Parents and pediatricians should routinely ask children with food allergy about bullying

NEW YORK – Nearly half of children diagnosed with food allergies who participated in a recent study are bullied, according to researchers at the Icahn School of Medicine at Mount Sinai. One third of those bullied specifically due to their food allergy. Almost eight percent of children in the U.S. are allergic to foods such as peanuts, tree-nuts, milk, eggs, and shellfish.

Nearly half of parents surveyed (47.9 percent) were not aware of the bullying—although both the bullied children and their parents reported experiencing higher stress levels and lower quality of life.

The study, titled, “Child and Parental Reports of Bullying in a Consecutive Sample of Children with Food Allergy,” appears in the online issue of Pediatrics on December 24. The study was led by Eyal Shemesh, MD, Associate Professor of Pediatrics and Psychiatry at the Icahn School of Medicine at Mount Sinai.  Dr. Shemesh and his team surveyed 251 pairs of parents and children. The patient and parent pairs were consecutively recruited during allergy clinic visits to independently answer questionnaires. Bullying due to food allergy or for any cause, quality of life, and distress in both the child and parent were evaluated using validated questionnaires.

“Parents and pediatricians should routinely ask children with food allergy about bullying,” said Dr. Shemesh. “Finding out about the child’s experience might allow targeted interventions, and would be expected to reduce additional stress and improve quality of life for these children trying to manage their food allergies.” Dr. Shemesh is Director of EMPOWER (Enhancing, Managing, and Promoting Well-being and Resiliency), a program within Mount Sinai’s Jaffe Food Allergy Institute. Dr. Shemesh is also Chief of the Division of Behavioral and Developmental Health in the Department of Pediatrics at The Mount Sinai Medical Center.

“When parents are aware of the bullying, the child’s quality of life is better,” said the senior author, Scott H. Sicherer, MD, Professor of Pediatrics, Chief, Division of Pediatric Allergy, Co-Director, EMPOWER program. “Our results should raise awareness for parents, school personnel, and physicians to proactively identify and address bullying in this population.”

Author: Mount Sinai, Researchers Survey Shows That Nearly Half of Children with Food Allergies Experience Bullying, December 24, 2012

The study, titled, “Child and Parental Reports of Bullying in a Consecutive Sample of Children with Food Allergy,” appears in the online issue of Pediatrics.

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Every year in the United States, there are more than 1.2 million poison exposures among children younger than 6 years. In recent decades, household cleaning products have consistently been one of the leading sources of pediatric poisoning. A new study conducted by the Center for Injury Research and Policy of The Research Institute at Nationwide Children’s Hospital found that from 1990-2006, an estimated 267,269 children younger than 6 years were treated in U.S. hospital emergency departments for injuries attributable to household cleaning products. During the 17-year study period, researchers noted a 46 percent decrease in the number of injuries.

Data from the study, being released online August 2 and appearing in the September issue of Pediatrics, show that most of the household cleaner-related injuries were poisonings, with children ages 1-3 years accounting for the majority (72 percent) of the injuries. Bleach was the cleaning product most commonly associated with injury (37.1 percent). While approximately one-third of the injuries occurred through contact with the cleaning product, the more frequent means was ingestion (62.7 percent), and spray bottles were the most common storage container (40.1 percent).

“Interestingly, spray bottles were the only major storage source that increased over the study period,” said study lead author Lara McKenzie, PhD, principal investigator at the Center for Injury Research and Policy at Nationwide Children’s Hospital. “Although rates of household cleaner-related injuries from regular bottles and original containers decreased during the study period, spray bottle injury rates remained constant. This area is worthy of further research.”

The good news is that the number of injuries decreased almost by half during the study period, but the bad news is that there were still nearly 12,000 children younger than 6 years who suffered injuries from household cleaning products in 2006.

“Young children are curious about their surroundings and tend to explore their environment by putting things in their mouths,” said Dr. McKenzie, also a faculty member of The Ohio State University College of Medicine. “This general sense of inquisitiveness, combined with increased mobility, the ubiquitous nature of household cleaning products and the ease of accessibility, place young children at high risk of injury.”

Parents and caregivers must do their part to prevent childhood poisonings. According to Heath Jolliff, DO, associate medical director of the Central Ohio Poison Center at Nationwide Children’s Hospital, parents should store poisonous substances in locked cabinets, out of sight and reach of children.

“It’s important to only purchase cleaners with child-resistant packaging, keep all products in their original containers and properly dispose of leftover or unused products,” Dr. Jolliff, also a faculty member at OSU College of Medicine, said.

Parents should also know what to do if they suspect their child has come in contact with a poison. Dr. Jolliff advises to immediately contact the Poison Center at 1-800-222-1222 (this national number will direct callers to their local Poison Center), unless the child is unconscious, not breathing, or having seizures, in which case parents should call 9-1-1.

This is the first published study using nationally representative data to examine poisonings from household cleaning products among children younger than 6 years for an extended time period. Data for this study were collected from the National Electronic Injury Surveillance System (NEISS), which is operated by the U.S. Consumer Product Safety Commission. The NEISS dataset provides information on consumer product-related and sports and recreation-related injuries treated in hospital emergency departments across the country.

Reference:

Nationwide Children’s Hospital, New National Study Finds Decrease in Pediatric Injuries Associated with Household Cleaners Children younger than 6 years still at high risk of poisoning, Columbus, OH – 8/2/2010.

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Further Articles about Children’s Health:

• Oil Spill: Kids in the Gulf
• Pesticides in kids linked to ADHD- Attention-Deficit/Hyperactivity Disorder, study finds
• Our Planet – Our Children – How are your Children doing?
• EPA releases Guide to help Scientists understand Children Exposure to Pollutants
• Common Plastics Chemicals linked to ADHD Symptoms

Dioxins and similar compounds, such as dioxin-like polychlorinated biphenyls (PCBs), include a range of toxic substances which are formed by burning – e.g. through waste incineration or forest fires – and some industrial processes. Their presence in the environment has declined since the 1970s, following concerted efforts at the EU level.

Dioxins are found at low levels in many foods. They do not cause immediate health problems, but long-term exposure to high levels of dioxins has been shown to cause a range of effects, including cancer. Their persistence and the fact that they accumulate in the food chain, notably in animal fat, therefore continues to cause some safety concerns.

The highest average levels of dioxins and dioxin-like PCBs in relation to fat content were observed for liver and liver products from animals. The highest average levels in relation to total product weight were for fish liver and products derived from fish liver. In animal feed, the highest average levels were found in fish oil.

Overall, 8% of the samples exceeded the different maximum levels set out in EU legislation. However, some of these samples clearly originated from targeted sampling during specific contamination episodes. There were also large variations between different groups of food and feed in terms of the proportion of samples which exceed maximum levels.

The report concludes that no clear trend can be established regarding changes in background levels of dioxins and related substances in food and feed over time, as there were increases in some categories but decreases in others. Furthermore, occasional contamination episodes and a lack of information on which samples resulted from targeted or random sampling make it difficult to assess such trends.

The current EU method for measuring overall dioxin levels is based on toxicity values for different types of dioxins recommended by the World Health Organisation (WHO) in 1998. EFSA was also asked to assess the impact on total dioxin levels of using toxicity values set out in WHO recommendations from 2005, which downgraded the relative toxicity of certain types of dioxins. The report finds that using the new values would reduce overall dioxin levels by 14%, although the extent of this reduction was very different across food and feed categories.

Finally, the report recommends continuous random testing of a sufficient number of samples in each food and feed group to ensure accurate assessments of the presence of dioxins and dioxin-like PCBs.

Author; EFSA, EFSA publishes European overview of dioxin levels in food and feed, March 31, 2010

• Full Report
• Results of the monitoring of dioxin levels in food and feed
• European Commission – Food Contaminants – Dioxins and PCBs

The disease MCS – Multiple Chemical Sensitivity (ICD-10 T78.4) is mentioned at the Thesaurus “Safety and Health at Work”, alphabetical Part, Status May 2009, as: 

Multiple Chemical Sensitivity (B02.19.00)     

At the systematic Part MCS – Multiple Chemical Sensitivity is found at the category B02:  

“Work related Disease and Occupational Disease/Disease”  

integrated in Part:  

• B02.19 Other Disease 
• B02.19.00 Multiple Chemical Sensitivity  

Chronic Fatigue Syndrome (CFS) is integrated analogue.  

MCS is not classified as a mental disease

To clear up occurring doubts, it is to point out that MCS – Multiple Chemical Sensitivity is not integrated into chapter B02.15: Mental diseases, Depression, Neurosis, Post traumatic Stress Disorder or psychosomatic diseases. 

Thesaurus “Safety and Health at Work”

The Thesaurus offers a quick overview on the broad group of themes “Safety and Health at Work”. It contains about 3 500 main keywords and is the joining of the keywords from the two previous Thesauri “Safety at Work” and “Occupational Medicine”. The Thesaurus is based on the practical work of the Library group, documentation at the content development and their research of technical literature. It is a tool for documentation.   

The Thesaurus is intended for all who search for literature about “Safety and Health at Work”. It is supportive for prearrangement of research inquiries at the data pool LITDOK and can be helpful for searching in topic related databases.  

Author: Silvia K. Müller, CSN – Chemical Sensitivity Network, July 23, 2009  

Reference:  Thesaurus „Sicherheit und Gesundheit bei der Arbeit“ Alphabetischer Teil, Systemischer Teil, Dortmund/Berlin/Dresden 2009. 

Research on Multiple Chemical Sensitivity (MCS)

Compiled by

Professor Anne C. Steinemann and Amy L. Davis

University of Washington

This document lists scientific citations for peer-reviewed journal articles that support a physiological basis for MCS:

1. Abdel-Rahman A., Shetty A.K., Abou-Donia M.B. 2002. Disruption of the blood-brain barrier and neuronal cell death in cingulate cortex, dentate gyrus, thalamus, and hypothalamus in a rat model of Gulf-War syndrome. Neurobiology of Disease 10(3): 306-26.
2. Abel-Rahman A., Abou-Donia S., El-Masry E., Shetty A., Abou-Donia M. 2004. Stress and combined exposure to low doses of pyridostigmine bromide, DEET, and permethrin produce neurochemical and neuropathological alteration in cerebral cortex, hippocampus, and cerebellum. Journal of Toxicology and Environmental Health Part A 67(2): 163-92.
3. Abdel-Rahman A., Dechkovskaia A.M., Goldstein L.B., Bullman S.H., Khan W., El-Masry E.M., Abou-Donia M.B. 2004. Neurological deficits induced by malathion, DEET, and permethrin, alone or in combination in adult rats. Journal of Toxicology and Environmental Health Part A 67(4): 331-56.
4. Abou-Donia M.B 2003. Organophosphorus ester-induced chronic neurotoxicity. Archives of Environmental Health 58(8): 484-97.
5. Abou-Donia M.B., Wilmarth K.R., Abdel-Rahman A.A., Jenseen K.F., Oehme F.W., Kurt T.L. 1996. Increased neurotoxicity following concurrent exposure to pyridostigmine bromide, DEET, and chlorpyrifos. Fundamentals of Applied Toxicology 34(2): 201-22.
6. Abou-Donia M.B., Dechkovskaia A.M., Goldstein L.B., Shah D.U., Bullman S.L., Khan W.A. July 2002. Uranyl acetate-induced sensorimotor deficit and increased nitric oxide generation in the central nervous system in rats. Pharmacology, Biochemistry, and Behavior 72(4): 881-90.
7. Abou-Donia M.B., Dechkovskaia A.M., Goldstein B., Abdel-Rahman A., Bullman S.L., Khan W.A. 2004. Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity. Pharmacology, Biochemistry, and Behavior 77(2): 253-62.
8. Abu-Qare A.W., Abou-Donia M.B. 2001. Combined exposure to sarin pyridostigmine bromide increased levels of rat urinary 3-nitrotyrosine and 8-hydroxy-2’deoxyguanosine, biomarkers of oxidative stress. Toxicology Letters 123(1): 51-58.
9. Abu-Qare A.W., Abou-Donia M.B. 2001. Biomarkers of apoptosis: release of cytochrome c, activation of caspase-3, induction of 8-hydroxy-2′-deoxyguanosine, increased 3-nitrotyrosine, and alteration of p53 gene. Journal of Toxicology and Environmental Health Part B, Critical Reviews 4(3): 313-32.
10. Abu-Qare A.W., Abou-Donia M.B. 2008. In vitro metabolism and interactions of pyridostigmine bromide, N,N-diethyl-m-toluamide, and permethrin in human plasma and liver microsomal enzymes. Xenobiotica 38(3): 294-313.
11. Anderson R.C., Anderson J.H. 1999. Sensory irritation and multiple chemical sensitivity. Toxicology and Industrial Health 15(3-4): 339-45.
12. Ashford N.A. 1999. Low-level chemical sensitivity: implications for research and social policy. Toxicology and Industrial Health 15(3-4): 421-47.
13. Baldwin C.M. and Bell I.R. 1998. Increased cardiopulmonary disease risk in a community-based sample with chemical odor intolerance: implications for women’s health and health-care utilization. Archives of Environmental Health 1998 53(5): 347-53.
14. Baldwin C.M., Bell I.R., O’Rourke M.K. 1999. Odor sensitivity and respiratory complaint profiles in a community-based sample with asthma, hay fever, and chemical odor intolerance. Toxicology and Industrial Health 15(3-4): 403-9.
15. Bascom R., Meggs W.J., Framptom M., Hudnell K., Kilburn K., Kobal G., Medinsky M., Rea W. 1997. Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation. Environmental Health Perspective 105 (Suppl. 2): 531-37.
16. Bell I.R., Miller C.S., and Schwartz G.E. 1992. An olfactory-limbic model of multiple chemical sensitivity syndrome: possible relationships to kindling and affective spectrum disorders. Biological Psychiatry 32(3): 218-42.
17. Bell I.R., Warg-Damiani L., Baldwin C.M., Walsh M.E., Schwartz G.E. 1998. Self-reported chemical sensitivity and wartime chemical exposures in Gulf War veterans with and without decreased global health ratings. Military Medicine 163(11): 725-32.
18. Bell I.R., Schwartz G.E., Peterson J.M. and Amend D. 1993. Self-reported illness from chemical odors in young adults without clinical syndromes or occupational exposures. Archives of Environmental Health. 48(1): 6-13.
19. Bell I.R., Schwartz G.E., Baldwin C.M., Hardin E.E. 1996. Neural sensitization and physiological markers in multiple chemical sensitivity. Regulatory Toxicology and Pharmacology 24(1), pt. 2: S39-S47.
20. Bell I.R., Baldwin C.M., Schwartz G.E.R. 2001. Sensitization studies in chemically intolerant individuals: implications for individual difference research. Annals of the New York Academy of Sciences 933:38-47.
21. Brandt-Rauf P.W., Andrews L.R., Schwarz-Miller J. 1991. Sick-hospital syndrome. Journal of Occupational Medicine 33(6): 737-39.
22. Bronstein A.C. 1995. Multiple chemical sensitivities—new paradigm needed. Journal of Toxicology: Clinical Toxicology 33(2): 93-94.
23. Brooks S.M., Weiss M.A., Bernstein I.L. 1985. Reactive airways dysfunction syndrome. Case reports of persistent airways hyperreactivity following high-level irritant exposures. Journal of Occupational Medicine 27(7): 473-76.
24. Brown-DeGagne A.M., McGlone J. 1999. Multiple chemical sensitivity: a test of the olfactory-limbic model. Journal of Occupational and Environmental Medicine 41(5): 366-77.
25. Buchwald D., Garrity D. 1994. Comparison of patients with chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities. Archives of Internal Medicine 154(18): 2049-53.
26. Caress S.M., Steinemann A.C. 2003. A review of a two-phase population study of multiple chemical sensitivities. Environmental Health Perspectives 111(12): 1490-97.
27. Caress S.M., Steinemann A.C. 2004. Prevalence of multiple chemical sensitivities: A population-based study in the southeastern United States. American Journal of Public Health 94(5): 746-47.
28. Caress S.M., Steinemann A.C. 2009. Prevalence of fragrance sensitivity in the American population. Journal of Environmental Health 71(7): 46-50.
29. Caress S.M., Steinemann A.C. 2009. Asthma and chemical hypersensitivity: prevalence, etiology, and age of onset. Toxicology and Industrial Health 25(1): 71-78.
30. Caress S.M., Steinemann A.C. 2004. A national population study of the prevalence of multiple chemical sensitivity. Archives of Environmental Health 59(6): 300-305.
31. Caress S.M., Steinemann A.C. 2005. National prevalence of asthma and chemical hypersensitivity: an examination of potential overlap. Journal of Occupational and Environmental Medicine 47(5): 518-22.
32. Caress S.M., Steinemann A.C., Waddick C. 2002. Symptomatology and etiology of multiple chemical sensitivities in the southeastern United States. Archives of Environmental Health 57(5): 429-36.
33. Davidoff A.L., Keyl P.M., Meggs W.J. 1998. Development of multiple chemical sensitivities in laborers after acute gasoline fume exposure in an underground tunneling operation. Archives of Environmental Health 53(3):183-89.
34. DeRosa C.T., Hicks H.E., Ashizawa A.E., Pohl H.R., Mumtaz M.M. 2006. A regional approach to assess the impact of living in a chemical world. Annals of the New York Academy of Sciences 1076:829-38.
35. Donnay A.H. 1999. On the recognition of multiple chemical sensitivity in medical literature and government policy. International Journal of Toxicology 18(6): 383-92.
36. Elberling J., Linneberg A., Dirksen A., Johansen J.D., Frølund L., Madsen F., et al. 2005. Mucosal symptoms elicited by fragrance products in a population-based sample in relation to atopy and bronchial hyper-reactivity. Clinical and Experimental Allergy 35(1): 75-81.
37. Farrow A., Taylor H., Northstone K., Golding J. 2003. Symptoms of mothers and infants related to total volatile organic compounds in household products. Archives of Environmental Health 58(10): 633-41.
38. Fernandez M., Bell I.R., Schwartz G.E. 1999. EEG sensitization during chemical exposure in women with and without chemical sensitivity of unknown etiology. Toxicology and Industrial Health 15(3-4): 305-12.
39. Gibson P.R., Elms A.N., Ruding L.A. 2003. Perceived treatment efficacy for conventional and alternative therapies reported by persons with multiple chemical sensitivity. Environmental Health Perspectives 111(12): 1498-1504.
40. Gilbert M.E. 1995. Repeated exposure to lindane leads to behavioral sensitivities and facilitates electrical kindling. Neurotoxicolgy and Teratology 17(2): 131-41.
41. Greene G.J., Kipen H.M. 2002. The vomeronasal organ and chemical sensitivity: a hypothesis. Environmental Health Perspectives 110 (Suppl 4): 655-61.
42. Haley R.W., Billecke S., La Du B.N. 1999. Association of low PON1 type Q (type A) arylesterase activity with neurologic symptoms complexes in Gulf War veterans. Toxicology and Applied Pharmacology 157(3): 227-33.
43. Heuser G., Mena I., Alamos F. 1994. NeuroSPECT findings in patients exposed to neurotoxic chemicals. Toxicology and Industrial Health 10: 561-71.
44. Jammes Y., DelPierre S., DelVolgo M.J., Humbert-Tena C., Burnet, H. 1998. Long-term exposure of adults to outdoor air pollution is associated with increased airway obstruction and higher prevalence of bronchial hyperresponsiveness. Archives of Environmental Health 53(6): 372-77.
45. Johansson A., Löwhagen O., Millqvist E., Bende M. 2002. Capsaicin inhalation test for identification of sensory hyperreactivity. Respiratory Medicine 96(9): 731-35.
46. Joffres M.R., Sampalli T., Fox R.A. 2005. Physiologic and symptomatic responses to low-level substances in individuals with and without chemical sensitivities; a randomized controlled blinded pilot booth study. Environmental Health Perspectives 113(9): 1178-83.
47. Kelly K.J., Prezant D.J. 2005. Bronchial hyperreactivity and other inhalation lung injuries in rescue/recovery workers after the world trade center collapse. Critical Care Medicine 33 (Suppl 1): S102-S106.
48. Kilburn K.H. 2003. Effects of hydrogen sulfide in neurobehavioral function. Southern Medical Journal 90(10): 997-1106.
49. Kilburn K.H. 1999. Measuring the effects of chemicals in the brain. Archives of Environmental Health 54(3): 150.
50. Koch F., Hughes J.M. 1998. Perioperative care of environmentally sensitive patients. AORN Journal 68(3): 375-82.
51. Lax M.B., Henneberger P.K. 1995. Patients with multiple chemical sensitivities in an occupational health clinic: presentation and follow-up. Archives of Environmental Health 50(6): 425-31.
52. Lieberman A.D., Craven M.R. 1998. Reactive Intestinal Dysfunction Syndrome (RIDS) caused by chemical exposures. Archives of Environmental Health 53(5): 354-58.
53. LoVecchio F., Fulton S.E. 2001. Ventricular fibrillation following inhalation of Glade Air Freshener. European Journal of Emergency Medicine 8(2): 153-54.
54. Mackness B., Durrington P.N., Mackness M.I. 2000. Low paraoxonase in Persian Gulf War Veterans self-reporting Gulf War Syndrome. Biochemical and Biophysical Research Communications 276(2): 729-33.
55. MacPhail R.C. 2001. Episodic exposures to chemicals: What relevance to chemical intolerance? Annals of the New York Academy of Sciences 933:103-11.
56. McKeown-Eyssen G., Baines C., Cole D.E.C., Riley N., Tyndale R.F., Marshall L, Jazmaji V. 2004. Case-control study of genotypes in multiple chemical sensitivity: CYP2D6, NAT1, NAT2, PON1, PON2 and MTHFR. International Journal of Epidemiology 33(5): 971-78.
57. Mckeown-Eyssen G.E., Baines C.J., Marshall L.M., Jazmaji V., Sokoloff E.R. 2001. Multiple chemical sensitivity: Discriminant validity of case definitions. Archives of Environmental Health 56(5): 406-12.
58. Meggs W.J., Cleveland C.H. Jr. 1993. Rhinolaryngoscopic examination of patients with the multiple chemical sensitivity syndrome. Archives of Environmental Health 48(1): 14-18. Meggs W.J., Dunn K.A.,
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60. Meggs W.J. 1993. Neurogenic inflammation and sensitivity to environmental chemicals. Environmental Health Perspectives 101(3): 234-38.
61. Meggs W.J. 1995. Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity. Environmental Health Perspectives 103: 54-56.
62. Meggs W.J. 1999. Mechanisms of allergy and chemical sensitivity. Toxicology and Industrial Health 15(3): 331-38.
63. Meggs W.J. 1997. Hypothesis for induction and propagation of chemical sensitivity based on biopsy studies. Environmental Health Perspectives 105 (Suppl 2): 473-78.
64. Meggs W.J. 1994. RADS and RUDS—the toxic induction of asthma and rhinitis. Clinical Toxicology 32(5): 487-501.
65. Meggs W.J. 1995. Multiple chemical sensitivities—chemical sensitivity as a symptom of airway inflammation. Journal of Toxicology. Clinical Toxicology 33(2): 107-10.
66. Miller C.S., Gammage R.B., Jankovic J.T. 1999. Exacerbation of chemical sensitivity: a case study. Toxicology and Industrial Health 15(3-4): 398-402.
67. Miller C., Ashford N., Doty R., Lamielle M. Otto D., Rahill A., Wallace L. 1997. Empirical approaches for the investigation of toxicant-induced loss of tolerance. Environmental Health Perspectives 102 (Suppl 2): 515-19.
68. Miller C.S. and Mitzel H.C. 1995. Chemical sensitivity attributed to pesticide exposure versus remodeling. Archives of Environmental Health 50(2): 119-29.
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Appendix: Related Articles

1. Anderson R.C. and Anderson J.H. 1997. Toxic effects of air freshener emissions. Archives of Environmental Health 52(6): 433-41.
2. Anderson R.C. and Anderson J.H. 1998. Acute toxic effects of fragrance products. Archives of Environmental Health 53(2): 138-46.
3. Anderson R.C. and Anderson J.H. 2000. Respiratory toxicity of fabric softener emissions. Journal of Toxicology and Environmental Health Part A 60(2): 121-36.
4. Anderson R.C. and Anderson J.H. 1999. Acute respiratory effects of diaper emissions. Archives of Environmental Health 54(5): 353-58.
5. Anderson R. and Anderson J. 2003. Acute toxicity of marking pen emissions. Journal of Toxicity and Environmental Health Part A 66(9): 829-45.
6. Anderson R.C., Anderson J.H. 2000. Respiratory toxicity of mattress emissions in mice. Archives of Environmental Health 55(1): 38-43.
7. Anderson R.C. and Anderson J.H. 1999. Respiratory toxicity in mice exposed to mattress covers. Archives of Environmental Health 54(3): 202-9.
8. Bridges B. 2002. Fragrance: emerging health and environmental concerns. Flavour and Fragrance Journal 17(5): 361-71.
9. Brown A.E. 1999. Developing a pesticide policy for individuals with multiple chemical sensitivity: considerations for institutions. Toxicology and Industrial Health 15(3/4): 432-37.
10. Cooper S.D., Raymer J.H., Pellizzari E.D., Thomas K.W. 1995. The identification of polar organic compounds found in consumer products and their toxicological properties. Journal of Exposure Analysis and Environmental Epidemiology 5(1): 57-75.
11. Destaillats H., Lunden M.M., Singer B.C., Coleman B.K., Hodgson A.T., Weschler C.J., Nazaroff W.W. 2006. Indoor secondary pollutants from household product emissions in the presence of ozone: a bench-scale chamber study. Environmental Science and Technology 40(14): 4421-28.
12. Duty S.M., Ackerman R.M., Calafat A.M., Hauser R. 2005. Personal care product use predicts urinary concentrations of some phthalate monoesters. Environmental Health Perspectives 113(11): 1530-35.
13. Muir T. and Zegarac M. 2001. Societal costs of exposure to toxic substances: economic and health costs of four case studies that are candidates for environmental causation. Environmental Health Perspectives 109 (Suppl 6): 885-903.
14. Steinemann A.C. 2009. Fragranced consumer products and undisclosed ingredients. Environmental Impact Assessment Review 29(1): 32-38.
15. Steinemann A. 2004. Human exposure, health hazards, and environmental regulations. Environmental Impact Assessment Review 24(7/8): 695-710.
16. Weschler C.J. 2009. Changes in indoor pollutants since the 1950s. Atmospheric Environment 43(1): 153-69.
17. Ziem G. 2005. Pesticide spraying and health effects. Environmental Health Perspectives 113(3): A150. (Letter to the editor)
18. Ziem G. 1999. Understanding patients with multiple chemical sensitivity. American Family Physician 59(8): 2101. (Letter to the editor)

Copyright:
Reprinted with personal permission. This document may not be republished in whole or part without the permission of Professor Anne C. Steinemann.

Searchable database shows pesticide residues still common

San Francisco, June 17, 2009 — Ever wonder about pesticides on your food? Or in your drinking water? In particular, which of those pesticides are most hazardous? A new tool from the nonprofit group Pesticide Action Network sheds new science-driven light on the invisible problem of pesticide residues.
 
Today’s launch of the What’s on My Food? database makes the results of government tests for pesticide residues in food available online in a searchable, easy-to-use format. The database shows what pesticides are found on each food, in what amount, and – for the first time – links those residues to the health effects associated with exposure to each of the chemicals.
 
“This kind of public visibility around pesticides is particularly needed in the U.S.,  since regulators base their decisions on toxicology studies that are almost all done by industry,” explains Dr. Brian Hill, Senior Scientist with Pesticide Action Network and the primary developer of the What’s on My Food? database. “Nearly 900 million pounds of pesticides are used in the U.S. every year, yet regulations depend on studies that are not peer-reviewed and are kept hidden behind the veil of ‘confidential business information.’” Hill notes that the 900 million figure is long overdue for updating, as the most recent pesticide use figures from the Environmental Protection Agency are for 2001.
 
In addition to highlighting the potential direct health effects of pesticide residues, the What’s on My Food? database points to the many problems associated with pesticide use before food reaches the kitchen table. Widespread use of agricultural chemicals threatens the health of workers and those in nearby communities and schools, as well as harming wildlife and contaminating ecosystems, according to the site.
 
“It’s time to shift away from reliance on these dangerous chemicals,” says Kathryn Gilje, Pesticide Action Network’s Executive Director. “In Europe governments have recognized that a healthy population and clean environment are worth more than short-term industry profits. They are moving toward safer and healthier ways to produce food, and we need to do the same.”
 
In the Take Action section of the site, Pesticide Action Network calls on consumers not only to vote with their dollars by choosing organic foods whenever possible, but also to become involved as “food citizens” demanding a clean, green and fair food production system.
 
Launch of the new database coincides with the release of Food, Inc., a film by the producers of An Inconvenient Truth that documents the dangerous health and environmental impacts of industrialized food production. Food reporter Michael Pollan calls Food, Inc. “the most important and powerful film about our food system in a generation.”
 

Reference: Pesticide Action Network North America, Searchable database shows pesticide residues still common, June 18, 2009

Resources:

• What’s On My Food? Database
• U.S. Department of Agriculture site re: food residue testing
• Food, Inc. “Hungry for Change” interactive cafeteria featuring WhatsOnMyFood? Database