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Air pollutants and cough.

Epidemiological studies have shown that exposure to air pollution is associated with respiratory symptoms and decreases in lung function. This paper reviews recent literature showing that exposure to particulate matter, irritant gases, environmental tobacco smoke (ETS), mixed pollutants, and molds is associated with an increase in cough and wheeze. Some pollutants, like particulate matter and mixed pollutants, appear to increase cough at least as much as wheeze. Others, like irritant gases, appear to increase wheeze more than cough. For ETS, exposure during childhood is associated with cough and wheeze in adulthood, suggesting that the pollutant permanently alters some important aspect of the lungs, immune system or nervous system. We have shown in animal studies that pollutants change the neural control of airways and cough. Second hand smoke (SHS) exposure lengthened stimulated apnoea, increased the number of stimulated coughs, and augmented the degree of stimulated bronchoconstriction. The mechanisms included enhanced reactivity of the peripheral sensory neurones and second-order neurones in the nucleus tractus solitarius (NTS). NTS effects were due to a substance P mechanism at least in part. Ozone and allergen increased the intrinsic excitability of second-order neurones in the NTS. The animal studies suggest that the cough and wheeze experienced by humans exposed to pollutants may involve plasticity in the nervous system.

Adult↗

Episodic air pollution is associated with increased DNA fragmentation in human sperm without other changes in semen quality.

BACKGROUND: This study examined potential associations between exposure to episodes of air pollution and alterations in semen quality. The air pollution, resulting from combustion of coal for industry and home heating in the Teplice district of the Czech Republic, was much higher during the winter than at other times of year with peaks exceeding US air quality standards. METHODS: Young men from Teplice were sampled up to seven times over 2 years allowing evaluation of semen quality after periods of exposure to both low and high air pollution. Routine semen analysis (sperm concentration, motility and morphology) and tests for sperm aneuploidy and chromatin integrity were performed, comparing measurements within each subject. Exposure was classified as high or low based on data from ambient air pollution monitoring. RESULTS: Using repeated measures analysis, a significant association was found between exposure to periods of high air pollution (at or above the upper limit of US air quality standards) and the percentage of sperm with DNA fragmentation according to sperm chromatin structure assay (SCSA). Other semen measures were not associated with air pollution. CONCLUSION: Exposure to intermittent air pollution may result in sperm DNA damage and thereby increase the rates of male-mediated infertility, miscarriage, and other adverse reproductive outcomes.

Abortion, Spontaneous↗

Air pollution and mortality in Philadelphia, 1974-1988.

Analyses involving data from many locations throughout the world have now been conducted to assess the association between air pollution and mortality. To date, six independent analyses of mortality data for Philadelphia, Pennsylvania, have been reported. In this new analysis of Philadelphia data for 1974-1988, Poisson regression models were developed to estimate the increased risk of daily mortality associated with air pollution while controlling for longer-term time trends and season and for weather. Model development was based on prior understanding of the effects of these factors on mortality and on consideration of model fit. The authors found moderate correlations of daily concentrations of total suspended particles (TSP), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO), and only slight correlations of ozone (O3) with other pollutants. When included individually in the model, the means of current and previous days' levels of TSP, SO2, and O3 had statistically significant effects on total mortality; pollutant increases of an interquartile range (34.5 micrograms/m3, 12.9 ppb, and 20.2 ppb, respectively) were associated with increases in mortality of around 1% for TSP and SO2, and of around 2% for O3. The effects of TSP and SO2 were diminished when both pollutants were simultaneously included in the model, whether pairwise or in the full multi-pollutant model. These analyses confirm the association between TSP and mortality found in previous studies in Philadelphia and show that the association is robust to consideration of other pollutants in the model.

Aged↗

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.

Air Pollutants↗

Effects of coal-smoke pollutants from different sources on the growth, chlorophyll content, stem anatomy and cuticular traits of Euphorbia hirta L.

Variations occurred in the growth, assimilate partitioning, chlorophyll content, stem anatomy and leaf cuticular traits of Euphorbia hirta L. on long-term exposure to coal-smoke pollutants prevailing at two sites, one situated close to a railway loco shed (site B) and another in the vicinity of a thermal power plant (site C). The Botanical Garden of Aligarh Muslim University, Aligarh, was considered as a control site (A). Site C possessed a greater load of coal-smoke pollutants than site B. The present study had shown that coal-smoke pollutants have led to a decrease in plant height, jeopardised the production of leaves and enhanced their fall, and caused a reduction in leaf area, leading to decreases of the total photosynthetic area of the plants, with increasing pollution load. The losses incurred in chlorophyll a were relatively more than chlorophyll b and, as a result, the total chlorophyll contents of leaves were decreased in polluted plants. The dry weights of stems, roots and leaves were decreased to different degrees, whereas the shoot/root dry weight ratio was found to increase in the polluted environment. The growth of stem cortex and pith were slightly affected on site B, but showed significant decreases on site C, due to a greater load of pollutants. Decreased area of xylem tissue was found to couple with an increasing number of vessels of reduced sizes. The stomatal density, pore size and index showed decreases, while the epidermal cells were larger and trichomes longer, on both surfaces of polluted leaves.

Journal Article↗

Current and historical relationships between the tissue nitrogen content of a snowbed bryophyte and nitrogenous air pollution.

Snowbed vegetation is under threat from atmospheric pollution. Most of the late lying snowbeds in Britain are in the central highlands of Scotland, coinciding with an area of very high deposition of nitrogenous air pollutants. Snow is a very efficient scavenger of atmospheric pollution and, due to the dynamics of snowmelt, much of the pollution load of a snow pack is released at very high concentrations in episodes known as 'acid flushes'. This study demonstrates the existence of a positive relationship between duration of snow-lie and tissue nitrogen content of Kiaeria starkei, a bryophyte characteristic of late snowbeds. An increase in the tissue nitrogen content of this bryophyte over this century is also shown, reflecting increasing air pollution. Maximum tissue nitrogen concentration in K. starkei is up to 50% greater than that recorded in other upland bryophyte species, demonstrating the exceptional threat of pollution to snowbed bryophytes. This has implications for the critical loads approach to pollution emission controls, as it indicates that some mountain communities are receiving higher pollution loadings than previously realised and therefore current exceedence of critical loads is probably greater than recognised at present.

Journal Article↗

Interaction patterns of major air pollutants in Hong Kong territory.

Air pollution in a metropolitan city like Hong Kong is a major obstacle to improve air quality and living environment due to the high population density and the vehicle emission increases. The high air pollutant levels impose harm to the human health and impair the city image. The characteristic analysis of air pollutants is very important and necessary to pollutant monitoring, forecasting and controlling. In this study, the interaction patterns of principle air pollutants, e.g. nitrogen dioxide (NO(2)), nitric oxide (NO), nitric oxides (NO(x)) and ozone (O(3)), a secondary pollutant, are investigated based on the measured database in four selected areas, which covers two urban types (i.e. residential area, mixed residential/commercial/industrial area) in Hong Kong, during the period of 1999-2001. The study involves analyzing the chemical and physical properties, the characteristics of air pollutants and the factors affecting such interactions using statistical method. The results reveal several routines in urban air pollutants' variations, interaction and trends from macro aspect.

Journal Article↗

Bottom sediments of the Arabian Gulf--II. TPH and TOC contents as indicators of oil pollution and implications for the effect and fate of the Kuwait oil slick.

Measurements of total petroleum hydrocarbon (TPH) concentrations in 77 core samples collected in 1992 from the bottom sediments of the Arabian Gulf were used to delineate oil pollution levels and their distribution in the region. Seven chronic moderately (TPH 50-89 microg g(-1)) and heavily (TPH 266-1448 microg g(-1)) polluted areas were identified; three in the northern part of the region and four in the southern part. Oil pollution in these areas was attributed to natural oil seepage, accidental damage to pipelines, accidental spillage from tankers, the Nowruz oil slick, and tanker deballasting. Present-day intermediate (TPH 50-114 microg g(-1)) and high (TPH 200-1122 microg g(-1)) pollution levels were identified in 10 areas. Of these, three polluted areas in the northeastern corner, offshore Saudi Arabia and offshore Bahrain, Qatar and United Arab Emirates are probably directly affected by the Kuwait oil slick. A new scenario is suggested for the movement and fate of the oil slick, in which additional large oil discharges from northern sources, as well as substantial quantities of eroded oiled sediments and oil floating from heavily impacted tidal flats along the Saudi Arabian coastline, serve as sources of oil pollution. A definite relationship exists between the grain-size distribution and the TPH content of bottom sediments, with the highest TPH concentrations in the muddy sediments, suggesting that adsorption onto muds is the primary mechanism of oil pollutant accumulation in the Arabian Gulf. Total organic carbon measurements do not correlate positively with the grain-size distribution and TPH contents of the sediments, and hence cannot be used as indicators for petroleum hydrocarbon pollution in the Arabian Gulf.

Journal Article↗

The effects of simultaneous large acidic and alkaline airborne pollutants on forest soil.

The effects of air pollutants on soil were studied in Scots pine (Pinus sylvestris L.) forests near the boundary of Russia and Estonia. The study area is characterized by large amounts of acidic and basic pollutants, mainly sulphur dioxide (SO(2)) and calcium (Ca). Several variables were measured in different horizons of the podzolic soil polluted by emissions from local sources in areas of several thousands of square kilometers. Alkalinization dominates the processes in the soil, since sulphur is absorbed only in small quantities and Ca is much better absorbed. Ca content in humus horizon may rise even to 100 000 mg kg(-1) and the pH of originally very acidic soil may rise to 8.3. Total aluminum (Al) content was high in the heavily polluted plots, since emissions contain much Al. On the other hand, the exchangeable Al was very low in these alkaline sites. A larger quantity of exchangeable Al occurred farther from the pollutant sources, even though total Al in these plots was low. These plots had acidic soils in which Al is in exchangeable form. Due to the neutralizing effect of acidic and basic pollutants, forest damage in the study area was not as serious as might be supposed. Complicated pollutant situations must be taken into consideration when pollution-caused environmental protection measures are planned. It is not reasonable to reduce only SO(2) emissions, but necessary to lower the basic emissions at the same time.

Journal Article↗

Passive sampling of ambient, gaseous air pollutants: an assessment from an ecological perspective.

During some past two decades there has been a growing interest among air pollution-vegetation effects-scientists to use passive sampling systems for quantifying ambient, gaseous air pollutant concentrations, particularly in remote and wilderness areas. On the positive side, excluding the laboratory analysis costs, passive samplers are inexpensive, easy to use and do not require electricity to operate. Therefore, they are very attractive for use in regional-scale air quality assessments. Passive samplers allow the quantification of cumulative air pollutant exposures, as total or average pollutant concentrations over a sampling duration. Such systems function either by chemical absorption or by physical adsorption of the gaseous pollutant of interest onto the sampling medium. Selection of a passive sampler must be based on its known or tested characteristics of specificity and linearity of response to the chemical constituent being collected. In addition, the effects of wind velocity, radiation, temperature and relative humidity must be addressed in the context of absorbent/adsorbent performance and sampling rate. Because of all these considerations, passive samplers may provide under- or overestimations of the cumulative exposures, compared to the corresponding data from co-located continuous monitors or active samplers, although such statistical variance can be minimized by taking necessary precautions. On the negative side, cumulative exposures cannot identify short-term (<few hours) pollutant episodes or regulatory non-compliance, where appropriate. Equally important, cumulative exposures (e.g. with ozone, a non-accumulating pollutant in plants) cannot account for the stochasticity and the dynamics of air pollutant exposure and plant (particularly deciduous vegetation) response. Although still being tested, statistical methods appear to be available to reconstruct passive sampler data to mimic the dynamics of the co-located continuous monitoring data. Regional level air quality and ecological risk assessments (multi-point models) as a whole should consider this type of approach in the future, using co-located passive samplers, with continuous monitors at selected locations as calibration points for mapping the air quality distribution on temporal and spatial scales.

Journal Article↗

Soil Bacterial Biomass, Activity, Phospholipid Fatty Acid Pattern, and pH Tolerance in an Area Polluted with Alkaline Dust Deposition.

Soil bacterial biomass, phospholipid fatty acid pattern, pH tolerance, and growth rate were studied in a forest area in Finland that is polluted with alkaline dust from an iron and steel works. The pollution raised the pH of the humus layer from 4.1 to 6.6. Total bacterial numbers and the total amounts of bacterial phospholipid fatty acids in the humus layer did not differ between the unpolluted control sites and the polluted ones. The number of CFU increased by a factor of 6.4 in the polluted sites compared with the controls, while the bacterial growth rate, measured by the thymidine incorporation technique, increased about 1.8-fold in the polluted sites. A shift in the pattern of phospholipid fatty acids indicated a shift in the bacterial species composition. The largest proportional increase was found for the fatty acid 10Me18:0, which indicated an increase in the number of actinomycetes in the polluted sites. The levels of the fatty acids i14:0, 16:1omega5, cy17:0, 18:1omega7, and 19:1 also increased in the polluted sites while those of fatty acids 15:0, i15:0, 10Me16:0, 16:1omega7t, 18:1omega9, and cy19:0 decreased compared with the unpolluted sites. An altered pH tolerance of the bacterial assemblage was detected either as a decrease in acid-tolerant CFU in the polluted sites or as altered bacterial growth rates at different pHs. The latter was estimated by measuring the thymidine incorporation rate of bacteria extracted from soil by homogenization-centrifugation at different pHs.

Journal Article↗

Atmospheric pollution due to mobile sources and effects on human health in Japan.

Following the rapid economic growth after World War II, diseases associated with environmental pollution frequently occurred due to delayed implementation of countermeasures against environmental pollution. These diseases are exemplified by Minamata disease, Itai-itai disease, chronic arsenic poisoning, and Yokkaichi asthma. After multiple episodes of these pollution-related diseases were experienced, the government and the private sector made joint efforts to reduce environmental pollution. As a result of these efforts and because of changes in the industrial structure, pollution-related diseases have declined. Instead, however, air pollution from automobile exhaust and the health effects of automobile exhaust on people living along roads with heavy traffic began to attract the public's attention after an increase in the use of automobiles. The epidemiological surveys carried out by the Environmental Agency and the Tokyo Metropolitan Government also have suggested unfavorable effects of automobile-caused air pollution on people living in large cities or along major roads. To solve this problem, it seems imperative to promote the reasonable use of automobiles and to work toward more efficient transportation of goods based on analyses of city structure, the life-styles of city dwellers, and the socioeconomic composition of cities. In addition, the discharge of pollutants from automobiles could be controlled.

Adult↗

Increased thyroid volume and prevalence of thyroid disorders in an area heavily polluted by polychlorinated biphenyls.

OBJECTIVE: To evaluate whether long-term exposure to heavy environmental pollution with polychlorinated biphenyls (PCBs) could result in impairment of thyroid status as evaluated by an epidemiological field survey. METHODS: Thyroid volume (ThV) was measured by ultrasound in 238 employees of a factory (EMP) which previously produced PCBs and 454 adolescents from the surrounding area polluted by PCBs. Controls (C) were 572 adults and 965 adolescents from much less polluted areas. In the 238 EMP and various numbers (shown in parentheses) of adult C the levels of thyroid-stimulating hormone (TSH) (n = 498), thyroxine (n = 498), thyroglobulin (n = 278) and thyroid antibodies (anti-peroxidase (TPO Ab), n= 517; anti-thyroglobulin (Tg Ab), n=455; anti-TSH receptor (TSHR Ab), n=238) were estimated in serum, while only TSH and TPO Ab were measured in 269 and 171 adolescents from polluted and control areas respectively. In several subjects in whom thyroid disease was suspected, total tri-iodothyronine or free thyroxine and tri-iodothyronine were measured. In a total of 362 adults and adolescents the urinary iodine was estimated. RESULTS: Using the Mann-Whitney test, ThV in EMP (mean+/-S.E. = 18.85+/-0.69 ml, median= 17.3 ml, upper quartile=22.9 ml, n=238) was significantly higher (P< 0.001) than that in C (13.47+/-0.48 ml, 11.5 ml, 15.3 ml, n = 486 respectively). Similarly, ThV in adolescents from the polluted area (9.37+/-0.17 ml, 8.9 ml, 11.0 ml, n = 454 respectively) was significantly higher (P< 0.001) than that in C (8.07+/-0.10 ml, 7.6 ml, 9.6 ml, n = 965 respectively). In adults, a significantly increased prevalence of TPO Ab (P<0.05) was found (using the chi-square test) in EMP women of all ages (54/190) vs C women (70/282), in EMP women aged 31-50 years (40/117 vs 70/282 respectively) and those aged 41- 50 years (28/77 vs 54/215 respectively). Compared with C, there was also a higher prevalence of Tg Ab in EMP women aged 31-60 years (36/169 vs 50/342 respectively) and of TSHR Ab (P< 0.001) in the group of EMP men and women (25/238) vs sex- and age-matched C (6/238). No difference between EMP and C was found in the level of thyroxine (mean+/-S.D = 116.1+/-31.2 nmol/l, n = 238 vs 112.2+/-37.0 nmol/l, n = 460 respectively), TSH in the range 0.1-4.5 mU/l(1.56+/-0.86 mUl/l, n = 219 vs 1.51+/-0.84 mU/l, n = 460 respectively), prevalence of TSH >4.5 (14/238 vs 28/498 respectively) and <0.1 mU/l(5/238 vs 10/498 respectively). The prevalence of individuals without any defined clinical or laboratory signs of thyroid disorders among EMP who had worked in the factory for 21-35 years (43/128, 33.6%) was significantly lower than that in twice as many matched C (118/256, 46.1%, P< 0.025) or in EMP who had worked for only 11-20 years (36/73, 49.3%, P< 0.05). In adolescents, no difference was found in the prevalence of TPO Ab or TSH >4.5 mU/l between the polluted (17/269, 6.3%, and 2/243, 0.8% respectively) and C areas (15/171, 8.5% and 4/140, 2.8% respectively). The median values of urinary iodine were in the optimal range (microg per dl/number of cases) and about the same in polluted (12.6/90 and 11.4/55) and C areas (14.1/80, 13.2/82 and 13.4/55). CONCLUSIONS: Since iodine intake in Slovakia is considered sufficient as a result of 45 years of well-monitored iodine prophylaxis, the increased ThVand prevalence of thyroid disorders in the polluted areas presumably results from long-term exposure to toxic substances rather than from a difference in life-long iodine intake. The increased prevalence of some thyroid antibodies may be related to the known immunomodulatory effects of PCBs.

Adolescent↗

Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution.

CONTEXT: Associations have been found between day-to-day particulate air pollution and increased risk of various adverse health outcomes, including cardiopulmonary mortality. However, studies of health effects of long-term particulate air pollution have been less conclusive. OBJECTIVE: To assess the relationship between long-term exposure to fine particulate air pollution and all-cause, lung cancer, and cardiopulmonary mortality. DESIGN, SETTING, AND PARTICIPANTS: Vital status and cause of death data were collected by the American Cancer Society as part of the Cancer Prevention II study, an ongoing prospective mortality study, which enrolled approximately 1.2 million adults in 1982. Participants completed a questionnaire detailing individual risk factor data (age, sex, race, weight, height, smoking history, education, marital status, diet, alcohol consumption, and occupational exposures). The risk factor data for approximately 500 000 adults were linked with air pollution data for metropolitan areas throughout the United States and combined with vital status and cause of death data through December 31, 1998. MAIN OUTCOME MEASURE: All-cause, lung cancer, and cardiopulmonary mortality. RESULTS: Fine particulate and sulfur oxide--related pollution were associated with all-cause, lung cancer, and cardiopulmonary mortality. Each 10-microg/m(3) elevation in fine particulate air pollution was associated with approximately a 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer mortality, respectively. Measures of coarse particle fraction and total suspended particles were not consistently associated with mortality. CONCLUSION: Long-term exposure to combustion-related fine particulate air pollution is an important environmental risk factor for cardiopulmonary and lung cancer mortality.

Adult↗

Ecological and toxicological effects of inorganic nitrogen pollution in aquatic ecosystems: A global assessment.

We provide a global assessment, with detailed multi-scale data, of the ecological and toxicological effects generated by inorganic nitrogen pollution in aquatic ecosystems. Our synthesis of the published scientific literature shows three major environmental problems: (1) it can increase the concentration of hydrogen ions in freshwater ecosystems without much acid-neutralizing capacity, resulting in acidification of those systems; (2) it can stimulate or enhance the development, maintenance and proliferation of primary producers, resulting in eutrophication of aquatic ecosystems; (3) it can reach toxic levels that impair the ability of aquatic animals to survive, grow and reproduce. Inorganic nitrogen pollution of ground and surface waters can also induce adverse effects on human health and economy. Because reductions in SO2 emissions have reduced the atmospheric deposition of H2SO4 across large portions of North America and Europe, while emissions of NOx have gone unchecked, HNO3 is now playing an increasing role in the acidification of freshwater ecosystems. This acidification process has caused several adverse effects on primary and secondary producers, with significant biotic impoverishments, particularly concerning invertebrates and fishes, in many atmospherically acidified lakes and streams. The cultural eutrophication of freshwater, estuarine, and coastal marine ecosystems can cause ecological and toxicological effects that are either directly or indirectly related to the proliferation of primary producers. Extensive kills of both invertebrates and fishes are probably the most dramatic manifestation of hypoxia (or anoxia) in eutrophic and hypereutrophic aquatic ecosystems with low water turnover rates. The decline in dissolved oxygen concentrations can also promote the formation of reduced compounds, such as hydrogen sulphide, resulting in higher adverse (toxic) effects on aquatic animals. Additionally, the occurrence of toxic algae can significantly contribute to the extensive kills of aquatic animals. Cyanobacteria, dinoflagellates and diatoms appear to be major responsible that may be stimulated by inorganic nitrogen pollution. Among the different inorganic nitrogenous compounds (NH4+, NH3, NO2-, HNO2NO3-) that aquatic animals can take up directly from the ambient water, unionized ammonia is the most toxic, while ammonium and nitrate ions are the least toxic. In general, seawater animals seem to be more tolerant to the toxicity of inorganic nitrogenous compounds than freshwater animals, probably because of the ameliorating effect of water salinity (sodium, chloride, calcium and other ions) on the tolerance of aquatic animals. Ingested nitrites and nitrates from polluted drinking waters can induce methemoglobinemia in humans, particularly in young infants, by blocking the oxygen-carrying capacity of hemoglobin. Ingested nitrites and nitrates also have a potential role in developing cancers of the digestive tract through their contribution to the formation of nitrosamines. In addition, some scientific evidences suggest that ingested nitrites and nitrates might result in mutagenicity, teratogenicity and birth defects, contribute to the risks of non-Hodgkin's lymphoma and bladder and ovarian cancers, play a role in the etiology of insulin-dependent diabetes mellitus and in the development of thyroid hypertrophy, or cause spontaneous abortions and respiratory tract infections. Indirect health hazards can occur as a consequence of algal toxins, causing nausea, vomiting, diarrhoea, pneumonia, gastroenteritis, hepatoenteritis, muscular cramps, and several poisoning syndromes (paralytic shellfish poisoning, neurotoxic shellfish poisoning, amnesic shellfish poisoning). Other indirect health hazards can also come from the potential relationship between inorganic nitrogen pollution and human infectious diseases (malaria, cholera). Human sickness and death, extensive kills of aquatic animals, and other negative effects, can have elevated costs on human economy, with the recreation and tourism industry suffering the most important economic impacts, at least locally. It is concluded that levels of total nitrogen lower than 0.5-1.0 mg TN/L could prevent aquatic ecosystems (excluding those ecosystems with naturally high N levels) from developing acidification and eutrophication, at least by inorganic nitrogen pollution. Those relatively low TN levels could also protect aquatic animals against the toxicity of inorganic nitrogenous compounds since, in the absence of eutrophication, surface waters usually present relatively high concentrations of dissolved oxygen, most inorganic reactive nitrogen being in the form of nitrate. Additionally, human health and economy would be safer from the adverse effects of inorganic nitrogen pollution.

Acid Rain↗

Estimating the effect of air pollution from a coal-fired power station on the development of children's pulmonary function.

Using geographical information systems (GIS) tools, the present study analyzed the association between children's lung function development and their long-term exposure to air pollution. The study covered the cohort of 1492 schoolchildren living in the vicinity of a major coal-fired power station in the Hadera sub-district of Israel. In 1996 and 1999, the children underwent subsequent pulmonary function tests (PFT) (forced vital capacity (FVC) and forced expiratory volume during the first second (FEV(1))), and the children's parents completed a detailed questionnaire on their health status and household characteristics. A negative association was found between changes in the results of PFT and the estimated individual levels of air pollution. A sensitivity test revealed a FEV(1) decline from -4.3% for the average pollution level to -10.2% for the high air pollution level. The results of a sensitivity test for FVC were found to be similar. Association with the reported health status was found to be insignificant. As we conclude, air pollution from a coal-fired power station, although not exceeding local pollution standards, had a negative effect on children's lung function development. As argued, previous studies carried out in the region failed to show the above association because they were based on zone approaches that assign average concentration levels of air pollutants to all individuals in each zone, leading to a misclassification bias of individual exposure.

Adolescent↗

Low levels of ambient air pollution during pregnancy and fetal growth among term neonates in Brisbane, Australia.

There is mounting evidence that maternal exposure to ambient air pollution during pregnancy is associated with adverse birth outcomes. We examined birth weight and small for gestational age (SGA <10th percentile for age and gender) among 26,617 singleton full-term births in Brisbane, Australia (July 2000-June 2003), in relation to ambient pollution during pregnancy. We also examined head circumference (HC) and crown-heel length (CHL) among a sub-sample (n=21,432) of the term neonates. Maternal exposure to PM(10), visibility reducing particles (bsp), O(3) and NO(2) was assessed by calculating average exposure estimates over months and trimesters of pregnancy based on a citywide average of the pollutants. Linear and logistic regression models were employed to examine the effect of these pollutants on the birth outcomes after adjusting for potential confounders and season of birth. The regression coefficients were based on an inter-quartile range (IQR) increase in exposure as well as quartiles of exposure with the lowest used as a reference category. Trimester- and monthly specific exposures to all pollutants were not significantly associated with a reduction in either birth weight or HC, or an increased risk of SGA. An IQR increase in NO(2) during the third trimester was associated with a reduction in CHL (beta=-0.15cm, 95% CI -0.25 to -0.05cm) and this was concentrated around exposure during month nine. No other pollutants were associated with a reduction in CHL. In conclusion, there was no strong evidence suggesting that ambient air pollution during pregnancy is associated with sub-optimal fetal growth in Brisbane.

Air Pollutants↗

Effects of wintertime ambient air pollutants on asthma exacerbations in urban minority children with moderate to severe disease.

BACKGROUND: Urban minority children with asthma are at higher risk for severe exacerbations leading to hospitalizations and deaths. Because multiple studies have reported associations between air pollution and asthma worsening, elevated levels of air pollution are cited as a possible trigger for increased asthma morbidity in urban areas. Few studies have prospectively followed panels of urban children with asthma to determine whether air pollution levels are associated with clinically relevant outcomes such as asthma exacerbations. OBJECTIVE: To determine the association between levels of ambient air pollutants and asthma exacerbations in urban poor children with moderate to severe asthma. METHODS: A school-based panel of children with difficult-to-control disease was followed over a period of 3 consecutive winters in Denver, Colo. The panel consisted of predominantly urban African American children with moderate to severe asthma. Levels of Environmental Protection Agency criteria air pollutants were measured on a daily basis with concurrent monitoring of lung function, bronchodilator use, symptoms, and asthma exacerbations. RESULTS: After controlling for time-varying factors such as upper respiratory infections and meteorologic factors, a weak association was found between ambient carbon monoxide levels and bronchodilator use. Ozone levels were associated with daytime symptoms only. No association was observed between daily air pollution concentrations and daily levels of FEV 1 , peak flow, nighttime symptom scores, or asthma exacerbations over the 3-year period. CONCLUSION: Ambient levels of Environmental Protection Agency criteria air pollutants in Denver do not lead to clinically significant asthma worsening in urban children with moderate to severe asthma during winter months when children are primarily indoors.

Air Pollutants↗