Dust and Human Health - Mineral Dust: A Key Player in the Earth System - page 387

may be equally involved in triggering the body's defense system to produce an
inflammatory response. Shins et al. ( 2004 ) observed that coarse particles (PM10)
from a rural setting produced greater inflammatory effects in rat lungs than fine
(PM2.5) particles from an industrial area and attribute the response to endotoxins
or related contaminants. There is some evidence that particle surface area may be a
more accurate measure of particle concentration than the mass (Ovrevik et al. 2005 ).
In a study to assess mineral dusts, Ovrevik et al. ( 2005 ) found that when cytokine
release was related to equal surface areas of the particles, there was no difference in
bioactivity between the two size fractions (i.e., PM10 and PM2.5).
The importance of a particle's biosolubility or biopersistence has also been
examined with respect to its ability to promote inflammation and toxicity, especially
for minerals associated with occupational exposures such as crystalline silica
and asbestos. Researchers commonly measure the production of cytokines and
other biomarkers following exposure of cell lines (i.e., cultures of physiologically
appropriate cell types such as lung epithelial cells) to particulate matter (Hetland
et al. 2001 ). Some of these studies indicate that biopersistent or poorly soluble
particles are a primary factor in terms of promoting inflammation, possibly due
to particle accumulation and/or overload, and longer retention times (Hetland et al.
2001 ; Muhle and Mangelsdorf 2003 ). Other studies indicate soluble components
(e.g., metals), may be more important (Adamson et al. 1999 ; Costa and Dreher
1997 ). Veranth et al. ( 2006 ) found a wide range of potency when examining cytokine
response to soil-derived particulate matter and suggested that it is the bioavailable
(amount that the body absorbs) metal fraction not the total metal concentration that
is the toxicologically relevant variable.

15.4.4 Exposure and Susceptibility

Other challenges relate to qualifying and quantifying environmental exposures
and individual susceptibility. Exposures to PM (and MD) may exacerbate existing
disease such as cardiovascular and respiratory ailments (Dockery et al. 1993 ; Pope
et al. 1995 ) resulting in the need for additional medications (Chimonas and Gessner
2007 ), emergency room visits (Mahboub et al. 2012 ), and hospitalizations (Kanatani
et al. 2010 ). Due to current scientific limitations, exposures are usually estimated
(Baxter et al. 2013 ). Although low-level environmental exposures may contribute to
common complex diseases, the relationship between exposure and health outcome
requires the integration of a wide range of factors—extrinsic (e.g., environmental),
intrinsic (e.g., genotype), and mechanistic (e.g., toxicological) (Hubal 2009 ).
Inhaled dusts, for example, that are cleared from the respiratory tract via the
mucociliary escalator and then ingested can also be a source of metal toxicant
uptake. Plumlee et al. ( 2013b ) showed that such an exposure route contributed to
a recent fatal outbreak of childhood lead poisoning associated with artisanal mining
in northern Nigeria. While the predominant exposure route was hand-to-mouth
transmission and inadvertent ingestion of particles from soils heavily contaminated