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Exposure to household air pollution (HAP) from cooking with solid fuels affects 2.8 billion people in developing countries, including children and pregnant women. The aim of this review is to propose intervention estimates for child survival outcomes linked to HAP.
Systematic reviews with meta-analysis were conducted for ages 0-59 months, for child pneumonia, adverse pregnancy outcomes, stunting and all-cause mortality. Evidence for each outcome was assessed against Bradford-Hill viewpoints, and GRADE used for certainty about intervention effect size for which all odds ratios (OR) are presented as protective effects.
Reviews found evidence linking HAP exposure with child ALRI, low birth weight (LBW), stillbirth, preterm birth, stunting and all-cause mortality. Most studies were observational and rated low/very low in GRADE despite strong causal evidence for some outcomes; only one randomised trial was eligible.Intervention effect (OR) estimates of 0.64 (95% CI: 0.55, 0.75) for ALRI, 0.71 (0.65, 0.79) for LBW and 0.66 (0.54, 0.81) for stillbirth are proposed, specific outcomes for which causal evidence was sufficient. Exposure-response evidence suggests this is a conservative estimate for ALRI risk reduction expected with sustained, low exposure. Statistically significant protective ORs were also found for stunting [OR=0.79 (0.70, 0.89)], and in one study of pre-term birth [OR=0.70 (0.54, 0.90)], indicating these outcomes would also likely be reduced. Five studies of all-cause mortality had an OR of 0.79 (0.70, 0.89), but heterogenity precludes a reliable estimate for mortality impact. Although interventions including clean fuels and improved solid fuel stoves are available and can deliver low exposure levels, significant challenges remain in achieving sustained use at scale among low-income households.
Reducing exposure to HAP could substantially reduce the risk of several child survival outcomes, including fatal pneumonia, and the proposed effects could be achieved by interventions delivering low exposures. Larger impacts are anticipated if WHO air quality guidelines are met. To achieve these benefits, clean fuels should be adopted where possible, and for other households the most effective solid fuel stoves promoted. To strengthen evidence, new studies with thorough exposure assessment are required, along with evaluation of the longer-term acceptance and impacts of interventions.
Household air pollution (HAP) from solid fuels (wood, dung, crop residues, charcoal and coal) used in simple stoves for cooking and heating, is recognized as a risk factor for several health outcomes with important consequences for child survival, including pneumonia [1] and low birth weight and stillbirth [2], in addition to a number of major non-communicable disease outcomes in adults [3,4].
Solid fuels were used by around 2.8 billion people in 2010 [5], a number which has changed little since 1980 due to global population increase, and is closely associated with poverty and high child mortality. Studies consistently show that exposure levels are very high, far exceeding WHO air quality guideline (AQG) levels for small particulate matter (PM2.5), and young children and women, including during pregnancy, are most at risk [6,7]. These factors imply that, if substantial intervention effects can be demonstrated, the removal of HAP exposure could bring large benefits for child survival.
Interventions for reducing HAP exposure include improved solid fuel stoves and clean fuels. Both present challenges for sustainable adoption at scale among the low income populations at risk [8]. For solid fuel stoves the key issues are achieving emissions low enough to deliver health benefits, as well as ensuring acceptability, sustained use, and affordability. Very low exposure would be assured if households used clean fuels such as LPG and electricity exclusively, but affordability and reliable supply remain key barriers. Recent initiatives to increase global access to clean household energy, including the UN Foundation Global Alliance for Clean Cookstoves [9], and the UN's Sustainable Energy for All [10], are now starting to address these issues in a coordinated way. More concerted action on and investment in technology development, stove standards [11], programme delivery, and evaluation can be expected over the next few years.
The objective of this review is to systematically review the evidence on HAP and child survival outcomes and to propose intervention impact estimates that would be suitable for the Lives Saved Tool [12]. While detailed assessment of intervention options, performance and policy for achieving sustained adoption is also important, these topics are beyond the scope of this review. These issues have been discussed elsewhere [8], and extensive review work is currently underway for new WHO Guidelines on household fuel combustion [13].
The scope of the review is as follows. For health outcomes, those listed by Walker et al [14] for children under 5 years and known or suspected to be linked to HAP were included, namely ALRI (pneumonia, including severe and fatal), low birth weight, pre-term birth, stillbirth, stunting, and all-cause mortality. Geographical coverage is global where the use of solid fuels for cooking has been studied. Although there is evidence that kerosene used in simple stoves and lamps is also highly polluting and a health risk for some of these outcomes [15], this was outside the scope of the review, except to note studies which included kerosene within the 'clean fuel' category.
Exposure assessment
A database of household energy, managed by WHO, draws information from nationally representative surveys including DHS, MICS, LSMS, World Health Survey, and national censuses on the primary fuel used for cooking. To date, data from some 586 surveys have been collated for 155 countries, spanning 1974 to 2010 [16,17]. Surveys obtain information on specific fuel types, but the main indicator used to assess exposure to household air pollution is use of solid fuel for cooking, and is available stratified by urban and rural settings within countries. It is recognized that this is a relatively crude measure of exposure, and one approach for improving this through modeling is considered further in the Discussion.
Reviews of health risks
We have previously published reviews for pneumonia [1] and adverse pregnancy outcomes (LBW, stillbirth and pre-term birth) [2]. The current report updates these published reviews using comparable methods, and includes new reviews conducted for stunting and all-cause mortality. The reviews cover the period from 1966 to July 2012. Search terms and databases used for all outcomes and study selection flowcharts are presented in Additional file 1; selection included around 10% independent checks of both selected and rejected titles and abstracts. Full duplicate data extraction and quality assessment using a modified Newcastle-Ottawa scale was conducted, with disagreements resolved by a third researcher. All study designs were eligible, but studies were excluded if outcome definitions were unclear (e.g. no differentiation between upper and lower respiratory infections). Analysis was carried out in RevMan (version 5.1), and pooling of studies used generic inverse variance weighting with fixed effects in the absence of statistical heterogeneity (I-squared < 10%), otherwise random effects meta-analysis was conducted. For outcomes with more than 4 studies, publication bias was assessed through statistical funnel plot asymmetry with Begg's and Eggar's tests using Stata Version 10 [18].
Additional file 1. Search terms and flow charts_HAP review_Bruce This file lists search terms and databases, and the flow charts to show numbers of studies selected and excluded at each stage.
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Assessment of the evidence for each of the outcomes using GRADE [19] was carried out by JD, DP, MD and NB in a 2-day workshop in July 2012. Recent debate on the application of GRADE in the assessment of studies of public health interventions suggests modifications may be needed for more appropriate rating of this evidence [20-22]. In this regard, it is useful to make a distinction between (i) the question of whether associations reported here are causal, for which Bradford-Hill viewpoints for distinguishing causation from association in environmental epidemiology (Figure 1) [23] are referred to, and (ii) the strength of evidence for the intervention effect size, for which GRADE has been used. While these assessments have much in common, it is quite possible to have strong evidence of causal associations between HAP exposure and one or more of the disease outcomes (and by implication that reducing exposure will reduce the risk of that disease), but rather weaker evidence as to the precise size of the effect of an intervention. As this debate on modifying GRADE for public health is ongoing, we have first referred to the Bradford-Hill viewpoints and then applied standard GRADE methodology, and consider the implications further in the Discussion.
Figure 1. Bradford-Hill viewpoints on assessing causation in environmental health
The majority of studies available are observational and report risks of high vs. low exposure, although in the context of this review we are interested in estimating the potential preventive impact of interventions. Only the single eligible RCT ('RESPIRE') has reported results in this way [24]. In order to achieve consistency across studies while avoiding potentially misleading changes to the existing published results, the Forest plots are presented as increased risk associated with higher exposure (as published by the incorporated studies), and for this purpose we have inverted the relative risks reported from our own work [24]. In the GRADE tables (Additional File 2) and reporting of these in the Results, all odds ratios are presented as preventive effects. Issues arising from estimating intervention effects from observational studies are considered further in the Discussion.
Additional File 2. GRADE Tabels_HAP review_Bruce This file shows the GRADE tables for all of the outcomes reviewed.
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A number of intervention studies are available, but most are restricted to measuring impacts on HAP and/or exposure, and do not include health outcomes. This information can, however, provide an indication of the expected health impacts as exposure-response evidence on key child survival outcomes becomes more available and robust. A systematic review of these studies, covering different types of solid fuel stoves and clean fuels, is being conducted for new WHO air quality guidelines [13] and will be reported separately. A selection of these studies showing the range of exposure reductions and post-intervention levels achieved are described in the current report, and related to the limited exposure-response evidence available on child ALRI. The trials that do report health outcomes are discussed in more detail.
In 2010, 41% of global households still relied primarily on solid fuels for cooking, a figure which has fallen from 62% in 1980, but because of population increases the actual number has remained steady at around 2.8 billion people [17]. Solid fuel use closely mirrors poverty and child mortality (Figure 2), and remains highly prevalent in South Asia and Africa, including more than 90% of homes in rural areas of many countries of Sub-Saharan Africa [5]. Regional trends show that, while the proportion of homes cooking with solid fuels has declined by around 25-35% in most regions since 1980, in Africa the decline has been only 10%, from 87% to 77% [17].
Figure 2. Households using solid fuels as the primary cooking fuel, by WHO region, 2010. Source: WHO Global Health Observatory: http://gamapserver.who.int/mapLibrary/Files/Maps/Global_iap_2010_total.png webcite
Child health outcomes
Child ALRI
A total of 26 eligible studies (28 estimates) were found for child ALRI, including all non-fatal ALRI (severity not defined), severe ALRI, and fatal ALRI outcomes (reported separately below). The pooled OR for all studies was 1.73 (95% CI=1.47, 2.03), and although there was evidence of publication bias (Egger's test p=0.046), this may be partly the result of larger effects for more severe and fatal outcomes being reported in smaller studies.
All non-fatal ALRI (severity not defined)
A total of 21 studies reported on non-fatal ALRI, without defining severity, including one RCT [24], 4 cross-sectional [25-28], 11 case-control [29-39] and 5 cohort studies [40-44], summarized by study design in Additional File 3, Table 1(a). The RCT by Hanna et al was not eligible as the outcome measures did not allow distinction of upper and lower respiratory infections [45]. The funnel plot suggests possible publication bias (Additional File 4, Figure 1), but Begg's (p=0.56) and Eggar's (p=0.091) tests were non-significant. There was significant heterogeneity (I2 = 61%, p<0.0001), and the pooled OR was 1.56 (1.33, 1.83), p<0.0001, Figure 3(a). Some duplication of cases in the RESPIRE trial occurs with the severe ALRI analysis below, but exclusion of this study results in a small increase in the effect estimate to 1.59 (1.34, 1.89). A concern with several studies in this review is inclusion of kerosene in the 'unexposed' group, which involves just the Indonesian DHS study for this outcome [25]: the pooled OR following exclusion of this study was 1.66 (1.41, 1.97) with I2 reduced to 52% (p=0.003). The GRADE assessment for the RCT was rated 'moderate' with a RR of 0·78 (0·59, 1·06), for which a statistically significant exposure-response relationship was also noted, while for the observational studies the rating was 'very low', with a protective OR of 0.63 (0.53, 0.75), Additional File 2, Table 1(a).
Additional File 3. Study summary tables_HAP review_Bruce This file provides summaries of all studies included in the review, listed by outcome.
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Additional File 4. Funnel plots__HAP review_Bruce This file illustrates the funnel plots for two outcomes (i) all pneumonia, and (ii) all-cause mortality.
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Figure 3. Forest plots All individual study results are presented as originally published (risk of outcomes for high exposure vs. low exposure) with the exception of the RESPIRE trial, for which relative risks have been inverted for consistency. Results in GRADE tables (Additional File 2) are all presented as protective effects. Figure 3(a): Forest plot for 20 studies of non-fatal ALRI, where severity is not defined Figure 3(b): Forest plot for 4 studies of severe ALRI Figure 3(c): Forest plot for 4 studies of fatal ALRI
Severe ALRI
Four studies, including one RCT [24] and three case-control studies [46-48] reported on severe ALRI, Additional File 3, Table 1(b). Heterogeneity was of borderline significance (I2=51%, p=0.10), and the pooled OR was 2.04 (1.33, 3.14) p=0.001, Figure 3(b). GRADE assessment for the RCT was 'high' with RR of 0·67 (0·45–0·98), again with significant exposure-response findings for this outcome, while the three observational studies were rated 'low' with a protective OR of 0.40 (0.25, 0.67), Additional File 2, Table 1(b).
Fatal ALRI
Four studies, including one RCT (9 events) [24], and three observational studies reported risk of fatal pneumonia [49-51], Additional File 3, Table 1(c). There was no evidence of statistical heterogeneity (I2=0), and the pooled OR was 2.80 (1.81, 4.34) p<0.0001, Figure 3(c). GRADE assessment rated the RCT as 'high' with a RR of 0.48 (0.12, 1.91) and the three observational studies as 'low', with a protective OR of 0.34 (0.22, 0.55), Additional File 2, Table 1(c).
Low birth weight
Seven studies, including one RCT (analyzed per protocol) [52] and six observational studies [53-58] reported on the risk of low birth weight (<2500 gm at term), Additional File 3, Table 2. Two studies provided separate, independent estimates for pre-term IUGR and term LBW [54,57]. There was no evidence of statistical heterogeneity (I2=0), nor of publication bias (Begg's p=0.348, Eggar's p=0.356). The pooled OR was 1.40 (1.26, 1.54) p<0.0001 for all births, Figure 4, and 1.36 [1.20, 1.54] for term births, while for pre-term the OR was slightly higher at 1.51 [1.25, 1.83]. Sensitivity analysis restricted to four studies carrying out adequate adjustment [52,56-58] had a larger effect for term LBW of 1.57 (1.33, 1.86). GRADE assessment rated the RCT as 'moderate' with a RR of 0.74 (0.33-1.66), while the observational studies were rated 'low' with a protective OR of 0.71 (0.64, 0.79), Additional File 4, Table 2.
Figure 4. Forest plot for 7 studies of low birth weight. Those marked (b) are separate estimates for pre-term IUGR
No new eligible studies of stillbirth were identified in the review update, Additional File 3, Table 3. The RCT by Hanna et al included stillbirth but was not eligible as this outcome was combined with infant mortality and miscarriage [45]. The Indonesian DHS-based study by Kashima et al was excluded as stillbirth was combined with miscarriage and abortion [25]. Among the four observational studies included there was no evidence of statistical heterogeneity (I2=0%), and the pooled OR was 1.51 (1.23, 1.85), Figure 5; GRADE assessment was 'low', with a protective OR of 0.66 (0.54, 0.81), Additional File 4, Table 3.
Figure 5. Forest plot for 4 studies of stillbirths
Pre-term birth
Only one study was identified with an estimate for pre-term birth [57]. This reported an OR of 1.43 (1.11, 1.84), Additional File 3, Table 4, and was rated 'low' in GRADE assessment, with a protective OR of 0.70 (0.54, 0.90), Additional File 4, Table 2.
Four studies reported on the risk of stunting, two for moderate stunting (-3 SD ≤ Z to -2 SD) [57,59], and two for severe stunting (Z < -3 SD) [59,60], Additional File 3, Table 5. One was based on an Indian cohort study [57], the others cross-sectional using DHS data for 7 countries [59], and India [60]; all studies provided adjusted estimates. For moderate stunting, there was no evidence of statistical heterogeneity (I2=0%), and the pooled OR was 1.27 (1.12, 1.43) p<0.0001, Figure 6(a). GRADE assessment was 'low' with a protective OR of 0.79 (0.70, 0.89), Additional File 2, Table 5. For severe stunting, there was evidence of significant heterogeneity (I2=83%, p=0.02), the pooled OR was 1.55 (1.04, 2.30), Figure 6(b), and GRADE assessment was rated 'very low' with a protective OR of 0.64 (0.43, 0.96), Additional File 2, Table 5. The study by Kyu et al combined DHS data from 7 countries with very different socio-economic conditions, including percentage use of solid fuels and children's nutritional status [59].
Figure 6. (a): Forest plot for 2 studies of moderate stunting Figure 6(b): Forest plot for 2 studies of severe stunting
All-cause mortality
Five studies provided estimates for all-cause mortality, two case control [61,62], two cross-sectional based on the DHS [25,63], and one cohort study [57], spanning several age groups, Additional File 3, Table 6. All five studies provide adjusted estimates. The RCT by Hanna et al assessed infant mortality, but has not been included for the reasons given in the Discussion [45]. There was significant heterogeneity across all studies (I2=72%, p<0.0001), in addition there was possible evidence of publication bias [(Begg's test p=0.466; Eggar's test p=0.081, Additional File 4, Figure 2. The pooled OR was 1.27 (1.07, 1.50) suggesting an overall significant impact on mortality (not shown); stratified analysis with all study estimates is shown in Figure 7. Two studies provided estimates for neonatal mortality, with an I2 =0% and a non-significant pooled OR of 1.14 (0.87, 1.48) [25,57], but both included kerosene in the 'unexposed' group. For the 1-12 month age group, three studies are included, although Tielsch et al focused on 0-6 months, and hence also covers the neonatal period. There was evidence of statistical heterogeneity (I2=54%, p=0.07), and the pooled OR of 1.08 (0.91, 1.28) was non-significant. All three studies included kerosene in the 'unexposed' group. Exclusion of the Tielsch et al estimate made little difference to the pooled estimate.
Figure 7. Forest plot for 5 studies of all-cause mortality, stratified by age group. Note: The estimate from Tielsch et al (2009) in the 1-12 month age group is for 0-6 months and includes the neonatal deaths: see text for further explanation.
The largest effect was seen in the 1-5 year age group, where there was significant statistical heterogeneity (I2=73%, p=0.01) with a significant pooled OR of 1.61 (1.21, 2.15). Only one of these studies included kerosene in the 'unexposed' group [62], while Wichmann et al included kerosene in the 'exposed' group [63].
GRADE assessment rated the evidence as 'very low', due to inconsistency and possible publication bias. The protective OR was 0.79 (0.67, 0.93), Additional File 2, Table 6. While assessment within age groups would be possible, this is unlikely to change the overall rating as significant heterogeneity was seen in the one age group with a significantly elevated risk (1-5 years).
Summary of effect estimates
Based on the findings of the review, consideration of the Bradford-Hill viewpoints, GRADE assessments and application of the Rules recommended by CHERG [14], the following effect estimates are proposed.
For ALRI, our earlier published review reported an OR of 1.78 (1.45, 2.18) [1], and the update has made little difference. The volume of evidence and reference to the Bradford-Hill viewpoints (including intervention impacts and exposure-response relationships), suggest a high level of confidence concerning causality. In a 2011 review, Po et al reported a much larger effect of 3.53 (1.94, 6.43) for child ARI but there were some important methodological differences [64]. Thus, Po et al grouped studies reporting ARI and ALRI, whereas we excluded studies not distinguishing upper and lower ARI and included others not cited by Po et al. We also did not include two studies cited by Po et al that reported surprisingly large estimates, the first as the unadjusted OR of 32.6 was stated as non-significant in adjusted analysis but not provided [65], while for the second study the OR for children of 7.98 (quoted by Po et al) used comparison with an 'unexposed' group of 'other members of the family' [66].
While the results of the RESPIRE trial are important, it would be inappropriate to base the effect estimate here on this single study. Furthermore, since the intervention group exposure remained high (relative to the WHO air quality guideline level), larger effects may be seen with community-wide use of clean fuels or low emission biomass stoves. Indeed, the exposure-response results from RESPIRE show that exposures below the intervention group mean were associated with considerably lower risk for all ALRI and severe ALRI [24]. These combined intention-to-treat and exposure-response findings from RESPIRE are consistent with the observational studies, both in terms of effect size and the greater effect on more severe outcomes.
These protective effect estimates for severe and fatal ALRI are relatively large, and require confirmation through further intervention studies before being considered as a basis for LiST. For the purpose of providing a realistic but conservative estimate given the current state of intervention-based evidence, it is proposed Rule 4 be used, taking the smallest of the pooled estimates, that for all non-fatal ALRI with severity not defined: 0.64 (0.55, 0.75). It is expected, however, that sustained, low exposure close to the WHO AQG level (annual mean PM2.5 of 10 µg/m3) would result in larger effects, especially for severe and fatal pneumonia. In this respect, it is noted that the recently published Global Burden of Disease 2010 comparative risk assessment used a larger relative risk for child ALRI than proposed here, but this was in the context of describing total population attributable risk with a counterfactual scenario of all homes using clean fuels and a mean PM2.5 exposure of less than 10 µg/m3 [4].
Adverse pregnancy outcomes
For low birth weight, the high degree of consistency across studies and the strong supportive evidence from other sources of combustion and animal studies [2] suggest a causal effect. Using Rule 6, with GRADE rating (moderate for the RCT and low for the observational studies), an intervention effect estimate of 0.71 (0.65, 0.79) is proposed. Evidence for stillbirth is less strong, but the consistency, supporting evidence from ambient air pollution and biological plausibility [2] are judged sufficient to support an intervention estimate using Rule 3 of 0.66 (0.54, 0.81). For pre-term birth, more studies are needed to strengthen causal inference, and we do not propose an intervention effect estimate at this time.
For stunting, two pooled estimates are available for both moderate and severe stunting, albeit data are drawn from seven countries in one study contributing to both outcomes [59], and further evidence is required to increase confidence about a causal effect. Accordingly, we do not propose an intervention effect estimate at this time.
All-cause mortality
The evidence on all-cause mortality suggests HAP exposure increases risk, with a significant pooled estimate across the whole under 5 year age group being 1.27 (1.07, 1.50). However, this is a heterogeneous set of studies, and a consistent effect across the different stages of the first 5 years of life, including the neonatal and post-neonatal periods, seems unlikely. Too few studies are available within each age group to provide risk estimates with any confidence. A causal effect on all-cause mortality is, however, highly likely given the strength of evidence on ALRI (including severe/fatal) as well as for adverse pregnancy outcomes, in particular low birth weight. We do not consider there is sufficient evidence to provide a reliable, direct intervention effect estimate for mortality at this time, and this should be a priority for future research.
Although much of the material in this review has been published previously, additional value derives from (i) updating of existing reviews by the same research group using comparable methods, (ii) stratification of ALRI by severe and fatal outcomes made possible by a number of new studies, (iii) adding stunting and all-cause mortality, (iv) bringing together all of the available child survival relevant outcomes in one review, and (v) the consistent application of GRADE to this evidence which hitherto, has not been attempted. The epidemiological evidence has a number of limitations, including study design bias (e.g. control selection), exposure misclassification, residual confounding, and variable outcome definitions, the implications of which we have discussed previously [1,2,6]. We found little evidence, however, of systematic over-estimation of effects in sensitivity analysis [1,2]. Almost all studies are observational, with only one eligible published RCT testing the impact of an effective intervention.
Strength of currently available evidence and GRADE assessments
One other recently reported trial from India used a stove with no impact on HAP due to technical limitations and low user valuation [45]. Although several outcomes potentially relevant to this review were included in that study, upper and lower ALRI could not be distinguished (therefore not meeting eligibility criteria) and still births were not presented separately from miscarriages and infant mortality, although infant mortality was reported separately. The reduction in exposure, measured using exhaled CO, was not reported for children under 5 years; that for all children was less than 10% (0.478 ppm), and non-significant. We have not incorporated any of the results from this trial in our review as we feel that the study does not add evidence regarding the impact of HAP reduction on child survival outcomes, and that this was equivalent to conducting an antibiotic or vaccine trial with an ineffective product. Prior to investigating health outcomes, the effectiveness of the candidate stove or cleaner fuel in delivering substantive exposure reductions in everyday use can and should be established, and over a period long enough to be confident that these effects will be sustained. The trial provides a valuable and timely warning of the importance of this, and that assumptions about so-called improved stoves must be tested prior to launching health studies and scaling-up adoption.
The predominance of observational designs means that effect estimates are based mainly on comparisons of rates in 'high' and 'low' exposure groups, rather than by directly measuring intervention impacts. Although some biases including poor control selection and residual confounding may overestimate effect sizes, inadequate exposure measurement will tend towards underestimation. In most studies, the lower-exposure group was often stated as using cleaner fuels such as LPG and electricity, but it is expected that these homes would have had exposures well above WHO AQG levels (annual mean PM2.5 of 10 µg/m3 [67]), for two reasons. First, many developing countries households that state their primary cooking fuel is clean (e.g. LPG) also use solid fuel for some cooking and maybe heating purposes, especially in rural areas [68]. Second, even where households use clean fuels (and perhaps exclusively), they are subject to pollution from neighbours using solid fuels, and in urban areas to annual average levels of ambient air pollution (from household combustion and other sources) that are known to exceed 50-100 µg/m3 PM10 in many developing country cities [69]. These suppositions are supported by studies reporting average concentrations in the range 50-150 µg/m3 (variously measuring PM10, PM4 and PM2.5) among LPG users [70-73]. High 'background' exposure in the 'clean fuels' groups will under-estimate risk, with effect estimates further biased towards the null by exposure misclassification. This latter point is emphasized by the substantial overlap of exposure distributions between control and intervention groups reported from the RESPIRE study [74].
It is recognised, therefore, that intervention effect estimates based on predominantly observational evidence may not be reliable, and that these are subject to a complex mix of bias. Related to this are the questions of (i) to what level exposure needs to be reduced in order to achieve the intervention impacts proposed here, and (ii) will any useful benefit accrue with lesser exposure reductions? For child ALRI, the RESPIRE exposure-response analysis suggests the function is relatively flat at high levels and the steep fall-off in risk only occurs at a level below that seen in the intervention (chimney stove) group [24]. Although derived from the trial this is effectively an (adjusted) observational analysis, but is consistent in shape with that reported earlier by Ezzati and Kammen [75]. Integration of ALRI risk data for PM2.5 arising from outdoor air pollution (OAP), second-hand smoke (SHS) and HAP (using RESPIRE results) has tended to confirm this conclusion; although details are yet to be published, this methodology was applied in the 2010 Global Burden of Disease (GBD) study comparative risk assessment [4].
In assessing the strength of evidence, we have drawn a distinction between confidence that associations are causal, and confidence about the size of the estimates proposed for intervention impacts. Based on the Bradford Hill viewpoints, we noted there was sufficient evidence for associations with ALRI, LBW and stillbirth being causal, while for others including pre-term birth and stunting further studies are needed for this purpose. GRADE assessments were mostly in the low and very low categories for all of these outcomes (and the single RCT could not be used alone), reflecting the lack of randomized trials and the way in which the current scoring system assesses observational evidence [20]. Furthermore, although observational evidence can be upgraded [21], this was only possible for severe and fatal pneumonia [see Additional File 2, Tables 1(b) and (c)]. Such generally low GRADE assessments imply that effect estimates are not established with confidence and that new evidence may well change these substantially. This may be correct, and for now justifies using the more conservative of the available results. On the other hand, exposure misclassification, the relatively high intervention group mean exposure in RESPIRE, and the emerging exposure-response evidence, suggest that larger impacts can be expected with sustained lower levels of exposure.
Improved population exposure assessment
The percentage SFU derived from the WHO database provides useful first line estimates of current levels of, and trends in, national and sub-national (e.g. urban/rural) exposure to HAP. Numerous HAP measurement studies, conducted across all WHO regions [76], have also provided unequivocal evidence of very high exposures in solid fuel using households, many times the recommended WHO AQG levels. However, few efforts have been undertaken to estimate population level exposures in quantitative terms.
Work carried out in India [Balakrishnan 2013, under review] and applied in the GBD 2010 comparative risk assessment [4] has been investigating the potential of using empirical HAP measurement studies to model population levels and variations of PM2.5 across India. Community studies in four states were used to collect data on area PM2.5, as well as on household level determinants such as, fuel and stove use, cooking location, etc., variables which are (or can be) collected in national surveys. A predictive model was then generated and applied to variables available from the Indian National Family and Health Survey (2005) to estimate HAP PM2.5 concentrations for each state. Future work will assess the potential for estimating personal exposures for women, children and other family members. While further validation is needed, this methodology offers the possibility of generating more nuanced estimates of HAP and exposure, and while the Indian model cannot be applied directly to other countries, the methodology can.
Prospects for interventions
We have indicated that, to deliver the estimated benefits reported here, interventions need to reduce HAP to low levels, probably with PM2.5 approaching WHO air quality guidelines although precision on this issue requires further study. Furthermore, these interventions need to be affordable and their use sustained. Addressing these questions in detail is beyond the scope of the current report; systematic reviews of both issues are underway for new WHO guidelines on household fuel combustion [13]. As noted in the Introduction, a range of interventions do exist, including both clean fuels and improved solid fuel stoves. For some socio-economically and geographically defined strata of solid fuel users, well-targeted policy could facilitate a relatively rapid transition to clean fuels such as LPG, though in practice this may be partial use for many with the aim of a more complete substitution over time. For others, however, solid fuels will continue to be relied upon and a key research and policy objective is to determine which solid fuel stove technologies can meet household needs and deliver all or most of the available health benefits.
Studies reporting the impacts of 'improved' solid-fuel stoves on HAP (including a mix of cross-sectional, before and after, quasi-experimental and randomized designs) have assessed a range of technologies and shown that many can substantially reduce PM2.5 concentrations in absolute terms, but post-intervention levels remain well above WHO AQG values in the range 100-300 µg/m3; see for example Dutta [77], Brandt [78], Chengappa [79] and Chowdhury [80]. Some chimney stoves have been reported to achieve kitchen PM2.5 levels close to the WHO annual IT-1 value of 35 µg/m3, for example Terrado [81], but these are the minority. Unfortunately, very few studies of advanced combustion solid fuel stoves (using forced ventilation) in everyday use are available. In summary, among solid-fuel stoves, those with chimneys have resulted in the lowest levels of HAP, but most seem unlikely to deliver very substantial reductions in risk of child ALRI until levels closer to the AQG are reached [24]. The point estimate of a 33% (95% CI: 2-55%) reduction in severe pneumonia from intention-to-treat analysis of the chimney (intervention) stove vs. open fire (control) in the RESPIRE trial is encouraging, but the confidence interval is wide and this requires confirmation [24]. In the absence of exposure-response evidence for other child survival outcomes, it probably should be conservatively assumed that the pneumonia scenario also applies to adverse pregnancy outcomes, child growth and mortality.
To fill these gaps, research is urgently required on the performance and acceptability of more advanced stove designs (with and without chimneys), the role modern fuels can play in advancing access to clean household energy, and on the impacts of these interventions on child health outcomes with studies that incorporate thorough exposure assessment.
Substantial evidence now exists that HAP increases the risk of a range of outcomes that are important for child survival. The predominance of observational evidence means that effect estimates may not yet be well estimated, but assessment of the various sources of bias suggests that these are unlikely to be exaggerated. Risk reductions of between 29% and 36% for the three outcomes (ALRI, LBW and stillbirth) with the strongest causal evidence are proposed. Interventions that deliver large reductions in HAP with PM2.5 close to WHO AQG levels can be expected to achieve these risk reductions, and quite possibly more, including for severe and fatal pneumonia. Where affordable, clean fuels provide the most certain means of achieving these benefits, but policy needs to actively support this transition. Improved solid fuel stoves may provide some intermediate or even large benefits, but substantial investments are needed in technology and measures to support adoption, and must be accompanied by robust evaluation of longer-term performance, acceptance and health impacts.
List of abbreviations used
ALRI: acute lower respiratory infection; AQG: air quality guideline; CHERG: Child Health Epidemiology Reference Group; GRADE: Grading of Recommendations, Assessment, Development and Evaluations; HAP: Household air pollution; LBW: low birth weight (less than 2,500 gm); OR: odds ratio; PM2.5: particulate matter with aerodynamic diameter of less than or equal to 2.5 microns; RCT: randomised control trial; WHO: World Health Organisation.
Competing interests
The authors declare they have no competing interests.
Funding for MD, conduct of the evidence review workshop including travel for JD and publication costs are from a grant from the Bill and Melinda Gates Foundation to the US Fund for UNICEF (Grant 43386 to "Promote evidence-based decision making in designing maternal, neonatal and child health interventions in low- and middle-income countries".
Authors' contributions
NB: planning and management of review work, drafting of manuscript.
MD: conduct of searches, data extraction and quality assessment.
JD: conduct of searches, data extraction and quality assessment.
HA-R: Global data on exposure assessment and contributions to systematic reviews.
KB: Methods and data for Indian exposure assessment modeling and contributions to systematic reviews.
ZB: planning and management of review and contributions to systematic reviews.
DP: systematic review, quality assessment and meta-analyses.
All authors read and approved the final manuscript.
We acknowledge the valuable contribution of Hamza Ansari and Anjali Tripathy, Aga Khan University, Karachi, who assisted JD with selection, extraction and quality assessment of studies.
The publication costs for this supplement were funded by a grant from the Bill & Melinda Gates Foundation to the US Fund for UNICEF (grant 43386 to "Promote evidence-based decision making in designing maternal, neonatal, and child health interventions in low- and middle-income countries"). The Supplement Editor is the principal investigator and lead in the development of the Lives Saved Tool (LiST), supported by grant 43386. He declares that he has no competing interests.
This article has been published as part of BMC Public Health Volume 13 Supplement 3, 2013: The Lives Saved Tool in 2013: new capabilities and applications. The full contents of the supplement are available online at http://www.biomedcentral.com/bmcpublichealth/supplements/13/S3.
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text:
Finally, when heading over to San Francisco one day, I found the Manta in the parking lot of the Alameda ferry terminal. Normally I don't like parking-lot shots for DOTS, but I'd had enough frustration trying to catch this Manta.
But then Akier took the initiative, tracking down the car's owner and convincing him to bring the car out to the former Alameda Naval Air Station for a photo session. I'm going to put my photos and the much more picturesque Akier shots in separate galleries. Hooray for our first DOTS Opel!
Here's what Akier has to say about this car: I first spotted this Manta near Mosswood Park in Oakland. I was driving by and did a cartoon double-take. Is that really an Opel ... ? After capturing the Opel Blitz firetruck a few weeks back, I suppose the ghost of Adam Opel must guide my hand. Evan rescued this from his friend's mom, who had bought it new and put only around 70,000 miles on it. It looked a little rough, and Evan's put some work into it to get it back up to a reasonable state of repair. A nice respray, yellow-coated inner headlights, a Weber instead of the fussy SU carb, and a lot of elbow grease and the old girl looks pretty nice. No tin worm, and despite admittedly needing a tune-up, the 1.9 growled nicely as we took a spin 'round Alameda Point. Designed to fight the Ford Capri and Vega Cosworth, the Manta shares much (i.e., all) of its running gear with its stablemates, the GT and 1900. There is the umbiquitous all-iron 4, with the semi-OHC setup - cams horizontal to the valves up in the heads, rather than on top of the valves - to make the engine surprisingly compact. Front discs and a well-designed live rear axle located by Panhard rods mean this light (<2200lbs) car handled pretty well back in the day. In Euro trim, the Manta made 90bhp, but the US versions made 75. With the Weber upgrade and a tune, Evan's is probably splitting the difference. Fittingly, this Manta lives in Alameda full-time, with a Corvair and a Valiant.

subset: commoncrawl


text: Grimturtle - Unregistered August 17, 2008 9:30 AM More electronics means different skills. Everyone is always pushing the limits regardless, which is where those with the best bike control and racing savvy rise to the top. That's why these guys are in motogp, because they can get on ANY bike and ride it fast.


text:
Academic Appointments
Emeritus Faculty, Acad Council, Biology
Professor Emeritus, Biology
We purified from pea (Pisum sativum) tissue an approximately 40 kDa reversibly glycosylated polypeptide (RGP1) that can be glycosylated by UDP-Glc, UDP-Xyl, or UDP-Gal, and isolated a cDNA encoding it, apparently derived from a single-copy gene (Rgp1). Its predicted translation product has 364 aminoacyl residues and molecular mass of 41.5 kDa. RGP1 appears to be a membrane-peripheral protein. Immunogold labeling localizes it specifically to trans-Golgi dictyosomal cisternae. Along with other evidence, this suggests that RGP1 is involved in synthesis of xyloglucan and possibly other hemicelluloses. Corn (Zea mays) contains a biochemically similar and structurally homologous RGP1, which has been thought (it now seems mistakenly) to function in starch synthesis. The expressed sequence database also reveals close homologs of pea Rgp1 in Arabidopsis and rice (Oryza sativa). Rice possesses, in addition, a distinct but homologous sequence (Rgp2). RGP1 provides a polypeptide marker for Golgi membranes that should be useful in plant membrane studies.
View details for Web of Science ID A1997XJ87600100
View details for PubMedID 9207152
From pea plasma membranes isolated by aqueous polymer two-phase partitioning we have purified 1,3-beta-D-glucan synthase [glucan synthase-II (GS-II) or callose synthase], an enzyme that several reports have suggested consists of between six and nine different subunits. The procedure involves (a) preliminary removal of peripheral proteins by 0.1% digitonin; (b) solubilization of GS-II with 0.5% digitonin; (c) precipitation of activity-irrelevant proteins from the digitonin extract by Ca2+, spermine and cellobiose, which are GS-II effectors needed in step (d); (d) product entrapment by formation of 1,3-beta-D-glucan from UDP-Glc by GS-II in the presence of the mentioned effectors, followed by centrifugal sedimentation of product micelles and elution of proteins therefrom with buffer; (e) preparative isoelectric focusing (IEF) of product-entrapped proteins; and (f) glycerol gradient centrifugation of the fractions of peak GS-II activity from IEF. The procedure yields 300-fold enrichment of GS-II specific activity over that in isolated plasma membranes, and 5500-fold over that in the original homogenate. Out of approximately six principal polypeptides that occur after the product entrapment step, the glycerol gradient GS-II activity peak contains only two major polypeptides, one of 55 kDa and another of 70 kDa, plus minor amounts of one or two others whose distribution and occurrence indicate are not responsible for GS-II activity. Antisera against either the 55-kDa or the 70-kDa polypeptide adsorb more than 60% of the GS-II activity from a product-entrapped preparation. After native gel electrophoresis, GS-II activity is associated with a single protein band of very large molecular mass, whose principal components are the 55-kDa and 70-kDa polypeptides, accompanied by minor amounts of a few other polypeptides most of which do not occur in enzyme preparations purified by the previously described procedure. The 55-kDa but not the 70-kDa component can be labeled by ultraviolet irradiation of the plasma membranes in the presence of [alpha-32P]UDP-Glc under GS-II assay conditions. It seems likely, therefore, that the 55-kDa and 70-kDa polypeptides form a large catalytic complex of which the 55-kDa component is the UDP-Glc-binding subunit.
View details for Web of Science ID A1994NB53000033
View details for PubMedID 8143748
Relative molecular size distributions of pectic and hemicellulosic polysaccharides of pea (Pisum sativum cv Alaska) third internode primary walls were determined by gel filtration chromatography. Pectic polyuronides have a peak molecular mass of about 1100 kilodaltons, relative to dextran standards. This peak may be partly an aggregate of smaller molecular units, because demonstrable aggregation occurred when samples were concentrated by evaporation. About 86% of the neutral sugars (mostly arabinose and galactose) in the pectin cofractionate with polyuronide in gel filtration chromatography and diethylaminoethyl-cellulose chromatography and appear to be attached covalently to polyuronide chains, probably as constituents of rhamnogalacturonans. However, at least 60% of the wall's arabinan/galactan is not linked covalently to the bulk of its rhamnogalacturonan, either glycosidically or by ester links, but occurs in the hemicellulose fraction, accompanied by negligible uronic acid, and has a peak molecular mass of about 1000 kilodaltons. Xyloglucan, the other principal hemicellulosic polymer, has a peak molecular mass of about 30 kilodaltons (with a secondary, usually minor, peak of approximately 300 kilodaltons) and is mostly not linked glycosidically either to pectic polyuronides or to arabinogalactan. The relatively narrow molecular mass distributions of these polymers suggest mechanisms of co- or postsynthetic control of hemicellulose chain length by the cell. Although the macromolecular features of the mentioned polymers individually agree generally with those shown in the widely disseminated sycamore cell primary wall model, the matrix polymers seem to be associated mostly noncovalently rather than in the covalently interlinked meshwork postulated by that model. Xyloglucan and arabinan/galactan may form tightly and more loosely bound layers, respectively, around the cellulose microfibrils, the outer layer interacting with pectic rhamnogalacturonans that occupy interstices between the hemicellulose-coated microfibrils.
View details for Web of Science ID A1992HC42800051
View details for PubMedID 16668637
Effects of indoleacetic acid (IAA) and of turgor changes on the apparent molecular mass (M(r)) distributions of cell wall matrix polysaccharides from etiolated pea (Pisum sativum L.) epicotyl segments were determined by gel filtration chromatography. IAA causes a two- to threefold decline in the peak M(r) of xyloglucan, relative to minus-auxin controls, to occur within 0.5 hour. IAA causes an even larger decrease in the peak M(r) concurrently biosynthesized xyloglucan, as determined by [(3)H]fucose labeling, but this effect begins only after 1 hour. In contrast, IAA does not appreciably affect the M(r) distributions of pectic polyuronides or hemicellulosic arabinose/galactose polysaccharides within 1.5 hours. However, after epicotyl segments are cut, their peak polyuronide M(r) increases and later decreases, possibly as part of a wound response. Xyloglucan also undergoes IAA-independent changes in its M(r) distribution after cutting segments. In addition, the peak M(r) of newly deposited xyloglucan increases from about 9 kilodaltons shortly after deposition to about 30 kilodaltons within 0.5 hour. This may represent a process of integration into the cell wall. A step increase in turgor causes the peak M(r) of previously deposited xyloglucan (but not of the other major polymers) to increase about 10-fold within 0.5 hour, returning to its initial value by 1.5 hours. This upshift may comprise a feedback mechanism that decreases wall extensibility when the rate of wall extension suddenly increases. IAA-induced reduction of xyloglucan M(r) might cause wall loosening that leads to cell enlargement, as has been suggested previously, but the lack of a simple relation between xyloglucan M(r) and elongation rate indicates that loosening must also involve other wall factors, one of which might be the deposition of new xyloglucan of much smaller size. Although the M(r) shifts in polyuronides may represent changes in noncovalent association, and for xyloglucan this cannot be completely excluded, xyloglucan seems to participate in a dynamic process that can both decrease and increase its chain length, possible mechanisms for which are suggested.
View details for Web of Science ID A1992HC42800052
View details for PubMedID 16668638
In pea membranes, UDP[14C]Glc glycosylates a approximately 40-kDa polypeptide doublet. This label rapidly disappears if excess unlabeled UDP-Glc, or UDP, is added, indicating that the glycosylation is reversible, and suggesting that the glycosylated polypeptides might be intermediates in a glycosyl transfer reaction. Glycosylation of the doublet requires a divalent cation, the effective ions being the same (except for Zn2+) as those that activate Golgi-localized beta-glucan synthase (GS-I) activity. Treatments that inhibit GS-I also inhibit doublet glycosylation. The doublet is associated with Golgi (and to a minor extent with plasma) membranes and occurs also in the soluble fraction. The Golgi-bound doublet may be a component of the GS-I system. Immunological, inactivation, and fractionation evidence indicates that at least one other polypeptide is required in GS-I activity.
View details for Web of Science ID A1991GP80400098
View details for PubMedID 1834664
Detergent-solubilized plasma membrane proteins from pea (Pisum sativum L.) stem tissue were separated by isoelectric focusing (IEF) using a Bio-Rad Rotofor cell, with the goal of identifying protein(s) involved in beta-1,3-glucan synthase (GS-II) activity. Ordinary IEF procedures result in membrane protein precipitation. Inclusion of 10% glycerol mitigates this problem in digitonin-solubilized preparations, but not in those solubilized in 3-[(-cholamidopropyl)dimethylammonio]-1-propanesulfonate. Loss of GS-II activity during IEF is minimized by improved cooling of the Rotofor cell. GS-II focuses at pH 5.1. Antiserum against a 55 kilodalton (kD) polypeptide that was recognized from other evidence as involved in GS-II activity, detects this polypeptide in exact correspondence with the GS-II activity peak. A presumptive P-type ATPase, detected using an antibody against corn root plasma membrane 97 kD ATPase, focuses at pH 5.3. In this digitonin/glycerol medium, most of the membrane proteins focus within the relatively narrow pH range of 4.5 to 6, compared to pH 5.5 to 8.5 for IEF in the presence of 9 molar urea, 2% Nonidet P-40 (NP-40), and 5% mercaptoethanol, a medium that inactivates GS-II. This latter medium increases the apparent isoelectric point (pl) values of the abovementioned 55 and 97 kD polypeptides to 5.8 and 7.3, respectively. In the digitonin/glycerol medium, membrane polypeptides apparently focus at pH values lower than their true pls, because of adhering negatively charged phospholipids, which can be at least partially removed by the detergent NP-40 in the presence of urea. These results provide independent evidence that the 55 kD polypeptide is associated with the GS-II activity and indicate that inclusion of urea and a strong nonionic detergent such as NP-40 is necessary if membrane proteins are to be focused at pH values near their true pls.
View details for Web of Science ID A1991FJ06700052
View details for PubMedID 16668130
By glycerol gradient centrifugation of a detergent-solubilized plasma membrane fraction from pea tissue, we find a polypeptide of 55 kDa that copurifies with beta-1,3-glucan synthase activity. An antiserum against this polypeptide adsorbs glucan synthase activity and the 55 kDa polypeptide from digitonin-solubilized plasma membrane. These results indicate that the 55 kDa polypeptide is involved in pea beta-1,3-glucan synthase activity.
View details for Web of Science ID A1991EX38500036
View details for PubMedID 1825066
The epidermis has been considered the site of auxin action on elongation of stems and coleoptiles. To try to identify mRNAs that might mediate auxin stimulation of cell enlargement, we compared, using in vitro translation assays, mRNA enhancement by indoleacetic acid (IAA) in the epidermis, with that in the internal tissues, of pea (Pisum sativum L., cv Alaska) third internode segments. We used seedlings that had been grown under red light, which enables the epidermis to be peeled efficiently from the internode. Most of the ;early' IAA enhancements previously reported using etiolated peas, plus several hitherto undescribed enhancements, occur in both the epidermis and the internal tissue of the light-grown plants after 4 hours of IAA treatment. These enhancements, therefore, do not fulfill the expectation of elongation-specific mRNAs localized to the epidermis. One epidermis-specific IAA enhancement does occur, but begins only subsequent to 1 hour (but before 4 hours) of auxin treatment. Similarly, the previously mentioned IAA enhancements common to epidermis and internal tissue do not begin, in the light-grown plants, within 1 hour of IAA treatment. Since IAA stimulates elongation in light-grown internodes within 15 minutes, it appears that none of these mRNAs can be responsible for auxin induction of elongation. We confirmed, with our methods, the previous reports that some of these mRNAs are enhanced by IAA within 0.5 hour in etiolated internodes. This indicates that we could have detected an early enhancement in light-grown tissue had it occurred.
View details for Web of Science ID A1990DK14100012
View details for PubMedID 16667484
Irradiation of etiolated pea (Pisum sativum L.) seedlings with white light affects two proteins, both of monomer molecular mass near 120 kDa. Both proteins have been detected in association with plasma membrane fractions. The first is identifiable in that it becomes heavily phosphorylated when the membranes are incubated with exogenous ATP. The second of these proteins is phytochrome, as determined by electrophoretic transfer (Western) blot analysis. Measurable phosphorylation and phytochrome (the latter detected by antigenicity) decline when the tissue is irradiated with white light prior to membrane isolation and in vitro phosphorylation. The phosphorylated protein is probably not phytochrome for three reasons. (i) It shows a slightly different distribution in sucrose gradients. (ii) Red light causes a gradual decline in the phytochrome that is associated with membrane fractions but has a negligible effect on the phosphorylatable protein; blue light, on the other hand, causes significantly slower loss of phytochrome than does red light but brings about a rapid decline in the phosphorylation signal. (iii) The molecular masses are not identical. The association of both proteins with membrane fractions is probably neither ionic nor, at least for the phosphorylatable protein, the consequence of entrapment of soluble proteins in vesicles formed during tissue extraction. Phytochrome is lost from the membrane fractions during irradiation, as judged by loss of antigenicity. Whether the phosphorylatable protein is lost, a specific kinase is lost, phosphatase activity increases, or phosphorylatable sites are blocked as a consequence of blue light treatment is not known.
View details for Web of Science ID A1988Q834100037
View details for PubMedID 16593988
Using (31)P nuclear magnetic resonance spectroscopy, we followed cytoplasmic and vacuolar pH in pea (Pisum sativum cv Alaska) internode segments during treatment with indoleacetic acid (IAA) or fusicoccin (FC) in continuously perfused, oxygenated buffer. Although IAA and FC induced normal H(+) extrusion, elongation, and glucan synthase activity responses during the measurements, neither the cytoplasmic nor the vacuolar pH showed significant change at any time between 5 minutes and 1 to 3 hours of treatment. Changes in cytoplasmic pH as small as about 0.04 pH unit were detected after treatment with 1-naphthyl acetate. Therefore, cytoplasmic pH changes do not appear to mediate IAA or FC stimulation of H(+) extrusion or other metabolic responses to these effectors.
View details for Web of Science ID A1988N466800041
View details for PubMedID 16666105
In pea stem segments whose cuticle has been made permeable by abrading it, actinomycin D (ActD) and 80S ribosomal protein synthesis inhibitors such as cycloheximide (CHI) inhibit enhancement by indole 3-acetic acid (IAA) of the activity of the cell wall biosynthetic enzyme, glucan synthase I (GS). This supersedes earlier, negative results with inhibitors, obtained with segments having an intact cuticle, which prevents adequate inhibitor uptake. Since these inhibitors also block IAA-stimulated H(+) extrusion, which according to earlier results is involved in the GS response, the significance of these inhibitions would be ambiguous without additional evidence. ActD does not inhibit fusicoccin (FC) enhancement of GS activity, which indicates existence of a post-transcriptional control mechanism for GS, but does not preclude involvement of transcription in the GS response to IAA. Although protein synthesis inhibitors such as CHI do not block FC-stimulated H(+) extrusion, they do inhibit FC enhancement of GS activity, indicating an involvement of protein synthesis in the GS response to FC, and presumably also to IAA. However, protein synthesis inhibitors (but not ActD) by themselves paradoxically elevate GS activity, less strongly than IAA does but resembling the IAA enhancement in several characteristics. These results suggest that IAA may enhance GS activity at least in part by inhibiting the synthesis or action of a labile repressor of the transcription of, or a labile destabilizer of, mRNA for GS or some polypeptide that enhances GS activity. However, resemblances between the IAA and FC effects on GS suggest that IAA also has a posttranscriptional GS-enhancing action like that of FC. Lipid biosynthesis may be involved in this aspect of the response since both IAA and FC enhancements of GS activity are inhibited by cerulenin.
View details for Web of Science ID A1987K590400038
View details for PubMedID 16665730
Fusicoccin (FC), like indoleacetic acid (IAA), causes Golgi-localized beta-1,4-glucan synthase (GS) activity to increase when applied to pea third internode segments whose GS activity has declined after isolation from the plant. This suggests that GS activity is modulated by H(+) extrusion; in agreement, vanadate and nigericin inhibit the GS response. The GS response is not due to acidification of the cell wall. Treatment of tissue with heavy water, which in effect raises intracellular pH, mimics the IAA/FC GS response. However, various treatments that tend to raise cytoplasmic pH directly, other than IAA- or FC-induced H(+) extrusion, failed to increase GS activity, suggesting that cytoplasmic pH is not the link between H(+) extrusion and increased GS activity. Although FC stimulates H(+) extrusion more strongly than IAA does, FC enhances GS activity at most only as much as, and often somewhat less than, IAA does. This and other observations indicate that GS enhancement is probably not due to membrane hyperpolarization, stimulated sugar uptake, or changes in ATP level, but leave open the possibility that GS is controlled by H(+) transport-driven changes in intracellular concentrations of ions other than H(+).
View details for Web of Science ID A1985AMN9000007
View details for PubMedID 16664267
(31)P-Nuclear magnetic resonance spectra of perfused maize (Zea mays L., hybrid WW x Br 38) root tips, obtained at 10-minute intervals over 12 hours or longer, indicate that no cytoplasmic or vacuolar pH changes occur in these cells in the presence of 25 millimolar K(2)SO(4), which induces extrusion of 4 to 5 microequivalents H(+) per gram per hour. In contrast, hypoxia causes cytoplasmic acidification (0.3-0.6 pH unit) without a detectable change in vacuolar pH. The cytoplasm quickly returns to its original pH on reoxygenation. Dilute NH(4)OH increases the vacuolar pH more than it does the cytoplasmic pH; after NH(4)OH is removed, the vacuole recovers its original pH more slowly than does the cytoplasm. The results indicate that regulation of cytoplasmic pH and that of vacuolar pH in plant cells are separate processes.
View details for Web of Science ID A1982NV81600020
View details for PubMedID 16662399
Polyadenylylated mRNA from etiolated pea stem segments treated with or without 20 muM indoleacetic acid (IAA) for various periods of time was assayed by translating it in a wheat germ extract containing [(35)S]methionine and separating the translation products by two-dimensional gel electrophoresis. Within 2 hr IAA causes at least five mRNA sequences to increase in translational activity, relative to initial levels and to simultaneous controls; three of these rise significantly within 20 min after exposure of tissue to IAA but are apparently not elevated at 10 min, whereas the others begin to increase at successive times later than 30 min, and still others begin to change only later than 2 hr. These observations indicate an early, highly selective IAA regulation of mRNA amounts or activities, becoming progressively more extensive with time. The earliest detected enhancement seems close to the primary action of IAA but appears not to be rapid enough to be responsible for auxin induction of cell enlargement.
View details for Web of Science ID A1982MZ45200045
View details for PubMedID 16593146
When 3- to 4-day-old dark-grown maize (Zea mays L. WF9 x Bear 38) seedlings are given red light, auxin-binding activity localized on endoplasmic reticulum membranes of the mesocotyl begins to decrease after 4 hours; by 9 hours, it falls to 50 to 60% of that in dark controls, on either a fresh weight or total particulate protein basis. Endoplasmic reticulum-localized NADH:cytochrome c reductase activity decreases in parallel. Loss of binding is due to decrease in number of sites, with no change in their affinity for auxin (K(d) 0.2 micromolar for naphthalene-1-acetic acid). Elongation of mesocotyl segments in response to auxin decreases with a similar time course. Elongation of segments from irradiated plants shows the same apparent affinity for auxin as that of the dark controls. Auxin-binding activity and elongation response also decrease in parallel down the length of the mesocotyl. These observations are consistent with a role of endoplasmic reticulum-localized auxin binding sites as receptors for auxin action in cell elongation.
View details for Web of Science ID A1981MV20300024
View details for PubMedID 16662103
In an effort to detect a pH-dependent release of polymers such as xyloglucans, thought to be involved in auxin-induced cell wall expansion during growth, radioactively labeled cell walls from pea stem tissue were incubated at different pH values, and changes in water-soluble, ethanol- or trichloroacetic acid-insoluble components were determined. This revealed the occurrence, at neutral pH, of a time- and pH-dependent binding of soluble pectin, in the walls, to a heat-labile, presumably protein, wall component, yielding a trichloroacetic acid-insoluble pectin-protein complex. This reaction, which can also be observed between polymers in water extracts of cell walls, is inhibited at low pH and by Ca(2+), and appears to be of a physical, possibly lectin-like, nature. Progressive binding of pectin or of the pectin-protein complex to the insoluble wall structure is also observed. These reactions may be involved in wall assembly during its deposition, and may participate in, or be analogous to pH-dependent physical interactions that participate in, wall extension during cell growth.
View details for Web of Science ID A1981LY62800032
View details for PubMedID 16661862
When radioactive UDP-glucose is supplied to 1-millimeter-thick slices of pea (Pisum sativum) stem tissue, radioactive glucose becomes incorporated into membrane-bound polysaccharides. Evidence is given that this incorporation does not result from breakdown of UDP-glucose and utilization of the resultant free glucose, and that the incorporation most likely takes place at the cell surface, leading to a specific labeling of the plasma membrane. The properties of the plasma membrane that are indicated by this method of recognition, including the association of K(+)-stimulated ATPase activity with the plasma membrane, resemble properties inferred using other approaches. The membrane-associated polysaccharide product formed from UDP-glucose is largely 1,3-linked glucan, presumably callose, and does not behave as a precursor of cell wall polymers. No substantial amount of cellulose is formed from UDP-glucose in this procedure, even though these cells incorporate free glucose rapidly into cellulose. This synthetase system that uses external UDP-glucose may serve for formation of wound callose.
View details for Web of Science ID A1978EZ63500004
View details for PubMedID 16660373
Golgi dictyosomal membranes isolated from pea (Pisum sativum) stem tissue, using a combination of rate zonal and isopycnic sucrose density centrifugation, were shown to bear cytidine diphosphate-choline:diglyceride phosphorylcholinetransferase, CDP-ethanolamine:diglyceride phosphorylethanolaminetransferase, and CTP:phosphorylcholine cytidyltransferase activities. Although the majority of the activity of the phospholipid-synthesizing enzymes was associated with the endoplasmic reticulum, the activity found in the Golgi system was about 25% of the total activity. These results suggest that Golgi dictyosomes probably synthesize at least part of the membrane phospholipids that they may need for their secretory function and for dictyosomal proliferation during cell growth, rather than importing this material entirely from the endoplasmic reticulum.
View details for Web of Science ID A1977CW61600025
View details for PubMedID 16659822
Dissociation coefficients of auxin-binding sites on maize (Zea mays L.) coleoptile membranes were measured, for 48 auxins and related ring compounds, by competitive displacement of (14)C-naphthaleneacetic acid from the binding sites. The sites bind with high affinity several ring compounds with acidic side chains 2 to 4 carbons long, and much more weakly bind neutral ring compounds and phenols related to these active acids, most phenoxyalkylcarboxylic acids, and arylcarboxylic acids except benzoic acid, which scarcely binds, and triiodobenzoic acids, which bind strongly. Specificity of the binding is narrowed in the presence of a low molecular weight "supernatant factor" that occurs in maize and other tissues. Activity of many of the analogs as auxin agonists or antagonists in the cell elongation response was determined with maize coleoptiles. These activities on the whole roughly parallel the affinities of the binding sites for the same compounds, especially affinities measured in the presence of supernatant factor, but there are some quantitative discrepancies, especially among phenoxyalkylcarboxylic acids. In view of several factors that can cause receptor affinity and biological activity values to diverge quantitatively among analogs, the findings appear to support the presumption that the auxin-binding sites may be receptors for auxin action.
View details for Web of Science ID A1977DZ19500029
View details for PubMedID 16660143
Characteristics of and optimum conditions for saturable ("specific") binding of [(14)C]naphthaleneacetic acid to sites located on membranous particles from maize (Zea mays L.) coleoptiles are described. Most, if not all, of the specific binding appears to be due to a single kinetic class of binding sites having a K(D) of 5 to 7 x 10(-7)m for naphthalene-1-acetic acid (NAA). Binding of NAA is insensitive to high monovalent salt concentrations, indicating that binding is not primarily ionic. However, specific binding is inhibited by Mg(2+) or Ca(2+) above 5 mm. Specific binding is improved by organic acids, especially citrate. Binding is heat-labile and is sensitive to agents that act either on proteins or on lipids. Specific binding is reversibly inactivated by reducing agents such as dithioerythritol; a reducible group, possibly a disulfide group, may be located at the binding site and required for its function. The affinity of the specific binding sites for auxins is modified by an unidentified dialyzable, heat-stable, apparently amphoteric, organic factor ("supernatant factor") found in maize tissue.
View details for Web of Science ID A1977CZ72100006
View details for PubMedID 16659851
Sites in maize (Zea mays L.) coleoptile homogenates that reversibly bind naphthalene-1-acetic acid with high affinity and may represent receptor sites for auxins are located primarily on cellular membranes that show the enzymic and buoyant density characteristics of membranes of the rough endoplasmic reticulum. The sites remain attached to the endoplasmic reticulum (ER) membranes after the ribosomes have been stripped off them. Binding sites for naphthylphthalamic acid, an inhibitor of auxin transport, are located on membranes different from those that carry the naphthalene-1-acetic-acid (NAA)-binding sites, and which are probably plasma membrane. The two kinds of binding sites can be largely separated by appropriate density gradient centrifugation. The results raise the possibility that primary auxin action occurs at ER membranes and could represent facilitation of the transfer of hydrogen ions and nascent secretory protein into the ER lumen followed by secretory transport of these products to the cell exterior via the Golgi system.
View details for Web of Science ID A1977DE35700015
View details for PubMedID 16659900
A pH microelectrode has been used to investigate the auxin effect on free space pH and its correlation with auxin-stimulated elongation in segments of pea (Pisum sativum) stem and maize (Zea mays var. Bear Hybrid) coleoptile tissue. Auxin induces a decrease in free space pH in both tissues. In maize coleoptiles, free space pH begins to fall within about 12 minutes of exposure to auxin and decreases by about 1 pH unit by approximately 30 minutes. In pea, pH begins to decrease within an average of 15 to 18 minutes of exposure to auxin and falls by about 0.9 pH unit by approximately 40 minutes. Auxin-stimulated elongation, measured in the same two tissues similarly prepared, appears in maize at the earliest 18 minutes after auxin application, while in pea it appears at the earliest 21 to 24 minutes after auxin application. The auxin analogs p-chlorophenoxyisobutyric acid and phenylacetic acid do not stimulate elongation above control levels in maize or pea tissue segments and do not cause a decrease in free space pH in either tissue. These findings are consistent with the acid secretion theory of auxin action.
View details for Web of Science ID A1976CE11300019
View details for PubMedID 16659648
Like indoleacetic acid, buffers of acidic pH, which stimulate elongation of pea (Pisum sativum var. Alaska) stem tissue, induce the appearance within the tissue of a watersoluble xyloglucan polymer that probably arises from previously deposited wall material. Neutral pH buffers, which inhibit the elongation response to indoleacetic acid in this tissue, inhibit indoleacetic acid-induced increase in soluble xyloglucan. The findings provide further evidence that release of soluble xyloglucan from the cell walls of pea results from the biochemical action on the cell wall that is responsible for wall extension. The data also indicate that treatment of tissue with either auxin or acidic pH has a similar biochemical effect on the cell wall. This is consistent with the H(+) secretion theory of auxin action.
View details for Web of Science ID A1975AQ95600007
View details for PubMedID 16659306
Turnover of cell wall polysaccharides and effects of auxin thereon were examined after prelabeling polysaccharides by feeding pea (Pisum sativum var. Alaska) stem segments (14)C-glucose, then keeping the tissue 7 hours in unlabeled glucose with or without indoleacetic acid. There followed an extraction, hydrolysis, and chromatography procedure by which labeled monosaccharides and uronic acids were released and separated with consistently high recovery. Most wall polymers, including galacturonan and cellulose, did not undergo appreciable turnover. About 20% turnover of starch, which normally contaminates cell wall preparations but which was removed by a preliminary step in this procedure, occurred in 7 hours. Quantitatively, the principal wall polymer turnover process observed was a 50% decrease in galactose in the pectinase-extractable fraction, including galactose attached to a pectinase-resistant rhamnogalacturonan. Other pectinase-resistant galactan(s) did not undergo turnover. No turnover was observed in arabinans, but a doubling of radioactivity in arabinose of the pectinase-resistant, hot-acid-degradable fraction occurred in 7 hours, possibly indicating conversion of galactan into arabinan. None of the above changes was affected by indoleacetic acid, but a quantitatively minor turnover of a pectinase-degradable xyloglucan was found to be consistently promoted by indole-acetic acid. This was accompanied by a reciprocal increase in water-soluble xyloglucan, suggesting that indoleacetic acid induces conversion of wall xyloglucan from insoluble to water-soluble form. The results indicate a highly selective pattern of wall turnover processes with an even more specific influence of auxin.
View details for Web of Science ID A1974T048500001
View details for PubMedID 16658765
Auxin promotes the liberation of a xlyoglucan polymer from the cell walls of elongating pea (Pisum sativum) stem segments. The released polymer can be isolated from the polysaccharide fraction of the water-soluble portion of tissue homogenates, thus providing as assay for this kind of metabolism. Promotion of xyloglucan metabolism by auxin begins within 15 minutes of hormone presentation. The effect increases with auxin concentration in a manner similar to the hormone effect on elongation. However, the xyloglucan effect of auxin occurs perfectly normally when elongation is completely blocked by mannitol. Metabolic inhibitors and Ca(2+), on the other hand, inhibit auxin promotion of elongation and of xyloglucan metabolism in parallel. The results suggest that the changes in xyloglucan reflect the means by which auxin modifies the cell wall to cause elongation.
View details for Web of Science ID A1974U470100014
View details for PubMedID 16658916
The 2- to 4-fold rise in particle-bound beta-glucan synthetase (uridine diphosphate-glucose: beta-1, 4-glucan glucosyltransferase) activity that can be induced by indoleacetic acid in pea stem tissue is not prevented by concentrations of actinomycin D or cycloheximide that inhibit growth and macromolecule synthesis. The rise is concluded to be a hormonally induced activation of previously existing, reversibly deactivated enzyme. The activation is not a direct allosteric effect of indoleacetic acid or sugars. It is blocked by inhibitors of energy metabolism, by 2-deoxyglucose, and by high osmolarity, but not by Ca(2+) at concentrations that inhibit auxin-induced elongation and prevent promotion of sugar uptake by indoleacetic acid, and not by alpha, alpha'-dipyridyl at concentrations that inhibit formation of hydroxyproline. Regulation of the system could be due either to an ATP-dependent activating reaction affecting this enzyme, or to changes in levels of a primer or a lipid cofactor.
View details for Web of Science ID A1973P452500002
View details for PubMedID 16658380
Treatment of pea stem segments with indoleacetic acid (IAA) causes within 1 hour a 2- to 4-fold increase in activity of particulate uridine diphosphoglucose-dependent beta-glucan synthetase obtainable from the tissue. The IAA effect is observable in tissue from all parts of the elongation zone of the pea stem, and also in older tissue that is not capable of a cell enlargement response to IAA. A large increase in activity is caused by IAA only if synthetase activity in the isolated tissue has first been allowed to fall substantially below the intact plant level, and only if sucrose is supplied along with IAA. Treatment of tissue with sucrose alone after a period of sugar starvation causes a transient rise of synthetase activity. The decline in synthetase activity in absence of IAA, the rise caused by IAA, and the transient rise caused by sucrose are all strongly temperature-dependent. IAA and sucrose do not affect the activity of isolated synthetase particles. Synthetase activity in vivo is sensitive to as low as 0.1 mum IAA and is increased by IAA analogues that are active as auxins on elongation but not by nonauxin analogues. Activity begins to rise 10 to 15 minutes after exposure to IAA, which places this among the most rapid enzyme effects of a plant growth regulator heretofore demonstrated, and among the most rapid known metabolic effects of auxins. The effect is seen also with polysaccharide synthetase activity using uridine diphosphate-galactose or uridine diphosphate-xylose as substrates, and to a lesser extent with guanosine diphosphoglucose-dependent glucan synthetase activity. Glucan synthetase from IAA-treated tissue appears to have a higher affinity for uridine diphosphate-glucose than the control.
View details for Web of Science ID A1973P452500001
View details for PubMedID 16658379
A variety of particle-bound synthetases that use sugar nucleotides as glycosyl donors for the formation of polysaccharides similar to those of the cell wall have been demonstrated in mung beans and other plant tissues,(1) but the particles in question have not been previously identified.(2, 3) The polysaccharide synthetase particles from peas that form mainly beta-1,4-glucan from UDPG and GDPG have now been separated from other cell particles by combinations of velocity and isopycnic density gradient centrifugation. The particles have an effective density of about 1.15 gm cm(-3), exhibit latent nucleoside diphosphatase activity upon IDP, UDP, GDP, and to a lesser extent upon ADP, and also possess acid phosphatase and weak ATPase activity. The isolated synthetase particles consist of somewhat condensed Golgi dictyosomes and free dictyosomal membranes bearing vesicles. It is concluded that the synthetase particles are Golgi membranes. The nucleoside diphosphatase activity of these particles may represent inactivated polysaccharide synthetase.
View details for Web of Science ID A1969E985200030
View details for PubMedID 16591795


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Both penalty boxes were frequently occupied the first two periods of the Oklahoma City Barons' 6-0 loss to the Chicago Wolves on Friday night at the Cox Convention Center.
OKC Barons, Chicago serve up a rash of penalties
Oklahoma City was whistled for seven penalties, Chicago six. The Wolves were 1-of-7 on the power play, the Barons 0-of-6.
"There wasn't a lot of flow. It's hard to get your guys going," said Barons coach Todd Nelson. "You'd like at least one rotation through your (four) lines to get everybody in the game. We couldn't do that tonight.
"We never scored any of our power-play chances. The reason we've been winning some games is our special teams have been really strong, but they weren't strong tonight."
Friday was Olivier Roy's first game as game as the Barons' No. 1 goaltender since Richard Bachman was called up to Edmonton last week. Roy lasted only two periods, allowing five goals on 21 shots before being replaced by Tyler Bunz at the start of the third period.
Roy is 1-2 this season, but was 9-9-1 last season with the Barons.
"It's on everybody," Nelson said. "Let's face it, we have to play better in front of our goaltenders. Four of the goals are tic-tac-toe plays where we were just standing around. A team like that will make you pay. And they have big bodies. You have to work for every inch of ice you get."
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