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Child health level in Moscow as related to ambient air pollution.

Ambient air in Moscow is characterised by high concentrations of nitric oxide and other pollutants. The level of air pollution varies from one neighbourhood of the city to another. This accounts for the variability of child health levels. In the most severely polluted areas the prevalence of childhood bronchial asthma is much higher; cases of dis-harmonious physical development among children are more frequent. A map of Moscow depicting the degrees of environmental hazards has been established on the basis of interrelated studies of ambient air quality and child health levels.

Air Pollution↗

Survey of air pollution in Cotonou, Benin--air monitoring and biomarkers.

Exposure to genotoxic compounds present in ambient air has been studied in Cotonou, Benin, a city where two-stroke motorbikes are the major form of transportation and gasoline quality is poor. Personal monitoring and biomarkers were used to assess the exposure. Non-smoking taxi-moto drivers (city) and village residents were the study subjects. Benzene exposure was significantly higher in the city, as compared to the village (76.0+/-26.8 microg/m(3) versus 3.4+/-3.0, p=0.0004). Urinary excretion of benzene and S-phenylmercapturic acid (S-PMA) were also highest in subjects living in the city, whereas 1-hydroxypyrene was not different. The level of total polycyclic aromatic hydrocarbons (PAHs), associated with particles, ranged from 76.21 to 103.23 in Cotonou versus 1.55 ng/m(3) for the village. Determination of DNA damage in lymphocytes showed that subjects from the city had elevated number of lesions compared to subjects in the village in terms of bulky DNA adducts, 8-hydroxy-2'-deoxyguanosine and 5-methylcytosine, whereas DNA fragmentations analysed by alkaline gel electrophoresis was not different between the subjects. In conclusion, this study shows that air pollution is pronounced in Cotonou, Bénin and is associated with elevated levels of DNA damage in residents of the city compared to people living in a non-polluted rural village.

Adult↗

The role of symptomatic colds in asthma exacerbations: Influence of outdoor allergens and air pollutants.

BACKGROUND: Both air pollutants and respiratory viral infections have been recognized to be important triggers of asthma exacerbations, but the possible interaction of these has not been assessed in an epidemiologic study. OBJECTIVE: In this study, we aimed to assess the possible associations of symptomatic colds with outdoor allergens and air pollutants in exacerbating asthma. METHODS: A total of 57 adults and children with asthma participated in a 1-year study in Vancouver, British Columbia. Diary cards recording symptoms of asthma and colds, medication usage, and peak expiratory flow rates were completed twice daily. Outdoor air pollutant levels and levels of pollen and fungal spores were measured. Levels were examined for associations with exacerbations of asthma with symptoms of a cold, as compared with asthma exacerbations with no cold symptoms and colds in the absence of asthma exacerbations. RESULTS: Of 130 asthma exacerbations, 47% were associated with cold symptoms (accounting for 44% of episodes of colds). Asthma exacerbations with colds were associated with higher levels of sulfur dioxide, and nitric oxide during March to November in comparison with asthma exacerbations without cold symptoms (P <.018). Cold-symptom days overall were more common in winter and were significantly associated with lower temperatures, lower ozone levels, and higher sulfur dioxide, nitrogen dioxide, nitrogen oxide (NO and NO(x)), and carbon monoxide levels. CONCLUSIONS: Asthma exacerbations are commonly associated with cold symptoms. These episodes are associated with higher levels of sulfur dioxide and nitrogen oxides from March to November in comparison with asthma exacerbations without cold symptoms.

Adolescent↗

Air pollution and daily mortality in three U.S. counties.

I used generalized additive models to analyze the time-series of daily total nonaccidental and cause-specific (cardiovascular, cerebrovascular, and chronic obstructive pulmonary disease) deaths over the period 1987-1995 in three major U.S. metropolitan areas: Cook County, Los Angeles County, and Maricopa County. In all three counties I had monitoring information on particulate matter [less than/equal to] 10 microm (PM(10)), carbon monoxide, sulfur dioxide, nitrogen dioxide, and ozone. In Los Angeles, monitoring information on particulate matter [less than/equal to] 2.5 microm (PM(2.5)) was available as well. I present the results of both single and multi-pollutant analyses. Air pollution was associated with each of the mortality end points. With respect to the individual components of the pollution mix, the results indicate considerable heterogeneity of air pollution effects in the different geographic locations. In general, the gases, particularly CO, but not ozone, were much more strongly associated with mortality than was particulate matter. This association was particularly striking in Los Angeles County.

Air Pollutants↗

[Carpeting and air pollution?].

After some introductory remarks concerning the frequency of the usage of textile floor-coverings from 1970 to 1979, the manufacturing processes and the composition of these coverings are briefly discussed with special regard to components which may pollute indoor air. As the back of the carpeting may be considered to be a source for air pollution, the composition of the most wide-spread coatings is given. Some difficulties in evaluating these data are due to the fact that it is difficult to analyze odours. During the last years the question of contamination of the air in kindergartens, schools and hospitals due to the use of carpets has been discussed. The results of different investigations which consider carpets to be the reason for either a decrease or an increase of the concentration of microorganisms in indoor air, are presented. Important criteria for evaluation are the frequency of use and the quality, intensity and frequency of cleaning. House-dust allergies are also discussed in relation to textile floor-coverings. The conclusion is drawn that a carefully manufactured carpet, when suitably used and well entertained, hardly adds to indoor air pollution.

Air Pollution↗

Chromosomal damage in peripheral blood lymphocytes of traffic policemen and taxi drivers exposed to urban air pollution.

Urban air contains a diversity of chemical compounds, some of which are genotoxins. An increased risk of cancer has also been reported in occupations with heavy exposure to traffic-related pollution. The aim of this study was to assess the cytogenetic effects of urban air pollution by analyzing the chromosomal aberration (CA) frequencies in lymphocytes and to estimate the polycyclic aromatic hydrocarbons (PAHs) exposure by measuring urinary 1-hydroxypyrene (1-OHP) levels. A total of 15 traffic policemen and 17 taxi drivers working in the city of Ankara were the exposed groups and 23 healthy men working in the office departments were the control group. The overall mean +/- S.D. values of 1-OHP excretions of traffic policemen, taxi drivers and control subjects were 0.59 +/- 0.40 micromol/mol creatinine, 0.32 +/- 0.25 micromol/mol creatinine and 0.57 +/- 0.36 micromol/mol creatinine, respectively. Urinary 1-OHP levels of non-smoking policemen were significantly greater than those of nonsmoking control subjects (p < 0.05). The overall mean +/- S.D. values for CA frequencies (%) from policemen, taxi drivers and control group were 1.29 +/- 1.59, 1.81 +/- 1.79, and 0.26 +/- 0.73, respectively. There was a significantly greater frequency of CAs in exposed groups relative to the matched control population (p < 0.05; p < 0.01). Age, sex and smoking habits have not influenced the cytogenetic end-point in this study. Our results demonstrate that occupational exposure to urban air pollutants leads to a significant induction of cytogenetic damage in peripheral lymphocytes of traffic policemen and taxi drivers.

Adult↗

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↗