Factors affecting the association between ambient concentrations and personal exposures to particles and gases

Results from air pollution exposure assessment studies suggest that ambient fine particles [particulate matter with aerodynamic diameter相似文献   

Effects of ambient ozone exposure on mail carriers' peak expiratory flow rates

The extent to which occupational exposure to ozone in ambient air can affect lung function remains unclear. We conducted a panel study in 43 mail carriers by measuring their peak expiratory flow rates (PEFRs) twice daily for 6 weeks in 2001. The daily exposure of each mail carrier to O3, particulate matter < 10 microm in aerodynamic diameter (PM10), and nitrogen dioxide was estimated by one air monitoring station in the center of the mail carrier's delivery area. Hourly concentrations of air pollutants during their exposure periods were 6-96 ppb for O3, 11-249 microg/m3 for PM10, and 14-92 ppb for NO2. Linear mixed-effects models were used to estimate the association between air pollution exposures and PEFR after adjusting for subject's sex, age, and disease status and for temperature and humidity. We found that night PEFR and the deviation in night PEFR were significantly decreased in association with 8-hr O3 exposures with a lag 0-2 days and by daily maximum O3 exposures with a lag of 0-1 day in our multipollutant models. By contrast, neither PM10 nor NO2 was associated with a PEFR reduction. Daily 8-hr mean concentrations of O3 had greater reduction effects on PEFR than did daily maximum concentrations. For a 10-ppb increase in the 8-hr average O3 concentration, the night PEFR was decreased by 0.54% for a 0-day lag, 0.69% for a 1-day lag, and 0.52% for a 2-day lag. We found that an acute lung function reduction occurs in mail carriers exposed to O3 concentrations below current ambient air quality standards and occupational exposure limits.     

The effects of ambient ozone on lung function in children: a reanalysis of six summer camp studies.

Studies of children attending summer camps often have observed relationships between daily outdoor ozone (O3) concentrations and decreased lung function that are qualitatively similar to results seen in human chamber studies. The former studies, focusing on the pulmonary effects of O3 and associated pollutants on children under natural conditions of exposure, are potentially of great importance to understanding the public health impact of ambient O3. However, a thorough assessment of the results of these studies has been hampered by differences in the analysis and reporting of data across the various studies. We obtained data sets from six summer camp studies carried out by three separate investigative groups, including two New Jersey studies performed by New York University, two studies in Ontario carried out by Health and Welfare Canada, and two studies in southern California. The data consisted of sequential, daily measurements of forced expiratory volume in 1 sec (FEV1), peak expiratory flow rate (PEFR), and 1-hr O3 concentration in the hour preceding lung function measurements for each child. We analyzed the relationships between lung function and O3 using linear regression models that fit subject-specific intercepts and a single, pooled O3 slope. These models were fit for each of the six studies separately and for all studies combined. All of the study-specific slopes of FEV1 on O3 were negative (i.e., increased O3 associated with decreased FEV1); five of six were statistically significant. Analysis of the combined six-study data set yielded a slope of -0.50 ml FEV1/ppb O3 (p<0.0001). Addition of time-trend variables to the combined-data analysis diminished, but did not eliminate, the FEV1-O3 relationship. Study-specific slopes for PEFR on O3 were more variable. Combined over studies, no significant relationship was observed between PEFR and O3. However, this negative finding appeared to be partially confounded by time trends in PEFR. The results of this reanalysis provide strong evidence that children exposed to O3 under natural conditions experience decreases in FEV1 of the kind demonstrated in laboratory studies, and raise concern that other acute respiratory effects observed in those studies (e.g., pulmonary inflammation) may also occur in young people exposed to ambient O3.     

Personal and ambient air pollution exposures and lung function decrements in children with asthma

BACKGROUND: Epidemiologic studies have shown associations between asthma outcomes and outdoor air pollutants such as nitrogen dioxide and particulate matter mass < 2.5 mum in diameter (PM(2.5)). Independent effects of specific pollutants have been difficult to detect because most studies have relied on highly correlated central-site measurements. OBJECTIVES: This study was designed to evaluate the relationship of daily changes in percent-predicted forced expiratory volume in 1 sec (FEV(1)) with personal and ambient air pollutant exposures. METHODS: For 10 days each, we followed 53 subjects with asthma who were 9-18 years of age and living in the Los Angeles, California, air basin. Subjects self-administered home spirometry in themorning, afternoon, and evening. We measured personal hourly PM(2.5) mass, 24-hr PM(2.5) elemental and organic carbon (EC-OC), and 24-hr NO(2), and the same 24-hr average outdoor central-site(ambient) exposures. We analyzed data with transitional mixed models controlling for personal temperature and humidity, and as-needed beta(2)-agonist inhaler use. RESULTS: FEV(1) decrements were significantly associated with increasing hourly peak and daily average personal PM(2.5), but not ambient PM(2.5). Personal NO(2) was also inversely associated with FEV(1). Ambient NO(2) was more weakly associated. We found stronger associations among 37 subjects not taking controller bronchodilators as follows: Personal EC-OC was inversely associated with morning FEV(1); for an interquartile increase of 71 mug/m(3) 1-hr maximum personal PM(2.5), overall percent-predicted FEV(1) decreased by 1.32% [95% confidence interval (CI), -2.00 to -0.65%]; and for an interquartile increase of 16.8 ppb 2-day average personal NO(2), overall percent-predicted FEV(1) decreased by 2.45% (95% CI, -3.57 to -1.33%). Associations of both personal PM(2.5) and NO(2) with FEV(1) remained when co-regressed, and both confounded ambient NO(2). CONCLUSIONS: Independent pollutant associations with lung function might be missed using ambient data alone. Different sets of causal components are suggested by independence of FEV(1) associations with personal PM(2.5) mass from associations with personal NO(2).     

Effects of chronic and acute ozone exposure on lipid peroxidation and antioxidant capacity in healthy young adults

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 O(3) 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.     

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.     

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.     

Experimental studies on human health effects of air pollutants. II. Four-hour exposure to ozone alone and in combination with other pollutant gases.

Eight adult male volunteers were exposed to ozone (O3) alone and then in combination with nitrogen dioxide and carbon monoxide under conditions simulating ambient air pollution exposures. Four "normal" men showed few or no effects from repeated exposures. Four male volunteers with a history of "hyperreactive" airways, but with normal base line pulmonary function spirometric studies, after O3 exposure developed definite symptoms and decrement in pulmonary function.     

Effects of submicrometer sulfuric acid aerosols on mucociliary transport and respiratory mechanics in asymptomatic asthmatics

The effects of a 1-hr inhalation of submicrometer sulfuric acid (H2SO4) aerosols via nasal mask on tracheobronchial mucociliary particle clearance and respiratory mechanics were studied in ten subjects with asthmatic histories. A brief inhalation of monodisperse 3.9-micron 99mTc-tagged Fe2O3 aerosol preceded the 1-hr H2SO4 (at 100, 300, and 1000 micrograms/m3) or a sham exposure. Thoracic retention of the gamma-tagged Fe2O3 was measured using external radiation detectors. Respiratory function was measured before, and 15 min and 3 hr after the H2SO4 or sham exposure. After exposure to 1000 micrograms/m3 of H2SO4, the six subjects not on routine medication exhibited a transient slowing of mucociliary clearance and also decrements in sGaw, FEV1/FVC, MMEF, and V25 (P less than 0.05) in both sets of measurements. The four asthmatics on daily medication exhibited stepwise mucociliary clearance that was too variable to allow detection of any H2SO4 effect on clearance. The 1000 micrograms/m3 of H2SO4 did produce decrements in V25 (P less than 0.05), but the variability of the other respiratory parameters in this small group was too great to permit detection of changes. Mucociliary clearance rates in both groups in the sham exposure tests were significantly slower than those of healthy nonsmokers studied previously using the same protocols. The extent of mucociliary clearance slowing following the 1000 micrograms/m3 exposure in the nonmedicated subjects was similar to that in the healthy nonsmokers. This similar change, from a reduced baseline rate of clearance, together with the significant change in respiratory function, indicate that asymptomatic asthmatics may respond to H2SO4 exposures with functional changes of greater potential health significance than do healthy nonsmokers.     

Repeated laboratory ozone exposures of volunteer Los Angeles residents: an apparent seasonal variation in response

This study was intended to help explain individual differences in susceptibility to irritant effects of ozone (O3), by determining whether prior ambient O3 exposures and/or recent acute respiratory illness modified response to laboratory O3 exposures. Response was measured in terms of lung function changes and irritant symptoms. Initially, 59 adult volunteer Los Angeles area residents underwent screening exposures in spring, before the season of frequent high ambient O3 levels. Unusually responsive and nonresponsive individuals (N = 12 and 13 respectively) underwent followup exposures in autumn (late in the high-O3 season) and in winter (low-O3 season). All exposures were to 0.18 ppm O3 for 2 hr with intermittent heavy exercise at 31 degrees C and 35% relative humidity. Nonresponders tended to remain nonresponsive throughout. In fall, responders had lost much of their reactivity, as if they had "adapted" to summer ambient O3 exposures. They did not regain reactivity by winter. Clinical laboratory findings suggestive of acute respiratory illness did not appear to correlate with O3 response. Eight responders and 9 nonresponders underwent another followup exposure in spring, about 1 yr after screening. By that time most responders had regained their reactivity; individual function changes were significantly correlated with changes 1 yr earlier. These results suggest that response to O3 is a persistent individual characteristic, but can be modified by repeated ambient exposures.     

Adverse cardiovascular effects with acute particulate matter and ozone exposures: interstrain variation in mice

OBJECTIVES: Increased ambient particulate matter (PM) levels are associated with cardiovascular morbidity and mortality, as shown by numerous epidemiology studies. Few studies have investigated the role of copollutants, such as ozone, in this association. Furthermore, the mechanisms by which PM affects cardiac function remain uncertain. We hypothesized that PM and O(3) induce adverse cardiovascular effects in mice and that these effects are strain dependent. STUDY DESIGN: After implanting radiotelemeters to measure heart rate (HR) and HR variability (HRV) parameters, we exposed C57Bl/6J (B6), C3H/HeJ (HeJ), and C3H/HeOuJ (OuJ) inbred mouse strains to three different daily exposures of filtered air (FA), carbon black particles (CB), or O(3) and CB sequentially [O(3)CB; for CB, 536 +/- 24 microg/m(3); for O(3), 584 +/- 35 ppb (mean +/- SE)]. RESULTS: We observed significant changes in HR and HRV in all strains due to O(3)CB exposure, but not due to sequential FA and CB exposure (FACB). The data suggest that primarily acute HR and HRV effects occur during O(3)CB exposure, especially in HeJ and OuJ mice. For example, HeJ and OuJ mice demonstrated dramatic increases in HRV parameters associated with marked brady-cardia during O(3)CB exposure. In contrast, depressed HR responses occurred in B6 mice without detectable changes in HRV parameters. CONCLUSIONS: These findings demonstrate that important interstrain differences exist with respect to PM- and O(3)-induced cardiac effects. This interstrain variation suggests that genetic factors may modulate HR regulation in response to and recuperation from acute copollutant exposures.     

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 microm). 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.     

Effects of multiday exposure to ozone on airway inflammation as determined using sputum induction

Single short-term exposures to ozone are known to cause acute changes in pulmonary function and neutrophilic airway inflammation. The respiratory health effects of repeated exposures are not as well studied. Pulmonary function decrements are known to attenuate, but it is less clear how injury and inflammation are affected. Using sputum induction (SI) to sample respiratory tract lining fluid after single- and multiday exposures, we designed a study to test the hypothesis that neutrophils would increase after multiday exposure compared with single-day exposure. In a randomized, crossover design, 15 normal healthy subjects were exposed to O3 (0.2 ppm) under two conditions: for 4 hr for 1 day (1D) and for 4 hr for 4 consecutive days (4D). Pulmonary function testing was performed immediately before and after each 4-hr exposure. The SI was performed 18 hr after the end of the 1D and 4D conditions. The symptom and pulmonary function data followed a pattern seen in other multiday O3 exposure studies, with the greatest changes occurring on the second day. In contrast to previous studies using bronchoalveolar lavage, however, there was a significant increase in the percentage of neutrophils and a significant decrease in the percentage of macrophages after the 4D condition compared with the 1D condition. Given that SI likely samples proximal airways better than distal lung, these results add to the body of evidence that differential airway compartmental responses to O3 occur in humans and other species.     

Combined effect of ozone and sulfuric acid on pulmonary function in man

A potential effect of the combination of ozone and sulfuric acid mist (H2SO4) on respiratory function has been postulated for humans simultaneously exposed to these two pollutants. Nine young men were exposed to 0.25 ppm ozone (O3), 1200-1600 micrograms/m3 sulfuric acid aerosol (H2SO4), and a combination of O3 and H2SO4. During the 2-hr exposures, the subjects exercised (ventilation = 30 L/min) three times for 20 min each. Air temperature was 35 degrees C and relative humidity 83%. Pulmonary function changes after exposure to ozone alone were not expected and were not demonstrated. If a reaction between the combination of O3 and H2SO4 and pulmonary function occurred, pulmonary function responses may have been anticipated following the combination exposure, but no significant changes were seen. It was concluded that the combination of ozone and sulfuric acid aerosol at levels in excess of Threshold Limit Values (TLV) levels do not cause pulmonary dysfunction.     

Relationships between nitrogen dioxide personal exposure and ambient air monitoring measurements among children in three French metropolitan areas: VESTA study

In epidemiological studies, investigators have routinely used ambient air concentrations, measured by air-quality monitoring networks, to assess exposure of subjects. When there is great spatial variability of ambient air concentrations or when there are specific indoor exposures, this approach may yield substantial exposure misclassification and distort the associations between exposure and the health endpoints of interest. In 3 French metropolitan areas, the cross-sectional relationships between 48 hr of nitrogen dioxide personal exposure of 73 children and the corresponding 48-hr background ambient air concentrations were analyzed. The crude correlation between ambient air concentrations and personal exposures was poor in all cities (r2 = .009 for Grenoble, r2 = .04 for Toulouse, and r2 = .02 for Paris). These correlations were improved when the authors took into account other ambient air or indoor air sources of nitrogen dioxide emissions (the corresponding multiple linear regression, r2, increased to .43 in Grenoble, .50 in Toulouse, and .37 in Paris). The main variables that explained personal exposures were an index of traffic intensity and proximity and use of a gas cooker at home. The results of this study confirm that ambient air-monitoring site measurements are poor predictors of personal exposure. Investigators should carefully characterize the proximity of roads occupied by dense traffic to the home/school as well as indoor sources of nitric oxide emissions; both of these careful characterizations will assist researchers in the prediction of personal exposure in epidemiological studies.     

Laboratory study of asthmatic volunteers exposed to nitrogen dioxide and to ambient air pollution

Adult volunteers with moderate to severe asthma (N = 59) underwent dose-response studies to assess their reactivity to nitrogen dioxide (NO2) in otherwise clean air. Exposure concentrations were 0.0 (control), 0.3 and 0.6 ppm. A subgroup (N = 36) also underwent exposures to Los Angeles area ambient air at times when NO2 pollution was expected. Concentrations of NO2 during ambient exposures were 0.086 +/- 0.024 ppm (mean +/- s.d.). All exposures took place in a movable chamber/laboratory facility. Each study lasted 2 hr, with alternating 10 min periods of exercise (mean ventilation rate 40 L/min) and rest. Lung function was measured prior to exposure and after 10 min, 1 hr and 2 hr of exposure. Symptoms were recorded prior to exposure, during exposure and for 1 week afterward. In some subjects bronchial reactivity to cold air was measured 1 hr after the end of exposure and again 24 hr later. Different exposure conditions were presented in randomized order, 1 week apart. No pollutant exposure produced statistically significant changes in lung function, symptoms, or bronchial reactivity, relative to clean air. Ambient air exposures produced the largest (still nonsignificant) mean changes in some lung function tests. Given the physiological and atmospheric variability, negative statistical results do not rule out a small unfavorable effect of ambient pollution on lung function. If any such effect occurred, it was not likely caused by NO2. Statistical results remained negative when the analysis was restricted to the 20 subjects with most severe lung dysfunction. In conclusion at least in the Los Angeles area, sensitivity to ambient concentrations of NO2 is not common, even among adult asthmatics with moderate to severe disease.     

Initiation of cell proliferation in livers of the viviparous fish Poeciliopsis lucida with 7,12-dimethylbenz[a]anthracene

Stimulation of liver cell proliferation by sublethal exposures to 7,12-dimethylbenz[a]anthracene (DMBA) is examined in the small, viviparous fish Poeciliopsis lucida. Poeciliopsis is susceptible to induction of liver tumors by repeated short-term exposures, under 24 hr, to waterborne DMBA at 5 ppm. Exposures to 5 ppm for 24 hr was lethal to fish under 1 month old and resulted in 60% mortality of adult females 20-25 mm in length. Response to 16-, 20-, and 22-hr exposures of 5 ppm DMBA, as measured by mitotic index, was similar in females of two size classes, 20-25 mm and 26-30 mm. Differences were observed in the onset of mitosis in livers of fish exposed for 16 hr vs 20 or 22 hr. Hepatocyte proliferation did not begin until 10-11 days after the 16-hr exposure and lasted for only 3 days. When exposure was increased to 20 or 22 hr, mitotic activity was observed earlier, 2 days following treatment, and continued for 6-8 days. The peak period of cell proliferation also varied, occurring 12 days after a 16-hr exposure, 4 days after a 20-hr exposure, and at least 10 days after a 22-hr exposure. The mitotic index was the highest on the final day specimens of the 22-hr treatment were collected. These results suggest that the toxic properties of DMBA in stimulating cell proliferation may function as an important cofactor in hepatocarcinogenesis.     

Urinary DEHP metabolites and fasting time in NHANES

Exposure assessment analyses conducted in Europe have concluded that the primary pathway of exposure to di(2-ethylhexyl) phthalate (DEHP) is through the diet. The purpose of this study is to evaluate whether urinary DEHP metabolite data from the 2007-2008 National Health and Nutritional Examination Survey (NHANES) demonstrate relationships with reported food-fasting time consistent with diet as the predominant exposure pathway. Previous controlled-dosing data demonstrate that DEHP metabolite concentrations in urine first rise and then decline over time, with first-order elimination becoming evident at about 6 h post exposure. Regression of the concentrations of four key DEHP metabolites vs reported fasting times between 6 and 18 h in adults resulted in apparent population-based urinary elimination half-lives, consistent with those previously determined in a controlled-dosing experiment, supporting the importance of the dietary pathway for DEHP. For fasting times less than about 6 h, sampling session (morning, afternoon, or evening) affected the measured metabolite concentrations. Evening samples showed the highest metabolite concentrations, supporting a hypothesis of recent daily dietary exposures from multiple meals, whereas morning and afternoon samples for fasting times less than 6 h were similar and somewhat lower than evening samples, consistent with less-substantial early day dietary exposure. Variations in children's bodyweight-normalized creatinine excretion and food intake rates contribute to a strong inverse relationship between urinary DEHP metabolite concentrations and age under age 18. Finally, a previously published pharmacokinetic model for DEHP demonstrates that time since previous urinary void, a parameter not measured in NHANES, is predicted to result in non-random effects on measured urinary concentrations.     

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.