RÉSUMÉ
The Pooled Uranium Miners Analysis (PUMA) study is the largest uranium miners cohort with 119,709 miners, 4.3 million person-years at risk and 7754 lung cancer deaths. Excess relative rate (ERR) estimates for lung cancer mortality per unit of cumulative exposure to radon progeny in working level months (WLM) based on the PUMA study have been reported. The ERR/WLM was modified by attained age, time since exposure or age at exposure, and exposure rate. This pattern was found for the full PUMA cohort and the 1960 + sub-cohort, i.e., miners hired in 1960 or later with chronic low radon exposures and exposure rates. The aim of the present paper is to calculate the lifetime excess absolute risk (LEAR) of lung cancer mortality per WLM using the PUMA risk models, as well as risk models derived in previously published smaller uranium miner studies, some of which are included in PUMA. The same methods were applied for all risk models, i.e., relative risk projection up to <95 years of age, an exposure scenario of 2 WLM per year from age 18-64 years, and baseline mortality rates representing a mixed Euro-American-Asian population. Depending upon the choice of model, the estimated LEAR per WLM are 5.38 × 10-4 or 5.57 × 10-4 in the full PUMA cohort and 7.50 × 10-4 or 7.66 × 10-4 in the PUMA 1960 + sub-cohort, respectively. The LEAR per WLM estimates derived from risk models reported for previously published uranium miners studies range from 2.5 × 10-4 to 9.2 × 10-4. PUMA strengthens knowledge on the radon-related lung cancer LEAR, a useful way to translate models for policy purposes.
Sujet(s)
Tumeurs du poumon , Tumeurs radio-induites , Maladies professionnelles , Exposition professionnelle , Radon , Uranium , Humains , Adolescent , Jeune adulte , Adulte , Adulte d'âge moyen , Études de cohortes , Radon/effets indésirables , Uranium/effets indésirables , Tumeurs du poumon/épidémiologie , Tumeurs du poumon/étiologie , Exposition professionnelle/effets indésirables , Tumeurs radio-induites/épidémiologie , Tumeurs radio-induites/étiologie , Protéines régulatrices de l'apoptose , Maladies professionnelles/épidémiologieRÉSUMÉ
Sujet(s)
Diabète/épidémiologie , Dépistage de masse/méthodes , Tuberculose/épidémiologie , Adulte , Sujet âgé , Glycémie/analyse , Études de cohortes , Diabète/diagnostic , Femelle , Humains , Incidence , Mâle , Adulte d'âge moyen , Programmes nationaux de santé , Études prospectives , Récidive , République de Corée/épidémiologie , Facteurs de risque , Tuberculose/diagnosticRÉSUMÉ
UNLABELLED: The scientific literature through 2005 on the effects of ventilation rates on health in indoor environments has been reviewed by a multidisciplinary group. The group judged 27 papers published in peer-reviewed scientific journals as providing sufficient information on both ventilation rates and health effects to inform the relationship. Consistency was found across multiple investigations and different epidemiologic designs for different populations. Multiple health endpoints show similar relationships with ventilation rate. There is biological plausibility for an association of health outcomes with ventilation rates, although the literature does not provide clear evidence on particular agent(s) for the effects. Higher ventilation rates in offices, up to about 25 l/s per person, are associated with reduced prevalence of sick building syndrome (SBS) symptoms. The limited available data suggest that inflammation, respiratory infections, asthma symptoms and short-term sick leave increase with lower ventilation rates. Home ventilation rates above 0.5 air changes per hour (h(-1)) have been associated with a reduced risk of allergic manifestations among children in a Nordic climate. The need remains for more studies of the relationship between ventilation rates and health, especially in diverse climates, in locations with polluted outdoor air and in buildings other than offices. PRACTICAL IMPLICATIONS: Ventilation with outdoor air plays an important role influencing human exposures to indoor pollutants. This review and assessment indicates that increasing ventilation rates above currently adopted standards and guidelines should result in reduced prevalence of negative health outcomes. Building operators and designers should avoid low ventilation rates unless alternative effective measures, such as source control or air cleaning, are employed to limit indoor pollutant levels.
Sujet(s)
Pollution de l'air intérieur/effets indésirables , Syndrome du bâtiment malsain/épidémiologie , Ventilation/statistiques et données numériques , Pollution de l'air intérieur/prévention et contrôle , Asthme/épidémiologie , Maladies transmissibles/épidémiologie , Logement , Humains , Communication interdisciplinaire , Infections de l'appareil respiratoire/épidémiologie , Établissements scolaires , Congé maladie/statistiques et données numériques , Lieu de travailRÉSUMÉ
Although the risks of tobacco smoking have been known for decades, the pandemic of tobacco use continues. There are an estimated 1.3 billion smokers worldwide, along with millions more using various oral tobacco products. Recent global estimates place the mortality burden from tobacco use at over 6 million annually, with nearly two-thirds of these deaths occurring in developing countries. If current patterns persist, there will be an estimated 1 billion deaths from tobacco during the twenty-first century. Part 1 of this two-part paper provides an overview of the tobacco pandemic, the scope of the pandemic, and its economic and health consequences. Part 2 reviews the history of tobacco control to date and addresses the current global strategy, based on the World Health Organization's (WHO's) Framework Convention on Tobacco Control and the MPOWER package of interventions. Part 2 ends with a consideration of scenarios for the future of the pandemic.
Sujet(s)
Trouble lié au tabagisme/économie , Trouble lié au tabagisme/prévention et contrôle , Réduction des dommages , Santé , Histoire du 20ème siècle , Humains , Législation médicale/histoire , Arrêter de fumer , Trouble lié au tabagisme/histoire , États-Unis , Organisation mondiale de la santéRÉSUMÉ
Although the risks of tobacco smoking have been known for decades, the pandemic of tobacco use continues. There are an estimated 1.3 billion smokers worldwide, along with millions more using various oral tobacco products. Recent global estimates place the mortality burden from tobacco use at over 6 million annually, with nearly two-thirds of these deaths occurring in developing countries. If current patterns persist, there will be an estimated 1 billion deaths from tobacco during the twenty-first century. Part 1 of this two-part paper provides an overview of the tobacco pandemic, the scope of the pandemic, and its economic and health consequences. Part 2 reviews the history of tobacco control to date and addresses the current global strategy, based on the World Health Organization's (WHO's) Framework Convention on Tobacco Control and the MPOWER package of interventions. Part 2 ends with a consideration of scenarios for the future of the pandemic.
Sujet(s)
Trouble lié au tabagisme/économie , Trouble lié au tabagisme/prévention et contrôle , Adolescent , Adulte , Facteurs âges , Sujet âgé , Pays en voie de développement , Femelle , Humains , Mâle , Adulte d'âge moyen , Facteurs sexuels , Fumer/économie , Fumer/épidémiologie , Facteurs socioéconomiques , Trouble lié au tabagisme/épidémiologie , Jeune adulteRÉSUMÉ
BACKGROUND: In Japan, tobacco smoking is one of the main avoidable causes of disease and death. Although the benefits of smoking cessation for reducing disease risk and increasing longevity have been extensively documented, a relatively low proportion of Japanese smokers currently express a willingness to quit. This study attempted to quantify future reduction in the burden of smoking-attributable disease that could result from increases in smoking cessation. METHODS: A simulation model was developed to project changes in mortality in Japan associated with increased quit attempts and use of nicotine replacement therapy (NRT) among smokers, incorporating data on smoking prevalence, cause-specific mortality rates, quitting behaviour and NRT use and effectiveness. RESULTS: Approximately 46 000 lung cancer deaths and 56 000 cardiovascular disease deaths could be avoided over 20 years if the proportion of smokers making a quit attempt per year gradually increased to current US levels over 20 years. If each of these quit attempts were aided by NRT, the estimates of avoidable deaths would increase to 64 000 for lung cancer and 78 000 for cardiovascular disease. In this model, negligible deaths were avoided due to decreased smoking initiation over the 20-year simulation. CONCLUSION: Smoking cessation can have measurable short-term impacts on the smoking-related mortality burden in Japan. However, to achieve these gains, tobacco control policies should focus both on increasing smokers' willingness to quit and providing the support and therapies to increase the likelihood that smoking cessation attempts will succeed.
Sujet(s)
Arrêter de fumer/statistiques et données numériques , Prévention du fait de fumer , Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Maladies cardiovasculaires/mortalité , Femelle , Prévision , Gangliostimulants/administration et posologie , Promotion de la santé/statistiques et données numériques , Promotion de la santé/tendances , Humains , Japon/épidémiologie , Tumeurs du poumon/mortalité , Mâle , Adulte d'âge moyen , Modèles statistiques , Nicotine/administration et posologie , Antagonistes nicotiniques/administration et posologie , Prévalence , Appréciation des risques , Fumer/mortalité , Résultat thérapeutiqueRÉSUMÉ
Exhaled breath collection is used to identify and monitor inflammatory or oxidative components in breath. Exhaled breath sample collection is noninvasive and would greatly benefit human pollutant exposure research. We demonstrate the efficacy of exhaled breath collection and analysis in two human exposure studies to ozone (O(3)) and diesel exhaust, respectively. O(3) study: we collected exhaled breath (gas phase) from healthy human volunteers (age 18-35 years, 12 subjects) immediately before and after exposure to filtered air or 0.4 ppm O(3) for 2 h with and without intermittent exercise. Six subjects received antioxidant supplementation for 2 weeks before their O(3) exposure, while the remaining six subjects received placebo treatments. We demonstrate increased amounts of non-polar carbonyls exhaled immediately post O(3) exposure. The O(3)-induced increase in exhaled carbonyl concentrations was attenuated in the group receiving antioxidants. Our data demonstrate that exhaled exposure biomarkers can be measured in the breath gas phase in humans exposed to O(3). Diesel study: we collected exhaled breath condensate (EBC; liquid phase) from healthy human volunteers (age 18-40 years; 10 subjects) immediately before, immediately after and 20 h post filtered air or diesel exhaust (106 ± 9 µg m(-3)) exposure. Clean air and diesel exposures were separated by 3 weeks to 6 months. We obtained reproducible intra-subject EBC volumes and total protein concentrations across our six collection time points. Diesel exposure did not affect either EBC volume or total protein concentrations. Our data demonstrated EBC volume and total protein reproducibility over several months. Volume and total protein concentration may serve as normalizing factors for other EBC constituents.
RÉSUMÉ
Epidemiological studies have implicated zinc (Zn2+) in the toxicity of ambient particulate matter (PM) inhalation. We previously showed that exposure to metal-laden PM inhibits protein tyrosine phosphatase (PTP) activity in human primary bronchial epithelial cells (HAEC) and leads to Src-dependent activation of EGFR signaling in B82 and A431 cells. In order to elucidate the mechanism of Zn2+-induced EGFR activation in HAEC, we treated HAEC with 500 microM ZnSO4 for 5-20 min and measured the state of activation of EGFR, c-Src and PTPs. Western blots revealed that exposure to Zn2+ results in increased phosphorylation at both trans- and autophosphorylation sites in the EGFR. Zn2+-mediated EGFR phosphorylation did not require ligand binding and was ablated by the EGFR kinase inhibitor PD153035, but not by the Src kinase inhibitor PP2. Src activity was inhibited by Zn2+ treatment of HAEC, consistent with Src-independent EGFR transactivation in HAEC exposed to Zn2+. The rate of exogenous EGFR dephosphorylation in lysates of HAEC exposed to Zn2+ or V4+ was significantly diminished. Moreover, exposure of HAEC to Zn2+ also resulted in a significant impairment of dephosphorylation of endogenous EGFR. These data show that Zn2+-induced activation of EGFR in HAEC involves a loss of PTP activities whose function is to dephosphorylate EGFR in opposition to baseline EGFR kinase activity. These findings also suggest that there are marked cell-type-specific differences in the mechanism of EGFR activation induced by Zn2+ exposure.
Sujet(s)
Bronches/métabolisme , Cellules épithéliales/métabolisme , Récepteurs ErbB/physiologie , Protein Tyrosine Phosphatases/antagonistes et inhibiteurs , Muqueuse respiratoire/métabolisme , Zinc/toxicité , Technique de Western , Cations divalents , Cellules cultivées , Humains , Phosphorylation , Muqueuse respiratoire/cytologie , Transduction du signal , Techniques de culture de tissus , src-Family kinases/métabolismeRÉSUMÉ
OBJECTIVE: To examine the effect of ozone exposure and vegetable juice supplementation on plasma and lung macrophage concentrations of carotenoids. DESIGN: A randomized trial. SETTING: Subjects were exposed to ambient air prior to antioxidant supplementation and to ozone after antioxidant supplementation or placebo. Exposures occurred while exercising intermittently in a controlled metabolic chamber at the Human Studies Division, US EPA. SUBJECTS: In all, 23 healthy subjects between ages of 18 and 35 y. INTERVENTIONS: Subjects consumed a low fruit and vegetable diet for 3 weeks. After the first week, subjects underwent a sham exposure to filtered air with exercise, followed by bronchoalveolar lavage (BAL). Subjects were randomly assigned into supplement (one can vegetable juice, vitamins C and E daily) or placebo (orange soda, placebo pill daily) groups for 2 weeks. After the 2-week intervention, subjects were exposed to 0.4 ppm (784 microg/m(3)) ozone for 2 h with exercise followed by BAL. Blood samples were drawn before, immediately after and 3 h postexposure on each exposure day. The concentrations of nine carotenoids were determined by HPLC in BAL macrophages and plasma samples. RESULTS: Plasma concentrations of all the carotenoids that were present in the vegetable juice (except cis-beta-carotene) increased significantly in the supplemented group. Lung macrophage alpha-carotene concentrations increased significantly, lycopene isomers increased slightly, and all other carotenoids decreased (nonsignificantly) in the supplementation group following the intervention. Ozone exposure resulted in decreases in several carotenoids in plasma of the placebo group, but not in the supplemented group. CONCLUSIONS: Lung macrophage concentrations of carotenoids can be manipulated by diet. Ozone is a potent environmental oxidant that appears to reduce plasma carotenoids in nonsupplemented individuals.
Sujet(s)
Antioxydants/administration et posologie , Caroténoïdes/administration et posologie , Caroténoïdes/sang , Régime alimentaire , Macrophages alvéolaires/effets des médicaments et des substances chimiques , Ozone/métabolisme , Adolescent , Adulte , Antioxydants/métabolisme , Antioxydants/pharmacologie , Lavage bronchoalvéolaire , Compléments alimentaires , Exercice physique/physiologie , Fruit , Humains , Macrophages/effets des médicaments et des substances chimiques , Macrophages/métabolisme , Macrophages alvéolaires/métabolisme , Oxydants photochimiques/effets indésirables , Oxydants photochimiques/métabolisme , Ozone/effets indésirables , Placebo , États-Unis , Environmental Protection Agency (USA) , LégumesRÉSUMÉ
OBJECTIVE: This paper reviews secondhand smoke (SHS) exposure and diseases and symptoms of the upper airway, including the sinuses. Risks to flight attendants, who were occupationally exposed until smoking was banned on all flights, are emphasised. DATA SOURCES: A systematic database search was conducted; the US Surgeon General's reports and other major reviews were evaluated. Literature summarised by National Research Council (NRC) reports on the airline cabin environment are included. STUDY SELECTION: A limited number of research publications on adults were identified; these are included. Many studies cited by the NRC were never published and information is taken directly from the reports. DATA EXTRACTION: Data from observational studies of cabin crews and the general public were extracted from surveys; exposure monitoring of cabin crews is reported. Data from controlled exposure studies are included; most are challenge studies using volunteers screened for sensitivity to SHS. DATA SYNTHESIS: Evidence shows that active and passive smoking cause upper airway diseases, including sinonasal and laryngeal cancers in adult active smokers. Experimental studies indicate that brief exposures to SHS result in nasal mucosa inflammation. However, direct evidence on sinusitis is limited. CONCLUSIONS: Evidence does not show a strong connection between active smoking and sinusitis, and active smokers have substantial exposures to SHS. However, extrapolation of these studies to cabin crews needs to be cautious, as other environmental conditions may increase risk for upper airway disease and symptoms. Surveys of cabin crews, while flawed, consistently indicate high rates of upper airway symptoms.
Sujet(s)
Maladies professionnelles/étiologie , Maladies de l'appareil respiratoire/étiologie , Pollution par la fumée de tabac/effets indésirables , Adulte , Médecine aérospatiale , Véhicules de transport aérien , Enfant , Maladies des oreilles/étiologie , Maladies des oreilles/physiopathologie , Humains , Maladies du nez/étiologie , Maladies du nez/physiopathologie , Maladies professionnelles/physiopathologie , Exposition professionnelle/effets indésirables , Maladies de l'appareil respiratoire/physiopathologie , Sinusite/étiologieSujet(s)
Polluants atmosphériques radioactifs , Pollution de l'air intérieur , Exposition environnementale , Tumeurs du poumon/mortalité , Tumeurs radio-induites/mortalité , Radon/effets indésirables , Logement , Humains , Tumeurs du poumon/étiologie , Mâle , Mine , Modèles théoriques , Facteurs de risqueSujet(s)
Polluants atmosphériques , Santé environnementale , Surveillance de l'environnement , Politique publique , Maladies de l'appareil respiratoire , Polluants atmosphériques/effets indésirables , Polluants atmosphériques/normes , Surveillance de l'environnement/législation et jurisprudence , Surveillance de l'environnement/méthodes , Surveillance de l'environnement/normes , Surveillance épidémiologique , Humains , Maladies de l'appareil respiratoire/épidémiologie , Maladies de l'appareil respiratoire/étiologie , Maladies de l'appareil respiratoire/mortalité , États-Unis/épidémiologieRÉSUMÉ
In this issue, Glantz and Ong offer a powerful analysis of the tobacco industry's attempt to discredit the scientific evidence on passive smoking, particularly the industry's use of the label "junk science." Environmental epidemiologic studies in other arenas have also been targets for the "junk science" label. Lessons for researchers involved in high-stakes issues in the public policy arena include a need for awareness of competing interests, for transparency concerning funding, and for adherence to rigorous quality assurance and peer review practices. The goal of "sound science" seems an admirable one; it should not, however, be used to dismiss available but uncertain evidence in order to delay action.
Sujet(s)
Conflit d'intérêts , Études épidémiologiques , Politique publique , Industrie du tabac/normes , Pollution par la fumée de tabac/effets indésirables , Cancérogènes/classification , Humains , Soutien financier à la recherche comme sujet , Appréciation des risques , États-Unis , Environmental Protection Agency (USA)RÉSUMÉ
This study tested the hypothesis that certain secretory phospholipase A(2) (sPLA(2)) isotypes act in a cytokine-like fashion through cell surface receptors to influence mast cell survival. Initial experiments revealed that sPLA(2) activity and sPLA(2) receptor expression are increased, and mast cells lost their capacity to maintain membrane asymmetry upon cytokine depletion. Groups IB and III, but not group IIA PLA(2), prevented the loss of membrane asymmetry. Similarly, group IB prevented nucleosomal DNA fragmentation in mast cells. Providing putative products of sPLA(2) hydrolysis to cytokine-depleted mast cells did not influence survival. Furthermore, catalytic inactivation of sPLA(2) did not alter its capacity to prevent apoptosis. Inhibition of protein synthesis using cycloheximide or actinomycin reversed the antiapoptotic effect of sPLA(2). Additionally, both wild-type and catalytically inactive group IB PLA(2) induced IL-3 synthesis in mast cells. However, adding IL-3-neutralizing Ab did not change Annexin V(FITC) binding and only partially inhibited thymidine incorporation in sPLA(2)-supplemented mast cells. In contrast, IL-3-neutralizing Ab inhibited both Annexin V(FITC) binding and thymidine incorporation in mast cells maintained with IL-3. sPLA(2) enhanced phosphoinositide 3'-kinase activity, and a specific inhibitor of phosphoinositide 3'-kinase reversed the antiapoptotic effects of sPLA(2). Likewise, sPLA(2) increased the degradation of I-kappaBalpha, and specific inhibitors of nuclear factor kappa activation (NF-kappaB) reversed the antiapoptotic effects of sPLA(2). Together, these experiments reveal that certain isotypes of sPLA(2) enhance the survival of mast cells in a cytokine-like fashion by activating antiapoptotic signaling pathways independent of IL-3 and probably via sPLA(2) receptors rather than sPLA(2) catalytic products.
Sujet(s)
Cellules de la moelle osseuse/immunologie , Mastocytes/immunologie , Phospholipases A/métabolisme , Récepteurs de surface cellulaire/métabolisme , Animaux , Annexine A5/métabolisme , Apoptose , Acide arachidonique/pharmacologie , Cellules de la moelle osseuse/cytologie , Survie cellulaire , Interleukine-3 , Isoenzymes/métabolisme , Lysophospholipides/pharmacologie , Mastocytes/cytologie , Souris , Facteur de transcription NF-kappa B/antagonistes et inhibiteurs , Inhibiteurs des phosphoinositide-3 kinases , Liaison aux protéines , Biosynthèse des protéines , Récepteurs à la phospholipase A2 , Transduction du signal , Transcription génétiqueRÉSUMÉ
BACKGROUND: Alcohol and tobacco, the primary etiologic agents for head and neck carcinoma (HNCA), cause other chronic diseases and may contribute to the high prevalence of comorbid conditions and generally poor survival of persons with HNCA. METHODS: The authors explored the prognostic role of comorbidity in persons with HNCA using Health Care Finance Administration Medicare (HCFA) files linked with the appropriate files of the Surveillance, Epidemiology, and End Results (SEER) Program. The Charlson comorbidity index was applied to in-patient data from the HCFA files. The SEER data were used to ascertain survival and identify persons with HNCA diagnosed from 1985 to 1993 (n = 9386). RESULTS: In a proportional hazards regression model adjusted for age and historic stage at diagnosis, race, gender, marital status, socioeconomic status, histologic grade, anatomic site, treatment, and pre-1991 diagnosis, Charlson index scores of 0, 1, and 2+ had estimated relative hazards (RHs) with 95 confidence intervals (CIs) of 1.00, 1.33 (95% CI, 1.21-1.47), and 1.83 (95% CI, 1.64-2.05), respectively (P value for trend < 0.0001). The adjusted RH for a Charlson index score of 1 or more compared with 0, using stratified models, was found to be greater in whites (RH, 1.55; 95% CI, 1.43-1.67) than blacks (RH, 1.24; 95% CI, 0.96-1.60), local (RH, 1.72; 95% CI, 1.50-1.96) versus distant stage (RH, 1.25; 95% CI, 1.00-1.56), and age 65-74 years (RH, 1.53; 95% CI, 1.38-1.69) versus age 85+ years (RH, 1.42; 95% CI, 1.09-1.84). CONCLUSIONS: This study establishes comorbidity as a predictor of survival in an elderly HNCA population and lends support to the inclusion of comorbidity assessment in prognostic staging of patients with HNCA diagnosed after 65 years of age.
Sujet(s)
Carcinome épidermoïde/mortalité , Tumeurs de la tête et du cou/mortalité , Sujet âgé , Sujet âgé de 80 ans ou plus , Carcinome épidermoïde/épidémiologie , Comorbidité , Femelle , Tumeurs de la tête et du cou/épidémiologie , Humains , Tumeurs du larynx/épidémiologie , Tumeurs du larynx/mortalité , Mâle , Tumeurs de la bouche/épidémiologie , Tumeurs de la bouche/mortalité , Tumeurs du pharynx/épidémiologie , Tumeurs du pharynx/mortalité , Pronostic , Modèles des risques proportionnels , Programme SEER , États-Unis/épidémiologieRÉSUMÉ
To investigate breast cancer risk in Hispanic and non-Hispanic White women, the authors conducted a population-based case-control study of New Mexican women during 1992-1994 using incident breast cancer cases aged 35-74 years and frequency-matched controls selected using random digit dialing. Activity type and weekly duration of usual nonoccupational physical activity were used to calculate weekly metabolic equivalent (MET)-hours of total and vigorous physical activity (> or =5 METs). Conditional logistic regression models were fitted to estimate the relative risk of breast cancer for levels of physical activity and to assess the difference in effects by ethnicity, body mass index, energy intake, and menopausal status. Vigorous physical activity was associated with reduced breast cancer risk in both Hispanic and non-Hispanic White women. Women in the highest category of vigorous activity had lower risk of breast cancer (adjusted odds ratio = 0.34, 95% confidence interval: 0.22, 0.51 for Hispanic; adjusted odds ratio = 0.60, 95% confidence interval: 0.41, 0.89 for non-Hispanic White women) compared with women reporting no vigorous physical activity. Both pre- and postmenopausal Hispanic women showed decreasing risk with increasing level of activity. Physical activity was protective only among postmenopausal non-Hispanic White women. The effects of physical activity were independent from reproductive factors, usual body mass index, body mass index at age 18, adult weight gain, and total energy intake.
Sujet(s)
Tumeurs du sein/épidémiologie , Exercice physique , Hispanique ou Latino/statistiques et données numériques , /statistiques et données numériques , Adulte , Sujet âgé , Indice de masse corporelle , Études cas-témoins , , Ration calorique , Femelle , Humains , Fonctions de vraisemblance , Modèles logistiques , Adulte d'âge moyen , Nouveau Mexique/épidémiologie , Enregistrements , Facteurs de risque , Enquêtes et questionnairesRÉSUMÉ
BACKGROUND: In the Collaborative Study on the Genetics of Asthma, 314 families with 2584 subjects were characterized for asthma and allergy. OBJECTIVE: The purpose of this investigation was to examine clinical heterogeneity observed in asthma and allergic characteristics among 3 ethnic groups (African American, white, and Hispanic family members). METHODS: Pulmonary function parameters and asthma associated phenotypes were compared among the ethnic groups. RESULTS: In comparison with the other groups, African American sibling pairs had a significantly lower baseline FEV(1) percent of predicted (P =.0001) and a higher rate of skin test reactivity to cockroach allergen (P =.0001); Hispanic sibling pairs had significantly more skin reactivity overall (P =.001); and white sibling pairs had significantly lower total serum IgE (P <.05). In addition, there were significantly more relatives with asthma among the African American families than among the white and the Hispanic families (P =.001). CONCLUSION: Although different environmental backgrounds should be considered, these clinical differences could be due to differences in genetic susceptibility among the ethnic groups, such as those suggested by our previous genome screen.