Arsenic - A Fatal Complication for Pandemic Flu - MUST READ

[Giuseppe]

Re: Argentina has the world?s highest rate of deaths associated with swine flu infections

Re: Argentina has the world?s highest rate of deaths associated with swine flu infections

I am not completely persuaded about the statement points Argentina as the country with the higher case-fatality rate.

Argentina 1587 - 26 / 99 - 3 [CFR=16,38 x 1,000]
Australia 4090 - 7 / 52 - 0 [CFR=1,71]
Brazil 680 - 1 / 228 - 1 [CFR=1,47]
Canada 7983 - 25 / 208 - 4 [CFR=3,13]
Chile 6211 - 12 / 1025 - 5 [CFR=1,93]
Colombia 93 - 2 / 5 - 0 [CFR=21,5]
Costa Rica 279 - 2 / 24 - 1 [CFR=7,16]
Dominican Republic 108 - 2 / 0 - 0 [CFR=18,51]
Mexico 8680 - 116 / 401 - 0 [CFR=13,36]
Philippines 861 - 1 / 0 - 0 [CFR=1,16]
Spain 717 - 1 / 176 - 1 [CFR=1,39]
Thailand 1414 - 3 / 640 - 3 [CFR=2,12]
United Kingdom 6538 - 3 / 2288 - 2 [CFR=0,45]
Uruguay 195 - 1 / 0 - 1 [CFR=5,12]

From Latest WHO case count update http://www.who.int/csr/don/2009_07_01a/en/index.html


There should be several biases in epidemiological surveillance.

What's about recent dengue hemorrhagic fever outbreaks in south America?

Are there data about incidence of dengue in regions currently badly hit by H1N1?

 

[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

Re: Discussion, high H1N1 CFR and elevated arsenic

http://www.sciencedirect.com/scienc...serid=10&md5=186a8ce9a62a1c8ea33b9d459f1a190f

doi:10.1016/j.scitotenv.2005.09.005


Copyright © 2005 Elsevier B.V. All rights reserved.


Occurrence of arsenic contamination in Canada: Sources, behavior and distribution
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References and further reading may be available for this article. To view references and further reading you must purchase this article.


<!-- refMsg -->Suiling Wang^a and Catherine N. Mulligan^,^a^,

<!-- authorsNoEnt -->^aDepartment of Building, Civil and Environmental Engineering, Concordia University, 1455 de Maisonneuve Boulevard W., EV 006-187, Montreal, QC, Canada H3G 1M8

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Received 16 February 2005;
<!-- articleText -->revised 2 September 2005;
<!-- articleText -->accepted 2 September 2005.
<!-- articleText -->Available online 3 October 2005.
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<!-- articleText -->Abstract

Recently there has been increasing anxieties concerning arsenic related problems. Occurrence of arsenic contamination has been reported worldwide. In Canada, the main natural arsenic sources are weathering and erosion of arsenic-containing rocks and soil, while tailings from historic and recent gold mine operations and wood preservative facilities are the principal anthropogenic sources. Across Canada, the 24-h average concentration of arsenic in the atmosphere is generally less than 0.3 μg/m³. Arsenic concentrations in natural uncontaminated soil and sediments range from 4 to 150 mg/kg. In uncontaminated surface and ground waters, the arsenic concentration ranges from 0.001 to 0.005 mg/L. As a result of anthropogenic inputs, elevated arsenic levels, above ten to thousand times the Interim Maximum Acceptable Concentration (IMAC), have been reported in air, soil and sediment, surface water and groundwater, and biota in several regions. Most arsenic is of toxic inorganic forms. It is critical to recognize that such contamination imposes serious harmful effects on various aquatic and terrestrial organisms and human health ultimately. Serious incidences of acute and chronic arsenic poisonings have been revealed. Through examination of the available literature, screening and selecting existing data, this paper provides an analysis of the currently available information on recognized problem areas, and an overview of current knowledge of the principal hydrogeochemical processes of arsenic transportation and transformation. However, a more detailed understanding of local sources of arsenic and mechanisms of arsenic release is required. More extensive studies will be required for building practical guidance on avoiding and reducing arsenic contamination. Bioremediation and hyperaccumulation are emerging innovative technologies for the remediation of arsenic contaminated sites. Natural attenuation may be utilized as a potential in situ remedial option. Further investigations are needed to evaluate its applicability.

<!-- articleText -->Keywords: Arsenic; Speciation; Biota; Canada; Mining; Soil; Sediments; Water

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<dl><dt>1. Introduction </dt><dt>2. Arsenic sources </dt><dl><dt>2.1. Natural sources </dt><dt>2.2. Anthropogenic sources </dt><dl><dt>2.2.1. Mining residues </dt><dt>2.2.2. Industrial emissions </dt><dt>2.2.3. Wood preserving </dt><dt>2.2.4. Coal combustion </dt><dt>2.2.5. Arsenical pesticides</dt></dl></dl><dt>3. Arsenic in air </dt><dl><dt>3.1. Reported concentrations </dt><dt>3.2. Arsenic species in air </dt><dt>3.3. Atmospheric deposition of arsenic</dt></dl><dt>4. Arsenic in soil and sediments </dt><dl><dt>4.1. Reported concentrations </dt><dl><dt>4.1.1. Soil </dt><dt>4.1.2. Sediments</dt></dl><dt>4.2. Arsenic species in soil and sediments </dt><dt>4.3. Arsenic association with solid phases </dt><dt>4.4. Mineral dissolution induced arsenic release</dt></dl><dt>5. Arsenic in water </dt><dl><dt>5.1. Reported arsenic concentrations </dt><dl><dt>5.1.1. Surface water </dt><dt>5.1.2. Groundwater </dt><dt>5.1.3. Porewater </dt><dt>5.1.4. Geothermal fluid </dt><dt>5.1.5. Seasonal variation</dt></dl><dt>5.2. Main arsenic species in water </dt><dt>5.3. Arsenic sorption behavior in water</dt></dl><dt>6. Arsenic in biota </dt><dl><dt>6.1. Arsenic uptake </dt><dt>6.2. Reported arsenic concentrations </dt><dt>6.3. Implications for arsenic remediation technologies </dt><dl><dt>6.3.1. Hyperaccumulation </dt><dt>6.3.2. Microbially mediated mobilization </dt><dt>6.3.3. Natural attenuation </dt><dt>6.3.4. Other technologies</dt></dl></dl><dt>7. Conclusions and recommendations </dt><dt>References</dt></dl>
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</td></tr></tbody></table>Fig. 1. Canadian arsenic production, 1885–1990 (modified from Cranstone, 2001).

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</td></tr></tbody></table>Fig. 2. A simplified diagram of arsenic cycle.

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</td></tr></tbody></table>Fig. 3. Arsenic release from NPRI reporting facilities, 1994–2001 (data sources: NPRI online database).

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</td></tr></tbody></table>Fig. 4. The Eh–pH diagram for arsenic at 25 °C and 101.3 kPa (modified from Ferguson and Gavis, 1972).

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Table 1. Estimated fluxes of arsenic transfer

(Mackenzie et al., 1979).

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Table 2. Arsenic concentrations measured in six mine tailings

(Wang and Mulligan, 2004a).

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Table 3. Arsenic concentrations in Canadian air

^a 24-h maximum concentrations.
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Table 4. Arsenic concentrations in Canadian soil

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Table 5. Arsenic concentrations in Canadian sediments

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Table 6. Arsenic concentrations in Canadian waters

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Corresponding author. Tel.: +1 514 848 2424x7925; fax: +1 514 848 7965.

 

[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

Re: Discussion, high H1N1 CFR and elevated arsenic

Interesting, many Inuit mothers have very high levels of contamination.

http://www.sciencedirect.com/scienc...serid=10&md5=0f11866494ac3a354c2f6653b7fe1c4a

doi:10.1016/j.scitotenv.2005.03.034


Crown copyright © 2005 Published by Elsevier B.V.
Review

Human health implications of environmental contaminants in Arctic Canada: A review
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References and further reading may be available for this article. To view references and further reading you must purchase this article.


<!-- refMsg -->J. Van Oostdam^a^,^,, S.G. Donaldson^a^,^b, M. Feeley^c, D. Arnold^c, P. Ayotte^d, G. Bondy^c, L. Chan^e, É. Dewaily^d, C.M. Furgal^f, H. Kuhnlein^e, E. Loring^g, G. Muckle^h, E. Mylesⁱ, O. Receveur^j, B. Tracy^k, U. Gill^l and S. Kalhok^m

<!-- authorsNoEnt -->^aEnvironmental Contaminants Bureau, Safe Environments Program, Health Canada, Rm 4-046, BMO Building, 269 Laurier Avenue W., AL4904B, Ottawa, ON, Canada K1A 0K9
^bCarleton University, 1125 Coloney By Drive, Ottawa, ON, Canada K1S 5B6
^cHealth Canada, Food Directorate, Bureau of Chemical Safety, Banting Research Center, Tunney's Pasture, Ottawa, ON, Canada K1A 0L2
^dUnité de recherche en santé publique (Centre hospitalier universitaire de Québec - Centre hospitalier de l'Université Laval), Université Laval, 945 Ave Wolfe, Ste. Foy, Québec, Canada G1V 5B3
^eCentre for Indigenous Peoples' Nutrition and Environment, Macdonald Campus of McGill University, 21,111 Lakeshore Road, Ste.-Anne-de-Bellevue, Quebec, Canada H9X 3V9
^fDépartment Science Politique et Unité de recherche en santé publique (Centre hospitalier universitaire de Québec - Centre hospitalier de l'Université Laval), Université Laval, 945 Ave Wolfe, Ste. Foy, Québec, Canada G1V 5B3
^gEnvironmental Contaminants Research Division, Inuit Tapiriit Kanatami, 170 Laurier Avenue West, 12th Floor, Ottawa, ON, Canada, K1P 5V5
^hÉcole de psychologie et Unité de recherche en santé publique (Centre hospitalier universitaire de Québec - Centre hospitalier de l'Université Laval), Université Laval, Ste Foy, Québec, Canada G1K 7P4
ⁱAXYS Environmental Consulting Ltd., Suite 300, 805 8th Ave SW, Calgary, Alberta, Canada T2P 1H7
^jFaculté de Medicin, Nutrition, Université de Montreal, CP6128, Succursale Centre Ville Montreal, QC, Canada H3C 3J7
^kHealth Canada, Environmental Health Directorate, Radiation Protection Bureau, 775 Brookfield Road, AL 6302D1, Ottawa, ON, Canada K1A 0L2
^lHealth Canada, Health Products and Food Branch, 2nd Floor, Qualicum Twr A, 2936 Baseline, AL 3302C Nepean, ON, Canada K1A 0K9
^mIndian and Northern Affairs, Northern Science and Contaminants Research Directorate, 10 Wellington Street, Gatineau, Quebec, Canada K1A 0H4

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Accepted 30 March 2005.
<!-- articleText -->Available online 16 November 2005.
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<!-- articleText -->Abstract

The objectives of this paper are to: assess the impact of exposure to current levels of environmental contaminants in the Canadian Arctic on human health; identify the data and knowledge gaps that need to be filled by future human health research and monitoring; examine how these issues have changed since our first assessment [Van Oostdam, J., Gilman, A., Dewailly, É., Usher, P., Wheatley, B., Kuhnlein, H. et al., 1999. Human health implications of environmental contaminants in Arctic Canada: a review. Sci Total Environ 230, 1–82]. The primary exposure pathway for contaminants for various organochlorines (OCs) and toxic metals is through the traditional northern diet. Exposures tend to be higher in the eastern than the western Canadian Arctic. In recent dietary surveys among five Inuit regions, mean intakes by 20- to 40-year-old adults in Baffin, Kivalliq and Inuvialuit communities exceeded the provisional tolerable daily intakes (pTDIs) for the OCs, chlordane and toxaphene. The most recent findings in NWT and Nunavut indicate that almost half of the blood samples from Inuit mothers exceeded the level of concern value of 5 μg/L for PCBs, but none exceeded the action level of 100 μg/L. For Dene/Métis and Caucasians of the Northwest Territories exposure to OCs are mostly below this level of concern. Based on the exceedances of the pTDI and of various blood guidelines, mercury and to a lesser extent lead (from the use of lead shot in hunting game) are also concerns among Arctic peoples. The developing foetus is likely to be more sensitive to the effects of OCs and metals than adults, and is the age groups of greatest risk in the Arctic. Studies of infant development in Nunavik have linked deficits in immune function, an increase in childhood respiratory infections and birth weight to prenatal exposure to OCs. Balancing the risks and benefits of a diet of country foods is very difficult. The nutritional benefits of country food and its contribution to the total diet are substantial. Country food contributes significantly more protein, iron and zinc to the diets of consumers than southern/market foods. The increase in obesity, diabetes and cardiovascular disease has been linked to a shift away from a country food diet and a less active lifestyle. These foods are an integral component of good health among Aboriginal peoples. The social, cultural, spiritual, nutritional and economic benefits of these foods must be considered in concert with the risks of exposure to environmental contaminants through their exposure. Consequently, the contamination of country food raises problems which go far beyond the usual confines of public health and cannot be resolved simply by risk-based health advisories or food substitutions alone. All decisions should involve the community and consider many aspects of socio-cultural stability to arrive at a decision that will be the most protective and least detrimental to the communities.

<!-- articleText -->Keywords: Arctic regions; Environmental monitoring; PCBs; Organochlorines; Mercury; Maternal; Infant; Monitoring environmental pollution; Northern populations; Public health; Risk factors; Risk-benefit management

<!-- articleText -->Article Outline

<dl><dt>1. Introduction </dt><dl><dt>1.1. Aboriginal peoples of Canada </dt><dt>1.2. Aboriginal perspectives on food and health </dt><dt>1.3. Factors that contribute to Aboriginal Northerners' exposure to country food contamination </dt><dt>1.4. Evaluation of research in CACAR and application to benefit and risk assessment/management </dt><dt>1.5. Research ethics</dt></dl><dt>2. Exposure assessment </dt><dl><dt>2.1. Country food consumption in the Arctic </dt><dt>2.2. Contaminant levels in people and their relationship to traditional food diets </dt><dl><dt>2.2.1. Tissue levels of contaminant results </dt><dt>2.2.2. Levels of mercury in hair and blood </dt><dt>2.2.3. Population groups and studies </dt><dt>2.2.4. Maternal hair </dt><dt>2.2.5. Maternal/cord blood </dt><dt>2.2.6. Levels of selenium in maternal blood </dt><dt>2.2.7. Levels of lead in maternal blood </dt><dt>2.2.8. Levels of cadmium in maternal blood </dt><dt>2.2.9. Radionuclide exposure </dt><dl><dt>2.2.9.1. Radiocesium </dt><dt>2.2.9.2. Lead-210 and polonium-210 </dt><dt>2.2.9.3. Summary of radionuclide exposures</dt></dl></dl><dt>2.3. Trends in traditional/country food dietary intakes and contaminant exposures</dt></dl><dt>3. Toxicology </dt><dl><dt>3.1. Priority contaminants </dt><dl><dt>3.1.1. Toxaphene </dt><dl><dt>3.1.1.1. Discussion</dt></dl><dt>3.1.2. Chlordane </dt><dl><dt>3.1.2.1. Discussion</dt></dl></dl><dt>3.2. Toxicological effects induced by exposure to food-chain contaminant mixtures </dt><dl><dt>3.2.1. Discussion</dt></dl><dt>3.3. Contaminant and dietary nutrient interactions </dt><dl><dt>3.3.1. Discussion</dt></dl></dl><dt>4. Epidemiology and human biomarkers </dt><dl><dt>4.1. Immune system function </dt><dl><dt>4.1.1. Clinical outcomes </dt><dt>4.1.2. Biomarkers </dt><dl><dt>4.1.2.1. Lymphocyte subsets and immunoglobulins </dt><dt>4.1.2.2. Antibody response following vaccination </dt><dt>4.1.2.3. Complement system </dt><dt>4.1.2.4. Cytokine production by Th1/Th2 Cells </dt><dt>4.1.2.5. Vitamin A status</dt></dl></dl><dt>4.2. Neurodevelopment </dt><dl><dt>4.2.1. Clinical outcomes </dt><dl><dt>4.2.1.1. Polychlorinated biphenyls (PCBs) </dt><dt>4.2.1.2. Methylmercury</dt></dl><dt>4.2.2. Biomarkers of developmental effects </dt><dl><dt>4.2.2.1. Cytochrome P4501A1 induction and DNA adduct formation </dt><dt>4.2.2.2. Thyroid hormones</dt></dl></dl><dt>4.3. Sex hormone disruption </dt><dl><dt>4.3.1. Clinical outcomes </dt><dl><dt>4.3.1.1. Sexual maturation of newborn males </dt><dt>4.3.1.2. Environmental risk factors for osteoporosis</dt></dl><dt>4.3.2. Hormonal biomarkers </dt><dl><dt>4.3.2.1. Hormone profiles</dt></dl></dl><dt>4.4. Oxidative stress</dt></dl><dt>5. Risk-benefit characterization, assessment and advice </dt><dl><dt>5.1. Contaminant exposure risks </dt><dl><dt>5.1.1. Contaminant intakes </dt><dl><dt>5.1.1.1. Persistent organic pollutants </dt><dt>5.1.1.2. Metals—mercury, cadmium, and lead </dt><dt>5.1.1.3. Contaminant tissue levels and guidelines</dt></dl></dl><dt>5.2. Special considerations for risk management in Arctic communities </dt><dl><dt>5.2.1. Nutritional benefits</dt></dl><dt>5.3. Social, cultural, spiritual and economic benefits of country food </dt><dt>5.4. Assessment of perceptions of risks, benefits and safety of country foods </dt><dl><dt>5.4.1. Perceptions of risks in the north </dt><dt>5.4.2. Research on the perceptions of food-chain contamination in the north </dt><dt>5.4.3. Impacts of these perceptions</dt></dl><dt>5.5. Risk-benefit characterization </dt><dl><dt>5.5.1. Risk management frameworks </dt><dt>5.5.2. Problem identification and context </dt><dt>5.5.3. Risk and benefit assessment </dt><dl><dt>5.5.3.1. Risk assessment </dt><dt>5.5.3.2. Benefit assessment</dt></dl><dt>5.5.4. Risk characterization </dt><dt>5.5.5. Assumptions/uncertainties of concern </dt><dt>5.5.6. Weighing benefits and risks—challenges in practice </dt><dt>5.5.7. Option analysis/evaluation </dt><dt>5.5.8. Selecting a risk management option </dt><dt>5.5.9. Implementation </dt><dt>5.5.10. Monitoring and evaluating the decision</dt></dl><dt>5.6. Risk and benefit communication</dt></dl><dt>6. Conclusions </dt><dl><dt>6.1. Aboriginal perspectives on food and health and interpretation of research results </dt><dt>6.2. Exposure assessment </dt><dt>6.3. Toxicology </dt><dt>6.4. Epidemiology and biomarkers </dt><dt>6.5. Risk and benefit characterization, assessment and advice</dt></dl><dt>7. Knowledge gaps </dt><dl><dt>7.1. Exposure assessment </dt><dt>7.2. Toxicology </dt><dt>7.3. Epidemiology </dt><dt>7.4. Risk and benefit characterization, assessment and advice</dt></dl><dt>Acknowledgements </dt><dt>References</dt></dl>
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</td></tr></tbody></table>Fig. 1.1.1. General locations of Arctic cultural groups (adapted from Van Oostdam et al., 1999).

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</td></tr></tbody></table>Fig. 1.1.2. Age distribution of Canadian Arctic population by ethnicity.

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</td></tr></tbody></table>Fig. 2.1.1. Communities participating in CINE dietary assessments.

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</td></tr></tbody></table>Fig. 2.1.2. Percentage of energy from traditional/country foods in the Yukon, Dene and Métis, and Inuit communities.

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</td></tr></tbody></table>Fig. 2.2.1. Contaminant studies in the Northwest Territories, Nunavut, and Nunavik.

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</td></tr></tbody></table>Fig. 2.2.2. Maternal contaminant levels in Arctic Canada: oxychlordane (μg/L plasma).

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</td></tr></tbody></table>Fig. 2.2.3. Maternal contaminant levels in Arctic Canada: hexachlorobenzene (μg/L plasma).

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</td></tr></tbody></table>Fig. 2.2.4. Maternal contaminant levels in Arctic Canada: total toxaphene (μg/L plasma).

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</td></tr></tbody></table>Fig. 2.2.5. Maternal contaminant levels in Arctic Canada: β-hexachlorocyclohexane (μg/L plasma).

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</td></tr></tbody></table>Fig. 2.2.6. Maternal contaminant levels in Arctic Canada: p,p′-DDE (μg/L plasma).

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</td></tr></tbody></table>Fig. 2.2.7. Maternal contaminant levels in Arctic Canada: PCBs (as Aroclor 1260) (μg/L plasma).

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</td></tr></tbody></table>Fig. 2.2.8. Adjusted mean organochlorine (OC) concentrations according of the year of birth: (a) PCBs; (b) DDE; (c) HCB; (d) oxychlordane (Dallaire et al., 2003a).

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</td></tr></tbody></table>Fig. 2.2.9. Maternal contaminant levels in Arctic Canada: total mercury (μg/L plasma).

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</td></tr></tbody></table>Fig. 2.2.10. Adjusted mean metal concentrations according to the year of birth for (a) lead and (b) mercury (Dallaire et al., 2003a).

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</td></tr></tbody></table>Fig. 4.1.1. Distribution of PCB 153 concentration in cord serum or plasma, 10 studies (Longnecker et al., 2003).

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</td></tr></tbody></table>Fig. 5.1.1. Mean intakes of chlordane, toxaphene, and mercury in northern Canada (μg/kg/day) (Kuhnlein et al., 2001b).

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</td></tr></tbody></table>Fig. 5.1.2. Mean intakes of toxaphene and chlordane in different regions (ages 20–40 years) (Chan et al., in preparation(a)).

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</td></tr></tbody></table>Fig. 5.1.3. Mean intakes of toxaphene and chlordane among different age groups in Baffin (Chan et al., in preparation(a)).

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</td></tr></tbody></table>Fig. 5.1.4. Maternal blood guideline exceedances for PCBs as Aroclor 1260 in Arctic Canada, by region and ethnicity (Van Oostdam, 2001).

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</td></tr></tbody></table>Fig. 5.1.5. Mean intake of total mercury in different regions (μg/kg/day) (Chan et al., in preparation(b)).

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</td></tr></tbody></table>Fig. 5.1.6. Maternal blood guideline exceedances for organic mercury in Arctic Canada, by region and ethnicity (Van Oostdam, 2001).

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</td></tr></tbody></table>Fig. 5.5.1. Framework for environmental health risk management (Presidential/Congressional Commission on Risk Assessment and Risk Management, 1997a and Presidential/Congressional Commission on Risk Assessment and Risk Management, 1997b).

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Table 1.1.1 Aboriginal peoples: population size and proportion of the total population in each region of Arctic Canada, 1996

Source: Statistics Canada (2001).
^a Data presented in this table are for those who identify with one or more Aboriginal groups (Metis, Inuit, or North American Indian).
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Table 2.1.1 Five country/traditional food items most often consumed (yearly average of days per week)

Source: Kuhnlein (2002).

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Table 2.2.1 Mean levels of organochlorine pesticides in maternal blood, by region and ethnic group (geometric means, range, μg/L plasma)

NA = Not available; nd = not detected.
^a Source: Butler Walker et al. (2003).
^b Source: Muckle, 2000 and Muckle et al., 2001b.
^c N = 25.
^d N = 42.
^e Four composites (n = 12, 12, 12 and 14; Seddon, 1996).
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Table 2.2.2 Mean levels of PCBs in maternal blood, by region and ethnic group (geometric means, range, μg/L plasma)

NA = Not available; nd = not detected.
^a Source: Butler Walker et al. (2003).
^b Source: Muckle (2000) and Muckle et al., 2001a and Muckle et al., 2001b.
^c Aroclor 1260 = 5.2 (PCB 153 + 138) (Weber, 2002).
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Table 2.2.3 Dioxins and furans and PCBs in maternal blood

^a TEQs = toxic equivalents.
^b D + F = dioxins and furans.
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Table 2.2.4 Cord and maternal contaminants (lipid weight basis)

Source: Van Oostdam (2001).
Abbreviations: B-HCH, beta-hexachlorocyclohexane; PCBs, polychlorinated biphenyls.
^a Sample size: cord–maternal pairs.
^b Concentration (μg/kg lipid, arithmetic mean).
^c Cord/maternal blood (paired data only).
^d Pearson's correlations.
^e Statistical significance of cord/maternal Pearson's correlations.
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Table 2.2.5 Worldwide comparisons of maternal blood levels of PCBs (Aroclor 1260) and β-HCH (geometric means, μg/L plasma)

^a Source: Butler Walker et al. (2003).
^b Source: Muckle (2000) and Muckle et al., 2001a and Muckle et al., 2001b.
^c Source: Deutch (2001).
^d Source: Deutch and Hansen (2000).
^e Source: Klopov et al. (1998).
^f Source: Klopov (2000), Klopov and Shepovalnikov (2000), and Klopov and Tchachchine (2001).
^g Source: Odland (2001).
^h Source: Sharma and Bhatnagar (1996).
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Table 2.2.6 Current and historic levels^a of mercury in maternal hair (μg/g)

Source: Snider and Gill (2001).
LOD: below analytical method detection limits (0.4 μg/g).
^a Peak exposure levels reported as parts per million (ppm) in hair.
^b GSD: Geometric mean standard deviation.
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Table 2.2.7 Mean concentrations of metals in maternal blood, by ethnicity and region (geometric mean (range), μg/L whole blood)

NA = Not available; nd = not detected.
^a Source: Butler Walker et al. (2005).
^b Source: Muckle et al., 2001a and Muckle et al., 2001b.
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Table 2.2.8 Worldwide comparisons of maternal blood mercury levels (μg/L whole blood) for women living in arctic regions

^a GM: geometric mean.
^b GSD: geometric standard deviation.
^c Source: Bjerregaard and Hansen (2000).
^d Source: AMAP (1998).
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Table 2.2.9 Radionuclide levels in caribou meat and people in the Canadian Arctic, and resulting radiation doses to people

Source: Tracy and Kramer (2000).
^a Doses based on measured whole-body concentrations of ¹³⁷Cs (Tracy et al., 1997).
^b Doses based on estimated caribou consumption in a typical northern diet and on human metabolic parameters. The higher ²¹⁰Po doses in the 1960s is not based on any changes in environmental levels of ²¹⁰Po but on an estimated higher consumption of caribou meat at that time (Tracy and Kramer, 2000).
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Table 3.1.1 Relative percent contribution to chlordane total

^a Buchert et al. (1989).
^b Marine mammal blubber average, 1993–1994.
^c As heptachlor epoxide.
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Table 3.1.2 Chlordane-induced mortality in sub-acute studies

Bondy et al., 2000 and Bondy et al., 2003.

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Table 3.2.1 Composition of the organochlorine mixture

Source: Ayotte (2001).
^a Mixture containing 2,4,4′-trichlorobiphenyl (320 mg), 2,2′,4,4′-tetrachlorobiphenyl (256 mg), 3,3′,4,4′-tetrachlorobiphenyl (1.4 mg), 3,3′,4,4′,5-pentachlorobiphenyl (6.7 mg), Aroclor 1254 (12.8 g), and Aroclor 1260 (19.2 g).
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Table 3.2.2 Composition of complex mixture based on human blood residues

Source: Bowers et al. (2003).
^a Containing PCBs 28, 52, 99, 101, 105, 118, 128, 138, 153, 156, 170, 180, 183, 187.
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Table 3.2.3 Comparison of PBTK-derived TDIs to estimated contaminant intakes

Source: Chan et al., 1997 and Chan et al., 2000. ND—not determined.

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Table 4.2.1 Comparison of mercury (total) concentrations in Nunavik with those observed in other cohorts

Source: Muckle et al. (2001b).
^a The average Hg concentration was reported in nmol/L, this concentrations was divided by 5 to transform to μg/L.
^b 95% confidence interval.
^c Women aged between 15 and 39 years old.
^d Arithmetic mean.
^e Standard deviation.
^f Among seafood consumers.
^g Among non-seafood consumers.
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Table 5.1.1 Sources of organochlorines in the Baffin Region (percent contribution)

Source: Kuhnlein and Receveur (2001).
^a Percent by weight of each species contributing to the traditional diet.
^b Percent of each contaminant contributed by each food.
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Table 5.1.2 Proportionate contributions of three main food sources of chlordane and toxaphene, in five Inuit regions, by food item

Source: Kuhnlein and Receveur (2001).

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Table 5.1.3 Population distribution of organochlorine intake in Qikiqtarjuaq (μg/kg bw/day)

Source: Kuhnlein and Receveur (2001).

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Table 5.1.4 Comparison of daily intake of selected contaminants in Qikiqtarjuaq in 1987–1988 and 1998–1999

^a Source: Kuhnlein et al. (1995a) and Chan et al. (1997).
^b Source: Kuhnlein et al. (2000).
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Table 5.1.5 Proportionate contributions of three main food sources of total mercury, and total mercury concentrations by food item in five Inuit regions

Source: Kuhnlein and Receveur (2001).

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Table 5.1.6 Population distribution of heavy metal intake in Qikiqtarjuaq (μg/kg bw/day)

Source: Kuhnlein and Receveur (2001).

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Table 5.1.7 Blood guideline exceedances for methyl mercury, lead, and cadmium in Arctic Canada, by region and ethnicity

NA = Not available.
^a Based on US EPA 1999 re-evaluation of methyl mercury.
^b Increasing risk range is 20–100 μg/L, Health Canada.
^c Guideline value of 5 μg/L is for occupational exposure.
^d Source: Butler Walker et al. (2005).
^e Source: Ayotte (2001).
^f ≥ 5.8 μg/L value.
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Table 5.2.1 Percent energy from macronutrients on days with or without traditional/country food (least square means ± S.E.M.)

Source: Kuhnlein et al. (2004).
<sup>

</sup> Different from with TF, p < 0.01.
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Table 5.2.2 Top three sources of selected nutrients from 24-h recalls (fall and late winter combined) in five Inuit regions

Source: Kuhnlein and Receveur (2001).

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Table 5.2.3 Reported daily fish consumption by gender and age group in three recent dietary surveys among Canadian Arctic indigenous peoples^a

Data adapted from Receveur et al., 1996 and Receveur et al., 1998a and Kuhnlein et al. (2000).
^a Estimates obtained by averaging food intake over all 24-h recalls collected in two seasons (Sep–Nov and Feb–Apr).
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Corresponding author. Tel.: +1 613 941 3570.

 

[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

Re: Discussion, high H1N1 CFR and elevated arsenic

http://www.questia.com/googleSchola...yPL3Hg0h!657527082!497993468?docId=5009311075

Mapping of Arsenic Content and Distribution in Groundwater in the Southeast Pampa, Argentina

Journal article by J.D. Paoloni, M.E. Sequeira, C.E. Fiorentino; Journal of Environmental Health, Vol. 67, 2005

Journal Article Excerpt

<TABLE id=rightTable border=0 cellSpacing=0 cellPadding=0><TBODY><TR><TD class=3text width=2></TD><TD class=3text>

Mapping of Arsenic Content and Distribution in Groundwater in the Southeast Pampa, Argentina.​

by J.D. Paoloni , M.E. Sequeira , C.E. Fiorentino

Introduction
The relationship between groundwater and the chemical, physical, and kinetic processes affecting the various rock and sediment components could be the reason for the appearance of arsenic in some sources of water supply (Toth, 2000). The content in water depends more on speciation than on the amount of arsenic present in the environment (Bhumbla & Keefer, 1994). Upper, or phreatic groundwater, tends to be highly mineralized water containing considerable amounts of arsenic, fluoride, boron, vanadium, and other minerals.
According to the World Health Organization (WHO, 1998), the carcinogenic effect of ingesting water containing inorganic arsenic above the recommended maximum level of 0.01 milligrams per liter (mg/L) is well demonstrated and is reflected in an increased incidence of skin cancer in humans.
Morras, Blanco, and Paoloni (2000) reported excessive levels of arsenic in the groundwater of the Chaco-pampa region in Argentina. A study by Sastre, Rodriguez, Varillas, & Salim (1997), surveyed a population that had resided in the Salta Chaco (northwest Argentina) for over 10 years and found that 8.6 percent of those surveyed were suffering from chronic regional endemic hydro-arsenism (CREHA).
Volcanic ash in quaternary sediments in the pampa plains of north La Pampa Province, Argentina, show high concentrations of arsenic (7 to 12 mg/L), as well as other oligoelements (Nicolli, Smedley, & Tullio, 1997; Smedley, Nicolli, Macdonald, Barros, & Tullio, 2002).
A considerable number of studies have been undertaken in Argentina on high arsenic content in water a...


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[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

Re: Discussion, high H1N1 CFR and elevated arsenic

Zimagail argues in post 7 that arsenic levels are not high in the city of Buenos Aries. While that may be true, the higher levels in other parts of the country coupled with the extremely high migration of people from outlying areas into Buenos Aries, where the levels are above the recommended rate, may explain the anomaly.

Two comments regarding arsenic and increased death rates.
1. Chaco may have a high arsenic level but that is not where the deaths are concentrated. Last I checked there were only 3 cases in Chaco.
2. Chile and Argentina both are mined heavily for gold, silver and copper, all extracted with arsenic.

 

[sharon sanders]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

I moved posts to this thread to solve a software problem on the other Arsenic discussion thread. Please post to this one. Thanks!

 

[AlaskaDenise]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Here's an article that includes costs to remove arsenic from water systems. It's an issue in some populated areas of Alaska.

http://www.adn.com/news/alaska/matsu/story/644794.html

(snipped)

According to the EPA, 967 water systems nationwide serving more than 1.3 million people were out of compliance with the new arsenic rule as of December 2008. That list includes eight water systems in Alaska affecting more than 1,400 people, most located in the Valley.

"Engineering estimates for remediation can run $50,000 to $100,000," Winkler said.

The cost of treatment depends on a lot of factors, he said. For some, a new well is the least-expensive answer. For others, more intensive treatment like installing a filtration system is required. The federal standards do not apply to private wells, but homeowners can likely treat the problem for between $400 and $4,000, Winkler said.

.....a system that sprays air into the water and filters it would be the backup plan. The estimated price tag would be around $100,000,

.

 

[Shannon Bennett]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

We have some evidence of elevated levels of arsenic in three of the areas hardest hit with CFR from H1N1. Why does an elevated arsenic level result in a higher CFR for H1N1 patients?

http://www.sciencedirect.com/scienc...serid=10&md5=7c366b5d39c29f7aec21579b6706b8d5

doi:10.1016/j.taap.2004.08.010


Copyright © 2004 Elsevier Inc. All rights reserved.


Implications of oxidative stress and hepatic cytokine (TNF-α and IL-6) response in the pathogenesis of hepatic collagenesis in chronic arsenic toxicity
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References and further reading may be available for this article. To view references and further reading you must purchase this article.


<!-- refMsg -->Subhankar Das, Amal Santra, Sarbari Lahiri and D.N. Guha Mazumder^,

<!-- authorsNoEnt -->Institute of Post Graduate Medical Education and Research, Kolkata, India

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Received 23 June 2004;
<!-- articleText -->accepted 23 August 2004.
<!-- articleText -->Available online 30 November 2004.
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<!-- articleText -->Abstract

Introduction:

Noncirrhotic portal fibrosis has been reported to occur in humans due to prolonged intake of arsenic contaminated water. Further, oxystress and hepatic fibrosis have been demonstrated by us in chronic arsenic induced hepatic damage in murine model. Cytokines like tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) are suspected to play a role in hepatic collagenesis. The present study has been carried out to find out whether increased oxystress and cytokine response are associated with increased accumulation of collagen in the liver due to prolonged arsenic exposure and these follow a dose–response relationship.
Methods:

Male BALB/c mice were given orally 200 μl of water containing arsenic in a dose of 50, 100, and 150 μg/mouse/day for 6 days a week (experimental group) or arsenic-free water (<0.01 μg/l, control group) for 3, 6, 9 and 12 months. Hepatic glutathione (GSH), protein sulfhydryl (PSH), glutathione peroxidase (GPx), Catalase, lipid peroxidation (LPx), protein carbonyl (PC), interleukin (IL-6), tumor necrosis factor (TNF-α), arsenic and collagen content in the liver were estimated from sacrificed animals.
Results:

Significant increase of lipid peroxidation and protein oxidation in the liver associated with depletion of hepatic thiols (GSH, PSH), and antioxidant enzymes (GPx, Catalase) occurred in mice due to prolonged arsenic exposure in a dose-dependent manner. Significant elevation of hepatic collagen occurred at 9 and 12 months in all the groups associated with significant elevation of TNF-α and IL-6. However, arsenic level in the liver increased progressively from 3 months onwards. There was a positive correlation between the hepatic arsenic level and collagen content (r = 0.8007), LPx (r = 0.779) and IL-6 (r = 0.7801). Further, there was a significant negative correlation between GSH and TNF-α (r = −0.5336)) and LPx (r = −0.644).
Conclusion:

Increasing dose and duration of arsenic exposure in mice cause progressive increase of oxystress and elevation of cytokines associated with increasing level of collagen in the liver.

<!-- articleText -->Keywords: Arsenic; Hepatotoxicity; Proinflammatory cytokines; Oxystress

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<dl><dt>Introduction </dt><dt>Materials and methods </dt><dl><dt>Experimental protocol </dt><dt>Estimation of hepatic thiol </dt><dt>Estimation of protein oxidation </dt><dt>Estimation of hepatic catalase and glutathione peroxidase (GSH-Px) </dt><dt>Estimation of hepatic lipid peroxidation (LPx) </dt><dt>Estimation of tissue collagen content </dt><dt>Estimation of cytokines </dt><dt>Estimation of hepatic arsenic (As) content </dt><dt>Estimation of protein </dt><dt>Statistical analysis</dt></dl><dt>Results </dt><dl><dt>Effect of chronic arsenic exposure on Hepatic Thiol </dt><dt>Effect on hepatic glutathione peroxidase (GSH-Px) and hepatic Catalase activity </dt><dt>Effect on hepatic lipid peroxidation </dt><dt>Glutathione (GSH) vs. lipid peroxidation (LPx) </dt><dt>Effect on hepatic protein carbonyl (PC) </dt><dt>Effect on hepatic collagen content </dt><dt>Correlation of hepatic collagen content with lipid peroxidation (LPx) and protein oxidation </dt><dt>Effect on hepatic arsenic </dt><dt>Correlation of hepatic arsenic content with lipid peroxidation and hepatic collagen level </dt><dt>Effect on Hepatic TNF-α and hepatic IL-6 </dt><dt>Glutathione (GSH) vs. tumor necrosis factor (TNF-α) </dt><dt>Hepatic IL-6 vs. hepatic collagen</dt></dl><dt>Discussion </dt><dt>Acknowledgements </dt><dt>References</dt></dl>
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</td></tr></tbody></table>Fig. 1. Data showing inverse correlation between GSH and LPx in the liver of control and experimental animals (r = −0.644, P < 0.001).

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</td></tr></tbody></table>Fig. 2. Concentration of total collagen in liver of control and experimental animals. Results are mean ± SD. a = P < 0.05, l = P < 0.001, sample size (n) = 10 in each group.

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</td></tr></tbody></table>Fig. 3. Data showing positive correlation between hepatic collagen content and MDA level of control and experimental animals (r = 0.7177, P < 0.001).

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</td></tr></tbody></table>Fig. 4. Data showing positive correlation between the levels of protein oxidation and collagen content in the liver of control and experimental animals (r = 0.8149, P < 0.001).

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</td></tr></tbody></table>Fig. 5. Hepatic arsenic (As) content of the control and experimental animals at different months of As feeding. Results are mean ± SD. l = P < 0.001, Sample size (n) = 10 in each group.

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</td></tr></tbody></table>Fig. 6. Data showing positive correlation between hepatic arsenic level and lipid peroxidation of control and experimental animals (r = 0.779, P < 0.001).

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</td></tr></tbody></table>Fig. 7. Data showing positive correlation between the concentration of arsenic and collagen in the liver of control and experimental animals (r = 0.8007, P < 0.001).

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</td></tr></tbody></table>Fig. 8. Concentration of TNF-α in the liver of control and experimental animals during different months of arsenic exposure. Results are mean ± SD. a = P < 0.05, d = P < 0.01, l = P < 0.001, sample size (n) = 10 in each group.

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</td></tr></tbody></table>Fig. 9. Concentration of IL-6 in the liver of control and experimental animals. Results are mean ± SD. d = P < 0.01, l = P < 0.001, sample size (n) = 10 in each group.

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</td></tr></tbody></table>Fig. 10. Data showing inverse correlation between GSH and TNF-α level in the liver of control and experimental animals (r = −0.5336, P < 0.001).

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</td></tr></tbody></table>Fig. 11. Data showing positive correlation between IL-6 and collagen content in the liver of control and experimental animals (r = 0.7801, P < 0.001).

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Table 1. Results of various components of antioxidant defense system during increasing dose and duration of arsenic (As) feeding in mice

Results are mean ± SD. α = P < 0.05., β = P < 0.02, δ = P < 0.01, λ = P < 0.001, Sample size (n) = 10 in each group.

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Corresponding author. 37/C, Block B, New Alipur, Kolkata-700053, India. Fax: +91 033 24751799.

 

[AlaskaDenise]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

What's the best immediate solution? Selenium?

.

 

[Shannon Bennett]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

I have lost my satellite connection. It will not be repaired until Saturday. Until then I am limited to a dial-up connection which will severely limit my ability to do more research.

As for the selenium, extreme caution needs to be taken as selenium toxicity may be irreversible and deadly. How much you are getting is dependent on soils in your area. Some places such as Kesterson in the Central Valley of California have extremely high amounts while the central plains of the U.S. have very low levels. Food grown in each of those areas will reflect how much is ingested.

 

[kiwibird]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

This should be very interesting to follow. Wherever you have grape growing areas here in New Zealand you have an increase in the aresenic content of local water supplies. Blenheim, in the north of the South Island, has a very high level of arsenic. It is used in the treatment of the wooden poles that support the wires for the vines. To top it off, New Zealand has virtually no Selenium in the soil. It is a very new, geologically speaking, country, we therefore know that one brazil nut a day is enough to supply the selenium needed in your diet (or a multivit), we also dose our farm animals. Argentina is a huge producer of very good wine. I wonder if they treat their poles the same way? Do the large cities get their water supplies from grape growing regions?

 

[Shannon Bennett]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Another point source for arsenic contamination is old cemeteries. From approx. 1860 until 1910, bodies were prepared for burial using an unregulated amount of arsenic. Sometims as much as 5 pounds was used per body. As groundwater moves through these graveyards it collects and moves arsenic into local waterways.

Yet one more point source are areas where treated lumber is stored. Copper arsenate is used to preserve lumber used for railroad tracks and myriad other uses where the wood was in contact with soils and thus subject to rapid deterioration.

 

[St Michael]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

We have some evidence of elevated levels of arsenic in three of the areas hardest hit with CFR from H1N1. Why does an elevated arsenic level result in a higher CFR for H1N1 patients?

http://www.sciencedirect.com/scienc...serid=10&md5=7c366b5d39c29f7aec21579b6706b8d5


Implications of oxidative stress and hepatic cytokine (TNF-α and IL-6) response in the pathogenesis of hepatic collagenesis in chronic arsenic toxicity

Abstract

Introduction:

Noncirrhotic portal fibrosis has been reported to occur in humans due to prolonged intake of arsenic contaminated water. Further, oxystress and hepatic fibrosis have been demonstrated by us in chronic arsenic induced hepatic damage in murine model. Cytokines like tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) are suspected to play a role in hepatic collagenesis. The present study has been carried out to find out whether increased oxystress and cytokine response are associated with increased accumulation of collagen in the liver due to prolonged arsenic exposure and these follow a dose?response relationship.

Cytokinemia -- TNF-α and IL-6 -- strikes again!

 

[Shannon Bennett]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Yup, we have a real aha! moment. Higher levels of arsenic mean an increased probability of both a reduction in vitamin D uptake and an increased cytokine response. Reduced vitamin D and you have a compromised immune system and yet another problem with pro-inflammatory cytokines. In essence a perfect storm.

 

[sharon sanders]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

I have lost my satellite connection. It will not be repaired until Saturday. Until then I am limited to a dial-up connection which will severely limit my ability to do more research.

As for the selenium, extreme caution needs to be taken as selenium toxicity may be irreversible and deadly. How much you are getting is dependent on soils in your area. Some places such as Kesterson in the Central Valley of California have extremely high amounts while the central plains of the U.S. have very low levels. Food grown in each of those areas will reflect how much is ingested.

Thanks Shannon.

 

[sharon sanders]

Re: Arsenic - A Fatal Complication for Pandemic Flu - MUST READ

I have moved this thread from discussion into the news forum.

It is a significant public health advisory.


Thank you to everyone on all the sites for working on this development.

 

[sharon sanders]

Re: Arsenic - A Fatal Complication for Pandemic Flu - MUST READ

Argentina Swine Flu thread -

http://www.flutrackers.com/forum/showthread.php?t=103168&page=3

 

[St Michael]

Re: Arsenic - A Fatal Complication for Pandemic Flu - MUST READ

Arsenic in drinking water and cerebrovascular disease, diabetes mellitus, and kidney disease in Michigan: a standardized mortality ratio analysis

Environmental Health 2007, 6:4doi:10.1186/1476-069X-6-4
2 February 2007

Abstract

Background

Exposure to arsenic concentrations in drinking water in excess of 300 μg/L is associated with diseases of the circulatory and respiratory system, several types of cancer, and diabetes; however, little is known about the health consequences of exposure to low-to-moderate levels of arsenic (10?100 μg/L).

Methods

A standardized mortality ratio (SMR) analysis was conducted in a contiguous six county study area of southeastern Michigan to investigate the relationship between moderate arsenic levels and twenty-three selected disease outcomes. Disease outcomes included several types of cancer, diseases of the circulatory and respiratory system, diabetes mellitus, and kidney and liver diseases. Arsenic data were compiled from 9251 well water samples tested by the Michigan Department of Environmental Quality from 1983 through 2002. Michigan Resident Death Files data were amassed for 1979 through 1997 and sex-specific SMR analyses were conducted with indirect adjustment for age and race; 99% confidence intervals (CI) were reported.

Results

The six county study area had a population-weighted mean arsenic concentration of 11.00 μg/L and a population-weighted median of 7.58 μg/L. SMR analyses were conducted for the entire six county study area, for only Genesee County (the most populous and urban county), and for the five counties besides Genesee. Concordance of results across analyses is used to interpret the findings. Elevated mortality rates were observed for both males (M) and females (F) for all diseases of the circulatory system (M SMR, 1.11; CI, 1.09?1.13; F SMR, 1.15; CI, 1.13,-1.17), cerebrovascular diseases (M SMR, 1.19; CI, 1.14?1.25; F SMR, 1.19; CI, 1.15?1.23), diabetes mellitus (M SMR, 1.28; CI, 1.18?1.37; F SMR, 1.27; CI, 1.19?1.35), and kidney diseases (M SMR, 1.28; CI, 1.15?1.42; F SMR, 1.38; CI, 1.25?1.52).

Conclusion

This is some of the first evidence to suggest that exposure to low-to-moderate levels of arsenic in drinking water may be associated with several of the leading causes of mortality, although further epidemiologic studies are required to confirm the results suggested by this ecologic SMR analysis.

 

[Lizw]

Re: Woods Hole Scientists Link Influenza A (H1N1) Susceptibility to Arsenic Exposure

Re: Woods Hole Scientists Link Influenza A (H1N1) Susceptibility to Arsenic Exposure

2.2.5. Feed additives

Almost hidden in this long list of links is a significant source of arsenic in US groundwater--an arsenic compound called Roxarsone which is fed to chickens. Quoting from a USGS article (my emphasis):

Organic arsenic compounds are extensively added to the feed of broiler chickens. The most commonly used arsenic compound is roxarsone (3-nitro-4-hydroxyphenylarsonic acid), which is fed to poultry to control coccidial intestinal parasites, thereby improving feed efficiency. Very little of the roxarsone is retained in the chicken meat (FDA limit is 0.5 parts per million in chicken muscle tissue). Most of the roxarsone is excreted unchanged; however, the degradation product, 3-amino-4-hydroxyphenylarsonic acid, has been detected in the urine of hens fed roxarsone. We estimate that approximately 106 kilograms (Kg) per year of roxarsone and its degradation products are introduced annually into the environment from the disposal of poultry litter spread onto agricultural fields near the chicken houses. This practice could result in localized arsenic pollution.

Another article from PubMed (my emphasis again):

Arsenic contamination of drinking water is a worldwide public health concern. The extent of the concern in some countries has reached a point such that some are calling this humanity?s largest mass poisoning (Bhattacharjee 2007). Even low levels of exposure to arsenic have been linked to increased cardiovascular disease and hypertension (Chen et al. 2007; Navas Acien et al. 2005). Although natural contamination of drinking water with inorganic arsenic represents the largest arsenical hazard to human health, environmental exposure to commercial organoarsenicals is a growing concern (Sapkota et al. 2007). Organoarsenicals such as roxarsone are widely used by the poultry industry (Arai et al. 2003; Brown et al. 2004; Chapman et al. 2002), with approximately 2.2 million pounds of roxarsone being fed to broiler chickens raised in the United States per year (Garbarino et al. 2003). The majority of roxarsone is excreted unchanged from chickens (Morrison 1969), while the remainder increases the total arsenic present in chicken tissue (Lasky et al. 2004). This residual roxarsone could amount to ingestion of 1.38?5.24 mg/day of arsenic at mean levels of chicken consumption (60 g/person/day) (Wallinga 2006). The excreted roxarsone may pose an environmental hazard, as microbes, including those residing in the gut microflora, can release inorganic arsenite (AsIII) from roxarsone (Stolz et al. 2007). The human health impacts of roxarsone have not been well studied, and the mechanisms for its biological effects in mammalian tissues are unknown. It has been suggested, however, that all of these biological effects require metabolism to inorganic AsIII (O?Connor et al. 2005).

A previous issue of the magazine Backyard Poultry published a critique of the poultry industry by Harvey Ussery, a well-known and widely respected organic gardener and writer. In the current issue of the magazine, a reader takes exception to Harvey and defends the industry that he criticised. Here is part of Harvey's rebuttal. In one of those odd examples of synchronicity, it was posted today in a mailing list I'm on.

America's commercial broiler flocks are fed two million pounds of
Roxersone per year, most of which is excreted unchanged, and the litter
is spread far and wide as fertilizer on croplands. Roxarsone is soluble,
that is, highly mobile in the environment, leaching to surface and
groundwater systems. Many environmental factors degrade Roxarsone to
inorganic forms of arsenic: mostly arsenate (toxic), but some arsenite
(highly toxic). Such factors include sunlight (seen any of that
around?), bacteria, presence of nitrates (plenty of that in chicken
litter), and especially anaerobic conditions, as found in big wet piles
of litter, subsoils, sediments under rivers and lakes, etc.

I have no idea whether Roxarsone is widely used in Argentina or Canada. It has been banned in Europe for a decade or more, but as far as I know, every commercial producer of broiler/fryers in the US uses it, and I'll be surprised if that isn't true for South America as well.

 

[Lizw]

Re: Arsenic - A Fatal Complication for Pandemic Flu - MUST READ

"When a normal person or mouse is infected with the flu, they immediately develop an immune response," says Hamilton, in which immune cells rush to the lungs and produce chemicals that help fight the infection. However, in mice that had ingested 100 ppb (parts per billion) arsenic in their drinking water for five weeks, the immune response to H1N1 infection was initially feeble, and when a response finally did kick in days later, it was "too robust and too late," Hamilton says. "There was a massive infiltration of immune cells to the lungs and a massive inflammatory response, which led to bleeding and damage in the lung." Morbidity over the course of the infection was significantly higher for the arsenic-exposed animals than the normal animals.]

My assumption as a layperson is that the phrase, "they immediately develop an immune response" refers to the innate immune system. Which makes the following even more interesting:

From this article on arsenic exposure in zebrafish:

What did they find? Arsenic exposure at both 2 and 10 ppb inhibited the zebrafish?s innate immune system, which allowed viral and bacterial infections to thrive in the exposed embryo as compared to the controls (graph below). One day after infection with the SHR virus, fish exposed to only 2 ppb arsenic had 57 times more virus particles growing inside them then did the control fish. Fish exposed to 10 ppb arsenic had 87 times more virus particles inside them.