HIPWOODS - Health Effects Related to Exposure to Particle Pollution From Woodburning Stoves (HIPWOODS)

Health Effects Related to Exposure to Particle Pollution From Woodburning

The study intends to focus on health effects and symptoms related to particle exposure from wood burning stoves

The objective is to determine whether moderate exposure to particles from wood smoke in a real life situation causes an systemic inflammatory response in peripheral blood or in lower airways. 24 healthy subjects (normal healthy subjects and mild asthmatics to study the asthmatic response) is selected for the study. A randomized double blind crossover procedure will be followed with a PM exposure concentration of 200ug/m3, 400ug/m3 or clean air as the control exposure. Exposure will take place in a climate chamber using wood burning in an appropriate wood stove.

Study Overview

• Status: Completed
• Conditions: Systemic Inflammation; Airway Inflammation
• Intervention / Treatment: Other: Wood smoke particles

Detailed Description

Public health is concerned with the physical, mental and environmental health of communities and populations at risk for disease and injury. Generally, the determination of health effects associated with indoor and outdoor exposures is difficult since documented cause-and-effect relationships are rare and the exposure and dosage data is sparse. Information about actual human exposure to different types of pollution has several important uses, including informing risk assessments, helping predict the potential consequences of exposures, and developing exposure criteria for regulations and other public policy guidance.

Wood-burning stoves have been a popular heating source for decades. Unfortunately, wood-burning stoves can emit substantial quantities of pollutants to outdoor and indoor air. Among the pollutants are: chlorinated dioxin, carbon monoxide, methane, volatile organic compounds (VOC), nitrogen oxides, polycyclic aromatic hydrocarbons (PAH), and fine particulate matter (PM10, PM2.5, fine and ultra fine particles). Recent studies indicate that the use of wood-burning stoves for heating of dwellings is one of the important outdoor particle sources [Glasius et al. 2004] in residential district in Denmark. This has resulted in an increase in public exposure to indoor and outdoor wood smoke related pollutants, which has prompted widespread concern about the adverse human health consequences that may be associated with wood smoke exposure.

Air pollution is a major aggravation of respiratory symptoms and disease. Effects are decreases in pulmonary function and evidence of inflammation as well as suggestions of increases in chronic respiratory disease. Orozco-Levi et al. (2006) showed strong association between wood smoke exposure and obstructive pulmonary disease. Several studies have shown that especially the small particles, has an effect on airways, and that asthmatic subjects may be the group at greatest risk from air pollutants. The awareness of the impact of airborne particles, particularly fine and ultra fine particles, on health is growing. In recent years, exposure to fine and ultra fine airborne particles has been identified as an important factor affecting human health [Seaton et al., 1995; Schwartz et al., 1996; Oberdörster et al., 1994; Alvin et al., 2000]. Several researchers hypothesize that an increased mortality is associated with the particle levels prevailing in urban air [Jamriska et al., 1999; Dockery et al., 1993]. Mølhave et al (2000; 2005) have suggested that reactive short-lived compounds resulting from reactions between ozone and particulate matter cause indoor air quality complaints and objective health effects such as impaired lung functions.

Particulate air pollution is also known to increase cardiovascular morbidity and mortality. Still the existing scientific knowledge and foundation for evaluating the underlying mechanisms and influence of particle exposure on human immune system are limited. Wood smoke particles, at levels that can be found in smoky indoor environments, seem to affect inflammation. Barregard et al observed a significant increase in S-Amyloid and Faktor VIII/vWf after 0, 3 and 20 hours of exposure to wood smoke. After 20 hours also and increase in Faktor VIII was registred. Surpise-lingly, an IL.-6 decrease was observed after 3 hours. [Barregard et al, 2006]. The particles may also act by increasing blood coagulation factors [Seaton et al 1995]. Both effects may be involved in the mechanisms whereby particulate air pollution affects cardiovascular morbidity and mortality.

• Study Type: Interventional
• Enrollment (Actual): 20
• Phase: Not Applicable

Contacts and Locations

Study Locations

• Denmark
  • Aarhus C, Denmark, 8000
    • Institute of Environmental and Occupational Medicine , Institute of Public Health , The Faculty of Health Sciences

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 18 years to 64 years (Adult)
• Accepts Healthy Volunteers: Yes
• Genders Eligible for Study: All

Description

Inclusion Criteria:

• Twenty-four, non-smoking atopic volunteers with normal lung function and bronchial reactivity are recruited for the study. Atopy is determined by skin-prick testing to common aeroallergens.

Exclusion Criteria:

• Smokers, pregnant women and other subjects with current or previous diseases, which could involve a risk for the subject or possibly influence the outcome measurements, will be excluded from the study.

Study Plan

How is the study designed?

Design Details

• Allocation: Randomized
• Interventional Model: Crossover Assignment
• Masking: Double

Number of Arms

3

Arms and Interventions

Participant Group / Arm	Intervention / Treatment
Sham Comparator: 1; Clean air	Other: Wood smoke particles; Subjects are exposed at rest to the exposures for 3 h in our climate chamber
Experimental: 2; Wood smoke particle concentration of 200 ug/m3	Other: Wood smoke particles; Subjects are exposed at rest to the exposures for 3 h in our climate chamber
Experimental: 3; Wood smoke particle concentration of 400 ug/m3	Other: Wood smoke particles; Subjects are exposed at rest to the exposures for 3 h in our climate chamber

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Time Frame
Different Inflammation Biomarkers	Baseline and follow up measurement after exposure 0 hours post, a 6 hours post and 20 hours post.

Secondary Outcome Measures

Outcome Measure	Time Frame
Baseline and follow up measurements are: spirometry, exhaled breath condensate, nasal lavage, nasal patency, blood sampling and symptoms.	Baseline and follow up measurement after exposure 0 hours post, a 6 hours post and 20 hours post.

Collaborators and Investigators

• Sponsor: University of Aarhus
• Collaborators: Aarhus University Hospital; University of Copenhagen
• Investigators: Principal Investigator: Torben Sigsgaard, Professor, Department of Environmental and Occupational Medicine , Institute of Public Health , The Faculty of Health Sciences

Study record dates

Study Major Dates

• Study Start: January 1, 2007
• Primary Completion (Actual): June 1, 2008
• Study Completion (Actual): November 1, 2009

Study Registration Dates

• First Submitted: May 5, 2008
• First Submitted That Met QC Criteria: May 5, 2008
• First Posted (Estimate): May 7, 2008

Study Record Updates

• Last Update Posted (Estimate): February 2, 2012
• Last Update Submitted That Met QC Criteria: February 1, 2012
• Last Verified: February 1, 2012

More Information

Terms related to this study

• Keywords: Human; Airway inflammation; Cardiovascular effects; Wood smoke; Health effects
• Additional Relevant MeSH Terms: Pathologic Processes; Inflammation
• Other Study ID Numbers: 2104-05-0003; Projekt nr: 0502-