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Air Quality in Alaska Asthma Studies

Air Quality in Alaska Asthma Studies. Mary Ellen Gordian, MD, MPH Institute for Circumpolar Health Studies. Ambient (Outdoors) Dust from roadways Exhaust from combustion engines including diesel. Pollen Dust and fumes from landfills and sewage lagoons. Indoor Air Smoking

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Air Quality in Alaska Asthma Studies

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  1. Air Quality in AlaskaAsthma Studies Mary Ellen Gordian, MD, MPH Institute for Circumpolar Health Studies

  2. Ambient (Outdoors) Dust from roadways Exhaust from combustion engines including diesel. Pollen Dust and fumes from landfills and sewage lagoons Indoor Air Smoking Storage of chemicals or gasoline Combustion heaters (diesel?) People and animals Cooking Types of Air Pollution

  3. How Arctic Conditions Relate to Air Pollution • Low temperatures increase incomplete combustion products. • Temperature inversions prevent air mixing. • Development increases traffic. • Energy efficient homes trap pollutants.

  4. Why are we concerned? • 90- 95% of our time is spent indoors. • Our homes are built air tight. • Indoor smoking causes fumes and particles. • Our gasoline contains 3-5% benzene. • Gasoline storage in house or in attached garage causes fumes throughout the house. • Furnaces in the garage can distribute air pollutants throughout the house.

  5. Respiratory Health of Children1997 survey of Alaska Native children grades 6-9 in YK Delta • 24% have asthma or asthma symptoms • 37% have chronic cough with sputum • 39% have no respiratory symptoms

  6. Anchorage indoor air benzene study, 1996 • Arithmetic mean 16 ppb of benzene. • 25% of homes about the mean. • Highest reading 344 ppb of benzene. • Alaskan children are exposed to benzene in their homes, automobiles and ambient air

  7. Indoor Pollutants • Carbon monoxide- from unventilated combustion. • Particulates from indoor smoking and wood stoves. • Biologicals –dust mites, animal dander germs • Benzene- evaporates from stored gasoline

  8. Carbon Monoxide (CO)A deadly killer indoors • Colorless, odorless. • Easily absorbed through the lungs • Forms carboxyhemoglobin in the blood • CO bonds with hemoglobin 240X stronger than oxygen’s bond with hemoglobin

  9. Normal Carboxyhemoglobin levels in humans • endogenous carboxyhemoglobin is 0.3-0.7% • smoker’s carboxyhemoglobin 0.8 -8.0% • after 8 hours continuous exposure to CO at 35ppm (workplace maximum), carboxyhemoglobin = 5% • the biological half-life of carboxyhemoglobin in human blood is 2 to 5 hours depending on respiratory rate.

  10. Health Effects of CO at different levels of Carboxyhemoglobin • Below 5% COHb no symptoms in healthy people. • If mother during pregnancy has COHb >0.7% oxygen to the baby is reduced-increasing risk. • Greater than 2.9% COHb increased angina with exertion in patients with heart disease. • Studies show hospitalization of elderly patients with heart disease increases when ambient CO increases.

  11. Particulate Pollution • Measured as PM10 or PM 2.5 • Volcanic ash and freeze-dried soil (PM10) • Re-suspended from roadways by traffic. • Combustion sources (PM2.5) • Diesel exhaust • coal • wood burning.

  12. What is Asthma? Asthma is a chronic respiratory disease characterized by: • eosinophilic inflammation of the airways; • bronchial hyper-responsiveness to stimuli.

  13. Different Types of Asthma • Allergic asthma is associated with allergy as much as 80% of childhood asthma is related to allergy. • Intrinsic asthma is not associated with allergy. • Post-infective asthma occurs after a lower respiratory infection. Frequently clears by age 5.

  14. Humoral T-helper 1 cells Immunoglobulin response- IgM, IgG Cytokine response- IFN-gamma Cell-mediated T-helper 2 cells Immunoglobulin response- IgE Cytokine response-IL4, IL5, IL 13 Immune Responses

  15. Tolerogenic Immune Response To survive in an environment full of foreign protein antigens, animals developed a method of response that minimized the energy needed to encounter non-infectious protein. Recognition and minimal response- IgA, Cytokine IL-10.

  16. Known Risk Factors for Asthma • Family history – genetic predisposition • Environmental tobacco smoke • Combination of family history and environmental tobacco smoke exposure is additive.

  17. Allergens associated with Asthma • Dust mite allergy has been associated with asthma. • Cockroach allergen are common in inner city children, associated with asthma. • Molds have been implicated. • Animal allergens (cat is ubiquitous) • Children with allergy have increased risk of asthma.

  18. World Wide Increase in Asthma • Multi-center surveys show that asthma is increasing worldwide. • Greatest increases in “westernized” English-speaking countries. • Urban areas have more asthma cases than rural areas. • Increase in both children and adults.

  19. Asthma Increasing Australia Costa Rica New Zealand Oman Peru Singapore United Kingdom United States No Asthma Increase Albania Estonia Indonesia Latvia Uzbekistan Asthma Rates

  20. What is Causing the Increase? • Dietary Hypothesis Changes in diet result in increased susceptibility to allergic response. • Hygiene Hypothesis Increased cleanliness reduces level of endotoxin which changes the immune system • Adjuvant Hypothesis Exposure to petroleum exhaust fumes changes the immune system

  21. Concerns for Dietary Hypothesis • Reduction in locally grown food. • Increases in chemically treated food. • Salt intake is increased. • Omega 3 fatty acids reduce allergic response in animals. • Early intake of cow’s milk protein or soy protein may increase risk of allergy.

  22. Hygiene Hypothesis Environmental exposure to endotoxin has a crucial role in developing tolerance to natural allergens

  23. Hygiene Hypothesis • Children living on farms have less risk of allergy and asthma. • Children in daycare have decreased risk. • Children with older siblings less risk. • Children with animal pets have less risk. • Increased amount of endotoxin exposure in farm homes, and homes with dogs

  24. The Icon of Westernization What is westernization? Individualization Independence Initiative and your own car!

  25. Adjuvant Theory The exposure to traffic results in changes in the immune system promoting cell-mediated Th2 immunity characterized by inflammation. There is direct experimental evidence for this.

  26. Evidence for Adjuvant Theory • Children living near to freeways in Holland have greater symptoms, reduced FEV1. • Children hospitalized for asthma live near high traffic areas as compared to children hospitalized for GI problems in U.K. • Children living near traffic have more cough in Japan.

  27. Laboratory Evidence • People experimentally exposed to diesel exhaust (DE) have 16 x greater response to ragweed allergen than people not exposed. • People exposed to DE make IgE to new antigen exposure, while people not exposed make IgA, IgG, but not IgE.

  28. What are we doing in Alaska? • Survey of Anchorage parents of children in kindergarten and first grade in 13 schools regarding asthma diagnoses, symptoms, demographics, home environment and family history. • Over 1100 surveys received. Minorities well represented. All socioeconomic classes represented. Geographically distributed.

  29. Study Design • 13 schools representing a range of traffic exposure and socioeconomic demographics • All kindergarten and first-grade students received surveys at registration, or in the classroom. (50-85% response rate) • Traffic data collected from state • Traffic measured on roads with no data.

  30. Traffic Variables • Nearest intersection to home is located on map. • Two buffer zones 100 meters and 300 meters around intersection is drawn and the length of each road falling within buffer is measured. • The length within the buffer is multiplied by the average daily traffic on that road in that segment.

  31. Some Unexpected Findings • A great many children do not live in the neighborhood school boundaries. • Children diagnosed with asthma have an increased number of respiratory illnesses. • There is variation in asthma rates between schools, highest 20%, lowest 6%.

  32. Table 1 Unadjusted results of 100 meter exposure Unadjusted (n=1043) OR (95% CI) * p-value † Traffic Exposure 0.210 Low Referent Medium 1.03 (0.65, 1.63) High 1.85 (0.96, 3.50)   *Maximum likelihood estimates and Wald-based 95% Confidence intervals for logistic regression models. †p-values are based on likelihood ratio tests for the inclusion of the entire factor.

  33. Table 2 Adjusted for Parental Asthma, Smoking, gender, income 100-meter Buffer300-meter Buffer Adjusted (n=927) Adjusted (n=927) OR (95% CI) * p-value † OR (95% CI) * p-value † Traffic Exposure 0.068 0.024 Low Referent Referent Medium 1.06 (0.64, 1.77) 1.37 (0.85,2.23) High 2.38 (1.19, 4.76) 2.74 (1.35, 5.56) *Maximum likelihood estimates and Wald-based 95% Confidence intervals for logistic regression models. †p-values are based on likelihood ratio tests for the inclusion of the entire factor.

  34. 100-meter Buffer300-meter Buffer OR (95% CI) * p-value † OR (95% CI) * p-value Gender 0.351 0.338 Male Referent Referent Female 0.81 (0.53, 1.25) 0.81 (0.52, 1.25) Parental Asthma <0.001 <0.001 No Referent Referent Yes 4.27 (2.74, 6.65) 4.30 (2.75, 6.72) Smoker in Home 0.203 0.177 No Referent Referent Yes 1.34 (0.86, 2.10) 1.37 (0.87, 2.15) Income 0.183 0.256 <$20K Referent Referent $20-49K 0.72 (0.43, 1.21) 0.76 (0.45, 1.28) $50-100K 0.49 (0.26, 0.93) 0.52 (0.27, 1.01) >$100K 0.81 (0.33, 1.94) 0.89 (0.37, 2.17)

  35. Conclusions • Exposure to traffic is a risk factor for childhood asthma. • The effect size of high traffic volume in a 100 meter radius of home is as great or greater than having a smoker in the house. • Residential housing and schools should be buffered from high traffic areas.

  36. Summary • Outdoor air pollution from combustion and traffic causes more problems in the Arctic because of temperature inversions. • Indoor air pollution is contributing to respiratory disease in Arctic homes. • Asthma may be affected by growing up close to traffic.

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