Aviation-Related Impacts on Ultrafine Particle Number Concentrations Outside and Inside Residences near an Airport.

Jet engine exhaust is a significant source of ultrafine particles and aviation-related emissions can adversely impact air quality over large areas surrounding airports. We investigated outdoor and indoor ultrafine particle number concentrations (PNC) from 16 residences located in two study areas in the greater Boston metropolitan area (MA, USA) for evidence of aviation-related impacts. During winds from the direction of Logan International Airport, that is, impact-sector winds, an increase in outdoor and indoor PNC was clearly evident at all seven residences in the Chelsea study area (∼4-5 km from the airport) and three out of nine residences in the Boston study area (∼5-6 km from the airport); the median increase during impact-sector winds compared to other winds was 1.7-fold for both outdoor and indoor PNC. Across all residences during impact-sector and other winds, median outdoor PNC were 19 000 and 10 000 particles/cm3, respectively, and median indoor PNC were 7000 and 4000 particles/cm3, respectively. Overall, our results indicate that aviation-related outdoor PNC infiltrate indoors and result in significantly higher indoor PNC. Our study provides compelling evidence for the impact of aviation-related emissions on residential exposures. Further investigation is warranted because these impacts are not expected to be unique to Logan airport.

Aviation Emissions Impact Ambient Ultrafine Particle Concentrations in the Greater Boston Area.

Ultrafine particles are emitted at high rates by jet aircraft. To determine the possible impacts of aviation activities on ambient ultrafine particle number concentrations (PNCs), we analyzed PNCs measured from 3 months to 3.67 years at three sites within 7.3 km of Logan International Airport (Boston, MA). At sites 4.0 and 7.3 km from the airport, average PNCs were 2- and 1.33-fold higher, respectively, when winds were from the direction of the airport compared to other directions, indicating that aviation impacts on PNC extend many kilometers downwind of Logan airport. Furthermore, PNCs were positively correlated with flight activity after taking meteorology, time of day and week, and traffic volume into account. Also, when winds were from the direction of the airport, PNCs increased with increasing wind speed, suggesting that buoyant aircraft exhaust plumes were the likely source. Concentrations of other pollutants [CO, black carbon (BC), NO, NO2, NOx, SO2, and fine particulate matter (PM2.5)] decreased with increasing wind speed when winds were from the direction of the airport, indicating a different dominant source (likely roadway traffic emissions). Except for oxides of nitrogen, other pollutants were not correlated with flight activity. Our findings point to the need for PNC exposure assessment studies to take aircraft emissions into consideration, particularly in populated areas near airports.

Short-term variation in near-highway air pollutant gradients on a winter morning.

Quantification of exposure to traffic-related air pollutants near highways is hampered by incomplete knowledge of the scales of temporal variation of pollutant gradients. The goal of this study was to characterize short-term temporal variation of vehicular pollutant gradients within 200-400 m of a major highway (>150 000 vehicles/d). Monitoring was done near Interstate 93 in Somerville (Massachusetts) from 06:00 to 11:00 on 16 January 2008 using a mobile monitoring platform equipped with instruments that measured ultrafine and fine particles (6-1000 nm, particle number concentration (PNC)); particle-phase (>30 nm) [Formula: see text], [Formula: see text], and organic compounds; volatile organic compounds (VOCs); and CO(2), NO, NO(2), and O(3). We observed rapid changes in pollutant gradients due to variations in highway traffic flow rate, wind speed, and surface boundary layer height. Before sunrise and peak traffic flow rates, downwind concentrations of particles, CO(2), NO, and NO(2) were highest within 100-250 m of the highway. After sunrise pollutant levels declined sharply (e.g., PNC and NO were more than halved) and the gradients became less pronounced as wind speed increased and the surface boundary layer rose allowing mixing with cleaner air aloft. The levels of aromatic VOCs and [Formula: see text], [Formula: see text] and organic aerosols were generally low throughout the morning, and their spatial and temporal variations were less pronounced compared to PNC and NO. O(3) levels increased throughout the morning due to mixing with O(3)-enriched air aloft and were generally lowest near the highway reflecting reaction with NO. There was little if any evolution in the size distribution of 6-225 nm particles with distance from the highway. These results suggest that to improve the accuracy of exposure estimates to near-highway pollutants, short-term (e.g., hourly) temporal variations in pollutant gradients must be measured to reflect changes in traffic patterns and local meteorology.

Controls on arsenic speciation and solid-phase partitioning in the sediments of a two-basin lake.

Arsenic (As) regeneration from sediments of Spy Pond, a two-basin lake near Boston, MA, continues to result in seasonally elevated As levels despite the several decades that have elapsed since the pond's historical contamination by a pulse input of As. Solid-phase speciation and partitioning of As in the sediments appear to be primary determinants of both potential As regeneration rate and, conversely, the rate at which long-term burial of the pond's As burden will occur. Although iron (Fe) chemistry often controls As speciation in lakes, a higher rate of As regeneration in the south basin, accompanied by the absence of a correlation between regenerated As and Fe in this basin, suggest that additional factors operate to control As cycling in this lake. Solid-phase As speciation was remarkably similar between sediments of the two basins of this lake, about 40% of sedimentary As in upper sediments being in relatively labile (ionically bound and strongly adsorbed) fractions and a larger fraction of As being associated with recalcitrant minerals, likely sulfides. Extraction, X-ray fluorescence, and acid-volatile sulfide data collectively suggest that sedimentary As cycling in both basins is largely controlled by the formation of sulfide minerals. An accounting of the size of sulfur (S) pools supports this conclusion, showing that sufficient S exists in the north basin to control both Fe and As, while the south basin has lower S levels resulting in seasonal accumulation of Fe in the porewater.

Human cell mutagenicity of chlorinated and unchlorinated water and the disinfection byproduct 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX).

Extracts of three water samples--humic acid-enriched water-both peatland water and drinking water, both with and without chlorination were tested for mutagenicity at the tk locus in MCL-5 cells, a line of human B-lymphoblastoid cells that express cytochrome P450 enzymes and microsomal epoxide hydrolase. Our results show that chlorination caused a 5.5-fold increase (P<0.0001) in the mutagenicity of the humic acid-enriched water. The unchlorinated peatland water was mutagenic at the two highest doses (240 and 480 microg equivalent total organic carbon (TOC)/ml), possibly due to polycyclic aromatic hydrocarbons (PAH) that were measured in the peat. In contrast, the chlorinated peatland water was non-mutagenic at low doses, while at the highest dose (240 microg equivalent TOC/ml) the sample was so toxic that an insufficient number of cells survived treatment to allow plating. The chlorinated and unchlorinated drinking water were both non-mutagenic. 3-Chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), a potent bacterial mutagen and chlorine-disinfection byproduct, was also tested in MCL-5 cells as well as in two other human B-lymphoblastoid cell-lines, AHH-1 TK+/- and h1A1v2 cells, which differ from each other and from MCL-5 cells in the amounts of cytochrome P450 enzymes they can express. MX was mutagenic to all three cell-lines, but there was no apparent correlation between cytochrome P450 enzyme expression and the mutagenicity of MX. Overall, our results show that samples of chlorinated humic acid-enriched water and MX, a model chlorine-disinfection byproduct, are moderately mutagenic to human cells.

Mutagenicity of C24H14 PAH in human cells expressing CYP1A1.

Relatively little is known about the mutagenicity of C24H14 PAH, a diverse group of five- and six-ring PAH, some of which are present at trace levels in the environment. To better understand the mutagenicity of this class of compounds, 11 C24H14 PAH, including benzo[a]perylene, benzo[b]perylene, dibenzo[a,e]fluoranthene, dibenzo[a,f]fluoranthene, dibenzo[j,l]fluoranthene, dibenzo[a,h]pyrene, dibenzo[a,i]pyrene, dibenzo[e,l]pyrene, naphtho[1,2-b]fluoranthene, naphtho[2,3-a]pyrene, and naphtho[2,3-e]pyrene, were tested in a mutagenicity assay based on human h1A1v2 cells. h1A1v2 cells are a line of human B-lymphoblastoid cells that have been engineered to express cytochrome P4501A1 (CYP1A1), an enzyme capable of metabolizing promutagenic PAH. Mutagenicity was measured at the thymidine kinase (tk) locus following a 72-h exposure period. Our results show that nine of the compounds were mutagenic. Benzo[a]perylene, dibenzo[a,e]fluoranthene, dibenzo[a,i]pyrene, and naphtho[2,3-a]pyrene were the most potent mutagens, having minimum mutagenic concentrations (MMC) (i.e., the dose at which the induced response was twice that of the negative controls) in the 1-5 ng/ml range. Benzo[b]perylene, dibenzo[a,h]pyrene, dibenzo[a,f]fluoranthene, and naphtho[2,3-e]pyrene were somewhat less potent mutagens, having MMC in the 10-30 ng/ml range. Dibenzo[e,l]pyrene, which had an MMC of 280 ng/ml, was the least potent mutagen. Dibenzo[j,l]fluoranthene and naphtho[1,2-b]fluoranthene were not mutagenic at the doses tested (1-3000 ng/ml). The most mutagenic compounds were also quite toxic. At the highest doses tested, benzo[a]perylene, dibenzo[a,e]fluoranthene, dibenzo[a,i]pyrene, dibenzo[a,h]pyrene, and dibenzo[a,f]fluoranthene induced > 60% killing, and naphtho[2,3-a]pyrene and naphtho[2,3-e]pyrene induced > 50% killing. Benzo[b]perylene, dibenzo[e,l]pyrene, dibenzo[j,l]fluoranthene, and naphtho[1,2-b]fluoranthene induced < 50% killing at the highest doses tested. Comparing these results to a previous study in which nine other C24H14 PAH were tested for mutagenicity in this same assay, it was found that dibenzo[a]pyrene isomers were generally more mutagenic than the other groups of C24H14 PAH tested. These observations are discussed with emphasis given to identifying C24H14 PAH that may be important environmental mutagens.

Hair analysis does not support hypothesized arsenic and chromium exposure from drinking water in Woburn, Massachusetts.

We hypothesized that residents of Woburn, Massachusetts, had been exposed to as much as 70 microg/l of arsenic (As) and 240 microg/l of chromium (Cr) in drinking water from municipal supply wells G and H. To test this hypothesis, we measured the concentrations of As and Cr in 82 hair samples donated by 56 Woburn residents. Thirty-six samples were cut between 1964 and 1979, the period during which wells G and H were in operation. The remainder were cut either before 1964 (1938-1963; n = 26) or after 1979 (1982-1994; n = 20). Washed hair samples were analyzed by instrumental neutron activation. Exposure to the well water--measured as access--was estimated using well pumping records and a model of the Woburn water distribution system. Our results show that access to wells G and H water was not significantly correlated (95% confidence interval) with As and Cr concentrations measured in the hair of Woburn residents, but As concentrations have declined significantly over the last half century. Linear regression of As concentrations (micrograms per gram) upon year of hair cut and access to wells G and H water yielded a standard coefficient for year of -0. 0074 +/- 0.0017 (standard error; p = 2.5 -multiple- 10(-5)) and -0.12 +/- 0.10 (p = 0.22) for access. The r2 value for the model was 0.19. The geometric mean concentrations (geometric standard deviation) of As and Cr in the hair of residents who had access (i.e., relative access estimate >0) to wells G and H water (n = 27) were 0.14 (2.6) and 2.29 (1.8) microg/g, respectively; the geometric mean concentrations of As and Cr in all of the hair samples from residents who did not have access (1938-1994; n = 55) were 0.13 (3.0) and 2.19 (2.0) microg/g, respectively.

Human cell mutagenicity of oxygenated, nitrated and unsubstituted polycyclic aromatic hydrocarbons associated with urban aerosols.

Polycyclic aromatic compounds (PAC) are ubiquitous pollutants in urban air that may pose risks to human health. In order to better assess the health risks associated with this class of compounds, a total of 67 PAC that either have been identified (55) or are suspected to be present (12) in urban aerosol samples were tested for mutagenicity in a forward mutation assay based on human B-lymphoblastoid cells. The cell line used (designated h1A1v2) constitutively expresses the cytochrome P4501A1, which is known to be necessary for the metabolism of many promutagens. The PAC tested included 39 polycyclic aromatic hydrocarbons (PAH). 19 oxygen-containing PAH (oxy-PAH) and nine NO2-substituted PAH (nitro-PAH). A total of 26 PAH were mutagenic. In comparing the minimum mutagenic concentrations of the mutagenic PAH with that of benzo[a]pyrene (B[a]P) it was found that dibenzo[a,l]pyrene (DB[al]P), cyclopenta[c,d]pyrene (CPP), naphtho[2,1-a]pyrene, dibenzo[a,e]pyrene (B[a]P) and 1-methylbenzo[a]pyrene were 24 +/- 21, 6.9 +/- 4.2, 3.2 + 3.0, 2.9 +/- 2.9 and 1.6+/- 1.4 times, respectively, more mutagenic than B[a]P, and that dibenzo[a,k]fluoranthene and B[a]P were approximately equally mutagenic. The 19 other mutagenic PAH were between approximately 2 and approximately 1800 times less mutagenic than B[a]P. Of the oxy-PAH tested only phenalenone, 7H-benz[d,e]anthracen-7-one, 3-nitro-6H-dibenzo[b,d]pyran-6-one, cyclopenta[c,d]pyren-3(4H)-one, 6H-benzo[c,d]pyren-6-one (BPK) and anthanthrenequinone were mutagenic; however, with the exception of BPK, these were over 50 times less active than B[a]P, BPK was approximately 3 times less active than B[a]P. Seven of the nitro-PAH were mutagenic including 9-nitroanthracene, 1-nitropyrene, 2-nitrofluoranthene, 3-nitrofluoranthene, 1,3-dinitropyrene, 1,6-dinitropyrene (1,6-DNP) and 1,8-dinitropyrene. 1,6-DNP was approximately 4 times less active than B[a]P; the six other mutagenic nitro-PAH were between 20 and 380 times less active than B[a]P. These results are discussed in terms of their relevance for determining the most important mutagens in ambient air. Based on reported concentrations of PAC in ambient aerosols, it is possible that CPP, DB[ae]P, DB[al]P and BPK could account for a greater proportion of the mutagenicity than B[a]P in some aerosols.

Elevated incidence of childhood leukemia in Woburn, Massachusetts: NIEHS Superfund Basic Research Program searches for causes.

Between 1966 and 1986, the childhood leukemia rate in Woburn, Massachusetts, was 4-fold higher than the national average. A multidisciplinary research team from MIT, which is being supported by the NIEHS Superfund Basic Research Program, has explored the possible importance of a temporal correlation between the period of elevated leukemia and a previously unrecognized mobilization of toxic metals from a waste disposal site in north Woburn. Residents of Woburn may have been exposed to arsenic (70 micrograms/l) and chromium (240 micrograms/l) at levels in excess of federal drinking water standards (50 micrograms/l for each metal) by consuming municipal groundwater contaminated with these metals. Research is currently underway a) to elucidate the mechanisms and the pathways by which these metals were transported from the waste disposal site to the drinking water supply; b) to determine the identity of the principal human cell mutagens in samples of aquifer materials collected from the site of the municipal supply wells; and c) to measure the extent of exposure and genetic change in residents who consumed the contaminated well water.