Introduction: Exposures to airborne microbial contaminants in sub-micrometer particles (PM1) have not been well characterized in different environments. Health effects due to these exposures are even more obscure.
Methods: Concentrations of airborne size specific (=1, 1-1.8, >1.8 µm) microbial contaminants (endotoxin, ß-glucan) were determined using cyclone samplers in two distinctly different environments: farms and homes. Using inhalable samplers and vacuum cleaners airborne inhalable and dust contaminants from these homes were collected. This approach was used to compare PM1 microbial contaminants in a particular home with those in inhalable particles and in dust inside the same home. Samples were analyzed with Limulus Amebocyte Lysate assays for endotoxin and ß-glucan. Walkthrough surveys and questionnaires determined home characteristics and other exposures. Airway inflammation was assessed in school-age children by measuring exhaled nitric oxide (eNO) levels with non-invasive nitric oxide monitoring system (NIOX-Flex). Skin-prick test were also employed to determine atopy.
Results: Relative proportions of PM1 (=1 µm) microbial contaminants from total airborne concentrations were significantly higher in homes despite their significantly higher actual concentrations on farms. In homes, PM1 and inhalable endotoxin concentrations correlated weakly with that in dust and with each other. PM1 endotoxin levels were not significantly associated with eNO levels in asthmatics but had significant inverse association with eNO levels in non-asthmatics. Among non-asthmatics, eNO levels were significantly lower for those children who lived in homes with levels of dog allergens above detection limits and for those with lower parental income.
Discussion: Moderate disturbance activities in homes preferentially allow PM1 microbial contaminants to predominate among total airborne particles compared to farming environments that have dynamic activity levels that cause re-suspension of large particles. In addition to dust, airborne PM1 or inhalable microbial contaminants may originate from outdoor sources. High PM1 endotoxin was protective only for non-asthmatics. It is well known that T-helper 1 cells predominantly mediate immune responses in non-asthmatics who do not have pre-existing airway inflammation. PM1 endotoxin exposures, therefore, may have a beneficial effect; along with dog allergens, these could possibly drive naïve immune systems away from inflammatory responses. For asthmatics, detectable dog allergens in homes may incite inflammatory response, possibly as irritants, in their already primed allergic immune systems. Among non-asthmatics from low-income parents, an adaptive immunity favoring Th1 immune response through higher microbial contaminant exposures may have favored protection against development of atopic response. This is in contrast to non-asthmatics from highest income parents who had significantly less microbial contaminant exposures. Subsequently, this may have led to predominantly Th2 adaptive immune response that is highly associated with atopy. Because atopy is a significant predictor of airway inflammation, it infers that non-asthmatics from lowest income parents had protective effects against airway inflammation compared to those non-asthmatics from highest income parents.
Conclusion: PM1 endotoxin may be a better predictor of health outcome than inhalable or larger particles. Exposures to PM1 endotoxin may protect against airway inflammation in non-asthmatic school-age children. Whether this protection is sustained, needs to be confirmed through follow-up studies.