SciELO - Scientific Electronic Library Online

 
vol.30 issue2Bronchiolitis obliterans organizing pneumoniaSmoking and its peculiarities during pregnancy: a critical review author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand

Journal

Article

Indicators

Related links

Share


Jornal Brasileiro de Pneumologia

Print version ISSN 1806-3713On-line version ISSN 1806-3756

J. bras. pneumol. vol.30 no.2 São Paulo Mar./Apr. 2004

http://dx.doi.org/10.1590/S1806-37132004000200015 

REVIEW ARTICLE

 

Biomass burning and its effects on health *

 

 

Marcos Abdo Arbex(TE SBPT); José Eduardo Delfini Cançado(TE SPBT); Luiz Alberto Amador Pereira; Alfésio Luís Ferreira Braga**; Paulo Hilário do Nascimento Saldiva

Correspondence

 

 


ABSTRACT

The first thought that comes to mind concerning air pollution is related to urban centers where automotive exhausts and the industrial chimneys are the most important sources of atmospheric pollutants. However a significant portion of the earth’s population is exposed to still another source of air pollution, the burning of biomass that primarily affects developing countries. This review article calls the attention of lung specialists, public authorities and the community in general to the health risks entailed in the burning of biomass, be it indoors or outdoors to which the population is exposed. This review describes the main conditions that lead to the burning of biomass and how the literature has recorded its effects on human health discussing the psychopathological mechanisms. Finally two recent studies are presented that emphasize an important type of biomass burning that of the sugar cane straw. This is a common practice in several regions of Brazil changing the respiratory morbidity standards of the population exposed.

Key words: air pollution, biomass, sugar cane, smoke, vegetation fires, respiratory disease.


 

 

Acronyms and abbreviations used in this paper
g/m3 - microgram per cubic meter
m - micrometer (one millionth of a meter)
BC- Black Carbon
CETESB – Companhia de Tecnologia de Saneamento Ambiental (Environamental Sanitation Technology Company)
FVC – Forced Vital Capacity disease
EPA – Environmental Protection Agency (USA)
FEF25-75% - Forced expiratory flow to 25-75% of the FVC
UAI - Upper airway tract infection
LAI - Lower airway tract infection
LPAE – Laboratório de Poluição Atmosférica Experimental (Experimental Atmospheric Pollution Laboratory)
WHO – World Health Organization
PM – Particulate matter
PM10 – Particulate matter with an aerodynamic diameter below 10 m
PM2.5 – Particulate matter with an aerodynamic diameter below 2.5 m
TAP – Total airborne particles
FEV – Forced expiratory volume
FEV1 – Expiratory volume at the first second of the forced vital capacity procedure

 

General aspects

Ever since the beginning of the last century, studies in the medical literature have witnessed a strong association between atmospheric pollution due to fossil fuel emission and human morbid-mortality increase in developed countries. This has been the case even for those air pollutant levels which have been considered as safe for the health of the exposed population (1). Nevertheless, only a handful of studies have aimed at the noxious effects produced by biomass burning (any material of either vegetable or animal provenance used as energy source). In 1985, a report issued by the WHO (2) questioned the seriousness and the extension of the damage caused by biomass-burning air pollution in rural areas of developing countries.

Biomass incineration is the biggest domestic energy source in developing countries (3). Approximately half of the Earth’s population, and over ninety percent of homes in rural areas of developing countries, keep making use of the energy from biomass burning, such as the burning of wood, charcoal, animal excrement and agricultural residues; thus, producing high levels of indoor air pollution, where children and women cooking can be found. This scenario gives rise to respiratory infections, the number one cause for infant mortality in developing countries (3, 4).

Deliberate or accidental vegetation burning, regardless of the considerable technological advancements in humanity—or maybe due to them—has become uncontrollable at times, reaching large extensions in forests, savannas and even in less dense vegetation areas. Fire has become an increasing problem, as far as the remaining tropical forests in the planet are concerned, and the pollution resulting from smoke has had a dramatic impact on the health of the exposed population. Such impact triggers rise in mortality, hospitalizations, emergency room care, medication usage due to cardiovascular and respiratory diseases, aside from reducing pulmonary function (4).

Even though there has been much effort spent in scientific research and in media attention regarding deforestation and forest fires, deliberate or accidental ones, the incidence and the effects of such fires have been ignored. Extensive forest fires in Borneo (1983 and 1997), Thailand (1997), Indonesia (1997), Roraima (1997-1998), Mato Grosso (1998) and Pará (1998), have raised the issue; however, the measures which were adopted in order to prevent, or even control, such fires have not been enough (5).

 

The Burning Process, Its Products and Physiopathological Consequences

Burning is a chemical procedure through which a material rapidly reacts to the oxygen in the air producing intense heat and light; in the case of biomass burning, it involves three stages: ignition, flaming (burning and smoking with flame), smoldering (burning and smoking without flame).

The biggest percentage of biomass burning, around eighty percent, occurs in tropical areas.  This burning is responsible for producing the main source of toxic gas, particulate matter and greenhouse-effect gases in the planet (6)—influencing the atmospheric physics and chemistry, producing chemical varieties that have significantly changed the pH of rainwater  (7, 8), affecting the atmosphere’s thermic balance by interfering on the amount of solar radiation reflected to outer space (9,10). Table 1 shows a concise description of the main pollutants resulting from the biomass burning process.

As it can be seen on Table 2, studies have shown that live beings that are exposed to several of these elements may end up producing, on the long as well as on the short-term, noxious effects to human health.

Among such elements, the most toxic pollutant and the one that has been studied the most is the particulate matter resulting from biomass burning, either from indoor or outdoor combustion. It is mostly (94%) made of fine and ultrafine particles (Figure 1), in other words, particles that are able to reach deep into the respiratory system, passing through the epithelial barrier, reaching the interstitial lung and triggering an inflammatory process (11-13) (Figure 2). Shi et al (14) infer that the adverse effects of the particulate matter to one’s health may be a result of the production of intracellular oxidizing agents; henceforth, being the first response and acting as the inflammation’s stimulating factor, as it is shown on Figure 3. Turn et al (15) have shown that forest fires convey pollutants that impact local as well as faraway areas due to its long distance reach; therefore, proportionally raising the impact on individuals.

 

 

 

 

 

 

Indoor Biomass Burning and its Effects on Health

There have been reports of indoor air pollution ever since pre-historic times when human beings started their search for temperate climates around 200 thousand years ago. The colder climate brought about the need to make use of shelters and caverns, as well as of fire for heating, cooking and lighting. Ironically, the same fire that allowed humans to enjoy the benefits of their shelters led their exposure to high levels of pollution, as it has been testified by the charcoal found in pre-historic caverns. The soot found in South African caverns suggests that the human race has been making use of fire since 1.5 million of years (16).

The effects on health due to long exposure to the smoke of indoor biomass burning have been associated to acute respiratory infections on children, chronic obstructive pulmonary disease (COPD), pneumoconiosis, cataract and blindness, pulmonary tuberculosis and adverse effects to pregnancy. All of these effects have been well studied in developing countries, where women and their children cook for long periods of time on wood-burning stoves without air openings to drive the smoke outwards. While developed countries mainly associate chronic obstructive pulmonary disease (COPD) with cigarette smoking, in the developing regions, where women cigarette smokers are less frequent, cross-sectional epidemiological and control-case studies suggest that exposure to smoke from biomass burning is the number one cause of chronic obstructive pulmonary disease. Padmavati et al (17, 18) from India, have shown the relationship between exposure to indoor pollutants and COPD, which may lead to cor pulmonale. These studies show that the Indian incidence rate of chronic cor pulmonale is similar between men and women even though 75% of men, as compared to only 15% of women, smoke. Analysis comparing the incidence of chronic cor pulmonale in men and women demonstrate that the pathology is more common among young women, the average age for women being between 10 to 15 years under those of the male sex. In 18 necropsies done on women who were nonsmokers, but who had been exposed to pollutants of biomass burning, showed that all of them presented pulmonary emphysema, 11 had bronchiectasis, 5 had chronic bronchitis, and 2 had tuberculosis (18).  The predominance of chronic cor pulmonale was lower in the southern states, compared to those in the north; this fact has been associated to better indoor ventilation in southern homes, higher temperatures during the summertime and no heating during its milder winter. A succeeding study confirmed these data (28[19]). Máster (20) assessed the inhabitants of local villages in New Guinea’s mountainous regions who nearly daily made use of biomass burning for heating purposes—78% of those interviewed and who were over 40 presented coughing, diffuse reduction in the vesicular murmur, crackling stertorous breathing and mainly obstructive ventilatory disorders. Anatomic-pathological studies that contain samples from exposed individuals showed incidence of center-lobular emphysema, pleural thickening, pulmonary fibrosis, hypertrophy of mucus glands, anthracotic pigment depositing.   In New Guinea(21,22), Anderson observed that the figures for adults over 45 who have a high incidence of respiratory symptoms are proportionally similar between men and women; additionally, 20% of men and 10% of women presented airflow obstruction with FEV1/ FVC below 60%. The author also emphasized that those patients whose clinical records showed COPD presented diffuse interstitial pulmonary fibrosis and bronchiectasis. In Nepal, the incidence of chronic bronchitis is proportional among men and women (18.9%) even though cigarette smoking is substantially higher among men (23, 24).  The incidence of chronic bronchitis is also considerable in Ladakh, India, as well as in Pakistan, where the incidence of women smokers is rare (25, 26). Control-case studies conducted in hospitals have shown that individuals who are exposed to smoke from biomass burning present a higher incidence record of airflow obstruction than those from the control groups (27-29).  This is a recurring fact of the research conducted in other communities (19, 30, 31). The research carried out in hospitals present severe obstruction and a significant, as well as positive, association to pollutant exposure levels (OR varying between 1.8 e 9.7).  One study carried out in a community showed an OR of 2.5(31). In Mexico, Regalado et al (30) have verified that biomass burning as an energy source was associated to a 4% reduction of the FEV1/FVC in individuals who had been exposed to a 1000 ug/m3 concentration of particulate matter in kitchens, as well as being associated to a 2% reduction of the FEV1. In India, the population that made use of biomass as energy source presented a lower FVC, as opposed to those who made use of gas or kerosene (19). Pandey et al (23, 24) reported an exposure-response relationship with a reduction in the FEV1 and FVC as the number of hours exposed to the pollutants would increase. In a cross-sectional study carried out by Menezes et al (32) in an urban area in southern Brazil, the aim was to determine the incidence of chronic bronchitis and its relationship to risk factors. Among the 1053 individuals over 40 who were interviewed, there was a significant association between the disease and the high levels of indoor pollution.

In the presented studies, exposure to pollutants was customarily estimated by means of questionnaires that would assess the daily number of hours, as well as the number of years, under exposure. A control-case study considered the figure hour-years (years of exposure multiplied by the hourly average of daily exposure). The incidence risk of chronic bronchitis exclusively and of chronic bronchitis associated with chronic airway obstruction increased linearly, proportionally to the hour-years of exposure to biomass smoke. The OR rate to an exposure above a 200 hour-years, comparing to those who had not been exposed, resulted in a 15.0 (CI 95%, 5.6-40) to chronic bronchitis and 75 (CI 95%, 18-306) to chronic bronchitis linked to chronic airway obstruction (29).  Few studies have quantified the particulate matter level in kitchens; therefore, confirming the high concentration of this pollutant (33, 30, 31). Narboo(25) has demonstrated the relationship between the number of hours spent in the kitchen and the individual level of carbon monoxide inhaled. These evidences, among others, have plotted the inclusion of indoor pollution due to biomass burning within the risk factors to the development of chronic obstructive pulmonary disease (COPD) presented at the “Global Strategy for The Diagnosis Management, and Prevention of Chronic Obstructive Lung Disease” (GOLD).

In 1991, Narboo et al (25, 34) demonstrated in Ladakh, India, individuals with a clinic-radiological record compatible to those with pneumoconiosis. Nevertheless, there were no mines or factories in their surrounding areas. Two factors were uncovered in explaining the development of such respiratory pathology: a) exposure to particles from sand storms, which are common during springtime, b) exposure to particulate matter from biomass burning used to heat the homes, without any ventilation, in order to face the region’s harsh winter. Clinical and radiological investigations (35) in 449 inhabitants of three different villages subject to light, moderate and severe intensity sand storms showed a pneumoconiosis incidence of 2.0%, 20.1% and 45.3%, respectively. The thoracic radiographs have shown radiological characteristics which were indistinguishable to the radiological standards present in individuals diagnosed with pneumoconiosis working in mines or factories. The particle concentration found in kitchens without any chimney varied between 3.22 and 11.30 mg/m3, averaging around 7.50 mg/m3. Detailed statistical studies have established that the incidence of pneumoconiosis is due to sand storms, exposure to products of biomass burning and age. Anthracosis and diffuse interstitial pulmonary fibrosis, two other diseases that are commonly associated with occupational exposure, have been frequently documented in necropsies of patients who were exposed to indoor biomass smoke (36, 37).

Acute lower respiratory tract infection (ALRI) is the number one cause for mortality among children under 5, adding up to 2 million annual deaths of children in this age group. Sixteen epidemiological studies, 11 of these being control-case studies and 5 being cohort studies, carried out for the last 20 years in developing countries, have shown an association between exposure to pollution from indoor biomass burning and acute lower respiratory tract infections in children. The criteria used by WHO and/or the radiological evidences were used to identify the LRI; nearly all studies assessed the following: the intensity to the exposure, including the type of stove and fuel used (38-46); if children were in contact with the smoke while the food was being prepared (47, 48); if mothers carried their infants on their back while cooking (49-51). As an example, Armstrong and Campbell (50) demonstrated that the pneumonia risk linked to smoke exposure had increased for girls, but not for boys. The authors inferred that this difference is a consequence of these girls’ longer exposure to smoke, not to the biological differences between both genders. In the topic’s most recent study, Ezzatti and Kammen (52, 53) observed 345 children in Kenya’s southern region (93 under 5 years of age) in 55 dwellings located in cattle ranches. These types of dwellers made use of biomass as an energy source through wood-burning stoves without any chimneys. The researchers evaluated the individual exposure of adults and children by combining an assessment of the symptoms that were weekly investigated to the criteria stipulated by the WHO for LRI. This was the first study to assess the relationship between particulate matter exposure and child (under 5) LRI incidence, as well as adults’ incidence. The disease risk was strongly associated to the high levels of exposure. The authors did not make the adjustments according to socio-economical level. In this study, the child LRI incidence was considerably higher, as compared to previous studies that had assessed similar populations.  A detailed review of the issue was published by Smith et al (54) who came to the conclusion that associating exposure to smoke caused by biomass burning and LRI may be considered as causal; however, the quantitative risks have yet to be portrayed.

Only one study links perinatal mortality (babies who died immediately before or after birth) to biomass. A link between these (OR of 1.5 CI 95%: 1.0-2.1 p= 0.05) has been adjusted to a broad variety of factors, even if there was no direct access to the exposure itself. Nonetheless, such findings have a marginal statistical meaning similar to the open air atmospheric pollution studies (55).

A project conducted in Guatemala demonstrated that the weight of newborn babies coming from homes that made use of biomass as fuel was 63 g (CI 95%: 0.4-127, p=0.049) below those newborn babies from homes that made use of “clean” fuel. This estimate has been adjusted to confusing factors; nevertheless, there was no direct access to the pollutant’s exposure (56).

The research projects associating indoor biomass burning and asthma conflict with one another. A control-case study among students in Nairobi, Kenya, has provided information showing an increasing number of individuals who have asthma in dwellings that are exposed to wood-burning smoke (57). In Nepal, a control-case study that evaluated individuals between the ages of 11 and 17 according to the ISAAC (International Study of Asthma and Allergies in Children) found an OR of 1.81(1.04-4.8) to asthma as compared to those individuals who have made use of biomass as energy source and those who used gas or kerosene (58). A cross-sectional study that evaluated 1058 individuals between the ages of 4 and 6 in Guatemala, also abiding by the ISAAC standards, has found an OR of 1.81 (CI 95%; 1.04-3.12) to students at any given period of time and of 2.35 (CI 95%; 1.08-5.13) to the students within the last 12 months of evaluation (59) who have been exposed to biomass burning.  Nonetheless, there are studies where such association has not been made (26, 33, 60).

Recent studies infer an association with indoor biomass burning and pulmonary tuberculosis (61-63). This association, if verified, would have serious implications on public health. The exposure to smoke from biomass burning could explain the significant difference found in India, once 59% of the cases of tuberculosis appear in rural areas, where biomass is largely used as fuel, while 23% of the cases appear in urban areas. The environmental exposure to particulate matter can be a potentializing agent in the binomial poverty/tuberculosis—which, up until today, has only been explained by means of malnutrition, overcrowding and inadequate access to health services.

India has the largest number of blind people as compared to any other country in the world. Aside from this fact, one out of every three cases of cataract in the world takes place in India. Cataract is responsible for 80% of the cases of blindness in that country. Eye irritation, conjunctival hyperemia, eye watering are some signs and symptoms universally associated with exposure to smoke, but they may also be a preliminary evidence leading to future blindness (64). Approximately 170 thousand individuals were observed in India and showed an OR of 1.32 (CI 95%; 1.16-1.50) when a complete or partial blindness evaluation was conducted comparing patients that mainly used biomass and patients who used other types of fuel—after taking geographic variation, housing and socio-economic conditions under consideration. However, cigarette smoking and nutritional state were not evaluated (65).

Up until the moment, the collected data do not present any association between cancer risks and high levels of exposure to smoke from biomass burning. Although the smoke from such procedure is potentially cancerous, its cancerous potential is still lower than that of smoke from automotive fuel burning. (16)

The research which approaches indoor air pollution in developing countries and its effects on health showed evidence of their important association even though there are methodological limitations, such as: a) lack of a better definition of exposure to pollution; b) all of the studies conducted were observational and c) the confusing elements, in general, were not properly assessed. However, aside from the limitations of these epidemiological studies, the evidence of the causal relationship between COPD and LRI is especially consistent when analyzed in conjunction with the previous findings related to cigarette smoking pollution and urban atmospheric pollution (considering the pollutant’s different compositions) as well as the evidence in animal studies.

Different research projects carried out in the United States have focused on the relationship between fireplace wood burning and the symptoms and/or measurements of pulmonary function. The majority of these projects concentrate on children under 5 since the susceptibility of this age group is higher due to their smaller pulmonary volume capacity and by their yet incomplete immune system development. In addition, their absence of active cigarette smoking and occupational exposure would eliminate these confusing factors.  Table 3 (66-72) presents the studies that have focused on the indoor issue more consistently. Other studies (Table 4) (73-78) have assessed the effects on health in communities where smoke from wood burning has contributed—although it is not the only one available—as a source of particulate matter in the atmosphere. 

Smoke produced by indoor biomass burning interferes in the mucociliary mechanism, decreasing the bactericide properties found in the pulmonary macrophage; thus, causing phagocytosis power reduction (79, 80).

Two animal toxicological studies infer that exposure to smoke from wood burning may increase the susceptibility to respiratory infections. In a study backed by the Environmental Protection Agency of the United States (EPA), Selgrade compared the effects of being exposed to an aerosol containing Streptococcus zooepidemicus, an agent that causes severe respiratory infection, on three groups of laboratory rats that had previously been exposed to one of these three scenarios: pure air or pollutants from either boiler fuel burning or wood burning. Two weeks after their exposure, 5% of the rats exposed to pure air and to boiler fuel burning died, while the rats that had been exposed to wood burning had a mortality rate of 26%. Judith Zelikoff, from New York University, and her cooperative team exposed rats to a 800 g/m3 concentration of smoke from oak-wood burning for one hour. Next, the same rats were exposed to Staphylococcus aureus by means of intratracheal instillation. One control group, which was not exposed to the smoke, had also received the same treatment. The bacteria seemed to be more virulent on the rats exposed to the smoke; the researchers have suggested that smoke suppresses the macrophage activity (81).

 

Outdoor Biomass Burning and Its Effects on Health

If the studies evaluating indoor pollution of biomass burning profusely demonstrate its adverse effects, this is not the case for outdoor pollution. Even the WHO recognizes that such intensity and seriousness depend upon a series of factors, such as: the characteristics of the pollutant as well as of the exposed population, individual exposure, the susceptibility of the exposed individual and the confusing factors (4). The smoke from outdoor biomass burning produces indirect adverse effects on health by reducing the photosynthesis and causing a reduction in the agriculture harvest; by blocking the A and B ultraviolet rays and causing an increase of pathogenic microorganisms in the air and in the water, as well as increasing the larvae of mosquitoes that are host to diseases (82-84).

In 1997, as a result of the “El Nino” phenomenon, the states of Kalimatan (Borneo) and Sumatra (Indonesia) were affected by uncontrollable forest fires that lasted for approximately two months (between July and September) leading to severe cases of air pollution, impacting the population over a broad area of Southwest Asia, including Indonesia, Malaysia, Singapore, South Thailand, Brunei and South Philippines. Approximately 1.500 fire spots led to the burning of 550,000 hectares of forest land and a total biomass burning area of 4,500,000 hectares. The haze covered an area of 3,000,000 hectares, affecting over 300 million people and running up a health treatment bill of 4.5 billion dollars. Such facts raised the attention of health authorities worldwide (85).

According to the Central Statistical Agency of Indonesia, between September and October of 1997, in 8 provinces of Indonesia totaling, approximately, 12,500,000 inhabitants, there was an increase of health-service demand related to bronchial asthma, chronic bronchitis and acute respiratory infection—reaching up to a total of 1,802,340 cases. The respiratory pathologies caused a total of 36,462 visits to emergency rooms, 15,822 hospitalizations and 2,446,352 days where people called in sick.  In several provinces, the TAP (Total Airborne Particles) exceeded the 260 um/m3 limit (which is considered acceptable), by a 15 fold. There was a massive concentration of particulate matter varying around 0.5 and 5 g in diameter in the areas surrounding the forest fire (86).

In Malaysia, children presented an increase of acute asthma crises and the pulmonary function in students decreased during the acute periods (87).

The Health Department in Singapore monitored the air quality in 15 different stations during the haze incident in 1997. The “Pollutant Standard Index” (PSI) was over 100 for 12 days, reaching a maximum of 138. The relationship between the PSI and the PM10 is as follows: a PSI of 100 corresponds, approximately, to a 150 g/m3 of PM10 (88). 94% of particles found in the haze had diameters below 2.5 g/m3. During the last week of September, when the levels of particulate matter reached their maximum, the Sanitation Enforcement Office from Singapore reported an increase of 30% of health services rendered in out-patient clinics related to respiratory pathologies. The increasing levels of PM10 from 50 g/m3 to 150 g/m3 were strongly linked to the increase of 13%, 19% and 26% in acute respiratory infections, asthma and rhinitis, respectively (89).

In the central region of Kalimantan (Borneo), one of the most affected areas by the haze for over six months—since July of 1997—the incidence of patients who were hospitalized due to pneumonia in September was 33 times higher than in the previous 12 months. Reports from the District Hospital of Jambi (Sumatra) presented facts that during the month of September, there was an increase in hospitalizations caused by bronchitis, acute laryngitis and bronchiectasis, in a fold of 1.6, 8.0 and 3.9, respectively, as compared to the average case history.

In Jambi (Sumatra), a sample population of 539 individuals answered a questionnaire that aimed at evaluating the effects of the air pollution on the population. Among these, 532 individuals (99.7%) reported some type of symptoms and 491 (91.1%) referred to respiratory symptoms. The reported symptoms were considered as medium intensity; however, the majority of those who were interviewed reported having had more than one symptom and 85.9% reported an accumulation of 10 symptoms. The interviewees who were over 60 reported having had severe symptoms and a significant reduction in their quality of life (90).

South Thailand was covered by the smoke from the forest fire for two months, between September and October of 1997. There was a significant increase of respiratory morbidity leading to an increase of hospitalizations and out-patient clinic visits. The percentage rate difference between the hospitalizations/clinic visits in the Southern region (the one affected by the smoke) and the Northern region (the control group) was 26:18, regarding the clinic visits due to respiratory diseases; and 33:18, for hospitalizations caused by respiratory diseases; 36:18, regarding hospitalizations caused by pneumonia; 40:28, for hospitalizations due to chronic obstructive pulmonary disease (COPD); and 12:9, for hospitalizations due to asthma. The monthly reports demonstrated that the morbidity caused by respiratory diseases had an approximate rise of 45,000 for out-patient clinic visits and 1,500 for hospitalizations in South Thailand during the haze period. Regression analysis models presented a strong association between the hospitalizations due to respiratory diseases and the monthly levels of PM10.  A rise of 10 g/m3  in the monthly average of PM10 led to an approximate hospitalization increase of 85%, 28%, 13% and 13% for respiratory diseases in general, pneumonia, chronic obstructive pulmonary disease (COPD) and bronchial asthma, respectively (91).

TAN et al (92) evaluated the number of leukocytes in 30 volunteers (military officers) who did not present a clinical history, by making use of peripheral blood samples and comparing those during the haze period (9/29 to 10/27/1997) to a period following the haze (11/21 to 12/5/1997) in Singapore. The findings demonstrated that the during the air pollution period, there was a relevant increase in the number of leukocytes due to a percentage rise of polymorphonuclear. This effect was more acute regarding the PM10 (the effects associated to the pollutant concentration on the day of the event and on the previous day) than regarding the SO2 (the effect associated with the pollutant concentration three to four days before the event). The researchers concluded that the atmospheric pollution triggered by biomass burning is linked to a rise in the number of white-blood cells in the peripheral blood as a consequence of a larger release of polymorphonuclear precursors in the bone marrow; this conclusion may contribute to the pathogenesis of cardiorespiratory morbidities associated with acute episodes of air pollution.

EEDEN et al (93), observing the same group of individuals, demonstrated that there was an increase in circulating cytokines; hence, verifying the hypothesis brought up by the research conducted by Tan and his team.

Previously to the Southwest Asia episode, the studies that assessed the exposure of the population to outdoor biomass burning were only a handful, and these were not properly considered. Reports of the adverse effects caused by the uncontrollable vegetation burning go all the way back to the 60’s, when GREENBURG et al (94) reported an episode that took place in New York nine years before—on November 3, 1952—when smoke coming from a forest fire “turned the sun off”. During those days, there was a mortality augmentation of 20% regarding the daily average observed in that month.

In 1987, a huge fire in California, USA, raised the TSP and PM10 levels to a rate of up to 1000 and 237 ug/m3, respectively. This fact triggered an increasing number of visits to emergency rooms due to asthma, chronic obstructive pulmonary disease (COPD), laryngitis, sinusitis among other respiratory infections around 40%; 30%; 60%; 30%; and 50%, respectively (95).

Individuals diagnosed with chronic respiratory pathologies seemed to be more susceptible to the effects of the pollution caused by the vegetation burning. During the forest fires of 1994 in Singapore, a 20% rise in emergency-room visits by asthmatic children was registered, in comparison to the annual average (96). As far as adults are concerned, the smoke from the vegetation and agricultural residue burning produced an aggravation of symptoms such as dyspnea, respiratory discomfort, coughing and wheezing to those individuals who had already been diagnosed as having moderate to severe airway obstruction (97).

There is evidence that not only those presenting previous pathologies are affected by air pollutants. Firefighters that combat forest fires make up an occupational group of individuals highly exposed to biomass burning. Studies carried out among these firefighters suggest an association between their exposure to particulate matter and the acute effects on their respiratory system, such as: irritation of the eye, nose and throat; decrease of the pulmonary function standards (FVC, FEV1, FEF25-75) (98-101). Prospective studies demonstrate that these effects can be reversible, after the individual’s withdrawal from the exposure to smoke.

It should be taken in consideration, however, that the forest-fire police are made up of a hearty portion of the population, by individuals who do not present history of diseases and, at least in principle, are healthier than the average population. Therefore, it is only reasonable to assume that similar effects may be observed in the general population during similar, or even lower, exposure to smoke.

 

Sugar Cane Straw Burning and Its Effects on Health

All of research projects carried out regarding open air vegetation burning relate to accidental episodes.  However, there is a region in the world where biomass burning is a programmed episode.  During the 70’s, in the midst of the petroleum crisis, the Brazilian government implemented a program called Proálcool (Pro-alcohol) aiming at producing an alternative, renewable, non-pollutant type of fuel: ethanol derived from sugar cane. The result of this program was a large production of alcohol-fueled vehicles starting in the 80’s, not to mention an increase harvesting of sugar cane. Back in 1996, only 5 states of the Brazilian Federation did not harvest sugar cane (Acre, Amapá, Pará, Rio Branco e Rondônia),  São Paulo being the biggest producer with an approximate figure of 65% of the nation’s total production. The increasing use of alcohol as car fuel brought about an improvement in the air quality of the large urban centers. Nonetheless, there was a downside: sugar cane harvesting is unique, once—due to productivity as well as safety—it is only done after burning the sugar cane plantation; thus, creating a large quantity of a black particulate matter called “cane soot”. This particulate matter modifies the environmental characteristics in the areas where sugar cane is planted, harvested and industrialized. These areas are natural laboratories where the population is exposed to the pollutants from biomass burning for approximately six months a year.

The Experimental Atmospheric Pollution Laboratory (LPAE) of the Pathological Department from the University of São Paulo Medical School (FMUSP) was the first, in Brazil, to assess the toxic effects of the pollutant emission caused by fossil fuel burning in large urban centers and its effects on human beings (102-104).  It was also the pioneer on assessing the toxic effects of alcohol combustion, the alcohol/gasoline mixture, as well as of the follow-up comparison of the toxic effects of gasoline combustion and the lead/gasoline mixture (105,106).

The potentially dangerous situation was persuasive enough to have the LPAE divert its research path, in other words, it undertook the task of estimating the effects of air pollution caused by biomass burning.

Two areas within the state of São Paulo were allocated to operate this research project: Araraquara and Piracicaba—two of the biggest worldwide producers of sugar cane. Reports from the Environmental Sanitation Technology Company (Cetesb) (107,108) compiled in 1986 and in 1999 on the air quality in Araraquara, demonstrated a significant increase of the total number of airborne particles and of the PM10 during the sugar cane harvesting, as opposed to the periods where there was no harvest.

From the medical point of view, the interest on the issue is exactly the fact that many chronic respiratory disease patients—especially those diagnosed with chronic bronchitis, emphysema and asthma—reported an aggravation of their symptoms in the period of the year in which the sugar-cane burning was taking place. But this is not all. Hearty individuals reported frequently having, in the same period of the year, upper airway tract irritation accompanied by nose and throat itching and burning. The presence of coarse residues in the atmosphere due to the sugar-cane burning seems to be, for the population as a whole, a clear evidence that the respiratory symptoms depend upon, or are aggravated by, the environmental pollution caused by such burnings. 

However, the problem is not as simple as it seems to be. The possibility that climate change, as one example, may also be responsible and aggravating for the respiratory symptoms of a portion of individuals within this population can not be discarded.

In 1992, Franco (109) formulated the following hypotheses:

1) During the sugar-cane burning period, the air quality in the region worsens.

2) The sugar-cane burning is not exclusively related to the aggravating conditions of the air quality, but due to the plantation’s extensive area and the burning’s extensive time—from the end of April to the beginning of November—the discharge of gas, among other pollutants, in the area’s atmosphere becomes a determining factor that cannot be ignored.

3) The population under risk, whose quality of life and health are dramatically affected by such adverse atmospheric condition, is quite significant.

4) The majority of the people that makes up the population under risk require a larger demand of doctor visits, out-patient clinic treatments, medications, as well as hospitalizations.  Such demand creates a considerable burden to the health care system, consequently weighing upon the medical services as well as the family’s economy.

Considering the scarceness of research projects that correlate the effects of the sugar cane burning, the real dimension of the risk population and the social, economical and medical burden, our research group has decided to tackle the issue.

A temporal epidemiological study with the purpose of evaluating the association between the particulate matter collected during the sugar-cane burning and a respiratory morbidity index in Araraquara (SP, Brazil) was conducted from May 26 to August 31, 1995. Furthermore, the daily number of patients requiring inhalation in one of the two major hospitals in the area was compiled and used in order to reach the respiratory morbidity. There was a significantly positive and dose dependent association between the number of inhalation treatments and the weight of sediment, which was used as a measurement to the particulate matter resulted by the sugar-cane burning. A rise of 10 mg in the weight of the sediment was associated with a relative risk to inhalation treatment of 1.09 (CI 95%: 1.01-1.18). On the days where the pollution was stronger, the inhalation treatment relative risk was 1.20 (1.03-1.39). These findings prove that the sugar-cane burning can trigger noxious effects to the exposed population’s health (110,111)

The LPAE continued its studies by analyzing the influence of atmospheric pollution caused by the sugar-cane-straw burning over the respiratory diseases in Piracicaba, in the Southeast of Brazil. The conditions found in that city were proper in order to conduct a research project aiming at evaluating the consequences not only of the biomass burning pollution, but of fossil fuel burning pollution as well, on the human health. Lara (112) collected particulate matter from April, 1997 to March of 1998, separating them according to their dimension—fine and coarse—then, analyzing and quantifying them into: BC, Al, Si, P, S, Cl, K, Ca, Ti, V, Cr, Mn, Fe, Ni, Cu, Zn, Br, Pb (112). At the same time, the daily hospitalizations rate due to respiratory diseases in children, teenagers (under 13), and elderly people (over 65) were also quantified through the data presented by the DATASUS. A Main Components Absolute Analysis identified that biomass burning and the re-suspension of the soil’s eroded matter (Factor 1) were accountable for 80% of the fine particulate matter (PM2.5). The hospitalization relative risk due to respiratory diseases for children and teenagers was significantly associated with the interquartile variation of PM10, PM2.5, BC, Al, Si, Mn, K, and S. A rise of 10.2 g/m3 in the PM2.5 was linked to an increase of 21.4% (95% CI 4.3; 38.5) regarding the hospitalizations due to respiratory diseases on children and teenagers. On the elderly, the hospitalization relative risk due to respiratory diseases was also significantly associated with an interquartile variation of the PM10, BC, and K. When the periods of sugar-cane burning were compared to those in which there is no such burning, the effect was 3.5 times higher during the burning period—evidencing the impact of such sweeping practice on the health of the population in the city of Piracicaba (113).

 

Conclusion

The physical and biological changes taking place on the environment due to anthropogenic activity have caused a dramatic impact on human health.  The extent of these changes—due to the overload required in the past and to the maintenance of erroneous policies—reflect upon our present, compromise our future and are far from being totally established.  For instance, the past emission of carbon monoxide, among other greenhouse-effect gases, and the depletion of the ozone layer in the stratosphere are still among our current problems that need to be faced every day. Likewise, the continuous demand of our ecological systems, which sustain human life, may be a worldwide threat to our health in the future. Due to the effect of the greenhouse gases, the Earth’s temperature has risen, approximately, 1.2°C since 1850—0.5°C between 1978 and today alone—constantly heating the surface of our oceans, causing changes in the direction of the deep oceanic currents, dramatically affecting regional climates, triggering problems such as the scarceness of water as well as of food.

Among the reasons for continual development of the human race, there is the protection of human health.  However, there still is a slowness regarding the evaluation and the implementation of sanitation measures as far the relationship to the environment and health, especially related to biomass burning, are concerned. According to the American Lung Association (114), over 800 of the new scientific studies associating the effects of airborne particulate matter from fossil fuel with human health were published between 1997 and 2001. Nevertheless, the literature is extremely parsimonious when assessing the effects of biomass burning on human health, regardless if the burning occurs indoors—means through which 3 billion people in the planet obtain their energy source—or if it occurs outdoors by vegetation burning, in which case there is no precise estimate as to how many people are affected to the exposure of the pollutants released in the air. Up until today, we still cannot determine 50% of the causes of forest and vegetation fires, making open air vegetation burning a recurring phenomenon in Asia, Latin America, Africa, among other regions in the world. Estimate figure show that in the year 2000, 351 million of hectares of worldwide vegetation were brought down by fire. On the other hand, the population affected by the products made by biomass burning, in general, corresponds to those individuals on the highest level of poverty, with the least possibility of having access to health care—making the already poor conditions of living even worse. The data presented in this review article should go beyond simply identifying the population most affected by biomass burning and  describing the complex mechanisms of health impacts; it should send a message to researchers aiming at expanding the limited amount of knowledge and, thus, enabling the creation of effective intervening programs with the objective to provide for a better quality of life to the individuals who are exposed to such pollutants.

 

References

1. Bascon R, Bromberg PA, Costa DA, Devlin R, Dockery DW, Frampton MW, Lambert W, Samet JM, Speizer FE, Utell M. Health effects of outdoor pollution. Am. J. Respir. Crit. Care Med 1996; 153: 3-50.        [ Links ]

2. De Koning HW, Smith KR, Last JM, Biomass fuel combustion and health. Bull. WHO 1985; 63:11-26.        [ Links ]

3. WHO Information, VEGETATION FIRES, 2000 Fact Sheet, n° 254        [ Links ]

4. WHO. Health Guidelines for Vegetation Fire Events, ed. Schwela DH Goldammer JG, Morawska LH, Simpson, O. Geneva, World Health Organization, 1999.        [ Links ]

5. Cochrane ME. O grande incêndio de Roraima. Ciência Hoje 2000; 27:26-43.        [ Links ]

6. Crutzen PJ, Andreae MO. Biomass burning in the tropics: Impacts on atmospheric chemistry and biogeochemical cycles. Science 1990; 250:1669-78.        [ Links ]

7. Lacaux JP, Loemba-Ndembi J, Lefeivere B. Biogenic emissions and biomass burning influences on the chemistry of the fogwater and stratiform precipitations in the African equatorial Forest. Atmospheric Environment 1992; 26:541-51        [ Links ]

8. Losno R, Bergametti G, Cartier P, et al. Major ions in marine rainwater with attention to sources of alkaline and acidic species. Atmospheric Environment 1991; 25:763-70        [ Links ]

9. Ward DE, Susott RA, Kauffmann JB, et al. Smoke and fire characteristics for cerrado and deforestation burns in Brazil- Base-B Experiment. Journal of Geophysical Research 1992; 97:14601-19        [ Links ]

10. Botkin D, Keller EA. Environmental Science: Earth as living planet. New York:1. ed., John Wiley & Sons, 1995        [ Links ]

11. Seaton A, MacNee W, Donaldson K, Godenn D. Particulate air pollution and acute health effects,. Lancet 1995; 345:176-8        [ Links ]

12. Peters A, Wichman HE, Tuch T, Heyder J. Respiratory effects are associated with the number of ultrafine particles. Am J Respir Crit Care Med 1997; 155:1376-83        [ Links ]

13. Donaldson K, Stone V, Clouter A, MacNee W. Ultrafine Particles. Occup Environ Med 2001; 58:211-6.        [ Links ]

14. Shi, MM, Godleski JJ, Paulauskis JD. Regulation of macrophage inflammatory protein-1 mRNA by oxidative stress. J. Biol. Chem 1996; 271: 5878-83        [ Links ]

15. Turn SQ, Jenkins BM, Chow JC, Pritchett LC, Campbell D, Cahill T, Whalen SA. Elemental characterization of particulate matter emitted from biomass burning: Wind tunnel derived source profiles for herbaceous and wood fuels. Journal of Geopysical Research 1997; 102: 2683-99        [ Links ]

16. Bruce N, Perez-Padilla R, Albalak R. Indoor air pollution in developing countries: a major environmental and public health challenge. Bull. WHO 2000; 78: 1078-92.         [ Links ]

17. Padmavati S, Pathak, SN. Chronic cor pulmonale in Delhi. Circulation 1959; 20:343-52.         [ Links ]

18. Padmavati S, Joshi, B. Incidence and etiolgy of chronic cor pulmonale in Delhi: a necropsy study. Dis Chest 1964; 46, 457-63        [ Links ]

19. Behera D, Jindal SK, Malhota HS. Ventilatory function in nonsmoking rural Indian women using different cooking fuels. Respiration 1994; 61:89-92.         [ Links ]

20. Master KM. Air pollution in New Guinea. Cause of chronic pulmonary disease among stone-age natives in the highlands. JAMA 1974; 228:1635.        [ Links ]

21. Anderson HR. Respiratory abnormalities and ventilatory capacity in a Papua New Guinea Island community. Am Rev Respir Dis. 1976; 114:537-48        [ Links ]

22. Anderson HR. Chronic lung disease in the Papua New Guinea highlands. Thorax 1979; 34:647-53.        [ Links ]

23. Pandey MR. Prevalence of chronic bronchitis in a rural community of the Hill Region of Nepal. Thorax 1984; 39:331-6.        [ Links ]

24. Pandey, MR. Domestic smoke pollution and chronic bronchitis in a rural community of the Hill Region of Nepal. Thorax 1984; 39:337-9.        [ Links ]

25. Norboo T, Yahya NB, Heady JA, Ball KP. Domestic pollution and respiratory illness in a Himalayan village. Int. J. Epidemiol 1991; 20:749-57.        [ Links ]

26. Qureshi K. Domestic smoke pollution and prevalence of chronic bronchitis/asthma in a rural area of Kashmir. Indian J Chest Dis Allied Sci 1994; 36: 61-72        [ Links ]

27. Dossing M. Risk factors for chronic obstructive lung disease in Saudi Arabia . Respir. Med 1994; 88:519-22        [ Links ]

28. Dennis RJ, Maldonado D, Norman S, Baena E, Martinez G. Woodsmoke exposure and risk for obstructive airways disease among women. Chest 1996; 109:115-9.        [ Links ]

29. Perez-Padilla R, Regalado J, Vedal S, Chapela R, Samspre 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; 154:701-6.        [ Links ]

30. Regalado J, Perez-Padilla R, Sansores R, Vedal S, Brauer M, Pare P. The effect of biomass burning on respiratory symptoms and lung function in rural women. Am J Resp Crit Car Med. 153 :A171        [ Links ]

31. Albalak R, Frisancho AR, Keeler GJ. Domestic biomass fuel combustion and chronic bronchitis in two rural Bolivian villages. Thorax 1999; 54:1004-8.        [ Links ]

32. Menezes AM, Victora CG, Rigatto M. Prevalence and risk factors for chronic bronchitis in Pelotas, RS, Brazil: a population-base study. Thorax 1994; 49:1217-21        [ Links ]

33. Ellegard, A. Cooking fuel smoke and respiratory symptoms among women in low-income areas of Maputo. Environ. Health Perspect 1996; 104:980-5.        [ Links ]

34. Narboo T, Angehuk p. Yahya m. Silicosis in a Himalaya Village population: Role of environmental dust. Thorax 1991; 46: 341-3.        [ Links ]

35. Saiyed HN, Sharma YK, Sadhu HG, Norboo T, Patel PD, Patel TS, Venkaiah K, Kashyap SK.Non-occupational pneumoconiosis at high altitude villages in central Ladarkh.Br J Ind Med 1991; 48:825-9.        [ Links ]

36. Grobbelar JP, Bateman ED.Hut lung: a domestically acquire pneumoconiosis of mixed etiology in rural women. Thorax; 1991; 46:334-40.        [ Links ]

37. Sandoval JJ, Salas MI, Martinez-Guerra A, Portales A, Palomar M, Villegas, Barrios R. Pulmonary arterial hypertension and cor pulmonale associated with domestic wood smoke inhalation. Chest 1993; 103: 12-20        [ Links ]

38. Cerquiero MC, Murtagh P, Halc M, Weissenbacher M. Epidemiologic risk factors for children with acute lower respiratory tract infection in Buenos Aires, Argentina: a matched case control study. Rev. Infect. Dis. 1990: 12, suppl 8: S1021-8.        [ Links ]

39. Collings DA, Sithole SD, Martin KS. Indoor air pollution in developing countries and acute respiratory infection in children. Tropical Doctor 1990; 20: 151-5.        [ Links ]

40. Mtango FD, Neuvians D, Broome CV, Hightowwer AW, Pio A. Risk factors for deaths in children under 5 years old in Bagamoyo district, Tanzania. Trop. Med. Parasitol 1992; 43:229-33.        [ Links ]

41. Johnson AW, Aderele WI. The association of household pollutants and socio-economic risk factors with the short-term outcome of acute lower respiratory infections in hospitalized pre- school Nigerian children. Ann. Trop. Paediatr 1992 12:421-32.         [ Links ]

42. Shah N, Ramankutty V, Premila PG & Sathy N. Risk factors for severe pneumonia in children in south Kerala: a hospital-based case-control study. J Trop Pediatr 1994; 40:201-6.        [ Links ]

43. Victora CG, Fuchs SC, Flores JA, Fonseca W, Irkwwood B. Risk factors for pneumonia among children in a Brazilian metropolitan area. Pediatrics 1994; 93:977-85.        [ Links ]

44. O´Dempsey T, McArdle TF, Morris J, Lloyd-Evans N, Bldehi, Laurence BE, et al. A study for pneumococcal disease among children in a rural area of West Africa. Int J Epidemiol 1996; 25:885-93.        [ Links ]

45. Wesley AG, Loening WE. Assessment and 2-year follow-up of some factors associated with severity of respiratory infections in early childhood. S. Afr. Med. J        [ Links ]

46. Lopez-Bravo IM, Sepulveda H, Valdes I. Acute respiratory illness in the first 18 months of life. Pan. Am. J. Public Health 1997; 1:9-17.        [ Links ]

47. Kossove D. Smoke-filled rooms and lower respiratory disease in infants. South Afr. Med. J 1982; 61:622-4.        [ Links ]

48. Pandey MR, Boleij JS, Smith KR, Wafula EM. Indoor air pollution in developing countries and acute respiratory infection in children. Lancet 1989; 1:427-9.        [ Links ]

49. Campbell H, Armstrong JR, Byass P. Indoor air pollution in developing countries and acute respiratory infection in children. Lancet 1989; 1:1012.         [ Links ]

50. Armstrong JR, Campbell H. Indoor air pollution exposure and lower respiratory infections in young Gambian children. Int. J. Epidemiol 1991; 20:424-9.        [ Links ]

51. De Francisco A, Morris J, Hall AJ, Armstrong-Schellenberg JR, Greenwood BM. Risk factors for mortality from acute lower respiratory tract infections in young Gambian children. Int. J. Epidemiol 1993; 22:1174-82.         [ Links ]

52. Ezatti M, Kammen D.Quntifying the effects of exposure to indoor air pollution from biomass combustion on acute respiratory infections in developing countries. Environmental Health Perspectives 2001; 109:481-8.        [ Links ]

53. Ezzati M, Kammen DM. Indoor air pollution from biomass combustion and acute respiratory infections in Kenyaan exposure response study. Lancet 2001; 358:619-24        [ Links ]

54. Smith KR, Samet JM, Romieu I, Bruce N. Indoor air pollution in developing coutries and aculte lower respiratory infections in children. Thorax 2000: 55: 518-32        [ Links ]

55. Mavalankar DV, Trivedi CR, Gray RH. Levels and risk factors for perinatal mortality in Ahmedabad, India. WHO Bulletin 1991; 69: 435-42.         [ Links ]

56. Boy E, Bruce N, Delgado H. Birth weight and exposure to kitchen wood smoke during pregnancy. Environ Health Perspective 2002; 110: 109-14        [ Links ]

57. Mohammed N, Ng´Ang´A L, Odhiambo J, Nyamwaya J, Menzies R. Home environment and asthma in Kenyan school children: a case-control study. Thorax 1995; 50:74-8        [ Links ]

58. Melson T, Brinch J, Hessen JO, Schei M etal. Asthma and indoor environment in Nepal. Thorax 2001; 56:477-81.         [ Links ]

59. Shei MA, Hessen JO, McCraken J, Lopez V, Bruce NG, Smith KR. Asthma and indoor air pollution among indigenous children in Guatemala. Proc Indoor air 2002,Monterey, CA (1st-7th July 2002).        [ Links ]

60. Azizi BH, Zulfkfli HI, Kasim S. Indoor air pollution and asthma in hospitalized children in a tropical environment. J. Asthma 1995; 32:413-8.        [ Links ]

61. Gupta Bn, Mathur N, Mahendra P, Srivastava A, Swaroop V, Agnihotri M. A study of the household environmental risk factors pertaining to respiratory disease. Energy Environ. Rev 1997; 13:61-7.        [ Links ]

62. Mishra VK, Retheford RD, Smith KR. Biomass cooking fuels and prevalence of tuberculosis in India. Int. J. Infect. Dis 1999; 3: 119-29.        [ Links ]

63. Perez-Padilla R, Perez-Guzman C, Baez-Saldana R, Torres-Cruz A. Cooking with biomass stoves and tuberculosis: a case control study. Int. J. Tuberc. Lung Dis 2001; 5:441-7.        [ Links ]

64. Ellegard A. Tears while cooking: an indicator of indoor air pollution and related health effects in developing countries. Environ. Res 1997; 45:12-22.         [ Links ]

65. Mishra VK, Retheford RD, Smith KR. Biomass cooking fuels and prevalence of blindness in India. J. Environ. Med 1999; 1:189-99.        [ Links ]

66. Honick RE, Osborne JS 3rd, Akpom CA. Symptom of respiratory Illness in young children and the use of wood-burning stoves for indoor heating. Pediatrics 1985; 75:587-93.        [ Links ]

67. Dockery D, Spengler J, et al. Association of health status with indicators of indoor air pollution from and epidemiologic study in six U.S. cities. International Conference on Indoor Air Quality and Climate , Berlin, Institute for Water Soil and Air Hygiene. 1987        [ Links ]

68. Butterfield P, LaCava G, Edumunston E, Penner J. Woodstoves and indoor air: the effects on preschoolers´upper respiratory systems. J. Environ Health 1989; 52: 172-3.        [ Links ]

69. Morris K, Morgenlander M, Coulehan Jl, Gahagen S, Arena VC. Wood-burning stoves and lower respiratory tract infection in American Indian children. Am. J. Dis. Child 1990; 144:105-8.        [ Links ]

70. Vedal S. Health effects of wood smoke. report to the provincial health office of British Columbia. Vancouver, BC, The University of British Columbia. 1993        [ Links ]

71. Ostro BD, Lipsett MJ, Mann JK, Wiener MB, Selner J. Indoor air pollution and asthma: Results from a panel study. Am J Respir Crit Care Medicine. 1994 149:1400-6        [ Links ]

72. Robin L, Lees PSJ, Winget M, Steinhoff M, Moulton, LH, Santosham M, Correa A. Wood-burning stoves and lower respiratory illness in Navajo children. Pediatric Infectious Disease Journal 1993; 15:859-65        [ Links ]

73. Heuman M, Foster LR, Johnson L, Kelly L. Wood smoke air pollution and changes in pulmonary function among elementary school children. 84th Annual Meeting of the Air and Waste Management Association, Vancouver, BC, Air and Waste Management Association. 1991.         [ Links ]

74. Johnson K, Gideon R, Loftsgaarden DO. Montana air pollution study: children´s health effects. J Official Stat. 1990; 5:391-408.        [ Links ]

75. Koenig J, Larson TV, Hanley QS, Rebolledo V, Dumler K, Checkoway H, Wang SZ, Lin D, Pierson WE. Pulmonary function changes in children associated with fine particulate matter. Environ Res 1993; 63:26-38.        [ Links ]

76. Schwartz J, Koenig J, Slater D. Particulate air pollution and hospital emergency room visits for asthma in Seattle. Am Rev Respir Dis 1993; 147:826-31.         [ Links ]

77. Lipsett M, Hurley S, Ostro B. Air Pollution and Emergency Room Visits for Asthma in Santa Clara County, California. Environmental Health Perspectives 1997; 105:216-22.         [ Links ]

78. Fairley D. The Relationship of Daily Mortality to Suspended Particulates in Santa Clara County, 1980-1986. Environ Health Perspect 1990; 89: 159-68.        [ Links ]

79. Fick RB, Paul ES, Merril WW, Reynolds HY, Loke JSO. Alteration in the antibacterial properties of rabbit pulmonary macrophages exposed to wood smoke. Am. Rev. Respir. Dis 1984; 129:76-81.         [ Links ]

80. Houtmeyers E, Gosselink R, Gayan-Ramirez G, Decramer M. Regulation of mucociliary clearance in health and disease. Eur. Respir. J. 1999; 13:1177-88.        [ Links ]

81. Brauer M. Health impacts of biomass air In: HEALTH GUIDELINES FOR VEGETATION FIRE EVENTS, Lima, Peru, 1998. Geneva, WHO, 1999; 186-220. (Background papers).        [ Links ]

82. Mims FM 3rd. Significant reduction of UVB caused by smoke from biomass burning in Brazil. Photochem Photobiol 1996; 64: 814-6        [ Links ]

83. Mims FM 3rd, Holben BN, Eck TF, Montgomery BC, Grant WB. Smoky skies, mosquitoes, and disease. Science 1997; 276: 1773-6 (in letters)        [ Links ]

84. Mims FM 3rd. Health effects of tropical smoke. Nature 1997; 390: 222-3        [ Links ]

85. Heil A, Goldameer JG. Smoke -haze pollution: A review of the 1997 episode in South East Asia. Journal of Regional Environmental Change 2001        [ Links ]

86. Dawud Y. Smoke Episodes and Assessment of Health impacts Related to Haze from Forest Fires: Indonesian Experience. In: HEALTH GUIDELINES FOR VEGETATION FIRE EVENTS, Lima, Peru, 1998. Geneva, WHO, 1999; 313-33. (Background papers).        [ Links ]

87. WHO Bi-Regional Workshop on Health Impacts of Haze-Related Air Pollution, Kuala Lumpur, Malaysia, 1998. Geneva, WHO, 1998, p.1-8 (Annex H).        [ Links ]

88. U.S. ENVIRONMENTAL PROTECTION AGENCY. Measuring Air Quality: The Pollutant Standards Index. Office of Air Quality Planning and Standards, Research Triangle Park, NC, EPA 451/K-94-001, 1994.        [ Links ]

89. Brauer M, Hisham-Hashim J. Indonesia Fires: Crisis and Reaction. Environ. Sci. Technol 1998; 32:404-7.        [ Links ]

90. Kunii O. Basic facts-determining downwind exposures and their associated health effects in practice: a case study in the 1997 forest fires in Indonesia. In: HEALTH GUIDELINES FOR VEGETATION FIRE EVENTS, Lima, Peru, 1998, Geneva, WHO, 1999; 295-312. (Background papers).        [ Links ]

91. Phonboon K, Paisarn-Uchapong O, Kanatharana P, Agsorn S. Smoke episodes emissions characterization and assessment of health risks related downwind air quality-case study, Thailand. In: HEALTH GUIDELINES FOR VEGETATION FIRE EVENTS, Lima, Peru, 6-9. 1998. Geneva, WHO, 1999; 334-58. (Background papers).        [ Links ]

92. Tan CW, Qiu D, Liam BL, NG, TP, Lee SL, Van Eeden, S.F.; D´Yachkova, Y.; Hogg, J.C. The human bone marrow response to acute air pollution caused by forest fires. Am. J. Respir. Crit. Care Med 2000; 161:1213-7.        [ Links ]

93. Eeden SF, Tan WC, Suwa T, et al. Cytokines involved in the systemic inflammatory response induced by exposure to particulate matter air pollutants (PM10). Am J Respir Crit Care Med 2001; 164: 826-30        [ Links ]

94. Greenburg L, Jacobs MB, Droletti BM, Field F, Braverman MM. Report of an air pollution incident in New York City, 1953. Public Health Reports 1962; 77: 7-16.        [ Links ]

95. Duclos P, Sanderson LM, Lipsett M. The 1987 Forest Fire Disaster in California: assessment of emergency room visits. Arch. Environ. Health 1990; 45: 53-8.        [ Links ]

96. Chew FT, Ooi BC, Hui JK, Saharom R, Goh D Lee BW. Singapore's haze and acute asthma in children. Lancet 1995; 346:1427         [ Links ]

97. Long W, Tate RB, Neuman M, Manfreda J, Becker AB, Anthonisen, NR. Respiratory symptoms in a susceptible population due to burning of agricultural residue. Chest 1998; 113:351-7.        [ Links ]

98. Rothman N, Ford DP, Baser ME, Hansen JÁ, O'Toole T, Tockman MS, Strickland PT. Pulmonary function and respiratory symptoms in firefighters. J. Occup. Med 1991; 33:1163-7.        [ Links ]

99. Liu D, Tager Ira B, Balmes JR, Harrison RJ. The effect of smoke inhalation on lung function and airway responsiveness in wildland fire fighters. Am. Rev. Respir. Dis 1992; 146:1469-73        [ Links ]

100.Reinhardt T, Ottmar R. Smoke exposure among wildland firefighters: A review and discussion of current literature, United States Department of Agriculture, Forest Service. Pacific Northwest Res. Station, 1997.        [ Links ]

101. Betchley G, Koening JQ, Van Belle G, Checkoway H, Reinhardt T. Pulmonary function and respiratory symptoms in forest firefighters. Am. J. Ind. Med 1997; 31:503-9         [ Links ]

102.Böhm G M, Saldiva PHN, Pasqualucci CA, Massad E, Martins MA, Zin WA, Cardoso WV, Criado PMP, Komatsuzaki M, Sakai RS, Nigri EM, Lemos M, Capelozzi VD, Crestana C, Silva R. Biological effects of air pollution in Sao Paulo and Cubatão. Environ. Res 1989; 49:208-16.        [ Links ]

103.Saldiva PHN, King M, Delmonte VLC, Macchione M, Parada MAC, Daliberto ML, Sakai RS, Criado PMP, Silveira PLP, Zin WA, Böhm GM. Respiratory alterations due to urban air pollution: an experimental study in rats. Environ. Res 1992; 57:19-33.        [ Links ]

104.Lemos M, Lichtenfels AJFC, Amaro Jr, E, Macchione M, Martins MA, King M, Böhm GM, Saldiva PHN. Quantitative patology of nasal passages in rats exposed to urban levels of air pollution. Environ. Res 1994; 66:87-95.        [ Links ]

105.Saldiva PHN, Massad E, Caldeira MPR, Calheiros DF, Saldiva CD, Nicolelis MAL, Böhm GM. Pulmonary function of rats exposed to ethanol and gasoline fumes. Braz. J. Med. Biol. Res 1985; 18:573-7         [ Links ]

106.Massad E, Böhn GM, Saldiva PHN. Ethanol fuel toxicity. In: CORN, M., Handbook of hazardous materials. New York, Academic Press 1993; 265-75.        [ Links ]

107.Cetesb. Superintendência de Qualidade Ambiental. Avaliação da qualidade do ar em Araraquara, 1986. São Paulo, CETESB, 1986.        [ Links ]

108.Cetesb. Departamento de Qualidade Ambiental. Resumo dos estudos em locais influenciados diretamente pelas queimadas de cana. São Paulo, CETESB, 1999. [Memorando].        [ Links ]

109.Franco AR. Aspectos epidemiológicos da queimada de canaviais na região de Ribeirão Preto. Centro de Estudos Brasileiros, Ribeirão Preto, 31/03/1992        [ Links ]

110. Arbex MA, Bohn GM, Saldiva PHN, Conceição GMS, Pope AC, Braga ALF. Assesment of the effects of sugar cane plantation burning on daily counts of inhalation therapy. J of Air Waste Manag Assoc. 2000; 50: 1745-9        [ Links ]

111. Arbex MA. Avaliação dos efeitos do material particulado proveniente da queima da plantação de cana-de-açúcar sobre a morbidade respiratória na população de Araraquara-SP. São Paulo. 188 p. Tese (Doutorado)-Faculdade de Medicina, Universidade de São Paulo, 2002        [ Links ]

112. Lara LBLS. Caracterização química da precipitação na Bacia do Rio Piracicaba: variabilidade espacial e temporal. 80 p. Tese (Doutorado)- Centro de Energia Nuclear na Agricultura, Universidade de São Paulo, 2000        [ Links ]

113. Cançado JED. A poluição atmosférica e sua relação com a saúde humana na região canavieira de Piracicaba-SP. São Paulo. 201 p. Tese (Doutorado)-Faculdade de Medicina, Universidade de São Paulo, 2003        [ Links ]

114. American Lung Association. Selected key studies on particulate matter and health: 1997-2001. Disponivel na Internet: < http: // www.lungusa.org>. Acesso em: março de 2003.        [ Links ]

 

 

Correspondence
Av. Dr. Arnaldo, 455, 1o Andar, Sala 108
Cerqueira César, CEP 01246-903, São Paulo, SP
Phone: (55) (16) 236-5228
E-mail: arbexma@techs.com.br.

Received for publishing on 9/12/03.
Certified, after editing, on 2/12/04.

 

 

* Research conducted at the Experimental Atmospheric Pollution Laboratory, FMUSP—Faculdade de Medicina da Universidade de São Paulo (University of São Paulo Medical School).
**This research project was financed by LIM05-FMUSP and UNISA.

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License