Dianne Meacher

A market basket survey of inorganic arsenic in food.

Dietary arsenic intake estimates based on surveys of total arsenic concentrations appear to be dominated by intake of the relatively non-toxic, organic arsenic forms found in seafood. Concentrations of inorganic arsenic in food have not been not well characterized. Accurate dietary intake estimates for inorganic arsenic are needed to support studies of arsenics status as an essential nutrient, and to establish background levels of exposure to inorganic arsenic. In the market basket survey reported here, 40 commodities anticipated to provide at least 90% of dietary inorganic arsenic intake were identified. Four samples of each commodity were collected. Total arsenic was analysed using an NaOH digestion and inductively coupled plasma-mass spectrometry. Separate aliquots were analysed for arsenic species using an HCl digestion and hydride atomic absorption spectroscopy. Consistent with earlier studies, total arsenic concentrations (all concentrations reported as elemental arsenic per tissue wet weight) were highest in the seafoods sampled (ranging from 160 ng/g in freshwater fish to 2360 ng/g in saltwater fish). In contrast, average inorganic arsenic in seafood ranged from less than 1 ng/g to 2 ng/g. The highest inorganic arsenic values were found in raw rice (74 ng/g), followed by flour (11 ng/g), grape juice (9 ng/g) and cooked spinach (6 ng/g). Thus, grains and produce are expected to be significant contributors to dietary inorganic arsenic intake.

Estimation of Multimedia Inorganic Arsenic Intake in the U.S. Population

Arsenic is widely distributed in the environment by natural and human means. The potential for adverse health effects from inorganic arsenic depends on the level and route of exposure. To estimate potential health risks of inorganic arsenic, the apportionment of exposure among sources of inorganic arsenic is critical. In this study, daily inorganic arsenic intake of U.S. adults from food, water, and soil ingestion and from airborne particle inhalation was estimated. To account for variations in exposure across the U.S., a Monte Carlo approach was taken using simulations for 100,000 individuals representing the age, gender, and county of residence of the U.S. population based on census data. Our analysis found that food is the greatest source of inorganic arsenic intake and that drinking water is the next highest contributor. Inhalation of airborne arsenic-containing particles and ingestion of arsenic-containing soils were negligible contributors. The exposure is best represented by the ranges of inorganic arsenic intake (at the 10th and 90th percentiles), which were 1.8 to 11.4 µg/day for males and 1.3 to 9.4 µg/day for females. Regional differences in inorganic arsenic exposure were due mostly to consumption of drinking water containing differing inorganic arsenic content rather than to food preferences.

Inhalation of Concentrated Ambient Particulate Matter near a Heavily Trafficked Road Stimulates Antigen-Induced Airway Responses in Mice

Abstract The goal of this study was to test the following hypotheses:(1) exposure to mobile emissions from mobile sources close to a heavily trafficked roadway will exacerbate airway inflammation and allergic airway responses in a sensitized mouse model, and (2) the magnitude of allergic airway disease responses will decrease with increasing distance from the roadway. A particle concentrator and a mobile exposure facility were used to expose ovalbumin (OVA)-sensitized BALB/c mice to purified air and concentrated fine and concentrated ultrafine ambient particles at 50 m and 150 m downwind from a roadway that was heavily impacted by emissions from heavy duty diesel-powered vehicles. After exposure, we assessed interleukin (IL)-5, IL-13, OVA-specific immunoglobulin E, OVA-specific immunoglobulin G1, and eosinophil influx as biomarkers of allergic responses and numbers of polymorphonuclear leukocytes as a marker of inflammation. The study was performed over a two-year period, and there were differences in the concentrations and compositions of ambient particulate matter across those years that could have influenced our results. However, averaged over the two-year period, exposure to concentrated ambient particles (CAPs) increased the biomarkers associated with airway allergies (IL-5, immunoglobulin E, immunoglobulin G1 and eosinophils). In addition, mice exposed to CAPs 50 m downwind of the roadway had, on the average, greater allergic responses and showed greater indications of inflammation than did mice exposed to CAPs 150 m downwind. This study is consistent with the hypothesis that exposure to CAPs close to a heavily trafficked roadway influenced allergic airway responses.

Inhalation of concentrated ambient particulate matter near a heavily trafficked road stimulates antigen-induced airway responses in mice.

Motor vehicle exhaust emissions are known to exacerbate asthma and other respiratory diseases. Several studies have demonstrated significant associations between living near highly trafficked roadways and increased incidence of asthma and increased severity of asthma-related symptoms, medication usage, and physician visits. This study tested the hypotheses that (1) exposure to particulate matter (PM) near a heavily trafficked Los Angeles freeway would enhance inflammatory and allergic responses in ovalbumin (OVA)-sensitized BALB/c mice compared to sensitized, clean air controls, and (2) there would be differences in response at two distances downwind of heavily traveled freeways because of greater toxicity of PM closest to the freeway. An ambient particle concentrator was used to expose ovalbumin (OVA)-treated BALB/c mice to purified air, to concentrated fine ambient particles, and to concentrated ultrafine airborne particles (CAPs) at 2 distances, 50 m and 150 m, downwind of a roadway that is impacted by emissions from both heavy-duty diesel and light duty gasoline vehicles. Tissues and biological fluids from the mice were analyzed after exposures for 5 days/wk in 2 consecutive weeks. The biomarkers of allergic or inflammatory responses that were assessed included cytokines released by Type 2 T-helper cells (interleukin [IL]-5 and IL-13), OVA-specific immunoglobulin E (IgE), OVA-specific immunoglobulin G1 (IgG1), and pulmonary infiltration of polymorphonuclear leukocytes and eosinophils. IL-5 and IgG1 were significantly increased in mice exposed to CAPs 50 m downwind of the road, compared to responses in mice exposed to purified air, providing evidence of allergic response. No significant increases in allergy-related responses were observed in mice exposed to CAPs 150 m downwind of the road. The biological responses at the 50-m site were significantly associated with organic and elemental carbon components of fine and ultrafine particles (p ≤ .05). The primary source of these contaminants at the roadway sites was motor vehicle emissions, suggesting that particulate matter from motor vehicle fuel combustion could exert adjuvant effects and promote the development of allergic airway diseases.

Arsenic binding proteins from human lymphoblastoid cells.

Arsenic is a ubiquitous contaminant of drinking water and food. The mechanisms of the toxic action of inorganic arsenic are unknown. We report the isolation of proteins having a high affinity for arsenic in the +3 oxidation state that are induced by arsenite (AsIII) in human lymphoblastoid cells. The arsenic-binding proteins were isolated using a p-aminophenylarsine oxide affinity column. At least four proteins of 50, 42, 38.5 and 19.5 kDa were isolated by elution with 10 or 100 mM 2-mercaptoethanol. Two proteins were tentatively identified as tubulin and actin on the basis of their molecular weights and previously reported affinity for the arsenic column. The identities of the remaining proteins are unknown. Heme oxygenase 1 was induced by AsIII but did not bind to the arsenic affinity column. We conclude that AsIII induces multiple proteins that have variable affinities for arsenic in the +3 state as judged by the concentration of 2-mercaptoethanol required for their elution. The arsenic binding motif of these proteins may involve three thiol groups arranged 3-6 A apart by the tertiary structure of the protein as suggested by others. These proteins may serve as high affinity binding sites for AsIII and may be involved in the biological action of AsIII.

Dietary Exposure to Inorganic Arsenic

Publisher Summary Background exposures to inorganic arsenic (Asi) have been estimated to be in the range of 16–19 μg/day with diet being the primary source. However, data on concentrations of inorganic Asi in food are scanty. Existing literature includes data for a limited number of foods, and suggests that daily dietary Asi intake for various age groups ranges from 8 to 14 μg/day in the United States, and from 5 to 13 μg/day in Canada. The current study was conducted to obtain data for a larger number and variety of foods, and to more precisely estimate background dietary exposure ranges in the United States. This analysis presented results of a market basket survey of 40 commodities selected to represent samples of most major food types and to account for the majority of dietary exposure to Asi. Samples were analyzed for total As using NaOH digestion and inductively coupled plasma–mass spectrometry. Separate aliquots were analyzed for As3+, As5+, MMA, and DMA using an HCl digestion and hydride atomic absorption. The highest Asi concentrations were found in grains and produce. Total As concentrations were the highest in seafood, and were consistent with results from previous studies; however, average inorganic arsenic concentrations in seafood were lower than previously reported. The data from the foods surveyed were coupled with a United States food consumption database to estimate the distribution of the dietary Asi intake among adults. For most adults, dietary Asi intake is predicted to fall within the range of 1–20 μg/day.

Part VIII • Chapter 19 – Air pollution and oxidative stress

November 2013 The Community Outreach and Education Core (COEC) increases awareness and understanding of environmental health research. Stakeholder Advisory Board members include:  Community Health and Social Services Center, Inc.  Detroit Department of Health and Wellness Promotion  Detroit Hispanic Development Corporation  Detroiters Working for Environmental Justice  Green Door Initiative  Henry Ford Health System  Imagine Creative Opportunities Now  Michigan Department of Community Health  Michigan Department of Environmental Quality  University of Michigan School of Public Health  Warren-Conner Development Coalition Project Coordinator: