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ObjectiveThis study describes associations of ozone and fine particulate matter with Parkinson's disease observed among farmers in North Carolina and Iowa.MethodsWe used logistic regression to determine the associations of these pollutants with self-reported, doctor-diagnosed Parkinson's disease. Daily predicted pollutant concentrations were used to derive surrogates of long-term exposure and link them to study participants' geocoded addresses.ResultsWe observed positive associations of Parkinson's disease with ozone (odds ratio = 1.39; 95% CI: 0.98 to 1.98) and fine particulate matter (odds ratio = 1.34; 95% CI: 0.93 to 1.93) in North Carolina but not in Iowa.ConclusionsThe plausibility of an effect of ambient concentrations of these pollutants on Parkinson's disease risk is supported by experimental data demonstrating damage to dopaminergic neurons at relevant concentrations. Additional studies are needed to address uncertainties related to confounding and to examine temporal aspects of the associations we observed.

Abstract: Exposure to air pollutants has been associated with adverse health effects. However, analyses of the effects of season and ambient parameters such as ozone have not been fully conducted. Residential indoor and outdoor air levels of polycyclic aromatic hydrocarbons (PAH), black carbon (measured as absorption coefficient [Abs]), and fine particulate matter <2.5μm (PM)2.5 were measured over two-weeks in a cohort of 5–6 year old children (n =334) living in New York City’s Northern Manhattan and the Bronx between October 2005 and April 2010. The objectives were to: 1) characterize seasonal changes in indoor and outdoor levels and indoor/outdoor (I/O) ratios of PAH (gas + particulate phase; dichotomized into ∑8PAHsemivolatile (MW 178–206), and ∑8PAHnonvolatile (MW 228–278)), Abs, and PM2.5; and 2) assess the relationship between PAH and ozone. Results showed that heating compared to nonheating season was associated with greater ∑8PAHnonvolatile (p <0.001) and Abs (p <0.05), and lower levels of ∑8PAHsemivolatile (p <0.001). In addition, the heating season was associated with lower I/O ratios of ∑8PAHnonvolatile and higher I/O ratios of ∑8PAHsemivolatile (p <0.001) compared to the nonheating season. In outdoor air, ∑8PAHnonvolatile was correlated negatively with community-wide ozone concentration (p <0.001). Seasonal changes in emission sources, air exchanges, meteorological conditions and photochemical/chemical degradation reactions are discussed in relationship to the observed seasonal trends. [ABSTRACT FROM AUTHOR]

Abstract: Relatively little is known about exposures to traffic-related particulate matter at schools located in dense urban areas. The purpose of this study was to examine the influences of diesel traffic proximity and intensity on ambient concentrations of fine particulate matter (PM2.5) and black carbon (BC), an indicator of diesel exhaust particles, at New York City (NYC) high schools. Outdoor PM2.5 and BC were monitored continuously for 4–6 weeks at each of 3 NYC schools and 1 suburban school located 40 km upwind of the city. Traffic count data were obtained using an automated traffic counter or video camera. BC concentrations were 2–3 fold higher at urban schools compared with the suburban school, and among the 3 urban schools, BC concentrations were higher at schools located adjacent to highways. PM2.5 concentrations were significantly higher at urban schools than at the suburban school, but concentrations did not vary significantly among urban schools. Both hourly average counts of trucks and buses and meteorological factors such as wind direction, wind speed, and humidity were significantly associated with hourly average ambient BC and PM2.5 concentrations in multivariate regression models. An increase of 443 trucks/buses per hour was associated with a 0.62 μg/m3 increase in hourly average BC at an NYC school located adjacent to a major interstate highway. Car traffic counts were not associated with BC. The results suggest that local diesel vehicle traffic may be important sources of airborne fine particles in dense urban areas and consequently may contribute to local variations in PM2.5 concentrations. In urban areas with higher levels of diesel traffic, local, neighborhood-scale monitoring of pollutants such as BC, which compared to PM2.5, is a more specific indicator of diesel exhaust particles, may more accurately represent population exposures. [Copyright &y& Elsevier]

Highway-building environments are prevalent in metropolitan areas. This paper presents our findings in investigating pollutant transport in a highway-building environment by combing field measurement and numerical simulations. We employ and improve the Comprehensive Turbulent Aerosol Dynamics and Gas Chemistry (CTAG) model to simulate the spatial variations of black carbon (BC) concentrations near highway I-87 and an urban school in the South Bronx, New York. The results of CTAG simulations are evaluated against and agree adequately with the measurements of wind speed, wind directions, and BC concentrations. Our analysis suggests that the BC concentration at the measurement point of the urban school could decrease by 43-54% if roadside buildings were absent. Furthermore, we characterize two generalized conditions in a highway-building environment, i.e., highway-building canyon and highway viaduct-building. The former refers to the canyon between solid highway embankment and roadside buildings, where the spatial profiles of BC depend on the equivalent canyon aspect ratio and flow recirculation. The latter refers to the area between a highway viaduct (i.e., elevated highway with open space underneath) and roadside buildings, where strong flow recirculation is absent and the spatial profiles of BC are determined by the relative heights of the highway and buildings. The two configurations may occur at different locations or in the same location with different wind directions when highway geometry is complex. Our study demonstrates the importance of incorporating highway-building interaction into the assessment of human exposure to near-road air pollution. It also calls for active roles of building and highway designs in mitigating near-road exposure of urban population.

Different estrogens vary in their carcinogenic potential despite having similar hormonal potencies; however, mechanisms of estrogen-induced carcinogenesis remain to be fully elucidated. It has been hypothesized that generation of reactive estrogen-quinones and oxidative stress, both of which result from metabolic activation of estrogens, play an essential role in estrogen-induced carcinogenesis. This hypothesis was tested using the estrogen-receptor (ER)-alpha-positive hamster kidney tumor (H301) and the human breast cancer (MCF-7) cell lines. Estrogens with differing carcinogenic potentials were compared in terms of their capacities to induce 8-iso-prostaglandin F(2alpha) (8- iso-PGF(2alpha)), a marker of oxidative stress. Tumor cells were treated with either 17beta-estradiol (E2), a carcinogenic estrogen or 17-alpha-ethinylestradiol (EE), a weakly-carcinogenic estrogen. Tumor cells were also treated with alpha-naphthoflavone, a cytochrome P450 inhibitor, or a combination of alpha-naphthoflavone and E2 to study the effect of metabolic activation of E2 on E2-induced oxidative stress. H301 cells treated with E2 displayed time- and dose-dependent increases in 8-iso-PGF(2alpha), compared to controls; treatment with 10 nM E2 resulted in a maximal 4-fold induction following 48 h of treatment. In contrast, H301 cells treated with EE did not display an increase in 8-iso-PGF(2alpha) compared with controls. In H301 cells cotreated with alpha-naphthoflavone and E2, alpha-naphthoflavone inhibited the E2-induced increase in 8-iso-PGF(2alpha). These data indicate that a carcinogenic estrogen shows strong oxidant potential, whereas a weakly-carcinogenic estrogen shows poor oxidant potential. Furthermore, inhibiting metabolic activation of a carcinogenic estrogen blocks its oxidant potential. Our data support the hypothesis that metabolic activation and subsequent generation of oxidative stress may play critical roles in estrogen-induced carcinogenesis., (Copyright 2004 Wiley Periodicals, Inc.)