Indoor pollutant exposures modify the effect of airborne endotoxin on asthma in urban children.

RATIONALE: The effect of endotoxin on asthma morbidity in urban populations is unclear. OBJECTIVES: To determine if indoor pollutant exposure modifies the relationships between indoor airborne endotoxin and asthma health and morbidity. METHODS: One hundred forty-six children and adolescents with persistent asthma underwent repeated clinical assessments at 0, 3, 6, 9, and 12 months. Home visits were conducted at the same time points for assessment of airborne nicotine, endotoxin, and nitrogen dioxide (NO2) concentrations. The effect of concomitant pollutant exposure on relationships between endotoxin and asthma outcomes were examined in stratified analyses and statistical models with interaction terms. MEASUREMENTS AND MAIN RESULTS: Both air nicotine and NO2 concentrations modified the relationships between airborne endotoxin and asthma outcomes. Among children living in homes with no detectable air nicotine, higher endotoxin was inversely associated with acute visits and oral corticosteroid bursts, whereas among those in homes with detectable air nicotine, endotoxin was positively associated with these outcomes (interaction P value = 0.004 and 0.07, respectively). Among children living in homes with lower NO2 concentrations (<20 ppb), higher endotoxin was positively associated with acute visits, whereas among those living in homes with higher NO2 concentrations, endotoxin was negatively associated with acute visit (interaction P value = 0.05). NO2 also modified the effect of endotoxin on asthma symptom outcomes in a similar manner. CONCLUSIONS: The effects of household airborne endotoxin exposure on asthma are modified by coexposure to air nicotine and NO2, and these pollutants have opposite effects on the relationships between endotoxin and asthma-related outcomes.

Breathing zone pollutant levels are associated with asthma exacerbations in high-risk children.

Background: Indoor and outdoor air pollution levels are associated with poor asthma outcomes in children. However, few studies have evaluated whether breathing zone pollutant levels associate with asthma outcomes. Objective: Determine breathing zone exposure levels of NO 2 , O 3 , total PM 10 and PM 10 constituents among children with exacerbation-prone asthma, and examine correspondence with in-home and community measurements and associations with outcomes. Methods: We assessed children's personal breathing zone exposures using wearable monitors. Personal exposures were compared to in-home and community measurements and tested for association with lung function, asthma control, and asthma exacerbations. Results: 81 children completed 219 monitoring sessions. Correlations between personal and community levels of PM 10 , NO 2 , and O 3 were poor, whereas personal PM 10 and NO 2 levels correlated with in-home measurements. However, in-home monitoring underdetected brown carbon (Personal:79%, Home:36.8%) and ETS (Personal:83.7%, Home:4.1%) personal exposures, and detected black carbon in participants without these personal exposures (Personal: 26.5%, Home: 96%). Personal exposures were not associated with lung function or asthma control. Children experiencing an asthma exacerbation within 60 days of personal exposure monitoring had 1.98, 2.21 and 2.04 times higher brown carbon (p<0.001), ETS (p=0.007), and endotoxin (p=0.012), respectively. These outcomes were not associated with community or in-home exposure levels. Conclusions: Monitoring pollutant levels in the breathing zone is essential to understand how exposures influence asthma outcomes, as agreement between personal and in-home monitors is limited. Inhaled exposure to PM 10 constituents modifies asthma exacerbation risk, suggesting efforts to limit these exposures among high-risk children may decrease their asthma burden. CLINICAL IMPLICATIONS: In-home and community monitoring of environmental pollutants may underestimate personal exposures. Levels of inhaled exposure to PM 10 constituents appear to strongly influence asthma exacerbation risk. Therefore, efforts should be made to mitigate these exposures. CAPSULE SUMMARY: Leveraging wearable, breathing-zone monitors, we show exposures to inhaled pollutants are poorly proxied by in-home and community monitors, among children with exacerbation-prone asthma. Inhaled exposure to multiple PM 10 constituents is associated with asthma exacerbation risk.

Bacterial DNA in house and farm barn dust.

BACKGROUND: Early in life, natural exposure to microbial components (eg, endotoxin) may mitigate allergy and asthma development in childhood. Bacterial DNA is a potent stimulus for the innate immune system; its immune stimulatory potential in dust is unknown. OBJECTIVES: We sought to quantify bacterial DNA and endotoxin content in dust from urban homes, rural homes, farm homes, and farm barns and to determine if dust DNA is immune-stimulatory. METHODS: Total DNA, bacterial DNA, and endotoxin were measured in 32 dust samples. To measure bacterial DNA content, a quantitative polymerase chain reaction assay specific for bacterial ribosomal DNA was developed. Peripheral blood mononuclear cells from 5 adults were stimulated with endotoxin-free dust DNA with/without lipopolysaccharide (LPS) from selected dust samples. IL-12p40, IL-10, and tumor necrosis factor-alpha were measured in cell supernatants by enzyme-linked immunosorbent assay. RESULTS: Bacterial DNA in dust correlated with endotoxin (r = 0.56, P <.001) and total DNA content (r = 0.51, P =.003). The highest bacterial DNA levels were measured in farm barns (mean, 22.1 microg/g dust; range, 1.3 to 56.2), followed by rural homes (6.3 microg/g; 0.2 to 20), farm homes (2.2 microg/g; 0.1 to 9.1), and urban homes (0.6 microg/g; 0.1 to 1.2). Farm barn DNA significantly potentiated (P < or =.05) LPS-induced IL-10 and IL-12 p40 but not tumor necrosis factor-alpha release (13-fold, 3-fold, and 1.5-fold increases, respectively). DNA from 6 urban homes did not demonstrate this LPS-potentiating effect. CONCLUSIONS: Endotoxin is a marker for bacterial DNA, which is also higher in locales of lower asthma and allergy prevalence. DNA from farm barn dust augments the immune modulatory effects of endotoxin and may combine with exposure to other such naturally occurring microbial components to mitigate allergy and asthma development.