Cancer deaths and cases attributable to lifestyle factors and infections in China, 2013.

BACKGROUND: The burden of cancer in China is high, and it is expected to further increase. Information on cancers attributable to potentially modifiable risk factors is essential in planning preventive measures against cancer. We estimated the number and proportion of cancer deaths and cases attributable to ever-smoking, second-hand smoking, alcohol drinking, low fruit/vegetable intake, excess body weight, physical inactivity, and infections in China, using contemporary data from nationally representative surveys and cancer registries. METHODS: The number of cancer deaths and cases in 2013 were obtained from the National Central Cancer Registry of China and data on most exposures were obtained from the China National Nutrition and Health Survey 2002 or 2006 and Global Adult Tobacco Smoking 2010. We used a bootstrap simulation method to calculate the number and proportion of cancer deaths and cases attributable to risk factors and their corresponding 95% confidence intervals (CIs), allowing for uncertainty in data. RESULTS: Approximately 718 000 (95% CI 702 100-732 200) cancer deaths in men and 283 100 (278 800-288 800) cancer deaths in women were attributable to the studied risk factors, accounting for 52% of all cancer deaths in men and 35% in women. The numbers for incident cancer cases were 952 500 (95% CI 934 200-971 400) in men and 442 700 (437 200-447 900) in women, accounting for 47% of all incident cases in men and 28% in women. The greatest proportions of cancer deaths attributable to risk factors were for smoking (26%), HBV infection (12%), and low fruit/vegetable intake (7%) in men and HBV infection (7%), low fruit/vegetable intake (6%), and second-hand smoking (5%) in women. CONCLUSIONS: Effective public health interventions to eliminate or reduce exposure from these risk factors, notably tobacco control and vaccinations against carcinogenic infections, can have considerable impact on reducing the cancer burden in China.

Maternal exposure to carbon monoxide and fine particulate matter during pregnancy in an urban Tanzanian cohort.

Low birthweight contributes to as many as 60% of all neonatal deaths; exposure during pregnancy to household air pollution has been implicated as a risk factor. Between 2011 and 2013, we measured personal exposures to carbon monoxide (CO) and fine particulate matter (PM2.5 ) in 239 pregnant women in Dar es Salaam, Tanzania. CO and PM2.5 exposures during pregnancy were moderately high (geometric means 2.0 ppm and 40.5 µg/m3 ); 87% of PM2.5 measurements exceeded WHO air quality guidelines. Median and high (75th centile) CO exposures were increased for those cooking with charcoal and kerosene versus kerosene alone in quantile regression. High PM2.5 exposures were increased with charcoal use. Outdoor cooking reduced median PM2.5 exposures. For PM2.5 , we observed a 0.15 kg reduction in birthweight per interquartile increase in exposure (23.0 µg/m3 ) in multivariable linear regression; this finding was of borderline statistical significance (95% confidence interval 0.30, 0.00 kg; P = 0.05). PM2.5 was not significantly associated with birth length or head circumference nor were CO exposures associated with newborn anthropometrics. Our findings contribute to the evidence that exposure to household air pollution, and specifically fine particulate matter, may adversely affect birthweight.

Childhood pneumonia and crowding, bed-sharing and nutrition: a case-control study from The Gambia.

SETTING: Greater Banjul and Upper River Regions, The Gambia. OBJECTIVE: To investigate tractable social, environmental and nutritional risk factors for childhood pneumonia. DESIGN: A case-control study examining the association of crowding, household air pollution (HAP) and nutritional factors with pneumonia was undertaken in children aged 2-59 months: 458 children with severe pneumonia, defined according to the modified WHO criteria, were compared with 322 children with non-severe pneumonia, and these groups were compared to 801 neighbourhood controls. Controls were matched by age, sex, area and season. RESULTS: Strong evidence was found of an association between bed-sharing with someone with a cough and severe pneumonia (adjusted OR [aOR] 5.1, 95%CI 3.2-8.2, P < 0.001) and non-severe pneumonia (aOR 7.3, 95%CI 4.1-13.1, P < 0.001), with 18% of severe cases estimated to be attributable to this risk factor. Malnutrition and pneumonia had clear evidence of association, which was strongest between severe malnutrition and severe pneumonia (aOR 8.7, 95%CI 4.2-17.8, P < 0.001). No association was found between pneumonia and individual carbon monoxide exposure as a measure of HAP. CONCLUSION: Bed-sharing with someone with a cough is an important risk factor for severe pneumonia, and potentially tractable to intervention, while malnutrition remains an important tractable determinant.

Regulation of FOXO3 subcellular localization by Kit ligand in the neonatal mouse ovary.

PURPOSE: Foxo3 protein is required in the oocyte nucleus for the maintenance of primordial follicles in a dormant state. PI3K/AKT-dependent phosphorylation of Foxo3 leads to its relocalization to the cytoplasm and subsequent follicular activation. However, the nature of the upstream signals controlling Foxo3 activity and subcellular localization remains unknown. We aimed to study the in vitro effects of Kit ligand (stem cell factor) on the subcellular localization of Foxo3 in primordial follicles within the postnatal mouse ovary. METHODS: This was an in vitro study using explants of intact neonatal mouse ovaries. The study was performed in laboratory animal facility and basic science research laboratory at a University Hospital. The animals used for this study were FVB mice. Neonatal FVB mice ovaries at postnatal day 7 (PD7) were harvested and incubated in culture medium (DMEM) at 37 °C and 5 % CO(2) for 60-90 min with (n = 3) or without (n = 3) Kit ligand at 150 ng/mL (8 nM). Similar experimental conditions were used to establish a dose-response curve for the effects of Kit ligand and assess the effects of imatinib (small molecule inhibitor of the Kit receptor). Immunofluorescence was used to identify the subcellular location of Foxo3 in oocytes. Proportions of cytoplasmic versus nuclear Foxo3 in primordial follicles were determined. RESULTS: Kit ligand treatment increased the cytoplasmic localization of Foxo3 from 40 % in the untreated ovaries to 74 % in the treated group (p = 0.007 in paired samples and p = 0.03 in unpaired samples). Furthermore, this effect was reversible with imatinib (p = 0.005). A dose-response curve for Kit ligand treatment showed that maximum effect was seen at 150 ng/mL. CONCLUSION: Kit ligand treatment in vitro increases the proportion of cytoplasmic Foxo3 in primordial follicles at PD7, lending support to the idea that Kit receptor/ligand controls Foxo3 activity in the context of primordial follicle activation.

Pharmacokinetics of dexmedetomidine combined with therapeutic hypothermia in a piglet asphyxia model.

BACKGROUND: The highly selective α2 -adrenoreceptor agonist, dexmedetomidine, exerts neuroprotective, analgesic, anti-inflammatory and sympatholytic properties that may be beneficial for perinatal asphyxia. The optimal safe dose for pre-clinical newborn neuroprotection studies is unknown. METHODS: Following cerebral hypoxia-ischaemia, dexmedetomidine was administered to nine newborn piglets in a de-escalation dose study in combination with hypothermia (whole body cooling to 33.5°C). Dexmedetomidine was administered with a loading dose of 1 µg/kg and maintenance infusion at doses from 10 to 0.6 µg/kg/h. One additional piglet was not subjected to hypoxia-ischaemia. Blood for pharmacokinetic analysis was sampled pre-insult and frequently post-insult. A one-compartment linear disposition model was used to fit data. Population parameter estimates were obtained using non-linear mixed effects modelling. RESULTS: All dexmedetomidine infusion regimens led to plasma concentrations above those associated with sedation in neonates and children (0.4-0.8 µg/l). Seven out of the nine piglets with hypoxia-ischaemia experienced periods of bradycardia, hypotension, hypertension and cardiac arrest; all haemodynamic adverse events occurred in piglets with plasma concentrations greater than 1 µg/l. Dexmedetomidine clearance was 0.126 l/kg/h [coefficient of variation (CV) 46.6.%] and volume of distribution was 3.37 l/kg (CV 191%). Dexmedetomidine clearance was reduced by 32.7% at a temperature of 33.5°C. Dexmedetomidine clearance was reduced by 55.8% following hypoxia-ischaemia. CONCLUSIONS: Dexmedetomidine clearance was reduced almost tenfold compared with adult values in the newborn piglet following hypoxic-ischaemic brain injury and subsequent therapeutic hypothermia. Reduced clearance was related to cumulative effects of both hypothermia and exposure to hypoxia. High plasma levels of dexmedetomidine were associated with major cardiovascular complications.

The small GTPase Rheb is required for spermatogenesis but not oogenesis.

The process of germ cell development is under the tight control of various signaling pathways, among which the PI3K-Akt-mTOR pathway is of critical importance. Previous studies have demonstrated sex-specific roles for several components of this pathway. In the current study, we aimed to evaluate the role of Rheb, a member of the small GTPase superfamily and a critical component for mTORC1 activation, in male and female gametogenesis. The function of Rheb in development and the nervous system has been extensively studied, but little is known about its role in the germ line. We have exploited genetic approaches in the mouse to study the role of Rheb in the germ line and have identified an essential role in spermatogenesis. Conditional knockout (cKO) of Rheb in the male germ line resulted in severe oligoasthenoteratozoospermia and male sterility. More detailed phenotypic analyses uncovered an age-dependent meiotic progression defect combined with subsequent abnormalities in spermiogenesis as evidenced by abnormal sperm morphology. In the female, however, germ-cell specific inactivation of Rheb was not associated with any discernible abnormality; these cKO mice were fertile with morphologically unremarkable ovaries, normal primordial follicle formation, and subsequent follicle maturation. The absence of an abnormal ovarian phenotype is striking given previous studies demonstrating a critical role for the mTORC1 pathway in the maintenance of primordial follicle pool. In conclusion, our findings demonstrate an essential role of Rheb in diverse aspects of spermatogenesis but suggest the existence of functionally redundant factors that can compensate for Rheb deficiency within oocytes.

Estimating the global and regional burden of suboptimal nutrition on chronic disease: methods and inputs to the analysis.

BACKGROUND/OBJECTIVES: Global burdens of cardiovascular disease (CVD), diabetes and cancer are on the rise. Little quantitative data are available on the global impact of diet on these conditions. The objective of this study was to develop systematic and comparable methods to quantitatively assess the impact of suboptimal dietary habits on CVD, diabetes and cancer burdens globally and in 21 world regions. SUBJECTS/METHODS: Using a comparative risk assessment framework, we developed methods to establish for selected dietary risk factors the effect sizes of probable or convincing causal diet-disease relationships, the alternative minimum-risk exposure distributions and the exposure distributions. These inputs, together with disease-specific mortality rates, allow computation of the numbers of events attributable to each dietary factor. RESULTS: Using World Health Organization and similar evidence criteria for convincing/probable causal effects, we identified 14 potential diet-disease relationships. Effect sizes and ranges of uncertainty will be derived from systematic reviews and meta-analyses of trials or high-quality observational studies. Alternative minimum-risk distributions were identified based on amounts corresponding to the lowest disease rates in populations. Optimal and alternative definitions for each exposure were established based on the data used to quantify harmful or protective effects. We developed methods for identifying and obtaining data from nationally representative surveys. A ranking scale was developed to assess survey quality and validity of dietary assessment methods. Multi-level hierarchical models will be developed to impute missing data. CONCLUSIONS: These new methods will allow, for the first time, assessment of the global impact of specific dietary factors on chronic disease mortality. Such global assessment is not only possible but is also imperative for priority setting and policy making.

Patterns and predictors of personal exposure to indoor air pollution from biomass combustion among women and children in rural China.

UNLABELLED: Indoor air pollution (IAP) from domestic biomass combustion is an important health risk factor, yet direct measurements of personal IAP exposure are scarce. We measured 24-h integrated gravimetric exposure to particles < 2.5 µm in aerodynamic diameter (particulate matter, PM2.5) in 280 adult women and 240 children in rural Yunnan, China. We also measured indoor PM2.5 concentrations in a random sample of 44 kitchens. The geometric mean winter PM2.5 exposure among adult women was twice that of summer exposure [117 µg/m³ (95% CI: 107, 128) vs. 55 µg/m³ (95% CI: 49, 62)]. Children's geometric mean exposure in summer was 53 µg/m³ (95% CI: 46, 61). Indoor PM2.5 concentrations were moderately correlated with women's personal exposure (r=0.58), but not for children. Ventilation during cooking, cookstove maintenance, and kitchen structure were significant predictors of personal PM2.5 exposure among women primarily cooking with biomass. These findings can be used to develop exposure assessment models for future epidemiologic research and inform interventions and policies aimed at reducing IAP exposure. PRACTICAL IMPLICATIONS: Our results suggest that reducing overall PM pollution exposure in this population may be best achieved by reducing winter exposure. Behavioral interventions such as increasing ventilation during cooking or encouraging stove cleaning and maintenance may help achieve these reductions.

The burden of cardiovascular disease associated with high body mass index in the Asia-Pacific region.

Studying obesity in the Asia-Pacific region is difficult because of the diverse ethnic background and different stages of economic and nutrition transition. The burden of cardiovascular disease associated with overweight (defined as body mass index ≥25 kg m(-2) ) was previously estimated for countries within the region. However, using the conventional cut-point of 25 kg m(-2) ignores the continuous association between body mass index and cardiovascular disease from approximately 20 kg m(-2) . By estimating the proportion of cardiovascular disease that would be prevented if the theoretical mean body mass index in the population was shifted to 21 kg m(-2) , nationally representative data from 15 countries suggested the population attributable fractions for cardiovascular disease were approximately three times higher than the previous estimates. Coronary heart disease attributable to body mass index other than 21 kg m(-2) ranged from 2% in India to 58% in American Samoa. Similarly, the population attributable fraction for ischaemic stroke ranged from 3% in India to 64% in American Samoa. If cardiovascular risk increases from 21 kg m(-2) applies to all populations, most countries in the region will need to aim towards substantially reducing their current population mean body mass index in order to lower the burden of cardiovascular disease associated with excess weight.

The impact of uterine leiomyomas on reproductive outcomes.

Uterine leiomyomas (fibroids, myomas) are a common benign disease of the uterus with a prevalence of 8-18%. Prevalence rates vary with race, and fibroids are most common in African American women. Uterine leiomyomas can also be present during pregnancy, which may occur more frequently than previously suspected, with prevalence rates reported of up to 10%. Recent evidence has emerged to clarify the relationship of uterine fibroids on fertility and obstetrical outcomes. In this paper we review evidence that uterine fibroids, specifically submucosal and intramural myomas, negatively impact fertility and are associated with adverse obstetrical outcomes such as: pain, preterm labor, placental abruption, malpresentation, postpartum hemorrhage, and cesarean section. Myomectomy performed for submucosal and intramural fibroids significantly improves fertility outcome, and current evidence suggests myomectomy is the treatment of choice in women desiring to conceive. For women that do not desire surgery, medical management of myomas is available. Treatment with GnRH agonists may be considered, however newer medications with fewer side effects give practitioners and patients more options. Progesterone antagonists, selective progesterone receptor modulators, and aromatase inhibitors have all shown promise as effective therapies. Non-pharmacologic treatments such as uterine artery embolization and MRI-guided ultrasound have also emerged as effective treatments for uterine fibroids. With such a wide range of new and emerging treatment options, it is important for providers to understand which fibroids are likely to respond optimally to a specific treatment, in order to individualize appropriate and effective management for patients.

Global and regional child mortality and burden of disease attributable to zinc deficiency.

BACKGROUND/OBJECTIVES: Zinc is an essential micronutrient and deficiency can lead to an increased risk for infectious diseases and growth retardation among children under 5 years of age. We aimed to estimate disease-specific and all-cause mortality attributable to zinc deficiency. SUBJECT/METHODS: We estimated the prevalence of zinc deficiency in Latin America, Africa and Asia, where based on zinc availability in the diet and childhood stunting rates, zinc deficiency is widespread. The relative risks of death among zinc-deficient children for diarrhea, malaria and pneumonia were estimated from randomized controlled trials. We used the comparative risk assessment methods to calculate deaths and burden of disease (measured in disability-adjusted life years, DALYs) from each of these three diseases attributable to zinc deficiency in these regions. RESULTS: Zinc deficiency was responsible for 453,207 deaths (4.4% of childhood deaths), and 1.2% of the burden of disease (3.8% among children between 6 months and 5 years) in these three regions in 2004. Of these deaths, 260,502 were in Africa, 182,546 in Asia and 10,159 in Latin America. Zinc deficiency accounted for 14.4% of diarrhea deaths, 10.4% of malaria deaths and 6.7% of pneumonia deaths among children between 6 months and 5 years of age. CONCLUSIONS: Zinc deficiency contributes to substantial morbidity and mortality, especially from diarrhea. Zinc supplementation provided as an adjunct treatment for diarrhea may be the best way to target children most at risk of deficiency.

Measuring the exposure of infants and children to indoor air pollution from biomass fuels in The Gambia.

UNLABELLED: Indoor air pollution (IAP) from biomass fuels contains high concentrations of health damaging pollutants and is associated with an increased risk of childhood pneumonia. We aimed to design an exposure measurement component for a matched case-control study of IAP as a risk factor for pneumonia and severe pneumonia in infants and children in The Gambia. We conducted co-located simultaneous area measurement of carbon monoxide (CO) and particles with aerodynamic diameter <2.5 microm (PM(2.5)) in 13 households for 48 h each. CO was measured using a passive integrated monitor and PM(2.5) using a continuous monitor. In three of the 13 households, we also measured continuous PM(2.5) concentration for 2 weeks in the cooking, sleeping, and playing areas. We used gravimetric PM(2.5) samples as the reference to correct the continuous PM(2.5) for instrument measurement error. Forty-eight hour CO and PM(2.5) concentrations in the cooking area had a correlation coefficient of 0.80. Average 48-h CO and PM(2.5) concentrations in the cooking area were 3.8 +/- 3.9 ppm and 361 +/- 312 microg/m3, respectively. The average 48-h CO exposure was 1.5 +/- 1.6 ppm for children and 2.4 +/- 1.9 ppm for mothers. PM(2.5) exposure was an estimated 219 microg/m3 for children and 275 microg/m3 for their mothers. The continuous PM(2.5) concentration had peaks in all households representing the morning, midday, and evening cooking periods, with the largest peak corresponding to midday. The results are used to provide specific recommendations for measuring the exposure of infants and children in an epidemiological study. PRACTICAL IMPLICATIONS: Measuring personal particulate matter (PM) exposure of young children in epidemiological studies is hindered by the absence of small personal monitors. Simultaneous measurement of PM and carbon monoxide suggests that a combination of methods may be needed for measuring children's PM exposure in areas where household biomass combustion is the primary source of indoor air pollution. Children's PM exposure in biomass burning homes in The Gambia is substantially higher than concentrations in the world's most polluted cities.

Reproductive ageing in women.

The traditional view in respect to female reproduction is that the number of oocytes at birth is fixed and continuously declines towards the point when no more oocytes are available after menopause. In this review we briefly discuss the embryonic development of female germ cells and ovarian follicles. The ontogeny of the hypothalamic-pituitary-gonadal axis is then discussed, with a focus on pubertal transition and normal ovulatory menstrual cycles during female adult life. Biochemical markers of menopausal transition are briefly examined. We also examine the effects of age on female fertility, the contribution of chromosomal abnormalities of the oocyte to the observed decline in female fertility with age and the possible biological basis for the occurrence of such abnormalities. Finally, we consider the effects of maternal age on obstetric complications and perinatal outcome. New data that have the potential to revolutionize our understanding of mammalian oogenesis and follicular formation, and of the female reproductive ageing process, are also briefly considered.

Regional, disease specific patterns of smoking-attributable mortality in 2000.

BACKGROUND: Smoking has been causally associated with increased mortality from several diseases, and has increased considerably in many developing countries in the past few decades. Mortality attributable to smoking in the year 2000 was estimated for adult males and females, including estimates by age and for specific diseases in 14 epidemiological subregions of the world. METHODS: Lung cancer mortality was used as an indirect marker of the accumulated hazard of smoking. Never-smoker lung cancer mortality was estimated based on the household use of coal with poor ventilation. Estimates of mortality caused by smoking were made for lung cancer, upper aerodigestive cancer, all other cancers, chronic obstructive pulmonary disease (COPD), other respiratory diseases, cardiovascular diseases, and selected other medical causes. Estimates were limited to ages 30 years and above. RESULTS: In 2000, an estimated 4.83 million premature deaths in the world were attributable to smoking, 2.41 million in developing countries and 2.43 million in industrialised countries. There were 3.84 million male deaths and 1.00 million female deaths attributable to smoking. 2.69 million smoking attributable deaths were between the ages of 30-69 years, and 2.14 million were 70 years of age and above. The leading causes of death from smoking in industrialised regions were cardiovascular diseases (1.02 million deaths), lung cancer (0.52 million deaths), and COPD (0.31 million deaths), and in the developing world cardiovascular diseases (0.67 million deaths), COPD (0.65 million deaths), and lung cancer (0.33 million deaths). The share of male and female deaths and younger and older adult deaths, and of various diseases in total smoking attributable deaths exhibited large inter-regional heterogeneity, especially in the developing world. CONCLUSIONS: Smoking was an important cause of global mortality in 2000, affecting a large number of diseases. Age, sex, and disease patterns of smoking-caused mortality varied greatly across regions, due to both historical and current smoking patterns, and the presence of other risk factors that affect background mortality from specific diseases.

Measuring the accumulated hazards of smoking: global and regional estimates for 2000.

OBJECTIVE: Current prevalence of smoking, even where data are available, is a poor proxy for cumulative hazards of smoking, which depend on several factors including the age at which smoking began, duration of smoking, number of cigarettes smoked per day, degree of inhalation, and cigarette characteristics such as tar and nicotine content or filter type. METHODS: We extended the Peto-Lopez smoking impact ratio method to estimate accumulated hazards of smoking for different regions of the world. Lung cancer mortality data were obtained from the Global Burden of Disease mortality database. The American Cancer Society Cancer Prevention Study, phase II (CPS-II) with follow up for the years 1982 to 1988 was the reference population. For the global application of the method, never-smoker lung cancer mortality rates were chosen based on the estimated use of coal for household energy in each region. RESULTS: Men in industrialised countries of Europe, North America, and the Western Pacific had the largest accumulated hazards of smoking. Young and middle age males in many regions of the developing world also had large smoking risks. The accumulated hazards of smoking for women were highest in North America followed by Europe. CONCLUSIONS: In the absence of detailed data on smoking prevalence and history, lung cancer mortality provides a robust indicator of the accumulated hazards of smoking. These hazards in developing countries are currently more concentrated among young and middle aged males.

Indoor air pollution from biomass combustion and acute respiratory infections in Kenya: an exposure-response study.

BACKGROUND: Acute respiratory infections (ARI) are the leading cause of the global burden of disease and have been causally linked with exposure to pollutants from domestic biomass fuels in less-developed countries. We used longitudinal health data coupled with detailed monitoring of personal exposure from more than 2 years of field measurements in rural Kenya to estimate the exposure-response relation for particulates smaller than 10 mm in diameter (PM(10)) generated from biomass combustion. METHODS: 55 randomly-selected households (including 93 infants and children, 229 individuals between 5 and 49 years of age, and 23 aged 50 or older) in central Kenya were followed up for more than 2 years. Longitudinal data on ARI and acute lower respiratory infections (ALRI) were recorded at weekly clinical examinations. Exposure to PM(10) was monitored by measurement of PM(10) emission concentration and time-activity budgets. FINDINGS: With the best estimate of the exposure-response relation, we found that ARI and ALRI are increasing concave functions of average daily exposure to PM(10), with the rate of increase declining for exposures above about 1000-2000 mg/m(3). After we had included high-intensity exposure episodes, sex was no longer a significant predictor of ARI and ALRI. INTERPRETATION: The benefits of reduced exposure to PM(10) are larger for average exposure less than about 1000-2000 mg/m(3). Our findings have important consequences for international public-health policies, energy and combustion research, and technology transfer efforts that affect more than 2 billion people worldwide.

Quantifying the effects of exposure to indoor air pollution from biomass combustion on acute respiratory infections in developing countries.

Acute respiratory infections (ARI) are the leading cause of burden of disease worldwide and have been causally linked with exposure to pollutants from domestic biomass fuels in developing countries. We used longitudinal health data coupled with detailed monitoring and estimation of personal exposure from more than 2 years of field measurements in rural Kenya to estimate the exposure-response relationship for particulates < 10 microm diameter (PM(10)) generated from biomass combustion. Acute respiratory infections and acute lower respiratory infections are concave, increasing functions of average daily exposure to PM(10), with the rate of increase declining for exposures above approximately 1,000-2,000 microg/m(3). This first estimation of the exposure-response relationship for the high-exposure levels characteristic of developing countries has immediate and important consequences for international public health policies, energy and combustion research, and technology transfer efforts that affect more than 2 billion people worldwide.

The contributions of emissions and spatial microenvironments to exposure to indoor air pollution from biomass combustion in Kenya.

Acute and chronic respiratory diseases, which are causally linked to exposure to indoor air pollution in developing countries, are the leading cause of global morbidity and mortality. Efforts to develop effective intervention strategies and detailed quantification of the exposure-response relationship for indoor particulate matter require accurate estimates of exposure. We used continuous monitoring of indoor air pollution and individual time-activity budget data to construct detailed profiles of exposure for 345 individuals in 55 households in rural Kenya. Data for analysis were from two hundred ten 14-hour days of continuous real-time monitoring of concentrations of particulate matter [less than/equal to] 10 microm in aerodynamic diameter and the location and activities of household members. These data were supplemented by data on the spatial dispersion of pollution and from interviews. Young and adult women had not only the highest absolute exposure to particulate matter (2, 795 and 4,898 microg/m(3) average daily exposure concentrations, respectively) but also the largest exposure relative to that of males in the same age group (2.5 and 4.8 times, respectively). Exposure during brief high-intensity emission episodes accounts for 31-61% of the total exposure of household members who take part in cooking and 0-11% for those who do not. Simple models that neglect the spatial distribution of pollution within the home, intense emission episodes, and activity patterns underestimate exposure by 3-71% for different demographic subgroups, resulting in inaccurate and biased estimations. Health and intervention impact studies should therefore consider in detail the critical role of exposure patterns, including the short periods of intense emission, to avoid spurious assessments of risks and benefits.

[Pulmonary involvement in Schonlein-Henoch's purpura]. / Manifestations pulmonaires du purpura rhumatoïde de Schonlein-Henoch, chez un enfant de huit ans.

A case of vascular purpura was observed in a 8 year-old girl. The clinical symptoms and pathological findings in kidneys and skin were compatible with Henoch-Schonlein syndrome. She presented with dyspnea and frequent acute pulmonary failure and the chest X-ray showed changing pulmonary infiltration. Despite treatment with corti-costeroids and cyclophosphamide, she died after 16 months. Pulmonary alveolar oedema, focal interstitial fibrosis and arterial fibrinoid thrombosis were found at autopsy. There was neither collagen lesion, nor fibrinoid necrosis.