Scale and causes of lead contamination in Chinese tea.

We investigated the scale and causes of Pb contamination in Chinese tea. Lead concentrations in 1,225 tea samples collected nationally between 1999 and 2001 varied from <0.2 to 97.9 mg kg(-1) dry weight (DW), with 32% of the samples exceeding the national maximum permissible concentration (MPC) of 2.0 mg kg(-1) DW and a significant difference between tea types. There was an increasing trend in tea Pb concentration from 1989 to 2000. Proximity to highway and surface dust contamination were found to cause elevated Pb concentrations in tea leaves. Furthermore, Pb concentration in tea leaves correlated significantly and positively with soil extractable Pb, and negatively with soil pH, suggesting that root uptake of Pb from soils also contributed to Pb accumulation in tea. Potential contributions to human Pb intake from drinking tea were small at the median or national MPC Pb values, but considerable at the highest concentration found in the study.

Genotoxic damage in mine workers exposed to diesel exhaust, and the effects of glutathione transferase genotypes.

This study was performed in an Estonian shale-oil mine with the purpose to develop and apply a number of biomarkers for occupational diesel-exhaust exposure monitoring. Increased breathing-zone exposures to exhaust from operators of diesel-powered trucks in the mine was confirmed in the environmental monitoring part of the study, showing a 7.5-fold higher exposure to particle-associated 1-nitropyrene (1-NP) in 50 underground workers compared with 42 surface workers [P.T.J. Scheepers, D. Coggon, L.E. Knudsen, R. Anzion, H. Autrup, S. Bogovski, R.P. Bos, D. Dahmann, P. Farmer, E.A. Martin, V. Micka, V. Muzyka, H.-G. Neumann, J. Poole, A. Schmidt-Ott, F. Seiler, J. Volf, I. Zwirner-Baier, Biomarkers for occupational diesel exhaust exposure monitoring (BIOMODEM)-a study in underground mining, Toxicol. Lett. 134 (2002) 305-317; P.T.J. Scheepers, V. Micka, V. Muzyka, R. Anzion, D. Dahmann, J. Poole, R.P. Bos, Exposure to dust and particle-associated 1-nitropyrene of drivers of diesel-powered equipment in underground mining, Ann. Occp. Hyg. 47 (2003) 379-388]. Analysis of DNA damage by the Comet assay on frozen blood samples was performed on the total study group and showed significantly higher levels (p=0.003) in underground workers (smokers) driving diesel-powered excavation machines (median 155 on a scale from 0 to 400, among 47 persons), compared with surface workers who smoked (median of 90, among 46 persons). The level of DNA damage in underground smokers was significantly higher (p=0.04) than in non-smokers. Samples from 2 of the 3 sampling weeks had significantly lower DNA damage compared with the third week, probably due to timely processing and freezing. These samples also showed significant differences (p<0.001) between underground workers (median 145, among 41 persons) and surface workers (median 60, among 30 persons). An HPLC method was developed for the analysis of (32)P-postlabelled 1-NP-DNA-adducts, and was applied to a sub-sample of 20 workers. No significant differences between surface and underground workers were found in this sub-sample with respect to the minor, unidentified adducts that had similar chromatographic properties to 1-NP adducts, and smoking did not have any effect on adduct levels. No significant effects of the genotypes of GSTM1, GSTP1 and GSTT1 on DNA-adducts and on DNA damage as measured by the Comet assay were found in the total study group. The study confirms an increased level of DNA damage in workers exposed to exhaust from truck-driving in the mine. However, the results of the environmental and biological monitoring of 1-NP did not correlate, suggesting that inhalation exposure to diesel exhaust is not reflected by an increase in 1-NP-DNA-adduct levels and/or that factors other than occupational exposure to diesel exhaust are primary determinants of these DNA-adduct levels.

Air pollution and atopy.

Relationships between air pollutants and atopy can be studied within 3 different settings. In vitro, exposure of pollen to air pollutants induce morphological changes and seems to facilitate extrusion on allergenic material out of the pollen grain. In animal as well as in human experiments, air pollutants, especially diesel exhaust particulates, are able to trigger an IgE-response. Epidemiological surveys also show that air pollutants trigger symptoms in patients. In contrast, whether or not air pollutants can induce de novo allergic diseases is still a matter of debate. Some surveys suggest that, in humans also, air pollutants, especially diesel-exhaust particulates, could trigger allergic sensitization and development of atopic diseases. At home, other pollutants can be involved: volatile organic compounds have pro-inflammatory properties and favour T-cell sensitization. Relationship between exposure to secondhand tobacco smoke or occupational hazards and atopic sensitization have led to discordant results.

Carbon monoxide poisoning from portable electric generators.

BACKGROUND: While the overall death rate from unintentional carbon monoxide (CO) poisoning has decreased in the United States due to improved automobile emissions controls and a decline in CO poisonings from motor vehicles, exposures have not changed from some sources of CO. One of these is the operation of portable electrical generators in poorly ventilated spaces. This study sought to describe the population poisoned from CO produced by portable electric generators, and to determine the reasons that generators are operated in a hazardous fashion. METHODS: Cases of CO poisoning referred for treatment with hyperbaric oxygen at Virginia Mason Medical Center in Seattle from November 1978 to March 2004 were reviewed. Those cases that resulted from portable generator use were selected for analysis. RESULTS: Sixty-three patients aged 2 to 85 years were treated for CO poisoning from portable electric generators. They included 34 males and 29 females who were poisoned in 37 separate incidents. Thirty-four lost consciousness with the exposure. Of the 63 total patients, 60 spoke English. Generators were typically used when normal electrical service was disrupted by a storm or in remote locations. In 29 of 37 incidents, the generator was operated in the home environment, most commonly in the garage. Lack of awareness of the dangers of CO poisoning or lack of knowledge of ventilation requirements were the most commonly identified reasons. CONCLUSIONS: CO poisoning from portable electric generators occurs in a characteristic population, in a few typical locations and for a limited number of reasons. This information may help target prevention efforts for this form of poisoning, such as warning labels or educational programs.

Complementary DNA microarray analysis in acute lung injury induced by lipopolysaccharide and diesel exhaust particles.

We have recently shown that diesel exhaust particles (DEP) synergistically enhance acute lung injury related to lipopoly-saccharide (LPS) in mice. The present study used cDNA microarray to elucidate the effects of DEP on the global pattern of LPS-related gene expression in the murine lung. The number of genes upregulated >/=2-fold as compared with their expression levels in the vehicle group was greater in the LPS group than in other groups, but treatment with DEP and LPS dramatically increased the number of the genes upregulated >/=6-fold. In particular, gene expression of metallothionein-1 and -2, S100 calcium-binding protein A9, lipocalin 2, and small inducible cytokine B family member 10 was higher by >/=20-fold in the DEP + LPS group than in the vehicle group. These results were concomitant with those obtained by real-time reverse transcription-polymerase chain reaction analysis in the overall trend. Our findings suggest that intense, focused expression of genes such as S100 calcium-binding protein A9, lipocalin 2, and small inducible cytokine B family member 10 relates to the synergistic aggravation of acute lung injury by LPS and DEP rather than weak, broad expression of various genes by exposure of LPS alone.

Particulate air pollutants and asthma. A paradigm for the role of oxidative stress in PM-induced adverse health effects.

Asthma is a chronic inflammatory disease, which involves a variety of different mediators, including reactive oxygen species. There is growing awareness that particulate pollutants act as adjuvants during allergic sensitization and can also induce acute asthma exacerbations. In this communication we review the role of oxidative stress in asthma, with an emphasis on the pro-oxidative effects of diesel exhaust particles and their chemicals in the respiratory tract. We review the biology of oxidative stress, including protective and injurious effects that explain the impact of particulate matter-induced oxidative stress in asthma.

Adjuvant activity of various diesel exhaust and ambient particles in two allergic models.

In the framework of an EU study entitled "Respiratory Allergy and Inflammation Due to Ambient Particles" (RAIAP), various collected particulate matter samples were to be tested for their adjuvant potency in two animal models of allergy. A pollen allergy model in the Brown Norway (BN) rat and an ovalbumin model in the BALB/c mouse were used in this study to compare the discriminatory value of these two models and to evaluate them for later studies of collected RAIAP-samples. Two different sources of diesel exhaust particles (DEP I and DEP II ), a residual oil fly ash source (ROFA), and two sources of ambient particles (Ottawa dust, EHC-93, and road tunnel dust, RTD) were tested. Rats were sensitized intratracheally with Timothy grass pollen (Phleum pratense, 200 microl, 10 mg/ml) on d 0, challenged on d 21, and examined on d 25. Mice were sensitized intranasally at d 0 and 14, challenged intranasally at d 35, 38, and 41 (50 microl, 0.4 mg ovalbumin/ml), and examined at d 42. Particulate matter (PM) was administered either during the sensitization phase only or during the sensitization and challenge phases (for mice only) or during the challenge phase only. In the pollen model, only DEP I, but not DEP II, ROFA, EHC-93, and RTD, stimulated the immunoglobulin (Ig) E and IgG1 response in serum to pollen allergens. In addition to this adjuvant effect noted, no other biomarkers in lung or bronchoalveolar lavage (BAL) revealed adjuvant activity in the pollen model. In the BAL of BN rats exposed to a combination of pollen and PM, the percentages of eosinophilic granulocytes were decreased compared to the BAL of BN rats immunized with pollen only. In the ovalbumin model, the IgE levels in serum were increased in mice after coexposure to ovalbumin and PM (including DEPI, DEPII, ROFA, EHC-93, and RTD) in the sensitization phase but not after coexposure during the challenge phase only. The inflammatory response was greater in the lung, predominantly the influx of eosinophilic granulocytes, as was observed by both histopathological examination and BAL analysis. In addition, BAL levels of inflammatory interleukin (IL)-4 were increased. Based on the IgE antibody response to ovalbumin, the ovalbumin model ranked the adjuvant capacity of the particles in the following order: RTD > ROFA > EHC-93 > DEPI > DEPII. In conclusion, the ovalbumin model is a sensitive system to detect adjuvant activity of airborne particles, whereas the pollen-induced allergy model in rat was less sensitive.

Rosmarinic acid inhibits lung injury induced by diesel exhaust particles.

Epidemiological and experimental studies have suggested that diesel exhaust particles (DEP) may be involved in recent increases in lung diseases. DEP has been shown to generate reactive oxygen species. Intratracheal instillation of DEP induces lung inflammation and edema in mice. Rosmarinic acid is a naturally occurring polyphenol with antioxidative and anti-inflammatory activities. We investigated the effects of rosmarinic acid on lung injury induced by intratracheal administration of DEP (500 microg/body) in mice. Oral supplementation with administration of rosmarinic acid (2 mg/body for 3 d) inhibited DEP-induced lung injury, which was characterized by neutrophil sequestration and interstitial edema. DEP enhanced the lung expression of keratinocyte chemoattractant (KC), interleukin-1beta, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1alpha, which was inhibited by treatment with rosmarinic acid. DEP enhanced expression of iNOS mRNA and formation of nitrotyrosine and 8-OHdG in the lung, which was also inhibited by rosmarinic acid. These results suggest that rosmarinic acid inhibits DEP-induced lung injury by the reduction of proinflammatory molecule expression. Antioxidative activities of rosmarinic acid may also contribute to its protective effects.

Factors associated with elevated blood lead concentrations in children in Karachi, Pakistan.

OBJECTIVES: To confirm whether blood lead concentrations in Karachi were as high as reported in 1989 and to identify which types of exposure to lead contribute most to elevated blood lead concentrations in children in Karachi. METHODS: A total of 430 children aged 36-60 months were selected through a geographically stratified design from the city centre, two suburbs, a rural community and an island situated within the harbour at Karachi. Blood samples were collected from children and a pretested questionnaire was administered to assess the effect of various types of exposure. Cooked food, drinking-water and house dust samples were collected from households. FINDINGS: About 80% of children had blood lead concentrations 10 g/dl, with an overall mean of 15.6 g/dl. At the 5% level of significance, houses nearer to the main intersection in the city centre, application of surma to children's eyes, father's exposure to lead at workplace, parents' illiteracy and child's habit of hand- to-mouth activity were among variables associated with elevated lead concentrations in blood. CONCLUSION: These findings are of public health concern, as most children in Karachi are likely to suffer some degree of intellectual impairment as a result of environmental lead exposure. We believe that there is enough evidence of the continuing problem of lead in petrol to prompt the petroleum industry to take action. The evidence also shows the need for appropriate interventions in reducing the burden due to other factors associated with this toxic element.

Outdoor air pollution, climatic changes and allergic bronchial asthma.

Both the prevalence and severity of respiratory allergic diseases such as bronchial asthma have increased in recent years. Among the factors implicated in this "epidemic" are indoor and outdoor airborne pollutants. Urbanisation with its high levels of vehicle emissions and Westernised lifestyle parallels the increase in respiratory allergy in most industrialised countries, and people who live in urban areas tend to be more affected by the disease than those of rural areas. In atopic subjects, exposure to air pollution increases airway responsiveness to aeroallergens. Pollen is a good model with which to study the interrelationship between air pollution and respiratory allergic diseases. Biological aerosols carrying antigenic proteins, such as pollen grains or plant-derived paucimicronic components, can produce allergic symptoms. By adhering to the surface of these airborne allergenic agents, air pollutants could modify their antigenic properties. Several factors influence this interaction, i.e., type of air pollutant, plant species, nutrient balance, climatic factors, degree of airway sensitisation and hyperresponsiveness of exposed subjects. However, the airway mucosal damage and the impaired mucociliary clearance induced by air pollution may facilitate the penetration and the access of inhaled allergens to the cells of the immune system, and so promote airway sensitisation. As a consequence, an enhanced immunoglobulin E-mediated response to aeroallergens and enhanced airway inflammation favoured by air pollution could account for the increasing prevalence of allergic respiratory diseases in urban areas.

Effects of birch pollen and traffic particulate matter on Th2 cytokines, immunoglobulin E levels and bronchial hyper-responsiveness in mice.

BACKGROUND: Health effects due to air pollution arising from motor vehicles are a major public and political concern world-wide. Epidemiological studies have shown that the manifestations of asthma are increased by air pollution in already affected individuals. OBJECTIVE: To investigate the potential role of air-polluted tunnel dust (traffic particulate matter, TPM) or pure carbon core particles in the initiation and persistence of experimental allergic inflammation. METHODS: BP2 mice were immunized with birch pollen alone (group B) or pollen together with TPM (group A), or with birch pollen and Al(OH)3 (group C), or with birch pollen and carbon core particles (group D). Before methacholine challenge they were challenged intranasally and thereafter bronchial hyper-reactivity (BHR) was evaluated in a whole-body plethysmograph. Levels of Th2 cytokines, fibronectin and lactate dehydrogenase (LDH) were determined, and differential counts were performed in the bronchoalveolar lavage (BAL) fluid. Sera were collected for determination of antibody titres and cytokine levels. RESULTS: Specific IgE titres, BHR, the number of recruited eosinophils and levels of fibronectin and LDH in BAL were increased in mice immunized and challenged with a mixture of birch pollen and TPM. However, mice immunized with birch pollen alone and challenged intranasally with pollen or a mixture of pollen and TPM demonstrated the highest levels of IL-4 and IL-5. CONCLUSION: This study highlights the importance of the exposure to a combination of particulate matters and pollen allergens, in the induction of allergic disease in the airways, and we have demonstrated that polluted tunnel dust has an effect on both the inflammatory and immunological components of experimental allergy. Immunization and challenge with carbon core particles together with birch pollen increased neither the BHR nor the specific IgE production significantly. Our results therefore strongly suggest that it is most likely to be the organic phase bound to the carbon core of the diesel exhaust particles that might have an important adjuvant effect in the induction of experimental allergy.

Effects of the inhalation of diesel exhaust, Kanto loam dust, or diesel exhaust without particles on immune responses in mice exposed to Japanese cedar (Cryptomeria japonica) pollen.

To assess the potential enhancement by air-pollutants of immune responses in mice, especially with regard to allergen-specific immunoglobulin E (IgE) antibody production, female BDF(1) mice (60 mice in each group) were exposed to diesel exhaust (particles, 3.24 mg/m(3); nitrogen dioxide, 1.0 ppm: DE group), Kanto loam dust (particles, 3.29 mg/m(3); nitrogen dioxide, 0.01 ppm: KLD group), diesel exhaust without particles (particles, 0.01 mg/m(3); nitrogen dioxide, 1.1 ppm: DEG group), or clean air (pollen and control groups) for 16 h/day, 5 days/wk for 24 wk, as well as to Japanese cedar pollen (JCP) (around 550,000 grains of JCP/m(3)) for 2 days/wk in the same period. The control group was exposed to clean air alone throughout the experiment. The mean values for Japanese cedar pollen allergens (JCPAs)-specific immunoglobulin E (IgE) antibody titers in mice sera measured by enzyme-linked immunosorbent assay (ELISA) in the DE, KLD, and DEG groups were higher than that for the pollen alone group, but not significantly, after both 12 and 24 wk of exposure time. The percentages of animals expressing more than the minimum ELISA titer of JCPAs-specific IgE antibodies in each group were 22% (DE and pollen groups) and 27% (KLD and DEG groups) of the totals at wk 12, and no statistical differences were observed among the groups. However, at wk 24 in the DE, KLD, and DEG groups the responders comprised 73%, 63%, and 67%, respectively, significantly higher than the 33% for the pollen alone group. No significant differences were observed among the DE, KLD, and DEG groups. A slight dose-dependent increase of proliferative responses of mouse cervical lymph node cells to JCPAs in both DE and KLD groups was observed, but not in the DEG group. Remarkable decrease of interferon-gamma and significant increase of interleukin-4 in the nasal lavage fluid were apparent after DE or DEG exposure, but not in the KLD group. These results suggest that these air pollutants (DE, KLD, and DEG) enhance the production of IgE antibodies in mice, with similar adjuvant activities in each case. Furthermore, in the early phase of exposure in which sensitization occurred with exposure to pollen, the fine particles and gas components are considered to have exhibited different enhancing mechanisms in mice as follows: (1) The fine particles augmented production of IgE antibodies through activation of T lymphocytes, and (2) the gas components exhibited almost no action on T lymphocytes, but directly induced disorders of the cytokine network and augmented the production of IgE antibodies.

Localization, release and bioavailability of pollen allergens: the influence of environmental factors.

Allergens are integral constituents of plants or animals and their normal functions and localization are being characterized. To trigger responses in humans, allergens must become bioavailable and the role of air pollutants--for example diesel-exhaust particles --in this process is causing concern. Finally, the fact that some pollen releases eicosanoid-like proinflammatory mediators may have wide implications.

Secretion of proinflammatory eicosanoid-like substances precedes allergen release from pollen grains in the initiation of allergic sensitization.

It is commonly believed that allergic sensitization starts when an allergen contacts the surface of an antigen-presenting cell in mucosal or skin epithelia. Most studies dealing with this aspect use allergen extracts as stimulus. Under natural exposure conditions, however, the bioavailability of allergen depends on allergen liberation from internal binding sites within the allergen carrier, e.g. pollen grains. In comparing total protein and major allergen release from timothy grass (Phleum pratense L.) pollen freshly collected on rural meadows or near high-traffic roads, there was a striking difference between the pollen, with higher allergen release rates from rural meadow pollen grains. Thus, allergen release does not explain the higher prevalence rates of atopic sensitization and disease observed in many epidemiological studies in children exposed to automobile exhaust. Therefore, other possible effectors from pollen grains were investigated. Pollen grains incubated in protein- free buffer were found to secrete significant amounts of eicosanoid-like substances, namely leukotriene (LT) B(4)-like and prostaglandin E(2)-like substances, in a pH-, time- and temperature-dependent fashion. The highest values of eicosanoid secretion were found in birch, grass and mugwort pollen, while pine (Pinus sylvestris L.) pollen showed only marginal eicosanoid-like secretion. Additionally, the release of these substances was significantly higher from pollen which had been collected near roads with heavy traffic, indicating a stronger proinflammatory activity of these pollen grains. In order to investigate the effects of air pollutants, native pollen grains were exposed in a dose- and time-dependent fashion in a fluidized bed reactor to traffic-related pollutants, e.g. volatile organic compounds (toluene, m-xylene), leading again to a significant increase in the secretion of LTB(4)-like immunoreactivity, in contrast to exposure with sulfur dioxide. This finding opens a new dimension of understanding of the early events in allergic sensitization, indicating that proinflammatory effects of the allergen carrier, e.g. the pollen grain itself, can lead to activation of the mucosal membrane. These findings might help to also explain the higher prevalence rates of pollen allergy in areas with high automobile exhaust emissions. Furthermore, the allergenic 'potency' of various allergens has to be redefined at the allergen carrier level with regard to different stages of allergen and mediator release prior to the contact with the host's immune system.

Blood lead levels of a population group not occupationally exposed to lead in Singapore.

A survey was conducted between 1995 and 1997 to assess the impact of introduction of unleaded petrol and other public health measures on the blood lead level of the population. The geometric mean blood lead level of 269 government employees as determined by graphite furnace atomic absorption spectroscopy, was 66.0 microg/l, much lower than that recorded before introduction of lead-free petrol. Using multiple regression analysis, factors significantly associated with blood lead levels were: exposure to traffic, age (>50 years) and active smoking. Passive smoking, exposure to recent paint work, consumption of alcohol and traditional medicine were found not to be significantly associated with the blood lead level.

[Importance of air purifiers in the prevention of respiratory allergy]. / Intérêt des purificateurs d'air dans la prévention de l'allergie respiratoire.

Prevention of respiratory allergy and thus diminution of its prevalence consists of the application not only of preventative measures on the allergens themselves, but also on atmospheric pollutants such as NO, CO and diesel particles. These modify the allergens and increase synthesis of allergen-specific IgE. Use of air purifiers, on condition that they have HEPA or ULPA filters may contribute to reduction of allergenicity linked to pollutants and are one of the not-negligible means of protection from respiratory allergy and asthma in particular.