1. Pediatric Environmental Health Evidence and Public Policy Joel Forman, MD Associate Professor of Pediatrics and Community and Preventive Medicine Mount Sinai School of Medicine February 4, 2009 Hartford, CT

2. With Gratitude Philip Landrigan, M.D. M.Sc. Ethel H. Wise Professor and Chair Department of Community and Preventive Medicine Professor of Pediatrics Mount Sinai School of Medicine Maida Galvez, M.D., M.P.H. Assistant Professor Department of Community and Preventive Medicine Director, Mount Sinai Pediatric Environmental Health Specialty Unit

3. Patterns of Disease in Children Have Changed As nations move toward industrial development, patterns of disease and death change. Prior to industrial development, infectious diseases were the major causes of illness and death MUCH OF AFRICA, LATIN AMERICA AND ASIA TODAY After development, life expectancy increases and chronic diseases become the major causes of illness and death USA AND WESTERN EUROPE TODAY

4. Patterns of Disease in New York City

5. Dying of Infectious Disease Streptococcus Septicemia 1911 Inpatient Record Rhode Island Hospital Providence, RI

6. The New Pediatric Morbidity A range of chronic disabling and sometimes life threatening conditions of complex and poorly defined origins that affect increasing numbers of American children today –Asthma –Obesity –Endocrine and Sexual Development Disorders –Cancer –Neurodevelopmental Disorders (e.g. Autism and ADHD) Increasing Evidence of Environmental Contribution

7. Unique Vulnerabilities of Children  Children consume more food, drink more water, and breath faster than adults  Children have unique behaviors, diets, and are closer to the ground  Children have immature metabolic pathways  Young children have unique windows of vulnerability – particularly in neurodevelopment  Children have a very long ‘shelf life’

8. Most chemicals to which children are exposed have not been tested for toxicity 80,000 + chemicals in commerce Approximately 3,000 produced in quantities of 1 million pounds or more per year (high production volume [HPV] chemicals) No basic toxicity information is publicly available for about half of HPV chemicals Information on developmental toxicity is publicly available for fewer than 20% of HPV chemicals --EPA: Chemical Hazard Data Availability Study, 1998

9. Improving Measures of Biologic Exposure (Biomonitoring) CDC’s 3 rd National Report on Human Exposure to Environmental Chemicals (http://www.cdc.gov/exposurereport/) –148 environmental chemicals –Noninstitutionalized, civilian U.S. population –2-year period 2001 - 2002 –Chemicals and their metabolites measured in blood and urine –Sample of NHANES

10. Permethrin Exposure Higher in Children Third Report on Environmental Exposure to Chemicals - CDC 2005

11. Chlorpyrifos exposure higher in Children Third Report on Environmental Exposure to Chemicals - CDC 2005

12. Asthma

13. Asthma prevalence, 1980-96, asthma lifetime diagnosis, current and asthma attack prevalence, 1997-2002: NHIS, children 0-17 years Asthma prevalence (4.3% per yr  ) Asthma lifetime diagnosis Asthma attack prevalence Current asthma prevalence

14. Asthma – Indoor/Outdoor Air Pollutants – Scientific Evidence Asthma Development Asthma Exacerbation House dust miteIncreased SHSIncreased cockroachMaybe IncreasedIncreased catMaybe IncreasedIncreased dogMaybe IncreasedProbably Increased Molds?Probably Increased VOCs?Probably Increased Nitrogen oxides?Probably Increased OzoneMaybe Increased*Probably Increased Particulates?Probably Increased Sulfur Dioxide?Probably Increased IOM Report 2000

15. Green Cleaning Cleaning to protect health without harming the environment Non-chemical products or less toxic products Can be just as effective and cost neutral For example: low VOC products can protect asthmatics from exacerbations

16. Developmental Disorders

17. The Prevalence of ASDs: Rising? Studies in the US prior to 1985 –2 per 10,000 for classic autism –4 to 5 per 10,000 for ASDs Analysis of 1992 -1994 NHANES data (Halfon et al, J AM Acad Child Adol Psychiatry. 1999;38:600-609) –3.8 per 10,000 for classic autism UK 2000 data (Chakrarbartiet al, JAMA 2001;285, 3093-3099) –16.8 per 10,000 for classic autism –62.6 per 10,000 for ASDs

18. Prevalence of ASDs cont. CDC study of autism in Brick Township, NJ in 1998 –Prompted by community concern about too many cases of ASDs and possible environmental causes –40 per 10,000 for classic autism –67 per 10,000 for ASDs Is this a cluster or a reflection of the true US prevalence rate?

19. Prevalence of ASDs cont. Metropolitan Atlanta Developmental Disabilities Surveillance Program Data (Yeargin- Alsop et al, JAMA. 2003;289:49-55) –Largest study to date in US –Prevalence of 34 per 10,000 for ASDs Likely an underestimate –Higher functioning children more likely to be missed –Low sensitivity for case identification in younger kids

20. Is the Rise in ASDs Real? Problems comparing new data with historical prevalence rates –Broadening definition from classic autism to ASDs –Varying case finding methodologies –Prevalence not Incidence data It is unlikely that this question can be definitively answered without prospective registries and cohort studies

21. Autism Prevalence Newschaffer, Pediatrics 2005 US Dept. of Ed. Office of Special Education Programs (OSEP) data Prevalence (cases per 10,000 population) of Autism among US children according to age and birth cohort

22. Other Health Impairment (e.g. ADHD) Prevalence Newschaffer, Pediatrics 2005 Prevalence (cases per 10,000 population) of OHI among US children according to age and birth cohort US Dept. of Ed. Office of Special Education Programs (OSEP) data

23. MR Prevalence Newschaffer, Pediatrics 2005 Prevalence (cases per 10,000 population) of MR among US children according to age and birth cohort US Dept. of Ed. Office of Special Education Programs (OSEP) data

24. Environmental Contributors to Developmental Disabilities Lead Mercury PCBs Pesticides Synergistic Effects of Mental Health Effects –Depression, Family Disruption, Social Disorganization –Disproportionate impact on poor children

25. Lead Principal source was Leaded Gasoline Currently, the principal source is lead paint and lead paint dust Other sources – toys, imported dinnerware Causes decreased IQ, shortened attention span, inability to concentrate, dyslexia and school failure Any amount of lead is dangerous – No level is safe

26. ADHD, SHS, and Lead Exposures to Environmental Toxicants and Attention Deficit Hyperactivity Disorder in US Children (Braun et al EHP 2006) Cross-sectional analysis of NHANES data Prenatal tobacco smoke exposure and BLL > 2 associated with ADHD –SHS attributable US cases 270,000 –Lead attributable US cases 290,000

27. Obesity

28. 1998 Obesity Trends* Among U.S. Adults BRFSS, 1990, 1998, 2007 (*BMI 30, or about 30 lbs. overweight for 5’4” person) 2007 1990 No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

29. Overweight and Obesity Source: Willet et al., New Eng J Med, 1999 Prevalence has nearly quadrupled in American children 2.5-fold increased risk of overall mortality 4-fold risk of cardiovascular mortality 5-fold risk of diabetes Risk of hypertension, gall bladder disease, and some cancers Environmental Factors Lifestyle (diet, exercise) Built Environment Endocrine Disrupters (BPA)?

30. Bisphenol A (BPA)

31. BPA Exposures are Widespread NHANES 2003-2004 (Calafat et al. EHP 2008) –US population ages 6-85 years (n=2517) –BPA present in 93% of population –Children 6-11 years (n=217) geometric mean BPA=4.3 ug/gram creatinine children >6 years old (p < 0.001) and adolescents (p < 0.003) had higher levels than adults

32. Adverse Effects in Lab Animals Even brief exposure to low levels of environmental estrogens early in life increases body weight as mice age. Newbold RR et al, Birth Defects Research 2005

33. Copyright restrictions may apply. Lang, I. A. et al. JAMA 2008;300:1303-1310. Estimated Mean Bisphenol A (BPA) Concentrations in Relation to Reported Diseases and Conditions

34. Endocrine Disruptors

35. Animal Data –DDT - Eagles –Phthalates - Hyperactivity in Rats –Bisphenol A - early female mice puberty DES - Clear cell Ca of Vagina/Cervix Dioxins + PCBs –Urogenital Anomalies –Intellectual impairment Pesticide exposure and low sperm count

36. Hypospadias Paulozzi et al, EHP Volume 107, Number 4, April 1999

37. Cancer

38. Environmental Contributors to Pediatric Cancer Ionizing Radiation Benzene Asbestos Certain Pesticides PCBs

39. SEER Delay-Adjusted Incidence and US Mortality All Childhood Cancers, Under 20 Years of Age Both Sexes, All Races, 1975-2005

40. Public Health Policy Evidence Based Interventions Can Work

41. Blood Lead Levels and Leaded Gasoline (EPA data)

42. Friedman, M. S. et al. JAMA 2001;285:897-905. Mean Levels of Major Pollutants Before, During, and After the 1996 Summer Olympic Games as a Percentage of the National Ambient Air Quality Standard (NAAQS)

43. Acute Asthma Events During 1996 Olympics - Atlanta Type of claim % change in mean # of Asthma claims per day % change in mean # of Non-Asthma claims per day Medicaid Hosp and ED Visits - 41.6%- 3.1% HMO ED, Urgent Visit, Hosp - 44.1%+ 1.3%

44. Reduction in Pesticide Exposure after EPA Ban on Chlorpyrifos Whyatt et al. EHP 2003 Maternal and Umbilical Blood Levels of Chlorpyrifos decreased 10 fold after the EPA Ban

45. PBDEs and Breast Milk: Effectiveness of regulation North America Sweden (In the United States, no federal regulatory action has been taken to ban or restrict PBDEs) In Sweden PBDE phase-out began in 1990 and accelerated in the end of the decade

46. Towards More Informed Decisions Getting Better Scientific Data for Policy Formulation

47. Case Study in Research : Rates of Heart Disease, Stroke and Lung Cancer Exploded after World War II To find out why, US public health authorities launched the Framingham Heart Study, a prospective epidemiological investigation to identify risk factors

48. The Framingham Heart Study Identified the major risk factors for lung cancer and cardiovascular disease: Cigarette smoking High cholesterol Hypertension Sedentary life style Diabetes The Result: Development of a blueprint for prevention that produced a massive (>50%) reduction in CVD incidence and mortality and parallel declines in cancer

50. The National Children’s Study A multi-year prospective epidemiological study that will follow 100,000 children from early in pregnancy to 18 years of age The Goals: 1. To discover the environmental exposures that cause disease and disability in childhood and throughout life 2. To translate this science into a roadmap for prevention Powerful Data Can Drive Public Health Policy

52. Where We Are Now New Diseases Increasing Children More Vulnerable Children Have Greater Exposure – Documented Evidence of Toxicity (Lab, Animal, High Dose Human Exposure) Epidemiologic Evidence of Association between Exposures and the ‘New Pediatric Morbidity’

53. What Can We Do Now Apply the Precautionary Principle as a philosophic approach to exposure prevention –Reduce exposures to known and suspected environmental toxins whenever possible –Integrated Pest Management (IPM) –Green Cleaning –Organic foods and produce –Choose foods low in PCBs and Mercury –Reduce exposures to SHS –Remove lead from children’s environments (Paint, Toys, Jewelry, etc.)

54. Where To Go From Here Support Public Policies that Reduce Children’s Exposures to Environmental Toxins and that Require Testing of Chemicals and Children’s Products for Safety Before Marketing Advocate for prospective registries of developmental disorders on large scales to define incidence rates and track prevalence Continue to expand population based cross-sectional biomonitoring (CDC Report) Carry out prospective cohort studies large enough to evaluate the relationship between our children’s multiple exposures and the development of developmental disorders

55. Thank You