Occupational/built environment and xenobiotic exposures
The role of the occupational environment seems to be important in many
CIDs[184,185]. For example, farmworkers and those who have close
contact with birds are more susceptible to hypersensitivity pneumonitis
(HP)[186]. Occupational asthma and HP may be related to exposures to
diverse substances, including chemicals, animal dander, plastic residue
and fungi[187].
The PHM hypothesis proposes that occupational and xenobiotic related
CIDs could at least sometimes be due to low level, often undetected PHM
colonization. In some cases, microbial antigens and PHM colonization
might be involved, in addition to the potentially synergistic effects of
non-microbial antigens and xenobiotics.
New research is revealing high levels of unknown microbes in built
environments[2,188,189]. A study using wearable sampling devices
found over 2500 species, and nearly half of the DNA information could
not be classified[190]. Gilbert et al[189] discussed how new
materials and diverse chemicals used in buildings could provide unique
selective pressures, potentially shaping microbial evolution. The new
species/strains that could result would fit the category of novel PHMs
and might be polyextremotolerant and more able to colonize humans.
Regarding experiments that evaluate the effect of xenobiotic exposures,
it is worth considering microbes and/or their antigens that are probably
present in the tested xenobiotics. So, it would be desirable for
toxicological studies to take this into account.
This need to address microbial contamination has become apparent in an
analogous situation in which microbial DNA is found in test kits used
for microbiological assays[191]. Research using the test kits use
controls and other methods so that reagent microbes do not bias the
study results.
Thus, xenobiotic’s effects could potentially result from a combination
of the xenobiotic itself and xenobiotic-associated microbes. Autoimmune
diseases may develop years after xenobiotic exposure[4]. This could
be partly explained, according to the PHM hypothesis, by the length of
time needed for colonizing xenobiotic-associated microbes to increase.
Also, with long-term colonization, microbial mutations could occur that
might aid microbial adaptation to the human tissue environment and
pathogenicity.