Environmental Engineering Reference
In-Depth Information
when sensitive animal models were used; (5) a lack of studies deining the relationship between
personal exposure and ambient air levels for most metal species; and (6) most controlled clinical
and laboratory animal exposure studies have been limited to one or a few days, which may not be
suficient to elicit responses of concern.
The subchronic CAPs inhalation studies in New York, Ohio, and California suggest that such
studies overall, and those with elevated concentrations of Ni and EC in particular, can yield
evidence that current levels of ambient air concentrations produce health effects of interest in terms
of public health. Furthermore, there are many toxicology studies of ROFA cited earlier, that are
buttressed by epidemiological studies (Hedley et al., 2002, 2004; Janssen et al., 2002; Lipfert et al.,
2006), suggesting a line of continuity between both types of studies with regard to damage from the
combination of V and Ni. There are also some studies showing oxidative stress and DNA damage
associated with V (Sorensen et al., 2005). If the inhalation of Ni, or Ni in combination with V, at
current, relatively low, ambient air concentrations, does appreciably affect cardiac function and
mortality in humans, one may wonder why the effects of such exposures have not previously been
recognized. One reason may be that the increment in cardiovascular mortality that they may have
produced is a relatively small part of the very large cardiovascular mortality. Also, it is possible that
other PM 2.5 components may account for the more numerous studies, not having speciation data,
showing associations of PM 2.5 mass with health effects because of the inluence of other components
alone or because the other components potentiate the effects of Ni.
Also, the statistically signiicant transient and progressive changes that Ni produced in
cardiovascular function in the ApoE −/− mice were relatively subtle, required advanced analytical
techniques for their detection, and are unlikely to be detected in the kinds of short-term exposure
studies that have previously been undertaken in laboratory animals.
In addition, the exact physical and chemical characteristics of Ni-bearing ambient PM have not
been determined. Based on the previous work at NYU, the fact that the potency of ultraine Zn
particles with a thin coating of sulfuric acid is much greater than uncoated acid particles (Amdur
and Chen, 1989), raises the likelihood that a speciic form of a metal that has not been reproduced
in the laboratory could be responsible for the observed biological effects.
Many studies have used ROFA as a surrogate for ambient PM in various in vivo and in vitro
experiments. ROFA contains many soluble metals, and since it is clear, from this review, that they
interact with each other, chemically and biologically, it should not be surprising that there are
inconsistent and confusing results. Although ROFA was useful in providing plausible evidence that
metals are important in eliciting adverse cardiopulmonary effects, it should not be the focus of future
studies. The experimental in vitro design of Maciejczyk and Chen (2005), in which CAPs were collected
in a biosampler impinger simultaneously with a series of daily CAPs inhalations, provided a sound
basis for parallel daily in vitro assays. Performing such assays in parallel with future animal inhalation
studies and/or human clinical studies, could provide opportunities for gaining a better understanding
of the source proile that may contribute to the adverse effects seen in animals and humans.
Much of the remaining skepticism concerning the biological plausibility of the premature mortality
and increased morbidity associated with ambient air PM 2.5 has been due to the paucity of exposure-
response data in laboratory studies involving PM 2.5 inhalation, and the heretofore seemingly impossible
task of identifying any speciic causal components. The subchronic CAPs inhalation studies that
were performed in Sterling Forest (Lippmann et al., 2005b, 2006; Sun et al., 2005) helped to establish
such plausibility, and have also developed a mechanistic base for the initiation and progression of
effects attributable to the long-range transported aerosol in the northeastern United States (Sun et al.,
2005). The consistency in these analyses and reexaminations of available data lead to the conclusions
that (1) Ni is a particularly inluential component of ambient PM 2.5 in terms of cardiac responses to
the inhalation of ambient air PM 2.5 ; (2) further research is needed on the speciic inluences of both
Ni and V, which are both generally most closely associated with residual oil combustion efluents, on
both acute and chronic respiratory and cardiovascular health effects; and (3) further research is also
needed on the currently unknown impacts of other toxic metals in ambient air.
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