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Children’s environmental healthNovember 9 2004
Don WigleInstitute of Population HealthUniversity of [email protected]
Outline
Environmental links to selected child health outcomes
• incident asthma, asthma episodes• neuropsychologic deficits among
school-age children at “low-level” lead exposure
• cancer– childhood cancer– adult cancers linked to childhood
exposures.
Level of epidemiologic evidence for causal relationships
Sufficient evidence - based on peer-reviewed reports of expert groups or authoritative reviews
Limited evidence - several epidemiologic studies, including at least one case-control or cohort study, showed fairly consistent associations and evidence of exposure-risk relationships after control for potential confounders
Inadequate evidence - epidemiologic studies limited in number and quality, inconsistent results, little or no evidence of exposure-risk relationships
Incident asthma
Sufficient evidence - house dust mite antigens
Limited evidence - ETS, cockroach antigen, outdoor air pollution (e.g., outdoor activities in high-ozone areas)
Inadequate evidence - pet allergens, endotoxins, fungi, pollen, VOCs, formaldehyde, pesticides
Main source: Institute of Medicine. Clearing the air. National Academy Press 2000
Asthma episodes
Sufficient evidence - ETS, cat, cockroach and house dust mite antigens, outdoor air pollution (e.g., personal NO2, ozone, PM10)
Limited evidence - dog antigens, indoor & outdoor molds, formaldehyde
Inadequate evidence - endotoxins, pollens, pesticides, VOCs, NO2, plasticizers
Main source: Institute of Medicine. Clearing the air. National Academy Press 2000
Neuropsychologic deficits in school-age children: low-level postnatal
lead exposure
Sufficient evidence - cognitive deficits, visual-motor integration deficits, attention deficits (? sufficient)
Limited evidence - fine motor function deficits, increased hearing threshold, central auditory processing deficits, problem behaviours (incl hyperactivity), academic achievement deficits
Childhood cancerSufficient evidence• a given radiation dose appears to double the excess
lifetime risk of fatal cancer for children compared to adults
• leukemia - prenatal x-ray pelvimetry (rel. high-dose)• thyroid cancer - incidence < 5 yr after Chernobyl
incident
Limited evidence• leukemia - parental and/or childhood pesticide
exposure, paternal smoking, childhood ionizing radiation (x-rays), nuclear testing fallout, EMF, paternal occupational exposure to solvents, paints and motor vehicle repair/related activities
• lymphomas - parental and/or childhood pesticide exposure, paternal smoking, parental occupational exposure to solvents and other petroleum products
Childhood cancer (limited evid, cont’d)
• brain - parental and/or childhood pesticide exposure, paternal smoking, paternal occupational exposure to paints
• Wilm’s tumour, Ewing’s sarcoma - parental occupational pesticide exposure
• neuroblastoma - parental occupational lead or pesticide exposure
Childhood cancer: inadequate evidence
• leukemia - lead, arsenic, indoor/outdoor air pollution (e.g. benzene), radon, RF radiation, chlorination disinfection by-products, paternal radiation exposure (ionizing, EMF)
• brain - radon, EMF, RF radiation, drinking water nitrate/nitrite, paternal exposure to EMF
Adult cancer: childhood exposures
Sufficient evidence• breast - atomic bomb survivors, fluoroscopy• brain, thyroid - radiotherapy of benign conditions• leukemia - atomic bomb survivors• melanoma - intense sun exposure
Limited evidence• thyroid - nuclear test radioactive fallout• lung - environmental tobacco smoke• stomach - H. pylori (waterborne infection)
Inadequate evidence• testicular - hormonally-active contaminants
To be ignorant of what happened before one was born is to remain ever a child
Cicero, 55 BC
Alice Hamilton (1869-1970)
- trained in medicine, pathology, bacteriology
- pioneer in industrial toxicology
- 1919 - first female professor at Harvard
May 20, 1925 meeting on TEL convened by US Treasury Dept
• Andrew Mellon, Treasury Secretary
– in charge of US Public Health Service
– major owner of Gulf Oil, holder of exclusive contract to distribute leaded gasoline in the southeastern USA
• Alice Hamilton stated that
– lead is a cumulative poison lacking obvious symptoms
– lead poisoning is a serious public health issue
December 1925: expert committee approved use of TEL
Lincoln, Nebraska, 1933
- test marketing of ethanol blends was common in the US Midwest
- failed due to the market dominance of oil companies
http://www.radford.edu/~wkovarik/papers/fuel.html
MMT (methylcyclopentadienyl manganese tricarbonyl)
– 1997: Canada bans MMT; Ethyl Corp sues Canada under NAFTA
– 1998: Canada apologizes to Ethyl, pays $13 million, reverses ban and states that MMT is not an environmental or health risk
MTBE (methyl tert-butyl ether)
– 1999: Calif announces MTBE phaseout starting in 2003; Vancouver-based Methanex Corp sues Calif for $970M under NAFTA
– 2002 - MTBE ban delayed until 2004
– 2003 - US Congress act states that no gasoline additive can be considered a "defective product”, virtually blocking lawsuits
Gasoline additives: the sequel
Evidence to action: role of scientists
• Identify important CEH knowledge gaps and seek research funding
• Support scientific organizations that advocate increased CEH research funding
• Educate the public on important research findings, knowledge gaps and their policy implications
Evidence to action: scientific barriers
Lack of consensus re epidemiologic evidence
• inadequate studies• unexplained inconsistencies between
well-conducted studies • unknown biologic mechanism• different perspectives of
multidisciplinary expert groups
Child health and the environment
Chapters
1. Child health and the environment
2. Environmental epidemiology
3. Risk assessment
4. Metals- lead
5. Metals- mercury, arsenic, cadmium, and manganese
6. PCBs, dioxins, and related compounds
7. Pesticides8. Hormonally active agents9. Radiation10. Indoor air11. Outdor air12. Water13. Conclusion
Oxford University Press 2003ISBN: 0-19-51355-98 http://www.mclaughlincentre.ca
Chapter structure
• Health effects - molecular mechanisms, prenatal outcomes, reproductive toxicity, neurotoxicity, cancer, other
• Exposure - internal dose (biomarkers), environmental contaminant levels, trends
• Risk management - major sources (air, water, food, dust/soil), standards/guidelines, uncertainties
• Conclusion - proven health outcomes, knowledge gaps, risk management issues
Reference, location
Design Exposure Results Associationa DRa Covariates
(Infante-Rivard et al. 1999), Montreal
Case-control study, 491 cases acute lymphoblastic leukemia (ALL), 491 controls, age < 10 yr; conducted PCR-RFLP and multiplex PCR to detect polymorphisms in CYP1A1, CYP2D6, GSTT1 and GSTM1 genes
Self-reported home use of pesticides in and around house during prenatal period (beginning 1 month before conception) and childhood; pesticides used likely included chlorpyrifos, diazinon, dichlorvos, malathion, cygon, propoxur, chlordane and 2,4-D
ALL associated with maternal prenatal use of herbicides in garden/yard or indoors (odds ratio, yes vs no); similar association for use during childhood
1.8 (CI 1.3-2.6)
Matched for age, sex, geographic region; adjusted for maternal age and education
Exposure-risk relationship between ALL and maternal prenatal use of herbicides indoors or in garden/yard (odds ratio, > 5 times vs 0)
3.7 (CI 0.7-19)
+ As above
ALL associated with maternal prenatal indoor use of plant insecticides (odds ratio, yes vs no); similar association for use during childhood
2.0 (CI 1.3-2.9)
As above
Exposure-risk relationship between ALL and maternal prenatal use of plant insecticides indoors or outdoors (odds
4.0 (CI 1.1-14)
+ As above
www.mclaughlincentre.ca