastern United States, the results did not support an association of chronic PM exposures with all-cause mortality and cardiovascular outcomes in models with time-varying covariates. Whether these findings suggest sex differences in susceptibility or the protective impact of healthier lifestyles and higher socioeconomic status requires additional investigation.     

Ozone dose-response effects of varied equivalent minute ventilation rates

While it is well known that exercise minute ventilation (V(E)) results in greater pulmonary function and subjective symptoms (SS) responses upon exposure to a given ozone (O3) dose, the magnitude of V(E) increase to produce a significant forced expiratory volume in 1 s (FEV1.0) response compared to that observed at a lower exercise V(E) for the same O3 concentration and exposure time is unclear, especially in prolonged (i.e., >2 h) exposures. Further, in prolonged exposures, the relationship of body size to FEV1.0 response to a given O3 exposure dose has not been systematically examined. In the present study, 30 young adults were exposed on four occasions for 6 h (during a 6.6-h period) to constant 03 levels of zero (filtered air, FA) or 0.12 parts per million (ppm). At the latter concentration, exercise V(E) was varied in exposures to 17, 20, and 23 l min(-1) m(-2) of BSA, respectively, for each individual to achieve an equivalent ventilation rate, EVR). In the FA exposure, EVR was 23 l min(-1) m2. Percent changes in FEV1.0 for the three 0.12 ppm O3 exposures were significantly greater than that for FA, but did not differ significantly from each other. For the 6.6-h exposures, exercise EVR at or in excess of 17 l min(-1) m(-2), SS values were significantly greater than those observed for the FA protocol. Further, SS values at 6.6 h of exposure to 0.12 ppm O3 for the exercise EVR of 23 l min(-1) m(-2) protocol were significantly greater than for the 0.12 ppm O3 exercise EVR of 17 l min(-1) m(-2) protocol. To achieve a widened EVR, two 1-h exposures to 0.30 ppm O3 with continuous exercise (CE) at a level necessitating an EVR of 17 and approximately 34 l min(-1) m(-2), respectively, were completed by each subject. All postexposure pulmonary function and SS responses were significantly greater for the higher 1-h EVR protocol. In all exposures with significant O3-induced changes in FEV1.0 and SS, it was found that the smaller subjects who exercised at the lowest absolute V(E) had significantly smaller responses than did the larger subjects. These results strongly suggest that for the O3 concentrations and exposure durations used in this study, the effect of V(E) on O3-induced FEV1.0 and SS responses is not body-size-dependent.