# Woodsmoke **and Human Health** 

**Ryan W. Allen, PhD** Associate Professor Faculty of Health Sciences Simon Fraser University Burnaby, BC, Canada allenr@sfu.ca National Educational Forum on the Residential Wood Heater NSPS November 8, 2012 Minneapolis, MN

# Presentation **Overview**

 

## What are the exposure/public **health impacts**  **of woodsmoke**  **?**  

## At what levels **and duration of time are**  **there health impacts?** 

 

## Some general comments on air pollution and health  

## How does woodsmok e dif fe r from pollution generated by other sources?  

## Wo odsmok

e and health  

### What do we know? What don’ t we know?  

### Emphasis from studies in developed countries  

### Ra nge of health effects and exposure - effect time scales

# Air **Pollution Epidemiology**  **Requires an**  **Exposure Gradient**

 

### Te mporal or spatial (or both)  

### Te mporal gradients  Hours to days  Provide information on “acute” effects of air pollution  Example: On days with more air pollution, more people die (“triggering”)  

### Spatial gradients  M to 1000s of KM  Provide information on “chronic” effects of air pollution  Example: People living in more polluted areas of a city die younger than those in less polluted areas (underlying disease?)

# Air **Pollution and Health** 

 

### Air pollution influences a wide ra nge of health outcomes and severities  

### Historical f

ocus on respiratory effects  Now also strong evidence of **cardiovascular** effects  Growing evidence of other impacts (e.g. birth effects)  

### Individual risks are small, but man y are exposed, so population impacts can be substantial  Example: air pollution vs. smoking

# How is Woodsmoke **Different?**

emitted ma ss inhaled ma ss fraction intake inhalation 

Reis, Brauer et al., 2009  

## Re sidential Woodsmoke Intake Fraction  

## Va ncouver study  

## 13 – 15 per million  

## Similar to vehicle emissions  

## ~7x higher than all - source PM

# How **is Woodsmoke**  **Different?**

Londahl et al., 2008, 2009 

### • Compared dose of deposited particles in airway for traffic exhaust and residential wood combustion particles. • Subjects breathed concentrations of 100 μg/m 3 

### • Traffic particle dose was **16x by number**, and **3x by surface area** . **WHY?** • Traffic particles have: • Higher deposition probability • Higher particle number and surface area per mass concentration **Particle toxicity influenced by size, composition, physical**  **properties, etc.**

### • **Epidemiologic Evidence:**  “ .....epidemiologic studies of indoor and communit y exposure to biomass smok

e indicate a generally consistent relationship between exposure and **increased respiratory**  **symptoms, increased**  **risk of respiratory illness,**  **including hospital**  **admissions and emergency**  **room visits, and decreased**  **lung function**  . Several studies suggest that **asthmatics are a particularly susceptible**  **subpopulation** with respect to smok e exposure.... ” Naeher et al., 2007 

# Woodsmoke and Health: **Evidence**

### • **General Conclusions**  “...at the present time **fine particles may represent**  **the best metric** to characterize exposures to smok e from residential wood combustion... ” “There is **no persuasive**  **evidence that**  **woodsmoke particles**  **are significantly less**  **dangerous for**  **respiratory disease**  than other major categories of combustion - derived particles in the same size range. ” “There is **too little evidence**  **available today**, however , to mak e a judgment about the relative toxicit y of woodsmoke particles with respect to **cardiovascular or cancer outcomes**  .” Naeher et al., 2007 

# Woodsmoke and Health: **Evidence**

# Woodsmoke and Health: **Evidence**  

## Constituents  

## Toxicology  

## Biomass burning in developing countries  

## Fo rest fires  

## Firefighters  

## Impacted communities  

## Communities impacted by agricultural burning  

## Controlled human **exposure studies**  

### Limitation: **only acute, reversible effects**  

## Communities **impacted by residential**  **woodsmoke**  

### Challenge: often small communities **(limited statistical power)**  Sarnat S. et al. , JA WMA, 2006

# Some Woodsmoke **Constituents**

*Indoor emissions from household combustion of biomass fu el (primarily wood) are categorized as a **Group 2** **A carcinogen**  (probably carcinogenic to humans – limited human evidence with supporting animal evidence) by the International Agency fo r Research on Cancer (IARC) . **Constituent Properties**  Pa rticulate Matter (PM 2.5 ) Inflammation, oxidative stress Carbon Monoxide Asphyxiant Nitrogen Dioxide Irritant Benzene Carcinogen*, mutagen PA Hs Carcinogen*, mutagen Aldehydes Irritant, carcinogen*, mutagen Phenols Irritant, carcinogen*, mutagen, teratogen Adapted from Larson & Koenig, 1994; Naeher et al., 2007

# Indoor Biomass Smoke

WHO, Fuel for Life, 2006  

### Indoor biomass (wood, crops) and coal smoke:  3 billion exposed  1.6 million premature deaths  2. 7% of global burden of disease  Strong evidence for:  Re spiratory infections  Obstructive lung disease (women)  Low birth weight  Cataracts  Limited evidence f

or:  Tu berculosis  Asthma  Otitis media  Lung cancer (biomass) **MUCH HIGHER EXPOSURES THAN IN**  **DEVELOPED WORLD**

# Controlled **Exposure Experiments** 

Barregard et al., 2006

# Controlled **Exposure Experiments** 

 

## 13 subjects exposed to wood smok

e and clean air  

## 240– 280 μ g/m 3  

## 4 - hour sessions, 1 week apart

Barregard et al., 2006

# Air **Pollution and Hospital**  **Admissions in Christchurch,**  **NZ**

 

### “Uniquely in Christchurch, more than 90% of particulate air pollution has been estimated to come from the city ’s47 ,000 wood burners and open fires that are used during the cold winters months”  

## McGowan et al. , 2002:  

### 3.37% increase in respiratory admissions and 1.26% increase in cardiac admissions per 15 μg/m 3 

### outdoor PM 10  

## Barnett et al. , 2006:  

### No significant effects of PM 10 

### on cardiac admissions Sarnat S. et al. , JA

WMA, 2006 McGowan et al., ANZJPH, 2002; Barnett et al., EHP, 2006• 

## 45 participants, 25 homes in Smithers , BC • 

## Portable HEPA filters 60%  in indoor PM 2.5 • 

### 11.2  4.6 ug /m 3 • 

## Increases in endothelial function and decreases in systemic inflammatory markers **Random Sel**  **ecti on**  **HEP A**  **Fi ltra**  **tio n**  **“Pl aceb**  **o” F**  **iltra tio**  **n**

**Day 0**  **Te chn**  **ic ian**  **Vi si**  **t Day**  **7 Te**  **chn ic**  **ia n**  **Vi si**  **t Day**  **1 4**  **Te chn**  **ic ian**  **Vi si**  **t Heal**  **th Measur** **em en**  **ts Heal**  **th Measur** **em en**  **ts Mo**  **ni to**  **rin g**  **Sessi on**  **2 Mo**  **ni to**  **rin g**  **Sessi on**  **1 Mo**  **ni to**  **rin g**  **Sessi on**  **2 Mo**  **ni to**  **rin g**  **Sessi on**  **1**

Allen et al., AJRCCM 201 1 

# Intervention **Studies**• ~30% reduction in winter PM 2.5 •  in childhood wheeze, itchy eyes, sore throat, cold, bronchitis, influenza, throat inf

ections • School absence associations inconsistent

**Libby , Montana stove exchange**  

# Intervention **Studies**

Noonan et al., HEI Report 162, December 201 1**Mobile Monitoring on Cold, Clear**  **Wi nter**  **Evenings**

Lo west third Middle third High est third Lo west third Middle third High est third **(~ 12,000 points)**

Larson et al. Environmental Science and T echnology

. 2007 Re is et al, Environmental Science and T echnology

. 2009 

# Mapping **Woodsmoke in Vancouver** **Outcome Exposure** 

**window N** 

**(n cases) Design**  **Mean Days**  **exposed [IQR]**  **Adjusted #**  **OR**

**(95% CI)** SGA birth All pregnancy 70,249 (6,939) Cohort 65 [43] 1.00 (0.91 - 1.09) Asthma 3 (0 – 48 mos. ) All pregnancy

0 - 12 months 37

,401 (3,482) Nested

C- C** 60 [33]

89 [17] 1.00 (0.94 - 1.07)

1.00 (0.98 - 1.02) **Bronchiolitis** 1 2 – 12 months 86,337 (10,485) Nested

C- C* 54 [45] **1.08 (1.04 -**  **1.11) Otitis**  **Media** 2 (1 – 24 mos. ) 1 month pre diagnosis 45,513

(19,115) Cohort 15 [16] **1.32 (1.27 -**  **1.36)** # per IQR increase, adjusted for covariates: Infant sex (SGA, B, OM) First Nations Status (SGA, B, OM), Parity (SGA, B, A), Mater nal age (SGA, B, OM), Maternal smoking during pregnancy (SGA, B, OM), Month -year of birth (SGA), maternal initiation of breastfeedin g at birth (B, OM, A), Income (SGA, B, OM, A), Maternal education (SGA, B, OM, A), older siblings (OM), birth season (OM), birthweight (OM, A), gestational duration (OM, A). *incidence - density matching (up to 1:10) on date of birth **matched 1:5 by sex, month -yr of birth 1 Karr et al. , AJRCCM 20009; 2 MacIntyre et al. , Epidemiology 2011; 3 Clark et al. , EHP



# Vancouver **Results**

# Summary  

## Biomass smok

e contains man y pollutants with known adverse ef

fe cts on health  

## Wo odsmok

e is an important source of air pollution in many communities  

### Emissions in populated areas  high “intake fraction”  

## Fo r respiratory outcomes, no evidence that woodsmok

e particles are less dangerous than other , similarly- sized particles  

### Short- term (≤24 hour) effects on symptoms, lung fu nction, admissions, & ED visits  

## Cardiovascular evidence is mixed (controlled exposure & in - home studies vs. population studies)  

## Emerging evidence that spatio - temporal va riations in woodsmok

e relate to important ef fe cts in children

# allenr@sfu.caKo cbach Bølling et al. 2009 21