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.