Background: Thallium is a metal that is ubiquitous in our natural environment. Despite its potential for high toxicity, thallium is understudied and not regulated in food. The California Department of Public Health was alerted to a household cluster of elevated urine thallium levels noted among a mother (peak 5.6 µg/g creatinine; adult reference: ≤0.4 µg/g creatinine) and her three young children (peak 10.5 µg/g creatinine; child reference: ≤0.8 µg/g creatinine). Objectives: This case report identifies questions raised after a public health investigation linked a household’s thallium exposure to a commercially available food product. We provide an overview of the public health investigation. We then explore concerns, such as gaps in toxicological data and limited surveillance of thallium in the food supply, which make management of individual and population exposure risks challenging. Methods: We highlight findings from a cross-agency investigation, including a household exposure survey, sampling of possible environmental and dietary exposures (ICP-MS analysis measured thallium in kale chips at 1.98 mg/kg and 2.15 mg/kg), and monitoring of symptoms and urine thallium levels after the source was removed. We use regulatory and research findings to describe the challenges and opportunities in characterizing the scale of thallium in our food supply and effects of dietary exposures on health. Discussion: Thallium can bioaccumulate in our food system, particularly in brassica vegetables like kale. Thallium concentration in foods can also be affected by manufacturing processes, such as dehydration. We have limited surveillance data nationally regarding this metal in our food supply. Dietary reviews internationally show increased thallium intake in toddlers. Limited information is available about low-dose or chronic exposures, particularly among children, although emerging evidence shows that there might be risks associated at lower levels than previously thought. Improved toxicological studies are needed to guide reference doses and food safety standards. Promising action towards enhanced monitoring of thallium is being pursued by food safety agencies internationally, and research is underway to deepen our understanding of thallium toxicity.
Diesel exhaust (DE) is a major traffic-related pollutant linked to adverse health outcomes, but existing methods for estimating indoor DE exposure fall short, as common surrogates like black carbon (BC), NOx, and PM2.5 are not sufficiently specific to diesel sources. 1-Nitropyrene (1-NP), a nitro-PAH preferentially formed during diesel combustion, has rarely been studied as an indoor exposure indicator. We measured 1-NP and isomeric nitro-PAHs (2-nitropyrene, 2-nitrofluoranthene) in indoor air and house dust from 40 homes in the eastern San Francisco Bay Area, CA, across two sampling events, alongside continuous indoor BC monitoring. We assessed 1-NP’s utility as a DE proxy using summary statistics, diagnostic nitro-PAH ratios, correlations with monitored pollutants, and single-predictor mixed-effects models relating 1-NP to spatial DE predictors. 1-NP was frequently detected in air (74%) and dust (97%), with median concentrations of 0.42 pg/m³ (IQR 0.32 - 0.54) and 340 pg/g (IQR 190 - 620), respectively. Air and dust 1-NP were moderately correlated (r=0.40, p = 0.02), as was BC with 1-NP (air r=0.38, dust r=0.47; p<0.01). Diagnostic ratios (2-NFl:1-NP <5) indicated dominant primary emission sources. Dust 1-NP showed numerous significant associations with spatial DE predictors, while air 1-NP showed fewer. Overall, 1-NP shows promise as a diesel-specific indoor exposure proxy integrating longer-term exposure and aligning with spatial DE predictors.
Diesel exhaust (DE) is a major traffic-related pollutant linked to adverse health outcomes, but existing methods for estimating indoor DE exposure are not validated. DE exposure indicators such as black carbon (BC), NOx, and PM2.5 are not sufficiently specific to diesel sources. 1-Nitropyrene (1-NP), an NPAH preferentially formed during diesel combustion, has rarely been studied as an indoor exposure indicator. We measured 1-NP and isomeric NPAHs (2-nitropyrene, 2-nitrofluoranthene) in indoor air and house dust from 40 homes in the eastern San Francisco Bay Area, CA, and conducted continuous indoor BC monitoring. We assessed 1-NP’s utility as a DE exposure indicator using summary statistics, diagnostic NPAH ratios, correlations with monitored pollutants, and single-predictor mixed-effects models relating 1-NP to spatial DE predictors. 1-NP was frequently detected in air (74%) and dust (97%), with median concentrations of 0.42 pg/m3 (IQR 0.32–0.54) and 340 pg/g (IQR 190–620), respectively. Air and dust 1-NP were moderately correlated (r = 0.40, p = 0.02), as was BC with 1-NP (air r = 0.38, dust r = 0.47; p < 0.01). Diagnostic ratios (2-NFl:1-NP < 5) indicated dominant primary emission sources. Dust 1-NP showed numerous significant associations with spatial DE predictors, while air 1-NP showed fewer. Overall, 1-NP shows promise as a diesel-specific indoor exposure indicator. Future studies with larger, geographically diverse cohorts are needed to further validate this metric.