Zhihua Fan

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

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

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

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

Nasal effects of a mixture of volatile organic compounds and their ozone oxidation products.

Objective:Our objective was to determine if low levels of a mixture of volatile organic compounds (VOCs) and their ozone (O3) oxidation products, similar to what might be found in “sick buildings,” cause nasal irritation and inflammation under controlled exposure conditions. Methods:Healthy, nonsmoking women (n = 130) completed 2-hour controlled exposures to VOCs, VOCs and O3, and a masked air “MA” control in random order at least 1 week apart. VOCs and O3 concentrations were approximately 25 mg/m3 and approximately 40 ppb, respectively. Nasal symptoms were rated before, during, and after exposure. Nasal lavage fluid was analyzed for polymorphonuclear cells, total protein, interleukin-6, and interleukin-8. Results:We found no significant differences in symptoms or markers of nasal inflammation between exposure conditions. Conclusions:Results suggest that VOCs and their oxidation products may not cause acute nasal effects at low concentrations.

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

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

Health Risk Assessment of Inhalation Exposure to Formaldehyde and Benzene in Newly Remodeled Buildings, Beijing

Objective To assess health risks associated with inhalation exposure to formaldehyde and benzene mainly emitted from building and decoration materials in newly remodeled indoor spaces in Beijing. Methods We tested the formaldehyde and benzene concentrations in indoor air of 410 dwellings and 451 offices remodeled within the past year, in which the occupants had health concerns about indoor air quality. To assess non-carcinogenic health risks, we compared the data to the health guidelines in China and USA, respectively. To assess carcinogenic health risks, we first modeled indoor personal exposure to formaldehyde and benzene using the concentration data, and then estimated the associated cancer risks by multiplying the indoor personal exposure by the Inhalation Unit Risk values (IURs) provided by the U.S. EPA Integrated Risk Information System (U.S. EPA IRIS) and the California Office of Environmental Health Hazard Assessment (OEHHA), respectively. Results (1) The indoor formaldehyde concentrations of 85% dwellings and 67% offices were above the acute Reference Exposure Level (REL) recommended by the OEHHA and the concentrations of all tested buildings were above the chronic REL recommended by the OEHHA; (2) The indoor benzene concentrations of 12% dwellings and 32% offices exceeded the reference concentration (RfC) recommended by the U.S. EPA IRIS; (3) The median cancer risks from indoor exposure to formaldehyde and benzene were 1,150 and 106 per million (based on U.S. EPA IRIS IURs), 531 and 394 per million (based on OEHHA IURs). Conclusions In the tested buildings, formaldehyde exposure may pose acute and chronic non-carcinogenic health risks to the occupants, whereas benzene exposure may pose chronic non-carcinogenic risks to the occupants. Exposure to both compounds is associated with significant carcinogenic risks. Improvement in ventilation, establishment of volatile organic compounds (VOCs) emission labeling systems for decorating and refurbishing materials are recommended to reduce indoor VOCs exposure.

Time-location patterns of a population living in an air pollution hotspot.

This study characterized the time-location pattern of 107 residents living in air pollution hotspots, the Waterfront South and Copewood/Davis Streets communities in Camden, NJ. Most residents in the two communities are minority and impoverished individuals. Results showed that employment status played the fundamental role in determining time-location patterns of this study population, and the variations of time-location pattern by season and by day-type were partially attributed to employment status. Compared to the National Human Activity Pattern Survey, the Camden cohort spent significantly more time outdoors (3.8 hours versus 1.8 hours) and less time indoors (19.4 hours versus 20.9 hours) than the general US population, indicating a higher risk of exposure to ambient air pollution for the Camden cohort. The findings of the study are important for understanding exposure routes and sources for the socioeconomically disadvantaged subgroup and ultimately help develop effective strategies to reduce community exposure to ambient air pollution in “hotspots”.

Characterization of Atmospheric Polycyclic Aromatic Hydrocarbons in a Mixed-Use Urban Community in Paterson, NJ: Concentrations and Sources

ABSTRACT Exposure to ambient polycyclic aromatic hydrocarbons (PAHs) is a potential health concern for communities because many PAHs are known to be mutagenic and carcinogenic. However, information on ambient concentrations of PAHs in communities is very limited. During the Urban Community Air Toxics Monitoring Project, Paterson City, NJ, PAH concentrations in ambient air PM10 (particulate matter ≤ 10 μm in aerodynamic diameter) were measured from November 2005 through December 2006 in Paterson, a mixed-use urban community located in Passaic County, NJ. Three locations dominated by industrial, commercial, and mobile sources were chosen as monitoring sites. The comparison background site was located in Chester, NJ, which is approximately 58 km west/southwest of Paterson. The concentrations of all of the individual PAHs at all three Paterson sites were found to be significantly higher than those at the background site (P < 0.05). The PAH profiles obtained from the three sites with different land-use patterns showed that the contributions of heavier PAHs (molecular weight > 202) to the total PAHs were significantly higher at the industrial site than those at the commercial and mobile sites. Analysis of the diagnostic ratios between PAH isomers suggested that the diesel-powered vehicles were the major PAH sources in the Paterson area throughout the year. The operation of industrial facilities and other combustion sources also partially contributed to PAH air pollution in Paterson. The correlation of individual PAH, total PAH, and the correlation of total PAHs with other air co-pollutants (copper, iron, manganese, lead, zinc, elemental carbon, and organic carbon) within and between the sampling sites supported the conclusions obtained from the diagnostic ratio analysis. IMPLICATIONS The study provides a valuable approach to understand potential exposure in a mixed land-use urban community. Data obtained from the study (i.e., concentration and source profiles of PAHs at different sites in Paterson) are useful in helping to identify air pollution sources of concern. The findings of this research project may also be helpful in assisting regulatory agencies in developing effective strategies to control sources of air pollution and to better address community concerns.

Hexavalent chromium in house dust: A comparison between an area with historic contamination from chromate production and background locations

In contrast to Cr(+3), Cr(+6) is carcinogenic and allergenic. Although Cr(+6) can occur naturally, it is thought that most soil Cr(+6) is anthropogenic, however, the extent of Cr(+6) in the background environment is unknown. Cr(+6)-containing chromite ore processing residue (COPR) from chromate manufacture was deposited in numerous locations in Jersey City (JC), New Jersey. In the 1990s, significantly elevated concentrations of total Cr (Cr(+6)+Cr(+3)) were found in house dust near COPR sites. We undertook a follow-up study to determine ongoing COPR exposure. We compared Cr(+6) in house dust in JC to selected background communities with no known sources of Cr(+6). Samples were collected from living areas, basements and window wells. Cr(+6) was detected in dust from all JC and background houses. In the JC homes, the mean (+ or - SD) Cr(+6) concentration for all samples was 3.9 + or - 7.0 microg/g (range: non-detect-90.4 microg/g), and the mean Cr(+6) loading was 5.8 + or - 15.7 microg/m(2) (range: non-detect-196.4 microg/m(2)). In background homes, the mean Cr(+6) concentrations of all samples was 4.6 + or - 7.8 microg/g, (range, 0.05-56.6 microg/g). The mean loading was 10.0 + or - 27.9 microg/m(2) (range, 0.22-169.3 microg/m(2)). There was no significant difference between Cr(+6) dust concentrations in Jersey City and background locations. Stratification by sample location within houses and sampling method gave similar results. Samples exceeding 20 microg/g were obtained only from single wood surfaces in different homes. Lower concentrations in window well samples suggests transport from outside is not the major source of indoor Cr(+6). Landscaping and groundcover may influence indoor Cr(+6). There appears to be a widespread low level background of Cr(+6) that is not elevated in Jersey City homes despite its historic COPR contamination. It is possible that house dust, in general, is a source of Cr(+6) exposure with potential implications for persistence of chromium allergic contact dermatitis.

Spatial/Temporal Variations and Source Apportionment of VOCs Monitored at Community Scale in an Urban Area

This study aimed to characterize spatial/temporal variations of ambient volatile organic compounds (VOCs) using a community-scale monitoring approach and identify the main sources of concern in Paterson, NJ, an urban area with mixed sources of VOCs. VOC samples were simultaneously collected from three local source-dominated (i.e., commercial, industrial, and mobile) sites in Paterson and one background site in Chester, NJ (located ∼58 km southwest of Paterson). Samples were collected using the EPA TO-15 method from midnight to midnight, one in every sixth day over one year. Among the 60 analyzed VOCs, ten VOCs (acetylene, benzene, dichloromethane, ethylbenzene, methyl ethyl ketone, styrene, toluene, m,p-xylene, o-xylene, and p-dichlorobenzene) were selected to examine their spatial/temporal variations. All of the 10 VOCs in Paterson were significantly higher than the background site (p<0.01). Ethylbenzene, m,p-xylene, o-xylene, and p-dichlorobenzene measured at the commercial site were significantly higher than the industrial/mobile sites (p<0.01). Seven VOCs (acetylene, benzene, dichloromethane, methyl ethyl ketone, styrene, toluene, and p-dichlorobenzene) were significantly different by season (p<0.05), that is, higher in cold seasons than in warm seasons. In addition, dichloromethane, methyl ethyl ketone, and toluene were significantly higher on weekdays than weekend days (p<0.05). These results are consistent with literature data, indicating the impact of anthropogenic VOC sources on air pollution in Paterson. Positive Matrix Factorization (PMF) analysis was applied for 24-hour integrated VOC measurements in Paterson over one year and identified six contributing factors, including motor vehicle exhausts (20%), solvents uses (19%), industrial emissions (16%), mobile+stationery sources (12%), small shop emissions (11%), and others (22%). Additional locational analysis confirmed the identified sources were well matched with point sources located upwind in Paterson. The study demonstrated the community-scale monitoring approach can capture spatial variation of VOCs in an urban community with mixed VOC sources. It also provided robust data to identify major sources of concern in the community.

Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution.

Type II diabetes is an established cause of vascular impairment. Particulate air pollution is known to exacerbate cardiovascular and respiratory conditions, particularly in susceptible populations. This study set out to determine the impact of exposure to traffic pollution, with and without particle filtration, on vascular endothelial function in Type II diabetes. Endothelial production of nitric oxide (NO) has previously been linked to vascular health. Reactive hyperemia induces a significant increase in plasma nitrite, the proximal metabolite of NO, in healthy subjects, while diabetics have a lower and more variable level of response. Twenty type II diabetics and 20 controls (ages 46–70 years) were taken on a 1.5hr roadway traffic air pollution exposure as passengers. We analyzed plasma nitrite, as a measure of vascular function, using forearm ischemia to elicit a reactive hyperemic response before and after exposure to one ride with and one without filtration of the particle components of pollution. Control subjects displayed a significant increase in plasma nitrite levels during reactive hyperemia. This response was no longer present following exposure to traffic air pollution, but did not vary with whether or not the particle phase was filtered out. Diabetics did not display an increase in nitrite levels following reactive hyperemia. This response was not altered following pollution exposure. These data suggest that components of acute traffic pollution exposure diminish vascular reactivity in non-diabetic individuals. It also confirms that type II diabetics have a preexisting diminished ability to appropriately respond to a vascular challenge, and that traffic pollution exposure does not cause a further measureable acute change in plasma nitrite levels in Type II diabetics.