Environmental Health Sciences

The Environmental Health Sciences (EHS) faculty include: Amy Kalkbrenner, Michael Laiosa, Todd Miller, and Kurt Svoboda. The EHS program conducts research on developmental and environmental toxicology, microbiology and environmental chemistry among other fields. The faculty lead several rigorous research laboratories: Kalkbrenner Lab (PI: Kalkbrenner), Laboratory for Developmental Immunotoxicology (PI: Laiosa), Laboratory for Developmental Neurobiology (PI: Svoboda), and Laboratory for Aquatic Environmental Microbiology and Chemistry (PI: Miller). Learn more about featured research projects by the EHS faculty:

Blue-green algae (cyanobacteria) toxins in lakes and drinking water production

Todd Miller, Michael Carvan, Gabriel Pinter

buoyThe number of lakes supporting accumulations of toxic blue-green algae (scientifically known as cyanobacteria) in the United States is rising due to changes in land use and climate. As a result there is increasing risk associated with lake recreational activities (e.g. swimming, boating), and consumption of fish. Environmental factors leading to toxin production by blue-green algae in lakes are ill-defined at time-scales relevant to human behavior and algal ecology (i.e. minutes to hours). Acute poisonings are well-documented, but chronic exposure to low levels of blue- green algal toxins in drinking water is not. This project is aimed at monitoring and modeling blue-green algal toxin production in Lake Winnebago and associated drinking water at a high temporal resolution using sensor equipped buoys and automated samplers.

Mechanisms underlying nicotine induced neuronal toxicity in zebrafish

Kurt Svoboda, Robert Tanguay

Embryonic exposure to nicotine has deleterious consequences on human development at various levels. Such exposure can lead to long term changes in the cognitive abilities and behaviors related to learning and memory. Various mammalian models have been utilized to understand how nicotine can exert such effects, but this is difficult because most mammalian behaviors and the nervous system underlying them are complex. We are studying the effects of nicotine exposure in a model vertebrate, the zebrafish, with the goal of linking behavioral abnormalities created by nicotine exposure to developmental alterations in spinal neurons and associated spinal musculature. Zebrafish embryos are sensitive to nicotine exposure (first published paper to document this; Svoboda et. al, 2002). Embryos acutely exposed to nicotine exhibit a swimming-like behavior at time when they typically do not swim. On the other hand, chronically exposing embryos to nicotine, results in paralysis. These two behavioral phenotypes point us toward candidate cell types that may be altered in zebrafish by embryonic nicotine exposure.

Water quality monitoring and modeling at Milwaukee beaches in partnership with the Milwaukee Health Department

John Hernandez, Chelsea Weirich, Sarah Bartlett, Todd Miller

john sampling
The United States Environmental Protection Agency requires regular monitoring of beaches for water quality indicators of microorganisms that may cause gastrointestinal illnesses. As a Lake Michigan coastal city, Milwaukee boasts some of the most popular beaches in the nation. To protect public health, the Miller Laboratory has partnered with the Milwaukee Health Department to conduct regular daily monitoring of Milwaukee beaches for fecal coliforms and other biological, chemical, and water quality indicators. In addition, we have worked closely with the Wisconsin Department of Natural Resources and the United States Geological Survey to construct nowcast models of water quality using high resolution climate and water quality data. This project was featured in the Milwaukee Journal Sentinel.

Air pollutants and autism: New pathways in analysis of windows of susceptibility

Amy Kalkbrenner, Marc Serre, Gayle Windham, Xuexia Wang, Julie Daniels

Environmental chemical exposures are suspected to contribute to autism, and one study has shown that living closer to freeways is associated with increasing autism risk. We will further understanding in this area by examining the association between 3traffic-related pollutants – course particulate matter, nitrogen dioxide, and ozone – with autism. This case-cohort design includes hundreds of children recognized to have autism in California and North Carolina by the autism surveillance program of the Centers for Disease Control and Prevention, combined with birth records representing the source population and air monitoring data. Notably, we will explore critical windows of susceptibility – exploring whether air pollutant exposures in early pregnancy, late pregnancy, or early childhood are more impactful.

In utero and childhood tobacco exposures and autistic traits

Amy Kalkbrenner, Joe Braun, Kim Dietrich, Kimberly Yolton, John T. Bernert, Bruce Lanphear

Studies have yielded inconsistent results about whether maternal cigarette smoking in pregnancy is associated with autism in the child. We will address prior limitations in research on this topic using a normal pregnancy cohort from Cincinnati, Ohio. We will evaluate whether second-handsmoke in pregnancy, maternal smoking in pregnancy, and second-hand exposure to the child after birth, are associated with autistic traits, after adjusting for a comprehensive set of confounders. In this cohort, tobacco exposures were well-characterized with biomarkers and questionnaires, and the full spectrum of autistic-like behaviors and related social and communication impairments at ages 4 and 5 years was measured using standardized psychometric tools.

Perinatal exposure to hazardous air pollutants and associations with autism phenotype

Amy Kalkbrenner, Heather Volk, Gayle Windham, Nora Lee

Three studies in different populations have suggested that some hazardous air pollutants may be risk factors for autism. Specifically, methylene chloride and some metals and solvents have been implicated. This study will build upon prior research using a large national sample of children with autism and their families, the Autism Genetic Resource Exchange. After obtaining a residential history for children in these families, we will historically reconstruct exposures to over a hundred volatile organic compounds and metals, using a census-tract based model of the Environmental Protection Agency. Air pollutant concentrations will be evaluated with regard to not only the diagnosis of autism, but the continuous phenotype of autism symptoms.

Social inequalities and toxic air pollution exposures in Milwaukee, WI

Amy Kalkbrenner, Lorraine Halinka Malcoe, D. Phuong Do, Brian Thayer

Air toxics – hundreds of airborne metals and volatile organic compounds – cause oxidative stress and systemic immune responses, biologic effects likely to underlie suboptimal birth outcomes such as infant mortality or preterm birth. Yet air toxics have been largely ignored by researchers studying these birth outcomes. This study will screen 187 toxic air pollutants from the EPA’s National-Scale Air Toxics Assessment and will lay the foundation for a full exploration of the intersection of air toxics and social inequalities in contributing to infant mortality and preterm birth. For this pilot study, the City of Milwaukee serves as the focal point – an ideal setting due to the City’s high degree of segregation, racial disparities in infant mortality, and large number of polluting sources. Levels, variations, and patterning of air toxics in Milwaukee by racial/ethnic and socioeconomic geographies will be identified. Illustrative maps will be produced to help communicate air pollutant “hotspots”, and importantly, identify and engage community partners for future collaborative research.