Alfheim I, Ramdahl T, Contribution of wood combustion to indoor air pollution as measured by mutagenicity in Salmonella and polycyclic aromatic hydrocarbon concentration, Environ. Mutagen 1984;6(2):121-130

Abstract: Samples of airborne particles have been collected in the same room when the room was heated by electricity and when heating was done by woodburning. These samples were compared with respect to mutagenic activity and concentration of polycyclic aromatic hydrocarbons (PAH). The effects of the various heating conditions were examined in the presence and absence of tobacco smoking. Whereas wood heating in an "airtight" stove was found to cause only minor changes in the concentration of PAH and no measurable increase of mutagenic activity of the indoor air, both these parameters increased considerably when wood was burned in an open fireplace, yielding PAH concentrations comparable to those of ambient urban air. Relatively high concentrations of moderately polar polycyclic aromatic hydrocarbon derivatives were also found in the indoor air when wood was burned in an open fireplace. Woodburning in the closed stove did, however, result in increased concentrations of mutagenic compounds and PAH on particles sampled in the vicinity of the house. The effects of wood burning in an open fireplace on the mutagenic activity of indoor air could still be considered moderate when compared to those resulting from tobacco smoking in the room. The extracts of particles collected when moderate smoking occurred were several times more mutagenic than samples from urban air collected close to streets with heavy traffic when measured in the Salmonella assay with strain TA98 with metabolic activation. >$/p>

Ardayfio Schandorf E, Women's health status in Africa -- environmental perspectives from rural communities, Health Care for Women International, 1993 Jul-Aug; 14(4): 375-86 (10 ref)

Health research used to be the exclusive domain of clinicians and medical specialists, who focused attention on the biomedical causes of disease. Socioeconomic and environmental considerations that have important bearing on the ill health of rural African women were rarely integrated with the methodology constructed to investigate disease patterns. However, it is becoming increasingly clear that physical environmental factors and malnutrition have important effects on women's health in rural Africa. I validated this assumption in an empirical study of 441 people (n = 294 women) in 15 different rural localities in Ghana. Apart from women-specific problems relating to biological health needs during pregnancy, childbirth, and lactation, sexually transmitted diseases, abortion, and mental health, environmental factors had a great impact on women's well-being in the study area. Sixty-two percent of the women reported that the endemic disease malaria is the most prevalent disease as far as they were concerned. Other community and household health hazards were found; for example, cooking over an open fuel wood stove resulted in an almost 50% greater chance of stillbirth among pregnant women.

Betchley C., Koenig J.Q., Vanbelle G., Checkoway H., Reinhardt T., Pulmonary Function and Respiratory Symptoms in Forest Firefighters, American Journal of Industrial Medicine, 31(5):503-509, 1997 May

Abstract : This study evaluated effects on respiratory, health of forest firefighters exposed to high concentrations of smoke during their work shift. This is the first study of cross-shift respiratory effects in forest firefighters conducted on the job. Spirometric measurements and self-administered questionnaire data were collected before and after the 1992 firefighting season. Seventy-six (76) subjects were studied for cross-shift and 53 for cross-season analysis. On average, the cross-season data were collected 77.7 days after the last occupational smoke exposure. The cross-shift analysis identified significant mean individual declines in FVC, FEV(1), and FEF(25-75). The preshift to midshift decreases were 0.089 L, 0.190 L, and 0.439 L/sec, respectively, with preshift to postshift declines of 0.065 L, 0.150 L, and 0.496L/sec. Mean individual declines for FVC, FEV(1) and FEF(25-75) of 0.033 L, 0.104 L, and 0.275 L/sec, respectively, also were noted in the cross-season analysis. The FEV(1) changed significantly (p<0.05). The use of wood for indoor heat also was associated with the declines in FEV(1).Although annual lung function changes for a small subset (n=10) indicated reversibility of effect, this study suggests a concern for potential adverse respiratory effects in forest firefighters. (C) 1997 Wiley-Liss, Inc. [References: 32] Browning KG, Koenig JQ,

Butterfield, P, LaCava, G. Edumunston E, Penner, J. 1989. Woodstoves and indoor air: the effects on preschooler’s upper respiratory symptoms. J. Environ. Health 52:172-73. (L&K, Ref 14)

Boone PM, Rossman TG, Daisey JM. The genotoxic contribution of wood smoke to indoor respirable suspended particles. Environment International 1989 15:361-368.

Browning KG, Koenig JQ, Checkoway H, Larson, TV, Peirson WE., A questionnaire study of respiratory health in areas of high and low ambient wood smoke pollution, Pediatr. Asthma All. Immunol. 4:183-91, 1990

Churg A., Brauer M., Human Lung Parenchyma Retains PM2.5, American Journal of Respiratory & Critical Care Medicine, 155(6):2109-2111, 1997 June.

Abstract: There is extensive epidemiologic evidence that increased levels of the inhalable particulate fraction of air pollution (PM10) are associated with increased morbidity and mortality. The mechanisms of these effects are unknown, and the exact types and sizes of particles responsible are a matter of intense dispute. To obtain an idea of the sizes of particles retained in human lung parenchyma, we used analytical electron microscopy to count, size, and identify particles in the upper lobe apical segment parenchyma of autopsy lung tissue from 10 never-smoking long-term residents of Vancouver. The overall geometric mean particle diameter (CSD) was 0.38 mu m (2.4); within this broad distribution, silica and silicate particles had a geometric mean diameter of 0.49 mu m (2.2), whereas metals had a geometric mean diameter of 0.17 mu m (2.0). Ultrafine particles (those with diameter less than or equal to 0.1 mu m) constituted less than 5% of the total, and most of these were metals. Translation of these projected area diameters into aerodynamic diameters (d(a)) revealed that 96% of the particles had d, less than 2.5. These data indicate that human lung parenchyma effectively retains PM2.5, suggesting that attempts to determine the particles responsible for chronic particulate pollutant effects should concentrate on this size range. These data also suggest that several different type/size classes of particle are present in human parenchyma, but that ultrafine particles make up only a small fraction of the total. [References: 19]

Collings DA, Sithole SD, Martin KS, Indoor woodsmoke pollution causing lower respiratory disease in children, Trop Doct, 1990 Oct;20(4):151-155

Abstract: Suggested aetiological factors were evaluated in 244 consecutive children presenting with lower respiratory disease at Marondera Hospital, Zimbabwe. Data obtained from these children were compared with information obtained from 500 children seen at the local well baby clinic. There were no differences in the prevalence of malnutrition, breast feeding, overcrowding, poor housing conditions and poverty in these two groups of children. A significant association was identified between lower respiratory disease and exposure to atmospheric woodsmoke pollution in young children. Air sampling within the kitchens of 40 children revealed levels of atmospheric pollution far in excess of the WHO recommended exposure limit. Elevated carboxyhaemoglobin concentrations confirmed childhood smoke inhalation. We suggest that in many Third World communities a chemical pneumonitis resulting from the inhalation of noxious constituents of woodsmoke predisposes to lower respiratory disease in children.

Cooper J.A., Environmental Impact of Residential Wood Combustion Emissions and its Implications, Air Pollution Control Association Journal, 30 (8), 855-861, 1980 Aug.

Abstract: Currently available information suggests a substantial environmantal impact from residential wood combustion emissions. Air pollution from this source is widespread and increasing. Current ambient measurements, surveys, and model predictions indicate winter respirable ( < 2 mm) emissions from residential wood combustions can easily exced all other sources. Both the chemical potency and deliverability of the emissions from this source are of concern. The emissions are almost entirely in the inhalable size range, and contain toxic and priority pollutants, carcinogens, co-carcinogens, cilia toxic, mucus coagulating agents, and other respiratory irritants sych as phenols, aldehydes, etc. This source is contributing substantially to the non-attainment of current particulate, carbon monoxide, and hydrocarbon ambient air standards, and will almost certainly have a significant impact on potential future standards such as inhalable particulates, visibliity, and other chemically specific standards. Emission from this growing source is likely to require additional expenditures by industry for air pollution control equipment in non-attainment areas.

Daigler G.E, Markello S.J, Cummings K.M, The effect of indoor air pollutants on otitis media and asthma in children, Laryngoscope 1991 Mar;101(3):293-296 Department of Pediatrics, State University of New York, Buffalo.

Abstract: This case-control study investigated the possible association between home environmental air pollutants and their effect on otitis media and asthma in children. Patients with physician-diagnosed otitis (n = 125, 74% response), with asthma (n = 137, 80% response), and controls (n = 237, 72% response) from a private pediatric practice seen between October 1986 and May 1987 were studied. A questionnaire inquired about housing characteristics (i.e., age, insulation, heating system) and sources of indoor air pollution such as cigarette smoking, use of woodburning stoves, household pets, etc. Analysis of the responses confirmed previous findings of significant relationships between maternal smoking (P = .021), and the presence of pets (P = .034) and the occurrence of asthma. A newly reported relationship between exposure to woodburning stoves and the occurrence of otitis (P less than .05) was reported. This implicates yet another risk factor (wood burning) in the etiology of otitis media.

Dean BS, Lopez G, Krenzelok EP, Environmentally-induced methemoglobinemia in an infant, J Toxicol Clin Toxicol 1992;30(1):127-133 Pittsburgh Poison Center, Children's Hospital of Pittsburgh, Pennsylvania 15213-2583.

Abstract: Acquired methemoglobinemia results from the exposure to various chemicals and drugs able to oxidize hemoglobin at a rate exceeding the normal enzymatic capacity for hemoglobin reduction. Levels of methemoglobin exceeding 60-70% may be associated with coma and death. We describe a case of complete, uneventful recovery involving a 10 week-old infant who presented to the Emergency Department with profound sudden onset of cyanosis, irritability, metabolic acidosis, and a lethal methemoglobin level of 71.4%. Intravenous administration of 12 mg methylene blue resulted in immediate resolution of the cyanosis and reduction of measured methemoglobin to 1.3%. The carboxyhemoglobin was negative. Sodium bicarbonate successfully corrected the acidosis. RBC reductase measurement was within normal limits, ruling out congenital methemoglobinemia. Family history revealed a wood-burning stove which emitted pine tar fumes as the potential environmental methemoglobin-producing source. The infant's cradle was situated five feet from the stove. The infant was discharged on day three of hospitalization with a methemoglobin level of 0.2%.

Dennis RJ, Maldonado D, Norman S, Baena E, Martinez G, Woodsmoke exposure and risk for obstructive airways disease among women, Chest 1996 Jan;109(1):115-119 Pontificia Universidad Javeriana, Bogota, Colombia.

Abstract: OBJECTIVE: To investigate if exposure to firewood smoke and other indoor pollutants is a potential risk factor for obstructive airways disease (OAD) among women in Bogota in whom cigarette smoking and other known risk factors may not be the most frequent. DESIGN AND SETTING: We conducted a hospital-based case-control study to identify risk factors for OAD among women in Bogota. An interview was conducted using a modified questionnaire recommended by the American Thoracic Society for epidemiologic studies. PATIENTS: We compared 104 OAD cases with 104 controls matched by hospital and frequency matched by age. ANALYSIS: The odds ratio (OR) was used as the basic statistic to evaluate risk. Multivariate analysis (MA) was conducted by the Mantel-Haenszel procedure and by logistic regression. MAIN RESULTS: Univariate analysis showed that tobacco use (OR = 2.22; p < 0.01), wood use for cooking (OR = 3.43; p < 0.001), passive smoking (OR = 2.05; p = 0.01), and gasoline use for cooking (OR = 0.52; p = 0.02) were associated with OAD. Trends for years of tobacco use and years of wood cooking were present (p < 0.05). After MA, variables remained significant except gasoline use. CONCLUSIONS: This study showed that among elderly women of low socioeconomic status in Bogota, woodsmoke exposure is associated with the development of OAD and may help explain around 50% of all OAD cases. The role of passive smoking remains to be clarified. This work may set the basis for interventional studies in similar settings.

Ellegard A., Cooking Fuel Smoke and Respiratory Symptoms Among Women in Low-Income Areas in Maputo, Environmental Health Perspectives, 104(9):980-985, 1996 Sep.

Abstract: The association between exposure to air pollution from cooking fuels and health aspects was studied in Maputo, Mozambique. Almost 1200 randomly selected women residing in the suburbs of Maputo were interviewed and 218 were monitored for air pollution. The fuels most commonly used were wood, charcoal, electricity and liquified petroleum gas (LPG). Wood users were exposed to significantly higher levels of particulate pollution during cooking time (1200 mu g/m3) than charcoal users (540 mu g/m(3)) and users of modern fuels (LPG and electricity) (200-380 mu g/m(3)). Wood users were found to have significantly more cough symptoms than other groups. This association remained significant when controlling for a large number of environmental variables. There was no difference in cough symptoms between charcoal users and users of modern fuels. Other respiratory symptoms such as dyspnea, wheezing, and inhalation and exhalation difficulties were not associated with wood use. Reducing wood use would Likely improve acute respiratory health effects in wood users and possibly improve the ambient air pollution conditions in Maputo. To reduce the health impact of wood smoke exposure, it appears that the least costly and quickest method would be to encourage charcoal use to a greater extent, high carbon monoxide levels would have to be addressed. Turning to modern fuels is beyond the means of most these households in the short term and could not be shown to be more effective. [References: 20]

EPA NSW. Environment Protection Authority New South Wales. Air Pollution from solid fuel home heaters. Jan. 1996.

Gharaibeh NS., Effects of Indoor Air Pollution on Lung Function of Primary School Children in Jordan, Annals of Tropical Paediatrics, 16(2):97-102, 1996 June

Abstract: Environmental exposure to tobacco smoke and contaminants from unvented cooking stoves has been linked to impaired pulmonary function and respiratory diseases. These risk factors exist to a greater extent in developing countries and, in the case of exposure to tobacco smoke, they are reported to be increasing. In this study, pulmonary function studies were performed on 1905 children in Jordan. The effect of exposure to these environmental factors on respiratory function was analyzed. A significant negative impact was found with regard to environmental exposure to both passive smoking and wood and kerosene unvented cooking stoves. The mean values of lung function in children exposed and not exposed to passive smoking were, respectively, FVC (L): 1.29-1.49; FEV(1) (L): 1.2-1.4; FEF(25-75) (L/S): 1.84-2.24; PEFR (L/S): 2.6-3.21, and to wood and kerosene were FVC (L): 1.02-1.32; FEV(1) (L): 0.91-1.25; FEF(25-75) (L/S): 1.24-1.86; PEFR (L/S): 1.67-2.64. This is a major problem in developing countries because of the increasing incidence of smoking and the high exposure to pollution risk factors. [References: 15]

Godleski J., Sioutas C., Katler M., Koutrakis P., Death from inhalation of concentrated ambient air particles in animal models of pulmonary disease, Proceedings of the Second Colloquium on Particulate Air Pollution and Human Health, Utah, 1996 May

Epidemiologic studies have found increased mortality associated with particulate air pollution. To test the biologic plausibility of this association, normal rats, rats with monocrotyline-induced pulmonary inflammation (50 mg/kg SC), and rats with SO2 induced chronic bronchitis (250 ppm SO2, 6 wks) were expose to concentrated air particles (CAPS) or filtered air for 3 consecutive days, 6 hours/day. The concentrating system of Sioutas et al, (Env Hlth Perspect 1995, 103:171) was used.

Group Control Monocrotyline Chronic Bronchitis
CAPS (mg/m3 SD) 245 70 228 89 288 64
% Mortality 0% 19% 37%
Pathologic Findings
on death or sacrifice
No inflammation
Minimal Broncho-
Acute inflammation in alveoli & interstitium
Some Broncho-constriction
Airway inflammation, increased mucus
Marked broncho-constriction
Interstitial edema
Pulmonary vascular congestion

Deaths occured during exposure and overnight. Inflammation was found in groups with disease, but animals exposed to CAPS exhibited increases in inflammatory parameters and broncho-constriction. Broncho-constriction, visible bucklling of the epithelium, was enumerated in all groups comparing the number of constricted airways in animals dying spontaneously with those who survived exposures but were killed afterwards. Animals with chronic bronchitis had the most evidence of airway constriction. In comparing death versus killed, broncho-constriction was significantly increased in the disease groups (monocrotyline p = 0.007; chronic bronchitis p = 0.02). Thus, ambient particle inhalation can cause death in rats with disease, and inflammation as well as airway constriction appear to be important in the response.

Table 1 from text of paper
Parameter Control - No Lung Disease Chronic Bronchitis
Concentration of Ambient Air Particles mg/m3 SD 254 45 272 40
% Mortality 0% 37%
% Significance (Log Rank Test) - p < 0.05
Pathologic Findings
on Death or Sacrifice
No inflammation
No Bronchoconstriction
Acute inflammation
Pulmonary vascular congestion
BAL (bronchial lavage) Findings no change compared to filtered air neutrophils increased 2X
compared to filtered air
Note: Table 1 from the text of the paper has been reproduced as well as the abstract. According to the first author, Dr Godleski, Table 1 contains a more accurate estimate of the particle concentration.

Guneser S, Atici A, Alparslan N, Cinaz P, Effects of indoor environmental factors on respiratory systems of children, J Trop Pediatr 1994 Apr;40(2):114-116 Cukurova University Medical Faculty, Department of Pediatrics, Adana, Turkey.

Abstract: Effects of indoor environmental factors on children's respiratory system and pulmonary function tests were investigated in this study. A total of 617 primary school children aged between 9-12 years were included. A standard questionnaire, which includes questions about respiratory symptoms and illness, indoor environmental determinants, family history of respiratory diseases, and smoking habits of the parents, was sent to homes of all children and information was obtained from parents. Children with a family history of asthma, bronchitis, or other chest troubles suffered morning and day/night coughs, shortness of breath, wheezing and asthma, bronchitis, or pneumonia more frequently. Children whose mothers smoked complained of blocked-runny nose and sinusitis more frequently. Pulmonary function levels were diminished in passive smokers and in children whose houses were heated by a wood-burning stove. As a result, passive smoking, using a wood-burning stove for heating, and family history of respiratory diseases are to be considered risk factors for the respiratory system.

Heumann M., Foster L.R., Johnson L, Kelly L., Woodsmoke Air Pollution and Changes in Pulmonary Function Among Elementary School Children, Air & Waste Management Association 84th Annual Meeting & Exhibition, Vancouver, British Columbia, 1991 June.

Hamada G.S, Kowalski L.P, Murata Y, Matsushita H, Matsuki H, Wood stove effects on indoor air quality in Brazilian homes: carcinogens, suspended particulate matter, and nitrogen dioxide analysis, Tokai J. Exp. Clin. Med. 1992 Oct;17(3-4):145-153

Abstract: The effects of wood burning stoves on indoor air quality was investigated in a rural community of southern Brazil, during the winter season of 1991. The concentrations of polycyclic aromatic hydrocarbons (PAHs), nitrogen dioxide (NO2) and suspended particulate matter (SPM) were assessed in houses with wood stoves and the results compared with levels found in houses with gas stoves. Strikingly higher (p < 0.01) levels of PAHs, and much higher (p = 0.07) levels of SPM were found in the kitchens with wood stoves. In contrast, NO2 concentrations in the kitchen as well in personal exposure, were found to be slightly higher in houses with gas stoves. All these differences were minimally affected by smoking, outdoor air pollution or other emissions from indoor combustion products. These findings appear to support the hypothesis that domestic wood burning stoves are risk factors for some upper digestive and respiratory tract cancers in Brazil.

Hogg J. C, Bronchiolitis obliterans and wood-burning stoves, Canadian Medical Association Journal,1997 Apr 15;156(8):1147-1148 Editorial, Comments on: Can Med Assoc J 1997 Apr 15;156(8):1171-3

Abstract The author reviews the features of bronchiolitis obliterans, a potentially fatal condition first described in 1901. There are 2 main types of the disease. In the "classic" type, polyps of granulation tissue form in the bronchiolar lumen, typically after a massive exposure to toxic fumes. In the "peribronchiolar" type an inflammatory response contricts the lumen but leaves the mucosa relatively intact; this is usually associated with a chronic exposure and progresses more slowly than the classic type. The author comments on the case report by Dr. David T. Janigan and colleagues in this issue of classic bronchiolitis obliterans in a man who used a wood-burning stove to dispose of construction materials.

Honicky RE, Osborne JS 3d, Akpom CA, Symptoms of respiratory illness in young children and the use of wood-burning stoves for indoor heating, Pediatrics 1985 Mar;75(3):587-593

Abstract: The occurrence of symptoms of respiratory illness among preschool children living in homes heated by wood-burning stoves was examined by conducting an historical prospective study (n = 62) with an internal control group (matched for age, sex, and town of residence). Exposures of subjects were not significantly different (P greater than .05) with respect to parental smoking, urea-formaldehyde foam insulation, and use of humidifiers. The control group made significantly greater use of gas stoves for cooking whereas the study group made greater use of electric stoves for cooking and of air filters (P less than .05). Only one home used a kerosene space heater. During the winter of 1982, moderate and severe symptoms in all categories were significantly greater for the study group compared with the control group (P less than .001). These differences could not be accounted for by medical histories (eg, allergies, asthma), demographic or socioeconomic characteristics, or by exposure to sources of indoor air pollution other than wood-burning stoves. Present findings suggest that indoor heating with wood-burning stoves may be a significant etiologic factor in the occurrence of symptoms of respiratory illness in young children.

Johnson KG, Gideon RA, Loftsgaarden DO, Montana air pollution study: children’s health effects. J. Official Stat. 5:391-407, 1990.

Koenig J.Q, Larson T.V, Hanley Q.S, Rebolledo V, Dumler K, Checkoway H, Wang S.Z, Lin D, Pierson W.E, Pulmonary function changes in children associated with fine particulate matter, Environ Res 1993 Oct;63(1):26-38 , Department of Environmental Health, University of Washington, Seattle 98195.

Abstract: During winter months many neighborhoods in the Seattle metropolitan area are heavily affected by particulate matter from residential wood burning. A study was conducted to investigate the relationship between fine particulate matter and pulmonary function in young children. The subjects were 326 elementary school children, including 24 asthmatics, who lived in an area with high particulate concentrations predominantly from residential wood burning. FEV1 and FVC were measured before, during and after the 1988-1989 and 1989-1990 winter heating seasons. Fine particulate matter was assessed using a light-scattering instrument. Analysis of the relationship between light scattering and lung function indicated that an increase in particulate air pollution was associated with a decline in asthmatic children's pulmonary function. FEV1 and FVC in the asthmatic children dropped an average of 34 and 37 ml respectively for each 10(-4) m-1 increase in sigma sp. This sigma sp increase corresponds to an increase in PM2.5 of 20 micrograms/m3. It is concluded that fine particulate matter from wood burning is significantly associated with acute respiratory irritation in young asthmatic children.

Kou Y.R., Lai C.J., Hsu T.H., Lin Y.S., Involvement of Hydroxyl Radical in the Immediate Ventilatory Responses to Inhaled Wood Smoke in Rats, Respiration Physiology, 107(1):1-13, 1997 Jan.

Abstract: Spontaneous inhalation of wood smoke (similar to 6 mi) via a tracheostomy immediately triggered either a slowing of respiration (SR, n = 51) or an augmented inspiration (AI, n = 32) in 83 anesthetized Sprague-Dawley rats studied. To investigate the involvement of hydroxyl radical (OH.) in evoking these immediate smoke-induced ventilatory responses, smoke challenges were repeated following intravenous infusion (0.05 ml/min for 20 min) of saline vehicle, dimethylthiourea (DMTU, 500 mg/kg), deferoxamine (DEF, 20 mg/kg), or iron-saturated DEF (DEF+Fe, 20 mg/kg). DMTU is a scavenger for OH.. DEF is an iron-chelator which prevents the formation of OH., whereas DEF saturated with iron results in the loss of its iron-chelating properties. In the vehicle group, both the SR (n = 8) and the AI (n = 7) were unaffected by the pretreatment. However, in the DMTU group, the SR (n = 23) was abolished in seven and attenuated in 16 rats, while the AI (n = 10) was eliminated in eight and unaffected in two rats. In the DEF group, the SR (n = 12) was abolished in three and attenuated in nine rats, while the AI (n = 8) was eliminated in six and unaffected in two rats. In contrast, in the DEF + Fe group, both the SR (n = 8) and the AI (n = 7) were not attenuated by the pretreatment. These results suggest that an increase in OH. burden following smoke inhalation is actively involved in evoking the acute irritant effects of wood smoke on breathing in rats. (C) 1997 Elsevier Science B.V. [References: 25]

Public-health impact of outdoor and traffic-related air pollution: a European assessment
N Kunzli, R Kaiser, S Medina, M Studnicka, O Chanel, P Filliger, M Herry, F Horak Jr, V Puybonnieux-Texier, P Quenel, J Schneider, R Seethaler, J-C Vergnaud and H Sommer Lancet 2000; 356: 795-801

The authors estimate the effects of air pollution on public health and its part in causing sickness and death in Europe. Their focus is on the economic aspects of this environmental factor, which are considerable.
COPYRIGHT 2000 The Lancet Ltd.


Background Air pollution contributes to mortality and morbidity. We estimated the impact of outdoor (total) and traffic-related air pollution on public health in Austria, France, and Switzerland. Attributable cases of morbidity and mortality were estimated.

Methods Epidemiology-based exposure-response functions for a 10 [micro]g/m3 increase in particulate matter (PM10) were used to quantify the effects of air pollution. Cases attributable to air pollution were estimated for mortality (adults ³ 30 years), respiratory and cardiovascular hospital admissions (all ages), incidence of chronic bronchitis (adults ³ 25 years), bronchitis episodes in children (<15 years), restricted activity days (adults ³ 20 years), and asthma attacks in adults and children. Population exposure (PM10) was modelled for each km2. The traffic-related fraction was estimated based on PM10 emission inventories.

Findings Air pollution caused 6% of total mortality or more than 40000 attributable cases per year. About half of all mortality caused by air pollution was attributed to motorised traffic, accounting also for: more than 25000 new cases of chronic bronchitis (adults); more than 290000 episodes of bronchitis (children); more than 0.5 million asthma attacks; and more than 16 million person-days of restricted activities.

Interpretation This assessment estimates the public-health impacts of current patterns of air pollution. Although individual health risks of air pollution are relatively small, the public-health consequences are considerable. Traffic-related air pollution remains a key target for public-health action in Europe. Our results, which have also been used for economic valuation, should guide decisions on the assessment of environmental health-policy options.

Lal K, Dutta KK, Vachhrajani KD, Gupta GS, Srivastava AK, Histomorphological changes in lung of rats following exposure to wood smoke, Indian J Exp Biol, 1993 Sep;31(9):761-764

Abstract: Rats were exposed to repeated, intermittent exposure to smoke generated from combustion of 1g wood/15 min, total period for 75 min daily under dynamic exposure conditions, over a period of 15, 30 and 45 days. First 15 days exposure caused mild bronchiolitis, hyperplasia and hypertrophy of bronchiolar epithelial lining cells, some necrosed lining cells desquamated into lumens, congestion of parenchymatous blood vessels, oedema, hyperplasia of lymphoid follicles, peribronchiolar and perivascular infiltration of polymorphonuclear cells, and mild emphysema. These lesions progressed further during 30 and 45 days of exposure, though emphysematous changes remain constant. By 30 days and 45 days, hyperplastic and hypertrophic changes of bronchioles become quite marked, with mononuclear cells infiltration and alveolar septa thickening. Hematological studies show marginal alterations in hemoglobin levels, ESR, PCV and TLCS during 15 days, where as significant changes in eosinophil were observed during 30 and 45 days, and ESR during 45 days only. The results indicate progressive pathomorphological pulmonary lesions with subsequent exposure to wood smoke in controlled conditions.

Larson T.V., Koenig J.Q., Wood Smoke - Emissions and NonCancer Respiratory Effects, [Review], Annual Review of Public Health, 15:133-156, 1994.

In conclusion, this review reveals much about the constituents and fate of wood smoke but not enough about the health effects. Animal toxicological studies show that wood smoke exposure can disrupt cellular membranes, depress macrophage activity, destroy ciliated and secretory respiratory epithelial cells, and cause aberrations in biochemical enzyme levels. With respect to the human epidemiological data, the literature summarized in Table 4 shows a coherence of the data from young children, with 7/8 studies especially in children with asthma, reporting increased respiratory symptoms, lower respiratory infection, and decreased pulmonary function as a result of exposure to wood smoke. As Bates (6) has discussed, coherence of the data, although not amenable to statistical tests, carries the weight of linkage and plausibility. These adverse respiratory effects associated with wood smoke exposure also comply with many of Brandon Hill's aspects of association necessary to establish causation (40). There is strength of association, consistency (7/8 studies showing positive associations), temporality, plausibility, coherence, and analogy (using ETS exposure; 70, 94). A biological gradient has not been shown, although one is suggested in the study of pulmonary function in wildfire fighters. We conclude that the preponderance of the data suggest a causal relationship between elevated wood smoke levels and adverse respiratory health outcomes in young children.

Lewtas J., Zweidinger R.B., Cupitt L., Mutagenicity, Tumorigenicity and Estimation of Cancer Risk from Ambient Aerosol and Source Emissions from Woodsmoke and Motor Vehicles, Air and Waste Management Association 84th Annual Meeting & Exhibition, Vancouver, British Columbia, 1991 June.

Lewis PR, Hensley MJ, Wlodarczyk J, Toneguzzi RC, Westley-Wise VJ, Dunn T, Calvert D. Outdoor air pollution and children's respiratory symptoms in the steel cities of New South Wales. Med J Aust. 1998 Nov 2;169(9):459-63.
Newcastle Environmental Toxicology Research Unit, University of Newcastle, NSW.

OBJECTIVE: To investigate the relationship between outdoor air pollution and the respiratory health of children aged 8 to 10 years.

DESIGN: A cross-sectional survey (between October 1993 and December 1993) of children's health and home environment. Summary measures of particulate pollution (levels of particles with an aerodynamic diameter less than 10 microns [PM10] each 6th day) and SO2 (daily mean and maximum hourly values) were estimated for each area (using air quality monitoring station data from July 1993 to June 1994).

Parents of 3023 primary school children (Years 3, 4 and 5) from industrial and non-industrial areas with air quality monitoring stations in the Hunter and Illawarra regions of New South Wales.
MAIN OUTCOME MEASURES: Reported occurrence of four or more chest colds, four or more attacks of wheezing, and night-time cough without a cold for more than two weeks, all within the previous 12 months.

RESULTS: 77% response rate, ranging by area from 66% to 88%. The average annual outdoor air pollution for the nine areas was 18.6-43.7 micrograms/m3 for PM10 and 0.16-0.90 parts per hundred million for SO2. The proportion of children reported to have the main outcome symptoms were: chest colds, 3.0%-9.7%; night cough, 12.3%-30.5%; and wheeze, 3.4%-11.3%. There was no significant association with SO2, but a significant increase in the odds of symptoms per 10 micrograms/m3 increase in PM10 on chest colds (odds ratio [OR], 1.43; 95% confidence interval [CI], 1.12-1.82) and night-time cough (OR, 1.34; 95% CI, 1.19-1.53), but not wheeze. Passive smoking was significantly associated with chest colds but not with the other symptoms. Maternal allergy was associated with all three respiratory symptoms, most strongly with wheeze.

CONCLUSION: These results provide evidence of health effects at lower than expected levels of outdoor air pollution in the Australian setting. They also suggest differences in contributions of environmental and hereditary factors to cough and chest colds compared with wheeze.

Lipsett M, Ostro B, Mann J, Wiener M, Selner J. 1991. Effects of exposures to indoor combustion sources on asthmatic symptoms. Proc 84th Annu. Meet. Air Waste Management Association, Vancouver, BC.

Lipsett M., Hurley S., Ostro B., Air Pollution and Emergency Room Visits for Asthma in Santa Clara County, California, Environmental Health Perspectives, 105(2):216-222, 1997 Feb.

Abstract : During the winters of 1986-1987 through 1991-1992, rainfall throughout much of Northern California was subnormal, resulting in intermittent accumulation of air pollution, much of which was attributable to residential wood combustion (RWC). This investigation examined whether there was a relationship between ambient air pollution in Santa Clara County, California and emergency room visits for asthma during the winters of 1988-1989 through 1991-1992. Emergency room (ER) records from three acute-care hospitals were abstracted to compile daily visits for asthma and a control diagnosis (gastroenteritis) for 3-month periods during each winter. Air monitoring data included daily coefficient of haze (COH) and every-other-day particulate matter with aerodynamic diameter equal to or less than 10 microns (PM10, 24-hr average), as well as hourly nitrogen dioxide and ozone concentrations. Daily COH measurements were used to predict values for missing days of PM10 to develop a complete PM10 time series. Daily data were also obtained for temperature, precipitation, and relative humidity. In time-series analyses using Poisson regression, consistent relationships were found between ER visits for asthma and PM10. Same-day nitrogen dioxide concentrations were also associated with asthma ER visits, while ozone was not. Because there was a significant interaction between PM10 and minimum temperature in this data set, estimates of relative risks (RRs) for PM10-associated asthma ER visits were temperature-dependent. A 60 mu g/m(3) change in PM10 (2-day lag) corresponded to RRs of 1.43 (95% CI = 1.18-1.69) at 20 degrees F, representing the low end of the temperature distribution, 1.27 (95% CI = 1.13-1.42) at 30 degrees F, and 1.11 (95% CI = 1.03-1.19) at 41 degrees F, the mean of the observed minimum temperatures. ER visits for gastroenteritis were not significantly associated with any pollutant variable. Several sensitivity analyses, including the use of robust regressions and of nonparametric methods for fitting time trends and temperature effects in the data, supported these findings. These results demonstrate an association between ambient wintertime PM10 and exacerbations of asthma in an area where one of the principal sources of PM10 is RWC. [References: 32]

Morgan, G. Daily Mortality and Air Pollution. Paper presented at the Health and Urban Air Quality Conference, Sydney, NSW, 3-4 June, 1996.

Morgan G, Corbett S, Wlodarczyk J, Lewis P. Air pollution and daily mortality in Sydney, Australia, 1989 through 1993. Am J Public Health 1998 May;88(5):759-764. New South Wales Health Department, Gladesville, Australia.

OBJECTIVES: This study examined the effects of outdoor air pollutants in Sydney, Australia, on daily mortality.
METHODS: Time-series analysis was performed on counts of daily mortality and major outdoor air pollutants (particulates, ozone, and nitrogen dioxide) in Sydney (1989 to 1993) with adjustment for seasonal and cyclical factors. Poisson regression was calculated with allowance for overdispersion and autocorrelation. The effects of lagging exposure by 0 to 2 days were assessed with single- and multiple-pollutant models.
RESULTS: An increase in daily mean particulate concentration from the 10th to the 90th centile was associated with an increase of 2.63% 95% confidence interval 0.87 to 4.41) in all-cause mortality and 2.68% (0.25 to 5.16) in cardiovascular mortality. An increase in daily maximum 1-hour ozone concentration from the 10th to the 90th centile was associated with an increase of 2.04% (0.37 to 3.73) in all-cause mortality and 2.52% (-0.25 to 5.38) in cardiovascular mortality. An increase in the daily mean nitrogen dioxide concentration from the 10th to the 90th centile was associated with an increase of 7.71% (-0.34 to 6.40) in respiratory mortality. Multiple-pollutant models suggest that the effects of particulates and ozone on all-cause and cardiovascular mortality, and of nitrogen dioxide on respiratory mortality, are independent of the effects of the other pollutants.
CONCLUSIONS: Current levels of air pollution in Sydney are associated with daily mortality.

Morris K, Morgenlander M, Coulehan J.L, Gahagen S, Arena V.C, Wood-burning stoves and lower respiratory tract infection in American Indian children, Am J Dis Child 1990 Jan;144(1):105-108

Abstract: Some studies suggest that home use of wood-burning stoves is an independent risk factor for lower respiratory tract infection in young children. To test this hypothesis in a population with a high prevalence of wood-burning stove use, we studied Navajo children with diagnosed pneumonia or bronchiolitis. We matched each case (less than or equal to 24 months of age) with a child of identical sex and age who was seen for well-child care or a minor health problem, and we interviewed an adult caretaker about family history and environmental exposures. Analyzing 58 case-control pairs, we found that home wood-burning stove use, recent respiratory illness exposure, family history of asthma, dirt floors, and lack of running water in the home increased the risk of lower respiratory tract infection. On multiple logistic regression analysis, however, only wood-burning stove use and respiratory illness exposure were independently associated with higher risk. Published erratum appears in Am J Dis Child 1990 Apr;144(4):490

Neas L.M., Dockery D.W., Ware J.H., Spengler J.D., Ferris B.G., Speizer F.E., Concentration of  Indoor Particulate Matter as a  Determinant of Respiratory Health in ChildrenAmerican Journal of Epidemiology, 139(11):1088-1099, 1994 June 1.

The effect of passive exposure to environmental tobacco smoke in the home on respiratory symptoms and pulmonary function level was studied in a cohort of white children aged 7-11 years examined in six US cities in 1983-1988. For 2,994 children with questionnaire-based exposure data, passive exposure to an additional pack of cigarettes smoked daily in the home was associated with increased incidence of lower respiratory symptoms (odds ratio (OR) = 1.25, 95% confidence interval (CI) 1.10-1.42). For 1,237 children with two consecutive 1-week measurements in both winter and summer, a 30-mu g/m(3) increase in the annual average indoor concentration of respirable particulate matter with an aerodynamic diameter of < 2.5 mu m (PM(2.5))-that is, approximately the effect of one pack per day of smoking-was marginally associated with an increased cumulative incidence of lower respiratory symptoms (OR = 1.13, 95% CI 0.99-1.30). Indoor measurements of PM(2.5) showed no direct association with children's pulmonary function measurements. Children whose mothers smoked during pregnancy showed a reduction of -2.6% (95% CI -5.2% to 0.1%) in volume-adjusted forced expiratory flow rates. Therefore, current indoor exposure to PM(2.5) increases the cumulative incidence of lower respiratory symptoms, but is only weakly associated with decreased pulmonary function level in preadolescent children. [References: 36]

Perez-Padilla R, Regalado J, Vedal S, Pare P, Chapela R, Sansores R, Selman M, Exposure to biomass smoke and chronic airway disease in Mexican women. A case-control study, Am J Respir Crit Care Med 1996 Sep;154(3 Pt 1):701-706 National Institute of Pulmonary Diseases, Mexico City, DF, Mexico.

Abstract: A case-control study was performed in women older than 40 yr of age to evaluate the risk of cooking with traditional wood stoves for chronic bronchitis and chronic airway obstruction (CAO). The subjects were recruited from patients attending a referral chest hospital in Mexico City. We selected 127 patients with chronic bronchitis or CAO, of which 63 had chronic bronchitis alone, 23 had CAO alone (FEV1 less than 75% of predicted), and 41 had both chronic bronchitis and CAO (cases). Four control groups were selected: 83 patients with pulmonary tuberculosis, 100 patients with interstitial lung diseases, 97 patients with ear, nose and throat ailments, and 95 healthy visitors to the hospital (controls). Exposure to wood smoke, assessed as any or none, and as hour-years (years of exposure multiplied by average hours of exposure per day) was significantly higher in cases than in controls. Crude odds ratios for wood smoke exposure were 3.9 (95% CI, 2.0 to 7.6) for chronic bronchitis only, 9.7 (95% CI, 3.7 to 27) for CAO plus chronic bronchitis, and 1.8 (95% CI, 0.7 to 4.7) for CAO only. Differences in exposure to wood smoke persisted after adjusting by stratification and logistic regression for age, income, education, smoking, place of residence, and place of birth. Risk of chronic bronchitis alone and chronic bronchitis with CAO increased linearly with hour-years of cooking with a wood stove; odds ratios for exposure to more than 200 hour-years compared with nonexposed were 15.0 (95% CI, 5.6 to 40) for chronic bronchitis only and 75 (95% CI, 18 to 306) for chronic bronchitis with CAO. The findings support a causal role of domestic wood smoke exposure in chronic bronchitis and chronic airflow obstruction.

Pierson W.E, Koenig J.Q, Bardana E.J Jr, Potential adverse health effects of wood smoke, West J Med 1989 Sep;151(3):339-342

Abstract: The use of wood stoves has increased greatly in the past decade, causing concern in many communities about the health effects of wood smoke. Wood smoke is known to contain such compounds as carbon monoxide, nitrogen oxides, sulfur oxides, aldehydes, polycyclic aromatic hydrocarbons, and fine respirable particulate matter. All of these have been shown to cause deleterious physiologic responses in laboratory studies in humans. Some compounds found in wood smoke--benzo[a]pyrene and formaldehyde--are possible human carcinogens. Fine particulate matter has been associated with decreased pulmonary function in children and with increased chronic lung disease in Nepal, where exposure to very high amounts of wood smoke occurs in residences. Wood smoke fumes, taken from both outdoor and indoor samples, have shown mutagenic activity in short-term bioassay tests. Because of the potential health effects of wood smoke, exposure to this source of air pollution should be minimal.

Ramage JE Jr, Roggli VL, Bell DY, Piantadosi CA. Interstitial lung disease and domestic wood burning. Am Rev Respir Dis 1988 May;137(5):1229-1232. Department of Medicine, Duke University Medical Center, Durham, NC 27710.

Abstract: A 61-yr-old woman was evaluated for dyspnea on exertion and interstitial lung disease. A unique association between inhaled particulates from wood burning and interstitial pneumonitis was demonstrated. Bronchoalveolar lavage revealed numerous particulates and fibers, as well as cellular and immunoglobulin abnormalities. The particles were shown to be carbonaceous by energy dispersive X-ray analysis (EDXA). Inflammation and fibrosis were found surrounding them on open biopsy. The particle source was traced to a malfunctioning wood-burning heater in the patient's home. We present this case to highlight the usefulness of BAL and EDXA in the elucidation of particle-associated lung disease.

Rao, C M, Qin, C, Robison, WG, Zigler, JS. Effect of smoke condensate on the physiological integrity and morphology of organ cultured rat lenses. Current Eye Research, 14:295-301, 1995.

Abstract: Smoke, either from cigarette smoking or from burning of organic fuels, has been proposed to be a major environmental risk factor for a variety of human diseases. Recently, smoke was implicated in cataract, an eye lens opacification which is a major cause of blindness. We have undertaken a study to investigate the effect of wood smoke condensate on the physiological integrity and morphology of organ cultured lenses. Lenses in organ culture are metabolically active and have functional defense systems, thus they provide an appropriate model for studying effects of smoke condensate. Our present study indicates that metabolites of wood smoke condensate accumulate in the lens. The ability of the lenses to accumulate rubidium-86 (mimic of potassium) and choline from the medium is compromised by exposure to smoke condensate. Rubidium efflux studies suggest that the damage is primarily at the uptake level and does not involve an overall increase in membrane permeability. Protein leakage experiments corroborate this suggestion. Histological data show distinct morphological changes such as hyperplasia, hypertrophy and multilayering of epithelial cells.

Robin L.F., Lees P.S.J., Winget M., Steinhoff M., Moulton L.H., Santosham M., Correa A., Wood-Burning Stoves and Lower Respiratory Illnesses in Navajo Children, Pediatric Infectious Disease Journal, 15(10):859-865, 1996 Oct.

Abstract: Background. Acute lower respiratory illnesses (ALRI) have been associated with exposure to domestic smoke. To examine further this association, a case-control study was conducted among Navajo children seen at the Public Health Service Indian Hospital at Fort Defiance, AZ. Methods. Cases, children hospitalized with an ALRI (n = 45), were ascertained from the inpatient logs during October, 1992, through March, 1993. Controls, children who had a health record at the same hospital and had never been hospitalized for ALRI, were matched 1:1 to cases on date of birth and gender. Home interviews of parents of subjects during March and April, 1993, elicited information on heating and cooking fuels and other household characteristics. Indoor air samples were collected for determination of time-weighted average concentrations of respirable particles (i.e. <10 mu m in diameter). Results. Age of cases at the time of admission ranged from 1 to 24 months (median, 7 months); 60% of the cases were male. Matched pair analysis revealed an increased risk of ALRI for children living in households that cooked with any wood (odds ratio (OR), 5.0; 95% confidence interval (CI), 0.6 to 42.8), had indoor air concentrations of respirable particles greater than or equal to 65 mu g/m(3) (i.e. 90th percentile) (OB 7.0, 95% CI 0.9 to 56.9), and where the primary caretaker was other than the mother (OR 9, 95% CI 1.1 to 71.4). Individual adjustment for potential confounders resulted in minor change (i.e. <20%) in these results. Indoor air concentration of respirable particles was positively correlated with cooking and heating with wood (P < 0.02) but not with other sources of combustion emissions. Conclusions. Cooking with wood-burning stoves was associated with higher indoor air concentrations of respirable particles and with an increased risk of ALRI in Navajo children. [References: 26]

Sandoval J, Salas J, Martinez-Guerra ML, Gomez A, Martinez C, Portales A, Palomar A, Villegas M, Barrios R. Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation. Chest 1993 Jan;103(1):12-20. Cardiopulmonary Department, Instituto Nacional de Cardiologia, Ignacio Chavez, Mexico City, Mexico.

Abstract: We describe the clinical, radiologic, functional, and pulmonary hemodynamic characteristics of a group of 30 nonsmoking patients with a lung disease that may be related to intense, long-standing indoor wood-smoke exposure. The endoscopic and some of the pathologic findings are also presented. Intense and prolonged wood-smoke inhalation may produce a chronic pulmonary disease that is similar in many aspects to other forms of inorganic dust-exposure interstitial lung disease. It affects mostly country women in their 60s, and severe dyspnea and cough are the outstanding complaints. The chest roentgenograms show a diffuse, bilateral, reticulonodular pattern, combined with normalized or hyperinflated lungs, as well as indirect signs of pulmonary arterial hypertension (PAH). On the pulmonary function test the patients show a mixed restrictive-obstructive pattern with severe hypoxemia and variable degrees of hypercapnia. Endoscopic findings are those of acute and chronic bronchitis and intense anthracotic staining of the airways appears to be quite characteristic. Fibrous and inflammatory focal thickening of the alveolar septa as well as diffuse parenchymal anthracotic deposits are the most prominent pathologic findings, although inflammatory changes of the bronchial epithelium are also present. The patients had severe PAH in which, as in other chronic lung diseases, chronic alveolar hypoxia may play the main pathogenetic role. However, PAH in wood-smoke inhalation-associated lung disease (WSIALD) appears to be more severe than in other forms of interstitial lung disease and tobacco-related COPD. The patients we studied are a selected group and they may represent one end of the spectrum of the WSIALD.

Stone R. Environmental toxicants under scrutiny at Baltimore meeting. (March 1995 Society of Toxicology conference) Science, March 24, 1995 v267 n5205 p1770(2)

Relevant Section of article:

Wood Smoke Fires Infections

The crackle of flames from a fireplace may warm the heart and kindle romance. But among those fuzzy feelings by the fireside might also be something not as nice - the beginnings of a nasty lung infection, caused by particles in wood smoke that appear to suppress the immune system. The reason for concern stems from two studies presented at the meeting linking exposure to wood smoke to an increased susceptibility to lung infections in rodents.

Part of the problem is that wood smoke is a witch's brew of carcinogens, including aldehydes and polycyclic aromatic hydrocarbons, carbon monoxide, and organic particles less than 10 microns in diameter, called [PM.sub.10]. [PM.sub.10]s have been implicated in increased morbidity and mortality on days of heavy air pollution. Epidemiological studies have also linked wood smoke to respiratory illness in preschoolers.

Two new studies lend biological credence to this statistical association. In one, immunotoxicologist Mary Jane Selgrade of the Environmental Protection Agency (EPA) found that mice breathing wood smoke were more susceptible to a flu bug than those exposed to emissions from an oil furnace, which releases fewer pollutants and less of them. After the mice spent 6 hours inhaling various combustion products, Selgrade exposed them to an aerosol of the bacterium Streptococcus zooepidemicus, which causes severe respiratory infections. After 2 weeks, 5% of the mice in the control group exposed to air and bacteria had died, along with a similar percentage of the mice breathing the oil fumes. But 21% of the wood-smoked mice were felled.

To measure the potency of the smoky pollutants, another group, led by New York University School of Medicine immunotoxicologist Judith Zelikoff, made use of a unique furnace developed by colleague Lung Chi Chen. Chen's furnace delivers known amounts of wood-smoke constituents directly to a rat's nose. Using the homemade furnace, Zelikoff's team exposed rats to small amounts of red-oak smoke, maintaining concentrations of particulate matter at 800 micrograms per cubic meter for one hour - levels "relevant to home burning," Zelikoff says.

NYU immunotoxicologist Mitchell Cohen then exposed some rats to Staphylococcus aureus, another respiratory pathogen. Although the rats' lungs showed little inflammation or other signs of insult, the bacteria were more virulent in the smokers than in the nonsmokers. Researchers attribute the result to a suppression in activity of the rats' macrophages, immune cells that roam the body, looking to engulf and destroy foreign particles. "It's really good data," says EPA toxicologist Gary Hatch.

Zelikoff says her findings emphasize the importance of inspecting wood-burning units for leaks and making sure rooms are properly ventilated. As for herself, Zelikoff says she and her husband intend to continue using their fireplace - unless, of course, they think they're coming down with something.

Main summary of Woodsmoke Health Effects

Schwartz J, Slater D, Larson T.V, Pierson W.E, Koenig J.Q., Particulate air pollution and hospital emergency room visits for asthma in Seattle, Am Rev Respir Dis 1993 Apr;147(4):826-831

U.S. Environmental Protection Agency, Washington, D.C.

Abstract: Recent studies have associated short-term exposure to respirable particulate matter (PM10) exposure with peak flow decrements, increased symptoms of respiratory irritation, increased use of asthma medications, and increased hospitalization for asthma. Increased mortality from chronic respiratory disease has also been reported. To help confirm whether PM10 exposure is a risk factor for the exacerbation of asthma, we compiled daily records of asthma emergency room visits from eight hospitals in the Seattle area. In Poisson regressions controlling for weather, season, time trends, age, hospital, and day of the week, the daily counts of emergency room visits for persons under age 65 were significantly associated with PM10 exposure on the previous day. The mean of the previous 4 days' PM10 was a better predictor (p < 0.005). The relative risk for a 30 micrograms/m3 increase in PM10 was 1.12 (95% confidence interval 1.20 to 1.04). Daily PM10 concentrations never exceeded 70% of the current ambient air quality standards during the period. The consistency of investigations of the health effects of PM10 suggest that increased attention should be given to the control of particulate matter air pollution.

Schwartz J., Dockery D.W., Neas L.M,. Is Daily Mortality Associated Specifically With Fine Particles?, Journal of the Air & Waste Management Association, 46(10):927-939, 1996 Oct.

Recent epidemiologic studies have consistently reported increased daily mortality associated with exposures to particulate air pollution. Currently, particulate mass is measured as particles smaller than 10 mu m (PM(10)). Fine (PM(2.5)) and coarse (PM(10) - PM(2.5)) mass and sulfate particle concentrations were measured in six eastern U.S. cities for eight years, and aerosol acidity concentrations were measured for approximately one year. Daily mortality for these metropolitan areas was combined with particulate air pollution and weather measurements. City-specific associations with each measure of particle pollution were estimated by Poisson regression, adjusting for time trends and weather by nonparametric methods. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. PM(10), PM(2.5), and SO4 = were each significantly associated with increased daily mortality, while no associations were found with coarse mass nor with aerosol acidity (H+) concentrations. The strongest association was found with PM(2.5) - A 10 mu g/m(3) increase in two-day mean PM(2.5) was associated with a 1.5% (95% CI 1.1% to 1.9%) increase in total daily mortality. Somewhat larger increases were found for deaths caused by chronic obstructive pulmonary disease (+3.3%) and by ischemic heart disease (+2.1%). These data suggest that increased daily mortality is specifically associated with particle mass constituents found in the aerodynamic diameter size range under 2.5 mu m, that is, with combustion-related particles. [References: 75]

Sobue T, Association of indoor air pollution and lifestyle with lung cancer in Osaka, Japan, Int. J. Epidemiol.,1990; 19 Suppl 1: S62-6

A hospital-based case-control study among non-smoking women was conducted to clarify risk factors in non-smoking females in Japan. Cases consisted of 144 non-smoking female lung cancer patients, and these were compared to 713 non-smoking female controls. The odds ratio (95% confidence interval) for use of wood or straw as cooking fuels when subjects were 30 years old was estimated as 1.77 (1.08 to 2.91). For those whose household members, other than husbands, had smoked, the odds ratio was estimated as 1.50 (1.01 to 2.32). For those whose mothers had smoked, the odds ratio was estimated as 1.28 (0.71 to 2.31). Use of heating appliances did not show an elevated risk. Some points to be noted in the study of low-risk agents for lung cancer are discussed.

Tuthill RW. 1984. Woodstoves, formaldehyde and respiratory diseases. Am. J. Emidemiol. 120:952-55.

van Houdt JJ, Daenen CM, Boleij JS, Alink GM, Contribution of wood stoves and fire places to mutagenic activity of airborne particulate matter inside homes, Mutat Res 1986 Aug;171(2-3):91-98

Abstract: Wood combustion produces compounds that are mutagenic in the Salmonella/microsome assay. As combustion products can be emitted in the home and the use of wood as a residential energy source is growing, an impact on human health might be of concern. In this study experiments were carried out to determine the contribution of wood combustion in stoves and fire places to indoor mutagenic activity under normal living conditions. Airborne particles from living rooms which were heated by stoves, or by fire places, and from outdoors were collected simultaneously. In each room two samples were collected during two consecutive weeks: one week the room was heated by central heating, the other week by wood combustion. Sampling took place in a total of 24 homes. Methanol extracts of the samples were tested in the Salmonella/mammalian microsome assay. Results show that mutagenic activity of outdoor air exceeds indoor mutagenicity. At the same time a correlation is found between in- and out-door mutagenicity, both with and without S9. However, a large difference is found between the ratio -S9/+S9 of in- and out-door mutagenic activity. Systematic differences in the ratio -S9/+S9 between control and experimental conditions are not observed. The use of wood stoves caused an increase of indoor mutagenicity in 8 out of 12 homes. It could be concluded that the use of an open fire consistently leads to an increase of mutagenic activity. This increase was caused by wood combustion products.

Volkmer R.E., Ruffin R.E. , Wigg N.R., Davies N., The Prevalance of Respiratory Symptoms in South Australian PreSchool Children, .2. Factors Associated with Indoor Air Quality, Journal of Paediatrics & Child Health. 31(2):116-120, 1995 April

Abstract: Objective: This study investigated the relationship between indoor air quality and the prevalence of respiratory symptoms in South Australian preschool children. Methodology: Data were collected from 14124 families with a child aged 4 years 3 months to 5 years of age. This sample represents 73% of the targeted State preschool population. At the time of a routine preschool health check, parents completed a questionnaire regarding: their child's respiratory health and place of residence (postcode), parental smoking, type of fuel used for cooking and heating and method used for home cooling. Results: For preschool children residing in the greater Adelaide region, logistic regression analyses found that having a natural gas stove compared to an electric stove was significantly associated with increased prevalence rates for: (i) asthma (odds ratio [OR] 1.24); (ii) wheezing in the preceding 12 months (OR 1.16); excessive colds (OR 1.14); and hay fever (OR 1.13). The use of a liquid petroleum gas stove compared to an electric stove was not associated with any respiratory symptoms. The use of a flueless gas heater compared to other forms of heating was significantly associated with increased prevalence rates for dry cough (OR 1.26), ever having wheezed (OR 1.15) and wheezing in the preceding 12 months (OR 1.18). The use of a wood fire/heater compared to other forms of heating was significantly associated with a reduced prevalence rate for dry cough (OR 0.84) and ever having wheezed (OR 0.82). Parental smoking was significantly associated with increased prevalence rates for bronchitis (OR 1.21) and ever having wheezed (OR 1.24). The form of home cooling used was not associated with prevalence rates, after accounting for geographic location. Socio-economic status (postcode level) was not generally associated with prevalence rates. Conclusions: These results suggest that respiratory symptom prevalence is related to the fuel used for cooking and heating and parental smoking. Prospective investigation regarding indoor air quality and respiratory symptoms is required. [References: 24]

Von Mutius E., Illi S., Nicolai T., Martinez FD., Relation of Indoor Heating with Asthma, Allergic Sensitisation, and Bronchial Responsiveness - Survey of Children in South Bavaria, British Medical Journal, 312(7044):1448-1450, 1996 June 8.

Objective-To investigate the relation between different types of heating and the prevalence of atopic diseases, skin test reactivity, and bronchial hyperresponsiveness. Design-Cross sectional survey-among school-children aged 9-11 years. Skin prick tests, pulmonary function tests, and bronchial challenge in the children and self completion of a written questionnaire by the children's parents.
Subjects-1958 children in a rural area in southern Bavaria, Germany.
Main outcome measures-Prevalence of asthma, hay fever, and atopic dermatitis as determined by parents' answers to a questionnaire; the atopic status of the child assessed by skin prick tests; and bronchial responsiveness to cold air challenge in the children.
Results-After possible confounders were controlled for, the risk of developing hay fever (odds ratio=0.57; 95% confidence interval 0.34 to 0.98), atopy defined as at least one positive reaction to a panel of common aeroallergens (0.67; 0.49 to 0.93), sensitisation to pollen (0.60; 0.41 to 0.87), and of bronchial hyperresponsiveness (0.55;0.34-0.90) was significantly lower in children living in homes where coal or wood was used for heating than in children living in homes with other heating systems.
Conclusions-Factors directly or indirectly related to the heating systems used in rural Bavarian homes decrease the susceptibility of children to becoming atopic and to developing bronchial hyperresponsiveness. [References: 18]

Zhang, J, Smith KR. Hydrocarbon emissions and health risks from cookstoves in developing countries. Journal of Exposure Analysis and Environmental Epidemiology, 6(2):147-161,1996.

The nonmethane hydrocarbon emissions from several types of cookstoves commonly used in developing countries were measured in a pilot study conducted in Manila, the Philippines. Four types of fuel, i.e., wood, charcoal, kerosene, and liquefied petroleum gas (LPG), were tested. Because kerosene was burned in three different types of stoves, there were six fuel/stove combinations tested. Fifty-nine nonmethane hydrocarbons were identified frequently In emissions of these cookstoves, with emission ratios to CO2 up to 5.3 x 10(-3). The emissions were quantitated with emission factors on both a mass basis (emissions/kg fuel) and a task basis (emissions/cooking task). On a task basis, combustion of biomass fuels (wood and charcoal) generally produced higher emission factors than combustion of fossil fuels (kerosene and LPG). One type of kerosene stove (wick stove), however, still generated the greatest emissions of some individual and classes of hydrocarbons, indicating that emissions were dependent on not only fuel types but also combustion devices. Some hydrocarbons, e.g., benzene, 1,3-butadiene, styrene, and xylenes, were of concern because of their carcinogenic properties. The lifetime risk from exposures to these compounds emitted from cookstoves was tentatively estimated by using a simple exposure model and published cancer potencies. Among the six fuel/stove combinations, wood stoves generated the highest cancer risk and LPG generated the least. Compared to the cancer risks of benzene and 1,3-butadiene, those of styrene and xylenes were negligible. The estimated cancer risk of benzene or that of styrene from use of a biomass cookstove exceeded published risk estimates from all sources of airborne benzene or styrene (excluding active tobacco smoking) in the United States. [References: 30]