Secondary sulfate effects?

Maynard et al. (2007) related mortality with ambient particulate black carbon (BC) and sulfate (SO4). They also associated SO4 in Boston, Massachusetts, with “secondary,” distant “coal combustion.” Their correlation of 0.44 between BC and SO4, however, suggests the importance of local source(s) of SO4, including vehicle exhaust (especially diesel).

Centrally monitored BC poorly characterizes exposure to traffic emissions and results in exposure misestimation, causing distorted or undetected health associations (Ito et al. 2004). Maynard et al. (2007) address this deficiency by geocoding BC estimates to a decedent’s residence; a central monitor characterizes SO4 exposure. In their single-pollutant models, BC and SO4 are associated with daily mortality, but in multipollutant models, only BC retains significance.

The association of mortality with SO4 is inconsistent. In a review of toxicologic studies, Schlesinger and Cassee (2003) suggested that SO4 is benign. In an in vivo study of PM2.5 (particulate matter ≤ 2.5 μm in aero-dynamic diameter) components, Seagrave et al. (2006) found that lung toxicity and inflammation correlated with vehicular but not secondary particles, including SO4. However, vehicular emissions are consistently associated with cardiac or other end points (Grahame and Schlesinger 2007). How does secondary SO4 cause mortality, if harmful biological mechanisms have not been found? Or could the mortality association with SO4 of Maynard et al. (2007) be linked with other local PM sources?

Maynard et al. (2007) cited mortality associations for coal and traffic tracers reported by Laden et al. (2000), but other study findings differ. In a reanalysis, Schwartz (2003) found that their traffic variable remained significant, but their regional “coal” variable became insignificant. We (Grahame and Hidy 2004) noted that among the six cities described by Laden et al. (2000), Boston had the lowest levels of the “coal tracer” (selenium); only Boston had a significant association with an apparent coal source. Similarly, only in Boston was an association with SO4 significant. Finding that local residual oil sources emitted over half the Se and SO4 in Boston, these authors (Grahame and Hidy 2004) concluded from toxicology that these results represented effects of residual oil emissions.

SO4 is elevated near major roadways. Reponen et al. (2003) showed an SO4 gradient that declined based on distance from a midwestern freeway; Riediker et al. (2004) found that among highway-related factors, only the “speed changing” factor, which included emissions from accelerating diesel engines, showed elevated SO4. These findings are relevant to the monitoring conditions of Maynard et al. (2007). Other Boston studies show commingling between SO4 and vehicular indicators. Clarke et al. (2000), for example, reported that loadings of BC are as high in an SO4 indicator as in the traffic indicator. Because coal plants emit virtually no BC (Edgerton E, Mueller P, Monroe L, Jansen J, Waid C, unpublished data), high BC in urban SO4 indicators reflects both SO4 and BC from diesels in an SO4 factor, derived from measurements near a thoroughfare. The SO4–BC correlation described by Maynard et al. (2007) thus suggests that SO4 associations reflect statistical comingling of vehicular and coal emissions.

Association of harm from traffic emissions, but not SO4 (or secondary aerosols generally), has been found in panel and epidemiology studies that a) precisely measure exposure to local vehicular emissions, and b) test effects of secondary PM2.5–SO4 compared with local emissions. Health end points in such studies include long-term mortality, heart rate variability reduction, ST-segment depression, cardiac effects, vasoconstriction, increased blood pressure, or morbidity [reviewed by Grahame and Schlesinger (2007)]. Kodavanti et al. (2005) found no effects only with the highest SO4 concentrations.

We suggest that findings of harmful exposure to secondary SO4 per se are tenuous until physiologic mechanisms are identified that support toxicity near ambient concentrations.