Search

Backyard chicken ownership is rapidly increasing in urban areas in the United States, largely as a way to provide eggs for household consumption. Despite elevated levels of environmental lead contamination in many US cities, the role of backyard chicken eggs as a pathway for lead exposure, particularly for children, has received limited scrutiny. To characterize lead exposure from consumption of backyard chicken eggs for children and predict related effects on blood lead level (BLL), we conducted a cross-sectional study of backyard chicken owners in the Greater Boston area (n = 51). We interviewed participants regarding egg consumption by household members and collected backyard eggs (n = 201) and coop soil samples (n = 48) for analysis. Inductively coupled plasma mass spectrometry (ICP-MS) was used to evaluate lead concentration in homogenized eggs and an X-ray fluorescence (XRF) portable device was used to assess soil lead levels in the laboratory. We used the USEPA's Integrated Exposure Uptake Biokinetic Model for Lead in Children (IEUBK) to assess the relative contribution of backyard egg consumption to aggregate BLL in children. Four scenarios were developed in the IEUBK model to address variability in egg consumption rates and egg lead contamination. Lead was detected in egg samples from 98% of the households that provided egg samples. Mean household lead concentration was 0.10 μg/g (SD: 0.18). Egg lead concentrations ranged from below the limit of detection (0.0014 μg/g) to 1.798 μg/g (1.4-1198 ppb). Egg lead levels were strongly positively correlated with lead concentration in coop soil (r = 0.64; p 0.001). In modeled scenarios where a child 7 years frequently ate eggs highly contaminated with lead, BLLs are predicted to increase by 0.9-1.5 μg/dL. In three other scenarios reflecting more moderate egg lead contamination and consumption rates, BLLs were predicted to increase from 0.1 to 0.8 μg/dL. Consumption of backyard chicken eggs can contribute to lead exposure in children. Soil lead remediation prior to chicken ownership may reduce lead exposure from backyard eggs.

In this study, we modeled concentrations of fine particulate matter (PM 2.5 ) and ozone (O 3 ) attributable to precursor emissions from individual airports in the United States, developing airport-specific health damage functions (deaths per 1000 t of precursor emissions) and physically-interpretable regression models to explain variability in these functions. We applied the Community Multiscale Air Quality model using the Decoupled Direct Method to isolate PM 2.5 - or O 3 -related contributions from precursor pollutants emitted by 66 individual airports. We linked airport- and pollutant-specific concentrations with population data and literature-based concentration-response functions to create health damage functions. Deaths per 1000 t of primary PM 2.5 emissions ranged from 3 to 160 across airports, with variability explained by population patterns within 500 km of the airport. Deaths per 1000 t of precursors for secondary PM 2.5 varied across airports from 0.1 to 2.7 for NOx, 0.06 to 2.9 for SO 2 , and 0.06 to 11 for VOCs, with variability explained by population patterns and ambient concentrations influencing particle formation. Deaths per 1000 t of O 3 precursors ranged from −0.004 to 1.0 for NOx and 0.03 to 1.5 for VOCs, with strong seasonality and influence of ambient concentrations. Our findings reinforce the importance of location- and source-specific health damage functions in design of health-maximizing emissions control policies.