The purpose of this study was to assess the effect of long-term ambient particulate matter (PM) on risk of fatal coronary heart disease (CHD). A cohort of 3,239 nonsmoking, non-Hispanic white adults was followed for 22 years. Monthly concentrations of ambient air pollutants were obtained from monitoring stations [PM < 10 μm in aerodynamic diameter (PM10), ozone, sulfur dioxide, nitrogen dioxide] or airport visibility data [PM < 2.5 μm in aerodynamic diameter (PM2.5)] and interpolated to ZIP code centroids of work and residence locations. All participants had completed a detailed lifestyle questionnaire at baseline (1976), and follow-up information on environmental tobacco smoke and other personal sources of air pollution were available from four subsequent questionnaires from 1977 through 2000. Persons with prevalent CHD, stroke, or diabetes at baseline (1976) were excluded, and analyses were controlled for a number of potential confounders, including lifestyle. In females, the relative risk (RR) for fatal CHD with each 10-μg/m3 increase in PM2.5 was 1.42 [95% confidence interval (CI), 1.06–1.90] in the single-pollutant model and 2.00 (95% CI, 1.51–2.64) in the two-pollutant model with O3. Corresponding RRs for a 10-μg/m3 increase in PM10-2.5 and PM10 were 1.62 and 1.45, respectively, in all females and 1.85 and 1.52 in postmenopausal females. No associations were found in males. A positive association with fatal CHD was found with all three PM fractions in females but not in males. The risk estimates were strengthened when adjusting for gaseous pollutants, especially O3, and were highest for PM2.5. These findings could have great implications for policy regulations.

In a cohort of 6338 California Seventh -day Adventists, we previously observed for males associations between long -term concentrations of particulate matter ( PM ) with an aerodynamic diameter less than 10 m (PM 10 ) and 15 -year mortality due to all natural causes ( ANC ) and lung cancer ( LC ) listed as underlying causes of death and due to nonmalignant respiratory disease listed as either the underlying or a contributing ( CRC ) cause of death. The purpose of this analysis was to determine whether these outcomes were more strongly associated with the fine ( PM 2.5 ) or the coarse ( PM 2.5 ± 10 ) fractions of PM 10 . For participants who lived near an airport ( n = 3769 ) , daily PM 2.5 concentrations were estimated from airport visibility, and on a monthly basis, PM 2.5 ± 10 concentrations were calculated as the differences between PM 10 and PM 2.5 . Associations between ANC, CRC, and LC mortality ( 1977 ± 1992 ) and mean PM 10 , PM 2.5 , and PM 2.5 ± 10 concentrations at study baseline ( 1973 ± 1977 ) were assessed using Cox proportional hazards models. Magnitudes of the PM 10 associations for the males of this subgroup were similar to those for the males in the entire cohort although not statistically significant due to the smaller numbers. In single -pollutant models, for an interquartile range ( IQR ) increase in PM 10 ( 29.5 g / m 3 ) , the rate ratios ( RRs ) and 95% confidence intervals ( CI ) were 1.15 ( 0.94, 1.41 ) for ANC, 1.48 ( 0.93, 2.34 ) for CRC, and 1.84 ( 0.59, 5.67 ) for LC. For an IQR increase in PM 2.5 ( 24.3 g / m 3 ) , corresponding RRs ( 95% CI ) were 1.22 ( 0.95, 1.58 ) , 1.64 ( 0.93, 2.90 ) , and 2.23 ( 0.56, 8.94 ) , and for an IQR increase in PM 2.5 ± 10 ( 9.7 g / m 3 ) , corresponding RRs ( 95% CI ) were 1. 05 ( 0.92, 1.20 ) , 1.19 ( 0.88, 1.62 ) , and 1.25 ( 0.63, 2.49 ) , respectively. When both PM 2.5 and PM 2.5 ± 10 were entered into the same model, the PM 2.5 estimates remained stable while those of PM 2.5 ± 10 decreased. We concluded that previously observed associations of long -term ambient PM 10 concentration with mortality for males were best explained by a relationship of mortality with the fine fraction of PM 10 rather than with the coarse fraction of PM 10 .

The consistency of EBNA-1 seropositivity with MS across racial/ethnic groups and between studies points to a strong biological link between EBV infection and MS risk. The association between past CMV infection and MS risk supports the broader hygiene hypothesis, but the inconsistency of this association across racial/ethnic groups implies noncausal associations.