Spatial variability in air pollution exposure in relation to socioeconomic indicators in nine European metropolitan areas: A study on environmental inequality.

A limited number of studies have addressed environmental inequality, using various study designs and methodologies and often reaching contradictory results. Following a standardized multi-city data collection process within the European project EURO-HEALTHY, we conducted an ecological study to investigate the spatial association between nitrogen dioxide (NO2), as a surrogate for traffic related air pollution, and ten socioeconomic indicators at local administrative unit level in nine European Metropolitan Areas. We applied mixed models for the associations under investigation with random intercepts per Metropolitan Area, also accounting for the spatial correlation. The stronger associations were observed between NO2 levels and population density, population born outside the European Union (EU28), total crimes per 100,000 inhabitants and unemployment rate that displayed a highly statistically significant trend of increasing concentrations with increasing levels of the indicators. Specifically, the highest vs the lowest quartile of each indicator above was associated with 48.7% (95% confidence interval (CI): 42.9%, 54.8%), 30.9% (95%CI: 22.1%, 40.2%), 19.8% (95%CI: 13.4%, 26.6%) and 15.8% (95%CI: 9.9%, 22.1%) increase in NO2 respectively. The association with population density most probably reflects the higher volume in vehicular traffic, which is the main source of NO2 in urban areas. Higher pollution levels in areas with higher percentages of people born outside EU28, crime or unemployment rates indicate that worse air quality is typically encountered in deprived European urban areas. Policy makers should consider spatial environmental inequalities to better inform actions aiming to lower urban air pollution levels that will subsequently lead to improved quality of life, public health and health equity across the population.

Characterization of the immune response to trivalent influenza vaccine in elderly men.

This study characterizes the time course of the immune response to influenza vaccine in elderly men. Sixty-two men aged 58 to 91 years (mean, 74.3 years) were vaccinated with trivalent inactivated influenza vaccine in the fall of 1983. Serum hemagglutinin-inhibiting (HAI) antibody titers were measured at various times up to 24 weeks postvaccination. Seroconversion frequencies determined at single times after vaccination were 28 to 46% of subjects, whereas cumulative seroconversion frequencies were greater than or equal to 70%. Eighteen to 28% of seroconversions occurred later than four weeks, and greater than or equal to 68% of those who seroconverted experienced greater than four-fold declines in peak HAI antibody titers by 24 weeks after vaccination. Consequently, 31 to 73% of subjects had HAI antibody titers greater than 40 throughout the study period. Measurement of HAI antibody titers at only one time after vaccination may not adequately reflect the immune response of this population or the degree of protection maintained through the influenza season.

Phenytoin therapy and immune response to influenza vaccine.

The effect of long-term phenytoin therapy on the immune response to inactivated influenza vaccine was evaluated. The patients were 31 white men who were receiving long-term phenytoin therapy for seizure disorders and 31 age-matched controls. Prevaccination blood samples were collected, and the patients were vaccinated subcutaneously with 0.5-mL inactivated whole-virion trivalent influenza vaccine. Venous blood samples were collected at 2, 4, 6, 9, 12, and 24 weeks after vaccination and stored at -20 degrees C until analysis. Total serum phenytoin concentrations were measured by fluorescence polarization immunoassay. Immune response was measured by assaying the sera for hemagglutinin-inhibiting antibody to each of the three antigenic strains. Seroconversion was defined as a fourfold or greater increase in serum antibody titer following vaccination. In the phenytoin-treated patients, the mean (+/- S.D.) serum phenytoin concentration before vaccination was 9.9 +/- 6.1 micrograms/mL. Prevaccination geometric mean titers were high enough in both groups to indicate that these patients had been exposed to these or related antigens, and medical records confirmed that some of the patients had been vaccinated the year before. The percent of patients demonstrating seroconversion to each antigen at week 4 was low in both groups, and there were no significant differences between the two groups. The cumulative seroconversion responses observed up to week 24 were also not significantly different. Long-term phenytoin therapy should not affect the efficacy of influenza vaccine in patients who have been previously exposed to infection or vaccination with identical or related strains.