Advancing environmental health surveillance in the US through a national human biomonitoring network.

The United States lacks a comprehensive, nationally-coordinated, state-based environmental health surveillance system. This lack of infrastructure leads to: • varying levels of understanding of chemical exposures at the state & local levels • often inefficient public health responses to chemical exposure emergencies (such as those that occurred in the Flint drinking water crisis, the Gold King mine spill, the Elk river spill and the Gulf Coast oil spill) • reduced ability to measure the impact of public health interventions or environmental policies • less efficient use of resources for cleaning up environmental contamination Establishing the National Biomonitoring Network serves as a step toward building a national, state-based environmental health surveillance system. The Network builds upon CDC investments in emergency preparedness and environmental public health tracking, which have created advanced chemical analysis and information sharing capabilities in the state public health systems. The short-term goal of the network is to harmonize approaches to human biomonitoring in the US, thus increasing the comparability of human biomonitoring data across states and communities. The long-term goal is to compile baseline data on exposures at the state level, similar to data found in CDC's National Report on Human Exposure to Environmental Chemicals. Barriers to success for this network include: available resources, effective risk communication strategies, data comparability & sharing, and political will. Anticipated benefits include high quality data on which to base public health and environmental decisions, data with which to assess the success of public health interventions, improved risk assessments for chemicals, and new ways to prioritize environmental health research.

Home Use of a Pyrethroid-Containing Pesticide and Facial Paresthesia in a Toddler: A Case Report.

Paresthesias have previously been reported among adults in occupational and non-occupational settings after dermal contact with pyrethroid insecticides. In this report, we describe a preverbal 13-month-old who presented to his primary care pediatrician with approximately 1 week of odd facial movements consistent with facial paresthesias. The symptoms coincided with a period of repeat indoor spraying at his home with a commercially available insecticide containing two active ingredients in the pyrethroid class. Consultation by the Northwest Pediatric Environmental Health Specialty Unit and follow-up by the Washington State Department of Health included urinary pyrethroid metabolite measurements during and after the symptomatic period, counseling on home clean up and use of safer pest control methods. The child's symptoms resolved soon after home cleanup. A diagnosis of pesticide-related illness due to pyrethroid exposure was made based on the opportunity for significant exposure (multiple applications in areas where the child spent time), supportive biomonitoring data, and the consistency and temporality of symptom findings (paresthesias). This case underscores the vulnerability of children to uptake pesticides, the role of the primary care provider in ascertaining an exposure history to recognize symptomatic illness, and the need for collaborative medical and public health efforts to reduce significant exposures in children.

Investigation of melamine and cyanuric acid deposition in pig tissues using LC-MS/MS methods.

Four LC-MS/MS methods were developed to quantify melamine (MEL) and cyanuric acid (CYA) in various pig tissues at or above the level of concern (2.5 mg/kg). Pigs treated with 200 mg/kg bw/day CYA daily for 7 days did not accumulate significant residue concentrations in muscle, liver or kidney. Pigs treated with 200 mg/kg bw MEL daily for 7 or 28 days had MEL residues in muscles (3-13 ppm), liver (2.8-14.1 ppm) and kidney (9.4-27.2 ppm). Treatment with MEL and CYA at 100 mg/kg bw of each triazine daily for 7 days resulted in MEL (26-59 ppm in muscle, 30-49 ppm in liver and 367-6300 ppm in kidney) and CYA (1.8-5.8 ppm in muscle, 2.6-6.5 ppm in liver and 303-7100 ppm in kidney). Treatment with MEL and CYA at 1, 3 or 10 mg/kg bw/day for 7 days did not result in residues greater than the level of concern in all tissues tested. Pigs dosed with 33 mg/kg bw/day of MEL + CYA for 7 days contained residues above the level of concern only in kidney. Deposition of MEL and CYA depends on the tissue type (muscles, liver and kidney), dosage and whether the triazines are given alone or in combination.

Determination of Urinary Creatinine in Washington State Residents via Liquid Chromatography/Tandem Mass Spectrometry.

A viable, quick, and reliable method for determining urinary creatinine by liquid chromatography/tandem mass spectrometry (LC/MS/MS) was developed and used to evaluate spot urine samples collected for the Washington Environmental Biomonitoring Survey (WEBS): part of the Washington State Department of Health, Public Health Laboratories (PHL). 50 µL of urine was mixed with a 1 : 1 acetonitrile/water solution containing deuterated creatinine as the internal standard and then analyzed by LC/MS/MS. Utilizing electrospray ionization (ESI) in positive mode, the transition ions for creatinine and creatinine-d3 were determined to be 114.0 to 44.1 (quantifier), 114.0 to 86.1 (qualifier), and 117.0 to 47.1 (creatinine-d3). The retention time for creatinine was 0.85 minutes. The linear calibration range was 20-4000 mg/L, with a limit of detection at 1.77 mg/L and a limit of quantitation at 5.91 mg/L. LC/MS/MS and the colorimetric Jaffé reaction were associated significantly (Pearson r = 0.9898 and R (2) = 0.9797, ρ ≤ 0.0001). The LC/MS/MS method developed at the PHL to determine creatinine in the spot urine samples had shorter retention times, and was more sensitive, reliable, reproducible, and safer than other LC/MS/MS or commercial methods such as the Jaffé reaction or modified versions thereof.