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Air Pollution from Household Fuel Use

Air Pollution from Household Fuel Use. Kirk R. Smith Professor of Global Environmental Health University of California, Berkeley. Expert Group. UC Berkeley: Kirk R. Smith, Heather Adair UC San Francisco: John Balmes Stanford: Sara Stern-Nezer Harvard: John McCracken, Joel Schwartz

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Air Pollution from Household Fuel Use

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  1. Air Pollution fromHousehold Fuel Use Kirk R. Smith Professor of Global Environmental Health University of California, Berkeley

  2. Expert Group • UC Berkeley: Kirk R. Smith, Heather Adair • UC San Francisco: John Balmes • Stanford: Sara Stern-Nezer • Harvard: John McCracken, Joel Schwartz • World Bank: Doug Barnes • Macro International: Vinod Mishra • Health Effects Institute: Sumi Mehta • NCI: Qing Lan • Liverpool University: Nigel Bruce, Dan Pope, Mukesh Dherani • WHO: Eva Rehfuess • Sri Ramakrishna University: Kalpana Balakrishnan • Peking University: Jinliang Zhang, Xiaoli Duan • Universidad Peruana de Ciencias Aplicadas: Claudio Lanata • Univ Maryland: Amir Sapkota

  3. Smith et al, CRA-2000

  4. Toxic Pollutants in Biomass Fuel Smokefrom Simple (poor) Combustion Source: Naeher et al, J Inhal Tox, 2007 • Small particles, CO, NO2 • Hydrocarbons • 25+ saturated hydrocarbons such as n-hexane • 40+ unsaturated hydrocarbons such as 1,3 butadiene • 28+ mono-aromatics such as benzene & styrene • 20+ polycyclic aromatics such as benzo()pyrene • Oxygenated organics • 20+ aldehydes including formaldehyde & acrolein • 25+ alcohols and acids such as methanol • 33+ phenols such as catechol & cresol • Many quinones such as hydroquinone • Semi-quinone-type and other radicals • Chlorinated organics such as methylene chloride and dioxin

  5. First person in human history to have her exposure measured doing one of the oldest tasks in human history Kheda District, Gujarat, India 1981

  6. Three Briefings • Progress in updating/expanding outcome assessments • Progress in updating/upgrading exposure assessments • Framing issues needing resolution

  7. Evidence for Outcomes • CRA-2000: ALRI in children, COPD, lung cancer from coal • Potential additions for CRA-2005 • Cataracts • Low birthweight • TB • Pneumonia in adults • Lung cancer from biomass • Upper aerodigestive cancers • Burns and scalds • Special case of heart disease

  8. CRA-2000 Outcomes • ALRI in children • New SR/MA published (Bruce et al., Bull WHO, 2008) • Guatemala RCT analyses completed • ITT and exposure-response analyses • COPD • New SR/MA completed and being prepared for publication • Lung cancer in coal • IARC review and monograph completed and in press • Formal MA underway (with biomass as well)

  9. *Number ofestimates available

  10. RESPIRE (Randomized Exposure Study of Pollution Indoors and Respiratory Effects) The plancha chimney wood stove, shown to reduce 48-hour kitchen PM2.5 by 80 - 90% Traditional open 3-stone fire: kitchen 48-hour PM2.5 levels of more than 1000 μg/m3

  11. RESPIRE Randomized Control Trial Guatemala Child Exposures

  12. MD-diagnosed ALRI RESPIRE- Guatemala Approximate Mean PM2.5 exposure in 100s of ug/m3

  13. SR/MA COPD Exclusion/Inclusion Criteria Population - individuals <15 years excluded, studies on non-human populations Exposure not indoor air pollution Outcome not defined as COPD using clinical or spirometrical definitions Effect measure not risk ratio; unable to combine with other studies (9 studies met inclusion criteria in final round of selection but could not be included in analysis) • 4,027 studies identified through Medline, Cochrane, DARE, LILAC, CINAHL and EMBASE for all studies published between 1950 and 2008 • Exclusion criteria applied in 3 rounds to those articles matching search terms • 28 articles published in peer-reviewed journals were selected for final inclusion in the analysis (22 cross-sectional, 2 cohorts, 4 case-control)

  14. Method - SRMA COPD (con’t) • Summary RR estimates calculated using both fixed effects and random effects models • Heterogeneity among studies assessed using general variance-based methods • Publication bias assessed using funnel plot, Eggers and Begg’s tests

  15. Forest Plot for all studies included in meta-analysis • Random effects model was used to account for significant heterogeneity between studies; 2=150.329, df=29 (p=0.000) • Overall effect measure for all studies 2.140 (1.777, 2.577)

  16. Subanalysis by fuel type Coal only • Studies vary significantly based on exposure assessment and design • Despite this variation, 19/28 studies included in final analysis showed an association between outcome and exposure that was statistically significant • Wood smoke was more strongly associated with COPD than coal, although confidence intervals for both effect estimates overlap 1.413 (1.180, 1.692) Wood only 2.276 (1.172, 4.419)

  17. Conclusions - IAP & COPD • Despite variation between studies, significant evidence exists to support an association between IAP and COPD • Many studies compare biomass fuels to “cleaner fuels”, such as LPG and paraffin but evidence exists that these fuels themselves may be associated with disease; thus the measured effect may underestimate the relationship between IAP and COPD • Presence or absence of ventilation is another factor which may account for heterogeneity across studies, but too few studies adjusted for ventilation to perform a subanalysis

  18. New Outcomes • TB: SR/MA done by others and three new case-control studies near finalized – combine? • LBW/SB: SR/MA completed • Cataracts: SR done and new exp-resp study in analysis • Adult pneumonia and upper aerodigestive cancers: SR/MAs underway • Burns and scalds: not yet determined how to include or whether they can be quantified

  19. IAP & TB Biological Mechanism • Smoke/particles generates inflammatory response- impairs the function of normal clearance of secretions on the tracheobronchial mucosal surface • This may allow TB bacteria to escape the first level of host defenses, which prevent bacilli from reaching the alveoli • Smoke also impairs the antibacterial properties of alveolar macrophages- such as ability to phagocytize bacteria and intracellular bactericidal processes • Alveolar macrophages isolated from the lungs of smokers have reduced phagocytoticability and secrete a lower level of pro-inflammatory cytokines

  20. Ex-smokers Current smokers Ever- smokers Ref: Bates et al. Arch Intern Med. 2007;167:335-342 21

  21. Association between solid fuel use relative to cleaner burning fuel or electricity and risk of Tuberculosis

  22. TB and Solid Fuel: Case Control Study (Results from Pokhara, Nepal)

  23. IAP &Cataract Mechanism The incomplete combustion of biomass fuels produces naphthalene. Naphthalene's intermediate, 1,2 napthaquinone, is a reactive species capable of producing reactive oxygen species (ROS) ROS produce superoxides (O2- ) who stimulate the production of H2O2 and OH- radicals and induce oxygen toxicity and oxidative reactions To reduce the damaging effect of ROS, different enzymes, vitamin E, vitamin C and NADPH are consumed The lack of NADPH, imbalances the ratio of protective enzymes and metabolites needed to maintain the supply of antioxidants available to protect the eye Some of the resulting oxidative damage within the eye includes: Lipid damage Protein aggregation thru cross-linking Hyperplasia, hypertrophy and multi-layering of epithelial cells Len discoloration & opacity All of the cellular damage listed above, and reduction of antioxidants for cell protection can lead to the formation of cataracts. Nuclear Cataract

  24. Association between solid fuel (SF)) use relative to cleaner burning fuel or electricity and risk of cataracts

  25. Biological Plausibility Role of Carbon Monoxide (CO) --Biomass combustion similar to tobacco smoke (COHb 2.5-13%; covering range for passive to heavy active smoking). Boy et al. 2002. --CO crosses placental barrier (haemoglobin in fetal blood has 10x more affinity for binding CO than for adults). Ritz et al. 1999. --Fetal elimination of CO slower than in the mother. Hill et al. 1977. Animal studies: --Retarded fetal growth from cigarette smoke (inc. CO). Bosley et al. 1981. --Inhaled CO in pregnant rabbits (90ppm) reduced birth weight by 11%. Astrup et al. 1972.

  26. Biological Plausibility Role of particulate matter (PM) Maternal PM exposure associated with decreased efficiency of transplacental function (restricted fetal development). Gliniania et al. 2004. Transplacental transfer of polyaromatic hydrocarbons (PAH) of ETS from mother to fetus. Perera et al. 1999. Increased PHA-DNA adduct levels from exposure to PAH from ambient air pollution (increase the potential for genetic fetal damage) reported in maternal and newborn white blood cells. Perera et al. 1999.

  27. Systematic review and meta-analyses of risk of low birth weight and stillbirth associated with indoor air pollution in developing countries Pope DP, Mishra V, Thompson L, Siddiqui AR, Rehfuess E, Weber M, Woodruff T, Bruce, NG

  28. Inclusion criteria Outcomes (1) Low birth weight (<2500g) or mean birth weight (2) Stillbirth or perinatal/ early neonatal deaths (first 7 days) Exposure: Direct/ indirect measurement of IAP exposure from solid fuel use

  29. 982 papers identified and screened by titles 953 papers excluded - not relevant 22 papers excluded outdoor pollution, not low birth weight 29 papers screened by abstract 7 papers reviewed 3 papers excluded outdoor pollution, tobacco smoke, not low birth weight 4 papers selected for inclusion 1 unpublished study selected for inclusion 5 studies included in the review Indoor air pollution and birth weight

  30. 171 papers identified and screened by titles 159 papers excluded - not relevant 9 papers excluded outdoor pollution, not stillbirth 12 papers screened by abstract 3 papers reviewed 1 papers excluded neonatal mortality 2 papers selected for inclusion 1 unpublished study selected for inclusion 3 studies included in the review Indoor air pollution and stillbirth

  31. Effect on low birth weight (odds ratio) of exposure to IAP from solid fuel use compared to cleaner fuels, or users of improved chimney stoves

  32. Details of studies for IAP and birth weight review Covariates: GA = Gestational age

  33. Details of studies for IAP and stillbirth review

  34. FUNNEL PLOT – ASSESSMENTOF PUBLICATION BIAS Effect on low birth weight of exposure to IAP from solid fuel use compared to cleaner fuels, or users of improved chimney stoves (Begg’s and Eggar’s tests NS – no evidence)

  35. Effect on mean birth weight (in gm.) of exposure to IAP from solid fuel use compared to cleaner fuels, or users of improved chimney stoves

  36. Effect on stillbirth (odds ratio) of exposure to IAP from solid fuel use compared to cleaner fuels

  37. Summary of pooled effects 1Sensitivity analysis excludes one study based on methodological quality 2Sensitivity analysis excludes one estimate using mother’s recall of birth weight

  38. Environmental Tobacco Smoke and birth weight Source: Leonardi-Bee et al. 2008

  39. Ambient Air Pollution and % LBW *Total Suspended Particles (TSP)

  40. [go to Exposure Slides]

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