Ken Sexton

Airborne emissions from numerous point, area, and mobile sources, along with stagnant meteorologic conditions, contribute to frequent episodes of elevated air pollution in Houston, Texas. To address this problem, decision makers must set priorities among ...

Differential exposure to mixtures of environmental agents, including biological, chemical, physical, and psychosocial stressors, can contribute to increased vulnerability of human populations and ecologic systems. Cumulative risk assessment is a tool for organizing and analyzing information to evaluate the probability and seriousness of harmful effects caused by either simultaneous and/or sequential exposure to multiple environmental stressors. In this article we focus on elucidating key challenges that must be addressed to determine whether and to what degree differential exposure to environmental mixtures contributes to increased vulnerability of exposed populations. In particular, the emphasis is on examining three fundamental and interrelated questions that must be addressed as part of the process to assess cumulative risk: a) Which mixtures are most important from a public health perspective? and b) What is the nature (i.e., duration, frequency, timing) and magnitude (i.e., exposure concentration and dose) of relevant cumulative exposures for the population of interest? c) What is the mechanism (e.g., toxicokinetic or toxicodynamic) and consequence (e.g., additive, less than additive, more than additive) of the mixture’s interactive effects on exposed populations? The focus is primarily on human health effects from chemical mixtures, and the goal is to reinforce the need for improved assessment of cumulative exposure and better understanding of the biological mechanisms that determine toxicologic interactions among mixture constituents.

Repeated measures of personal exposure to 14 volatile organic compounds (VOC) were obtained over 3 seasons for 70 healthy, nonsmoking adults living in Minneapolis–St. Paul. Matched data were also available for participants' time–activity patterns, and measured VOC concentrations outdoors in the community and indoors in residences. A novel modeling approach employing hierarchical Bayesian techniques was used to estimate VOC concentrations (posterior mode) and variability (credible intervals) in five microenvironments: (1) indoors at home; (2) indoors at work/school; (3) indoors in other locations; (4) outdoors in any location; and (5) in transit. Estimated concentrations tended to be highest in “other” indoor microenvironments (e.g., grocery stores, restaurants, shopping malls), intermediate in the indoor work/school and residential microenvironments, and lowest in the outside and in-transit microenvironments. Model estimates for all 14 VOC were reasonable approximations of measured median concentrations in the indoor residential microenvironment. The largest predicted contributor to cumulative (2-day) personal exposure for all 14 VOC was the indoor residential environment. Model-based results suggest that indoors-at-work/school and indoors-at-other-location microenvironments were the second or third largest contributors for all VOC, while the outside-in-any-location and in-transit microenvironments appeared to contribute negligibly to cumulative personal exposure. Results from a mixed-effects model indicate that being in or near a garage increased personal exposure to o-xylene, m/p-xylene, benzene, ethylbenzene, and toluene, and leaving windows and doors at home open for 6 h or more decreased personal exposure to 13 of 14 VOC, all except trichloroethylene.

We assessed concurrent exposure to a mixture of > 50 environmental chemicals by measuring the chemicals or their metabolites in the blood of 43 ethnically diverse children (3–6 years of age) from a socioeconomically disadvantaged neighborhood in Minneapolis. Over a 2-year period, additional samples were collected every 6–12 months from as many children as possible. We analyzed blood samples for 11 volatile organic compounds (VOCs), 2 heavy metals (lead and mercury, 11 organochlorine (OC) pesticides or related compounds, and 30 polychlorinated biphenyl (PCB) congeners. The evidence suggests that numerous VOCs originated from common sources, as did many PCBs. Longitudinal measurements indicate that between-child variance was greater than within-child variance for two VOCs (benzene, toluene), for both heavy metals (Pb, Hg), for all detectable OC pesticides, and for 15 of the measured PCB congeners (74, 99, 101, 118, 138–158, 146, 153, 156, 170, 178, 180, 187, 189, 194, 195). Despite the relatively small sample size, highest measured blood levels of 1,4-dichlorobenzene, styrene, m-/p-xylene, Pb, Hg, heptachlor epoxide, oxychlordane, dichlorodiphenyldichloroethene (p,p′-DDE), trans-nonachlor, and PCB congeners 74, 99, 105, 118, 138, 146, 153, 156, 170, and 180 were comparable with or higher than 95th percentile measurements of older children and adults from national surveys. Results demonstrate that cumulative exposures to multiple environmental carcinogens and neurotoxins can be comparatively high for children from a poor inner-city neighborhood.

The Minnesota Children's Pesticide Exposure Study is a probability-based sample of 102 children 3-13 years old who were monitored for commonly used pesticides. During the summer of 1997, first-morning-void urine samples (1-3 per child) were obtained for ...