Pediatric Environmental HealthEvidence and Public Policy

Joel Forman, MDAssociate Professor of Pediatrics and Community and Preventive MedicineMount Sinai School of Medicine

February 4, 2009Hartford, CT

With Gratitude

Philip Landrigan, M.D. M.Sc.Ethel H. Wise Professor and Chair Department of Community and Preventive MedicineProfessor of PediatricsMount Sinai School of Medicine

Maida Galvez, M.D., M.P.H.Assistant ProfessorDepartment of Community and Preventive MedicineDirector, Mount Sinai Pediatric Environmental Health Specialty Unit

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

Patterns of Disease in New York City

Dying of Infectious Disease

Streptococcus Septicemia1911

Inpatient Record Rhode Island HospitalProvidence, RI

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

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’

Most chemicals to which children are exposed have not beentested 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

Improving Measures of Biologic Exposure (Biomonitoring) CDC’s 3rd 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

Permethrin Exposure Higher in Children

Third Report on Environmental Exposure to Chemicals - CDC 2005

Chlorpyrifos exposure higher in Children

Third Report on Environmental Exposure to Chemicals - CDC 2005

Asthma

Asthma prevalence, 1980-96, asthma lifetime diagnosis, current and asthma attack prevalence, 1997-2002: NHIS, children 0-17 years

0

20

40

60

80

100

120

140

1980 1985 1990 1995 2000

Pre

vale

nce

per 1

,000

chi

ldre

n

Asthma prevalence (4.3% per yr )

Asthma lifetime diagnosis

Asthma attack prevalence

Current asthma prevalence

Asthma – Indoor/Outdoor Air Pollutants – Scientific Evidence

Asthma Development

Asthma Exacerbation

House dust mite Increased Increased

SHS Increased Increased

cockroach Maybe Increased Increased

cat Maybe Increased Increased

dog Maybe Increased Probably Increased

Molds ? Probably Increased

VOCs ? Probably Increased

Nitrogen oxides ? Probably Increased

Ozone Maybe Increased* Probably Increased

Particulates ? Probably Increased

Sulfur Dioxide ? Probably Increased

IOM Report 2000

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

Developmental Disorders

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

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?

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

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

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

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

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

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

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

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

Obesity

1998

Obesity Trends* Among U.S. AdultsBRFSS, 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%

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)?

Bisphenol A (BPA)

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

Adverse Effects in Lab AnimalsEven 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

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

Endocrine Disruptors

Endocrine Disruptors

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

Hypospadias

Paulozzi et al, EHP Volume 107, Number 4, April 1999

Cancer

Environmental Contributors to Pediatric Cancer

Ionizing Radiation Benzene Asbestos Certain Pesticides PCBs

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

Public Health Policy

Evidence Based Interventions Can Work

Blood Lead Levels and Leaded Gasoline (EPA data)

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)

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%

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

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

Towards More Informed Decisions

Getting Better Scientific Data for Policy Formulation

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

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 CVDincidence and mortality and parallel declines in cancer

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

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’

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.)

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

Thank You