Transcript How Green and How Clean? Environmental

Pediatric Environmental Health
Evidence and Public Policy
February 4, 2009
Hartford, CT
Joel Forman, MD
Associate Professor of Pediatrics and
Community and Preventive Medicine
Mount Sinai School of Medicine
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
Patterns of Disease in Children
Have Changed
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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
Septicemia
1911
Inpatient Record Rhode Island Hospital
Providence, 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
–
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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
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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 been
tested for toxicity
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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
Asthma lifetime diagnosis
140
Prevalence per 1,000 children
120
Current asthma prevalence
100
80
Asthma prevalence (4.3% per yr )
60
Asthma attack prevalence
40
20
0
1980
1985
1990
1995
2000
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
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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
US Dept. of Ed. Office of Special Education Programs (OSEP) data
Prevalence (cases per 10,000
population) of OHI among US
children according to age and
birth cohort
MR Prevalence
Newschaffer, Pediatrics 2005
US Dept. of Ed. Office of Special Education Programs (OSEP) data
Prevalence (cases per 10,000
population) of MR among US
children according to age and
birth cohort
Environmental Contributors to
Developmental Disabilities
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Lead
Mercury
PCBs
Pesticides
Synergistic Effects of Mental Health Effects
– Depression, Family Disruption, Social
Disorganization
– Disproportionate impact on poor children
Lead
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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
Obesity Trends* Among U.S. Adults
BRFSS, 1990, 1998, 2007
(*BMI 30, or about 30 lbs. overweight for 5’4” person)
1998
1990
2007
No Data
<10%
10%–14%
15%–19%
20%–24%
25%–29%
≥30%
Overweight and Obesity
• 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
Environmental Factors
• Risk of hypertension, gall
•Lifestyle (diet, exercise)
bladder disease, and some
•Built Environment
•Endocrine Disrupters
cancers
(BPA)?
Source: Willet et al., New Eng J Med, 1999
Bisphenol A (BPA)
BPA Exposures are Widespread
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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 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
Estimated Mean Bisphenol A (BPA) Concentrations in Relation to
Reported Diseases and Conditions
Lang, I. A. et al. JAMA 2008;300:1303-1310.
Copyright restrictions may apply.
Endocrine Disruptors
Endocrine Disruptors
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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
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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)
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)
Friedman, M. S. et al. JAMA 2001;285:897-905.
Acute Asthma Events During
1996 Olympics - Atlanta
% 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%
Type of claim
Reduction in Pesticide Exposure
after EPA Ban on Chlorpyrifos
Maternal and Umbilical Blood
Levels of Chlorpyrifos decreased
10 fold after the EPA Ban
Whyatt et al. EHP 2003
PBDEs and Breast Milk:
Effectiveness of regulation
•(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
North America
Sweden
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:
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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
The National Children’s Study
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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’
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What Can We Do Now
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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
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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