Biomed% Pharmacother(1990)44.4434% 0 Elsevier.Parts
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ossier espiratory effects of pollution F Philip-Joet Service de Pneumologie-Allergologie. CHU Nord 13326 Marseille Cedex 15, France
(Received 19 June 1990; accepted 27 August 1990)
Summary - Atmospheric poilution is increasingly responsible for chronic airway disease. Although outdoor pollution has decreased somewhat in recent years, indoor pollution has increased. Outdoor pollution results essentially from the combustion of coal and other fuels used for heating. industrial production and motor vehicles. The major sources of indoor pollution are heating and cooking devices. The main pollutants are suspended particulates, S@. NOz in indoor pollution and ozone which is linked to the photochemical effects. Transient increases ht pollution cause transient decreases in pulmonary airflow. Chronic pollution seems to lead to an increase in the prevalence of lower and upper respiratory airway symptoms. In young children early exposure to pollution contributes to the development of chronic airways disease later in life. Asthmatics are at greater risk for pollution-related complications and several pollutants are known to increase bronchial reactivity. Further efforts are needed to reduce in pollution indoor and outdoor environments in particular with regard to tobacco smoke and
especially for children. pollution / airway diseases R&urn6 - Les effets respiratoires de la pollution. La pollution atmosphdrique est responsable dune augmentation des maladies des voies akriennes. La pollution ext&ieure a diminud au cows des derni&es an&es. Ceci a augment6 l’importance relative de la pollution a’omestique. Les sources de pollution extkrieure sont essentiellement la combustion du charbon et des differents combustibles utilis& pour le chauffage. l’industrie ou les ve’hicules automobiles. Les sources de pollution domestiques sent essentiellement reprt%entkes par les chauffages et les cuisinkkes. Les principaux polluants sont les fumCes noires. le SOz, le NO2 lid d la pollution domestique, l’ozone lie ri la pollution photochimique. Les augmentations transitoires de pollution sent souvent ci l’origine de variations transitoires de dkbits ae’riens expires, tandis que la pollution chronique serait responsable dune augmentation de la pkvalence des signes d’atteinte des voies aCrienne inf&ieures et supbieures. Chez l’enfant la pollution est responsable &infection des voies respiratoires et celles-ci sont ci l’origine datteintes honiques des votes respiratoires dans les anne’es ultkrieures. Les asthmatiques sent plus expost% que les autres et nombre de pollutants augmentent leur hyperr6activittZbronchique. La lutte contre la pollution doit s’attacher autant au microenvironnment individuel qu’d la pollution extt+ieure, en particulier la fumee de cigarettes, spkiaiement pour les enfants. pollution I maladies des voies adriennes
Introduction Atmospheric pollution results from the presence in the air of foreign substances and/or important variations in the normal composition. There is substantial evidence implicating pollution in the onset of chronic airway disease [17]. Thirty years ago urban pollution was the most important pollutant. Today, cigarette smoking and indoor pollution have emerged as the dominant factors
PI.
Pollution can occur in the form of either a gas or an aerosol ie of solid particles or liquid in suspension. It can be natural or man-made. Natural pollution made pollution
is more
abundant
than man-
There are two major sorts of natural po!lutants; the first includes dust, ashes and erosion products originating from land masses eg deserts and volcanoes, the second includes nitrogen dioxide,
F Philip-Joet carbon monoxide and hydrocabons from the oceans and plant life. Natural pollution accounts for only 2% of sulfur dioxide. It is more diffuse and less concentrated than human pollution in urban areas. Man-made pollution In urban and industrial areas, man-made pollution results from combustion of coal and other fuels for vehicles, electricity production, heating or industrial activities such as petroleum refineries and waste treatment. In rural areas the source of manmade pollution is less clear. Although farming and livestock raising may produce some pollution, storage in silos and the use of composts or pesticides are probably the major sources. Fortunately rare, some spectacular ecological disasters have occurred. In Bohpal, India, massive exposure to toxic gases led to extensive injury and death. At Nyos Lake in the Cameroons, the sudden release of CO2 caused 2000 fatalities. Dramatic events also took place in Seveso, Italy, with dioxin and in Chernobyl, USSR, with radioactivity. Climatic conditions Meteorologic conditions affect the concentration of the pollutants (wind, temperature gradients, rain) or their modification through chemical reactions (temperature, sunlight, rain). Winds dissipate pollution or carry it in certain directions and areas. Rain dissolves some pollutants and can transform them into nitric or sulfuric acids (acid rain). Air stagnation and cold temperatures during atmospheric pollution inversions cause pollutants to collect at ground level. These episodes have been associated with excessive acute mortality in the elderly, infants and subjects with chronic cardiopulmonary diseases. Association of sun with temperature inversion can trigger photochemical reactions (photochemical smog) [21]. The legendary London pea-soup of the latter part of the 19th century was a result of black smog and sulfur dioxide from incomplete combustion of coal in factories and homes which in combination with the high relative humidity prevailing in winter led to the formation of irritant species of particulates including sulfuric acid WI. Recently, the photochemical Los Angeles smog complex has been studied. It results from an interaction between hydrocarbons (vehicles, industrial activity) and nitrogen oxides in sunlight to produce a highly complex mixture containing
ozone and organic oxidants. Diesel vehicles have been shown to contribute to the concentrations of the black smoke currently found in London [23. Primary and photochemical pollutants usually co-exist in the atmosphere. In developed countries, untransformed pollutants reach maximum concentration in winter while the photochemical pollutants reach their highest values in summer. Pollutants The main primary pollutants released into the atmosphere are sulfur dioxide, nitrogen monoxide and dioxide (NO, NOz), carbon monoxide, hydrocarbons, dust, ash and heavy metals (Pb, Cd). Secondary pollutants like sulfates, nitrates and ozone are products of chemical reactions in the atmosphere. Sulfur and nitrogen acid occur principally from the combustion of fuel and coal. High ozone levels are generally associated with photochemical pollution. Since the concentration of outdoor pollutants has decreased in the last few decades, indoor pollution plays an increasingly important role in total exposure. Rising fuel costs have encouraged people in developed countries to insulate their homes and to reintroduce traditional heating systems such as wood stoves and kerosene heaters. As a result, pollutants are often trapped inside and exposure is high [6]. In developing countries, wood is the major source of domestic energy and burning under inefficient conditions with minimal ventilation results in high indoor concentrations. Indoor pollutants such as nitrogen dioxide, formaldehyde and biologic agents have also been associated with respiratory effects. Another important source of indoor pollution is tobacco smoke [28].
Respiratory effects of pollution Acute pollution The most dramatic example of acute pollution is the Nyos accident, but other less spectacular episodes have been observed in conjunction with meteorologic factors that increase the level of some pollutants. In 1952, in London the coincidence of an increase in sulfur dioxide and suspended particulate matter coupled with a dense fog led to the death of 3500 people. Acid fog contains multiple stimuli that may be capable of inducing
Respiratcry effects of pollution bronch~onst~ction [3]. By monitoring pollutant levels and applying strict admission standards, such incidents can be avoided. This can temporarily reduce the dirty industrial activities or private vehicles.
The relationship between chronic pollution and mortality or morbidity has been demonstrated in numerous studies. Postmen working in urban areas displayed more symptoms of chronic b~nchitis than postmen living in less polluted areas 1161.In Cracow, respiratory symptoms were more frequent in polluted areas particularly in smokers [24]. During childhood MMEF (maximal mid-expiratory flow) was shown to be lower in polluted areas 1293.Similar results were reported in France and pollution was correlated with increased prevalence of respiratory s~ptoms both in adults and children [14, 15, 261. Wheexing crises and incidence of severe asthma are siguificantly higher in children living in polluted areas
Ia It seems that transient peaks in pollution lead to ~nsient decreases in pulmonary function data while chronic exposure increases the prevalence of bronchial symptoms without any effect on pulmonary function 116, 271. In the Gardanne coal basin, an increase in SO2 level was correlated with a decrease in FEVl/FVC in school children [7] and with an increase in the prevalence of ENT and respiratory symptoms [S, l] as compared with non-polluted areas. Suspended particulate matter and SO2
In most areas, suspended p~iculate matter and SO2 increase in parallel. PAARC study (French national survey Pollution atmosphbrique ef affections respiratoires chroniques) showed relationships between the SO2 levels and the prevalence of bronchial symptoms, lower airway diseases in adults and upper airway diseases in children 114, 151. Likewise, a negative correlation was observed between SO2 level and FEV1.0. Other studies also implicate these factors in the decrease of FEVl and FVC in children living in moderately polluted areas in comparison with those living in low polluted areas 1253. In an urban communism the association between SO2 pollution and respiratory deaths has been demonstrated [ll]. A study performed in children from six US cities showed strong correlations between the prevalence of coughing, bronchitis and airway
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diseases and suspended particle matter (less than 15 microns and less than 2.5 microns aerodynamic diameter), aerosol sulfate and, to a lesser degree, SO2 and NO2. No association was found between pollutant concentration and any of the pulmonary function measurements considered. Earache tended to be associated with particulate concentration. Children with a history of wheezing or asthma had a much higher prevalence of respiratory symptoms [12]. The mortality from asthma and chronic bronchitis seems to decrease when sulfur oxide pollution decreases 1181. Nitrogen oxide
Nitrogen oxide result from the combustion of gas. Levels are often greater indoors than outdoors 1231.Epidemiologic studies do not clearly implicate nitrogen oxides in ~spi~to~ disease flO]. They could be responsible for bronchial epitltelium alterations 1131 and also lower defences against viral or bacterial infections. Acute exposure to NO2 seems to increase the nonspecific carbacholine hyperreactivity iu asthmatic patients f22]. Ozone
Photochemical pollution reportedly aggravates respiratory disease 811. Ozone is one of the most important factors in photochemical pollution. An increase in the frequency of aspirator signs and a decrease of respiratory function measurements has been observed in subjects submitted to high concentrations (0.5 ppm). No such increase was noted with levels around 0.1 ppm which prevail in numerous towns 1201. Children exhibit transient ~te~tions in spi~me~c data when ozone levels increase [ 19]. SO;?, particulate pollution, NO2 and photochemical pollution linked to ozone are the main pollutants causing respiratory diseases. Numerous studies have shown that concentrations of S& and suspends particle matter have conside~bly decreased over the Iast 20 years. Supposedly Safe levels have been defined. However, although some studies indicate that no manifeStatiOnOCCUrS below certain levels, others show a relationship between the SO2 concentrations and the prevalence of ,symptoms f 151 no matter what the level. Au important point that must be emphasized is that childhood infections are liuked to general pollution and that this increases the risk of developing chronic airway disease 14, 285
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Measures must be taken to further reduce mean concentrations of pollutants as well as to prevent accidents near industrial plants in urban areas. Indoor pollution can be lowered by improving heating ventilation but the most important factor is tobacco smoke.
Referemes 1 Amdur MO (1989) Health effects of air pollutants:
sulfuric acid, the old and the new. Environ Health Perspect 89, 109 2 Ball DJ, Hume R (1977) The relative importance of vehicular emissions of dark smoke in Greater London in the mid 1970’s, the significance of smoke shade measurements and an explanation of the relationship of smoke shade to gravimetric measurements of particulaies. Atmos Environ 11, 1065 3 Balmes JR, Fine JM, Gordon T, Sheppard D (1989) Potential bronchoconstrictor stimuli in acid fog. Environ Health Perspect 79, 163 4 Barker DJP, Osmond C (1986) Childhood respiratory infection and adult chronic bronchitis in England and Wales. Br Med J 293, 1271 5 Berciano FA, Dominguez J, Alvarez FV (1989) Influence of air pollution on extrinsic childhood asthma. Ann Allergy 62, 135 6 Boleij JS, Brunckreef B (1989) Domestic pollution as a factor causing respiratory health effects. Chest 96, 3688 7 Charpin D, Kleisbauer JP, Fondarai A, Francheterre A, Fondarai J, Graland B, Viala A (1988) Acute effects of air pollution changes in schoolchildren: the Gardanne coal basin study. Int J Biometeorol32, 275 8 Charpin D, Kleisbauer JP, Fondarai J, Graland B, Viala A, Gouezo F (198X) Respiratory symptoms and air pollution changes on children. The Gardanne coal basin study. Arch Environ Health 43, 22 9 Chretien J (1989) Pollution (atmospheric, domestic, and occupational) as chronic airways disease. Chest 96, 3165 10 Dawson SV, Schenker MB (1979) Health effects of inhalation of ambient concentrations of nitrogen dioxide. Am Rev Respir Dis 120, 281 11 Derriennic F, Richardson S, Mollie A, Lellouch J (1989) Short term effects of sulfur dioxide pollution on mortality in two French cities. Inc J Epidemiol 18, 186 12 Dockery DW, Speizer FE, Stram DO, Ware JH, Spengler JD, Ferris BG (1989) Effects of inhalable particles on respiratory health of children. Am Rev Respir Dis 139, 587 13 Goings SAJ. Kulle TJ, Bascom R, Sauder LR, Green DJ, Hebel JR, Clements ML (1989) Effect of nitro-
gen dioxide exposure to influenza A virus infection in healthy adults. Am Rev Respir Dis 139, 1075 14 Groupe cooperatif PAARC (1982) Air pollution and chronic respiratory diseases I - Methods and material. Bull Eur Physiopathol Respir 18, 87 15 Groupe cooperatif PAARC (1982) Air pollution and chronic respiratory diseases II - Results and discussion. Bull Eur Physiopathol Respir 18, 101 16 Holland WW, Stone RW (1965) Respiratory disorder in United States east cost telephone men Am J Epidemiol 82, 92 17 Holland WW, Bennett AE, Cameron IR, Florey C, Leeder SR, Schilling RS, Swan AV, Wailer RE (1979) Health effects of particulate pollution: reappraising the evidence. Am J Epidemiol 110, 525 18 Imai M, Yoshida K, Kitabtake M (1986) Mortality from asthma and chronic bronchitis associated with change in sulfur oxides air pollution. Arch Environ Health 41,29 19 Kinney PL, Ware JH, Spengler JD (1988) A critical evaluation of acute zone epidemiology results. Arch Environ Health 43, 168 20 Kinney PL, Ware JH, Spengler JD, Dockery DW, Speizer FE, Ferris BG (1989) Short term pulmonary function change in association with ozone levels. Am Rev Respir Dis 139, 56 21 Mills CA (1957) Respiratory and cardiac deaths in Los Angeles smogs. Am J Med Sci 233, 379 22 Orehek J, Massari JP, Gayrard D, Grimaud C. Charpin J (1976) Effect of short term low level nitrogen dioxide exposure on bronchial sensitivity of asthmatic patients. J Clin Invest 57, 301 23 Samet JM, Marbury MC, Spengler JD (1987) Health effects and sources of indoor air pollution part I. Am Rev Respir Dis 136, 1486 24 Sawicki F (1969) Chronic non-specific respiratory disease in the city of Cracow. Statistical analysis of air pollution by suspended particulate matter and sulfur dioxide. Epidemiol Rev 23, 221 25 Stem B, Jones L, Raizenne M, Burnett R, Meranger JC, Franklin CA (1989) Respiratory health effects associated with ambient sulfates and ozone in two rural Canadian communities. Environ Res 49, 20 26 Teculescu D, Pham QT. Aubry C, Chau N, Viaggi MN, Henquel JC, Manciaux MM (1989) Sante respiratoire des enfants et pollution atmosph&ique. II. Fonction ventilatoire. Rev Ma1 Respir 6, 221 27 Van der Lende R, Huygen C, Jansen-Koster EJ, Knispstra S, Peset R, Quanjer PH, Wolfs EHE, Orie NJM (1977) Description d’enquetes kpidemiologiques r&entes aux Pays-Bas. Rev Fr Ma1 Respir 5, 95 28 Waller RE (1989) Ahnospheric pollution. Chest 96,363s 29 Zapleptal A, Jech J, Kaspar J, Samanek M (1977) Courbes debit volume et detection de l’obstruction des voies abriennes chez les enfants d’une zone poll&e. Bull Eur Physiopathol Respir 13, 803